(Lib-Ebooks Com) 050420202258 PDF

Clinical
Manual of Surgery
S. Devaji Rao MS MNAMS FICS

Teaching Faculty, National Board of Examinations, Senior Consultant in
General Surgery, Surgical Gastroenterology and Surgical Oncology, St. Isabel’s
Hospital,
Chennai Meenakshi Multispecialty Hospital Ltd., and Kauvery Hospital,
Chennai, India
Table of Contents
Cover image
Title page
Copyright
Dedication
Contributors
Contributors of photographs
Preface
Acknowledgements
Abbreviations used
1. General
1. Introduction
1.1 How to use this manual
2. Patient and the surgeon
2.1 Introduction
2.2 Appearance
2.3 Behaviour
2.4 Doctor-patient relationship
2.5 Examination of the patient
2.6 Frank communication
2.7 Counselling
2.8 Management of patients in the hospital
2.9 Maintenance of records
2.10 Surgical ethics
2.11 Informed consent
3. Eliciting history
3.1 Introduction
3.2 Chief complaint*
3.3 History of present illness
3.4 Previous history of present complaint
3.5 Past medical history
3.6 History of drug intake and allergies
3.7 Social and personal history
3.8 Family history
3.9 History of immunization
3.10 Analysis of symptoms
3.11 Examining a child
3.12 Difficulties in history taking

4. General physical examination
4.1 Introduction
4.2 At the time of patient’s entry or separately
4.3 Eliciting history
4.4 Height and weight measurements
4.5 Examination of the patient on the couch
4.6 General system examination
4.7 Method of general physical examination
4.8 Conclusion
2. Symptoms and Signs
5. Dysphagia
5.1 Introduction
5.2 Surgical anatomy of oesophagus
5.3 Causes of dysphagia
5.4 Diseases of oesophagus
5.5 Clinical evaluation
6. Constipation
6.1 Introduction
6.2 Pathophysiology of constipation
6.3 Etiology of constipation
6.4 Organic causes of constipation
7. Obstructive jaundice
7.1 Introduction
7.2 Bilirubin metabolism
7.3 Anatomy of biliary system
7.4 Obstructive jaundice
7.5 Causes of obstructive jaundice
8. Gastrointestinal haemorrhage
8.1 Introduction
8.2 Causes of gastrointestinal haemorrhage
8.3 Pathological conditions
Summary
9. Lumps and swellings

9.1 Definition
9.2 Classification
9.3 Swellings of skin
9.4 Swellings of subcutaneous tissue
10. Ulcers
10.1 Definition
10.2 Parts of ulcer
10.3 Classifications of ulcers
10.4 Traumatic ulcers
10.5 Inflammatory ulcers
10.6 Vascular ulcers

10.7 Neoplastic ulcers
10.8 Miscellaneous ulcers
11. Sinuses and fistulae

11.1 Definitions
11.2 Aetiological classification of sinuses
11.3 Aetiological classification of fistulae
11.4 Regional classification of sinuses and fistulae
11.5 Sinuses and fistulae of parotid region
11.6 Sinuses and fistulae of mandibular and submandibular regions
11.7 Sinuses and fistulae of midline of neck
11.8 Sinuses and fistulae of lateral sides of neck
11.9 Sinuses and fistulae of chest
11.10 Sinuses and fistulae of abdomen
11.11 Sinuses and fistulae of loins
11.12 Sinuses and fistulae of groins
11.13 Sinuses and fistulae of right iliac fossa
11.14 Sinuses and fistulae of male genitalia
11.15 Sinuses and fistulae of perineal region
Sinuses of the back
11.16 Sinuses of bones and joints
11.17 Sinuses of feet
3. System and Region Based Diseases
12. Lymphatic system

12.1 Anatomy of lymphatic system
12.2 Causes of lymphadenopathy
12.3 Diseases of lymphatic system
12.4 Diseases of lymphatics
12.5 Diseases of lymph nodes
13. Arterial system

13.1 Surgical anatomy of arterial system
13.2 Diseases of arterial system
13.3 Symptoms of arterial system diseases
13.5 Special tests
14. Venous system

14.1 surgical anatomy of venous system
14.2 venous haemodynamics
14.3 diseases of venous system
14.4 symptoms of pathologies of venous system
14.5 clinical evaluation
14.6 special tests
15. Burns
15.1 Definitions
15.2 Anatomy of skin
15.3 Pathophysiology of burns
15.4 Classification of burns
15.5 Metabolic effects of burns
16. Brain
16.1 Development of brain
16.2 Surgical anatomy of brain
16.3 Intracranial lesions
16.4 Symptoms of intracranial lesions
17. Head injuries

17.1 Introduction
17.2 Surgical anatomy
17.3 Pathophysiology of unconsciousness in brain injury
17.4 Varieties of head injuries
17.5 Symptoms of head injuries
18. Face and oral cavity

18.1 development of face and oral structures
18.2 surgical anatomy of face
18.3 diseases of face
18.4 surgical anatomy of oral structures
18.5 diseases of oral cavity
18.6 symptoms of oral cavity pathologies
19. Injuries of face
19.1 surgical anatomy of facial skeleton
19.2 fractures of facial skeleton
20. Nose, nasal cavities and paranasal sinuses

20.1 development of nose, nasal cavities and paranasal sinuses
20.2 surgical anatomy
20.3 diseases of nose, nasal cavities and paranasal sinuses
20.4 diseases of nose
20.5 diseases of nasal cavities
20.6 diseases of paranasal sinuses
20.7 symptoms of pathologies of nose, nasal cavities and paranasal sinuses
21. Ears
21.1 development of ear and auditory canal
21.2 surgical anatomy of ear and auditory canal
21.3 diseases of external ear and auditory canal
21.4 diseases of middle ear
21.5 diseases of inner ear (affecting hearing)
21.6 diseases of inner ear (affecting balance)
21.7 symptoms of pathologies of ears
22. Pharynx and larynx

22.1 development of pharynx and larynx
22.2 surgical anatomy of pharynx and larynx
22.3 diseases of pharynx
22.4 diseases of larynx
22.5 diseases of larynx in adults
22.6 diseases of larynx in children
22.7 symptoms of pathologies of pharynx and larynx
23. Salivary glands

23.1 Development of salivary glands
23.2 Anatomy of salivary glands
23.3 Diseases of salivary glands
23.4 Symptoms of salivary gland diseases
24. Thyroid
24.1 Development of thyroid
24.2 Surgical anatomy of thyroid
24.3 Physiology
24.4 Diseases of thyroid
24.5 Symptoms of thyroid diseases
25. Neck
25.1 surgical anatomy of neck
25.2 midline swellings of neck
25.3 lateral swellings of neck

26. Thorax
26.1 Development of respiratory tract
26.3 Diseases of chest wall
26.4 Diseases of pleura
26.5 Diseases of trachea and bronchi
26.6 Diseases of lungs
26.7 Diseases of mediastinum
26.8 Symptoms of pathologies of chest
27. Thoracic injuries

27.1 Injuries of chest wall
27.2 Injuries of pleura
27.3 Injuries of lung parenchyma
27.4 Injuries of mediastinal structures
27.5 Symptoms of chest injuries
28. Breasts
28.1 Development of breasts
28.2 Surgical anatomy of breast
28.3 Physiology of breasts
28.4 Diseases and abnormalities of the breasts
28.5 Symptoms of breast diseases

29. Spine and spinal cord

29.1 Development of spine and spinal cord
29.2 Surgical anatomy of spine and spinal cord
29.3 Disorders and diseases of spine
29.4 Disorders of sacroiliac joints
29.5 Disorders and diseases of spinal cord
29.6 Abnormalities of craniovertebral junction
29.7 Symptoms of spine and spinal cord pathologies
30. Acute abdomen

30.1 Introduction
30.2 Acute inflammatory conditions of abdomen
30.3 Perforated bowel pathologies
30.4 Intestinal obstruction
30.5 Diseases causing intestinal obstruction
30.6 Adynamic lesion
30.7 Vascular conditions
30.8 Haemorrhagic conditions
30.9 Torsions
30.10 Colics
30.11 Extra abdominal causes of abdominal pain
30.12 Symptoms of patients with acute abdomen
31. Chronic abdominal illnesses
31.1 Introduction
31.2 Diseases of oesophagus, stomach and duodenum
31.3 Diseases of gallbladder
31.4 Diseases of pancreas
31.5 Diseases of intestines
31.6 Diseases of any part of gastrointestinal system
31.7 Symptoms of patients with chronic abdominal illnesses
32. Abdominal injuries

32.1 Introduction
32.2 Injuries of abdominal organs
32.3 Symptoms of injuries of abdominal organs
33. Abdominal lumps

33.1 Introduction
33.2 Lumps of abdominal wall
33.3 Lumps in the right hypochondrium
33.4 Lumps in the left hypochondrium
33.5 Lumps in the epigastrium
33.6 Lumps in the lumbar regions
33.7 Lumps in the umbilical region
33.8 Lumps in the iliac fossae
33.9 Lumps in the hypogastrium
34. Rectum and anal canal
34.1 Surgical anatomy of rectum and anal canal
34.2 Aetiological classification of anorectal diseases
34.3 Anorectal diseases
34.4 Symptoms of anorectal pathologies
34.5 Rectal examination
Remember
35. Herniae
35.1 Introduction
35.2 Classification of herniae
35.3 General features of herniae
35.4 Anatomical nomenclature
35.5 Groin herniae
35.6 Ventral herniae
35.7 Other herniae
35.8 Symptoms of hernia
36. Male genitalia

36.1 development of male genitalia
36.2 surgical anatomy of male genitalia
36.4 diseases and abnormalities of testis and epididymis
36.5 diseases of scrotum
36.6 symptoms of diseases of male genitalia
37. Urinary system
37.1 Development of urogenital system
37.2 Kidney and renal pelvis
37.3 Diseases of kidney and renal pelvis
37.4 Ureters
37.5 Diseases of ureters
37.6 Urinary bladder
37.7 Diseases of urinary bladder
37.8 Prostate
37.9 Diseases of prostate
37.10 Urethra
37.11 Diseases of urethra
37.12 Symptoms of urinary tract pathologies
Remember
38. Female genital system

38.1 Development of female genital tract
38.2 Surgical anatomy of female genital tract
38.3 Physiological response of female genital tract
38.4 Diseases of female genital tract
38.5 Symptoms of diseases of female genital tract
Remember
Remember
39. General orthopaedics

39.1 Introduction
39.2 Diseases of bones
39.3 Symptoms of pathologies of bones
40. Shoulder and arm

40.1 Shoulder joint
40.2 Traumatic lesions (fractures)
40.3 Nonfracture lesions of shoulder joint
40.4 Nontraumatic lesions of shoulder joint
40.5 Fracture of shaft of humerus
40.6 Symptoms of shoulder joint pathologies
41. Elbow and forearm

41.1 Elbow joint
41.4 Traumatic lesions of elbow joint
41.5 Nontraumatic lesions of elbow joint
41.6 Extra-articular disorders of elbow
41.7 Fractures of shafts of forearm bones
41.8 Symptoms of elbow joint pathologies
42. WRIST, hand and fingers

42.1 Wrist joint
42.2 Bones of the hand
42.3 Joints of the hand

42.4 Traumatic articular lesions of WRIST and hand
42.5 Traumatic lesions of carpal bones
42.6 Traumatic lesions of metacarpal bones
42.7 Traumatic lesions of phalanges
42.8 Nontraumatic articular lesions of wrist and hand
42.9 Extra-articular disorders of wrist and hand
42.10 Symptoms of pathologies of wrist, hand and fingers
43. Hands (soft tissues)

43.1 Development of hands
43.2 Surgical anatomy of hands
43.3 Diseases of hands
43.4 Symptoms of pathologies of hands
44. Pelvis, hip and thigh

44.1 Hip joint
44.2 Deformities of hip
44.3 Congenital lesions
44.4 Traumatic lesions of pelvis and hip
44.5 Nontraumatic lesions of hip joint
44.6 Extra-articular disorders of hip
44.7 Fracture of shaft of femur
44.8 Symptoms of hip joint pathologies
45. Knee and leg
45.1 Knee joint
45.2 Deformities of knee
45.3 Traumatic lesions of knee joint
45.4 Soft tissue injuries of knee joint
45.5 Nontraumatic lesions of knee joint
45.6 Extra-articular disorders of knee
45.7 Fractures of shafts of leg bones
45.8 Symptoms of knee joint pathologies
46. Ankle, foot and toes

46.1 Ankle joint
46.2 Anatomy of foot
46.3 Deformities of foot
46.4 Traumatic lesions of ankle joint
46.5 Soft tissue injuries of ankle joint
46.6 Injuries of tarsal bones
46.7 Nontraumatic lesions of ankle and foot
46.8 Extra articular disorders of ankle and foot
46.9 Symptoms of ankle, foot and toe pathologies
47. Feet (soft tissues)

47.1 Development of feet
47.3 Diseases of the feet
47.4 Symptoms of pathologies of feet

48. Muscles, tendons and fasciae

48.1 Introduction
48.3 Diseases of muscles, tendons and fasciae
48.4 Symptoms of pathologies of muscles, tendons and fasciae
49. Peripheral nerves

49.1 Surgical anatomy of nerves of upper limb
49.2 Surgical anatomy of nerves of lower limb
49.3 Causes of peripheral nerve disorders
49.5 Symptoms of peripheral nerve pathologies
4. Polytrauma
50. Polytrauma
50.1 Introduction
50.2 Preparation
50.3 Receiving the patient
50.4 Primary survey and resuscitation
50.5 Secondary survey
50.7 Conclusion
Index
Copyright
Clinical Manual of Surgery, 1/e
Rao
© 2015 Reed Elsevier India Private Limited. All rights reserved.
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This book and the individual contributions contained in it are protected under
copyright by the Publisher (other than as may be noted herein).
Illustrations rendered by Dr Kirthana Devaji Rao, BDS.
ISBN: 978-81-312-3795-3
e-Book ISBN: 978-81-312-3871-4
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Dedication
Dedicated to the parents and teachers of all the contributors
Contributors
N. Anandan, MS FRCS Dip Urol (Lon)
Consultant Urologist, Andrologist and Laparoscopic Surgeon St. Isabel’s
Hospital, Kauvery Hospital and Nova Specialty Hospital
Former Professor of Urology Sri Ramachandra Medical College and Research
Centre Chennai

S.M. Balaji, MDS PhD, Oral and Faciomaxillary Surgeon and Director
Balaji Dental and Craniofacial Hospital Chennai

A. Chandrasekhar Rao, MS FICS FAIS FRSH FAGE FIC, Consultant
Surgeon St. Isabel’s Hospital & Apollo Specialty Hospital Chennai

Chithra Subramanian, MBBS DGO DNB, Consultant Obstetrician &
Gynecologist St. Isabel"s Hospital, Chennai

S. Devaji Rao, MS MNAMS FICS
Consultant Surgeon St. Isabel’s Hospital; Chennai Meenakshi Multispecialty
Hospital Ltd. and Kauvery Hospital
Former Surgeon Apollo Specialty Hospital & Institute Hospital, IIT, Chennai
Teaching Faculty National Board of Examinations of India

M. Harish, MD
Assistant Professor Department of Pulmonology Sree Balaji Medical College
and Hospital, Chennai
Consultant Pulmonologist Chennai Meenakshi Multispecialty Hospital and
Kauvery Hospital Chennai

Jacinth Cornelius, MS DLO
Former Professor of ENT Surgery Madras Medical College
Consultant ENT Surgeon St. Isabel’s Hospital Chennai

V. Jayaraman, MS MCh MNAMS DNB PhD FICS, Professor and Head
Burns, Plastic and Reconstructive Surgery Kilpauk Medical College; K. K.
Childs Trust Hospital; Sooriya Hospital Chennai

Lakshmi Nagarajan, MBBS DGO, Consultant Obstetrician and
Gynecologist St. Isabel’s Hospital Chennai

N. Mohan, MS FICS FAIS
Emeritus Professor Tamil Nadu Dr. MGR Medical University
Former Professor and Head of Surgery Kilpauk Medical College and Govt.
Royapettah Hospital
Consultant Surgeon BRS Hospitals, Chennai

R. Priya, MD DM, Consultant Neurophysician Trichy, Tamil Nadu

M.G. Rajamanickam, MS MCh
Professor of Urology Sri Ramachandra Medical College and Research Centre
Former Professor of Urology Kilpauk Medical College and Govt. Royapettah
Hospital
Consultant Urologist St. Isabel’s Hospital and Bharathiraja Hospitals Chennai

R. Ravi, MS MCh, Consultant Plastic Surgeon St. Isabel’s Hospital and
Chennai Meenakshi Multispeciality Hospital Ltd. Chennai

K.S. Ravishankar, MS FICS
Professor of Surgery Sree Balaji Medical College and Hospital
Consultant Surgeon St. Isabel’s Hospital Chennai

N. Sekar, MS MNAMS MCh FICS
Consultant Vascular Surgeon Malar Hospital and Apollo Hospital
Former Professor of Vascular Surgery Madras Medical College and Govt.
General Hospital Chennai

G. Sivakumar, MS FICS FAIS
Former Professor of Surgery Madras Medical College and Govt. General
Hospital
Consultant Surgeon BSS Hospital and St. Isabel’s Hospital Chennai

K. Sridhar, MS MCh
Vice President (Medical) and Director Institute of Craniofacial Surgery and
Department of Plastic Surgery SRM Institutes for Medical Sciences, Chennai
Former Senior Consultant Plastic Surgeon Apollo Hospitals
Senior Advisor, VHS Leprosy Project
Former Assistant Professor of Plastic Surgery Stanley Medical College and
Govt. Stanley Hospital Chennai

A.V. Srinivasan, MD DM PhD FAAN FIAN FRCP
Emeritus Professor Tamil Nadu Dr. MGR Medical University
Former Head Madras Institute of Neurology Madras Medical College and Govt.
General Hospital Chennai

V. Srinivasan, MS FICS
Former Professor of Surgery Sri Ramachandra Medical College and Research
Centre
Consultant Surgeon VK Nursing Home Chennai

Sripriya Rajan, MS MRCS MNAMS DNB (Surgical Oncology),
Consultant in Minimally Invasive Surgery and Surgical Oncology Apollo
Specialty Hospital Chennai

K.R. Suresh Bapu, MS MCh
Consultant Neurosurgeon St. Isabel’s Hospital, and Apollo Speciality Hospital
Former Professor of Neurosurgery Madras Medical College and Govt. General
Hospital Chennai

V. Thulasiraman, MS D Ortho
Former Professor of Orthopedic Surgery Madras Medical College and Govt.
General Hospital
Consultant Orthopedic Surgeon Trinity Acute Care Hospital, Chennai

P.S. Venkatesh Rao, MS DNB FICS
Consultant Endocrine and Laparoscopic Surgeon Kadri Clinic, MSR Memorial
Hospital and Columbia Asia Hospital, Bangalore
Former Teaching Faculty CMC Vellore; AIMS and UCMS, New Delhi; MS
Ramiah Medical College, Bangalore

Contributors of photographs
C.T. Alagappan, MS D Ortho, Orthopedic Surgeon Chennai Meenakshi
Multispecialty Hospital Chennai
Bhavna Devaji Rao, BDS, Dental Surgeon Smile Forum Dental Clinic
Chennai
K. Dakshinamoorthy, MS FACS FICS FAIS, Consultant Surgeon Nagai
Hospitals Nagapattinam, Tamil Nadu
R. Emmanuel, MD, Consultant Radiologist and Director Bharat Scans,
Chennai
V. Ganesan, MBBS DMRD, Consultant Radiologist VG Scans, Chennai
M. Kanagavel, MBBS MRCS DNB, Consultant Surgeon St. Isabel’s
Hospital Chennai
Kirthana Devaji Rao, BDS
Dental Surgeon St. Isabel’s Hospital, Smile Forum and Smile Craft Dental
Clinics
Former Lecturer Sathyabama University Dental College Chennai
B. Loganathan, BSc MD DV, Former Professor and Head Dept. of Sexually
Transmitted Diseases Kilpauk Medical College and Govt. Royapettah Hosital
Chennai
K.M. Lakshmipathy, MBBS PGDNM MNCSI PhD, Specialist in Nuclear
Medicine and PET–CT Vijaya Nuclear Scans and Therapy Chennai
M. Mahender, BSC MBBS DLO MS, Consultant ENT Surgeon Prabhu
ENT Clinic; BSS Hospital Chennai
Mani Veeraraghavan, MBBS Dip in Endosurgery, Endoscopist and
Director The Endoscopy Centre Chennai
T.V. Raja, MBBS D Ortho DAc DCr FAMS FRSH, Orthopedic Surgeon
and Foot Specialist Visa Hospital Chennai
R. Rajaraman, MS MCh
Professor and Head Centre for Oncology and Department of Surgical Oncology
Govt. Royapettah Hospital
Consultant Surgical Oncologist Apollo Specialty Hospital and Rai Memorial
Medical Centre Chennai
RavisankarG.Pillai, MBBS MRCS MD (Urology) Dip Urology ChM (Urol)
FEBU, Specialist Urologist Royal Bahrain Hospital, Al Salmaniya Manama,
Kingdom of Bahrain
N. Sivakataksham, MD DM, Cardiologist Siva’s Cardio Care Chennai
Usha Dorairajan, MS FRCS FMAS, Professor of Surgery Govt. Kilpauk
Medical College and Hospital Chennai
Preface
S. Devaji Rao, Chennai 2015
Many textbooks in surgery are available today, but manuals in clinical surgery
are only few. Methods of clinical examination in surgery remain to be the same,
but newer diagnostic techniques have pushed them to the backseat and changed
the scenario. It appears that high-tech investigations have reduced the necessity
of clinical examination in many spheres of medicine, but in reality, it is not true.
“The diagnostic problem of today

Has greatly changed – the changes have come to stay;
We all have to confess, though with a sigh
On complicated tests we much rely
And use too little hand and ear and eye”
(The Acute Abdomen in Rhyme, Zachary Cope, 1881–1974)
Improper and hurried clinical examination puts the patient in wrong

directions, and confusion and havoc are the final results. Also, the clinician may
end in the court of law. Jules Henri Poincare, France’s greatest mathematician,
theoretical physicist and a philosopher of science said, “a small error in the
former will produce an enormous error in the latter”, which aptly fits here.
We have to better ourselves and need to learn every day, however much one is
experienced, and it should be realized, the more curious we are, more we find to
learn. With the advent of the Internet, patients are also better informed, and feel
that they have the right to know about their illnesses. We need to communicate
in a simple language to make them understand their problems. For all this, a
strong foundation in clinical examination continues to be necessary.
General surgery has branched and branched, to have many specialties and
super specialties, and making a book like this by one person is very difficult. I
have utilized the knowledge of super specialists in the preparation of this first of
its kind multi-author book. All the contributors are keen willing teachers in their
own spheres and have a flare to see that the younger generation benefits.
The chapters have been designed in such a way that the students orient with
the developmental and surgical anatomy (which they have already learnt in
detail) and various pathologies (which they are going to learn in ensuing days)
before they start eliciting the history, so that, they know what to ask. Colour
photographs are used mostly to enhance clarity and reality, as many cases in
surgery are spotters. After coming to a reasonable differential diagnosis from the
history, they analyse the symptoms mentally to arrive at a reasonable diagnosis.
The following physical examination gives the working clinical diagnosis. They
should ask for the relevant investigations to make a final diagnosis. However, it
is emphasized that the details of pathologies given in this manual do not replace
those in a standard textbook. The value addition to this manual is the analysis of
symptoms done individually in every chapter for making the understanding very
clear.
William Fry (1889–1963) said, “God gave you ears, eyes and hands, use them
on the patient in that order”, which is very relevant for clinical examination.
This manual should be read cover to cover, without omitting any detail, to
have a complete understanding, which will help the students to develop the skills
in communication, clinical examination, objective assessment, investigation and
treatment planning, as they continue to be important as ever.
Preparing such a manual is not an easy task, and has taken years of
preparation and homework, and the team of contributors have made honest
contributions. It is said, “Teamwork divides the task and doubles the success”.
This manual has been evolved to rekindle the interest in students, the desire to
improve the art of clinical diagnosis, and hope this achieves the desired result.
Acknowledgements
S. Devaji Rao, Chennai 2015
The desire to make a book of this nature was driven by the non-availability of a
down-to-earth fundamental book on clinical surgery. The dwindling of clinical
examination methods among the students, who seem to be depending on the
newer expensive investigations have motivated me to make a book dealing with
the basic fundamentals of clinical examination. Today, as specializations have
mushroomed to a great extent and one man to write a book of this nature may
not be adequate, hence, the involvement of many contributors who are greats in
their respective specialities.
My sincere thanks go to all my colleagues, who have given me the support by
contributing the chapters and photographs to the book. My special thanks go to
my colleagues Dr Mala Shankar, Dr Ranjani Nandakumar, Dr K. S. Ravishankar
and Dr N. Mohan who took the responsibility of going through some chapters
and gave suggestions and corrections.
Detailed chapter corrections were done by my daughter Dr. Bhavna Rao, and
above all, I express my very sincere thanks to my daughter Dr Kirthana Rao for
patiently drawing the computer-aided illustrations.
I had to borrow a sizeable number of photographs from many of my
colleagues (listed on page ix), and I immensely thank Dr R. Emmanuel of Bharat
Scans, Chennai for arranging to supply the radiology photographs coordinating
with his colleagues, Dr Karthikeyan, Dr H. Ramesh, Dr Sathyan, Dr Thanuja and
Dr Reena Yadav.
My grateful thanks to my beloved wife, Kalpana, for the extreme patience and
tolerance to my involved preoccupation during the long years of preparation of
this manual.
I am grateful to all those working for Elsevier, for their expertise in shaping
this edition.
Abbreviations used
ACTH Adrenocorticotrophic hormone
AFP Alpha fetoprotein
AFRS Allergic fungal rhino sinusitis
ANF Antinuclear factor
AOM Acute otitis media
APD Acid peptic disease
Beta-HCG Human chorionic gonadotrophin
BPV Benign positional vertigo
CBD Common bile duct
CECT Contrast-enhanced computerized tomography
CMV Cytomegalovirus
COPD Chronic obstructive pulmonary disease
CSF Cerebrospinal fluid
CSOM Chronic suppurative otitis media
CT Computerized tomography
DIP joint Distal interphalangeal joint
DNA Deoxyribonucleic acid
DSA Digital subtraction angiography
DVT Deep vein thrombosis
E coch gram Electro-cochleo gram
EBV Ebstein–Barr virus
ELISA Enzyme-linked immunosorbent assay
ENG Electronystagmo gram
ERCP Endoscopic retrograde cholangiopancreatography
ESR Erythrocyte sedimentation rate
EUS Endoscopic ultrasound
FESS Fiberoptic endoscopic sinus surgery
FNAC Fine needle aspiration cytology
FTA-Abs test Fluorescent treponemal antibody absorption test
GCS Glasgow coma scale
GERD Gastroesophageal reflux disease
GH Growth hormone
GIST Gastrointestinal stromal tumour
HbF Fetal haemoglobin
HbS Haemoglobin of sickle cell anaemia
HIDA Hepatobiliary iminodiacetic acid
HIV Human immunodeficiency virus
HPE Histopathological examination
HRCT High-resolution computerized tomography
IBS Irritable bowel syndrome
ICP Intracranial pressure
ICT Intracranial tension
IgA Immunoglobulin A
ITP Idiopathic thrombocytopenic purpura
IVU Intravenous urography
LP Lumbar puncture
MDCT Multi-detector computerized tomography
MEN Multiple endocrine neoplasia
MPR Multiplanar reformation
MRA Magnetic resonance angiography
MRCP Magnetic resonance cholangiopancreatography
MRI Magnetic resonance imaging
NSAID Non-steroidal anti-inflammatory drug
OME Otitis media with effusion
PCR Polymerase chain reaction
PET Positron emission tomography
PIP joint Proximal interphalangeal joint
PSC Primary sclerosing cholangitis
PTA Post traumatic amnesia
PTC Percutaneous transhepatic cholangiography
RBC Red blood corpuscle
RNA Ribonucleic acid
SAP Serum alkaline phosphatase
SEPS Subfascial endoscopic perforator surgery
SNHL Sensorineural hearing loss
SOL Space occupying lesion
TPHA test Treponema pallidum haemagglutination test
TRH Thyrotropin-releasing hormone
TRUS Transrectal ultrasonography
TSH Thyroid-stimulating hormone
TUR Trans-urethral resection
UDCA Ursodeoxycholic acid
US Ultrasonography
VDRL Venereal Diseases Research Laboratory
VGP Visible gastric peristalsis
VP shunt Ventriculo-peritoneal shunt
PA R T I
General
OUTLINE
1. Introduction
2. Patient and the surgeon
3. Eliciting history
4. General physical examination

CHAPTER 1
Introduction
CHAPTER OUTLINE
1.1. How to use this manual 02
• While evaluating an organ 02
• While evaluating a symptom 03
• While evaluating a sign 03
Clinical examination is the cornerstone of good clinical practice, more so the

history taking. Good doctors are still admired for their ability to distil the
information from history, their clinical skills, their attitude towards patients, and
their knowledge of diseases and disorders.
The patients quickly recognise doctors who demonstrate interest, empathy and
concern. They seek out to doctors who possess appropriate skills and attitude
towards them. History taking is an art by itself, which is the first step in clinical
evaluation of the patient. This consists of the doctor listening to the patient,
analyzing the information heard, and then addressing them leading questions
without hurting their sentiments. At the end, the doctor’s mind is flooded with
information about the patient, but he distils the right and appropriate
information, before he touches the patient for examination.
The doctors, with this state of mind, approach the patients’ body without
hurting them during their physical examination, and also giving adequate
privacy. The mind of the doctor gets further loaded with the physical findings to
enumerate the list of illnesses the patient could have, and investigate or treat
accordingly.
While examining a child, it should be remembered that the doctor needs to
consider the anxious parents also.
The tact of clinical examination can be summarized by an acronym HELP.
• H–History
• E–Examination
• L–Logical deduction
• P–Plan of management
By the invention and introduction of newer technologies in medicine, clinical
medicine is given lesser importance, and errors in clinical diagnosis have
become aplenty. This has led to more of unwanted and unwarranted
investigations, which may dilute the entire issue, lead to erroneous diagnosis,
and increased expenditure to the patients. The clinical medicine, though given a
second priority, still is the most important and undisputed part of clinical
practice.
In this manual, some of common symptoms like dysphagia and constipation,
and signs like gastrointestinal hemorrhage are dealt with special attention. Every
system in the human body is taken into consideration for clinical examination, as
a surgeon, whichever speciality he is interested in, may ultimately have to know
everything about every part of human body as they are all interlinked. Each
chapter starts with a comprehensive presentation of the developmental and
surgical or applied anatomy to replenish the minds of the fresh clinical students,
who are already familiar with them. The pathologies are given in a concise form,
so as to give an idea of what they are going to face in the forthcoming
examination procedure. The symptoms of all the systems are analysed in detail,
at the appropriate places, so as to make the history eliciting meaningful and
patient friendly. Every step of examination is made extremely fundamental so
that there is no ambiguity.
1.1 How to use this manual
While evaluating an organ (e.g., breast)

• The students should go directly to Chapter 28, read it from the beginning to
understand the basics of development, anatomy and pathology, so that they
are ready with all the details of breast diseases.
• The next step is to read the symptom analysis which will guide them as to
how they should go about evaluating the patient.
• With all these details in mind, they should ask the patient the questions listed
in the manual, and analyze the symptoms to get a reasonable diagnosis.
• After that, the doctors should physically examine the patient as described in
the manual to reach a clinical diagnosis by analyzing the physical findings.
• Relevant investigations are advised based on the clinical diagnosis, taking
guidance from the list provided at the end of the chapter.
While evaluating a symptom

• Some symptoms may denote the system without any confusion, for example,
hematuria indicates pathology of urological system, and the student may go
direct to Chapter 37, and go on with the examination of the patient.
• Many symptoms, like abdominal and back pain, do not indicate one particular
system, and the clinical examination has to be thoughtful and logical. In such
a case, the student is advised to go to the index and reach the appropriate
chapters, and then on to the exact location in the book to clinch the
diagnosis. The classical example is the abdominal pain, the colic (Chs. 30
and 37). A fresh clinical student may not know what to ask the patient, and is
directed to go to the chapter on acute abdomen, and then on to the urological
system, if it is a ureteric colic. Likewise, intercostal neuralgic pain should
direct the student to go the chapter on acute abdomen (Ch. 30) and then on to
the chapter on spine (Ch. 29).
While evaluating a sign (e.g., lump)

The classical signs of surgical illnesses, lumps and swellings, ulcers, and sinuses
and fistulae have been given separate chapters, as it is done in any conventional
clinical surgery book. Even here, for evaluating a lump in the neck, the student
may have to go through the chapters on lump (Ch. 9), neck (Ch. 25), lymphatic
system (Ch. 12), ear (Ch. 21), nose (Ch. 20), throat (Ch. 22), salivary glands
(Ch. 23), and thyroid (Ch. 24). This makes it clear how important it is to know
about every system.
Road traffic accidents have become common today, so also the trauma to
multiple organs (Polytrauma), and hence a separate chapter is allotted to deal
with this, but at the end of this manual, for easy reference, beginning from the
end.
CHAPTER 2
Patient and the surgeon

N. Mohan
CHAPTER OUTLINE
2.1. Introduction 04
2.2. Appearance 04
2.3. Behaviour 04
2.4. Doctor-patient relationship 04
2.5. Examination of the patient 05
2.6. Frank communication 05
2.7. Counselling 05
2.8. Management of patients in the hospital 05
2.9. Maintenance of records 05
2.10. Surgical ethics 05
2.11. Informed consent 05
2.1 Introduction
Patients do not feel like normal human beings because they suffer from an
ailmen, major or minor. The term ‘major or minor’ is what people in the medical
field look at. But to the patient it is the illness that causes concern. Beside, what
patients hear from friend, colleagues and relatives about the ‘problem’ add to
their fears. Each patient has physical or organic problems and psychological
fallout.
Who is a patient? The word ‘Patient’ in Latin means ‘To suffer’; a patient is a
person who suffers. This sufferer seeks help from doctor, who should realise that
—
‘A PATIENT is NOT dependent on doctor, they are dependent on patients;
A PATIENT is NOT an interruption in doctor’s work; he is the PURPOSE of it;
Doctors are not doing a favour by serving hi, but the patient is doing the doctor
a favour by giving him the opportunity to do so;
A PATIENT is NOT someone to argue or match wits with; nobody has ever
won an argument with a patient;
A PATIENT is a person who brings doctors his wants; it is doctors’ duty to
handle them profitably to him and to themselves.’*
Patients come to the doctor with worrie, anxiet, fear of the unknow, wrong
ideas and myth, doubt, querie, etc, and a doctor should help patients handle and
resolve them. The fear and anxiety of the patients is multifold when they go to a
surgeo, than to a physicia, as the word ‘operation’ could mentally shatter them.
The surgeon to allay the patient’s fear should follow some ethics and
discipline.
2.2 Appearance
Most patients are influenced by the appearance of the doctor. In the hospital set
u, the doctors are expected to be in their white coat with the name badge, which
show their positions. The surgeons should give special attention to their
appearance and outfit. It is the outward expression of their mental makeup and
goes a long way in instilling confidence in patients.
2.3 Behaviour
Manners and body language count a lot! The physician should always wear a
smile—‘a smile goes miles’! A welcome note or even a gestur, like a nod and
offering the patient a chair make a lot of difference. The doctor should be a good
listener and give attention to all details. Patients are satisfied and feel
comfortable when the doctor hears them out. Doctors who behave and dress well
are often successful in establishing good professional relationships.
2.4 Doctor-patient relationship

This relationship must be mature, if one wants to be a good doctor and a
surgeon. It is a matter of mutual trust. Politeness and language go a long way in
developing the bond. When a doctor is able to communicate in the language the
patient understand, an instant rapport is developed.
2.5 Examination of the patient

After eliciting adequate information from what the patient has sai, also from
leading question, it becomes necessary to examine the patient. A doctor should
not go by the investigation reports the patient is carryin, as it could influence the
diagnosis.
• Etiquette: Always permission should be sought from the patients to examine
the, especially while loosening or removing the dress. Patients should be told
about the nature of the investigation and the discomfort they may experienc,
so that the patients are not taken by surprise. If not explained politel, they
will only get annoyed and not cooperat, e.g. rectal examination.
2.6 Frank communication

This is an art and must be developed well if one wants to be a good doctor and a
surgeon. It is better to be frank with the patients and tell them about their illness
and the details relating to it clearly in simple words so that it is well understood.
When told in a refined wa, it will be taken well. If the illness is cance, it should
be told in a more polite way with guarded sentence, which will not scare them.
Toda, there are many cancer, which have a total cure. The doctor should drive
the point that cancer is not the end of everythin, and offer encouraging words.
2.7 Counselling
According to the Oxford Dictionary ‘Counsel’ means consultatio, plan of actio,
advic, professional recommendation, etc. Many a time a patient is new to the
doctor/ surgeon. Henc, it is imperative to gain the patient’s confidence with soft
word, patient listenin, explaining various aspects of the disease and its
managemen, and the pros and cons of the various modalities of treatment (if
available). Today’s patient is well-informed and has a right to know.
2.8 Management of patients in the hospital

A patient needs to be admitted in the hospital for:
• Serious conditions and emergencie, e.g. shoc, dehydratio, com, blunt injuries
of abdomen and thorax.
• Problems requiring detailed investigations.
• Problems that need conservative managemen, but need close monitorin, e.g.
appendicular mass or abscess.
• Difficulty in commuting from home.
It is always a good policy not to waste too much time on formalities; the
procedures for such occasions must be simplified.
2.9 Maintenance of records

The records must be complete and in order. All the details must be noted dow,
including adverse situations.
• All the observations should be entered in the chronological order clearly with
date and time. Systematic and correct entries are very helpful.
• Diagrammatic representation is more informative than words.
• Diagnosis must be written in capital letters and boxed.
• Investigations with dates and results are to be recorded separately.
• Prescriptions are to be written clearly and legibly.
• Proper documentation is a MUST.
• Opinion from specialists and other experts should be clearly entered.
• Operation notes should be elaborat, with all the details and observations with
procedures done. Status of the patient at the time of shifting the patient out of
the theatre should be clearly noted.
• Pad, instruments and gauze counts have to be verified and entered in the case
records.
• Post-operative records must be full and up-to-date till sutures are removed.
Condition of the wound and the patient are to be noted.
• Discharge summary should contain all details and should be in order; advice
on discharge depending on the condition treated and the procedure
performed.
2.10 Surgical ethics

Surgery and Ethics go hand in hand. A surgeon also uses a knife producing
injury; but the purpos, is to cure. The harm done to the body is incidental. The
patient must be made to understand the details of the disease and its proposed
treatmen, including surgery. No decision or treatment should be forced on the
patient. The patient has the right to make the decision. It is a different situation
during emergencie, where the surgeon can take the decision in the interest of
saving the life of the patient. If the treatment is refuse, it is better to record the
unwillingness and get the patient’s signature on it.
2.11 Informed consent

This includes the provision that the patient has been informed of all aspects of
the disease and treatmen, and the patient has understood all the implications well
and has given consent. Legal implication, if an, must also be ascertained. When
the patient does not understand or is in an unconscious stat, doctors should
obtain the consent from relatives or friends. In case of childre, consent of parents
or guardian is a must. All the details must be kept CONFIDENTIAL.
Research and academic activities are secondary compared to the welfare of
the patient.
In al, the surgeon should maintain professional and personal integrity and
standard, and constantly update.
*Adapted from the speech by Mahatma Gandhi in South Africa in 1890— “A
customer is the most important visitor on our premises. He is not dependent on
us. We are dependent on him. He is not an interruption of our work. He is the
purpose of it. He is not an outsider of our business. He is part of it. We are not
doing him a favour by serving him. He is doing us a favour by giving us the
opportunity to do so.”
CHAPTER 3
Eliciting history
S. Devaji Rao, A. Chandrasekhar, Rao
CHAPTER OUTLINE
3.2. Chief complaint 06
3.3. History of present illness 07
3.4. Previous history of present complaint 07
3.5. Past medical history 07
3.6. History of drug intake and allergies 08
3.7. Social and personal history 08
3.8. Family history 08
3.9. History of immunization 08
3.10. Analysis of symptoms 08
• Pain 09
3.11. Examining a child 09
3.12. Difficulties in history taking 09
3.1 Introduction
A patient visits a doctor with a specific problem (symptom). The doctor should
first listen and then ask further questions relating to the illness to know the
details of the problem. The doctor will next examine the patient in a systematic
manner, to arrive at the clinical diagnosis. After thinking about other possibilities
(differential diagnosis), and the most probable diagnosis, the doctor arrives at a
clinical diagnosis. Doctors should request for appropriate cost effective
investigations to confirm their clinical diagnosis and institute appropriate
treatment (management). Managing a patient involves four steps:
• Careful history taking;
• Systematic clinical examination;
• Requesting for appropriate cost effective investigations; and
• Administering the most effective treatment option.
History taking becomes the most important factor to make a diagnosis. It is
also the basis to set priorities in clinical examination, subsequent investigations
and management. Building the confidence of the patient, who generally gets
nervous about visiting a doctor, is another important factor. It should be
remembered that the communication is a two-way process. There are two ways
of beginning to take history.
1. The patient can be asked to talk about his or her illness first, or
2. The doctor can get the background details before hearing the patient.
If a non-medical front office is available, details such as name, sex, marital
history, address, religion and occupation may be recorded there. If not, doctors
record them in any order they wish, to make it informal, but no detail should be
left out, as each has its own relevance. It is wise to have a proforma to fill up, so
that every detail is recorded. The front office staff should restrict to general
information given in Table 3.1 and not ask about the medical problems.
TABLE 3.1
Patient Particulars and Their Relevance
Particulars Relevance Examples
Name Since more patients can have the same name, the Srinivas Jayanth Raghavan, Shyam Jayaram
(expanded expansion of initials is necessary Raghavan, Somu Jagan Raghavan
initials)
Age Newborns – Congenital anomalies Cystic hygoma, Cleft lip
Infants Wilm’s tumour
Young adults Acute arthritis, Acute osteomyelitis
Elderly patients Osteoarthritis, Prostatic hypertrophy
Sex Diseases related to sex organs Penile cancers in men and ovarian pathologies in
women
Diseases related to particular sex or have sex Hemophilia affects only men, breast cancers are
predominance more common in women
Religion Diseases or habits related to religious habits Carcinoma of penis is rare in Muslims due to routine
should be considered circumcision on religious grounds
Social status Certain diseases are more common in certain Tuberculosis is common in people of low social
social strata status
Marital Diseases related to marital status should be Extra marital diseases like syphilis
history considered
Address Certain diseases are prevalent in certain areas Peptic ulcer in south India, urolithiasis in north India
Detailed address will help in further
communications
Occupation Occupational disorders can be understood Varicose veins in men who stand for long hours
(Policemen)
The medical staff, especially the assistant doctors of the consultant can go into
the details given in Table 3.2 as they are expected to be working closely with the
consultant and will maintain secrecy.
TABLE 3.2
History of Illness
Chief complaint
History of present illness
Previous history of present complaint
Past medical history
History of drug intake and allergies
Social and personal history
Family history
History of immunization
3.2 Chief complaint*

The patient is asked what brings him or her to the doctor and is requested to
mention the problems in chronological order, when there is more than one
symptom. They are recorded, in chronological order, the symptom with the
shortest duration first.
Example
• Fever–10 days
• Weight loss–3 months
• Swelling–1 year
It is important that the doctor listens to the patient attentively, without
distraction, when patients are describing the problems in their own language. It
is also important to know if the patient was in perfect health before all these
symptoms developed. At this juncture, patients generally make some
modifications in their symptoms after a little thought. The change is usually with
regard to duration. This will help the examiner to get the more accurate duration
of the illness (how long the patient has been suffering).
3.3 History of present illness

Having listened to the complaints carefully, the doctor has to get more details, by
asking questions relevant to the complaints (leading questions).
Example
• Mode of onset (e.g. sudden or gradual)
• Progression of disease (e.g. uniform progression or with remissions)
• Treatment (e.g. mode of treatment)
If it is felt that the patient is in distress or depression and not interested in
giving further details, it is wise to ask the accompanying close relative or friend
who knows about it. Remember not to ask these questions when the patients are
talking about their symptoms and illness, as it may interrupt the flow of recall.
3.4 Previous history of present complaint

A similar complaint might have been present years ago, and the patient might
think that it is irrelevant to talk about it now. Questions should be asked to
ascertain this and the treatment received (e.g. tuberculosis).
3.5 Past medical history

All the diseases and operations, however trivial and minor should be enquired
into, and a note be made. It is not uncommon to find a direct relationship
between the past medical history and the present condition, which may not be
apparent to the patient. For example, a patient with acute abdominal pain may
have had minor attacks recurrently in the past, indicating an ongoing process of
obstruction (e.g. colonic malignancy), or a completed treatment for tuberculosis
may be presenting as a recurrence of disease at some other site.
3.6 History of drug intake and allergies
Doctors should note all drugs the patient has been taking, their dosages and the
period of consumption. They should also look into the drug allergies, so that
those drugs can be avoided during treatment. Also, the illness the patient is
suffering now may itself be a drug allergy.
3.7 Social and personal history

The personal history should record the following:
• Tobacco usage – smoking (beedies, cigarettes, cigars), chewing (pan),
quantity per day, and the duration
• Alcohol consumption – quality, quantity per day and the duration
• Diet – pattern of diet, its regularity
• Difficulties with job, finances and family
• In women
• Menstrual history (e.g. regularity, nature and quantity of menstrual flow,
last menstrual period)
• Gynaecological history (e.g. discharge, pain etc.)
• Obstetric history (e.g. number of children, nature of childbirth, last
childbirth)
3.8 Family history

Since many diseases run in families, the details of the suffering family members
and those who lost their lives due to the illness can be a good clue to make a
diagnosis (e.g. malignancies of the breasts and colon have a familial
distribution).
3.9 History of immunization

This has great relevance, especially in diseases like hepatitis, with a special
significance in patients belonging to the paediatric age group.
3.10 Analysis of symptoms

After a proper and detailed interrogation of the patient, it is the duty of the
examiner to take each main symptom and analyze in detail. If in case the
examiner feels that there is a need to know more, he or she should not hesitate to
ask but politely, so that the patient is not tired of the whole process. It should be
noted that no question should upset the patient emotionally or sentimentally.
There are many non-verbal clues, such as holding the breath, restlessness,
abnormal limb and eye movements, which will be good indicators of systemic
illnesses. By this time, the student should be able to identify the disturbance of
function (physiological) and anatomical structure responsible for all the trouble.
Many a time, it is worthwhile to talk to the relatives and friends to get further
information, preferably not in the presence of the patient. The common
symptoms in relation to various systems of the human body are given in Table
3.3.
TABLE 3.3
Various Symptoms of Human Body Relating to Surgical Illnesses
System Symptom
General Weight gain or loss
Appetite gain or loss
Disturbances of sleep
Upper gastrointestinal tract Upper abdominal pain
Nausea or vomiting
Flatulence or postprandial fullness
Dysphagia
Heartburn
Lower gastrointestinal tract Diarrhoea or constipation
Lower abdominal or flank pain
Hepatobiliary system Jaundice
Right upper quadrant pain
Fever with rigor
Urinary system Disturbances in urination
Hematuria
Loin pain
Fever with rigor
Cardiovascular system Palpitations
Chest pain
Dyspnoea
Cough
Pedal edema
Respiratory system Cough with expectoration
Chest pain
Breathing disturbances
Wheeze
Genital system Discharges in females
Lower abdominal pain
Pain in the genitals
Fever
Pain
By far the commonest complaint, which brings a patient for consultation to a
doctor, is pain. Careful analysis of pain can take the examiner close to the
diagnosis in many cases.
The pain can be of various types:
• Vague pain–it may not have any specific feature
• Burning pain–characteristic of acid peptic disease
• Scalding pain–cystitis, urethritis
• Throbbing pain–acute pyogenic abscess
• Shooting pain–nerve root pain like sciatica
• Stabbing pain–acute perforation of bowel
• Constricting pain–angina pectoris
• Colicky pain–colics
• Twisting pain–torsions
The other features of pain are analysed and tabulated in Table 3.4.
TABLE 3.4
Analysis of Pain
Character Examples
Site The site pointed by the patient with a finger tip many times determines the anatomical structure causing
the pain (focal): e.g. pain in the quadrants of the abdomen, diffuse pain e.g. headache in intracranial
lesions, referred pain – visceral nerve impulses simulating the somatic afferent pathways of same
dermatome, e.g. shoulder pain from disease under the diaphragm
Intensity Dull pain may indicate low grade pathologies or slow growing tumours, severe pain may indicate colic,
e.g. biliary colic
Radiation It may radiate along the peripheral nerve it involves in the disease process, e.g. renal pain radiating to
the genitalia (ureteric colic)
Duration Short duration e.g., colics, long duration e.g., malignancies
Aggravating Food may aggravate gastric ulcer pain, breathing may aggravate pleural pain
factors
Relieving Food may relieve duodenal ulcer pain, rest may relieve cardiac pain
factors
Many a time, the diagnosis may be almost reached from the history alone.
Since the examination can give what was present at that moment like a snap
shot, history is more important than the physical examination.
The symptoms are discussed in the appropriate chapters.
3.11 Examining a child

In the case of children, parents should be addressed. The child’s age is always a
key feature in the history and examination as it determines:
• The nature and presentation of illnesses.
• The way in which the history taking and examination are conducted.
• The way in which any further management is organized.
While making note of the history of a child’s illness,
• Know the gender of the child.
• Ask how the child prefers to be addressed.
• Determine the relationship of the accompanying adults.
• Establish rapport with the family.
• Ensure that questioning is friendly and unthreatening.
• If the child is more comfortable in the parent’s arms or lap, do not disturb.
• Have some toys, for the child and observe the way the child handles it.
• If older children want privacy, tactfully send the parents out of the consulting
room.
It should be remembered that pediatrics is a specialty governed by age. They
are divided into
• Neonates (< 4 weeks)
• Infants (> 4 weeks to 1 year)
• Toddlers (approx 1–2 years)
• Preschool children (2–5 years)
• School age children (5–10 years)
3.12 Difficulties in history taking

Generally, a doctor faces difficulties in history taking while dealing with:
• Mentally retarded patients
• Hearing and visually impaired patients
• Agitated patients
• Anxious patients
• Patients wanting quick diagnosis even before examination
• Patients who do not want to reveal their personal problems
• Women who avoid personal questions
• Small children
Doctors can always take a complete history, if they show concern and
sympathy to the patient’s suffering. Patience and creating confidence are the key
factors to get a complete history from a patient.
*
The symptom presentation should be in the patient’s own words.
CHAPTER 4
General physical examination

S. Devaji Rao
CHAPTER OUTLINE
4.2. At the time of patient’s entry or separately 10
• Gait 10
• Posture 10
• Clothing 10
4.3. Eliciting history 10
4.4. Height and weight measurements 11
4.5. Examination of patient on the couch 11
• Physique 11
• Facies 11
• Complexion 11
• Scratch marks 11
• Body odour 11
4.6. General system examination 11
• Skin 11
• Eyes 11
• Oral cavity 12
• Hands and feet 12
• Anaemia 13
• Jaundice 13
• Cyanosis 14
• Pulse, temperature, respiration 14
• Blood pressure 15
• Lymphatic system 15
• Chest and abdomen 15
4.7. Method of physical examination 15
• Examining a child 16
4.8. Conclusion 16
4.1 Introduction
There is no correct sequence of performing a physical examination, and it is
important that the doctors develop their own approach. But the time-honoured
sequence for examination consists of:
• Inspection
• Palpation
• Percussion
• Auscultation
These can be integrated into the examination and can be altered as deemed
necessary by the examiner.
4.2 At the time of patient’s entry or separately
Gait
The gait of patients who can walk should be paid attention to, as the patient
enters the consulting room. A surgical patient especially with acute illness has a
very characteristic gait according to the disease, e.g. a patient with a painful
corn, a diabetic foot, or lower limb fractures may exhibit a limp, and acute
anorectal conditions produce a wide gait.
Posture
In the outpatient department, when the patients are offered a seat, they adopt
peculiar postures which can be informative, e.g. patients with anorectal painful
conditions sit at the edge of the seat or to one side of it, while some may not
even sit but remain standing. A patient with pain due to acute pancreatitis may
stoop over the table, or one with distended abdomen will sit in a lordotic posture,
unable to sit properly. Patients in surgical wards adopt postures which can be
informative. Severely ill patients slip down in bed, patients with peritonitis lie
still, and those with colicky pain are restless.
Clothing
The clothing of the patient will describe the state of mind the patient is in. When
the illness is acute and the patients are severely disturbed, they may not even
wear their clothes properly, and keep their hair unkempt. There may even be
feculent soiling of the garments in anorectal infective pathologies.
4.3 Eliciting history

The history is elicited as given in Chapter 3. If the patient is uncomfortable
sitting due to some reason, the history eliciting should be done only after making
the patient lie down on the bed.
4.4 Height and weight measurements

If the patients are not acutely ill, the height and weight measurements should be
done before they get onto bed.
4.5 Examination of the patient on the couch

The patient is made to lie down comfortably on an examination couch in the
consulting room. When examined in a hospital ward, patients should be made to
lie comfortably relaxed. As the patient gets on to the examination couch, the gait
and movement, and the method of getting on to the couch are to be recorded
again.
Physique
General examination of the physique gives abundant information, both towards
diagnosis and treatment planning, especially those with surgical illnesses. It is
wise to note the following:
• Is the appearance consistent with the age? e.g. Mental retardation.
• Is he or she tall, short, fat, thin, wasted and tired? e.g. Short and fat patients
are difficult to be examined physically and also are high risk patients for
major surgeries.
• Is there any deformity? e.g. Congenital anomalies may indicate the presence
of some other congenital abnormality in the patient – cleft lip and
hypospadias can coexist.
• Do the height and weight correlate? e.g. Dwarfs of hypopituitarism or
Gigantism of hyperpituitarism, thyroid disorders.
Note
Height should be roughly equal to the fingertip-to-fingertip length of
outstretched arms and twice the length of the leg from the pubis to heel.
Facies
The patient may present with a winced face when he or she is acutely ill, e.g.
colics, or a worried and disgusted facies when suffering from a chronic illness
without much relief, e.g. malignancies.
Complexion
The examiner should make a general survey of the patient with special reference
to the skin. The skin may show some obvious discolourations due to varied
conditions, generally noticed by friends and relatives. The examples are given in
Table 4.1.
TABLE 4.1
Skin Discolourations in a Patient
Condition Skin Colour
Bluish colourations Cyanosis, sulfhemoglobinemia, methemoglobinemia, dapsone toxicity

Cherry red colouration Carbon monoxide poisoning
Yellow colouration Mepacrine, carotene, jaundice
Red colouration Clofazamine toxicity
Slate gray colouration Phenothiazines toxicity
Scratch marks
Presence of scratch marks on the skin may be an indicator of a hypersensitive
reaction probably to the intake of drugs. When associated with yellowish
discolouration of the skin, it may indicate severe and longstanding jaundice.
Body odour
Normally the body produces an odour, which arises from apocrine sweat
contaminated by diphtheroid bacteria. Poor personal hygiene exaggerates this
odour, which may be exaggerated by soiled clothes or infected discharging
wounds or ulcers, e.g. diabetic foot ulcers.
4.6 General system examination
Skin
Examination of the skin is a very important part of general examination. There
can be a variety of external features suggestive of an internal or a generalized
illness. They are:
• Pallor (e.g. anaemia)
• Yellow discolouration (e.g. jaundice)
• Bluish discolouration (e.g. cyanosis)
• Pigmentation [e.g. Von Recklinghausen’s disease, spider naevi (Fig. 4.1)]
• Eruptions (e.g. macule, papule, vesicle, bulla, etc.,)
• Nodules (e.g. Heberden’s nodes of osteoarthrosis)
• Visible veins (e.g. Visible neck veins of cardiac overload, caput medusae of
portal hypertension)
FIGURE 4.1 Spider naevi of hepatic failure.
Eyes
Some of the features may suggest an internal or a generalized disease: External
examination of eyes is done in an organized manner. The steps are:
• Orbital region
• Prominence of eye balls [e.g. exophthalmos of thyrotoxicosis (Fig. 4.2)]
• Sunken eyeballs (e.g. dehydration)
• Eyelids
• Puffiness (e.g. trauma, renal pathology)
• Colour (e.g. black eye of head injuries)
• Conjunctivae
• Colour (e.g. pale in anaemics)
• Sclera
• Colour (e.g. yellow in jaundiced patients)
• Cornea and iris
• Opacities and ulcers (e.g. trauma, infections)
• Pupils
• Size, shape, symmetry and reaction to light (e.g. changes in cranial nerve
lesions)
FIGURE 4.2 Exophthalmos Source: (Courtesy Dr P S Venkatesh Rao).
Oral cavity
While examining the oral cavity (Fig. 4.3), a definite plan should be adopted. It
should be done in the following order:
• Lips
• Colour and texture (e.g. cracked lips of exposure to extreme cold)
• Pigmentation (e.g. telangiectasia)
• Gums
• Colour (e.g. blue line of lead poisoning)
• Texture (e.g. inflammation due to gingivitis)
• Pigmentation (e.g. hemorrhages due to leukemia)
• Teeth
• Colour and pigmentation (e.g. mottled yellow colour of flurosis)
• Number and health status of the teeth (e.g. Hutchinson’s teeth of
congenital syphilis)
• Tongue
• Colour (e.g. blue colour of central cyanosis)
• Texture (e.g. smooth tongue of vitamin B12 deficiency)
• Ulcer (e.g. aphthous ulcers)
• Movements (e.g. hyplossal nerve palsy)
• Hard palate and soft palate
• Colour (e.g. anaemia)
• Cleft (e.g. cleft palate)
• Ulcer (e.g. malignancy)
FIGURE 4.3 Examination of oral cavity.
Halitosis (Bad breath) may be due to poor oral hygiene or even oral
pathologies, e.g. oral cancers, or bronchopulmonary pathologies, e.g. lung
abscesses.
Hands and feet

• Hands of the patient should be examined carefully, like –
• Shape of the hands (e.g. characteristic shape of Dupuytren’s contracture,
Tetany)
• State of the joints [e.g. deformed joints of rheumatoid arthritis (Fig. 4.4A)]
• Shape and colour and deformity of fingers [e.g. clubbing (Fig. 4.4B) or
nicotine staining of chronic smokers]
• Nails (e.g. koilonychia of iron-deficiency anaemia)
• Abnormal movements of fingers (e.g. tremors of thyrotoxicosis)
• Feet of the patient are generally tucked under the bedclothes and their
examination should not be forgotten. Examination may reveal –
• Oedema, unilateral (e.g. filarial leg) and bilateral (e.g. hypoproteinemia)
(Fig. 4.5A)
• Skin changes (e.g. pigmentation or ulcers due to ischemia) (Fig. 4.5B)
• Ulcers (e.g. trophic ulcers) (Fig. 4.5C)
FIGURE 4.4A Rheumatoid hand.

FIGURE 4.4B Clubbing of fingers.
FIGURE 4.5A Oedema of lower limbs—(A) Filarial, (B) Hypoproteinaemia.
FIGURE 4.5B Vasculitis.
FIGURE 4.5C Trophic ulcer in a deformed foot.
Anaemia
A patient’s relatives and close friends observe the increasing pallor, which may
be an early feature of progressive anaemia due to malignancies. Pallor is
examined by examining the mucous membranes, commonly the conjunctiva, by
asking the patient to look up (Fig. 4.6). Examination of nails to certain extent is a
reliable indicator of pallor (Fig. 4.7).
FIGURE 4.6 Examination of conjunctiva for anaemia.
FIGURE 4.7 Examination of hands and nails.
Jaundice
Jaundice is the yellowish discolouration of the sclera and skin due to the
presence of bile pigments. When the jaundice is longstanding, a distinct greenish
colour develops in the sclerae and skin due to the presence of biliverdin. The
patient’s sclerae are examined by asking the patient to look down (Fig. 4.8).
FIGURE 4.8 Examination of sclera for jaundice.
Cyanosis
Cyanosis is a bluish colour of the skin and mucous membranes due to reduced
haemoglobin in the blood. There are two varieties of cyanosis:
1. Central cyanosis is due to a central cause, like a heart disease producing
imperfect oxygenation of blood. The cyanosis is generalized but the
extremities remain warm.
2. Peripheral cyanosis is due to reduced amounts of oxyhaemoglobin in the
capillaries due to reduction of circulation.
Note
In central cyanosis, bluish discolouration is generalized (including the
tongue), but the extremities remain warm. In peripheral cyanosis, the tongue
does not show the discolouration, and the extremities are cold.
To summarise, the points to note in general physical examination are:

Pallor, Icterus, Cyanosis, Clubbing, Koilonychia, Lymphadenopathy and pedal
Edema (mnemonic: PICKLE).
Pulse, temperature and respiration

Pulse should be counted for a full minute and the following are to be noted:
• Rate
• Rhythm
• Volume
• Abnormalities
Normal rate of pulse varies from 60 beats to 80 beats per minute, during the
stress of a medical examination. Tachycardia (Rapid pulse) may be seen after
recent exercise, anxiety, thryotoxicosis, acute infections and cardiac conditions.
Rhythm abnormalities (arrhythmias) and abnormal pulses may be seen in cardiac
illnesses.
Temperature recording is an essential part of general examination.
• Hyperpyrexia(Increase in temperature) may indicate acute infective illnesses;
mild elevations are seen in malignancies
• Hypopyrexia (Low temperature) may indicate shock and volume loss.
Respiration is a very important part of the general examination. This can be
counted concurrently when the patient’s pulse is counted, that is, for a full
minute. Though wide variations occur, the normal rate is 14–18 per minute.
Tachypnoea (increased respiratory rate) occurs in exertion, anxiety, high fever,
cardiopulmonary problems, diseases of the chest wall like injuries, and
abdominal pathologies like peritonitis and gross ascites.
Blood pressure
Recording of blood pressure is a very useful exercise while examining a surgical
patient. It helps in finding out the acuteness of the situation (e.g. hypotension of
shock patients), or hypertensive diseases (e.g. Cushing’s syndrome,
Pheochromocytoma). Associated essential hypertension may help in the
planning of surgery and anaesthesia.
Lymphatic system
Examination of the lymphatic system is an essential part of the general
examination. Enlargement of lymph nodes, whatever group they belong to, or a
generalized lymphadenopathy has a very great significance in arriving at a
diagnosis. The details of the lymphatic system illnesses and the methods of
examination of the lymphatic system are given in Chapter 12.
Chest and abdomen

The chest and abdomen are examined fully following the pattern of inspection,
palpation, percussion and auscultation. It is very important to examine the
rectum.
Summary
In summary, the general scheme of physical examination is given in Table 4.2.
TABLE 4.2
General Scheme of Physical Examination
At the Time of Entry or Separately Gait
While eliciting history Posture

Clothing
Before getting on the couch Height and weight measurements
On the couch Physique
Facies
Complexion
Scratch marks
Body odours
Skin Anaemia
Eyes Jaundice
Oral cavity Cyanosis
Hands and feet
Pulse, temperature and respiration
Blood pressure
Lymphatic system
Chest and abdomen (including genitalia and rectum)
4.7 Method of general physical examination
A good physical examination can be done in the following set up:
Ambience
• Quiet, well-lit room.
• An examination couch (with adjustable height if possible) with a stool for
easy access (for elderly patients). Adjustable back-rest will be an added
advantage while examining patients who become breathless on lying flat.
Patient
For a complete examination, the patient should be asked to undress completely
and lie on the couch covered with a sheet. Once the general examination is over,
the part of the body that needs to be examined in detail alone should be exposed
and the rest covered with a sheet or blanket (Fig. 4.9). The examination should
be done with the patient lying supine, with upper limbs on both sides. Thighs
may be flexed to 45 degrees for the relaxation of the lower part of abdomen. A
nurse is essential while examining a female patient (Fig. 4.10). Or else, it is
better to keep one relative to stay behind, especially if the patient is a child and
has any difficulty in communication.
FIGURE 4.9 Exposure of entire abdomen including genitalia for clinical
examination of abdomen.
FIGURE 4.10 Examining a female patient.
Equipments required (Fig. 4.11)

• Thermometer, Sphygmomanometer
• Weighing scale
• Stethoscope
• Measuring tape
• Tongue depressor
• Pen-torch
• Ophthalmoscope, otoscope, proctoscope, illuminoscope
• Disposable gloves and lubricant jelly
• Tendon hammer, tuning fork, cotton wool and pins
FIGURE 4.11 Equipments required for general examination.
Method of examination
The examiner should do the following while examination:
• Watch the way the patient gets on to the couch.
• Watch the way the patient undresses.
• Follow the scheme given in Table 4.2.
Examining a child
Examining a child needs special tact, as the examiner has to obtain the child’s
cooperation for examination. How to obtain it? The following points will help:
• Make friends with the child.
• Be gentle and avoid scolding or dominating the child.
• Short mock examination will help, e.g. examining the parent or a toy.
• Explain the procedure well in a language the child can understand and obtain
permission.
During the physical examination, the examiner may have to adapt to the
child’s age, and do the following:
• Babies in the first few months of age are best examined on the couch with a
parent next to the child.
• A toddler is best examined on the mother’s lap.
• Pre-school children are best examined on the couch.
• Older children who expect privacy need to be examined alone, but female
children are best examined in the presence of their mother or nurse.
Developmental skills are assessed while the children are playing, may be with
the toys. Careful observation is the key to success in examining children. Very
sick children should be examined quickly and rapidly.
It should be remembered that the white apron and a stethoscope generally
scare the children, as doctors are projected to be injection givers. A casual dress
for the examiner is always welcomed by a sick child.
4.8 Conclusion
The general physical examination is performed to get an overall impression of
the patient’s health status, and also to exclude abnormalities. Sometimes, general
physical examination gives excellent clue for the diagnosis (e.g. cervical
lymphadenopathy in an asymptomatic carcinoma of the stomach, or in
symptomatic abdominal tuberculosis). The general physical examination should
be followed by a detailed system-wise examination, starting with the system
suspected to be involved (detailed in appropriate chapters) based on the
presenting complaint of the patient.
PA R T I I
Symptoms and Signs
OUTLINE
5. Dysphagia
6. Constipation
7. Obstructive jaundice
8. Gastrointestinal haemorrhage
9. Lumps and swellings
10. Ulcers
11. Sinuses and fistulae

CHAPTER 5
Dysphagia
S. Devaji Rao
CHAPTER OUTLINE
5.2. Surgical anatomy of oesophagus 18
5.3. Causes of dysphagia 18
5.4. Diseases of oesophagus 19
• Oesophageal atresia 19
• Strictures of oesophagus 19
• Reflux oesophagitis 21
• Fungal infections 21
• Benign tumours 22
• Oesophageal malignancy 23
• Scleroderma 24
• Diffuse oesophageal spasm 25
• Achalasia 25
• Paterson-Kelly syndrome 25
• Diverticula 26
• Hiatus hernia 27
• Schatzki’s ring 27
• Pressure from extrinsic pathologies 28
• Foreign bodies, bolus obstruction 29
5.5. Clinical evaluation 29
• Eliciting history 29
• Physical examination 30
• General examination 30
• Systemic examination 30
5.1 Introduction
Normal swallowing is a very complex mechanism consisting of co-ordination of
four elements. They are:
1. Voluntary muscular contractions of oropharynx;
2. Protection of the larynx and respiratory passages by its striated muscles;
3. Relaxation of oesophageal sphincters; and
4. Peristaltic wave.
Dysphagia may occur due to the derangement of one or more of the above
four elements, or the narrowing of the lumen by stricture, tumour, or extraneous
causes.
Dysphagia is defined as a difficulty in swallowing.
It is a very reliable symptom and should never be dismissed as psychological,
unless proved otherwise.
For clinical purposes, dysphagia is divided into two varieties:
1. Oro-pharyngeal
2. Oesophageal
Patients with dysphagia complain of the sensation of food sticking somewhere
in the passage to the stomach, usually at the level of obstruction, but many times
point at the suprasternal notch, even though the level of obstruction is far below.
Pain can accompany dysphagia, if there is associated oesophageal spasm.
Very severe pain may occur, which may be radiating to the base of the neck,
angles of the jaw, arms, epigastrium, and the back. Oesophageal pain may mimic
cardiac pain.
Heartburn is a retrosternal sensation of burning and discomfort, which
occurs due to regurgitation of stomach contents into the normally empty
oesophagus, which may reach even the pharynx if the quantity is large.
5.2 Surgical anatomy of oesophagus

Oesophagus is a muscular tube connecting the pharynx and the stomach, guarded
by sphincters at both ends. It is lined by the squamous epithelium, except in its
lower part and the oesophago-gastric junction, where it is lined by the columnar
epithelium. It lies anterior to the cervical vertebrae and in the posterior
mediastinum, and enters the abdomen through a hiatus – ‘oesophageal hiatus’ of
the diaphragm. The oesophagus is devoid of a serosal layer. Gastro oesophageal
reflux is prevented by the lower sphincter and the acute gastro-oesophageal
angle, and the oesophagus normally remains empty.
5.3 Causes of dysphagia

Neuromuscular disorders are the most common causes of oropharyngeal
dysphagia (e.g. cerebrovascular accidents with pseudobulbar palsy, myasthenia
gravis and myotonic dystrophies). Causes of dysphagia are given in Table 5.1.
TABLE 5.1
Causes of Dysphagia
Etiology Oral cavity Pharynx Larynx Oesophagus

Congenital Macroglossia Pharyngeal pouch Subglottic stenosis, Atresia
laryngomalacia
Traumatic Injuries of oral Impacted foreign Injuries to larynx/ Post operative and corrosive strictures,
cavity bodies (coin, laryngopharynx, foreign bodies, radiotherapy
tooth, dentures) impacted
foreign bodies
Inflammatory Stomatitis, Acute pharyngitis, Acute epiglottitis, Reflux oesophagitis, post-chemotherapy
tonsillitis, retropharyngeal tuberculous fungal infections
peritonsillar abscess, cervical laryngitis
abscess lymphadenopathy
Neoplastic Minor salivary Benign tumours
benign gland
tumours
Neoplastic Carcinoma Carcinoma Carcinoma larynx Oesophageal malignancy
malignant tongue, hypopharynx
cancers of
oral cavity
Miscellaneous Paralysis of Paterson-Kelly Vocal cord palsy, Scleroderma, diffuse oesophageal spasm,
soft palate syndrome neuroasthenia achalasia, Paterson-Kelly syndrome,
(bulbar diverticula of the oesophagus, para-
palsy) oesophageal hiatus hernia, pressure
from extrinsic pathologies
Conditions of the oral cavity, pharynx and larynx, which contribute to

dysphagia are discussed in appropriate chapters (Chs. 19 and 22).
Dysphagia is almost always caused by diseases in and adjacent to the
oesophagus and rarely by the lesions in the pharynx or stomach. Oesophageal
narrowing causes dysphagia when the lumen is not able to expand beyond a
diameter of about 10 mm. Chronic obstructions of oesophagus, like achalasia
cardia, allow the patients to compensate and present at a very late date, but by
this time, there is marked weight loss and severe undernutrition.
5.4 Diseases of oesophagus
Osophageal atresia
Incidence and aetiology
• Congenital anomaly in which there is interruption of elongation, and
partitioning of oesophageal and tracheal tubes.
• Occurs in 1 in 4000 births.
• Oesophageal atresia (Fig. 5.1A) is classified as:
• Type A–Pure oesophageal atresia (8%).
• Type B–Oesophageal atresia with upper pouch fistula to the trachea (1%).
• Type C–Oesophageal atresia with lower pouch fistula to the trachea (86%)
(Fig. 5.1B).
• Type D–Oesophageal atresia with upper and lower fistulae (1%).
• Type E–Fistula without atresia (4%).
• Associated congenital anomalies occur in 20% patients.
FIGURE 5.1A Oesophageal atresia.
FIGURE 5.1B Incidence of oesophageal atresia.
Clinical presentation
• Child presents with inability to retain the food intake resulting in vomiting,
aspiration, choking, cyanosis, and respiratory distress.
• Maternal history of polyhydramnios is usually present.
• The abdomen progressively distends due to the air entry through the fistula.
Relevant investigations
• Passing the nasogastric tube is impossible.
• Administration of contrast through the tube will clinch the diagnosis (Fig.
5.2).

FIGURE 5.2 Barium swallow—Oeosphageal atresia with trachea-
oesophageal fistula.
Treatment
• Medical: Head up position, intravenous fluids, antibiotics
• Surgical: Transthoracic approach: Transpleural or extrapleural
• Excision of fistula with end to end anastomosis.
• Oesophageal replacement using stomach, colon or jejunum may be
required to fill long gaps.
• Feeding gastrostomy may be necessary if surgery is delayed.
Strictures of oesophagus
Strictures are caused by:
• Corrosives
• Surgery
• Radiotherapy
• Reflux oesophagitis
Dysphagia, particularly to solids
• Barium swallow is the best investigation and is diagnostic (Figs. 5.3A and B).
• A computed tomography (CT) with oral contrast is useful in determining the
oesophageal wall thickness (Fig. 5.3C).
• Endoscopy (Figs. 5.4 and 5.5) is confirmatory and useful in obtaining biopsy,
if needed.

FIGURE 5.3A-B Barium swallow—(A) Stricture oesophagus. (B) Corrosive
stricture.
FIGURE 5.3C CT—Stricture oesophagus after radiotherapy for
malignancy.
FIGURE 5.4 Oesophagoscopy—Stricture of cervical
oesophagus Source: (Courtesy Dr Mani Veeraraghavan).
FIGURE 5.5 Oesophagoscopy—Stricture of lower oesophagus with
ulcerations Source: (Courtesy Dr Mani Veeraraghavan).
Treatment
• Endoscopic dilatation where possible.
• Bypass procedures using stomach and colon are reserved for impassable
strictures.
Reflux oesophagitis (gastro-oesophageal reflux

disease – gerd)
• Incompetence of the oesophago-gastric junction, which allows the acidic
gastric contents into the lower oesophagus, causes oesophagitis.
• Although this oesophagitis is superficial, it may result in:
• Stricture.
• Metaplastic change (Barrett’s oesophagus), which is a precursor of
adenocarcinoma at that region.
• Heartburn is a predominant symptom, and sometimes present as water-brash
in the mouth, more commonly on stooping or lying down soon after food
intake.
• Dyspepsia, upper abdominal discomfort and dysphagia are associated.
• Barium meal of the stomach (Fig. 5.6) may show reflux in the Trendelenburg
position.
• Oesophageal manometry is useful.
• Oesophagoscopy is diagnostic to see the reflux (Fig. 5.7), and also for
Barrett’s oesophagus (Fig. 5.8).
• Histopathology confirms oesophagitis.

FIGURE 5.6 Barium meal—reflux oesophagitis.
FIGURE 5.7 Oesophagoscopy—Severe esophagitis Source: (Courtesy Dr Mani
Veeraraghavan).
FIGURE 5.8 Oesophagoscopy—Barrett’s oesophagus Source: (Courtesy Dr
Mani Veeraraghavan).
Treatment
• Proton pump inhibitors with gastrokinetics along with advice regarding
position in the post prandial period are effective.
• Surgical correction by Nissen’s fundoplication (Open or laparoscopic) is for
refractory cases.
Fungal infections of oesophagus

• Fungal infections occur in the oesophagus most commonly during
chemotherapy due to immune deficiency.
• Infections cause severe oedema of the oesophageal mucosa.
• It can be a presentation in acquired immune deficiency syndrome (AIDS).
• Dysphagia associated with pain.
• The fungal infection concomitantly occurs in the oral cavity, and presents
with glossitis and pharyngitis with ulcers in the oral cavity.
• Fungal cultures and swabs taken through oesophagoscopy (Fig. 5.9) are
useful in making the diagnosis (affected areas appear as white patches).
FIGURE 5.9 Oesophagoscopy—Candidiasis of

oesophagus Source: (Courtesy Dr Mani Veeraraghavan).
Treatment
• Administration of anti-fungal agents is curative.
Benign tumours
Benign tumours are rare. They are classified based on the layer of origin.
• Mucosa
- Epithelium–papilloma, adenoma
- Lamina propria–mucus retention cyst, fibrovascular polyp
- Smooth muscle–leiomyoma
• Submucosa
- Mucous gland–mucous retention cyst, adenoma
- Connective tissue–fibrovascular polyp
- Blood vessels–hemangioma
- Nervous tissue–neurilemmoma, granular cell tumour
• Muscularis
- Striated muscle–rhabdomyoma
- Smooth muscle–leiomyoma
- Nervous tissue–neurilemmoma, granular cell tumour
• Adventitia
- Connective tissue–fibroma
- Neural tissue–neurilemmoma
• Of these leiomyomas are the most common. Most of them occur in the lower
half.
• Generally asymptomatic.
• Large lesions cause dysphagia.
• CT and endoscopic ultra sonography (EUS) are useful in differentiating
from malignancy.
• Barium swallow (Fig. 5.10) and oesophagoscopy (Fig. 5.11) are diagnostic.

FIGURE 5.10 Barium swallow—Leiomyoma of oesophagus.
FIGURE 5.11 Oesophagoscopy—Lipoma of oesophagus Source: (Courtesy Dr
Treatment
• Simple enucleation is the treatment of choice.
Oesophageal malignancy
• Affects males more than the females.
• Frequency increases with age, peaking in the sixth decade.
• Common in the middle (40%–50%) and lower (40%–50%) third of the
oesophagus.
• The risk factors are:
• Smoking
• Alcohol consumption
• Dietary deficiency
• Fungal infections
• Paterson-Kelly (Plummer-Vinson) syndrome
• Achalasia cardia
• Oesophageal diverticula
• Chronic oesophagitis
• Human papilloma virus types 16 and 18
• Macroscopically, the tumour appears:
• Nodular
• Ulcerative
• Diffusely infiltrative (results in stricture with proximal dilatation)
• Microscopically, it may be:
• Squamous cell carcinoma (common)
• Adenocarcinomas (in the lower end in uncorrected reflux disease, against a
background of glandular metaplasia of Barrett’s oesophagus)
• Stromal tumours and lymphomas (rare)
• Oesophageal cancer spreads by various routes:
• Longitudinally and circumferentially within the oesophagus.
• Submucosal spread leads to diffuse infiltration and also skip lesions.
• Direct spread to mediastinal structures, like trachea, main bronchi, lungs,
pleura, vertebrae and great vessels.
• Lymphatic spread:
- Upper third tumours to deep cervical and supraclavicular nodes
(Virchow’s nodes).
- Middle third tumours to mediastinal, paratracheal and subcarinal nodes
- Lower third tumours to celiac nodes below the diaphragm
• Hematogenous spread to liver, lungs, and bones, with the liver being the
commonest.
• Symptoms:
• Progressive dysphagia (for solids to start with and to liquids later)
• Weight loss
• Anaemia
• Loss of appetite is a very common symptom
• Signs
• Signs of undernutrition
• Stigmata of chronic liver disease in alcoholics
• Hepatomegaly may suggest hepatic metastases
• Enlarged supraclavicular lymph nodes if there is spread (Troisier’s sign)
• Barium swallow (Figs. 5.12A and B), CT (Fig. 5.12C) and magnetic
resonance imaging (MRI) of thorax are diagnostic.
• Oesophagoscopy (Fig. 5.13) with biopsy is confirmatory.
• X-ray Chest to assess aspiration pneumonitis, and intrathoracic metastases.
• CT and MRI of upper abdomen for assessment of hepatic metastases.
• Bronchoscopy to exclude invasion of posterior tracheal wall and left main
bronchus.

FIGURE 5.12A-B Barium swallow—(A) Oesophageal malignancy mid
third and (B) lower third.
FIGURE 5.12C CT—Oesophageal malignancy upper third.
FIGURE 5.13 Oesophagoscopy—Malignant growth (OG
Junction) Source: (Courtesy Dr Mani Veeraraghavan).
Treatment
• Surgery (oesophago-gastrectomy for lower third tumours) and Ivor Lewis
two stage oesophagectomy for middle third tumours) /or radiotherapy is the
treatment of choice.
• Palliative:
• Combined chemoradiation (CRT) is used for inoperable tumours.
• Chemotherapy as a curative treatment is not advised excepting for
synchronous CRT.
• Dilatation and stenting are for inoperable malignancies.
• Laser application is useful for restoration of passage, in very advanced
cases (Laser rebore).
• Feeding gastrostomy is done as palliation for impassable strictures or for
nutritional supplementation during radiotherapy
Scleroderma
• The commonest systemic disease to affect the oesophagus, which is
characterized by fragmentation and homogenization of the submucosal
connective tissue elements, and motor failure is characteristic.
• Commonly affects the inferior oesophageal sphincter.
• Dysphagia, regurgitation and heartburn are characteristic symptoms.
• Oesophageal motility studies are indicative of diagnosis.
Treatment
• Coritcosteroids are useful in the management.
Diffuse oesophageal spasm

• Exact etiology is not known.
• Chest pain (mimicking a cardiac pain) and dysphagia.
• Contrast studies may show exaggerated oesophageal contractions giving a
‘cork screw’ appearance (Fig. 5.14).
• Oesophagoscopy is generally normal.
• Oesophageal manometry is diagnostic.

FIGURE 5.14 Corkscrew oesophagus.
Treatment
• Drugs like nitrates and calcium channel blockers which reduce smooth
muscle contractions are used.
• Long oesophageal myotomy in which all layers (excepting mucosa) are
divided may be helpful.
Achalasia (cardiospasm)
• Common in third decade.
• An uncommon motility disorder of the oesophagus with aperistalsis, and
failure of lower oesophageal sphincter relaxation while swallowing.
• Occurs due to degeneration of ganglion cells of myenteric plexus resulting in
the non-relaxation of the lower oesophageal sphincter during deglutition,
with the bolus being retained in the lower oesophagus for some time.
• It can be a forerunner for malignancy.
• Rarely associated with alacrimation and Addison’s disease (Triple A
syndrome).
• Infection with Trypanozoma cruzi may produce a similar syndrome which is
common in South America.
• Progressive dysphagia to liquids and solids.
• Regurgitation of food several hours after intake, probably due to the dilated
oesophagus acting as a reservoir and eject its contents when the intra-
oesophageal pressure reaches its maximum.
• Retrosternal pain (caused by fermentation of food).
• Weight loss is common.
• X-ray chest is usually normal, but when the disease progresses, it shows a
widened mediastinum with air fluid level in the dilated oesophagus.
• Barium swallow (Fig. 5.15) shows a smooth tapering of distal oesophagus
(Bird’s beak appearance).
• Oesophagoscopy (Fig. 5.16) shows disproportionate amount of food residue
at the oesophago-gastric junction and is essential to differentiate it from
malignant disease, especially in older patients.
• Blood smear may show T. cruzi.
FIGURE 5.15 Barium swallow—Achalasia.

FIGURE 5.16 Oesophagoscopy—Achalasia showing retained fluid
level Source: (Courtesy Dr Mani Veeraraghavan).
Treatment
• Balloon dilatation of oesophago-gastric junction resolves majority of lesions.
• Cardiomyotomy (Heller’s operation) is the treatment of choice and it is
curative in majority of cases.
• Anti-reflux procedures may be needed in some cases.
Paterson-kelly (plummer-vinson) syndrome

• A complex described by Paterson and Kelly in 1919, and Plummer and
Vinson’s name got associated with the syndrome later.
• The patient is middle aged.
• An edentulous woman.
• Atrophic oral mucosa
• spoon shaped fingers with brittle nails
• longstanding anaemia (iron deficiency)
• dysphagia
• Barium swallow (Fig. 5.17A) and endoscopy (Fig. 5.17B) demonstrate a
fibrous web obstructing the lumen in an eccentric fashion just below the
cricopharyngeus muscle.
FIGURE 5.17A Barium swallow—Oesophageal web.
FIGURE 5.17B Oesophagoscopy—Oesophageal web.
Treatment
• Correction of anaemia and dilatation of oesophagus is useful.
Diverticula
The oesophageal diverticula are of acquired variety and are protrusions of
epithelial lined mucosal pouches. They are of three varieties:
• Pharyngo-oesophageal pouch (Pharyngeal pouch/Zenker’s diverticulum)–
located in the midline, protruding between the oblique fibers of the inferior
pharyngeal constrictor and the transverse fibers of cricopharyngeus in the
proximal oesophagus (Killian’s dehiscence).
• Parabronchial pouch–occurs at the mid-oesophageal level due to traction by
the lymph nodes of tuberculosis or histoplasmosis of the subcarinal region.
• Epiphrenic diverticulum–a pulsion diverticulum usually occurs in the distal
oesophagus, typically within 10 cms of the cardia. The hernial sac consists of
mucosa and submucosa covered by thin bands of attenuated oesophageal
musculature.
• Pharyngeal pouch–sensation of high cervical obstruction is the most common
symptom. Regurgitation of the recently consumed food with offensive odour
is a characteristic symptom.
• Parabronchial pouch–usually asymptomatic, unless complicated. They rarely
cause dysphagia.
• Epiphrenic diverticulum–many are asymptomatic, but dysphagia,
regurgitation and retrosternal pain are the common symptoms.
• Barium swallow (Fig. 5.18) is diagnostic.
• Oesophagoscopy (Fig. 5.19) is confirmatory.
• Oesophageal manometry is diagnostic.
FIGURE 5.18 Barium swallow—Oesophageal diverticula (A) Zenker’s
diverticulum, (B) Parabronchia pouch, (C) Epiphrenic diverticulum.
FIGURE 5.19 Oesophagscopy—Oesophageal diverticulum Source: (Courtesy
Dr Mani Veeraraghavan).
Treatment
• Pharyngeal pouch
• Cricopharyngeal myotomy is effective for small diverticula.
• Excision is effective for large diverticula.
• Parabronchial pouch–large diverticula need excision.
• Epiphrenic diverticulum–excision is curative.
Note
Severely symptomatic diverticula of any region of the oesophagus need
excision.
Hiatus hernia
• This is a herniation of the stomach along the oesophagus through the
oesophageal hiatus into the chest.
• Hiatus hernia is of three types (Fig. 5.20):
• Sliding or oesophagogastric (most common)
• Rolling or paraesophageal
• Mixed
• Obesity, pregnancy (increase in intra-abdominal pressure) and old age may be
contributory factors.
• Strangulation is not uncommon.
FIGURE 5.20 Hiatus hernia types.
• Usually asymptomatic.
• Postprandial fullness of stomach, vomiting and dysphagia if the hernial sac is
very big.
• Barium contrast studies (Figs. 5.21A and B) and CT are diagnostic.
• Oesophagoscopy (Fig. 5.21C) is confirmatory.
FIGURE 5.21A Barium swallow—sliding hiatus hernia.
FIGURE 5.21B X Ray—Paraesophageal hernia.
FIGURE 5.21C Oesophagoscopy—Sliding hiatus hernia Source: (Courtesy Dr
Treatment
• Severely symptomatic patients require surgical correction (reduction of
herniated stomach, re-establishment of the oesophago-gastric angle and an
anti-reflux procedure – fundoplication).
Schatzki’s ring
• A ring like constriction of the lower oesophagus.
• Majority remains asymptomatic, but dysphagia is a common symptom.
• Barium swallow and oesophagoscopy (Fig. 5.22) are diagnostic.
FIGURE 5.22 Oesophagoscopy—Schatzki’s ring Source: (Courtesy Dr Mani

Veeraraghavan).
Treatment
• Endoscopic dilatations are useful, though repeated dilatations may be
required.
Pressure from extrinsic pathologies

Malignant tumours of the mediastinum, like lymph node enlargements are a
common cause of extrinsic pathologies to press on the oesophagus.
• Dysphagia is the commonest symptom.
• Associated symptoms relating to the primary disease may be elicitable.
• X-ray and CT are diagnostic.
• Barium swallow is informative.
• Oesophagoscopy (Fig. 5.23) is diagnostic.
FIGURE 5.23 Oesophagoscopy—Extrinsic pressure on normal

oesophagus. Source: (Courtesy Dr Mani Veerarahavan).
Treatment
• Treatment of the primary cause relieves dysphagia.
Foreign bodies, bolus obstruction

• Swallowing of foreign bodies, like coins is common in small children, and the
dentures in the very elderly.
• Bolus of food can also cause oesophageal obstruction.
• Dysphagia of acute form following the ingestion of the foreign body, or large
bolus of food.
• Plain radiographs are useful in identifying the metal objects.
• Oesophagoscopy is (Fig. 5.24) useful in identifying the obstructing agent and
removal of the same.
FIGURE 5.24 Oesophagoscopy—Foreign body Source: (Courtesy Dr Mani

Veeraraghavan).
Treatment
• Small objects pass without any difficulty.
• Obstructed large or impacted foreign bodies may be removed using an
endoscope.
• Rarely, surgery is required to remove the foreign bodies.

The chief complaint is dysphagia (difficulty in swallowing).
Eliciting history
• History of present illness: For how long the patient is suffering from
dysphagia and is it persistent or intermittent?
The period of presence of dysphagia is very important. Longstanding
dysphagia indicates a benign pathology, whereas, a short history especially in an
elderly may indicate malignancy. Remissions in dysphagia is seen in spastic
lesions like Paterson-Kelly syndrome.
• Previous history of present complaint: Is dysphagia specific to intake of
certain forms of food?
Difficulty in swallowing of recent onset, particularly to solid food is indicative
of an obstructive lesion. Dysphagia progressing from solids to liquids indicates a
progressive pathology like malignancy. Whereas, dysphagia to liquids first and
later on to solids is characteristic of cardiospasm.
Related questions
• Association of pain: Does the patient have pain, and if so, its location and
nature?
Pain is commonly present at the level of obstruction (e.g. reflux oesophagitis).
Severe pain radiates to the root of the neck, angles of the jaw, arms, epigastrium
and back. Pain in the oropharyngeal dysphagia is due to infective pathologies,
like tonsillitis and quinsy.
• Association of vomiting or regurgitation: Has the patient been bringing
out the food being consumed?
The patient might regurgitate or vomit the food in cases of achalasia cardia
with gross oesophageal dilatation and para-oesophageal hernia, as the proximal
dilated oesophagus and the large hernia sac store the food before it is ejected;
hence the vomitus may contain food particles taken hours ago.
• Association of blood in the vomitus: If the patient has been vomiting, does
or did the vomitus contain blood?
Association of blood in the vomitus is seen in pathologies, like oesophagitis,
para-oesophageal hernia and malignancies.
• Association of cough: Does the patient cough during the period of present
illness?
Cough is an unusual accompaniment of dysphagia. It may be present in cases
of tracheo-oesophageal fistula, or after regurgitation or vomiting due to irritation
of the pharynx or aspiration pneumonitis.
• Association of fever: Has the patient been having fever during the period of
dysphagia?
Presence of fever with pain is associated with infective pathologies, like
tonsillitis and quinsy. Fever may be present in patients with aspiration
pneumonitis.
• Loss of appetite and weight: Is there any loss of appetite and weight during
the course of illness?
Loss of appetite and weight are indicative of illnesses, like malignancies and
longstanding cases of achalasia cardia.
• Past medical history: Has the patient suffered from any chronic or major
illness, which required hospitalization?
This question will answer the history of previous surgeries performed on the
oro-pharyngo-oesophageal tract and also the stomach. Post operative or post-
radiotherapy strictures cause severe dysphagia. Cerebrovascular accidents
causing bulbar palsy are other causes of dysphagia. Accidental or intentional
consumption of corrosives (suicidal attempt of psychiatric patients) might have
warranted prolonged hospitalization.
• History of drug intake and allergies: Has or is the patient on a prolonged
drug intake?
Patients who have consumed drugs for prolonged periods develop an acid
peptic disease and gastro-oesophageal reflux which cause dysphagia.
• Social and personal history: Has the patient been taking balanced diet and
also been using tobacco?
Patients consuming severely spicy food are known to develop oesophagitis
and strictures. Tobacco usage has direct link with oesophageal malignancies.
• Family history: Has any other family member suffered from a similar
illness?
A family history of chronic anaemia and malignancies has to be noted.
Physical examination
General examination
• Examination of eyes
• Sunken eyes indicate dehydration and undernutrition (e.g. malignancy)
• Jaundice may be an indicator of metastatic liver disease. (e.g. oesophageal
malignancy with liver metastases).
• Pallor a feature of anaemia (e.g. Paterson-Kelly syndrome) and
undernutrition (e.g. malignancy).
• Examination of skin
• Dry scaly skin (e.g. dehydration and undernutrition)
- Scratch marks may indicate obstructive jaundice (e.g. oesophageal
malignancy with liver metastases).
- Scleroderma.
• Generalized oedema (anasarca) may be seen in patients with
hypoproteinemia.
• Recording of pulse and blood pressure
• Hypertension (e.g. anasarca of malignancies)
• Recording of temperature
• Elevated temperature (e.g. infective pathologies and malignancies)
Systemic examination
• Examination of oral cavity–a systematic examination of oral cavity is
essential (e.g., glossitis, aphthous ulcers, atrophic oral mucosa, tonsillitis,
pharyngitis)
• Examination of neck–a systematic examination of the neck is required (e.g.,
thyromegaly, lymph nodes of the neck)
• Examination of pharynx–a systematic examination of pharynx and larynx is
required to rule out malignancies, quinsy etc.
• Examination of chest
• Auscultation: Adventitious sounds may indicate aspiration penumonitis of
oesophageal malignancy
• Examination of abdomen–examination for determination of hepatomegaly
(e.g. nodular hard hepatomegaly of malignancy)
Examination of lymphatic system

The lymphatics and lymph nodes of the entire body should be examined in detail
with special attention to supraclavicular and axillary nodes for metastasis.
Enlargement of other groups of lymph nodes may indicate tuberculosis or
lymphomas. Examination of the liver and spleen completes the lympho reticular
system, which is useful in diagnosis.
CHAPTER 6
Constipation
S. Devaji Rao
CHAPTER OUTLINE
6.2. Pathophysiology of constipation 31
6.3. Etiology of constipation 31
6.4. Organic causes of constipation 31
• General 33
• Local 33
6.1 Introduction
Constipation means different things to different people:
• Straining to pass stool
• Sense of incomplete evacuation
• Passing stools of hard consistency
• Diminished frequency of bowel movements
Constipation is defined as a frequency of bowel movements of three or less in
a week with the need to strain at quarter or more of all bowel movements.
6.2 Pathophysiology of constipation
Table 6.1 highlights the various factors for constipation.
TABLE 6.1
Causes of Constipation
Factor Pathologies
Psychosocial Lack of childhood toilet training

Depression
Physiologic Delayed colonic transit (Colonic or hindgut inertia)
Impaired rectal motor function
Reduced rectal filling
Outlet obstruction
Absent gastrocolic reflex
Idiopathic megacolon and megarectum
Irritable bowel syndrome
The patients with constipation are divided into two categories:

1. Patients with normal colon and
2. Patients with organic pathology
6.3 Etiology of constipation

In patients with normal colo, constipation is caused by various factors of
systemic causes. They are listed in Table 6.2.
TABLE 6.2
Causes of Constipation in Patients with Normal Colon
Cause Conditions
Endocrine Hypothyroidis, hyperparathyroidis, hypercalcemi, hyperglucagonom, pheochromocytoma
Metabolic Diabetes mellitus
Nervous system Autonomic neuropathie, high spinal cord transectio, cauda equina syndrom, multiple sclerosi,
disorders Parkinson’s disease
Medications Anticholinergic, antidepressants
6.4 Organic causes of constipation
Patients with organic pathology in and around the colorectum present with
constipation due to various causes. They are listed in Table 6.3.
TABLE 6.3
Causes of Constipation in Patients with Organic Local Pathologies
Intraluminal Intramural Extramural
Fecal impaction Colorectal malignancies Uterine tumours

Polyps Anorectal infections Prostatic enlargement
Foreign bodies Strictures Pelvic metastases
Post anal dermoid
Pessaries
In patients with megacolon and megarectu, the causes are:

• Hirschprung’s disease (Congenital megacolon)
• Chagas’ disease
• Neurological diseases
• Endocrine and metabolic diseases
• Acquired megacolon
Clinical features
• The presenting symptom is constipation (number of bowel movements less
than three per week).
• Abdominal discomfor, pai, distensio, nausea are frequent accompaniments.
• Rectal bleeding may be associated with lesion, like colorectal cancer, solitary
rectal ulcers and hemorrhoids.
Clinical examination
• Abdominal examination may show:
• Palpable fecal masses in the sigmoid colon.
• Palpable malignant growths of colon.
• Rectal examination may show:
• Fecal soiling of perineu, due to overflow incontinence around a hard fecal
mass in the rectum.
• Palpable growth in the rectum.
Note
Constipation dating back to childhood is habitual and needs no special
investigatio, wherea, constipation of recent onset or short duratio, and a
change in the pattern of chronic constipation needs special attentio, especially
in the elderly.

• The chief complaint is constipation.
Eliciting history
• Description of constipation: Please describe the symptoms which the
patient presents as constipation.
The patients should be asked to describe in their own word, what they means
by constipatio, because each person has his or her own version.
• Number and frequency of stools: At what frequency does the patient pass
stools and how many times a wee, and does he or she have to strain to pass
stools?
Frequency of less than three stools per week with the need to strain at a
quarter or more of all bowel movement, is defined as constipation.
• History of present illness: For how long is the patient suffering from
constipatio, and is it different than before?
Long periods of constipatio, almost dating back to the childhood or pubert,
eliminate the possibility of diverticulosis and malignancy. Worsening of the
situation may indicate a patholog, especially in the elderl, and the development
of malignancy.
• Previous history of present complaint: Is constipation specific to intake of
certain forms of food?
Constipation may be associated with certain varieties of foo, like food low in
fibre content.
Related questions
• Association of pain: Does the patient have pain and if s, its location and of
what nature?
Abdominal pain may be present with constipation due to incomplete
evacuation and flatulent distensio, like in obstructive lesions. Local pai, like in
the perineum may be seen in constipation associated with anal fissur, anorectal
infections and low rectal or anal tumours.
• Association of blood in the stools: Has the patient been passing stools with
bleeding?
Passing fresh blood not mixed with hard stools is associated with injurie,
internal hemorrhoid, anal fissure, and anal carcinoma. Hard stools mixed with
blood and mucus is seen in colo-rectal malignancies.
constipation?
Presence of fever with pain is associated with infective pathologie, like
anorectal abscesses.
Loss of appetite and weight are indicative of illnesse, like malignancies and
longstanding cases of diverticulosis.
illnes, which required hospitalization?
This question will answer the history of previous surgeries performed on the
colon for malignancies. Post operative or post-radiotherapy strictures cause
severe constipation.
drug intake?
Patients who have consumed drug, like antidepressants for prolonged periods
develop constipatio, and the consumption of laxative for a longtime indicates
habitual constipation.
• Social and personal history: Has the patient been taking a balanced diet
and also been using tobacco?
Patients consuming low fibre food are known to develop constipation.
illness?
A family history of chronic constipation and malignancies has to be noted.
General examination
• Sunken eyes indicate dehydration and undernutrition; seen in uremia.
• Jaundice may be an indicator of metastatic liver disease.
• Pallor a feature of malignancy.
• Dry scaly skin (e.g. dehydration and undernutrition).
• Scratch marks may indicate uremia or obstructive jaundice.
• Generalized oedema(anasarca) may be seen in patients with metastatic
disease.
Local examination
• Examination of abdomen: Examination for determination of hepatomegaly
(e.g. nodular hard hepatomegaly of metastatic liver).
• Rectal examination: Rectal examination and proctoscopy are inherent parts
of the clinical examination of patients with constipation (e.g. anorectal
pathologies).
Examination of the lymphatic system

with special attention to inguinal nodes for metastasis. Enlargement of other
groups of lymph nodes may indicate tuberculosis or lymphomas. Examination of
the liver and spleen completes the lympho reticular syste, which is useful in
diagnosis.
CHAPTER 7
Obstructive jaundice
S. Devaji Rao
CHAPTER OUTLINE
7.2. Bilirubin metabolism 34
7.3. Anatomy of biliary system 34
7.4. Obstructive jaundice 34
7.5. Causes of obstructive jaundice 35
• Biliary atresia 35
• Choledochal cyst 36
• Benign strictures 38
• Sclerosing cholangitis 38
• Hepatocellular carcinoma 39
• Cholangiocarcinoma 39
• Periampullary carcinoma 40
• Carcinoma head of pancreas 40
• Metastatic liver disease 40
• Metastatic lymph nodes 40
• Choledocholithiasis 41
• Parasitic diseases 42
• General 44
• Abdomen 44
7.1 Introduction
Jaundice is defined as the yellowish discolouration of body tissues due to an
excess of circulating bilirubin.
• Normal serum bilirubin levels range from 0.5 to 1.0 mg%.
• Jaundice is detected clinically when serum bilirubin levels go above 2.0 mg%.
• The discolouration is most evident in tissues abundant in elastic collagen
tissu, such as mucous membranes (bulbar conjunctive over the scler, oral
cavity and undersurface of tongue) and skin.
7.2 Bilirubin metabolism

Bilirubin metabolis, and its defects and diseases are given in Figure. 7.1
FIGURE 7.1 Bilirubin metabolism.
Note
Malabsorption of Vitamin K is a consequence of poor dietary absorptio, which
leads to decreased hepatic synthesis of clotting factor, particularly
prothrombin. Impairment of blood clotting is not so great that it will cause
spontaneous haemorrhag, but there is significant risk of haemorrhage during
surgery or invasive procedures.
7.3 Anatomy of biliary system

Bile canaliculi form a network surrounding the hepatocyte, and unite to form
intralobular and interlobular ductules. These ductules converge to form the left
and right hepatic ducts. The hepatic ducts unite to form the common hepatic
duct. The cystic duct joins the common hepatic duct to form the common bile
duct (CBD). The common duct lies most anterior in the lesser omentum and
travels down through the posterior substance of the pancreas and is joined by the
pancreatic duct. The confluence is flask shaped and is called ampulla of Vater.
The duct ultimately opens in the postero-medial part of the duodenum. This
opening is surrounded by a circular muscl, Sphincter of Oddi (Fig. 7.2).
FIGURE 7.2 Anatomy of biliary system.

7.4 Obstructive jaundice
Extra-hepatic obstruction producing cholestasis and jaundice is otherwise called
Surgical or Obstructive cholestatic jaundice.
The causes of obstruction are mechanical and are shown in Figure 7.3 A.
FIGURE 7.3A Causes of mechanical obstruction of biliary system.
The surgeon is concerned with surgical jaundice as it requires surgical

intervention to remove the cause and/or relieve the obstruction.
7.5 Causes of obstructive jaundice

Causes of obstructive jaundice can be classified based on its aetiology (Table
7.1).
TABLE 7.1
Aetiological Classification of Obstructive Jaundice
Aetiology Pathology
Congenital Biliary atresia
Choledochal cyst
Traumatic Traumatic strictures
Inflammatory Sclerosing cholangitis
Neoplastic Hepatocellular carcinoma
Cholangiocarcinoma
Periampullary carcinoma
Carcinoma head of pancreas
Metastatic liver disease
Metastatic lymph nodes
Metabolic and miscellaneous Gallstones
Parasitic diseases
Biliary atresia
• There are two types of biliary atresia
• Fetal type: present at the time of birth.
• Perinatal type: develop around 2nd to 4th week of life.
• Exact aetiology is not known
• Suggested triggering factors are:
• Viral or bacterial infection
• Immune deficiency
• Abnormal bile component
• Error in development of biliary system
• The undeveloped biliary duct system may be at single or multiple point,
causing obstruction and jaundic, leading to liver failure and deat, generally in
the first year of life.
Persistent and progression of jaundice beyond first two weeks after birth.
• Serum bilirubin (serial estimations) levels are diagnostic
• Ultra sound (US) is informative.
• HIDA scan and liver biopsy are confirmatory.
Treatment
• Hepatic porto-enterostomy (Kasai operation) is the treatment of choice
within 60 days of birth.
• Liver transplantation is warranted for deteriorating liver functions.
Choledochal cyst
• Cystic dilatations of the biliary system.
• Can involve the extrahepatic radicles or intrahepatic radicles or both.
• Reported frequency rates range from 1 case per 100,000–150,000 to 1 case
per 2 million live births.
• Choledochal cysts are relatively rare in Western countrie, but more prevalent
in Asia.
• Shows female predominance.
• No definite aetiology is known.
• Pathogenesis is probably multifactorial.
• Anomalous junction of pancreatic duct with the bile duct leading to reflux
pancreatic juice causes activation of pancreatic proenzyme, damaging the
bile duct wall
• Defects in epithelialization and recanalization of the developing bile ducts
and congenital weakness of the ductal wall also have been implicated
• These anomalies are classified according to the system published by Todani
and coworkers. Five major classes of choledochal cysts (Fig. 7.3B) exist (i.e.
types I-V, with subclassifications for types I and IV (i.e. types I, I, IC; types
IV, IVB)
• Type I cysts are the most common and represent 80-90% of choledochal
cysts. They consist of saccular or fusiform dilatations of the common bile
duc, which involve either a segment of the duct or the entire duct.
- Type IA is saccular in configuration and involves either the entire
extrahepatic bile duct or the majority of it
- Type IB is saccular and involves a limited segment of the bile duct
- Type IC is more fusiform in configuration and involves most or all of the
extrahepatic bile duct.
• Type II cysts appear as an isolated diverticulum protruding from the wall of
the common bile duct. The cyst may be joined to the common bile duct by
a narrow stalk
• Type III cysts arise from the intraduodenal portion of the common bile duct
and are described alternately by the term ‘choledochocele’.
• Type IV cysts are multiple dilatations of bile ducts
- Type IVA cyst consist of multiple dilatations of the intrahepatic and
extrahepatic bile ducts.
- Type IVB cysts are multiple dilatations involving only the extrahepatic
bile ducts.
• Type V (Caroli disease) consists of multiple dilatations limited to the
intrahepatic bile ducts.
FIGURE 7.3B Choledochal cysts.
Complications
• Children – pancreatiti, cholangitis and hepatocellular damage.
• Adults – cholangiti, hepatic abscesse, recurrent pancreatiti, cholelithiasi,
cholangiocarcinoma
Infants
• Early infancy: Jaundice and acholic stools may prompt a workup for biliary
atresia.
• Palpable mass in the right upper quadrant of the abdome, accompanied with
hepatomegaly.
Children
• Clinical picture of intermittent biliary obstruction or recurrent bouts of
pancreatitis.
• A palpable right upper quadrant mass and jaundice.
• Intermittent attacks of colicky abdominal pain.
Adults
• Adults with choledochal cysts can present with one or more severe
complications
• Frequentl, adults with choledochal cysts complain of vague epigastric or right
upper quadrant pain and can develop jaundice or cholangitis.
• The most common symptom in adults is abdominal pain.
• A classic triad of abdominal pai, jaundic, and a palpable right upper quadrant
abdominal mass has been described in adults with choledochal cysts but is
found in only 10-20% of patients.
• Leucocytosis in cholangitis.
• Raised alkaline phosphatase in some cases.
• Serum amylase may be increased when there is pancreatitis.
• US abdomen is informative.
• CT (Fig. 7.4A) and MRI abdomen can delineate the biliary anatomy.
• MRCP (Fig. 7.4B) has very high sensitivity.
• ERCP and PTC are useful investigations.
FIGURE 7.4A CT—Choledochal cyst.
FIGURE 7.4B MRCP—Choledochal cyst – Type 1.
Treatment
• Antibiotics when cholangitis or pancreatitis occur.
• Excision of cyst with biliary enteric anastomosi, and varies according to
type:
• Type I: Complete excision of the involved portion of the extrahepatic bile
duct with Roux-en-Y hepaticojejunostomy
• Type II: The dilated diverticulum comprising a type II choledochal cyst is
excised in its entirety. The resultant defect in the common bile duct is
closed over a T-tube
• Type III (choledochocele): The choice of therapy depends upon the size
the cyst.
- Choledochoceles measuring 3 cm or less can be treated effectively with
endoscopic sphincterotomy
- Lesions larger than 3 cm typically produce some degree of duodenal
obstruction. These lesions are excised surgically through a
transduodenal approach. If the pancreatic duct enters the choledochocel,
it may have to be reimplanted into the duodenum following excision of
the cyst.
• Type IV: The dilated extrahepatic duct is completely excised and a Roux-
en-Y hepaticojejunostomy is performed to restore continuity. Intrahepatic
ductal disease does not require dedicated therapy unless hepatolithiasi,
intrahepatic ductal stricture, and hepatic abscesses are present. In such
instance, the affected segment or lobe of the liver is resected.
• Type V (Caroli disease): Disease limited to one hepatic lobe is amenable to
treatment by hepatic lobectomy. When this occur, the left lobe usually is
affected. Hepatic functional reserve should be examined carefully in all
patients before committing to such therapy. Patients with bilobar disease
who begin to manifest signs of liver failur, biliary cirrhosi, or portal
hypertension may be candidates for liver transplantation.
• Lilly technique: Occasionall, the cyst adheres densely to the portal vein
secondary to long-standing inflammatory reaction. In this situatio, a complet,
full-thickness excision of the cyst may not be possible. In the Lilly techniqu,
the serosal surface of the duct is left adhering to the portal vei, while the
mucosa of the cyst wall is obliterated by curettage or cautery. Theoreticall,
this removes the risk of malignant transformation in that segment of the duct.
Benign strictures
Majority of strictures of CBD are due to a previous surgery of biliary system.
Right upper quadrant pain with obstructive jaundice.
• US and CT may reveal the dilated intra-hepatic radicals.
• ERCP (Fig. 7.5) and MRCP (Fig. 7.6) will reveal the level and severity of
stricture.
• PTC is useful in impassable strictures.
• MDCT with the MPR technique has sensitivity of about 90 – 95% in
localizing the causes of biliary obstruction.
FIGURE 7.5 ERCP—Benign stricture of CBD.

FIGURE 7.6 MRCP—Benign stricture of CBD.
Treatment
• Stenting of the bile duct is the preferred treatment.
• Surgical treatment is required for impassable strictures.
• Resectable strictures can be resected with primary anastomosis.
• Strictures of the retropancreatic region require choledocho-duodenostomy.
• Strictures of the common hepatic duct require hepatico-jejunostomy.
Primary sclerosing cholangitis (PSC)

• Rare condition of autoimmune origin.
• Results in progressive fibrosis of the biliary system.
• Causes luminal narrowing and progressive obstructive jaundice and secondary
cirrhosis.
• Strongly associated with inflammatory bowel diseas, ulcerative colitis (75%
of patients with PSC have inflammatory bowel disease and 7.5% with
ulcerative colitis have PSC).
• Risk of malignant transformation (cholangiocarcinoma) is 15%.
• Progressive obstructive jaundice.
• Low grade fever with chills and/or sweats.
• CT and ERCP are diagnosti, and classically show diffuse stricturing and
beading involving both intra and extrahepatic bile duct, but indistinguishable
from cholangiocarcinoma.
• Liver biopsy may show the characteristic lesion of concentric fibrosis around
the small bile duct, termed ‘onion skin’ fibrosis.
• Peripheral antineutrophil cytoplasmic antibody (pANCA) is detected.
Treatment
• May settle spontaneously
• May respond to antibiotics and UDCA.
• Stenting of the biliary tree is very useful.
• Liver transplantation is used widely for advanced disease.
Hepatocellular carcinoma
(Detailed in Chapter 33)
Cholangiocarcinoma
• Malignancy arising from the epithelium lining the intra-hepatic or the extra-
hepatic parts of the biliary ductal system.
• Common in males of 50 to 70 years of age.
• Infestation with liver flukes (Clonorchis sinensis in Hong Kon,
Opisthorchis viverrini in Thailand)
• Oriental cholangiohepatitis
• Hepatolithiasis
• Congenital biliary anomalies
• Microhamartomas
• Thorotrast (historical importance only)
• Macroscopically,
• Upper third tumours of extrahepatic biliary tree tend to be diffusely
sclerosing.
• Middle third tumours tend to be nodular.
• Lower third tumours tend to be papillary.
• Microscopically, they are adenocarcinomas.
• Hilar adenocarcinoma refers to the tumour arising from the main hepatic duct
or one of its lobar branches in the hilum of liver (Klatskin tumour).
• Spread of cholangiocarcinoma can be by various routes:
• Direct: Upper third is to the liver and lower third is to the duodenum and
pancreas.
• Lymphatic: to hila, superior mesenteric and celiac lymph nodes.
• Hematogenous: to live, lungs and bones.
Symptoms
• Painless progressive obstructive jaundice.
• Pruritu, dark urine and pale stools.
• Weight loss and weakness are common accompaniments.
Signs
• Gallbladder may be palpable (positive Courvoisier’s sign) (See page 41)
• Smooth hepatomegaly.
• Serial determinations of bilirubi, alkaline phosphatas, SGO, SGP, SGGT.
• Tumor markers: Carcinoembryonic antigen (CEA) and cancer antigen (CA
19/9) are usually elevate, but not specific.
• CT (Fig. 7.7) and MRCP (Fig. 7.8) show the level of obstruction.
• ERCP (Fig. 7.9) is useful in permitting tissue diagnosis and temporary or
permanent biliary decompression by stenting. Histopathology may be
difficult due to the fibrous nature of the disease involving the duct wall.
• PTC (Fig. 7.10) is useful in certain situation, when ERCP is not possible.
• Positron emission tomography (PET, endoscopic ultrasound and
laparoscopic ultrasound are newer imaging modalities used today.
FIGURE 7.7 CT—Cholangiocarcinoma.

FIGURE 7.8 MRCP—Cholangiocarcinoma.
FIGURE 7.9 ERCP—Stricture due to cholangiocarcinoma.
FIGURE 7.10 PTC—Cholangiocarcinoma.
Treatment
Curative
• Pancreato-duodenectomy (Whipple’s procedure) with reconstruction
procedures is done for distal tumours.
• Local resection (with hepatic resection) and hepatico-jejunostomy is done
for hilar lesion.
• Hepatic resection is required for intrahepatic lesion.
Palliative
• Stenting (endoprosthesis) (Ref Fig. 7.10) is useful for unresectable tumours.
• Choledochojejunostomy to relieve jaundice in cases not amenable to
endoscopic or percutaneous procedures.
Periampullary carcinoma
• Adenocarcinoma arising from the ampulla of Vater.
• Forms a polypoid lesion projecting into the duodenal lumen.
Fluctuating jaundic, as the tumour is friable and tends to bleed insidiously.
• Fecal occult blood test is positive in many cases.
• US may show a dilated biliary system.
• CT (Fig. 7.11A) localizes the tumour and also makes diagnosis about the
lymph nodal involvement.
• MRCP (Fig. 7.11B) helps in localizing the tumour.
• Duodenoscopy (Fig. 7.12) and biopsy are diagnostic.
FIGURE 7.11A CT—Periampullary carcinoma.
FIGURE 7.11B MRCP—Polypoid periampullary carcinoma.
FIGURE 7.12 Duodenoscopy—Periampullary carcinoma Source: (Courtesy Dr
Treatment
Pancreato-duodenectomy (Whipple’s operation) is the treatment of choice.
Carcinoma head of pancreas


Metastatic lymph nodes

• The tumours of the hepatobiliary region metastasise to the lymph nodes in the
porta hepati, which may cause extraneous pressure on the ductal system to
cause obstructive jaundice.
• Presenting symptom is painless progressive jaundice.
• Investigations should target to find the primary tumour.
• U, CT and upper gastrointestinal (GI) endoscopy may be conclusive.
Treatment
• This advanced disease needs only palliation by chemotherapy.
• Bypass procedures are needed for obstructing primary tumours.
• PTC and ERCP stenting may be useful in relieving jaundice.
Choledocholithiasis (gallstones in bile ducts)

• Stones within the CBD are usually formed in the gallbladder and pass on to
the CBD.
• Primary stones in the CBD are usually of the soft brown pigmented type and
result due to stasis of bile.
The gallstones originate in the gallbladde, pass through the cystic duct and lodge
in the CBD. Many small stones pass into the duodenum without causing
symptom, but some enlarge in the CB, due to stasi, and cause obstruction to bile
outflo, and cause obstructive jaundice. A stone in the CBD can give rise to two
varieties of obstructive jaundice:
1. Progressive jaundice due to impaction of stone
2. Intermittent jaundice due to ball-valve action of the stone
Gallstones obstructing the bile outflow in the bile duct can cause a variety of
clinical conditions. They are given in Table 7.2.
TABLE 7.2
Clinical Presentation of Gallstones in the CBD
Degree of Obstruction Clinical Condition Clinical Presentation

Chronic obstruction associated with Ascending cholangitis Abdominal pai, swinging pyrexia and jaundice
infection
Acute chronic obstruction with severe Acute suppurative Abdominal pai, swinging pyrexia and jaundic,
infection cholangitis toxemia
Obstruction at the duodenal papilla Acute pancreatitis Abdominal pai, jaundic, shock syndrome
In a jaundiced patien, the gallbladder is not distended and palpable when the
disease is due to stone, as chronic cholecystitis leads to fibrosis and contracture
and does not allow the distention. Wherea, it becomes palpably enlarged if the
obstruction is chronic and progressive as in tumours of head of pancreas. This is
called ‘Courvoisier’s law’.
• Increased and fluctuating levels of serum bilirubin.
• Raised levels of alkaline phosphatas, SGG, SGO, SGPT.
• Transabdominal ultrasonography has a detection rate of 70–80% in
choledocholithiasis.
• Endoscopic ultrasound (EUS) (Fig. 7.13) has a sensitivity rate of 98% and is
not the most preferred investigation.
• MRCP has the accuracy rate similar to EU, and most of the stones missed by
MRCP are less than 6 mm in diameter.
• CT cholangiography (Fig. 7.14) has the accuracy rate less than that of either
EUS or MRCP.
• ERCP (Fig. 7.15) is accurate in more than 90% of patient, but should be
performed only as a preliminary therapeutic procedure [sphincterotomy (Fig.
7.16A) and basketing (Fig. 7.16B, or balloon extraction (Fig. 7.16C)] an, as
complications like acute pancreatiti, bleeding and perforation occur.
• PTC is used for establishing the upper level of obstruction caused by
impacted stone, which also can be used as a drainage procedure in inoperable
and very sick patients.
• Isotope studies of the biliary system will indicate the physiology.
FIGURE 7.13 Endoscopic US—stone in the CBD.
FIGURE 7.14 CT—stone at the distal CBD.

FIGURE 7.15 ERCP—multiple stones in CBD.
FIGURE 7.16 (A) Sphincterotomy. (B) Basketing of CBD stone. (C)
Balloon extraction of bile duct stones.
Treatment
• Endoscopic treatment
• ERCP sphincterotomy and basketing is used for removal of obstructing
gallstones.
• Endoscopic lithotripsy during ERCP or extra-corporeal lithotripsy in
combination with ERCP are for management of large stones.
• Surgical management
• Choledocho-duodenostomy is performed for multiple stones and grossly
dilated CBD.
• Urgent decompression by ERCP sphincterotomy and drainage are
required for the management of suppurative cholangitis.
• Open CBD procedures are rarely performed these days.
Parasitic diseases
• After ingestion of the eggs of Ascaris lumbricoide, larvae are liberated into
the small intestin, which migrate into the bloodstream to the lungs.
• They ascend the bronchial tree and are swallowe, and return to the jejunum.
• During this proces, the adult worms may enter the bile duct, and obstruct the
bile outflow causing obstructive jaundice.
• More common in children.
• Hydatids are also known to cause obstructive jaundice.
• Obstructive jaundice with bouts of intestinal or biliary colic.
• Stool examination for ova may reveal the presence of worms.
• US or CT of hepatobiliary system is diagnostic.
• Casoni’s test and immunoelectrophoresis are useful in hydatid diseases.
Treatment
• ERCP sphincterotomy and extraction of worm is the treatment of choice.
• Administration of anti-helminthic is mandatory.
• Scolicidal drugs are necessary for the treatment of hydatid disease.

Chief complaint is jaundice (yellowish discolouration of eyes).
Eliciting history
• History of present illness: For how long the patient is jaundiced and is it
persistent or fluctuant?
The period of presence of jaundice is very important. Longstanding jaundice
indicates a progressive diseas, and fluctuation in levels of jaundice is an
indicator of periampullary carcinoma (ball valve obstruction) or gallstones in
CBD.
• Previous history of present complaint: Did the patient suffer from jaundice
at any time in the past?
If the patient had suffered from jaundice in the pas, then the nature of virus
should be known. Hepatitis B infection in the past is a precursor for cirrhosis and
hepatocellular carcinoma. It should be remembered that hepatitis A infections do
not give immunity to hepatitis B and C infection, and vice versa.
Related questions
• Association of abdominal pain: Does the patient have abdominal pain and
if s, its location and of what nature?
Painless jaundice occurs in viral hepatiti, periampullary and pancreatic head
carcinoma. Painless progressive jaundice may indicate malignancy. Constant
pain in the abdomen or in the back may indicate a pancreatic malignancy.
Colicky pain in the right subcostal area may indicate gallstones causing
obstructive jaundice.
jaundice?
Presence of fever with chills associated with abdominal pain indicates
cholangitis and is an accompaniment of gallstones in the bile duct (Charcot’s
triad).
• Association of pruritus: Has the patient been having itching?
Association of pruritus with jaundice indicates obstruction of bile ducts due to
irritation of the cutaneous nerves by the retained bile salts.
• Bowel habits: Has the patient been passing stools without strai, and is
defecation associated with rectal bleed?
Recent history of constipation or altered bowel habits with or without rectal
bleed may indicate colo-rectal malignancies metastasizing to the liver to cause
jaundice. Characteristic ‘putty’ or ‘clay coloured’ stools is seen in cholestasis due
to the absence of stercobilin and bile acids which darken the stools.
Loss of appetite and weight are indicative of illnesse, like malignancie, and
chronic hepatocellular damage also causes loss of weight.
illnes, which required hospitalization?
Some chronic illnesses or major surgerie, which require a prolonged hospital
stay and blood transfusions may be a cause of viral B hepatitis. Previous history
of biliary surgery may be a good clue to traumatic stricture of bile ducts or
residual gallstones as a cause of jaundice. A past history of upper GI
haemorrhages may indicate portal hypertension and variceal bleed.
• History of drug intake and allergies: Is the patien, or has bee, on a
prolonged drug intake?
Sometimes the patients are not aware of the illnesses they have suffered in the
pas, but have been on prolonged drug intak, like the hepatinics (indicating a
hepatic illness) or drugs administered for some other illness which are
hepatotoxic and may be the cause for jaundice (e.g. Chlorpromazine for
psychiatric illness).
• Social and personal history: Has the patient been taking a balanced diet
and also been consuming alcohol?
Patients of low economic groups and frequent travellers may consume
unprotected water and foo, which may be a cause of viral A and E hepatitis.
Unprotected injections may be a cause of viral B and C hepatitis. Consumption
of alcohol has a direct link to cirrhosis and hepatocellular carcinoma. Drug
addicts have a high incidence of hepatitis , which may progress to cirrhosis and
hepatocellular carcinoma.
• Family history: Has any other family member suffered from jaundice?
A family history of chronic anaemi, gallstones and a history of splenectomy
may indicate hereditary spherocytosi, or any form of congenital
hyperbilirubinemia.
• History of immunization: Has the patient received any immunization
towards hepatitis virus?
History of immunization may help to eliminate some viral afflictions of the
liver.
General examination
• General build
• Emaciated–Malignant causes of jaundice
• Distended abdomen–Ascites
• Eyes (to be examined in natural illumination)
• Sclerae for the depth of jaundice (Ref. Fig. 4.8).
• Conjunctivae for pallor and anaemia (Ref. Fig. 4.6).
• Skin
• Dry scaly skin–Malignancies
• Scratch marks–Obstructive jaundice
• Xanthomas
• Examination for signs of liver failure
• Palmar erythema
• Spider naev, ascites
• Fetor hepaticus
• Gynecomazia
• Testicular atrophy
• Clubbing of fingers
• Pedal oedema
• Flapping tremor
Vital signs
• Recording of pulse and blood pressure.
• Recording of Temperature
• Elevated temperature (e.g. high–chalangiti, viremi, septicemia and liver
abscess; mild–hepatic malignancies).
Examination of abdomen
• Examination of abdominal wall
• Scars may indicate previous surgery.
• Caput medusae indicate liver failure and portal hypertension.
• Examination of abdomen–Examination should include procedures for
determination of:
• Ascites or free fluid in the abdomen (e.g. liver failure and/or malignancy)
(See Chapter 31).
• Hepatomegaly (e.g. fine nodular liver of cirrhosis and/or nodular hard
hepatomegaly of malignancy) (See Chapter 31).
• Splenomegaly (e.g. congenital hemolytic anemi, portal hypertension) (See
Chapter 31).
• Enlargement of gallbladder (e.g. malignancy of pancreas or gallbladder).
• Intra-abdominal lumps (e.g. malignancy and/or lymph node enlargement).
• Rectal examination–Rectal examination is mandatory and is useful in
determining the presence of primary rectal malignancy or malignant deposits
in the pouch of Douglas.

(e.g. tuberculosis or lymphoma). Examination of the liver and spleen completes
the lympho reticular system which is useful in diagnosis.
A flowchart for the evaluation of obstructive jaundice is shown at the end of
the chapter.
Flowchart for Evaluation of Obstructive Jaundice

CHAPTER 8
Gastrointestinal haemorrhage
S. Devaji Rao
CHAPTER OUTLINE
8.2. Causes of gastrointestinal haemorrhage 46
8.3. Pathological conditions 48
• Oesophageal varices 48
• Mallory Weiss tears 48
• Gastroduodenal polyps 48
• Gastric lymphoma 49
• Vascular malformations 49
• Radiation enterocolitis 49
• Benign tumours of small bowel 50
• Malignant tumours of small bowel 50
• Acute infections and inflammations 51
• Colorectal polyps 51
• Local examination 53
8.1 Introduction
Gastrointestinal (GI) haemorrhages, called major haemorrhages when they are in
large quantities, present either as vomiting of blood or passage of blood per
rectum.
• Vomiting blood, called haematemesis may be fresh or partly altered. Altered
blood is dark in colour (contact of blood with hydrochloric acid produces
haematin), and has the typical appearance of ‘coffee grounds’.
Haematemesis usually occurs due to pathologies proximal to the duodeno-
jejunal flexure at the ligament of Treitz. Some blood passes down the
alimentary tract, and is subjected to digestion, to pass per rectum as altered
blood called ‘melena’ The blood should remain in the gut for approximately
eight hours to produce melena, but when the bleeding from the upper
gastrointestinal tract (GIT) is large and rapid, and when the GI transit time is
prolonged, bleeding from small bowel and even ascending colon can pass
rectally as black stools, and as melena. Approximately about 60 ml of blood
is required to produce a single black stool; loss of more than this amount can
cause melena for more than three days. Even after the colour of the stools
returns to normal, the test for occult blood in the stool may remain positive
for a week or longer. Haematemesis and melena usually co-exist.
• On the contrary, bleeding per rectum usually occurs due to the pathologies
distal to the duodeno-jejunal flexure, and it is bright red in colour. This is
called haematochezia. Rarely, melena is the sole clinical presentation of
upper GI bleed. Occult bleeding from GIT is common, but can be identified
only by stool examination, but the bleed should be atleast 10 ml.
The blood loss due to GI haemorrhage is divided into three types:
1. Mild–less than 500 ml
2. Moderate–500 to 1,500 ml
3. Severe–more than 1,500 ml
Mild haemorrhages are rarely associated with systemic signs. When the blood
loss approaches about 40% of the blood volume, shock ensues. The volume of
blood loss either by vomiting or through rectum, is not a very reliable measure,
as large amounts stay in the bowel. Whatever be the external visible loss, signs
of hypovolemia should be watched for.
8.2 Causes of gastrointestinal haemorrhage

The causes of GI haemorrhage are given in Table 8.1 and shown in Figure 8.1.
FIGURE 8.1 Causes of gastrointesnal bleeding.
TABLE 8.1
Causes of Gastrointestinal Hemorrhage and Their Clinical
Presentation
Part of GIT Pathology Clinical Presentation
Upper Oesophagus Reflux oesophagitis Haematemesis and/or melena

Oesophageal varices
Mallory Weiss tears
Stomach and Acid peptic disease
duodenum
Gastric polyps
Gastric lymphoma
Carcinoma stomach
Lower Small bowel Angiodysplasia Melena/Hematochezia
Diverticulitis
Radiation enteritis
Infections and
inflammations
Ischemic disease
Intussusception
Richter’s hernia
Benign tumours
Malignant tumours
Angiodysplasia Haematochezia (diarrhoea/constipation as per
aetiology)
Diverticulitis
Radiation colitis
Infections and
inflammations
Ischemic disease
Ulcerative colitis
Benign polyps
Malignant tumours
Rectum and anus Polyps Hematochezia (constipation)
Malignant tumours
Haemorrhoids, fissures
Note
Lower GI haemorrhages do not present with haematemesis.
The pathological conditions which have the potential to bleed are discussed
separately in appropriate chapters. However, a few conditions, which do not
present with any clinical finding other than the bleed, are detailed below.
8.3 Pathological conditions
Oesophageal varices
• Occurs usually due to portal hypertension secondary to cirrhosis of liver.
• Any disease causing portal hypertension (e.g. portal vein thrombosis,
idiopathic portal hypertension, non-cirrhotic portal fibrosis) can cause
oesophageal varices.
• Sudden and massive upper GI bleed.
• Chronic blood loss due to bleeding varices is rare.
• Recurrent bleeds are common.
• Barium swallow (Fig. 8.2A) is informative.
• Oesophagoscopy (Fig. 8.2B) is diagnostic.
• Other investigations related to liver pathology should be performed to
identify the cause of varices.
FIGURE 8.2A Barium swallow—Oesophageal varices.
FIGURE 8.2B Oesophagoscopy—oesophageal varices Source: (Courtesy Dr
Treatment
• Acute bleeds require medical management with measures to stop the
bleeding (compression with Sengstaken-Blakemore tube), and blood
transfusions.
• Once the acute crisis is managed, oesophagoscopy and
sclerotherapy/banding controls the bleeding.
• Surgical procedures are required to prevent recurrences.
Mallory weiss tears

• Refers to a longitudinal tear in the region of oesophago-gastric junction,
majority just below the junction.
• The tear follows retching and related to alcohol intake.
• Retching and vomiting of normal gastric contents followed by haematemesis
and or melena.
• Oesophagoscopy (Fig. 8.3) is diagnostic.
FIGURE 8.3 Oesophagoscopy—bleeding from Mallory Weiss

tear Source: (Courtesy Dr Mani Veeraraghavan).
Treatment
• Initial treatment is supportive and expectant.
• In a small minority of cases, persistent bleeding requires suturing of
laceration through gastrotomy.
Gastroduodenal polyps
• Gastric polyps are small, benign hyperplastic growths.
• They may be single or multiple, and occur anywhere in the stomach.
• They are potentially malignant.
• Generally asymptomatic, but rarely presents with minor bleeds.
• Found incidentally on barium studies or endoscopy (Fig. 8.4).
FIGURE 8.4 Gastroduodenoscopy—duodenal polyp Source: (Courtesy Dr Mani
Veeraraghavan).
Treatment
• Endoscopic excision is the treatment of choice.
Gastric lymphoma
• Lymphomas constitute about 10% of gastric malignancies, and H. pylori
infection is closely associated with the lymphoid hyperplasia, which may
progress to lymphoma.
• They infiltrate the stomach wall diffusely.
Loss of appetite, upper abdominal dyspepsia and upper GI bleed.
Barium meal and Gastroscopy (Fig. 8.5) biopsy are conclusive.
FIGURE 8.5 Gastroscopy—bleeding gastric lymphoma Source: (Courtesy Dr

Treatment
• Low-grade lymphomas resolve by H. pylori eradication.
• Chemoradiation is the treatment of choice in some cases.
Vascular malformations
• They are tiny hamartomatous vascular lesions in the bowel wall.
• Since this presents in the later part of life, the origin is thought to be
degenerative than congenital.
• Similar lesions may be present in the large bowel.
Severe bleeding that is out of proportion to the size of the lesion, and may be
recurrent.
• Endoscopy (Figs. 8.6A and B) is diagnostic.
• Selective mesenteric arteriography may show the source of bleeding.
FIGURE 8.6A Colonoscopy—bleeding angiodysplasia of large
bowel Source: (Courtesy Dr Mani Veeraraghavan).
FIGURE 8.6B Colonoscopy—haemangioma of rectum Source: (Courtesy Dr
Treatment
• Therapeutic embolisation of localized bleeding lesions using selective
angiography is useful.
• If unsuccessful, the affected segment is resected.
Radiation enterocolitis
Inflammation of the intestine especially in those patients undergoing radiation
for malignancy in the adjacent areas.
Abdominal pain and frequent blood stained mucous stools.
• Endoscopy is diagnostic (Fig. 8.6C).
• Capsule endoscopy is diagnostic.
FIGURE 8.6C Colonoscopy—radiation colitis Source: (Courtesy Dr Mani

Veeraraghavan).
Treatment
Usually self limiting, and undergoes spontaneous resolution.
Benign tumours of small bowel

• Small bowel tumours are rare.
• They can be:
• Adenomas
• Endocrine tumours (carcinoids)
• Stromal tumours
• Lipoma
• Vascular tumours (hemangioma)
• Neurogenic tumours
• Tumours of lymphoid tissue
• Beingn polyps (Peutz-Jeghers syndrome)
• Many lesions are asymptomatic.
• Presentation depends on size and location.
• Large lesions are usually of villous type. and present with intestinal
obstruction and intussusception (Ref Fig. 30.21A)
• Ulcerated lesions may present with bleeding.
Capsule endoscopy is diagnostic (Fig. 8.7)
FIGURE 8.7 Capsule endoscopy—ileal lipoma.
Treatment
Excision with resection of bowel is the treatment for symptomatic tumours.
Malignant tumours of small bowel

• Lymphomas of small intestine are uncommon, but account for 30% of small
bowel malignancies.
• Adenocarcinomas of small intestine are much rarer than carcinoma of
stomach and large intestine.
• Periampullary region and duodenum are most common sites.
• Most cancers arise within a pre-existing adenoma.
• Carcinoid tumours account for about one third of all small intestinal tumours.
• They are more common in the duodenum and ileum.
• They are slow growing and produce narrowing.
• Malignant Gastrointestinal stromal tumours (GISTs) and vascular tumours
(angiosarcoma) are rare.
• Malignant tumours can ulcerate.
• Many lesions are asymptomatic.
• Presentation depends on size and location.
• Large lesions are usually of villous type, and present with intestinal
obstruction and intussusception.
• Ulcerated lesions may present with bleeding.
Relevant investigation
Capsule endoscopy is diagnostic (Fig. 8.8).
FIGURE 8.8 Capsule endoscopy—bleeding from small bowel lymphoma.
Treatment
• Excision with resection of bowel is the treatment for symptomatic tumours.
• Adjuvant chemotherapy is useful.
Acute infections and inflammations

• Acute infections of the colon are caused by viruses, bacteria (Shigella, E. coli)
and parasites (E. histolytica).
• Antibiotic associated colitis (pseudomembranous colitis) is a common entity.
Fever, lower abdominal pain and bloody diarrhoea.
Demonstration of incriminating organisms is necessary.
Treatment
Administration of appropriate antibiotic is curative.
Colorectal polyps
• Most colorectal polyps are benign adenomas.
• More common in males.
• Uncommon before the age of forty.
• All polyps have the potential for malignant change.
• They are either pedunculated or sessile.
• Histologically they are of three types:
• Tubular;
• Villous; and
• Tubulo-villous.
• Multiple colonic polyps occur in some syndromes (Table 8.2).
TABLE 8.2
Syndromes Associated with Colorectal Polyps
Malignant
Disorder Features
Potential
Peutz Jeghers syndrome Diffuse GI polyposis, mucocutaneous pigmentation of lips, gums Benign
Gardner’s syndrome Osteomas, soft tissue tumours, sebaceous cysts, multiple colonic polyps Premalignant
Familial polyposis coli Multiple polyps of stomach, small and large bowel, autosomal dominant Premalignant
Turcot’s syndrome Glioblastomas or medulloblastomas, multiple colonic polyps Premalignant
Cronkhite-Canada’s Alopecia, atrophy of nails, pigmentation, watery diarrhoea, multiple Premalignant
syndrome colonic polyps
• Polyps remain generally asymptomatic.
• Symptomatic polyps present with rectal bleeding, sometimes leading to iron
deficiency anaemia.
• Distal lesions may cause tenesmus and may prolapse through the anus.
• Barium enema (Fig. 8.9) reveals most polyps of significant size.
• Colonoscopy (Figs. 8.10A, B and C) is diagnostic.
• Histopathology is confirmatory.
FIGURE 8.9 Barium enema—colonic polyp.
FIGURE 8.10A Colonoscopy—bleeding colonic polyp Source: (Courtesy Dr
FIGURE 8.10B Colonoscopy—pedunculated colonic polyp Source: (Courtesy
FIGURE 8.10C Colonoscopy—pedunculated colonic polyp Source: (Courtesy
Treatment
• Colonic polyps have to be removed for the fear of malignancy.
• Polyps can be snared through colonoscopy.
• Large polyps may require snaring in several pieces. Histopathology
examination is essential for diagnosis and for determining the completeness
of excision. Incomplete removal of malignant polyps requires bowel
resection. Patients who have undergone snaring should have colonoscopy the
next year and then every 3–5 years.

Chief complaint is haematemesis and/or melena (upper GI aetiology) and
haematochezia and or melena (lower GI aetiology).
It is important to establish whether there has actually been haematemesis. The
measures are:
• Eliminate swallowed blood (e.g. bleed from nasal or oral cavities).
• Examination of vomitus/fecal matter.
• Rectal examination for altered blood.
Eliciting history
• History of present illness: For how long the patient has been vomiting or
passing blood per rectum?
Acute GI bleeding carries a risk of death from hypovolemic shock, and
chronic bleed leads to anaemia and its effects.
• History of present complaint: What is the quantity of the blood loss?
The amount of blood loss is very important (e.g. Bleeding from oesophageal
varices and vascular malformations is very large and life threatening, and should
be taken as a warning for a rebleed of a similar nature. This warrants treatment
in intensive care and a quick diagnosis, so the rebleed is avoided. Bleeding from
haemorrhoids is generally in small quantities).
Related questions
• Association of pain: Does the patient have pain and if so, its location and of
what nature?
Upper GI haemorrhage associated with pain is usually due to acid peptic
disease, and variceal bleed is generally not associated with pain. Dull abdominal
pain may be an accompaniment of bleed due to tumours. Abdominal pain is a
constant feature in ulcerative colitis.
• Association of dysphagia or retrosternal burning with haematemeis: Does
the patient have associated dysphagia or retrosternal burning?
Retrosternal burning may be an accompanying symptom in patients with
reflux oesophagitis, and dysphagia is a symptom of obstructing lesions, like
malignancies.
• Association of constipation or diarrhoea with rectal bleed: Does the
patient have altered bowel habits, like constipation and or diarrhoea?
Obstructing lesions, like tumours present with constipation, whereas,
infections of the lower GIT, like tuberculosis, Crohn’s disease and ulcerative
colitis present with diarrhoea. Alternating constipation and diarrhoea is an
indicator of partially obstructing tumours of the large intestine. Constipation is
usually the cause for haemorrhoidal bleed.
GI bleed?
Presence of fever with upper GI bleed could be due to malignancies, like
lymphoma, and with lower GI bleed could be due to active infections, like
tuberculosis, Crohn’s disease, acute amoebiasis and ulcerative colitis.
Loss of appetite and weight are indicative of illnesses, like tuberculosis and
malignancies.
• Past medical history: Has the patient suffered from a similar illness or any
chronic or major illness which required hospitalization?
This question will answer the history of previous treatments given for similar
GI bleeds. Perusal of previous records is extremely important for diagnosis and
treatment planning
drug intake?
Patients who have consumed drugs (e.g. NSAIDs) for prolonged periods
develop acid peptic disease and gastro-oesophageal reflux, which cause severe
gastritis and upper GI bleed. The GI bleeds are life threatening in patients on
anti-coagulants and aspirin.
• Social and personal history: Has the patient been taking balanced diet, and
also been using tobacco and or alcohol?
Patients consuming severely spicy food are known to develop oesophagitis
and acid-peptic disease. Tobacco and alcohol usage have direct link with acid
peptic disease and oesophageal malignancies.
illness?
Colonic polyps and malignancies have a familial preponderance.
General examination
• Sunken eyes indicate dehydration and undernutrition.
• Yellowish discolouration of sclera (jaundice) may be an indicator of liver
disease, like cirrhosis.
• Pale conjunctivae may indicate anaemia.
• Dry skin indicates dehydration and undernutrition.
• Generalized oedema (anasarca) may indicate severe hypo-proteinemia.
• Caput medusae and spider naevi (See Fig. 4.1) may indicate liver failure.
• Pulse rate indicates hypovolemia and shock of acute GI bleeds.
• Blood pressure is a more reliable indicator of blood loss (e.g. variceal
bleed).
• Recording of Temperature
• Elevated temperature may indicate infective pathologies.
Local examination
• Examination of oral cavity–A systematic examination of oral cavity is
essential to eliminate local causes in the oral cavity which can be mistaken
for haematemesis (e.g. acute ginigivitis or dental caries).
• Examination of neck–A systematic examination of the neck is required (e.g.
metastatic lymph nodes of the neck from gastric malignancies).
• Examination of pharynx–A systematic examination of pharynx and larynx is
required to rule out local causes like malignancies.
• Examination of chest: Auscultation–Adventitious sounds may indicate
aspiration pneumonitis.
• Examination of abdomen–Examination should include procedures for
determination of hepatomegaly (e.g. nodular hard hepatomegaly of
malignancy) and splenomegaly (e.g. portal hypertension).
• Rectal examination (Digital and proctoscopy)–Examination of the rectum is
performed to rule out primary rectal diseases, like haemorrhoids and
malignancies, and also haemorrhoids secondary to portal hypertension.

with special attention to supraclavicular nodes for metastasis. Enlargement of
other groups of lymph nodes may indicate tuberculosis or lymphomas.
Examination of the liver and spleen completes the lympho reticular system,
which is useful in diagnosis.
Summary
In a case of GI bleed, the initial history taking and clinical examination should
be brief and quick. Detailed history taking and clinical evaluation can be done
later if the patient is acutely ill and in shock. Resuscitation measures should be
given priority.
Note
In spite of the availability of all the investigations, a small minority will not
show a demonstrable cause, and require close follow up and repeat of
investigations as and when necessary.
CHAPTER 9
Lumps and swellings

S. Devaji Rao
CHAPTER OUTLINE
9.1. Definition 54
9.2. Classification 54
• Anatomical 54
• Aetiological 54
9.3. Swellings of skin 56
• Dermoid cyst 56
• Haemangioma 58
• Implantation dermoid 59
• Haematoma 59
• Erysipelas 60
• Furuncle 60
• Wart 61
• Condyloma acuminata 61
• Papilloma 61
• Moles or naevi 62
• Keratoacanthoma 63
• Solar keratosis 63
• Bowen’s disease 64
• Fibroma 64
• Neurofibroma 65
• Schwannoma 65
• Basal cell carcinoma 66
• Squamous cell carcinoma 67
• Malignant melanoma 67
• Sarcoma 68
• Sebaceous cyst 68
• Hypertrophic scar and Keloid 69
• Granuloma pyogenicum 70
• Histiocytoma 70
• Callosity or corn 71
• Seborrhoeic wart 71
9.4. Swellings of subcutaneous tissues 71
• Cellulitis 71
• Acute abscess 72
• Carbuncle 72
• Chronic abscess or antibioma 73
• Cold abscess 73
• Lipoma 73
• Liposarcoma 74
• Lump / swelling 76
• General 86
9.1 Definition
A lump is defined as the vague mass of body tissue. A tumour or a neoplasm is
an abnormal and independent purposeless growth of mass of cells, which may
stop to grow or continue to grow in an atypical manner even after the stimulus
has ceased to work.
All lumps are not tumours and all tumours do not necessarily mean lumps.
9.2 Classification
Anatomical classification
The lumps of skin and subcutaneous tissues can be classified based on their
anatomical origin. The classification is given in Table 9.1.
TABLE 9.1
Anatomical Classification of Lumps of Skin and Subcutaneous
Tissues
Skin
Epidermis Benign Papilloma
Warts
Seborrhoic keratosis
Keratoacanthoma
Moles and naevi
Premalignant Solar keratosis
Bowen’s disease
Erythroplasia of Queyrat
Malignant Squamous cell carcinoma
Basal cell carcinoma
Malignant melanoma
Dermis Benign Pyogenic granuloma
Keloid
Malignant Secondary carcinoma
Appendages Benign Epidermal cyst
Dermoid cysts
Pilonidal abscess
Benign/malignant Appendage tumours
Subcutaneous Tissues
Fat Benign Lipoma
Malignant Liposarcoma
Blood vessels Benign Spider naevi, Haematoma, Aneurysm, AV malformation, Haemangioma
Malignant Haemangiosarcoma
Lymphatics Benign Cystic hygroma, Lymph cyst, Lymphangioma
Malignant Lymphangiosarcoma, Lymphoma, Metastatic lymph nodes
Nerves Benign Schwannoma, Neuroma
Malignant Malignant schwannoma, Neurosarcoma
Fasciae, muscles Benign Fibroma, Rhabdomyoma
Malignant Fibrosarcoma, Rhabdomyosarcoma
Bones and joints Benign Osteoma, Chondroma, Osteochondroma
Malignant Osteosarcoma, Ewing’s tumour, Chondrosarcoma
Aetiological classification
Based on aetiology, the lumps can be classified as:
1. Congenital
2. Traumatic
3. Inflammatory
4. Neoplastic
5. Degenerative
Congenital swellings: These are divided into two groups:
• present at the time of birth (e.g. meningocoele, exomphalos, teratoma,
dermoid).
• present later in life but not present obviously at birth (e.g. polycystic kidney,
cystic hygroma, branchial cyst and thyroglossal cyst)
Traumatic swellings: These are caused by direct or indirect injury.
• Acute–swellings which occur immediately after injury (e.g. haematoma)
• Subacute–swellings which occur slowly and after repeated trauma (e.g.
chronic haematoma)
• Chronic–swellings which occur months or years after trauma (e.g. false
aneurysms, implantation dermoid)
Inflammatory swellings: Inflammatory swellings are caused by infections.
• Acute–Acute infections present with the five cardinal signs of acute
inflammation:
1. redness (rubor)
2. pain (dolor)
3. heat (calor)
4. swelling (tumour)
5. loss of function (functio laesa)
and constitutional symptoms like fever and leukocytosis.
Brawny induration and oedema are almost always present (e.g. abscess and
acute lymphadenitis).
• Subacute–Mild infections present with a little subdued picture of acute form
of infection (e.g. chronic abscess).
• Chronic–Present months or years after infection with conspicuous absence of
signs of acute inflammation. Brawny induration and oedema are
conspicuously absent (e.g. tuberculosis, HIV infections or deeply embedded
foreign bodies).
Neoplastic swellings: These are new growths.
• Benign–Arise from any tissue from the skin down to the bone, and behave in
an innocent pattern (e.g. lipoma, fibroma and neuroma).
• Malignant–Arise from any tissue from the skin down to the bone and have a
potential to spread.
• Locally invasive (e.g. rodent ulcer and osteoclastoma).
• Invade to other distant tissues (e.g. carcinoma and sarcoma)
The differentiating features of benign and malignant swellings are given in
Table 9.2.
TABLE 9.2
Differentiating Features of Benign and Malignant Swellings
Characteristic Feature Benign Swelling Malignant Swelling
Symptom
Rate of growth Slow Rapid
Pain Absent Absent in the initial stages
Loss of appetite and weight Absent Usually present
Loss of function Absent Usually present
Sign
Surface Smooth Irregular
Margin Smooth and well defined Irregular and ill defined
Consistency Soft to firm Firm to hard, variable
Mobility Freely mobile Restricted mobility
Pressure effects Absent unless very large Present
Lymphatic involvement Absent Present when spread through lymphatics
Distant metastasis Absent Present
Incidence of recurrence Nil May recur
It should be noted that many benign swellings have malignant potential, when
triggering factors are influenced (e.g. fibroma can become fibrosarcoma).
The malignant transformation is identified clinically by the following factors:
1. Sudden increase in size
2. Development of pain
3. Increase in vascularity and rise of local temperature
4. Decreased mobility and recent fixity of the swelling
5. Secondary changes like ulceration, bleeding or itching as in malignant
melanoma
6. Involvement of regional lymph nodes
7. Appearance of distant metastases
Lumps can be clinically of two types:
• Solid lumps (e.g. fibroma and bone tumours).
• Cystic lumps may contain:
• blood (e.g. haemangioma)
• lymph (e.g. lymph cyst), or
• pus (e.g. abscess).
Both anatomical and aetiological classifications of lumps are correlated in
Table 9.3.
TABLE 9.3
Correlation of Aetiological and Anatomical Classifications of Lumps
Tissue of Origin
Subcutaneous tissue
Aetiology Skin Fat Blood vessels Lymphatics Nerves
Congenital Dermoid cyst Aneurysm Cystic hygroma

Haemangioma
AV
malformation
Glomus tumour
Traumatic Implantation Aneurysm Traumatic lymph cyst
dermoid haematoma
Acute Erysipelas, furuncle Cellulitis, Acute vasculitis Acute lymphangitis Acute neuritis
inflammatory acute
pyogenic
abscess,
carbuncle
Chronic Warts, condyloma Chronic Chronic vasculitis Chronic lymphangitis Chronic neuritis
inflammatory acuminata abscess or
antibioma,
cold
abscess
Benign Papilloma, moles, Lipoma Haemangioma Lymphangioma Neuroma,
neoplastic keratoacanthoma schwannoma
solar keratosis,
Bowen’s
disease,
erythroplasia of
Queyrat
Malignant Basal cell Liposarcoma Haemangiosacroma Lymphangiosarcoma, Neurosarcoma
neoplastic carcinoma, primary and
squamous cell secondary lymph
carcinoma, node malignancies
malignant
melanoma
Others Sebaceous cyst,
keloid,
granuloma
pyogenicum,
histiocytoma,
callosity or corn,
seborrhoeic wart
Note
Blood vessels, lymphatics and nerves are present in the skin also, and their
pathologies occur in the skin and subcutaneous tissues, with equal
preponderance.
During the diagnosis of lumps on the body, the students should be able to
identify from which plane the swelling is originating from. The following
description of each disease will help them to identify the same. The swellings
arising from the skin and subcutaneous tissues are detailed below and the others
are detailed in appropriate chapters.
9.3 Swellings of skin
Dermoid cyst
• Otherwise called ‘sequestration dermoid’.
• Results from cystic change in epithelial remnants left behind at the lines of
embryonic fusion.
• Can occur anywhere in the midline (Fig. 9.1A) or commonly in the line of
fusion–
• At the outer angle of the orbit it is called ‘external angular dermoid’ (Fig.
9.1B).
• Behind the pinna of the ear (Fig. 9.1C) it is called ‘post auricular
dermoid’.
FIGURE 9.1A Midline dermoid of forehead Source: (Courtesy Dr Usha

Dorairajan).
FIGURE 9.1B External angular dermoid.
FIGURE 9.1C Postauricular dermoid Source: (Courtesy Dr Usha Dorairajan).
This can occur in the midline below the tongue and is called ‘sublingual
dermoid’.
• A well defined cystic swelling.
• Transillumination is absent as the contents are pultaceous.
• On the skull it can present in various forms:
• a cystic swelling entirely on the outside of the skull.
• a cystic swelling attached to the dura mater inside the skull through a defect
in the bone.
• a cystic swelling outside the skull and interconnected to another cystic
swelling inside the skull (dumb-bell shaped).
• Longstanding dermoids may show erosion of bone on which it is sitting due
to constant pressure.
Investigations
X rays and CT scan may reveal bone defects, if any, and will show intracranial
extensions.
Treatment
Excision is the treatment of choice mostly for cosmetic reasons or for the fear of
infections of the cyst.
Haemangioma
These are vascular malformations or hamartomas of cutaneous blood vessels
(capillary, artery or vein). They are classified as:
• Capillary haemangioma
• Portwine stain
• Salmon patch
• Spider naevus
• Strawberry angioma
• Cavernous haemangioma
• Plexiform or cirsoid haemangioma
• Capillary haemangioma–Presents as purple or bright red coloured patches of
varying sizes. They are flat with the surface of the surrounding skin.
Application of pressure blanches the lesion and the colour reappears on
release of pressure.
• Portwine stain–present since birth; diffuse telangiectatic patch with no
swelling (Fig. 9.2A).
• Salmon patch–present since birth, usually on the forehead and disappears
completely within a year.
• Spider naevus–central red spot with radiating blood vessels resembling a
spider (See Fig. 4.1).
• Strawberry angioma–sessile lobulated circumscribed swelling, red in
colour (Fig. 9.2B).
• Cavernous haemangioma–Present as large soft spongy swelling of dilated
spaces containing blood, which is compressible and reappears after release of
pressure; commonly seen on the lips cheek and face (Figs. 9.2C, D and E)
• Plexiform or cirsoid haemangioma–Appears like a bag of worms; systolic
bruit may be present
FIGURE 9.2A Salmon patch Source: (Courtesy Dr N. Sekar).

FIGURE 9.2B Strawberry angioma.
FIGURE 9.2C Cavernous haemangioma of face and lip.
FIGURE 9.2D Cavernous haemangioma of lip Source: (Courtesy Dr K.
Sridhar).
FIGURE 9.2E Cavernous haemangioma of lip Source: (Courtesy Dr R.
Devakanthan).
No special investigations may be necessary.
Treatment
• Small and tiny haemangiomata may be left alone without treatment.
• Disfiguring lesions need excision.
• Large haemangioma may be reduced in size by injecting sclerosants, and
excision and reconstructive surgery at a later date.
Implantation dermoid
• Follows a trivial penetrating sharp trauma.
• Occurs when the ectoderm is driven into the subcutaneous tissue.
A cystic swelling at the areas that are prone to trauma, like fingers (Fig. 9.3).
FIGURE 9.3 Implantation dermoid.
Investigations
No special investigation is necessary.
Treatment
Excision is the treatment of choice.
Haematoma
Injury to the skin and subcutaneous tissue can damage the capillaries in that
region, and blood can collect in the intradermal or subcutaneous plane.
Irregular bluish patch, rarely raised above the surface of skin (Fig. 9.4)
FIGURE 9.4 Haematoma of medial aspect of arm.
Coagulation profile may be needed for recurrent attacks.
Treatment
• Many of them resolve on their own.
• Thrombolytic creams are helpful.
Erysipelas
This is the spreading cuticular lymphangitis of the skin following trauma and
infection by Streptococcus pyogenes.
• Starts as a rose rash, followed by vesicular eruptions (Fig. 9.5)
• When this occurs in regions where loose areolar tissue is found, it resembles
cellulitis.
• The differentiating features of erysipelas and cellulitis are given in Table 9.4.
FIGURE 9.5 Erysipelas.
TABLE 9.4
Differentiating Features of Erysipelas and Cellulitis
Feature Erysipelas Cellulitis
Rose rash Disappears on pressure Does not disappear on pressure

Better felt than seen Better seen than felt
Vesicles Contain serous fluid Contain pus
Note
In the face, erysipelas does not involve the pinna, whereas, cellulitis involves
the pinna of the ear (See Chapter 21).
Isolation of the organism in culture.
Treatment
Appropriate antibiotics cure the lesion.
Furuncle
• Infection of the hair follicle by Staphylococcus aureus.
• Furuncle may be a source of systemic sepsis in diabetics.
• Cavernous sinus thrombosis is rare but a serious complication of furuncle on
the face above the line drawn from the angle of the mouth to the tragus of the
ear.
• A painful indurated swelling at the hair root with surrounding oedema (Fig.
9.6).
• This swelling may contain pus in due course and draining lymph nodes may
be involved.
• Cellulitis is seen in immunocompromised individuals and diabetics.

FIGURE 9.6 Furuncle.
Culture of the pus and identifying the incriminating organism is necessary.
Treatment
• The abscess may burst spontaneously.
• Some may need surgical drainage.
Wart
• A simple overgrowth of the skin with hyperkeratosis.
• Believed to be of viral aetiology (Papilloma virus).
• Familial preponderance is also seen.
• Warty projections on the skin (Fig. 9.7).
• Kiss lesions may appear.
FIGURE 9.7 Wart.
Treatment
• Burning the warts with electrocautery or liquid nitrogen is curative.
• Small lesions may be excised.
Condyloma acuminata
Clinical manifestation of secondary syphilis.
• A warty, sessile moist growth at the muco-cutaneous junctions like the angle
of the mouth, vulva and anus (Fig. 9.8).
FIGURE 9.8 Condyloma acuminata of anus.
Biospy may be required to establish diagnosis.
Treatment
• Application of podophyllum or burning the tissue with electrocautery or
liquid nitrogen is curative.
Papilloma (squamous cell papilloma, skin tag)

• An overgrowth of all the layers of skin.
• Consists of loose connective tissue core covered by normal, keratinised
epithelium.
• It may ulcerate, bleed and turn malignant.
• Can occur on any part of the body.
• Common on the trunk, neck, axillae and groins.
• A pedunculated growth with villous processes (Fig. 9.9).
• It moves with the skin, and the base is free and not indurated as in epidermoid
carcinoma.
FIGURE 9.9 Papilloma.
No special investigation is required.
Treatment
• Excision biopsy is the treatment of choice.
• Removal by electrocautery is a good alternative.
Moles or naevi
• Lesions are mostly congenital and some appear later in life.
• Moles have excess quantity of melanin, derived from melanocytes, which
migrate to the ectoderm from the neural crest during embryonal
development.
• Since these grow only on excessive stimulation of growth-limiting factors
(differ from tumours which grow without any stimulation), they are called
‘pseudotumours’ or ‘hamartomas’.
• These harmartomatous cells may appear in the epidermis, dermis, or both to
form raised pigmented lesions, called moles or naevi.
• Clinically they are of two types:
1. Hairy mole–It is a flat or slightly raised lesion with hair growing from
its surface (Fig. 9.10A).
2. Smooth mole–It is a flat lesion without hair on it (Fig. 9.10B).
• Appear as black spots on any part of the body, face and limbs being common
areas (Figs. 9.10C to E).
FIGURE 9.10A Hairy mole.
FIGURE 9.10B Smooth mole on the scalp.
FIGURE 9.10C Naevus mammary region.
FIGURE 9.10D Naevus on the neck Source: (Courtesy Dr K. Sridhar).
FIGURE 9.10E Naevus on the scalp.
Histologically, the moles or naevi are classified into five types. The
characteristics are shown in Table 9.5.
TABLE 9.5
Characteristics of Various Moles
Type Period of Clinical Presentation Layer of Skin Benign /

Appearance Malignant
Junctional Before or at Deep pigmented lesion Junctional or basal layer Potentially
naevus puberty of epidermis malignant
Intradermal After puberty Less deeply pigmented lesion From junctional layer Benign
naevus migrate into dermis
Compound At or after Appearance intermediate between Combination of Potentially
naevus puberty junctional and intradermal naevus junctional and malignant
intradermal
components
Blue naevus Before puberty Flat hairless, appears blue in colour (due Deep in the dermis Benign
to optical effect) with smooth and
shiny overlying skin
Juvenile Any age, usually Deep pigmented lesion In the dermis Benign
naevus in the young
Lentigo (plural = lentigenes) – This is a large, dark pigmented patch with a
smooth surface with junctional activity. It is found to be common in middle age,
especially over the face and neck. This is also called ‘Hutchison’s freckle’. It is
benign, but may predispose to superficial spreading type of malignant
melanoma.
Naevi, which show sudden increase in size, ulceration, bleeding or itching
should raise suspicion of malignancy. The criteria for suspicion of malignancy
can be summarized as:
• A – Asymmetry
• B – Border irregularity/Bleeding
• C – Colour variation
• D – Diameter >6 mm
• E – Elevation
Biopsy is required for any naevus which shows sudden increase in size, pruritus
or bleeding to eliminate malignant transformation.
Treatment
Lesions suspicious of malignancy should be excised with clear margins in all
directions.
Keratoacanthoma (molluscum sebaceum)

• A tumour composed of keratinized squamous cells of the sebaceous glands.
• Originates in the dermis and is covered by intact epidermis; both are
connected at one point.
• Seen on the exposed areas of the skin.
• The predisposing factors are:
• Sunlight
• Mineral oil and tar
• Infection
• A firm, rounded reddish papule or a nodule, with a rubbery consistency (Fig.
9.11).
• The centre has a horny plug, which falls off after sometime and ulcerates.
• Whole lesion regresses spontaneously after about 8 weeks.

FIGURE 9.11 Keratoacanthoma.
Treatment
Excision with a margin of surrounding normal skin is done if spontaneous
regression does not occur.
Solar keratosis (intra epidermal carcinoma)

• Seen in people who work outdoors, like fishermen.
• Common in fair skinned people living in tropical and subtropical regions.
• Histologically, the keratin layer (hyperkeratosis) and the prickle cell layers
(acanthosis) are markedly thickened. This shows abnormal mitotic activity
and predisposes to squamous cell carcinoma.
• It is premalignant and more than half develop malignancy in 8 years.
• Flat, well demarcated, brown crusty or scaly lesions with an erythematous
base, often multiple in numbers (Fig. 9.12).
• They bleed easily when traumatized.
FIGURE 9.12 Solar keratosis.
Biopsy is advised.
Treatment
Excision is required, as this is a premalignant condition.
Bowen’s disease
• Occurs in any part of body, particularly at the sites of repeated trauma.
• Common in old age.
• It is squamous cell carcinoma in situ.
• Bowen’s disease occurring on the glans penis or prepuce is called
‘Erythroplasia of Queyrat’ (See Ch. 36).
• Causes include solar damage, immunosuppression, viral infection (HPV),
chronic skin injury and dermatoses.
• A brown indurated thickened mass covered with crust with well-defined edge.
• It oozes serosanguinous fluid when crusts are removed (Fig. 9.13).
FIGURE 9.13 Bowen’s disease.
Biopsy confirms diagnosis.
Treatment
• Excision is required as this is a premalignant condition.
• Photodynamic therapy, cryotherapy or local chemotherapy are other
alternatives
Fibroma (see also chapter 48)

• A tumour of fibrous tissue.
• They are combined with other mesodermal tissues, like:
• fat (fibrolipoma)
• muscles (fibromyoma)
• nerve sheath (neurofibroma)
• Paget’s recurrent fibroid (Desmoid tumour) is an unusual tumour arising from
rectus sheath, and has a potential to become malignant (See Chs. 33 and 48).
• A painless, firm, circumscribed swelling moving freely on underlying
structures (Figs. 9.14A and B).
• The consistency varies from soft to hard, depending on the amount of fibrous
tissue.
FIGURE 9.14A Fibroma of lip Source: (Courtesy Dr K. Sridhar).
FIGURE 9.14B Fibrolipoma.
• Biopsy confirms diagnosis.
• Wedge biopsy is needed for large tumours.
Treatment
• Excision is curative.
Neurofibroma
This tumour contains both neural and fibrous elements.
• Neurofibromas occur in multiple, but single tumours are also common.
• Multiple neurofibromatosis occur in Von Recklinghausen’s disease, a
congenital autosomal dominant disease – tumours arising from perineureum
and epineureum, and this can be a part of multiple endocrine neoplasia
(MEN Type II – neurofibromas of lips, eyelids and face associated with
medullary carcinoma of thyroid and pheochromocytoma).
• Plexiform neurofibromatosis show myxofibromatous degeneration.
• Pachydermatocoele is a variety of plexiform neurofibromatosis.
Complications: Cystic degeneration and sarcomatous changes (very rare).
• Solitary tumour–a smooth, firm nodule with or without pain, and mobile if it
arises from subcutaneous plane, but not if it is from the skin. When it arises
from a specific nerve in the subcutaneous plane, the mobility can be
demonstrated in the plane vertical to the course of the nerve. Paresthesia
along the distribution of the nerve is common.
• Multiple tumours (generalized neurofibromatosis – Von Recklinghausen’s
disease)–multiple cutaneous nodules with light brown pigmentation of skin
(Café au lait patch), acoustic neuroma, pheochromocytoma). The number
and size of nodules vary (Fig. 9.15A) and may increase as age advances. The
consistency of the nodules varies from soft to firm to hard.
• Plexiform neurofibromatosis–Unsightly irregular swellings predominantly on
the face in connection with the fifth cranial nerve, and also on the upper limb
(Fig. 9.15B).
• Pachydermatocoele–presents with unsightly loosely hanging soft tissue,
predominantly in the neck.

FIGURE 9.15A Multiple neurofibromata.
FIGURE 9.15B Plexiform neurofibroma face Source: (Courtesy Dr K.
Sridhar).
• Diagnosis is obvious and investigations are required only if MEN is
suspected.
Treatment
• Excision is the treatment of choice.
• Plastic reconstructive procedures are required for lesions like plexiform
varieties.
Schwannoma
• A benign tumour arising from the Schwann cell of neurilemma.
• Ectodermal in origin.
• Can have its origin in the cutaneous or subcutaneous nervous tissue, and can
occur in any part of the body, commonest site being the acoustic nerve (See
Chs. 16 and 21).
• Mediastinum and retroperitoneum are other common sites.
• A well circumscribed encapsulated tumour, usually globular in shape (Fig.
9.16).
• It can also be ovoid or fusiform when it occurs on a large nerve.
• Pain may be a predominant feature.
FIGURE 9.16 Schwannoma left axilla Source: (Courtesy Dr K. Sridhar).

• MRI is useful is diagnosing lesions in critical areas.
Treatment
• Excision is the treatment of choice.
Basal cell carcinoma

• This low-grade malignant lesion arises from the basal layer of the rete
Malphigi of the skin.
• Ultraviolet rays, especially those present in the sunlight are supposed to be the
stimulating factor
• The types are:
• Nodular
• Cystic
• Cicatricial
• Infiltrative
• Micronodular
• Superficial
• Pigmented
• Rodent ulcer
• Fibroepithelioma of Pinkus
• Polypoid
• Pore-like
• Aberrant
• Nodulo ulcerative
• Commonly on the face, especially in the Caucasians living in countries like
Australia.
• Starts as a firm nodule with a shiny surface with capillaries.
• Later it ulcerates, and the edges become raised with a beaded appearance.
• The margin is locally infiltrating the surrounding and the deeper tissues,
and derives the name ‘Rodent ulcer’ (See Fig. 10.13).
• Morphoeic
• Slowly expanding yellow/white waxy plaque with an ill defined edge.
• Superficial
• Most often on the trunk, that are pink/brown multiple scaly plaques with a
fine ‘whipcord edge’.
• Pigmented
• Specs of brown or black pigment may be present in any type (Figs. 9.17A
and B ).
• It is locally infiltrating.
• It does not infiltrate the lymphatic tissue; hence the regional lymph nodes
are not enlarged.
FIGURE 9.17A Basal cell carcinoma Source: (Courtesy Dr R. Rajaraman).

FIGURE 9.17B Pigmented basal cell carcinoma Source: (Courtesy Dr R.
Rajaraman).
• No special investigation is required.
Treatment
• Excision biopsy with 0.5 cm margin is the treatment of choice.
• Mohs micrographic surgery gives better results.
• Reconstructions by plastic procedures may be required if the defect is large.
• Chemotherapy, immunotherapy, radiation, cryotherapy and
electrodesiccation with curettage are good alternatives.
Squamous cell carcinoma (epidermoid

carcinoma)
• A malignant lesion of the skin.
• Common in the elderly.
• Can occur anywhere on the body and also organs lined by stratified squamous
epithelium, like mouth, tongue, etc.
• In the skin, it arises from the prickle cell layer.
• Irritants like chemicals and dyes (e.g. Carcinoma scrotum in chimney
sweeps in nineteenth century);
• Irradiation of the skin (e.g. while radiating cancers of other organs);
• Scar from burns (e.g. Marjolin’s ulcer); and
• Ultraviolet ray exposure (e.g. solar keratosis).
• A sessile cauliflower growth with or without ulceration (Fig. 9.18).
• When ulcerated,
• Edges are raised and everted, and
• Base is indurated.
• If it is secondarily infected, it may discharge blood or pus.
• Regional lymph nodes are often involved and are firm to hard in consistency,
which may show local invasion.
FIGURE 9.18 Squamous cell carcinoma of foot Source: (Courtesy Dr A.
Chandrasekhar Rao).
• Biopsy will be needed to establish the diagnosis.
Treatment
• They respond well to radiotherapy.
• Small lesions are to be excised, with adequate tumour free margins.
• Regional lymph nodes (Block dissection) need to be removed when possible.
Malignant melanoma
• A malignant tumour of the melanocytes, it originates from the neural crest,
and is ectodermal in origin.
• May arise de novo in apparently normal skin or in a pre-existent naevus
(junctional and compound varieties) (See Page 63).
• Spreads by lymphatics (to lymph nodes) and blood (to lungs, liver and brain).
• Can occur at any age.
• Suggested causes are:
• DNA damage in melanocytes caused by ultra violet (UV) radiation; results
in neoplastic transformation.
• Inherited mutations are identified in CDKN2A and CDK4 (tumour
suppressor genes) in a rare familial melanoma syndrome, which is
autosomal dominant.
• Sudden growth of a pre-existing naevus.
• A firm itchy lesion, varying from brown to black in colour (Fig. 9.19).
• Most common in the foot, but rarely in the eye and mucocutaneous junction,
e.g., anus.
• Some may ulcerate or bleed.
• Regional lymph nodes are involved quite early.
• Satellite nodules may be seen in the areas between the primary lesion and the
lymphatic area.
• Hepatomegaly (liver metastases).
FIGURE 9.19 Malignant melanoma foot Source: (Courtesy Dr N.
Sivakataksham).
• Biopsy is needed for confirmation of diagnosis.
• X ray of the chest to assess lung metastases.
• Ultra sonography (US) and CT abdomen to assess liver metastases.
Treatment
• Wide local excision with 1 cm margins is required, followed by chemo
radiation, if indicated.
• Mohs micrographic surgery gives better results.
Sarcoma
• It is a malignant tissue of connective tissue and occurs from any structure
derived from mesoblastic origin:
• Blood vessel–haemangiosarcoma
• Lymph tissue–lymphangiosarcoma
• Fibrous tissue–fibrosarcoma
• Fibrous and nervous tissue–neurofibrosarcoma
• Synovial membrane, tendon sheath or bursa–synovial sarcoma
• Occurs in younger age.
• It has the potential to spread both locally and through blood; lung metastases
are common.
• Lymphatic invasion occurs late (carcinomas spread through lymphatics).
• The tumours attain a large size quickly, and the skin is breached and ulcerated
(Figs. 9.20A and B).
• They are very vascular and bleed profusely.
• They are soft to hard, depending on the tissue of origin.
FIGURE 9.20A Dermatofibrosarcoma right arm Source: (Courtesy Dr N.
Mohan).
FIGURE 9.20B Fungated osteosarcoma femur Source: (Courtesy Dr R.
Rajaraman).
• X rays may show calcification.
• MRI details the spread of tumour locally.
• Biopsy is conclusive.
• Chest X rays are needed to identify pulmonary metastases.
Treatment
• Wide excision is the treatment of choice.
• Local radiotherapy is useful.
Sebaceous cyst
• This is a collection of sebum in the sebaceous gland due to the blockage of its
duct.
• It can occur anywhere on the body, except the palms and soles.
Complications
1. Infection to form an abscess (Figs. 9.21A and B)
2. Ulceration
3. Sinus formation (Fig. 9.21C)
4. Calcification
5. Malignant change
6. Sebaceous horn (Fig. 9.21D)
7. Cock’s peculiar tumour (Fig. 9.21E)
FIGURE 9.21A Inflamed sebaceous cyst.

FIGURE 9.21B Grossly infected sebaceous cyst low back.
FIGURE 9.21C Sinus of sebaceous cyst interscapular region.
FIGURE 9.21D Sebaceous horn—thigh Source: (Courtesy Dr V. Srinivasan).
FIGURE 9.21E Cock’s peculiar tumour.
• A bluish coloured cystic swelling with a black depressed spot on the swelling
(obstructed opening of the duct) called ‘punctum’ (Fig. 9.21 F), which is the
diagnostic feature of a sebaceous cyst.
• The skin is usually free, except at the punctum.
• The lesion is fluctuant, but not transilluminant as the contents are thick.
FIGURE 9.21F Sebaceous cyst back.
Treatment
• Excision of the cyst is the treatment of choice.
Hypertrophic scar and keloid

Overgrowth of fibrous tissue formed by excessive collagen deposition in the
dermis; they are seen in the healing process of wounds.
• When the scar alone is involved, it is called ‘hypertrophic scar’.
• When the overgrowth of fibrous tissue extends into the adjacent normal skin it
is called ‘keloid’.
It is commonly seen in the presternal region and in the dark skinned
population.
• Hypertrophic scar–A thickened scar of a previous wound (Fig. 9.22A).
• Keloid–Are extensions into the surrounding skin to produce finger like
extensions (Fig. 9.22B).
FIGURE 9.22A Hypertrophic scar after surgery.
FIGURE 9.22B Multiple keloids developed on every surgical scar.
There is a history of small boils, burn scars, and previous surgery (Fig.
9.22D). Usually they follow deep burns (Fig. 9.22E) and wounds with infection
and sloughing.
The properties of hypertrophic scar and keloid are given in Table 9.6.
TABLE 9.6
Properties of Hypertrophic Scar and Keloid
Property Hypertrophic Scar Keloid

Pruritus Not present Present
Spread to surrounding areas Not present Present
Tenderness Absent Present
Vascularity Absent Present
• No special investigation is necessary.
Treatment
• Intralesional corticosteroid injections are useful in reducing the swelling and
the pruritus.
• Excision is not advocated as this will also result in a keloid.
• Low dose radiotherapy is useful.
Granuloma pyogenicum
• Overgrowth of the granulation tissue stimulated by chronic inflammation
arising in response to minor penetrating injuries, like thorns and needles.
• Commonly seen on the hands and feet, rarely on gums and lips.
• A solitary, red or reddish blue, firm nodule of 1–2 cm with ulceration which
bleeds easily (Fig. 9.23).
• If infected, it is painful.
FIGURE 9.23 Granuloma pyogenicum of finger.
Treatment
• Excision biopsy small lesions may be excised. is required to eliminate
malignancy, and the base curetted or cauterized to prevent a recurrence.
Histiocytoma (dermatofibroma)
• Painless skin lesion containing numerous lipid-filled macrophages
(histiocytes).
• Firm reddish brown nodules, about 5 mm in diameter.
• Biopsy is needed to distinguish from malignant melanoma.
Treatment
• Three-dimensional excision.
Callosity or corn
• Callosity is a raised patch of hyperkeratosis and increased thickening of the
epidermis, particularly of the stratum corneum and the granular layer. It is
commonly seen in areas of excessive pressure or repeated trauma
(Gardener’s hand). Callosities are frequently seen on the fingers of those
who drive two-wheelers.
• Corn is a circumscribed horny thickening, conical in shape with the base at
the surface and the apex deep inside. They are commonly seen on the soles
of the feet due to ill-fitting footwear. Corn is composed of keratin masses
with intact basal layers.
• Callosity presents as a thick skin in the areas of excessive pressure (Fig.
9.24A).
• Corn presents as a thickened tissue, mostly in the soles (Fig. 9.24B).
FIGURE 9.24A Callosity.
FIGURE 9.24B Multiple corns (black arrows) both feet and callosity
(red arrow) right foot.
Treatment
• Callosity–Wearing properly fitting footwear and removal of the pressure
points will help in the treatment; urea containing creams soften the skin.
• Corns can be treated with local salicylic acid, while some require excision.
Seborrhoic wart (seborrhoic keratosis)

• A benign overgrowth of basal layer of epidermis containing swollen abnormal
epithelial cells; commonly seen in the elderly.
• A familial disease transmitted by a dominant autosomal gene.
• Sometimes they are indistinguishable from superficial spreading malignant
melanoma.
• A raised, hypertrophic papilliferous lesion varying from a few millimeters to
about 2 cm in size (Fig. 9.25).
• It bleeds to trivial trauma and becomes painful when infected.

FIGURE 9.25 Seborrhoiec wart.
• Excision biopsy is required.
Treatment
• Shaving the lesion or curettage and cautery gives good cosmetic result.
9.4 Swellings of subcutaneous tissue
Cellulitis
• Spreading inflammation of the subcutaneous and fascial tissues.
• Commonly due to Streptococcus pyogenes.
• Organism gains entry through broken skin due to trauma.
• Diabetics are mostly affected.
• Affected part appears grossly swollen, painful and red (Fig. 9.26A).
• It is very tender.
• Constitutional symptoms, like fever and toxemia are common.
• The lymphatics may appear inflamed and appear as red streaks, and lymph
nodes may be enlarged and tender.
• Abscesses may form in the subcutaneous plane and the skin may undergo
avascular necrosis and become gangrenous (Fig. 9.26B).
FIGURE 9.26A Cellulitis foot.
FIGURE 9.26B Patchy gangrene of the leg.
• Organisms should be isolated in culture from discharge if any.
Treatment
• Appropriate antibiotics are necessary to control infection.
Acute pyogenic abscess

• Abscess is defined as the collection of pus.
• Incomplete resolution of cellulitis and lymphadenitis are the causes.
• A painful swelling.
• There will be signs of inflammation on and around the swelling (Fig. 9.27).
• On examination, it is tender and may show fluctuation if the pus is liquid.
• When this occurs as a part of pyemia, they are multiple in numbers.
• Constitutional symptoms, like fever, rigor and toxemia will be predominant.
FIGURE 9.27 Acute abscess leg.
• No special investigation is required if it is solitary.
• Isolation of organism in blood by culture, if suspected to be part of pyemia.
• Diagnostic aspiration may be helpful in localizing deep seated abscess.
Treatment
• Incision and drainage of pus will be curative under cover of appropriate
antibiotics.
Carbuncle
• An infective gangrene of subcutaneous tissue.
• Caused by Staphylococcus aureus.
• Commonly seen in diabetics.
• Commences as a painful swelling with marked induration.
• The skin becomes red and oedematous, with the appearance of pustules on it.
They burst to form multiple discharging sinuses like a ‘sieve’ (Fig. 9.28), a
characteristic feature of carbuncle.
• The slough may involve the deeper structures.
FIGURE 9.28 Carbuncle back.
• Isolation of organism in pus by culture.
• Determination of blood sugar levels is mandatory.
Treatment
• Control of diabetes is necessary.
• Drainage of pus and excision of slough under cover of appropriate
antibiotics is curative.
Chronic abscess or antibioma

• Occurs when the acute abscess is inadequately treated with inadequate
antibiotics.
• A painless fluctuant swelling, mostly a pre-existing swelling without the signs
of acute inflammation (Fig. 9.29).
FIGURE 9.29 Cold abscess in the thigh.
Investigations
• Isolation of the causative organism is essential.
Treatment
• Appropriate antibiotics for adequate period.
• Proper drainage of pus is necessary.
Cold abscess
• This is due to tuberculous lymphadenitis getting converted into a pus filled
abscess, a process called ‘caseation’.
• Can also result from a tuberculous lesion of the bone, vertebra or joint.
• A fluctuant swelling mostly where lymphoid tissues are abundant, like the
neck (Fig. 9.29) and axilla.
• Does not exhibit any sign of acute inflammation unless it is secondarily
infected.
Investigations
• Diagnostic aspiration of pus:
• Smear for acid fast bacilli.
• Isolation of acid fast bacilli in culture.
• PCR test for Mycobacterium tuberculosis.
Treatment
• Antitubercular treatment is curative.
Lipoma
• A cluster of overactive fat cells.
• Can occur anywhere in the body, mostly on the nape of the neck, shoulder,
forearm and back.
• Lipomas are also seen in other planes, like intermuscular, subfascial,
parosteal, subserous, submucous, intra-articular, subsynovial, subdural, and
extradural planes of the spinal cord.
• Encapsulated lipoma
• Appears as a painless, slow growing lobulated soft swelling (Fig. 9.30).
• The edge is definite and slips under the examining finger (Slip sign) (Fig.
9.31A).
• Multiple lipomas are not uncommon (Fig. 9.31B).
• Though lipomas are not fluctuant, they may show slight fluctuation
(pseudofluctuation) and may also transilluminate.
• Some subcutaneous lipomas may get complicated, namely,
- Myxomatous degeneration
- Saponification
- Calcification
- Infection
- Ulceration
- ? Malignant transformation (liposarcoma)
• Diffuse lipoma
• When the lipoma is not clearly encapsulated and merges into the
surrounding tissue, it is called ‘Diffuse lipoma’ (Fig. 9.31C).
FIGURE 9.30 Lipoma—left scapular region.
FIGURE 9.31A Slip sign of lipoma.
FIGURE 9.31B Multiple lipomata forearm.
FIGURE 9.31C Diffuse lipoma in the medial aspect of upper part of
right thigh.
When they occur as painful lumps, they may be a part of nervous tissue, and
are called ‘neurolipomata’. Multiple painful lipomata is a variety called
‘Adiposis dolorosa’ or ‘Dercum’s disease’.
• No special investigation is required, except in lipomata, which shows sudden
increase in size.
• MRI is useful for intermuscular lipomas.
• Biopsy may be needed in such situations to rule out malignant transformation.
Treatment
• Excision may be needed for cosmetic reasons. Recurrence is known to occur
with diffuse variety, as part of finger like projections may have been missed
during excision.
Liposarcoma
• A malignant tumour of fatty origin.
• Common sites being the thigh, retroperitoneum, and inguinal region.
• Usually arise de novo, and extremely rarely from a pre-existing lipoma.
• A typically soft, slow-growing, ill-defined non-tender mass.
• Biopsy is confirmatory.
Treatment
• Radical excision is the treatment of choice.

The presenting complaint is a lump.
Eliciting history
General particulars
• Age–Malignancies like carcinoma are more common in the elderly, and
sarcomas are common in the young.
• Sex–Testicular tumours in males, and uterus and ovaries related tumours in
females should be considered in the analysis of abdominal lumps.
• Race and religion–Jews and Muslims who perform religious circumcisions
have a low incidence of carcinoma of the penis.
• Occupation–Occupations which need prolonged kneeling cause bursitis of
knees. In housemaids it is called ‘Housemaid’s knee’, and in priests it is
called ‘Clergyman’s knee’.
• Place of residence–Certain areas show endemicity for certain illnesses like
filariasis.
Questions to be addressed to the patient

• Duration of swelling: When did the patient first notice the swelling?
This will give the duration of this present illness – short duration represents
acute pathology, like acute infections, and long duration indicates chronic
pathology, like benign tumours.
• Mode of onset: Was it a sudden event or gradual in developing, and was
there any trauma preceding the swelling?
Sudden origin indicates acute pathology, like infections, and gradual
development indicates chronic pathology, like benign tumours. History of trauma
indicates traumatic pathology (e.g. haematoma). Sometimes trauma draws the
attention of the patient to a pre-existing swelling.
• Size at the time of onset: What was the nature of the swelling?
Description of the size of the swelling will permit the examiner to compare its
growth if any, and can be correlated with the duration of the illness, which may
indicate acute or chronic pathologies. Likewise, decrease in size may indicate
resolving infections (e.g. resolving cellulitis and resolving haematoma).
• Association of pain and discharge: Was or is the swelling painful and does
or did it discharge any fluid at anytime?
Lumps of acute infectious pathology, like cellulitis, abscess. etc., are
associated with pain of varying intensity and nature. Dull pain may indicate
swellings due to chronic pathologies, like tuberculosis, or even malignancy.
Some swellings may discharge fluid. The fluid may be of varying nature, like
serous (e.g. lymphangitis), serosanguinous (e.g. resolving hematoma), bloody
(e.g. haematoma), or purulent (e.g. pyogenic abscess). Discharge of the sticky
and malodorous material ‘sebum’ is the hallmark of sebaceous cyst.
• Variation in size: Does the lump remain in the same size always or does it
show some variation in size?
Some lumps increase on coughing or sneezing (e.g. hernia), or while eating
(e.g. salivary gland adenitis), or decrease on lying down (e.g. uncomplicated
hernia). Some lumps show a rapid increase in size and stop progressing, some
decrease in size (e.g. infective swellings on treatment), or remain static without
any variation in size (e.g. solitary thyroid nodule). The rate of progression in size
is a useful indicator, as rapid progression in size represents a very active disease
and slow progression indicates a chronic disease.
• Association of fever: Is or was it associated with fever?
Association of high grade fever may indicate a infective pathology (e.g.
cellulitis), or low grade fever may indicate malignancies (e.g. lymphomas).
• Pressure effects: Is it producing any pressure effect on neighbouring
structures?
Association of pressure effects will indicate its local invasiveness and the
inward growth which is not seen from the outside (e.g. thyroid swellings press
the trachea to cause dyspnoea and the oesophagus to cause dysphagia), and also
indicate the urgency of treatment required. It may also indicate the relevant
investigations to be performed to facilitate the correct treatment.
• Loss of function: Is there any loss of function?
Lumps like neuromas of the extremities can cause sensory loss.
• Loss of appetite and weight: Is there any loss of appetite and weight in the
course of illness?
malignancies.
• Treatment for the illness: Has any treatment been given to the illness?
The information of any treatment received in the past for this illness will give
a clearer picture of diagnosis (e.g. failed treatment will help in the elimination
from differential diagnosis, and success will help in confirmation of the
diagnosis and continuation of the treatment).
• Past history: Was there any similar illness in the past which required any
treatment?
If the patient had suffered a similar illness in the past, which was successfully
treated, will indicate the examiner to reconsider the diagnosis like tuberculosis,
and eliminate diagnosis like viral infections, like mumps, as they give immunity.
illness or had any treatment?
Diseases like tuberculosis occur in closely living families and a positive
history may be a good indicator for the present diagnosis.
• Personal history: Questions regarding personal habits?
Personal habits like smoking and drinking alcohol may be the causative factor
of the present illness (e.g. bronchogenic carcinoma with cervical lymph node
metastases).
• Any other relevant question: This is left to the choice of the examiner to
match the situation, like extramarital contact if the lump is suspected to be of
syphilitic aetiology.
Symptoms related to the swellings of the skin and subcutaneous tissues are
tabulated in Tables 9.7 and 9.8.
TABLE 9.7
Correlation of Symptoms with Swellings of the Skin
Symptom
Lesion Duration Pain Fever Increase in Loss of Past
size appetite history
and
weight
Congenital Dermoid cyst Since Absent Absent May be Absent Absent
birth present
Haemangioma Since Absent Absent May be Absent Absent
birth present
Traumatic Implantation Long Absent Absent May be Absent Absent
dermoid present
Haematoma Very May be Absent May be Absent Absent
short present present
Acute inflammatory Erysipelas Short Present Present Absent Absent Nil
Furuncle Short Present Present Present Absent Nil
Chronic inflammatory Wart Long Absent Absent Increase in Absent Nil
number
Condyloma Long Absent Absent Absent Absent Nil
acuminata
Benign/Premalignant Papilloma Long Absent Absent Present Absent Nil
neoplastic
Moles/Naevi Long Absent Absent Present Absent Nil
Kerato Long Absent Absent Absent Absent Nil
acanthoma
Solar keratosis Long Absent Absent Absent Absent Absent
Bowen’s disease Long Absent Absent Absent Absent Absent
Fibroma Long Absent Absent Absent Absent Absent
Neurofibroma Long Absent Absent Absent Absent Absent
Schwannoma Long Absent Absent Absent Absent Absent
Malignant neoplastic Basal cell Long Absent Absent Present Absent Nil
carcinoma
Squamous cell Short Absent May be Present May be Nil
carcinoma present present
Malignant Short Absent Absent Present May be Mole
melanoma present
Sarcoma Short May be May be Significant May be Previous
present present present lump
Others Sebaceous cyst Long Absent Absent Absent Absent Nil
Hypertrophic Long Absent Absent Absent Absent Nil
scar or
Keloid
Granuloma Long Absent Absent Absent Absent Nil
pyogenicum
Histiocytoma Long Absent Absent Absent Absent Nil
Callosity and Long Absent Absent Absent Absent Nil
corn
Seborrhoeic Long Absent Absent Absent Absent Nil
Wart
TABLE 9.8
Correlation of Symptoms and Lesions of Subcutaneous Tissues
Symptom
Lesion Duration Pain Fever Increase in Loss of Past history Family

size appetite
and
weight
Acute Cellulitis Short Present Present May be Absent Absent Nil
inflammatory present
Acute Short Present Present May be Absent Absent Nil
pyogenic present
abscess
Carbuncle Short Present Present Present Absent Absent Nil
Chronic Chronic Long Absent Absent Absent Absent Absent Nil

inflammatory abscess
Cold abscess Long May be May be May be May be Respiratory TB
present present present present tuberculosis
Benign Lipoma Long Absent Absent Absent Absent Absent Nil
neoplastic
Malignant Liposarcoma Long Absent Absent Present May be May be present Nil
neoplastic present
Lump/swelling
The steps for examination of swellings are:
• Inspection
• Palpation
• Percussion
• Auscultation
Inspection
The examiner should never be hasty to touch the patient with great desire of
making the diagnosis. Inspection forms the first part of the examination. The
points to note during inspection are:
• Location or site of swelling–Observe the location of the swelling in relation
to the anatomical landmarks. Location gives great amount of clue to the
diagnosis.
• Swelling in the midline of neck (e.g., midline dermoid).
• Swelling in the submandibular region (e.g. submandibular salivary gland).
• Number of swellings–The number gives adequate clue in diagnosis.
• Solitary swellings (e.g. dermoid and thyroglossal cyst).
• Multiple swellings (e.g. lymph node swellings in the neck).
Note
Swellings like lipoma and neurofibroma can be single or multiple and occur
elsewhere also.
• Shape and size of the swelling–Lumps have three dimensions and all the
three should be noted down. Deeply placed lumps may cause difficulty in
measuring the depth. Shape is also three dimensional, but can be described in
descriptive terms, like oval, globular, irregular, etc.
• Globular or round swellings usually indicate:
- Cystic (e.g. dermoid cyst).
- Solid swellings of benign nature (e.g. lipoma).
• Irregular swellings indicate malignancies.
Note
Irregular swellings that have more than three dimensions, like the thyroid
swellings, may indicate the tissue or organ of origin, which may be useful in
diagnosis.
• Skin over the swelling–Careful attention has to be given to the skin over the
swelling to note the following:
• Colour
- Redness indicates acute inflammation.
- Dark pigmentation may indicate a melanoma.
- Discolouration may be seen in vascular tumours due to high vascularity.
- Colour changes are seen in necrotic tumours.
- Blue colour is seen in ranula and sebaceous cysts.
• Texture of skin
- A shining or glistening skin over the swelling indicates the stretch on
the skin by the swelling (e.g. sebaceous cyst).
- Oedema of the skin over the swelling (e.g. peau d’orange meaning
orange peel in French) is seen in malignant swellings of the breast with
lymphoedema.
- Scaly skin may indicate eczematous reactions.
• Changes on the surface
- Ulcers (e.g. tuberculosis).
- Prominent scars or keloids (e.g. indicate previous surgery).
- Punctum (e.g. sebaceous cyst).
- Sinuses (e.g. tuberculous lymph nodes).
• Prominent veins
- Engorgement of the veins in the subcutaneous plane may indicate fast
growing tumours like large sacromas, which block the venous drainage.
• Hair loss
- Hair loss is seen in sebaceous cysts of the scalp.
• Surface of the swelling–The surface of the lump provides some indication
of its aetiology, and is described in easily understandable terms, like
smooth and regular, rough and irregular, or in any combination.
• A smooth surface indicates cystic or benign swellings.
• An irregular or lobulated surface may indicate pathologies like
tuberculosis or malignancy.
If the swelling is obviously in the subcutaneous plane, it may stretch the
overlying skin and create some skin changes. Swellings which arise from the
structures of the skin, like the sebaceous cyst, may show the punctum which is
the hallmark of its diagnosis.
• Edge of the swelling–The edge or margin may be flattened or projecting, or
ill-defined. Some swellings have the potential to invade locally, like
malignancies, or the inflammatory reaction itself can involve the surrounding
tissues.
• Well defined or circumscribed margins indicate benign swellings.
• Ill defined margins may indicate inflammation or malignancies.
• Movements–Movements like pulsations and peristalsis may be naturally
present or may be induced by acts like bringing the muscles into contraction
or acts like coughing, sneezing.
• Movements noticed at rest
- Expansile pulsations: Pulsations caused by vascular tumours, like
aneurysms.
- Transmitted pulsations: Pulsations caused by tumours sitting on
pulsating blood vessels.
- Peristalsis: Intestinal movements (e.g. hernia sac).
• Movements noticed during normal acts like respiration/deglutition
- Intra abdominal lumps show movement when they lie in relation to the
diaphragm; thyroid swellings move during deglutition.
• Movements noticed during induced acts
- Impulse on coughing, sneezing or straining (e.g. pharyngeal pouch in
the neck, empyema in the thorax, herniae in the abdomen, and
meningocoele in the spine).
- Movements during muscular contractions (e.g. tumours arising from
muscles, like ruptures or hematomas).
Examination of the relevant areas: This becomes important in the clinical
evaluation of swellings especially of the lymphatic system (e.g. face needs to be
examined in neck swellings and vice versa).
Palpation
This step is to physically feel the lump and the surrounding areas with the
fingers or the hand in an organized stepwise method, to get a better idea of the
nature of the pathology. Palpation is done in the following steps:
• Palpation of the skin over the swelling
• Temperature: Warmth or cold–The skin over the swelling is palpated
gently by the dorsum of the examining fingers or hand, and also compared
with the normal skin (Fig. 9.32).
• Tenderness–Expressed by the patient with a wince on the face or by verbal
expression, when gentle pressure is applied over the skin (Fig. 9.33).
• Sensation is tested if there are any depigmented patches on a swelling, as
in Leprosy.
• Skin involvement is tested by two methods:
- Gliding test: The skin is rolled over the swelling by a finger to see
whether it is fixed or not (Fig. 9.34A).
- Pinching test: The skin is pinched with the thumb and the index finger to
see its adherence to the lump (Fig. 9.34B).
• Palpation of the swelling itself
• The swelling is felt with little more firm pressure.
• Exact size is determined in two directions (measured by tape) (Fig. 9.35).
• Surface is assessed by running the pulp of the examining fingers over the
swelling (Fig. 9.36).
• Edges are assessed by running the index finger along the edges (Fig. 9.37).
• Palpation to analyse the contents of the swelling (consistency): The swelling
is palpated to determine the contents of the swelling. The contents of the
swelling could be:
• Solids (soft – lipoma; firm – lymph node swellings; hard – bone swellings).
• Gas (soft – subcutaneous or surgical emphysema, bowel in a hernia sac).
• Liquid (soft and cystic swellings).
• Fluctuation is a hallmark of fluid or gas filled enclosed lump. When pressure
is applied to one side of a fluid filled lump, the fluid tends to spread to all
other directions, and when it cannot escape into any other compartment, it
bulges from the other side. This sign is called ‘fluctuation’. This is tested by
the following methods:
• Index fingers of both hands (for small swellings)–This is a standard
method for determining fluctuation. After fixing the swelling, the tip of
the index finger of one hand is kept at one side of the swelling and the tip
of the index finger of the other hand is kept at the other side of the
swelling. When one of the index fingers is pressed, the pressure is felt by
the other index finger and also by a visible movement. This has to be done
in two planes, at right angles to each other. This is called positive when
both the acts are positive (Fig. 9.38A). Both can be combined by using the
thumb and index fingers of both hands at the same time (Fig. 9.38B ).
• Paget’s test (for moderate size swellings)–The thumb and the index finger
of the left are kept on the periphery of the swelling and a gentle push is
given by the right index finger at the centre of the swelling, between the
fingers of the left hand. The displacement is felt by the fingers of the left
hand if it is positive for fluctuation (Fig. 9.39).
• Match-stick test (for very small swellings)–This test is done for very
small swellings, i.e. those less than 1 cm in size. Since there is not enough
space for the finger pulps to be kept over the swelling, two matchsticks are
used instead of the fingers. A gentle push on one matchstick is seen as a
displacement of the other matchstick if it is positive for fluctuation (Fig.
9.40).
• Thumb and middle finger of left hand and index and middle fingers of
the right (for large swellings)–Since the pressure induced by the right
index finger alone may not be adequate, the swelling is held with the
thumb and the middle finger of the left hand, and the pressure is induced
by the index and middle fingers of the right hand. Displacement of the
fingers of the left hand is seen when it is positive for fluctuation (Fig.
9.41).
• Thumb and fingers of both hands (for mobile swellings)–When the
swelling is mobile, the swelling is fixed with the thumb and the other
fingers of the left hand, and the pressure is applied by the thumb and other
fingers of the right hand. Displacement of the fingers of the left hand is
seen when it is positive for fluctuation (Fig. 9.42).
• Three finger tap test (for hydatid cyst)–The index, middle and the ring
fingers of the left hand are kept on the swelling near the periphery, and a
gentle tap is given by the right index finger at the centre. A wave is felt by
the fingers of the left hand and this is called ‘hydatid thrill’ which is
characteristic for a hydatid cyst.
• Cross fluctuation: Shift of fluid from one compartment of a cyst to the other
when they are intercommunicating (e.g. compound ganglion of the wrist and
plunging ranula).
• Transillumination: This test is done only when the fluctuation is positive.
This test is done in a dark room; the light transmitted by a beam of torch is
seen through a fine tube prepared by folding a card board or a X ray film
called ‘illuminoscope’ (Fig. 9.43).
• Brilliantly transilluminant swellings (e.g. cystic hygroma and vaginal
hydrocoele).
• Translucent swellings (e.g. lipoma and chylocele).
• Opaque swellings (e.g. sebaceous cyst, haematocoele and abscess).
FIGURE 9.32 Feeling the swelling for warmth.

FIGURE 9.33 Testing for tenderness.
FIGURE 9.34A Skin gliding test for skin involvement.
FIGURE 9.34B Skin pinching test for skin involvement.
FIGURE 9.35 Measuring the swelling in two directions.
FIGURE 9.36 Feeling the surface of the swelling.
FIGURE 9.37 Feeling the edge of the swelling.
FIGURE 9.38A Eliciting fluctuation with index fingers of both hands.
FIGURE 9.38B Eliciting fluctuation with fingers of both hands.
FIGURE 9.39 Paget’s test.
FIGURE 9.40 Matchstick test.
FIGURE 9.41 Eliciting fluctuation of a large swelling.
FIGURE 9.42 Eliciting fluctuation with the thumb and index fingers of
both hands.
FIGURE 9.43 Method of eliciting transillumination.
Note
• The lump should be big enough and the torch should have a unidirectional
beam.
• Non-cystic lesions, like lipomas may also exhibit transillumination, and
hydrocoeles with thick walls may not transilluminate.
• Cutaneous transmission of light should not be mistaken for
transillumination, and to prevent this, the torch should be kept firmly against
the skin of the swelling.
• Abnormal feel: Some swellings exhibit abnormal feels, like indentation

(pitting on pressure) and crepitus (crackling feel).
• Indentation–This happens due to the displacement of fluid from
oedematous tissues, or when the contents of the lump are soft-solid or
semi-solid and not very tense. This is determined by applying pressure
with the pulp of the index finger on a bony area underneath. Small
indentations are better felt than seen. This can also be demonstrated by
compressing faeces in the palpable colon per abdomen. Some sebaceous
cysts and dermoids show this sign due to displacement of the pultaceous
material within.
• Crepitus–The examiner feels a very funny crackling feel. This can be of
various types. They are:
- Crepitus of surgical emphysema: This is felt as a crackling feel in the
subcutaneous plane. This can occur due to the presence of air in the
subcutaneous plane following: (i) rupture of air passage (injury to
tracheobronchial tree); (ii) disease (ruptured bulla); (iii) infection (gas
gangrene); (iv) surgery (post laparoscopic procedures)
- Crepitus of bone: This is felt as a crackle (e.g. fracture, or ‘eggshell
crackling in osteoclastoma).
- Crepitus of joints: The crackle is felt when the joint is moved (e.g.
Charcot’s joint and osteoarthritis).
- Crepitus of tendons: A click may be felt when the finger is moved –
when the tendon nodule is pulled through a narrow area of tendon
sheath (e.g. tenosynovitis – Trigger Finger).
• Movements: A swelling can exhibit movements. They may be:
• Present at rest (e.g. pulsations or peristalsis).
• Noticed during normal physiological acts like respiration and deglutition.
• Noticed during induced acts (e.g. muscular action, coughing or sneezing).
Movements at rest
• Pulsations
• Transmitted pulsations–Pulsations caused by tumours sitting on pulsating
blood vessels. This is determined by keeping the index fingers of both
hands on the swelling as above, and the transmitted pulsations push the
fingers away from the swelling, but do not push the fingers away from
each other (Fig. 9.44A).
• Expansile pulsations–Pulsations caused by vascular lesions, like
aneurysms. This is determined by keeping the index fingers of both hands
on the swelling and the expansile pulsations push the fingers away from
the swelling and away from each other (Fig. 9.44B).
• Peristalsis–Intestinal movements. While examining the abdomen, they can be
felt with the examining hand.
FIGURE 9.44 Methods of eliciting (A - Transmitted pulsation, B -
Expansile pulsation).
Movements noticed during normal physiological acts

• Respiration–Intra abdominal lumps of hepatobiliary origin move up and
down with respiratory movements when they lie in relation to the diaphragm
• Deglutition–Thyroid swellings move during deglutition due to their
relationship with the pretracheal fascia.
Movements noticed during induced acts

• Coughing, sneezing or straining–Pharyngeal pouch in the neck, empyema in
the thorax, herniae in the abdomen, and meningocoele in the spine become
prominent on coughing, sneezing or straining since they are in continuity
with the cavity from which they arise. This is called ‘Cough Impulse’.
• Muscular action–Tumours arising from the muscle become more prominent
(haematomas), whereas, those arising from below the muscle fibres become
less prominent. This should be confirmed by palpation. The methods of
putting some of the muscles of the body into contraction are given in figures
9.45A to C.
FIGURE 9.45A Trapezius.

FIGURE 9.45B Latissimus dorsi.
FIGURE 9.45C Pectoralis major.
Sometimes it may be possible to bounce large abdominal masses

anteroposteriorly (kidney lumps) or in side to side direction (mesenteric cysts)
termed ‘ballottement’.
• Changes on application of pressure
• Reducibility–The swelling disappears and does not reappear even after the
release of pressure (applied by the examiner’s hand), but reappears when it
is induced by acts like coughing or sneezing (e.g. reducible hernia) (Fig.
9.46).
• Compressibility–The swelling reduces partly and remains so as long as the
pressure (applied by the examiner’s hand) is applied, but reappears
spontaneously on release, without any specific act which will make it
reappear (e.g. haemangioma).
Note
Both features can be seen in saphena varix, as it is compressible by
application of pressure and also reducible by limb elevation.
FIGURE 9.46 Demonstration of reducibility of a swelling.
• Blanching–Reduction in size and colour occurs due to emptying of blood

vessels when firm pressure is applied, and refilling occurs after the release
of pressure (e.g. capillary naevi). Both changes can be demonstrated with
the help of a glass slide (Figs. 9.47 Aand B).
• Palpation for its mobility: The mobility of a lump generally depends on its
tethering or fixation to the surrounding structures. The mobility of the lump
from deeper structures, can be determined by moving the lump with the
thumb and the index fingers while at rest (Fig. 9.48A), and also putting the
structures underneath in tension (Fig. 9.48B). When the mobility is restricted
at rest, it indicates its involvement to deeper structures, like the deep fascia.
If mobility is restricted when the underlying tissues are tense, it indicates its
origin or involvement to that tissue, e.g. lumps attached to linear structures
like a tendon, nerve or muscle move tangential to the direction of the
structure only and do not move in the direction of the axis of the tendons
(Fig. 9.49).
• Palpation of surrounding areas: The surrounding areas are examined with
the palm of the examining hand (Fig. 9.50) for any other lumps, the effects
on the surroundings tissues (induration – thickening and firmness of
surrounding tissues), vessels and lymphatics (pitting oedema – due to
vascular or lymphatic obstruction), nerves (motor and sensory
abnormalities), and bones (erosion – due continued pressure).
FIGURE 9.47A Capillary haemangioma of left palm.

FIGURE 9.47B Blanching of capillary haemangioma (elicited by
pressing with a glass slide).
FIGURE 9.48A Testing for mobility of swelling at rest.
FIGURE 9.48B Testing for mobility of swelling after keeping the
muscle taut.
FIGURE 9.49 Testing for mobility of ganglion.
FIGURE 9.50 Examining the surrounding areas of the swelling.

The draining lymph nodes must always be palpated as a part of examination of
lumps, which means the cervical, axillary and inguinal lymph nodes. It should be
remembered that the drainage area of testicular lumps is para-aortic lymph
nodes, and the abdomen should be palpated specifically for this group.
The physical examination findings and swellings of the skin are correlated in
Tables 9.9 and 9.10.
TABLE 9.9
Correlation of Physical Examination Findings with Swellings of the
Skin
Lesion Examination
Inspection Palpation Pathognomonic feature

Congenital Dermoid cyst Globular Soft At the lines of embryonic fusion
Haemangioma Irregular Soft Erythematous colour
Traumatic Implantation Globular Soft History of trauma
dermoid
Haematoma Irregular Soft Bluish discolouration
Acute Inflammatory Erysipelas Vesicles discharging Tender skin Rosy red rash with fever
fluid
Furuncle Pus filled lesion at Tenderness Hair root lesion
hair root
Chronic inflammatory Warts Single or multiple Soft to firm Warty appearance
warty growths
Condyloma Warty lesions at the Soft to firm History of sexual contact
acuminata muco-cutaneous
junctions
Benign/Premalignant Papilloma Pedunculated Soft with narrow Absence of induration
neoplastic growth stalk
Moles Flat or raised; Nontender Brown to black colour, with or
solitary or without hairs
multiple black
lesions
Kerato Papule or nodule Firm and rubbery Presence in sun exposed areas,
acanthoma with central coal tar exposure
crater
Solar keratosis Flat, brown, scaly Firm Presence in sun exposed areas
lesions
Bowen’s disease Brown indurated Firm Serosanguinous discharge
mass
Fibroma Globular Firm Nil specific
Neurofibroma Globular Firm May be multiple, pain
Schwannoma Globular Soft to firm Nil specific
Malignant neoplastic Basal cell Ulcerated swelling Soft to firm at its Commonly on face – areas
carcinoma with rounded base exposed to sun
edges
Squamous cell Ulcerated swelling Firm at its base Bleed to trivial trauma or touch,
carcinoma with raised and presence of induration
everted margin
Malignant Solitary or multiple Firm to touch History of pre-existing mole
melanoma black lesions with pruritus, bleeding or
sudden increase in size
Others Sebaceous cyst Solitary or multiple Soft and fluctuant Presence of punctum
cystic lesions without trans
illumination
Keloid or Thickened scar with Firm to hard History of previous surgery or
Hypertrophic or without drainage
scar infiltration of
skin
Granuloma Red firm nodule in Soft Bleeds to touch
pyogenicum granulation
Histiocytoma Reddish brown Firm and Resemble malignant melanoma
nodules nontender
Callosity and Hardened skin Firm Ill-fitting footwear or in the
corn areas of repeated trauma
Seborrhoic wart Overgrowth of skin Soft to firm Disease of the elderly
TABLE 9.10
Correlation of Physical Examination Findings with Swellings of the
Subcutaneous Plane
Lesion Examination
Inspection Palpation Pathognomonic feature

Acute Cellulitis Generalized Soft and History of trauma
inflammatory swelling tender
Acute abscess Localized Soft and History of previous cellulitis
swelling tender
Carbuncle Localized Soft and Multiple sinus openings discharging pus
swelling tender
Chronic Chronic abscess or Localized Soft and History of previous acute abscess
inflammatory Antibioma swelling nontender
Cold abscess Localized Soft and History of pulmonary tuberculosis at present
globular nontender or in the past or in family
swelling
Benign Lipoma Globular Soft and Slip sign
neoplastic nontender
Malignant Liposarcoma Irregular Firm History of lipoma in the past in that region
neoplastic
Percussion
Percussion is done in swellings which are in relation to the abdomen, thorax and
neck.
• Hyper resonant note indicates presence of gas (e.g. gas filled bowel loops).
• Dull note indicates the presence of fluid or solid matter in the swelling (e.g.
enlarged urinary bladder, pregnant uterus).
• Distended abdomens due to ascites (fluid in peritoneal cavity) are dull to
percussion. When the fluid is large, a tap on one side of the abdomen will
give a vibration on the other hand called ‘fluid thrill’ (Fig. 9.51). Since
the vibrations can travel through the subcutaneous fat, the patient or a
third person should place the side of one hand at the midline to block the
movement.
• When the fluid is in moderate quantity, it maintains a horizontal level. The
dull area will become resonant when the patient shifts positions, as the
area occupied with fluid is occupied by floating intestines. This is called
‘shifting dullness’ (Fig. 9.52).
FIGURE 9.51 Eliciting fluid thrill.

FIGURE 9.52 Method of eliciting shifting dullness.
Auscultation
Auscultation means hearing. This can be done with or without a stethoscope.
• Intestinal peristalsis is heard as sounds called ‘Borborygmi’, which do not
require the help of stethoscope.
• When a lump is vascular, and is in connection with an artery, it produces a
bruit or a murmur, which can be heard with the help of a stethoscope (Fig.
9.53).
FIGURE 9.53 Auscultation of a swelling.
General examination
It should be remembered that the presence of one or more lumps in one part of
the body presenting clinically for examination, may be an indicator of a systemic
illness, like tuberculosis or syphilis. General physical examination should
include all that has been described in the chapter, along with the examination of
chest and abdomen and all areas of lymph nodes.
CHAPTER 10
Ulcers
S. Devaji Rao
CHAPTER OUTLINE
10.1. Definition 87
10.2. Parts of ulcer 87
10.3. Classifications 87
• Aetiological classification 87
• Clinical classification 88
10.4. Traumatic ulcers 88
10.5. Inflammatory ulcers 88
• Tuberculous ulcer 88
• Lupus vulgaris 89
• Syphilitic ulcer 90
• Gummatous ulcer 90
• Soft chancre (Chancroid) 91
• Oriental sore (Delhi boil) 91
• Meleney’s ulcer 91
10.6. Vascular ulcers 91
• Arterial (ischemic) ulcer 91
• Venous (varicose) ulcer 92
10.7. Neoplastic ulcers 92
• Basal cell carcinoma 92
• Squamous cell carcinoma 92
• Marjolin’s ulcer 92
10.8. Miscellaneous ulcers 93
• Diabetic ulcer 93
• Trophic ulcer 93
• Tropical ulcer 94
• Martorell’s ulcer 94
• Bazin’s ulcer (Erythema induratum) 94
• Ulcer 95
• Vaginal and rectal examination 99
10.1 Definition
An ulcer is the break in the continuity of the epithelium. The covering may be
the skin or mucous membrane.
10.2 Parts of ulcer

An ulcer consists of the following parts (Fig. 10.1A):
• Floor: It is the exposed surface of the ulcer.
• Edge: It is the junction between the normal and ulcerated epithelium.
• Margin: It is the surface between the edge and the floor of the ulcer.
• Base: It is the area on which the ulcer rests.
FIGURE 10.1A Parts of ulcer.
The parts of an ulcer can be understood better by referring it to a vessel (Fig.

10.1B).
FIGURE 10.1B Part of ulcer referred to as a vessel.
10.3 Classifications of ulcers

Ulcers are classified based on their aetiology and clinical presentation.
Aetiological classification
Traumatic
The injury may be due to various causes –
• Mechanical (e.g. irregular tooth or denture)
• Chemical (e.g. alkalis or acids)
• Thermal (e.g. burns)
• Electrical (e.g. shock)
• Radiation (e.g. radiation necrosis of skin)
Inflammatory
The inflammation may be caused by –
• single organism, like M. tuberculosis (e.g., tuberculous ulcer) and T. pallidum
(e.g., chancre).
• more than one organism (e.g. Meleney’s ulcer).
Vascular
The vascular causes may be –
• arterial, which produces undernutrition (e.g. ischemic ulcer).
• venous, like varicose vein (e.g. varicose ulcer).
• lymphatic, like filarial lymphangitis (e.g. filarial ulcer).
Neoplastic
Neoplastic causes may be –
• Primary malignancy, like squamous cell carcinoma, basal cell carcinoma and
malignant melanoma.
• Secondary metastatic malignancy, which may ulcerate.
Miscellaneous
• Trophic ulcers (e.g. peripheral neuritis).
• Metabolic causes (e.g. diabetic foot ulcers).
Clinical classification
1. Acute (spreading) ulcer
2. Healing ulcer
3. Chronic ulcer
The differentiating features between each are given in Table 10.1.
TABLE 10.1
Differentiating Features of Acute, Healing and Chronic Ulcers
Type of Ulcer
Healing
Feature Acute ulcer Chronic ulcer
ulcer
History
Duration Short Weeks Months
Pain Marked Mild Absent
Fever Marked Absent May be present
Loss of function Severe Little Variable
Physical signs
Inspection
Shape Variable Regular Variable
Discharge Profuse, offensive Thin serous Seropurulent
Floor Slough Absent Absent May be present
Granulation Absent Bright red Unhealthy and pale
Edge Ragged Sloping Variable
Surrounding skin Erythematous Normal Pigmented
Palpation
Tenderness Present Absent Minimal
Edge Ragged, inflamed Normal thin Thick indurated
Bleeding on touch Present Present Absent if it is not
malignant
Induration and fixity to surrounding Absent Absent Present
structures
Regional lymph nodes Enlarged and Not palpable Enlarged and nontender
tender
10.4 Traumatic ulcers

Results due to direct trauma, like –
• Mechanical
• Chemical
• Thermal
• Electrical
• Radiation
• Features of acute ulcer.
• Radiation ulcers present with changes of pigmentation and dermatitis in the
surrounding skin (Fig. 10.2)
FIGURE 10.2 Traumatic ulcer.
• Proper history evaluation and examination is required to localize the
incriminating agent.
Treatment
• Ulcers heal when the incriminating agent is removed, followed by
administration of antibiotics and dressings.
10.5 Inflammatory ulcers
Tuberculous ulcer
• Caused by Mycobacterium tuberculosis.
• Results following the burst of a cold abscess or tuberculous lesions of the
bones and joints.
• Usually multiple.
• Shape is irregular.
• Edges are undermined (Fig. 10.3).
• Floor is covered with pale granulation tissue (apple jelly appearance).
• Surrounding skin may show pigmentation.
• Regional lymph nodes may be enlarged, which are firm, non-tender and
matted.
• There may be associated systemic evidence of tuberculosis in the lungs or
other parts of the body.
FIGURE 10.3 Undermined edge of tuberculous ulcer.
• Bacteriological examination may identify M. tuberculosis, which is
established by Ziel Nielson staining.
• Culture in Lowenstein-Jensen medium.
• Polymerase chain reaction (PCR) test for tuberculosis.
• X ray chest may identify the pulmonary lesions.
• Mantoux test may be useful.
Treatment
• Anti-tubercular drugs are mandatory.
• Antibiotics are needed to treat secondary infections.
• Dressings are needed to cover the ulcers.
Lupus vulgaris
• Tuberculosis of skin, seen mostly in children and young adults.
• Single or multiple cutaneous nodules, with ulcerations.
• Common on the face and occasionally on the arm.
• Ulcers remain active at the periphery, but show signs of healing at the centre.
• Biopsy of the ulcer for tubercle bacilli.
Treatment
• Anti-tubercular drugs are mandatory.
• Antibiotics are needed to treat secondary infections.
• Dressings are needed to cover the ulcers.
Syphilitic ulcer
• Caused by Treponema pallidum.
• Transmitted by sexual contact.
• Ulceration is a manifestation of the first stage of the disease.
• Manifests about 3–4 weeks after infection, at the point of entry of infection.
• A single, painless ulcer on the genitalia (Hard chancre) (Fig. 10.4).
• Found on the coronal sulcus, frenum, and rarely on the glans and shaft.
• Has a characteristic hard feel like a button with well-defined margins.
• Regional lymph nodes are mobile, discrete and shotty in nature with no
tendency to suppurate.
• Extragenital chancres are also seen on the lips, tongue, nipple and rectum,
according to the point of entry.
FIGURE 10.4 Primary chancre penis Source: (Courtesy Dr B Loganathan).
• Dark field microscopy of the exudates demonstrates Treponema pallidum.
• Wassermann reaction and Kahn tests are positive in the primary stage.
• Enzyme immunoassay (EIA) for T. pallidum is specific for primary syphilis.
Treatment
• Chancres heal spontaneously but may recur at a later stage.
Gummatous ulcer
• A late manifestation of syphilis (tertiary syphilis).
• Occurs 3–12 years after primary infection, and is due to inflammatory
reaction in perivascular lymphatics of the terminal vessels producing
obliterative endarteritis, necrosis and fibrosis.
• A single painless ulcer.
• Common on the areas of thin skin over the bones, like sternum, tibia, ulna and
skull (Fig. 10.5).
• Edges are round in shape and punched out.
• Floor is covered by yellowish gray (wash-leather) slough.
• Lymph nodes are rarely involved, unless secondarily infected.
FIGURE 10.5 Gummatous ulcers on the leg.
• Wassermann reaction and Kahn tests are positive.
Treatment
• Aqueous procaine penicillin is the standard drug of choice.
• Doxycycline is a good alternative.
Soft chancre (chancroid)

• Caused by Haemophilus ducreyi.
• Spreads through sexual contact.
• Develops about 3–7 days after the exposure.
• Single (Fig. 10.6) or multiple painful ulcers (School of fish or rail road track
appearance).
• The ulcers are soft.
• Margins are undermined.
• Edges are oedematous.
• Floor is covered by typical yellow slough.
• Base is non-indurated.
• Discharge copious and purulent.
• Bleeds readily to touch.
• Inguinal lymph nodes are generally enlarged.
• They are hard and tender.
• May form inguinal abscess, ulcer or sinus.
FIGURE 10.6 Chancroid Source: (Courtesy Dr B Loganathan).
• Smear examination (Gram’s, Unna Pappenheim’s and Wright’s staining).
• Culture with special media can isolate the organism.
• PCR tests are useful.
Treatment
• Ciprofloxacin, ceftriaxone, azithromycin and erthromycin are effective
drugs.
• Abscesses need drainage.
Oriental sore (Delhi boil)

• Caused by infestation by a protozoal parasite, Leishmania tropica.
• An indurated papule on the face and hand.
• If not treated, breaks down to form ulcer.
• Identifying the organism in the ulcer discharge.
Treatment
• Heal spontaneously leaving an ugly scar.
Meleney’s ulcer
• Occurs due to symbiotic action of micro-aerophilic non-hemolytic
streptococci and Staphylococcus aureus.
• This was described by Meleney.
• A gangrenous patch on the postoperative wound following surgeries of septic
conditions (e.g. empyema and peritonitis).
• Becomes an acutely spreading painful ulcer.
• Edge is undermined and burrowing in nature.
• Floor is covered by an unhealthy granulation tissue with foul smelling
discharge.
• Surrounding area has inner purple zone and outer reddish zone.
• The patient may be toxic.
• Causes mortality if untreated.
• Identification of the causative agent is necessary.
Treatment
• Antibiotics are mandatory.
• Local care of ulcer with excision of slough.
10.6 Vascular ulcers
Arterial (ischemic) ulcers

• Develops due to impaired blood supply as in thrombo-angiitis obliterans and
atherosclerosis.
• Common in chronic smokers.
• A dry punched out painful ulcer on the feet, especially on the toes (Fig. 10.7).
• Penetrates the deep fascia.
• History of intermittent claudication and discolouration of other toes may
suggest arterial aetiology.
• The floor is covered with minimal granulation tissue, and also reveals the
underlying structures, like tendons and nerves.
• Absent pulses of the lower limbs is conclusive.
FIGURE 10.7 Ischemic ulcers.

• Arteriography, plethysmography and Doppler studies are useful in diagnosis.
Treatment
• Vasodilators are essential.
• Thromboembolectomy is the treatment of choice if the arteriography does not
show enough collaterals.
Venous (varicose) ulcers

• These ulcers develop due to increased hydrostatic pressure in the vein
(Gravitational ulcer).
• Commonly in the lower limbs.
• Ulcerations occur due to defective exchange of oxygen and metabolites
following oedema.
• Solitary ulcer, usually seen on the lower leg.
• More common on the medial aspect of lower leg at the level of the
perforators, where there is maximum hydrostatic pressure. Not uncommon
on the lateral aspect of the leg (Fig. 10.8).
• It is a superficial ulcer.
• Margin is thin and blue due to the growing epithelium.
• Edge is sloping and pale purple blue in colour.
• Floor is covered with pale, unhealthy granulation.
• Discharge is scanty.
• Surrounding skin is pigmented and shows evidence of dermatitis.
• Varicose veins are always present.
• There may be associated oedema of the lower limb.
• Regional lymph nodes are not enlarged unless the ulcer is infected.
FIGURE 10.8 Varicose ulcers.
• Doppler studies and venography are diagnostic.
Treatment
• Phlebotonic drugs and limb elevation are useful.
• Compression bandages or stockings are essential.
• Local care for ulcers.
• Antibiotics are required if there is evidence of infection.
10.7 Neoplastic ulcers

Basal cell carcinoma (rodent ulcer)
See Chapter 9.
Squamous cell carcinoma

See Chapter 9.
Marjolin’s ulcer
A low-grade epidermoid carcinoma arising from the epithelium covering the scar
tissue (commonly burns), keloid or longstanding benign ulcers, like venous
ulcer.
• A very slow growing painless ulcer (Fig. 10.9) that does not metastasize as the
scar tissue is devoid of nerves and lymphatics.
• When the ulcer involves the normal skin, the lymph nodes may get involved.
• Clinically it mimics a squamous cell carcinoma, but the edge is not raised and
the floor does not contain florid granulation tissue.
FIGURE 10.9 Marjolin"s ulcer.
Treatment
• Wide excision.
10.8 Miscellaneous ulcers
Diabetic ulcer
• Develops due to neuro-vasculopathy.
• This is a metabolic neuropathy associated with atheroslerotic changes,
causing microangiopathy.
• Starts as a painless ulcer usually on the toes or the heel of the foot (Figs.
10.10A and B).
• It becomes deep and penetrating due to repeated infections.
• Edge is inflamed and indurated.
• Floor may contain seropurulent discharge.
• Base may be fixed to the deeper structures. It becomes painful when
infected.
FIGURE 10.10A Diabetic ulcer.

FIGURE 10.10B Diabetic ulcer.
• Determination of blood glucose levels is necessary.
Treatment
• Treatment for diabetes mellitus.
• Local care of ulcer.
Trophic ulcer
• Occurs due to neuropathy, producing loss of sensation commonly in the foot.
• A painless punched out ulcer.
• Common at the pressure points, like heads of metatarsals (Fig. 10.11A) and
sacral region (bedsore) (Fig. 10.11B).
• Begins as thickened skin, a callosity, which suppurates and discharges pus.
• Central part is deep and burrows deep into the tissues, creating a foul
smelling slough.
• Edge is thickened and corny.
• Surrounding skin is anesthetic, which is a characteristic finding.
FIGURE 10.11A Trophic ulcer of foot.

FIGURE 10.11B Bedsore in the sacral region.
• Nerve conduction studies may be required to confirm the diagnosis.
Treatment
• Excision of slough and allowing the wound to heal by secondary intention is
commonly followed.
• Reconstruction with skin flaps is required for large defects.
Tropical ulcer
• Occurs due to the infection of Vincent’s organisms (Bacteroides fusiformis).
• Starts from an insect bite, which causes a small breach in the skin.
• A papule-pustule with a zone of surrounding inflammation and induration.
• These lesions burst in 2–3 days to form painful foul-smelling ulcers, with
undermined and raised edges (Fig. 10.12).
• Pain is a notable feature.
• Ulcer becomes indolent and refuses to heal for months to years.
• Squamous cell carcinoma may supervene.
FIGURE 10.12 Tropical ulcer on the anterior aspect of leg.
• Determination of blood glucose levels to rule out diabetes.
Treatment
• Heals spontaneously after a long period, leaving behind a characteristic
circular pigmented scar.
Martorell’s ulcer
• Occurs in hypertensive, atherosclerotic patients.
• Starts as a local necrosing patch of skin on the calf, sloughing away to form a
punched out ulcer extending deeper.
• Can be bilateral.
• Surprisingly, the pulses are present.
• Arteriography may be useful.
Treatment
• Heals spontaneously but takes months to years.
• Administration of vasodilators may be useful.
Bazin’s ulcer (erythema induratum)

• Supposed to be due to localized fat necrosis.
• Starts as erythematous, purplish nodules on the calves, which break down to
become indolent and refuse to heal.
• Shape is irregular.
• Margin is thin and undermined.
• Floor covered with watery granulation.
• Discharge is serosanguinous.
• Identification of incriminating organism is necessary.
• Tubercle bacilli may be isolated in some cases.
Treatment
• Anti tubercular treatment is necessary if tubercle bacilli are isolated.
• Appropriate antibacterials may be needed.
• They heal but take a very long time.
Eliciting history
• Duration of ulcer: When did the patient first notice the ulcer?
Acute ulcers will be present for a short period and chronic ulcers are present
for a longtime. The examiners should direct their questions towards the
information of incubation period in infective pathology (e.g. Chancres develop
after 3–4 weeks after exposure; chancroid develops after 3–7 days after
exposure).
• Mode of onset: Was the onset of the ulcer a sudden event or gradual in
developing, and was there any trauma preceding the ulcer?
Some ulcers develop following a low-grade infection in the neck or axilla (e.g.
tuberculous ulcer, traumatic ulcer – a sharp tooth producing an ulcer).
• Situation at the time of onset: Was there a swelling at the time of
development of the ulcer?
Some infections may form an abscess which may burst to form an ulcer on the
skin (e.g. tuberculosis and actinomycosis).
• Association of pain: Was or is the ulcer painful?
Some ulcers are characteristically painless (e.g. syphilitic ulcer), some are
moderately painful (e.g. tuberculosis), and some are very acutely painful (e.g.
inflammatory ulcers and traumatic ulcers).
• Nature of discharge: What is the nature of discharge?
The nature of discharge is useful in arriving at the diagnosis (e.g. purulent
discharge of acute ulcers, serous discharge of healing ulcers, and foul smelling
discharge of severely infected ulcers).
• Variation in discharge:Does the discharge reduce from time to time?
The discharge can vary in quantity till complete healing takes place (e.g.
serous discharge of healing ulcers may turn foul smelling when they get infected
and discharge pus).
Presence of fever at the time of examination indicates active infection (e.g.
superadded bacterial infection in tuberculous ulcers may cause fever).
It should be enquired whether any treatment was given for the illness. Non
healing ulcers indicate inadequate or improper treatment or persistence of a
focus as the cause of non healing (e.g. infection and foreign body).
• Loss of appetite and weight: Is there associated loss of appetite and loss of
weight?
Loss of appetite and weight may indicate malignant pathology (e.g. secondary
metastatic lymph nodes presenting with ulcers, or tuberculosis of the lymph
nodes).
• Personal history: Does the patient smoke cigarettes?
This question has relevance, as smokers develop thrombangiitis obliterans,
which can cause ischemic ulcers especially of the feet. History related to calf
muscle pain (claudication pain) and claudication distance should be clearly
elicited.
treatment?
treated, it will indicate the examiner to reconsider the diagnosis like tuberculosis.
Diseases like tuberculosis occur in closely living families and a positive
Ulcers
The steps for carrying out examination of the patient with ulcers are:
1. Inspection
2. Palpation
Inspection
The following points are to be noted during the inspection of the ulcers:
• Position–Observe the position of the ulcer.
• Ulcers in the neck are generally tuberculous.
• Rodent ulcers on the face occur above the line joining the outer canthus of
the eye and the lobule of the ear (Fig. 10.13).
• Chancres–ulcers on the genitalia.
• Number–The number of ulcers is relevant.
• Single ulcer may be due to trauma caused by a constant irritant, like a
sharp tooth (Fig. 10.14).
• Multiple ulcers may be due to infections (Fig. 10.15).
• Shape, size and depth–Shape of the ulcer varies in different conditions.
• Varicose ulcers are oval in shape (Fig. 10.16).
• Tuberculous ulcers may be regular or irregular.
• Post traumatic ulcers are irregular (Fig. 10.17A).
• Malignant ulcers are irregular in shape (Fig. 10.17B).
FIGURE 10.13 Rodent ulcer.

FIGURE 10.14 Single ulcer due to sharp tooth.
FIGURE 10.15 Multiple aphthous ulcers of the tongue.
FIGURE 10.16 Oval shaped varicose ulcer.
FIGURE 10.17A Irregular post traumatic ulcer.
FIGURE 10.17B Irregular malignant ulcer.
Determination of the size and depth will help in the assessment of the progress
of the ulcers.
• Floor of the ulcer–It is the exposed surface of the ulcer which can be clearly
seen. The tissue covering the floor of the ulcer differs in various conditions
(Figs. 10.18A, B and C). They are given in Table 10.2.
• Discharge–Discharges from the ulcers vary according to the pathology.
• Serous discharge–healing ulcer.
• Sero-sanguinous discharge–tuberculous ulcer.
• Bloody discharge–malignant ulcer.
• Margin of the ulcer–The margin should be inspected for infiltration.
• Edge of the ulcer–This is an important property of an ulcer which needs
special attention, as it by itself gives a good amount of clue to the diagnosis.
There are five types of edges seen in ulcers. They are:
1. Undermined edge–When the deeper penetration of the disease is faster than
the destruction of the skin, it gives this appearance of an overhanging edge
Fig. 10.19 [e.g. pressure sore, tuberculous ulcer].
2. Punched out edge–The disease process limits itself to the ulcer itself and
does not tend to spread to the surrounding tissues. It gives the punched out
appearance (Fig. 10.20) (e.g., ischemic ulcer and gummatous ulcer).
3. Sloping edge–The healing ulcers give the appearance of sloping edge, as the
edge starts showing the signs of regeneration [e.g. healing ulcer (Fig10.21)].
4. Raised and pearly white edge–The edge develops into an invasive disease,
whereas, the centre becomes necrotic [e.g. Basal cell carcinoma (Fig. 10.22)].
5. Rolled out edge–The disease overgrows the edge of the ulcer and this tissue
heaps up and spills over the normal skin to produce an everted edge [e.g.
malignant ulcer (Fig. 10.23)].
FIGURE 10.18A Healthy granulation tissue of healing ulcer.

FIGURE 10.18B Ulcer with slough.
FIGURE 10.18C Ulcer with hypertrophic granulation.
FIGURE 10.19 Undermined edge Source: (Courtesy Dr K. Sridhar).
FIGURE 10.20 Punched out edge.
FIGURE 10.21 Sloping margin of healing ulcer.
FIGURE 10.22 Rolled and beaded edge of rodent ulcer.
FIGURE 10.23 Rolled margin of malignant ulcer.
TABLE 10.2
Appearance of Floor of Various Ulcers
Appearance of the floor of ulcer Condition

Slough with profuse foul smelling discharge Acute spreading ulcer
Healthy granulation with scanty discharge Healing ulcer
Smooth pale granulation with serous discharge Chronic ulcer
Smooth pale granulation with serosanguinous discharge Tuberculous ulcer
Wash leather slough Gummatous ulcer
Nodular granulation raised above surface Epithelioma
Blackish colour tissue Melanoma
Deeper tissues may be exposed Trophic ulcer
The edge and margin are separate entities and should not be confused with
each other
• Surrounding area–The skin surrounding the ulcer may show some changes
(e.g. red and inflamed skin around an acute ulcer, pigmentation and
dermatitis around a varicose ulcer (Fig. 10.24).
FIGURE 10.24 Pigmented areas surrounding the ulcer.
Palpation
The following points are to be noted by palpation. The examiner should always
wear gloves while examining the ulcers as the discharge may contaminate the
fingers of the examiner.
• Size of the ulcer–The exact size of the ulcer should be measured at least in
two directions and recorded in a diagrammatic way, as repeated
measurements will be useful in assessing the progress of healing (Fig.
10.25).
• Tenderness of the ulcer–The ulcer should be held between the thumb and
index finger and gentle pressure should be exerted (e.g. tenderness is elicited
in acute ulcers) (Fig. 10.26).
• Edge of the ulcer–The edge should be palpated between the thumb and index
finger and the edge should be assessed as various pathologies have various
characteristics of edges (Fig. 10.26).
• Base of the ulcer–The ulcer should be held between the thumb and index
finger and the base (the structure on which ulcer is situated) should be
assessed [e.g. induration is felt in chronic ulcers; feeling of hardness is
experienced in malignant ulcers and chancres (Fig. 10.26)].
• Mobility–The examiner should try to move the ulcer over the underlying
structures [e.g., ulcers like gummatous ulcers from the bone cannot be
moved, but those on the soft tissues like muscles can be moved (Fig. 10.26)].
FIGURE 10.25 Measuring the size of ulcer.
FIGURE 10.26 Palpation of ulcer for tenderness and edges.
Lymphatic system
Of drainage area
It is always mandatory to examine the area of lymphatic drainage of the ulcer,
which will give useful information, e.g. an ulcer in the neck may be a part of
multiple tuberculous lymph node swellings, and malignant ulcers may
metastasize to the local lymph nodes.
Note
Enlarged lymph nodes in malignancies may also be due to secondary infection
and not necessarily due to the malignant spread.
Of other lymph nodes

(e.g. tuberculosis). Examination of the liver and spleen completes the lympho
reticular system, which is useful in diagnosis.
General examination
General physical examination will give clues for diagnosis, like evidence of
pulmonary tuberculosis, and may direct the cause for non healing ulcers in the
neck or bone, or a tuberculous intestinal fistulae.
Rectal and vaginal examination

Rectal examination (digital examination and proctoscopy) should be performed
in perianal ulcers, and vaginal examination for ulcers around the genitalia in
females.
C H A P T E R 11
Sinuses and fistulae

S. Devaji Rao
CHAPTER OUTLINE
11.1. Definitions 100
11.2. Aetiological classification of sinuses 101
11.3. Aetiological classification of fistulae 102
11.4. Regional classification of sinuses and fistulae 103
11.5. Sinuses and fistulae of parotid region 103
• Preauricular sinus 103
• Parotid fistula 103
11.6. Sinuses and fistulae of mandibular and submandibular
regions 103
• Alveolar sinus 103
• Cervico-facial actinomycosis 103
• Chronic osteomyelitis of mandible 105
• Submandibular salivary fistula 105
11.7. Sinuses and fistulae of midline of neck 105
• Median mental sinus 105
• Burst sublingual dermoid 106
• Thyroglossal sinus or fistula 106
11.8. Sinuses and fistulae of lateral side of neck 106
• Branchial fistula 106
• Pharyngeal fistula 106
• Tuberculous sinus 107
11.9. Sinuses and fistulae of chest 107
• Postoperative sinus (Sternal region) 107
• Broncho-pleuro-cutaneous fistula 107
• Thoracic actinomycosis 108
• Tuberculous sinus of chest wall 108
• Osteomyelitis of ribs 108
• Malignant sinuses of chest wall 108
11.10. Sinuses and fistulae of abdomen 109
• Umbilical sinus 109
• Patent vitello-intestinal duct 109
• Urachal sinus and fistula 109
• Malignant fistula of umbilical region 110
• Postoperative sinus (midline) 110
• Postoperative gastrointestinal fistulae 110
• Postoperative urinary fistulae 112
11.11. Sinuses and fistulae of loins 112
• Urinary fistulae of loins 112
• External biliary fistula 112
• Colocutaneous fistulae of the loins 113
• Tuberculous sinus (Pott’s spine) 113
11.12. Sinuses and fistulae of groins 114
• Postoperative sinus (mesh) 114
11.13. Sinuses and fistulae of right iliac fossa 114
• Small intestinal fistulae of right iliac fossa 114
• Actinomycosis of right iliac fossa 114
• Colocutaneous fistulae of right iliac fossa 114
11.14. Sinuses and fistulae of male genitalia 115
• Testicular sinus 115
11.15. Sinuses and fistulae of perineal region 115
• Urethral fistula 115
• Anal fistulae 116
11.16. Sinuses of the back 116
• Pilonidal sinus 116
11.17. Sinuses of the feet 117
• Maduramycosis 117
• Chronic osteomyelitis of metatarsals 117
• Sinus due to retained foreign body 117
• Sinus/Fistula 118
• General 121
• Rectal and vaginal examination 121
11.1 Definitions
Sinus is defined as a blind track extending from the exterior to the tissues, which
may be lined by granulation tissue or epithelial tissue (Fig. 11.1).
FIGURE 11.1 Anatomy of a sinus.
Fistula is defined as a track communicating two epithelial surfaces.

• When it connects a viscus to the exterior, it is called external fistula (Fig.
11.2).
• When hollow internal organs are connected by a track, it is called internal
fistula (Fig. 11.3).
FIGURE 11.2 External fistula.
FIGURE 11.3 Internal fistula.
Like a sinus, the granulation tissue lining the track of a fistula may get
epithelialized.
11.2 Aetiological classification of sinuses

The sinuses are classified based on its aetiology:
1. Congenital–A discharging sinus presenting due to a congenital cause [e.g.
preauricular sinus (Fig. 11.4)].
2. Traumatic–A sinus may follow trauma like surgery or an implanted foreign
body [e.g. prosthesis in orthopedic surgery (Figs. 11.5A and B); mesh in
hernia surgery (Fig. 11.6)].
3. Inflammatory–A sinus caused by a infective pathology (e.g. osteomyelitis,
tuberculosis and actinomycosis).
4. Neoplastic–A sinus caused by malignant tissue undergoing degeneration [e.g.
malignancy of the breast (Fig. 11.6A)]
5. Miscellaneous–Variable causes, like hair [e.g. pilonidal sinus (Fig. 11.7)].
FIGURE 11.4 Pre auricular sinus Source: (Courtesy Dr K. Sridhar).

FIGURE 11.5A Sinus after internal fixation of fracture tibia.
FIGURE 11.5B Sinus after surgery for fracture femur Source: (Courtesy Dr C. T.
Alagappan).
FIGURE 11.6 Sinus following surgery for incisional hernia (Mesh).
FIGURE 11.6A Sinus from breast malignancy Source: (Courtesy Dr Usha
Dorairajan).
FIGURE 11.7 Pilonidal sinus in a hairy individual.
11.3 Aetiological classification of fistulae

The fistulae are classified based on its aetiology:
1. Congenital–Present at the time or soon after birth due to developmental
defects [e.g. branchial fistula, thyroglossal fistula (external fistula), tracheo-
oesophageal fistula (internal fistula) (Fig. 11.8)].
2. Traumatic–A communication of a hollow viscus or a duct with the exterior
following a surgical procedure [e.g. pancreatic fistula (external fistula), faecal
fistula, biliary fistula or a communication between two or more organs (e.g.
gastro jejuno colic fistula)].
3. Inflammatory–Inflammatory focus causing the communication of a hollow
viscus with the exterior [e.g. appendicular fistula, fistula in ano (external
fistula), colo-vesical fistula (internal fistula)].
4. Neoplastic–Neoplasms of internal organs may extend to the exterior [e.g. oro-
cutaneous fistulae following oral cancer (external fistula), carcinoma cervix
entending into the urinary bladder, e.g. recto-vesical fistula (internal fistula)].

FIGURE 11.8 Oesophageal atresia with tracheo oesophageal fistula.
Note
The sinuses and fistulae are complications of various pathologies per se, or
they occur following trauma or surgery.
11.4 Regional classification of sinuses and

fistulae
The sinuses and fistulae have a specific regional occurrence, and this is depicted
in the Fig. 11.9. To know about the pathology of the respective diseases, the
student is advised to refer to the appropriate pages in the book in other chapters
also.
FIGURE 11.9 Regional distrbution of sinuses and fistulae.

11.5 Sinuses and fistulae of parotid region
Preauricular sinus
• Occurs due to imperfect fusion of the six tubercles, which form the pinna.
• When the sinus is blocked, a cyst is formed which may get infected to form an
abscess (Fig. 11.10).
FIGURE 11.10 Preauricular sinus with abscess formation.

• The sinus opening is seen at the root of the helix or the tragus of the ear (Fig.
11.4).
• Ulceration of skin around the sinus opening is not uncommon.
Treatment
• Surgical excision is curative.
Parotid fistula
• Usually an aftermath of incision of parotid abscess, a penetrating injury or
after parotidectomy.
• A pinpoint opening in the parotid region discharging saliva, with a history of
an abscess, trauma or surgery.
• The discharge is of extreme discomfort as it is associated with a meal and the
smell of good food.
• Skin excoriation may be present around the fistulous opening (Ref Fig.
23.13A).
• Sialography is diagnostic.
Treatment
• Excision of fistula is needed if it is from the major duct.
11.6 Sinuses and fistulae of mandibular and

submandibular regions
Alveolar sinus
• Results as a complication of an untreated alveolar (periapical) abscess
(maxilla or mandible).
• An opening below the mandible, with the history of an acute abscess (severe
toothache) or without any symptom (chronic alveolar abscess).
• X ray of the tooth is contributory.
Treatment
• Excision of fistulous tract along with extraction of diseased tooth is
necessary.
Cervico-facial actinomycosis
• The commonest form of actinomycosis.
• Caused by Actinomyces israelii, an aerobic Gram positive branching
filamentous organism, which lives as a harmless parasite in the tonsillar
crypts and dental cavities of a normal mouth.
• Lower jaw is commonly affected; often adjacent to carious tooth.
• The gum becomes indurated, and induration extends to the skin of face and
neck.
• A soft swelling in the submandibular region, with multiple soft areas
(abscesses).
• May burst into sinuses surrounded by bluish skin.
• A recent history of tooth extraction, signs of tooth decay, or poor oral hygiene
aid in the diagnosis.
• Isolation of organism is necessary.
Treatment
• Prolonged administration of antibiotics is curative.
Chronic osteomyelitis of mandible

• Inadequately treated acute osteomyelitis, resulting from a root abscess of the
mandible results in chronic osteomyelitis, producing a sinus.
• A discharging sinus opening on the mandible or close to it.
• The sinus may be fixed to the mandible, which may show local swelling and
tenderness.
• X rays show abnormal bone with rarefaction and sclerosis. A separate area of
dense bone lying in the cavity may appear called ‘sequestrum’.
• Computed tomography (CT) scan may give useful information about the
‘sequestrum’.
Treatment
• Excision of the sinus tract along with removal of sequestrum
(sequestrectomy) and all dead tissue under cover of antibiotics is the
treatment of choice. The cavity may be filled with bone grafts.
Submandibular salivary fistula

• Results due to bursting of a submandibular salivary abscess due to total
obstruction of the Wharton’s duct by a calculus.
• Can also occur after the surgery of submandibular salivary gland, or after
trauma or radiotherapy to the neck.
• Clinical Presentation: An opening in the submandibular region discharging
saliva (Fig. 11.11) or pus, with the history of drainage of abscess or surgery.
FIGURE 11.11 Submandibular salivary fistula due to irradiation to tongue.
• No investigation may be necessary.
• Fistulogram may be of use.
Treatment
• Excision of fistulous tract, along with the remnants of salivary gland is
curative.
11.7 Sinuses and fistulae of midline of neck
Median mental sinus

• Usually secondary to intra-oral infections, especially of the tongue or teeth
(periodontal abscess).
• A painful and tender lump in the midline near the mandible in the submental
region. When the lump bursts, it forms a discharging sinus.
• Examination of the oral cavity for oral infections.
• Identifying the incriminating organism by culture from discharge is
necessary.
Treatment
• Broad spectrum antibiotics will have to be administered.
• If abscesses are found in the dental planes, they have to be drained with or
without dental extractions.
• Excision of sinus is necessary if it does not heal.
Burst sublingual dermoid

• Occurs from a rare lesion, median sublingual dermoid, a developmental
deformity and occurs at the line of fusion.
• A discharging sinus with a previous history of a smooth soft cystic swelling in
the submental region.
• Sinogram will be diagnostic.
Treatment
• Complete excision of the sinus is the treatment. The division of mylohoid
muscle at the line of its raphe will help easy excision.
Thyroglossal sinus or fistula (see also chapter

24)
• Thyroglossal cysts result from failure of atrophy of the thryoglossal tract.
• Thyroglossal sinus or fistula results due to bursting of an infected cyst, either
spontaneously or after surgical drainage.
• A discharging orifice in the infrahyoid region (Fig. 11.12), rarely above the
hyoid bone.
• The specific diagnostic test is the pulling up of the orifice on protrusion of the
tongue; rarely when the tongue is pulled with traction.
FIGURE 11.12 Thyroglossal fistula Source: (Courtesy Dr Usha Dorairajan).
• Sinogram or fistulogram may be useful.
Treatment
• Excision of the sinus or fistula is curative.
11.8 Sinuses and fistulae of lateral sides of neck
Branchial fistula
• It can be present at or soon after birth, due to persistence of remnants of
cervical sinus.
• Or a sinus may also result from drainage of a cyst either spontaneously or
after surgery (See also Ch. 25).
• The tract passes between the internal and external carotid arteries, above the
hypoglossal nerve and below the glossopharyngeal nerve to open into the
tonsillar fossa
• A discharging orifice on the anterolateral aspect of the neck, at the anterior
border of the lower part of the sternomastoid muscle.
• The fistula undergoes recurrent infection and discharges.
• Fistulogram may be useful.
Treatment
• Excision of fistula is curative.
Pharyngeal fistula
Results when the infected pharyngeal pouch (See also Ch. 25)
• bursts.
• is incised.
• Following a reconstructive surgery after pharyngectomy for malignant
tumours of the pharynx.
• A discharging sinus with a history of incision of a cystic swelling in the neck,
or with a history like pharyngectomy for tumours.
• Fistulogram is useful in diagnosis.
• CT or Magnetic resonance imaging (MRI) of the neck with a fistulogram is
diagnostic.
Treatment
• Small fistulae heal spontaneously and large ones require surgical excision.
Tuberculous sinus
• Caused by bursting of caseating lymph nodes; infection caused by M.
tuberculosis (See Ch. 12).
• A discharging sinus opening anywhere in the neck (Fig. 11.13), with a
previous history of a lump at the site or near the opening.
FIGURE 11.13 Tuberculous sinus in the neck.
• Lymphocytosis, raised erythrocyte sedimentation rate (ESR), and positive
Mantoux test are suggestive of diagnosis.
• X ray and CT scan of the chest help in the diagnosis of associated pulmonary
tuberculosis.
• Acid Fast Bacilli (AFB) may be demonstrated in the discharge.
• Polymerase chain reaction (PCR for Mycobacterium tuberculosis) is useful
in diagnosing tuberculosis.
• Excision biopsy of the sinus is conclusive.
Treatment
• Anti-tubercular treatment is curative.
11.9 Sinuses and fistulae of chest
Postoperative sinus (sternal region)

• Results after cardiac surgery, where sternotomy is closed with a stainless steel
wire.
• Chronic infection and persistence of the foreign body aggravates this
condition.
• A discharging sinus on the operative wound in the sternal region, with a
history of previous surgery by sternotomy.
• Culture of discharge may show the incriminating organism.
Treatment
• Appropriate antibiotics and dressings are curative.
Broncho-pleuro-cutaneous fistula (thoracic

region)
Causes of broncho-pleuro-cutaneous fistula are:
• Postoperative (operations involving resection of lung tissue)
• Spontaneous (infections)
• Pneumonia (associated with AIDS)
• Lung abscess
• Tuberculosis
• Spontaneous pneumothorax
• Traumatic (penetrating injuries or blunt airway injury)
• Symptoms develop towards the end of the first week after surgery; fever and
blood-stained sputum are the first signs.
• A small leak allows air entry through the fistula into the pleural cavity to
produce pneumothorax and collapse of lung.
• Larger fistulae give rise to serious flooding of bronchial tree and a tension
pneumothorax results.
• Bronchogram is diagnostic.
• Bronchoscopy, CT and radionuclide ventilation scanning are useful to
confirm the diagnosis and aetiology of fistula.
Treatment
• Repeated aspirations control small leaks and healing is possible.
• Open surgery and resuturing of bronchus, with muscle graft is required for
larger fistulae.
• Broad spectrum antibiotics or anti-tubercular treatment is mandatory.
Thoracic actinomycosis
• The infecting organism, Actinomyces israelii is aspirated into the lungs. It
occasionally spreads downwards from the pharynx or neck, or upwards
through the diaphragm.
• The disease extends through the lungs to the pleura and chest wall, and ends
up in sinuses.
• Resemble tuberculosis.
• Multiple discharging sinuses on the chest wall.
• Isolation of organism in culture of sputum or the discharges from the sinuses
is conclusive.
Treatment
• Prolonged administration of penicillin is curative.
• Clindamycin and erythromycin are good alternatives.
Tuberculous sinus of chest wall

This sinus results as a complication of tuberculous infection of:
• The pleural cavity forming a chronic empyema, due to bronchiectasis or lung
abscess.
• Intercostal lymph nodes, spine, ribs and sternum. The sinus forms cold
abscesses, which rupture and track a considerable distance, and present at the
anterior axillary line.
• Symptoms are vague, like general malaise, mild fever and anaemia.
• Clinical examination shows a sinus opening on the chest wall (Fig. 11.14).
• Signs of tuberculosis of lungs may be present.
FIGURE 11.14 Sinus following tuberculous osteomyelitis of
sternum Source: (Courtesy Dr V. Thulasiraman).
• X ray chest is diagnostic.
• Biopsy of the sinus is confirmatory.
Treatment
• Antitubercular treatment is curative in many cases.
• Excision is warranted for chronic sinus.
Osteomyelitis of ribs
• Caused by spread of infection from chronic empyema (tuberculosis and
fungal infections).
• A discharging sinus adherent to the rib, with or without tenderness (Fig.
11.15).
FIGURE 11.15 Sinus of osteomyelitis of rib.
• X ray of the underlying rib and the chest will help in diagnosis.
Treatment
• Excision of the involved rib is needed.
• Decortication may be needed for underlying empyema.
Malignant sinuses of chest wall
• Results due to direct extension of bronchogenic carcinoma to the pleura and
chest wall.
• Cough, haemoptysis, dyspnoea and wheezing.
• A discharging sinus opening may be seen on the chest wall with or without a
fungating tumour underneath it.
• Chest X ray and CT are diagnostic.
• Biopsy of the sinus is confirmatory.
• CT aided sinogram is useful.
Treatment
• Management of the underlying malignancy is the treatment of choice.
11.10 Sinuses and fistulae of abdomen
Umbilical sinus
• Recurrent or chronic infections of umbilicus produce umbilical granuloma,
and form a sinus to the skin.
• Pilonidal sinus can occur at the umbilical region in hairy people (Fig. 11.16).
FIGURE 11.16 Pilonidal sinus of umbilicus (tuft of hair is
seen) Source: (Courtesy Dr N Mohan).
• A foul smelling discharge from the umbilicus.
• Careful examination may reveal the sinus opening.
• Sinogram or probing the fistula is useful in diagnosis.
Treatment
• Excision of sinus is curative with broad-spectrum antibiotics.
Patent vitello-intestinal duct
• During fetal development, the vitello-intestinal duct communicates with the
midgut. This tract closes before birth.
• Occasionally, this tract may persist as a fistula (umbilical fistula) between the
(Meckel’s diverticulum) small bowel and the umbilicus.
• When the tract closes at the small bowel and remains open at the umbilicus, it
is called ‘umbilical sinus’.
• The umbilical fistula discharges mucus and or faeces, whereas, the umbilical
sinus discharge mucus only.
• The everted edges of the sinus may form an adenoma (Raspberry tumour).
• Fistulogram or sinogram may be useful in diagnosis.
Treatment
• Excision of the fistula or sinus together with Meckel’s diverticulum, if
present, is the treatment of choice.
Urachal sinus and fistula

• During fetal development, the urogenital sinus communicates with the
allantois via the urachus. This tract closes before birth.
• Occasionally, this tract may persist as a fistula (urachal fistula. between the
urinary bladder and the umbilicus.
• When the tract closes at the urinary bladder and remains open at the
umbilicus, it is called ‘urachal sinus’ (Ref Fig. 37.32).
• An opening in the lower anterior abdominal wall, close to the umbilicus;
discharging urine (urachal fistula), or seropurulent material (urachal sinus),
recurrently.
• Fever may be associated.
• Sinogram through the sinus opening, cystography, and CT with sinogram
or fistulogram are useful in diagnosis.
Treatment
• Small fistulae heal with appropriate antibiotics.
• Excision of sinus or fistula is curative.
Malignant fistula of umbilical region

• This fistula results due to extension of malignant tumours of intra-abdominal
organs, like stomach, colon or ovary.
• A fistula in the umbilicus discharging serosanguinous fluid.
• Sinogram and CT of abdomen are diagnostic.
Treatment
• Treatment of underlying malignancy is the treatment of choice.
Postoperative sinus (midline)

Postoperative sinus is formed due to:
• A persistent foreign body like a suture (e.g. non-absorbable suture material,
polypropylene mesh) or a foreign body (a calculus in the wound left behind
while extracting a gallbladder with stones during laparoscopic surgery).
• Infection of the wound.
• Single or multiple discharging sinus openings in one part of the wound (Figs.
11.17A and B) not responding to treatment.
FIGURE 11.17A Single sinus opening after incisional hernia repair with
mesh.
FIGURE 11.17B Multiple sinuses following inguinal hernia repair with
mesh.
• Sinogram may be useful.
• Ultrasonography (US) of the abdominal wall may show retained stones.
• Isolation of organism from the discharge may be useful.
Treatment
• Exploration of the sinus is needed for removal of retained foreign bodies.
• Appropriate antibiotics are necessary.
Postoperative gastrointestinal fistulae
• Postoperative enterocutaneous fistulae form about 75–80% of all
gastrointestinal fistulae, occurring commonly after operations (especially
emergency) for:
• Cancer
• inflammatory bowel disease
• lysis of adhesions
• pancreatitis
• Occur at the midline or in the flanks corresponding to the incision of the
previous surgery and the places of drains.
• They can be:
• Gastrocutaneous or duodenocutaneous fistulae
• Ileocutanous fistulae
• Appendicocutaneous fistulae (Fig. 11.18)
• Colocutaneous fistulae
• External biliary fistulae
• External pancreatic fistulae
FIGURE 11.18 Appendicocutaenous fistula (Post appendicectomy).
• Patients have a sluggish postoperative period, and present with severe
abdominal pain, tenderness and fever.
• The drain exit wound shows signs of inflammation with a copious discharge
of frank enteric contents in the wound, drain (Fig. 11.19) and dressing.
• Prolonged and large output from the fistulae causes severe nutritional
depletion.
• Diagnosis is established by the nature of discharge, its quantity and the details
of previous surgery.
FIGURE 11.19 Biliary leak (bile in the drain) Source: (Courtesy Dr A.
Chandrasekhar Rao).
• Barium contrast studies (Figs. 11.20A and B) are useful in bowel fistulae.
• Fistulography (Fig. 11.21) is useful in establishing the origin and localization
of the tract.
• Contrast enhanced CT (Fig. 11.22) is useful in localizing many fistulae.
• Radionuclide scans are useful especially in biliary fistulae.
FIGURE 11.20A Barium enema—gastrojejunocolic fistula (stomach filled
with contrast).

FIGURE 11.20B Barium enema—colovesical fistula.
FIGURE 11.21 Fistulogram—ileocutaneous fistula.
FIGURE 11.22 CT—rectovescial fistula from rectal malignancy.
Treatment
• Most fistulae heal spontaneously in a period of about 6–12 weeks, if there is
no distal obstruction or severe sepsis.
• Supportive treatment with hyperalimentation and control of sepsis is
necessary for the healing.
• Non healing fistulae require surgical management, and excision of fistulae
with or without intestinal resections.
Postoperative urinary fistulae

• Injury to the urinary tract, like the ureter during surgery may result in a fistula
in the operation wound.
• Urinary fistulae in the midline may occur after surgery of the urinary bladder
itself.
• Patient presents with leakage of urine through the operation wound in the
immediate postoperative period.
• There may be associated high grade fever.
• Determination of urea content of the fluid determines the presence of urine
in the discharge.
• Intravenous urography may be diagnostic to localize the level of leak.
Treatment
• Fistulae from the urinary bladder heal by urethral catheterization.
• Ureteric fistulae need stenting if possible. or procedures like primary
suturing, uretero-ureterostomy or uretro-neocystostomy are required for
delayed identification of fistulae.
11.11 Sinuses and fistulae of loins
Urinary fistulae of loins

Urinary fistulae in the loin result from:
• Perforating or penetrating wounds.
• Renal infections like pyonephrosis (e.g. tuberculosis).
• Percutaneous renal surgeries like nephroscopy.
• Operative injuries of ureter.
• Leakage of urine in the loin through a small sinus opening.
• Eliciting history carefully may give the diagnosis.
• Intravenous urogram, CT (Fig. 11.23) and fistulogram are diagnostic.
FIGURE 11.23 Urocutaneous fistula.
Treatment
• If there is no distal obstruction, renal fistulae heal.
• Tuberculous sinuses heal with anti-tuberculous treatment.
• Ureteric fistulae need stenting if possible. or procedures like primary suturing,
uretero-ureterostomy or uretro-neocystostomy are required for delayed
identification of fistulae.
External biliary fistula

Occurs due to:
• Spontaneous leakage of bile or bileoma to the exterior.
• Surgical drainage of bileoma.
• Distal obstruction of common bile duct (CBD) (stone or malignancy).
• High grade fever.
• Discharge of bile from wound or drain site.
• Severe excoriation of skin around fistulous opening (Fig. 11.24).
• Signs of electrolyte imbalance.
FIGURE 11.24 External biliary fistula with severe skin excoriation.
• US will demonstrate dilated biliary radicles.
• CT and MRI may demonstrate the pathology at the distal CBD.
• Fistulography or MR fistulography may demonstrate the pathology at the
distal CBD.
• Magnetic resonance cholangiopancreatography (MRCP) is useful.
• Percutaneous transhepatic cholangiography (PTC) is useful when the ductal
system is dilated.
• Isotope studies, apart from the origin of fistulous tract, gives the index of liver
function and biliary secretion.
Treatment
• Medical
• Correction of electrolyte and fluid imbalance
• Correction of malnutrition
• Control of skin excoriation
• Control of intra abdominal infection
• Surgical
• Relief of obstruction of CBD (ERCP sphincterotomy and basketing of
stone).
• Total disruption of CBD warrants fistulo-jejunostomy or choledocho-
jejunostomy.
• Malignancy requires pancreato-duodenectomy.
Colocutaneous fistulae of the loins

Colocutaneous fistulae result after:
• a surgical procedure, such as leaking anastomosis.
• incision and drainage of an abscess (pericolic abscess due to perforated
diverticulitis).
• due to erosion of the anterior abdominal wall by colonic malignancy.
• Patient presents with a fistulous opening discharging faeces.
• There may be associated fever, abdominal mass, obstruction and rectal
bleeding.
• Barium enema with thin water-soluble contrast may demonstrate the fistula.
• Fistulogram (Fig. 11.25) with or without CT abdomen is useful.
FIGURE 11.25 Fistulogram—fistulae leading to an abscess cavity after

colonic surgery.
Treatment
• Control of sepsis with antibiotics is necessary.
• Most fistulae heal spontaneously if constipation is taken care with adequate
laxatives.
• Surgical treatment consists of diversion procedures.
• Rarely colonic resections are required.
Tuberculous sinus (pott’s spine)

• Commonest form of skeletal tuberculosis, with infection starting at the
anterior margin of a vertebral body near the intervertebral disc.
• There is complete destruction of intervertebral disc with partial destruction of
two adjacent vertebrae, resulting in anterior collapse and kyphosis.
• Pus from the abscess formed from the diseased lower vertebra tracks down
behind the psoas sheath and presents in the iliac fossa.
• Rupture leads to a non healing sinus.
• Patient presents with a discharging sinus in the iliac fossa, with a history of
stiffness of back, backache, and sometimes kyphosis.
• X ray of spine reveals the narrowing of intervertebral space and local
vertebral osteoporosis.
• CT and MRI are diagnostic.
Treatment
• Spine needs special attention for its deformity and the neurological defects.
11.12 Sinuses and fistulae of groins
Postoperative sinus (mesh)

• The sinus results due to the presence of foreign body at the inguinal region
following mesh application for hernioplasty, or after Bassini repair with a
non-absorbable suture material.
• Patient presents with a discharging sinus with the previous history of surgery
for hernia in the groin (Ref Fig. 11.17B).
• Culture of discharge may show the incriminating organism.
Treatment
• Appropriate antibiotics and dressings should suffice.
• Rarely, the mesh or the non absorbable suture material used to fix the mesh
may have to be removed.
11.13 Sinuses and fistulae of right iliac fossa
Small intestinal fistulae of right iliac fossa

External small bowel fistulae are due to:
• Appendicular abscess (drained surgically).
• Diseases like Crohn’s disease, tuberculosis and ischemic bowel disease.
• Patients may present with single or multiple fistulous openings in the
abdominal wall, discharging varying amounts of intestinal fluid, usually
through the drain site.
• They tend to have a sluggish postoperative course with fever and
leucocytosis.
• Administration of non absorbable marker (charcoal or Congo red) or by a
fistulogram, can be diagnostic.
Treatment
• Nothing by mouth, nasogastric aspiration and intravenous antibiotics are
important.
• Correction of malnutrition and electrolytes is necessary for recovery.
• Drainage of localized collections of pus.
• Surgery is indicated when there is obstruction, active disease or interruption
of bowel continuity and spontaneous closure becomes unlikely, especially
when the closure has not occurred by 4–6 weeks.
• Surgery is the excision of fistulous tract with a part of the involved or
diseased bowel.
Actinomycosis of right iliac fossa

• Actinomycosis develops when a breach of the mucous membrane occurs due
to disease or trauma, which permits the entry of Actinomyces israelii into the
deeper layers.
• Suppuration occurs and the disease spreads into the retroperitoneal tissues and
eventually the abdominal wall becomes the seat of multiple sinuses.
• Liver may get affected through portal venous spread.
• Usually a mass forms in the right iliac fossa following appendicectomy, which
discharges through sinuses.
• The discharge is thin and watery to start with and later becomes thick and foul
smelling due to secondary infection.
• The discharge is granular and yellowish (sulfur granules) or black in colour.
• Pus demonstrates sulfur granules when allowed to trickle down the test tube.
• Bacteriological examination of the pus is mandatory.
Treatment
• Medical
• Prolonged intensive course of penicillin or tetracycline is curative.
• Clindamycin and erythromycin are good alternatives.
• Hyperbaric oxygen combined with antibiotic therapy is successful.
• Surgery may be needed to drain the lesion.
Colocutaneous fistulae of right iliac fossa

Colocutaneous fistulae are caused by a complication of:
• surgical procedures (ruptured appendicular stump).
• leaking anastomosis.
• incision and drainage of an abscess (appendicular abscess, abscess following
perforated cecal diverticulitis).
Occasionally, this can be due to erosion of the anterior abdominal wall of a
colonic malignancy.
• Patient presents with a fistulous opening discharging faeces.
• There may be associated fever, abdominal mass, obstruction and rectal
bleeding.
• Barium enema with thin water-soluble contrast may demonstrate the fistula.
• CT of abdomen with fistulogram is useful.
Treatment
• Control of sepsis with antibiotics is necessary.
• Most fistulae heal spontaneously if constipation is taken care with adequate
laxatives.
• Surgical treatment consists of diversion procedures. like ileostomy,
especially for large fistulae.
• Bowel resections are rarely required.
11.14 Sinuses and fistulae of male genitalia
Testicular sinus
Testicular sinus is caused by:
• Chronic inflammation of the epididymis and testis caused by tuberculosis.
• After orchidectomy (due to retained suture).
Patient may present with:
• a sinus in the posterior aspect of scrotum (Fig. 11.26A), following an abscess
of the epididymis (cold abscess). The sinus may have shown signs of
healing, but reopen several times. Beading of vas deferens and grossly
enlarged prostate and seminal vesicles point towards tubercular pathology.
• a sinus on the anterior aspect of scrotum especially on the operation scar is
seen after orchidectomy (Fig. 11.26B) or drainage of testicular abscess.
FIGURE 11.26 (A) Tuberculous testicular sinus. (B) Postoperative
testicular sinus.
• Biopsy of the sinus is diagnostic.
• Evidences of tuberculosis of urinary system may be contributory.
• X ray of chest may demonstrate pulmonary tuberculosis.
Treatment
• Antitubercular treatment is mandatory and curative.
11.15 Sinuses and fistulae of perineal region
Urethral fistula
• Most frequent cause of an acquired extenal urethal fistula is bursting or
incision of a periurethral abscess.
• There may be an associated stricture in the distal part of urethra.
• Patient presents with a single or multiple fistulous openings on the shaft or at
the penoscrotal junction, discharging urine.
• Ascending urethrography is diagnostic.
Treatment
• Repeated dilatations of urethra cure most urethral fistulae.
Anal fistulae
• Generally the end product of ano rectal sepsis.
• The varieties of anal fistulae are given in Figure 34.4.
• Recurrent fistulae are caused by infections like tuberculosis and Crohn’s
disease.
• The patient presents with intermittent anal discharge, purulent or blood
stained.
• Pain may be present during discharge free intervals.
• On examination it presents as a discharging opening in the perianal skin (Fig.
11.27). The internal opening may be felt as an indurated nodule or a
depression seen at proctoscopy.
FIGURE 11.27 Multiple fistulous openings in the perianal region.
• Special investigations are necessary in recurrent fistulae.
Treatment
• Anal fistulectomy is the treatment of choice.
• Recurrent fistulae caused by infections like tuberculosis and Crohn’s disease
need appropriate medical treatment.
11.16 Sinuses of the back

Pilonidal sinus
• This sinus occurs due to the entry of a broken hair into the skin (due to
negative pressure caused by the up and down movement of the buttocks) or
in the mouth of sudoriferous glands.
• Commonly seen in hairy individuals at the level of sacrum and coccyx, mostly
in the midline.
• A small opening (Ref Fig. 11.7) in the sacrococcygeal region discharging
serous material.
• A piece of hair may be found in the sinus opening.
• Infected sinus discharges pus (Fig. 11.27A).
• An abscess may form (Fig. 11.27B) preceding the episode and burst to form a
sinus.
• There may be fibrosis in longstanding cases as in vehicle drivers called ‘jeep
driver’s bottom’ similar to ‘barber’s hand’.
FIGURE 11.27A Pilonidal sinus discharging pus.
FIGURE 11.27B Pilonidal abscess.
• Sinogram may be useful to distinguish the sinus from anal fistula.
• MRI sinogram is contributory.
Treatment
• Excision of sinus.
Sinuses of bones and joints

Discussed in Chapter 39 - General Orthopedics.
11.17 Sinuses of feet
Maduramycosis (madura foot)

• Chronic granulomatous disease characterized by infection of subcutaneous
tissue and bone.
• Named mycetoma, because it forms a tumour like mass.
• Caused by Nocardia madurae, a normal soil inhabitant.
• Entry gained through a prick in the foot in people who walk barefoot (e.g.
agriculture workers).
• The first manifestation is a firm, pale and painless nodule.
• Vesicles develop on the nodules which burst to form sinuses, discharging
watery fluid containing yellow, red or black granules (Fig. 11.27C).
• There is no lymphatic involvement.

FIGURE 11.27C Maduramycosis of foot Source: (Courtesy Dr K.
Dakshinamoorthy).
DD: Osteomyelitis, tuberculosis, leishmaniasis and syphilis.
• Microscopy and culture of exudates can identify the organism.
• Skin biopsy is useful.
• Serology and DNA sequencing are newer modalities of identification.
• X rays of foot show extensive soft tissue or bone disruption. Periostitis and
sclerosis sometimes occur. Intra-articular bone fusion may lead to a melting
snow appearance.
• MRI scan provides better assessment of bone and soft tissue involvement.
Treatment
• Medical
• Broad-spectrum antibiotic to control the secondary infection followed by a
prolonged course of Dapsone is useful.
• Rifampicin is useful in resistant cases.
• Surgical
• Debridement and amputations are necessary for severe infections with
deformity.
Chronic osteomyelitis of metatarsals

• Nearly always follows acute osteomyelitis.
• Caused by staphylococcus, streptococci, pneumococci and typhoid organisms.
Complications: chronic bone abscess (Brodie’s abscess).
• Purulent discharge from a sinus over affected bone (continuous or
intermittent).
• Pain in the affected area.
• ‘Flare up’ – pain, fever and abscess is common.
• On examination, scars and sinuses are seen on the foot; the bone is palpably
thickened.
• X rays show thickening of bone, and irregular and patchy sclerosis.
Sequestrum appears as a dense loose fragment with irregular but sharply
demarcated edges, lying within a cavity in the bone (Fig. 11.28).
FIGURE 11.28 X ray—chronic osteomyelitis of proximal phalanx of great

toe.
Treatment
• Rest and antibiotics will help acute flare–ups.
• Drainage of abscess.
• Sequestrectomy for sequestrum.
Sinus due to retained foreign body

• Sinus may be caused by a persistent foreign body. like a piece of glass, staple,
or wood pricked while walking barefoot.
• Commonly seen in diabetics.
A discharging wound in the plantar aspect of the foot, with or without history of
trauma (generally the diabetics are not aware of the prick due to the
hypoesthesia), discharging foul smelling pus.
• Culture of the discharge to identify the incriminating organism.
• X rays to identify the foreign body.
• MRI is useful.
Treatment
• Appropriate antibiotics and removal of foreign body will help the sinus to
heal.
• Tight control of diabetes is necessary.
Eliciting history
• Duration of sinus or fistula: When did the patient first notice the sinus or
fistula?
Sinuses may be present since birth (e.g. preauricular sinus), may follow an
infection and persist for a longtime (e.g. chronic non healing sinus due to a
foreign body or infection like tuberculosis).
• Mode of onset: Was the sinus or fistula of a sudden event or gradual in
developing, and was there any trauma preceding the sinus or fistula?
Some sinuses develop following a low grade infection in the neck or axilla, like
tuberculosis and form a sinus (e.g. tuberculosis), and injuries in which
embedded foreign bodies like stone, glass may form a chronic non-healing
sinus or fistula (e.g. road traffic accidents).
• Situation at the time of onset:Was there a swelling at the time of
development of the sinus or fistula?
Some infections may form an abscess and the abscess may burst to form a sinus
on the skin (e.g. tuberculosis and actinomycosis).
• Association of pain:Was or is the sinus or fistula painful?
The acute sinuses or fistulae may exhibit pain due to infection, while chronic
sinuses and fistulae do not exhibit severe pain. However, when the external
opening gets closed, the pent up secretions inside the sinus or fistula may
cause severe pain. The pain reduces or disappears once the external opening
lets out the discharge (e.g. fistula in ano).
The nature of discharge is useful in arriving at the diagnosis (e.g. purulent
discharge of fistula in ano, necrotic bone chips in chronic osteomyelitis, bile
in biliary fistula, and faeces in faecal fistula).
• Variation in discharge:Does the discharge reduce from time to time?
The sinuses or fistulae discharge some material intermittently or continuously.
The discharge usually varies in its quantity (e.g. fistula in ano), but the
quantity remains constant or increases when it is communicating with an
abscess or a hollow viscus (e.g. enterocutaneous fistulae and pancreatic
fistula). The gastrointestinal fistulae close over a period of time if there is no
distal obstruction.
Presence of fever at the time of examination indicates active infection (e.g.
superadded bacterial infection in tuberculous sinus or fistulae, and
appendico-cutaneous fistula following acute perforated appendicitis).
• Treatment for the illness:Has any treatment been given to the illness?
It should be enquired whether any treatment was given for the illness. Non
healing sinuses and fistulae indicate inadequate or improper treatment, or
persistence of a focus as the cause for non healing (e.g. infection or foreign
body).
weight?
Loss of appetite and weight may indicate malignant pathology (e.g. secondary
metastatic lymph nodes presenting with sinuses, or tuberculosis of the lymph
nodes).
• Past history:Was there any similar illness in the past which required any
treatment?
treated, it will indicate the examiner to reconsider the diagnosis, like
tuberculosis.
• Family history:Has any other family member suffered from a similar
Diseases like tuberculosis occur in closely living families and a positive history
may be a good indicator for the present diagnosis.
Sinus / fistula
The steps for carrying out examination of the sinus or fistula are:
1. Inspection
2. Palpation
3. Probing of the fistula
Inspection
The following points are to be noted during the inspection of the sinuses or
fistulae:
1. Position–Observe the position of the sinus opening.
• Sinuses in the neck are generally tubercular (Ref Fig. 11.13).
• In the perineum may be due to Crohn’s disease (Ref Fig. 11.27), but usually
follows perianal abscess.
2. Number–The number of openings of the fistulae or sinuses is relevant.
• Single sinus may be due to retained foreign body (Ref Fig. 11.5).
• Multiple may be due to tuberculosis (Fig. 11.28A) or Crohn’s disease.
3. Discharge–Discharges from the sinus openings vary (Figs. 11.29 A, B and C)
according to the pathology.
• Pus in infective pathology.
• Serosanguinous in retained foreign body.
• Urine in urinary fistula.
• Faecal matter in faecal fistula.
• Bile in biliary fistula.
4. Opening of the sinus–Opening of the sinus may show changes according to
the pathology.
• Sprouting granulation tissue (Fig. 11.30A) suggests foreign bodies like
suture, sequestrum, etc.
• Undermined edges in tuberculosis (Ref Fig. 11.26A).
5. Surrounding skin–The skin surrounding the fistulous opening may show
some changes
• Healed scar (Fig. 11.30B) indicating a chronic or recurrent disease, like
tuberculosis.
• Excoriation of skin around the sinus opening (Ref Fig. 11.24).
• Pigmentation is characteristic of Crohn’s disease or actinomycosis.
FIGURE 11.28A Multiple tuberculous sinuses Source: (Courtesy Dr K Sridhar).

FIGURE 11.29A Bloody discharge from sinus.
FIGURE 11.29B Seropurulent discharge from sinus.
FIGURE 11.29C Purulent discharge from sinus.
FIGURE 11.30A Sprouting granulation around the sinus opening.
FIGURE 11.30B Recurrent gluteal sinus.
Palpation
The following points are to be noted by palpation:
• Tenderness of the external opening–The opening of the sinus should be held
between the thumb and index finger and gentle pressure should be exerted
[e.g. tenderness is elicited in inflammatory sinuses like osteomyelitis) (Fig.
11.31)]
• Palpation of the sinus tract–The sinus tract should be palpated with the
fingers of the examining hand as far as it is palpable [e.g. thickness indicates
chronic pathology like tuberculosis) (Fig. 11.32)].
• Base of the sinus–The base of the sinus should be assessed by examining the
structure on which it is lying [(e.g. lymph node swelling in tubercular
sinuses) (Fig. 11.33)]
• Mobility–The examiner should try to move the sinus track over the
underlying structures [(e.g. sinuses from the bone cannot be moved, those on
the soft tissues like muscles can be moved) (Figs. 11.34A, B and C)].
FIGURE 11.31 Eliciting tenderness of sinus opening.

FIGURE 11.32 Palpation of sinus tract.
FIGURE 11.33 Feeling the base of sinus.
FIGURE 11.34A Demonstrating the adherence of sinus on the
bone Source: (Courtesy Dr V. Thulasiraman).
FIGURE 11.34B Demonstrating the adherence of sinus to soft tissues.
FIGURE 11.34C Testing for mobility of sinus.
Note
During palpation, the discharge may appear at the sinus opening (Fig. 11.35),
and sometimes splash on the clothes of the examiner.
FIGURE 11.35 Discharge during palpation of sinus.
Probing the sinus or fistula

Introduction of a probe through the external opening is called probing. This is
done with a probe (Fig. 11.36) made of malleable material so that there is no
undue pressure exerted during probing. This may indicate the length of fistula or
sinus which will be useful for treatment planning. No force should be exerted
while probing as it will create a false passage and complicate or worsen the
fistula or sinus.
FIGURE 11.36 Probing a fistula.
Lymphatic system
Of drainage area
It is always mandatory to examine the area of lymphatic drainage of the sinus
which will give useful information (e.g. sinus in the neck may be a part of
multiple tubercular lymph node swellings).

The lymphatics and lymph nodes of the entire body should be examined in
detail, e.g. tuberculosis. Examination of the liver and spleen completes the
lympho reticular system which is useful in diagnosis.
General examination
General physical examination will give clues for diagnosis, like evidence of
pulmonary tuberculosis, and may direct the cause for a non healing sinus in the
neck or bone, or a tuberculous intestinal fistulae.
Rectal and vaginal examination

Rectal examination (digital examination and proctoscopy) should be performed
in perianal sinuses and fistulae, and vaginal examination for sinuses or fistulae
around the genitalia in females.
PA R T I I I
System and Region Based Diseases
OUTLINE
12. Lymphatic system
13. Arterial system
14. Venous system
15. Burns
16. Brain
17. Head injuries
18. Face and oral cavity
19. Injuries of face
20. Nose, nasal cavities and paranasal sinuses
21. Ears
22. Pharynx and larynx
23. Salivary glands
24. Thyroid
25. Neck
26. Thorax
27. Thoracic injuries
28. Breasts
29. Spine and spinal cord
30. Acute abdomen
31. Chronic abdominal illnesses
32. Abdominal injuries
33. Abdominal lumps
34. Rectum and anal canal
35. Herniae
36. Male genitalia
37. Urinary system
38. Female genital system
39. General orthopaedics
40. Shoulder and arm
41. Elbow and forearm
42. WRIST, hand and fingers
43. Hands (soft tissues)

44. Pelvis, hip and thigh
45. Knee and leg
46. Ankle, foot and toes
47. Feet (soft tissues)
48. Muscles, tendons and fasciae
49. Peripheral nerves

CHAPTER 12
Lymphatic system
S. Devaji Rao
CHAPTER OUTLINE
12.1. Anatomy of lymphatic system 124
• Lymphatics 124
• Lymph nodes 124
• Lymphatic drainage 125
12.2. Causes of lymphadenopathy 125
12.3. Diseases of lymphatic system 125
12.4. Diseases of lymphatics 129
• Primary lymphoedema 129
• Post operative lymphoedema 130
• Acute lymphangitis 130
• Lymphoedema of tropics 131
• Lymphangioma 132
• Lymphangiosarcoma 132
12.5. Diseases of lymph nodes 132
• Lymph cyst (Cystic hygroma) 132
• Acute lymphadenitis 133
• Filarial lymphadenitis 134
• Tuberculous lymphadenitis 134
• Lymphadenitis due to venereal infections 136
• Lymphadenitis due to AIDS 136
• Primary lymphomas 137
• Secondary metastatic lymphadenopathy 138
• Lymph nodes (cervical/axillary/inguinal) 139
• Other systems 143
12.1 Anatomy of lymphatic system

The lymphatic system is the pathway for the return of the tissue fluid to the
systemic circulation.
FIGURE 12.2 Lymph nodes of axilla.

The lymphatic system consists of two parts:
1. Lymphatics
2. Lymph nodes
Lymphatics
Lymphatic vessels start blindly from the tissues. They contain valves and direct
lymph only in one direction.
In the limbs, they form –
• superficial and deep lymphatic plexuses in the dermis of the skin, and
• subfascial plexus in the muscles.
The dermal lymphatics drain into subcutaneous lymph vessels, which follow
the course of superficial veins.
• The lymphatics drain into the lymph nodes of the corresponding area (e.g.
lower limb lymphatics into the inguinal lymph nodes).
• The lymph from the head and neck is collected by the right and left jugular
lymph trunks.
• On the left side, this trunk drains into the thoracic duct, while on the right
side, it ends in the right lymphatic duct.
• The lymph from the body and the limbs ultimately drain into the thoracic
duct, which in turn drains into the left subclavian vein.
Lymph nodes
Lymph nodes are the sites where phagocytosis of particles occurs, and foreign
matter is exposed to the immune system.
Lymph nodes of the head and neck

The lymph nodes of the head and neck are divided into superficial and deep
nodes (Fig. 12.1A).
FIGURE 12.1A Cervical lymph nodes.
Superficial cervical lymph nodes

• Submental group
• Submandibular group
• Buccal nodes
• Superficial parotid group
• Retroauricular group
• Occipital group
Deep cervical lymph nodes

Most of these nodes lie deep to the sternomastoid muscle (Table 12.1).
TABLE 12.1
Deep Cervical Lymph Nodes and their Locations
Group Location
Superior (Jugulodigastric nodes) Lie behind the posterior belly of digastric and anterior to the internal jugular vein
Inferior (Jugulo-omo-hyoid nodes) Lie behind the intermediate tendon of omohyoid on the internal jugular vein
Clinically, the lymph nodes of the neck are classified by the levels of
involvement (Fig. 12.1B). The classification is as follows:
FIGURE 12.1B Levels of cervical lymph nodes.
Level 1
• A–submental nodes
• B–submandibular nodes
Level 2
• Superior spinal accessory, superior jugular and Jugulodigastric nodes (base of
skull to hyoid bone).
Level 3
• Midjugular nodes between hyoid bone and cricoid cartilage.
Level 4
• Juguloomohyoid and inferior jugular nodes between cricoid cartilage and
clavicle (Virchow’s nodes).
Level 5
Nodes in posterior triangle –
• A–inferior spinal accessory (upper half).
• B–Transverse cervical (lower half).
Level 6
Paratracheal/Pretracheal nodes (Delphian nodes).
Level 7
Anterior mediastinal nodes (between common carotid arteries; and below top
of manubrium) and infraclavicular.
The other lymph nodes of the body and their locations are given in Table 12.2.
TABLE 12.2
Lymph Nodes of the Body and their Locations
Group Location
Axillary lymph nodes (Fig.
12.2)
Anterior or interpectoral Under the anterior axillary fold along the lateral thoracic vein
Central or medial Lie on the chest wall
Apical Apex of the axilla
Posterior or subscapular Under posterior axillary fold along the subscapular vessels
Lateral or humeral Close to the neck of humerus
Inguinal lymph nodes
Superficial
Horizontal Parallel and on inguinal ligament
Vertical Along the upper end of saphenous vein
Deep Deep to fascia lata along the femoral vein (lymph node in the femoral canal – Cloquet’s
node)
Thoracic lymph nodes
In relation to thoracic wall
Parasternal nodes Anterior ends of intercostal spaces along the internal thoracic artery
Intercostal nodes Posterior ends of intercostal spaces
Diaphragmatic nodes Thoracic surface of the diaphragm
In relation to thoracic contents
Brachicephalic nodes Superior mediastinum, in front of brachiocephalic veins
Posterior mediastinal nodes In relation to oesophagus and descending thoracic aorta
Tracheo-bronchial nodes Along the trachea and bronchi
Abdominal lymph nodes
Pancreatico splenic nodes Along the splenic artery
Left gastric nodes Along the left gastric artery
Right gastro-epiploic nodes Along the right gastro-epiploic artery
Pyloric nodes Lie in the angle between the first and second parts of duodenum
Pancreatico-duodenal nodes Inside the curve of duodenum
Mesenteric nodes Along the superior mesenteric artery and its branches
Appendicular and ileocolic Along the ileo-colic artery
nodes
Epicolic nodes On the wall of the colon
Paracolic nodes Along the inner border of the colon
Hepatic nodes Along the hepatic artery
Pre-aortic nodes
Celiac nodes Along the celiac axis (at its origin)
Superior mesenteric nodes Along the superior mesenteric artery (at its origin)
Inferior mesenteric nodes Along the inferior mesenteric artery (at its origin)
Lateral aortic nodes Sides of the abdominal aorta
External iliac nodes Along the external iliac artery
Internal iliac nodes Along the internal iliac artery
Common iliac nodes Along the common iliac artery
Lymphatic drainage
The lymphatic drainage of the body is given in tables 12.3, 12.4 and 12.5.
TABLE 12.3
Lymphatic Drainage of the Head and Neck
Region Superficial Lymphatic System Deep Lymphatic System
Scalp Occipital, retroauricular, Deep cervical nodes
superficial parotid nodes
Ears
Auricle and External meatus
Upper half of cranial surface Retroauricular nodes Deep cervical nodes
Upper half of lateral surface Superficial parotid nodes
Lower half of both surfaces Superficial cervical nodes
Parotid nodes
Auditory tube
Face
Forehead, lateral parts of eyelids, lateral part of Superficial and parotid lymph Deep cervical nodes
cheeks nodes
Central part of face, medial parts of eyelids and Buccal and submandibular
cheeks, nose, lateral parts of lips nodes
Median part of lower lip, chin and floor of the Submental nodes and then to
mouth submandibular nodes
Nose and nasal cavities
External nose and upper part of nasal cavities Submandibular nodes Deep cervical nodes
Paranasal sinuses
Posterior part of nasal cavities and nasopharynx Retropharyngeal nodes
Palate
Hard palate, soft palate and nasopharynx Retropharyngeal nodes Deep cervical nodes
Tonsil Jugulodigastric nodes
Floor of mouth
Floor of mouth, gums and teeth Submandibular nodes Deep cervical nodes
Anterior part of floor of mouth Submental nodes
Tongue
Tip Submental nodes Jugulodigastric and jugulo-
omohyoid lymph nodes
Lateral borders Submandibular nodes
Central and posterior parts
Pharynx, trachea and oesophagus
Pharynx Retropharyngeal nodes Deep cervical nodes
Cervical part of trachea Pretracheal and paratracheal
nodes
Cervical part of oesophagus Paratracheal nodes
Thyroid
Upper part Prelaryngeal and pretracheal Upper deep cervical nodes
nodes
Lower part Para tracheal nodes Lower deep cervical nodes
Larynx Deep cervical nodes
TABLE 12.4
Lymphatic Drainage of Limbs, Chest Wall and Abdominal Wall
Region Superficial Lymphatic Deep Lymphatic System

System
Upper limbs
Little finger, medial half of ring finger, medial side of palm, Supratrochlear nodes Axillary nodes
dorsum of hand, forearm
Lower limbs
Superficial tissues of lower limb, skin of scrotum and penis Vertical chain of Deep group of inguinal nodes
superficial group of and Iliac nodes
inguinal nodes
Deep tissues of lower limb, glans penis Deep group of inguinal External iliac nodes →
nodes common iliac nodes →
lateral aortic nodes
Lateral side of foot, lateral part of calf and knee joint Popliteal nodes → Deep
group of inguinal
nodes
Medial side of foot
Chest and Abdominal walls
Area extending from clavicle to umbilicus, breast Axillary nodes Supraclavicular nodes
Anterior abdominal wall below the umbilicus, genitalia, Horizontal chain of Deep group of inguinal nodes
perineum, buttock, mucous membrane of urethra, some superficial group of and Iliac nodes
parts of anus and vagina inguinal nodes
TABLE 12.5
Lymphatic Drainage of Abdomen and Thorax
Abdomen
Superficial lymphatic
Region Deep lymphatic system
system
Stomach, most of the duodenum, Left gastric, Celiac lymph nodes

liver, extrahepatic biliary pancreaticosplenic, right
apparatus, pancreas, spleen gastroepiploic, pyloric,
hepatic nodes
Part of duodenum, small bowel, Mesenteric, preileal, ileal Superior mesenteric nodes
appendix, large bowel upto the nodes
transverse colon
Descending colon, sigmoid and Epicolic, rectal Inferior mesenteric nodes
upper part of rectum
Pelvic organs and deeper tissues of Internal iliac nodes Common iliac nodes → Lateral aortic nodes
perineum
Posterior abdominal wall, kidneys Lateral aortic nodes
and ureters, testes and ovaries,
uterus and fallopian tubes
Thorax
Chest wall muscles and costal Intercostal nodes
pleura (posterior part)
Skin near the sternum, chest wall Parasternal nodes Broncho mediastinal trunk * (joins right lymphatic
muscles and costal pleura duct in the right and may join the thoracic duct
(anterior part), thymus in the left) → subclavian vein
Thymus, heart Brachiocephalic nodes
Heart, pericardium, lungs, thymus, Tracheobronchial nodes
trachea and bronchi
Thoracic surface of diaphragm Diaphragmatic nodes →
parasternal and posterior
mediastinal
Oesophagus Posterior mediastinal nodes
The thoracic duct carries lymph from both sides of the body below the
diaphragm, and from the left side above the diaphragm (Fig. 12.3). The thoracic
duct opens into the junction of the subclavian vein and the internal jugular vein
on the left side.
FIGURE 12.3 Lymphatic drainage of the body.
12.2 Causes of lymphadenopathy

Lymphadenopathy can be generalized or localized. Some of the important causes
are given in Table 12.6.
TABLE 12.6
Causes of Lymphadenopathy
Category Cause Pathology

Generalized lymphadenopathy Infective Viral Cytomegalovirus, HIV, Epstein Barr virus
Bacterial Brucellosis, Syphilis, Tuberculosis
Protozoal Toxoplasmosis
Neoplastic Primary Lymphomas
Others Sarcoidosis, Systemic lupus erythematosus
Localized lymphadenopathy Infective Viral Infections
Bacterial
Neoplastic Secondary metastatic, Lymphomas
Note
Small discrete lymph nodes can be felt in normal individuals.
12.3 Diseases of lymphatic system

The diseases of the lymphatic system can be classified based on its aetiology
(See Table 12.7).
TABLE 12.7
Aetiological Classification of Diseases of Lymphatic System
Aetiology Lymphatics Lymph Nodes

Congenital Primary lymphoedema Lymph cyst
Traumatic Post operative lymphoedema
Acute inflammatory Acute lymphangitis Acute viral lymphadenitis
Acute bacterial lymphadenitis
Acute filarial lymphadenitis
Chronic inflammatory Lymphoedema of the tropics Tuberculous lymphadenitis
Chronic filarial lymphadenitis
Syphilitic lymphadenitis
Lymphadenitis due to AIDS
Benign neoplastic Lymphangioma
Malignant neoplastic Lymphangiosarcoma Primary lymphomas
Secondary metastatic lymphadenopathy
12.4 Diseases of lymphatics

Primary lymphoedema
• Occurs due to congenital anomalies of the lymphatic system.
• Has female preponderance.
• The types of primary lymphoedema are:
• Aplasia–Total absence of subcutaneous lymph channels.
• Hypoplasia–Progressive obliteration of lymphatics.
• Hyperplasia–Enlargement and dilatation of lymphatics.
• Varies according to the aetiology –
• Aplasia–Generally swollen body; present since birth (e.g. lymphoedema
congenitalia).
• Hypoplasia–Progressive swelling of the limbs presenting in the teens (e.g.
lymphoedema praecox).
• Hyperplasia–Enlarged, dilated and tortuous lymphatics, resembling
varicose veins (they discharge chyle through the skin).
Duplex studies help to differentiate from the vascular cause.
Treatment
Limb elevations and compression bandages are useful in managing the oedema
of the limbs.
Note
Hypoproteinemia, cardiac failure, renal failure and hepatic failure are
common causes of bilateral pedal oedema (Fig. 12.4).
FIGURE 12.4 Generalised lymphoedema of hypoproteinemia. (A) lower
limbs (B) Upper limbs.
Post operative lymphoedema

They are common after radical surgery of the lymph nodes secondary to
malignancies.
• Upper limb oedema after radical mastectomy (Fig. 12.5).
• Scrotal oedema (Fig. 12.6) after bilateral inguinal block dissection.
FIGURE 12.5 Oedema of upper limb after radical mastectomy (axillary
clearance).
FIGURE 12.6 Scrotal oedema after bilateral inguinal block dissection.
• Patient gives history of previous surgery.
• The region draining into the lymphatic (operated) area shows progressive
swelling, pitting to start with and later non-pitting. (e.g. upper limb swelling
after mastectomy; scrotal swelling after inguinal block dissection).
Ultra sonography (US) and Computed tomography (CT) of the operated area
may be needed to look for recurrence.
Treatment
Limb elevations and compression bandages are useful in managing the oedema
of the limbs.
Acute lymphangitis
In the tropics, the main causes are:
• filariasis and
• tuberculosis.
• Swelling of the limbs and genitalia associated with fever and rigor.
• On examination, the limbs are swollen and erythematous with weeping
eruptions (Fig. 12.7A).
• Secondary infections can lead to localized patchy gangrene (Fig. 12.7B).

FIGURE 12.7 (A) Acute lymphangitis. (B) Gangrenous patches in acute
lymphangitis.
Peripheral smear for microfilaria.
Treatment
Antifilarial treatment and compression bandages.
Lymphoedema of the tropics

In the tropics, the main causes of chronic lymphangitis and lymphoedema are:
• filariasis and
• tuberculosis.
• Swelling of the lower limbs, sometimes to massive proportions, a condition
called ‘elephantiasis’ (Fig. 12.8).
• The skin becomes hyperkeratotic, nodular (Fig. 12.9A) and fissured giving a
pachydermous appearance (Fig. 12.9B).
• The scrotum may be enormously enlarged (Fig. 12.10), so also the labia in the
female.
• It can affect the upper limbs and breasts.
FIGURE 12.8 Elephantiasis of left lower limb.

FIGURE 12.9 Elephantiasis—(A) nodular, (B) pachydermous.
FIGURE 12.10 Filarial scrotum.
Peripheral smear for microfilaria.
Treatment
• Medical
• Antifilarial treatment.
• Compression stockings are useful if the oedema is pitting.
• Surgical
• Various plastic surgical procedures are available for limb swellings and
genitalia
Lymphangioma
• Benign hamartomatous tumours of the lymphatic vessels.
• More common in the neck.
They are of three types:
1. Capillary lymphangioma
2. Cavernous lymphangioma
3. Cystic lymphangioma (Cystic hygroma)
• Capillary lymphangioma
• Superficial, shiny, wart like lesion of skin (Fig. 12.11).
• Common on the face, mucosa of lips and tongue.
• Serous fluid oozes out of the lesion.
• Cavernous lymphangioma
• Soft and sessile lobulated swelling.
• Common on the neck, lip, tongue and axilla.
• In the tongue, it presents as macroglossia (See Fig. 18.33C).
• Cystic lymphangioma
• Big cystic swelling.
• More common in children.
• Common on the neck and axilla.
• Cervical lesions may extend into the mediastinum or oral cavity.
• It is brilliantly transilluminant.
FIGURE 12.11 Capillary lymphangioma of abdominal wall Source: (Courtesy
Dr Ramji Gupta).
• CT and magnetic resonance imaging (MRI) may be required for large
lesions.
Treatment
• Small lymphangiomas resolve spontaneously.
• Large lesions require surgical excision.
Lymphangiosarcoma
• Malignant transformation of longstanding lymphoedema.
• Extremely rare.
• This condition progresses to be fatal.
• Lymphoedema of the limb, with a localised firm nodule or thickening.
Biopsy of the suspicious area is conclusive.
Treatment
Early extensive amputation of limb, if feasible.
12.5 Diseases of lymph nodes
Lymph cyst (cystic hygroma)

These can occur anywhere in the body, especially where the lymphatic tissue is
in abundance.
• Congenital lymph cysts are called ‘cystic hygromas’.
• Common in the neck and axilla.
• Large cystic hygromas of the neck can cause difficulties during delivery.
• A soft cystic swelling in the neck or axilla (Fig. 12.12). Brilliantly
transilluminant.
FIGURE 12.12 Cystic hygroma of neck.
Diagnostic aspiration may be done to confirm the presence of lymph.
Treatment
• Therapeutic aspiration is sufficient for small lymph cysts, but recurrences are
not uncommon.
• Surgical excision is needed for cosmetic reasons for larger lesions.
Acute lymphadenitis
Caused by –
• viruses, commonly by rhinovirus.
• bacteria, secondary to oral cavity infections, may result into abscesses.
• Acute painful enlargement of lymph nodes mostly of the anterior cervical
group (Figs. 12.13 and 12.14)
• Clinical examination reveals a tender soft to firm swelling with signs of
inflammation on the skin (Fig. 12.15).
• Examination of the drainage area is essential to assess the primary cause (e.g.
acute pharyngitis or dental infections causing secondary enlargements of
neck glands).
FIGURE 12.13 Acute viral lymphadenitis of neck.
FIGURE 12.14 Acute bacterial lymphadenitis of neck.
FIGURE 12.15 Inguinal lymphadenitis (Right).
• No specific investigation is required in short lived cases.
• Biopsy may be needed to differentiate persistent swellings from other causes.
• Diagnostic aspiration is useful in abscesses.
Treatment
• No treatment is required for viral lymphadenitis as they resolve
spontaneously.
• Broad spectrum antibiotics are required to cure bacterial infections.
• Incision and drainage is warranted for abscesses.
Filarial lymphadenitis
• Acute and recurrent or chronic attacks are common.
• Caused by thread like parasitic filarial worms, Wuchereria bancrofti or Brugia
malayi.
• Worms lodge in the lymphatic system, and live for 4–6 years, producing
millions of immature microfilariae that circulate in the blood.
• Transmitted by mosquitoes, Culex fatigans (develop and reach the infective
stage in 7–21 days and migrate to biting mouth parts).
• Causes severe inflammation of the lymphatics and they settle down in the
lymph nodes, commonly in the inguinal group.
• High grade fever with rigor.
• Swelling of the lower limbs and inguinal lymphadenopathy.
• Recurring attacks of varying grades of fever, with or without rigor.
• Swelling of the lower limbs and genitalia, with non pitting oedema and
inguinal lymphadenopathy.
• Presentation with swelling of scrotum (hydrocoele) (Fig. 12.16) is common.
• Scrotum and penis may appear sunken under the hard thickened skin. In
endemic areas, the clinical picture is atypical. Penis takes the form
‘Ramhorn penis’ (Fig. 12.17).
FIGURE 12.16 Filarial hydrocoele.
FIGURE 12.17 Filarial scrotum and Ramhorn penis Source: (Courtesy Dr K.
Sridhar).
• Midnight peripheral blood smear, or particularly during the time of fever,
may demonstrate microfilariae.
• Card test to detect circulating parasite antigens with finger prick blood,
anytime of the day.
• US may show the presence of adult parasite in the inguinal lymph nodes and
in the lymphatics of cord structures.
Treatment
• Medical
• Antifilarial drugs, like Diethyl carbamazine citrate (DEC), for longer
periods of time are useful to control the attacks of fever.
• Antibiotics are useful in controlling secondary infection in acute
lymphadenitis.
• Compression bandages are useful in the management of pitting oedema.
• Surgical
• Surgery is required for conditions like hydrocele.
• Scrotoplasty is performed for filarial scrotums which are grossly swollen.
• Procedures to divert lymph into the circulation (e.g. nodo-venous shunt)
are performed for chronic non-pitting lymphoedema of the lower limbs.
• Very large and recurrent scrotal enlargement will need complete extirpation
of the scrotum with implantation of testes in the thighs, which may make
the patient sterile.
Tuberculous lymphadenitis
• Infection caused by M. tuberculosis, mostly by the air-borne route.
• The infection usually enters the body through the respiratory tract and settles
in the lungs.
• From the lungs, the infection spreads to other organs of the body, and also to
the lymph nodes.
• Neck nodes are infected through the tonsils.
• The lymph node enlargement consists of four stages (Figs. 12.18A and B):
• Stage I: Discrete solid lymph node swellings.
• Stage II: The nodes get matted due to periadenitis.
• Stage III: The central part of the nodes get caseated and become soft (cold
abscess), which may erode the deep cervical fascia, eventually releasing
the pus beneath the superficial fascia forming a dumb bell arrangement
(Collar stud abscess).
• Stage IV: Sometimes it may burst through the skin to form a sinus or an
ulcer, which may refuse to heal without anti-tubercular treatment.
FIGURE 12.18A Stages of tuberculous lymphadenopathy with ulcer
formation.
FIGURE 12.18B Stages of tuberculous lymphadenopathy with sinus
formation.
• Chronic cough with expectoration.
• Enlarged lymph nodes, commonly in the neck (Fig. 12.19A), mediastinum,
axillae, mesentery and inguinal regions.
• May present as chronic abscess (Fig. 12.19B).
• Discharging sinus appears when the abscess bursts (Fig. 12.19C).
FIGURE 12.19A Multiple lymph node swellings in the neck.
FIGURE 12.19B Cold abscess.
FIGURE 12.19C Tuberculous sinus.
• Lymphocytosis, raised erythrocyte sedimentation rate (ESR), and positive
Mantoux tests are suggestive of diagnosis.
• MRI of neck is occasionally required for lymph node evaluations.
• X ray and CT scan of the chest is useful in diagnosing associated pulmonary
tuberculosis, and the diagnosis becomes highly suggestive.
• Diagnostic aspiration is useful [the pus appears pale yellow and thin in
consistency (different from the non-tubercular pus) (Fig. 12.20)].
• Smear and culture of aspirated pus may grow Acid Fast Bacilli (AFB).
• Polymerase chain reaction test (PCR for Mycobacterium tuberculosis) is
useful in diagnosing tuberculosis.
• Biopsy of the node is conclusive.
FIGURE 12.20 Aspiration of cold abscess.
Treatment
Anti-tubercular treatment is curative.
Lymphadenitis due to venereal infections

• The infections are sexually transmitted.
• The infections spread through the lymphatics to the inguinal lymph nodes.
• Enlarged inguinal lymph nodes, with or without an ulcer on the genitalia
[e.g.Chancre and chancroid (Fig. 12.21)], or white discharge per urethra
(gonococcal urethritis) or vaginitis in females.
• The enlarged lymph nodes (Fig. 12.21) have different clinical features in
different infections –
• Chancre–small, discrete, painless and rubbery feel.
• Chancroid–firm and ulcerate.
• Lymphogranuloma venereum–firm (Groove’s sign of Greenblatt); may
suppurate (multiloculated).
• Granuloma inguinale–firm and discrete.
FIGURE 12.21 Inguinal lymphadenopathy of lymphogranuloma venereum.
• Wasserman test and Kahn test are diagnostic.
• Demonstration of Treponema pallidum is diagnostic.
• Treponema pallidum Hemaglutination Assay (TPHA) and FTA-Abs are
confirmatory for syphilis.
Treatment
Antibiotics, especially of the penicillin group (cephalosporin and quinolones) are
useful in curative treatment.
Lymphadenitis due to AIDS

• Acquired immunodeficiency syndrome (AIDS) caused by human
immunodeficiency virus (HIV) – 1.
• In most cases the infections are sexually transmitted.
• Blood borne infections through injections and vertical transmission through
pregnancy are common.
• The primary cell infected is the CD4 lymphocyte.
• HIV syndrome occurs 3–6 weeks after infection.
• Fever, sweats, sore throat and oral ulcers (candidiasis).
• Skin lesions (purple lesions of Kaposi’s sarcoma).
• Enlarged lymph nodes.
• Weight loss.
• Muscle and joint pains.
• Diarrhoea.
• Symptoms of any opportunistic illness (pneumocystis carinii and tubercular
infection of lungs, CMV infection, cryptococcal meningitis or toxoplasmosis
of brain).
• Dementia (HIV encephalopathy) and depression.
HIV antibody tests (antibodies appear 2 weeks to 6 months after original
infection).
• Enzyme linked immunosorbent assay (ELISA)–If positive, repeated again to
confirm.
• Western blot–Done to confirm positive ELISA tests.
• PCR–Finds genetic material DNA or RNA of HIV; may be positive even if
other tests are negative for the virus.
• Indirect fluorescent antibody (IFA)–Done to confirm positive ELISA tests
(more expensive).
Note
Testing is done at 6 weeks, 3 months and 6 months after exposure to detect
infection.
Treatment
The goal of treatment is to keep CD4 count above 200/ml, and to prevent or
control opportunistic infections.
• When viral loads are high and significant, anti retroviral drugs (nucleoside
analogues, e.g. Zidovudine, Zalcitabine, Lamivudine and Stvudine, and
protease inhibitors, e.g. Indinavir, Ritonavir, Nefinavir and Saquinavir) are
used.
• Triple therapy (two nucleoside analogues with one protease inhibitor) is used
to reduce the viral load.
Primary lymphatic malignancies

• The primary lymphatic malignancies occur at different age groups and the
exact cause is not known.
• They are classified as:
• Hodgkin’s lymphoma and
Non-Hodgkin’s lymphoma, The differentiating factor being the presence of
Reed Sternberg cell, specific to Hodgkin’s lymphoma (Fig. 12.22
).
• The former affects the young and the latter the elderly.
FIGURE 12.22 Histology—Reed Sternberg cell.
Hodgkin’s lymphoma
The cancerous cells are of B-cell lymphocyte origin
• In 40–50%, Epstein-Barr virus is the cause.
• More prevalent in those who have contracted infectious mononucleosis.
• Suggested links with measles virus.
• Interleukin-12, a natural cytokine may be overproduced in Hodgkin’s
lymphoma.
• More common in two age groups (early adulthood – 15 to 40, late adulthood –
after 55).
• Rare under the age of 5.
Non-hodgkin’s lymphoma
• Encompass over 29 types of lymphoma; distinction based on type of cancer
cells.
• 95% occur in the elderly over the age of 65.
• Clinically classified as aggressive (fast growing) and indolent (slow growing).
• Pathologically classified as T-cell (15%), B-cell (85%), Large cell and
Follicular cell.
Ann arbor staging of lymphoma
• Stage I–involving one lymph node area (I), or one area of one organ outside
the lymph system (I E).
• Stage II–two or more lymph node areas on the same side of the diaphragm
(II), or one lymph node area and one organ on the same side of diaphragm
(IIE).
• Stage III–lymph node areas on either side of diaphragm (III), with or without
spread to nearby organs (IIIE) or spleen (IIIS), or both (IIIS or E).
• Stage IV–spread to more than one spot to an organ or organs outside the
lymph system, or to only one organ with lymph nodes far away from the
organ involved.
Note
The absence or presence of fever, night sweats, or unexplained loss of 10% or
more of body weight in the preceding 6 months are to be denoted in all cases
by suffix letters A and B, respectively.
• Fever is usually intermittent (Pel-Ebstein fever), with generalized
lymphadenopathy (Fig. 12.23).
• Appetite loss and weight loss may be present.
• Mediastinal, mesenteric and intra-abdominal lymph nodal enlargements are
rarely present clinically.
• Splenomegaly may be present, either due to the disease process or secondary
to liver involvement.
FIGURE 12.23 Hodgkin’s lymphoma.
• Leukocyte count and ESR may be raised.
• X ray chest may show involvement of hilar lymph nodes.
• US, CT and MRI scans are useful tools for diagnosing the lymph nodal
enlargement in the thorax and abdomen (Fig. 12.24).
• Fine needle aspiration cytology (FNAC) and biopsy are confirmatory.
• PCR and immunohistochemistry are diagnostic for specific tissue diagnosis.
• A positron emission tomography (PET) scan will show hot spots of cellular
activity.
• Gallium scan is useful in localizing lesions.
• Bone marrow aspiration will indicate infiltration.
• Lymphangiogram to assess the lymphatics of pelvis.
FIGURE 12.24 CT—right axillary and retroperitoneal lymph node swellings
with splenomegaly in a patient of non-Hodgkin’s lymphoma.
Treatment
• Many of the lymphomas respond to chemotherapy.
• Hodgkin’s lymphoma (ABVD – Adriamycin, Bleomycin, Vinblastine and
Dacarbazine).
• Non-Hodgkin’s lymphoma (CHOP – Cyclophosphamide,
Hydroxydoxorubicin, Oncovin and Prednisolone).
• Bone marrow transplant (BMT) or peripheral blood stem cell transplant
(PBSCT), for Hodgkin’s lymphoma, aggressive Non-Hodgkin’s lymphoma
and relapse after standard chemotherapy.
• Immunotherapy (monoclonal antibody and vaccine therapy)
• Radiation
• Hodgkin’s Lymphoma is radiosensitive.
• Surgery is usually not required in most cases.
Secondary metastatic lymphadenopathy

Malignancies spread through the lymphatics to the corresponding lymph nodes.
• The patient presents with enlarged lymph nodes.
• Nodes are generally firm to hard in consistency, sometimes fungating through
the skin (Figs. 12.25A and B).
• There are associated symptoms relating to the malignancy of the organ in the
drainage area, e.g. cervical lymph node swellings of nasopharyngeal
carcinoma (Fig. 12.25C) or laryngeal cancer and inguinal nodes of
carcinoma penis.
• Sometimes the primary is occult.
FIGURE 12.25A Fungating secondary lymph nodes neck ( Source: Courtesy
Dr Jacinth Cornelius).
FIGURE 12.25B Fungating secondary nodes of carcinoma
penis Source: (Courtesy Dr R. Rajaraman).
FIGURE 12.25C Bilateral lymph node swellings secondary to
nasopharyngeal carcinoma.
• FNAC and Biopsy are confirmatory.
• Examination of the drainage area is essential to look for the primary
malignancy associated with histopathological confirmation.
• Tumour marker study or immunohistochemistry may be needed to confirm
the exact histopathological diagnosis.
Treatment
• Radiotherapy, chemotherapy and or surgery of the primary malignancy with
the secondaries as en bloc dissection, depending upon its sensitivity.
• Radiotherapy or chemotherapy may be administered pre or post operatively,
as per the tissue diagnosis and stage of disease.
Eliciting history
Eliciting the history in a patient suggestive of having lymph nodal swelling or
swellings is very important. Apart from the general information, like the age and
occupation, the history should include the following:
Swelling
• Site of the swelling: Where did the swelling originate?
The site of origin is important (e.g. tuberculosis is common in the neck and
lymphogranuloma inguinale is common in the inguinal region).
• Duration of swelling: Since how long has the swelling been present?
Short duration is common in acute inflammatory lesions and long duration is
common in chronic conditions like tuberculosis.
• Progress of the swelling: Has the swelling been increasing in size, and if so
is it rapid?
Rapid progress indicates acute inflammatory lesions and slow progress
indicates chronic conditions like tuberculosis.
Other related questions

• Association of pain: Is there pain associated with the swelling?
Pain is common in acute inflammatory lesions, and absence of pain may
indicate chronic conditions, like tuberculosis, syphilis or neoplastic diseases.
• Association of fever: Is there fever since the appearance of swelling? If so,
describe?
Fever is seen in a variety of lymphatic diseases, acute high grade fever in viral
and acute bacterial diseases, evening rise of temperature in tuberculosis,
intermittent fever (Pel-Ebstein fever) in lymphomas, and high grade fever with
rigor in filariasis.
malignancies.
• Treatment for the illness: Has any treatment (medical or surgical) already
been given to the illness?
The information on any treatment received in the past for this illness will give
a clearer picture of diagnosis (completely responded swellings which have
reappeared may indicate a recurrence of tuberculosis or malignancy).
• Past history: Was there any similar illness in the past which required
treatment?
If the patient had suffered a similar illness in the past many years ago, which
was successfully treated, will indicate the examiner to reconsider the diagnosis,
like recurrence of tuberculosis.
Diseases like swellings due to tuberculosis occur in families and a positive
match the situation, like extramarital or premarital contact, or if the lump is
suspected to be of syphilitic aetiology. History relating to trauma should also
be elicited.
The symptoms of lymphatic system are correlated with history in Table 12.8
TABLE 12.8
Correlation of Symptoms of Lymphatic System with History
Lesion Symptom
Duration Pain Fever Loss of Loss of Past history
appetite weight
Congenital Lymph cyst Since Nil Nil Nil Nil Nil
birth
Acute Acute viral Short May be Present Nil Nil Nil
Inflammatory lymphadenitis present
Acute Bacterial Short May be Present Nil Nil Nil
lymphadenitis present
Acute filarial Short May be Present with Nil Nil Nil
lymphadenitis present rigor
Chronic Tubercular Long May be May be May be May be May be
inflammatory lymphadenitis present present* present present present
Lymphadenitis of Long May be Usually Absent Absent Sexual
venereal present absent exposure
infections
Lymphadenitis due to Long May be May be May be May be Sexual
AIDS present present present present exposure,
injections
or drug
abuse
Primary Lymphoma Long May be May be May be May be May be
malignancy present present present present present
**
Secondary Metastatic Variable May be May be May be May be May be
malignancy lymphadenopathy present present present present present
*Evening rise of temperature

** Intermittent fever (Pel- Ebstein fever)
Lymph nodes
This consists of two parts:
1. Inspection
2. Palpation
Inspection
The examiner should inspect the swelling without touching it and should record
visibly the following and record the observations (to be examined in line with
examination of swellings in general – Chapter 9).
• The node’s location
• Size
• Number
• Skin over the swelling–it may be involved and fix itself to the node; or when
inflamed it will show signs of inflammation.
• Pressure on neighbouring structures–the blood vessels may be distended
due to the pressure on them, like in lymph node secondaries of the thyroid.
Likewise, they may exert pressure on the oesophagus to produce dysphagia
or the trachea to produce dyspnoea.
• Pulsations–Pulsations may be seen on lymph node swellings sitting on the
artery, like the carotid.
Palpation
The palpation of various groups of lymph nodes is performed in different ways
by the examiner. By this method of examination, the examiner confirms the
findings of inspection.
• The size and the number are exactly determined.
• The consistency of the swellings is determined by palpation. It can be –
• Soft (e.g. cyst or abscess).
• Firm (e.g. syphilitic lymph node).
• Hard (e.g. metastastic lymph node).
• Soft swellings of lymphatic system
Soft swellings may show fluctuation indicating it is cystic (e.g. lymph cyst or
abscess), but show transillumination only if they contain clear fluid (e.g. lymph
cyst).
Transillumination is a characteristic finding in soft swellings containing clear
fluid, like in a lymph cyst or a cystic hygroma.
The various consistencies of lymph node swellings and their properties are
correlated in Table 12.9.
• Firm swellings–It is essential to determine whether the swellings are discrete
and matted to each other. Matting is a hallmark of tuberculosis.
• Skin involvement: By pinching the skin over the swelling, the involvement
of the skin is determined. The swellings are moved with the index and
thumb of the examiner to determine its fixity to the surrounding structures
and deeper structures. The fixity is commonly seen in malignancies
involving the lymph nodes.
• Temperature and tenderness should be elicited (e.g. warmth and tenderness
are present in acute inflammations like acute lymphadenitis).
• Pulsations–Transmitted pulsations may be seen if the lymph nodes are
sitting on a pulsating blood vessel (e.g. nodes on the carotid artery).
TABLE 12.9
Properties of Lymph Node Swellings
Consistency Fluctuation Transillumination Example of Pathology

Cystic Present Present Cystic hygroma
Soft Present Absent Abscesses
Elastic* Absent Absent Hodgkin’s disease
Firm* Absent Absent Syphilis
Hard* Absent Absent Neoplastic diseases
*Fluctuation and Transillumination should not be attempted in swellings which are not soft and
cystic.
Cervical lymph nodes

• The palpation of neck glands should be performed both from the front and
behind the patient. When the swellings are not visible clearly, they are best
palpated from the back. Since the patient has a natural tendency to lift the
head, which will obscure the swellings, it is better to keep the patient’s neck
slightly flexed and tilted to the side of examination, which will relax the
muscles of the neck and make the examination easy (Fig. 12.26A). The right
hand is used for the right side and vice versa. The palpation is done is an
organized way, so no area is left unexamined.
• It can be supplemented by examining the neck from the front (Fig. 12.26B).
• Supraclavicular lymph nodes are best palpated from behind (Fig. 12.26C).
FIGURE 12.26A Palpation of neck for lymph nodes swellings from behind.
FIGURE 12.26B Palpation of neck from the front.
FIGURE 12.26C Palpation of left supraclavicular lymph nodes.
Axillary lymph nodes
• Examination of right axilla: If the right axilla of the patient is to be

examined, the examiner should stand in front of the patient. The patient is
asked to rest his or her right hand on the left forearm of the examiner (Figs.
12.27 A–E ), which is the examining hand for the first three steps. The
examiner should support the right shoulder of the patient with the right hand,
so that the shoulder muscles relax and allow the examiner to examine the
axilla. The examiner should follow a specific pattern to examine all the
groups so that nothing is left unexamined. The examiner should examine
(Step I) the anterior part of the axilla behind the pectoral muscles for anterior
pectoral group of nodes; (Step II) then the medial group (on the chest wall)
and then (Step III) push the fingers into the apex of the axilla for apical
group of nodes. For examining the lateral group of nodes on the right side
the examiner should go behind the patient and put the left hand at the neck
and shaft of the right humerus (Step IV). And lastly, to examine posterior
group of the same axilla, the examiner should put the right hand in front of
the latissimus dorsi muscle (Step V). The last two steps are done from behind
the patient.
• Examination of left axilla: The same procedure is followed for the other
axilla. From the front, the left axilla is examined with the right hand for the
first three steps, and from behind with the right hand for the fourth step and
the left hand for the last step.
FIGURE 12.27A Palpation of anterior group of axillay nodes.
FIGURE 12.27B Palpation of medial group of axillary lymph nodes.
FIGURE 12.27C Palpation of apical group of axillary lymph nodes.
FIGURE 12.27D Palpation of lateral group of axillary lymph nodes.
FIGURE 12.27E Palpation of posterior group of axillary lymph nodes.
Note
An experienced examiner can complete the examination without changing his
or her hand.
Inguinal lymph nodes

The examiner stands to the right of the patient and examines both the inguinal
regions with the right hand (Fig. 12.28). Slight flexion of the hip will relax the
muscles and the fascia, which will ease the examination process. The
examination should be in the same lines of the examination of swellings in
general (see Chapter 9).
FIGURE 12.28 Palpation of inguinal lymph nodes.
Auscultation
Though it is not a useful method in lymph node swellings per se, it may be
useful in soft swellings to differentiate from aneurysms by the absence of bruit.
Other systems
The examination of the lymphatic system is never complete without the
examination of the following:
• Examination of the corresponding drainage area for primary pathology (e.g.
oral cavity and ear, nose, throat (ENT) cancers present with cervical node
swellings; breast cancers present with axillary node swellings).
• Examination of the other groups of lymph nodes to evaluate general
lymphatic disorders, like tuberculosis and primary lymphatic malignancies.
• Examination of the abdomen, especially for enlargement of liver and spleen
as they form part of lympho-reticular system, and stomach cancers present
with supraclavicular lymphadenopathy.
• Examination of external genitalia (e.g. penile cancers present with inguinal
node swellings).
• Examination of the lungs for primary focus of tuberculosis or disseminated
malignancies.
The examination findings are correlated with the pathologies of the lymphatic
system in Table 12.10.
TABLE 12.10
Correlation of Physical Examination Findings with Lymph Node
Swellings
Lesion Examination Findings
Inspection Palpation Significant feature

Congenital Lymph cyst Globular Soft Brilliantly transilluminant
(Cystic
hygroma)
Acute Viral Solitary or multiple Soft to firm Associated fever
Inflammatory lymphadenitis swellings
Bacterial Solitary or multiple Soft to firm Signs of pathology in the
lymphadenitis swellings drainage area
Filarial Solitary or multiple Soft to firm Associated lymphoedema
lymphadenitis swellings
Chronic Tuberculous Multiple swellings in Firm and matted (soft Associated pulmonary
inflammatory lymphadenitis multiple groups if abscess formed) pathology
Filarial Solitary or multiple Soft to firm Associated non pitting
lymphadenitis swellings lymphoedema
Syphilitic Multiple swellings in Soft to firm History of pre or extramarital
lymphadenitis multiple groups sex
Lymphadenitits Multiple swellings in Soft to firm History of pre or extramarital
due to AIDS multiple groups sex or blood transfusions
Neoplastic Lymphomas Multiple swellings in Soft to firm Hepato-splenomegaly may be
one or more present
groups
Secondary Multiple swellings in Firm to hard Associated malignancy in the
malignancies one group drainage area
In summary,
1. Ascertain that the swelling is a lymph node.
2. Examine the other lymph nodes of the same group and record.
3. Examine the other anatomically described lymph node groups and record.
4. Always look for the enlargement of liver and spleen.
5. Also examine the areas where lymphatic tissue is concentrated, e.g. right iliac
fossa.
CHAPTER 13
Arterial system
N. Sekar
CHAPTER OUTLINE
13.1. Surgical anatomy of arterial system 144
• Upper limb 144
• Lower limb 144
13.2. Diseases of arterial system144
• Acute ischaemia 144
• Chronic lower limb ischaemia (CLI) 146
• Buerger’s disease 148
• Non-specific aortoarteritis 148
• Chronic upper limb ischaemia 149
• Thoracic outlet syndrome (TOS) 149
• Subclavian steal syndrome 151
• Vasculitis 151
• Scleroderma 152
• Giant cell arteritis (Temporal arteritis) 152
• Aneurysms 152
• Abdominal aortic aneurysm 153
• Popliteal aneurysm 153
13.3. Symptoms of arterial system diseases 154
• Analysis of symptoms 154
• Arterial system 156
• General 158
• Neurologic system 158
13.5. Special tests 158
13.1 Surgical anatomy of arterial system
Upper limb
Blood supply to the upper limb(Fig. 13.1A) is by the subclavian artery. From
the outer border of the first rib, it continues as the axillary artery.
FIGURE 13.16 Feeling the pulsations—(A) Aorta. (B) External iliac
artery. (C) Common femoral artery. (D) & (E) Popliteal artery. (F)
Posterior tibial artery. (G) Anterior tibial artery. (H) Dorsalis pedis.
FIGURE 13.15 Feeling the pulsations—(A) Superficial temporal artery.
(B) Carotid artery. (C) Subclavian artery. (D) Axillary artery. (E)
Proximal brachial artery. (F) Distal brachial artery. (G) Radial artery.
(H) Ulnar artery.
FIGURE 13.1A Arteries of upper limb.
It runs along the medial side of arm as brachial artery, and just below and
posteromedial to the biceps tendon in the elbow, it divides into the radial and
ulnar arteries.
The radial artery passes along the outer side of the forearm to the wrist,
crosses the palm to form the deep palmar arch and unite with the deep branch of
the ulnar artery.
The ulnar artery runs down along the inner side of forearm to the wrist,
crosses the palm to form the superficial palmar arch and unite with the
superficial palmar artery (branch of radial artery).
The palmar arches supply the fingers and the digital vessels anastomose
freely with each other
Lower limb
Blood supply to the lower limb (Fig. 13.1B) is by the external iliac artery,
which crosses the groin and continues as the femoral artery in the thigh. It is
named popliteal artery at the lower third of thigh. The popliteal artery divides
into:
• the anterior tibial artery, which runs along the front of the leg, crosses the
front of the ankle joint and supplies the front of the foot as the dorsalis pedis
artery.
• the tibioperoneal trunk which divides into posterior tibial and peroneal
arteries. The posterior tibial artery crosses the back of the ankle joint to enter
the sole of the foot to divide into:
• Medial plantar artery and
• Lateral plantar artery
FIGURE 13.1B Arteries of lower limb.
The plantar arteries divide into the metatarsal and digital arteries. The
arteries around the ankle joint anastomose freely with one another to form
networks of vessels.
13.2 Diseases of arterial system
Acute ischaemia
• Causes of acute ischaemia are:
• Acute thrombosis
- Occurs in a vessel with pre existing atherosclerosis due to plaque rupture
or due to hypercoagulable condition.
- Can occur de novo in a normal artery due to thrombophilia.
• Embolism–Emboli originate from:
- Heart (e.g. Myocardial infarction and rheumatic heart disease with atrial
fibrillation, commonest; atrial myxoma, rare).
- Proximal artery (e.g. Arterial emboli arise from an ulcerated
atheromatous plaque or from an aneurysm – Popliteal aneurysm and
subclavian aneurysm following thoracic outlet compression). The
common sites for emboli are the brachial bifurcation and common
femoral artery bifurcation. Multiple showers of emboli in the foot
produce the characteristic trash foot.
• Dissection–Seen in patients with hypertension or connective tissue
disorders, like Marfan’s syndrome. There is a tear in the intima which
allows the blood to enter between the intima and the media (false lumen)
causing the true lumen to occlude. It usually starts in the arch of aorta and
extends all the way upto the iliac arteries.
• Arterial trauma–Can be homicidal or iatrogenic (e.g. surgical intervention,
accidents). The arterial injury may be laceration, transection, contusion,
thrombosis or spasm. There is usually an associated bony and or soft
tissue injury.
• Rapid changes occur in the tissues distal to the occlusion and the limb
survival depends on the presence of collaterals.
• Skeletal muscle and nerve tissue are the most sensitive to hypoxia and suffer
damage early.
Complications
• Compartment syndrome, acute renal failure (acidosis) and muscle contracture
(Volkmann’s ischaemic contracture).
• Acute ischaemia produces classical symptoms (6 Ps) –
• Pain–Usually excruciating, sudden at onset and continuous.
• Pallor–Affected limb appears pale due to lack of blood.
• Pulselessness–Pulses distal to the block are absent.
• Paresthesia–Due to nerve damage.
• Paralysis–Sensory motor deficit due to ischaemic nerve damage secondary
to severe ischaemia (a late sign).
• Poikilothermia–The affected limb appears cold.
• Affected muscle gets swollen and tense, and is very tender due to persistent
ischaemia.
• On palpation, muscle gives a characteristic rubbery feel [can be mistaken for
deep vein thrombosis (DVT)].
• Later skin changes, like mottling (Fig. 13.2A) and blisters start, and ultimately
the limb becomes gangrenous (Fig. 13.2B).
FIGURE 13.2A Mottling of ischaemic limb.

FIGURE 13.2B Acute ischaemia of left lower limb.
All investigations should be done without delay.
• Duplex scan is done to confirm diagnosis in early cases.
• Angiogram for treatment planning.
• Tests for thrombophilia.
• Hyperkalemia, when renal shut down ensues.
Note
Those who present late should be taken up for surgery without imaging, and
intraoperative angiogram should be done to reduce time delay.
Treatment
• Acute arterial occlusion is a surgical emergency. Usually irreversible damage
occurs by 4–6 hours. Hence, revascularization should be done within 6–8
hours for limb salvage (Golden hour).
• Intravenous heparin should be administered as soon as the diagnosis of
acute ischaemia of the limb is made. Best results are seen in those who
undergo revasculariztion within 6–8 hours after the onset of ischaemia.
• Embolism is best managed by embolectomy done through the brachial
artery at the elbow or the femoral artery at the groin.
• Acute arterial thrombosis can be managed by surgical bypass or by
catheter directed thrombolytic therapy. Frequently, both modalities may
be required to achieve revascularization.
• Fasciotomy will be required to avoid muscle damage in compartment
syndrome caused by delayed revascularization.
• Early amputation for limbs with irreversible ischaemia.
Chronic lower limb ischaemia (CLI)

• Common causes of chronic lower limb ischaemia are:
• Atherosclerosis
• Buerger’s disease
• Nonspecific aortoarteritis
• Neglected arterial trauma
• Congenital cause–Popliteal artery entrapment; and
• Miscellaneous causes–Vasculitis, and cystic degeneration of popliteal
artery.
In developed countries, 80–90% of the cases of CLI are due to atherosclerosis,
whereas, in developing nations, Buerger’s disease is still the major cause of CLI.
• In atherosclerosis, cholesterol deposits in the subintimal layer of the artery
cause a thick plaque, which causes luminal narrowing. The plaque is prone to
ulcerate and discharge cholesterol emboli. Ulcerated plaque is prone to
develop a thrombus, which can also embolise distally. Sudden thrombosis
can also cause total occlusion of the artery and lead to acute ischaemia.
• Common sites for atherosclerotic stenosis are:
• Aortoiliac bifurcation
• Superficial femoral artery at adductor hiatus
• Popliteal artery trifurcation and
• Carotid artery bifurcation.
• Major predisposing causes are
• Diabetes mellitus
• Hypertension
• Hyperlipidemia
• Tobacco smoking and
• Familial causes.
• Vascular disease is a systemic disease and 30–40% of patients with peripheral
vascular disease have associated coronary, cerebral or visceral arterial
involvement.
• Lerische’s syndrome refers to an aortoiliac block with gluteal claudication
and impotence.
Symptoms
• Claudication, or pain in a group of muscles on walking a particular distance,
is the most common presentation of CLI. This is due to accumulation of
anaerobic metabolites in the muscle. If the block is mild the pain disappears
on continued walking due to vasodilatation and wash out of the metabolites.
As the severity of the block increases, the pain becomes more pronounced,
forcing the patient to stop to get relief from pain. As the ischaemia becomes
more severe, the claudication distance gradually comes down and ultimately
the pain comes even on walking a few steps.
• ‘Rest pain’ refers to pain in the muscle even at rest. Rest pain is felt more at
night forcing the patient to get up from bed and walk, or keep the limb
hanging by the side of the bed to get relief from the pain.
• The site of arterial occlusion can be predicted by the site of pain –
• Foot and Instep–Tibial block.
• Calf muscle–Femoro popliteal block.
• Thigh–Common femoral block.
• Gluteal–Aortoiliac block.
• Ulcer or gangrene. At this stage even a trivial trauma can precipitate an ulcer
(Fig. 13.3) or gangrene in an ischaemic limb (Fig. 13.4). Once these develop,
the pain shifts to the ulcer or gangrene.
FIGURE 13.3 Ischaemic ulcer.
FIGURE 13.4 Gangrene of toes due to ischaemia.
Signs
• Absence of pulse distal to the block (all accessible pulses to be felt).
• Decreased blood pressure distal to the block (all four limb pressures to be
recorded).
• Signs of chronic ischaemia –
• Muscle wasting
• Loss of hair
• Atrophic skin and
• Nail changes.
Note
History related to coronary, cerebral or visceral arterial insufficiency to be
elicited.
• Haemogram–Polycythemia and erythrocytosis.
• Renal function test–Contrast cannot be used in patients with elevated renal
parameters.
• Lipid profile–To identify dyslipidemia.
• Electrocardiography (ECG) and ECHO–To assess the cardiac function.
• Imaging–
• Noninvasive(for anatomical and physiological data and help towards
diagnosis, treatment planning, and follow up) –
- Ankle Brachial Index.
- Doppler tracing.
- Duplex scan: color Doppler.
• Invasive–Angiogram, done only when some intervention is planned, and
not for diagnosis.
- Conventional angiogram: Using Seldinger’s technique the artery is
cannulated and contrast is injected. Femoral, brachial or radial arteries
are commonly punctured for the angiogram.
- Digital subtraction angiogram (DSA): Computer aided deletion of bony
shadows gives better visualization of the arteries.
- Computed tomography (CT) angiogram: Rapid sequence CT imaging
with intravenous contrast is done and arteries are reconstructed by the
computer. It gives excellent 3D visualization of the arteries (Fig. 13.5).
- Magnetic resonance angiogram (MRA): Gadolinium, which is not
nephrotoxic, is used as contrast and hence is the imaging of choice in
those with nephropathy.
FIGURE 13.5 CT angiogram —Aortoarteritis.
Treatment
Medical
• All patients with claudication should be treated medically.
• Abstinence from tobacco smoking and regular exercises (walking) are the
main stay of medical management.
• Drugs–
• Antiplatelet drugs: Aspirin and Clopidogrel.
• Haemorrheological agents: Pentoxyphyllin and Cilostazol.
• Foot care: Proper footwear; care of the ulcer and the skin.
• Treatment of comorbid conditions–Diabetes, hypertension, dyslipidemia,
cardiac or renal failure.
Interventional
Indicated in limb threatening ischaemia, interventional treatment helps in
incapacitating claudication and arterioarterial embolism.
Intervention can be open, surgical or endovascular depending on the site and
length of occlusion.
• Endovascular treatment–Balloon angioplasty, Stenting or Percutaneous
placement of covered stents (Stent graft).
• Surgical treatment–Endarterectomy and bypass surgery using reversed or in
situ saphenous vein graft or prosthetic graft (PTFE and Dacron). In
selected patients lumbar sympathectomy can be performed.
Note
Regular medical treatment and follow up are needed to maintain limb salvage.
Buerger’s disease
• An inflammatory disease involving all layers of the arterial wall (pan
arteritis), causing segmental arterial occlusion.
• Affects young males who are heavy smokers.
• Characterized by remission and relapses.
• Relapses are related to resumption of smoking.
• Disease starts in the small and medium sized arteries and gradually spreads to
involve even major arteries.
• The disease affects both upper and lower limbs.
• Veins can also be involved; migrating phlebitis is one of the early features.
Symptoms
• Claudication pain in the foot.
• Painful non healing ulcer and blackish discolouration of toes (Fig. 13.6) and
fingers.
FIGURE 13.6 Dry gangrene of great toe.
Signs
• Absent pedal and/or wrist pulses.
• Gangrene of toes and/or fingers.
• The diagnostic criteria are –
• Onset before the age of 50.
• Infra popliteal involvement.
• Absence of atherogenic risk factors, except smoking.
• Thrombophlebitis.
• Upper limb involvement.
• Angiogram shows segmental occlusion of the artery, and typical tree root
appearance and corkscrew collaterals (Fig. 13.7).
FIGURE 13.7 Corkscrew collaterals.
Treatment
• During the acute stage the disease is treated with anticoagulation,
prostaglandins and foot care.
• In the chronic stage, bypass surgery and sympathectomy can be done.
• Total abstinence from tobacco is needed to prevent relapse.
Non-specific aortoarteritis
• An inflammatory arterial disease.
• More common in Asian countries.
• More common in females of 20–40 years.
• Exact aetiology is not known, but an autoimmune mechanism has been
suggested.
• The disease usually affects major elastic arteries, mainly aorta and its
branches.
• Inflammatory cell infiltration of the arterial wall causes thickening of the
media and the adventitia in the acute stage. In later stages there is extensive
fibrosis. This can cause both arterial block, as well as aneurysm.
• Inflammation of the arch of aorta and occlusion of the ostia of
brachiocephalic, carotid and subclavian arteries resulting in the absence of
pulses of both subclavian and wrist (hence called ‘pulseless disease’).
• In the acute stage –
• Fever, malaise and joint pain.
• The affected artery is swollen and tender.
• Carotidynia is very characteristic of this disease.
• In the chronic stage the symptoms are related to the arterial occlusion and
the organ involved.
• Stroke, blindness, upper limb exertional pain, renovascular hypertension,
mesenteric ischaemia, and lower limb claudication are common
presentations.
• Aortic aneurysm is also commonly seen.
• Death is usually due to uncontrolled hypertension, cerebral haemorrhage,
and cardiac or renal failure.
• Erythrocyte sedimentation rate (ESR) is elevated.
• C reactive protein (CRP) is elevated in the acute stage and indicates
continuing inflammatory activity.
• Color doppler and arteriogram are needed to assess the extent of arterial
involvement.
Treatment
• Immunosuppressants, like corticosteroids and antimetabolites are given to
control the inflammatory process in acute stage.
• Balloon angioplasty and stenting can be performed in selected cases with
arterial occlusion.
• Bypass grafting is done for long segment occlusion.
• Aneurysm can also be managed by the endovascular method or by open
surgery.
Chronic upper limb ischaemia

• Major vessel occlusion is relatively uncommon in the upper limb.
• Common causes of chronic upper limb ischaemia are:
• Atherosclerotic disease
• Thoracic outlet syndrome
• Nonspecific aortoarteritis
• Vasculitis and Vasospastic disorders
• Atherosclerotic disease and nonspecific aortoarteritis usually affect the
proximal major artery (subclavian and axillary), whereas, small vessel
occlusion is due to a variety of causes and is more common.
• Ischaemia in the upper limb is more insidious because there are well
developed collaterals around the scapula, elbow and wrist.
Thoracic outlet syndrome (TOS)

• It is a symptom complex produced by neurovascular compression at the
thoracic outlet.
• Compression at –
• interscalene triangle formed by the scalenus anticus and medius muscles
with the first rib as the base (common).
• costoclavicular space.
• pectoralis minor tendon.
• Compression is due to –
• soft tissue causes:
- Hypertrophied muscle (scalenus anticus, medius, minimus, subclavius
and pectoralis minor); and
- Abnormal slips, insertion and fibrous bands.
• bony causes:
- Cervical rib
- Prominent C7 transverse process
- Abnormal first rib
- Callus from fracture of the first rib or clavicle and
- Tumours at the thoracic outlet can also cause compression (rare).
95% of the patients present with neurogenic symptoms, and 5% with vascular
symptoms which may be due to arterial or venous compression.
• Neurogenic symptoms depend on the cord compressed.
• Lower cord (C8, T1) compression (most common) produces pain and
paresthesia along the inner side of forearm reaching up to the little and
ring fingers and weakness of the hand.
• Upper cord (C5, C6) compression produces pain along the outer aspect of
the arm, shoulder and nape of the neck.
• Symptoms come during the end of the day and are more common in
younger women. Usually there is a history of loss of weight or whiplash
injury in the recent past.
• Examination reveals a long neck, fullness in the supraclavicular fossa,
tenderness over the scalene muscle, and wasting of the small muscles of
the hand.
• Symptoms may be reproduced by hyperabduction and external rotation of
the shoulder (90o AER).
• Arterial compression is usually due to a complete cervical rib. The second
part of subclavian artery gets compressed between the scalenus anticus and
the cervical rib. The artery distal to that develops dilatation (Post stenotic
dilatation). Due to the turbulence plaque and thrombus develop, which may
embolise distally.
• Symptoms develop only when the embolization starts. Micro emboli
produce Raynauds symptoms in the fingers. Larger emboli cause acute
ischaemia.
• Examination reveals prominent subclavian pulse in the supraclavicular
fossa, bruit over the artery, absent distal pulses and ischaemic changes
distally (Fig. 13.8). Adson’s test will be positive.
• Venous compression usually occurs at the costo clavicular space where the
subclavian vein gets compressed. In early cases, swelling of the limb occurs
on exertion, which subsides gradually after rest.
• More often, patient presents with sudden onset pain and swelling of the
upper limb usually after heavy exertion with the upper limb due to sudden
thrombosis of the subclavian vein (Paget Shroetter Syndrome).
• The limb is oedematous and cyanosed, and the superficial veins may
become prominent.
FIGURE 13.8 Cervical rib with ischaemic changes in the upper limb.
• X rays of the neck for cervical rib (Figs. 13.9A and B).
• Nerve conduction studies and MR imaging of the neck are needed to
confirm nerve root compression and to identify the cause.
• Colour Doppler study and arteriogram are needed to plan revascularization
in patients with arterial compression.
• Axillary subclavian venogram is needed for patients with venous
compression.
FIGURE 13.9A X ray —Unilateral cervical rib.

FIGURE 13.9B X ray —Bilateral cervical ribs.
Treatment
• A trial of medical management is offered to all patients with neurogenic
symptoms which include shoulder bracing exercises, avoiding
hyperabduction and analgesics.
• Surgery needs decompression of the thoracic outlet which may be excision of
cervical rib, first rib, scalene muscle and bands.
• For arterial symptoms, excision of the rib, repair of the subclavian artery
and distal embolectomy is done.
• For venous compression, excision of the first rib is advised in early cases.
Once thrombosis occurs, the patient is given anticoagulation or
thrombolytic therapy. In selected patients, endovascular treatment is
recommended.
Subclavian steal syndrome
• In patients with stenosis of the subclavian artery proximal to the vertebral
artery the upper limb circulation is maintained by reversal of flow in the
vertebral artery stealing the blood from the posterior circulation.
• Upper limb exercise causes more blood to be diverted to the arm from the
brain.
• Giddiness, ataxia and visual disturbance (Vertebro basilar insufficiency).
Vasculitis
• Small vessel occlusion is seen in autoimmune diseases due to deposition of
immune complexes, periarterial inflammation and thrombosis.
• Both cutaneous and visceral vessels are known to be affected.
• Commonly seen in connective tissue disorders, like rheumatoid arthritis,
scleroderma, polyarteritis nodosa (PAN) and giant cell arteritis.
• Thromboangiitis obliterans (Buerger’s Disease) and Aortoarteritis are also
considered as a type of vasculitis involving medium and large arteries.
• Cutaneous vasculitis may be the first manifestation of underlying connective
tissue disorder.
• Fever, malaise, joint pain and rashes.
• Toe or fingertip ischaemia and paronychia (Fig. 13.10A).
• Raynaud’s phenomenon (Fig. 13.10B).
• Multiple painful ulcers (Fig. 13.10C).
FIGURE 13.10A Vasculitis.
FIGURE 13.10B Raynaud’s phenomenon.
FIGURE 13.10C Multiple ulcers of vasculitis.
• Immunological tests for connective tissue disorder.
Treatment
• Anticoagulants.
• Immunosuppresants.
• Vasodilators.
Scleroderma
• Collagen vascular disease.
• Common in women between 20 and 30 years.
• Histologically, the artery shows fibrinoid necrosis, round cell infiltration and
arterial narrowing.
• Progresses to fibrosis of subcutaneous tissue.
• Leads to visceral involvement [pulmonary fibrosis, oesophageal motility
disorder, renal failure, bowel ischaemia, bowel perforation and gastro
intestinal (GI) bleed].
• CREST Syndrome refers to Calcinosis, Raynauds syndrome, Esophageal
disorder, Sclerodactyly and Telangiectasia.
• The initial presentation may be Raynaud’s symptoms and recurrent
paronychia.
• Atrophy of finger tips and pulp.
• Later finger tip gangrene.
• Tightening of skin and characteristic facial appearance (due to subcutaneous
fibrosis) (Fig. 13.11A).
FIGURE 13.11A Scleroderma.
• Immunological tests for connective tissue disorder.
Treatment
• Anticoagulants.
• Immunosuppresants.
• Vasodilators.
Giant cell arteritis (temporal arteritis)

• Arterial inflammation shows predominantly giant cells.
• Commonly older men are affected.
• Involvement of ophthalmic artery can cause sudden blindness due to
inflammation and thrombosis.
• Severe head ache.
• On examination, temporal artery is swollen and cord like (Fig. 13.11B).
• Tenderness over the artery.
FIGURE 13.11B Temporal arteritis.
• Temporal artery biopsy is needed to confirm the diagnosis.
Treatment
• The condition resolves with corticosteroids
• Treatment should be started immediately, to prevent blindness.
Aneurysms
Dilatation of the artery, more than one and a half times the diameter, is called
an aneurysm.
• The dilatation may involve –
• a part of the wall of the artery (saccular) (Fig. 13.12A).
• the whole circumference (fusiform) (Fig. 13.12B).
• Aneurysm can be of two types –
• True aneurysm–The wall of the aneurysm contains all the components of
the arterial wall.
• False aneurysm–The wall is made of compressed clot and the surrounding
soft tissue, and is usually due to trauma.
• Causes of aneurysms are:
• Congenital (Rare)
- Berry aneurysm (cerebral, splenic, renal);
- Congenital arteriovenous fistula; and
- Marfan’s syndrome.
• Acquired
• Degenerative:Atherosclerosis (most common).
• Inflammatory: Aortoarteritis and Vasculitis.
• Infective (Mycotic): misnomer. Causative organism is usually bacterial.
• Traumatic: Arterial trauma and Cervical rib.
• Dissecting aneurysm– Blood flows between the intima and the media through
a tear in the intima and causes the dilatation. This is commonly seen in
patients with hypertension and those with connective tissue disorders.
• Common aneurysms are –
• Abdominal aortic aneurysm and
• Popliteal artery aneurysm.
FIGURE 13.12A CT —Saccular left renal artery aneurysm.
FIGURE 13.12B CT —Fusiform abdominal aortic aneurysm.
Abdominal aortic aneurysm (AAA)

• Majority occur in the infra renal aorta.
• Most commonly due to atherosclerosis.
Complications
• Erosion of vertebra, inferior vena cava (aorto-caval fistula), bowel (aorto-
enteric fistula), rupture and distal embolization.
Symptoms
• 70–80% of abdominal aortic aneurysms are asymptomatic and are detected
during routine clinical examination or ultrasound (US) screening.
• Dull backache (due to erosion of vertebra).
• Severe pain (due to rapid enlargement and rupture).
• Symptoms of shock (due to rupture).
• Symptoms of cardiac failure (due to aortocaval fistula).
• Gastrointestinal bleed (due to aortoenteric fistula).
Signs
• A mass with expansile pulsation just above the umbilicus.
• It is possible to get above the swelling in infra renal aneurysms.
• Common iliac involvement is suspected if the swelling extends below the
umbilicus.
• Bruit over the aneurysm indicates associated arterial stenosis.
• Distal pulses must be checked to rule out associated peripheral vascular
disease or embolization.
DD: Tortuous aorta in a thin individual; retroperitoneal mass with transmitted
pulsation.
Popliteal aneurysm
• Most common peripheral aneurysm.
• It could be bilateral.
• Frequently associated with aneurysm elsewhere (aortic and femoral).
Complications
• Distal embolization and ischaemia, rupture (rare), thrombosis
• Mass in the popliteal fossa with expansile pulsations (Fig. 13.13A).
• Symptoms and signs of distal embolization and ischaemia (sudden thrombosis
and acute ischaemia is known).
• Tense swelling with shiny inflamed skin (due to rupture); may be mistaken for
abscess.

FIGURE 13.13A Popliteal aneurysm.
DD: Baker’s cyst and abscess.
• US and colour Doppler are diagnostic.
• CT (Fig. 13.13B) and MR angiograms are used frequently for diagnosis and
treatment planning.
• Invasive angiogram (Fig. 13.13C) is needed only in the presence of
complications.
• Angiogram is needed for popliteal aneurysm to plan distal
revascularization.
FIGURE 13.13B CT —Abdominal aortic aneurysm.

FIGURE 13.13C Arteriogram —Popliteal artery aneurysm.
Treatment
Abdominal aortic aneurysm
• Treatment of asymptomatic AAA depends on its size.
• All aneurysms 5.5 cm or more should be operated because the risk of
rupture is higher than the risk of surgery
• (AAA less than that could be managed with regular follow up and beta
blockers).
• All symptomatic aneurysms should be operated irrespective of their size.
• Open surgery with replacement of the aorta with a prosthetic Y graft has
been the mainstay of treatment till recently.
• Endovascular aneurysm repair (EVAR) has recently been introduced and
is gaining popularity.
Popliteal aneuryms
• All popliteal aneurysms should be operated irrespective of their size in view
of the high risk of embolization.
• Exclusion bypass with reversed saphenous vein graft has been the most
common operation performed.
• Thrombolytic therapy is needed for thrombosed aneurysm and distal
embolization.
• Loss of limb depends on the patency of the distal artery, and may warrant
amputations.
13.3 Symptoms of arterial system diseases

1. Pain
2. Colour changes in limb
3. Ulceration
4. Symptoms related to arterial insufficiency
Analysis of symptoms
Pain
Pain is the most common symptom of arterial occlusion.
• Intermittent claudication: Pain in the muscle, usually calf, on walking,
which forces the patient to stop or limp (Claudio literally means ‘to limp’).
This occurs in chronic arterial occlusion with ischaemia to the muscles.
Muscles switch to anaerobic metabolism in the absence of adequate oxygen
leading to accumulation of metabolites, which cause the pain. Typically, the
patient gets pain on walking a particular distance called ‘claudication
distance’, and gets relieved by resting which allows the metabolites to get
washed away. In mild ischaemia, when there are enough collaterals, the pain
may be mild and the patient will be able to walk with the pain; sometimes it
might even disappear on continued walking. When the severity of ischaemia
increases, the claudication distance becomes shorter or pain may appear even
at rest. Sometimes, a trivial trauma or minor surgery can precipitate an ulcer
or gangrene and the rest pain shifts to the ulcer area.
• Rest pain: It is felt more at night. Patient may be forced to walk or sit with
the leg hanging by the side of the bed to get some relief from the pain. This
causes the leg to develop gross oedema which can worsen the ischaemia and
tissue damage.
• Pseudoclaudication: Patients with lumbar canal stenosis also can complain
of pain in the legs on walking. Careful history is needed to differentiate it
from true claudication. In pseudoclaudication, the pain usually starts from
the lower back or gluteal region and moves down along the posterior aspect
of the thigh and leg. Pain is not completely relieved by rest and quickly
returns once the patient starts to walk.
• Sudden onset pain: Pain of sudden onset is more suggestive of acute arterial
occlusion. The patient may notice that the limb has become cold and pale.
This is a surgical emergency.
• Paresthesia: Some patients may not have typical claudication pain and
instead will complain that the leg becomes tight and numb and are unable to
walk any further. This is more often seen in diabetics who have associated
neuropathy.
Colour changes in limb

• On exposure to cold, toes and fingers become pale, then turn blue, and finally
develop redness with intense burning pain. This is seen in vasospastic
disorders and in diseases of small vessel occlusion, like Buerger’s disease,
cervical rib with arterial compression, and distal embolization. In vasospastic
disorders, this symptomatology will be seasonal during winter and in those
living in colder places. This is called ‘Raynaud’s phenomenon’.
• Gangrene–Severe vascular impediment giving rise to blackish discolouration
of the skin.
Ulceration
• Ulceration can occur after a trivial trauma or even spontaneously, especially
in those with compromised arterial blood supply (e.g. Buerger’s disease and
atherosclerosis).
• Site of the ulcer–Ischaemic ulcers are seen more in the feet. The edges will be
unhealthy, and the base will be covered with slough and pale granulation,
with no signs of healing. The surrounding skin also shows signs of
ischaemia.
Symptoms related to arterial insufficiency

Arterial disease is a systemic disease and will involve other areas also. 30–40%
of patients with peripheral vascular disease have coronary, carotid or visceral
artery involvement. The symptoms may be related to specific arterial system
involvement. Some examples are:
• Carotid artery– Motor weakness, slurring of speech, giddiness and sudden
transient blindness (amurosis fugax).
• Coronary artery– Chest pain and exertional dyspnoea.
• Renal artery– Hypertension (sudden uncontrolled).
• Mesenteric artery– Postprandial pain, food fear and loss of weight.
• Aorotiliac arteries– Impotence (Leriche’s syndrome).
Upper limb ischaemic diseases and symptoms:
• Neck and shoulder pain, radiating to hands and fingers.
• Muscle weakness and inability to hold objects.
• Raynaud’s symptoms.
• Swelling in supraclavicular area.
Eliciting history
The detailed history taking starts with the presenting symptom, followed by
questions relating to other symptoms.
• Age
• Aortoarteritis and Buerger’s disease are more common in the younger age
group (20–40 years).
• Atherosclerosis is generally seen in older age group (>50 years), though
premature atherosclerosis is increasingly seen in India.
• Sex
• Buerger’s disease occurs in males
• Scleroderma is common in females
Pain in the limb

• Sites of pain: In which part of the limb does the patient complain of pain?
From the site of pain, it is easy to predict the level of arterial occlusion.
• Foot and instep claudication– Tibial and pedal artery disease, commonly
seen in Buerger’s disease.
• Calf claudication– Popliteal artery occlusion.
• Thigh claudication–Common femoral occlusion.
• Gluteal claudication– Iliac artery occlusion.
• Duration of pain: When did the pain start?
The duration of pain will indicate the chronicity of the problem. Pain of short
duration may indicate acute pathology (e.g. acute arterial occlusion) and long
duration (e.g. Buerger’s disease).
• Precipitating factors: Does the pain become severe on walking or standing,
or is relieved by any exercise?
Walking can aggravate ischaemic pain of the lower limb (e.g. claudication
pain), and standing for a longtime may precipitate pain of venous origin (e.g.
varicose veins).
• Treatment: Has any treatment been given for the pain?
Administration of treatment for the pain will give the severity of the pain and
the relief the patient had with the intake of drugs.
Colour changes
• Colour changes: Has the patient seen any change in colour of the toes or
fingers?
Colour changes occur in Raynaud’s phenomenon and progressive arterial
occlusion (e.g. atherosclerosis).
Ulcer on the lower limb

If an ulcer is present in the limb, it should be evaluated in line with any ulcer in
general (See Chapter 11), and the questions are directed towards it evaluation,
and some are given below
• Duration of ulcer: For how long has the ulcer been present?
Ulcers which are present for a short duration are generally due to trauma, and
those of longer duration, are due to repetitive trauma.
• Site of the ulcer: In which part of the foot is the ulcer present?
Ulcer on the medial or lateral aspect of ankle is more due to varicose ulcer.
Trophic ulcers occur at pressure points, and ischaemic ulcers occur at the
terminal part of the toes, where the vascularity is the minimum. Ulcers due to
vasculitis can occur in the upper leg also.
• Association of pain: Is the ulcer painful or painless?
Trophic ulcers are painless, while acute ischaemic ulcers are painful.
Infection is the common cause of pain in the ulcer.
• Nature of treatment: Has any treatment been given for the ulcer?
Applications of strong chemicals and native medicines can delay healing,
and also detailed history regarding the treatment taken will give an idea
about the chronicity of the ulcer.
• Association of fever: Is or was this associated with fever?
Association of high grade fever may indicate infective pathology, like
cellulitis of foot and thrombophebitis.
Loss of appetite and weight are indicative of illnesses like malignancies (e.g.
intra-abdominal lumps producing arterial obstruction).
• Treatment for the illness: Has any treatment (medical or surgical) been
given to the illness?
The information of any treatment received in the past for this illness will
give a clearer picture of diagnosis (e.g. embolism and vasospastic illness).
• Past history: Was there any similar illness in the past which required a
treatment?
If the patient had suffered a similar illness in the past, which was
successfully treated, will indicate the examiner to reconsider the diagnosis,
like embolism and vasospastic illness.
• Personal history: Is the patient a smoker and suffer from any disease?
Tobacco usage (smoking) predisposes to peripheral arterial disease. History
of pre existing hypertension, diabetes mellitus, hyperlipidemia and
hypothyroidism are known to be associated with peripheral vascular disease.
Abdominal aortic aneurysm is more common in patients with chronic
obstructive pulmonary disease.
Diabetes and dyslipidemia may be genetic and can run in families.
Abdominal aortic aneurysm is known to be more common amongst first
degree relatives.
match the situation, like consumption of drugs (e.g. aspirin). Questions, like
the presence of chest pain, breathlessness and giddiness have to be asked as
they may indicate coronary or carotid disease.
Arterial system
Pre-requisites for physical examination
• Patient should be undressed to enable the limbs to be examined.
• Opposite limb should be exposed for comparison.
• Adequate knowledge and orientation of the limb and its anatomy is
mandatory.
For examination of the lower limbs, the patient is requested to stand evenly on
a flat surface and both the lower limbs are examined from the front, back and
sides, and compared.
Physical examination consists of three parts:
1. Inspection
2. Palpation
3. Auscultation
Inspection
Skin
• Texture of skin–Dry skin (e.g. chronic arterial disease)
• Colour of skin
• Pallor (e.g. light coloured skin of vasospastic disease and acute ischaemia).
• Reddish colour (e.g. critical ischaemia when the limb is kept in a
dependent position to get pain relief).
• Dark colour–Cyanosis (e.g. acute ischaemia).
• Gangrene
- Dry gangrene: dry mummified with a line demarcating the dead and
viable tissues (line of demarcation) (Fig. 13.14A).
- Wet gangrene: no line of demarcation, with the tissue adjacent to
gangrenous area oedematous, cyanosed and infected (Fig. 13.14B).
• Hair–Hair loss is common in chronic ischaemia.
• Veins–They appear guttered in chronic ischaemia.
• Nails–They are brittle and ridged in chronic ischaemia.

FIGURE 13.14 (A) Dry gangrene. (B) Wet gangrene.
Swelling
• Generalized swelling–One foot (e.g. filariasis or cellulitis, post operative).
Ulcers
• The ulcer is examined in lines with general ulcers (Ch. 10).
Palpation
The following signs are elicited in palpation:
• Temperature–Is tested with the back of the hand – ischaemic limb will be
colder; confirmed by comparing with the other limb.
• Capillary filling–Ttested by pressing the nail bed.
• Venous refilling–Tested by elevating the limb; lowering the limb will fill the
vein. The normal time taken is less than 5 seconds.
• Tenderness
• Tenderness over the artery indicates site of embolus or thrombus.
• Tender mass over carotid artery is seen in aortoarteritis (carotidynia).
• Muscle tenderness indicates acute ischaemia or myonecrosis.
• Swellings and ulcers are examined in line with any swelling or ulcer in
general (see Chs. 9 and 10)
• Arterial pulsations–Always compared with the opposite side.
The locations where various pulsations are best felt and the bones against
which they are felt are given in Table 13.1.
TABLE 13.1
Locations of Various Pulsations Which can be Felt in the Body
Bone against
Pulsations Location
which felt
Superficial temporal artery (Fig. In front of tragus Temporal bone

13.15A)
Carotid artery (Fig. 13.15B) In the carotid triangle Tubercle of C6
vertebra
Subclavian artery (Fig. 13.15C) At the supraclavicular fossa above the mid point of clavicle First rib
Axillary artery (Fig. 13.15D) In the apex of axilla Head of
humerus
Proximal brachial artery (Fig. 13.15E) Just posteromedial to the biceps muscle along the medial side Shaft of
of the upper arm humerus
Distal brachial artery (Fig. 13.15F) Just proximal to the elbow crease medial to the biceps tendon Medial condyle
of humerus
Radial artery (Fig. 13.15G) Proximal to the wrist crease Lower end of
radius
Ulnar artery (Fig. 13.15H) Proximal to the wrist crease medial to the flexor carpi ulnaris Lower end of
ulna
Aorta (Fig. 13.16A) At the epigastrium and at the umbilical region in the midline Vertebral
bodies
External iliac artery (Fig. 13.16B) Just above the inguinal ligament
Common femoral artery (Fig. 13.16C) Below the inguinal ligament at midpoint between anterior Neck of femur
superior iliac spine and pubic symphysis
Popliteal artery (distal) (Fig. 13.16D) In the lower part of popliteal fossa with the knee flexed in Tibial condyle
supine position
Mid popliteal artery (Fig. 13.16E) In the upper part of popliteal fossa with the knee flexed in Femoral
prone position condyle
Posterior tibial artery (Fig. 13.16F) Behind the medial malleolus; midway between the medial Calcaneum
malleolus and the tendoachilles
Anterior tibial artery (Fig. 13.16G) At lower leg, anteriorly, midway between the two malleoli, just Lower end of
proximal to the ankle and lateral to the extensor hallucis tibia
longus tendon
Dorsalis pedis artery (may be absent Just lateral to the extensor hallucis longus tendon, at the Navicular and
in about 5–10% of population) proximal end of first web space mid
(Fig. 13.16H) cuneiform
bone
Peroneal artery (rarely felt) (Fig. In front of lateral malleolus
13.27)
Note
Thrill indicates stenosis, expansile pulsation denotes aneurysm. Easily
palpable popliteal pulse could indicate popliteal aneurysm.
Auscultation
It is essential to auscultate over all the major arteries.
• Systolic bruit indicates turbulence due to a stenosis.
• Continuous machinery murmur is typically heard in arteriovenous fistula.
General examination
• Detailed general examination is essential to rule out limb changes due to
cardiac, renal, hepatic and neurological diseases.
• Blood pressure examination is to be done in all four limbs, as the arterial
disease is a systemic illness and may involve more than one limb.
Neurologic system
Both, the central and peripheral neurologic systems are to examined in detail,
(e.g. peripheral artery disease may be associated with cerebrovascular ischaemia.
Ischaemic neuropathy is a common accompaniment of acute ischaemia. Small
muscles of palm may be wasted in thoracic outlet syndrome (See Ch. 49).
FIGURE 13.17 Feeling the peroneal artery pulsations.
13.5 Special tests
Tests for arterial insuffiency

Buerger’s test
The patient’s leg is raised and the colour of the foot and nail bed is watched. In
normal individuals, the colour is maintained, but in an ischaemic limb, the foot
becomes pale. When the limb is lowered, the colour returns and will develop a
cyanotic hue and rubor. This test is best seen in daylight and in fair skinned
individuals (Fig. 13.18A and B).
FIGURE 13.18A Limb elevation in Bureger’s test.

FIGURE 13.18B Limb depression in Buerger’s test.
Allen’s test
• Step 1: The patient is asked to make a tight fist. Both ulnar and radial arteries
are compressed by the examiner at distal forearm (Fig. 13.19A).
• Step 2: The patient is asked to open the fist, and the palm looks pale (Fig.
13.19B).
• Step 3: The compression on radial artery is released, and if the colour returns
to normal, it indicates the patency of radial artery. The same procedure is
repeated to determine the patency of ulnar artery (Fig. 13.19C).
FIGURE 13.19 Allen’s test. (A) Step 1. (B) Step 2. (C) Step 3 —ulnar
artery released.
Inference
• If the palmar arch is incomplete, the entire palm will not regain its colour.
Test for vasospasm

Cold exposure test
When the hand is dipped in cold water and taken out of it, it becomes pale due to
severe vasoconstriction. Then gradually it becomes cyanotic and ultimately turns
hyperemic, hot and painful. This sequence of events is called ‘Raynaud’s
syndrome’. This is commonly seen in connective tissue disorders and
vasospastic diseases. This can also be seen in small vessel occlusion.
Test for AV fistula

Branham nicoladoni’s sign
This test is performed in patients with arterivenous fistula. Pulse rate drops when
the feeding artery of the fistula is compressed to stop the flow through the
fistula. This is usually seen in traumatic (acquired) AV fistula.
Tests for thoracic outlet obstruction

Elevated arms stress test (east)
The arm is elevated and the patient is asked to do exercise by making a fist.
Patients with thoracic outlet syndrome develop fatigue quickly. The hand
becomes cold and pale if there is arterial occlusion (Fig. 13.20).
FIGURE 13.20 Elevated arms stress test.
Adson’s test
The patient is asked to turn the head to the affected side and take a deep breath
while the upper limb is pulled down and the radial pulse is examined. The pulse
will weaken or disappear if there is compression at the thoracic outlet.
Unfortunately, there are significant false positives for this test (Fig. 13.21).
FIGURE 13.21 Adson’s test.
Abduction and external rotation manoeuvre (90 o AER)

Radial and subclavian pulses are examined at rest. The arm is abducted by 90o
and externally rotated. If there is arterial compression the pulse will disappear or
a bruit may appear over the subclavian artery. Patients with neurogenic
compression at the thoracic outlet will get the typical pain (Fig. 13.22).
FIGURE 13.22 Abduction and external rotation manoeuvre.
CHAPTER 14
Venous system
N. Sekar
CHAPTER OUTLINE
14.1. Surgical anatomy of venous system 162
• Lower limb 162
• Upper limb 164
14.2. Venous haemodynamics 164
14.3. Diseases of venous system 165
• Congenital vascular malformations 165
• Capillary malformation 165
• Venous malformation 165
• Congenital arteriovenous malformation 166
• Lymphatic malformation 166
• Combined malformations 167
• Acquired arteriovenous fistula 167
• Infantile haemangioma 168
• Venous thrombosis 168
• Superficial thrombophlebitis 168
• Deep vein thrombosis 169
• Phlegmasia alba dolens 170
• Phlegmasia cerulea dolens 170
• Post phlebitic syndrome 170
• Axillary vein thrombosis 171
• Varicose veins 171
• Venous ulcers 172
14.4. Symptoms pathologies of venous system 173
• Venous system 175
• General 176
• Abdomen 176
14.6. Special tests 176
14.1 surgical anatomy of venous system
Lower limb
Venous system of the lower limb consists of three parts:
1. Superficial venous system–A set of superficial veins in the subcutaneous
plane.
2. Deep venous system–Veins located deep to deep fascia.
3. Perforators–Veins joining these two systems.
Superficial venous system

The superficial veins (Fig. 14.1A) consist of –
1. Great saphenous or long saphenous vein
2. Short saphenous vein
3. Communicating veins
FIGURE 14.1A Superficial venous system of lower limb.
Great saphenous vein (GSV)

It starts as the continuation of the dorsal vein of the foot in front of the medial
malleoleus. It rises along the medial side of the leg and drains into the common
femoral vein at the groin. Position of the saphenous opening in the deep fascia is
variable, but is usually located about 1 cm below the mid inguinal point.
The important tributaries of the GSV are:
In the leg:
• Anterior accessory great saphenous vein.
• Posterior accessory great saphenous vein (Leonard’s vein).
In the thigh:
• Anterior circumflex vein of the thigh.
• Posterior circumflex vein of the thigh.
In some patients, short saphenous vein drains into posterior circumflex vein of
the thigh (Giacomini’s vein).
• Tributaries at the sapheno-femoral junction are:
• Superficial external pudendal;
• Superficial epigastric; and
• Superficial circumflex iliac.
They may drain into the GSV, and in some cases enter directly into common
femoral vein. During flush ligation, all these tributaries should be identified and
ligated, or otherwise there is a risk of recurrence of varicosities.
The saphenous nerve runs along the GSV from the knee upto the medial
malleolus. Thus, during stripping of GSV, the nerve could be injured.
Short saphenous vein (SSV)

This vein starts lateral to tendoachilles behind the lateral malleolus, and runs in
the superficial plane at midline on the posterior aspect of the calf. At the
popliteal fossa it penetrates the deep facia to join the popliteal vein.
In 60% of the patients the sapheno-popliteal junction is located 5 cms
proximal to the popliteal crease. In 10–15% of the patients the SSV joins the
GSV through the Giacomini’s vein. There are perforator veins along the course
of the SSV draining into the deep veins.
The sural nerve runs along the SSV at the distal leg and hence is likely to be
injured during the stripping of the SSV.
Communicating veins
There are many veins which communicate between the great saphenous and
short saphenous veins.
Deep venous system

Deep venous system (Fig. 14.1B) consists of –
• Anterior tibial vein
• Posterior tibial vein
• Peroneal vein (paired)
FIGURE 14.1B Deep venous system of lower limb.
They join together to form the popliteal vein, which may also be double in
many cases. Soleal and gastrocnemius muscles are drained by tiny veins (Calf
veins), which are devoid of valves. They enter the tibial veins or the popliteal
vein.
• Popliteal vein continues as superficial femoral vein (SFV).
• Deep femoral vein (DFV) or profunda vein joins the SFV to form the
common femoral vein (CFV) at the femoral triangle.
• The common femoral vein runs up deep into the inguinal ligament and
continues as the external iliac vein (EIV).
• Internal iliac vein (IIV) joins the EIV to become the common iliac vein. The
left common iliac vein is crossed in front by the right common iliac artery
and may be partially compressed (May Thurner syndrome).
This could be a reason for DVT to be more common on the left side.
Perforators
These veins penetrate the deep fascia and join the superficial veins with the deep
veins. They have valves which allow blood to flow from the superficial to the
deep vein only. There are many perforators (Fig. 14.1C), but the constant named
ones are:
FIGURE 14.1C Perforating veins of lower limb.
At the ankle
• Medial (Cockett’s perforator I), lateral and anterior perforating veins.
At the lower leg
• Anterior and lateral perforating veins.
• Medial perforating veins–
• Posterior tibials (Cockett’s perforators II and III).
• Paratibials (Boyd – Sherman perforator).
• Posterior perforating veins –
• Intergemellary (May’s perforator).
• Achilles’ (Bassi’s perforator).
At the knee
• Popliteal fossa perforating vein.
At the thigh
• Medial thigh perforating veins (Hunter or Dodd’s perforator).
At the gluteal region
• Lower gluteal, midgluteal and superior gluteal perforating veins.
Upper limb
Veins of the upper limb also have a set of
• Superficial veins and
• Deep veins.
Superficial veins
The superficial veins of upper limb (Fig. 14.2) are:
• Cephalic vein and
• Basilic vein.
FIGURE 14.2 Superficial venous system of upper limb.
Cephalic vein starts at the anatomical snuff box and runs along the lateral
border of the forearm and enters the deltopectoral groove in the upper arm. It
drains into the axillary vein after piercing the clavipectoral fascia.
Basilic vein is formed on the ulnar side of the wrist and runs along the medial
side of the forearm. It pierces the deep fascia at the elbow and runs parallel to
the brachial artery, and joins the brachial vein at the anterior axillary fold to form
the axillary vein.
Deep veins
• Paired radial and ulnar veins join to form the brachial vein at the elbow.
• Basilic vein joins the brachial vein to form the axillary vein.
• Axillary vein crosses the costoclavicular space to become the subclavian
vein.
The vein can get compressed at this space leading to axillary subclavian
venous thrombosis (Effort vein thrombosis or Paget Shroetter syndrome).
14.2 venous haemodynamics
The direction of blood flow in the vein is always towards the heart and from the
superficial to the deep system. This is ensured by a series of valves in the veins,
which maintain the unidirectional flow. These valves contain two cusps, which
oppose and close the lumen if there is reversal of flow.
• Internal jugular vein, cerebral veins, veins of portal system, inferior vena cava
and common iliac veins do not have any valves.
• External iliac and the common femoral veins have a valve each.
• In about 70–80% of patients both sapheno-femoral and sapheno-popliteal
junctions are guarded by a valve.
• The deep veins distal to the sapheno femoral (SF) junction have many valves.
In the erect position the venous pressure in the leg is equivalent to the distance
from the right atrium to the foot (about 100–120 cm of H2O). During exercise,
the muscles squeeze the deep veins and empty them creating a low pressure so
that blood drains from the superficial vein to the deep vein (calf muscle pump).
Thus, the venous pressure is reduced by exercise if the valves are competent. If
the valves are incompetent, blood leaks from the deep to the superficial system
causing an increase in venous pressure.
14.3 diseases of venous system

Diseases of the venous system can be classified as:
1. Congenital vascular malformations
2. Arteriovenous fistula (acquired)
3. Infantile haemangioma
4. Venous thrombosis
5. Varicose veins
Congenital vascular malformations

Congenital vascular malformation is due to errors of embryonic development
that may affect any segment of the vascular tree, including arterial, venous,
capillary and lymphatic vessels. The embryonic vascular system consists of:
• a primitive capillary network (First stage), which coalesce into
• larger plexiform structure (Second stage). This later matures into
• veins, arteries and capillaries (Third stage).
Depending on the stage at which failure of development occurs, various
malformations manifest.
They are classified into five types:
1. Capillary malformation
2. Venous malformation (including dysplasias and cavernous venous
malformations)
3. Congenital arteriovenous malformation
4. Lymphatic malformation
5. Combined malformations – Slow flow anomalies Fast flow anomalies
Capillary malformation
• These are dermal vascular anomalies.
• Occur in 0.3% of newborns.
• Present at birth or appear within a year.
• Also known as ‘portwine stain’.
• They may be associated with other anomalies, like the Klippel Trenaunay
syndrome, Parkes Weber Syndrome and Sturge Weber syndrome.
• Deep purple patch blanching on compression (Ref Fig. 9.2A).
• There may be few surrounding dilated veins.
• They usually grow with the child and can become nodular, and may be
associated with soft tissue and bony hypertrophy.
• Capillary malformation may be a signal of underlying structural abnormality.
• MRI may be needed when other anomalies are suspected.
Treatment
• Treatment is difficult.
• Laser photocoagulation and cosmetic surgical correction have been tried
with variable results.
Venous malformation
• Cavernous venous malformations are the most common of all vascular
anomalies.
• Often mistakenly called cavernous haemangioma, which is inappropriate
because they are not tumours.
• They are composed of thin walled dilated sponge like abnormal venous
channels.
• Although present at birth, they may manifest later.
• They increase with age.
• They have a predilection for the trunk, palm and soles of the feet.
• They are also known to occur in the gastrointestinal (GI) tract.
• Symptoms depend on the site of involvement.
• May present as dilated venous channels in the subcutaneous, as well as deeper
planes (Fig. 14.3). They empty on elevation.
• Phleboliths may be palpable.
• Disfigurement, bleeding, painful phlebitis and painful movement of muscles
are common symptoms.
FIGURE 14.3 Venous malformation.
• MRI is the best modality to assess the true extent of involvement.
• Plain X ray will reveal phlebolith.
Treatment
• Sclerotherapy and excision in selected cases.
• Compression garments for extremities.
Congenital arteriovenous malformation (avm)

• Congenital AVMs may not be apparent at birth and remain dormant for years.
• Lower limb is most commonly involved, but involvement of upper limb, head
and neck are not infrequent.
• Hormone changes of puberty or local trauma seem to trigger expansion.
Complications
• Ulceration, bleeding and distal ischemia due to steal phenomenon, and high
output heart failure (rare in congenital AVM in contrast to acquired AV
Fistulas).
• May start as a pink patch in the skin with an underlying thrill or bruit (Fig.
14.4).
• They grow with the child and manifest with the classical symptoms of dilated
pulsatile veins, local warmth, gigantism and continuous murmur.
FIGURE 14.4 Congenital arteriovenous malformation of right hand.
• Plain X ray to look for bony erosion.
• CT or MR angiogram to delineate the true extent of the lesion and the
feeding vessels.
Treatment
• Treatment of congenital AVM is difficult.
• The indications for intervention are bleeding, ulceration, distal ischemia,
functional impairment, and heart failure due to shunting.
• Transcatheter embolization of the nidus and all feeding vessels is the
procedure of choice.
• Surgical excision is possible for some amenable lesions.
• Surgical ligation of feeding arteries away from the lesion should never be
done since the lesion will refill through collaterals and access for subsequent
embolization is lost forever.
Lymphatic malformation
• Traditionally called ‘cystic hygromas’ or ‘lymphangiomas’.
• They are localized or diffuse malformations of lymphatic channels presenting
as micro or macro cystic spaces or both.
• Most common in the axilla and cervico facial regions.
• Congenital lymphedema is due to aplasia or hypoplasia of lymphatics and
should also be included in the lymphatic malformation.
Complications
• Ulceration, bleeding and infection.
• Cystic translucent swelling, which can enlarge in the presence of infection
(Ref Fig. 12.13).
• Symptoms occur due to compression of the adjacent structures.
• CT is needed to assess the true extent.
Treatment
• Antibiotics are needed to control the infection.
• Sclerotherapy and surgical excision are needed to achieve cure, but
recurrences are common.
Combined malformation
Combined lesions contain both venous and arterial malformations with
overgrowth of soft tissue and bone. They are classified according to the flow
anomalies.
Slow flow anomalies

• Klippel Trenaunay syndrome (KT Syndrome) (Fig. 14.5) is a combined
capillary lymphatico venous anomaly associated with soft tissue and skeletal
hypertrophy.
• Capillary malformation is usually on the lateral side of the leg and thigh.
• Venous malformation has large venous channels devoid of valves; present
also on the lateral side draining into the profunda or the pelvic veins.
There are also deep vein anomalies.
• Lymphatic malformation is lymphatic hypoplasia leading to lymphedema.
FIGURE 14.5 Klippel Trenaunay syndrome.
• Symptoms and signs of thrombophlebitis and pulmonary embolism.
• Local gigantism and limb lengthening.
• Colour Doppler of venous system.
• MR venogram.
Treatment
• Conservative – compression stockings.
• Sclerotherapy, if needed.
• Excision of the abnormal veins can be done in selected cases.
Fast flow anomalies

Park Weber syndrome is almost similar to the KT Syndrome, but it has a
component of capillary AV fistula. The lesion is obvious at birth with limb
hypertrophy, pink warm stain with underlying bruit or thrill.
Acquired arterio venous fistula

• Result from penetrating injuries, either gunshot or stab wounds.
• Once a track forms between the artery and the vein, blood continues to flow
from the high pressure artery to the low pressure vein.
• The veins dilate and the high flow produces a turbulence causing the thrill and
the characteristic machinery murmur.
• Over a period of time the fistula enlarges and can become aneurysmal.
• Because of excessive shunting there is ‘steal’ of blood from the distal
circulation, causing distal ischemia.
• Increased venous return causes high output cardiac failure.
• This complication is more common in the proximal artery AV fistulas.
• Scar due to the penetrating trauma.
• Pulsatile swelling over the artery.
• Palpable thrill and bruit.
• Dilated pulsatile veins.
• Closure of the fistula by compressing the inflow artery leads to fall in the
pulse rate (Branham’s sign). This is because of the drop in the venous
return, which causes the peripheral resistance and arterial pressure to go up
leading to drop in the pulse rate. This sign is classically seen in the acquired
AV fistulas.
• An angiogram evaluates the fistula well.
Treatment
• Surgical disconnection of the artery and the vein, with repair of vein.
• Endovascular stent graft placement is the recent development.
• Management by quadruple ligation is now given up.
Infantile haemangioma
• A benign vascular neoplasm different from the congenital vascular
malformation.
• The differences are shown in Table 14.1.
• About 20% of them are at multiple sites.
• Infants with multiple tumours are likely to have tumours in the GIT and the
liver
• There are three stages in the natural history of infantile haemangiomas. They
are:
• In the first stage (Proliferative stage), i.e. in the first year of life, they
rapidly grow. They can become dangerous to life due to compression of
airway in the neck, cause massive enlargement of the liver or spleen with
congestive heart failure, or produce GI bleed depending on the site of
involvement.
• In the second stage, the growth slows down and is proportional to the
growth of the child.
• In the third stage, spontaneous involution occurs and can last for 1–7
years. During this stage the proliferative endothelium is replaced by loose
fibrofatty tissues.
• Most haemangiomas are small and they regress spontaneously without any
need for intervention.
TABLE 14.1
Differences Between Haemangioma and Vascular Malformation
Lesion
Property Haemangioma Vascular malformation
Nature Neoplasm Congenital anomaly
Appearance 30% present at birth, rest appear by 3 months All present at birth
Growth Rapid in first year of life Gradual
Sex incidence (female:male) 5:1 1:1
Pathology Endothelial proliferation cellular stroma Flat endothelium
Increased mast cells No mast cells
Involution Spontaneous by 7 years in 95% No involution
Soft tissue hypertrophy Rare Local gigantism
Complications
• Ulceration, bleeding, respiratory obstruction, proptosis, visual disturbance, GI
bleed and high output heart failure. Thrombocytopenia and bleeding occurs
due to platelet trapping in Kasabach Merritt Syndrome.
• Typically appear around the first or second week of life.
• Present as a pink macular stain, pale spot or a purplish ecchymotic patch (Fig.
14.6).
• They involve the dermis, and the skin looks elevated or bosselated.
• They are firm in consistency and cannot be compressed.
• They are most commonly located in the head and neck region (60%),
followed by trunk (25%) and extremities (15%).
FIGURE 14.6 Infantile haemangioma.
• CT or MRI is contributory.
Treatment
Options are many:
• Systemic corticosteroids, interferons, laser coagulation and intra-lesional
sclerosants.
• Angiogram and embolization.
• Surgical excision and plastic reconstruction.
Venous thrombosis
Both superficial and deep veins are prone to develop thrombosis. Thrombosis in
the superficial veins is usually associated with inflammation, and hence the
thrombus is adherent and less likely to cause pulmonary embolism as compared
to the deep vein thrombosis.
Superficial thrombophlebitis
• More common in the lower limbs.
• Usual causes are:
• Infection
• Varicose veins
• Malignancy
• Hormone therapy
• Direct injury
• Auto immune disorders
• Intravenous infusion
• Superficial phlebitis migrans is a spontaneous phlebitis at various sites. It is
typically seen in patients with Buerger’s disease, malignancy and connective
tissue disorder.
• Mondor’s Disease is a superficial phlebitis of the vein over the anterior chest
wall (Fig. 14.7) and the dorsal vein of penis.
FIGURE 14.7 Mondor’s disease.
Complications
• Deep vein thrombosis
• The overlying skin of the thrombosed vein is inflamed (Fig. 14.8).
• The vein feels like a cord.
FIGURE 14.8 Superficial thrombophlelbitis.
• No specific investigation is necessary.
Treatment
• Conservative involves rest, anti-inflammatory drugs and anti-platelet drugs;
rarely heparin is needed.
• Surgical disconnection of vein is needed for phlebitis of superficial veins
close to the junction with the deep system (saphenofemoral or
saphenopopliteal junction) in order to prevent the spread to the deep system.
• The infected thrombus and the vein are removed when abscess is formed and
causing septicemia.
Deep vein thrombosis (DVT)

• A serious life threatening condition as it can cause pulmonary embolism.
• The possible causes are:
• Venous stasis, hypercoagulable state and endothelial injury (Virchow’s
triad).
• Prolonged immobilization
• Surgery (pelvic and orthopaedic surgery)
• Sepsis
• Malignancy
• Medical condition needing intensive care
• Hormone intake
• Varicose veins
• Thrombophilia
• Post partum condition
• Usually more than one causative factor is operative to produce DVT.
• In majority of the patients the clot starts in the soleal plexus (calf veins) and
gradually spreads to involve the proximal veins.
• Left lower limb is more commonly involved than the right because of the
compression of the left common iliac vein by the right common iliac artery.
Complications
• Phlegmasia alba dolens, phlegmasia cerulea dolens and postphlebitic
syndrome.
• Low grade fever, leg swelling (Figs. 14. 8A and B) and pain are the common
symptoms.
• Calf muscle tenderness, pain on passive stretch of calf muscle (Homan’s
sign), tenderness over the deep vein and oedema are the diagnostic signs.
• High index of clinical suspicion is needed to diagnose DVT, especially in
postoperative patients where the classical signs and symptoms may not be
present.
FIGURE 14.8A Deep vein thrombosis of left leg.
FIGURE 14.8B Left iliofemoral DVT.
DD: Calf muscle tear, ruptured Baker’s cyst and cellulitis.
• Duplex scan can show the thrombus and its proximal extent.
Treatment
• Bedrest, elevation and adequate heparinization, and low molecular weight
heparins.
• Compression stockings are used once the signs of inflammation have
subsided. It helps in recanalization.
Note
Oral anticoagulation is to be continued for at least 6 months to avoid
recurrence.
Phlegmasia alba dolens (white leg)

This is a complication of the Ilio femoral DVT. The entire lower limb is swollen,
tense and is pale in colour. This is because of spasm of the artery and associated
lymphatic occlusion leading to increased oedema and pallor.
Phlegmasia cerulea dolens (blue leg, venous gangrene)
• Occurs due to extensive ilio femoral DVT with occlusion of even the pelvic
veins.
• Since all the venous outflows are blocked, the interstitial tissue pressure
becomes higher than the capillary pressure and the arterial flow stops.
• Severe bursting pain of the entire limb.
• On examination, the limb becomes tense and cyanosed (Fig. 14.9).
• Soon gangrene sets in and spreads to the level where there is still arterial flow.
FIGURE 14.9 Phlegmacia cerulea dolens.
Treatment
• Treatment for this condition is an emergency, as the patient is in shock due to
massive sequestration of fluid and blood in the lower limb.
• Adequate fluid replacement is needed.
• Open venous thrombectomy or catheter directed thrombolyic therapy may
be required to decompress the veins.
• Fasciotomy also will be needed to reduce compartment pressure.
• Anticoagulation has to be continued for at least 6 months.
Post phlebitic syndrome

• Sequel of deep vein thrombosis.
• Late complication appearing after 3–5 years.
• Occurs due to incomplete lysis of clot with unrelieved obstruction or
destruction of valve with incompetence of the deep vein.
• Venous claudication, itching, pigmentation and painful ulceration.
• Clinical examination reveals varicose veins with perforator blowouts,
lipodermatosclerosis, stasis eczema and ulcer (Figs. 14.9A and B).
FIGURE 14.9A Post phlebitic leg.
FIGURE 14.9B Post phlebitic legs.
• Duplex scan and venography are confirmatory.
Treatment
• Treatment is very difficult.
• Conservative–Proper wound care, multilayered bandaging, graded
compression stockings and intermittent elevation of leg.
• Surgical –
• Flush ligation, varicose vein stripping, perforator ligation, sclerotherapy
and split skin grafting are available methods.
• Surgery for deep veins also can be done in selected cases.
Note
High incidence of recurrence of ulceration is known.
Axillary vein thrombosis (paget shroetter syndrome, effort

vein thrombosis)
Occurs
• After excessive use of upper limb.
• As a part of the thoracic outlet syndrome due to compression at the costo
clavicular space
• After central venous cannulation
• Typically it occurs in a young or middle-aged male
Complication: Pulmonary embolism (rare)
• Arm swells up suddenly and becomes painful (Fig. 14.10).
• Superficial veins of the arm and the upper chest become prominent.
FIGURE 14.10 Thrombosis of right axillary vein.
• Duplex scan is confirmatory.
Treatment
• Medical–Anti coagulation or thrombolytic therapy.
• Surgical–First rib resection is useful in patients with costoclavicular
compression.
• Lytic therapy with endovascular stenting of the vein is useful in select cases.
Varicose veins
Veins, which become dilated, tortuous, elongated and thin walled due to valvular
incompetence are called ‘varicose veins’.
• Extremely common.
• Nearly 25% of the population suffers from some form of venous disease.
• The risk factors are–
• Age–Incidence increases with age. Nearly 70% of adults over the age of 70
suffer from telangiectesia or varicosities.
• Heredity–Varicose veins are familial. There is no genetic susceptibility, but
if both the parents have varicose veins the chances of developing
varicosities is 80%.
• Gender–More common in women.
• Pregnancy–Multiple pregnancies increase the chances of developing
varicosities due to the effect of hormones on the vein wall and
compression on the iliac vein by the growing foetus.
• Height–Taller persons are more prone to develop varicose veins.
• Lifestyle–Sedentary life makes the calf muscles and the muscle pump
weak, promoting venous stasis and dilatation. Similarly, those who stand
for long hours are also prone to develop varicose veins.
• Exact cause of valvular incompetence is not known, but congenital and
environmental factors have been suggested.
• Varicose veins are of two varieties:
• Primary varicose veins (without any identifiable cause); and
• Secondary varicose veins (mostly due to deep vein thrombosis,
arteriovenous fistula, incompetence of the saphenofemoral valve or
sapheno popliteal valve or perforator valve or a combination of these, and
primary deep vein valve incompetence).
Complications
• Bleeding, superficial thrombophlebitis, pigmentation, eczema, itching and
painful ulceration.
Symptoms
• Many remain asymptomatic.
• Aching, discomfort or restless legs, especially during the end of the day,
dependent oedema and calf cramps at night are the common symptoms.
• Symptoms become more pronounced after the onset of complications.
Signs
• Dilated and tortuous veins of the lower limbs (Figs. 14.11A and B).
• Recurrent ulceration and fibrosis are known to produce varus deformity of the
foot.
• Detailed clinical examination can reveal the system involved and the status of
the deep veins. Various clinical tests have been described for evaluation (Ref
page 176).

FIGURE 14.11 Varicose veins—(A) Great saphenous system. (B) Short
saphenous system.
• Duplex Doppler study is informative. This test can show the anatomy of the
veins, confirm valve reflux, study the deep veins and rule out deep vein
thrombosis.
Treatment
• Conservative treatment involves
• graded compression stockings and intermittent elevation of the legs for
uncomplicated and asymptomatic varicose veins.
• Surgical
• Flush ligation, stripping of the vein and multiple ligation and excision of
varicosities are the procedures for symptomatic primary varicose veins
involving superficial veins
• Endovenous laser coagulation and radiofrequency ablation of the
saphenous vein are becoming popular.
• Perforator ligations by open surgery or by endoscopic method (Subfascial
endoscopic perforator surgery - SEPS) are for perforator incompetence.
• Sclerotherapy is useful for recurrent or residual veins.
Venous ulcer
• Extremely common.
• Nearly 60–70% of all ulcers in the leg are due to venous causes.
• Upto 1.5% of adults suffer from a venous ulcer at some point in their life.
• Various theories have been put forward for the development of venous ulcers
–
• Valvular incompetence causes venous hypertension, which causes damage
to the capillaries and protein leaks through the pores. The leaked fibrin
forms a cuff around the capillary, preventing oxygen diffusion leading to
ischemia and ulceration (Fibrin cuff theory of Browse).
• Trapping of white cells and release of free radicals lead to capillary damage
(White cell trapping theory).
• Majority of the patients with venous ulcer have perforator incompetence.
• Only 17% of the patients have isolated superficial vein incompetence. Nearly
50% of them show evidence of old DVT on investigations.
• Ulcer in the perimalleolar or gaiter area and rarely on the dorsum (Fig. 14.12).
• Onset is spontaneous or after a trivial injury or skin infection.
• They are painful.
• On examination,
• Chronic ulcers have fibrotic edges (due to protein causing characteristic
lipodermatosclerosis).
• The ulcer base is made of healthy granulation.
• Surrounding skin shows pigmentation and dermatitis [due to haemosiderin
from the leaked red blood cells (RBCs)].
FIGURE 14.12 Varicose veins with ulcer.
• Duplex Doppler and contrast venogram are useful in delineating the deep
veins and identifying the perforator incompetence.
Treatment
• Conservative–Rest, elevation of the leg, wound care and compression
bandages. But once the patient resumes normal activities it quickly recurs.
• Surgical treatment of the underlying cause for the venous hypertension is
needed.
• Stripping and multiple ligations are done for superficial vein
incompetence.
• Subfascial ligation or by SEPS for perforator incompetence.
• Valve repair or vein transplant are useful for deep vein incompetence, but
it is difficult to manage.
Note
In spite of best treatment, recurrence is common.
14.4 symptoms of pathologies of venous

system
• Pain in the limb
• Swelling of limb
• Itching, pigmentation and stasis dermatitis
• Ulceration
• Bleeding
Pain in the limb
• Acute pain: The pain is acute and bursting and involves the entire limb in
DVT, and becomes severe while walking and stretching the calf muscle. The
pain may extend along the course of the vein. Deep vein thrombosis of the
inferior vena cava will produce pain in the back and iliac fossa. The pain can
be acute in superficial phlebitis.
• Aching type of pain: The pain of this nature is felt in the leg and foot, mostly
on standing for long hours or towards the end of the day, and is common
with varicose veins. The pain is relieved by rest or limb elevation.
• Crampy pain: Muscle cramps, especially at night may occur in varicose
veins.
• Burning pain: Those who have venous ulcers have severe burning type of
pain. This pain is localized to the gaiter area and gets worse on standing.
Pain may sometime precede ulcer development.
• Localized pain: The pain is localized to an area of the limb when there is
phlebitis, and the vein gets engorged.
• Venous claudication: Pain and swelling of the limb on walking in some
patients with DVT.
Swelling of limb
The swelling of the limb can be generalized or localized.
Generalized swelling
• Generalized swellings of lower limbs are caused by oedema and the causes
are:
• Both lower limbs–bilateral pedal oedema of cardiac, hepatic or renal
pathology.
• One lower limb–filariasis, local infective pathology like abscess, and DVT.
• Gigantism–large arterio-venous malformations.
Oedema
• Oedema occurring by the end of the day or after prolonged standing is
common in varicose veins. This type of oedema is relieved by limb elevation
or in the mornings.
• Sudden onset oedema of a limb should alert one to the possibility of DVT,
but pain is usually present.
• Oedema has regional distribution –
• In popliteal and superficial femoral vein thrombosis, the leg and foot are
swollen.
• In calf vein thrombosis, calf alone is swollen.
• In ileofemoral thrombosis, oedema extends upto the thigh.
• When pelvic veins are thrombosed, the genitals are also oedematous.
Note
Generalized swellings of the limb reduce on elevation in venous and
lymphatic pathologies.
Localized swelling
• Localized varicosities
• Abscesses
• Arteriovenous malformations
• Haemangiomas
Itching, pigmentation and stasis dermatitis

These symptoms are common in long standing varicose veins and in post
phlebitic legs.
Ulceration
• Ulceration can occur after a trivial trauma or even spontaneously.
• Ulcers are very painful.
• Ulcers heal with rest and recur quickly after resuming work.
Bleeding
Bleeding occurs spontaneously, probably due to trivial trauma, and occurs
without any pain. It stops only by compression and elevation of the limb.
Eliciting history
• Age
• At birth (e.g. Congenital vascular malformations like portwine stain)
• Neonatal period (e.g. Congenital haemangiomas)
• Childhood (e.g. Congenital arteriovenous fistulas)
• Middle age (e.g. Varicose veins)
• Occupation–Prolonged standing has been considered a possible cause for the
onset of varicose veins. They are more common in policemen
Pain in the limb

• Site of pain: In which part of the limb does the patient complain of pain?
Pain may be present in some localized area (e.g. superficial thrombophlebitis),
or may be in the whole limb (e.g. deep vein thrombosis).
duration may indicate acute pathology (e.g. acute thrombophlebitis and deep
vein thrombosis) and long duration (e.g. chronic deep vein thrombosis).
• History of trauma: Is there a preceding history of trauma?
Nature of trauma and its severity will indicate the pathology (e.g. muscle
ruptures, sprains and fractures).
• Precipitating factors: Does the pain become severe on walking or standing
Walking can aggravate ischaemic pain of the lower limb (e.g. claudication
pain), and standing for a longtime may precipitate pain of venous origin (e.g.
varicose veins). Exercise relieves pain of venous origin due to venous return of
blood. In DVT, pain will be aggravated by walking.
the relief the patient had with the intake of drugs.
Swelling of limb
If a swelling is present in the limb, it should be evaluated in line with any
swelling in general (see Ch. 9), and the questions are directed towards its
evaluation.
Ulcer on the lower limb

If an ulcer is present in the limb, it should be evaluated in line with any ulcer in
general (see Ch. 11), and the questions are directed towards its evaluation, some
of them are given below:
• Duration of ulcer: For how long has the ulcer been present?
those of longer duration are due to repetitive trauma, uncorrected venous stasis,
etc.
Ulcer on the medial or lateral aspect of ankle is more due to varicose ulcer.
Trophic ulcers occur at pressure points, and ischemic ulcers occur at the terminal
part of the toes, where the vascularity is the minimum.
Trophic ulcers are painless, and acute ischemic ulcers are painful. Infection is
the common cause of pain in the ulcer. Venous ulcers are also painful.
Applications of strong chemicals and native medicines can delay healing. A
detailed history regarding the treatment taken will give an idea about the
chronicity of the ulcer.
Itching, pigmentation and bleeding

• Itching, pigmentation and bleeding: Is there any symptom like itching or
bleeding from any part of the limb?
Itching is one of the predominant symptoms of venous stasis, and is caused
due to the seepage of proteinaceous matter in the subcutaneous tissue. Repeated
itching episodes may lead to oozing of blood and a resultant change in the colour
of the skin. Break in the integrity of the skin due to repeated itching can cause an
ulcer, which may refuse to heal.

Association of high grade fever may indicate infective pathology, like
cellulitis of foot and thrombophebitis.
Loss of appetite and weight are indicative of illnesses like malignancies (e.g.
intra-abdominal lumps producing venous obstruction and pedal oedema).
a clearer picture of diagnosis (e.g. recurrence of DVT, and recurrence of
retroperitoneal malignancies).
treatment?
If the patient had suffered a similar illness in the past and was successfully
treated, it will indicate the examiner to reconsider the diagnosis, like recurrence
of DVT.
• Personal history:
Did the patient have any difficulties during pregnancy?
Women should be asked about the obstetric history, white leg, etc.
Diseases like varicose veins can occur in families and the positive history may
be a good indicator for the present diagnosis. Deep vein thrombosis in other
members of the family suggests an underlying hypercoagulable state.
match the situation, like consumption of drugs such as oral contraceptives
(e.g. DVT). Questions like the presence of chest pain, breathlessness and
haemoptysis may indicate pulmonary embolism, a complication of DVT.
Long distance travel in a sitting posture is a known cause of DVT.
Venous system
• Patient should be undressed upto the costal margins (abdomen and lower
limbs exposed).
• Adequate knowledge and orientation of the limb and its anatomy is
mandatory.
In general, the patient should be examined in the following position:
• Standing: Patient is requested to stand evenly on a flat surface and both feet
are examined from the front, back and sides and compared.
Physical examination consists of two parts:
• Inspection
• Palpation
Inspection
Skin
• Texture of skin – Dry scaly skin (e.g. stasis dermatitis).
• Colour of skin
• Reddish colour (e.g. Cellulitis)
• Red streaks (e.g. lymphangitis and phlebitis).
• Dark colour–Cyanosis (iliofemoral DVT; may be a sign of phlegmasia
cerulia dolens).
• Gangrene–Warm oedematous limb with absent pulses and distal gangrene
is more suggestive of venous gangrene (arterial gangrene is associated
with cold limb with guttering of veins, and oedema occurs late).
• Scratch marks–Feature of venous stasis.
Swelling
• Generalized swelling
• One foot (e.g. filariasis, cellulitis, and post operative).
• Both feet (e.g. medical conditions).
• Localized swelling (e.g. incompetent perforators, and oedema at malleolar
level).
Ankle flare is more common in venous hypertension.
• Erythematous lesions (e.g. telangiectasia or spider veins).
• Prominent dilated tortuous veins [e.g. varicosities–longstanding DVT gives
rise to secondary varicosities; abdominal varicosities indicate Inferior Vena
Caval (IVC) thrombosis and pubic collaterals indicate iliofemoral DVT].
Note
The presence of varicosities at abnormal sites may indicate secondary
varicose veins and congenital anomalies (e.g. large venous channel on the
lateral aspect of leg and thigh along with capillary venous malformation and
pigmentation may be a part of Klippel Trenaunay syndrome).
Ulcers
• Site of the ulcer–ulcers on medial aspect of ankle (e.g. varicose ulcer of GSV)
and lateral aspect (varicose ulcer of SSV) can also occur on the dorsum.
• The ulcer is examined in lines with general ulcers (see Ch. 10).
Palpation
1. Temperature and site of maximum tenderness.
2. Foot arterial pulsations.
3. Venous and nail bed filling.
4. Induration in the base of ulcers.
5. Assess the degree of sensation (touch, pain and joint and position sense).
A swelling in the limb is described in line with any swelling in general (see
Ch. 9).
• If there is oedema, it should be determined whether it is pitting (e.g. early
stages) or non-pitting (e.g. chronic stages).
• Palpation of vein–It is done along its entire length. It is usually soft and
compressible. Even when there is oedema, the veins are not visible, but they
can be felt.
• Palpate for
- Thickening or indurated mass (e.g. phlebolith or thrombus).
- Tenderness over the vein (vein is tender in phlebitis; tenderness over the
popliteal vein or femoral vein is a classical feature of DVT).
• Calf muscle tenderness–This can be elicited by–
• Squeezing the calf muscle (e.g. DVT).
• Dorsiflexing the foot to cause stretching of calf muscle.
Pain in the calf indicates positive Homan’s sign (Due to the stretching of the
inflamed thrombosed vein, and other inflammatory conditions).
Lymphatic system
Lymph from the lateral aspect of the foot and fourth and fifth toes drain to the
popliteal nodes, while the foot predominantly drains to the inguinal vertical
chain. The examiner should remember to examine the above lymph nodes,
especially when there is an ulcer in the leg.
General
Detailed general examination is essential to rule out limb changes due to cardiac,
renal, hepatic and neurological diseases.
Abdomen
Abdomen should be examined for any lump which may be causing pressure over
the venous system causing varicose veins in the lower limbs.
14.6 special tests
Tests for saphenofemoral incompetence

Cough impulse test (morrissey’s sign)
A finger is kept over the saphenofemoral junction or over the varicosity in the
thigh and the patient is asked to cough. If the saphenofemoral valve is
incompetent, an impulse is felt by the examining finger. If there is gross reflux
and dilatation of the vein, the impulse can also be seen (Fig. 14.13).
FIGURE 14.13 Morrissey’s sign.
Brodie trendelenberg’s test for saphenofemoral

incompetence
• Step 1: The patient is asked to lie down and the vein emptied by limb
elevation (Fig. 14.14A).
• Step 2: A tourniquet is tied just distal to the saphenofemoral opening and the
patient is asked to stand (Fig. 14.14B)
• Step 3: The tourniquet is released and the venous filling is observed (Fig.
14.14C).
FIGURE 14.14A Brodie Trendelenburg test (Step 1).
FIGURE 14.14B Brodie Trendelenburg test (Step 2).
FIGURE 14.14C Brodie Trendelenburg test (Step 3).
Inference
• If the vein rapidly fills from the top it indicates sapheno femoral
incompetence.
Note
The first step to check for sapheno-popliteal incompetence can be done also
by tying the tourniquet distal to the saphenopopliteal junction. Care must be
taken to block the great saphenous vein since reflux in that vein may be
transmitted to the short saphenous vein through the communicating veins
between the two.
Test for incompetence of valves in the vein
Schwartz test (percussion or tap sign)
With the patient standing, the fingers of one hand are placed over the
saphenofemoral opening and the varicosity at ankle is tapped with the fingers of
the other.
Inference: The test is considered positive when the impulse is felt by the
fingers, if the valves in the vein are incompetent, and the tap impulse is
transmitted by the uninterrupted column of blood. The same test can be repeated
by tapping at the saphenofemoral opening and the impulse can be felt at the
ankle (Fig. 14.15).
FIGURE 14.15 Schwartz test.
Tests for perforator incompetence

Brodie trendelenberg’s test for perforator incompetence
• Step 1: The patient is asked to lie down and the vein emptied by limb
elevation (Fig. 14.16A), and a tourniquet is tied just distal to the
saphenofemoral opening.
• Step 2: The patient is asked to stand. The tourniquet is not released and the
venous filling is observed (Fig. 14.16B)
FIGURE 14.16A Brodie Trendelenburg test for perforator incompetence
(Step 1).
FIGURE 14.16B Brodie Trendelenburg test for perforator incompetence
(Step 2).
Inference
• If the vein fills slowly from the distal leg, it indicates presence of perforator
incompetence.
Multiple tourniquets test

• Step 1: The patient is asked to lie down and the veins are emptied by limb
elevation (Fig. 14.17A).
• Step 2: A tourniquet is tied just distal to the saphenofemoral junction and
others at lower thigh, upper and lower leg levels (Fig. 14.17B).
• Step 3: The patient is asked to stand and the venous filling is noted (Fig.
14.17C).
FIGURE 14.17A Multiple tourniquets test (Step 1).

FIGURE 14.17C Multiple tourniquets test (Step 3).
FIGURE 14.17B Multiple tourniquets test (Step 2).
Inference
• If a segment of vein between two tourniquets fills up, it indicates
incompetence of a perforator or perforators in that particular segment. The
test can be repeated by bringing the tourniquets closer in that segment and
localizing the perforator level exactly.
Fegan’s test
Perforators go through a defect in the deep fascia. This fascial defect becomes
big when the perforator dilates due to incompetence. This defect in the deep
fascia can be felt when the finger is run along the dilated varicosities.
Pratt’s test
This is another test to know the position of the perforator. The veins are emptied
and a tourniquet is applied just distal to the saphenofemoral junction to prevent
reflux. A compression bandage is applied from groin to ankle and the patient is
made to stand. The compression bandage is gradually released from the ankle
and the venous refilling is observed.
Inference
• When the vein fills as the bandage is released, it must be from the
incompetent perforator just below the level of release of bandage.
Test for patency of deep veins

Perthe’s test
A tourniquet is tied at the upper thigh to block the saphenous vein and the patient
is asked to walk. If the deep veins are occluded, the patient complaints of a
bursting type of pain along with tightness in the leg. The superficial vein
becomes prominent.
CHAPTER 15
Burns
R. Ravi, V. Jayaraman
CHAPTER OUTLINE
15.1. Definitions 180
15.2. Anatomy of skin 180
15.3. Pathophysiology of burns 181
15.4. Classification of burns 181
15.5. Metabolic effects of burns 182
• Burnt area 186
• General 187
• Systemic examination 187
15.1 Definitions
Burns is defined as the damage to the skin by coagulation necrosis caused by
heat, cold, electricity, radiation and chemicals.
• Thermal burns–Heat denatures cellular proteins by coagulation necrosis. The
damage is directly related to the intensity of heat and the duration of contact
of the incriminating agent. Usually the damage is partial thickness or full
thickness.
• Electrical burns–Electricity (high and low voltage) causes deep tissue
destruction, both at the point of entry and at the point of exit. Muscle tissue
destruction is an integral part, but it cannot be assessed accurately in the
initial stages.
• Radiation burns–Radiation causes full thickness dermal injury due to the
deep penetration of ionizing radiation.
• Chemical burns–Chemicals cause cell necrosis and the damage depends on
the concentration of the chemical and the duration of contact with the skin.
The damage ceases only when the agent is chemically expended, and
majority of the times the damage is full thickness.
FIGURE 15.7 Infected burns wound. Source: (Courtesy Dr K. Sridhar).

FIGURE 15.8 Keloid formation after burns Source: (Courtesy Dr K. Sridhar).
FIGURE 15.9 Post burn contracture of neck ( Source: Courtesy Dr K. Sridhar).
FIGURE 15.10A Post burn contractures Source: (Courtesy Dr K. Sridhar).
FIGURE 15.10B Post burn scarring resulting in syndactyly Source: (Courtesy
Dr K. Sridhar).
FIGURE 15.10C Post burns scarring resulting in disability Source: (Courtesy
Dr K. Sridhar).
FIGURE 15.10D Post burns contracture of axillary folds Source: (Courtesy Dr
K. Sridhar).
15.2 Anatomy of skin
The skin is the largest organ of the body and covers a wide area, 0.25 sq. m in
newborns and 1.25 sq. m in adults. It varies in thickness at various places, and is
the thickest on the palms, soles and back. It is thinnest on the glans penis and the
eyelids.
It protects the body and transmits information from the environment to the
nervous system. The skin plays a large role in immunity, and the immune cells in
the skin alert the body to antigens invading the skin. The skin consists of
1. Epidermis
2. Basement membrane
3. Dermis
4. Subcutaneous fat
Epidermis, the uppermost layer of skin replaces itself every four weeks, and
the predominant cells being keratinocytes. The epidermis consists of four layers
of cells (Table 15.1). They are:
1. Stratum corneum–Cornified envelope (outermost layer)
2. Stratum granulosum–Granular layer
3. Stratum spinosum–Spinous layer
4. Stratum basale–Basal layer (innermost layer)
TABLE 15.1
Layers of Epidermis and Their Functions
Layer of Skin Components Function
Epidermis Stratum corneum Keratinocytes Holds moisture within skin and protects cells
Stratum Cells develop keratohyalin granules and lamellar bodies for joining the
granulosum next layer
Stratum Attach one cell to another (by desmosomes), and control growth and
spinosum migration of cells
Stratum basale Form keratinocytes and are displaced upwards towards the skin surface
In addition to keratinocytes, the cells of the epidermis are –

• Melanocytes – responsible for pigmentation of skin and hair, which
proliferate in response to ultraviolet light and produce melanin in packets
called ‘melanosome’s;
• Langerhans cells–dendritic cells that take an active role in immunity; and
• Merkel’s cells–slow growing touch receptors associated with sensory nerves.
Basement membrane separates the epidermis and dermis, but anchors them
with a collagen called ‘Laminin 5’. Other collagens are of the types IV and VII.
Dermis can be separated into upper (papillary) dermis and the lower (reticular
dermis). The dermis consists of connective tissue (collagen – types I and III and
elastic fibres), cells and ‘ground substance’, which fills spaces between the
connective tissue and cells. The predominant cells are fibroblasts. Mast cells and
lymphocytes are also found in the dermis. Other cells found in the dermis are
endothelial cells, veil cells and pericytes, Schwann’s cells, monocytes,
macrophages, and dermal dendritic cells. Specialized structures of the dermis
are: hair follicles, sebaceous glands, and sweat (epocrine and accrine) glands.
The anatomy of the skin is shown in Fig. 15.1.
FIGURE 15.1 Structure of skin.
15.3 Pathophysiology of burns
Jackson postulated three concentric areas of tissue damage –
1. Area of hyperaemia;
2. Zone of stasis; and
3. Zone of coagulation.
Severe burn injuries produce venous stasis, microthrombi formation and
vascular endothelial sloughing. As the viscosity of the blood changes, white cells
marginate and red cell rouleaux formation occurs, creating a physical barrier
which compromises oxygen, antibody and phagocytic delivery to the burned and
live tissue inter-phase.
In acute phase reaction and the process of inflammation, venous circulation
gets compromised in the zone of stasis. Neutrophils adhere to the vessel wall and
platelet adherence occurs. Microthrombi formation occurs in the capillaries,
which occlude microcirculation, and furthers cell death. Chemical mediators
released from the polymorphonuclear (PMN) leucocytes are responsible for the
development of typical inflammatory response. The localized response, the
inflammation, is accompanied by a large number of systemic and metabolic
changes, which are collectively referred to as ‘acute phase response’. This acute
phase response is characterised by a set of hepatic disturbances, which include
marked variation in the concentration of some plasma proteins. Oedema
formation that is seen in acute burns is mainly due to the effect on the vascular
compartment by the acute phase proteins.
15.4 Classification of burns
The burn wounds are classified into four degrees, as given in Table 15.2. The
clinical photographs are shown in figures 15.2 to 15.6.
FIGURE 15.2 Superficial burns.

FIGURE 15.3 Mixed second and third degree burns.
FIGURE 15.4 Deep burns of the forearm.
FIGURE 15.5 Acid burns of the face Source: (Courtesy Dr K Sridhar).
FIGURE 15.6 Thermal burns caused by direct heat Source: (Courtesy Dr S
Devaji Rao)
TABLE 15.2
Classification of Burn Wounds and Their Clinical Features
Clinical Presentation Tests

Layer of Skin
Degree of Burn
Involved Capillary
Pain Colour Blisters Touch Pressure
filling
First degree Epidermis Severe Erythema Absent Present Present Present

(superficial)
Second degree Superficial Severe Erythema/Pallor Present Present Present Present
(partial (superficial
thickness) dermis)
Deep (deep reticular Moderate Pallor Usually Absent Present Present
dermis) absent
Third degree burn Epidermis and Absent Pallor Absent Absent Absent Absent
(Full thickness) Dermis
Fourth degree burns Skin and Absent Pallor Absent Absent Absent Absent
subcutaneous
structures
Note
In any patient of burn injury, a combination of degrees occurs. This is
important while treating a patient of burns, and repeated assessment and
scrutiny of the wounds is necessary.
The depth of burns varies depending on the incriminating agent and its
duration of contact with the skin (Table 15.3).
TABLE 15.3
Burns Based on Its Aetiology
Agent Exposure Time Depth of Burns Appearance Pain
Hot liquids Short exposure Superficial dermal Wet, pink, blisters Severe
Long exposure Deep dermal Wet, red, dark Minimal
Flame Flash exposure Partial thickness Wet pink blisters Severe
Direct contact Full thickness Dry, white, waxy or brown, black leathery Minimal
Chemicals Direct contact Full thickness Light brown to light grey Severe
15.5 Metabolic effects of burns

Burn injuries cause severe damage to the body structures and its metabolism.
They are shown in Table 15.4.
TABLE 15.4
Metabolic Disturbances Associated with Burns
Category Period Clinical Condition Reason Clinical Presentation
General Immediate Hypovolemic Extracellular Tachycardia, tachypnoea, hypotension, pre-renal

effects shock accumulation of uremia, oliguria
water and
excessive
evapouration
from burnt area
Hemoconcentration Loss of water and
plasma from burnt
area
Dehydration Excessive
evapouration of
water from burnt
area
Electrolyte Retention of sodium Altered sensorium, uremia, oliguria
imbalance and excessive
excretion of
potassium
Asphyxia and Due to burn of Difficulty in breathing
cyanosis respiratory
passages
Late Septicemia (Multi Systemic spread of High grade fever, tachycardia, tachypnoea,
organ failure) infection hypotension oliguria, death
Acute renal failure Fluid loss and Altered sensorium, uremia, oliguria or anuria
electrolyte
imbalance
Stress ulcers Reason not known Haematemesis and melena
Local Immediate Tissue damage Direct injury of cells Extensive wounds
effects
Oedema Excessive Swollen areas surrounding or below the burnt
accumulation of areas
fluid in the
extracellular
spaces
Water and Excessive loss from Large dry wounds
electrolyte loss the burnt area
from large
wounds
Local sepsis Bacterial growth on Purulent discharge or slough formation
the burnt area (Fig.15.7), fever with rigors
Late Delayed healing Inadequate and Chronic wound with unhealthy granulation
improper
treatment,
diabetes mellitus
Keloid formation Severe scarring Elevated thick irregular skin lesion (Fig. 15.8)
Marjolin’s ulcer Low grade A very slow growing painless ulcer, on the scar
epidermoid without lymphatic spread., resembling
carcinoma arising squamous cell carcinoma, but the edge is not
from the raised and floor does not contain florid
epithelium granulation tissue (Ref Fig. 10.9)
covering the scar
tissue after burns
Contractures Fibrosis of burnt Contracted areas with restricted mobility (Fig.
areas around 15.9)
neck, joints
Disability Pain and restricted Extensive fibrotic tissues resulting in debility
mobility due to (Figs. 15.10A to D)
contractures
Strictures of Annular healing by Dysphagia, if oesophagus is involved and
tubular organs fibrosis of tubular dyspnoea, if trachea is involved
structures
Eliciting history
The patient may be brought to the casualty in various stages, varying from a
normal looking person with small patchy areas of burns to in a state of shock
with varying grades of consciousness. Hence, the history taking should be
precise and rational, and the examination quick. The resuscitative measures
should be started immediately, as the situation can take a turn to the worse in a
very short time.
The patient’s attendants (who were at the scene) may be requested to narrate
the entire incident in detail in their own words. Further, leading questions are
required to complete the history taking, for exact evaluation.
• Cause of burns: What is the incriminating agent of burns? How long was
the agent in contact with the patient?
Burns can be caused by different agents, commonly heat, cold, electricity,
radiation or chemicals, and each has its own effect in the morbidity of the
patient. The duration of contact of the agent with the skin is important, as
longer the contact, larger the damage.
• Time and place of incident: When and where did the incident occur?
This will answer the time duration since the incident. In a case of burns, time
of commencement of treatment is very important, as it should be given at the
earliest, to avoid complications. Location of the incident gives the
information, such as usually at the workspot, like furnace, is accidental.
• Patient’s activity: What was the patient doing at the time of incident?
It is important to know the patient’s activity at the time of incident (e.g.
cooking, working in a furnace, etc.), as it may also, to certain extent, indicate
whether it is accidental, suicidal or homicidal. It is also better to know
whether the patient was standing, working at a height, sitting or sleeping
during the incident, as there may be associated injuries, like fractures due to
a fall, in a standing person. Panic reaction leads to more injuries, including
head injuries due to a fall from a height, especially in electrical burns.
• Patient’s clothes: What type of clothes was the patient wearing during the
incident?
The type of clothes the patient was wearing during the incident is important,
as synthetic materials tend to stick to the skin and create more damage to the
skin.
• Type of incident: Is it accidental or otherwise?
It is important to know whether it is accidental or otherwise, like suicidal or
homicidal. Accidental injuries are relatively lesser in intensity as there is
always an attempt to extinguish the fire either by the victim or by the
relatives and neighbours, whereas, in other varieties, the victim or the
relatives refuse to co-operate to extinguish, as the intent is motivated. Hence
the damage is more.
• Initial treatment: Was any first-aid given?
Many times, first aid is administered by relatives or neighbours, but it may
not be the right one. Misunderstood methods like applying ink or coffee
powder may only complicate the situation and the surgeon finds it difficult to
treat such patients.
• Association of pain: Has the patient been having pain at the site of burns?
Association of pain is generally seen in all patients of burns, especially of the
superficial variety. Since all degrees of burns are present in one patient at one
time, pain may not be an indicator of intensity of burns, but administration of
analgesics is an important step in the management.
• Association of fever: Has the patient been having fever after the incident?
Association of fever with or without chills is an indicator of associated
infection. More the time taken to present to the doctor, more is the incidence
of infections.
• Past history: Is there any similar incident in the past?
Some patients attempt to burn themselves repeatedly, due to constant family
problems. An unsuccessful attempt in the past may motivate the person for
another attempt. The intensity of such incidents is severe as the victim does
not want this attempt also to fail. A careless epileptic may sustain burn
injuries repeatedly.
• History of drug intake and allergies: Is the patient on a prolonged drug
intake? Is the patient allergic to any drug?
Patients may be on prolonged drug intake for epilepsy or diabetes, as these
medications have to be continued during treatment. Epileptic patients are
prone to accidental burn injuries when working close to a fire. Knowledge of
drug allergies will help in the administration of drugs, especially antibiotics.
• Social and personal history: Has the patient been consuming alcohol?
Patients consuming alcohol may have associated psychological problems,
like depression and have suicidal tendencies.
• Family history: Is there any history of family problems like quarrels?
Family quarrels and domestic problems predispose to suicidal and homicidal
burns. Such injuries tend to be severe as the intent is motivated.
• Any other relevant history: (in women): Is the patient pregnant?
Pregnant women require special care, including medication.
Clinical examination of a patient of burns should be done quickly, but in detail.
Preliminaries before examination
• The patient should be weighed using a trolley weighing machine
(determination of weight is necessary to calculate the fluid requirement).
• The patient should be sedated well after ensuring the airway patency, and if
required intubated.
• The patient should be completely undressed (Fig. 15.11).
• Two intra-venous portals should be established for fluid resuscitation and
medication.
FIGURE 15.11 Nursing a burns patient Source: (Courtesy Dr K. Sridhar).
Note
For circumferential burn injuries (around the chest and limbs), especially the
third degree burns, escharatomy will have to be performed, or otherwise
respiratory embarrassment and ischemic necrosis of limbs may occur.
Burnt area
The patient should be examined head to foot, with special attention to the areas,
like the axillae, groins and the perineum. The extent of damage, both by area and
depth should be assessed quickly and precisely, as this helps in the determination
of fluid replacement.
• Extent of area of burns–This is calculated in two ways:
• For small, multiple and scattered areas– ‘Rule of hand’ is used;
determination of surface area of burns, using the patient’s own hand (with
adducted fingers), which is equal to 1%.
• For large areas– ‘Wallace’s rule of nine’ is used (Fig. 15.12A). For
children, the rule is modified (Fig. 15.12B), as the surface of area of the
head is bigger relative to the other parts of the body.
• Depth of tissue damage–This can be done by inspecting the burnt area (see
Table 15.2), and reasonable conclusions may be reached. It should be
remembered that various degrees of tissue damage co-exist in the same
patient.
• Cutaneous sensation is tested by pricking the burnt area (sterile needle test)
with a sterile needle (Fig. 15.13). Presence of sensation is diagnostic of
partial thickness burns, but it is not pathognomonic.
FIGURE 15.12A Wallace’s rule of nine for adults.

FIGURE 15.12B Modified rule of nine for children.
FIGURE 15.13 Assessing depth with painful stimuli.
Plucking the hair from the burnt area can show the depth. In full thickness
burns, the hair can be plucked easily, whereas, in partial thickness burns it is not.
General examination
• Examination of sensorium–Usually the sensorium remains normal and not
willing to answer may indicate a psychiatric problem (e.g. depression or
withdrawal). Inability to answer may indicate state of unconsciousness or
altered sensorium (e.g. shock, hyponatremia or uremia).
• Examination of face–Eyes–Sunken eyes indicate dehydration and
undernutrition. Examination of conjunctivae will reveal anaemia. Hairy
areas–Surging of hair in eyebrow, moustache or over the forehead will
indicate respiratory burns.
• Examination of skin–The skin should be examined for dehydration and
undernutrition. Generalized oedema may be seen in severely burnt patients.
• Examination of tongue–Dry tongue indicates dehydration.
• Recording of vital signs– Tachycardia may indicate infection or
hypovolemia. An elevated temperature may indicate associated infections
and toxemia (usually seen in the second week). Hyperventilation may
indicate hydration and hypovolemia, and is predominant in respiratory burns.
Hypotension may indicate hypovolemia.
Systemic examination
• Examination of oral cavity–A systematic examination of oral cavity is
essential (e.g., chemical burns, burns due to inhalation of gases)
• Examination of chest– Auscultation–Adventitious sounds may indicate
aspiration penumonitis or respiratory infections.
CHAPTER 16
Brain
K. R. Suresh Bapu
CHAPTER OUTLINE
16.1. Development of brain 188
16.2. Surgical anatomy of brain 188
16.3. Intracranial lesions 190
• Encephalocoele and meningocoele 190
• Hydrocephalus 190
• Craniosynostosis 191
• Arachnoid cyst 191
• Brain abscess 191
• Tuberculoma of brain 192
• Neurocysticercosis 192
• Intracranial aneurysms 193
• Arteriovenous malformations 193
• Cerebral infarcts and haemorrhage 193
• Meningioma 194
• Pituitary adenoma 194
• VIII nerve schwannoma 195
• Low grade glioma 195
• Craniopharyngioma 196
• Colloid cyst 196
• Cerebellar haemangioblastoma 196
• High grade gliomas 196
• Cerebral metastases 197
• Medulloblastoma 197
• Pseudotumour cerebri 198
• Chronic subdural haematoma 198
• Normal pressure hydrocephalus 198
16.4. Symptoms of intracranial lesions 199
• Cranial nerves 202
• Motor coordination 208
• Motor function 210
• Sensory function 212
• Stance and gait 212
• Skull 212
16.1 Development of brain
The neural tube is divisible into an enlarged cranial part which forms the brain,
and a caudal tubular part which forms the spinal cord. As the embryo grows the
spinal cord increases in length. The cavity of the developing brain shows three
dilatations, namely:
• Prosencephalon–subdivides into –
• Telencephalon (consists of right and left telencephalic vesicles)
• Dienchephalon
• Mesencephalon
• Rhombencephalon–subdivides into –
• Metencephalon (cranial part) Myelencephalon (caudal part)
The parts of the brain develop from the subdivisions of the neural tube, and
are shown in Table 16.1.
TABLE 16.1
Neural Tube and Its Derivatives
Parts of neural tube Parts of brain

Prosencephalon Telencephalon Cerebral cortex, corpus striatum Lateral ventricle
Diencephalon Thalamus, hypothalamus optic stalk, pars nervosa of Third ventricle
hypophysis
Mesencephalon Midbrain Aqueduct
Rhombencephalon Metencephalon Pons and cerebellum Fourth ventricle
Myelencephalon Medulla oblongata
16.2 Surgical anatomy of brain

The brain (Figs. 16.1 and 16.2), covered by pia-arachnoid and dura mater with
cerebrospinal fluid (CSF) in the subarachnoid space, lies in the intracranial
cavity protected by the bony skull all round. The intracranial cavity is partitioned
by the tentorium cerebelli into –
1. the supratentorial compartment housing the cerebral hemispheres, and
2. the infratentorial compartment housing the brainstem and cerebellum.
FIGURE 16.1 Brain anatomy.
FIGURE 16.2 Brain anatomy.
The right and left cerebral hemispheres are separated by falx cerebri. When a
space occupying lesion arises in one compartment, as the skull in not expansile,
herniation of brain tissue from that compartment occurs across the falx cerebri
and across the tentorial hiatus. Uncus of the medial temporal lobe, as it herniates
across the tentorial hiatus, presses on the brain stem and the third nerve causing
depression of consciousness and pupillary dilatation. This phenomenon called
‘coning’ forms the anatomical basis of unconsciousness in brain tumours,
traumatic intracranial haematomas and other space occupying lesions. Normally
the cephalic end of central reticular core of the brain stem is, to a large extent,
responsible for the conscious state by its ascending reticular activating system.
Some of the functions of the brain, like gross memory, intelligence and
emotions are performed by several parts of the brain; certain functions are
performed exclusively by specific parts of the brain and are collectively termed
as the ‘eloquent areas’ of the brain:
• Motor cortex controls voluntary movement of contralateral limbs;
• Sensory cortex controls the finer aspects of sensation from contralateral
limbs;
• Medial occipital lobe is responsible for visual perception from contralateral
hemifield;
• Language functions are done by the dominant (usually left) hemisphere;
• Speech is controlled by the posterior part of the inferior frontal lobe on left
side (Broca’s area); and
• Language comprehension is controlled by the left angular gyrus.
When a space occupying lesion (SOL) involves the eloquent area of the brain,
specific neurologic deficits occur early in the course of illness. When a SOL
involves the ‘silent areas’ of the brain (e.g. right frontal pole, right temporal pole,
right posterior parietal lobe and intra ventricular space), focal neurologic deficits
do not occur and patients present with features of raised intracranial pressure
only.
The brain stem is compact with all long tracts connecting cerebral
hemispheres and spinal cord; they contain nuclei of cranial nerves 3 to 12 and
most importantly, the cardio-respiratory and autonomic centres. Even minimal
involvement of the brain stem leads to profound deficits and can lead to coma
and death.
Anatomically, the motor tract crosses at the lower most part of the medulla,
and hence a focal lesion on one side of the brain stem will cause ipsilateral
cranial nerve palsy and contralateral haemiparesis called ‘crossed haemiplegia’.
The cerebellar hemisphere is responsible for the co-ordination of movements
of the ipsilateral limbs.
The arterial supply to the brain is through the internal carotid arteries and
vertebral arteries forming the Circle of Willis at the base of the brain.
Venous drainage is through the superior sagittal sinus, inferior sagittal sinuses
and straight sinus becoming the transverse-sigmoid sinuses draining into the
internal jugular vein.
Lymphatic drainage exists only for extradural space; CSF acts as the lymph
for the brain. There is neither CSF nor lymphatics in the subdural space, and
hence any bleeding restricted to the subdural space will expand into chronic
subdural haematoma as the degradation products are not carried away.
The brain itself is insensitive, and hence the space occupying lesions within
the brain do not cause headache until they stretch the basal dura and the Circle of
Willis, which have pain fibres and nerve endings.
The intracranial lesions are classified according to the aetiology (Table 16.2).
TABLE 16.2
Aetiological Classification of Intracranial Lesions
Congenital and Encephalocele, Meningocele, Hydrocephalus, Craniosynostosis, Arachnoid cyst

developmental
Traumatic (Discussed separately in Chapter 17)
Infective Brain abscess, tuberculoma, cysticercosis
Vascular Intracranial aneurysm and arteriovenous malformation, cerebral infarct and intracerebral
haemorrhage
Benign tumours Meningioma, vestibular and trigeminal schwannoma, pituitary adenoma, craniopharyngioma,
dermoid and epidermoid cysts, colloid cyst, choroid plexus papilloma, low grade glioma
Malignant High grade glioma, PNET (cerebral hemispheric PNET, medulloblastoma, ependymoblastoma,
tumours pinealoblastoma), cerebral metastases from systemic primary lesions
Miscellaneous Chronic subdural haematoma, pseudotumour cerebri (Idiopathic intracranial hypertension), normal
pressure hydrocephalus
16.3 Intracranial lesions
Encephalocele and meningocele

• Rare compared to spinal myelo-meningocele.
• They are the result of defective closure of midline in the embryo.
• The two common locations are the occipital region and frontonasal junction.
• Present from birth, they are covered by whole skin and thinned out meninges.
• When it contains the CSF only it is called ‘meningocele’ and with the brain
tissue, it is called ‘encephalocele’.
• Globular swelling near the root of the nose (Fig. 16.3A) or on the occiput
(Fig. 16.3B).
• When CSF is the only content (meningocele), they are brilliantly
transilluminant.
• Areas of brain tissue in the cavity (encephalocele) can be seen as darker areas
on transillumination.
• Impulse on crying will suggest communication with intracranial cavity.
FIGURE 16.3A Meningocoele Source: (Courtesy Dr K. Sridhar).

FIGURE 16.3B Meningocoele Source: (Courtesy Dr N. Dakshinamoorthy).
• Magnetic resonance imaging (MRI) of the brain will delineate the size,
shape and extent of lesion, and nature of contents.
Treatment
• Surgical excision and repair.
Hydrocephalus
• Progressive dilatation of ventricles commonly due to obstruction to CSF
pathway.
• Site of obstruction is usually the aqueduct.
• In post-inflammatory obstruction of basal cisterns, dilated ventricles
communicate with spinal subarachnoid space called ‘communicating
hydrocephalus’.
• In infants, progressive enlargement of head occurs with wide open fontanelle,
and ‘sunset sign’ (down looking eyes) develops.
• Loss of acquired developmental milestones and mental functions, and
presentation of raised intracranial pressure, viz., headache, vomiting, gait
ataxia and optic disc oedema are seen in children and adults.
• Computed Tomography (CT) (Fig. 16.4) or MRI of the brain is diagnostic.
FIGURE 16.4 CT—hydrocephalus.
Treatment
• Endoscopic third ventriculostomy is preferred for aqueductal obstruction.
• CSF diversion - ventriculo-peritoneal shunt is done in most cases.
Craniosynostosis
• It is rare and occurs due to premature fusion of coronal or sagittal sutures with
excess skull growth at unfused sutures.
• Asymmetry and deformity of skull is the presenting symptom (Fig. 16.5),
such as,
• Brachycephaly in coronal synostosis;
• Scaphocephaly in sagittal synostosis; and
• Tower skull deformity at anterior fontanelle in pansynostosis.
• In neglected cases optic atrophy and visual loss occurs.
• Developmental milestones are normal, which differentiates it from
microcephaly due to mental retardation.
FIGURE 16.5 Craniosynostosis Source: (Courtesy Dr K. Sridhar).
• X ray skull and CT (bone window study) will show fused sutures.
• 3-D images of CT will show the skull deformity.
Treatment
• Excision of sutures before 2 years of age is preferred.
• When detected later in life, cosmetic reconstruction of skull base or orbit and
optic nerve decompression will be indicated depending upon the clinical
presentation.
Arachnoid cyst
• Usually an incidental finding when CT or MRI brain is done for seizure
disorder or head injury.
• When large, focal skull bossing in the temporal region is seen.
• CT or MRI of the brain.
Treatment
• In large cysts with mass effect, fenestration into basal cisterns or
cystoperitoneal shunt will be needed.
Brain abscess
• Spread of infection can be –
• contiguous from midd–le ear or mastoid or frontal sinus;
• blood-borne from infections elsewhere in the body;
• direct from compound depressed fracture with dural tear; or
• due to cyanotic congenital heart disease (lack of pulmonary filter,
secondary polycythemia and hypercoagulable state facilitate abscess
formation).
• Headache, vomiting, and/or seizures for a few days in the presence of the
above mentioned predisposing factors should raise the suspicion of brain
abscess.
• Focal neurologic signs are mild and depend on location of the abscess.
• CT or MRI of brain (Plain and contrast) will show the lesion. Round shape,
smooth inner wall thinner medially towards the ventricle will differentiate
the abscess from a tumour (Fig. 16.6).
FIGURE 16.6 CT—brain abscess.

Treatment
• Burr hole drainage and appropriate antibiotics for several weeks will
provide a cure in most cases.
Tuberculoma of brain
• Caused by Mycobacterium tuberculosis, and spreads from lungs or other foci.
• Tuberculoma is very common in India especially in children, and in adults
with decreased body resistance, e.g. diabetics, postpartum women, steroid
therapy and in HIV patients.
• Focal fit is the commonest presentation.
• Focal neurologic deficit and/or raised intracranial pressure occurs when the
lesion is large.
• CT or MRI of the brain (plain and contrast study) will show the nodular ring-
enhancing lesion anatomically. Pathological nature is guessed from
multiplicity, concomitant lesion elsewhere in the body, conglomerate
appearance in CT and sometimes MR spectroscopy
• Polymerase Chain Reaction (PCR tests) may be useful.
• CT guided stereotactic biopsy or serial CT after 6 to 8 weeks of therapeutic
trial are needed to differentiate tuberculoma from tumour.
Treatment
• Antitubercular therapy is the mainstay of treatment.
Neurocysticercosis
• Ingestion of larval form of Taenia saginata in contaminated vegetables leads
to cysticercosis.
• The commonest cause of granuloma of the brain in India.
• Focal fit is the commonest presentation.
• Multiple lesions with oedema can lead to the syndrome of raised intracranial
pressure.
• CT and MRI of brain will be diagnostic (Fig. 16.7). Differentiation from
tuberculoma is by
• smaller size
• less mass effect, and
• better clinical condition.
• Immunological tests may be useful.
FIGURE 16.7 CT—cysticercosis.
Treatment
• A course of albendazole is usually given to eradicate any systemic infection
which does not influence the cerebral lesion.
• Control of seizures is the main aim of treatment.
Intracranial aneurysms
• Saccular aneurysms of the Circle of Willis arise at defective media at points
of bifurcation or branching.
• Ruptured aneurysm is the commonest cause of spontaneous (non-traumatic)
subarachnoid haemorrhage.
• In about 18% cases, the leak is severe leading to death before hospitalization.
• Acute onset of violent headache, brief loss of consciousness, and vomiting
with neck stiffness and without focal neurologic deficit is the classical
clinical presentation of an aneurysmal bleed.
• CT brain will show subarachnoid haemorrhage.
• Cerebral angiogram [CT – angio/MR – angio/Digital subtraction
angiography (DSA)] is needed to identify the details of aneurysm (Fig. 16.8)
• Lumbar puncture (LP) and CSF study is indicated when CT is non-
contributory.
FIGURE 16.8 Angiogram—aneurysm.
Treatment
• Patients should be investigated and treated while they are conscious.
• Obliteration of aneurysm by surgical clipping of the neck or by
endovascular coiling is needed at the earliest to avoid rebleed.
• Volume expansion is needed to counteract delayed vasospasm.
Arteriovenous malformations
• Cerebral arteriovenous malformations are congenital and enlarge over the
years.
• The nidus is often compact with feeding from branches of middle cerebral,
anterior cerebral, or posterior cerebral arteries.
• Venous drainage into superficial or deep venous system is the usual source of
bleeding.
• Remain asymptomatic for several years.
• Seizures, intra cerebral haemorrhage in the age group of 20–40 years are the
common presentations.
• Depending on the size and location of haemorrhage neurologic deficits occur.
• Cerebral angiogram (Fig. 16.9) is the investigation of choice.
FIGURE 16.9 Angiogram—AV malformation.
Treatment
• Embolization of nidus followed by surgery or gamma knife therapy is the
preferred method of treatment.
Cerebral infarcts and cerebral haemorrhage

• Commonest neurological illness in adults.
• Common aetiological factors are –
• Hypertension
• Diabetes mellitus
• Cardiac disease
• Atherosclerosis
• Hypercholesterolemia
• Focal neurologic deficits of abrupt onset.
• CT or MRI brain is diagnostic.
Treatment
• Many times management is medical.
• Surgical decompression will be needed in selected cases when the mass
effect is severe causing coning.
Meningioma
• Commonest benign neoplasm arising from arachnoidal cap cells and attached
to convexity dura, parasagittal sinus, basal dura, lesser wing of sphenoid or
the tentorium cerebelli, and rarely at the atrium of lateral ventricle.
• Common after 30 years of age with slight female preponderance.
• Focal fits becoming generalized is the initial symptom in the majority. With
increasing size of the tumour, local pressure effect and oedema cause focal
neurologic deficit.
• When the tumour is over the non-eloquent area of the brain, presentation of
raised intracranial pressure will be the only presentation.
• CT or MRI brain (plain and contrast study) will show a bun shaped,
homogenously and densely enhancing extra axial, dural based tumour with
mass effect (Fig. 16.10).
FIGURE 16.10 MRI—Meningioma.
Treatment
• Craniotomy and excision of the tumour is needed in most patients.
Pituitary adenoma
• 2–5% of primary intracranial tumours.
• These tumours are classified into –
• Functioning tumours [e.g. Prolactinoma, growth hormone (GH) secreting
adenoma and adrenocorticotropic hormone (ACTH) secreting adenoma].
• Non-functioning tumours (e.g. Chromophobe adenoma).
• Functioning tumours produce specific endocrine-excess syndrome even
when the tumour is small (Microadenoma).
• Prolactinoma–Infertility, impotence, and galactorrhea-amenorrhea.
• GH-secreting adenoma–acromegaly (large hands and feet, and
prognathism) in adults and gigantism in children.
• ACTH-secreting adenoma–Cushing’s syndrome (moon like face and
hypertension).
• Non-functioning adenomas cause a headache and pressure effect on a normal
pituitary, and later as the tumour grows into the suprasellar region, it
compresses the optic chiasm producing bitemporal hemianopia leading on to
progressive visual loss.
• CT or MRI (plain and contrast) will delineate the tumour anatomically (Fig.
16.11).
• Serum prolactin, growth hormone and cortisol levels, and 24 hrs urinary
cortisol excretion are raised in specific syndromes.
FIGURE 16.11 MRI—Pituitary tumour.

Treatment
• Prolactinoma can often be treated with dopamine agonists.
• Transphenoidal excision is done for all other tumours.
VIII nerve schwannoma

Chapter 21 - Ears.

• 1–2% of primary intracranial tumours.
• Mostly the tumours are unilateral, except in Neurofibromatosis Type II where
the tumours are bilateral.
• As the tumour grows into a cerebello-pontine angle, pressure on the
trigeminal nerve, brain stem and cerebellum occurs.
• Hydrocephalus occurs in late stages.
• Tinnitus, followed by unilateral sensorineural hearing loss, occurs in most
patients when the tumour is confined to the internal auditory canal.
• Surprisingly, VII nerve function is retained for a long period.
• Imbalance on walking.
• Headache and optic disc oedema occur in the late stages.
• CT or MRI brain (plain and contrast study) will show all the details of the
tumour (Fig. 16.12).
• Audiological tests and brain stem evoked potential studies are done to
document the defects.
FIGURE 16.12 MRI—acoustic neuroma.
Treatment
• Retrosigmoid craniectomy and excision of tumour is the choice of treatment
in most cases.
• Translabyrinthine excision is possible in selected cases.
• Gamma-knife treatment is available for small tumours.
Low grade gliomas

• Gliomas constitute the majority of primary brain tumours.
• The common types are –
• Astrocytomas
• Oligodendrogliomas
• Ependymomas
• Grade I and II gliomas occur more often in children and young adults.
• Low grade gliomas occur in the cerebral hemisphere, cerebellum,
hypothalamo-chiasmal region and brainstem.
• Cerebral gliomas present as seizures most often.
• Cystic cerebellar astrocytoma presents as raised intracranial tension (ICT)
with cerebellar signs in children.
• Gliomas in the central neuraxis present with progressive focal neurologic
deficit, depending on the location of the tumour.
• CT or MRI brain (plain and contrast) (Fig. 16.13) is diagnostic.
FIGURE 16.13 MRI—low grade glioma.
Treatment
• Total excision is done wherever possible.
• CT-guided stereotactic biopsy followed by radiotherapy is preferred for
tumours in locations like brainstem, optic chiasm. etc.
Craniopharyngioma
• Occurs mostly in children in the suprasellar region.
• Hypothalamic dysfunction, viz., growth retardation, hypogonadism and
diabetes insipidus.
• Visual disturbances, viz., visual field defects and progressive visual loss.
• Hydrocephalus with presentation of raised intracranial pressure (ICP) is
another method of presentation.
• In adults, craniopharyngiomas present without much hypothalamic
disturbances.
• X ray and CT (Fig. 16.14) show typical suprasellar calcification.
• MRI delineates the extent of the tumour and pressure effect on the brain.
FIGURE 16.14 MRI—craniopharyngioma.
Treatment
• Surgery followed by radiotherapy is the usual mode of treatment.
Colloid cyst
• Occurs as a round cyst in the anterior third ventricle; it blocks the foramen of
Munro producing hydrocephalus.
• Symptoms and signs of raised ICP.
• It can present as sudden coma and even death in some patients.
• CT or MRI (Fig. 16.15) is confirmatory.
FIGURE 16.15 MRI—colloid cyst.
Treatment
• Surgical excision by transcallosal approach.
Cerebellar haemangioblastoma
• Can present as part of Von Recklinghausens’ disease.
• When the lesion is large, it produces mass effect
• Because of multiplicity of lesions, the whole brain and spine survey with
MRI is indicated periodically (Fig. 16.16).
FIGURE 16.16 MRI—cerebellar haemangioblastoma.

Treatment
• Surgery is mandatory.
High grade gliomas

• Commonest of primary intracranial tumours.
• They can arise de novo or can mutate from low-grade gliomas.
• Affects the age group > 40 years.
• The high grade gliomas are –
• Grade III and IV astrocytomas
• High grade oligodendrogliomas
• Malignant ependymomas
• Glioblastoma multiforme
• They do not metastasize outside the brain.
• Survival for glioblastoma multiforme is about 15 months only.
• Seizures, raised intracranial pressure, rapidly progressive focal neurologic
deficit, and progressive impairment of mental functions occur over a period
of a few weeks.
• CT or MRI of brain (plain and contrast study) will give the size, shape,
location and extent of the lesion and its mass effect (Fig. 16.17).
• CT-guided stereotactic biopsy will be needed often to differentiate it from
tuberculoma, metastasis, lymphoma, etc.
FIGURE 16.17 MRI—high grade glioma.
Treatment
• Surgical debulking followed by radiotherapy is the mainstay in the
management
Cerebral metastases
• In autopsy series, metastases are commoner than primary brain tumours.
• Multiple metastases are common, though solitary lesions are sometimes seen.
• The common sites of primary lesion are lungs, breast, thyroid, ovary,
gastrointestinal (GI) tract and soft tissue sarcomas.
• In known patients with primary, any significant headache, vomiting or
seizures should raise the suspicion of brain metastasis.
• When there is no history or clinical evidence of systemic primary, the
presentation is similar to high grade glioma and only a biopsy will establish
the pathology of the lesion.
• CT or MRI brain (Fig. 16.18) will show single or multiple densely enhancing
lesions with severe surrounding oedema.
FIGURE 16.18 MRI—cerebral metastasis.
Treatment
• Steroids, anticonvulsants and radiotherapy form the mode of therapy.
• Craniotomy and surgical excision of solitary metastasis is preferred in select
situations.
Medulloblastoma
• Highly malignant primary tumour occurs in children between 3 and 12 years
affecting the vermis of cerebellum.
• Desmoplastic variety occurs in older children and young adults, affecting the
cerebellar hemisphere, and carries better prognosis.
• Incessant vomiting, headache and ataxia are the cardinal presentations of
midline cerebellar tumours in children.
• CT or MRI of the brain (Fig. 16.19) will show the vermian mass with a
homogenous dense enhancement causing hydrocephalus.
• Differentiation from other midline cerebellar tumours, viz., ependymoma,
astrocytoma, haemangioblastoma and tuberculoma is most often possible
with CT or MRI.
FIGURE 16.19 MRI—medulloblastoma.

Treatment
• Total excision followed by radiotherapy and chemotherapy offers a disease
free interval for several years.
Pseudotumour cerebri
• Condition caused by cerebral vasodilatation/diffuse oedema due many
aetiological factors.
• Symptoms and signs of raised intracranial pressure, viz., headache, vomiting
and papilloedema.
• CT or MRI excludes space occupying lesions or hydrocephalus.
• LP-CSF manometry, if done, will show an increased CSF pressure.
Treatment
• Anti-oedema measures along with treatment of primary pathology.
• In chronic cases, when persistent papilloedema is leading to visual decline,
lumbo-peritoneal shunt will be indicated.
Chronic subdural haematoma

• History of trivial injury 2 to 4 months earlier is available only in 60% of
patients.
• Chronic subdural haematoma occurs mostly in patients with brain atrophy:
old age, alcoholics, past h/o brain insult.
• Progressive decline in mental functions, difficulty in walking, progressive
haemiparesis, urinary incontinence – all these symptoms occurring over a
period of 1 to 3 weeks.
• CT or MRI (Fig. 16.20) is diagnostic
FIGURE 16.20 CT—chronic subdural haematoma.
Treatment
• Burr-hole and drainage gives excellent results.
Normal pressure hydrocephalus
• An uncommon disease.
• A treatable cause of dementia and gait ataxia.
• Gait apraxia, dementia and urinary incontinence form the triad of normal
pressure hydrocephalus.
• CT or MRI will show ventricular dilatation with periventricular oedema.
Relative obliteration of cortical sulci differentiates it from senile cortical
atrophy.
• CSF pressure study, nuclear scan and CSF flowmetry are useful.
Treatment
• Ventriculo-peritoneal shunt using programmable valve will give satisfactory
results.
16.4 Symptoms of intracranial lesions

• Headache
• Vomiting
• Seizures
• Impaired mental functions
• Focal neurologic deficit
Headache
• Headache is a common symptom of many illnesses without intracranial
pathology. Common causes of such headache are –
• Episodic–Unilateral headache with vomiting with/without aura in young
patients will suggest migraine.
• Tension headache– Pain localized to suboccipital region; not associated
vomiting and the headache does not disturb sleep, but gets aggravated by
stress factors at home or at work place.
• Psychogenic headache–Lasts for several years and is localized to the
vertex and not associated with vomiting, but associated with insomnia,
depression and anxiety. It does not respond to common analgesics, but
responds to a course of anti depressants.
• Headache of systemic fever–It is usually associated with a generalized
bodyache.
• Headache of sinusitis–Is localized to the region of affected paranasal sinus
and may be more on bending the head forwards, and fever may also be
present.
• Headache due to refractory error–Is generally associated with
disturbances in visual acuity.
• Headache is the presenting symptom of intracranial lesions
• Headache due to increased intracranial pressure is often bifrontal and is
of a few days or weeks duration. It is the maximum in the early morning
hours soon after waking up from sleep (During sleep there is relative
depression of breathing with relative hypercarbia and cerebral
vasodilatation). Headache can occur during sleep and wakeup the patient,
and such a clinical situation is an indication for urgent CT/MRI of the
brain. Headache is aggravated by cough and bending forward, and
associated with vomiting. Vomiting can relieve headache transiently (Post-
vomiting hyperventilation leads to relative hypocarbia, cerebral venous
constriction and decrease in intracranial pressure). Common analgesics
give relief of headache for a few days. There is no association with stress
factors. With tonsillar herniation, there will be nuchal pain with stiffness
associated with torticollis.
• Headache due to benign tumours without increase of intracranial
pressure can be localized to the region of tumour, e.g. occipital pain in
posterior fossa tumours and bitemporal pain in pituitary tumours.
• Headache due to intracranial haemorrhage (Aneurysmal subarachnoid
haemorrhage and hypertensive intracranial hypertension), is acute and
very severe and associated with vomiting, altered sensorium and neck
stiffness. In aneurysmal subarachnoid haemorrhage, there will be no
haemiplegia, whereas, in hypertensive intracranial hypertension, there
will be haemiplegia.
Vomiting
• Vomiting associated with nausea is common in –
• Disorders of GI tract.
• Systemic illnesses, particularly in children.
• Vomiting associated with vertigo and nausea is common in even mild
vestibular system dysfunction.
• Vomiting without nausea is caused by increased intracranial pressure.
• Projectile vomiting, especially in the early hours of the day is characteristic of
increased intracranial pressure.
Note
If there is no obvious GI tract disease or vestibular dysfunction, intracranial
cause should be suspected. Incessant vomiting without apparent cause is an
indication for CT/MRI to exclude intracranial space occupying lesions.
Seizures
• Seizures of idiopathic epilepsy–Seizures start before 15 years of age, with or
without family history; the pattern of seizure remains the same and there is
very little post-ictal palsy.
• Seizure due to transient intracranial insults (e.g. febrile fits, poisoning, and
traumatic impact seizures).
• Seizures due to intracranial tumours– Onset after the age of 20 years,
starting as focal fits and becoming generalized with prolonged post-ictal
palsy (e.g. Focal fits arising in the lower limb will indicate lesion near
contralateral parasagittal motor cortex, such as parasagittal meningioma). As
tumour grows, the epileptogenic focus changes and the pattern of seizures
changes over time: instead of focal fits becoming generalized, it can be
generalized from the beginning of episode or vice versa.
• Aura or onset of convulsions may give a clue to the location of lesion (e.g.
Visual aura of formed objects will indicate occipital lobe tumour, whereas,
visual aura of unformed objects will indicate temporal lobe tumour.
Olfactory and gustatory aura will indicate medial temporal lobe lesion).
Impaired mental functions

Higher mental functions
• Memory–Remote memory is preserved in many diseases and hence patients
can easily recall events that happened several years ago. Recent memory will
be impaired.
• Orientation–Orientation to place, time and persons may be affected.
Focal neurological deficit

Focal neurological deficit aids in localizing the lesion –gradual onset and
progression of neurologic symptoms will suggest a space occupying lesion [e.g.
anosmia (loss of olfaction) in midline frontal basal meningioma, visual field loss
in pituitary tumours, diplopia in extraocular palsy, unilateral hearing loss in VIII
Nerve Schwanomma, and subtle weakness of contralateral limbs in pyramidal
tract involvement].
The symptoms of neurological illnesses have a very characteristic onset and
progression. They are shown in Table 16.3.
TABLE 16.3
Characteristics of Temporal Profile of Neurological Illnesses
Aetiology Onset and progression
Congenital Symptoms present from birth and usually progress very slowly
Traumatic Sudden onset from time of significant injury; further deterioration over 2 to 8 days; if patient
survives, improvement +/− over a period of weeks/months
Infections Gradual onset over a few days in acute infections and over a few weeks in chronic infections with
rapid progression over a few days. No spontaneous recovery
Cerebral infarcts Focal neurologic deficit (haemiplegia) is abrupt during onset over a few seconds to minutes. When
and cerebral mass effect is the maximum on fourth to sixth day, patient’s consciousness may deteriorate
haemorrhage further due to coning. In surviving patients, partial recovery will occur after a few weeks
Benign tumours Gradual onset and slow progression of symptoms over weeks or months
Malignant Gradual onset of symptoms over a few days with rapid progression within a few days; no
tumours spontaneous recovery
Degenerative Gradual onset and progression over months or years. Usually bilateral (e.g. Parkinsons disease,
diseases cerebellar degeneration and Alzheimer’s disease)
Demyelinating Onset over a few days (as in infections) but spontaneous recovery +. Past h/o similar illness + with
diseases spontaneous recovery
Eliciting history
• Age − Certain intracranial pathologies occur at certain age groups −
• Young children–medulloblastoma
• Young adults–low grade gliomas
• Elderly–high grade glioma, chronic subdural haemorrhage with brain
atrophy.
• Sex−Meningiomas are slightly more common in women
Headache
• Site of headache: Which part of the head is aching?
The patient should be asked to show the region of headache (e.g. increased
intracranial pressure causes bifrontal headache, occipital benign lesions cause
occipital pain, etc.). Headache is unilateral in migraine.
• Duration of headache: How long is the patient suffering from headache?
If the patient has been suffering from headache for a very long period of time,
it indicates chronicity (e.g. migraine), whereas, short duration may suggest a
neoplastic condition (e.g. tumours). Episodic headache is suggestive of migraine.
• Description of headache: Can you describe the ache?
Headache has a variety of presentations− Severe pain (e.g. migraine) and dull
pain (e.g. sinusitis).
• Recent change in the quality, intensity of headache: Is there a change in
its quality, periodicity or intensity of ache or not?
Recurrent attacks of migraine may change to a constant pain when there is
associated appearance of malignant lesion.
• Shift or Radiation of pain: Has the pain changed its place from its point
where it started?
Headache may shift to the neck (e.g. tonsillar herniation).
• Timing of headache: At what time of the day does the headache occur?
Early morning headache occurs in increased intracranial tension and sinusitis.
Waking up in the nights due to headache occurs in increased intracranial tension.
• Effects of movements, stress, food or habits: Is there any factor, such as
food which relieves or makes the pain worse?
The headache gets aggravated by certain factors, like bending (e.g. increased
intracranial pressure), intake of fatty food (e.g. migraine) and analgesics relieve
the episodic or migrainous headache. The pain of increased intracranial pressure
may be relieved transiently by analgesics. Psychogenic headache is not relieved
by analgesics. The headache may get aggravated by stress at workplace or at
home.
Nausea and vomiting

• Frequency: How frequently is the patient been vomiting?
Vomiting is a common feature of migraine. Projectile vomiting without nausea
is characteristic of increased intracranial pressure.
• Relationship to food: Is vomiting related to food intake?
Fatty food induces vomiting in migraine. Food has no relationship with
vomiting in increased intracranial pressure.
• Relationship to headache: Does this vomiting relieve or aggravate
headache?
Vomiting gives transient relief from headache in increased intracranial
pressure, but significant relief in migraine.
• Presence of nausea: Is there preceding nausea to the attack of vomiting?
Preceding nausea is characteristic of GI or vestibular pathologies, and the
absence of nausea is characteristic of increased intracranial pressure.
Seizures
• Onset of seizures: Since when are the attacks of seizures happening?
The first attack of seizure after the age of 15 usually is suspicious of
intracranial neoplasm, and that at a very young age is suspicious of epilepsy.
• Frequency: Were the seizures frequent, and if so with what frequency?
Frequent attacks of seizures for a very long period is suspicious of epilepsy,
but for a short period is suspicious of increased intracranial pressure.
• Nature of seizures: Were the seizures limited to one anatomical area or
generalized?
Seizures limited to one anatomical area are probably focal fits (e.g. neoplasm),
and generalized seizures indicate epilepsy. Focal fits can become generalized in
situations where the tumour grows in size and the epileptogenic focus shifts.
• Post ictal palsy: For how long was the patient lying quiet after the attack of
seizures?
Post ictal palsy is short in epilepsy and prolonged in seizures due to
intracranial tumours.
• Presence of aura: Was there any aura present before the attack of seizure?
Aura before seizures may give a clue to the location of lesion (e.g., Visual
aura of formed objects will indicate an occipital lobe tumour, whereas, visual
aura of unformed objects will indicate a temporal lobe tumour. Olfactory and
gustatory aura will indicate medial temporal lobe lesion).
Mental functions
• Memory– Recent memory may be lost, but remote memory is preserved in
many cases.
• Orientation– Orientation to place, time and person may be affected.
Note
Higher mental functions can be tested only if patient is fully conscious,
cooperative and with intact language functions.
• Reasoning and judgement−As history is elicited, a patient can be asked how

he or she is going to manage responsibilities at work and at home; and from
the answer one can assess higher mental functions.
• Comprehension−Understanding of written and spoken language can be
assessed by serial commands like:
- Lift the head
- Lift the head and close the eyes, and
- Lift the head, close the eyes and stand up.
• Expression: Spoken language is assessed as the patient talks, by fluency and
coherence of speech. Naming of objects can be tested by showing a pen,
torch, comb, etc. Writing is tested by asking the patients to write their name
and address.
Note
Progressive impairment of higher mental functions, memory, judgement,
emotion, orientation, calculation, comprehension, speech, writing, etc., can be
easily made out as the physician talks to the patient and close relatives; it will
localize the lesion to specific cerebral lobes. Language dysfunction will
indicate lesion in the left hemisphere.
Focal neurological deficit

• Focal deficit: Does the patient have any difficulty in any act or movement?
The patient may express difficulty in certain acts, like buttoning the shirt,
walking, etc.
Fever
• Fever: Does or did the patient have fever during the course of this illness?
Association of low grade fever may be present (e.g. lymphomas and
malignancies) with an evening rise of temperature (e.g. tuberculosis). High grade
fever may be a symptom of meningitis or encephalitis.
Past history
• Treatment in the past: Was there any similar illness in the past, which
required any treatment?
treated, it will indicate the examiner to reconsider the diagnosis, like
tuberculosis.
Family history
Tuberculosis occurs in closed knit groups living together, and can affect more
people in a family.
match the situation.
Elicitation of neurologic signs is an art but can be easily learnt and practiced.
Cranial nerves
Olfactory (I) nerves
The basic function of olfactory nerve is the sense of smell or olfaction.
Method of testing olfactory nerve function
It is assessed by checking if the patient can appreciate smell of common items,
like coffee powder, camphor, etc.
Note
It is less important to determine whether the patient can correctly identify a
particular smell than whether the presence or absence of the stimulus is
perceived.
Causes of anosmia
• Blocked nasal passage (any cause)
• Head injury
• Frontal lesions (glioma, meningioma)
Optic (II) nerves

The basic function of optic nerves is vision.
Methods of testing the optic nerve function
• Visual acuity–Determines the focal distance of vision.
• Method: It is tested by counting fingers at varying distances and by reading
the Snellen’s chart. Normally, a small newspaper print can be read at a
distance of 32 inches.
• Visual fields–It is another measure of the integrity of the optic nerves, optic
chiasm, optic tracts and optic radiations through the hemispheres.
• Confrontation testing − Patient and examiner stand at eye level at about
arm’s length. The patient is asked to close his or her left eye. The
examiner’s left arm is extended and then brought inwards from the side;
the patient should say how many fingers are shown, the moment he or she
sees them. The patient and the examiner should see the fingers at the same
time. The same is repeated for the other eye, with the right eye covered by
the right hand. All four quadrants are tested for each eye (Fig. 16.21A).
FIGURE 16.21A Confrontation technique for testing visual fields.
Inference: Visual field defects (Fig. 16.21B) and their relevance are given in
Table 16.4.
• Fundus examination is done by using an ophthalmoscope (Fig. 16.22) and
the examiner
FIGURE 16.21B Visual field defects (1) Ispliateral blind eye, (2)
Bitemporal haemianopia, (3) Homonymous haemianopia, (4) and (5) Upper
and lower homonymous quantranopia, (6) Homonymous hemianopia with
macular sparing.
FIGURE 16.22 Examination of fundus of eye (Inset – ophthalmoscope).
TABLE 16.4
Visual Field Defects and Their Relevance
Visual field defect Anatomical basis
Ipsilateral blind eye Pre-chiasmatic lesion

Bitemporal haemianopia Pressure over optic chiasm (chiasmatic lesions) by pituitary tumours,
suprasellar meningiomas
Homonymous haemianopia Lesion involving contralateral visual pathway beyond optic chiasm (post-
chiasmatic lesions)
Upper homonymous quadranopia Lesions in the temporal lobe optic radiation
Lower homonymous quadranopia Lesions in the parietal lobe optic radiation
Homonymous haemianopia with Lesions in the occipital cortex
macular sparing
looks for −
• Loss of venous pulsations
• Retinal lesions
• Abnormalities of vessels
• Colour of optic nerve head
• Blurring of disc margins (papilloedema) is a very important sign of increased
intracranial pressure
• Consensual constriction: Relative Afferent Pupillary Defect (RAPD):
Swinging flashlight test– By swinging the flashlight from one eye to other
sequentially (Fig. 16.23); incomplete visual loss can be diagnosed by
pupillary dilatation of the defective eye. This is an important test as it is the
only clinical method of diagnosing optic nerve injury in unconscious
patients.
• Pupillary reflexes–a normal pupil will constrict –
1. in response to direct light (direct light reflex).
2. as a consensual response to light in the opposite eye (consensual light
reflex).
3. to accommodation.
FIGURE 16.23 Swinging flash light test.
Note
Light shown in the ipsilateral eye will cause constriction of both pupils,
provided both II and III cranial nerves are intact.
Oculomotor (iii), trochlear (IV) and abducent (VI) nerves
Functions
The III, IV and VI cranial nerves take care of the muscles of the eyeball, the
oculomotor function (Table 16.5).
• The third nerve also contains visceral efferents (parasympathetic) that
innervate the intrinsic ocular muscles. It also innervates the levator palpebrae
superioris that elevates the upper eyelid.
• Trochlear nerve is a motor nerve that innervates a single muscle in the orbit,
the superior oblique.
TABLE 16.5
Functions of III, IV and VI Cranial Nerves
Function Symptoms Signs

Cranial Nerve
Autonomic Motor
Oculomotor Intrinsic – ocular Extrinsic– extraocular muscles Ptosis diplopia Loss of
(III nerve) muscles (through (superior, inferior and medial adduction,
parasympathetic) recti, and inferior oblique) elevation
and levator palpebrae and
superioris depression
Pupillary
dilation
Trochlear (IV Superior oblique muscle, but the Severe diplopia with Loss of
nerve) nerve crosses to the opposite downward gaze, depression
side and innervates which improves of adducted
contralateral trochlear when head tilted to eye
nucleus contralateral side
Abducent (VI Lateral rectus muscle, which Diplopia Loss of
nerve) results in abduction of eye abduction
Method of testing the III, IV and VI cranial nerves

The patient and the examiner should be at the same eye level.
The extraocular movements are tested in the following manner. The methods
are:
• Primary gaze– The patient is asked to look straight ahead, and the symmetry
of position of the light reflection off the two corneas are noted (Fig. 16.24A).
• Volitional eye movements– The examiner should put a hand on the patient’s
forehead and should ask the patient to follow the fingers. The examiner
should move the index finger of the other hand horizontally, then up and
down on either side, tracing the letter ‘H’ (six directions) (Figs. 16.24B and
C).
FIGURE 16.24A Testing for primary gaze.
FIGURE 16.24B Testing for volitional movements of eye.
FIGURE 16.24C Checking conjugate eye movements.
Conjugate eye movements are checked with both eyes open, and in all six
directions of gaze.
• Doll’s head maneuver– The examiner should hold the patient’s head firmly
and rotate from side to side, then up and down (the eyelids should be held
open) (Ref Fig. 17.3). If the brainstem is intact, the eyes will move
conjugately away from the direction of turning. This maneuver is performed
if the patient is unresponsive or unable to perform volitional eye movements.
Note
• Direct light reflex is lost when the parasympathetic fibres in the third nerve
are damaged
• A pupil that reacts to accommodation, but not to light, is an Argyll-
Robertson pupil, signifying a lesion in the tectum of midbrain.
• Gaze palsy to right or left side can occur in acute insults of contralateral
frontal eye field (Area 8) or ipsilateral pontine gaze centre, the causes being
head injury or infarct or intracerebral haemorrhage.
• Diplopia and squint are present in extraocular nerve palsies, whereas, in
supranuclear gaze palsies, diplopia and squint are absent.
• Pupil-sparing III nerve palsy occurs in diabetes and demyelination, whereas,
pupil-involving III nerve palsy occurs in trauma, tumour and aneurysm of
posterior communicating artery.
• VI nerve palsy is an important false localizing sign and is due to stretching
of nerve in ICT.
• Abnormalities of eye movements can result from lesions other than cranial
nerve involvement, anything from muscular (ocular myopathy),
neuromuscular disease (myasthenia gravis) to central lesions in the cortex or
brainstem (e.g. after a stroke, horizontal movements may remain conjugate,
but gaze at rest may be directed to one side – toward the side of lesion if it is
cortical, and away if the lesion is in the brainstem).
Causes of oculomotor nerve lesions

• Skull base fractures
• Increased intracranial pressure
• Aneurysms or tumours compressing the nerve
Trigeminal (V) nerve

This nerve is a sensory nerve with some motor component and arises from the
trigeminal ganglion and has three divisions.
• Ophthalmic (V1)–supplies the skin of upper nose, eyelid, forehead and scalp.
Cornea, conjunctiva, mucosa of frontal, ethmoidal and sphenoidal sinuses,
and upper part of nasal cavity.
• Maxillary (V2)–supplies the lower eyelid, dura of middle cranial fossa, upper
part of cheek, adjacent part of nose and upper lip, mucosa of upper mouth
and nose, roof of pharynx, maxillary, ethmoid, and sphenoid sinuses, gums,
teeth and palate.
• Mandibular (V3)
• Sensory–supplies dura of middle and anterior cranial fossa, teeth and gums
of lower jaw, lower lip and cheek, mucosa of cheek and floor of mouth,
epithelium of anterior 2/3 of tongue, and temporomandibular joint.
• Motor–muscles of mastication, anterior belly of digastric, mylohoid, tensor
veli palatini and tensor tympani.
Methods of testing trigeminal nerve function

• Sensory
• Test for light touch, pain and temperature in the area of nerve supply
(forehead V1, cheek V2, jaw V3 (Fig. 16.25A). Sensory loss over the same
side of face, except over angle of mandible can be elicited.
• Corneal reflex– Nasociliary branch of V1 is the afferent and facial (VII)
nerve is efferent. Touching the cornea evokes a response by a contraction
of orbicularis oculi. The corneal reflex is bilateral, direct and consensual
because of interneural connections.
FIGURE 16.25A Testing for pain in trigeminal nerve distribution.
Method: A wisp of cotton is lightly swept across the lateral surface of the eye
from the sclera to cornea (Fig. 16.25B). As soon as the stimulus reaches the
sensitive cornea, the patient will wince and blink vigorously if V and VII nerves
are intact. Absence of corneal reflex is a very sensitive sign.
• Motor
• Wasting of masseter and temporalis can be seen easily, and the muscles,
while clenching the teeth.
• On opening the mouth, the jaw deviates to the side of paralysis due to the
pulling action of unopposed pterygoids of the opposite side.
• For more subtle weakness, the patient is asked to open the mouth against
resistance. Jaw deviates to the side of paralysis.
FIGURE 16.25B Testing the corneal reflex.
Causes of trigeminal nerve loss

• Meningiomas and schwanomma affecting V nerve (e.g. Trigeminal
schwanomma, cerebellopontine (CP) angle tumours, petrous apex
meningioma, etc.)
• Skull fractures
• Surgery on the face
• Cavernous sinus lesions
• Lesions at petrous apex
Facial (VII) nerve

The facial nerve has three functions –
• Motor–Supplies muscles of facial expression (Upper part of the face has
motor supply from contralateral and ipsilateral motor cortex, whereas, the
lower part has supply only from contralateral motor cortex).
• Secreto motor–Lacrimal gland, submandibular and sublingual salivary glands.
• Sensory–Taste of anterior two third of the tongue.
Methods of testing facial nerve function

Motor
• Observe –
• The face at rest for any facial asymmetry (Fig. 16.26).
• Facial tics and symmetry of eye blinking or eye closure.
• During smiling.
• Action: Ask the patient to –
• close the eyes (watch the palpebral fissures and nasolabial folds) and
wrinkle the forehead (Fig. 16.26A).
• show teeth, by saying ‘cheese’ (watch the angles of the mouth for
deviation) (Fig. 16.26B).
• blow out the cheeks with lips closed (Fig. 16.26C).
FIGURE 16.26 Facial asymmetry in left LMN facial palsy.
FIGURE 16.26 (A) Patient is asked to close the eyes closed tightly. (B)
Patient is asked to say ‘cheese’. (C) The eyes are attempted to open and
the cheeks are pressed.
Mild force is applied to open the closed eyelids and compress the cheeks to
expel the air. If the strength is not normal, the eyelids can not be opened, lips
cannot be forced apart and air can not be expelled from the mouth.
• Inference
• In LMN palsy, the eyelids are not completely closed and the eyeball rolls
up. This is called Bell’s phenomenon (Ref Fig. 18.28).
• On the side of facial palsy, the patient cannot wrinkle the forehead.
• Angle of mouth deviates to normal side while showing teeth.
• Patient cannot blow the cheeks as air escapes from affected side.
Secretomotor
• Schirmer’s test– A small piece of blotting paper is put on the eyelid on both
sides. They are removed within 5 minutes. On the affected side, the paper
may not be damped at all, or less damped compared to normal side.
Sensory
• Test for taste on the tongue: Place sweet, bitter and sour substances on the
protruded tongue on one side, followed by the other (Electrogustometry is
available now).
Facial nerve loss

This occurs in –
• Traumatic–temporal bone fracture, surgery of middle ear, parotid and skull
base.
• Inflammatory–viral (herpes zoster oticus), malignant otitis externa and
cholesteatoma.
• Neoplastic–cerebellopontine angle tumours and parotid tumours.
• Miscellaneous–brainstem infarction, multiple sclerosis and idiopathic (Bell’s
palsy).
Note
• A central ‘supranuclear’ lesion [upper motor neuron (UMN) facial palsy],
such as stroke, will preserve forehead wrinkling and cause only mild
weakness of eye closure, while the lower face is severely involved.
• UMN facial lag is seen in lesions affecting pyramidal tract above pons.
• A peripheral lesion of the VII nerve [lower motor neuron (LMN) facial
palsy] will cause weakness of the entire hemiface and the eyelid closure will
be impaired.
• Unilateral slow or delayed blinking of eye is an early sign of LMN facial
palsy.
Vestibulo-cochlear (VIII) nerve

Basic functions of vestibulo-cochlear nerve are:
• Vestibular–balancing the body
• Cochlear–hearing
Major symptoms of vestibular nerve affection are:
• Vertigo
• Vomiting
• Nausea
Methods of testing the vestibular nerve

• The patient is asked to stand erect with eyes open and eyes closed, and
observe whether the patient is waving to one or the other side.
• The patient is asked to walk in a straight line, keeping a minimum distance in
two steps (eyes open and closed) and observe waving.
Romberg test: The patient is asked to keep the eyes closed and lift the left and
right foot alternately off the ground. Approximately 80 to 90 steps are repeated
in a minute. During the process, the patient deviates from the original position,
which is measured. A patient with a defect in vestibular apparatus is unable to
maintain the original position and deviates.
Unterberger test: The patient is asked to close the eyes, keep the hands
stretched in front, and step up and step down the feet alternately 80 to 100 times
on the point the patient is standing. The patient with a defect in vestibular
apparatus is unable to maintain the original position and deviates. This is a
modification of the Romberg test.
Caloric testing (Hallpike and Dix test): The patient should lie supine on a
table, head elevated by 30 degrees, so as to make the horizontal semicircular
canal, vertical in position. The ear is irrigated with cold and hot water, which
causes change in temperature of endolymph and sets up convection currents in
the endolymph which stimulate the labyrinth, and a vestiulo-ocular reflex, is
elicited. Cold water causes nystagmus to the opposite side and warm water to the
same side. This is called ‘COWS (Cold Opposite Warm Same) response’.
Duration of nystagmus is noted and plotted on a graph called ‘calorigraph’.
Normal duration of nystagmus is 1.5 to 2.5 minutes.
Methods of testing the auditory nerve

• Whispering close to the ear is tested with the other ear closed. It is an
important early sign of VIII nerve schwanomma.
• Sensorineural hearing loss should be differentiated from conductive hearing
loss in which bone conduction is better than air conduction (Rinne’s test)
(See Ch. 21).
• Inability to use one ear for telephonic conversation will indicate that ear has
no serviceable hearing
Vestibulo cochlear nerve loss

The nerve loss occurs in –
• Infective–vestibular neuronitis and labyrinthitis
• Traumatic–skullbase fractures and surgery of labyrinth
• Toxic–drugs (streptomycin and kanamycin)
• Tumours–acoustic neuroma
Glossopharyngeal (IX) and vagus (X) nerves

Glossopharyngeal nerve has three functions
• Motor–supply stylopharyngeus muscle.
• Sensory–lining of middle ear cavity, Eustachian tube, mucosa of pharynx and
tonsil, and conveys taste sensation from posterior one third of the tongue.
• Sensorimotor–parotid gland.
Vagus nerves supply

• Motor–Muscles of upper pharynx and soft palate, and intrinsic muscles of
larynx including cricopharyngeus.
• Sensory–Dura mater of posterior cranial fossa and posterior wall of external
auditor canal.
Methods of testing IX and X cranial nerves

Sensory
• The soft palate is touched lightly with the tip of a cotton swab and the patient
is asked whether he or she is feeling the touch.
• Loss of taste sensation over posterior part of tongue is another sign.
Motor
• The patient is asked to say ‘Ah’. The palate is watched for full and
symmetrical elevation (not deviation). If one side is weak, it will fail to
elevate and will be pulled toward the normal side.
• Gag reflex: The posterior pharyngeal wall is gently touched on each side with
a cotton swab which causes reflex contraction of palatal and pharyngeal
muscles leading to elevation of palate and pharynx, and the vigour of gag is
compared (For the gag reflex, the IX nerve is afferent and X nerve is
efferent).
Loss of function of these nerves occurs in
• Jugular foramen tumours. Due to the close proximity of the IX cranial to
vagus and accessory nerves, isolated lesions of IX cranial nerve are rare.
Spinal accessory (XI) nerve
Spinal accessory nerve is a pure motor nerve and supplies sternomastoid and
trapezius.
Method of testing spinal accessory nerve

• Sternomastoid– The patient’s jaw is pressed with a hand and the patient is
asked to turn and push the hand against resistance. This is done for both
sides.
• Trapezius– The patient is asked to shrug the shoulders against resistance and
the power is noted on each side.
Accessory nerve weakness causes weakness of sternomastoid and trapezius.
Accessory nerve weakness is seen in –
• Foramen magnum and jugular foramen region lesions
• Skull base tumours
• Progressive bulbar palsy
• Accidental injury in radical neck dissection
Hypoglossal (XII) nerve

Hypoglossal nerve supplies the muscles of tongue on the same side.
Methods of testing hypoglossal nerve

• Atrophy or fasciculations– The patient is asked to open the mouth and rest
the tongue on the floor of the mouth. Atophy and fasciculations (worm like
quivers and twitches) are watched for.
• Deviation of tongue–The patient is asked to protrude the tongue which is
watched for deviation. The tongue deviates to the paralysed side due to
unopposed action of contralateral genioglossus muscle (Fig.16.27A).
• Test for subtle weakness– The patient is asked to push the tongue into each
cheek against external resistance. Strength of protrusion to one side is a
measure of the power of the opposite hypoglossal muscle (Fig. 16.27B).
FIGURE 16.27A Testing for movements of hypoglossal nerve.
FIGURE 16.27B Testing the power of hypoglossal nerve.
XII Nerve dysfunction causes wasting of one half of the tongue with
deviation of tongue to the side of paralysis. Tongue weakness is manifested by
slurring, particularly the lingual sound (la-la-la).
XII nerve palsy is seen in intracranial and extracranial skull base lesions.
Motor coordination
Cerebellar hemispheres are responsible for coordination and fine tuning of
movements, and control the ipsilateral appendages, particularly the arms.
Methods of testing the cerebellar functions

• Finger to nose test– The patient is asked to touch the nose and the examiner’s
forefinger of outstretched hand alternately. Overshoot or an oscillating
‘hunting’ tremor is looked for, and the latter tends to increase if the distance
between the finger and the nose are shortened. These abnormalities are
termed ‘dysmetria’ (Fig. 16.28).
• Finger-tapping or toe-tapping test– The patient should be asked to tap the
fingers and toes as evenly and rhythmically as possible on the thighs and
floor respectively, and irregularities in rhythm and force are to be noted (Fig.
16.29).
• Rapid alternating movements– The patient is asked to strike the thigh
rhythmically and rapidly, alternating between the palms and the backs of
hands, and also touch the thumb to each finger in succession, or rapidly
wiggle the protruded tongue from side to side. Dysrythmias of any of these
tasks is termed ‘dysdiadochinesia’ (Fig. 16.30).
• Rebound test– The patient is asked to flex the arm as strongly as possible and
hold the arm extended against resistance. The examiner should suddenly let
go of the arm. If the arm flies upward and toward the face, this signifies that
the patient is unable to check the abrupt imbalance between flexors and
extensors (Fig. 16.31).
• Heel knee shin test– The patient is asked to place one heel against the
opposite knee, tap the knee, and with the heel run smoothly down the tibia to
the ankle (Fig. 16.32).
FIGURE 16.28 Finger nose test.
FIGURE 16.29 Finger tapping and toe tapping test.
FIGURE 16.30 Rapid alternating movements test.
FIGURE 16.31 Rebound test.
FIGURE 16.32 Knee shin heel test.
Methods of testing functions of cerebellar vermis

Cerebellar vermis takes care of postural stability and gait.
• In lesions of this area, the gait will be wide-based and ataxic (staggering), and
it may be difficult to sit upright without support.
Method of testing: The patient is asked to stand normally, and the distance
between the feet is noted. The examiner should support the patient with extended
arms, and should be asked to bring the feet together until they touch, which the
patient may not be able to perform without losing balance (Fig. 16.33).
• Tandem walking– The patient is asked to walk in a straight line. Tandem
walking will be impaired in vermis tumours (Fig. 16.34).
• Tandem hopping– The patient is asked to hop in a straight line (Fig. 16.35).
Inability indicates minimal defects.
• Nystagmus can occur in cerebellar, brain stem and vestibular system diseases.
• Jerky nystagmus in horizontal gaze with larger amplitude while looking to
the side of lesion is a sign of cerebellar disease.
• Vertical nystagmus will indicate brain stem disease.
FIGURE 16.33 Test for stability.

FIGURE 16.34 Tandem walking test.
FIGURE 16.35 Tandem hopping test.
Testing the function of basal ganglia

• Disorders of basal ganglia may result in the inability to initiate motor activity,
correct postural imbalance, and control abnormal movements like tremors.
Method of testing: The abnormal movements are watched for during rest, arm
extension or during movements
Testing sympathetic system

• Horner’s syndrome (partial ptosis, meiosis, enophthalmos) will occur
whenever the sympathetic fibres descending from the hypothalamus to the
cervicodorsal cord are affected. The fibres do not cross, and hence Horner’s
will be seen on the same side of the lesion.
Motor function
Unlike in stroke in which haemiplegia is dense and obvious, in intracranial
tumours weakness of upper and lower limbs is minimal and has to be elicited
carefully.
Motor function is evaluated (See Chapter 49) by assessing the following:
• Tone
• Power
• Reflexes
Muscle tone
Arm muscle tone: The patient’s elbow of the bent arm is cupped with one hand;
then the forearm is flexed and extended, then pronated and supinated (Fig.
16.36). The forearm is then grasped, the wrist is flopped back and forth, and the
arms are raised as if tossing into the air, and then abruptly let go, and watch how
fast and symmetrically they drop.
FIGURE 16.36 Testing the arm muscle tone.
Screening tests for motor deficits in the limbs:

• Upper Limb
• Arm drift– Both arms of the patient are lifted to 90 degrees and kept for 1–
2 minutes and the weak arm will drift down and out (Fig. 16.37A).
• Finger grip power–The finger of the examiner is gripped by the patient and
both hands are compared (Fig. 16.37B).
• Finger spanning power–The stretched out fingers of both hands are
squeezed by the examiner (Fig. 16.37C).
• Alternate movement rate of fingers–Rapid, rhythmic opposition of thumb
and index finger is done with both hands (Fig. 16.37D) and any
slowness/clumsiness noted.
• Lower Limb
• Tandem walking–Walking in a straight line with one foot immediately in
front of the other (Fig. 16.34).
• Hopping with either leg–The patient is asked to hop on one leg and the
minimal weakness of the leg can be elicited by this test (Fig. 16.35).
• Foot tapping–The patient is asked to tap the feet on the floor continuously
and they are then compared (Fig. 16.38).
• Toe wriggling–will be impaired in subtle weakness.
FIGURE 16.37A Arm drift test.

FIGURE 16.37B Testing the finger power.
FIGURE 16.37C Testing the finger spanning power.
FIGURE 16.37D Opposition of fingers.
FIGURE 16.38 Foot tapping test.
Muscle power
Detailed grading of power of muscles in upper and lower limbs will be needed
when roots are involved (See Chps. 29 and 49).
Reflexes
A deep tendon reflex is the reaction of a muscle being passively stretched by
percussion on the tendon, and it is a measure of the integrity, both of the afferent
and efferent peripheral nerves and of their central inhibitory controls (See Ch.
49).
Note
• In lesions involving pyramidal tract, the deep tendon jerks (Biceps, triceps
and supinator jerks in upper limb and knee, and ankle jerks in lower limb)
will be exaggerated on the opposite side of brain lesion.
• Abdominal reflexes and cremasteric reflexes will be absent.
• Plantar response will be extensor.
In general,
• UMN weakness involves distal movements more than proximal movements.
• Extensors in upper limb and flexors in lower limb are preferentially affected.
• Hypotonia is seen in acute cerebellar lesions.
Sensory function
Sensory function is evaluated (See Ch. 49) by assessing the following:
• Touch
• Pain
• Temperature
• Position
• Vibration
Note
• Primary modalities of sensations are preserved in hemispheric lesions.
• Loss of cortical sensation in contralateral limbs occurs in parietal lobe
lesions.
• In brain-stem lesions, loss of pain and temperature sensations carried by
spino-thalamic tract can be elicited on contralateral limbs.
Stance and gait

Watching the patient walk is an important part of neurologic examination. The
varieties of gaits are –
• Steppage gait (Foot drop)–The patient elevates the flexed hip and knee
abnormally to clear the ground while walking.
• Cerebellar gait–Wide based, irregular and staggering or reeling gait, as if
drunk.
• Sensory-ataxic gait–Wide-based, short and uneven gait, characterized by high
steps and slapping down of the feet, with glueing of eyes to the ground (e.g.
tabes dorsalis).
• Haemiplegic gait–The spastic leg is extended and internally rotated, the foot
is inverted and plantar flexed, and the leg circumducts at the hip to allow the
foot to clear the ground.
• Paraplegic gait–Slow stiff and shuffling gait with the toes scraping and the
legs ‘scissoring’ due to increased adductor tone associated with spasticity
(e.g. myelopathy).
• Dystrophic gait–Waddling and lordotic posture while walking (e.g. pelvic
muscle weakness).
• Parkinsonian gait–Slow and short shuffling steps with a tendency to
accelerate as if chasing the centre of gravity.
• Apraxic gait–Similar to Parkinsonian gait, but if it is severe it will make the
patient stand glued to the ground, as if drawn by magnetic force.
• Antalgic gait–Response to pain, favouring one leg by putting as little weight
as possible on it.
• Choreic gait–Lurching or dancing gait; falls are surprisingly rare.
The minimal screening examination for stance and gait should include and
evaluate the following:
• ‘Normal’ gait across the room;
• ‘Heel walking’ with ankles dorsiflexed;
• ‘Toe walking’ on the balls of the feet with heels elevated; and
• ‘Tandem gait’ – walking with one foot in front of the other, heel to toe, on an
imaginary line.
Skull
It is usually unremarkable. except in encephalocele and skull tumours. However,
bossing of skull may be seen in convexity meningiomas and arachnoid cyst.
Bony metastases of skull bones may be seen and felt by palpation.
Summary
The screening neurologic examination should include –
• Cognitive function
• Gait
• Cranial nerves
• Motor system
• Sensory system
• Reflexes
CHAPTER 17
Head injuries
K. R. Suresh Bapu
CHAPTER OUTLINE
17.2. Surgical anatomy 213
17.3. Pathophysiology of unconsciousness in brain injury 213
17.4. Varieties of head injuries 213
• Brain injury 214
• Fractures of skull 214
• CSF fistulae 215
• Vascular injuries 216
• Scalp injuries 216
17.5. Symptoms of head injuries 216
• Physical Examination 218
• In unconscious patients 218
• In conscious patients 219
17.1 Introduction
It is important to remember the following in patients with head injuries:
• Resuscitation procedures should be carried out simultaneously along with
clinical evaluation.
• Repeated clinical evaluation every 10–15 minutes is essential in unconscious
patients in the acute stage of head injury for the first 48 hours to detect
evolving intracranial haematomas which will need evacuation before any
permanent damage occurs to the brain.
• History eliciting may not be possible as informants will not be available.
• Total evaluation of patient including chest, abdomen, spine and limbs is
mandatory.
• Hypovolemic shock is unlikely to be due to head injury alone in adults and it
is important to look for systemic injuries.
• Clinical signs of abdominal injury, like rigidity and tenderness may be
masked in unconscious patients.
Brain covered by pia-arachnoid and dura mater with cerebrospinal fluid (CSF) in
the subarachnoid space lies in the intracranial cavity protected by the bony skull
all round. The intracranial cavity is partitioned by the tentorium cerebelli into –
• The supratentorial compartment housing the cerebral hemispheres and
• The infratentorial compartment housing the brainstem and cerebellum.
The right and left hemispheres are separated by the falx cerebri. When a
haematoma forms in one compartment, as the skull cannot expand, herniation of
brain tissue from that compartment occurs across the falx cerebri and across the
tentorial hiatus. Uncus of the medial temporal lobe as it herniates across the
tentorial hiatus presses on the upper brainstem and the third nerve, causing
depression of consciousness and pupillary dilatation. This phenomenon called
‘coning’ forms the anatomical basis of unconsciousness in traumatic intracranial
haematomas and other space occupying lesions.
17.3 Pathophysiology of unconsciousness in
brain injury
Consciousness is the function of central reticular core at the upper end of
brainstem with constant stimulation of cerebral hemispheres through ascending
reticular activating system. When this system is affected either by primary injury
occurring at the time of accident or later by secondary insults due to coning,
hypoxia, ischaemia, or water and electrolyte imbalance, unconsciousness sets in.
17.4 Varieties of head injuries
Head injuries are classified into
• Brain injury
• Fractures of skull
• CSF Fistula
• Injuries of cranial nerves
• Vascular injuries (rare)
• Scalp injuries.
Brain injury
For the purpose of understanding the pathophysiology, brain injury is subdivided
into –
• Primary brain injury and
• Secondary brain injury.
Primary brain injury is further classified into –
• Concussion brain
• Diffuse axonal injury
• Primary brain stem injury
• Contusions and lacerations of brain
These injuries occur depending on the severity and direction of impact force,
movement of head and type of injury: closed or penetrating injury. With impact
force/acceleration-deceleration force, the brain moves within the cranial cavity –
the cerebrum moves over the brainstem leading to deformation of neuronal-
synaptic membranes at the central reticular core.
• Mild force causes concussion of brain characterized by transient loss of
consciousness, post traumatic amnesia and confused state, and the patient
recovers completely.
• Severe force causes diffuse axonal injury characterized by prolonged
unconsciousness and neurologic deficits.
• More severe force causes primary brain stem injury. With extremely severe
impact force, fatal injury occurs with death at the accident spot itself.
• To-and-fro movement of the head shakes various parts of the brain within the
skull causing different injuries: gray matter moves over white matter;
subcortical white matter moves over basal ganglia; brain surface hits against
the rough floor of cranial fossa floor and sharp edges of falx and tentorium
leading to contusions of the brain. When the pia-arachnoid is torn it is
termed ‘laceration’.
Secondary brain injury is characterized by the following injuries:
• Hypoxic-Ischemic injury to the brain because of impaired breathing,
aspiration, airway obstruction, chest injury, cervical spine injury,
hypotension, etc.
• Intracranial haematomas (viz., acute extradural haematoma, acute subdural
haematoma and acute intracerebral haematoma), or expanding contusions
and brain oedema can cause brain shifts and increased intracranial pressure.
• Metabolic abnormalities of glucose, sodium, acid-base, etc.
Acute extradural haematoma vs acute subdural

haematoma
• Acute extradural haematoma occurs at the site of impact and hence the scalp
injury or fracture skull will give a clue to the location of extradural
haematoma.
• Bleeding is usually from the middle meningeal branches or from the fracture
edges.
• Acute subdural haematoma is 6–8 times more common than extradural
haematoma, and is often due to acceleration and deceleration injury.
• Subdural haematoma can be contracoup, i.e. its location can be diagonally
opposite to the site of scalp injury. The bleeding is from the cortical veins.
• Due to associated severe primary brain injury, prognosis is, in general, poor
compared to isolated extradural haematoma.
Fractures of skull
• Skull fracture indicates that the force of injury was severe but does not
indicate the severity of brain injury.
• Skull fractures are classified into –
• Fractures of skull vault, which can be –
- Linear fracture (Fissured fracture) and
- Depressed fracture.
• Fractures of skull base, which can involve –
- Anterior cranial fossa;
- Middle cranial fossa; and
- Posterior cranial fossa.
• They can also be classified into –
• Simple (or closed) fractures and Compound (or open) fractures (depending
on the absence or presence of communication to atmospheric air through
breach of skin or air containing cavities in the skull).
• Fractures of skull vault will indicate the location of the underlying extradural
haematoma, when present.
• Compound depressed fractures are potential sources for the spread of
infection leading to brain abscess, meningitis, and epidural/subdural abscess.
• Depressed fractures of vault can lead to direct brain contusions and
haematomas.
• Fractures of anterior cranial fossa (Fig. 17.1) can cause –
• Ecchymosis of the upper eyelids appearing after 24 hours or so.
• Subconjuctival haemorrhage in anterior skull base fractures is pointed
towards the cornea, and posterior limit will not be seen.
• In contrast, in ‘Black Eye’ where the injury is directly over the orbit, the
ecchymoses occur in both upper and lower eyelids and appear within
minutes of injury.
• The subconjuctival haemorrhages are actually conjuctival in plane and will
move with the conjunctiva.
• Cranial nerve palsies occur in fractures of the base of the skull across or near
the cranial nerve exit foraminae.
• Fracture of temporal bone can explain 7th and 8th nerve palsies.
• Fracture of superior orbital fissure can explain spread of injuring force
close to 3rd, 4th and 6th nerves.
• Fractures near jugular foramen can cause lower cranial nerve palsies
• CSF rhinorrhea occurs in fractures involving the cribriform plate or
paranasal sinuses.
• CSF otorrhea occurs in fractures of the temporal bone. CSF leaks have the
risk of meningitis.
• Pulsatile proptosis in a head injury can be due to carotico cavernous fistula or
more commonly comminuted fracture of orbital roof with normal pulsation
of brain being transmitted to orbit. In carotico-cavernous fistula bruit may be
present over the orbit.
FIGURE 17.1 Fracture of anterior cranial fossa.
Note
Cranial nerve palsies can occur without a skull fracture, e.g. olfactory nerve
injury or optic nerve injury.
• X rays [anteroposterior (AP), lateral and oblique views] and computed
tomography (CT) of skull (Figs. 17.1A and B) are diagnostic.
FIGURE 17.1A CT—fracture of frontal sinus.

FIGURE 17.1B CT—subdural haematoma.
Treatment
• Closed depressed fractures over the forehead may need elevation for
cosmetic purposes.
• Compound fractures will need debridement to prevent brain abscess.
CSF fistulae
• Leak of CSF is caused by –
• Fractures involving the cribriform plate or paranasal sinuses can lead to
CSF rhinorrhea.
• Fractures of temporal bone leading to CSF otorrhea and through the
Eustachian tube CSF rhinorrhea.
Complications
• Meningitis
• Watery discharge is pathognomonic of CSF leak.
• Estimation of sugar in the nasal discharge and presence of sugar confirms
the CSF leak.
• CT of paranasal sinuses after intrathecal contrast is useful.
Treatment
• Lumbar pucture and CSF drainage intermittently for 10–20 days.
• Surgical repair is necessary if leak persists.
Vascular injuries
Injuries to carotids and venous sinuses are rare, but can cause aneurysms, AV
fistulae, infarcts and sinus thrombosis, and raised intracranial pressure.
Scalp injuries
Scalp injuries indicate the sites of impact force.
They are of three types –
1. Contusions
2. Lacerations
3. Haematomas
• Subpericranial–Confined to an area of one cranial bone and fixed.
• Subaponeurotic or subgaleal–More diffuse, and extend beyond the
margins of the bones.
• Subcutaneous–Superficial and moves with the scalp.
• Fractures beneath a scalp injury in unconscious patients suggest the
possibility of underlying extradural haematoma.
• Scalp injury over the occipital region may give a clue to posterior fossa
haemorrhage.
• The centre of scalp haematomas may liquefy in the centre after a few days
and often give a false impression of a depressed fracture to the palpating
finger.
• Swelling in the head with or without external injury to the scalp.
Treatment
• Immediate suturing of the wound, as the vessels are prevented from normal
contraction by fixation of their walls to fibrous stroma of scalp.
Note
When there is scalp laceration, before wound closure, the depressed fracture
has to be excluded clinically under aseptic precautions.
17.5 Symptoms of head injuries

• Loss of consciousness
• Headache
• Vomiting
• Loss of memory
• Seizures
• Bleeding ENT
• Cranial nerve palsies
Loss of consciousness
• A patient who is deeply unconscious from the time of injury (e.g. injury
sustained is severe or caused by primary brain injury).
• If the patient was unconscious for a few seconds or minutes only after the
injury and continues to be conscious (e.g. concussion brain).
• If the patient’s consciousness level has deteriorated after initial improvement,
it signals secondary insults to the brain and needs urgent evaluation and
treatment.
• ‘Lucid interval’ is the term used to indicate the period of the fully conscious
state occurring between the initial concussion and later occurrence of
unconsciousness due to coning. It is highly suggestive of extradural
haematoma, but can also occur in other conditions.
Headache
• Localized headache (e.g. local scalp injury or skull fracture at that site, or
underlying extradural haematoma).
• Diffuse headache suggests the possibility of an intracranial bleed.
• Increasing severity of headache with associated vomiting is highly
suggestive of evolving intracranial haematoma.
• Headache along with nuchal pain and neck stiffness indicates
asubarachnoid bleed.
Vomiting
• Vomiting can occur due to an intracranial bleed or vestibular dysfunction, the
former associated with headache and latter associated with vertigo.
• Vomiting of fresh blood suggests injury to the nasal cavity, paranasal sinuses,
oral cavity or fracture of the skull base.
• Vomiting of altered blood can be due to irritation of the stomach by
swallowed blood.
Loss of memory
• Registration and recall of events are affected at the time of injury and for a
variable period after the injury, leading to loss of memory.
• Loss of memory for events that happened immediately prior to injury is
known as ‘retrograde amnesia’.
• The term ‘post-traumatic amnesia’ (PTA) is used to indicate the loss of
memory from the time of injury till the return of continuous memory.
Note
• The duration of PTA and duration of unconsciousness depends on the
severity of injury and is a good indicator of prognosis.
• Duration of PTA is in general 2–4 times that of loss of consciousness.
• Retrograde amnesia shrinks over time, whereas PTA persists.
Seizures
• Generalized seizures occur more often than focal seizures.
• Seizure occurring within a few minutes of injury is called ‘impact seizure or
immediate epilepsy’.
• Seizures occurring one hour or later, but before two weeks are termed ‘early
post traumatic epilepsy’.
Note
Impact seizure does not increase the risk of late post-traumatic epilepsy.
However, early post traumatic epilepsy increases the risk of late post
traumatic epilepsy. Occurrence of seizure may be the first sign of evolving
haematoma, brain oedema or electrolyte imbalance. Clinically it causes an
abrupt decline in the conscious level and also increases the risk of aspiration
and asphyxia.
Bleeding ENT
• History of bleeding from the ear or nose will indicate either local injury or
fracture of the skull base. Bleeding ear-nose-throat (ENT) can lead to
aspiration; swallowed blood can irritate the stomach.
• A H/o nasal bleed warns the surgeon the possibility of not only injury to the
olfactory nerves but also of CSF rhinorrhea occurring later.
• A H/o ear bleed warns the surgeon the possibility of CSF otorrhea or the
associated 8th nerve injury (hearing loss and vertigo) and the possibility of
delayed facial palsy.
Cranial nerve palsies

Cranial nerve palsies in head injuries are caused by –
• Fractures of the base of skull across or near the cranial nerve exit foraminae.
• 7th and 8th nerve palsies can occur in the fracture of the temporal bone.
• 3rd, 4th and 6th nerve palsies can occur in fractures of the superior orbital
fissure.
• Lower cranial nerve palsies can occur in fractures near the jugular
foramen.
• Injuries of nerves directly to Olfactory and optic nerves.
Quick assessment of patient as a whole [including glasgow coma score (GCS),
pupils, developmental eye movement and limb movement] and resuscitation
should be carried out simultaneously and will get priority over detailed history
eliciting especially in unconscious patients.
Eliciting history
• Mode of Injury: How did the patient sustain injury? (with details)
Head injuries can be caused by various ways (e.g. road traffic accident, fall
from height, fall of heavy object overhead, assault with sharp weapon/blunt
weapon, or gunshot injury).
• Level of Consciousness immediately after injury:
• Is the patient unconscious from the time of injury?
• Was the patient able to talk/walk/understand what was told?
• Is conscious level of the patient improving or deteriorating?
• Was there a period of complete consciousness before becoming
unconscious again (lucid interval)?
As each question has its own relevance in diagnosis and management, the
answers should be determined in detail (See Page 216).
• Post traumatic amnesia and retrograde amnesia (tested only in conscious
patients):
• Can the patient recollect the events that happened immediately before the
injury?
• Can the patient recall the exact events at the time of injury?
• Can the patient recall events that happened immediately after the injury?
Each question has its own bearing in diagnosis and management and the
answers should be determined in detail (See Page 216)
• Headache: In conscious patients, details of headache have to be obtained.
• Where is the head ache? Is it just over the injured scalp or deep inside the
skull?
• Is the intensity of headache increasing in the last few hours?
Each question being asked by the examiner has its own significance in
diagnosis and management; therefore the responses should be determined in
detail (See Page 216).
• Vomiting: Vomiting in unconscious patients often leads to asphyxia,
aspiration and respiratory abnormalities.
• Has the patient vomited?
• Is the vomitus mixed with fresh blood or altered blood?
• Is it associated with headache or positional vertigo?
Vomiting is a very reliable sign in head injuries and the details have to be
determined (See Page 216).
• Bleeding from ear or nose: Is there any bleeding from the ear or nose?
Bleeding from ENT usually indicates local injury to the ENT or a fracture of
the skull base, and may warn the surgeon of a delayed nerve palsy, and also
cause aspiration into lungs (See Page 217).
• Seizures: Did the patient have seizures after the injury?
Seizures after head injuries have great relevance and determine the prognosis.
The details have to be determined (See Page 217).
• Cranial nerve deficits: Does the patient have any disturbance of smell,
vision, hearing or speech?
History of loss of smell, loss of vision, diplopia, facial numbness, facial palsy,
hearing loss, vertigo, or swallowing difficulties may indicate appropriate cranial
nerve injuries directly or caused by fractures.
• Past History: History of head injury in the past multiplies the effect of the
current injury in causing brain damage.
• Personal History: Alcohol consumption is the commonest cause of single
vehicular accident. Sometimes a patient develops a stroke, syncope or
idiopathic seizure and falls down at home sustaining scalp injury and
clinically mimicking head injury; detailed history of events at the onset of
neurologic event will clarify the cause of unconsciousness in most instances.
Position of patient is an important aspect in physical examination.
Note whether the patient is lying –
• Flaccid with the jaw relaxed (serious condition) or
• Curled up on the side and is irritable (favourable condition).
In unconscious patients
Examination of an unconscious patient has to be done systematically in a few
steps, remembering that resuscitation has to be done simultaneously.
Step 1
Determination of level of consciousness
This is done using the Glasgow Coma Score (GCS) (Table 17.1).
TABLE 17.1
Glasgow Coma Score
Eye Opening Verbal Response Motor Response
E1–No eye opening E2– V1–No response V2– M1–No response M2–Decerebrate (extension of UL and
Eye opening to pain Incomprehensible LL) M3–Decorticate (flexion of UL and extension of
E3–Eye opening to call (moaning and groaning) LL) M4–Withdrawal response (flexion of UL and LL)
E4–Spontaneous eye V3–Inappropriate V4– M5–Localizing pain M6–Obeys commands
opening Confused V5–Oriented
The GCS
• in fully conscious patient is E4 M6 V5, and
• in totally unconscious patient GCS is E1 M1 V1
(When intubated or tracheostomy is done, the verbral response is indicated as
VET or VT)
Step 2
Examination of eyes
• Evidence of haemorrhage (See Step 6).
• Pupils–Tested by applying a beam of light with a torch, and the examiner
looks for the size and reaction to light.
Inference
• Unconscious patients (Fig. 17.2) with –
• Normal pupillary size and light response have very good chance of
recovery, as it indicates an intact brain stem.
• A unilaterally dilated and non-reacting pupil indicates tentorial herniation
due to acute intracranial haematoma or expanding contusions until proved
otherwise, and is an urgent indication for surgical intervention.
• Bilateral mid dilated unresponsive pupil is a sign of irreversible brain stem
damage.
• Pinpoint pupils occur in pontine injury.
• A unilateral small light responsive pupil (Horner’ syndrome) indicates
ipsilateral sympathetic palsy due to carotid artery injury or T1 root injury.
FIGURE 17.2 Pupillary reactions.
Relative afferent pupillary defect

Detected by swinging a flashlight from one eye to the other; it is the clinical
method to diagnose optic nerve injury in unconscious patients. When light is
thrown from the normal eye to the ‘blind’ eye, the pupils dilate (See Ch. 16).
Step 3
Reflex eye movements (provided there is no cervical spine injury) in
unconscious patients are checked by rotating the head side to side. The
movement of the eyes to the contralateral side is termed ‘Doll eye movement’
(Fig. 17.3).
• Intact ‘Doll eye movement’ indicates an intact brain stem.
• Absent ‘Doll eye movement’ indicates an injury to the medial longitudinal
fasciculus of the brain stem and carries extremely poor prognosis.
FIGURE 17.3 Doll eye movements.
Ice-caloric test
This is done by injecting 10–20 ml of ice-cold water into the external ear canal
with the patient’s head tilted up by 60o. In unconscious patients, nystagmus does
not occur, but the eye will deviate to the side of the injection. If there is no eye
movement, it is diagnostic of brain stem dysfunction and carries very poor
prognosis.
Step 4
Limb movements are assessed in all patients with motor response of 4, 5 and 6
(See Ch. 49). With stimulus over supra orbital margin or sternum, the
movements of both sides can be compared and any haemiparesis can be
diagnosed. The presence of haemiparesis is suggestive of injury to the
contralateral corticospinal tract.
Step 5
Signs of intracranial tension (ICT)
Increased intracranial pressure leads to bradycardia, tachypnea and
hypertension. Monitoring of pulse, respiratory rate and blood pressure (BP) are
essential in all head injury patients.
Step 6
Examination of scalp, eyelids and conjunctiva are very important in many
ways –
• Scalp
• Hair may have to be shaved to visualize the scalp injuries.
• Look for contusions, haematomas and lacerations.
• Eyelids
• Eyelids are swollen and ecchymotic in anterior cranial fossa injuries. The
ecchymoses occur in both upper and lower eyelids and appear within
minutes of the injury.
• Conjunctivae
• The subconjuctival haemorrhage in the upper eyelid in the anterior skull
base fractures is pointed towards the cornea and the posterior limit will not
be seen.
• In contrast, in ‘Black Eye’, where the injury is directly over the orbit, The
subconjuctival haemorrhages are actually conjuctival in plane and will
move with the conjunctiva.
Step 7
Look for injuries to the rest of the body:
• Cervical spine injury is deemed to be present in all unconscious head injured
patients until proved otherwise by an X ray or CT scan.
• Any unconscious adult patient with hypovolemic shock is deemed to have a
chest injury, an abdominal injury, or a fractured pelvis or femur and a goal
oriented clinical examination is done to exclude these injuries.
• As clinical signs, like muscle guarding, tenderness, etc., may be absent due to
head injury, specific investigations will be needed.
Recognition of emergency situations

• Deteriorating level of consciousness
• Asymmetric unresponsive pupil
• Abnormal motor posturing
• Impaired doll eye movement
• Bradycardia and respiratory distress
In conscious patients
Detailed neurological evaluation is possible in conscious patients.
• Mental Functions
• Memory impairment
• Language disturbances
• Orientation to time, place and persons
• Calculation ability, and
• Other higher mental functions.
Duration of retrograde amnesia and post traumatic amnesia are determined.
• Cranial nerve Examination (See Ch. 16)
• Olfactory nerve– Anosmia due to olfactory nerve injury is a very common
condition.
• Optic nerve– Visual impairment has to be quantified by a detailed neuro-
ophthalmic evaluation for visual acuity and visual field charting as there
may be an indication for urgent steroid therapy.
• III, IV and VI nerves– Eye movements are checked.
• V nerve– Facial sensations, corneal reflexes, and tests for muscles of
mastication are done.
• Facial nerve– Facial paresis can be missed in the acute stage when there is
facial oedema. Delayed facial palsy can occur in the fracture of the
temporal bone. The early signs of facial paresis are incomplete/delayed
closure of the eyelids.
• Auditory nerve– Hearing is assessed by simple whispering sounds or words
while masking the other ear by alternating pressure on tragus.
• Glossopharyngeal and vagus nerves– Palatal movements are checked by
asking the patient to say ‘Aah’. The palate will deviate to the side opposite
the lesion pulled by normal muscles.
• Hypoglossal nerve– The tongue deviates to the side opposite the lesion.
• Spinal sensory and motor examination
• Weakness of limbs can be subtle and can be brought out by simple tests,
like arm drift, finger spanning power, standing on one leg, hopping with
either leg, etc.
Development of fresh focal neurologic deficit is a sign evolving intra cranial
haematoma.
• Examination of the scalp, eye lids and conjunctiva, and examination of
other systems are done as in unconscious patients.
CHAPTER 18
Face and oral cavity

S.M. Balaji
CHAPTER OUTLINE
18.1. Development of face and oral structures 220
18.2. Surgical anatomy of face 221
18.3. Diseases of face 221
18.4. Surgical anatomy of oral structures 222
18.5. Diseases of oral cavity 223
• Clefts 224
• Fordyce’s granules 225
• Ranula 225
• Haemangiomas 226
• Ankyloglossia 227
• Torus 227
• Cysts of newborn 227
• Burns 228
• Denture stomatitis 228
• Amalgam tattoo 228
• Ankylosis 228
• Herpetic lesions 229
• Angular cheilitis 229
• Ginigivitis 229
• Aphthous ulcers 230
• Angioneurotic oedema 231
• Ludwig’s angina 231
• Noma/Gangrene 231
• Tuberculosis 232
• Epulis 232
• Foreign body granuloma 232
• White lesions 233
• Oral submucous fibrosis 233
• Oral candidiasis 234
• Necrotising sialometaplasia 234
• Chronic osteomyelitis of jaws 235
• Cervicofacial actinomycosis 235
• Dental cyst 235
• Lymphangioma/Macrochelia/Cystic Hygroma 236
• Ameloblastoma 236
• Salivary gland tumours of oral cavity 237
• Malignant lesions of oral structures 238
• Verrucous carcinoma 239
• Malignant tumours of jaws 240
• Oral manifestations of anaemia 241
18.6. Symptoms of oral cavity pathologies 241
• General 244
• Face 244
• Lips 246
• Oral mucosa 248
• Tongue 250
• Floor of the mouth 253
• Buccal mucosa 254
• Gingiva 256
• Palate 256
• Pharynx and larynx 258
• Teeth 258
• Jaws 262
18.1 development of face and oral structures
About the sixth week of fetal life, a depression appears at the front of the head.
Around this depression called ‘stomodeum’ (primitive mouth), five processes
appear; one at the cephalic end (frontonasal process) and on each side, a
maxillary and a mandibular process (Figs.18.1A and B). The frontonasal process
becomes subdivided, by the appearance of olfactory pits (future nostrils), into a
solitary median nasal process (future nose) and two lateral nasal processes
(future alae of the nose). The median nasal process becomes bluntly bifurcated,
forming the processus globularis. The central part of the processus globularis
forms the philtrum. The union of the two maxillary processes (future cheeks)
and the median nasal process forms the upper lip. The union of two mandibular
processes forms the soft tissues covering the lower jaw and also the lower lip.
FIGURE 18.1A Development of face.
FIGURE 18.1B Development of face.
Tongue: The anterior two-third of the tongue is formed by the fusion of –

• The tuberculum impar and
• The two lingual swellings.
and the posterior one third is derived from the third arch mesoderm.
Palate: The palate is formed by the fusion of –
• The palatal process from the maxilla on each side and
• The primitive palate from the frontonasal process.
Teeth: Epithelial thickenings (dental laminae) give rise to milk teeth or
deciduous teeth. The permanent teeth develop from the buds from the dental
laminae.
18.2 surgical anatomy of face
The face extends from the hairline above to the chin below, and is bounded on
the sides by the ears.
The four orifices of the face are the orbits, nose, and the mouth, which are
guarded by the eyelids, nostrils and lips respectively. Each of them contains a
group of circular muscles, which act as sphincters and dilators. The muscles are
highly differentiated and are responsible for expressions.
The face has a rich vascular supply with abundant anastomosis within them,
and the veins do not have valves. The rich arterial supply helps in quick wound
healing, and the absence of valves in the veins predispose to infections spreading
to the cavernous sinus inside the skull.
18.3 diseases of face
The diseases of the face are many and are classified on its aetiological basis
(Figs. 18.1C and D). The aetiological classification is given in Table. 18.1.
FIGURE 18.1C Macrostomia.
FIGURE 18.1D Hairy nevus.
TABLE 18.1
Aetiological Classification of Lesions of the Face
Aetiology Swellings Ulcers Sinuses and Fistulae Others

Congenital Meningocoele Preauricular sinus Clefts
Median dermoid Naevus
Angular dermoid Macrostomia
Preauricular dermoid
Haemangioma
Lymphangioma
Traumatic Haematoma Ulcers Orocutaneous fistula Fractures
Acute inflammatory Cellulitis Ulcers
Erysipelas
Abscess
Chronic Lupus vulgaris Cancrum oris Chronic osteomyelitis
Lymphadenitis Parotid fistula
Actinomycosis
Alveolar sinus
Tuberculosis
Benign neoplastic Mole
Lipoma
Fibroma, neurofibroma
Malignant neoplastic Squamous cell carcinoma Squamous cell carcinoma Squamous cell carcinoma
Malignant melanoma Basal cell carcinoma Orocutaneous fistulae
Miscellaneous Sebaceous cyst
Fibrous dysplasia
The differential diagnosis is detailed in appropriate chapters, the clinical

evaluation and physical examination are done in lines with the examination of
swellings, ulcers, sinuses and fistulae in general (See Chs. 9, 10, and 11).
18.4 surgical anatomy of oral structures

The oral structures consist of the lips (upper and lower), tongue, palates (hard
and soft), floor of the mouth, tonsils, and the jaws with the teeth forming the
masticatory apparatus together (Fig.18.2). The tongue is a movable, muscular
organ of taste and speech. The oral and perioral musculature form part of the
muscles of facial expression and are inserted into the skin.
FIGURE 18.2 Anatomy of oral cavity.
The mucous membrane lining the oral cavity consists of a layer of stratified
squamous epithelium and a sub-epithelial layer, the lamina propria, which
consists of a fibrous connective tissue and contains capillaries, nerves and the
minor salivary glands. The minor and major salivary glands form an integral part
of the oral cavity and their ductal orifices drain into the mouth. The
submandibular and submental lymph nodes form the lymphatic drainage system.
The skin of the face, like the mucous membrane, also possesses two layers –
the epidermis and the underlying corium with its associated appendages, the
sweat and sebaceous glands, and the hair follicles.
The bones of the region include the maxilla, the mandible, the zygoma and
vomer, and the palatine, sphenoid, hyoid, and temporal bones, as well as the
cervical vertebrae. The maxilla and the mandible form the skeletal framework of
the oral cavity. The mandible articulates with the temporal bone (glenoid fossa)
at the temporomandibular joint and is elevated and depressed by the masticatory
muscles, namely the masseter, temporalis, pterygoids, digastric and the genial
muscles.
The muscle systems with which the oral diagnostician must be familiar are
those of facial expression, mastication, and swallowing, as well as those
involved in movements of the head and neck. Not only do these muscles,
alongwith the bony and cartilaginous structures and vessels, provide landmarks
that facilitate an effective examination, they also, with the fascial planes, tend to
mechanically obstruct or guide the invading and spreading disease processes,
such as infections and neoplasms. Consequently, the examiner must be aware of
the exact location and plane of each muscle and the extent of its normal
movements during function.
18.5 diseases of oral cavity

The aetiological classification of disorders of oral cavity is tablulated in Table
18.2.
TABLE 18.2
Aetiological Classification of Disorders of Oral Cavity
Soft Tissue Hard Tissue

Lesion
Lips Oral mucosa Tongue Palate Jaws/TMJ Teeth
Congenital Cleft Fordyce Ankyloglossia Cleft Micrognathia Agenesis

granules
Lip pits Ranula Fissured Torus Macrognathia Mottled
tongue
Double lip Haemangioma Papillary Cysts Agnathia
atrophies
Macrostomia Scleroderma Lingual thyroid
Microstomia Macroglossia
Microglossia
Traumatic Ulcers Ulcer/burns Ulcer Ulcer, fracture Fractures Fractures
Burns Amalgam Contact Arthritis
tattoo stomatitis
Contact Ankylosis
stomatitis
Denture Aneurysmal
stomatitis bone cyst
Acute Herpes Gingivitis Acute Abscess Disc Pulpitis,
inflammatory superficial displacement periodontitis
glossitis
Allergy Aphthous ulcer Aphthous ulcer Aphthous ulcer Ludwig’s angina
Cheilitis Abscess
Chronic Noma Tuberculosis Candidiasis Gumma Myalgia Cysts, pulpitis,
inflammatory periodontitis
Syphilis Cysts Osteomyelitis
Epulis Benign Necrotising Actinomycosis
migratory sialometaplasia
glossitis
Granuloma Median Smoker’s palate,
rhomboid candidiasis
glossitis
White lesions Leukoplakia
Sarcoidosis Submucous
fibrosis
Benign Lymphangioma White lesions Papilloma Adenoma Ameloblastoma
neoplastic
Fibroma Lymphoid Fibrous
nodules dysplasia
Papilloma Lymphangioma
Keratoacanthoma Haemangioma
Neurofibroma
Malignant SCC SCC SCC Kaposi’s sarcoma SCC
neoplastic
BCC Salivary gland Salivary gland Osteosarcoma
tumours tumours
Melanoma Verrucous Verrucous
carcinoma carcinoma
Metabolic Anaemia Anaemia Paget’s disease, Fluorosis
gout
Clefts
• Oral and orofacial clefts are congenital malformations of the face, more
commonly the lip and palate, where there is a failure of fusion of median
nasal process, maxillary and lateral nasal processes.
• Incidence being 1 in 600 live births.
• Clefts of the face also occur rarely, often in the lateral facial regions (Figs.
18.3 and 18.4).
• Mandibular clefts are extremely rare.
• These children also may present with other anomalies, some are–
• Isolated cleft palate with micrognathia (Pierre Robin’s syndrome).
• Children with isolated cleft palate with congenital cardiac anomalies, like
interrupted aortic arch (Velo-cardio-facial syndrome).
• Midline clefts may be associated with meningocoele.
• Van der Woude’s Syndrome is characterized by pits in the lower lip.
FIGURE 18.3 Lateral facial cleft.

FIGURE 18.4 Bilateral alar cleft.
Cleft lip may be –
• unilateral or bilateral (Figs.18.5A and B);
• complete or incomplete (Fig. 18.6); or
• associated with cleft palate (Figs.18.7A and B).
FIGURE 18.5A Complete unilateral cleft lip.
FIGURE 18.5B Complete bilateral cleft lip.
FIGURE 18.6 Incomplete unilateral cleft lip.
FIGURE 18.7A Cleft of hard palate.
FIGURE 18.7B Cleft of soft palate.
• MRI, CT scan, and other investigations as indicated to rule out the presence
of associated craniofacial and other anomalies.
Treatment
• Surgical correction of respective clefts.
• Multidisciplinary management may be required to correct all the associated
cranio-facial and speech problems.
Fordyce’s granules
• Heterotropic collections of sebaceous glands at various sites in the oral cavity.
• Commonly seen in the buccal mucosa, lip, tongue, gingiva and palate.
• The granules are more apparent in adults than children because the sebaceous
glands and hair system do not reach maximal development until puberty.
• Appear as small yellow spots or large plaques projecting slightly above the
tissue.
• Histopathology is conclusive.
Treatment
• No treatment is generally necessary.
• Excision is indicated for keratin filled pseudocyst or benign sebaceous gland
adenoma.
Ranula
• Mucous or salivary retention cyst of submandibular or sublingual salivary
gland.
• May arise due to duct blockage or development of ductal aneurysm.
• Slowly enlarging painless bluish mass, often resembling a frog’s belly, in the
floor of the mouth (Fig.18.8A).
• Tongue is elevated, causing difficulty in speech and mastication.
• Swelling appearing on one side of the midline causes deviation of the tongue
to the opposite side.
• Transillumination is positive (Fig. 18.8B).
FIGURE 18.8A Simple ranula.
FIGURE 18.8B Demonstration of transillumination in ranula.
• Fine needle aspiration cytology (FNAC) is conclusive.
Treatment
• Excision or marsupialization of swelling.
Haemangiomas
• Benign tumours of blood vessels occurring on the skin of face and neck; also
on the tongue, buccal mucosa and lip.
• The bone, viscera and the central nervous system (CNS) may be involved.
• Majority of the lesions are present at birth.
• Haemangiomas are blue, purple, or purplish red in colour, usually blanch
when pressure is applied (Fig. 18.9A-C).
• Haemangiomas of the tongue present as macroglossia. If it is traumatized, it
bleeds profusely and may present as an ulcer.
FIGURE 18.9A Haemangioma of upper lip.

FIGURE 18.9B Haemangioma of nose.
FIGURE 18.9C Mandibular haemangioma.
• Haemangiomas are usually diagnosed clinically and no investigations are
necessary for the majority of lesions.
• MRI or angiography are useful to rule out intracranial extensions and to
identify the feeder artery.
Treatment
• They can grow for up to 18 months after which they start regressing. This
period may extend even from 3 to 10 years and is termed Regression.
Almost all the childhood haemangiomas involute spontaneously without any
treatment.
• However, some haemangiomas can be disfiguring and psychologically
distressing, and require medical intervention. The various treatment
modalities available are: surgery, radiation therapy, sclerosing agents,
cryotherapy, carbondioxide snow and compression.
Ankyloglossia
• Occurs as a result of fusion between the tongue and the floor of the mouth or
short lingual frenum attached too near to the tip of the tongue (Fig.18.10).
FIGURE 18.10 Ankyloglossia.
• Movements of the tongue are restricted leading to slurred speech.
Treatment
• Lingual frenectomy.
Torus
• Developmental exostosis of the mandible (torus mandibularis) or palate (torus
palatinus).
• Occurs in the middle age with predominance in women.
• Hard, smooth, slow growing mass occurring beneath the premolars in the
lingual aspect of the mandible above the mylohyoid line.
• In the palate, it occurs in the midline (Fig. 18.11A).
• Mandibular tori occur bilaterally (Fig.18.11B).
FIGURE 18.11A Palatal tori.

FIGURE 18.11B Mandibular tori.
• Radiographs are contributory.
Treatment
• Removal warranted if it interferes with denture reconstruction, speech or
mastication.
Cysts of newborn
Cysts occur along the midline and originate from epithelial remnants of the –
• dental lamina (gingival cyst);
• salivary gland (Bohn’s nodules); or
• epidermis (epidermoid cyst).
These developmental cysts are found in the newborns.
Fluctuant swelling –
• at the alveolar ridge (gingival cyst);
• at the junction of hard and soft palate (Bohn’s nodules);
• in the anterior portion of the floor of the mouth (epidermoid cyst); or
• at midpalatine raphe (Epstein’s pearls).
The epidermoid cyst occuring in the floor of the mouth may be mistaken for
a ranula, but ranula has thinner wall. They are neither tender nor painful, but
slightly movable.
• Aspiration reveals cheesy exudates.
Treatment
• Bohn’s nodules and gingival cysts disappear spontaneously by opening onto
the surface.
• Epidermoid cyst will require marsupialization.
Burns
• Burns may occur due to contact of chemicals, like aspirin, sodium perborate,
eugenol, formoacresol, hydrogen peroxide, or pyrazone in the oral mucous
membrane.
• Burns of the oral mucous membrane manifest as gingivostomatitis, ulceration
of oral tissues, or necrosis of bone, as per severity.
DD: White lesions, candidiasis, acute necrotising ulcerative gingivitis
(ANUG).
Treatment
• Palliative treatment.
Denture stomatitis
• Caused by Candida albicans in denture wearers.
• Aggravated by denture trauma, continuous denture wearing, poor oral
hygiene, and possibly dietary and systemic alterations.
• Mucosa beneath the denture becomes extremely red, swollen, smooth, or
granular and painful.
• Redness of the mucosa is sharply outlined and restricted to the tissue actually
in contact with the denture.
Treatment
• Antifungal therapy followed by palliative treatment and replacement of
denture.
Amalgam tattoo
• Usually produced when the gingiva is abraded at the time a tooth is prepared
for restoration or inclusion of amalgam filling in sockets after extraction.
• Most common locations: gingiva, alveolar mucosa and buccal mucosa.
• Asymptomatic dark bluish lesion, usually seen on the gingiva in which the
teeth have been restored with silver amalgam.
DD: Superficial Melanomas, Melanomas
• Excision biopsy.
Treatment
• Removal of restoration may be needed to prevent further damage to tissues.
Ankylosis
• Abnormal immobility of the joint due to fusion (fibrous or bony) between the
articular surface (glenoid fossa) at the base of the skull and the condylar
process.
• Usually preceded by a history of trauma to the temporomandibular joint.
• Progressive decrease in mouth opening.
• Bilateral cases present with micrognathia, small lower jaw with typical bird
like face.
• Unilateral ankylosis presents with deviation of the face, hemimandibular
hypoplasia, deviation of the mouth opening, malocclusion and facial
asymmetry (Fig.18.12).
FIGURE 18.12 TMJ ankylosis—flattened left side face with deviation of
chin to right side.
DD: Submucous fibrosis
• Radiographs reveal obliteration of joint space.
Treatment
• Gap arthroplasty with interposition of graft material to prevent reankylosis
Herpetic lesions
• Caused by Herpes Simplex Virus Type I.
• Common in young age groups.
• A cluster of small discrete grey or white vesicles without red erythematous
halo.
• Vesicles quickly rupture forming small punctate ulcers.
• Ulcers are round in shape.
• Lesions are found in the skin of the corner of the mouth, keratinized mucosa,
hard palate (Fig. 18.12A), gingiva and alveolar ridge (Fig.18.12B).
FIGURE 18.12A Herpetic lesions on hard palate.
FIGURE 18.12B Herpetic lesions on the gingiva.
DD: Shingles, aphthous ulcers, erythema multiforme, epidermolysis bullosa,

Koplick’s spots and burns.
• Immunofluroscence test and cytological examination.
Treatment
• Antiviral therapy, if severe.
Angular cheilitis
• Caused by Candida albicans.
• Discrepancy in the vertical height of denture.
• Riboflavin deficiency.
• Feeling of dryness and burning sensation at the corners of the mouth.
• One or more deep fissures or cracks at the corner of the mouth (Fig.18.13).
• The fissures do not involve the mucosal surface of the commissures inside the
mouth, but stop at the mucocutaneous junction.
FIGURE 18.13 Angular cheilitis.
DD: Basal cell carcinoma and rhagade.
Treatment
• Correction of primary cause.
Gingivitis
Gingival enlargement is of two types –
• Fibrous enlargement of the gingiva occurs due to –
• intake of drugs (phenytoin, nifidepine, cyclosporine);
• ill fitting denture;
• poor oral hygiene;
• prolonged orthodontic treatment;
• pregnancy;
• idiopathic; and
• diabetes worsens existing periodontal disease and fulminates it.
Fibromatosis gingiva is a congenital condition.
• Inflammatory enlargement of gingiva is caused by leukemia and scurvy.
It may involve a single tooth, a few teeth or an entire arch (Fig. 18.14A).
FIGURE 18.14A Gingival enlargement.
• The gingival papillae are oedematous and shiny-red, with loss of stippling of
the interdental gingiva with bulging of the normal, knife edged papilla.
• Gingival enlargement due to chronic gingivitis (Fig.18.14B) is accompanied
by bleeding.
FIGURE 18.14B Chronic gingivitis.
Treatment
• Gingivectomy and gingivoplasty.
Aphthous ulcers
There are four types of aphthous ulcers. They are –
• Recurrent aphthous major
• Recurrent aphthous minor
• Recurrent herpetiform ulcerations
• Recurrent ulcers associated with Behçet’s syndrome
Aetiology could be –
• Bacterial infection
• Viral infection
• Immunologic abnormalities
• Deficiency of iron, vitamin B12 and folic acid
• Stress
In women, it is found to be hormone related also.
Predominantly found on non-keratinized, free, mobile mucosa, like the cheek,
labial mucosa, tongue and soft palate (Figs.18.15A and B).
• Recurrent aphthous major
• Large painful ulcers of size 1–3 cm usually 1–10 in number on the lips,
cheek, tongue, soft palate or fauces.
• Recurrent aphthous minor
• Appears as one or more small nodular (3–10 mm), vesicle like lesions
containing mucus, which rupture to present as single or multiple
superficial erosions with a well circumscribed margin, covered by a grey
membrane and surrounded by a characteristic, erythematous halo.
• Also presents a generalized oedema of the oral cavity.
• Recurrent herpetiform ulcerations
• Characterized by crops of multiple, small (1–3 mm), shallow ulcers, often
upto 100 in number, which may occur at any site in the oral cavity.
• Recurrent ulcers associated with Behcet’s syndrome
• Small pinhead sized erosions that gradually enlarge and coalesce.
• Features of Behcet’s syndrome (oral ulcers, genital ulcers, and eye and skin
lesions).
FIGURE 18.15A Aphthous ulcer on the faucial pillar.
FIGURE 18.15B Aphthous ulcer of tongue.
DD: Herpes, traumatic ulcers, herpangina, and hand-foot mouth disease.
• Immunofluorescent serological techniques and cytologic smears.
Treatment
• Recurrent aphthous major ulcers heal spontaneously, but leave a scar,
whereas, recurrent aphthous minor ulcers also heal spontaneously and do
not leave a scar.
• In severe cases, mouthwash (prednisolone 5 mg or povidone iodine) is
warranted.
Angioneurotic oedema
• Manifestation of allergic reaction.
• Usually hereditary (absence of C1 esterase enzyme, endocrine disturbance).
• This may also occur due to psychological disturbances.
• Smooth, diffuse, oedematous swelling, particularly involving the face around
the lips, chin, eyes, tongue, and also hands and feet.
• Swelling usually occurs around the eyes and lips.
• Affected person may unable to open the eyes due to swelling.
• Itching or pricking sensation may be present.
DD: Cellulitis and fracture.
Treatment
The condition usually persists for 24–48 hours and subsides after elimination of
causative agent
• Palliative treatment–antihistamines.
• Emergency tracheostomy may be needed for severe cases causing oedema of
glottis.
Ludwig’s angina
• Severe cellulitis beginning usually in the submandibular space, secondarily
involving the submental and sublingual spaces.
• Caused by periapical or periodontal infection of mandibular molar,
penetrating injury of the floor of the mouth or osteomyelitis in compound
jaw fracture.
• Rapidly developing board-like swelling of the floor of the mouth and
consequent elevation of the tongue.
• The swelling is firm, painful, diffuse, showing no evidence of localization
(Fig.18.16).
• There is difficulty in eating and swallowing, as well as breathing.
• As the swelling involves the neck, oedema of glottis may occur.
FIGURE 18.16 Ludwig’s angina—swelling of bilateral submandibular,

submental, left masseteric, infratemporal and temporal spaces.
• Biochemical investigations and cytological smear.
Treatment
• Incision and drainage.
• Appropriate antibiotic therapy.
• Tracheostomy, if needed.
Noma/gangerene (cancrum oris)

A rapidly spreading gangrene of the oral and facial tissues caused by Vincent’s
organisms (Borrelia vincentii), that occurs usually in debilitated or nutritionally
deficient persons.
• Noma usually begins as a small ulcer of the gingival mucosa, which rapidly
spreads and involves the surrounding tissues of jaws, lips and cheeks by
gangrenous necrosis.
• The initial site is commonly the area of stagnation around a fixed partial
denture, overlying skin becomes inflamed, oedematous, and finally necrotic,
with a result that a line of demarcation develops between the healthy and
dead tissue.
• Large masses of tissue may slough out leaving the jaw exposed.
• Foul odour is present.
• Patients have hyperpyrexia during the course of disease, suffer secondary
infection, and may die from toxemia or pneumonia.
• Cervical lymph nodes are enlarged and tender.
DD: Carcinoma and actinomycosis.
• Periodic Acid Schiff Test (PAS test).
Treatment
• Antibiotic therapy works in the initial stages.
• Tissue debridement
Tuberculosis
• Tuberculous ulcer may occur in any region of the oral cavity.
• Most common on the tongue, palate, lips, buccal mucosa, gingiva and
frenulum.
• Tuberculous gingivitis is an unusual form of tuberculosis (TB), which may
present as diffuse, hyperemic, nodular, papillary, proliferation of gingival
tissues.
• TB may also involve the bone of the maxilla and mandible causing a
tuberculoma.
• The usual tuberculous lesion is an irregular, deep painful ulcer, with
undermined edge, which tends to increase slowly in size.
DD:
Traumatic ulcer and gumma.
• Mantoux test, biochemical investigations and cytological smear.
Treatment
• Anti tubercular treatment.
Epulis
• Epulis describes a localized swelling on the gingiva (Fig.18.17A).
• Three main types of epulis are recognized –
• Fibrous epulis;
• Giant cell epulis; and
• Vascular epulis.
• Risk factor: chronic irritation.
FIGURE 18.17A Epulis.
Whatever the type, there are similarities in clinical presentation.
• It presents as a localized swelling.
• Ulceration of overlying epithelium is common.
The various swellings of gingiva are shown in Table 18.3.
TABLE 18.3
Swellings of Gingiva and Their Clinical Features
Swelling Clinical Features

General appearance Colour Sessile or
pedunculated
Fibroma Elevated lesion with smooth surface; it is painless Normal colour Sessile
Papilloma Exophytic growth made up of numerous small finger like Normal colour Pedunculated
projections; it is a circumscribed tumour
Pyogenic Elevated mass; smooth or lobulated or warty surface; frequent Deep red or purple Pedunculated or
granuloma ulceration; bleeds upon slight trauma sessile
Gingival cyst of Resembles a superficial mucocele; well circumscribed, small Translucent Sessile
adults and painless swelling
Peripheral Peripheral slow-growing solid; firmly attached gingival mass Normal colour Sessile
odontogenic
fibroma
Giant cell Small, raised, pedunculated, papillary lesion less than 1 cm in Normal colour Pedunculated
fibroma diameter; asymptomatic; seen for many years
Pregnancy Identical to pyogenic granuloma; occurs during pregnancy; Deep red or purple Pedunculated or
tumour may not regress after delivery sessile
Peripheral giant Seems to originate from periodontal ligament or Dark red and Sessile
cell mucoperiosteum (Between 0.5–o 1.5 cm) haemorrhagic
granuloma
Peripheral Commonly appears interdentally; rarely superficial erosion of Normal/slightly Sessile or
ossifying bone reddened pedunculated
fibroma
Lateral Overlying mucosa is normal; most commonly seen in Normal colour Sessile
periodontal mandibular premolar region
cyst
Lateral It is related to preexisting periodontal pocket; pus exudation Normal colour or Sessile
periodontal might be seen through the gingival cervice; in acute cases slightly
abscess tooth will be tender to percussion reddened
Treatment
Foreign body granuloma

• Hyperplastic reaction (infective or inflammatory) of the mucous membrane of
the oral cavity as a consequence of any foreign body inclusion.
• Small, nodular, polypoid mass in the oral cavity; commonly in the gingival.
DD: Pyogenic granuloma (Fig. 18.17B ), fibroepithelial polyp or fibroma and
papilloma.
FIGURE 18.17B Pyogenic granuloma.
Treatment
• Excision.
White lesions
• Can occur at any age.
• May or may not be associated with tobacco abuse.
• Some of the white lesions are precancerous in nature.
• White lesions are usually found in the buccal mucosa.
• It may also be found in other areas of the oral mucosa.
• Lichen planus–Reticular pattern of white lines with a dot at points of
intersection; bilateral, dermal presentation.
• Leukoplakia–Homogenous white plaques; unilateral; associated with
tobacco use.
• Leukoedema–Filmy opalescence of buccal mucosa in early stages to more
delicate, greyish white cast with coarsely wrinkled surface; bilateral;
follows course of linea alba.
• Candidiasis–Thick white plaque with submucosal erythema; associated
with poor oral hygiene, xerostomia and mycotic vaginitis.
• Histopathological examination of the lesion.
Treatment
• According to the lesion.
Oral submucous fibrosis (osmf)

• Chronic disease affecting any part of the oral cavity, sometimes the pharynx,
occasionally preceded by or associated with vesicle formation leading to
epithelial atrophy which results in stiffness of the oral mucosa causing
progressive loss in mouth opening and trismus.
• Common in the age group between 20–40 years.
• Associated with betel nut chewing, vitamin B deficiency, protein deficiency
and high intake of chillies.
• A precancerous condition.
• Burning sensation of mouth, particularly when eating spicy food.
• Accompanied by formation of vesicles (palate), ulcerations or recurrent
stomatitis with excessive salivation or xerostomia, and defective gustatory
sensation ultimately resulting in trismus. Mucosa eventually becomes
blanched, opaque; sometimes fibrotic bands appear involving the buccal
mucosa (Fig.18.18), soft palate, lips and tongue.
• The mucous membrane loses its elasticity and becomes board-like.
• Inability to protrude the tongue and evert the lips is characteristic.
FIGURE 18.18 Oral submucous fibrosis—completely edentulous with

restricted mouth opening.
DD: Systemic sclerosis and scleroderma.
• CT scan reveals fibrotic bands.
Treatment
• Medical–Systemic corticosteroids, local injection of placentrex and
fibrinolytic agents.
• Surgical– Excision of fibrotic bands and covering the defect with skin graft
(nasolabial or tongue flap).
Oral candidiasis
• Caused by Candida albicans or Monilia.
• Occurs in –
• Children as opportunistic infection (oral thrush);
• The elderly;
• Immunosuppressed or immunocompromised patient (Most common in
AIDS); and
• Patient on steroid therapy.
• Soft, white, slightly elevated plaques most frequently involving the buccal
mucosa, tongue (Fig. 18.19A), palate, gingiva and floor of the mouth.
• The lesion is scrapable, which will leave a raw, eroded and erythematous area.
FIGURE 18.19A Fungal infection of tongue.
DD: White lesions of the oral cavity.
• PAS test.
Treatment
• Antifungal therapy.
Necrotizing sialometaplasia
• A benign, inflammation of salivary gland.
• It is mainly due to local ischaemia.
• Most common in men.
• An ulcer or a perforation in the palate.
• It is often mistakenly diagnosed as carcinoma, though it is a self-healing ulcer.
DD: Mucoepidermoid carcinoma and carcinoma.
• Cytological smear.
Treatment
• Self-limiting; heals by secondary intention.
Chronic osteomyelitis of jaws

• Chronic inflammation of the medullary portion of the bone.
• Mandible is affected more often than the maxilla.
• In the majority of cases, an alveolar abscess or peridental suppuration leads to
infection of the medullary cavity and Haversian systems, and extends to
involve the periosteum of the affected area.
• Causes rapid destruction of bone with enlargement of medullary spaces.
• Causes of chronic osteomyelitis are–
• Radiation
• Tuberculosis
• Syphilis or
• Actinomycosis.
• Intense pain, paresthesia, focus of infection (odontogenic, traumatic or
ballistic), oedema of the soft tissues, suppuration, multiple perforating
sinuses draining pus into the oral vestibule or burrowing into the overlying
musculature and forming abscesses.
DD: Actinomycosis, osteolytic osteosarcoma and Ewing’s sarcoma.
• X rays (Fig.18.19B) show the ‘moth eaten’ appearance.
FIGURE 18.19B X ray—chronic osteomyelitis mandible.
Treatment
• Medical– Antibiotics.
• Surgical–Saucerisation and sequestrectomy.
Cervicofacial actinomycosis
Caused by Actinomyces israelii, an aerobic Gram positive branching,
filamentous organism which lives as a harmless parasite in the tonsillar crypts
and dental cavities of a normal mouth.
• The commonest form of actinomycosis.
• Lower jaw is commonly affected, often adjacent to carious tooth.
• The gum becomes indurated, and the induration extends to the skin of face
and neck.
• A soft swelling in the submandibular region, with multiple soft areas
(abscesses).
• May burst into sinuses surrounded by the bluish skin.
• A recent history of tooth extraction, signs of tooth decay, or poor oral hygiene
aid in the diagnosis.
• Isolation of organism is necessary.
Treatment
• Prolonged administration of antibiotics is curative.
Dental cyst
• Apical periodontal cyst represents a chronic inflammatory process arising
from a dental infection and develops only over a prolonged period of time.
• Swelling in relation to a non-vital tooth, the focus of the infection.
• Sinus discharging pus usually at the periapical region of the non-vital tooth or
the muco-gingival sulcus. Rarely increases in size and therefore no
expansion of the cortical plates.
• The swelling may develop on the buccal or lingual side of the alveolar process
and will be covered with normal mucosa.
• Initially it will be bony hard to palpation, but later it may demonstrate a
crackling sound as the cortical plates become thinned. In these cases, clinical
swelling is rubbery and fluctuant.
• Root resorption is also seen.
• Pain is present on percussion of the associated tooth.
DD: Periapical granuloma, periapical cementoma and traumatic bone cyst.
• X rays show a well circumscribed, periapical radiolucency (Fig.18.20).
FIGURE 18.20 X ray—dental cyst.
Treatment
• Apicoectomy with retrograde sealing of the root canal.
Lymphangioma/macrochelia/cystic hygroma
• A benign tumour of the lymphatic vessels.
• May be congenital and it may also be found in the ages of 15–20 yrs
• The varieties of lymphangioma are –
• Simple lymphangioma
• Cavernous lymphangioma
• Cellular lymphangioma
• Diffuse systemic lymphangioma, and
• Cystic hygroma.
Commonly occurs in the tongue; also in palate, gingiva and buccal mucosa.
Superficial lesions are papillary, whereas, the deeper lesions are diffuse nodules
and masses.
• If it affects the tongue, it presents as macroglossia (Irregular nodularity of the
tongue surface with grey and pink projections).
• If it involves the lip, it manifests as macrochelia.
• Cystic hygroma is a common distinct entity appearing as a large, deep,
diffuse, swelling.
• It is lesser blue than the haemangioma ranging from normal mucosal pink
to bluish.
• It is not reducible, but soft, fluctuant and translucent.
• Trans illumination is positive.
DD: Cavernous haemangioma, lipoma, neurofibroma and cystic lesions.
• Aspiration yields a clear yellow fluid (lymph).
Treatment
• Surgical excision is the treatment of choice, where possible.
Ameloblastoma
• A benign tumour of odontogenic origin.
• Occurs at any age, but more in the fourth decade.
• Usually unicentric, non-functional and intermittent in growth.
• Molar ramus area of the mandible is the most common site of occurrence.
• In the maxilla, it presents more often in the molar area and the floor of the
nose.
• Peripheral ameloblastoma may present as epulis-like fibrous nodules in the
gingiva.
• Ameloblastoma of maxilla occurs in the older age group and has a poorer
prognosis.
• A painless, slow growing tumour (Fig.18.21).
• Causes migration and loosening of teeth associated with root resorption and
paresthesia of the lip.
• It only expands and does not perforate the bone.
• On palpation, it may feel –
• firm if it is of the solid type (fine, granular, firm consistency); or
• soft and fluctuant if it has undergone cystic degeneration.
FIGURE 18.21 Ameloblastoma—left side mandible.
DD: Lesions presenting with multilocular radiolucencies: Odontogenic

keratocyst, dentigerous cyst, central giant cell granuloma, fibrous dysplasia,
cherubism (familial fibrous dysplasia), central haemangioma of bone,
odontomes, Paget’s disease, and osteosarcoma.
• Aspiration yields straw coloured fluid if the lesion is cystic.
• X rays show multilocular radiolucency (Fig. 18.22A) and expansion of the
lingual cortex, producing jaw expansion, thinning of cortical bone and
tipping of the teeth with resorption of the roots of the teeth.
• CT (Fig. 18.22B) and MRI are diagnostic.
FIGURE 18.22A OPG—ameloblastoma.
FIGURE 18.22B CT—ameloblastoma of mandible.
Treatment
• Wide excision and reconstruction (recurrence rate is high).
Salivary gland tumours of oral cavity

• Form only a small proportion of tumours arising from major salivary glands,
whereas, forms the major proportion of tumours arising from minor salivary
glands.
• The relative prevalence of tumours of salivary glands are shown in Table 18.4
(Ref Fig. 23.8).
• The commonest malignancy is the mucoepidermoid carcinoma.
• Others include –
• Adenoid cystic carcinoma (Fig. 18.23A);
• Acinic cell carcinoma; and
• Squamous cell carcinoma.
FIGURE 18.23A Adenoid cystic carcinoma of the right maxilla involving

the orbit.
TABLE 18.4
Relative Prevalence of Salivary Gland Tumours
Salivary Gland Prevalence Benign Tumours Malignant Tumours
Parotid 80 80 20
Submandibular 10 20 80
Sublingual 2 0 100
Minor salivary 8 20 80
Malignant tumours of intra-oral minor salivary glands present with cervical

lymph node metastases.
• A rapidly enlarging, firm and painless swelling in the oral cavity (Fig.
18.23B).
• Pain suggests infection or a rapidly growing malignant tumour.
FIGURE 18.23B Polymorphous low grade adeno carcinoma of palate.
• CT is useful.
Treatment
• Wide excision of the tumour is the treatment of choice.
• Block dissections are needed for lymph nodal involvement.
Malignant lesions of oral structures

• Malignancy can occur in any part of the oral cavity.
• Majority of them are squamous cell carcinomas.
• Malignant lesions of oral cavity spread locally and metastasize to neck nodes.
• There are a variety of precipitating factors and predisposing conditions, as
shown in Table 18.5.
TABLE 18.5
Precipitating Factors and Predisposing Conditions of Intraoral
Malignancies
Region Precipitating Factors Predisposing Condition
Lip Sunlight, tobacco smoking Actinic cheilitis

Tongue Tobacco smoking, betel leaves and betel nut chewing Leukoplakia
Palate Tobacco smoking Leukoplakia
Buccal mucosa Tobacco smoking, betel leaves and betel nut chewing Submucous fibrosis, leukoplakia
Floor of the mouth Tobacco smoking, betel leaves and betel nut chewing
• Malignant lesions may present as non-healing ulcers or exophytic growths of
the oral cavity.
• Characterized by rapid growth, variation in the surrounding mucosa,
induration and infiltration of adjoining tissues (Figs.18.24A to 18.24 I).
• The clinical presentation of various malignancies is given in Table 18.6.
FIGURE 18.24A Carcinoma of retromolar region.
FIGURE 18.24B Carcinoma upper surface of tongue.
FIGURE 18.24C Carcinoma upper surface of tongue.
FIGURE 18.24D Carcinoma lateral border of tongue.
FIGURE 18.24E Carcinoma buccal mucosa.
FIGURE 18.24F Carcinoma of buccal mucosa.
FIGURE 18.24G Carcinoma buccal mucosa infiltrating the cheek.
FIGURE 18.24H Carcinoma floor of the mouth.
FIGURE 18.24I Carcinoma of tongue.
TABLE 18.6
Clinical Presentation of Intraoral Malignancies
Differential
Location Presentation Associated Symptoms Complications
Diagnosis
Lips Non healing ulcer Bleeding, spread Keratoacanthoma

Tongue Small warty Pain, salivation, Bleeding, Papilloma, angioma,
outgrowth/ulcer/fissure/indurated ankyloglossia, secondary lipoma,
mass, more on the lateral dysphagia, difficulty infection, myoblastoma
margins of the anterior two thirds in articulation, fetor lymphatic
spread
Palate Ulcer, growth Bleeding Perforation Necrotising
sialometaplasia,
extension of
maxillary antral
tumours
Buccal Ulcer, growth or indurated mass Pain, fetor Perforation, Actinomycosis
mucosa orocutaneous
fistula
Floor of Ulcer, growth or indurated mass Pain, salivation, Perforation, Actinomycosis
the difficulty in orocutanous
mouth articulation, fetor fistula
• Histopathologic confirmation after biopsy.
Treatment
• Surgical excision, radiotherapy or chemotherapy in various combinations.
Verrucous carcinoma
• Most commonly occurs in the buccal mucosa, alveolar ridge and gingiva,
tongue, floor of the mouth, and palate of elderly patients.
• Exophytic, keratinized tumours
• Surface dimensions are of several centimetres, but show superficial spreading
type rather than invasion to deeper tissues.
• The colour of the surface may be white or red depending on the degree of
surface keratinization, and ulceration may be present.
• On palpation, the margins are usually well defined and characteristically
show a rim of slightly elevated normal mucosa where the tumour has been
pushed under the edge of the normal tissue and has undermined it slightly.
• Histopathologic confirmation after biopsy.
Treatment
• Surgical excision, radiotherapy or chemotherapy in various combinations.
Malignant tumours of jaws
• Majority are squamous cell carcinomas.
• Can arise de novo from the epithelium lining the maxillary antrum, or from
the epithelium overlying the hard palate, from a tooth socket or from the
gums.
• The other variety is columnar cell carcinoma.
• Occurs equally in both sexes.
• Metastases occur relatively late; upper jugular nodes are the first to be
invaded.
• Lymphadenopathy is the first presentation in one third of cases.
• Osteogenic sarcoma is another malignant tumoir of maxilla and mandible.
• Tooth pain is predominant when the growths originate on the floor of the
antrum.
• A foul, purulent and blood stained discharge from the nose is common.
• The clinical features vary depending on its spread (Figs. 18.25A and B)–
• Posterior spread–causes no specific symptom or deformity.
• Medial spread–nasal obstruction and epiphora.
• Antero-lateral spread: swelling and deformity of the face; atypical facial
pain due to trigeminal nerve involvement.
• Spread to the floor–bulge in hard palate.
• Upward spread–proptosis, diplopia and cranial nerve palsies.
FIGURE 18.25A Tumour of maxillary sinus.
FIGURE 18.25B Malignancy of right maxilla with lateral extension.
• X rays, CT or MRI (Fig. 18.25C) are diagnostic.
FIGURE 18.25C Malignancy of right maxillary antrum. (A) Extension into
orbit and nose. (B) Extension into the hard palate.
Treatment
• Radiotherapy, surgery and chemotherapy in various combinations.
Note
• Primary malignant tumours are more common in the maxilla when compared
to mandible.
• Direct spread of advancing carcinoma of tongue or of the floor of the mouth,
or spread of carcinoma of lip through the mental foramen to the mandible
are known.
• Rarely, a metastatic cervical lymph node can directly invade the mandible.
Oral manifestation of anaemia

• Glossodynia, glossopyosis, beefy red (pernicious anaemia), bald tongue, pale
tongue and palate, and cracks and fissures at the corners of the mouth.
• Symptoms may vary from a tender to a burning tongue to extreme
glossodynia.
• Frequently, the tongue is intensely red initially and then becomes smooth due
to atrophy of its papillae.
DD: Median rhomboid glossitis, xerostomia, lichen planus, psoriasis,
geographic tongue, and Reiter’s syndrome.
• Haematocrit.
Treatment
• Supplement therapy.
18.6 symptoms of oral cavity pathologies

• Swelling
• Ulcer
• Pain
• Discharge
• Discolourations
• Teeth problems
• Occlusal problems
• Bad taste
• Bad breath
• Bleeding
• Burning sensation
• Paresthesia/anesthesia
Swelling
The swellings related to oral cavity lesions have certain specific characteristics –
• Swelling related to mastication or food intake (e.g. salivary retention or
sialolithiasis).
• Swelling with growth.
• Slow growth (e.g. reactive hyperplasia, cysts and benign tumours).
• Moderate growth (weeks to few months) (e.g. chronic infections, cysts and
malignant tumours).
• Rapid growth (hours to days) (e.g. abscesses, infected cysts, aneurysmsand
haematomas).
• Swelling with fever (e.g. infections and lymphomas).
• Swelling with pain (e.g. abscess and infected cyst).
• Swellings of certain locations (Table 18.7).
TABLE 18.7
Lesions of Oral Cavity Presenting as Swellings
Location Pathology
Lips Mucous cyst, haemangioma, lymphangioma, lipoma, neurofibroma, papilloma, verrucous

carcinoma, squamous cell carcinoma
Oral mucosa Mucocoele, developmental cysts, minor salivary gland tumours, squamous cell carcinoma
Tongue Haemangioma, lymphangioma, squamous cell carcinoma
Floor of the mouth Ranula, sublingual dermoid, deep plunging ranula
Mandible and Ameloblastoma, torus, dentigerous cyst, fibrous dysplasia, aneurysmal bone cyst, alveolar abscess,
alveolar margin osteomyelitis, osteosarcoma
Gingivae Fibroma, papilloma, pyogenic granuloma, gingival cyst, giant cell fibroma, lateral periodontal
cyst, lateral periodontal abscess, epulis
Palate Torus palatinus, palatal abscess
Ulcer
Ulcers are other common presentations of oral cavity pathologies. The lesions
which present as ulcers are shown in Table 18.8.
TABLE 18.8
Lesions of Oral Cavity Presenting as Ulcers
Location Pathology
Lips Traumatic ulcers, herpetic ulcers, aphthous ulcers, syphilitic ulcers, tuberculous ulcers,
malignancy
Oral mucosa Traumatic ulcer, squamous cell carcinoma
Tongue Aphthous ulcer, squamous cell carcinoma
Floor of the mouth Aphthous ulcer, squamous cell carcinoma
Mandible and alveolar Squamous cell carcinoma
margin
Palate Squamous cell carcinoma
Pain
Pain is a common symptom in oral cavity pathologies, many times associated
with lesions like swellings or ulcers. It is also a determinant of duration of the
lesion. Carcinomatous lesions are not painful unless infected.
• Acute pain–traumatic lesions and infective lesions like herpes.
• Chronic pain–tuberculous ulcers and syphilitic chancre.
• Painless lesions–gumma and neoplasms.
Discharge
Discharges can be from a wound, ulcer, sinus, fistula or a suppurated cystic
lesion. Common types of discharges are shown in Table 18.9.
TABLE 18.9
Types of Discharges from Intraoral Pathologies
Nature of
Lesions
Discharge
Serous Parotid fistulae

Haemorrhagic Ulcerated haemangioma, traumatic bone cyst, aneurysmal bone cyst
Serosanguinous Carcinomatous ulcer
Mucous Submandibular salivary fistula, ruptured mucocoele, ruptured dentigerous cyst, ruptured sebaceous
cyst
Purulent Ruptured abscess
Sulfur granules Actinomycosis
Discolourations
Discolourations are commonly seen in intraoral pathologies and they are shown
in Table 18.10.
TABLE 18.10
Discolourations of Intraoral Pathologies
Generalized
Cyanosis, Addison’s Disease, Haemochromatosis, Argyria
Discolourations
Localized discolourations
Colour of Pathology Clinical presentation Age of History
lesion onset
Brown, Melanoplakia Nevus of varying size and shape Congenital Less than 1 year
bluish
or Amalgam Impregnation of amalgam particle in Any age History of amalgam
black tattoo restoration
Petechiae Sub-epithelial bleeding spots Any age Recent trauma,
ecchymosis blood
dyscrasias
Melanoma Malignant neoplasm of melanocytes > 50 years Slow growing patch
Junctional Nevus with malignant potential > 40 years Starts growing
nevus during
malignant
transformation
Peutz Jegher’s Melanocytic papules on the lips, buccal mucosa Puberty Colicky abdominal
syndrome (autosomal dominant disorder) pain, GI
bleeding
Albright’s Polyostotic fibrous dysplasia of bone, café au lait 6–10 years Short stature, round
syndrome pigmentation of skin, mental retardation face, difficulty
in walking,
bony
overgrowth
Red or Varix Elevated patch may not blanch Any age May not blanch due
bluish to pigmented
red thrombus
Haemangioma Blanching lesion Any age Congenital
Kaposi’s Elevated lesion, swelling/ulceration Any age Immunosuppression
sarcoma
Yellow Fordyce’s Circumscribed lesions in clusters on buccal mucosa or Any age
granules lips
White Lichen planus Reticular pattern of white lines with a dot at points of Any age Bilateral, dermal
intersection presentation
Leukoplakia Homogenous white plaques Any age Unilateral,
associated with
tobacco use
Leukoedema Filmy opalescence of buccal mucosa in early stages to Any age Bilateral, follows
more delicate, greyish white cast with coarsely course of linea
wrinkled surface alba
Candidiasis Thick white plaque with submucosal erythema Any age Poor oral hygiene,
xerostomia,
mycotic
vaginitis
Diffuse Nicotinic Red inflammatory lesion to start with, diffuse greyish Puberty or Seen in hard palate
greyish stomatitis white thick multinodular appearance with small old age of pipe or cigar
white red spot at the centre of each nodule; fissures and smokers
cracks may appear with wrinkled or irregular
surface
Teeth problems
The patient may present with problems related to the teeth that are enumerated in
Table 18.11.
TABLE 18.11
Lesions Presenting with Teeth Problems
Condition Lesions
Anomalies in number* Anodontia, supernumerary teeth, supplementary teeth

Anomalies in shape* Talon cusp, taurodontism Hutchinson’s teeth
*Many of the anomalies are associated with other anomalies and form part of various syndromes
Occlusal problems
Various types of malocclusion occur. They are –
• Open bite
• Deep bite
• Cross bite
• Crowding
• Spacing
• Proclination
Bad taste
Bad taste is a manifestation of many intra-oral lesions –
• Purulent infections like abscess
• Stomatitis
• Candidiasis
• Acute necrotising ulcerative gingivitis
• Drugs
Bad breath
Bad breath (Halitosis) may occur due to various causes in the oral cavity. They
are tabulated in Table 18.12.
TABLE 18.12
Lesions Presenting with Bad Breath
Intra-oral Causes Extra-oral Causes

Stomatitis Respiratory tract infections
Gingivitis Alcoholic breath
Extensive dental caries Acetone breath in diabetics
Chronic smoking Aromatic substances excreted through lungs
Poor oral hygiene
Bleeding
Bleeding from the oral cavity is seen in –
• gingival and periodontal infections;
• ulcers in the mouth; and
• coagulation disorders.
Burning sensation
Burning sensation is a manifestation in some intra-oral conditions –
• Oral submucous fibrosis;
• Lesions coming in contact with spicy food; and
• Burning mouth syndrome.
Paresthesia/anaesthesia
Change in sensation is seen in the following conditions –
• Lesions involving the nerves (e.g. malignancy and post surgery).
• Compromised blood supply.
• Local anesthesia.
Eliciting history
• Age–Lesions, like clefts are congenital, and malignancies are common in the
elderly.
• Sex– Salivary gland diseases are more common in females, and diseases
related to stress and smoking are more common in males.
• Occupation– Occupation may play a role in some instances; exposure to
harmful substances should be especially noted.
• Race– Some races, especially some tribes have the habit of tattooing or
causing self inflicted injuries for religious reasons.

• Duration of illness: For how long is the patient suffering from this illness?
• Pain–Recurrent episodes of pain in the teeth may be due to dental caries.
• Swelling
– Acute swellings of the oral cavity are seen in abscesses, and gradual
increase in benign cystic lesions. Multiple swellings can occur in the oral
cavity in tori (e.g. mandibular tori).
• Ulcer– Painful multiple ulcers of short duration occur in aphthous ulcers,
traumatic ulcers and painless solitary ulcers of long duration occur in
chancre. Malignancy can present as ulcerative lesion in the tongue or
cheek.
• Sinus– Sinus can occur and last for a longtime in tuberculous aetiology, or
in salivary fistulae.
• Discharge– Discharges from the sinus may be of short duration in those of
pyogenic origin and last for longer duration in tuberculous aetiology.
• Association of fever: Is or was it associated with fever, and if so for how
long?
Association of high grade fever may indicate an acute infective pathology
(e.g. acute alveolar abscess) and low grade fever in TB.
Loss of appetite and weight are indicative of illnesses like TB and
malignancies.
given to the illness, in particular self medication?
give a clearer picture of diagnosis (sinuses with previous history of surgery
may indicate a tuberculous pathology), and the patient’s attitude and
response to the previous treatment. History of self-medication: application of
aspirin for toothache may cause aspirin burns.
treatment?
successfully treated, it will indicate the examiner to reconsider diagnosis,
like recurrence of TB. Even recurrent malignancies should be considered.
Diseases like sinuses due to clefts occur in families and the positive history
may be a good indicator for the present diagnosis.
Personal habits like smoking (e.g. smoker’s palate), betel nut chewing (e.g.
submucous fibrosis) and tobacco chewing (e.g. malignancies of oral cavity)
should be enquired.
match the situation, like oral sex if the disease is suspected to be of syphilitic
aetiology. History relating to trauma should also be elicited.
• Patient should be made to sit comfortably on a chair; acutely ill patients
should be made to lie on the bed.
• The examiner should sit comfortably and the patient’s oral cavity should be at
the examiner’s eye level.
• Adequate illumination is necessary.
• A pen torch and a tongue depressor are mandatory equipments for
examination of the oral cavity.
• Adequate knowledge and orientation of the oral cavity and its related anatomy
is mandatory.
General
• Sunken eyes indicate dehydration and undernutrition, or facial trauma.
• Jaundice may be an indicator of metastatic liver disease (oral
malignancies).
• Pallor is a feature of blood loss (e.g. anaemia/facial trauma).
• Dry scaly skin (e.g. dehydration/undernutrition/hypothyroidism).
• Oedema of the face may be seen in patients with fractures of facial bones
(Fig. 18.26).
• Hypotension (e.g. hypotension in facial trauma).
• Elevated temperature (e.g. infective pathologies and malignancies).
FIGURE 18.26 Swelling of face in trauma patient.
Face
Look for–
• Asymmetry– Asymmetry may occur due to skeletal or soft tissue
abnormalities (Figs.18.27 A to F) or due to nerve lesions resulting in loss of
motor innervation of the muscles.
• Skeletal asymmetry–Skeletal asymmetry is caused by–
• Condylar hyperplasia
• Hemimandibular hypoplasia
• Occlusal discrepancies
• Condylar fracture
• TMJ ankylosis
• Hemifacial hypertrophy
• Neoplasm (Fig. 18.27E)
• Inflammation (Fig. 18.27F)
• Fibrous dysplasia
• Asymmetry in facial movements: Facial palsy and Bell"s phenomenon
(Figs.18.28A and B).
FIGURE 18.27A Facial asymmetry.

FIGURE 18.27B Neurofibromatosis.
FIGURE 18.27C Lymphangioma.
FIGURE 18.27D Tessiers cleft (3, 4, 5, 6 and 7).
FIGURE 18.27E Juvenile cemento—ossifying fibroma.
FIGURE 18.27F Cellulitis face.
FIGURE 18.28 Facial palsy—Bell"s phenomenon.
Examination should be carried out in presence of external light source to
evaluate any pigmented (red, brown, black), ulcerated, raised or firm areas of the
skin, hair bearing regions of the face and scalp. Region of occurrence will give
clue for diagnosis of the condition (e.g., basal cell carcinoma; Fig. 18.28C).
FIGURE 18.28C Basal cell carcinoma in the inner canthus of right eye.
Eyes: As part of the cranial nerve examination, extraocular movements should

be tested in each direction as well as visual acuity (See Page 202). Any deficits
should be carefully noted, as they may result from an invasive cancer. Any
swelling of the eye or periorbital area should be noted and can be a late sign of a
cancer which may have started in the palate, maxillary or ethmoid sinuses.
Drainage from the lacrimal system (epiphora), may be a sign of an obstructing
mass in the maxillary sinus, nose or facial soft tissue. In case of facial trauma,
periorbital odema and subconjunctival haemorrhage are noted.
Lips
Most lesions of the lip can be identified on just visual inspection of the
condition. Some lesions can be deceptive and can lead to a wrong diagnosis if
not visualized under good lighting. It is a good practice to thoroughly examine
the lesion and the surrounding structures (Table 18.13) before coming to a
conclusive diagnosis.
TABLE 18.13
Various Appearances of Lip Lesions
Contour of the Lip Pathology
Dysmorphology Cleft lip, double lip, macrochelia
Generalized swelling Angioneurotic oedema, macrochelia
Localized swelling Inflammation, abscess, haemangioma, lymphangioma, carcinoma
Any abnormality on symmetry, contour, colour or texture in lip should be

evaluated. Vermilion border of the lower lip should be paid special attention, as
this is the prime site of oral cancers. Difficulty in opening the mouth occurs in
submucous fibrosis and post surgery status (Fig. 18.29).
FIGURE 18.29 Oral submucous fibrosis—difficulty in opening the mouth.
Method of examination: First, the lower lip is everted and the inner surface is
inspected (Fig.18.30A).
FIGURE 18.30A Examination of inner surface of lower lip by eversion.
Look for–
• The colour of labial mucosa– Normal labial mucosa should be smooth and
uniform in colour. Note any signs of tobacco use (ulcers, red or white
discolourations, texture variations) on the labial mucosa. Vitiligo of the lip
suggests solar keratosis or tobacco abuse.
• Localized lesions on the labial mucosa– If a lesion is found, the following
are to be noted:
• Colour of the lip lesion– Various coloured lesions are listed in Table 18.14.
• Number of lesions on the labial mucosa– Varieties of pathologies present as
single (Fig. 18.30B) or multiple localized lesions on the labial mucosa (Fig.
18.30C). Kiss lesions are known to occur from one lip to the other.
• Nature of lesions on the labial mucosa: The lesions on the lip are of various
types. They are listed in Table 18.15.
• Ulcers on the labial mucosa– Ulcers are one of the common presentations of
lip lesions. They are listed in Table 18.16.
FIGURE 18.30B Mucous cyst lower lip.
FIGURE 18.30C Multiple vesicles of herpes simplex on upper lip.

TABLE 18.14
Coloured Lesions of Lip
Colour of the
Pathology
Lip Lesion
Reddish Inflammatory lesions, haemangioma, granuloma, Struge-Weber syndrome (port wine stain), Kaposi’s
sarcoma, Rendu-Osler-Weber syndrome
Blackish or Smoker’s lip lesion, solar keratosis, melanoma, nevus, Peutz-jegher’s syndrome, melanoma
brownish
Whitish Leukoplakia, vitiligo, lichen planus, candidiasis, actinic chelitis, focal epithelial hyperplasia (Heck’s
disease)
Blanched Submucous fibrosis, anaemia
TABLE 18.15
Localized Lesions of the Labial Mucosa
Localized Lesions Pathology
Elevated lesions Fibroma, lipoma, minor salivary gland tumours, nasolabial cyst, blisters (herpetic)
Depressed lesions Lip pits, ulcers, scars
Vesicle Herpes, allergic manifestation
Blister Mucocoele, chicken pox, burns, cyst
Nodule Haemangioma (reddish), nevus (blackish), granuloma (bleeding, purplish), lipoma, neurofibroma
Plaque Candidiasis
Fungating Squamous cell carcinoma, candidiasis
Verrucous Papilloma, verrucous carcinoma
TABLE 18.16
Ulcers on the Labial Mucosa
Prodromal
Aetiology Number Borders/pathognomonic Sign Onset
Symptoms
Traumatic Single or Raised/reddish with yellowish necrotic surface on the Acute Absent
multiple base
Herpetic Multiple Multiple vesicles, rupture and coalesce to ulcerate Acute Fever
Aphthous Single or Yellow base, erythematous halo Acute Malaise
grouped
Carcinoma Single Non-healing ulcer, rolled or everted border (commonly Chronic Cachexia
lower lip)
Actinic cheilitis Multiple Rounded nodule with umbilication and depressed central Chronic Absent
(keratoacanthoma) core or plug, heals spontaneously
Syphilitic Multiple Punched out margins, serpiginous outline and with Chronic Absent
stringy non-purulent exudates
Tuberculous Multiple Undermined edges with lymphadenopathy Chronic Fever, weight
loss
Note
Ulcers on the labial commissures suggest nutritional deficiency or loss of
vertical dimension in a denture wearer.
• Frenum of the lip– Normally the frenum of the lip is in the midline.
• Gingivolabial sulcus, the gingival mucosa, and the teeth– With the lip still
retracted, one can also inspect the gingivolabial sulcus, the gingival mucosa,
and the teeth.
• Repeat these steps for the upper lip (Fig.18.30D).
FIGURE 18.30D Examination of inner surface of upper lip by eversion.
Palpation of lip lesion

Any lesion of the lip should be carefully palpated. While benign neoplasms are
firm and lobulated, carcinoma of the lip is stony hard in consistency, whereas,
Hunterian chancre is rubbery. When an ulcer of lip is suspected for carcinoma,
the base of the ulcer should be held with the index finger and thumb to determine
its consistency (Fig. 18.31A)
FIGURE 18.31A Feeling the consistency of lip lesion.
which is always hard if it is a malignant condition. We should also look for its
fixation with the underlying structures. This is done by fixing the lip with one
hand and trying to move the lesion against the lip with the other hand.
Carcinoma is almost always fixed. Mucous retention cyst is often seen on the
inner surface of lip. Fluctuation and transillumination test are positive when the
cysts are large, but not easy to perform in lip lesions. For fluctuation test one
should follow the technique for small swellings (See Ch. 9).
Oral mucosa
For this portion of the examination, the patient positioning can vary.
• Dental patients tend to lie on their backs, while the dentist examines the oral
cavity.
• On the other hand, physicians usually make their patient to sit up straight and
examine them by facing eye-to-eye.
It is imperative that the mouth be examined with an external light source,
which allows both hands free for bimanual palpation or to hold gauze or tongue
blade(s) for improved visualization. If a handsfree light source is not available,
an assistant may provide invaluable help in visualization of difficult areas such
as the posterolateral border of the tongue and floor of mouth (Fig. 18.31B).
FIGURE 18.31B Examination of oral mucosa with external source of light.
Before beginning this part of the examination, the patient should be asked
to remove all dental appliances.
Examination of the mucosal surface should be carried out after gently drying
the surface using gauze or air syringe to appreciate any change in colour and
texture. Clinicians should look out for any red and white lesions as this may turn
into malignant lesions on the oral mucosa. Many studies reported that the earliest
manifestation of many oral and oropharyngeal squamous cell cancers is a
persistent erythroplastic lesion.
The Oral mucosa is examined for –
• Cause of the lesion
• Alterations in colour (Table 18.17)
• Texture
• Contour
• Swellings and
• Ulcers.
TABLE 18.17
Various Causes Which Produce Coloured Lesions on the Oral
Mucosa
Cause Clinical Findings Lesions Differentiating Features

Intravascular Blanch on pressure; Varix Blue in colour; elevated; may not blanch due to
blood compressible pigmented thrombus
Haemangioma Red to blue in colour
Kaposi’s Clinical and historical evidence of
sarcoma immunosuppression
Extravascular Does not blanch on pressure; Haematoma Surface elevation or submucosal enlargement; firm
blood short history; history of to palpation
trauma may be present
Ecchymosis Subepithelial; no enlargement; not palpable
Petechiae Focal; red in colour; subepithelial; multiple;
nonpalpable
Melanin Do not blanch; persistent Ephelis oral Non-palpable
melanotic
macule
Lentigo If non-palpable, can be differentiated from ephelis
simplex or melanotic macule; if palpable, cannot be
differentiated from nevus or melanoma
Naevus Palpable; may be raised
Melanoma Unless large or ulcerated, cannot be differentiated
from naevus
Tattoo Does not blanch; history of Tattoo History; mostly not palpable
injury; radioopacity may be
evident radiologically
Colour
The examiner must be familiar with the normal characteristic colour of each
region in the oral cavity. The examiner must be aware of the normal variations in
colour and shadings these tissues can assume, and certainly must be able to
recognize the colour changes that signal abnormal conditions in a particular area.
The normal colour of the oral mucosa is pink, because healthy stratified
squamous epithelium is semitransparent and transmits the red colour of the
blood in the extensive capillary bed.
Generalized discolourations of the oral mucosa indicate various systemic
disorders. They are –
• Bluish colour–Cyanosis
• Bronze colour–Addison’s disease
• Grey or bronze colour–Haemochromatosis
• Greyish silver colouration–Argyria
Localized discolourations on the oral mucosa may present as specific lesions.
They are shown in Table 18.18.
TABLE 18.18
Localized Discolourations on the Oral Mucosa
Brownish, Bluish or Black Lesions Yellow White Lesions

Lesions
Melanoplakia Amalgam tattoo Petechiae ecchymosis Melanoma Fordyce’s Lichen planus Leukoplakia
Junctional naevus Peutz-Jegher’s syndrome Albright’s syndrome granules Nicotinic stomatitis
Leukoedema
Note
The soft palate in many persons appears quite yellow.
White lesions of the oral cavity can be differentiated as per the age of
occurrence, history, habits, physical and nutritional condition of the patient,
immunosuppression, fetid odour and the presence of other skin lesions.
When the mucosa appears white, it may be due to a deposition of debris, due
to hyperkeratosis or due to decrease in vascularity. While necrotic debris can
be flushed or scraped out, the keratotic lesions are adherent to the epithelium.
The submucous lesions often present more as blanched mucosal lesions.
Contour
Swellings of the oral mucosa vary with the site of occurrence. Swellings of the
gingiva are distinct. They should be examined for number, size, site, shape,
mucosa over the swelling, borders, presence of pedicle, discharge and the
surrounding mucosa.
• Macule is the result of a localized colour change produced by the deposition
of pigments or slight alterations in the local vasculature or other minimal
local changes.
• Papule, nodule, polypoid, or papillomatous mass results due to hyperplasia
and hypertrophy.
An ephelis or freckle is a brownish macule that histologically represents only
an increased production of melanin by the normal number of melanocytes. On
the other hand, an intradermal or intramucosal naevus histologically shows a
significantly increased number of naevus cells producing melanin and an
increased amount of collagen in the subepithelial area. Hence, both hypertrophy
and hyperplasia are present and the lesion appears clinically to be pigmented and
elevated.
Some of the swellings of the oral mucosa are –
• Mucocoele
• Developmental cysts
• Minor salivary gland abscess
• Gingivitis, and
• Epulis.
Tongue
Inspection
• Anterior 2/3 of the tongue (dorsum)–The patient is asked to open the mouth
fully and asked to put out the tongue to see the dorsum of the anterior two-
third of the tongue (Fig. 18.32A).
• Lateral aspects of the tongue– To see the lateral aspect of the tongue, the
patient is asked to take the tongue to the sides (Figs. 18.32B and C).
• Posterior third of the tongue– Examined with a mouth mirror (Fig. 18.32D).
• Undersurface of the tongue– The patient is asked to lift the tongue so as to
touch the hard palate (Fig. 18.32E).
FIGURE 18.32A Dorsal surface of anterior third of tongue.
FIGURE 18.32B Left lateral border of tongue.
FIGURE 18.32C Right lateral border of tongue.
FIGURE 18.32D Examination of posterior third of tongue with a mouth
mirror.
FIGURE 18.32E Undersurface of tongue.
Note
Inability to protrude the tongue may be due to ankyloglossia and infiltrating
malignancy, or when tongue is involved in oral submucosal fibrosis.
Look for:
• Colour [e.g. red in glossitis (Fig. 18.33A), geographic tongue (Fig.18.33B)].
See Table 18.19 for red lesions of tongue.
• Size [e.g. macroglossia (Fig.18.33C)]
• Ulcerations [e.g. traumatic ulcers due to sharp teeth (Fig.18.33D) and
dentures, glossitis, malignancy (Fig. 18.33E)].
• Fissures (e.g. transverse fissures in congenital fissured tongue, longitudinal
fissures in syphilitic lesions).
• Swellings [e.g. lingual thyroid (Fig.18.33F), haemangioma (Fig. 18.33G),
papilloma, malignancy (Figs. 18.33H and I)].
• Other abnormalities (e.g. post op deformities – haemiglossectomy).
FIGURE 18.33A Glossitis.

FIGURE 18.33B Geographic tongue.
FIGURE 18.33C Macroglossia.
FIGURE 18.33D Traumatic ulcer tongue due to sharp tooth.
FIGURE 18.33E Ulcer undersurface of tongue.
FIGURE 18.33F Lingual thyroid.

FIGURE 18.33G Haemangioma of tongue.
FIGURE 18.33H Carcinoma of tongue.
FIGURE 18.33I Swelling—carcinoma tongue.
Table 18.19
Red Lesions of the Tongue
Lesion Site Appearance Age Confirmation

Migratory Dorsum; lateral Irregular circinate areas which gradually widen, 5–84 Loss of
glossitis surface change shape, migrate over the tongue years filiform
papillae at
the red
atrophic
areas
Median Dorsum; midline Dusky red, smooth, nodular or fissured 15–84 Devoid of
rhomboid anterior to years filiform
glossitis circumvallate papillae
papilla
Iron Entire tongue Bald red tongue, pain, burning sensation Any Anaemia
deficiency
Xerostomia Entire tongue Dusky red; atrophic; ulcerated Any Absence of
saliva
Strawberry Dorsum Bright red papillae standing out of a thick white fur; Any Scarlet fever
tongue later white coat disappears leaving enlarged
papillae on a bright red surface
Note
Normal circumvallate papillae and lingual tonsils are often mistaken for
pathologic lesions.
• Movements of the tongue: While examining the tongue, free movement of

tongue like protrusion, retraction, side-to-side movement and any restriction
in movement should be checked. In case of paralysis of the hypoglossal
nerve, the tongue deviates to the side of the lesion (Fig. 18.34).
FIGURE 18.34 Left hypoglossal nerve palsy.
One of the most common sites of oral cancer is on the lateral aspect of the
tongue, and it must be evaluated completely. This often requires using a gauze to
pull the tongue out and roll it from side to side (Fig. 18.35) while retracting the
cheek with a tongue blade. Alternatively, two tongue blades can be used to push
the tongue away from the lower teeth allowing visualization of every part of the
mucosal lining to the tonsil and base of tongue. A mouth mirror may be
necessary to visualize the base of the tongue (part of the oropharynx)
FIGURE 18.35 Inspection of tongue by holding it with a piece of gauze
and rolling it sideways.
Palpation
The dorsum and lateral margins of the tongue are palpated by running the index
finger on them (Fig.18.36). Being careful not to gag the patient, the lingual
tonsils are palpated.
FIGURE 18.36 Palpation of a tongue lesion.
Look for:
• Firm areas (e.g. indurated lesions) and
• Swellings.
Note
It is desirable that the tongue should lie relaxed and at rest within the mouth
during palpation, as the act of protrusion puts the muscles into contraction and
may give a false impression of induration and lead to error in diagnosis.
Floor of the mouth

The floor of the mouth is a horseshoe-shaped area that extends from the alveolar
ridge of the mandible to the ventral aspect of the tongue.
Inspection
This area is inspected while the tongue is elevated. The patient is asked to open
the mouth and touch the palate with tip of the tongue (Fig. 18.37).
FIGURE 18.37 Examination of floor of mouth.
Look for:
• Colour of the mucosa.
• Swellings (e.g. mucous cysts, fungating mass of verrucous carcinoma and
haemangioma (Figs. 18.38A and B ) (Table 18.20).
• Frenulum linguae (e.g. short frenulum and ulcers of chronic cough).
• Orifices of submandibular ducts on either side of the frenulum (e.g.
discharge of pus).
• Ampulla of the duct (e.g. calculus seen as a white or yellow bleb distending
an oedematous hyperemic ampulla).
• Lingual gingiva.
FIGURE 18.38A Haemangioma floor of the mouth.

FIGURE 18.38B Haemangioma of lower lip.
TABLE 18.20
Swellings of the Floor of the Mouth
Lesion Position Transillumination

Ranula Unilateral, bluish cyst over which Wharton’s duct may be seen Positive
Sublingual dermoid Midline; frequently extends into the submental region Negative
Deep plunging ranula Cervical prolongation into submandibular area Positive
Note
Varicosities of the floor of the mouth are common in elderly people. Keep in
mind that this is one of the most common places for oral cancers to hide.
Palpation
• Bidigital palpation– A gloved finger is inserted into the mouth along the
groove between the alveolus and the tongue as far back as possible and then
pressed on the floor of the mouth. With the help of the fingers of the other
hand placed under the jaw, the gland and then the duct are palpated from
behind forward. Submandibular glands and the entire submental region are
palpated bidigitally. This helps to differentiate an enlarged submandibular
salivary gland from enlarged lymph nodes in that area (Fig.18.39).
FIGURE 18.39 Bidigital palpation of submandibular swelling.
Buccal mucosa
Buccal mucosa is defined as the mucosa lining the cheeks.
Common lesions of the buccal mucosa
• Aphthous ulcers
• White Lesions
• Cysts, mucocoeles
• Papilloma
• Carcinoma
• Catarrhal stage of measles
• Addison’s disease
• Neurofibroma
• Submucous fibrosis
Inspection
• Method 1– The cheeks must be spread away from the teeth and gums by
retracting outwards with a cheek retractor or a pair of tongue blades to see
the buccal mucosal surface of the cheek and also the buccal side of gingiva
and buccal sulcus, the area which connects the gums (gingiva) and the buccal
mucosa (Fig.18.40A).
• Method 2– Insert the index and middle fingers inside the patient’s mouth on
the buccal mucosa and the thumb on the cheek, and while spreading it wide,
both the gutters along the upper and lower jaws can be inspected well (Fig.
18.40B).
• Method 3– An assistant can use both the hands to spread the cheek so as to
make the examination clear for the examiner (Fig.18.40C).
FIGURE 18.40A Examination of cheek mucosa.

FIGURE 18.40B Examination of cheek mucosa.
FIGURE 18.40C Examination of cheek mucosa.
One side is examined followed by the other. It is not uncommon to see a

white line here arising from a habit of biting the inside of the cheek.
• Colour (e.g. white lesions of the cheek – lichen planus and leukoplakia
(Figs.18.41A and B).
• Surface (e.g., elevated lesion of verrucous carcinoma, fungating lesions of
squamous cell carcinoma)
• Texture (e.g. leukoplakia and submucous fibrosis)
• Irregularity [e.g. leukoplakia, submucous fibrosis and malignancy
(Fig.18.41C)].
• Swellings [e.g. mucous cyst (Fig.18.41D)].
• Opening of parotid duct (Stenson’s duct) – opposite the upper second molar
and should secrete clear saliva from both sides when the parotid gland is
milked.
FIGURE 18.41A Lichen planus.
FIGURE 18.41B Leukoplakia of cheek mucosa.
FIGURE 18.41C Malignancy of buccal mucosa.
FIGURE 18.41D Mucous cyst of cheek.
Note
Be sure to examine the entire buccal mucosa from the labial commissure back
to the anterior tonsillar pillar.
Palpation
Both the skin surfaces and mucous surfaces of the cheek should be carefully
palpated to determine whether an ulcer or growth at the mucous surface has
invaded the skin of the cheek or not. A gentle grip of the cheek between the
index and thumb fingers will help in palpating the buccal mucosa for any hidden
masses (Fig.18.42).
FIGURE 18.42 Palpating the cheek for hidden masses.
Gingiva
The commonest symptoms of gingival disease are –
• Bleeding
• Swelling
• Pain or
• Loss of attachment to the teeth.
Normal colour of the gingiva is coral pink. Margins of the gingiva are
scalloped.
Gingiva has three parts –
• Attached gingiva
• Free gingiva or marginal gingiva, and
• Interdental papilla
Examination of the gingiva should begin with the examination for the debris,
plaque and calculus to estimate the oral hygiene. The commonest cause of
gingival diseases is plaque or calculus resulting from bad oral hygiene. The
collection of food debris primarily forms a mucinous, tendinous film called
‘plaque’, which later forms a calcified microbial mass around the cervical region
of the teeth. Poor oral hygiene rules out the possibility of other aetiological
factors in the manifestation of the disease.
The gingival attachment is evaluated by measuring the depth of the gingival
sulcus using special periodontal probes.
• Normal depth of the gingival sulcus, the distance between the gingival
attachment to the tooth and the cemento-enamel junction (neck of the tooth)
is 0.5 mm.
• The mobility of the teeth can be graded in 3 degrees according to the severity.
Look for:
• Gingival enlargement (fibrous or inflammatory).
• Epulis–While examining an epulis it is important to note whether it is sessile
or pedunculated, bleeds on provocation, has any surface ulceration, fibrotic,
soft or hard, arises from the free gingiva, attached gingiva or the pulp, or
associated with other periodontal pathology or systemic condition.
• Recession of gingiva–Recession of the gums is caused by periodontitis,
which pushes the gingiva from the normal level of attachment and causees
migration of the attachment apically. This results in exposure of the roots and
cementum. Severe loss of periodontal attachments may result in alveolar
bone loss, mobility or migration of teeth.
Palate
To examine the palate, the patient is asked to put the head right back and keep
the mouth wide open.
Inspection
The hard palate and soft palate are inspected and the position of the uvula is
noted. A mouth mirror may be used if required (Fig. 18.43).
FIGURE 18.43 Inspection of palate with mouth mirror.
Hard palate
The hard palate is seen for –
• Colour
• Shape (e.g. clefts and fractures)
• Bulge [e.g. nasopharyngeal or maxillary antral malignancy (Fig.18.43A)].
• Texture.
• Swellings confined to –
• One side–herpes zoster of maxillary division of 5th nerve, palatal abscess
(Fig.18.43B).
• Midline-gumma
• Both sides–minor salivary gland enlargements.
• Any area–malignancy (Fig.18.43C).
• Ulcerations (e.g. malignancy).
FIGURE 18.43A Bulging hard palate due to nasopharyngeal malignancy.
FIGURE 18.43B Palatal abscess.
FIGURE 18.43C Infiltration of hard palate by right maxillary antral
malignancy.
Soft palate
For direct examination of the soft palate, the patient is placed facing the light
with the mouth open and a tongue depressor is introduced (Fig. 18.44A). One
must watch the movements of the soft palate during phonation. Ask the patient
to say ‘Ah’! Observe whether both sides of the palate arch upwards. If one side
is paralysed, it will remain flat and immobile, and the median raphe will be
pulled towards the other side. In bilateral paralysis, the whole palate is
motionless. Ask whether the patient notices regurgitation of fluids through the
nose when making an attempt to swallow, a common symptom in total paralysis
of the soft palate.
FIGURE 18.44A Examination of soft palate by depressing the tongue.
Note
Regurgitation of fluids may also be present in individuals with a cleft palate.
The position of the uvula is unreliable, as deviation is not uncommon even in
good health.
The nasality in the voice is evaluated for velopharyngeal incompetence which

is a common finding in individuals with a cleft palate. Remnant oro-nasal
fistulae may be present in cleft palate cases even after the repair of the palate.
The patients may also present a naso-labial fistula if they have an alveolar cleft
and bone grafting has not been performed.
Get the patient to say ‘Ah’ which raises the soft palate and increases the
visibility of fauces, tonsils, oropharynx for a good view for any ulcers, erythema
or vesicles.
Palpation
Palpation of the hard palate is done by running the index finger on it
(Fig.18.44B). Swellings and ulcers are examined in the usual pattern. Tender
swellings denote inflammatory lesions (e.g. a tender fluctuating swelling close to
the alveolar process is an alveolar abscess, and towards the midline is palatal
abscess), and induration and hardness of lesion indicate malignancy.
FIGURE 18.44B Palpation of palate by running the index finger on it.
Palpation of the posterior part of the oral cavity is unpleasant for the patient as
it usually causes gagging and it is thus left until last. As before, the index finger
is used and run over the structures as rapidly as possible. One is concerned with
detecting a small or hidden carcinoma in these sites, so feel for any irregularity
or ulceration, particularly induration.
Common lesions of the palate:
• Tori
• Smoker’s palate
• Syphilitic chancre
• Syphilitic gumma
• Cleft palate
• Malignant ulcer
• Infectious swelling
• Traumatic swelling
• Cyst
• Haematoma
Pharynx and larynx

The details of examination of pharynx and larynx are given in Chapter 22.
Teeth
Evaluation of the dental health status of a patient is essential and mandatory
while evaluating the illnesses of the oral cavity. A thorough dental examination
and history may provide valuable clues to detect the nature of the underlying
disease, and hence should not be ignored.
• Firstly, the age of the patient and the dental age should be compared.
• Secondly, if the number of the teeth present is less than the actual numbers for
that age then a developmental disturbance or extraction should be suspected.
Hence, it is essential for the practitioners to know the chronology of tooth
eruption in order to identify any delayed eruption or exfoliation for the
corresponding age. The anomalies in number of teeth are given in Table
18.21.
• Thirdly, the clinician should know to differentiate between deciduous and
permanent dentition (Table 18.22) as in the case of mixed dentition
(Fig.18.45).
FIGURE 18.45 Types of dentition.
TABLE 18.21
Anomalies in Number of Teeth
Associated
Condition Clinical Features Associated Features
Syndrome
Anodontia Complete absence of Hereditary Dry skin; absence of sweat glands; hair of scalp and
teeth ectodermal eyebrows scanty; depressed nasal bridge; prominent
dysplasia supra-orbital ridge; frontal bossing; protruded lips
Supernumerary Extra teeth which do not Gardner’s Multiple polyposis of intestine; osteomas of long bones;
teeth resemble the normal syndrome multiple sebaceous cysts esp of scalp; multiple
teeth desmoid tumours
Supplementary Extra teeth which
teeth resemble the normal
teeth and help in
mastication
TABLE 18.22
Differences Between Deciduous Teeth and Permanent Teeth
Property Deciduous Teeth Permanent Teeth

Number 20 32
Colour Milky white Yellowish white
Mamelons Absent Present
Spacing Normal spacing No space is present
Impacted tooth (tooth not erupted) may be due to a dentigerous cyst (common
with mandibular and maxillary third molar followed by maxillary canine).
Next, the shape of the teeth should be noted. Many generalized conditions of
the body, such as syphilis may cause abnormality in the shape of the teeth. Shape
of the teeth may also get altered due to wearing off, i.e. attrition, abrasion and
erosion. They are shown in Table 18.23.
TABLE 18.23
Anomalies in Shape of Teeth
Associated
Condition Features Associated Features
Syndrome
Talon cusp An anomalous structure projects lingually Rubinstein Developmental retardation; broad
from the cingulum areas of a maxillary or Taybi thumb; great toes; thin long
mandibular permanent incisor syndrome arms and legs; prognathic jaws
Taurodontism Body of the tooth is enlarged at the expense Klinefelter’s Occur more commonly in males;
of the root syndrome mental retardation; patient is
tall; thin long arms and legs;
prognathic jaws
Hutchinson’s Peg shaped lateral incisors; mulberry molars Congenital Interstitial keratitis; 8th nerve
tooth syphilis deafness; irregular thickening of
clavicle; saddle nose
Anomalies in structure and discolouration of teeth (Figs.18.46 A to C ) are

shown in Tables 18.24 and 18.25.
FIGURE 18.46A Dental flurosis.
FIGURE 18.46B Tetracycline stains.

FIGURE 18.46C Nicotine stains (D) indicates denture.
TABLE 18.24
Anomalies in Structure of Teeth
Associated
Condition Features Associated Features
Syndrome
Dentigogenesis Colour of teeth may range from grey to Osteogenesis Fragile bone; prone to fractures;
imperfecta brownish violet or yellowish brown; imperfecta pigmented choroids (blue
exhibitsunusual translucent or sclera); deafness due to
opalescent hue; enamel fractures off osteosclerosis; laxity of
easily; rapid attrition of dentin ligaments; peculiar shape of
skull; abnormal electric
reaction of the muscles
TABLE 18.25
Discolourations of Teeth (Fig. 18.46A to C)
Discolouration Cause Features
External
Yellowish Chlorhexidine
mouthwash
Brownish black Tobacco History of tobacco usage
Green Chromogenic Due to food products
bacteria
Internal
White spots to Fluorosis Cannot be removed easily
brownish
discolouration
Blackish Dental caries Tooth structure demineralized, sometimes with pain
discolouration
Reddish or Congenital Excretion of red urine; photosensitivity; vesicular or bullous eruptions on the
brownish porphyria face, back of hands and other parts
discolouration
Pinkish hue Internal resorption Inflammatory vascular pulp filling the resorbed area and showing through the
tooth substance; Associated with pulpal infection; hyperplasia of pulp
Reddish yellow hue Non-vital tooth Breakdown products of blood scatters in dentin and shows off through enamel
Greenish grey Tetracycline Tetracycline gets incorporated in the developing tooth of the foetus
intake during
pregnancy
Inspection
To determine the –
• Nature of teeth (e.g. deciduous or permanent or mixed).
• Number of teeth (e.g., anodontia and supernumerary teeth).
• Shape of teeth (e.g. Talon cusp, Hutchinson’s tooth).
• Discolourations (e.g. tetracycline, fluorosis and tobacco stains).
• Surfaces of teeth (e.g. dental caries).
Palpation
The teeth can be palpated for their mobility (e.g. extruded tooth in apical
abscess). This can be done in one of the following ways:
• The tooth can be gently pushed with the help of the mouth mirror handle (Fig.
18.47A).
• A probe can be pressed on the occlusal surface of the tooth and moved (Fig.
18.47B).
• The tooth may be held with the mouth mirror or its handle on one side and the
probe on the other and moved (Figs. 18.47C and D).
• The tooth may be moved by holding with the mouth mirror handle and the
index finger (Fig. 18.47E).
FIGURE 18.47 Testing the mobility of tooth—(A) with mouth mirror handle;
(B) probe on occlusal surface; (C) with mouth mirror and probe; (D) with
mouth mirror handle and probe.
FIGURE 18.47E Testing the mobility of tooth with mouth mirror handle and
a finger.
Pain on palpation of the gingiva of the involved tooth can help to determine if
there is an associated apical abscess. Biting on to a gauze or rubber (Fig.18.48)
can be used to elicit pain due to cracked tooth. Mobility of the tooth increases as
the bone support decreases like in cases of periodontal disease, fracture of the
root or the supporting bone.
FIGURE 18.48 Biting a piece of gauze for evaluation of tooth pain.
Percussion
Percussion is carried out by gently tapping the suspected and the adjacent teeth
with the handle of a mouth mirror to elicit pain (Fig.18.49). A positive sign
indicates the presence of periapical periodontitis or a lesion.
FIGURE 18.49 Percussing the tooth with the handle of the mouth mirror.
Pulp vitality tests

Integrity of nerve and blood supply of a tooth can be examined by various pulp
vitality tests, like application of cold, application of heat, electric pulp testing
and test cavity preparation.
Oral hygiene
Oral hygiene of the patient should be evaluated; periodontal attachment of every
single tooth should be assessed. This can be done by using a periodontal probe.
Pocket depth of more than 5 mm is an indication of periodontal disease. Diabetes
mellitus more commonly manifests as a periodontal disease orally. Secondly,
diabetic patients might have acetone breath.
Dental caries
Each tooth surface must be examined for the presence of dental caries and the
integrity of restorations if any. Dental caries is a sugar-dependent infectious
disease of the hard tissues of the oral cavity. The initial lesion appears as a white
spot, most commonly on the occlusal surface of the tooth. This white spot is a
result of demineralization of the enamel. This gradually develops into an
advanced carious lesion (Fig.18.50).
FIGURE 18.50 Dental caries.
Occlusion of dental arches

The occlusion is evaluated by asking the patient to close the jaws together. The
different types of malocclusion (Figs.18.51 A to D) are shown in Table 18.26.
FIGURE 18.51A Open bite.
FIGURE 18.51B Deep bite.
FIGURE 18.51C Cross bite.
FIGURE 18.51D Proclination.
TABLE 18.26
Varieties of Malocclusion
Malocclusion Presentation
Open bite (anterior or Teeth of upper and lower jaw do not interdigitate
posterior)
Deep bite The teeth of upper jaw overlap the teeth of lower jaw excessively
Cross bite (anterior or The teeth of upper jaw are present lingual to the teeth of lower jaw
posterior)
Crowding Occurs when mesio-distal width of all the teeth present in the jaw is more than the available
space in the jaw
Spacing Occurs when mesio-distal width of all the teeth present in the jaw is less than the available
space in the jaw
Proclination Upper anterior teeth are protruded.
Centric occlusion is described as that occlusion of the jaws when the cusps are
in maximum interdigitation.
Look for –
• Relationship between the arches and
• Path of closure for obvious prematurities or displacements.
Note
Improper occlusion can be the root cause of many other problems, like bad
oral hygiene, dental caries, TMJ disorders and poor esthetics.
Jaws
The bones of the jaws are membranous bones; there is no cartilage. The diseases
of jaws are broadly classified as –
• Inflammatory
• Alveolar abscess
• Osteomyelitis
• Odontogenic
• Dental cyst
• Dentigerous cyst
• Ameloblastoma
• Bone tumours
Benign
• Fibro-osseous group (e.g.fibrous dysplasia and osteoma)
• Osteoclastoma
• Giant cell granuloma
Malignant
• Osteosarcoma
• Carcinoma of maxillary antrum
The salient features of the above are tabulated in Table 18.27.
TABLE 18.27
Salient Features of Diseases of Jaws
Lesion Clinical Features Radiological and Histological Feature
Dentigerous cyst A fluctuant; swelling commonly in Unilocular radiolucent area associated with well defined
the third molar area; associated border with the crown of an unerupted tooth
with crown of an unerupted tooth; Histology: 2–4 layers of flattened non-keratinising
may be extensive to cause cells with loosely arranged connective tissue
‘hollowing out of the mandible’
Odontogenic Most common in the ramus and third Multilocular radiolucent area with defined smooth and
keratocyst molar region; pain; soft tissue corticated margins Histology: (i) Corrugated
swelling; expansion of bone; parakeratin surface 6–10 cells thickness of epithelium
drainage; paresthesia of lip or without rete pegs formation. (ii) Polarized palisaded
tooth basal layer of cells
Ameloblastoma Central lesion of bone, slowly : Multilocular radiolucency
destructive expands the bone; •Small loculations ‘Honey Comb’.appearance
extremely disfiguring •Large loculations ‘Soap bubble’ appearance
Expansion of buccal and lingual cortical plates
Histology:Islands; cords or sheets of epithelium in a
mature fibrous connective tissue stroma
Calcifying epithelial Asymptomatic; painless swelling : Unilateral or multilocular radiolucency with scalloped
odontogenic margins; Specks of calcification give a ‘driven-snow’
tumour appearance Histology: Islands; strands or sheets of
polyhedral epithelial cells in a fibrous stroma;
calcifications form concentric rings and fuse to form
large complex masses
Benign Most commonly affects the Circumscribed dense radio-opaque mass with a thin
cementoblastoma mandibular first molar tooth; translucent line; associated with resorption of the
associated tooth is vital; slow involved root Histology: Sheets of thick trabeculae of
growing; may cause expansion of mineralized material with irregularly placed lacunae
cortical plates of bone and multinucleated giant cells
Paget’s disease Progressive enlargement of the skull ‘Cotton wool’ appearance Histology: ‘Jigsaw puzzle’
and deformities of the spine, appearance or ‘mosaic’ pattern
femur and tibia; maxilla
progressively enlarges;
pathological fractures; bone pain;
patient assumes a simian
appearance
Fibrous dysplasia Occurs mostly in children as a ‘Ground glass’ or ‘Peau d’ orange’ appearance Histology:
painless swelling or bulging of Trabeculae are ‘chinese letter’ pattern
the jaw involving labial or the
buccal plate; mucosa is intact
over the lesion
Cherubism Most commonly seen in early Bilateral; multilocular expansile radiolucencies Histology:
childhood often by the age of 3 or Vascular fibrous tissue with multinucleated giant cells;
4 years; there is progressive perivascular eosinophilic cuffing of small capillaries
painless symmetric swelling of
the jaws; firm to hard on
palpation
Central gaint cell Predominant in children and more Unilocular or multilocular radiolucency with non-
granuloma common in females; slight to corticated margins Histology: Multinucleated giant
moderate bulging of the mandible cells are seen with few or several dozen nuclei
(mostly) with no pain; history of
trauma is present
Osteomyelitis Manifest as severe pain with Diffuse lytic changes seen in the bone
elevation of temperature and
regional lymphadenopathy
Traumatic swelling Severe pain and oedema due to Fracture line might be seen
fracture of bone or injury to soft
tissue
Masseteric Unilateral hypertrophy in case of Normal
hypertrophy congenital facial hemi
hypertrophy; bilateral
hypertrophy due to unusual
muscle function through habit or
necessity
The clinical examination of jaws conforms to the examination of the oral

cavity for their intra-oral presentations and other swellings, ulcers and sinuses in
general for their extra-oral presentation.
Other systems
When the clinical presentation is related to pathologies of oral cavity and jaws,
the following systems should be clinically evaluated for completion and more
information –
• Neck (e.g. secondary lymph node metastases in oral cancers)
• Chest (e.g. TB and pulmonary metastases in oral cancers)
• Abdomen (e.g. lymphoma)
• Lymphatic system in general (e.g. TB and lymphoma)
• General physical examinationContinuedContinued
CHAPTER 19
Injuries of face
S.M. Balaji
CHAPTER OUTLINE
19.1. Surgical anatomy of facial skeleton 264
19.2. Fractures of facial skeleton 264
• Fractures of midface 268
• Fractures of mandible 272
• Teeth 273
19.1 surgical anatomy of facial skeleton

The understanding of the surgical anatomy of the facial skeleton and the adjacent
structures is extremely important in understanding the fracture, the displacement
of the fractured bone fragments, and the factors necessary for uncomplicated
healing.
Traditionally, the face (Fig. 19.1) is divided into –
• Upper facial skeleton;
• Mid facial skeleton; and
• Lower facial skeleton
FIGURE 19.1 Facial skeleton.
The upper facial skeleton is the frontal bone making up the superior orbital
margin and orbital roof. The base extends backwards and is angled downwards
at approximately 45 degrees where the frontal bone articulates with the
sphenoid. Mid facial skeleton articulates with this sloping plane and the
cribriform plate of the ethmoid.
The mid facial skeleton is made up of complex of bones, and is defined as an
area bounded superiorly by a line drawn across the skull from the fronto-
zygomatic sutures across the frontonasal and frontomaxillary sutures to
frontozygomatic suture on the opposite site, and inferiorly by the occlusal plane
of the upper teeth (alveolar ridge in edentulous person). It extends backward as
far as the pterygoid plates of the sphenoid. The area of mid facial skeleton is
made of the following bones:
• Two maxillae
• Two zygomatic bones
• Two zygomatic processes of the temporal bones
• Two palatine bones
• Two nasal bones
• Two lacrimal bones
• Vomer
• Ethmoid and its attached conchae
• Two inferior conchae
• Pterygoid plates of the sphenoid
The lower facial skeleton essentially comprises of the mandible.
Applied anatomy
Injuries of the upper facial skeleton cause injury to the brain directly or
indirectly. Injuries of the mid facial skeleton is almost always composite, but
takes considerable force and acts as a cushion for trauma to the brain, whereas,
injuries of the mandible are directly transmitted to the base of the skull through
craniomandibular articulation, and cause surprising degree of head injury.
19.2 fractures of facial skeleton

Fractures of mid face
• The fracture of facial skeleton is usually due to direct injury.
• Types of fractures of mid face are –
• Zygomatic
• Nasal
• Maxillary [Le Fort classification (Fig. 19.2)]
- Le Fort I (Low level fracture): This is horizontal fracture above the level
of the nasal floor
- Le Fort II (Pyramidal or subzygomatic fracture): The fracture runs from
the thin middle area of the nasal bones down either side crossing the
maxillary processes into the medial wall of each orbit
- Le Fort III (High transverse or suprazygomatic fracture): The fracture
runs from near the frontonasal suture transversely backwards, parallel with
the base of the skull and involves the full depth of the ethmoid, including
the cribriform plate
FIGURE 19.2 Fractures of maxilla.
Fractures of mandible
Fracture of the mandible (Fig. 19.3) can be divided according to the anatomical
location into eight types –
1. Dento alveolar
2. Condylar
3. Coronoid
4. Ramus
5. Angle
6. Body
7. Parasymphysis
8. Symphysis
FIGURE 19.3 Fractures of mandible.
The mandibular fractures can be –

• Unilateral
• Bilateral
• Multiple
• Comminuted
History
• History of the injury and hearing or feeling of a bone crack. The nature of
impact (direct violence, indirect violence or excessive muscular contraction)
should be determined.
Symptoms
• Pain and loss of function.
• Loss of function may not be a feature of an impacted fracture.
Signs
• Tenderness of the bone on applying pressure.
• Swelling and ecchymosis (Fig. 19.4A).
• Nasal bleed (Fig. 19.4B) and cerebrospinal fluid (CSF) rhinorrhoea (Fig.
19.4C) are common in associated base of skull fractures.
• Subconjunctival haemorrhage occurs in orbital bone fractures (Fig. 19.4D).
• Blebs on the skin overlying the fractured site.
• Deformity–This is elicited by inspection, palpation and measurement. This is
the most important sign of a fracture. The deformity in case of a flat bone is
either depression or elevation, and in case of a long bone this is angular,
lateral, longitudinal or rotatory. Hard palate is deformed in Le Fort I fracture
(Figs. 19.5A and B).
• Dental alignment is lost in displaced fractures (Fig. 19.6).
• Abnormal mobility–This is present in case of impacted fractures.
• Crepitus–Also present in case of impacted fractures and should be elicited
gently.
• Loss of function–For example, if the maxilla or the mandible is fractured, the
patient may not be able to masticate properly.
FIGURE 19.4A Characteristic raccoon eyes of Le Fort II and III—
periorbital oedema and ecchymosis.
FIGURE 19.4B Injury of midface.
FIGURE 19.4C Periorbital oedema associated with frontal and naso-
orbital-ethmoid fracture. Note clear fluid from right nostril possibly CSF
rhinorrhea.
FIGURE 19.4D Zygomatic fracture.
FIGURE 19.5A Le Fort I fracture.
FIGURE 19.5B Parasagittal palatal fracture associated with Le Fort I
fracture.
FIGURE 19.6 Displaced mandibular fracture.
• X rays (Figs. 19.7A to C) and computed tomography (CT) (Figs. 19.8A and
B) are diagnostic.
FIGURE 19.7A X ray—fracture of ramus of mandible.
FIGURE 19.7B X ray—fracture of condyle of mandible.
FIGURE 19.7C X ray—zygomatic fracture.

FIGURE 19.8A CT—zygomatic fracture.
FIGURE 19.8B CT—fracture of orbital bones.
The clinical examination of patient with maxillofacial injuries takes place in
three stages –
1. Immediate assessment and treatment of any condition constituting a threat to
life.
2. General clinical examination of the patient.
3. Local examination of the maxillofacial region.
Patients with maxillofacial injuries may have sustained other bodily injury
which may constitute an actual threat to life or be of higher priority than facial
trauma. Hence, it is always essential to make ainitial rapid assessment of an
injured patient and establish emergency resuscitation before a detailed
examination.
Maxillofacial injury rarely threatens the patient’s airway and constitutes the
highest concern in the management.
In the case of injuries of the face, before a detailed examination is done, the
face must be gently cleaned with warm water and swabs to remove blood clots,
dirt, etc., in order to make an accurate evaluation of any soft tissue injury.
The following reasons may compromise airways in patients with maxillofacial
injuries:
• Obstruction of nasal and oral airways by blood clot, saliva, bone, teeth and
part of dentures.
• Inhalation of any of the above.
• Obstruction of the nasopharynx and oropharynx by backward displacement of
tongue and its attachments in symphyseal fractures of the mandible.
• Occlusion of the oronasopharynx by downward and backward displacement
of a fractured maxilla.
• Soft tissue oedema of the face.
Midface
Extra oral examination
Pre-requisites
• The blood and debris from the fractured site are cleaned for a better view and
examination.
• During the cleaning of the face, the cranium and the cervical spine are
carefully inspected and then palpated for signs of injury.
Inspection
The cardinal signs of midfacial fracture (Figs. 19.9A to C) are–
• Face–Swelling, ecchymosis, deformity. When there is a considerable
displacement temporomandibular joint (TMJ) injuries or middle cranial fossa
(MSF) injuries may manifest as bleeding from the external auditory canal.
Basilar skull fractures may result in CSF otorrhea. Any perforation and
bulging of the tympanic membrane (Haemato tympanum) usually indicates
basilar skull fracture. Ecchymosis behind the ear is known as ‘Battle’s sign’,
which is also an indicative of basilar skull fracture involving the middle
cranial fossa.
• Eyes–Periorbital oedema, ecchymosis and subconjunctival haemorrhage. The
examiner should never neglect a small laceration which may indicate a
penetrating wound of the upper or lower eyelid and they should assume that
such injuries may be associated with a globe injury. Bilateral periorbital
ecchymosis (raccoon eyes) is commonly seen as a result of the fracture of the
base of the anterior cranial fossa.
• Nose–Haemorrhage or CSF leak. CSF is usually associated with bleeding.
However, the presence of CSF in the blood can be detected with the help of a
simple test. A drop of fluid is placed on a handkerchief and the classic ‘bull’s
eye’ sign or ‘ring test’ develops. It is also identified by the tram-line pattern.
• Mouth–Haemorrhage and the inability to close the mouth due to deformity
and pain. A penetrating wound of the soft palate may be extended into the
middle cranial fossa and the transverse penetrating injury in the neck region
must be assumed to injure a major vessel, and requires arteriogram for
evaluation.
FIGURE 19.9A Circumorbital oedema.
FIGURE 19.9B Periorbital ecchymosis.
FIGURE 19.9C Periorbital echymosis in relation to frontal and skull base
fracture. Note the sutured laceration in forehead, right CSF otorrhea.
Palpation
The back of the head and the cranium should be explored gently for wounds
and bony injuries.
Palpation should be done to identify the bony injuries, which manifest as – (i)
break in the continuity of the bone; (ii) tenderness; or (iii) crepitus.
• Bimanual palpation of the maxilla: One hand is placed over the forehead
for stabilizing the head and the maxilla is manipulated with the other hand to
check its mobility. Movement of the maxilla within the soft tissue indicates
maxillary fracture.
• Palpation over the naso-frontal suture helps to diagnose fracture in that area,
which is indicative of Le Fort II (Pyramidal) or Le Fort III (Craniofacial
dysjunction) maxillary fracture. Le Fort I (horizontal or Guerin) fracture is
diagnosed by manipulating the buccal fold with the help of the thumb and
index finger.
• Lack of mobility of maxilla does not rule out a maxillary fracture; hence, it
can be impacted. Such fractures can be mobilized with the help of
disimpaction forceps under general anesthesia.
• The infraorbital rim is palpated for the presence of step deformity which may
indicate either an isolated fracture of zygoma or a Le Fort II level injury. The
area of the frontozygomatic suture is now palpated.
• Displacement of the lateral orbital bone may displace the lateral canthal
ligament resulting in diplopia. Lateral orbital rim fracture can occur either
alone or in association with the zygoma fractures. Hence, it is always safe to
evaluate the visual acuity and extraocular movements.
Examination of the zygomatic complex is done by palpation of the zygomatic
arch and buttress. Any injury to the zygomatico-facial or zygomatico-temporal
nerve in this region would result in anesthesia or paraesthesia of the soft tissues
in case of zygomaticarch fracture. Intraoral palpation of the zygomatic buttress
may disclose a step deformity, which is a common finding in the fractures of the
zygoma.
Method of palpation: It is done by running the fingers of both the hands
simultaneously on each half of the face with gentle pressure. The order of
palpation (Figs.19.10A to H) is –
• Back of the head and cranium
• Forehead
• Orbits: From midline run laterally along the rim of the orbit
• Zygomatic bones and arch (Fig. 19.11)
• Nasal complex
• Temporomandibular joints and
• Mobility of maxilla.
FIGURE 19.10 Methods of palpation—(A) Supraorbital margins. (B)
Infraorbital margins. (C) Lateral orbital margins. (D) Zygomatic arches. (E)
Nasal bones. (F) Temporomandibular joints. (G) Zygomatic buttress
intraorally. (H) Maxilla for mobility.
FIGURE 19.11 Zygomatic arch fracture with clinical deformity.
Examination of eyes: The eyelids are gently separated and the extent of the
subconjunctival ecchymosis is confirmed. Measurement of the intercanthal
distance beyond 32 mm may indicate the presence of traumatic telecanthus.
Combination of obtuse medial canthal angle, increased intercanthal distance, and
flattened nasal bridge is indicative of a fracture of naso-orbital-ethmoidal (NOE)
complex. Severe injuries of the NOE complex might be an indication of
fractures involving the frontal bone and the associated sinus.
In a conscious patient, the following are tested:
• Vision in each eye;
• Movements of the eyeball–The patient is asked to follow the clinician’s
finger with his or her eyes and asked to inform if diplopia occurs (Fig.
19.12A).
FIGURE 19.12A Enopthalmos and restriction in eye ball elevation in the
right eye.
With the help of a torch, the following are noted:

• Any alteration in the size of the two pupils, and
• Light reflex.
Globe position: Simple testing of pupil axis using a straight instrument
(Figs.19.12B & C).
FIGURE 19.12B Enopthalmos, hypoglobus, flattening of malar eminence
on right side and depressed nasal bridge.
FIGURE 19.12C Note the step deformity on the right side of the chin
indicating parasymphysis fracture.
Forced duction test (Traction test) (Fig. 19.12D): Diplopia caused due to
oedema or haematoma of the extraocular muscles usually resolves in 5–7 days,
but diplopia as a result of failure to rotate the eyes superiorly indicates paralysis
or entrapment of the muscle within the fractured segments. To differentiate
between these two causes of diplopia, forced duction test is carried out under
sedation, local anesthesia (LA) or general anesthesia (GA).
FIGURE 19.12D Forced duction test.
Hold the tendon of the inferior rectus muscle with the tissue holding forceps
and ask the patient to carry out an entire range of eye movements. Any failure to
rotate the eyes superiorly indicates paralysis or entrapment of the muscle within
the fractured segment.
Finally, the examiner should test both the cheeks for areas of anesthesia in the
distribution of infra orbital nerve.
Intra oral examination

Pre-requisites
• Lukewarm mouthwash is given in order to remove the clotted blood and for a
better view.
• Clotted blood and any fragment of teeth, bone or denture must be removed
carefully and gently with the help of forceps.
• The mouth should be examined for loose or broken teeth or dentures. If a
denture is fractured, the fragments should be collected carefully, and should
see that no part of the denture has been swallowed by the patient
accidentally.
• Good illumination is mandatory.
Inspection
Look for:
• Derangement of the bite
• Lacerations
• Ecchymosis
• Damage to the teeth or
• Damage to the alveolus (Fig. 19.13).
FIGURE 19.13 Alveolar fracture involving right maxillary dental segment.
Palpation
Look for:
• Areas of tenderness
• Bony irregularities
• Crepitus
• Mobility of teeth or
• Integrity of the alveolus.
A finger and thumb are placed over the fronto-nasal suture line and movement
of the facial skeleton is demonstrated by the pressure of the fingers on the palate.
Percussion
• Next, the teeth are tapped and the cracked-pot sound is elicited if there is
fracture above the teeth.
Mandible
Extra oral examination
Pre-requisites
• They are the same as that of midface extraoral examination.
Inspection
The cardinal signs of mandibular fracture are –
• Swelling
• Ecchymosis
• Haemorrhage through oral cavity
• Deformity–When there is a considerable displacement.
• Inability to close the mouth–Due to deformity and pain.
Palpation
Palpation should be done bilaterally in the condylar region and then should
continue downwards towards the lower border of the mandible, to identify –
• Break in the continuity of the bone
• Tenderness and
• Crepitus.
Intra oral examination

Pre-requisites
• They are the same as that of midface intraoral examination
Inspection
• Step 1: Examination of buccal sulcus, lingual sulcus and floor of the mouth.
Look for:
• Ecchymosis in the thebuccal and the lingual sulci–Submucosal
extravasation of blood is often indicative of an underlying fracture.
• Ecchymois on the lingual side of the mucosa of the floor of the
mouth–Since it overlies the periosteum of the mandible, which if
breached, causes leakage of blood into the body of the mandible (e.g. a
linear haematoma, particularly in the region of the third molar indicates an
adjacent fracture).
• Step 2: Occlusal plane or the alveolar ridge.
Step defect in the occlusion or alveolus is seen along with any obvious
laceration of the overlying mucosa.
Neurological examination
The nerves commonly injured as a result of oral and perioral trauma are –
• Inferior alveolar nerve–Frequently injured as a result of mandibular
fractures and cause lip anesthesia on the affected side, which may be
permanent.
• Lingual nerve–This nerve is less commonly injured. Injury to the lingual
nerve results in anesthesia or paraesthesia of the anterior two-thirds of the
tongue. In addition, since the chorda tympani fibers are carried by the lingual
nerve, injury to this structure also results in alteration in taste.
Palpation
The back of the head and the cranium should be explored gently for wounds and
bony injuries.
• All the teeth are examined for any fracture, crack, loose fillings, missing
crown, and luxation or subluxation. Fractured sites are gently tested for
mobility by placing the finger and thumb on each side and using pressure to
elicit unnatural mobility.
Percussion
• Next, the teeth are tapped and the cracked-pot sound is elicited if there is
fracture below the teeth.
Movements
If possible the patient is asked to carry out a full range of mandibular
movements, and any pain or limitation of movement is recorded. Occasionally,
this examination also fails to confirm a mandibular fracture which is suspected
from the history and presence of haematoma. In such cases, the flat of both
hands should be placed over the two angles of the mandible and gentle pressure
exerted. This manoeuver would elicit pain when even a crack fracture is present.
Teeth
Dental examination
Finally, if the patient has teeth they are examined with a mirror and probe to
demonstrate the following:
• Fractures, either horizontal or vertical.
• Mobility, either due to root fracture or periodontal problem.
• Bleeding from the gingival crevice, either due to trauma or periodontal
disease.
• Missing teeth. If teeth are missing, chest and abdominal radiographs must be
reviewed. Although displaced teeth are usually swallowed, the main stem
bronchi and the lungs should be carefully evaluated.
CHAPTER 20
Nose, nasal cavities and paranasal

sinuses
Jacinth Cornelius
CHAPTER OUTLINE
20.1. Development of nose, nasal cavities and paranasal sinuses
274
• Nose 275
• Nasal cavities 275
• Paranasal sinuses 275
20.3. Diseases of nose, nasal cavities and paranasal sinuses 276
20.4. Diseases of nose 276
• Congenital anomalies 276
• Injuries of nose 276
• Nasal fractures 277
• Lupus vulgaris 278
• Rhinophyma 278
• Carcinoma of nose 279
20.5. Diseases of nasal cavities 279
• Nasal septal deviation 279
• Choanal atresia 280
• Nasal glioma 280
• Meningocele/encephalocele 280
• Nasal septal haematoma and abscess 280
• Furunculosis / vestibulitis 281
• Rhinitis 281
• Allergic rhinitis 281
• Nonallergenic eosinophilic rhinitis 282
• Atrophic rhinitis 282
• Chronic granulomatous rhinitis 282
• Rhinosporidiosis 282
• Simple nasal polyps 283
• Adenoidal hypertrophy 283
• Inverted papilloma 284
• Angiofibroma 284
• Carcinoma of postnasal space (nasopharynx) 285
• Foreign bodies 285
20.6. Diseases of paranasal sinuses 285
• Acute sinusitis 285
• Chronic sinusitis 286
• Malignant tumours 286
20.7. Symptoms of pathologies of nose, nasal cavities and
paranasal sinuses 287
• Nose 291
• Nasal cavities 293
• Postnasal space 293
• Paranasal sinuses 295
20.1 development of nose, nasal cavities and

paranasal sinuses
External nose
receives contributions from the frontonasal process, and from the medial and
lateral nasal processes of the right and left side (Ch. 18). When the frontonasal
process gradually becomes narrow, the deeper part ultimately forms the nasal
septum. The nose becomes prominent due to heaping up of the mesoderm. A
groove appears between the region of the nose and bulging forebrain. As the
nose become prominent, the external nares come to open downward instead of
forward.
Nasal cavity is formed by extension of nasal pits. The nasal pits deepen to
form the nasal sacs, which expand both dorsally and caudally. The bucconasal
membrane separates the nasal sacs from the stomatodeum, which ultimately
breaks, to open ventrally into external nares and posteriorly into the pharynx.
Paranasal sinuses appear as diverticula from the nasal cavity, which
gradually invade the bones after which they are named. The ethmoidal sinuses
are well developed at birth, maxillary sinuses develop during secondary
dentition, the frontal and sphenoidal sinuses develop after 8 years.
20.2 surgical anatomy
Nose
The nose is a pyramidal projection of face. It has:
• A tip
• A root at its junction with the forehead
• A dorsum which is pyramidal and rounded towards the base and tip
• Nostrils or nares are a pair of apertures at the inferior surface of the external
nose separated by columella
The nose is supported by a framework of bones (two nasal bones, articulating
with each other and the nasal processes of frontal bone) in the upper part and
cartilages in the lower part. The cartilaginous part consists of:
• Upper nasal cartilage
• Lower nasal cartilage
• Alar cartilages
Nasal cavities
The nasal cavity extends from nostrils (anterior nares) to choanae (posterior
nares), and opens into the nasopharynx. It is divided into two halves by a
septum. Each half of the nasal cavity has:
• A roof
• A floor
• Medial wall
• Lateral wall
The formation of boundaries of nasal cavity is given in Table 20.1.
TABLE 20.1
The Walls of the Nasal Cavity
Roof Floor Medial Wall (Septum) Lateral Wall
•Nasal •Anterior two •Bony part Nasal surface of maxilla and a number
process of thirds Vomer posteroinferiorly and of bones which articulate with it
frontal Palatine perpendicular plate of ethmoid such as:
bone process of postero-superiorly •lateral mass of ethmoid
•Cribriform maxillae •Cartilaginous part Septal cartilage •lacrimal bone
plate of •Posterior •ascending process of maxilla
ethmoid third •perpendicular plate of palatine
•Body of Horizontal •medial pterygoid process of
sphenoid process of sphenoid posteriorly
palatine
The inner surface of the lateral wall of nose is divided into three regions:
• Vestibule (lowest part of nose—lined by skin and covered by hair)
• Atrium and middle meatus (just above the vestibule)
• Region of conchae (three scroll-like projections—superior, middle and
inferior) and three corresponding meatuses (openings below and lateral to the
respective conchae—superior, middle and inferior)
Sphenoethmoidal recess: Lies between upper part of septum and superior
turbinate about 1.5 cm superior to choana in adults. Sphenoid ostium is located
here.
Superior meatus: Lies between superior and middle turbinates. Ostia of
posterior ethmoids drain here.
Middle meatus: Space between middle and inferior turbinates (harbours
ostiomeatal complex) contains ostia of anterior group of sinuses viz., frontal,
maxillary and anterior ethmoidal sinuses which are situated in two prechamber
areas of the sinuses viz., frontal recess of infundibulum. Frontal sinus and agger
nasi open into frontal recess.
Bulla ethmoidales and maxillary ostia open into infundibulum. Infundibulum
is covered by uncinate process posterior to lacrimal bone. Posterior to uncinate is
a semilunar groove called hiatus semilunaris. The bleb posterior to it is bulla
ethmoidales with middle group of ethmoidal cells. Anteroinferior to bull is the
ostium of maxillary sinus.
Note
The nasolacrimal duct which drains the lacrimal sac opens in the anterior part
of the inferior meatus.
Nerve supply is derived from anterior ethmoidal nerve, a branch of V cranial

nerve and branches of sphenopalatine ganglion. Olfactory nerves are present in
olfactory mucosa and are responsible for smell.
Arterial supply is from branches of external and internal carotid arteries.
• External carotid artery branches:
• Sphenopalatine, greater palatine, supralabial—Little’s area
• Infraorbital and superior dental—antrum
• Pharyngeal branches of maxillary artery—sphenoid
• Internal carotid artery branches:
• Anterior and posterior ethmoidal—nasal septum, ethmoidal and frontal
sinuses
Venous drainage is through:
• Ophthalmic veins and through them into the cavernous sinus
• Sphenopalatine vein
• Anterior facial vein
Paranasal sinuses
These air-filled spaces are present around the nasal cavity in pairs (Fig. 20.1).
They are:
• Frontal
• Maxillary
• Ethmoidal
• Sphenoidal
FIGURE 20.1 Surgical anatomy of paranasal sinuses.
The sinuses are lined by ciliated columnar epithelium, which is continuous

with that of the nasal cavity, and the direction of ciliary beat is towards the
natural ostium into the nasal cavity, so that the secretions are drained into the
nasal cavity.
The functions of the sinuses are:
• Moisten and warm the inspired air
• Add resonance to the voice
• Make facial bones lighter
Nerve supply
• Frontal and Sphenoidal—ophthalmic nerve
• Ethmoidal and Maxillary—maxillary nerve
The lymphatic drainage
is ultimately into the cervical nodes both superficial and deep cervical nodes
(Chs. 12 and 26). With relevance to the spread of malignancies of the oral cavity,
nose and nasal cavity, pharynx and larynx, the neck nodes are divided into seven
levels (Table 20.2).
TABLE 20.2
Lymph Nodes of Neck (Ref Fig. 12.1B)
Level Nodes
1 Submental and submandibular nodes
2 Jugular nodes up to the carotid bifurcation (upper group—jugulodigastric nodes)
3 Lymph nodes between the carotid bifurcation and omohyoid muscle (middle group—jugulo-omohoid nodes
4 Nodes between omohyoid muscle and clavicle—lower jugular group of nodes
5 In posterior triangle, between posterior border of sternomastoid and anterior border of trapezius and clavicle
6 Anterior compartment group—visceral group consisting of para and pretracheal, perilaryngeal and prelaryngeal
nodes
7 Lymph nodes in upper mediastinum
20.3 diseases of nose, nasal cavities and

paranasal sinuses
The diseases of the nose, nasal cavity and paranasal sinuses can be classified
based on their aetiologies (Table 20.3).
TABLE 20.3
Aetiological Classification of Lesions of Nose, Nasal Cavity and
Paranasal Sinuses
Diseases
Aetiology
External nose Nasal cavity Paranasal sinuses
Congenital Anomalies of Nasal septal deviation Agenesis or hypoplasia
nose
Bifid nose Nasal glioma
Flattened nostril Meningocele
With cleft lip and Choanal atresia
palate
Dermoid cyst Mucociliary
and sinuses dyskinesia
Traumatic Injuries of nose Nasal septal Le Fort fracture of mid face involving maxillary
haematoma and and malar complex or fracture of ethmoidal
abscess complex or frontal sinus
Nasal fractures
Inflammatory Acute Furunculosis, Acute infections Acute sinusitis
vestibulitis (viral, bacterial,
fungal)
Chronic Lupus vulgaris Chronic rhinitis Chronic sinusitis
Lupus pernio Atrophic rhinitis
Rhinophyma Chronic
granulomatous
rhinitis
Simple nasal polyps
Neoplastic Benign Papilloma,
haemangioma,
osteoma,
adenoma, fibroma
Inverted papilloma
Angiofibroma
Malignant Carcinomas Carcinomas of nasal Malignant tumours of sinuses
cavity
Carcinoma of
postnasal space
Others Foreign bodies
Obstructive sleep
apnoea
20.4 diseases of nose
Congenital anomalies
• Nasal dermoid cyst—due to failure of (upper part) median nasal folds
• Bifid nose—due to failure of (lower part) median nasal folds. They are
infrequent
• Cleft lip and palate extending to the nose—occurs due to failure of fusion of
maxillary processes with the frontonasal process, and this anomaly is not
very rare
• Haemangioma—vascular malformation
• Nasal dermoid cyst—a globular swelling on the bridge of the nose. A fistula
may often be present
• Bifid nose (Fig. 20.2) and cleft lip and palate extending to the nose
—midline cleft running through the tip, bridge, septum and columella or
through philtrum of lip or through entire palate or as bifid uvula
• Haemangioma (Fig. 20.2A.)—irregular vascular swelling blanches on
pressure
FIGURE 20.2 Bifid nose. Source: (Courtesy Dr K. Sridhar)

FIGURE 20.2A Cavernous haemangioma of nose. Source: (Courtesy Dr
Lakshmi Nagarajan)
• CT for nasal dermoid cysts
• Fistulogram for fistula
Treatment
Cosmetic surgery
Injuries of nose
• Common occurrence due to trauma
• Caused by direct physical violence, cricket ball injury, road traffic accidents,
etc.
• Fractures of nasal bones may be associated
External nasal deformity with incised or lacerated wounds (Fig. 20.3) depending
on the nature of violence
FIGURE 20.3 Laceration of external nose. Source: (Courtesy Dr K. Sridhar)
X-rays
for associated nasal bone fractures
Treatment
Primary suturing
with good cosmetic result for open wounds
Nasal fractures
• Common in young males
• Probably due to the higher incidence of head injuries in road traffic accidents
and contact sports
• The bony pyramid is injured alone or in combination with the cartilaginous
septum
• Head injuries may be associated with cerebrospinal fluid (CSF) leak
• Painful soft swelling of nose
• Asymmetry or deformity of external nose (Fig. 20.4) may be present
• When haematoma develops, nasal obstruction is predominant
• Nasal bleeding (epistaxis) is present
• CSF rhinorrhoea indicates anterior cranial fossa (skull base) fracture
• There may be displacement of nasal bones, with crepitus on palpation
FIGURE 20.4 Deviation in fracture nasal bones. Source: (Courtesy Dr K.
Sridhar)
X-rays (Fig. 20.5) and CT are diagnostic
FIGURE 20.5 X-ray—nasal bone fracture.
Treatment
• Reduction of displaced fracture, especially within 10 days, or when the soft
tissue swelling settles
• Reduction by external manipulation under local or general anesthesia is
done for simple fractures
• Open surgical correction and fixation is required for complex fractures
Lupus vulgaris
• Caused by inoculation of Mycobacterium tuberculosis possibly through nose
pricking
• Perforation of the cartilage of nasal septum can occur with severe scarring in
longstanding cases
Red or brown patches or nodules on the nose (apple jelly nodules)
Mantoux test, biopsy and histopathology are confirmatory
Treatment
Antitubercular chemotherapy
Rhinophyma
• Associated with acne rosacea
• Usually seen in elderly
Lobulated masses (Fig. 20.6) centred around the bulbous nasal tip with coarse
and pitted skin
FIGURE 20.6 Rhinophyma anterior and lateral views. Source: (Courtesy Dr V.
Srinivasan)
Microscopic examination
shows excessive hypertrophy of sebaceous glands
Treatment
Dermabrasion or surgical shaving is the treatment of choice
Carcinoma of nose
• Majority are basal cell carcinomas
• Squamous cell carcinomas and melanomas also occur
Warty or ulcerating lesions (Fig. 9.17B) on the nose
Biopsy
is confirmatory
Treatment
Wide excision and radiotherapy is the treatment of choice
20.5 diseases of nasal cavities
Nasal septal deviation

• Usually occurs due to a differential growth of the midfacial skeleton
• Rarely after trauma to the nose
• The deviation can be ‘C’ or ‘S’ shaped
• May involve cartilage or bone or both
• Angulated sharp projection formed at the junction of cartilage and bone is
called ‘spur’
• Caudal dislocation of septal cartilage into nasal cavity may be seen when
displaced from the groove
• Many are asymptomatic and it is an incidental finding
Symptoms
• When symptomatic, nasal obstruction can occur on the deviated side, and
paradoxical intermittent blockage on the unobstructed side due to turbinal
hypertrophy
• Rarely, the obstruction on the deviated side can cause obstruction to free flow
of secretions and cause maxillary and ethmoidal sinusitis
• Pressure headaches due to contact with lateral nasal wall may be present
(Sluder neuralgia)
• Epistaxis may occur from prominent vessels over sharp spur
• Anterior deviation to an imaginary line between nasal process of frontal bone
and maxilla, obliterates the inner nasal valve (limen nasi) and causes
inspiratory obstruction
• Snoring and sleep disturbance
Signs
• Nasal speculum examination shows the deviation (Fig. 20.7)
• Cottle test is diagnostic of anterior deviation (p. 294)
• Cold spatula test reveals obstruction during exhaling
FIGURE 20.7 Speculum examination—deviated nasal septum.
Nasoendoscopy (Fig. 20.8) and CT are confirmatory
FIGURE 20.8 Nasoendoscopy—deviated nasal septum with spur touching
the inferior turbinate.
Treatment
• Always surgical
• Submucosal resection of the septum, leaving a frame of inferior and
anterior cartilaginous strut to maintain the profile of the nose may be done
• Septoplasty (realignment of septum) is useful for anterior deviations, and
in symptomatic deflections below 18 years of age
Choanal atresia
• Results due to persistence of buccopharyngeal membrane across the
nasopharynx
• May be membranous or bony
• Bilateral atresia may be associated with other congenital abnormalities of the
eye, ear and heart
• Neonates with bilateral atresia present as respiratory emergency
• Unilateral atresia goes unnoticed till late in life
• Adults complain of mucoid nasal discharge
• Since there is no air flow through the nose, the discharge is free of air bubbles
• Inability to pass a nasal catheter from nasal cavity into nasopharynx
• Fibre-optic nasoscopy is useful
• CT may be needed to diagnose the nature of atresia
Treatment
Surgical corrections
are necessary, with respiratory and feeding support
Nasal glioma
Rare congenital tumour due to persistent dural process
• A tumour mass:
• projecting into the nasal cavity or
• extranasally over the bridge of the nose
• On examination it resembles a polyp intranasally
Nasoendoscopy and CT are useful
Treatment
Surgical excision
Meningocele/encephalocele
Occurs due to herniation of meninges (meningocele) or brain (encephalocele)
through a dehiscence of frontal bone
A smooth globular mass at the root of nose with cough impulse (Ref Fig. 16.3A),
or as a polypoidal mass deep in the nasal cavity from the roof
• CT is diagnostic
• Endoscopy, aspiration and CSF analysis are useful
Treatment
Excision and closure of bony defect
Nasal septal haematoma and abscess

• Trauma can cause a haematoma in the nasal septum
• More common in patients with bleeding disorders
• The mucoperiosteum or perichondrium gets stripped from the septal cartilage,
from which it receives its blood supply
• If this is ignored and untreated, the cartilage may get eroded and haematoma
of septum forms
• The haematoma can get infected to form an abscess, and nasal collapse
becomes inevitable
Complications: Cavernous sinus thrombosis and meningitis
• Painful widening of nasal septum (Fig. 20.9A) with blocking sensation of
both nasal passages
• The external nose may be collapsed (Fig. 20.9B)
FIGURE 20.9A Nasal septal haematoma.

FIGURE 20.9B Collapsed nose.
Aspiration of pus and culture
Treatment
• Immediate surgical drainage supported by antibiotics is the treatment of
choice
• Bilateral compression nasal packs to avoid recurrence
Furunculosis / vestibulitis
• Caused by Staphylococcus aureus
• Usually due to nose picking
Complication: Cavernous sinus thrombosis
• Acute pain and localized swelling in the nasal vestibule
• Examination reveals:
• Mucopurulent or purulent discharge, with congested nasal mucocutaneous
junction
• A localized tender swelling in the vestibule (Fig. 20.9C)
• Fissuring of the vestibular skin is characteristic of vestibulitis

FIGURE 20.9C Furunculosis vestibule of nose.
No specific investigation is necessary
Treatment
Topical and systemic antibiotics
Note
Nasopalatine and nasolabial cysts present as cystic lesions and push on to
vestibule obliterating nasolabial fold externally. These can be excised through
sublabial route.
Rhinitis
• Inflammation of the nasal mucosa, which may extend to the sinuses
• It may be acute or chronic
• Acute rhinitis (coryza)—caused by viruses (rhinovirus, adenovirus,
coronavirus, influenza virus, coxsackie virus [commonly seen in
unhygienic surroundings and in people with lowered resistance])
• Chronic rhinitis—caused by recurrent nasal infections, vasomotor rhinitis,
nasal obstruction and allergy
• Nasal obstruction, discharge, disturbances in smell and heavy feeling of nose
• On examination, the mucosa appears congested
Blood count and nasal smear cytology are useful
Treatment
Decongestants, antihistaminics, steam inhalations, antibiotics, analgesics and
nasal douches
Note
Nasal decongestants can be used only when necessary and for a maximum
period of 10 days for fear of precipitation of rhinitis medicamentosa.
Allergic rhinitis
It is an IgE mediated hypersensitivity disease and may be:
• seasonal (caused by allergy to grass or tree pollens)
• perennial (caused by allergens encountered all through the year—house dust)
It may be mild, moderate or severe depending on how much it affects the
routine of patient.
• Sneezing
• Itching of the nose and eyes, serous nasal discharge and intermittent nasal
obstruction (present in most cases)
• Examination reveals a pale mucosa with increased secretions
Skin tests
may demonstrate the allergen
Treatment
• Avoidance of allergens where possible, may be of some benefit
• Medical
• Oral antihistamines are useful especially during acute episodes
• Topical steroids are useful
• Surgical: Submucous diathermy and trimming of the turbinates is rarely
indicated and may improve the airway in select cases
Nonallergenic eosinophilic rhinitis

Diagnosed on the basis that the symptoms are that of allergic rhinitis when no
obvious allergens are implicated
• Itching of the nose and eyes, serous nasal discharge and intermittent nasal
obstruction (present in most cases)
• Examination reveals pale and oedematous mucosa with increased thick
greenish or yellow secretions
• Skin tests may demonstrate no allergen
• Nasal cytology reveals eosinophilic infiltration
Treatment
• Medical: Antihistamines and diethyl carbamazine citrate are useful in some
patients
• Surgical: Submucous diathermy and trimming of the turbinates is rarely
indicated and may improve the airway in select cases
Atrophic rhinitis
• Chronic inflammation of nasal mucosa causing atrophy of nasal mucosa and
underlying bone
• It can be primary or secondary
• Primary
- Hereditary
- Autoimmune
• Secondary
- Endocrine dysfunction
- Iron and vitamin deficiencies
- Infections
- Previous surgery
• Roomy nose, epistaxis, anosmia, sensation of obstruction, foul stench crusts
and greenish yellow discharges
• Examination reveals atrophic mucosa and turbinates
Venereal Disease Research Laboratory (VDRL) test, Mantoux test, X-rays are
useful
Treatment
• Medical: Nasal douches, Kemicitine nasal drops
• Surgical: Young’s operation, Lauenslager operation and Wittmack’s operation
are useful
Chronic granulomatous rhinitis

Can be caused by:
• Specific causes—tuberculosis, leprosy, sarcoid and rhinoscleroma
• Nonspecific causes—Wegener granulomatosis, Stewart’s granuloma, Churg–
Strauss syndrome
Symptoms
• Serosanguinous discharge, nasal obstruction, nasal crusting and sometimes
nasal deformity
• Sensation of blocking of ears, hoarseness and stridor may be present
Signs
• External nose may look collapsed, nasal cavity may be filled with bloody
crusts and the mucosa is friable and bleed when removed
• Perforation of cartilaginous septum may be seen
• Adhesions between the lateral wall and the septum may cause meatal stenosis
• Eardrum may show the features of middle ear effusion
• Larynx may show features of granular laryngitis and subglottic stenosis may
be present
• Rhinoscleroma starts with purulent foetid rhinorrhoea, crusting and atrophic
changes of nasal mucosa and progresses to nodularity and finally, scars
causing adhesion and cicatrisation
• Antineutrophil cytoplasmic antibody test for Wegener granulomatosis
• Biopsy of nasal mucosa and Kveim test for sarcoid
• Biopsy and PCR and culture of nasal tissue for tuberculosis, rhinoscleroma
and leprosy are useful
Treatment
Treatment is towards the cause
Rhinosporidiosis
• Chronic fungal disease caused by Rhinosporidium seeberi
• Endemic in India and Sri Lanka
• In Tamil Nadu, it is endemic in Madurai, Ramnad, Rajapalayam and
Sivaganga
• Usually occurs in those who take bath in ponds
• Nasal obstruction, epistaxis and nasal discharge
• On examination, friable red polypoid mass studded with sporangia
resembling strawberry are seen. Bleeds on probing
Smear for histopathology examination and special staining
Treatment
• Excision and diathermy or laser coagulation
• Dapsone reduces recurrence rates
Simple nasal polyps

• Prolapsed, hypertrophic, pedunculated oedematous fluid-filled mucosa of
nose and paranasal sinuses, usually due to allergy
• More common in men and in asthmatics
• Frequently bilateral and sometimes unilateral
• Depending on the site of origin, they are classified into antrochoanal and
ethmoidal polyps
• Nasal obstruction, with rhinorrhoea and sneezing
• On examination, they appear as semitranslucent whitish grey, pedunculated
insensitive masses by speculum examination (Fig. 20.10) and nasoscopy
(Fig. 20.11)
• They do not bleed on touch
• Allergic fungal rhinosinusitis (AFRS) presents with greenish mucinous
discharge between polyps or with fungal balls
FIGURE 20.10 Speculum examination—nasal polyp.

FIGURE 20.11 Nasoendoscopy—nasal polyp.
The differences between the ethmoidal and antrochoanal polyps are given in
Table 20.4.
TABLE 20.4
Differences between Ethmoidal and Antrochoanal Polyps
Property Ethmoidal Polyps Antrochoanal Polyps
Cause Allergic Infective

Origin Ethmoidal labyrinth Maxillary antrum
Number Multiple Single
Site Anterior Posterior
Nasal obstruction Bilateral Unilateral
Disturbances in smell More pronounced Not significant
Recurrence Common Rare
Allergy tests and CT are useful
Treatment
• Medical: Intranasal corticosteroids are useful
• Surgical: When they do not regress to medical treatment, excision (simple
polypectomy) will improve the airway. Functional endoscopic sinus surgery
(FESS) is the current treatment
Adenoidal hypertrophy
Adenoids are lymphoid aggregations in nasopharynx
• Variety of symptoms occur:
• Hypertrophy causes nasal obstruction, discharge and hyponasal voice,
blocking sensation of ears due to eustachian dysfunction, mouth breathing
or halitosis
• Ectopic choanal adenoids with hypertrophic nasopharyngeal adenoids
causes severe snoring and sleep apnoea
• On examination, the adenoids are enlarged (Fig. 20.12)
FIGURE 20.12 Nasoendoscopy—adenoid hypertrophy.
X-rays of nasopharynx (lateral views) will show adenoidal enlargement (Fig.
20.12A.)
FIGURE 20.12A X-ray lateral view—adenoid enlargement. Source: (Courtesy
Bharat Scans)
Treatment
Adenoidectomy is indicated, if nasal symptoms are severe, and tonsillectomy is
done along with it
Inverted papilloma
• Rare, exclusive, epithelial tumour
• No definite aetiology
• Potentially malignant
• Unilateral nasal obstruction of very long duration
• Bleeding may be present occasionally
• Examination will reveal a fleshy pale polypoidal leafy growth in the nasal
cavity (Fig. 20.13)
FIGURE 20.13 Inverted papilloma.
• Biopsy is conclusive
• CT demonstrates the involvement of adjacent sinuses
Treatment
• Excision is the treatment of choice
• Tumours extending into the sinuses need extensive surgery through lateral
rhinotomy earlier
• Endoscopic removal is the modern treatment
Angiofibroma
• Rare vascular tumour arising from sphenopalatine foramen and its
neighbourhood
• Exclusively presents in boys before puberty
Symptoms
• Nasal obstruction
• Spontaneous, unprovoked and profuse epistaxis
• Local spread may cause ‘frog face’ deformity, proptosis, hyponasal speech
and eustachian blocks
Signs
• Postnasal space shows a dusky red fleshy lobulated mass in the nasopharynx
• Anterior rhinoscopy reveals pinkish fleshy mass with engorged vessels
occupying the nasal cavity pushing the septum, if large
• Cheek swelling above zygoma and proptosis if extensive
• CT and MRI are useful is determining its extent
• Carotid angiography reveals the feeding vessel and shows the typical
‘tumour blush’
• Excision biopsy is conclusive
Treatment
Wide surgical excision (external approach or endoscopic)
Carcinoma of postnasal space (nasopharynx)
• A tumour more common in South China
• Presents at any age, but more in the third and fourth decades
• Squamous cell carcinoma is the commonest
• Has environmental and genetic aetiology
• Epstein Barr (EB) virus plays a role in its aetiology
• Enlarged lymph nodes in the neck
• Usually, nasal obstruction and epistaxis are present
• Unilateral serous otitis media due to eustachian tube block may occur
• Multiple cranial nerve palsies are seen
• Postnasal examination reveals the growth usually arising from fossa of
Rosenmuller and occupying the nasopharynx
• CT and MRI are needed to assess the extensions
• Biopsy is necessary to confirm the diagnosis
• IgA to EB virus is useful for follow up
Treatment
• Radiotherapy is the mainstay of treatment
• Neck dissection may be necessary for nodes in the neck
Foreign bodies
• Foreign bodies are commonly inserted by small children while playing or in
adults who are psychologically disturbed
• Foreign bodies vary from organic matter (e.g. vegetable seeds) to inorganic
matter (e.g. button cells)
• Pain and bloodstained discharge may be caused when the foreign body is
pushed inside forcibly
• Longstanding foreign bodies cause unilateral mucopurulent discharge and
form concretions to form ‘rhinolith’
• Examination will reveal the foreign body (Fig. 20.14)
FIGURE 20.14 Nasoendoscopy—foreign body nasal cavity.
• Diagnostic nasoendoscopy is necessary in some cases
• X-ray paranasal sinuses are useful
Treatment
Urgent removal is necessary and those in the anterior compartment can be
removed with a blunt curved probe
20.6 diseases of paranasal sinuses
Acute sinusitis
• Infections of paranasal sinuses are caused by:
• Viruses
• Bacteria (Haemophilus influenzae, staphylococci, streptococci)
• Fungi
• Acute viral rhinitis may spread to the sinus mucosa
• Ethmoiditis is common in children and maxillary sinusitis is common in
adults
• Isolated maxillary sinusitis may be of dental origin
Complications:
• Suppuration of ethmoidal and frontal sinusitis may cause intracerebral
abscesses
• Sphenoid sinus disease may cause visual disturbances. Proptosis and
intracranial invasion into anterior cranial fossa may take place in AFRS
• Orbital cellulitis or abscess
• Mucoceles of sinuses
• Osteomyelitis of maxilla or frontal bone (Pott’s puffy tumour)
• Discharge
• Pressure or pain over face
• Heaviness of head
• Disturbances of smell
• Cough and postnasal drip
• Ear block
• Halitosis
Pain of sinusitis in general is exacerbated by bending.
Fever and malaise are common symptoms of:
• Severe ethmoiditis—red, swollen orbit with the displacement of orbit down
and outwards
• Other sinusitis causes pain in the affected sinus
• Sphenoidal sinusitis causes a variety of headaches
• Frontal sinusitis causes headache as soon as patient gets up in the morning
and disappears by noon
Clinical examination, reveals tenderness over the affected sinus, maxillary
sinusitis may discharge pus through the middle meatus in the nose. In maxillary
sinusitis, dental causes have to be ruled out.
Diagnostic nasal endoscopy, X-rays and CT of paranasal sinuses are diagnostic
Treatment
• Decongestants and steam inhalation are helpful
• Broad spectrum antibiotics are necessary, when the symptoms last for more
than 3 days
• Antral washouts and endoscopic middle meatal antrostomy may be
necessary, if suppuration occurs
Chronic sinusitis
Chronic sinusitis may be caused by:
• Unresolved acute bacterial infections (e.g. primary ciliary dyskinesia, immune
deficiency)
• Fungal infections—aspergillus and mucormycoses (e.g. immune deficiency)
• Nasal polyps
• Ostiomeatal anatomical blocks
General malaise, headache, nasal block and pus discharge, cough, postnasal
discharge, halitosis, ear block, smell disturbance
X-rays (Fig. 20.14A), CT scan and diagnostic nasal endoscopy are good
diagnostic aids
FIGURE 20.14A X-ray paranasal sinuses—chronic maxillary sinusitis.
Treatment
• Caldwell-Luc operation (sublabial antrostomy), and establishment of sinus
drainage by fronto-ethmoidectomy were done earlier
• FESS is the procedure of choice today
• Antibiotics are necessary initially
Benign tumours
Fibro-osseous dysplasia may cause cosmetic deformity of face and can be
removed after puberty.
Malignant tumours
• Varieties of malignancies occur in this region (Ch. 19)
• Squamous cell carcinoma of maxilla is the commonest
• Adenocarcinoma of the ethmoid sinuses occur in people working in leather
industry
A foul, purulent and bloodstained discharge from the nose is common.
The clinical features vary depending on its spread of maxillary malignancy:
• Posterior spread—causes trismus in maxillary antral tumours
• Medial spread—nasal obstruction and epiphora (Fig. 20.15A)
• Anterolateral spread—swelling and deformity of the face, atypical facial pain
due to trigeminal nerve involvement (Fig. 20.15B and C)
• Spread to the floor—bulge in hard palate (Fig. 20.15D), dental loosening
• Upward spread—proptosis and diplopia (ethmoid and high antral tumours),
cranial nerve palsies
FIGURE 20.15A Maxillary antral malignancy causing obliteration of
nasofacial groove.
FIGURE 20.15B Maxillary antral malignancy causing a swelling.
FIGURE 20.15C Maxillary antral malignancy causing a visible swelling.
FIGURE 20.15D Maxillary antral malignancy infitrating the hard palate.
• Diagnostic nasal endoscopy, radiographs, CT and MRI (Ref Fig. 18.25C)
are diagnostic
• Histopathology is conclusive
Treatment
Radiotherapy, surgery and chemotherapy in various combinations
20.7 symptoms of pathologies of nose, nasal

cavities and paranasal sinuses
• Anterior nasal discharge (rhinorrhoea)
• Postnasal discharge
• Sneezing and itching
• Pain
• Alteration in smell
• Halitosis
• Voice change
• Bleeding per nose (epistaxis)
• Swelling and deformity
• Falling of crusts from nose
Some symptoms, which are not specific to pathologies of nose, nasal cavity
and paranasal sinuses, but may be closely related, are:
• Headache
• Double vision (diplopia)
• Snoring
• Change in voice
• Fever
• Mouth breathing and dryness of throat
Nasal obstruction
Sense of nasal blockage is mediated by cold receptors (e.g. menthol). Sensation
of nasal blockage can be:
• Continuous (e.g. space occupying lesions of nasal cavity)
• Fluctuating (e.g. allergic rhinitis, vasomotor rhinitis)
Anterior nasal discharge (rhinorrhoea)

The anterior nasal discharge can be:
• Watery clear (e.g. CSF rhinorrhoea)
• Serous (e.g. allergic rhinitis)
• Mucoid (e.g. rhinitis)
• Mucopurulent (e.g. chronic rhinitis, sinusitis)
• Purulent (e.g. bacterial infection, green pus—Gram negative infection)
Note
• A unilateral discharge in a child is usually caused by a foreign body unless
otherwise proved.
• A clear watery discharge after head injury is considered to be CSF unless
otherwise proved.
• Bilateral discharge in a child may be due to enlarged adenoids.
• Foul smelling discharge is suggestive of purulent sinusitis, atrophic rhinitis
or foreign body (crust may fall out with bleeding in atrophic rhinitis).
• Serosanguinous discharge is suggestive of malignancy.
Postnasal discharge
The postnasal discharge may be watery clear (e.g. allergic rhinitis) to green pus
(e.g. Gram negative infection), as in anterior nasal discharge.
Sneezing and itching

Irritation of the nasal cavity causes sneezing, a protective reflex, which can be in
a row of sneezes. Occasional sneezing is normal. More than eight to ten sneezes
at a time without any obvious reason are considered abnormal. Very frequent
attacks of sneezing are seen in allergic rhinitis.
Pain
Pain is a common symptom as the head and neck have very rich nerve and blood
supply, and the sensory impulses of the nose and sinuses are mediated by the
trigeminal nerve.
• Pain of the nose and paranasal sinuses may refer to these structures
• Frontal headache may arise due to pathology in the sinus, septum or
turbinates
• Migrainous pain may arise from nasal pathology
• Pain in the cheek may indicate acute maxillary sinusitis
• Pain in the nose may be due to vestibulitis or furuncle nose
Alteration in smell
Loss of sensation of smell can be:
• Complete loss of sense of smell
• Anosmia (e.g. head injury, functional, intracranial tumour)
• Merciful anosmia (e.g. atrophic rhinitis)
• Incomplete loss of sense of smell:
• Hyposmia—reduced sense of smell (e.g. rhinitis, nasal allergy, polyps, old
age, tobacco)
• Parosmia—altered sense of smell (e.g. functional, recovery from head
injury, drugs)
• Cacosmia—sensation of foul smell (e.g. chronic sinusitis, foreign bodies,
malignancy)
Halitosis
Offensive odour may be caused by:
• atrophic rhinitis
• leprosy
• tuberculosis
• granulomatous lesions such as Wegener granulomatosis
Voice change
The voice change is generally nasal intonation (rhinolalia clausa or aperta)
Epistaxis
• Epistaxis is defined as bleeding from nose
• It can be:
• Unilateral (e.g. rupture of vessels from Little’s area, foreign body)
• Bilateral (e.g. atherosclerosis, hypertension, coagulopathies)
Children have a tendency to scratch the nose and bleeding can occur from the
Little’s area— epistaxis digitorum. The causes of epistaxis are shown in Table
20.5.
TABLE 20.5
Causes of Epistaxis
Aetiology Local General

Congenital Telangiectasia Von Willebrand’s disease
Traumatic Nose picking
Foreign bodies
Fractures of nose and midface
Surgical trauma
Infective All infections
Neoplastic Benign and malignant tumours Leukaemia
Angiofibroma Bone marrow infiltration with secondaries
Carcinoma of postnasal space
Vascular Little’s area Coagulopathies
Posterior degeneration of elderly Thrombocytopenia
Blood vessel disorders
Metabolic Sarcoidosis
Wegener granulomatosis
Drugs Tobacco Chemotherapeutic drugs
Heroin Anticoagulants, aspirin, phenytoins
Cocaine
Eliciting history
Since most illnesses of the nose present with symptoms related to the system, the
detailed history taking starts with the presenting symptom, followed by
questions relating to other symptoms of the ear, nose and throat illnesses as well.
• Age: Congenital anomalies, tonsillar enlargement, adenoid hypertrophy, are
seen in children. Malignancies are seen in older age
• Sex: Simple nasal polyps are more common in males
• Occupation: Workers in humid and polluted areas are prone to allergic
rhinitis. Furniture workers, wood workers are predisposed to nasal
malignancy
• Residence: Rhinosporidosis is common in some areas of Tamil Nadu, Kerala,
Madhya Pradesh and West Bengal. In Tamil Nadu, it is common in Madurai,
Ramnad, Sivaganga and Rajapalayam

Nasal obstruction
• Nature of obstruction: Is the sense of obstruction continuous or
intermittent?
The sensation of nasal obstruction can be continuous (e.g. obstructive mass
lesions) or intermittent (e.g. allergic rhinitis), sporadic (e.g. common cold)
• Unilateral or bilateral: Is the sense of obstruction in both sides of nose?
Unilateral obstruction is seen in foreign bodies, unilateral choanal atresia,
gross nasal septal deviation, choanal polyp or unilateral nasal mass and
bilateral obstruction in allergic rhinitis, bilateral mass lesions such as
ethmoidal polyps, bilateral sinusitis, atrophic rhinitis, adenoid hypertrophy,
nasopharyngeal malignancy, bilateral choanal atresia
• Other symptoms: Is there any other symptom associated with the feel of
obstruction?
Sneezing and itching are seen in allergic rhinitis, or also headache as in
common cold
Anterior nasal discharge

The nature of discharge varies from clear watery (e.g. CSF rhinorrhoea),
serous fluid (e.g. allergic rhinitis), serosanguinous (e.g. antral and nasal
malignancy), thick mucus (e.g. common cold), greenish purulent (e.g.
eosinophilic sinusitis, bacterial infections), greenish-golden yellow (e.g.
AFRS) to bloody (e.g. trauma, angiofibroma, bleeding polyps)
• Unilateral or bilateral: Is the discharge from one side or both sides?
Unilateral purulent discharge may indicate infective pathology (e.g. foreign
body in a child, unilateral sinusitis and mass lesions), bilateral in severe bacterial
infections of nose, adenoids and bilateral mass lesions
Postnasal discharge
The postnasal discharge drips on to the pharynx and the patient brings it out
by coughing. It is usually mucoid nature, but may vary in colour indicating the
nature of infection (e.g. rhinitis, sinusitis, adenoiditis, nasal polyposis). Watery
salty-tasting discharge (CSF leak)
Sneezing and itching

• Number and frequency: What is the number of sneezing episodes and how
frequent?
Five or more sneezes in a row occurring more than once in a week, is
considered pathological. Whether it is seasonal or perennial according to the
type of allergy
• What are the precipitating factors? Under what circumstances the
sneezing increases?
Some factors such as dust, pollen and pets can increase the sneezing attacks,
as they are allergens, and cold temperature causes sneezing in vasomotor
rhinitis
Pain
• Location of pain: What is the location of pain?
Location of pain may indicate the pathology, as a furuncle or nasal septal
abscess cause pain in the nose. Maxillary sinusitis causes infraorbital facial pain,
frontal sinusitis causes supraorbital pain, ethmoidal sinusitis causes pain between
the eyes and sphenoidal sinusitis causes occipital or retroocular pain
Alteration in smell
• Change: Is there any change in the nature of smell?
Nasal mucosal disease often reduces the sense of smell. Acute viral infections
and head injury can cause complete loss of smell. Acute rhinitis may cause
temporary alteration of smell. Atrophic rhinitis may cause temporary anosmia
due to blockage by crusts
Epistaxis
• Quantity and nature: What is the quantity of bleed?
The blood loss is usually insignificant. In children, it is usually from the
anterior nasal septum (Little’s area), and in adults, it may be due to
atherosclerosis and hypertension or coagulopathies
• Unilateral or bilateral: Is the bleeding from one side or both sides?
Unilateral epistaxis occurs commonly in children due to foreign body and
bilateral bleeding occurs in coagulopathies
• Other bleeding episodes: Were there any other large bleeding episodes?
Patients with coagulopathies give history of bleeding from other areas such as
gums (e.g. leukaemia) or following trauma (e.g. haemophilia), spontaneous,
unprovoked profuse bleeding is encountered in JNA
• Positions of patient and examiner
Patient should be made to sit comfortably on a chair, with his legs together
along the side of the table opposite the examiner and the patient’s nose
should be at the examiner’s eye level (Fig. 20.16)
• Illumination
• Bull’s eye lamp (Fig. 20.16A): It consists of a heavy base stand and a
cylindrical box with an electrical bulb and a planoconvex lens. It is located
behind the left side of the patient
• Head mirror (Fig. 20.16B): It has a circular concave mirror with a focal
length of 23.6 cm (9 inches) and a headband attached to it. The mirror is 9
cm in diameter and has a central 2 cm diameter hole for the examiner to
see
• Clark’s headlight (Fig. 20.16C): It has a concave mirror attached to the
headband and a 6 volt bulb, working on a surgical transformer
• Headlight: Available with focus options due to inbuilt lens, bulb and
transformer (Fig. 20.16D)
FIGURE 20.16 Positions of patient and examiner for examination of nose.
FIGURE 20.16A Bull"s eye lamp.
FIGURE 20.16B Head mirror.
FIGURE 20.16C Clark’s headlight.
FIGURE 20.16D Headlight.
Bull’s eye lamp is not needed when headlights are used.

• Aids for examination
• Thudicum’s nasal speculum (Fig. 20.17A): A ‘U’ shaped metallic strip
with blades at its tips for retraction (available in various sizes)—for
examination of the anterior nose and nasal cavity
• Killian’s speculum (long bladed self-retaining nasal speculum) (Fig.
20.17B):For examination of the anterior nose and nasal cavity
• Postnasal mirror (St. Clair Thompson mirror) (Fig. 20.18): Similar to
laryngeal mirror but has two bends in the shaft—used for posterior
rhinoscopy
• Tongue depressor (Fig. 20.19): A metal strip used to depress the tongue
and also to assess the air entry in the nasal cavity
• Diagnostic nasal endoscope 0 and 30 degrees (Fig. 20.20): An illuminated
endoscope for examining the anterior and posterior nasal cavity and
nasopharynx
• Aids for therapy
• Nasal packing forceps (Tilley’s forceps) (Fig. 20.21): Used for packing of
nose, removal of foreign bodies or crusts
• Adequate knowledge and orientation of the nose and its related anatomy is
mandatory
FIGURE 20.17A Thudicum’s nasal speculum.

FIGURE 20.17B Killian’s nasal speculum.
FIGURE 20.18 Postnasal mirror.

FIGURE 20.19 Tongue depresssor.
FIGURE 20.20 Nasoendoscope.

FIGURE 20.21 Tilley’s forceps.
Nose
The face as a whole should be inspected, as even a maxillary pathology may
give an impression of asymmetry of nose though it is normal (See Ch. 18)
External nose
The nose has to be examined from the front and sides
Inspection
• Deformity (Fig. 20.21A.)
• Congenital deformities (e.g. bifid nose, nasal dermoid cyst or sinus)
• Acquired deformities (e.g. collapsed nose due to necrosis of nasal cartilage,
deviated nose, crooked nose tip, saddle nose of syphilis)
• Scars
• On the nose (e.g. posttraumatic, postsurgical)
• Swellings, ulcers, sinuses
• Presence or absence of nasofacial or maxillary or nasolabial groove
FIGURE 20.21A Inspection of nose—postsurgical

deformity. Source: (Courtesy Dr K. Sridhar)
Palpation
Swellings, ulcers and sinuses should be assessed as described in appropriate
Chapters (Chs. 9, 10 and 11). Crepitus and tenderness indicate fracture of nasal
bones
Vestibule of nose
The vestibule can be seen lifted up, by gently drawing the nose upwards (Fig.
20.22)
• Assess the vestibular opening of nose
• Assess the vestibular skin
• Look for furuncle
FIGURE 20.22 Examination of vestibule of nose.
Assessment of air flow

• Method 1: A cold, well chrome-plated metal tongue depressor is held
horizontally just beneath the nasal vestibule, the mist formed on the
depressor blade is watched (Fig. 20.23)
• Method 2: The air flow on each side can be assessed by the displacement of
cotton wool during respiration (Fig. 20.24)
• Method 3: Cottle’s test: Septal deviation at nasal valve is detected on the
affected side by pulling the cheek on that side outward to open the airway
(Fig. 20.25)
FIGURE 20.23 Assessment of airflow with tongue depressor.

FIGURE 20.24 Assessment of airflow with cottonwool.
FIGURE 20.25 Cottle’s test.
Nasal cavities
Anterior rhinoscopy
The anterior nasal cavity is examined using a Thudicum’s nasal speculum.
Method: The speculum is held with the left index finger, supported by the
thumb, and the limbs are pressed by left middle finger and ring finger, and the
flanges are negotiated into the skin lined nostril of the patient and the limbs are
released (Fig. 20.26).
FIGURE 20.26 Anterior rhinoscopy.
By this method, the following structures are seen:

• Nasal septum
• Inferior turbinate and inferior meatus
• Middle turbinate and middle meatus
• Floor
Note
Superior turbinate and superior meatus are not generally seen in normal
conditions.
Look for:
• Discharge: Discharges vary from watery to purulent
• Nasal mucosa
• Colour
- Pink and moist—normal mucosa
- Pale mucosa with profuse watery secretions—allergy
- Bright red mucosa—infections
• Polyps: Polyps are greyish peeled grape-like masses usually seen in middle
meatus. Large polyps distort the shape of the nose
• Growths: Malignant growths are reddish masses, friable and bleed on touch
• Nasal septum: Nasal septum is generally in the midline. It may be deviated to
one side (nasal septal deviation), which may be cartilaginous or bony or
both. Sometimes, deviation is found anteriorly obliterating inner nasal valve.
‘C’ or ‘S’ shaped deviation may also be seen. Prominent spurs are also seen.
Prominent blood vessels may be found in Little’s area (Fig. 20.26A.) in
children
• Lateral wall (Figs. 20.27 and 20.28A-D)
• Inferior turbinate—largest turbinate highly sensitive to touch and firm to
feel. It is hypertrophied in rhinitis and sinusitis
• Inferior meatus—nasolacrimal duct opens into it
• Middle turbinate—second largest and the neck has to be extended to view
it
• Middle meatus—frontal, maxillary, anterior and middle ethmoidal sinuses
open into it, and discharge may be seen
FIGURE 20.26A Little’s area.
FIGURE 20.27 Scopy—hypertrophy of middle turbinate.
FIGURE 20.28 Scopy—(A) Pus middle meatus. (B) Inferior turbinate
hypertrophy. (C) Normal middle meatus. (D) Congested inferior turbinate in
allergic rhinitis.
Note
• Masses other than angiofibroma inside the nose may be probed to find out
their attachment, sensitivity and bleeding nature.
• A unilateral polyp may be antrochoanal polyp.
• Polyps, which are friable and bleed on touch, should make one suspect
malignancy.
• It may be necessary to aspirate any discharge to have a proper assessment of
nasal cavity.
• Though foreign bodies are easily identifiable, longstanding ones are difficult
to be identified when calcium deposits are found on it. Surrounding
inflamed granulation tissue may cause bleeding when probed. Grating
sensation is felt.
• Meningo-encephalocele may also present as polyps. Aspiration of CSF
confirms it.
• Choanal polyps can be from maxillary antrum and from sphenoidal and
posterior ends of turbinates.
Postnasal space
Posterior rhinoscopy
The posterior nasal cavity is examined using an angled mirror called postnasal
mirror. Method: The method has to be explained to the patient in advance. The
postnasal mirror is optimally warmed to prevent condensation of patient’s breath
on the mirror, and should be tested by the examiner on his or her body that it is
not over heated. A tongue depressor is held with the left hand and the tongue is
depressed anteriorly, and the warm mirror is negotiated into the oral cavity
behind uvula. The mirror is rotated in various angles without touching the
posterior pharyngeal wall or base of tongue to view nasopharynx (Fig. 20.29).
FIGURE 20.29 Posterior rhinoscopy.
By this method, the following structures are seen:

Note
• Superior turbinate and superior meatus are not generally seen in normal
conditions.
• In the roof of nasopharynx the adenoids can be seen in children.
Nasopharyngoscopy: Fibre-optic nasopharyngoscopy (Fig. 20.30) is a better

method to visualize both the anterior and posterior nasal spaces with least
discomfort.
FIGURE 20.30 Nasoendoscopy in progress.
Paranasal sinuses
Inspection
The sinus area may be occasionally swollen and inflamed when the pathology is
acutely infective, a swelling may also be seen when there is expansion of the
sinus towards the exterior due to a mass (e.g. malignancy).
Palpation
Sinuses when acutely inflamed become tender and it can be elicited by
application of firm pressure on the corresponding areas as follows:
• Maxillary sinus—the thinnest area of the anterior wall of sinus (canine fossa)
• Frontal sinus—roof of orbit, above medial canthus in the floor of frontal
sinus medial to supraorbital notch
• Ethmoid sinus—medial to medial canthus on the lateral side of the bridge of
the nose
Note
Sphenoidal sinus—tenderness cannot be elicited as it is inaccessible.
Transillumination
Normal sinuses contain only air and conduct light. When a source of light is kept
inside the closed mouth in a dark environment, the light is transmitted through
the maxillary sinus as ‘pupillary glow’ or ‘infraorbital crescent’. When the sinus
contains fluid, mass or a large polyp, it is not transilluminant and the test is
considered negative. It is not routinely done.
Other systems
When the clinical presentation is related to pathologies of ear, nose and throat,
information
• Neck (e.g. secondary lymph node metastases in nasopharyngeal cancers)
• Chest (e.g. tuberculosis, COPD)
• Lymphatic system in general (e.g. tuberculosis, lymphoma)
• Neurological system (e.g. intracerebral extension of nasal pathology)
CHAPTER 21
Ears
Jacinth Cornelius
CHAPTER OUTLINE
21.1. Development of ear and auditory canal 296
21.2. Surgical anatomy of ear and auditory canal 297
21.3. Diseases of external ear and auditory canal 297
• Haematoma auris 299
• Injury to the earlobe 300
• Perichondritis 300
• Cellulitis 301
• Otitis externa 301
• Keratosis Obturans 302
• Malignant otitis externa 302
• Osteoma 302
• Impacted wax 303
• Chondrodermatitis nodularis helicis 303
21.4. Diseases of middle ear 304
• Trauma to tympanic membrane, middle ear and temporal bone
304
• Acute otitis media 304
• Otitis media with effusion 305
• Chronic suppurative otitis media 305
• Acute mastoiditis 306
• Otosclerosis 307
21.5. Diseases of inner ear (affecting hearing) 308
• Traumatic diseases (including noise) 308
• Otitic labyrinthitis 309
• Presbycusis 309
• Acoustic neuroma 309
21.6. Diseases of inner ear (affecting balance) 309
• Benign positional vertigo 309
• Ménière’s disease 310
• Vestibular neuronitis 310
21.7. Symptoms of pathologies of ears 310
• External ear 316
• Preauricular area 316
• Postaural area 316
• External auditory canal 316
• Tympanic membrane (eardrum) 317
• Assessment of hearing 320
21.1 development of ear and auditory canal

• Pinna (auricle) is formed from about six mesodermal thickenings called
tubercles or hillocks that appear on the mandibular and hyoid arches, around
the opening of the dorsal part of the first ectodermal cleft. The mandibular
arch forms only the tragus and a small area around it, rest of the auricle is
formed from the hyoid arch
• External auditory meatus is a remnant of the first branchial groove
• Middle ear and eustachian tube develop from the tubotympanic recess
between the first and the second visceral arches
• Malleus and incus are derived from the dorsal end of Meckel’s cartilage
• Stapes is formed from the dorsal end of the cartilage of the second
pharyngeal pouch
• Tensor tympani is derived from the mesoderm of the first pharyngeal arch
and the stapedius from that of the second arch
• Inner ear
• Membranous labyrinth is derived from a specialized area of surface
ectoderm overlying the developing hindbrain. Ectoderm invaginates to
form the auditory pit and later auditory vesicle. Membranous labyrinth is
formed from the vesicle or otocyst. Otocyst differentiates into
endolymphatic duct, sac and utricular saccular portions. Semicircular
ducts develop from outpouching of utricle. By the 8th week, cristae of
semilunar ducts, maculae of utricle and saccule, organ of Corti of
cochlea are formed
• Bony labyrinth is formed from the mesenchyme surrounding the
membranous labyrinth, and becomes condensed to form the otic capsule.
The periotic tissue, around the utricle and saccule, disappears to form a
space called the vestibule
• The periotic tissue around the semicircular ducts also disappears to form
the semicircular canals. The membranous labyrinth is filled with a fluid
called endolymph while the periotic tissue surrounding it is filled with
perilymph. Inner ear attains full adult size by 4th fetal month
21.2 surgical anatomy of ear and auditory

canal
The ear (Fig. 21.1) consists of three parts. They are:
• External ear
• Middle ear
• Internal ear
FIGURE 21.1 Anatomy of the ear.
External ear consists of the pinna (auricle) and the external auditory meatus
and canal. The pinna is a cartilaginous structure covered by skin. The skin is
firmly attached to the underlying perichondrium. The pinna has a helix and
antihelix with a separate tragus in front of the meatus. The lobule is composed of
fat and varies in shape. The external auditory canal has a somewhat S-shaped
course (the auricle has to be pulled upwards and backwards to straighten the S
shape while examination in adults). Outer third is cartilaginous and contains hair,
sebaceous and ceruminous glands. Inner two thirds is bony and lined by the
sensitive skin. Furuncle and other varieties of external otitis are encountered in
outer cartilaginous canal.
Middle ear is a narrow slit-like cavity in the petrous part of the temporal bone
separating the external ear from the internal ear. It consists of tympanic cavity
with its extensions and the auditory ossicles. The three auditory ossicles
(malleus, incus and stapes) lie within the tympanic cavity, transmit sound
vibrations from the external ear to internal ear. The tympanic membrane
(eardrum) separates the middle ear from the external ear, placed obliquely
making an angle of about 55° with the floor of the external meatus. It is about 1
cm in diameter and more or less circular. It is pearly grey in colour and
anteroinferiorly a shiny cone of light is present. Malleus handle is firmly
attached to fibrous layer of tympanic membrane.
Inner ear consists of:
• An inner membranous labyrinth
• An outer bony labyrinth
Membranous labyrinth: Cochlear portion of the labyrinth is concerned with
hearing, and the vestibular portion with balancing. The membranous labyrinth
consists of a closed system of intercommunicating membranous sacs and ducts
within the bony labyrinth, and is filled with endolymph. The cochlear duct, the
saccule and the utricle (membranous sacs) are the components, the latter two
being responsible for static equilibrium and kinetic equilibrium. There are three
semicircular ducts, anterior, posterior and lateral, and all the three open into the
utricle. They are responsible for dynamic equilibrium (movements of the head).
Bony labyrinth: This consists of three parts:
• Bony cochlea
• Bony vestibule and
• Bony three semicircular canals
The nerve supply, arterial supply and lymphatic drainage are given in
TABLE 21.1
Nerve Supply of Ears
Area Nerve supply
External ear Facial nerve—small region in the root of concha

Auricular nerve—concha and antihelix
Auriculotemporal nerve—tragus, crus of helix and adjacent helix
Great auricular nerve—medial surface and posterior portion of lateral surface
Lesser occipital nerve—superior part of medial surface
Middle ear Tympanic branch of glossopharyngeal nerve
Superior and inferior caroticotympanic rami from the sympathetic plexus
Branches of facial nerve
Meningeal branch of mandibular nerve
TABLE 21.2
Arterial Supply of Ears
Area Main artery Branches

External ear External carotid artery Superficial temporal artery
Posterior auricular artery
Occipital artery
Maxillary artery Deep auricular branch
Middle ear External carotid artery Tympanic branch of maxillary artery—anterior part, tympanic membrane,
malleus and incus
Stylomastoid branch of posterior auricular artery—posterior part
Middle meningeal branch—roof of mastoid and attic
Ascending pharyngeal—inferior part of mesotympanum
Internal carotid artery Tympanic branches—meso- and hypotympanum
Inner ear Vertebral / Basilar artery / Labyrinthine branch (anterior vestibular, vestibulocochlear and cochlear
AICA arteries)
TABLE 21.3
Lymphatic Drainage of the Ears
Area Lymph nodes
External ear Preauricular, mastoid and deep cervical

Middle ear Parotid, retropharyngeal, upper deep cervical
21.3 diseases of external ear and auditory

canal
Classification of the lesions of the external ear: The diseases of the external
ear can be classified based on their aetiology as given in Table 21.4.
TABLE 21.4
Aetiological Classification of the Diseases of the External Ear
Aetiology Diseases
Congenital Anomalies of the external ear
Traumatic Haematoma auris
Inflammatory Perichondritis
Cellulitis
Otitis externa
Malignant otitis externa
Neoplastic Osteoma
Malignant tumours
Impacted wax
Chondrodermatitis nodularis helicis
• Occur due to abnormal, incomplete fusion of the nodules
• Usually isolated and rarely a part of familial disease such as Treacher Collins
syndrome, where the deformity is severe and usually involves the external
ear and the proximal part of the eardrum and ossicle, sparing the inner ear
• Preauricular sinus (Ref Fig. 11.4) is generally an isolated deformity (See Ch.
11)
• Minor variations of the auricle (Fig. 21.2A) are common
• Gross anomalies of the external ear canal (Fig. 21.2B) may cause stenosis
(Fig. 21.2C) or atresia of its length partially or in its whole length
FIGURE 21.2A Minor anomaly of the pinna.
FIGURE 21.2B Major anomalies of the pinna Source: (Courtesy Dr K. Sridhar).
FIGURE 21.2C Microtia.
• Cosmetic defects such as microtia, anotia, macrotia, bat ears / lop ears or an
accessory auricle seen as a small tag of skin covering the cartilage in front of
the ear
• Major defects may be associated with hearing loss, especially when the defect
is bilateral
• Tests related to hearing may be useful
• CT and MRI may exhibit the developmental defects
Treatment
• No treatment for small accessory tags, excepting for cosmetic reasons
• Correction of hearing loss is needed when warranted
• Otoplasty can be considered for cosmetic defects in pinna
Haematoma auris
• Trauma can cause swelling of the ear
• Blood lifts the perichondrium away from the cartilage and renders it
ischaemic
• The cartilage can get necrosed
• When the haematoma organizes, the end result is a ‘cauliflower ear’ (Fig.
21.3)
• Pseudocyst is a nontender serous collection in subperichondrial region
mimicking this condition
FIGURE 21.3 Cauliflower ear.
Pain, swelling and deformity are the characteristic features
• No specific investigation is necessary
• Coagulation profile in select cases
Treatment
• No treatment is needed for small haematomas, as they resolve spontaneously
• Aspiration or surgical drainage, with compression will cure large ones
• Broad-spectrum antibiotics are needed
Injury to the earlobe

• Injuries to the earlobe are common
• Acute injuries occur due to sudden pull and chronic tears occur due to heavy
ear hangings
Complications: Hypertrophic scar and keloid formation (See Ch. 9)
Acute tears present with a bleeding laceration (Figs. 21.4A and B) starting at the
pierced site, and the chronic tears (Fig. 21.5) lengthen the pierced site thereby
enlarging the opening
FIGURE 21.4A Acute partial tear of the earlobe Source: (Courtesy Dr S. Devaji
Rao).

FIGURE 21.4B Acute avulsion of the earlobe Source: (Courtesy Dr K. Sridhar).
FIGURE 21.5 Chronic tear earlobe.
No specific investigation is necessary.
Treatment
• Immediate suturing is done for acute tears
• Plastic repair is done for chronic tears
Perichondritis
Occurs following:
• Trauma
• Any infection
• Surgery of mastoid when the cartilage of the external ear is involved
• Connective tissue diseases (rare) in which case it is bilateral
Ear is swollen and painful and often hot to touch (Fig. 21.6). The earlobe is
always spared (see cellulitis)
FIGURE 21.6 Perichondritis.
Treatment
• Systemic broad-spectrum antibiotics with antibiotic ear drops
• Window operation with drainage, removal of necrotic cartilages and
compression dressings
Cellulitis
Usually occurs following infections of the external ear, such as otitis externa
Ear is swollen and painful and often hot to touch (Fig. 21.7). The earlobe is
always involved (see perichondritis)
FIGURE 21.7 Cellulitis.

Treatment
• Systemic broad-spectrum antibiotics with antibiotic ear drops
• Incision and drainage is done for localized collections of pus
Otitis externa
• Caused by a variety of reasons, manifesting as a furuncle or even a diffuse
exudative oedema
• The common causes are:
• Infections
- Viral (e.g. herpes zoster and herpes simplex)
- Bacterial (e.g. staphylococcus, Gram-negative bacilli)
- Fungal (Candida albicans and Aspergillus niger)
• Allergy (e.g. ear drops, hair colouring agents)
• Skin diseases (e.g. seborrhoeic dermatitis and psoriasis)
• Irradiation
• Furuncle presents with an acutely painful swelling in the external ear canal
(Fig. 21.8)
• Discharge (serous or seropurulent, rarely bloody) may be present in severe
otitis externa
• On examination, the ear canal may be oedematous with debris, crusts and
desquamation with discharge (Fig. 21.9A)
• Otomycosis presents with itching and fullness of the ear. It looks like a wet
newspaper in the ear canal (Fig. 21.9B)
FIGURE 21.8 Otitis externa.
FIGURE 21.9 Otoscopy—(A) Bacterial otitis externa. (B) Fungal otitis
externa.
Aural swab and histopathology
Treatment
• Glycerine and ichthammol or magnesium sulphate application with a wick
is done for furuncle in the external canal
• Aural toilets may be necessary and appropriate antibiotic therapy is instituted
• Steroid and antibiotic preparations may be required as an external
application
• Antihistamines are required if the aetiology is allergic
• Antifungal topical agents are applied after aural toileting in cases of
otomycosis
Keratosis obturans
Wax and desquamated epithelium accumulate at the deeper bony meatus due to
migratory failure of epithelium and expand the bony canal. When the infection
sets in, pus and granulation are produced
• Pain and hearing loss
• On examination, granulations and pus may be seen in the external ear canal
in the midst of keratinous debris and wax
Treatment
Removal under general anaesthesia (GA)
Malignant otitis externa

• A very aggressive condition mimicking a tumour, and has significant
morbidity and mortality
• Starts as cellulitis of the external canal and progresses onto fleeting
granulations, which erode the neighbouring bone and cartilage, and spread to
the skull base and involve the lower cranial nerves (VII, IX, X, XI and XII)
• The implicating organism is usually Pseudomonas aeruginosa, common in:
• Diabetics
• Immunocompromised patients
• Painful, mucopurulent or purulent and bloodstained discharge associated with
granulations in the external ear canal may be associated with headache
• Cranial nerve palsies are found in severe cases
• Blood sugar levels should be determined
• Pus culture, biopsy of granulations
Treatment
• Hospitalization and intravenous antibiotics (e.g. ciprofloxacin) are necessary
• Ear should be cleaned and dressed
• Control of diabetes is necessary
• Surgery is to remove the necrotic bone and tissue
Osteoma
• Arise from the deep bony canal
• Two types of osteomata occur, they are:
• pedunculated
• diffuse (common in swimmers in cold water)
• Debris in the medial part of the canal can cause otitis externa
• Painless swelling
• Large ones block the ear canal, causing conductive deafness
CT is diagnostic.
Treatment
• No treatment is required for most osteomas
• Surgical removal is done for large osteomas
Note
Other benign tumours, papilloma, fibroma, chondroma and angioma rarely
occur. Occasionally, adenomas viz. sebaceous adenoma or ceruminoma are
known to occur.
Malignant tumours
• Squamous cell carcinomas and basal cell carcinomas occur in the pinna
• Common in fair-skinned people
• Swelling on the pinna with bloody discharge
• Examination shows:
• Painful friable ulcerating mass on the external ear canal
• Enlarged pre- and postauricular lymph nodes with cervical
lymphadenopathy
• Facial nerve paralysis may occur
• CT is useful
• Biopsy is diagnostic
Treatment
• Wide surgical excision with or without local radiotherapy
• Preoperative radiotherapy and radical excisions (petrosectomy) along with
block dissections of neck for large lesions
Foreign bodies
• Various types of foreign bodies including paper, plastic, metal and organic
material are found
• Most are inserted deliberately, commonly in children
• Insects may crawl into the canal
• Otitis externa may develop
Seeds may swell and insects may buzz and cause pain
Otoscopy is diagnostic (Fig. 21.10)
FIGURE 21.10 Otoscopy—foreign body in the external auditory canal.
Treatment
• Depends on the type of foreign body:
• Insectsshould be killed and then syringed out
• Foreign bodies may be syringed or hooked out or removed with suction
• Children may require GA for safe removal of foreign bodies
Impacted wax
• Wax is produced by ceruminous glands in the outer third of the ear and the
quantity decreases and becomes hard as the person ages
• Wax can get impacted due to use of ear buds
• Blockage or slight decrease in hearing
• Examination reveals dark brown or black-coloured wax plugging the external
meatus
No special investigation is necessary
Treatment
• Wax is syringed with water
• Hard wax may be softened and then syringed or removed manually, either
under direct vision or under microscope with suction
Chondrodermatitis nodularis helicis

A painful and chronic nodular lesion on the outer pinna and may be confused
with a tumour, but the skin is normal
Painful nodules on the upper outer edge of helix (Fig. 21.11) covered by
adherent crust over the exposed necrotic cartilage
FIGURE 21.11 Chondrodermatitis helicis nodularis.
Biopsy is diagnostic
Treatment
Local excision with a wedge of underlying cartilage
21.4 diseases of middle ear

The diseases of the middle ear can be classified based on its aetiology (Table
21.5).
TABLE 21.5
Diseases of the Middle Ear
Aetiology Diseases
Congenital syndrome, Treacher Collins syndrome
Fused, abnormal or absent ossicles
Dehiscent jugular plate, dehiscent fallopian canal, persistent stapedial artery
Traumatic Foreign bodies, perforation of the eardrum, ossicular disconnection, barotraumatic
otitis media, temporal bone fracture
Inflammatory Acute otitis media
Otitis media with effusion
Chronic suppurative otitis media
Complications of chronic Extracranial Intra Acute mastoiditis, acute labyrinthitis, facial nerve
suppurative otitis media temporal palsy, petrositis
Extra Cervical abscesses
temporal
Intracranial Extra- and subdural abscess, meningitis, brain abscess, venous sinus
thrombosis
Trauma to tympanic membrane, middle ear and

temporal bone
• Perforations of the tympanic membrane—caused by open-handed blow, blast
injury, barotraumas or syringing, sometimes ossicular dislocation may also
occur
• Injury to the middle ear:
• chorda tympani injury
• jugular bulb injury
• Ossicular disruption may be caused by surgical trauma
• facial nerve injury
• Temporal bone fractures
• Perforations of the tympanic membrane—conductive hearing loss
• Injury to the middle ear:
• chorda tympani—taste disturbances
• jugular bulb injury—bleeding
• ossicular disruption—conductive hearing loss
• facial nerve paralysis—inability to close the eye, deviation of the angle of
the mouth, etc.
• Temporal bone fractures: Present with cerebrospinal fluid (CSF) leak, meatal
skin injury and bleeding, conductive deafness if the eardrum and ossicles are
involved, vertigo, facial paralysis or sensorineural hearing loss (SNHL)
High resolution computed tomography (HRCT) may be helpful in localizing
the site of trauma
Treatment
• Perforations of the tympanic membrane:
• Heal on their own
• Secondary infections may have to be prevented by substitution with
antibiotics and oral decongestants while maintaining the ear dry. Topical
eardrops are avoided
• If spontaneous closure of perforation does not take place within 3 months
or ossicular disruptions are suspected, surgery would be necessary
• Temporal bone fractures: Control of secondary infection and surgical
correction may be needed
Acute otitis media

• Very common problem in children and usually follows upper respiratory
infection
• Though the initial inflammation is viral, secondary infection by Gram-
positive cocci follows
• Children with congenital HIV infection present with recurrent otitis media
during the first year of life
• Primary immune deficiency is another cause of otitis media
Complications: Tympanosclerosis, erosion or fixation of ossicles, adhesive
otitis and permanent perforations. SNHL is rare.
• Acute severe pain deep in the ear is the predominant symptom
• Examination reveals a bulging and congested eardrum (Fig. 21.12)
FIGURE 21.12 Otoscopy—acute otitis media.
Perforation of eardrum relieves the pain, and presents with discharge.
Otoscopy is diagnostic
Treatment
• Broad-spectrum antibiotics for 5–7 days relieves most patients
• Myringotomy relieves pain immediately
Otitis media with effusion
• More common in children
• The aetiology is debated and various factors are suggested. They are:
• Eustachian tube dysfunction
• Adenoidal hypertrophy
• Associated base of skull abnormalities
• Cleft palate
• In adults, this can follow:
• Common cold
• Sinusitis
• Barotraumas
• Nasopharyngeal tumour blocking the eustachian tube
• Allergy
• Children present with intermittent hearing loss, with preceding history of pain
in the ear and acute otitis media (AOM)
• In very young children speech may be delayed and the child may remain
inattentive and withdrawn
• Adults complain of deafness and blockage of the ear, with clicking or
bubbling noise (due to eustachian tube dysfunction or middle ear fluid)
• Otoscopy reveals a lustreless tympanic membrane with loss of cone of light
(‘glue’ ear) (Fig. 21.13A). Occasionally, a fluid level is seen (Fig. 21.13B)
• Audiometry demonstrates conductive loss, especially for lower frequencies,
with air—bone gap. Impedance audiometry (tympanometry) shows a flat ‘B’
type curve due to decreased compliance and negative middle ear pressure
FIGURE 21.13 Otoscopy—(A) Glue ear. (B) Acute otitis media with fluid
level. (C) Grommet in situ.
Treatment
Surgical treatment consists of myringotomy and insertion of a ventilation tube
(grommets) into the affected tympanic membrane (Fig. 21.13C)
Chronic suppurative otitis media

Chronic suppurative otitis media (CSOM) is of two types. They are:
• Tubotympanic (caused by bacterial suppuration and perforation of pars tensa
following upper respiratory infections)
• Atticoantral (caused by longstanding chronic nonsuppurative disease with
chronic eustachian tube dysfunction resulting in retraction of the eardrum in
the attic or posterior segment and invasion or migration or implantation of
epithelium):
• Congenital: Arises from embryonic epithelial cell rest in the mastoid or
middle ear (seen as a white mass behind the intact eardrum) or petrous
part of the temporal bone (no history of otorrhoea)
• Acquired:
- Primary: It is a ball of keratinous debris lined by fibrous stroma
accumulated in attic, which expands and exerts pressure, and erodes the
ossicles or facial nerve canal or the bony labyrinth, usually via the
lateral semicircular canal. If the floor of the middle fossa is eroded,
intracranial suppuration can occur
- Secondary: Occurs due to ingrowth of epithelium into destroyed
tympanic membrane following necrotizing otitis media
Complications
• Intracranial: Meningitis, lateral sinus thrombosis, intracranial abscess, otitic
hydrocephalus, extra or subdural abscess
• Extracranial:
• Intratemporal: Facial nerve palsy, suppurative labyrinthitis, acute
mastoiditis, Gradenigo syndrome (apex petrositis: diplopia, retroocular
pain and profuse otorrhoea, mastoiditis)
• Extratemporal: Wilde’s subperiosteal mastoid abscess, Citelli’s abscess,
Luc’s abscess, Bezold’s abscess
Symptoms
• Deafness: Anterior and central perforations cause less deafness than the
posterior perforation. When ossicles are involved, hearing loss is greater
• Discharge: It is profuse, mucoid and nonoffensive in tubotympanic disease. It
is scanty and offensive in atticoantral disease
• Greenish discharge occurs due to Pseudomonas pyocyaneus infection
• Blood-stained discharge may occur from granulations arising due to osteitis
induced by erosion of scutum in atticoantral cholesteatoma
• Tinnitus: Rare
• Vertigo: In patients with lateral semicircular canal involvement
• Pain: Pain may occur due to complications:
• Neurological complications are rarely caused by central perforations
• Facial nerve paralysis occurs when fallopian canal is involved
Signs
• Otoscopy (tubotympanic CSOM) may reveal:
• Pus (Fig. 21.14A)
• Perforations
- Central perforation—perforation in pars tensa
- Attic or marginal perforations / retraction pockets can be associated
with white flaky fetid cholesteatoma, sensitive, sessile, bleeding (Figs.
21.14B–H) granulations
FIGURE 21.14 Otoscopy—(A) Chronic suppurative otitis media. (B) Dry

attic perforation. (C) Posterior central perforation. (D) Inferior central
perforation. (E) Subtotal central perforation. (F) Large total perforation. (G)
& (H) Cholesteatoma.
Note
Atticoantral type is unsafe because the attic is lined by cuboidal epithelium,
crowded with head of malleus, body of incus and mucosal folds which impede
drainage and is related to the neighbourhood of brain, labyrinth and VII nerve.
• Insensitive pedunculated polyps, not bleeding on touch, arising from the

middle ear mucosa
• Inactive ear would be dry
• Audiometry reveals the cochlear reserve (hearing potential) and type of
hearing loss
• Aural swab culture reveals causative organisms
• X-ray mastoids: Law’s lateral oblique view reveals asymmetry, abnormal
anatomy and pathological changes in mastoid
• HRCT of temporal bones elucidates the extent of damage and intracranial
invasions
• Oto endo/microscopy confirms the findings
Treatment
• Tympanomastoid exploration, disease clearance and hearing augmentation
• Surgical treatment of cholesteatoma may vary from marginectomy and
excision of retraction pocket to atticotomy or atticoantrostomy or modified
radical mastoidectomy or radical mastoidectomy according to the extent of
disease
Acute mastoiditis
• Acute infection of mucoperiosteum of middle ear cleft
• May be a sequel to infection of the middle ear or due to cholesteatoma in
children
• Fever, pain, hearing loss and swelling over the mastoid region (Fig. 21.15)
• On examination, sagging of posterosuperior meatal wall can be seen
• Three-point mastoid tenderness can be elicited by digital pressure over cymba
concha, mastoid tip and posterior emissary vein area in the region of sigmoid
sinus
FIGURE 21.15 Acute mastoiditis.
• X-ray is diagnostic (Fig. 21.15A)
• CT scan (Fig. 21.15B) is conclusive (cavity due to cholesteatoma or
destruction of bony architecture and ossicles reveals intracranial extension)
Treatment
• High-dose antibiotics, drainage of abscess
• Cortical mastoidectomy, if conservative treatment fails
• Modified radical mastoidectomy may be indicated in the presence of
cholesteatoma
Otosclerosis
• A disease of the otic capsule affecting the area around the footplate of the
stapes
• Spongy new bone replaces the ivory compact bone, and the increased
metabolic activity causes hearing loss
• More common in females and may get worse during pregnancy
• Majority of them are familial
• Manifests with conductive deafness
• May progress into mixed deafness. In active stages, tinnitus may be present
• On examination, the eardrum is usually normal. Schwartz sign denotes
flamingo pink hue of promontory due to increased vascularity in active stage.
Paracusis of Willis is a phenomenon by which these patients hear better in
noisy environment owing to raised voices
• Audiometry shows conductive loss. Mixed deafness is observed when the
disease extends into cochlea
• Carhart’s notch seen as a dip in 2 kHz
Treatment
• No treatment if the hearing loss is not severe
• Use of hearing aid is a good choice
• Stapedectomy is the surgical treatment of choice
• Sodium fluoride may be tried during active stage
21.5 diseases of inner ear (affecting hearing)

• The inner ear degenerates with age, and this is the commonest cause of
sensorineural damage
• Inner ear can be damaged by various factors:
• Congenital (poorly developed cochlea)
• Trauma
• Hypoxia
• Infections
• Connective tissue disorders
• Noise
• Diseases of the inner ear affecting hearing and balance (Table 21.6)
TABLE 21.6
Diseases of the Inner Ear Affecting Hearing and Balance
Diseases affecting
Hearing Balance
Trauma (including noise) Benign positional vertigo

Otitic labyrinthitis Ménière’s disease
Presbycusis Vestibular neuronitis
Acoustic neuroma Trauma
Ototoxicity Otitic labyrinthitis
Ossicular dysfunction Acoustic neuroma
Ménière’s disease Vestibulotoxicity
Traumatic diseases (including noise)

• Inner ear is subjected to varieties of trauma, which can be:
• Sudden injury (direct injuries to the skull or barometric trauma)
• Chronic, the common cause being noise (high-impulse noise and ultrasonic
shock waves can damage cochlea)
• Damage depends on some characteristics of sound, such as:
- Type
- Intensity
- Duration
- Rest period between stimuli
- Sensitivity of cochlea
• Inner ear function is usually lost in very severe injuries (e.g. temporal bone
fractures)
• Sudden deafness with tinnitus
• Profound prostrating vertigo may be apparent when the inner ear ruptures into
the middle ear
• Constant noise produces gradual hearing loss affecting high frequencies first
and low frequencies later
• On examination, the eardrum is normal
• Audiometry is necessary
• Brainstem audiometry is necessary in some cases
• CT may be indicated in temporal bone fractures
Treatment
• Sudden hearing loss due to trauma is an emergency and needs inpatient
care
• If fistula is diagnosed, a tympanotomy and repair is needed
• Where noise is the cause, noise levels are monitored and minimized
• Hearing aids are necessary to restore normal hearing, though the restoration
is not complete in noise-induced hearing loss, after a trial of conservative
treatment with steroids etc.
Otitic labyrinthitis
• Infections of inner ear are caused by:
• Viruses (e.g. mumps, measles)
• Bacteria (as a complication of the middle ear infections, meningitis),
syphilitic infections can be congenital or acquired
• These may result from bony erosion, trauma or direct spread through the
windows
• Vertigo, nystagmus, hearing loss
• Fistula test is positive, if a fistula between the middle and inner ear is present
and the vestibular sense organs are viable
• Audiometry will show sensorineural loss of variable degree
• Further investigations are directed towards aetiology
Treatment
• Treatment is towards the cause
• Antibiotics and sedatives are given during acute stage
• Middle ear infections should be adequately treated and cholesteatoma should
be surgically managed without delay, to prevent further loss in hearing
Presbycusis
• Degenerative disease of the cochlea
• The three main causes are:
• Age
• Exposure to noise
• Vascular insufficiency
• Inability to discriminate sounds and conversation amidst background noise,
with a sense of blocked ears
• Hearing loss is sensorineural in type
Audiometry is conclusive, and reveals deafness to higher frequencies first and
lower frequencies later
Treatment
• Home environment should be made more comfortable without noise
• Hearing aids are helpful
Acoustic neuroma
• Neuromas are schwannomas of the 8th cranial nerve
• Asymptomatic in most cases
• They are seen in 5% of postmortem cases
• Neuromas occur in the superior vestibular nerve, 80% in the bony canal and
the rest in the cranial cavity
• All patients with unilateral SNHL should be suspected for this disorder, unless
otherwise proved
• Progressive SNHL and tinnitus
• Large tumours may involve other cranial nerves, especially the 5th nerve, with
loss of corneal reflex
• Large tumours present with features of increased intracranial pressure and
cerebellar symptoms
• Facial paralysis also may be seen
• Vertigo is gradually progressive
• Audiometry will show unilateral SNHL
• Brainstem audiometry will show a delay in nerve conduction
• Caloric tests will show a canal paresis
• Plain X-rays of the internal auditory meatus may show funnelling of meatus
• CT and MRI (Fig. 21.16) are confirmatory

FIGURE 21.16 CT—acoustic neuroma.
Treatment
• Excisional surgery is the treatment of choice, if the patient is young
• Follow-up with annual screening is advised for older patients, and sudden
increase will warrant surgery
• Radiotherapy with gamma knife is indicated when sudden increase is noted
21.6 diseases of inner ear (affecting balance)
Benign positional vertigo

• Benign positional vertigo (BPV) occurs when otoliths become dislodged from
macula of the utricle and saccule and embed into the cupula of the posterior
canal
• More common in females above 40
• Head injury
• Aging
• Surgical sequelae
• Vertigo when the head is turned to affected side
• Dix–Hallpike manoeuvre detects affected side by manifestation of fatigable
transient nystagmus and vertigo occurrences
Audiometry, caloric tests and radiographs are normal and are done to exclude
other causes
Treatment
• Particle reposition manoeuvre such as Semont or Epley manoeuvre are
useful, and the disease resolves spontaneously after a few months, though
recurrences are common
• Rarely singular neurectomy may be indicated
Ménière’s disease
• An autoimmune or idiopathic disorder
• More common in men
• Affects people between 40 and 60 years of age
• Episodes of tinnitus followed by vertigo and hearing loss
• Attacks occur in clusters and affect one ear initially, and may become bilateral
• Vertigo is the worst symptom, causing nausea and vomiting
• The SNHL is reversible initially, later fluctuant and become permanent as the
disease advances
• Hyperacusis and recruitment are common accompaniments of deafness
• During attacks, the patients may have noise intolerance
• Nystagmus beating to the affected side may be elicited during the attack
• Audiometry will show SNHL, caloric test may show canal paresis
• Bekesy audiogram—type II curve
• Recruitment positive
• Glycerol test may be positive
• Echogram shows negative summation potential
• Electronystagmography (ENG)
Treatment
• Medical: Vasoactive compounds (e.g. betahistine) and labyrinthine sedatives
(e.g. cinnarizine), diuretics
• Surgical
• Hearing preserving surgeries: Endolymphatic sac decompression, shunt
procedures, sacculotomy, Grommet insertion
• Hearing destructive surgeries: Labyrinthectomy (chemical or surgical) and
vestibular neurectomy
Vestibular neuronitis
Presumed to be of viral aetiology.
• Preceded by an attack of upper respiratory catarrh
• Patients complain of profound continuing vertigo, nausea and vomiting
lasting for many weeks
• Movements of head make it worse, but vertigo is present at rest in many cases
• Clinical examination reveals normal hearing
• Audiometry is normal
• ENG and caloric test will reveal a canal paresis
Treatment
Labyrinthine sedatives are of help with reassurance
21.7 symptoms of pathologies of ears
• Hearing loss (deafness)
• Itching
• Pain in the ear (otalgia)
• Discharge (otorrhoea)
• Dizziness
• Ringing in the ears (tinnitus)
• Blocked sensation in the ear
• Facial palsy
Some symptoms which are not specific to ear pathology, may be closely
related. They are:
• Nausea and vomiting
• Light headedness
• Headache
• Fever
• Visual disturbances (diplopia)
• Inability to close the eye and deviation of the angle of the mouth (facial palsy)
Deafness
Deafness is defined as an impairment of hearing. This may be realized by the
patient himself or may be pointed out by others. In a prelingual child, deafness
manifests as inattention or delayed language development and behavioural
problems.
The onset of deafness may be:
• Sudden (e.g. wax in the external ear, viral disease, barotraumas, trauma to
temporal bone blast injury)
• Slow and progressive
• Conductive deafness in chronic otitis media
• Conductive and sometimes sensorineural deafness in otosclerosis
• Sensorineural deafness in presbycusis, senile deafness and ototoxicity
• Fluctuating
• Secretory otitis media—varies according to position of the head and
viscosity of effusion
• Perilymph fistula
• Ménière’s disease—deafness increases before vertigo and returns to normal
after the attack of vertigo
The deafness varies in degrees. The characteristics are tabulated in Table 21.7.
• Paracusis of Willis is a phenomenon occurring in persons with conductive
deafness, wherein they hear better in noisy environment because the speakers
raise voice above the ambient noise to make themselves audible
• Recruitment is a phenomenon where loud sounds are heard louder in patients
with cochlear hearing loss (e.g. Ménière’s disease)
• Diplacusis is the difference in the pitch of a tone between the two ears (e.g.
Ménière’s disease). Deafness increases with flare up of the disease. During
ossicular disruption, the fluid forms a conductive medium to improve
hearing
• Autophony is an abnormal perception of patient’s own breath and voice
sounds and feels like echo (patulous or dysfunctional eustachian tube)
TABLE 21.7
Characteristics of Various Degrees of Deafness
Degree of deafness Tuning fork test Audiogram Hearing

256 512 1024
Mild Negative Positive Positive 25–40 dB loss Difficulty to hear a whisper
Moderate Negative Negative Positive 40–55 dB loss Difficulty to hear normal conversation
Severe Negative Negative Negative 55–70 dB loss Difficulty to hear loud conversation
Profound Negative Negative Negative Above 90 dB loss
The higher frequencies are usually affected earlier, and the ability to
appreciate consonants is lost first, and is usually bilateral. Unilateral deafness
usually follows trauma, and left-sided deafness is usually seen in rifle users as
the left ear is closer to the muzzle of the rifle. History of familial tendencies
(otosclerosis) and exposure to noise and medical history of drugs intake
(ototoxicity) are to be elicited in particular.
The causes of sensorineural and conductive deafness are given in Tables 21.8
and 21.9.
TABLE 21.8
Causes of Sensorineural Deafness
Aetiology Pathology
Genetic Alport syndrome
Pendred syndrome
Usher syndrome
Trisomy 18
Congenital Inner ear aplasia
Traumatic Head injuries
Hypoxia during birth
Noise
Infective Rubella
(congenital)
Toxoplasmosis
Cytomegalovirus
Syphilis
Infective Viral (mumps, measles, influenza, herpes zoster)
(acquired)
Bacterial (syphilis, suppurative infections of middle ear, tuberculous meningitis)
Neoplastic Acoustic neuroma
Degenerative Age
Metabolic Hypoxia during birth
Neonatal jaundice
Ménière’s disease
Diabetes mellitus
Drugs Ototoxic drugs (aminoglycosides, quinine, salicylates, cis-platinum)
Iatrogenic Stapes surgery
Others Haematological—anaemia, embolism, coagulation disorders
Endolymphatic hydrops—Ménière’s disease
Connective tissue disorders—polyarteritis nodosa, Coagan’s disease, multiple sclerosis, sarcoidosis,
amyloidosis, lateral sclerosis
TABLE 21.9
Causes of Conductive Deafness
Aetiology Pathology
Genetic Treacher Collins syndrome

First arch syndromes
Otosclerosis
Congenital Defects of the external and middle ear
Traumatic Head injuries
Barotraumas
Infective Otitis externa
Acute otitis media
Secretory otitis media
Chronic otitis media
Neoplastic Osteoma of external canal
Carcinoma
Iatrogenic Cholesteatoma surgery
Wax and debris
Itching
• Mild irritation to itching (e.g. otitis externa, otomycosis, dry scaly wax)
Pain in the ear

The pain in the ear can be of various types. They are:
• Continuous (dull or throbbing pain occurs in furunculosis)
• Intermittent (occurs in otitis media with effusion (OME). Pain is increased
while lying down due to venous congestion. On sitting up or swallowing it
disappears)
• Paroxysmal (throbbing pain occurs in AOM or lancinating pain
glossopharyngeal neuralgia)
• AOM pain is sudden in onset, and is often severe and resolves spontaneously
when bulging drum perforates
• Severe pain—otitis externa and perichondritis because the skin is adherent to
periosteum, AOM
• Pain followed by vesicular eruptions on skin—herpes zoster
• Pain followed by vesicular eruptions on eardrum—myringitis bullosa (with
bleeding or serous discharge)
Note
Pain is not a feature of chronic otitis media per se.
Referred pain: Pain may be referred to the ear from other non-otological
problems through V, IX and X cranial and upper cervical nerves:
• Oropharyngeal pathologies in children
• Tonsillitis
• Osteoarthritis of cervical spine in elderly
• Temporomandibular joint pathologies
• Dental diseases
• Tonsillar, laryngeal, posterior third of tongue and pharyngeal tumours in
adults
Discharge
The discharge can be:
• Unilateral
• Bilateral
The colour and consistency of the discharge can be:
• Serous (e.g. otitis externa), watery (e.g. CSF otorrhoea)
• Mucoid (e.g. chronic otitis media from the middle ear is sticky in nature)
• Mucopurulent (e.g. acute or chronic otitis media)
• Purulent (e.g. furunculosis, cholesteatoma)
• Bloodstained (e.g. trauma, glomus jugulare tumour, atticoantral lesions,
malignancy)
• Serosanguinous (e.g. AOM)
• Blackish, yellowish or whitish (e.g. otomycosis)
• Greenish (e.g. Pseudomonas infections)
The quantity of discharge can be:
• Scanty (e.g. atticoantral disorders). The tip of the swab alone is stained
• Moderate (e.g. tubotympanic disease). Discharge fills the floor of the canal
and drains out
• Profuse (e.g. mastoid reservoir). Discharge drains out and stains the pillow
Smell of the discharge may be foul smelling if it is due to bony necrosis or
cholesteatoma.
Note
• Discharge of the external ear occurs after pain in otitis externa, whereas, the
pain reduces after discharge from AOM.
• A clear watery discharge after a head injury should be considered as CSF,
unless otherwise proved.
• Wax may be mistaken when discharge is brownish and soft:
• Active stage—discharging ear
• Inactive stage—dry ear
• Quiescent stage—intermittent discharge
Dizziness
Dizziness is an imbalance and vertigo is a hallucination of the movement of the
body or surrounding. Vertigo can last for a few seconds to several hours to
several days. The causes of vertigo are given in Table 21.10.
TABLE 21.10
Causes of Peripheral (Labyrinthine) Vertigo
Aetiology Pathology
Traumatic Head injury
Barotrauma
Infective Viral (e.g. herpes zoster), vestibular neuronitis
Bacterial (e.g. syphilis, suppurative otitis media)
Degenerative Benign positional vertigo
Metabolic Ménière’s disease
Cochlear otosclerosis
Drugs Ototoxic drugs (aminoglycosides)
Iatrogenic Middle ear and inner ear surgeries, perilymph fistula
Note
• When vertigo fluctuates over several hours, associated with a feeling of
pressure in one ear, with tinnitus and hearing loss, it indicates Ménière’s
disease.
• When vertigo lasts for several days and not associated with hearing loss, it
may indicate vestibular dysfunction or neuronitis.
• When vertigo is associated with discharge, it may indicate chronic otitis
media with cholesteatoma causing labyrinthine fistula.
• When vertigo is precipitated by certain position of the head, BPV must be
borne in mind.
• Vertigo without deafness occurs in vestibular neuronitis.
Tinnitus
Tinnitus is defined as a purposeless sound generated from within the ear or
auditory pathway or simply ringing in the ear. It varies in quality and intensity.
It may be:
• Subjective:
• Whistling
• Ringing due to cochlear or auditory neural pathways
• Hissing
• Objective:
• Roaring—glomus tumour
• Clicking—palatal myoclonus, Costen syndrome
It can be:
• Unilateral (e.g. acoustic neuroma)
• Bilateral (e.g. bilateral otosclerosis)
It can be:
• Continuous
• Intermittent
Any pathology of the ear starting from wax to acoustic neuroma can cause
tinnitus and is frequently associated with deafness, especially when it is due to
inner ear pathology. It is also associated with tiredness and consumption of
alcohol and caffeine, or may be induced by drugs such as quinine or
aminoglycoside and exposure to continuous noise.
Blocked sensation in ear

This sensation may be experienced by patients with secretory otitis media or in
early phases of AOM, impacted wax or otomycosis.
Facial palsy
Facial palsy with:
• otorrhoea occurs in CSOM
• deafness occurs in acoustic neuroma
• intact ear drum and ear free disease occurs in Bell’s palsy
Eliciting history
• Age: Congenital anomalies are seen in children. Otosclerosis is seen in
adolescents and middle aged. Malignancies, presbycusis and otosclerosis are
seen in older age
• Sex: Otosclerosis is more commonly seen in females
• Occupation: Workers in noisy areas are prone to develop SNHL
• Residence: Middle ear infections are common in crowded areas and lower
socioeconomic group

Deafness
• Impairment of hearing: What is the onset of deafness? Was it gradual or
sudden?
Gradual loss of hearing is seen in chronic illnesses such as chronic otitis
media, otosclerosis, whereas sudden loss is seen in perforation of eardrum,
barotraumas, viral diseases and sound blasts
• Unilateral or bilateral: Is the impairment of hearing in one ear or in both
the ears?
Unilateral deafness may be seen in Ménière’s disease or trauma. Bilateral
deafness may be seen in otosclerosis. Acoustic neuroma must be ruled out in
case of unilateral SNHL
• Exposure to noise or drugs:Is there a history of exposure to noise or
drugs?
Noise exposure by the duration predisposes to hearing loss. Drugs such as the
aminoglycosides cause sensorineural deafness
Itching
• Itching: Is there any itching in the ear and if so, of what nature?
Itching can be present in various forms and can be unilateral or bilateral (e.g.
fungal infections, eczematous otitis externa, dry wax)
Pain in the ear

• Severity and onset: How severe is the pain and what is its type? Was it
sudden or gradual?
Pain in the ear can be mild and described by the patient to be boring and deep.
It can be continuous (e.g. boil), intermittent (e.g. OME or paroxysmal (e.g.
glossopharyngeal neuralgia)). It can be sudden (e.g. AOM) or develop gradually
(e.g. acute mastoiditis. In otitis externa, dull aching pain gradually becomes
severe and increases with yawning or movement of the ear)
• Pain and discharge: Is the pain associated with any discharge and what is
its relationship to pain?
Pain of otitis externa is generally before or at the time of discharge, whereas
the pain is often relieved by discharge (e.g. perforation of AOM)
• Ear pain and symptoms of throat: Are there any symptom of illness of
throat?
In children, adenotonsillitis is known to cause ear pain, and in adults,
malignant tumours of oropharynx, larynx and pharynx can be associated with ear
pain, but they may be associated with sore throat/voice change and/or dysphagia.
Dental caries, temporomandibular joint arthritis or malocclusion and cervical
spondylosis may also present with referred ear pain (referred otalgia)
Discharge
• Unilateral or bilateral: Is the discharge in one ear or in both ears?
Discharge from the ear can be unilateral or bilateral (e.g. external canal or
middle ear cleft)
• Nature and quantity: What is the nature and quantity of discharge?
The quantity varies considerably. The ear discharges can be serous (e.g.
external ear pathology), and mucoid, mucopurulent or purulent (e.g. otitis
media). It can be bloody (e.g. trauma). Scanty and offensive discharges occur
due to cholesteatoma. Clear watery discharge after head injury may be due to
CSF. Mild to copious discharge in CSOM
• Association with pain: Is the discharge related to ear pain?
The pain of otitis externa is generally before or at the time of discharge,
whereas the pain is often relieved by discharge (e.g. AOM). CSOM is painless,
pain indicates complications
Dizziness
• Nature and duration: What is the nature of the dizziness—is it vertigo or
unsteadiness? How long does it last?
Vertigo is a false sense of rotation. It is usually present with vestibular
disturbances. BPV lasts for a few seconds, whereas, it lasts for hours in
Ménière’s disease. Vertigo of labyrinthitis or neuronitis lasts for several days or
weeks. Unsteadiness occurs due to inadequacies in visual, vestibular and
proprioceptive inputs (e.g. travel sickness, hyperventilation, drugs and iatrogenic
causes)
• Nausea and vomiting: Is dizziness associated with vomiting?
Acute vestibular imbalances cause nausea and vomiting
• Unconsciousness: Is dizziness associated with unconsciousness?
Peripheral vertigo is never associated with unconsciousness. Circulatory
disorders cause dizziness along with unconsciousness
• Discharge: Is there any associated discharge from the ear?
Discharge is an associated symptom of vertigo in CSOM in the form of
cholesteatoma eroding the lateral semicircular canal
• Hearing loss: Is there any associated loss in hearing?
Vertigo is associated with hearing loss with a feeling of pressure in the ear in
Ménière’s disease. In BPV and vestibular neuronitis, there is no loss of hearing
• Systemic symptoms: Are there any symptoms related to nervous system,
eyes or circulation?
Diseases of CNS, eyes and circulation are also involved with balance and so
the symptoms relating to them are to be evaluated
Tinnitus
• Quality and intensity: What is the quality and intensity of tinnitus?
It can vary in quality and intensity. It can be tonal or like noise. It can be
continuous or intermittent and can be in one or both ears
• Precipitating factors: When does it become worse?
The precipitating factors of tinnitus are alcohol, caffeine or tiredness. It
becomes more audible and worse when the surroundings are quiet
• Other symptoms of ear: Are there any symptoms related to the ear?
Tinnitus occurs occasionally in CSOM. Glomus tympanicum presents with
roaring tinnitus
Other symptoms
• Nausea: Is there associated nausea?
Nausea is a symptom of labyrinthitis, vestibular neuronitis or Ménière’s
disease
• Vomiting: Is there associated vomiting?
Acute labyrinthitis causes severe nonprojectile vomiting in contrast to that of
intracranial pathologies
• Headache: Is there associated headache?
Although headache per se is not a complication of an ear disease, it can reflect
an intracranial complication such as meningitis, intracerebral abscess secondary
to chronic secretory otitis media
• Fever: Is there associated fever?
AOM is a common condition to cause fever, but fever with severe headache
and vomiting should suggest an intracranial complication. Picket fence type of
fever is seen in sigmoid sinus thrombosis. Hypothermia may be experienced in
brain abscess
Positions of patient and examiner
Patient should be made to sit comfortably on a chair, with his or her legs together
along the side of the table opposite the examiner and the patient’s ear should be
at the examiner’s eye level (Fig. 21.17).
FIGURE 21.17 Positions of the patient and doctor for examining the ear.
Illumination (p. 333):

• Bull’s eye lamp (Ref Fig. 20.16A)
• Head mirror (Ref Fig. 20.16B)
• Clark’s headlight (Ref Fig. 20.16C)
• Headlight (Ref Fig. 20.16D)
AIDS for examination of the ears

• Aural speculum (Fig. 21.18): It is a conical and funnel-shaped tube with a
dull finish in its interior—it is used to see the external ear canal and eardrum
• Siegel’s speculum (Fig. 21.19): The aural speculum with a rubber bulb,
rubber tubing and an adapter with lens for attaching to the speculum—it is
used to see the external ear canal and eardrum, test the mobility of eardrum
and for conducting fistula test
• Otoscope (Fig. 21.20): It consists of an ear speculum with a magnifying lens
with batteries—it is used to see the external ear canal and eardrum magnified
• Tuning forks: Tuning forks of 256, 512, 1024 Hz frequencies are necessary.
They have a strong metallic base, stem and prongs (Fig. 21.21). They are
used to perform Weber’s test, Rinne’s test
FIGURE 21.18 Aural speculum.

FIGURE 21.19 Siegel"s speculum.
FIGURE 21.20 Otoscope.

FIGURE 21.21 Tuning fork.
AIDS for therapy

• Cerumen spud (Fig. 21.22A)—long spatula-like instrument used for removal
of foreign body or wax
• Jobson Horne probe (Fig. 21.22B)—used for removal of wax
• Cotton buds (Fig. 21.23)—used for removing discharges
• Aural dressing forceps (Fig. 21.24)
FIGURE 21.22A Cerumen spud.

FIGURE 21.22B Jobson Horne probe.
FIGURE 21.23 Cotton buds.
FIGURE 21.24 Aural dressing forceps.
Adequate knowledge and orientation of the ear and its related anatomy is
mandatory.
External ear
Inspection
Carefully inspect the external ear or pinna and look for:
• Presence (absence of pinna—anotia)
• Size (microtia—small in Down syndrome, macrotia—large pinna)
• Shape (absence of antihelix—bat ear, lop or cup ears)
• Deformity (may be congenital or acquired):
• Congenital deformities (e.g. absence of pinna—anotia, accessory auricles,
low placement in Down syndrome)
• Deformities following trauma (e.g. cauliflower ear)
• Scars:
• On the lobule (e.g. repair)
Preauricular area
Look for three ‘S’s:
• Sinus—preauricular sinus at the root of helix
• Scar—operated scar
• Swelling—preauricular adenitis
Postaural area (behind the ear)

Posterior surface of the ear and the mastoid area are inspected by lifting the
external ear forward and look for three ‘S’s:
• Sinus—postmastoidectomy sinus (Fig. 21.25)
• Scar—operated scar of postaural approach surgeries of the ear
• Swelling—subperiosteal abscess, postauricular adenitis, Battle’s sign
(contusion following temporal bone fracture), Grissinger sign (swelling due
to thrombosis of emissary vein in lateral sinus thrombosis)
FIGURE 21.25 Examination of postaural area—postmastoidectomy sinus.
Note
Retroauricular sulcus is obliterated in furunculosis by oedema unlike
subperiosteal abscess where postauricular groove is maintained.
External auditory canal

The external canal can be seen right up to the eardrum, by straightening the S-
shaped canal, by gently drawing the pinna upwards, outwards and backwards
(Fig. 21.26) in adults and downwards, outwards and backwards in children.
FIGURE 21.26 Examination of the external ear.
Look for:
• Change in diameter of the canal
• Examine the roof, floor and the walls
• Wax debris, foreign bodies, furuncle, cellulitis, soft tissue tumours, osteoma,
keratosis obliterans
Note
Moving the external ear in a patient with otitis externa or furuncle will be
extremely painful. Tragal sign is positive in external otitis.
The external auditory canal can be examined using the aural speculum and the
otoscope (see below). In patients who have undergone modified radial
mastoidectomy, the meatus is wider and directly leads into mastoid cavity.
Tympanic membrane
Examination with aural speculum
Proper size ear speculum is chosen and gently negotiated in the ear canal with
rotatory movements and passed just beyond the junction of the bony and
cartilaginous ear canal (Fig. 21.27).
FIGURE 21.27 Examination with aural speculum.
Examination with otoscope

The otoscope is held like a pen and the little finger is extended and used to
anchor the examining hand on the face. The left hand should hold the otoscope
to examine the left ear and the right hand for the right ear. The scope should be
directed into the canal, and the largest speculum that is comfortable should be
used (Fig. 21.28).
• Normal eardrum is a shallow concave disc pearly grey in colour, and oval in
shape (Fig. 21.28A)
• Next is to identify the handle of malleus, which extends vertically
downwards and backwards (terminal part ends in a knob-like structure called
umbo)
• Prominent knuckle-like process is the lateral process of malleus
• The fold of tympanic membrane, which runs from the anterior part of annular
rim to lateral process of malleus is called anterior malleolar fold and the one
which runs posteriorly to the annular rim to the handle of malleus is called
posterior malleolar fold
• The incidental light may get reflected from a triangular area at the
anteroinferior lower portion of the drum with its apex at the umbo and base
at the periphery, which is called the cone of light
• The area of tympanic membrane above the malleolar folds is called pars
flaccida and that below the malleolar folds is called pars tensa
FIGURE 21.28 Examination with otoscope.
FIGURE 21.28A Otoscopy—normal tympanic membrane.
For convenience and understanding, the eardrum is divided into four unequal
quadrants (Fig. 21.28B).
FIGURE 21.28B Quadrants of tympanic membrane.
Mobility of tympanic membrane

Mobility of the tympanic membrane can be elicited by two methods:
Siegalization: The Siegel’s speculum is attached to the ear speculum and is
introduced into the ear canal. With the help of the inflatable bulb (Fig. 21.29),
the pressure is increased and decreased alternately, and the mobility is tested.
When the tympanic membrane and the middle ear pressure are normal, the
membrane is fully mobile. The movement is restricted in adhesive otitis media,
secretory otitis media etc.
FIGURE 21.29 Siegalization.
Valsalva manoeuvre: Valsalva manoeuvre increases the pressure in the

nasopharynx which is transmitted to the middle ear through the eustachian tube.
This is seen as mobility of the tympanic membrane. When the tube is not patent
or during middle ear disease, this movement may be restricted or absent.
Method: This is done by asking the patient to inflate his or her cheek with his or
her nose and mouth closed (Fig. 21.30).
FIGURE 21.30 Valsalva manoeuvre.
Toynbee manoeuvre: This is done by asking the patients to swallow with his
or her nose and mouth closed. The negative pressure created in the middle ear
causes mobility of eardrum inwards (Fig. 21.31).
FIGURE 21.31 Toynbee manoeuvre.
Abnormalities of tympanic membrane

• Colour varies considerably:
• Dull grey or amber (e.g. secretory otitis media)
• Flamingo tint (e.g. otosclerosis)—not commonly seen in Indian ears
• Rising sun appearance (e.g. glomus jugulare tumour)
• Chalky white (e.g. myringosclerosis)
• Red (e.g. AOM)
• Bluish.(e.g. trauma)—haemotympanum, high jugular bulb, cholesteatosis
• Blood vessels are generally not found on the surface of the eardrum, but radial
blood vessels indicate an effusion of the middle ear in AOM
• Cone of light is distorted or lost in middle ear pathologies due to retraction of
the drum
• Granulations may be found on the eardrum in myringitis granulosa (attic and
postero-superior marginal granulations of the eardrum are accompanied by
perforation, cholesteatoma and hearing loss)
• Vesicles on the eardrum are seen in myringitis bullosa
• Plaques may be found in myringosclerosis or tympanosclerosis
• Polyps: Pedunculated, insensitive, non-bleeding oedematous mucosal polyps
arise from the middle ear mucosa. Abnormally bleeding polyp may be a
glomus tumour
• Pars tensa: Perforations—the perforations should be described taking into
consideration the following (Fig. 21.32):
Type and location (Figs. 21.14B–D):
• Central (they have a margin of pars tensa around the perforation)
- Anterior—anterior to the handle of malleus
- Posterior—posterior to the handle of malleus
- Inferior—below the level of umbo
• Marginal (they do not have a margin of eardrum around it, but expose the
bony annulus)
Size: Assessment of size is based on clinical judgement. Roughly, they can be
described as:
• Small—when it occupies less than a quadrant of the eardrum
• Moderate—when it occupies about half the size of the eardrum
• Large—when it occupies more than three fourths of the eardrum
• Subtotal (a large part of pars tensa is lost, which is usually central and
kidney shaped)
• Total (entire eardrum is lost)
• Multiple perforations are seen in tuberculosis (TB) otitis media
Shape: It is usually oval, round or kidney shaped
Margins:
• Regular in chronic otitis media
• Irregular in traumatic perforation with blood clots
Structure seen through perforations:
• Anterior superior perforation—eustachian tube crater
• Posterior perforation—incudostapedial joint or stapedius tendon
• Middle ear mucosa (normal, congested or oedematous or polypoid mucosa
in subtotal perforation)
• Malleus may be vertically placed or foreshortened and ankylosed to
promontory
FIGURE 21.32 Perforations of tympanic membrane.
Retraction pockets and cholesteatoma

Sometimes, there may not be any perforation but a retraction pocket may be
found with foul smelling debris (cholesteatoma). Assessment of retraction
pocket and access to the fundus is important to decide on treatment.
Granulations
They are seen as red sessile sensitive patches which bleed on touch, and are
due to underlying osteitis.
Polyps
Polyps may arise from the middle ear mucosa over promontory, ossicles,
fallopian canal, eustachian tube. They are pedunculated and insensitive and do
not bleed on touch.
• Pars flaccida: This part of the tympanic membrane known as ‘attic’ may
show retraction pouch with cholesteatoma. Perforations and granulations
may also be seen, and attic perforations are unsafe.
Note
To assess the perforation, the secretions should be cleaned with the help of
suction or swab under operating microscope, the mucosa and the structures of
the middle ear may be assessed through the perforation.
Fistula test
The fistula in the labyrinth (a communication between the middle and inner ear)
is usually caused by cholesteatoma. This test is designed to establish its
presence. Method: This is tested by pressing the tragus of the patient repeatedly
against the ear canal or by Siegalization. Inference: If the patient develops
nystagmus or complains of giddiness, nausea or vomiting during this procedure,
it indicates the presence of a fistula in the labyrinth and the test is considered
positive.
Note
False negativity occurs when there is a fistula but the labyrinth is dead. False
positivity is seen due to endolymphatic hydrops where there is no fistula but
adhesion between endosteal membrane of oval window and saccule, which
initiates a vestibulo–ocular reflex in the absence of a fistula. The positive sign
is also called Hennebert’s sign.
Assessment of hearing
The hearing can be assessed on an outpatient basis. This can be done by two
methods:
• Tuning fork tests
• Free field speech assessment
Tuning fork tests

Equipment: Tuning forks of 512 and 1024 Hz are routinely used to assess
hearing, because these frequencies fall within normal speech frequency which
ranges from 500 to 2000 Hz.
Rinne’s test: The prong of tuning fork is struck on the bony prominence of
elbow or knee and vibrating prong is now held 1 " away from the external
auditory meatal acoustic axis to check air conduction. When the patient indicates
the perception of sound by raising a finger, the base of the tuning fork is
transferred to be placed on mastoid process in repetitions. Normally, hearing by
air conduction is heard longer than bone conduction. In conductive deafness,
bone conduction is better (Figs. 21.33A and 21.33B). Modified Rinne’s test is by
assessing the intensity. The vibrating prong is kept near the external auditory
meatus and immediately the base is transferred to mastoid process to assess
whichever is loudest. Interpretation of Rinne’s test is shown in Table 21.11.
FIGURE 21.33A Holding the tuning fork near the external meatus.
FIGURE 21.33B Placing the tuning fork on the mastoid process.
TABLE 21.11
Interpretation of Rinne’s Test
Rinne’s
Patient’s response Interpretation
test
Air conduction louder than bone Positive Normal hearing or slight sensorineural loss
conduction
Bone conduction louder than air Negative Conductive hearing loss (becomes negative only if conductive loss is
conduction >15 dB)
Note
False negativity occurs in unilateral SNHL due to crossover of the bone
conduction to normal ear. Rinne’s infinitive is when patient appreciates only
air conduction and no bone conduction. Rinne’s equal indicates mild
conductive deafness in AC = BC intensity.
The hearing loss may also be quantified (Table 21.12).
TABLE 21.12
Quantification of Hearing Loss
Frequency Conductive deafness

256 512 1024
Negative Positive Positive Mild
Negative Negative Positive Moderate
Negative Negative Negative Severe
Weber test: A vibrating tuning fork (Fig. 21.34) is kept in the midline of the
skull anywhere from the occiput to the chin or alternatively on the exposed front
teeth. Sound is not lateralized in normal or identical hearing losses.
FIGURE 21.34 Weber test.
Note
In conductive deafness, Weber is lateralized to worse hearing ear. In SNHL,
Weber is lateralized to better hearing ear.
Free field speech assessment

The examiner should stand behind the patient (to avoid any visual clue), and
phonetically balanced words are uttered, at varying intensities (whisper—30 dB
to conversational tone—60 dB), and the patient is asked to repeat.
• Speech reception threshold (SRT):The lowest intensity level at which 50% of
presented words are repeated by the patient
• Speech discrimination score (SDS): When single syllable words are
presented at 20–40 dB above SRT the percentage of words repeated correctly
forms SDS. In normal persons with conductive deafness, SDS is 90–100%. It
is less than 90% in persons with SNHL
Other systems
When the clinical presentation is related to pathologies of the ear, nose and
throat, the following systems should be clinically evaluated for completion and
more information:
• Neck (e.g. secondary lymph node metastases in ear cancers, Bezold or
Citelli’s abscess)
• Chest (e.g. TB)
• Lymphatic system in general (e.g. TB, lymphoma)
• Neurological system (e.g. intracerebral extension of middle ear pathology)
CHAPTER 22
Pharynx and larynx

Jacinth Cornelius
CHAPTER OUTLINE
22.1. Development of pharynx and larynx 322
22.2. Surgical anatomy of pharynx and larynx 322
22.3. Diseases of pharynx 323
• Pharyngeal pouch 323
• Pharyngitis 323
• Acute tonsillitis 324
• Membranous tonsillitis 324
• Chronic tonsillitis 324
• Acute retropharyngeal abscess 324
• Chronic retropharyngeal abscess 325
• Parapharyngeal abscess 325
• Peritonsillar abscess (quinsy) 326
• Malignancies of tonsils 326
• Carcinoma of hypopharynx 327
• Foreign bodies of pharynx 327
22.4. Diseases of larynx 328
22.5. Diseases of larynx in adults 328
• Acute laryngitis 328
• Chronic laryngitis 328
• Papilloma larynx 329
• Carcinoma larynx 329
• Vocal nodules 330
• Vocal cord paralysis 330
22.6. Diseases of larynx in children 331
• Subglottic stenosis and laryngomalacia 331
• Acute epiglottitis 331
• Acute laryngotracheobronchitis 331
• Juvenile laryngeal papillomatosis 331
• Foreign bodies of larynx 332
22.7. Symptoms of pathologies of pharynx and larynx 332
• Pharynx and larynx 333
22.1 development of pharynx and larynx

Pharynx is derived from the cranial-most part of the foregut. With the
establishment of the palate and mouth, the pharynx shows a subdivision into
nasopharynx, oropharynx and laryngopharynx.
Larynx develops from the cranial-most part of the respiratory diverticulum
called the tracheobronchial groove. The communication between the
diverticulum and the pharynx persists as the inlet of the larynx. The
hypobronchial eminence forms the epiglottis. The thyroid, cricoid and arytenoid
cartilages are derived from the fourth and sixth pharyngeal arches. The laryngeal
muscles are derived from branchial mesoderm.
22.2 surgical anatomy of pharynx and larynx

Pharynx is a passage common to the upper ends of digestive and respiratory
tracts. It is about 10–15 cm in length and extends from the undersurface of the
basi-occiput to the level of sixth cervical vertebra which corresponds to the
lower border of cricoid cartilage beyond which the pharynx continues as the
oesophagus.
Based on its anterior communications, it is divided into three parts (Fig. 22.1):
• Nasopharynx (behind the nasal cavity—entirely respiratory)
• Oropharynx (behind the oral cavity—respiratory and alimentary)
• Laryngopharynx or hypopharynx (behind and along the sides of larynx—
respiratory and alimentary)
FIGURE 22.1 Surgical anatomy of pharynx and larynx.
Arterial supply is from:

• Tonsillar branch of facial artery (chief arterial supply to tonsil)
• Ascending pharyngeal branch of external carotid
• Ascending palatine branch of internal maxillary artery and
• Greater palatine branch of maxillary artery
Venous drainage is through the pharyngeal plexus into internal jugular vein.
Nerve supply is from:
• Sensory—glossopharyngeal nerve
• Motor—vagus and sympathetic plexus
Lymphatic drainage
• Retropharyngeal nodes
• Jugulodigastric nodes
• Deep cervical nodes
Larynx is an organ for respiration and phonation (voice box). It lies in the
middle of the anterior part of the neck opposite the fourth, fifth and sixth
cervical vertebrae, and becomes continuous with the trachea at the level of sixth
cervical vertebrae.
Larynx is formed by a rigid framework of cartilages and ligaments. There are
three single (thyroid, cricoid and epiglottis) and three sets of paired cartilages
(arytenoid, corniculate and cuneiform).
The ligaments are both extrinsic (thyrohyoid membrane, cricotracheal
membrane and hyoepiglottic ligament) and intrinsic (quadrangular membrane,
cricovocal membrane).
The three parts of larynx above downwards are:
• Vestibule
• Ventricle or sinus
• Infraglottic cavity
22.3 diseases of pharynx
Diseases of pharynx are classified based of the aetiology (Table 22.1).
TABLE 22.1
Aetiological Classification of Lesions of Pharynx
Aetiology Diseases
Congenital Pharyngeal pouch
Inflammatory Pharyngitis, tonsillitis
Retropharyngeal abscess
Neoplastic Carcinoma of hypopharynx
Pharyngeal pouch
• Rare condition
• Represents a pulsion diverticulum resulting from the muscular weakness at
the posterior pharynx between the two components of inferior constrictor
muscle (thyropharyngeus and cricopharyngeus), called Killian’s dehiscence
(Ch. 25)
• A cystic swelling mostly at the midline but deviates to the side later, mostly to
the left
• Larger pouches present with regurgitation or obstruction of the upper
oesophagus
• Aspiration may give rise to pneumonia or lung abscess
• Halitosis and cough are usually present
• CT or MRI of the neck will be diagnostic
• Oral contrast enhancement will be contributory
Treatment
• Total excision with proper exploration of the neck (cricopharyngeal myotomy
will be needed during the procedure)
• Endoscopic division of diverticulo oesophageal septum is also practiced
(Dohlman’s operation)
Pharyngitis
• Causative organism is usually virus
• Bacterial and fungal infections are also common
• Purulent post nasal drip secondary to sinusitis is a common cause
• Acid reflux (gastroesophageal reflux disease (GERD))
• Sore throat and a variable degree of difficulty in swallowing
• Examination will reveal a red and congested oropharynx and hyperemic
lymphoid follicles in posterior pharyngeal wall
• Inflammation may spread to tonsils and larynx also
Throat swab for culture of organisms will be useful
Treatment
• No specific treatment is needed for viral pharyngitis
• Antibiotics are needed for bacterial infections
• Antifungals are needed for fungal infections
• Antireflux treatment for GERD
Acute tonsillitis
• A very common disease of children between 4 and 10 years of age
• Over 50% are caused by β-haemolytic streptococcus
• Majority of others are caused by viruses, superadded by staphylococci and
pneumococci
Complications:Pharyngitis, peritonsillar abscess, parapharyngeal abscess,
poststreptococcal rheumatic fever or glomerulonephritis or subacute bacterial
endocarditis
Symptoms
• Sore throat
• Dysphagia
• Pain on swallowing
• Ear pain, associated with fever and general malaise
Clinical examination reveals:
• Congested anterior pillar of tonsils and pharyngeal mucosa
• Tonsils are often enlarged (Fig. 22.1A) with discrete microabscesses or
exudates
• Jugulodigastric lymph nodes may be enlarged and tender
FIGURE 22.1A Acute tonsillitis.
• Leucocytosis is common
• Throat swab and culture to detect the pathogen
Treatment
Bed rest, antibiotics and hydration are important in the management
Membranous tonsillitis
• Exudates of crypts coalesce to resemble a membrane
• The conditions which resemble membranous tonsillitis are given in Table 22.2
TABLE 22.2
Membranous Lesions of Tonsils
Condition Symptoms Clinical features Associated features

Acute follicular Fever, Membranous tonsillitis
tonsillitis odynophagia,
referred
otalgia
Acute diphtheritic Mild fever, Greyish-green pseudomembrane across soft
tonsillopharyngitis malaise palate, pharynx and tonsils bleeds on
removal. Stridor occurs on spread to
larynx
Vincent’s angina Sore throat, Slough across shallow ulcers of tonsils and Ulcerative gingivitis
fever, palate
bleeding
gums and
foetid odour
Agranulocytosis Fever, headache, Necrotic ulcers with slough Leucopenia, follows intake
odynophagia of drugs such as
chloramphenicol,
phenylbutazone
Infectious Low-grade fever, Oedematous ulceromembranous formation Cervical lymph nodes,
mononucleosis headache, over palate splenomegaly
malaise, sore
throat
Leukaemia Fever, bleeding Slough covered ulcers over gums, oral cavity Bilateral cervical
tendencies and pharynx lymphadenopathy,
hepatosplenomegaly
Keratosis pharyngitis Asymptomatic Keratinous horny outgrowths adherent to
mucosa of tonsils, pharynx
Chronic tonsillitis
Persistent subclinical or clinical tonsillitis for more than 6 months leads on to
chronic tonsillitis
• Subdued symptoms of tonsillitis persistent beyond 6 months
• Examination reveals:
• Chronically inflamed and enlarged or small and fibrotic tonsils
• Anterior pillar appears flushed; pressure over anterior pillar expresses
cheesy material of exudates from the crypts, which is called ‘Irwin Moore
sign’. When the tonsils are huge and obstructive, they may progress to
cause sleep apnoea
• Painless upper cervical lymphadenopathy
• Acute attacks cause tender adenitis
• No investigation may be useful
• Cephalometry and polysomnography are used to assess sleep apnoea
Treatment
Tonsillectomy
Acute retropharyngeal abscess

Condition follows a perforation of the pharynx by:
• a foreign body (FB)
• suppuration of retropharyngeal lymph node, following upper respiratory
infection in children
• Pain and dysphagia are commonly present
• Examination may reveal a bulge in the posterior wall of pharynx
• Plain X-rays of neck (lateral view) will reveal widened prevertebral soft
tissue shadow of swelling in the posterior pharyngeal wall and pockets of air
shadow
• MRI is diagnostic
Treatment
Incision of pharyngeal wall and drainage of pus with appropriate antibiotics is
curative
Chronic retropharyngeal abscess

Cold abscesses from cervical spine tuberculosis may also present as chronic
retropharyngeal abscess
• Mild pain and dysphagia
• Examination may show a bulge in the midline of posterior wall of pharynx
• Plain X-rays of neck (lateral view) will reveal widened prevertebral soft
tissue shadow
• MRI (Fig. 22.2) is diagnostic
FIGURE 22.2 MRI Cervical spine—C2, C3, C4 caries spine with
prevertebral soft tissue swelling. Source: (Courtesy Dr K. R. Suresh Bapu)
Treatment
Drainage of pus and antitubercular treatment
Parapharyngeal abscess
Infection of the tissue space lateral to the pharynx secondary to:
• acute tonsillitis
• infection of third molar teeth
• Pain in the throat, dysphagia and trismus
• Examination reveals the tonsil pushed medially with a tender neck swelling
in the upper part (Fig. 22.2A)
FIGURE 22.2A Parapharyngeal abscess.
CT and MRI are diagnostic
Treatment
Incision and drainagevia the neck supported by intravenous antibiotics
Peritonsillar abscess (quinsy)

Always a unilateral condition and follows tonsillitis caused by streptococcal
infection
• Severe pain (odynophagia), total dysphagia with fever
• Examination (Fig. 22.3) reveals:
• Medial and downward displacement of tonsil
• The soft palate looks oedematous
• Uvula is pushed to opposite side
FIGURE 22.3 Peritonsillar abscess.
Note
Parapharyngeal tumours also push the tonsils medially but they present with
diffuse lateral neck swelling.
Leucocytosis is present
Treatment
• Incision and drainage of the abscess offers immediate relief
• Abscess tonsillectomy was practiced
• Interval tonsillectomy is preferable to avoid recurrence
Malignancies of tonsils
• Unilateral enlargement of a tonsil or ulcers on tonsils should make one
suspect of a malignancy
• Common malignancies are:
• Lymphoma
• Squamous cell carcinoma
• Unilateral enlargement of tonsil, with or without mucosal ulcerations
• In lymphoma, the mucosa over the tonsil is smooth (Fig. 22.4) and has a
rubbery consistency, whereas squamous cell carcinoma appears as
ulceroproliferative friable growth of tonsil (Fig. 22.5) and has an indurated
feel more so in tonsillolingual sulcus
• Jugulodigastric nodes may be palpable due to spread
FIGURE 22.4 Lymphoma tonsil. Source: (Courtesy Dr R. Rajaraman)
FIGURE 22.5 Squamous cell carcinoma tonsil.
• CT is useful in assessing the lymph node involvement in the neck
• Biopsy clinches the diagnosis
Treatment
• Tonsillectomy and biopsy decides the histology
• Radiotherapy and chemotherapy are used for lymphomas
• Radical neck dissection with radiotherapy is the treatment of choice for
squamous cell carcinomas
Carcinoma of hypopharynx
• More than 50% occur in pyriform fossa, 40% in the postcricoid region and
less than 10% occur in posterior pharyngeal wall
• Arises in a predisposing postcricoid oesophageal web. This forms a part of
Plummer Vinson syndrome, where it is associated with iron deficiency
anaemia and achlorhydria
• High intake of alcohol and smoking are predisposing factors
• Mild dysphagia to solids is a common complaint. Progressive dysphagia
occurs as the lumen is narrowed
• Hoarseness of voice and weight loss are common
• Pyriform fossa:
• Commonly presents as an ulcerative growth in medial wall of pyriform
fossa
• Pooling of saliva may be present
• Growth extending to lateral part of pyriform fossa may present as swelling
on lateral wall of neck and move up on deglutition, unlike neck nodes
• Referred otalgia would be present. Fixation of hemilarynx may be present
(transglottic growth involves supraglottic, glottis and subglottic areas)
• Post cricoid area:
• Apart from post cricoid fullness, proliferative growth may be seen with
pooling of saliva
• Indirect laryngoscopy (IDL) reveals oedematous and popped up arytenoids
• Laryngeal crepitus would be absent (Boca’s sign)
• Posterior pharyngeal wall
• Present as ulceroproliferative growth, which can be seen by depressing the
tongue
• Lymph node swellings in the neck indicate advanced disease
• Endoscopy biopsy is diagnostic
• CT is contributory
• Barium swallow is useful
Treatment
• Total laryngo-pharyngo-oesophagectomy and reconstruction
• Neck nodes require block dissection
• Chemoradiation is an alternate treatment
Foreign bodies of pharynx

• Accidental swallowing of FBs (fish or meat bone) is common
• Lesions in the oesophagus such as webs and strictures predispose to
impaction of FBs
• Pain associated with pooling of saliva is the commonest complaint
• Fish bones are usually seen in the tonsils
• Indirect and direct laryngoscopy are diagnostic
• Plain X-rays (Figs. 22.6 and 22.7) are useful
FIGURE 22.6 Foreign body larynx.
FIGURE 22.7 X-ray—chicken bone in hypopharynx.
Treatment
If the FB is found, it should be removed (if no FB is found, but there is evidence
of mucosal tear) which should be managed by nasogastric tube feeding till it
heals
22.4 diseases of larynx
Diseases of larynx are classified based on the aetiology (Table 22.3).
TABLE 22.3
Aetiological Classification of Lesions of Larynx
Aetiology Diseases
Adult Children
Congenital Subglottic stenosis and laryngomalacia
Inflammatory Acute laryngitis Acute epiglottitis
Chronic laryngitis Acute laryngotracheobronchitis
Neoplastic Laryngeal papilloma Juvenile laryngeal papillomatosis
Carcinoma of larynx
Others Vocal nodules FBs
Vocal cord paralysis
22.5 diseases of larynx in adults
Acute laryngitis
Infection of larynx is caused by:
• Viruses
• Bacteria
• Purulent postnasal drip secondary to sinusitis is a common reason
• Sore throat, hoarseness of voice and pain
• Irritating cough
• Fever may be present
• IDL shows congested and swollen laryngeal mucosa
Video laryngoscopy is diagnostic.
Treatment
• Voice rest, steam inhalations
• Broad-spectrum antibiotics
Chronic laryngitis
• Chronic laryngitis occurs in people who:
• Smoke
• Voice abuse for long periods (singers, teachers)
• After chronic rhinosinusitis
• Tuberculosis, sarcoidosis and other granulomatous diseases are other causes
• Hoarseness of voice after prolonged use is the common symptom
• Examination may reveal:
• Hyperemic laryngeal mucosa
• Oedematous vocal cords (Reinkie’s oedema) (22.8A) or polyps (Fig.
22.8B)
• Nodules at the junction of anterior 1/3 and posterior 2/3 of vocal cords may
be present bilaterally in singers (Fig. 22.8C)
• Keratinising horny projections of hyperkeratosis may also be seen
• Intubation granuloma is seen in posterior part of vocal cords
FIGURE 22.8 Scopy—(A) Chronic hypertrophic laryngitis. (B) Polyp of
vocal cord. (C) Singer’s nodules.
• Endoscopy biopsy is diagnostic
• Thyroid function tests, autoimmune profiles may be necessary
Treatment
• Voice rest, steam inhalation
• Hyperkeratosis, polyps and nodules have to be removed, followed by speech
therapy
• Phonomicro-laryngeal surgery with laser gives functional results
Note
Posterior laryngitis is usually due to GERD. Tuberculous involvement causes
ulcerations, mouse nibbled appearance of vocal cords, turban-shaped
epiglottis, interarytenoid mammillations and oedematous appearance.
Papilloma larynx
• Solitary lesion
• More common in adults
• A premalignant condition
Warty growth in anterior commissure or from anterior third of vocal cord or
ventricular band
Video laryngoscopy (Fig. 22.9)
FIGURE 22.9 Scopy—laryngeal papilloma.
is diagnostic
Treatment
Microlaryngeal excision
Carcinoma larynx
• Carcinoma of supraglottic larynx
• Majority of them are squamous cell carcinomas
• Common in chronic smokers
• Lesions can be exophytic or ulcerative affecting the epiglottis, arytenoids,
false cords
• They may spread locally or metastasize to neck nodes
• Carcinoma of vocal cord
• Progresses to anterior commissure and into pre epiglottic space or laterally
to paraglottic space to become transglottic growth by progression into
supra- and infraglottis
• Difficulty in swallowing, FB sensation, haemoptysis and referred otalgia are
present in supraglottic malignancy
• Persistent hoarseness of voice is the common symptom in glottic involvement
• Swellings in the neck indicate lymph node metastases (cervical lymph node
metastases occur commonly in supra- and infraglottic malignancies, whereas,
it is uncommon in glottic malignancy)
• Subglottic growth presents with stridor
• Direct laryngoscopy (Fig. 22.10) biopsy is diagnostic. Cord movements may
be restricted due to involvement of laryngeal muscles, cricoarytenoid joint or
recurrent laryngeal nerve
• CT determines the extent of the disease including lymph node metastases in
the neck
FIGURE 22.10 Scopy—advanced vocal cord malignancy. Source: (Courtesy
Dr Mani Veeraraghavan)
Treatment
• Early lesions are treated by radiotherapy
• Large lesions require total laryngectomy
• Cervical lymph node metastases require block dissection
Vocal nodules
• Vocal nodules are hyperkeratotic nodules of both the vocal cords at the
junction of the anterior third and posterior two thirds
• Commonly seen in those who use their voice excessively such as singers and
teachers
• GERD also plays a great role in aetiology
DD: Intubation and contact granuloma occur over vocal processes of
arytenoids
Voice change with tiredness in phonation, and discomfort in the throat
Laryngoscopy (Fig. 22.8C) is diagnostic
Treatment
• Treat GERD if present
• Voice rest and speech therapy are useful
• Microlaryngeal surgery may be warranted, in select cases
Vocal cord paralysis

Common causes of vocal cord palsy are
• malignancies (bronchial, oesophageal, thyroid or skull-base tumours)
• surgical trauma (thyroid or cardiothoracic surgery—disruption of recurrent
laryngeal nerve)
• other causes are Ortner syndrome and idiopathic
• Husky and hoarse voice
• Symptoms depend on the position of the paralysed vocal cord and the ability
of the unaffected vocal cord to compensate (Fig. 22.11)
• Bilateral paralysis causes stridor
• Recurrent chest infections occur due to aspiration of food and secretions when
there is laryngeal incompetence
• Laryngoscopy shows the various positions of vocal cords (Table 22.4)
FIGURE 22.11 Vocal cord paralysis.
TABLE 22.4
Positions of Vocal Cords
Position name Actual position of vocal cords

Median position Vocal cords in midline during phonation
Paramedian Vocal cords are 3.5 mm away from midline (seen in strong whisper)
position
Cadaveric Vocal cords are 7 mm away from midline, the position after death. (seen in complete vocal cord
position paralysis due to vagal paralysis)
Gentle Vocal cords are 13.5 mm away from midline (seen in quiet respiration)
abduction
Full abduction Vocal cords are 19 mm away from midline (seen during deep respiration)
Direct laryngoscopy, stroboscopy
Treatment
• Treatment depends on the cause
• Idiopathic palsies recover spontaneously
• Tracheostomy with speaking valve would be immediate answer, for stridor
due to bilateral abductor paralysis
• Arytinoidectomy or posterior cordotomy with laser offer good relief
• Thyroplasty improves the voice in unilateral vocal cord palsy
22.6 diseases of larynx in children
Subglottic stenosis and laryngomalacia

• Subglottic stenosis may be congenital or may occur due to intubation in
neonates (premature or low birthweight children)
• Laryngomalacia is a condition, where the supraglottic larynx is flaccid
Infants present with stridor, some children show respiratory distress and cyanosis
while feeding
• Direct laryngoscopy is diagnostic
• CT is useful
Treatment
• Tracheostomy may be rarely required to relieve obstruction. Widening of
lumen may be done by surgery in select cases
• Laryngomalacia requires reassurance mostly
• Laser surgery to reduce the flaccidity is rewarding
Acute epiglottitis
Potentially life-threatening condition is common in children, and is caused by
Haemophilus influenzae
• A normal child suddenly becomes dyspnoeic, febrile and develops stridor
• The child becomes distressed, restless and sweaty and sits upright trying to
take in more air. IDL may cause fatal glottic spasm
X-ray lateral view of neck shows thumb’s sign (soft tissue shadow of epiglottis
appears enlarged to the size of thumb)
Treatment
• Recognition is important and quick intubation is necessary, and if needed a
tracheostomy
• Intravenous antibiotics is mandatory
• Steroids are useful
Acute laryngotracheobronchitis
• Affects children of 6 months to 3 years
• Viral in aetiology
• Children have brassy cough and are very unwell
• Clinical examination is noncontributory
X-ray of the neck
shows narrowing of airway (Steeple’s sign)
Treatment
• Humidified oxygen administration by mask is necessary
• Intubation may be needed in severe cases
• Steroids are useful in reducing the airway oedema
• Antibiotics if superadded infections are present
Juvenile laryngeal papillomatosis

• Benign tumours of larynx
• It is multiple and warty in appearance
• Caused by genital human papilloma virus, contamination of airway caused
during birth
• Total airway obstructions are not uncommon
Hoarseness and stridor
Video laryngoscopy is diagnostic
Treatment
Excision of these tumours by microlaryngeal CO2 laser or cold steel
techniques
Foreign bodies of larynx

FBs in the larynx are rare
Stridor is the symptom
X-ray of the neck (Fig. 22.6), CT and laryngoscopy are required
Treatment
Tracheostomy and immediate removal is the treatment or death may supervene
the laryngospasm
22.7 symptoms of pathologies of pharynx and

larynx
• Sore throat
• Pain in the throat
• Change of voice
• Noisy breathing (stridor)
• Difficulty in swallowing (dysphagia)
• Lump in the throat
• Snoring and sleep disturbance
Sore throat
• Sore throat accompanied by fever may indicate infectious pathology
• Supraglottic malignancy also starts with irritation or soreness in the throat
• GERD or laryngopharyngeal reflux disease also causes sore throat or
discomfort especially at nights
Pain in the throat

Pain in the throat, especially while swallowing is of varying degrees.
Association of fever may indicate infections such as tonsillitis and pharyngitis.
Usually, the pain from the larynx and pharynx may be referred to the ear, TB
larynx or quinsy present with odynophagia.
The causes of pain in the throat are:
• Traumatic (e.g. injury to larynx)
• Inflammatory (e.g. acute tonsillitis, quinsy, perichondritis, acute epiglottitis,
perichondritis, retropharyngeal abscess, parapharyngeal abscess)
• Neoplastic (e.g. malignancy of larynx, oropharynx and hypopharynx)
• Miscellaneous (e.g. FBs, aphthous ulcers)
Change of voice
• Hoarseness of voice may be a common accompaniment of vocal fold
pathology. Persistent or progressive hoarseness should make one suspect a
laryngeal malignancy, especially in chronic smokers. More commonly
encountered in teachers, preachers and vendors due to voice abuse and
consequent vocal nodules. Invariably, history of GERD or laryngopharyngeal
reflux is a frequent accompaniment
• Huskiness suggests vocal cord paralysis
• Mogiphonia or phonic spasm occurs in professional speakers who suddenly
become aphonic
• Spasmodic dysphonia causes strained voice made with an effort
• Functional aphonia occurs in hysteria
• Phonoasthenia causing progressive loss of voice towards the end of the day
occurs in Myasthenia gravis
• Hypernasal voice (e.g. velopharyngeal incompetence—disorders of palate)
Stridor
Stridor may be encountered in any age group:
• Inspiratory (e.g. lesion above the glottis)
• Biphasic (e.g. lesion at glottis, subglottis and cervical trachea)
• Expiratory (e.g. lesion of intrathoracic trachea and bronchi)
Stridor may be caused in:
• Neonates and infants: Subglottic stenosis or laryngomalacia
• Children (e.g. epiglottitis or croup or FBs)
• Adults (e.g. laryngeal malignancy, post thyroidectomy)
Dysphagia
Malignant lesions of pharynx and oesophagus cause dysphagia, starting with
solids progressing onto liquids. Neurogenic dysphagia is often worse for liquids
than solids. In recurrent tonsillitis and pharyngitis, patient is able to take food
despite the discomfort. Dry swallowing is noted in globus pharyngeus.
Snoring and sleep disturbance
Large tonsils and redundant soft palate
Eliciting history
Since, most illnesses of throat present with symptoms related to the system, the
questions relating to other symptoms of the ear, nose and throat illnesses.
• Age: Croup and laryngomalacia are seen in children. Malignancies are seen in
old age
• Sex: Postcricoid carcinoma of hypopharynx is more common in females
• Occupation: Chronic laryngitis and vocal nodules are seen in people who use
their voice excessively, e.g. teachers, singers. Laryngeal malignancy may be
seen with asbestosis
• Residence: Recurrent tonsillitis and pharyngitis are seen in lower
socioeconomic people who live in crowded areas
Sore throat and throat pain

• Duration: How long is it present?
Short duration may indicate illnesses such as viral pharyngitis, and
longstanding pain may indicate malignancy
• Type and nature: Is it mild or severe and is it present continuously?
Intermittent pain may indicate inflammatory aetiology, and continuous pain
may indicate chronic fungal pharyngitis or chronic granulomatous lesions or
neglected malignancy
• Dysphagia: Is it associated with difficulty in swallowing?
Painful swallowing (odynophagia) may indicate acute inflammatory oedema
(e.g. quinsy, TB larynx)
• Earache: Is there associated ear pain?
Sometimes the pain from the teeth and larynx, cervical spine,
temporomandibular joint and pharynx may be referred to the ear, but it is
associated with normal looking ear on otoscopy
• Fever: Is there associated fever?
Fever indicates infective pathology (e.g. acute tonsillitis or acute pharyngitis)
• Neck pain: Is there associated pain in the neck?
Neck movements may cause pain when complications such as quinsy and
parapharyngeal abscess occur following acute follicular tonsillitis
Hoarseness
Short duration may indicate illnesses due to infection, and longstanding
hoarseness may indicate malignancy
Hoarse voice is heard in laryngitis, vocal nodules and glottic malignancies.
Intermittent hoarseness may indicate allergic aetiology or recurrent infections,
and continuous hoarseness may indicate malignancy of vocal cord. People, who
use their voice continuously for long hours, may have hoarseness free spells in
the morning and it gets worse as the abuse continues. Persistent hoarseness may
indicate malignancy, especially in smokers. Breathy and harsh voice is heard in
vocal cord palsy
• Cough: Is there associated cough and if so what is the nature of cough?
Normal cough is present despite complete loss of voice in hysterical aphonia,
whereas, the nature of cough changes to a characteristic ‘bovine cough’ with
weak voice in patients with laryngeal palsy. Generally cough is present in TB
laryngitis, vocal cord paralysis and malignancies due to aspiration
Stridor
Sudden onset indicates allergic acute glottic oedema. Short duration indicates
acute epiglottitis in children and long duration may indicate slow growing
malignancy of subglottic area or bilateral abductor paralysis
Stridor has relationship to phases of respiration. Inspiratory stridor is a
symptom of lesions of supraglottic area, whereas intra laryngeal lesions produce
biphasic stridor. A FB in larynx causes sudden severe stridor
• Dyspnoea: Is there associated difficulty in breathing?
Dyspnoea may be present with lesions of lumps due to pressure or due to
aspiration, or coexisting infection or secondaries
• Positions of patient and examiner
The patient should be made to sit comfortably on a chair, with his or her legs
together along the side of the table opposite the examiner and the patient’s oral
cavity should be at the examiner’s eye level
• Illumination (p. 292, Chapter 20)
• Bull’s lamp (Ref Fig. 20.16A)
• Head mirror (Ref Fig. 20.16B)
• Clark’s headlight (Ref Fig. 20.16C)
• Headlight (Ref Fig. 20.16D)
• Aids for examination
• Tongue depressor (a bent metallic blade) (Ref Fig. 20.19)—used for
depressing the tongue to examine the oral cavity and oropharynx
• Laryngeal mirror (a small circular plane mirror fixed to a straight handle at
an angle to a long shaft) (Fig. 22.12)—used for examination of larynx
• Aids for therapy
• Suction cannula (Fig. 22.13)—used for clearing the secretions in throat
FIGURE 22.12 Laryngeal mirror.

FIGURE 22.13 Suction cannula.
Note
Adequate knowledge and orientation of the larynx and pharynx and their
related anatomy is mandatory, as during IDL, the mirror image of the larynx is
seen by the examiner.
Pharynx and larynx

The larynx and pharynx can be examined by various methods:
• Indirect laryngoscopy (IDL): Method: It is performed using the laryngeal
mirror, which is gently heated (to prevent condensation of patient’s breath).
The seated patient’s tongue is held with the help of gauze with the thumb and
middle finger. With the help of the index finger the upper lip is retracted.
Warmed laryngeal mirror is held like a pen in the other hand and introduced
into the oral cavity and held at the base of uvula without touching the
posterior pharyngeal wall. The mirror image of the larynx is viewed, hence it
is called IDL (Fig. 22.14)
FIGURE 22.14 Indirect laryngoscopy.
Vocal cord movements are examined during:

• gentle breathing
• phonation
• forced inspiration
• coughing and at rest
• The structures which cannot be viewed by this procedure are:
• Laryngeal ventricles
• Subglottic area
• Post cricoid area
• Direct laryngoscopy: The larynx can be examined directly using a rigid
laryngoscope (Fig. 22.15). This is done under local or general anesthesia.
Mild sedation, analgesics and vagolytic premedication should supplement
local anesthesia. Macintosh’s laryngoscope (Fig. 22.16) with beak facilitates
hypopharyngeal examination while anterior commissure laryngoscope
delineates laryngeal inlet, ventricles and vocal cords
FIGURE 22.15 Direct laryngoscopy.

FIGURE 22.16 Mackintosh’s direct laryngoscope.
The differences between IDL and direct laryngoscopy are given in Table 22.5.
• Flexible fiberoptic direct nasopharyngo laryngoscopy: Method: After
anaesthetizing the nose with xylocaine spray, the scope is passed along the
floor of the nasal cavity on the patent side. Once the posterior choana is
reached, it is advanced over the soft palate and down into the pharynx. The
base of the tongue and epiglottis are identified. The larynx and most of the
pharynx can be visualized
• Video endolaryngoscopy: A telescope with attachment to camera and
monitor is introduced into the oropharynx to visualize the larynx (Fig. 22.17)
• Stroboscopy: Video endolaryngoscopy during pulsed illumination
synchronizing with vocal cord vibration is done to identify the wave pattern
and space occupying lesions of vocal cord
FIGURE 22.17 Video endolaryngoscopy.
TABLE 22.5
Differences between Indirect and Direct Laryngoscopy
Indirect laryngoscopy Direct laryngoscopy
There is foreshortening in antero-posterior diameter There is no foreshortening in antero-posterior diameter

True or false vocal cords appear to be in contact with each True and false vocal cords are separated by ventricles
other
Inverted mirror image is seen There is only direct visualization
Vocal cords look flat and white with sharp margins Vocal cords look pinkish and appear slightly rounded
Mobility of cricoarytenoid joint cannot be checked Mobility of cricoarytenoid joint can be checked by
probing
It is an outpatient procedure It is done in operation theatre
Other systems
When the clinical presentation is related to pathologies of ear, nose and throat,
information:
• Oral cavity (e.g. discolourations, tumours)
• Neck (e.g. secondary lymph node metastases in throat cancers)
• Chest (e.g. tuberculosis, pulmonary metastases in throat cancers)
• Lymphatic system in general (e.g. tuberculosis, lymphoma)
• Neurological system (e.g. parapharyngeal tumours)
CHAPTER 23
Salivary glands
G. Sivakumar
CHAPTER OUTLINE
23.1. Development of salivary glands 336
23.2. Anatomy of salivary glands 336
23.3. Diseases of salivary glands 336
• Acute viral parotitis 337
• Acute suppurative sialadenitis 337
• Chronic recurrent parotitis 338
• Chronic submandibular sialadenitis 338
• Pleomorphic adenoma 339
• Warthin’s tumour 340
• Primary malignant tumours 340
• Metastatic tumours 341
• Mikulicz’s disease 343
• Sjögren’s syndrome 343
• Sialadenosis/Sialosis 343
• Salivary calculi 343
• Salivary fistulae 344
23.4. Symptoms of salivary gland disorders 344
• Salivary glands 346
• Relevant areas 348
23.1 Development of salivary glands

The salivary glands develop as outgrowths of the buccal epithelium, which are
solid at first and later get canalized. They branch repeatedly to form the duct
system, and the terminal parts of the ductal system develop into secretory acini.
• The outgrowth of the parotid gland arises in relation to the line of fusion of
maxillary and mandibular processes to form the cheek (ectodermal origin)
• The outgrowths for the submandibular and sublingual glands arise in
relation to the linguogingival sulcus (endodermal origin)
23.2 Anatomy of salivary glands

The salivary glands are divided into major and minor salivary glands:
• The major salivary glands are paired and include the parotid, submandibular
and sublingual glands
• The minor glands are about 600–1000 in number and are located in the
oropharyngeal mucosa
Parotid gland is the largest salivary gland and is situated in the parotid space,
which is bound superiorly by the zygoma, posteriorly by the external auditory
canal, inferiorly by the styloid process, styloid muscle and great vessels. The
gland is innervated by a branch of the auriculotemporal nerve, which carries
postganglionic parasympathetic fibres from the otic ganglion. The gland is
divided into superficial and deep lobes by the facial nerve. Tumours arising
from the superficial lobe present on the surface, whereas the tumours from the
deep lobe present in the parapharyngeal space, as a bulge in the lateral
pharyngeal wall. Malignant tumours invade the facial nerve to cause its
paralysis. The duct draining the parotid gland (Stensen’s duct) is approximately
5 cm long and opens in the upper labial sulcus near the second molar tooth.
Parotid gland (serous glands) produces serous saliva.
Submandibular salivary gland is situated in the submandibular triangle and
lies on either side of the mylohoid muscle. This gland is closely associated with
the lingual nerve. Its duct (Wharton’s duct) runs in the floor of the mouth and
opens on either side of the frenulum of the tongue. Submandibular gland (mixed
glands) produces seromucous saliva.
Sublingual salivary glands are situated under the tongue (mucous glands),
produce mucous saliva and drain via many small ducts.
Minor salivary glands are present all over the oral cavity.
23.3 Diseases of salivary glands

The diseases of the salivary glands can be classified based on their aetiology
(Table 23.1).
TABLE 23.1
Aetiological Classification of Diseases of Salivary Glands
Aetiology Diseases
Infective inflammatory Acute Acute viral sialadenitis
Acute suppurative sialadenitis
Chronic Chronic recurrent parotitis
Chronic submandibular sialadenitis
Neoplastic Benign Pleomorphic adenoma
Warthin’s tumour
Malignant Primary Mucoepidermoid carcinoma
Adenocystic carcinoma
Acinic cell carcinoma
Squamous cell carcinoma
Secondary Metastatic tumours
Degenerative Mikulicz’s disease
Sjögren’s syndrome
Metabolic and degenerative Metabolic and endocrine disorders
Others Ranula
Salivary calculi
Salivary fistulae
Acute viral parotitis (epidemic parotitis, mumps)

• Most common viral disease of the salivary gland
• Most common cause of a parotid swelling
• Viruses which affect the salivary glands are:
• Coxsackie A
• Cytomegalovirus
• HIV
Complications: Pancreatitis, meningitis and orchitis (uncommon)
• Bilateral parotid swellings with fever, malaise, myalgia and headache
• There may be dull ache below the ears
• The opening of the parotid duct is puffy and reddened
Tests to demonstrate antibodies to the mumps S and V antigens and to the
haemagglutination antigen
Treatment
• Symptomatic
• Mumps can be prevented by vaccination with MMR (mumps, measles,
rubella) vaccine
Acute suppurative sialadenitis

• Occurs generally in
• people with poor oral hygiene
• postoperative patients
• dehydration and reduced or obstructed salivary flow
• by ascending infection from oral flora, usually Streptococcus viridans or
pneumococci
• Parotid gland is usually involved
• Submandibular gland may also be involved
• Acute parotitis
• Painful unilateral parotid swelling with trismus, fever and tachycardia
• On examination, the parotid appears diffusely enlarged as a brawny
swelling (Fig. 23.1) and extremely tender with purulent discharge through
the Stensen’s duct
• Acute submandibular sialadenitis
• Painful swelling of the submandibular gland
• On examination, the gland appears enlarged and tender (Fig. 23.2);
purulent discharge through the Wharton’s duct
• Obstructing calculus may be seen or felt in the floor of the mouth (Fig.
23.3)
FIGURE 23.1 Acute suppurative parotitis.
FIGURE 23.2 Submandibular salivary gland abscess.
FIGURE 23.3 Calculus in the Wharton’s duct. Source: (Courtesy Dr Jacinth
Cornelius)
No special investigation is required
Treatment
• Broad-spectrum antibiotics are necessary
• If an abscess is formed, external drainage is necessary without waiting for
fluctuation to establish
Chronic recurrent parotitis

• Caused by low-grade infection affecting one or both glands
• The duct is dilated with terminal sacculation, known as ‘sialectasis’, the cause
being stenosis of the duct orifice by trauma or a calculus
Recurrent attacks of pain in the parotid gland with swelling
Sialography is diagnostic
Treatment
• Ductoplasty will relieve stenosis of the orifice
• Dilatation with balloon catheter is done for remote ductal stenosis
• Superficial parotidectomy is done for chronic unsightly swelling of the
parotid
Chronic submandibular sialadenitis

• Occurs when the duct is obstructed and dilated and becomes fibrotic due to a
calculus
• Attacks of pain before and after meals (salivary colic), with a swollen gland
(Fig. 23.4)
• Tender submandibular salivary gland (felt by bidigital palpation) with a foul
smelling purulent discharge through its duct
• Calculus may be felt in the course of the Wharton’s duct
FIGURE 23.4 Right submandibular salivary gland.
• Plain X-ray (Fig. 23.5) may show the obstructing calculus
• CT (Fig. 23.5A) is useful in identifying the calculus and defining the gland
parenchyma
• Sialography shows the dilated and obstructed ductal system
FIGURE 23.5 X-ray—submandibular salivary duct stone.
FIGURE 23.5A CT—left submandibular sialadenitis with obstructing
calculus. Source: (Courtesy Dr M. Kanagavel)
Treatment
Removal of the obstructing calculus (Fig. 23.5B) under cover of antibiotics is
curative
FIGURE 23.5B Submandibular duct calculus.
Salivary gland neoplasms

General features:
• Worldwide incidence varies from 0.4 to 13.5 cases per 100,000 people
• Majority are epithelial in origin (90%)
• Pleomorphic adenoma is the commonest (65%) of all tumours
• Parotid gland is the commonest site of occurrence of salivary gland tumours
• Primarily occur in older adults
• Females are commonly affected, except Warthin’s tumour
• The smaller the salivary gland, the higher the proportion of malignant
tumours
• Tumours have the highest chance of being malignant if they arise from the
retromolar area, floor of mouth, tongue and sublingual gland
Pleomorphic adenoma
• Commonest neoplasm of salivary glands
• Affects most commonly the superficial part of parotid glands
• More common in females of 4th–6th decades
• This is a benign tumour
• Histology shows columns of neoplastic epithelial cells separated by
myxomatous connective tissue stroma and this varied histological
appearance, derives the name, pleomorphic adenoma
• Facial nerve palsy and lymph nodal involvement are seldom seen
• General features of parotid tumours are:
• 80% parotid tumours are benign
• 80% of parotid tumours are pleomorphic adenomas
• 80% of pleomorphic adenomas occur in the parotid
• 80% of parotid pleomorphic adenomas occur in the superficial lobe
• 80% of pleomorphic adenomas are benign
Though rare, pleomorphic adenomas develop malignancy, and the features
suggesting this transformation are (mnemonic—‘PAROTID’):
• Pain
• Altered consistency
• Rapidity of growth
• Onset of facial palsy
• Tethering of skin
• Involvement of bone
• Development of nodes
• A slow-growing painless lump in the parotid region, lifting the earlobe (Fig.
23.6)
• The growth may be intermittent
FIGURE 23.6 Pleomorphic adenoma.
• US and biopsy may be useful
• CT if malignancy is suspected
Treatment
Superficial parotidectomy is the treatment of choice (facial nerve should be
safeguarded)
Warthin’s tumour (adenolymphoma)

• Second most common tumour in salivary glands
• Composed of bilayered oncocytic and basaloid epithelium forming cystic
structures sharply demarcated from lymphoid stroma
• Male predominance
• Risk factor—tobacco smoking
• Exclusively occurs in the parotid gland
• Believed to develop from neoplastic transformation of heterotopic salivary
duct in the lymph node (intraglandular lymph node is constant in parotid
gland)
• Multicentric tumours are also seen (25%)
• Bilateral occurrence (5–8%)
• Rarely, either the epithelial or lymphoid component can undergo malignant
change (0.1%)
• Many are asymptomatic
• Pain, facial weakness, ipsilateral ear symptoms (tinnitus, earache and
deafness)
• Lump in the inferior pole of parotid gland (Fig. 23.7)
• Sudden increase in pain (due to leakage of fluid into surrounding tissues and
retrograde infection from oral cavity via Stensen’s duct)
• On examination, the lump is typically doughy to cystic

FIGURE 23.7 Warthin’s tumour right side: (A) front view and (B) lateral
view.
• US and biopsy may be useful
• CT is done if malignancy is suspected
Treatment
• No treatment is required if it is not unsightly
• Superficial parotidectomy is curative
Malignant primary salivary tumours

• Malignant salivary tumours form only a small proportion of tumours arising
from major salivary glands, whereas, they form the major proportion of
tumours arising from minor salivary glands
• The relative prevalence of tumours of salivary glands are shown in Table 23.2
and Fig. 23.8
• Microscopically, the malignancies of salivary glands are:
• Mucoepidermoid carcinoma (commonest)
• Adenoid cystic carcinoma
• Acinic cell carcinoma
• Ulceration, fixation and facial nerve palsy are common and unfavourable
prognostic factors
FIGURE 23.8 Incidence of primary salivary gland tumours.
TABLE 23.2
The Relative Prevalence of Tumours of Salivary Glands
Salivary gland Prevalence Benign Tumours Malignant Tumours

Parotid 80 80 20
Submandibular 10 20 80
Sublingual 2 0 100
Minor salivary 8 20 80
The clinical presentation of various malignancies of salivary glands is given in
Table 23.3.
• Rapidly enlarging hard painless swelling in the region of the salivary gland
(Fig. 23.9)
• Pain suggests infection or a rapidly growing malignant tumour
• Fungation (Figs. 23.10A and B) and cervical lymphadenopathy may be
presenting symptoms
• Malignant tumours may present with cervical lymph node metastases (Fig.
23.10C)
• Malignant parotid tumours present with facial nerve palsy
FIGURE 23.9 Malignant parotid tumour. Source: (Courtesy Dr R. Rajaraman)
FIGURE 23.10A Advanced malignant submandibular salivary

tumour. Source: (Courtesy Dr R. Rajaraman)
FIGURE 23.10B Fungated malignant parotid tumour. Source: (Courtesy Dr R.
Rajaraman)
FIGURE 23.10C Submandibular malignancy with cervical lymph node
metastases. Source: (Courtesy Dr R. Rajaraman)
TABLE 23.3
Clinical Presentation of Malignancies of Salivary Glands
Examination Local
Type Common sites Symptoms Metastases
Findings Infiltration
Mucoepidermoid Parotid, palate Low grade is slow- Firm mass, High grade is Lymph node
growing, high grade facial nerve infiltrative (75%),
is rapid-growing paralysis distant
painless swelling (33%)
Adenoid cystic Parotid, Slow-growing painful Tender firm Common Distant
submandibular swelling mass and metastases
and palate facial nerve more
palsy common
than local
lymph node
metastases
Acinic cell Parotid, Slow-growing mass, with Firm mass, Uncommon Local metastases
submandibular, or without pain facial nerve often
buccal mucosa, palsy is rare delayed
upper lip and
palate
Squamous cell Parotid, Fast-growing mass, with Hard and fixed Common Local metastases
carcinoma submandibular ulceration mass, facial common
nerve palsy
common
• CT (Fig. 23.11) and MRI of salivary glands are diagnostic
• Biopsy (open biopsy / core biopsy more reliable than FNAC) is confirmatory
• X-ray and CT of chest are used to stage the disease
FIGURE 23.11 CT—parotid malignancy.
Treatment
• Wide resection of gland is the treatment of choice
• Total parotidectomy is the treatment of choice for malignant parotid tumours
(facial nerve is usually sacrificed)
• Block dissection is done for lymph nodal involvement
• Postoperative radiotherapy may be useful to prevent local recurrence,
especially in adenoid cystic carcinoma
Metastatic tumours
• Usually squamous cell carcinoma
• Metastatic squamous cell carcinoma outnumbers primary squamous cell
carcinoma of the salivary glands
• Lymph nodes in the parotid gland may be involved by secondary deposits
from tumours of scalp and face, and likewise, the nodes in the submandibular
area or gland may be involved by oral cancers
• Two thirds occur in the parotid gland and rest in the submandibular gland
• Ulceration, fixation and facial nerve palsy are common and unfavourable
prognostic factors
• Prior radiation therapy for acne, tumours of thymus, thyroid or tonsils are
predisposing factors in some cases
• A fast-growing, hard, fixed mass, with ulceration
• Regional lymph nodal involvement and facial nerve palsy are common
• Examination of the oral cavity may show the primary pathology
CT is diagnostic
Treatment
Radical surgery of the primary lesion with excision of the involved salivary
gland is the treatment of choice
Mikulicz’s disease
• Uncommon lesion exhibiting both inflammatory and neoplastic characteristics
• An autoimmune disease in which the patient’s own salivary gland becomes
antigenic
• Common in females, more common in aged women
• Unilateral or bilateral enlargement of parotid gland with mild local
discomfort, occasional pain and xerostomia
• Associated with fever, upper respiratory tract infections
Biopsy—histopathology—lymphocytic infiltration destroying or replacing the
acini
Treatment
• No treatment is required for mild cases
• Surgical excision and radiation are administered for persistent disease
Sjögren’s syndrome
• An autoimmune disease
• Other factors suggested are:
• Genetic
• Hormonal
• Infectious
• Immunologic
• It has been found to be associated with HLA system—HLA DR3 and DR4
• Various secretory glands may be involved—trachea, pharynx, larynx, nose
(bucco-pharyngo-laryngitis sicca)
Dryness of mouth and eyes and burning sensation in the oral mucosa, vagina
may also be involved with dryness.
• Primary Sjögren’s syndrome: Parotid enlargement with lymphadenopathy,
purpura, myositis and kidney involvement
• Secondary Sjögren’s syndrome: Rheumatoid arthritis, lymphadenopathy
• Sialography
• Biopsy of minor salivary glands (lip mucosal biopsy) reveals a lymphocytic
infiltrate with acinar atrophy
Treatment
• Artificial saliva and tear drops
• Symptomatic treatment
• Surgery is reserved only for patients with severe discomfort
Sialadenosis/sialosis
Sialadenosis or Sialosis is a noninflammatory, non-neoplastic enlargement of
salivary glands
• Usually affects the parotid
• Common between 40 and 70 years of age
• Cause is unknown, but suggested to abnormal tissue growth factor and is
often associated with malnutrition, obesity and alcoholic cirrhosis
• Hypothyroidism, diabetes mellitus, Cushing’s disease, AIDS, acromegaly and
certain drugs are known to cause such enlargement
Sialosis presents as diffuse enlargement of the glands, with symptoms related to
other systemic disorders
No special investigation is necessary, excepting those related to the metabolic
diseases
Treatment
Treatment is directed towards the metabolic or endocrine cause
Salivary calculi
• Occur more commonly in the submandibular gland and duct, because of their
mucinous secretion and elongated duct, travelling against gravity
• They vary in size and may occupy any part of the duct
• Intermittent pain and swelling of the salivary gland (Fig. 23.4), especially at
mealtimes
• Enlargement of the submandibular gland is established by bidigital palpation
• Stone itself may be palpable in the course of the duct
• Plain X-rays (occlusal and oblique views) will demonstrate most calculi (Fig.
23.5)
• Sialography is useful when stone is not clearly seen
• CT sialography is useful in assessing the size of stone
Treatment
• Most stones can be removed (ductotomy) through the intraoral approach
• Sialadenectomy is required for stones in the gland proper and in the proximal
duct
Salivary fistulae
• Parotid fistula is usually an aftermath of:
• incision of parotid abscess
• penetrating injury
• parotidectomy
• Submandibular salivary fistula results due to:
• bursting of a submandibular salivary abscess
• total obstruction of the Wharton’s duct by a calculus
• surgery of submandibular salivary gland
• Presents with a pinpoint opening in the parotid (Fig 23.12) or submandibular
region discharging saliva (Ref Fig. 11.11) with a previous history of an
abscess, trauma or surgery
• The discharge is of extreme discomfort as it is associated with a meal, and the
smell of good food
• Skin excoriation may be present around the fistulous opening
• The fistula is better demonstrated by asking the patient to chew a piece of
lime and suck a little of the juice
FIGURE 23.12 Parotid fistula. Source: (Courtesy Dr V. Srinivasan)
Sialography is diagnostic
Treatment
The fistula needs to be excised if it is from the major duct
23.4 Symptoms of salivary gland diseases

• Swelling in the region of the salivary glands
• Pain in the region of the salivary glands
• Salivary fistula
• Intraoral discharge
Swelling in the region of the salivary glands
The swelling can have different characteristics:
Parotid region Submandibular region

Parotid swelling Submandibular salivary gland swelling
Preauricular lymph node swellings (infections, primary and Facial lymph node swelling (infections, primary and
secondary malignancies) secondary malignancies)
Idiopathic masseter muscle hypertrophy
Sebaceous cyst
Preauricular cyst or abscess
Cyst of the parotid
• Soft and cystic—cysts, Warthin’s tumour

• Smooth and firm—pleomorphic adenoma
• Hard and irregular—malignancy
Pain in the region of the salivary glands

Pain in the salivary glands can be:
• Acute (e.g. acute parotitis, abscess)
• Acute and recurrent.(e.g. chronic recurrent sialadenitis)
• Dull and short period (e.g. viral parotitis, malignancy)
• Dull and long period (e.g. chronic sialadenitis)
Salivary fistula
Salivary fistula occurs due to trauma, surgery
The nature of discharge can be:
• Watery—saliva
• Pus—burst salivary gland abscess
Intraoral discharge
Intraoral discharges can occur from:
• The natural ductal orifice
• Internal salivary fistula (postoperative)
Eliciting history
General particulars
• Age: Malignancies such as carcinoma are more common in the elderly
• Sex: Sjögren’s syndrome is common in females

Swelling
This will give the duration of this present illness—short duration represents
acute pathology such as acute infections, and carcinomas and the long duration
indicate chronic pathologies such as benign tumours including pleomorphic
adenoma and chronic sialadenitis
• Site of swelling: Where did the patient notice the swelling first?
Warthin’s tumour usually starts at the lower pole of the parotid while ectopic
salivary tumours occur in the palate and buccal mucosa
Sudden origin indicates acute pathology such as infections, and gradual
development indicates chronic pathology such as benign tumours, including
pleomorphic adenoma
Description of the size of the swelling will permit the examiner to compare its
growth, if any, and can be correlated with the duration of the illness, which may
indicate acute or chronic pathologies. Likewise, decrease in size may indicate
resolving infections, e.g. viral parotitis
• Variation in size: Does the lump remain the same size always or show some
variation in size?
Viral infections show regression is size, bacterial infections show regression
in response to antibiotic therapy, but neoplasms show a steady increase in size.
The rate of progression in size is a useful indicator, as rapid progression in size
represents malignancy and slow progression indicates a benign disease
Pain
• Nature of pain: Was or is the swelling painful and how severe it is?
Acute infectious pathology such as acute suppurative parotitis and parotid
abscess are associated with pain of varying intensity and nature. Dull pain may
indicate swellings due to chronic pathologies such as sialadenitis
• Duration of pain: Was the pain present along with the onset of the swelling
or did it precede or follow the appearance of the swelling?
Pain and prodromal symptoms suggest viral parotitis such as mumps, and
development of pain in a pre-existing swelling suggests malignancy
• Precipitating factors: What is aggravating the pain?
Recurrent pain and swelling during mastication suggests chronic sialadenitis
secondary to ductal dilatation
Discharge from external fistula

• Nature of discharge: Was or is the swelling painful, and does or did it
discharge any fluid anytime?
Burst parotid abscess discharges pus through the overlying skin, in the form of
a fistula (parotid salivary fistula). Watery discharge suggests salivary fistula
• History of previous surgery or trauma: Did the patients undergo any
surgery for the salivary gland disorder or did they sustain any injury?
External salivary fistulae are associated with surgery or trauma
Intraoral discharge
• Nature of discharge: What is the nature of the discharge?
Purulent discharge through the salivary duct orifice occurs in sialectasia and
ductal obstructions. Bloody discharge is rare. Tiny stones or gravel-like material
may be discharged through the orifice after a colicky pain, commonly through
the Wharton’s duct

Association of high-grade fever may indicate an infective pathology (e.g.
acute suppurative parotitis, parotid abscess) or low-grade fever may indicate
malignancies
• Pressure effects: Is it producing any pressure effect on or infiltrating
neighbouring structures?
Association of pressure effects will indicate its local invasiveness (e.g.
malignant parotid tumours involve the facial nerve, malignant submandibular
salivary malignancies involve the hypoglossal nerve), and also the urgency of
treatment required. It may also indicate the relevant investigations to be
performed to facilitate the correct treatment
Malignant lumps of parotid may cause facial palsy and those of the
submandibular gland may cause hypoglossal nerve palsy
course of illness?
Loss of appetite and weight are indicative of illnesses such as malignancies
a clearer picture of diagnosis (failed treatment will help in the elimination from
differential diagnosis and success will help in confirmation of the diagnosis and
continuation of the treatment)
• Past history: Was there any similar illness in the past, which required any
treatment?
treated will indicate the examiner to reconsider the diagnosis such as recurrent
ranula and malignancies and eliminate diagnosis such as viral infections such as
mumps as they give immunity
Diseases such as tuberculosis occur in closely living families and the presence
of it may be a good indicator for the present diagnosis
Personal habits such as tobacco smoking have relationship to Warthin’s
tumour
Any other relevant question: This is left to the choice of the examiner to
match the situation, such as extramarital contact if the lump is suspected to be of
aetiology like syphilis or AIDS.
Salivary glands
The examination of the patient should be carried out in the following steps:
1. Inspection
2. Palpation
3. Auscultation
4. Examination of relevant areas
Inspection
The examiner should never be hasty to touch the patient with the desire of
making the diagnosis. Inspection forms the first part of the examination. The
points to note during inspection are:
Dentures, if any, should be removed before examination, as there may be
lesions underneath them
• Location or site of swelling: Observe the location of the swelling in relation
to the anatomical landmarks.
• Location gives great amount of clue in the diagnosis, e.g. swelling in the
parotid region (parotid pathology) and swelling in the submandibular
region (submandibular salivary pathology)
• Lifting of earlobe is a very important sign of a parotid swelling, which is
best seen from behind (Fig. 23.13). The swelling fills the furrow between
the mandible and the mastoid. Parotid swellings become more prominent
when masseter is contracted, by clenching the jaws, as the gland lies above
it
FIGURE 23.13 Lifting of earlobe by left parotid swelling (best seen from
behind).
Note
Masseteric muscle hypertrophy may rarely mimic parotid enlargement.
• Number of swelling: The number gives adequate clue in diagnosis

• Solitary swellings (salivary gland tumours)
• Multiple swellings (usually lymph node swellings)
• Shape and size of the swelling: Lumps of salivary origin have three
dimensions and all the three should be noted down; deeply placed lumps may
cause difficulty in measuring the depth
Shape is also three dimensional, but can be described in descriptive terms
such as oval, globular, irregular etc.
• Globular or round swellings usually indicate cysts
• Irregular swellings indicate malignancies
• Skin over the swelling: Careful attention has to be given to the skin over the
• Colour: Redness indicates acute inflammation (e.g. acute parotitis)
• Texture of skin: Shiny glistening skin over the swelling indicates its stretch
or oedema of the overlying skin (e.g. parotid abscess). Tethering of skin
suggests malignancy
• Changes on the surface: Prominent scars (e.g. indicate previous surgery;
Fig. 23.14), fistula (e.g. parotid fistula), ulcerations (e.g. burst parotid
abscess)
• Prominent veins: The engorgement of veins in the subcutaneous plane may
indicate fast-growing tumours creating venous blockage
• Surface of the swelling: The surface of the swelling provides some indication
of its aetiology, and is described in easily understandable terms such as
smooth and regular, rough and irregular or in any combination. Smooth
surface indicates cystic or benign swellings and irregular or lobulated surface
may indicate malignancy
• Margin of the swelling: The edge or margin may be flattened or projecting or
ill-defined. Well-defined or circumscribed margins indicate benign swellings
and ill-defined ones indicate inflammation or malignancies
• Movements: Movements of facial muscle may be absent in malignant tumour
infiltrating the facial nerve
• Examination of the related areas: This becomes important in the clinical
evaluation of the salivary swellings.
• Face needs to be examined for:
- Facial palsy in parotid swellings
- Swellings of other salivary glands
• Tongue for its paralysis in submandibular salivary swellings
• Oral cavity: The orifices of salivary glands (buccal mucosa opposite the
upper 2nd molar tooth for parotid duct, and floor of the mouth for the
submandibular duct) should be examined, and the two sides compared.
Look for oedema, inflammation, impacted stone, purulent discharge. If no
obvious pathology is found, the flow of saliva should be stimulated. The
flow of saliva can be stimulated in two ways:
- Applying pressure and massaging the salivary gland
- By placing some lime juice on the tongue and viewing the orifice
FIGURE 23.14 Recurrent swelling of right parotid.
Note
If the salivary gland is not obviously visible, but described to be appearing
only before or during meals, chewing a piece of lime would make it appear, a
foolproof test for a salivary duct obstruction. Free flow of clear saliva through
the orifice indicates that there is no obstruction of the duct.
Palpation
The swelling is palpated as described in Chapter 9, Lumps and Swellings.
Note
Benign tumours from deep lobe are immobile. Parotid swellings cannot be
moved beyond the zygoma, as the parotid fascia is attached to the zygomatic
process.
• Bidigital palpation
• Submandibular salivary gland swellings are bidigitally palpable
(palpation using two fingers)
Method:
Position of the patient: The patient’s head should be tilted to the affected side
to relax the musculature
Procedure:
Right submandibular gland: The gloved right index finger is introduced into
the mouth, the pulp of the finger being placed upon the internal surface of the
alveolus. The finger is passed backwards along the alveolus till its posterior
extremity. The tip of the finger is insinuated between the alveolus just behind the
last molar tooth and the side of the posterior third of the tongue, and rotated
anticlockwise through a right angle, so that the pulp gets directed downwards.
The gland is felt at this area. The gland is pushed with the left index finger from
outside, and its size, consistency, mobility and tenderness are assessed with both
the index fingers (Fig. 23.15). The left submandibular gland is palpated with
the gloved left index inside and the right index outside.
FIGURE 23.15 Bidigital palpation of right submandibular gland.
(This method is exclusively useful in differentiating the submandibular

salivary gland swellings from the lymph nodes of the neck, as the gland lies
on either side of the mylohoid muscle whereas the lymph node is superficial
to it)
• Salivary ducts should be bidigitally palpated (palpation with two fingers) in
their course for calculi
• Stensen’s duct lies about one fingerbreadth below the inferior border of the
zygomatic bone. The anterior part of the duct can be felt satisfactorily
between the index finger and thumb (Fig. 23.16), but major part of the
duct is made inaccessible by the masseter muscle
• Wharton’s duct lies in the floor of the mouth and is felt in the same way as
it is used for the submandibular gland, with the finger advancing towards
the frenulum of the tongue
FIGURE 23.16 Method of palpating Stenson’s duct.
(Palpation of the ducts is performed from the back towards the front of the
mouth to avoid displacement of a mobile stone into the gland substance)
Auscultation
Highly vascular tumours may produce bruit in the tumour, when auscultated with
a stethoscope.
Relevant areas
Face
The face is examined for the facial nerve function (e.g. facial nerve palsy is seen
in malignant tumours of parotid). Lacrimal glands are enlarged along with
salivary glands in Sjögren’s syndrome.
Oral cavity, nasal cavity and external autditory canal

• Oral cavity is systematically examined with special attention to the orifices of
the salivary ducts, for inflammation and discharges. Application of pressure
over the gland may express purulent discharge. Deep lobar swellings of
parotid gland should be assessed by intraoral palpation (Fig. 23.17). Tonsil
and lateral pharyngeal wall may get pushed inside by the tumours of deep
lobe of the parotid
• Nasopharynx is examined for nasopharyngeal tumours, as its secondaries in
Level II (Trotter’s triad) can masquerade parotid swelling
• External auditory canal is examined to eliminate infections, e.g. furuncle,
which can cause swellings of lymph nodes in the preauricular region
FIGURE 23.17 Intraoral palpation of deep lobe swelling of parotid gland.

Neck
The neck is examined systematically for lymph node enlargements secondary to
salivary gland tumours.
Abdomen
Examination of the abdomen both by inspection and palpation has to be done for
splenic enlargement (Frey syndrome).
Lymphatic system
(e.g. non-Hodgkin’s lymphoma of parotid). Examination of the liver and spleen
completes the lymphoreticular system, which is useful in diagnosis.
Systemic examination to rule out organ involvement in Sialosis is important.
CHAPTER 24
Thyroid
P. S. Venkatesh Rao
CHAPTER OUTLINE
24.1. Development of thyroid 349
24.2. Surgical anatomy of thyroid 349
24.3. Physiology 350
24.4. Diseases of thyroid 350
• Thyroglossal cyst / sinus / fistula 350
• Lingual thyroid 351
• Retrosternal ectopic / accessory thyroid 352
• Suppurative thyroiditis 353
• De Quervain’s thyroiditis 354
• Subacute lymphocytic thyroiditis and postpartum thyroiditis 354
• Hashimoto thyroiditis 354
• Riedel’s thyroiditis 355
• Neoplasms 355
• Adenoma 355
• Follicular carcinoma 355
• Papillary carcinoma 356
• Anaplastic carcinoma 357
• Medullary carcinoma 357
• Lymphoma 357
• Nontoxic goitre 358
• Thyrotoxicosis 359
24.5. Symptoms of thyroid diseases 360
• Thyroid 364
• Relevant areas 370
• General 373
24.1 Development of thyroid
The thyroid gland is derived from the epithelial proliferation called medial
anlage in the floor of the pharynx, as an offshoot of the primitive alimentary
tract, from a point called foramen caecum, at the junction of anterior two-thirds
and posterior one-third of the tongue in the midline. The median anlage as a
tubular structure descends from the floor of pharynx down into the neck, where
it is joined by a pair of lateral components developing from the ultimobranchial
bodies, which arise as a diverticulum of the fourth pharyngeal pouch. These
provide the neuroendocrine C cells.
The gland descends into the neck in front of the foregut, and lies anterior to
the trachea, and during this migration it is attached to its point of origin by a
narrow tube called thyroglossal duct. The thyroglossal duct disappears around 6
weeks of age. Any part of this duct may persist to form a ‘thyroglossal cyst’.
24.2 Surgical anatomy of thyroid

Thyroid is a butterfly-shaped gland with two lobes, one on either side of the
trachea, invested by pretracheal fascia, which sends septa into the substance of
the gland. It is attached to the larynx, which makes the gland rise on swallowing.
• Isthmus is the thyroid tissue which connects the two lobes of thyroid
• Pyramidal lobe is a vertical tongue of the thyroid and extends from the
isthmus towards the hyoid bone. It is a remnant of the embryological descent
of the gland
• Aberrant (ectopic) thyroid tissue may be found anywhere in the path of
descent, near the midline:
• If undescended, at the back of the tongue (lingual thyroid)
• If excess descent in the anterior mediastinum (retrosternal ectopic thyroid)
• Rarely elsewhere in the neck, chest or abdomen
Accessory thyroid tissue, in addition to normal thyroid can also occur in any
of these locations.
Relations
• Parathyroid glands, a pair on each side, are situated posterior to the lobes of
the thyroid and receive branches from the inferior thyroid artery
• External branch of superior laryngeal nerve is closely related to the superior
pole and its damage may lead to interference in high notes in speech and
singing
• Recurrent laryngeal nerve lies in the tracheoesophageal groove, and passes
between the branches of inferior thyroid artery, damage of which results in
hoarseness (unilateral damage) and stridor (bilateral damage)
Blood supply is very rich to the thyroid gland, derived from superior and
inferior thyroid arteries, which are branches of the external carotid artery and
thyrocervical trunk, respectively.
Venous drainage is through the superior, middle and inferior thyroid veins
draining into the facial, internal jugular and brachiocephalic veins, respectively.
Lymphatic drainage of the thyroid occurs through middle and lower deep
cervical (Levels 3 and 4), pretracheal, prelaryngeal (Delphic nodes), paratracheal
(Level 6) and mediastinal nodes.
Histology
The thyroid is composed of acini (follicles), which are spherical, and lined with
the epithelial cells. These cells secrete thyroid hormones, which are stored in the
colloid of the follicle. C cells, also called parafollicular cells, are found between
the follicles and they secrete calcitonin.
24.3 Physiology
Two hormones are secreted by the thyroid gland. They are:
• Thyroxin and its analogues
• Calcitonin
Thyroxin and its analogues

Follicular cells first synthesize a unique dimorphic glycoprotein, thyroglobulin
(colloid) that remains confined to the thyroid follicle except in certain thyroid
cancers (and hence may be used as a tumour marker) and in some cases of
Graves’ disease. Antibodies against thyroglobulin are found in Hashimoto"s
thyroiditis and Graves’ disease, and are of diagnostic significance.
Iodine trapped by follicular cells is bound to tyrosine on the thyroglobulin by
the enzyme peroxidase, forming monoiodotyrosine (MIT) and diiodotyrosine
(DIT). They are coupled to yield tri-iodotyrosine (T3 = MIT + DIT) and thyroxin
(T4 = DIT + DIT). T4 is converted into T3 both inside the thyroid and in the
periphery by 5-deiodinase. Lysosomal proteases release T3 and T4 from the
colloid. The thyroid hormones are regulated by hypothalamic-thyroid axis
through thyrotropin-releasing hormone (TRH) from the hypothalamus, which
promotes the release of thyroid stimulating hormone (TSH) from the pituitary. T3
and T4 in turn regulate the secretion of TRH and TSH (Fig. 24.1). Thyroid
hormones cause a variety of metabolic and physiologic effects, leading to
symptoms observed during excess release (thyrotoxicosis) and deficiency
(myxoedema).
FIGURE 24.1 Thyroid physiology.
There are three groups of actions of thyroxin:

1. Increased metabolic activity in all cells
2. Increased beta-adrenergic receptor sensitivity
3. Stimulation of growth during the growth period
Calcitonin
It acts to reduce the concentration of calcium, by inhibiting osteoclast-directed
bone absorption and by increased renal excretion of calcium.
Physiological demands of the thyroid are more during growth, pregnancy and
following trauma.
24.4 Diseases of thyroid
The diseases of the thyroid gland can be classified based on their aetiology Table
24.1.
TABLE 24.1
Aetiological Classification of Thyroid Disorders and Diseases
Aetiology Diseases
Congenital Persistence of duct Thyroglossal cyst / sinus / fistula
Failure of descent Lingual thyroid
Excessive descent Retrosternal ectopic thyroid
Inflammatory Acute Suppurative thyroiditis
Subacute De Quervain’s thyroiditis
Subacute lymphocytic thyroiditis and postpartum thyroiditis
Chronic Hashimoto thyroiditis
Riedel’s thyroiditis
Neoplastic Benign Adenoma
Malignant Follicular carcinoma
Papillary carcinoma
Anaplastic carcinoma
Medullary carcinoma
Lymphoma
Metabolic Nontoxic goitre Colloid goitre, nodular goitre, Graves’ disease, secondary thyrotoxicosis
Thyrotoxicosis
Thyroglossal cyst / sinus / fistula

• Persistence of part of the thyroglossal duct leads to formation of a
thyroglossal cyst
• It can lie anywhere along the course of the thyroglossal tract, which extends
from the foramen caecum in the posterior tongue down through the neck
along the anterior midline lying close to the hyoid bone up to the
suprasternal notch (Fig. 24.2)
• The entire duct can persist as a sinus (or fistula if it opens inferiorly)
• It occurs in early childhood or adulthood
FIGURE 24.2 Path of descent of thyroid gland.
Complications: Infection of cyst, thyroglossal fistula (See Ch. 11)
• A globular cystic swelling in the infrahyoid region (Fig. 24.3A), rarely above
the hyoid bone
• It lies in the midline or very close to it
• When infected, skin over the cyst is hyperaemic (Fig. 24.3B) and tender to
palpation
• When the infected cyst bursts spontaneously or is incised surgically, it results
in a sinus or a fistula if there is an open communication at foramen caecum
called thyroglossal fistula, discharging purulent fluid (Ref Fig. 11.12)
• The specific diagnostic test is the pulling up of the cyst or fistula on
protrusion of the tongue, rarely when the tongue is pulled with traction (Fig.
24.3C)
FIGURE 24.3A Thyroglossal cyst.

FIGURE 24.3B Infected thyroglossal cyst.
FIGURE 24.3C Thyroglossal cyst pull up on putting out the tongue.
• Sinogram or fistulogram may be useful
• Isotope scan (Fig. 24.3D) is conclusive
FIGURE 24.3D Isotope scan—thyroglossal cyst.
Treatment
• Uncomplicated cysts should be excised. The excision should include the body
of hyoid bone (Sistrunk’s operation)
• Infected cysts may have to be incised under antibiotic coverage to let out the
pus followed by excision at a later date. Incision of infected cyst has a high
incidence of forming a fistula (thyroglossal fistula)
• Sinus or fistula requires excision
Lingual thyroid
• Occurs due to the failure of descent of the thyroid tissue from its place of
origin at the junction of anterior two-thirds and posterior third of the tongue
• The normal thyroid is absent in the neck
• Difficulty in swallowing, with dyspnoea and occasional bleeding
• Clinical examination reveals a globular swelling in the midline of the
posterior part of the tongue (Fig. 24.4A)
FIGURE 24.4A Lingual thyroid Source: (Courtesy Dr K. Dakshinamoorthy).
• Radioiodine scan reveals the presence of the thyroid tissue (Fig. 24.4B) in the
posterior part of the tongue, with no isotope activity in the neck
• MRI is useful (Fig. 24.4C)
FIGURE 24.4B Isotope scan—lingual thyroid Source: (Courtesy Dr S. Devaji
Rao).
FIGURE 24.4C MRI—lingual thyroid.
Treatment
• Excision and reimplantation of the lingual thyroid in the neck, preferably
between the fibres of the sternomastoid muscle
Retrosternal ectopic/accessory thyroid

• Occurs due to excessive descent of the thyroid tissue into the superior
mediastinum, retrosternally
• Any disease of the thyroid can affect it and cause it to enlarge and become
symptomatic
A swelling in the suprasternal region with hypo- or hyperthyroid symptoms,
pressure symptoms
• X-ray of the chest (Fig. 24.5A) and isotope scan (Fig. 24.5B) reveal the
presence of the thyroid tissue in the lowest part of the neck, and in the
retrosternal region
• CT of the neck and thorax delineates the swelling better (Fig. 24.5C)

FIGURE 24.5A Chest X-ray—retrosternal goitre.

FIGURE 24.5B Isotope scan of retrosternal thyroid.
FIGURE 24.5C CT—retrosternal goitre.
Treatment
Excision of the retrosternal thyroid tissue if it shows signs of hyperactivity or
enlargement with pressure effects
Suppurative thyroiditis
• Uncommon disease
• Occurs due to pyogenic infections and rarely due to tuberculosis
• Often proceeds to an abscess
• Pain, fever, dysphagia, dysphonia, cough and history of recent upper
respiratory illness
• On examination, there is a warm and tender goitre especially in the midline
(isthmic) and on left side, with erythema of overlying skin (Fig. 24.6)
FIGURE 24.6 Suppurative thyroiditis.
• Leucocyte count and erythrocyte sedimentation rate (ESR) are elevated
• Ultrasonography (US) may be needed to identify an abscess
• Fine-needle aspiration cytology (FNAC) and culture of pus are necessary
Treatment
• Appropriate antibiotics may resolve the process
• Incision and drainage if abscess is formed
De quervain’s thyroiditis
• Uncommon acute inflammatory disorder caused by viral infection
• The inflammatory reaction is in the form of histiocytes, multinucleate giant
cells and granuloma formation
• It is also called subacute granulomatous thyroiditis
• Acute pain in the neck, with malaise and pyrexia, and thyrotoxicosis
following an episode of flu
• On examination, the thyroid is enlarged, tender and soft
• Lymph nodes may be enlarged and tender
• ESR may be elevated
• Thyroid hormones may show transient elevation with decreased TSH
• Thyroid antibodies are absent
Treatment
Analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs) will suffice, as
the disease is usually self-limiting
Subacute lymphocytic thyroiditis and

postpartum thyroiditis
These are considered by some as variants of Hashimoto thyroiditis but they are
usually transient. Postpartum thyroiditis (also called silent thyroiditis) occurs
within a year of pregnancy and lasts several weeks or months. They are painless
and present with hyperthyroidism initially, which is followed by hypothyroidism
and eventually often returns to euthyroid state.
Hashimoto"s thyroiditis
• An autoimmune disease of unknown aetiology also called chronic
lymphocytic thyroiditis
• Commonest cause of thyroiditis
• The thyroid is diffusely infiltrated by lymphoid and plasma cells with
destruction of thyroid follicles
• There may be family history of thyroiditis or other autoimmune diseases such
as diabetes, rheumatoid arthritis
• It may be associated with lymphoma of the thyroid
• Varying degrees of activity of the thyroid, but hypothyroidism is typical
• Clinical examination reveals a diffuse goitre, firm in consistency with an
irregular or bosselated surface (Fig. 24.6A)
FIGURE 24.6A Hashimoto"s thyroiditis.
• Thyroid hormones are decreased
• TSH levels are increased
• Antithyroid antibodies for thyroglobulin and microsomes are markedly
elevated
• Radioisotope scan shows less activity (Fig. 24.6B)

FIGURE 24.6B 99Tc scan—decreased activity of
hypothyroidism. Source: (Courtesy Dr K. M. Lakshmipathy)
Treatment
Thyroxin administration is required for life
Riedel’s thyroiditis
• Very rare disease of unknown aetiology
• Dense fibrosis of the gland and the surrounding tissues in the neck is
predominant
• May occur in isolation or with disorders such as retroperitoneal fibrosis,
mediastinal fibrosis or sclerosing cholangitis
• Rapidly increasing goitre with tracheal and oesophageal compression
• Clinical examination shows goitre, hard and woody on palpation
• Biopsy at surgery is required
• Histopathology examination of isthmusectomy specimen
Treatment
Isthmusectomy is used to release tracheal constriction
Neoplasms
Neoplasms of the thyroid are classified as shown in Algorithm 24.1.
ALGORITHM 24.1 Classification of thyroid neoplasms.
Adenoma
An autonomous lesion, which may show varying grades of thyroid activity
A solitary nodule or unilateral enlargement of the thyroid gland (Fig. 24.7)
FIGURE 24.7 Thyroid adenoma.
• Isotope scan may show a cold or euthyroid nodule
• US reveals a solid lesion
• FNAC is unreliable in differentiating from a carcinoma
Treatment
Excision by hemithyroidectomy is the treatment of choice for the fear of missing
malignancy
Follicular carcinoma
• A well-encapsulated solitary tumour of the thyroid follicles, distinct from an
adenoma
• The diagnosis is based on the extracapsular or venous invasion
• Histologically, this shows nuclear polymorphism and increased nuclear to
cytoplasmic ratio
• Haematogenous spread can occur especially to the bones
• A swelling of the thyroid gland limited to one lobe
• May present with metastases (Fig. 24.8). These have large vessels and are
warm, pulsatile and noncompressible
• Lymph node swellings of the neck rarely occur
FIGURE 24.8 Metastases in the skull secondary to follicular carcinoma of

thyroid.
• Thyroid hormones remain normal
• Serum thyroglobulin is often raised
• FNAC is useful, but unreliable in differentiating it from an adenoma
• US shows a solid lesion
Treatment
• Total thyroidectomy is the treatment of choice
• Completion total thyroidectomy has to be done, if the diagnosis is made after
hemithyroidectomy
• Postoperative thyroxin replacement at a high suppressive dose is mandatory
• 131I ablation is warranted for any residual thyroid tissue and distant
micrometastases
• Large metastases need excision
Papillary carcinoma
• Two-thirds of all thyroid malignancies are papillary type, and have multifocal
origin
• Histologically, they show finger-like papillae and psammoma bodies are
typical
• The tumour spreads predominantly through lymphatics
• A slow-growing (over months/years) swelling of the thyroid gland involving
one or both lobes (Fig. 24.9A)
• Lymph node swellings of the neck may occur
FIGURE 24.9A Papillary carcinoma of thyroid with cervical lymph node
metastases Source: (Courtesy Dr V. Srinivasan).
• Thyroid hormones remain normal
• Serum thyroglobulin is often raised
• FNAC is useful
• US and MRI (Fig. 24.9B) shows a solid lesion and enlarged lymph nodes if
present
FIGURE 24.9B MRI—papillary carcinoma with lymph node metastases.
Treatment
• Total thyroidectomy with central compartment dissection is the treatment of
choice
• Postoperative thyroxin replacement at a high suppressive dose is mandatory
• Modified radical neck dissection if lymph nodes are involved
Anaplastic carcinoma
• Aggressive tumours believed to arise from unrecognized differentiated
tumours
• Common in endemic areas and present in the elderly over the age of 60
A hard woody enlargement of the thyroid (Fig. 24.10) fixed to the surrounding
structures
FIGURE 24.10 Anaplastic carcinoma of thyroid Source: (Courtesy Dr R.

Rajaraman).
DD: Riedel’s thyroiditis, lymphoma, calcified lesions
FNAC or open biopsy is confirmatory
Treatment
Excision of tumour as much as possible especially the isthmus, with
radiotherapy
Medullary carcinoma
• Malignancy derived from C cells
• Incidence of 5–10% of thyroid malignancies
• They produce calcitonin to detectable levels in blood
• Majority of them occur sporadically and the rest have a familial tendency
• Familial medullary carcinoma has some peculiar features:
• Autosomal dominant inheritance
• Multifocal origin
• Can be associated with pheochromocytoma and parathyroid hyperplasia
(multiple endocrine neoplasia [MEN] 2 syndrome)
• A lump in the neck with lymph node (Fig. 24.11) or distant metastases
• Diarrhoea can occur due to high levels of calcitonin
• Familial history is elicited
FIGURE 24.11 Medullary carcinoma of thyroid with lymph node
metastases Source: (Courtesy Dr R. Rajaraman).
• Plasma calcitonin and carcinoembryonic antigen (CEA) may be elevated
• FNAC of the thyroid mass or cervical lymph nodes is necessary
• Whole body isotope 99Tc scan is useful in identifying distant metastases
• Plasma and urine metanephrine, urinary catecholamines to detect
pheochromocytoma
• Serum parathormone to detect hyperparathyroidism
• Ret test (genetic screening for ret point mutations) for MEN 2
Treatment
• Total thyroidectomy and thyroxin replacement
Local recurrence requires surgery and distant metastases radiotherapy.
Lymphoma
• Extremely rare in the thyroid (less than 1% of the thyroid malignancies)
• Typically, affects the elderly females
• Longstanding Hashimoto thyroiditis is the only known risk factor
• A rapidly growing nodule
• Hard woody enlargement (Fig. 24.12) of the thyroid fixed to the surrounding
structures, if Hashimoto thyroiditis pre-exists
• Cervical lymph nodes may be palpable
FIGURE 24.12 Non-Hodgkin’s lymphoma of thyroid Source: (Courtesy Dr R.

Rajaraman).
DD: Riedel’s thyroiditis, anaplastic carcinoma

FNAC or open biopsy is confirmatory
Treatment
Concurrent chemotherapy and radiation is the treatment of choice
Nontoxic goitre
An enlargement of the thyroid is named goitre
It can present as:
1. Diffuse goitre: A simple swelling of the thyroid caused by hyperplasia due to
stimulation of the thyroid by raised levels of TSH, with female preponderance
in the ratio of 6:1
• The swelling may be transient as in physiological goitre or permanent as in
colloid goitre
• The causes are:
• Iodine deficiency in endemic areas (gland’s attempt to extract iodine from
a diet insufficient in iodine)
• Physiologic demands (puberty and pregnancy, following severe illness,
physical and emotional stress)—raised TSH concentration, stimulation of
thyroid by beta-human chorionic gonadotropin (HCG) (structurally similar to
TSH)
• Drugs and dietary factors (e.g. goitrogens—drugs and chemicals found in
foods such as cabbage)
• Enzyme malfunction in the thyroid (dyshormonogenetic goitre)
(peroxidase deficiency, as part of Pendred syndrome—associated with
deafness)
2. Multinodular goitre: The constant stimulation and nonuniform regression
causes multinodularity. Five to ten per cent of multinodular goitres undergo
malignant change. Chronic thyroiditis or toxic goitre after prolonged
treatment with drugs or after radioiodine ablation may present as a nodular
goitre
• Diffuse goitre:
• A painless enlargement of the thyroid, with gradual progression
• Clinical examination may reveal uniform enlargement (Fig. 24.13) of the
thyroid with smooth surface
• Multinodular goitre:
• Painless enlargement with gradual progression
• Dyspnoea (due to compression of the trachea) and dysphagia (due to
compression of the oesophagus)
• Clinical examination may reveal a solitary nodule (Fig. 24.14) or multiple
nodules (Fig. 24.15)
• Trachea may be shifted from the midline due to uneven enlargement of the
gland
• There may be a retrosternal extension larger than the goitre in the neck
• Distended veins may be seen due to obstruction of the superior vena caval
system
• Regional lymphadenopathy and hoarseness of voice suggest malignant
change
FIGURE 24.13 Diffuse enlargement of thyroid.

FIGURE 24.14 Solitary thyroid nodule.
FIGURE 24.15 Multinodular goitre.
• Thyroid function tests to establish the activity of the thyroid (euthyroid,
hyperthyroid or hypothyroid)
• US identifies cysts from solid lesions, size and extent of the goitre
• X-ray of the soft tissues of the neck is useful to identify tracheal shift or
compression
• FNAC is indicated in doubtful lesions to rule out malignant change
• MRI (Fig. 24.16) and isotope scans are useful in identifying retrosternal
extensions
FIGURE 24.16 MRI—diffuse goitre.
Treatment
• No treatment is required for small euthyroid goitres
• Hormone supplements for hypothyroid goitre
• Surgery is required for hyperthyroid and pressure causing multinodular
goitres:
• Hemithyroidectomy for hyperthyroid goitres (unilobular lesions or solitary
nodule of one lobe)
• Total thyroidectomy for bilobar multinodular goitre to prevent pressure
effects and for fear of suspected malignant transformation, followed by
life-long thyroxin
Thyrotoxicosis
Thyrotoxicosis is a symptom complex, which results from peripheral actions of
increased levels of circulating thyroid hormones, with a female preponderance.
The causes are:
• Diffuse enlargement of thyroid: Primary thyrotoxicosis or Graves’ disease
(an autoimmune disease with autoantibodies against TSH receptors that act
as long-acting thyroid stimulators—LATS)
• Toxic multinodular goitre: Plummer syndrome
• Toxic solitary thyroid nodule
Secondary thyrotoxicosis: The differentiating features of primary and
secondary thyrotoxicosis are given in Table 24.2.
TABLE 24.2
Differentiating Features of Primary and Secondary Thyrotoxicosis
Primary thyrotoxicosis Secondary thyrotoxicosis
Usually in the young (15–45 years) women Occurs later in life between 45 and 65 years
Symptoms appear before swelling and are more severe Symptoms are less severe and appear long after the swelling
Thyroid is uniformly enlarged and smooth Thyroid is larger in size, nodular and asymmetric
Tremors, exophthalmos and eye signs are common Cardiac symptoms are common
• Graves’ disease: Smooth generalized enlargement of the thyroid gland (Fig.
24.17) with ophthalmic features (Graves’ ophthalmopathy) and dermatologic
symptoms (Graves’ dermopathy). Associated autoimmune diseases (e.g.
vitiligo, rheumatoid arthritis)
• Toxic multinodular goitre: Multinodular thyroid swelling, with cardiac
arrhythmias and heart failure
• Toxic solitary thyroid nodule: A solitary swelling in one lobe of thyroid, with
cardiac manifestations
FIGURE 24.17 Graves’ disease.
• Thyroid function tests to establish its overactivity
• Thyroid autoantibodies may be present in autoimmune disorders
• Radioisotope scans show activity of nodule (A and B)

FIGURE 24.18 99Tc scan—diffuse toxic goitre Source: (Courtesy Dr K. M.
Lakshmipathy).
FIGURE 24.19A 99Tc scan—hot nodule Source: (Courtesy Dr K. M.
Lakshmipathy).

FIGURE 24.19B 99Tc scan—cold nodule Source: (Courtesy Dr K. M.
Lakshmipathy).
Treatment
• Antithyroid drugs are required to manage thyrotoxicosis
• Beta-blockers are useful in managing the effects of T4 on the sympathetic
system
• 131I radio ablation therapy is a convenient and permanent therapy
• Thyroidectomy is indicated when the enlargement is huge and causes pressure
effects, and also for toxic multinodular goitre. Failure of compliance to
treatment is also an indication for surgery
24.5 Symptoms of thyroid diseases

The presenting complaints of patients with thyroid diseases are:
• Swelling in the region of the thyroid
• Sinus or fistula in the midline of the neck
• Pressure symptoms
• Cardiac symptoms (thyrocardiac disease)
• Ophthalmic symptoms (ophthalmopathy)
• Dermatologic symptoms (dermopathy)
• General symptoms of thyroid malfunction
• Swellings in other areas of the neck or elsewhere (metastases)
Swelling in the region of the thyroid
The commonest presentation of a thyroid disorder is in the form of a swelling in
the lower part of the neck, in the region of the thyroid, just lateral to the midline.
The swelling is in different forms:
• Single nodular swelling: Solitary thyroid nodule
• Multiple nodular swellings (usually on both sides): Multinodular goitre
• Smooth enlargement of the thyroid: For example Graves’ disease (need not
be symmetrical)
• Smooth globular swelling in the midline: Thyroglossal cyst
Sinus or fistula in the midline of neck

Thyroid pathologies can present in the form of a discharging sinus or fistula (e.g.
thyroglossal fistula).
Pressure symptoms
Since thyroid gland is located in the neck closely related to the structures such as
trachea and oesophagus, pressure symptoms may be caused by:
• Goitres of massive size
• Goitres with large intrathoracic extension
• Chronic thyroiditis
• Infiltration by thyroid malignancies
And the symptoms related to pressure on the neighbouring structures are:
• Dyspnoea (choking sensation with cough)—pressure on trachea:
• Positional dyspnoea (on flexing the neck forwards or laterally)
• Nocturnal dyspnoea (on lying flat at night)
• Dysphagia—pressure on oesophagus
• Dysphonia (hoarseness of voice)—pressure or infiltration of recurrent
laryngeal nerve
• Stridor (whistling sound)—narrowing of trachea due to pressure or malignant
infiltration of trachea
Cardiac symptoms
Cardiac symptoms are associated with thyrotoxicosis. Hypermetabolism of the
peripheral tissues increase both the metabolic and nonmetabolic (heat loss)
circulatory load, whereas direct effect of the thyroid hormones on the
myocardium increases the force, velocity and rate of ventricular contraction. The
symptoms and signs are tabulated in Table 24.3.
TABLE 24.3
Symptoms and Signs of Cardiac System Associated with
Thyrotoxicosis
Symptoms Signs
•Palpitation •Sinus tachycardia

•Precordial chest pain •Tachydysrhythmias
•Atrial fibrillation
•High-output cardiac failure
•Digitalis resistant cardiac failure
Ophthalmic symptoms
The eyes may be involved in thyrotoxicosis, possibly due to a cross reaction
between thyroid stimulating antibodies in the eye muscles and intra-orbital
tissues. The ocular signs are thought to result from sympathetic overstimulation,
and subside when thyrotoxicosis is corrected. The symptoms and signs of eye
involvement are tabulated in Table 24.4.
TABLE 24.4
Symptoms and Signs of Eye Involvement Related to Thyrotoxicosis
Symptoms Signs
•Double vision Grade 1: Mild
•Grittiness in the eye
•Protrusion of eyes •Upper sclera visible due to eyelid retraction
(exophthalmos) •Lid lag on looking down
•Characteristic stare with widened palpebral fissures
Grade 2: Moderate
•Exophthalmos and failure to wrinkle the brow on upward gaze
Grade 3: Severe
•Ophthalmoplegia (palsy of superior and lateral recti and oculomotor nerves)
•Congestive oculopathy (chemosis, conjunctivitis, periorbital swelling, corneal
ulcerations, optic neuritis, optic atrophy)
Grade 4: Progressive
•Progressive protrusion of eye balls (malignant exophthalmos)
Note
The term exophthalmos is used in thyrotoxicosis, which is bilateral and the
term ‘proptosis’ denotes protrusion of the eyes due to numerous other intra-
orbital and periorbital causes and is often unilateral. Werner’s classification
has grades 0–6.
Dermatologic symptoms
Dermatologic symptoms are common in Graves’ disease (Graves’ dermopathy),
and usually manifest over the dorsum of feet and legs, and is called pretibial
myxoedema. The affected area is well demarcated from the normal skin with a
characteristic appearance. It is raised, thickened, has a peau d’orange
appearance, may be pruritic and hyperpigmented. Dermal changes may be
accompanied by clubbing (thyroid acropachy) and signs of other associated
autoimmune diseases.
In hypothyroidism (e.g. autoimmune) there is a generalized myxoedema.
General symptoms of thyroid malfunction

The general symptoms vary according to the activity of the thyroid gland and the
effect of the thyroid hormones on tissues. Excessive activity is collectively
termed hyperthyroidism and reduced activity hypothyroidism.
Note
Goitre with hypothyroidism may occur in thyroiditis, dyshormonogenesis,
multinodular goitre and drug-induced goitre.
The symptoms of thyroid malfunction are tabulated in Table 24.5.
TABLE 24.5
Symptoms of Thyroid Malfunction
Symptom Hyperthyroidism Hypothyroidism

Change in weight Weight loss in spite of excessive appetite Weight gain in spite of decreased appetite
and appetite
Tolerance to Intolerance to heat Intolerance to cold
temperature
Neuromuscular Nervousness, anxiety, irritability, insomnia, Lethargy, slowing of intellectual and motor
tremors and muscle weakness activity, myalgia, fatigue
Cardiovascular Palpitations, dyspnoea on exertion, chest pain Bradycardia, dyspnoea, pedal oedema
Ophthalmic Poor visual acuity, double vision, grittiness in the Periorbital puffiness
eye
Gastrointestinal Frequent passage of stools Constipation
Gynaecological Oligomenorrhoea, amenorrhoea Menorrhagia
Dermatological Warm and moist skin, fine silky hair Dry skin, loss of hair especially outer
eyebrows
Orthopaedic Arthralgia
Voice Coarse voice
Pain
Pain is a very rare accompaniment of the thyroid pathologies excepting in those
of infective inflammatory aetiology such as de Quervain’s thyroiditis.
The symptom analysis is tabulated in Table 24.6.
TABLE 24.6
Analysis of Symptoms of the Thyroid Disorders
Incidence
Rate of
Lesion Pain Other features
F:M Growth
Age
ratio
Simple Goitre
Diffuse goitre 5–20 5:1 Very slow Painless
Multinodular goitre 20–40 6:1
Thyroiditis
Acute and subacute 30–50 2:1 Rapid Pain, fever Preceding URI, mild toxicity
thyroiditis
Chronic
Hashimoto thyroiditis At menopause Variable Mild pain Hypothyroid, associated autoimmune
diseases
Riedel’s thyroiditis 40–70 Rare Slow Painless Early pressure symptoms
Diffuse toxic goitre 20–40 8:1 Thyrotoxicosis
Neoplastic
Adenoma 20–40 4:1 Slow Usually
painless
Papillary carcinoma 30–50 4:1 Pain in late
stages
Follicular carcinoma 40–60 3:1 Bone pain (metastases)
Anaplastic carcinoma 50–70 1.5:1 Rapid Pain present Early distant metastases
Medullary carcinoma 50–70 3:1 Family history, MEN 2, metastases
(nonfamilial)
Lymphoma 50–70 1:3 (rare) Pain in late Preceding Hashimoto thyroiditis
stages
Note
Endemic, sporadic, drug-induced and multinodular goitres, solitary thyroid
nodule, early thyrotoxicosis and Hashimoto thyroiditis may present without
any symptom excepting a swelling in the thyroid.
Eliciting history
General particulars
• Age: Thyroglossal cyst is common in young age; simple goitre is more
common at puberty and malignancies are more common in the elderly
• Sex: Most thyroid disorders are common in females
• Place of residence: Iodine deficiency goitres are endemic in some areas such
as Himalayas, Nilgiris in India and mountainous areas in the world. There is
a higher incidence of thyrotoxicosis, thyroiditis, thyroid tumours in these
areas

Swelling
This will give the duration of the present illness—short duration represents
acute pathology such as acute infections (e.g. De Quervain’s thyroiditis), and
carcinomas (e.g. anaplastic carcinoma) or a haematoma in a pre-existing lesion
and long duration indicates chronic pathologies such as simple colloid goitre,
multinodular goitre, chronic thyroiditis and benign tumours such as adenoma.
Swellings presenting soon after birth or in young age may be congenital in
aetiology (e.g. goitres of cretinism, thyroglossal cyst, lingual thyroid)
• Site of swelling: Where did the patient notice the swelling first?
Tumours or solitary cysts develop as unilateral swelling in one of the lobes,
i.e. on one side of the neck or midline (e.g. lesion in the isthmus). Bilateral
development of swelling of the thyroid is seen in other causes of goitre, though
this may be symmetrical or asymmetrical
Stress and anxiety may precipitate thyrotoxic goitre. Viral upper respiratory
infection usually precedes De Quervain’s thyroiditis. Trauma to the neck may
lead to a haematoma
• Variation in size: Does the lump remain the same in size always or shows
some variation?
Non-neoplastic thyroid swellings may show regression in size, in response to
the therapy, but neoplasms show a steady increase in size. The rate of
progression in size is a useful indicator, as rapid progression in size represents
malignancy (e.g. anaplastic tumours), slow progression indicates a benign
disease (e.g. adenoma), and a sudden progression may indicate haemorrhage in a
cyst and a change from slow to rapid progression indicates malignant change or
dedifferentiation of a differentiated cancer
Discharge from external sinus / fistula

• Nature of discharge: Was or is the swelling painful and does or did it
discharge any fluid at any time?
Burst thyroglossal abscess discharges pus through the overlying skin, in the
form of a sinus or fistula (e.g. thyroglossal sinus or fistula)
• History of previous surgery or trauma: Did the patient undergo any
surgery in the neck or did he sustain any injury?
Incision and drainage of thyroglossal cyst is known to result in a sinus or
fistula. Thyroglossal fistula is also known to recur after surgery
Pressure symptoms
• Dyspnoea: Does the patient have difficulty in breathing? If so, is it related
to any posture?
Any thyroid swelling can press the trachea or even compress it almost
circumferentially and cause difficulty in breathing. Since, thyroid swellings are
predominant on the sides of the trachea, the dyspnoea is pronounced when the
patient lies on his or her sides or on the side of a unilateral goitre. Severe
narrowing of the trachea can create noise during breathing, called stridor.
Malignant swellings infiltrate the trachea and cause the same effect
• Dysphagia: Does the patient have difficulty in swallowing?
A thyroid swelling due to its proximity to the oesophagus can press the
oesophagus from the sides and cause dysphagia, more so when it is malignant
• Hoarseness: Does the patient complain of change in voice?
Hoarseness of voice is seen with patients with hypothyroidism and also when
malignancies infiltrate or press on the recurrent laryngeal nerves which run in
the tracheoesophageal grooves. Longstanding multinodular goitre or Hashimoto
thyroiditis developing hoarseness should indicate malignant change
Cardiac symptoms
• Cardiac symptoms: Does the patient complain of symptoms such as
palpitations, chest pain, swelling of the feet, related to cardiac system?
Cardiac symptoms such as palpitations and chest pain can, and those of
cardiac failure such as dyspnoea, pedal oedema etc., manifest with
thyrotoxicosis and may indicate the activity of the lesion
Ophthalmic symptoms
• Ophthalmic symptoms: Does the patient have any symptom related to the
eyes?
Development of symptoms related to the eye such as diplopia, diminution of
visual acuity may be indicative of thyrotoxicosis
Dermatologic symptoms
• Skin changes: Does the patient complain of any changes in the skin?
Variety of dermal changes are seen both in hyperthyroidism and
hypothyroidism
General symptoms
The examiner should be familiar with the general symptoms of thyroid diseases
and should direct questions in relation to those.
Swellings in other parts of the neck

• Swellings in the neck: Does the patient complain of any other swelling in
the neck?
Lymph node swellings can occur as metastatic nodes secondary to thyroid
malignancies or as part of lymphoma of the thyroid
Pain
Pain is an uncommon symptom of thyroid disorders.
• Nature of pain: Was or is the swelling painful and how severe is it?
Acute and subacute thyroiditis are associated with the pain of varying
intensity and nature
• Duration of pain: Was the pain present along with the onset of the swelling
or did it precede or follow the appearance of the swelling?
Pain and prodromal symptoms suggest viral thyroiditis, and development of
pain in a pre-existing swelling suggests malignancy, or haemorrhage in a cyst.
Pain may follow FNAC
• Precipitating factors: What is aggravating the pain?
Pain may be felt only on deglutition. Pain on movements of the neck may
indicate infiltrating malignancies of the thyroid
• Radiation of pain: Is there any radiation of pain?
Pain of thyroid pathology may radiate to the ears or jaws

Associated fever may indicate an infective pathology (e.g. suppurative or viral
thyroiditis)
• Appetite and weight: Is there any change or loss of appetite and weight in
Loss of appetite and weight are indicative of illnesses such as malignancies.
Increased appetite and weight loss is seen in hyperthyroidism and the reverse in
hypothyroidism
• Treatment for the illness: Has any treatment been given for the present
illness?
a clearer picture of diagnosis (e.g. intake of goitrogens, antithyroid drugs can
alter the signs and symptoms; treated primary toxic goitre may feel nodular;
recurrence of goitre may recur after hemi / partial thyroidectomy)
• Past history: Was there any other illness in the past, which required any
treatment? Was there exposure to radiation?
If the patient had suffered any other illness in the past, which required any
treatment (e.g. radiation to head, neck or thymus in the childhood can predispose
to thyroid malignancy)
Many thyroid diseases run in families (e.g. iodine or enzyme deficiency,
primary thyrotoxicosis, medullary carcinoma, various autoimmune disorders
associated with Hashimoto thyroiditis)
• Personal history: Questions regarding personal habits:
Personal habits such as smoking and drinking alcohol do not have any direct
relationship to thyroid pathologies, but dietary history has a very great relevance
(e.g. iodine deficient diet, goitrogenics in diet)
• Any other relevant question: This is for the examiner (clinician) to decide
likely exposure to tuberculosis
Thyroid
The examination of the patient should be carried out in the following steps:
1. Inspection
2. Palpation
3. Percussion
4. Auscultation
Pre-requisites
• Position of the patient: Patient should be made to sit comfortably on a chair,
with his or her arms down and the neck extended
• Position of the examiner: The examiner should sit comfortably and the
patient’s face and neck should be at the examiner’s eye level (Fig. 24.20)
• Adequate illumination is necessary
• Adequate knowledge of the thyroid and its related anatomy is mandatory
FIGURE 24.20 Examination of thyroid gland.
Inspection
The examiner should never be hasty to touch the patient with an urge to make
the diagnosis. Inspection forms the first part of the examination. The points to
note during inspection are:
• Location or site of swelling: The location of the swelling is observed in
relation to the anatomical landmarks, both from the front and sides. Swelling
located in the region of the thyroid, or in the path of descent of the thyroid
(e.g. thyroglossal cyst—suprahyoid or infrahyoid, retrosternal goitre). In
obese and short-necked individuals, the thyroid gland is more visible by
Pizillo’s method (the patient should place his or her clasped hands behind his
or her head on the occiput, and push back against them with his or her head)
(Fig. 24.21)
• Number of swelling: The number gives a clue to diagnosis:
• Solitary swellings (e.g. thyroglossal cyst in the midline, solitary thyroid
nodule lateral to the midline)
• Multiple swellings: Unilateral or bilateral (e.g. multinodular goitre) (Fig.
24.15)
• Shape of the swelling: Shape is three dimensional, but can be described in
descriptive terms such as butterfly shaped, oval, globular, irregular, etc.
FIGURE 24.21 Pizillo’s method.
• Symmetrically enlarged butterfly shaped on both sides (e.g. diffuse goitre)

• Asymmetrical:
- Unilateral, single, oval or globular (e.g. solitary nodule)
- Multiple nodules (e.g. multinodular goitre)
- Irregular swellings (e.g. multinodular goitre, malignancies)
• Size of the swelling: Lumps of thyroid origin have three dimensions and all
the three should be visually estimated and noted down
• Skin over the swelling: Careful attention has to be given to the skin over the
• Colour: Redness indicates acute inflammation (e.g. acute thyroiditis)
• Texture of skin: Shiny glistening skin over the swelling indicates the
stretching of skin, oedema of the skin over the swelling (e.g. infected
cyst). Tethering of skin suggests malignancy
• Changes on the surface: Prominent scars (e.g. indicate previous surgery),
fistula (e.g. thyroglossal fistula)
• Prominent veins: Engorgement of the veins in the subcutaneous plane may
indicate fast-growing tumour creating venous blockage (e.g. large
thyromegaly obstructing the superior vena caval system) (Fig. 24.22A).
This can be confirmed by asking the patient to lift both arms so as to touch
the sides of his or her face, and maintain for a minute (Fig. 24.22B).
Prominence of veins indicates superior vena caval obstruction at the
thoracic outlet (Pemberton’s sign). When the intrathoracic extension is
large and occludes the thoracic outlet ‘thyroid cork phenomenon’, the
face looks congested, swollen and unhealthy called ‘facial plethora’
• Horner syndrome (Fig. 24.22C) suggests involvement of sympathetic
trunk. It is characterized by:
- Slight sinking of the eyeball into the orbit (enophthalmos due to paralysis
of Muller’s muscle)
- Drooping of upper eyelid (pseudoptosis due to sympathetic trunk
paralysis)
- Contraction of pupil ( myosis due to paralysis of sympathetic fibres)
- Absence of sweating (anhidrosis)
- Flushing of face and nasal congestion due to vasodilatation
• Surface of the swelling: The surface of the swelling provides some indication
of its aetiology, and is described in easily understandable terms such as
smooth and regular, rough and irregular or in any combination:
• Smooth surface indicates cystic swellings, diffuse goitre
• Irregular or lobulated surface may indicate multinodularity
• Margin of the swelling:
• The edge or margin may be flattened or projecting, well defined or ill
defined
• Well-defined or circumscribed margins indicate benign swellings
• Ill-defined margins indicate poorly differentiated malignancies (e.g.
anaplastic carcinoma)
FIGURE 24.22A Prominent veins due to thoracic outlet obstruction by
large thyroid swelling.
FIGURE 24.22B Method of eliciting Pemberton’s sign.
FIGURE 24.22C Horner syndrome.
If the lower margin of the goitre is not seen it should be looked for during
deglutition.
• Movements: Since the thyroid is enclosed by the pretracheal fascia attached
to the oblique line on the thyroid cartilage and the arch of cricoid cartilage,
the swelling moves with deglutition (Fig. 24.22D)
FIGURE 24.22D Thyroid moving up on deglutition.
Note
• Subhyoid bursa, pretracheal and prelaryngeal lymph nodes and swellings of
larynx and trachea (e.g. laryngocele), which are also enclosed in the
pretracheal fascia will move with deglutition.
• Thyroglossal cyst moves up with protrusion of the tongue.
• A goitre which is very large or fixed or with large retrosternal component
may not move with deglutition.
Palpation
Patient continues to be seated with arms down and neck now slightly flexed,
instead of the extended position used for inspection and the face rotated to the
side under palpation to relax the sternomastoid muscle on that side.
• Palpation of the skin over the swelling:
• Warmth: In abscess and acute thyroiditis the thyroid feels warm, when felt
by the back of the hand
• Tenderness: Thyroid swelling is tender to palpation in thyroiditis and
abscess, elicited by gentle palpation
• Skin involvement is tested by two methods:
- Gliding test (Fig. 24.23)—the skin is rolled over the swelling to see
whether it is fixed or not
- Pinching test (Fig. 24.24)—the skin is pinched with the thumb and the
index finger to see its adherence to the lump
• Palpation of the thyroid gland: Examination should be done both from the
front and from behind:
FIGURE 24.23 Gliding test for assessing skin involvement.

FIGURE 24.24 Skin pinching test for assessing skin involvement.
• From behind: The examiner should go behind the seated patient and the
patient is asked to flex the neck slightly. The examiner should keep both the
hands on the sides of the neck, with the thumbs on the nuchal line and the
pulps of the fingers on the lobes of thyroid. The gland is palpated by running
the pulps of the fingers on them (Fig. 24.25)
• From front: The examiner should stand in front of the seated patient, and
each lobe is palpated with the thumb, right thumb for the right lobe and
left thumb for the left lobe. Next, the lobes are pushed individually to one
side for palpation (Lahey’s method). For palpating the left lobe, the
examiner should push the lobe laterally by the left hand, and the lobe is
palpated with the right hand (Fig. 24.26). For the right lobe, the lobe is
pushed laterally by the right hand and is palpated with the left hand. A
unilateral goitre can also be palpated when standing on the opposite side
of the patient
FIGURE 24.25 Examination of thyroid from behind.
FIGURE 24.26 Lahey’s method of examination of thyroid.
The following are noted; inspection findings of number, shape etc. are
confirmed:
• Site: It is determined whether the whole of the thyroid is enlarged or there is a
localized swelling
• Exact size: The exact size is determined in two directions (measured by tape
—Fig. 24.27A), and also the circumference of the neck will help (Fig.
24.27B)
• Surface: Assessed by running the pulp of the examining fingers over the
swelling. Otherwise, the patient may be asked to swallow while palpating the
gland with a thumb, with the gland between the thumb and other fingers
(Crile’s method—Fig. 24.28)
• Margins: Determined by running the index finger along the margins (Fig.
24.29). When the sternomastoid muscles are over the thyroid swelling, the
muscles can be displaced laterally by the palpating fingers or by the other
hand. Starting high in the neck to ensure that a high-placed goitre is not
missed, the fingers are moved laterally starting from the cricoid cartilage,
then to the upper border of the isthmus inferior to it and then along the
borders of the thyroid. The fingers are moved in a circular and rubbing
movement. Then, with the hands held steady, the patient is asked to swallow
repeatedly
• Palpation of lower border of the thyroid: The lower border is generally felt in
the neck close to the suprasternal notch. This is determined by placing the
index finger on the lower border of the gland (Fig. 24.30). When it is not felt,
the neck should be hyperextended. If still not palpable, the patient is asked to
swallow and if the lower border is now felt, it indicates small amount of
retrosternal extension. In large extensions the lower border is never felt
• Consistency: This is determined by applying firm pressure on the swelling
(e.g. benign tumours are firm and malignant tumours are hard in consistency)
• Mobility of overlying skin: Skin over the swelling is pinched up. If it is
indurated and fixed, it cannot be pinched up, and it may indicate an
underlying malignancy or inflammation. Thyroglossal cyst moves up with
protrusion of the tongue and an upward tug is felt if it is held back between
the fingers pinching above it (Fig. 24.31)
• Plane: Patient is asked to push chin down against resistance thus causing
contraction of both sternocleidomastoids and strap muscles. Thyroid
swellings, lymph nodes etc. that lie deep to these muscles become less
prominent
• Palpation for its mobility: The swelling is held between the thumb and index
finger and moved in all directions. Lack of mobility indicates fixity to deeper
structures (e.g. malignant tumours)
• Fixity to trachea or larynx: Fixity to trachea or larynx leads to differential
mobility in transverse direction but not in vertical direction
• Fixity to sternomastoid: Fixity to sternomastoid is checked by asking the
patient to swallow while pinching the relaxed muscle and feeling the pull on
the muscle by the adherent thyroid
• Kocher’s test: This test is used to detect narrowing of the trachea due to the
pressure effect of the goitre. By application of pressure on both lobes of a
goitre, the trachea gets further narrowed and causes the characteristic noise
of breathing ‘stridor’ (Fig. 24.32)
• Testing the surrounding structures:
• Tracheal deviation: When the thyroid swelling is unilateral and the
trachea is visible, the index finger and the ring finger are kept on the
heads of the clavicles and the middle finger is run along the trachea and its
rings starting as high as possible, till it reaches the suprasternal notch. If
the finger reaches the midline, there is no tracheal shift. If the finger
reaches close to one of the clavicular heads, the trachea is considered
deviated to that side (Fig. 24.33). When the trachea is covered by the
thyroid tissue, the trachea is felt in the midline at the suprasternal notch,
and the deviation assessed.
FIGURE 24.27A (A) Measuring the vertical enlargement of thyroid. (B)
Measuring the circumference of neck.
FIGURE 24.28 Crile’s method.
FIGURE 24.29 Feeling the margins of the thyroid swelling.
FIGURE 24.30 Palpating the lower border of thyroid to determine.

FIGURE 24.31 Feeling of upward tug on thyroglossal cyst.
FIGURE 24.32 Kocher’s test for stridor.
FIGURE 24.33 Method of palpating the trachea.
Note
A large isthmic nodule or a retrosternal extension with gross deviation can
make it difficult to palpate the trachea. Auscultation for tracheal sounds helps
to locate the trachea.
• Muscles: Sternomastoid muscles may become thinned out due to large

thyroid swellings stretching them. The bulk and the power can be tested by
asking the patient to turn the head to one side against resistance, applied by
the examiner’s hand (Fig. 24.34).
• Arteries: Normally, the common carotid artery is felt at the level of the upper
border of thyroid cartilage over Chassaignac tubercle on the transverse
process of C6 vertebra (Fig. 24.35). This gets displaced posteriorly by a
benign thyroid swelling. Malignant swellings of thyroid may infiltrate the
carotid sheath and the carotid pulse may become impalpable (Berry’s sign).
FIGURE 24.34 Feeling the bulk and power of sternomastoid muscle.
FIGURE 24.35 Feeling the carotid pulse.
Note
• In individuals with thin long neck, the cricoid cartilage and thyroid gland lie
at a higher level and the goitre may be missed or the size is overestimated.
• In elderly individuals with kyphosis or emphysema, the cricoid cartilage and
thyroid gland lie very low almost hidden by the sternum and the size may be
underestimated.
• A low-lying goitre may be detected only on palpating the lower anterior neck
during swallowing.
• The pyramidal lobe may lie lateral to the midline and may be mistaken for
an enlarged lymph node.
• If nodules are felt only during swallowing, they should be trapped between
the fingers and felt after the act of swallowing is complete for details.
• The upper pole of thyroid lobe is felt by pinching it up with the thumb and
index finger.
• A pad of fat in the anterolateral neck especially in the obese may resemble
goitre but it does not move with deglutition (pseudogoitre).
Percussion
Percussion over the manubrium sterni will give a dull note when retrosternal
thyroid or any other retrosternal mass (DD) is present.
Auscultation
• Auscultation over the thyroid, swelling may demonstrate:
• A bruit (Fig. 24.36), indicating increasing vascularity, a feature of
malignant tumours
• A continuous low-pitched venous hum over the goitre in Graves’ disease
• Tracheal breath sounds help to locate trachea and any shift in its position
• Auscultation over the carotid artery may demonstrate:
• A bruit indicating compression
FIGURE 24.36 Auscultation of thyroid for bruit.
Relevant areas
Face
The face is examined for the signs of thyroid malfunction:
• Hyperthyroidism:
• Characteristic stare with widened palpebral fissures (frightened facies)
• Failure to wrinkle the brow on upward gaze
• Hypothyroidism:
• Dull expressionless face
• Rough, dry and doughy skin
• Sparse hair (loss of outer third of eyebrows)
• Puffiness of the face with pouting of lips
Scalp
• Checked for metastases (warm, pulsatile, smooth well-defined lump)
Eyes
• Hyperthyroidism
Thyroid ophthalmopathy is usually graded as mild, moderate, severe and
progressive. Werner’s classification has grade 0–6. They appear in the
following order:
1. Signs of mild ophthalmopathy:
(a) Infrequent blinking, staring look and widened palpebral fissures
(Stellwag’s sign)
(b) Lid retraction: Due to spasm of Muller’s muscle (a smooth muscle
adjoining the levator palpebrae superioris), the upper eyelid remains at
a higher level so that the sclera is visible above the iris (Dalrymple’s
sign) (Fig. 24.37A)
(c) Lid lag: The patient’s head is stabilized with examiner’s left hand and
the patient is asked to follow the examiner’s right index finger which
is slowly moved downwards from patient’s eye level. The upper eyelid
lags behind the pace of movement of the eyeball exposing the upper
sclera (von Graefe’s sign) (Fig. 24.37B)
2. Signs of moderate ophthalmopathy:
(a) Exophthalmos: The eyeball is pushed forward, exposing the sclera
both above and below the iris (Figs. 24.37C and D). Mild
exophthalmos is detected by the examiner standing behind the patient,
with the patient’s head tilted backwards, and the eyeballs visible
(Naffziger’s sign) (Fig. 24.37E)
(b) Due to exophthalmos, the patient can look up without wrinkling the
forehead even when the face is inclined downwards (Joffroy’s sign)
(Fig. 24.37F)
(c) Upper eyelid eversion is difficult or absent in exophthalmos (Gifford’s
sign) but is easy in proptosis
3. Signs of severe ophthalmopathy:
(a) Failure for convergence: Patients have diplopia and are unable to
converge their eyes. The patient’s head is stabilized with examiner’s
left hand and examiner’s right index finger is moved from a distance
towards the root of the patient’s nose between the eyes. The patients
are asked to keep looking at the approaching fingertip and their ability
to converge their eyes is looked for. (Moebius’s sign) (Fig. 24.37G)
(b) Ophthalmoplegia: Due to oedema and cellular infiltration of the eye
muscle and oculomotor nerves, leading to weakness of the superior
and lateral rectus and inferior oblique muscles of the eye preventing
upward and lateral gaze (Fig. 24.37H)
4. Signs of progressive ophthalmopathy:
(a) Congestive oculopathy (chemosis, conjunctivitis, periorbital swelling,
corneal ulcerations, optic neuritis, optic atrophy)
FIGURE 24.37A Dalrymple’s sign.

FIGURE 24.37B von Graefe sign.
FIGURE 24.37C Exophthalmos relation of eyelids to the iris.
FIGURE 24.37D Exophthalmos.
FIGURE 24.37E Naffziger sign.

FIGURE 24.37F Joffroy sign.
FIGURE 24.37G Moebius sign.
FIGURE 24.37H Ophthalmoplegia.
Numerous other eye signs have been described:

• Hypothyroidism:
• Periorbital puffiness
Neuromuscular system
• Nervousness
• Anxiety
• Irritability
• Tremors (Fig. 24.38)
• Muscle weakness
• Warm moist hands (sympathetic hyperactivity)
• Brisk deep tendon reflexes
• Hypothyroidism:
• Lethargy
• Slowing of intellectual and motor activity
• Slow tendon reflex (hung reflex)
FIGURE 24.38 Examining for tremors.
Cardiovascular system
• Tachycardia, increased sleeping pulse rate (grade 1—up to 90 /min, grade 2
—90–110/min, grade 3—110/min)
• Hypertension
• Irregularity of heart rate
• Signs of cardiac failure
• Hypothyroidism:
• Bradycardia
Skeletal system
• Examined for metastases and pathological fractures
Oral cavity
Oral cavity is examined for large tongue (e.g. myxoedema), pale tongue (e.g.
anaemia), tongue tremor (thyrotoxicosis), lingual thyroid.
Note
Look for tongue tremor inside the mouth. Fasciculation of intrinsic muscles
may be mistaken for tremors, when the tongue is protruded.
Neck
The neck is examined systematically for lymph node enlargements secondary to
the thyroid gland tumours. In hypothyroidism, there is fat deposition on the back
of the neck and shoulders.
Auditory system
The ears are examined for hearing loss (e.g. hypothyroidism). Pendred syndrome
—cretinoid goitre associated with deafness.
Chest
The chest should be examined for bronchial sounds or absence of breath sounds
in lung parenchymal disorders (e.g. metastases), decreased air entry, dullness on
percussion and absence of breath sounds (e.g. malignant pleural effusion).
Abdomen
Examination of the abdomen both by inspection and palpation has to be done for
splenic enlargement (e.g. lymphoma), hepatosplenomegaly (e.g. Hashimoto
thyroiditis, Graves’ disease, liver metastases).
Lymphatic system
(e.g. lymphoma of thyroid). Examination of the liver and spleen completes the
lymphoreticular system, which is useful in diagnosis.
General examination
General examination of the patient includes checking for:
• Associated anaemia, jaundice etc.
• Pretibial myxoedema
• Coarse voice and inspiratory stridor
• Change in body weight
• Increased respiratory rate in hyperthyroidism
The signs in thyroid disorders are analysed in Table 24.7.
TABLE 24.7
Analysis of Signs in Thyroid Disorders
Lesion Symmetry Laterality Surface Feel Fixity Other features

Nontoxic goitre
Diffuse goitre Symmetrical Bilateral Smooth Soft Nil Mild hypothyroidism
Multinodular goitre Asymmetrical Bilateral Nodular Variable Nil Pressure effects if
large
Thyroiditis
Acute and subacute Either Usually Irregular Soft Nil Tender, lymph nodes
thyroiditis bilateral
Chronic
Hashimoto thyroiditis Asymmetrical Bilateral Lobular Woody Rare Late hypothyroidism
Riedel’s thyroiditis Irregular Hard Early Pressure effects,
hypothyroid
Diffuse toxic goitre Symmetrical Bilateral Smooth Soft, firm Thyrotoxic, bruit
initially later
Neoplastic
Adenoma Asymmetrical Unilateral Smooth Firm Nil Nil
Papillary carcinoma Unilateral Irregular Late Lymph nodes
Follicular carcinoma Late Distant metastases
Anaplastic carcinoma Unilateral Hard Early Pressure effects,
initially metastases
Medullary carcinoma Unilateral Late Lymph nodes,
(nonfamilial) metastases
Lymphoma Bilateral Early Lymph nodes
Table 24.8 summarizes some points to remember, which will help in clinical
evaluation of the thyroid swellings.
TABLE 24.8
Points to Remember While Examining Thyroid Gland
Sign / Symptom Probable cause
Stridor Narrowing of trachea due to carcinoma of the thyroid, retrosternal goitre, scabbard trachea of
longstanding multinodular goitre and Riedel thyroiditis
Warmth and Inflammation or haemorrhage
tenderness
Unilateral goitre Adenomas and carcinomas, sometimes Riedel’s thyroiditis
Bilateral goitre Simple goitres, thyroiditis, Graves’ disease
Symmetrically Neonatal, childhood, early endemic, sporadic goitres, thyroiditis and Graves’ disease
smooth and
lobular
Nodular or Multinodularity is seen in late endemic, sporadic goitres and occasionally in medically treated
irregular Graves’ disease, chronic thyroiditis and carcinoma
Non palpable Retrosternal extension
lower border
Consistency (not a Colloid goitre and goitre of Graves’ disease are usually soft. Benign thyroid nodules when calcified
very reliable and tense cysts feel hard. In Riedel’s thyroiditis and malignancy, the thyroid gland may be stony
sign) hard
Mobility Fixation of the thyroid gland usually indicates the presence of carcinoma though occasionally it may
occur in thyroiditis. Overlying skin may be adherent to the goitre due to inflammation, infiltration
due to cancer, or scarring due to previous surgery
Pulsation, thrill The common carotid artery pulsations are normally felt at the level of the upper border of the thyroid
cartilage. A large goitre displaces it posteriorly. It is absent (Berry’s sign) when a malignant
thyroid tumour encloses the carotid sheath. Vascular thrill, if felt over the thyroid, is suggestive of
hyperthyroidism
Tracheal position Lateral deviation can be due to a large thyroid lobe, a substernal goitre or other intrathoracic
abnormalities
Horner syndrome Indicates involvement of the sympathetic nerve trunk on the affected side and consists of:
I.enophthalmos (due to paralysis of Muller’s muscle)
II.drooping of upper eyelid (pseudoptosis)
III.myosis (due to paralysis of dilator pupillae) and absence of spinociliary reflex
IV.absence of sweating on the affected half of the face (anhidrosis)
V.flushing of the face and nasal congestion due to vasodilatation
Lymph nodes Nodes in the central compartment also move with deglutition. Cervical lymph nodes may be palpable
in carcinoma thyroid (especially papillary carcinoma), Hashimoto thyroiditis, acute thyroiditis
CHAPTER 25
Neck
S. Devaji Rao
CHAPTER OUTLINE
25.1. Surgical anatomy of neck 375
25.2. Midline swellings of neck 375
• Submental lymph node 375
• Thyroglossal cyst 376
• Subhyoid bursa 376
• Pharyngeal pouch 377
• Plunging ranula 378
• Laryngocele 378
• Median dermoid 378
• Retrosternal goitre 379
• Thymic swelling 379
25.3. Lateral swellings of neck 379
• Lymph nodes 379
• Salivary glands 380
• Thyroid swellings 380
• Branchial cyst 380
• Carotid body tumour 381
• Carotid artery tortuosities and aneurysm 381
• Cystic hygroma 381
• Sternomastoid tumour 381
• Tumours of muscles, neural or fatty tissue 381
• Cervical rib 382
• Innominate tortuosity and aneurysm 383
• Subclavian aneurysm 383
• Neck 385
25.1 surgical anatomy of neck

The neck is divided into two halves, the left and the right (Table 25.1) (Fig.
25.1). Each half of the neck is divided further into triangular anatomical
landmarks, called triangles. The broad sternomastoid muscle divides the neck
into anterior and posterior triangles. These major triangles are further divided.
• Anterior triangle is divided into three further subdivisions:
• Inferior border of the mandible, and the two bellies of the digastric muscle
form a triangle called digastric triangle
• Posterior belly of digastric, superior belly of the omohyoid muscles along
with the anterior border of sternomastoid form the carotid triangle
• Superior belly of omohyoid and anterior belly of digastric with the midline
forms the muscular triangle
• Posterior triangle is divided into two further divisions, by the inferior belly
of omohyoid muscle, as occipital triangle above and supraclavicular or
subclavian triangle below.
FIGURE 25.1 Surgical anatomy of neck.
TABLE 25.1
Triangles of the Neck, their Contents and Lesions
Triangle Anatomical Boundaries Contents Lesions

Anterior Triangle
Digastric Inferior border of the Submandibular salivary glands Submandibular salivary gland
mandible swellings
Anterior and posterior Facial artery
bellies of digastric
muscle Lymph nodes Lymph node swellings
Carotid Superior belly of Common carotid artery dividing into Carotid body tumour Carotid
omohyoid the external and internal carotid tortuosity Carotid
arteries aneurysm
Posterior belly of Internal jugular vein
digastric
Anterior border of Vagus nerves
sternomastoid
Lymph nodes Lymph node swellings
Muscular Superior belly of Larynx Laryngocele
omohyoid
Midline Thyroid gland Goitre
Lymph nodes Lymph node swellings
Anterior belly of Innominate vein Innominate tortuosity and
digastric aneurysm
Posterior Triangle
Occipital Anterior border of Lymph nodes Lymph node swellings
trapezius
Posterior border of
sternomastoid
Inferior belly of
omohyoid
Supraclavicular or Inferior belly of Lymph nodes Lymph node swellings
subclavian omohyoid
Upper border of middle Accessory nerve
third of clavicle
Posterior border of Subclavian vessels Subclavian aneurysm
sternomastoid
The superficial or investing layer of the deep cervical fascia splits to envelop
the sternomastoid muscle, and turning the head to the side against resistance
tenses the fascia and helps to distinguish whether a swelling is superficial or
deep to the fascia.
Immaterial to its presence either superficial or deep to the fascia, for
convenience, the swellings of the neck (Figs. 25.2 and 25.3) are classified (Table
25.2) as:
• Midline swellings
• Lateral swellings
FIGURE 25.2 Midline swellings of neck.
FIGURE 25.3 Lateral swellings of neck.
TABLE 25.2
Relationship of the Neck Swellings to the Deep Fascia
Swellings Superficial to the Deep

Swellings Beneath the Deep Fascia
Fascia
Midline or lateral swellings Midline swellings Lateral swellings
Sebaceous cysts Submental lymph node Lymph nodes

Lipomas Median dermoid Salivary glands
Neurofibromas Thyroglossal cyst Thyroid swellings
Some lymph nodes Subhyoid bursa Branchial cysts
Pharyngeal pouch Carotid body tumour
Plunging ranula Carotid tortuosity and aneurysm
Laryngocele Cystic hygroma
Goitre of the isthmus or pyramidal Sternomastoid tumour
lobe
Median dermoid Tumours of muscles, neural or fatty
tissue
Retrosternal goitre Cervical rib
Thymic swelling Innominate tortuosity and aneurysm
Subclavian aneurysm
25.2 midline swellings of neck
Submental lymph node

Usually secondary to intraoral infections especially of the tongue or teeth
• A painful and tender lump in the midline near the mandible in the submental
region
• Oral cavity examination is mandatory
• Culture of pus and identifying organism
Treatment
• Broad-spectrum antibiotics
• Incision and drainage, if abscesses are found in the dental planes, with or
without dental extractions
Thyroglossal cyst
Detailed in the Chapter 24, Thyroid.
Subhyoid bursa
This rare lesion is the prominence of the existing bursa
A soft cystic globular swelling in the subhyoid region, closely adherent to the
body of the hyoid bone
CT or MRI of the neck will be diagnostic
Treatment
• Total excision is the treatment of choice
• Incision and drainage of infected bursa (with antibiotic coverage),
followed by excision at a later date
Pharyngeal pouch
• Rare condition
• Represents a pulsion diverticulum resulting from the muscular weakness at
the posterior pharynx between the two components of inferior constrictor
muscle (thyropharyngeus and cricopharyngeus), called Killian’s dehiscence
• A cystic swelling mostly at the midline but deviates to the side later, mostly to
the left
• Large pouches present with regurgitation or obstruction of the upper
oesophagus
• Barium swallow (Fig. 25.4) is diagnostic
• Oesophagoscopy is confirmatory
FIGURE 25.4 Barium swallow—pharyngeal pouch.
Treatment
• Total excision with proper exploration of the neck (cricopharyngeal myotomy
will be needed during the procedure)
Plunging ranula
Rare condition occurs due to myxomatous or mucoid degeneration of the
sublingual salivary gland
• A bluish-grey or a translucent swelling in the floor of the mouth
• It may enlarge downwards to insinuate itself laterally to the submandibular
region or through the fibres of mylohyoid muscle towards the midline
CT (Fig. 25.5) or MRI of the oral cavity and neck will be diagnostic
FIGURE 25.5 CT—plunging ranula.
Treatment
• Total excision of the swelling through the oral route
• Deroofing or marsupialization is effective when excision is not possible
Laryngocele
Uncommon condition, an example of pulsion diverticulum, occurring more in
players of wind instruments
• A soft variable unilateral or bilateral swelling arising above the thyroid
cartilage
• It will empty on compression and will reappear on Valsalva manoeuvre
CT or MRI of the neck will be diagnostic
Treatment
Complete excision is the treatment of choice
Median dermoid
• Rare lesion
• A developmental deformity
• Occurs at the line of fusion
A smooth soft cystic swelling in the midline (Fig. 25.6) of the neck or oral cavity
FIGURE 25.6 Midline dermoid Source: (Courtesy Dr Usha Dorairajan).
CT of the neck and oral cavity will be diagnostic
Treatment
Complete excision
Retrosternal goitre
Detailed in the Chapter 24, Thyroid.
Thymic swelling
See in Chapter 26, Thorax.
25.3 lateral swellings of neck

Lymph nodes
Lymph node swellings are the commonest swellings in the neck and can be due
to varied causes (Table 25.3)
TABLE 25.3
Causes of Cervical Lymph Node Swellings
Pathology Cause
Inflammation Acute Infections of oral cavity (bacterial and fungal), pharynx, larynx, salivary glands
Superficial infections of skin of head and neck
Viral infections
Chronic Tuberculosis
Sarcoidosis
Malignancies Primary Lymphomas (Hodgkin’s and non-Hodgkin’s)
Secondary Primary malignancy of aerodigestive tract, tumours of head and neck, rarely from other sites
of body
• Discrete, matted or conglomerate swellings in the neck with or without pain,
depending on the aetiology (discussed separately) (Ref Fig. 12.20A)
• Squamous cell carcinomatous lumps may present as firm to hard swellings
(Figs. 25.7A and B) and may even fungate through the skin (Fig. 25.8A)
• Malignant enlargement of lymph nodes of the head and neck malignancies are
firm in consistency (Fig. 25.8B)
FIGURE 25.7A Bilateral lymph node swellings of lung malignancy.
FIGURE 25.7B Metastatic lymph node of laryngeal malignancy.
FIGURE 25.8A Fungating squamous cell carcinomatous lymph
node Source: (Courtesy Dr A. Chandrasekar Rao).
FIGURE 25.8B Lymph node metastases from thyroid malignancy.
They remain as indicators of systemic illnesses in the body excepting in

primary lymphomas or as secondaries to primary malignancies elsewhere
Note
Normal lymph nodes without disease are not palpable.
Variety of investigations may have to be done (Fig. 25.9) (discussed separately)
FIGURE 25.9 CT neck—bilateral cervical lymph node swellings with

necrosis.
Treatment
• Medical management for benign systemic illnesses presenting with cervical
lymph node swellings
• Chemoradiation is required for primary lymphatic malignancies
• Surgery and chemoradiation are for secondary lymph node swellings
depending on the primary, its site and histopathology
Salivary gland swellings

Detailed in Chapter 23.
Thyroid swellings
Branchial cyst
• A congenital anomaly
• Arises from congenital remnants of the second pharyngeal pouch or branchial
cleft
• Initially an empty sac of embryological tissue, and over the years, epithelial
debris accumulates and infection may occur, thus becoming more prominent
• It presents commonly in the third decade, more frequently in men
• A soft, ovoid, painless, fluctuant swelling in the lateral side of neck lying
between the carotid sheath and the sternomastoid muscle, bulging into the
carotid triangle from beneath the anterior border of the sternomastoid muscle
(Fig. 25.10) at the junction of its upper one-third and lower two-thirds
• Infected cyst may be hard and tender
• Aspiration of the cyst will show a yellow coloured fluid which on microscopy
will show large amount of cholesterol crystals, hence they do not
transilluminate
FIGURE 25.10 Branchial cyst Source: (Courtesy Dr K. S. Ravishankar).
CT (Fig. 25.11) and MRI will be diagnostic
FIGURE 25.11 CT—right branchial cyst.
Treatment
Excision is the treatment of choice
Carotid body tumour

• These are chemodectomas and arise from the chemoreceptor cell of the
carotid body
• They form a part of a group of tumours arising from glomus tissue,
paraganglionomas, which include tumours of the vagus body, the glomus
jugulare and phaeochromocytomas
• There is autosomal dominant genetic tendency, especially in bilateral tumours
• They are seen more in areas of hypoxemia (high-altitude habitants), which is
known to cause carotid body hyperplasia
• More common in elderly women
• Common in the fourth decade
• Slow-growing painless lump in the neck
• On examination:
• A hard, regular mass at the bifurcation of the carotid artery—at the level of
hyoid bone—presenting transmitted pulsation
• Rarely, it can cause local nerve damage resulting in the palsies of seventh,
ninth, tenth, eleventh and twelfth cranial nerves
CT and MRI will be diagnostic
Treatment
• Excision of the tumour especially if they are locally invasive and cause
carotid insufficiency
• During excision carotid vessels may need grafting, if the procedure involves
removal of part of vessels
Carotid artery tortuosities and aneurysm

• They are rare
• Majority of them are iatrogenic, arising in relation to surgical trauma, some
are due to atherosclerosis
• May sometimes be associated with Takayasu’s disease
• Pulsatile swelling in the neck with pain
• Symptoms related to embolic phenomenon
• When it is part of Takayasu’s disease, it is tender
CT and MRI with angiography (Fig. 25.12) are diagnostic
FIGURE 25.12 Angiogram—common carotid artery aneurysm.
Treatment
Excisional surgery with grafting of carotid artery is done for aneurysms
Cystic hygroma
Detailed in Ch. 12.
Sternomastoid tumour
• It is either an organizing haematoma or an area of fibrosis secondary to
ischaemia in the middle third of the sternomastoid muscle
• It is also thought to be a sequel to a breech presentation and birth injury or an
intrauterine phenomenon
• In adults, muscular tumours such as rhabdomyosarcoma may be the cause
• It is seen soon after birth
• A smooth, fusiform swelling in the middle third of the sternomastoid muscle
or may present with torticollis after about 3–6 weeks
• Due to fibrotic shortening of the muscle, the head gets turned away from the
affected side and slightly upwards (Fig. 25.13)
FIGURE 25.13 Torticollis Source: (Courtesy Dr K. Sridhar).
DD: Traumatic lesions of the sternomastoid muscle, and lesions lying over or
under the muscle
CT and MRI will be diagnostic
Treatment
Excision of muscle or myotomy followed by physiotherapy
Tumours of muscles, neural or fatty tissue
Tumours (both benign and malignant) arising from the muscles, neural and fatty
tissue can occupy any region of the neck
• A lump according to its type (Figs. 25.14 and 25.15A–C )
• Many of them are painless
FIGURE 25.14 Lipoma.
FIGURE 25.15A Venous malformation.

FIGURE 25.15B Neuroma.
FIGURE 25.15C Schwannoma.
• CT and MRI are useful in diagnosis
• Fine-needle aspiration cytology (FNAC) and wedge or excision biopsy are
required for confirmation of pathology
Treatment
Excision
Cervical rib
• This is the prominent transverse process of the last cervical vertebra
• When the lower trunk of brachial plexus and / or the subclavian vessels pass
over the rib, they may get compressed to produce neurovascular deficiency
called ‘thoracic outlet syndrome’
• Cervical ribs may be palpable, usually bilateral, as a mass in the lower neck
• Neurovascular deficiency in the form of pain, weakness, paraesthesia may
occur in the ulnar aspect of the forearm
• Compression of the subclavian vein may cause Raynaud’s phenomenon (Fig.
13.8)
• Plain X-ray (Ref Figs. 13.9A and B) will demonstrate the cervical ribs
• CT and MRI of neck demonstrate the compression of nerve roots and the
artery
• Nerve conduction studies may be useful in determining the degree of nerve
compression
Treatment
• Medical management and physiotherapy are useful in many
• Excision of the cervical rib is curative, in severely symptomatic patients
Innominate tortuosity and aneurysm

They are rare but may occur due to hypertension and atherosclerosis
A pulsatile mass (Fig. 25.16) in the muscular triangle with bruit, may give rise to
embolic phenomena
FIGURE 25.16 Innominate artery aneurysm.
CT and MRI with angiography are diagnostic
Treatment
Excisional surgery with grafting of innominate artery is curative for aneurysms
Subclavian aneurysm
Rare but may occur as a poststenotic dilatation in thoracic outlet syndrome
A pulsatile mass in the supraclavicular fossa with bruit and may give rise to
embolic phenomena
• Plain X-rays may show cervical ribs
• CT and MRI with angiography (Fig. 25.17) are diagnostic
• Duplex ultrasonography (US) is useful
FIGURE 25.17 Angiogram—subclavian artery aneurysm.

Treatment
Excisional surgery with grafting of carotid artery is curative for aneurysm
Eliciting history
Eliciting the history in a patient with a swelling in the neck should be precise to
arrive at a clinical diagnosis. Apart from the general information, the history
should include the following points:
• Duration of lump: When did the patient first notice the lump?
Lumps seen in childhood or immediately after birth are congenital in origin
(e.g. cystic hygroma). Lumps of infective pathology will be present for a short
period (e.g. acute lymphadenitis) and benign tumours are present for a long
time (e.g. lipoma)
• Progression of lump: Was the lump of the same size since it was seen for
the first time or has it increased in size?
Benign lumps such as neurofibroma remain the same, some increase in size
gradually (e.g. thyroid swellings) and malignant tumours grow in size in a very
short period (e.g. lymphomas, secondary lymph nodes)
• Association of pain: Is or was the lump painful?
Some lumps are characteristically painless (e.g. lipomas, lymphomas), some
are moderately painful (e.g. tubercular nodes) and some are very acutely
painful (e.g. acute lymphadenitis)
Presence of infection at the time of examination indicates active infection
(e.g. superadded bacterial infection in tubercular nodes)
It should be enquired whether any treatment was given for the illness.
Nonresponsiveness will help in revising the diagnosis, or reorganizing the
treatment
weight?
Loss of appetite and weight may indicate malignant pathology, e.g.
secondary metastatic lymph nodes, tuberculosis of the lymph nodes
• Personal history: Does the patient smoke cigarettes?
This question has relevance, as smokers develop bronchogenic carcinoma,
which can manifest with cervical lymph nodes
treatment?
successfully treated will indicate the examiner to reconsider the diagnosis such
as tuberculosis
Diseases such as tuberculosis occur in closely living families and the
presence of it may be a good indicator for the present diagnosis
The findings of the history are correlated with the swellings of the neck in the
TABLE 25.4
Correlation of Symptoms with Midline Swellings of the Neck
Symptom
Lesion
Loss of Loss of Past Family Associated
Duration Pain Fever
appetite weight history history symptom
Ludwig’s angina Short Present Present Nil Nil Nil Nil Tooth pain
Submental Short Present Present Nil Nil Nil Nil Intraoral
lymph node pathology
Median dermoid Long Absent Absent Nil Nil Nil Nil Nil
(present (present
when when
infected) infected)
Thyroglossal Since birth / Absent Absent Nil Nil Nil Nil Moves when
cyst later in (present (present tongue is
life when when protruded
infected) infected)
Subhyoid bursa Anytime in Absent Absent Nil Nil Nil Nil Nil
life
Pharyngeal Since birth Absent Absent Nil Nil Nil Nil Nil
pouch (present (present
when when
infected) infected)
Plunging ranula Long Nil Nil Nil Nil Nil Nil Nil
Laryngocele Long Absent Absent Nil Nil Nil Nil Common in
windblowers,
compressible
Goitre of the Short Absent Absent Nil Nil Nil Nil Thyroid-related
isthmus or symptoms
pyramidal
lobe
Retrosternal Short Absent Absent Nil Nil Nil Nil Thyroid-related
goitre symptoms
Thymic swelling Short Absent Absent Nil Nil Nil Nil Myasthenia
gravis
TABLE 25.5
Correlation of Symptoms and Lateral Swellings of the Neck
Symptom
Lesion
Past Family
Duration Pain Fever Loss of appetite Loss of weight
history history
Lymph nodes Short Present Present Present in Present in May be May be
when when tuberculosis tuberculosis present present
infected infected and and
malignancies malignancies
Salivary glands Short / long in Present Present May be present May be present Nil Nil
benign when when in in
pathologies infected infected malignancies malignancies
Thyroid swellings Variable Absent Absent May be present May be present Nil May be
in in present
Branchial cyst Since birth Absent Absent Absent Absent Nil Nil
Carotid body Variable Absent Absent May be present May be present Nil Nil
tumour in in
Cystic hygroma Since birth Absent Absent Absent Absent Nil Nil
Sternomastoid Since birth May be May be Absent Absent Nil Nil
tumour present present
Tumours of Variable May be Absent Absent Absent Nil Nil
muscles, present
neural or fatty
tissue
Cervical rib Variable Absent Absent Absent Absent Nil Nil
Neck
This consists of four parts:
• Inspection
• Palpation
• Percussion
• Auscultation
Inspection
The neck needs to be exposed in full for proper examination, and clothes should
be removed from the patient up to the level of nipples. If a lump is seen, the
student should observe the following and record them carefully:
• Location
• Size
• Number
• Skin over the swelling
• Pressure on neighbouring structures
• The neck should be observed for sinuses, fistulae or ulcers
Location: Location of the swelling is important as this will help in narrowing
the differential diagnosis. The swellings in the neck may be classified in relation
to the triangles in the neck.
Size: Size of the swelling is not a very significant factor in making a clinical
diagnosis, as this factor is very inconsistent. However, a sudden increase in size
or its development in a very short time is significant, as this is a common
symptom in malignant pathologies.
Number: Majority of the swellings of the neck are solitary excepting the
lymph nodal swellings, which are many times multiple, whatever the pathology.
Skin over the swelling: The skin over the swelling looks normal when it is
not complicated. Acute inflammatory changes make the skin look red and
erythematous. The skin may break in inflammatory lesions into an ulcer or a
sinus or fistula discharging pus or serosanguineous discharge, a common finding
is tuberculous cold abscesses, acute or chronic osteomyelitis of mandible,
thyroglossal fistula or a branchial fistula. Scars may indicate healed sinuses or
previous surgery.
Pressure on the neighbouring structures: The swelling may exert pressure
on the neighbouring structures such as the jugular vein causing a facial oedema,
on the carotid artery to produce syncopal attacks or on a nerve causing wasting
of muscles supplied by the nerve. Examination of the face and surrounding
structures become necessary.
Ulcers, sinuses and fistulae: Ulcers, sinuses and fistulae may present at any
part of the neck discharging varieties of liquid material (discussed in the
following paragraphs).
Palpation
The whole neck should be examined first and then attention is directed to the
lump.
Palpation of neck in general
Where to start?
• Start at the chin with both hands comparing both sides
• Palpate the suprahyoid region and submandibular regions
• Next, palpate posteriorly over the parotid glands
• Move along the occiput, where the fingers come together again
• Next, palpate the posterior triangles, moving along the anterior border of the
trapezius and reach the supraclavicular fossa
• The anterior triangle is examined next. Start in front of the sternomastoid
muscle just below the angle of the mandible and move down to the
suprasternal notch, gently pushing the sternomastoid laterally to feel under it
• Next to feel are the structures in the midline, starting at the thyroid gland and
move upwards towards the chin (Fig. 25.18)
FIGURE 25.18 Examination of neck.
Palpation of neck swellings

Visible swellings may be examined from the front or from the back, for
convenient assessment (Figs. 25.19A and B). The neck in general, should be
palpated from behind the patient.
FIGURE 25.19A Examination of neck from the front.
FIGURE 25.19B Examination of neck from the back.
The examiner should keep his or her left hand on the patient’s head and make
him or her look down and tilt the head to the right when the right side is to be
examined (Fig. 25.20) and vice versa. This will relax the muscles on the side of
the lesion.
FIGURE 25.20 Examination of one side of neck by tilting towards that
side.
By this method of examination, the examiner confirms his or her findings

found on inspection.
The following are to be noted by the examiners:
• Size and number: Size and number are exactly determined. The examiners
should run their fingers of the right hand on the swelling to determine its
exact size (e.g. solitary swellings—branchial cyst, dermoid, multiple
swellings—lymph nodes)
• Shape: Some swellings such as cysts are globular, but inflamed tissues and
malignant tumours may be irregular
• Surface: Examiners should run the pulp of their examining fingers on the
surface of the swelling (e.g. cystic swellings have a smooth surface, but
malignant tumours and calcified lymph nodes are irregular due to
calcification)
• Margins: They are felt by passing the examining finger along the
circumference of the lump (e.g. a well-defined margin is felt in benign
swellings such as neurofibroma and irregular in matted lymph nodes)
• Consistency: Consistency of the swelling is determined by applying gentle
pressure on the swelling during palpation. (e.g. cystic swellings are soft,
lymph nodes are firm and calcified swellings are hard)
• Compressibility: Compressibility is determined by the application of pressure,
and the size of the swelling especially the soft swellings reduce considerably
and fill up slowly on its own, a characteristic of haemangioma
• Reducibility: Some swellings reduce on pushing by the examiner’s fingers but
do not appear on their own, but reappear on acts of straining such as
coughing and sneezing, a property called reducibility (e.g. laryngocele)
Note
The spontaneous reappearance of lesion without strain differentiates
compressibility from reducibility.
• Cough impulse: Some swellings appear or become prominent on coughing,

which is felt by the examining fingers (e.g. laryngocele may show impulse
on coughing)
• Fluctuation: Any fluid containing cyst will show fluctuation
• Translucency: For example cystic lesions containing clear fluid such as cystic
hygroma show transillumination
• Pulsations: Examined by keeping the fingers on the swelling. Some swellings
may exhibit pulsations as in vascular tumours especially those, which are
directly connected to the lumen of an artery, such as aneurysm, which shows
expansile pulsation. Carotid body tumour shows transmitted pulsation
• Mobility: This is determined by moving the lump with index finger and
thumb of the examiner. When a swelling is not fixed and mobile, it is
essential to find whether it is moving on any fixed axis or in all directions.
Mobility in one single axis is a property of swellings arising from a linear
structure such as an artery or nerve or tendon (e.g. carotid body tumour).The
fixity is commonly seen in malignancies involving the lymph nodes. The
palpation of the various groups of lymph nodes in the neck are performed in
different ways by the examiner but it is better to follow a sequence
• Skin involvement: Skin involvement is determined by pinching the skin over
the swelling
Percussion
This is not a very relevant method of examination of the lesions of the neck
excepting in laryngocele, which may show tympanic note because of its
connection with the larynx.
Auscultation
A bruit may be heard in lesions, which have communication with the vascular
structures. In the neck, carotid aneurysm or an arteriovenous fistula may exhibit
this finding.
The physical findings of examination are correlated with the swellings of the
neck in Tables 25.6 and 25.7.
TABLE 25.6
Correlation of Physical Findings and Midline Swellings of the Neck
Lesion Inspection Palpation Pathognomonic Feature

Submental lymph node Ovoid Firm Midline swelling at the submental region
Median dermoid Globular Soft Midline swelling, fluctuant not transilluminant
Thyroglossal cyst Globular Soft Pulled up when the tongue is protruded
Subhyoid bursa Globular Soft Below hyoid bone
Pharyngeal pouch Globular Soft Cough impulse
Plunging ranula Globular Soft Transilluminant
Laryngocele Globular Soft Reducibility
Goitre of the isthmus or pyramidal lobe Irregular shape Soft to firm Moves with deglutition
Retrosternal goitre Regular shape Soft to firm Lower border is not felt
Thymic swelling Regular shape Soft to firm Lower border is not felt
TABLE 25.7
Correlation of Physical Findings and Lateral Swellings of Neck
Lesion Inspection Palpation Pathognomonic Feature
Lymph nodes Single or Variable Soft—abscess Firm and tender—inflammatory Firm and
multiple consistency nontender—chronic inflammatory, neoplastic Hard—
calcified, metastatic
Salivary glands Globular Soft to firm Parotid—lifting of earlobe Submandibular—location,
discharge through Wharton’s duct
Thyroid swellings Unilateral or Variable Soft—goitre Hard—anaplastic malignancy
bilateral
Branchial cyst Globular Soft Location
Carotid body tumour Globular Firm Transmitted pulsations Positive Valsalva manoeuvre
Cystic hygroma Globular Soft Transilluminant
Sternomastoid tumour Globular Firm to hard Becomes less prominent on tensing the muscle
Tumours of muscles, Globular or Firm to hard Fixity to deeper structures
neural or fatty irregular
tissue
Cervical rib Regular Hard Symptoms of neurovascular insufficiency in the ipsilateral
upper limb
Innominate tortuosity Irregular Soft Expansile pulsation
and aneurysm
Subclavian aneurysm Irregular Soft Expansile pulsation
The swellings in the neck can be classified in general based on their

consistencies (Table 25.8).
TABLE 25.8
Classification of Neck Swellings Based on Consistency
Midline Swellings Lateral Swellings
Cystic Solid Cystic Solid

Median dermoid Submental lymph node Branchial cyst Lymph nodes
Plunging ranula Retrosternal goitre Carotid tortuosity and Salivary glands
aneurysm
Thyroglossal cyst Thymic swelling Cystic hygroma Thyroid swellings
Subhyoid bursa Goitre of the isthmus or Subclavian aneurysm Carotid body tumour
pyramidal lobe
Cysts of the isthmus or Innominate tortuosity and Sternomastoid tumour
pyramidal lobe aneurysm
Cold abscess Tumours of muscles, neural or
fatty tissue
Laryngocele Cervical rib
Pharyngeal pouch
Other systems
• Examination of oral cavity: A systematic examination of oral cavity is
essential to eliminate local causes in the oral cavity (e.g. oral sepsis)
• Examination of pharynx: A systematic examination of pharynx and larynx is
required to rule out local causes such as infection and malignancies
• Examination of chest: Auscultation: Adventitious sounds may indicate
tuberculosis and malignancy of lungs, absent breath sounds may indicate
pleural effusion (e.g. tuberculosis, malignancy)
• Examination of abdomen: Examination should include procedures for
determination of hepatomegaly (e.g. nodular hard hepatomegaly of
malignancy)
Lymphatic system
if the swellings are thought to be of the lymphatic origin (Ch. 12).
CHAPTER 26
Thorax
(Excepting Heart, Great Vessels and
Oesophagus)
M. Harish
CHAPTER OUTLINE
26.1. Development of respiratory tract 389
26.3. Diseases of chest wall 392
• Rib anomalies 392
• Anomalies of sternum 393
• Pectus excavatum 393
• Pectus carinatum 393
• Infection of costal cartilages 393
• Osteomyelitis of sternum 394
• Abscesses 394
• Tietze’s syndrome 394
• Benign tumours of ribs 395
• Malignant tumours of ribs 395
26.4. Diseases of pleura 395
• Pleurisy 395
• Pleural effusion 396
• Acute empyema 397
• Pneumothorax 397
• Pleural tumours 397
26.5. Diseases of trachea and bronchi 399
• Tracheal stenosis 399
• Tracheo-oesophageal fistula 399
• Acute tracheitis and laryngotracheobronchitis 400
• Bronchiectasis 400
26.6. Diseases of lungs 403
• Pulmonary agenesis/hypoplasia 403
• Cystic fibrosis 403
• Aspiration pneumonia 403
• Hospital acquired pneumonia 403
• Lung abscess 404
• Pulmonary tuberculosis 404
• Fungal infections 405
• Metastatic lung disease 406
• Sarcoidosis 406
• Acute respiratory distress syndrome 407
• Pulmonary embolism 407
26.7. Diseases of mediastinum 408
• Acute mediastinitis 408
• Chronic mediastinitis 408
• Mediastinal tumours 408
26.8. Symptoms of pathologies of chest 410
• General 412
• Chest 412
26.1 Development of respiratory tract
Pleura
Embryologically, the paired pleural cavities become separated from the
pericardial cavity, by the development of pleuropericardial membrane. The
pleural cavity is continuous with the peritoneal cavity/coelomic cavity also, and
separates from it by the development of pleuroperitoneal membrane and septum
transversum.
Trachea, bronchi and lungs

By the fourth week, laryngotracheal diverticulum buds out from the primitive
pharynx, and its blind end forms the lung bud. The lung bud continues to
elongate and branch into bronchial buds, secondary bronchi etc. The left and
right lung buds push into the pericardioperitoneal canals (primordia of pleural
cavity), followed by the descent of heart and lungs into thorax. Pleuroperitoneal
foramen closes. By the seventh week, enlargement of liver stops the descent of
the heart and lungs. By 3–6 months, lungs appear glandular, followed by the
proliferation of respiratory bronchioles to end in alveolar ducts and sacs. The
lungs develop in five sequential stages namely, embryonic, pseudoglandular,
canalicular, terminal sac and alveolar stages. Development of this system is not
completed until late fetal life.
Thorax is the upper part of the trunk and is like a truncated cone. It has two
apertures:
• Upper aperture called thoracic outlet
• Lower aperture
Thorax is flattened anteroposteriorly and protected by a rib cage.
Thorax is divided into:
• Chest wall
• Pleural space
• Lungs
• Mediastinum
Each lung communicates with the structures in the mediastinum through the
root of the lung.
Chest wall
The chest wall includes the bony thorax and associated musculature (Fig. 26.1)
• Bony thorax consists of:
• Ribs and costal cartilages: There are 12 pairs of ribs
- Seven true ribs—first to seventh ribs (i.e. they articulate with sternum
directly through costal cartilages)
- Three false ribs—8,9,10 ribs articulate with a combined cartilage at
seventh costal cartilage
- Two floating ribs—eleventh and twelfth ribs, which have no anterior
articulation
• Sternum (flat bone and is in the midline anteriorly) consists of:
- Manubrium sterni (articulates with clavicles)
- Body (four pieces and articulates with second to seventh costal
cartilages)
- Xiphisternum
The manubrium and body meet at the angle of Louis and this
corresponds to second rib articulation
• Twelve thoracic vertebrae
• Below the skin and subcutaneous tissue lies the chest wall musculature that
includes:
• Anteriorly: Pectoralis major and minor
• Posterolaterally: Serratus anterior, latissimus dorsi, paraspinal muscles
FIGURE 26.1 Anatomy of chest.
Pleural space
• Pleura is a two-layered serous membrane which surrounds the lung and
separates it from the chest wall, and covers those portions of the diaphragm
and mediastinum which are contiguous to the pleural space
• The two layers are:
• Visceral pleura invests the lung and mediastinum
• Parietal pleura lines the thoracic cavity
• Parietal pleura is further subdivided into:
• Costal pleura (lining the lateral thoracic wall from the sternum to the
vertebral bodies behind)
• Diaphragmatic pleura (covering the superior surface of diaphragm)
• Mediastinal pleura (lining the lateral aspect of mediastinum)
• Cervical pleura (projects into the neck above the thoracic inlet)
• Pleural cavity is a closed space and contains pleural fluid
• Normal pleural fluid volume is 10–15 ml and the intrapleural pressure is
usually −5 to −8 cm H2O. Whenever fluid or air accumulates inside the
pleural space, there is reduction in lung volume and expansion of the
hemithorax producing a restrictive lung defect in proportion to the amount of
liquid or air in the cavity
• There should be an accumulation of more than 300 ml of fluid before there is
restriction of chest wall movement, dullness on percussion and reduction of
breath sounds
• Pleura has a generous vascular, lymphatic and nervous supply, and also pain
sensitive nerve fibres (only to parietal pleura) supplied by the intercostals
Intercostal spaces are wider anteriorly than posteriorly. There are 11
intercostal spaces, of which third is the widest. Each space has three intercostal
muscles—internal, external, transverse thoracic muscle and a neurovascular
bundle that runs along the inferior border of the rib
Respiratory tract
Respiratory tract is divided into upper and lower tracts
• Nose, nasopharynx and larynx (externally up to lower border of cricoid
cartilage) form the upper respiratory tract (detailed in Chs. 20 and 22)
whereas
• Trachea and bronchi form the lower respiratory tract
• These form an interconnecting tree of conducting airways via terminal
bronchioles, with the alveoli to form acini, which are the gas exchange units
of the lung
Tracheobronchial tree
Trachea starts from the level of C6 vertebra and ends at the level of T4 vertebra,
where it divides into two main bronchi, the left and right. Trachea is a tube made
of cartilaginous and membranous areas measuring about 10–12 cm in length in
adults.
The divisions of the bronchi are depicted in the Fig. 26.2 and also in the Table
26.1.
FIGURE 26.2 Anatomy bronchial tree.
TABLE 26.1
Divisions of Bronchi
Right Main Bronchus (RMB) Left Main Bronchus (LMB)
Right middle
Right upper lobe bronchus lobe Left upper lobe bronchus
Right lower lobe bronchus (RLL)
(RUL) bronchus (LUL)
(RML)
1 2 3 4 5 6 7 8 9 10 1 and 2
Apical Posterior Anterior Lateral Medial Apical Medial Anterior Lateral Posterior Apicoposterior
basal basal basal basal
Lungs
• Lungs constitute the organs of respiration, and situated one on each side of the
mediastinum
• Right lung is divided into three lobes (upper, middle, lower) separated by
two fissures (oblique and horizontal)
• Left lung is divided into two lobes (upper and lower separated by oblique
fissure)
Mediastinum
The thick median septum which separates the right and left pleural cavities is
called the ‘mediastinum’. This space is bounded by mediastinal pleura and the
lungs on either side, diaphragm inferiorly and thoracic outlet superiorly (Fig.
26.3)
FIGURE 26.3 Mediastinum.
It is divided into:
• Superior mediastinum (part lying above the horizontal plane passing through
the sternal angle and the disc below the fourth thoracic vertebra)
• Inferior mediastinum (part lying below the level of sternal angle)
• Middle mediastinum (part behind the body of sternum and bodies of T5–
T9 vertebrae—occupied by the heart and major vessels)
• Anterior mediastinum (narrow coronal cleft between the heart and body of
sternum)
• Posterior mediastinum (between the heart and diaphragm in front and T5–
T12 vertebrae behind)
• The structures of the mediastinum are:
• Heart
• Great vessels
• Oesophagus
• Trachea
• Nerves (vagus and phrenic)
• Thoracic duct
• Thoracic aorta
26.3 Diseases of chest wall

They can be classified based on their aetiology (Table 26.2).
TABLE 26.2
Aetiological Classification of Diseases of Chest Wall
Aetiology Pathology
Congenital Rib anomalies

Anomalies of Pectus excavatum
sternum
Pectus carinatum
Inflammatory Infection of costal cartilages
Osteomyelitis of sternum
Abscesses
Tietze’s syndrome
Neoplastic Benign Soft tissues Tumours of skin, subcutaneous tissue and nervesa
Bony structures Chondroma, osteochondroma, fibrous dysplasia
Malignant Soft tissues Tumours of skin, subcutaneous tissue and neurofibrosarcomaa
Bony structures Chondrosarcoma, osteogenic sarcoma, Ewing’s sarcoma, multiple
myeloma, metastases
a
Discussed in detail in Chapter 9, Lumps and Swellings.
Predominantly, the chest wall lesions present as swellings and sinuses. They
are tabulated in Table 26.3. The swellings may be solid and cystic in
consistency.
TABLE 26.3
Swellings of Chest Wall
Solid Swellings Cystic Swellings
Swellings of skin and subcutaneous swellings Cold abscess
Swellings of nerves Empyema necessitates
•Neurofibroma of intercostals nerves
•Ganglioneuroma of sympathetic chain
Swellings of bone Herniation of lung
•Primary—chondroma, osteoma, osteoclastoma, chondrosarcoma, osteosarcoma, etc.
•Secondary metastatic tumours
Swellings of joints
•Costochondritis
Sinuses of chest wall occur due to various reasons (detailed in Ch. 11). They
are:
• Tuberculous sinus (bursting of cold abscess)
• Sinus from a chronic empyema—broncho pleurocutaneous fistula
• Sinus due to actinomycosis
• Sinus from underlying rib or lung malignancy
Rib anomalies
• Vary from those that are of no clinical significance to extensive areas of
deficiencies, often associated with hemivertebrae
• Commonest anomaly is the presence of a cervical rib and bifid ribs
• Large deficiencies lead to severe spinal curvature (scoliosis) and impaired
respiratory function
• Cervical rib can present with pain and neurocirculatory symptoms in the arm
(p. 149, Ch. 13 - Arterial System)
X-rays (Fig. 13.9B) are diagnostic
Treatment
• Large deficiencies can be corrected by plastic procedures
• Division of scalene muscle often relieves circulatory symptoms of cervical
rib
Anomalies of sternum
• Anomalies of sternum result due to varying degrees of imperfect fusion of
two sternal bars, resulting in a cleft
• Midline clefts can be partial or complete, and may be associated with ectopia
cordis
Obvious visible deformity
• X-rays and CT are diagnostic
• Echocardiogram may show cardiac anomalies
Treatment
• Clefts can be corrected by surgery if not accompanied by ectopia cordis
• Major surgical procedures are required to correct cardiac anomalies, which
carry high degree of mortality
Pectus excavatum (funnel chest, cobbler’s

chest)
• A funnel-shaped deformity (depression of sternum and curving inward of
medial portion of adjacent costal cartilages), resulting in a small
anteroposterior measurement of chest cage with a tendency to
kyphoscoliosis, due to lack of muscle layer of anterior diaphragm which gets
replaced by fibrous tissue
• The heart gets displaced to the left
• It has some familial tendency
• Obvious deformity of the chest (indrawn depression in the sternum) (Fig.
26.4A)
• Cardiac output may reduce after exercise
• Causes psychological disturbances especially in boys

FIGURE 26.4A Pectus excavatum.
Treatment
The deformity can be corrected by plastic procedures (Ravitch and Nuss
procedures)
Pectus carinatum
• Rare deformity (referred to as ‘pigeon breast’), with a keel-like protrusion of
the sternum, resulting due to disproportionate rib growth or abnormal
diaphragmatic pull and obliteration of sternal sutures at early age (Fig.
26.4B)
• May be associated with neuromuscular lesions or Marfan syndrome
FIGURE 26.4B Pectus carinatum.
Obvious deformity
Treatment
The deformity can be corrected by plastic procedures
Infection of costal cartilages

• Costal cartilages are hyaline cartilages, which do not contain any blood vessel
or nerve, but derive nutrition from lymph
• Because of its avascularity, this tissue is very vulnerable to infection
• Infection may be caused by pyogenic organisms, tubercle bacilli and fungi
• Extensive wound infection after surgery of breast (e.g. radical mastectomy) is
another cause
Severe pain is the presenting symptom, which may get worse on deep inspiration
X-rays and CT are usually normal
Treatment
• Antibiotics and analgesics are useful
• Subperichondrial resection of a cartilage may be necessary
Osteomyelitis of sternum
• Results due to direct extension of infection from adjacent areas or secondary
to costochondritis
• Surgical procedures which involve the sternum may result in an infected
wound of the sternum (e.g. thoracotomy for cardiac surgery)
• Chronic infections may destroy the sternum exposing the great vessels
• Severe pain, swelling and fever
• Symptoms are mild when it is due to tuberculosis
• Tenderness depends on the severity of infection
• Pulsations of underlying great vessels can be felt when the sternum is
destroyed. A sinus may form
X-ray and CT are diagnostic
Treatment
Appropriate antibiotics and resection of the involved portion of sternum is the
treatment of choice
Abscesses
• Abscess can occur due to various causes. They are:
• Intrathoracic infection penetrating the chest wall—tuberculosis, fungal
infection
• Secondary to infections of chest wall—osteomyelitis of ribs and sternum
• Subpectoral abscess may occur due to suppurative lymphadenitis below
pectoral muscles
• Sinus results when a tuberculous abscess bursts spontaneously or after
dependent wide bore surgical drainage
Fluctuant swelling with pain
• X-ray, computed tomography (CT) and magnetic resonance imaging (MRI)
(Fig. 26.5) are diagnostic
• Diagnostic aspiration is confirmatory
FIGURE 26.5 MRI—left subpectoral abscess.
Treatment
• Treatment of underlying cause
• Acute abscess needs incision and drainage
• Tubercular abscess needs nondependent drainage
• Broad spectrum antibiotics are necessary
Tietze’s syndrome
• A disease of unknown aetiology (probably viral)
• The second costal cartilage is frequently affected
DD: Cartilagenous tumours
• Painful, nonsuppurative swelling
• Tenderness is marked
X-ray and CT are required to exclude cartilaginous tumours
Treatment
• Analgesics control pain
• Usually self-limiting, but recurrences are common
• If symptoms persist, excision of costal cartilage is warranted
Benign tumours of ribs

The common benign tumours of ribs are:
• Chondroma—25% of benign tumours of chest wall, anteriorly at the
costochondral junction
• Osteochondroma—less common than in other parts of body
• Fibrous dysplasia—most common chest tumour, generally involves the
posterior part of rib
Nontender swelling
X-rays and CT
are diagnostic
Treatment
• Wide excision is the treatment of choice in all tumours
• Excision of the entire rib is warranted in some cases
Malignant tumours of ribs

The malignant tumours of ribs are:
• Chondrosarcoma—the most common malignant tumour, between 30 and 40
years of age, anteriorly at the costochondral junction
• Osteogenic sarcoma—10% of all osteogenic sarcoma occur in chest wall,
between 20 and 30 years of age
• Ewing’s sarcoma—8% of all malignant tumours of chest wall, commonly in
children
• Multiple myeloma—predominantly between 50 and 60 years of age
• Metastases—from a variety of malignancies—breast, bronchi, prostate and
kidneys
• Excepting Ewing’s sarcoma, others present as painless swelling
• On examination, Ewing’s sarcoma is warm and tender
• Systemic manifestations such as fever and malaise are frequently present in
Ewing’s sarcoma
• X-ray and CT are diagnostic
• Isotope scan (Fig. 26.6) is diagnostic
• Biopsy is confirmatory
FIGURE 26.6 Isotope scan—multiple bone secondaries including ribs.
Treatment
• Radical excision is the treatment of choice for all tumours
• Chemoradiation is the treatment of choice in tumours such as Ewing’s
sarcoma, osteogenic sarcoma and metastatic tumours
26.4 Diseases of pleura
They can be classified based on their aetiology. They are tabulated in Table 26.4.
TABLE 26.4
Aetiological Classification of Diseases of Pleura
Aetiology Pathology
Inflammatory Acute Pleurisy
Pleural effusion
Empyema
Spontaneous pneumothorax
Chronic Empyema
Neoplastic Benign Fibroma, solitary fibrous tumour
Malignant Fibrosacroma, malignant mesothelioma
Pleurisy
• A simple term denoting the pleural involvement of any disease giving rise to
pleuritic pain or evidence of pleural friction
• Common feature of pleural invasion by pulmonary tuberculosis or
bronchogenic carcinoma
• Pain characteristically inspirational
• On examination, the chest movement may be restricted locally with an
audible pleural rub better heard at basal regions. Other features depend on
the nature of underlying cause
X-ray of the chest is useful in identifying the underlying cause
Treatment
Analgesics are required to treat pleuritic pain with treatment focused towards the
primary cause
Pleural effusion
Denotes accumulation of serous fluid in the pleural space, which results due to:
• Increased hydrostatic pressure or decreased osmotic pressure (transudative
effusion). The causes are:
• Cardiac failure (postmyocardial infarction)
• Hepatic failure
• Renal failure
• Increased microvascular permeability due to disease of pleura or adjacent
lung (exudative effusion). The causes are:
• Infections (bacterial, tuberculous, fungal, parasitic, viral)
• Immunological disorders (rheumatoid, lupus)
• Malignancy (mesothelioma, lung cancer, metastases)
• Pulmonary embolism
• Abdominal disease (e.g. pancreatitis, subphrenic abscess)
• The effusion can be:
• Unilateral (e.g. tuberculosis, malignancy)
• Bilateral (e.g. cardiac failure, hypoproteinemia)
• Symptoms and signs of pleurisy often precede the development of effusion
• Breathlessness is the commonest symptom
• Physical signs include reduced chest wall movement on the affected side,
stony dullness on percussion and reduced or absent breath sounds and vocal
resonance
• Large effusions shift the trachea to the opposite side
• Chest X-ray shows a dense uniform opacity in the lower and lateral parts of
haemithorax, shading off above and medially into translucent lung (about
200 ml is required to blunt the costodiaphragmatic angle) (Ellis S curve)
(Fig. 26.7A)
• Ultrasonography (US) is very useful in differentiating the effusion and
tumour
• CT (Fig. 26.7B) is diagnostic
• Aspiration of pleural fluid is necessary for:
• Nature (blood—malignancy, embolus, milky—chyle, pus—empyema,
straw coloured—tuberculosis)
• Microbiology—culture sensitivity
• Cytology
• Biochemistry
- Exudate(Light’s criteria)
1. Pleural fluid protein / serum protein ratio. 0.5
2. Pleural fluid lactate dehydrogenase (LDH)/serum LDH
ratio > 0.6
3. Total proteins >3 g%
- High levels of:
1. Triglycerides >110 mg%—chylothorax
2. Amylase—pancreatitis
• Bronchoscopy biopsy, thoracoscopy and biopsy of enlarged lymph nodes
may be needed to identify the primary cause
• Pleural biopsy yields good results
FIGURE 26.7A Right pleural effusion.
FIGURE 26.7B CT—pleural effusion (left).
Treatment
Aspiration of pleural fluid may be necessary to relieve breathlessness, but
treatment of underlying cause is necessary
Acute empyema
• Empyema indicates pus in the pleural space, which may involve a part
(loculated) or the whole of it
• Always secondary to infection in a neighbouring structure, usually the lung
(bacterial pneumonia and tuberculosis)
• Other causes being, infection of haemothorax or rupture of subphrenic abscess
or liver abscess
Complications: Bronchopleural fistula, empyema necessitans, (empyema
burrowing through the chest wall to present as an opening externally),
pleurocutaneous fistula, pericarditis, mediastinal abscess
• High intermittent pyrexia, with rigors, sweating, malaise and weight loss
• Pleural pain, breathlessness and cough with purulent sputum
• Clinical signs are those of pleural effusion
• Tenderness over the chest on palpation
• Chest X-ray is diagnostic
• US and CT give invaluable information
• Aspiration of pus is confirmatory
• Pleural aspirate WBC count 10,000/ml is diagnostic
• Isolation of organism from sputum or pleural aspirate is useful in treatment
Treatment
• General—supportive respiratory care, physiotherapy
• Drainage of pleural space (thoracentesis or close drainage) and irrigation
with normal saline is necessary to clear the pleural space of the pus, under
cover of appropriate antibiotics
• Underlying causes such as pneumonia and tuberculosis need active
treatment
Pneumothorax
• Pneumothorax is presence of air in the pleural cavity
• Spontaneous pneumothorax can be:
• Primary—without any obvious evidence of pulmonary pathology (e.g.
rupture of small emphysematous bulla)
• Secondary—due to underlying pulmonary pathology (e.g. chronic
obstructive pulmonary disease (COPD), tuberculosis)
• Traumatic pneumothorax:
• Noniatrogenic—barotrauma, chest injury
• Iatrogenic—biopsy, pleurocentesis
• This is a sudden event, with sudden unilateral chest pain or breathlessness
• Small pneumothorax shows no clinical signs, whereas, large ones show
decreased movement of chest wall, hyper resonant percussion note and
decreased or absent breath sounds
• Chest X-ray shows sharply defined edge of the deflated lung with complete
translucency between the line and the chest wall with no lung markings (Fig.
26.8)
• CT is useful in defining the underlying pathology
FIGURE 26.8 X-ray—right pneumothorax.
Treatment
• Percutaneous needle aspiration of air is necessary for full lung expansion
• Intercostal tube drainage with underwater seal may be needed
• Smoking should be completely avoided and the underlying pathology
treated
Pleural tumours
• Primary tumours
• Commonest pleural tumour is mesothelioma
• Arises from mesothelial cells of pleura
• Occurs at any age, most common in the 50–70 year age group
• Usually unilateral
• They can be divided into localized and diffuse types:
- Localized tumour is generally benign and is either a fibroma or a
mesothelioma
- Diffuse malignant mesothelioma simulates pleural effusion
• Malignant mesothelioma of pleura is linked to blue asbestos (crocidolite),
with a time lag of over 20 years between the contact and tumour
development
• Malignant mesothelioma invades adjacent structures such as underlying
lung, overlying chest wall, pericardium and contralateral haemithorax
• Lymphatic spread and distant metastases are uncommon
• Secondary tumours
• Usually associated with lung metastases
Symptoms
• Localized tumour causes no symptoms till it attains a large size (Fig. 26.9)
• Benign mesothelioma may cause severe hypoglycemia
• Chest pain is the presenting symptom in some cases
• Breathlessness may occur due to pleural effusion which is bloodstained
• Dry cough and systemic symptoms such as anorexia, weight loss and fever
may occur
FIGURE 26.9 Mesothelioma right pleura Source: (Courtesy Dr S Devaji Rao).
Signs
• Finger clubbing, if there is prior asbestosis
• Reduced chest expansion, dullness to percussion and reduced breath sounds
on the affected side
• X-ray of the chest (Fig. 26.10) and CT thorax are diagnostic (Figs. 26.11A
and B)
• Percutaneous pleural aspirate may be blood stained and high in protein. A
high level of hyaluronic acid (> 50 mg/L) is common. Cytological
examination may show malignant mesothelial cells
• Pleural biopsy (US or CT guided) is confirmatory
FIGURE 26.10 X-ray—mesothelioma right side Source: (Courtesy Dr S Devaji
Rao).
FIGURE 26.11A CT—mass from pleura left side.
FIGURE 26.11B CT—pleural metastatic nodule with effusion.
Treatment
• No curative treatment for mesothelioma, pleurectomy is done in some
patients
• Radiotherapy is of value in palliating chest pain
• Chemotherapy (cisplatin, premetrexed) is useful
• Immunotherapy (imatinib, bevacizumab, IL2, IF8) is useful
• Simple drainage of pleural effusion gives adequate symptomatic relief
26.5 Diseases of trachea and bronchi

They can be classified based on the aetiology (Table 26.5).
TABLE 26.5
Aetiological Classification of Diseases of Trachea and Bronchi
Aetiology Pathology
Congenital Tracheal stenosis, tracheal agenesis, tracheobronchomegaly, bronchogenic cysts
Tracheo-oesophageal fistula
Inflammatory Tracheitis
Laryngotracheobronchitis
Bronchiectasis
Neoplastic Benign Papilloma
Malignant Carcinoma
Miscellaneous Foreign bodies, arteriovenous malformation
Tracheal stenosis
• Congenital
• Developmental defect due to deficiency of membranous trachea and the
wall consists of complete cartilaginous rings
• Often associated with other anomalies of tracheobronchial tree
• Acquired
• Postintubation (cuffed tubes cause local ischaemia, ulceration and fibrosis)
• Posttraumatic (e.g. complete avulsion of trachea from larynx)
• Postinfectious (e.g. tracheobronchial tuberculosis, diphtheria)
• Neoplastic (e.g. malignant tumours)
• Difficulty in breathing may be present
• Clinical examination may demonstrate rhonchi, stridor
• Bronchoscopy is diagnostic
• Spiral CT with reconstruction is the investigation of choice
Treatment
• Dilatation
• Dilatation and stenting
• Resection with primary reconstruction
Note
Mounier-Kuhn syndrome—tracheobronchomegaly, Williams-Campbell
syndrome—tracheobronchomalacia
Tracheo-oesophageal fistula
This fistulous communication can occur in:
• Newborn infants as a congenital abnormality
• Adults due to malignant lesions in the mediastinum such as infiltrating
oesophageal carcinoma or lymphoma
• Cough and fever are common symptoms due to the entry of swallowed food
into the respiratory tract
• Choking and cyanotic spells after food intake
Barium swallow
(Fig. 26.12) allows the contrast to enter the trachea and bronchi, and is
diagnostic

FIGURE 26.12 Barium swallow—tracheo-oesophageal fistula.
Treatment
• Surgical closure of a congenital fistula is usually successful
• Malignant fistulae are difficult to handle and death becomes inevitable due to
pulmonary infection
Acute tracheitis and laryngotracheobronchitis

(croup)
• Usually follows acute coryza (common cold)
• Usually due to parainfluenza I and III virus infection
• Acute laryngotracheobronchitis in children is fatal, due to superinfection with
bacteria such as Streptococcus pneumoniae and Staphylococcus aureus
• Initially the cough is unproductive accompanied by retrosternal discomfort
• Inspiratory stridor and bark such as cough
• When bronchi are involved, chest tightness, wheeze and breathlessness occur
• Fever may be associated
• Sputum is initially scanty and mucoid, later becomes more copious
Microbiological analysis of sputum may be useful
Treatment
• Cough suppressants such as codeine is useful
• Antibiotics are mandatory
• Bronchodilators may be necessary to relieve bronchospasm
• Endotracheal intubation is necessary for acute laryngotracheobronchitis in
children with maintenance of hydration
• Nebulization with racemic epinephrine, steroids and humidified air
Bronchiectasis
• Bronchiectasis denotes abnormal permanent dilatation of medium sized
bronchi, which may be due to various causes. They are:
• Congenital—ciliary dysfunction, cystic fibrosis, primary
gammaglobulinaemia, tracheobronchomalacia, tracheobronchomegaly
• Acquired
- Children—pneumonia, primary tuberculosis, foreign body
- Adults—suppurative pneumonia, pulmonary tuberculosis, bronchial
tumours
• Bronchiectatic cavities may be lined by granulation tissue with inflammatory
changes in the deeper layers of the bronchial wall with hypertrophy of
bronchial arteries. Surrounding lung tissue may show chronic inflammatory
and fibrotic changes
• It may involve any part of the lung but these complications are more severe
with lower lobar lesions due to gravity
• Chronic productive cough, with three-layered sputum, more in the mornings
is common
• Fever, malaise occur when there are inflammatory changes
• Haemoptysis is not uncommon
• Coarse leathery mid inspiratory crackles on auscultation
• Persistent purulent bronchiectasis causes weight loss, anorexia and failure to
thrive in children. Clubbing of fingers is commonly seen
• X-ray of the chest shows cystic spaces (ring shadow, tram track appearance,
gloved finger appearance) when the disease is gross
• High-resolution computed tomography (HRCT) chest (Fig. 26.13) is
diagnostic
• Bacteriological and mycological examination of sputum and ciliary function
studies are necessary in most cases
• Bronchoscopy and bronchogram may be needed in select cases
FIGURE 26.13 CT—bronchiectasis.
Treatment
• Postural drainage of sputum (aided by chest physiotherapy), under cover of
appropriate antibiotics is necessary
• Surgery is indicated in small number of cases especially when the disease is
limited to one lobe or a segment
• Surgical resection is needed in few cases with persistent or life threatening
haemoptysis
Benign tumours
Benign tumours are rare.
They are generally classified based on the tissue of origin:
• Epithelial
• Polyp
• Papilloma
• Mucous gland adenoma
• Mesodermal
• Chondroma
• Fibroma
• Lipoma
• Leiomyoma
• Schwannoma
• Haemangiopericytoma
• Unknown
• Hamartoma
• Clear cell tumour
• Others
• Plasma cell granuloma
• Germ cell tumour
• Xanthoma
• Amyloid
• Mixed tumours
• Usually asymptomatic
• Chance finding
• X-ray of the chest may show a solitary lung nodule
• CT and fine-needle aspiration (FNA) are useful
Treatment
Simple excision
Malignant tumours
• Attributed to exposure of bronchial epithelium to inhaled carcinogens
• Tobacco smoking (90%)—related to duration and intensity of smoking
• Pollution
• Chemicals such as chromate, arsenic and nickel and asbestos
• The malignancies are divided (Fig. 26.14) into:
• Small cell carcinoma (25%)
• Non small cell carcinoma (75%)
- Squamous cell carcinoma (40%)
- Adenocarcinoma (30%)
- Large cell anaplastic carcinoma (5%)
• Others
- Carcinoid
- Salivary gland tumours
- Sarcomatous
• The genetic predispositions are:
• Squamous cell carcinoma (loss of heterozygosity of the p53 gene)
• Small cell carcinoma (over expression of C-myc and loss of heterozygosity
of the p53 gene)
• Disruption of Rb gene is universal in lung cancer
• EGFR (+) in 84% of SCCs
• HER2/neu (+) and K-ras (+) frequest in adenocarcinomas, infrequent in
SCCs
• The tumour spreads
• Locally to extend proximally to carina and trachea, and distally to visceral
pleura, chest wall or diaphragm. Circumferential spread leads to bronchial
obstruction, leading to lobar or segmental collapse of lung. Stasis of
secretions leads to secondary infection, manifesting as pneumonia. Spread
to mediastinal structures such as the oesophagus, pericardium, heart, great
vessels and vertebral bodies are common
• Lymphatically to mediastinal lymph nodes and to supraclavicular lymph
nodes
• Haematogenously to the adrenals (50%), liver (30%), brain and bones
FIGURE 26.14 Incidence of primary malignant tumours of lungs.
Symptoms
• Persistent cough (due to irritation of bronchi by tumour)
• Haemoptysis (slight streaking to frank haemorrhage due to ulceration of
tumour)
• Dyspnoea (due to pleural effusion, bronchial obstruction)
• Chest pain (pleuritic pain or ache)
• Recurrent chest infections
• Appetite and weight loss are common
• Hoarseness occurs when recurrent laryngeal nerve is involved
• Stridor due to airway obstruction
Signs
• No physical signs may be elicited
• General examination may show clubbing and nicotine staining of fingertips
• Neck may show enlarged lymph nodes
• Signs of pleural effusion may be present
• Horner’s syndrome may occur when cervical sympathetic nerves are involved
at T1 level
• X-ray of the chest may show discrete opacities, hilar lymphadenopathy,
pulmonary collapse, consolidation and pleural effusion
• Contrast-enhanced CT (CECT) (Fig. 26.15) and MRI are diagnostic and
determine the spread
• Sputum cytology may be useful
• Bronchoscopy (Fig. 26.16) and washings and brushings for cytology
• Bronchoscopy biopsy is confirmatory, excepting in peripheral lesions
• Fine-needle aspiration cytology (FNAC) is useful for peripheral lesions
• Isotope bone scan is useful to assess bone metastases
• Mediastinoscopy is useful is assessing the operability of tumour staging
• Indirect laryngoscopy to assess the recurrent laryngeal nerve involvement by
examining the vocal cords
FIGURE 26.15 CT—bronchogenic carcinoma right side.
FIGURE 26.16 Endobronchial view of carcinoid in right intermediate
bronchus.
Treatment
Lobectomy or pneumonectomy with or without chemoradiation
is the treatment of choice, for malignancies up to stage IIIA. Larger lesions are
not resectable
Foreign bodies
• Foreign bodies get lodged in the trachea and bronchi accidentally, and are
more common in:
• children than in adults
• the bronchus than the trachea
• the right bronchus than the left, as the right bronchus is a direct
continuation of trachea and is wider than the left bronchus
• In children, the objects are in the form of seeds, buttons, cells, etc., and in
adults, they are dentures, loose teeth, etc.
• In adults, accidental lodging when they are under the influence of alcohol
• Foreign bodies act like a valve and cause symptoms (Table 26.6)
TABLE 26.6
Pathogenesis of Foreign Body Obstruction in Lower Respiratory
Tract
Mechanism Pathophysiology
Stop valve Foreign body causes total obstruction and does not allow air entry (ingress) or allow air and secretions to
escape (egress). The lobe of lung may collapse and consolidate
Bypass When the foreign body is small or has a hole, it allows ingress and egress of air
valve
Ball valve During inspiration, the bronchi dilate allowing air to enter (ingress), but do not allow air to escape (egress)
as the bronchi constrict during expiration. The trapped air caused pneumothorax or emphysema
Dyspnoea, cough, stridor, cyanosis and fever are common
• X-rays reveal the radio-opaque foreign bodies, and collapsed lungs
• Bronchoscopy is diagnostic
Treatment
Bronchoscopic removal (using a rigid bronchoscope) is curative
26.6 Diseases of lungs
They can be classified based on their aetiology. They are tabulated in Table 26.7.
TABLE 26.7
Aetiological Classification of Diseases of Lungs
Aetiology Pathology
Congenital Pulmonary agenesis, pulmonary hypoplasia
Cystic fibrosis, sequestration
Inflammatory Acute Suppurative pneumonia
Hospital-acquired pneumonia
Lung abscess
Chronic Tuberculosis
Fungal infections
Neoplastic Malignant Metastatic lung disease
Interstitial and infiltrative Sarcoidosis
Due to systemic diseases Acute respiratory distress syndrome
Pulmonary embolism
Pulmonary agenesis/hypoplasia
• Pulmonary agenesis may be unilateral or varying degrees of hypoplasia may
occur. Other congenital anomalies may be present
• Conditions causing reduced intrathoracic space in utero cause hypoplasia
Dyspnoea of varying degrees are present
Treatment
No treatment is possible, but may be indicated in select cases to treat
haemoptysis and superimposed chronic infection or because of associated
congenital cardiac disease
Cystic fibrosis
Most common severe autosomal recessive disease, due to mutation affecting a
gene that codes for CFTR (located on the long arm of chromosome 7)
Symptoms are due to complications:
• Respiratory—spontaneous pneumothorax, nasal polyps, cor pulmonale,
chronic infection, haemoptysis
• Gastrointestinal—malabsorption, biliary cirrhosis, gallstones, DIOS
• Others—diabetes, male infertility, amyloidosis, arthropathy
Repeated lung infections lead to respiratory failure and death
• X-ray, CT chest and chromosomal analysis
• Sweat chloride test (>70 mEq/L) is diagnostic
Treatment
Chest physiotherapy, antibiotics and nebulization of recombinant human
DNAse (mucolytics)
Aspiration pneumonia
• Suppurative pneumonia or pneumonic consolidation denotes destruction of
lung parenchyma by inflammatory process with microabscess formation on
histology
• Staphylococcus aureus and Klebsiealla pneumoniae infections cause
suppuration, which may follow inhalation of septic material during
endotracheal anesthesia or by aspiration of gastric contents
• Aspiration may lead to severe acute respiratory distress syndrome (ARDS)
• Suppuration has an insidious onset whereas aspiration is acute
• Productive cough (fetid or blood stained)
• Pleural pain may be present
• High remittent pyrexia is common
• Chest examination may show signs of consolidation, with pleural rub
Chest X-ray (Fig. 26.17) shows homogenous lobar or segmental opacity. A
cavity with fluid level may indicate an abscess
FIGURE 26.17 X-ray—aspiration pneumonia right lung.
Treatment
• Broad-spectrum antibiotics form the mainstay of treatment
• Surgical intervention may be required for abscess, which does not respond to
medical therapy
Hospital acquired pneumonia

Refers to a new episode of pneumonia, 48 h after admission to hospital, not
incubating at the time of admission. The predisposing factors for the
development of pneumonia are:
• Immunocompromised state (e.g. corticosteroid treatment, malignancy, AIDS)
• Reduced cough reflex (e.g. postoperative)
• Aspiration of gastric contents (e.g. vomiting, severe reflux, nasogastric
intubation)
• Endotracheal intubation (e.g. mechanical ventilation)
• Bacteraemia (e.g. sepsis)
• Cough with purulent expectoration is the predominant symptom
• Breathlessness and cyanosis will appear soon
• On examination, crepitations are heard on auscultation
• Leucocytosis is present
• Sputum culture and Gram staining are useful
• Chest X-ray will show bilateral nonhomogenous opacities
Treatment
• Broad-spectrum intravenous antibiotics are necessary
• Physiotherapy is mandatory in immobile patients
Lung abscess
• A suppurative focus within the lung associated with necrosis > 2 cm in
diameter
• Bacteria responsible for a lung abscess may reach the lung through various
routes. They are:
• Aspiration down the tracheobronchial tree (e.g. aspiration pneumonia)
• By blood (e.g. septicaemia)
• Trauma (e.g. penetrating trauma)
• Extension of adjacent suppurative focus (e.g. liver abscess)
• Other causes are:
• Tumours of bronchus (e.g. bronchogenic carcinoma)
• Suppuration of haematoma (e.g. penetrating trauma)
• Appear acutely ill
• Cough with foul smelling purulent expectoration
• Haemoptysis may occur
• Postural variation of symptoms
• Sputum for culture and acid-fast bacillus (AFB) smear
• Bronchoscopic washings for AFB smear and culture
• X-ray and CT are diagnostic (Fig. 26.18)
FIGURE 26.18 X-ray—lung abscess.
Treatment
Antimicrobial therapy resolves most abscesses
Surgical intervention (lobectomy or segmentectomy), is reserved for those
which do not respond
Pulmonary tuberculosis
• Infection caused by Mycobacterium tuberculosis
• Lungs are the commonest of the sites involved, others being the lymph nodes,
skin and soft tissues
• The mode of entry is through infected droplets of air
• More common in HIV-infected individuals
• From the primary focus, it can spread to:
• mediastinal lymph nodes
• direct extension of primary focus
• extension to pleura
• blood borne to bones, genitourinary tract (months or years later), and to
meninges or widespread in the body (miliary tuberculosis)
• Complications are:
• Consolidation or collapse of lung
• Bronchiectasis
• Cavitation of lung
• Pleural effusion or empyema
• Miliary spread
• Many may remain asymptomatic
• Chronic cough with or without haemoptysis, with pyrexia is common
• Weight loss and general debility may be presenting symptoms
• Bacteriological examination of sputum, bronchoalveolar lavage or
transbronchial biopsy for AFB smear and culture
• X-ray of the chest may show consolidation, cavitation, or collapse, with or
without pleural effusion (Figs. 26.19A to C)
FIGURE 26.19A X-ray—right upper lobe atlectasis.
FIGURE 26.19B X-ray—left upper lobe fibrocavity disease.
FIGURE 26.19C X-ray—destroyed left lung.
Treatment
Antitubercular treatment is mandatory, for effective cure
Fungal infections
• Aspergillosis forms the commonest fungal infection of lungs, caused by
hypersensitivity reactions to Aspergillus fumigatus, more commonly in
asthmatics
• Other fungi which can invade the lungs are:
• Candida
• Histoplasma
• Coccidiomyces
• Blastomyces
Fever, breathlessness and productive cough are common symptoms
• Chest X-ray (Fig. 26.20) shows changes of bronchiectasis in the upper lobes
• Bronchoscopy is useful
• Serum precipitins to A. fumigatus may be shown in almost all patients
• Serum IgE levels
FIGURE 26.20 X-ray—aspergilloma.
Treatment
• Corticosteroids are used to suppress immunological responses, optimal
control of asthma with adequate physiotherapy
• Specific antifungal therapyis necessary
• Surgerymay be needed for persistent cavity disease and complications
Metastatic lung disease

• Lung is the most common site of metastasis for all malignancies
• Most often develop following haematogenous spread
• Majority of them have micrometastases at multiple sites
• Isolated lung metastases occur in up to one third of patients of malignancies
• Most metastases are peripheral lesions
• Metastases can be of various types (Table 26.7A.)
TABLE 26.7A
Types of Metastatic Lung Disease
Primary Nodular Lymphangitis Central Cavitation Intra Bronchial Tumour Emboli Lepidic
Carcinomatosis Masses Pattern
Breast Stomach SCC of Breast Breast Colon
aerodigestive
tract
GIT Breast Colon Kidney Stomach Pancreas
Kidney Choriocarcinoma Leiomyosarcoma Colon Liver
Sarcoma Pancreas Choriocarcinoma
Melanoma Prostate
• Most patients are asymptomatic
• Diagnosis is usually made on follow-up chest X-ray after resection of primary
tumour
• X-ray chest (Fig. 26.21) is suggestive or metastases, appear as ‘cannon balls’
due to haematogenous spread
• CT chest (Fig. 26.22) is useful in detecting smaller lesions
FIGURE 26.21 X-ray—coin shadow right middle zone.
FIGURE 26.22 CT—multiple lung metastases.
Treatment
• Curative options are few for metastatic lung lesions
• Surgical resection is appropriate when:
• The primary tumour is successfully controlled
• All metastases are possible to be resected
• There is no extrathoracic metastases
Sarcoidosis
• A multisystem granulomatous disease
• Uncertain aetiology
• Most common in cold climates
• Lungs are affected in more than 90% cases
• Histologically, the lesions resemble tuberculosis, but caseation and tubercle
bacilli are absent
• The mediastinal lymph nodes, liver, spleen, skin, eyes and parotid glands are
most frequently affected
• Acute form may present with erythema nodosum, peripheral neuropathy,
uveitis and bilateral hilar lymphadenopathy
• Chronic form presents with cough, exertional breathlessness
• Mantoux test remains negative and is useful in eliminating tuberculosis
• Serum angiotensin generating enzyme is usually elevated
• Kveim’s test is diagnostic
• Transbronchial lung biopsy is confirmatory in majority of cases
• Radionuclide scan is useful in diagnosis
• X-ray and CT chest show characteristic findings (Fig. 26.23)
FIGURE 26.23 X-ray—sarcoidosis.
Treatment
• Rarely required for early cases
• Steroids such as prednisolone are useful in management of advanced cases
• Methotrexate and hydroxychloroquine are effective second line drugs
Acute respiratory distress syndrome (ARDS)

• Indicates the acute diffuse pulmonary inflammatory response to either direct
or indirect insults from extrapulmonary pathology
• Direct—via airway or injury to chest (e.g. aspiration, toxic gases,
pneumonia)
• Indirect—blood-borne insults (e.g. sepsis, polytrauma, severe burns, drugs)
• Frequently associated with multiple organ (kidney, liver, intestines)
dysfunction
• Pathophysiology is complex
They are not specific, but share many things with other pulmonary pathologies
• Blood gas analysis (PaO2/FiO2 of less than 200 mg Hg)
• X-ray of the chest shows bilateral diffuse infiltrates
• Pulmonary capillary wedge pressure (less than 18 mm Hg)
Treatment
Current treatment is supportive and no specific therapy exists to modulate the
sequence of events of ARDS
• Monitoring
• Monitoring of all vitals
• Ventilatory management
• Mechanical ventilation to permit adequate oxygen uptake
• Nonventilatory management
• Treatment of underlying risk factors
• Enteral feeding
• Maintenance of haemodynamic stability and cardiac output
Pulmonary embolism
Majority of pulmonary emboli result from deep venous thrombosis of lower
limbs, and they can be acute (minor and massive) or chronic
The symptoms and signs are tabulated in Table 26.8
TABLE 26.8
Symptoms and Signs of Pulmonary Embolism
Type Symptoms Examination Findings

Acute Shortness of breath and haemoptysis— Pleural rub and signs of pleural effusion
minor pleurisy
Acute Central chest pain, apprehension, low Sinus tachycardia, hypotension and peripheral vasoconstriction
massive cardiac output and syncope
Chronic Exertional dyspnoea, syncope and chest Pulmonary hypertension, loud pulmonary component of second
pain over months and years heart sound and a right ventricular heave
Chest radiographs, ECG, arterial blood gases, ventilation-perfusion lung
scanning and pulmonary angiography are useful investigations
Treatment
• General—opiates to relieve pain and distress, resuscitation by external
cardiac massage, with oxygen support
• Anticoagulation is necessary at least for 5 days
• Thrombolytic therapy is used in acute massive types
26.7 Diseases of mediastinum
Acute mediastinitis
Acute mediastinitis occurs due to varied causes. They are:
• injury to cervical or thoracic oesophagus
• extension of cervical infections
• secondary to osteomyelitis of ribs and sternum
• extension of retroperitoneal infections
• suppuration of mediastinal lymph nodes
• Chest pain, fever and chills are commonly present
• Symptoms related to primary cause are usually present
• X-ray of the chest (Fig. 26.24) may show mediastinal widening
• CT chest is diagnostic, especially of the primary cause
FIGURE 26.24 X-ray—mediastinitis.
Treatment
• Broad-spectrum antibiotics are necessary with anaerobic coverage
• Immediate surgery with adequate mediastinal drainage for oesophageal
injuries
Chronic mediastinitis
Chronic granulomatous infections of mediastinal lymph nodes, especially
tuberculosis and fungal infections are the causes of chronic mediastinitis
• Chest pain, fever and chronic cough are common symptoms
• Superior vena cava may be obstructed in upper mediastinal lesions
• Constriction of pulmonary veins may lead to cardiocirculatory signs
• X-ray chest shows mediastinal widening
• CT chest is diagnostic, especially of the primary cause
Treatment
Appropriate antibiotics with surgical drainage of any localized abscess or
excision of necrotic granulomatous lymph tissue
Mediastinal tumours
Variety of tumours occur in the mediastinum and they are shown in Table 26.9
TABLE 26.9
Tumours of Mediastinum
Mediastinum Tumours
Benign Malignant
Anterior •Thymoma (most •Thymic carcinoma

common) •Thyroid malignancy
•Thymic cyst •Germ cell tumours (teratomas, seminomas and nonseminomatous
•Thymic hyperplasia germ cell tumours)
•Thyroid neoplasms •Lymphoma
•Cystic hygroma •Thymic carcinoid
•Parathyroid neoplasms
Middle •Cysts •Lymphoma
•Oesophageal mass •Metastases
•Hiatus hernia •Oesophageal malignancy
•Cardiac and vascular •Thyroid malignancy
structures
•Lipomas
•Ectopic thyroid
Posterior •Neurofibroma •Neuroblastoma
•Schwannoma
•Chemodectoma
•Foramen of Bochdalek
hernia
•Meningocele
•Cysts
Anterior mediastinum
• Thymomas are the commonest tumours of anterior mediastinum
• Teratomas are the most common germ cell tumours of the mediastinum
(common in men of 40)
• Primary mediastinal malignant nonseminomatous tumours occur in young
men and may be associated with Klinefelter syndrome
• Both Hodgkin’s and non-Hodgkin’s lymphomas can occur as primary
malignancies, but usually a part of disseminated lymphoma
Middle mediastinum
• Most common masses of middle mediastinum are lymphatic (infection,
inflammation or primary or metastatic neoplasms)
Posterior mediastinum
• Most common posterior mediastinal masses are neurogenic
Symptoms
• Thymomas: Cough, chest pain, dyspnoea, hoarseness and superior vena cava
syndrome and myasthenia gravis
Signs
• No specific clinical finding is elicitable in most mediastinal masses unless
they are large
• Radiology
• X-ray chest (Fig. 26.25A) shows a soft tissue mass in the mediastinum.
Combinations of fat, fluid, soft tissues and calcium deposits (teeth or
bones) is highly suggestive of a teratoma
• CT (Fig. 26.25B) and MRI give enormous information (MRI better than
CT) of mediastinal tumours
• Radionuclide studies
• Isotope scanning (thallium 201, technetium-99m—sestamibi imaging) is
useful for thyroid tumours
• Positron emission tomography (PET) scanning is useful
• Biochemistry
• Thymomas: Serum anti acetyl choline receptor antibodies are raised
• Seminomas: Beta hCG levels are occasionally raised
• Nonseminomatous tumours: Alpha fetoprotein and beta hCG levels are
used in most cases
• Endoscopy
• Cervical mediastinoscopy
• Anterior mediastinoscopy
• Thoracoscopy
• Exploratory thoracotomy
• Bronchoscopy
• Endoscopic ultrasonography
• Oesophagoscopy
• Histopathology
• CT-guided FNA
• Biopsy
FIGURE 26.25A X-ray—hilar lymph nodes.
FIGURE 26.25B CT—hilar lymph nodes secondary to breast malignancy.
Treatment
• All mediastinal masses need to be excised, malignant ones radically
• Multidisciplinary treatment is needed for germ cell tumours and lymphatic
malignancies
26.8 Symptoms of pathologies of chest

• Cough with expectoration
• Difficulty in breathing
• Chest pain
• Haemoptysis
Cough with expectoration
Cough is the most frequent symptom of respiratory disease. It is caused by
sensory nerve stimulation in the mucosa of the entire tract. Rarely, stimulation of
parietal pleura can cause cough. Various varieties of cough and their causes are
given in Table 26.10. The varieties of expectoration (sputum) and their causes
TABLE 26.10
Causes and Characteristics of Cough
Nature of Cough Pathologies

Dry cough Pleural and mediastinal diseases, interstitial lung disease
Productive cough Chronic bronchitis, suppurative lung disease
Brassy cough (metallic cough) Extrinsic compression of trachea by intrathoracic SOL
Bovine cough Paralysis of recurrent laryngeal nerve
Staccato cough (paroxysmal cough) Whooping cough
Barking or seal-like cough Laryngotracheobronchitis
TABLE 26.11
Causes and Characteristics of Expectoration (Sputum)
Nature of Sputum Pathologies
Green-coloured sputum Allergic conditions, pseudomonas infection

Pink frothy sputum Pulmonary oedema
Anchovy sauce sputum Rupture of amoebic liver abscess into lung
Red currant jelly sputum Klebsiella pneumonia
Dyspnoea (breathlessness)
It is defined as an unpleasant and subjective awareness of the sensation of
breathing
• It is a common symptom of cardiac and respiratory diseases, but can occur in
disorders of other systems, e.g. diabetic ketoacidosis
• Some important respiratory causes of dyspnoea are given in Table 26.12
TABLE 26.12
Causes of Dyspnoea
Acute Dyspnoea at Rest Chronic Exertional Dyspnoea

Acute obstructive airway disease Chronic obstructive airway disease
Pneumothorax Bronchial carcinoma
Acute pneumonia Interstitial lung disease
Pulmonary embolism Pleural effusion
Lobar collapse
Chest pain
Chest pain is a major manifestation of cardiac and respiratory disease
• In general, lung diseases give rise to chest pain only when there is pleural or
chest wall involvement (peripheral)
• Chest pain of respiratory origin may be central (tightness) or peripheral. They
are shown in Table 26.13
TABLE 26.13
Causes of Chest Pain of Respiratory Origin
Chest Pain
Central Peripheral
Obstructive airway disease Pulmonary infarction

Tracheitis Pneumonia
Pneumothorax
Tuberculosis
Malignancy
Connective tissue disorders
Haemoptysis
Coughing up blood is defined as haemoptysis. It must always be considered
serious till the cause is established. Causes of haemoptysis are tabulated in Table
26.14.
TABLE 26.14
Causes of Haemoptysis
Bronchial Lung Parenchymal Lung Vascular

Carcinoma Tuberculosis Pulmonary infarction
Bronchiectasis Suppurative pneumonia Pulmonary embolism
Acute bronchitis Trauma
Bronchia adenoma Lung abscess
Foreign body Fungal infections
Note
• Pneumococcal pneumonia causes usually rust coloured sputum.
• Bronchiectasis and intracavity aspergilloma (fungal ball) can cause
catastrophic haemorrhage.
• Cardiovascular diseases (e.g. acute left ventricular failure, mitral stenosis
and aortic aneurysm) and blood disorders (e.g. leukaemia, haemophilia, and
anticoagulants) can cause haemoptysis.
• Spurious haemoptysis—haemoptysis due to upper respiratory causes.
• Pseudohaemoptysis—due to the pigment prodigiosin produced by a Gram
negative organism—Serratia marcescens.
• Endemic haemoptysis—infection with lung fluke (Paragonimus
westermanii).
Eliciting history
Cough with expectoration
• Duration of cough: How long has he or she been suffering from cough?
Acute or transient cough mostly indicates viral infection affecting the
respiratory tract (e.g. laryngitis, bronchitis), and can be due to other reasons
(e.g. pneumonia, aspiration), but they have other clinical features and clinical
situations. Chronic cough may indicate tuberculosis, COPD
• Nature of cough: Is the cough associated with expectoration?
Dry cough usually indicates upper respiratory pathology (e.g. tracheitis),
whereas, expectoration indicates diseases such as bronchitis, tuberculosis,
bronchiectasis. Persistent expectoration may indicate malignancy, especially
in the elderly and smokers
• Nature of expectoration: What is the nature of expectoration?
The expectoration may be in varying quantities. Expectoration may increase
in certain postures (e.g. pneumonia, bronchiectasis), may be purulent (e.g.
suppurative pneumonia) or pink and frothy (e.g. pulmonary oedema)
• Postural variation: Does the expectoration vary with postures?
Lung abscess related expectoration will be more when the patient is lying on
the side opposite the lesion
• Seasonal variation: Does the cough and expectoration increase in various
seasons?
Allergic conditions will show increased cough and expectoration during cold
reasons
Difficulty in breathing
• Duration: How long has he or she been suffering from difficulty in
breathing?
Dyspnoea of acute onset may indicate acute events (e.g. spontaneous
pneumothorax, acute pulmonary oedema) and longer duration in diseases
such as COPD, chronic asthma and malignancy
• Nature of dyspnoea: Is the dyspnoea present at rest or related to exertion?
Dyspnoea at rest indicates acute events (e.g. cardiac—myocardial ischaemia,
respiratory—acute asthma, pneumothorax, pneumonia, lobar collapse), and
exertional dyspnoea may indicate events such as (e.g. cardiac—chronic heart
failure, respiratory—COPD, interstitial lung disease)
• Postural and seasonal variations: Does the cough and expectoration
increase in various seasons?
Dyspnoea of COPD will be more on lying down and during cold seasons
Chest pain
• Duration: How long has the patient been complaining of chest pain?
Chest pain of short duration may indicate acute pathology (e.g. acute
bronchitis) and longer duration may indicate chronic pathology (e.g.
myocardial ischaemia, COPD)
• Nature: Is the chest pain severe or mild?
Severe chest pain is seen in acute event such as pulmonary embolism and
dull ache may be seen in malignancy
• Location: What is the location of pain?
Central pain is seen in pathologies such as myocardial ischaemia or
infarction, aortic dissection, oesophagitis or tracheitis. Peripheral pain is seen
in diseases of lungs (e.g. pulmonary infarction, pneumonia, pneumothorax,
tuberculosis) and pleura (e.g. pleurisy). It should be noted that herpes zoster
or prolapsed intervertebral disc may present with unilateral peripheral chest
pain
• Relationship to respiration: Is the pain related to respiration?
Pleuritic pain may get aggravated during deep inspiration, whereas the
herpes zoster pain may be constant
Haemoptysis
• Blood in the sputum: Does the patient cough out blood in the sputum?
Presence of blood in the sputum indicates erosion of a bronchial vessel in the
lung. The commonest cause of haemoptysis is tuberculosis. Others are
bronchiectasis, pneumonia and malignancy. Amount of blood in sputum is to
be noted
• Duration: How long has the patient been coughing blood in the sputum?
Repeated small haemoptyses, or blood streaking of sputum, is highly
suggestive of carcinoma
• Nature: What is the nature of bleed?
Blood streaking of sputum is suggestive of carcinoma—pink frothy sputum
suggests pulmonary oedema

• Association of fever: Is there any presence of fever?
Association of fever may indicate an infection (e.g. pneumonia), low-grade
infection may indicate infections such as tuberculosis, malignancy
Loss of appetite and weight are indicative of illnesses such as tuberculosis
and malignancies
give a clearer picture of diagnosis (e.g. tuberculosis, malignancy)
treatment?
successfully treated will indicate the examiner to reconsider the diagnosis
such as recurrence of tuberculosis and recurrent malignancies
Diseases such as tuberculosis occur in families especially in the lower
economic group and who live in crowded areas and the positive history may
be a good indicator for the present diagnosis
match the situation, such as extramarital contact or blood transfusions, if the
symptom is suspected to be in relation to AIDS. History relating to trauma
(part of fight or shooting incident) should also be elicited (detailed in Ch. 28)
Pre-requisites:
• The patient is undressed, so that the chest can be examined fully
• Good illumination
• Noiseless examination room
General
General appearance
• Restlessness (e.g. severe dyspnoea in pulmonary infarction)
• Air hunger (e.g. electrolyte disturbances)
• Severe pain on respiratory movements (e.g. fracture ribs)
• Pursed lip breathing (e.g. COPD, emphysema)
• Sunken eyes may indicate malignant cachexia, dehydration
• Dry skin may indicate malnutrition
General physical examination Look for pallor, icterus, cyanosis, clubbing,
koilonychia, lymphadenopathy, pedal oedema (mnemonic—PICKLE)
Vital signs
Pulse, BP, JVP, respiratory rate and temperature
Chest
Inspection
The chest should be inspected over the entire area with special attention to the
back and axillae. The abdomen should be observed from different positions at
different angles
1. Shape The normal chest is bilaterally symmetrical and elliptical in cross
section
• Asymmetry: Congenital deformities (e.g. pectus excavatum)
• Localized swellings can be seen in swellings of chest wall (e.g. cold
abscess)
• Flattening or hollowing of chest (e.g. tuberculosis)
2. Skin The skin has to be given special attention for sinuses and scars
• Scars: Special attention should be given to the scars on the chest wall,
which may indicate the nature of treatment administered in the past (e.g.
healed scars of empyema drainage)
3. Trachea: Prominence of sternomastoid muscle (lower part) may suggest
tracheal deviation to that side (Trail’s sign)
4. Movements of the chest wall Respiratory excursions: The chest wall moves
regularly and smoothly with respiration. The normal rate of respiration in a
relaxed adult is about 14–16 breaths per minute. When the movements of the
chest wall are normal, it indicates the absence of any gross collections in the
pleural cavity or any painful conditions on the chest wall
• Restricted movements to chest in general (e.g. pneumothorax and pleural
effusion)
• Restricted movements to certain localized areas indicate local pathology
(e.g. herpes zoster)
5. Sounds during respiration
• Noisy breathing/wheeze/stridor (e.g. obstructive airway disease)
6. Spinal deformity
Note
Use of accessory muscles of respiration such as intercostals, sternomastoids
during breathing should be noted.
Palpation
• Trachea: Usually it is in the central position in the neck. Hence, look for
deviation in the upper mediastinum by placing the middle finger in the
suprasternal notch and pushing down and back and insinuating it between the
tracheal and sternomastoid muscle. A gap indicates the shift to opposite side.
(e.g. trachea deviates to the side of lesion in collapse of lung and to away
from the side of lesion (e.g. pneumothorax, pleural effusion)
• Tactile vocal fremitus: Method: The patient is asked to repeat a phrase such
as ‘ninety nine’, and the vibrations are felt with the ulnar aspect of the hand
on the chest wall, indicating the transmission of voice sounds from the
central airways to the chest wall (e.g. reduced in pneumothorax or pleural
effusion)
• Apex beat of the heart is felt at the fifth intercostal space 1/2″ medial to the
left midclavicular line. Shift indicates shift of inferior mediastinal structures
(shift of apex beat to the opposite side in pneumothorax, pleural effusion and
to the same side in collapse of the lung) (Fig. 26.26A)
• Movements of the chest: Normal chest moves equally on both sides.
Movements may be restricted during disease conditions. This can be
determined by keeping the fingertips of both hands on the chest so that the
thumbs meet at the midline. The inspiratory movements separate the thumbs
from the midline and comparison of both sides will show the impaired
movement. This can be done anteriorly and posteriorly (Fig. 26.26B).
Minimal difference in movement can be assessed by a similar procedure, but
by holding a skin fold in the midline with the thumbs. When expansion takes
place on deep inspiration, the skin fold will disappear on the side of good
expansion (Fig. 26.26C)
FIGURE 26.26A Palpation of apex beat.
FIGURE 26.26B Demonstration of chest movements—Method 1.
FIGURE 26.26C Demonstration of chest movements—Method 2.
Percussion
Percussion of the chest is done at intervals of 1.5–2 inches comparing both sides
systematically, moving backwards and forwards from one side to the other, and
not all the way down one side and then down the other. Method: The middle
finger of the left hand (called pleximeter) is placed flat on the part to be
percussed and the back of its middle phalanx is then struck with the tip of the
middle finger of the right hand (called plexor) (vice versa for the left handed
examiner). The strike should be perpendicular to the finger of the left hand (Fig.
26.26D)
FIGURE 26.26D Percussion of chest.
The points to note are:

• Impaired (e.g. fibrosis)
• Hyper resonance (e.g. pneumothorax)
• Stony dullness (e.g. pleural effusion, empyema)
• Widened area of dullness of sternal region (e.g. mediastinal mass)
• Widened area of dullness of cardiac area (e.g. pericardial effusion)
Note
The normal degree of resonance varies between individuals and in different
parts of a normal individual. On the right side, there is loss of lung resonance
inferiorly as the liver is encountered, and on the left lower area, the lung
resonance changes to tympanitic resonance due to stomach.
Auscultation
The chest is auscultated with the diaphragm (more sensitive than the bell) of the
stethoscope, asking the patient to take deep breaths in and out through the
mouth. The auscultation should be done in comparable positions to each side
alternately, switching back and forth from one side to the other to compare (Fig.
26.26E).
FIGURE 26.26E Auscultation of chest.
Look for:
• Breath sounds (e.g. diminished in pleural effusion/pneumothorax)
• Heart sounds (e.g. muffled in pericardial effusion)
• Pericardial crunch—sounds which synchronise with heartbeat (e.g.
pneumomediastinum or small left pneumothorax)
• Added sounds:
• Polyphonic in obstructive airway disease
• Monophonic in fixed airway obstruction, e.g. endobronchial mass, FB
The physical findings of examination of chest are given in Table 26.15.
TABLE 26.15
Physical Findings of Examination of Chest
Findings
Lesion
Tracheal deviation Chest expansion Percussion note Auscultation
Pneumothorax Away from the side Decreased or fixed in Hyperresonance Diminished or dull
of lesion hyperextension
Fibrosis Towards the lesion Decreased Impaired Diminished
Consolidation Midline Normal Dull Bronchial
Pleural Away from the side Decreased Dull, especially posteriorly Normal if small,
effusion of lesion (stony dull) diminished if large
Lung collapse Towards the lesion Decreased Normal May be reduced
Lymphatic system
detail, for example, tuberculosis and lymphoma. Examination of the liver and
spleen completes the lymphoreticular system, which is useful in diagnosis.
CHAPTER 27
Thoracic injuries
Sripriya Rajan, S. Devaji Rao
CHAPTER OUTLINE
27.1. Injuries of chest wall 415
• Rib fractures 415
• Flail chest 415
• Sternal fracture 417
27.2. Injuries of pleura 418
• Pneumothorax 418
• Surgical emphysema 418
• Haemothorax 418
27.3. Injuries of lung parenchyma 419
• Lung contusion / laceration 419
27.4. Injuries of mediastinal structures 419
• Injuries of thoracic aorta 419
• Injuries of myocardium 420
• Oesophageal injuries 420
• Diaphragmatic injuries 421
27.5. Symptoms of chest injuries 421
• General 422
• Chest 423
• Head, neck and abdomen 424
27.1 Injuries of chest wall
Rib fractures
• This constitutes the most common chest injury
• Minor fractures are those confined to one or two ribs
• Mechanism of injury
• Upper rib injuries involve major energy transfer and are often associated
with injuries to major vessels, brachial plexus and tracheobronchial tree
• Fractures of lower ribs are frequently associated with liver and splenic
injuries
• Rib fractures in the elderly can occur after relatively low-energy transfers
as the bones are of low density and chest wall compliance is poor
Symptoms
• Severe pain on deep inspiration and coughing, poor inspiratory effort, and
progressive atelectasis and pneumonia due to underlying lung contusion
Signs
• Crepitus and bony tenderness
• Skin bruises should give the suspicion (Fig. 27.1)
• The hallmarks of rib fractures are intense pain, poor inspiratory effort and
progressive atelectasis and pneumonia due to underlying lung contusion
FIGURE 27.1 Bruises on the skin with underlying rib fractures.
• X-ray of the chest shows the site and number of fractures (Fig. 27.2),
underlying pleural and lung injuries
• Computed tomography (CT) of the chest gives clearer view of fractures (Fig.
27.3)
FIGURE 27.2 X-ray—fractures of lower ribs.
FIGURE 27.3 CT chest—fractures of 7, 8, 9 and 10th ribs (yellow arrows
denote surgical emphysema).
Treatment
Centers around pain management
• Oral and / or parenteral analgesics
• Intercostal nerve blocks
• Epidural analgesia especially in elderly or patients undergoing abdominal
surgeries
Flail chest
• When three or more ribs are fractured, each in more than one place, producing
a free floating section of the chest wall with or without separation of the
costochondral junction it is called a flail chest (Fig. 27.4)
• The flail segment interferes with the ventilatory function by ineffective chest
wall motion (paradoxical movement), i.e. movement inward with inspiration
and outward with expiration, producing pain and splinting and thereby a fall
in tidal volume, hypoxia and hypercarbia
• Other causes for flail chest are:
1. Traumatic disruption of ligaments and cartilages of ribs not seen on X-
ray
2. Destruction of ribs from malignant disease, e.g. multiple myeloma
3. Metabolic disease—osteitis fibrosa cystica
4. Nonclosure of median sternotomy wound
FIGURE 27.4 Flail chest.
Dyspnea, paradoxical respiration and hypoxia
• X-ray of the chest: To assess fracture, lung injury, haemopneumothorax
• Arterial blood gas analysis: To aid treatment of respiratory insufficiency
(ventilation perfusion mismatch)
Treatment
• Treatment of flail chest is shown in Table 27.1
TABLE 27.1
Treatment of Flail Chest
Segment of flail Respiratory distress Respiratory function Treatment

Small No Good Pain relief and observation
Moderate Severe Moderate Mechanical ventilation and analgesics
Large Severe Bad Chest wall reconstruction and mechanical stabilization
Sternal fracture
• Occurs mostly at the manubriosternal junction and is associated with very
high velocity trauma
• Injury to aorta, oesophagus, bronchi, myocardium and spine need to be kept
in mind
• Patient presents with severe pain over the anterior chest wall
• Pain and crepitus over the fracture site are characteristic
X-ray of the chest lateral view (Fig. 27.5A) and CT (Fig. 27.5B) demonstrate the
fracture
FIGURE 27.5A Fracture sternum.
FIGURE 27.5B Traumatic sternal fracture with
pneumomediastinum. Source: (Courtesy Dr M Harish)
Treatment
• Sternal fractures can be managed conservatively with pain relief
• Rarely, in case of persistent chest wall instability, fixation may be necessary
27.2 Injuries of pleura
Pneumothorax
• This is defined as air in the pleural cavity
• The types (Fig. 27.6) are:
• Closed pneumothorax: Air in the pleural cavity and has no external
communication (e.g. rupture of emphysematous bulla)
• Open pneumothorax: Air in the pleural cavity and has external
communication (e.g. penetrating chest wall injury or rib fracture)
• Tension pneumothorax: Continued entry of air into the pleural cavity,
increasing the intrapleural pressure above the atmospheric pressure, which
results in the shift of the mediastinum away from the side of injury
FIGURE 27.6 Types of pneumothorax.
Symptoms
• Chest pain, dyspnoea and tachycardia
Signs
• On examination, the neck veins are distended, the trachea and apex beat are
shifted away from the side of tension, breath sounds become distant or
absent on the side of tension, due to the presence of air between the chest
wall and the lung substance
• The chest on the affected side is more resonant (DD—haemothorax,
hydrothorax) on percussion
• X-ray chest (Ref Fig. 26.8) is conclusive, with shift of mediastinal structures
away from the side of the pathology, with air shadow lateral to the lung
parenchyma on the side of the pathology
Treatment
• Open pneumothorax: The external wound is closed with a tape to convert it
into a closed variety, supported by intercostal drainage
• Closed and tension pneumothorax: Simple aspiration of air from the pleural
space followed by tube thoracostomy
Note
Large chest wall wounds more than 75% the diameter of trachea allow
preferential air entry through the chest wall. Any attempt to ventilate leads to
movement of air in and out of the defect. No ventilation is achieved, and
severe respiratory compromise occurs.
Surgical emphysema
• Defined as air in the subcutaneous tissues due to the air entry from the injured
lung or external injuries such as fractured rib
• The entrapped air gradually spreads along the fascial planes into the neck,
mediastinum but, rarely down into the scrotum producing a pneumoscrotum
Subcutaneous tissues appear swollen and crepitus is a classical finding
• X-ray is diagnostic and reveals the air shadow in the subcutaneous plane, and
also the underlying cause (e.g. rib fracture)
• CT (Fig. 27.3A) is diagnostic
Treatment
• Small emphysema resolves spontaneously
• Hemodynamic instability warrants surgical intervention
• Treating the underlying cause
Haemothorax
Defined as blood in the pleural space, which is usually due to external (blunt or
penetrating) trauma
• Chest pain, dyspnoea and tachycardia
• On examination
• Neck veins are distended
• Trachea and apex beat are shifted away from the side of lesion
• The chest on the affected side is less resonant or dull (DD—pneumothorax)
on percussion
• Breath sounds become distant or absent on the side of lesion, due to the
presence of blood between the chest wall and the lung substance
• Hypotension and shock may be evident depending on the amount of blood
loss (bleeding from lung parenchyma is usually small but those from the
intercostals and internal mammary arteries may be large)
• X-ray chest (Fig. 27.7) is conclusive, with shift of mediastinal structures away
from the side of the pathology, with haziness with obliteration of
costophrenic angle
FIGURE 27.7 X-ray—right haemothorax. Source: (Courtesy Dr M Harish)
Treatment
• Small collections of blood may be aspirated under aseptic conditions
• Large collections need intercostal drainage
• Thoracotomy is needed for massive bleeds (initial bleed of more than 1–1.5
L), or continued bleeds of more than 200–300 ml/h, to control the source of
bleeding
27.3 Injuries of lung parenchyma
Lung contusion / laceration

• While contusions of the lungs are produced by blunt chest injury with
haemorrhage and edema in the lung parenchyma, lung lacerations are due to
penetrating injuries
• There may be associated injury to larger airways:
• Blunt injury usually produces injuries within 2.5 cm of the carina
• Penetrating injuries may be at any level
• Alveolar microhemorrhages are responsible for the poor ventilatory status
• Tracheobronchial injuries may coexist
Complications: Mediastinal emphysema in case of major airway injury and
hemopneumothorax in case of peripheral bronchial injuries
• Dyspnoea, tachycardia and chest pain
• Small lacerations produce no symptoms
• Chest X-ray is diagnostic, which shows vague opacification in the injured
area (usually within 1–2 h of injury)
• CT and magnetic resonance imaging (MRI) are conclusive
• Bronchoscopy is needed to evaluate tracheobronchial injuries
Treatment
• Most lacerations of the lung resolve spontaneously and need no treatment
• Large lacerations may require resuscitation and tube thoracostomy
• Bronchial injuries involving more than one third circumference of the
bronchus require surgery
• Mechanical ventilation is warranted when there is profound V/Q mismatch
27.4 Injuries of mediastinal structures
Injuries of thoracic aorta

• Thoracic aorta is vulnerable for injuries at its three fixed sites
• Annulus
• Ligamentum arteriosum—isthmus
• Aortic hiatus
• The most common sites being
• the ascending aorta proximal to innominate artery
• the descending aorta at the point beyond the origin of left subclavian artery
(ligamentum arteriosum)
• Mechanism of injury:
• Penetrating: More common and may involve other great vessels
• Blunt: Rapid deceleration produces shear at the fixed portions of the aorta,
or by anteroposterior compression
• Almost 80% die on the way to the hospital
• Severe respiratory distress
• Examination reveals features of massive haemothorax
• Signs of shock may be evident
• Neurological signs of cord compression may be present
• Chest X-ray and CT are diagnostic with the following findings:
• Widening of superior mediastinum
• Depression of left main stem bronchus
• Loss of aortic knob
• Massive hemopneumothorax
• Look for associated first rib fracture, flail chest, sternal fracture and
fracture of thoracic spine
• Arteriography is useful for definitive diagnosis of location, extent of injury
Treatment
• Resuscitation is the primary and emergent treatment
• Resection of damaged segment of aorta and repair/interposition grafts is
curative
Note
Injuries distal to innominate artery may show pseudocoarctation syndrome
(upper extremity hypertension and hypotension and low pulse in lower limbs).
Injuries of myocardium
• Myocardial injuries are caused by:
• Penetrating injuries (e.g. gunshot or stab injuries) where the outcome of
injury depends on size of pericardial defect
• Blunt injuries
- Rupture into the pericardium producing pericardial tamponade
- Myocardial contusion
- Arrhythmias
• Commotio cordis is the condition of sudden cardiac death or near sudden
cardiac death after blunt, low-impact chest wall trauma in the absence of
structural cardiac abnormality. Ventricular fibrillation is the most commonly
reported induced arrhythmia in commotio cordis.
• Blunt impact injury to the chest with a baseball is the most common
mechanism and does not result solely from the force of a blow as it is not
seen in association with any rib or sternal fracture. It is largely the result of
the exquisite timing of the blow during a narrow window within the
repolarization phase of the cardiac cycle, 15–30 msec prior to the peak of the
T wave. Survival rates for commotio cordis are low, even with prompt CPR
and defibrillation.
• Dyspnoea and cyanosis
• Examination reveals, distension of jugular veins, hypotension and narrowing
pulse pressure and distant heart sounds (Beck’s triad)
• The jugular venous distension raises paradoxically on deep inspiration
(Kussmaul’s sign), because the increased venous return cannot be
accommodated within the constricted heart
• Signs of shock may be evident
• Pulsus paradoxus is a cardinal sign (drop in systolic BP > 10 mm during
inspiration due to CO2 absorption)
• Chest X-ray is contributory with cardiomegaly
• ECG may remain normal for over 36 h but exhibit features of ischaemia,
dysrhythmia later
• Echocardiography (ECHO) is done to assess regional wall motion
abnormalities
• CPK-MB values show elevation (check values at admission, 24 h, 48 h)
Treatment
• Cardiac monitoring and resuscitation are important
• Cardiac tamponade warrants pericardiocentesis/ subxiphoid pericardial
window
• Thoracotomy is done to create an opening of pericardial sac
Oesophageal injuries
• Oesophageal injuries are caused by:
• Penetrating injury: may occur at any level and should be suspected when
the injury crosses the midline (e.g. in sword swallowers as circus act,
during oesophagoscopy)
• Blunt injury: Usually following severe blow to the sternum or epigastrium.
The common site of injury is at the lower one-third oesophagus
• Fever, dyspnoea (due to mediastinitis or mediastinal emphysema) or
tachypnoea
• Features of surgical emphysema (spread of mediastinal emphysema to neck,
face and chest wall) may supervene, with signs of hypoxia about 3–4 days
later
• X-ray of the chest may reveal
• Pneumomediastinum
• Air in the prevertebral space
• Left pleural effusion
• Hemo or pneumothorax in the absence of rib fracture
• Gastrograffin swallow may show the leak
• Oesophagoscopy may show the injury
• Intercostal drainage shows particulate food matter, and show air leak during
both phases of respiration
Treatment
• Intercostal drainage is mandatory
• Early operative repair of the oesophageal tear is necessary
Diaphragmatic injuries
• Injuries of diaphragm are caused by:
• Blunt injuries produce large radial tears and herniation of abdominal
viscera in to the chest
• Penetrating injuries are small initially and enlarge over a period of time
Diagnosis is difficult unless the tears are large and allows herniation of
abdominal contents into the chest cavity—dyspnoea and tachycardia
• Chest X-ray is contributory and may show:
• Bowel loops in the chest (in herniation of small bowel)
• Double shadow overlying the diaphragm
• Nasogastric tube in the chest in patients with gastrothorax
• Contrast studies and CT of chest are conclusive
Treatment
Surgical repair with or without mesh is mandatory
27.5 Symptoms of chest injuries

• Chest pain
• Difficulty in breathing
• Palpitations
• Passage of blood in sputum (haemoptysis)
• Symptoms of shock
• Haematemesis
• Melena
The complaints can occur in various combinations depending on the organ
injured, the severity and type of injury and the time of injury.
Eliciting history
Before questioning the patient or the relatives, the patient’s general condition
should be assessed. If the patient is in shock, he or she should be mobilized to
the intensive care unit for immediate resuscitation and no time should be wasted
in eliciting history. Resuscitation may be required in acutely ill patients, which is
done in the pattern ABCDE (Ch. 51):
• Airway
• Breathing
• Circulation
• Disability
• Exposure
If the patient is stable, the history can be elicited. All cases of chest injury
should be admitted in the hospital and observed.
The patient or the attendants should be allowed to describe the accident or
trauma in their own words. The following details should be elicited, by direct
questioning, if not already told by the patient. The relevant questions should
relate to the following:
• Nature of injury: Penetrating (e.g. gunshot or knife injury) or nonpenetrating
injury (e.g. hit by a blow, or a fall)
• Mechanism of injury (e.g. fall from a height, deceleration injury)
• Time of injury (e.g. time elapsed has relevance)
Gunshot injuries may produce life-threatening injuries due to shock waves
that produce spontaneous rupture of many organs distant from the site of entry.
Chest pain
• Chest pain: Where does it hurt on the chest and point it with one finger?
The patient should be asked to point the area of pain with one finger and this
has great relevance in diagnosis (e.g. rib fractures)
• Radiation of pain: Does the pain radiate to any specific area?
Radiation of chest pain is characteristic in certain situations (e.g. radiation to
the back is seen in aortic injuries)
• Relationship to breathing: Does the pain become more on deep
inspiration?
Chest pain after trauma is aggravated by deep inspiration in rib fractures
Difficulty in breathing
• Difficulty in breathing: Is there any difficulty in breathing?
Dyspnoea is a constant symptom in chest injuries. Both chest wall (e.g. rib
fractures cause severe pain, pneumo and haemothorax cause restricted expansion
of lungs), and structures of chest cavity (e.g. lung parenchymal injuries) injuries
cause restricted expansion, mediastinal injuries cause mediastinal emphysema,
myocardial injuries cause haemopericarium)
Note
Tachypnoea is an increased respiratory rate observed by the doctor, while
dyspnoea is the symptom of breathlessness experienced by the patient.
Palpitation
• Palpitation: Does the patient have palpitation?
Palpitation is a symptom of tachycardia and is commonly an accompaniment
of dyspnoea in chest injuries due to fear and also in certain pathological
conditions (e.g. myocardial injuries, mediastinitis, mediastinal emphysema,
shock syndrome)
Passage of blood in sputum (haemoptysis)

• Blood in the sputum: Does the patient cough out blood in the sputum?
Presence of blood in the sputum may indicate injuries to the tracheobronchial
tree or lung parenchyma
Symptoms of shock
• Symptoms of shock: Does the patient complain of giddiness or blackouts?
The patient may complain of persisting giddiness (e.g. major vessel injuries
producing shock) or giddiness at the time of injury and recovered later (e.g.
vasovagal attack)
Passage of blood in vomitus (haematemesis)

• Vomiting: Has the patient vomited or has been continuously vomiting since
the incident?
Vomiting may indicate peritoneal irritation or peritonitis (e.g. bowel injury in
multiple injuries, thoracoabdominal injuries) and persistent vomiting may
indicate increasing soiling of the peritoneum (e.g. large leaks causing
peritonitis)
• Hematemesis: Does the vomitus contain blood and if so in what quantities?
When was the last vomit?
Haematemesis may indicate hollow organ injury (e.g. gastric injury) and large
quantities of bleed may indicate major vessel injury (e.g. avulsion of major
vessels in the chest). The period between the last vomit and the time of
examination is important, as longer interval may indicate control of bleeding
Passage of blood per rectum (melena)

• Melena: Has the patient passed blood per rectum and if so what is the
quantity? When was the last bleed?
Passing of blood after chest injury indicates gastrointestinal injury (e.g.
thoracoabdominal injury involving the large bowel), and this should alert the
clinician. Quantity of bleeds is not very relevant as the melena seen outside is
only an indication of the nature of injury and there may be a large quantity of
blood in the bowel. The period between the last bleed and the time of
examination is important, as longer interval may indicate control of bleeding
Abdominal distension
• Abdominal distension: Has the abdomen distended since the accident and
if so, is it progressive?
Abdominal distension may indicate leakage of contents of the bowel or urine
(e.g. bowel injury in thoracoabdominal injuries or multiple injuries) or even
paralytic ileus (e.g. retroperitoneal rupture of duodenum, spinal injury)
• Association of fever: Is or was fever after the accident?
Association of fever may indicate an infection (e.g. mediastinitis after
mediastinal injury or peritonitis after bowel injury)
• Treatment for the injury: Has any treatment (first aid or surgical) been
given to the accident victim?
The information of any treatment received at the accident site or in a nearby
hospital or clinic will provide more information and records should be obtained
for further management and for medicolegal purposes (e.g. suturing of a wound
on the chest wall, blood transfusions)
• Past history: Was there any illness in the past, which required any surgical
treatment?
If the patient had any illness in the past which required organ removal (e.g.
pneumonetomy for previous accident or illness), will help in the diagnosis. If the
patient has been on medication (e.g. antiepileptics) in the past, the examiner will
find it easy to relate this to the cause and nature of injury (e.g. fall from a height)
match the situation (e.g. family problems, property matters etc.)
Pre-requisites:
• The patient should be fully undressed, so that the entire body can be examined
• Good illumination is necessary
• Noiseless examination / emergency room
General
1. General appearance
• Lying quiet (e.g. as in peritonitis)
• Restlessness (e.g. intraperitoneal haemorrhage)
• Air hunger (e.g., electrolyte disturbances)
• Severe pain on respiratory movements (e.g. fracture ribs)
2. Examination of eyes
• Sunken eyes may indicate dehydration
• Pallor (e.g. severe blood loss)
• Cyanosis (e.g. hypoxia)
3. Examination of skin
• Dry skin may indicate dehydration and undernutrition
• Oedema and swelling of skin may indicate injuries such as surgical
emphysema, haematoma
4. Recording of pulse and blood pressure
• Tachycardia, low volume pulse may indicate hypovolemia
• Hypotension may indicate hypovolemia
5. Recording of temperature
• Elevated temperature may indicate associated infection
Chest
Inspection
The chest should be inspected over the entire area with special attention to the
back and axillae. The chest should be observed from different positions at
different angles
1. Shape
The shape of the chest varies according to the nature of the injury to the chest
wall and the thoracic contents
The normal chest is bilaterally symmetrical and elliptical in cross section
• Asymmetry: Large areas of injury to the chest wall distort the shape of the
chest and lead to asymmetry (e.g. flail chest, large haematoma)
Diffuse swelling of the chest: The whole of the chest may look full and
swollen (e.g. surgical emphysema)
• Localized swellings can be seen in localized injuries (e.g. haematoma)
2. Skin
The skin has to be given special attention for colour, bruises, abrasions and
lacerations, tyre or belt marks, puncture wounds and scars.
• Colour: Red erythematous skin (e.g. haemothorax or subcutaneous
extravasation of blood)
• Bruises, abrasions and lacerations: These marks may indicate the nature of
injury (bruises and abrasions of a fall from height, lacerations in injuries
where the subject is hit by an object)
• Tyre or seat belt marks: Run-over accidents may indicate tyre marks of the
vehicle and seat belt marks indicate that the nature of accident and possible
damage. Impressions made by clothes of the victim will indicate the nature
of injury (London’s sign)
• Punctured wounds: Punctured wounds such as gunshot wounds indicate the
points of entry and exit (entry point appears more charred than the exit point
by the heat of the missile). If a large puncture wound is seen, it should be
quickly occluded with a sterile pad and strapped to prevent further effects of
open pneumothorax
• Scars: Special attention should be given to the scars on the chest wall, which
may indicate the nature of injury especially when the patient is seen late.
Nature of treatment administered can be made out (e.g. healed or infected
suture marks)
• Impalement injury: This is a penetrating injury where the patient presents
with penetrating object in situ (e.g. iron rod, long glass piece)
3. Movements of the chest wall
Respiratory excursions
The chest wall moves regularly and smoothly with respiration. The normal rate
of respiration in a relaxed adult is about 14–16 breaths per min. When the
movements of the chest wall are normal, it indicates the absence of any gross
collections in the pleural cavity or any painful conditions on the chest wall.
• Restricted movements to chest in general (e.g. hemo or pneumothorax)
• Restricted movements to certain localized areas indicate local pathology (e.g.
rib fracture)
• Paradoxical respiration (e.g. flail chest)
Sounds during respiration

• Noisy breathing/stridor (e.g. large airway injury. Tracheal injury usually
produces inspiratory stridor)
• Loud sucking wounds with bubbling usually indicate a pleural injury and
require immediate attention
Note
Use of accessory muscles of respiration such as intercostals, sternomastoids
during breathing should be noted.
Palpation
• Trachea:.Usually it is in the central position in the neck. Hence, look for
deviation in the upper mediastinum by placing a finger in the suprasternal
notch and pushing down and back. (e.g. trachea deviates to the side of lesion
in collapse of lung and away from the side of lesion in hemothorax,
pneumothorax)
• Sternum is felt for any fracture. The fingers are run by the examiner on the
anterior surface of sternum (Fig. 27.8) and crepitus is felt in fractures,
deformity in displaced fractures. If sternal fracture is diagnosed, the spine
should be examined for coexisting fractures as they frequently occur
• Skin for subcutaneous emphysema is felt as a crepitus to the examining
finger
• Ribs are palpated sequentially by running the finger on each rib (Fig. 27.9) or
over a tender rib and looked for bony tenderness, crepitus and irregularity.
The number of ribs involved and the presence of any flail segment should be
noted
• Compression test: This test is done, when the patient is not able to localize
the exact site of pain in a rib fracture Method: Patient stands or sits with
both hands above the head. The clinician compresses the chest
anteroposteriorly with one hand on the sternum and other on the spine
(Fig. 27.10). This compressive movement causes pain at the site of
fracture
• Tactile vocal fremitus: The patient is asked to repeat a phrase such as ‘ninety
nine’, and the vibrations are felt with the hand on the chest wall, indicating
the transmission of voice sounds from the central airways to the chest wall
(e.g. reduced in pneumo or haemothorax)
• Apex beat of the heart: Method is explained in page 417 (Ref Fig. 26.26A)
FIGURE 27.8 Palpation of sternum for tenderness.
FIGURE 27.9 Palpation of ribs for tenderness.
FIGURE 27.10 Compression test.
Percussion and auscultation

The methods of percussion and auscultation are described on page 417 and 418
(Ref Figs. 26.26D and E)
The physical findings of examination of chest are given in Table 27.2
TABLE 27.2
Physical Examination Findings of Chest in Trauma
Lesion Findings
Tracheal deviation Chest expansion Percussion note Auscultation (breath
sounds)
Tension Away from the side of Decreased or fixed in Hyperresonance Diminished or dull
pneumothorax lesion inspiration
Simple Nil Decreased Usually normal, may be May be diminished
pneumothorax hyperresonant
Haemothorax Away from the side of Decreased Dull, especially Normal if small,
lesion if large posteriorly diminished if large
Contusion of lung Nil Normal Normal Normal, may have
crackles
Lung collapse Towards the lesion Decreased Normal May be reduced
Note
The size of the injury, and position of the patient will affect the clinical
findings. For example, a small haemothorax may have no clinical signs at all.
A moderate haemothorax will be dull to percussion with absent breath sounds
at the bases in the erect patient, whereas signs will be posterior in the supine
patient. This is also reflected in chest X-ray findings.
Head, neck and abdomen

• Head and face for associated injuries
• Oral cavity for foreign bodies, secretions, mucosa for cyanosis
• Neck for associated injuries and the veins (e.g. distended in haemothorax,
pericardial tamponade, collapsed in hypovolemia)
• Abdomen for associated injuries
CHAPTER 28
Breasts
S. Devaji Rao, V. Srinivasan
CHAPTER OUTLINE
28.1. Development of breasts 425
28.2. Surgical anatomy of breast 425
28.3. Physiology of breasts 426
28.4. Diseases and abnormalities of the breasts 426
• Amazia (amastia) and athelia 426
• Polymazia (polymastia) and polythelia 427
• Small or large breasts 429
• Traumatic fat necrosis 429
• Haematoma of breast 429
• Mastitis and cyclical mastalgia 430
• Acute breast abscess 430
• Antibioma and chronic breast abscess 430
• Tuberculosis of breasts 431
• Duct papilloma 431
• Fibroadenoma 431
• Cystosarcoma phyllodes 432
• Primary malignancy 432
• Paget’s disease of breasts 436
• Fibroadenosis 436
• Galactocoele 437
• Mammary duct ectasia 437
• Mamillary fistula 438
• Gynecomastia 438
28.5. Symptoms of breast diseases 439
• Breasts 441
• Axillae and supraclavicular areas 448
• Abdomen 448
• Chest 448
• Skeletal system 448
• Pelvis 448
28.1 Development of breasts
In women, breasts, the secondary sex organs, are subjected to a constant
dynamic role of physical changes related to menstrual cycle, from menarche to
death, and hence called a dynamic organ. They show regular growth pattern and
involutionary changes during every menstrual cycle. Such physiological
disturbances contribute to a variety of benign breast disorders, which may
disturb the woman. Incidentally, breast cancer is the commonest malignancy in
women, which is of extreme concern to the surgeons, oncologists and the
radiotherapists.
Breasts or mammary glands are modified sweat glands and develop from a
distinct linear elevation called ‘mammary ridge or milk line’, that runs from the
axilla to the groin on both sides (Fig. 28.1). Breasts originate as lens shaped
thickenings on the milk line. The line disappears rapidly excepting the
thickening in the pectoral region, which develops into a breast.
FIGURE 28.1 Milk lines.
28.2 Surgical anatomy of breast

It normally lies on the chest wall (Fig. 28.1A) extending from the second to the
sixth ribs vertically, and from near the midline to the anterior axillary line
horizontally. The breast may be divided into nipple, areola and four quadrants
(upper inner, lower inner, lower outer and upper outer) with the axillary tail
projecting from the upper outer quadrant (UOQ), which passes to the axilla. The
lactiferous ducts originate from the glands and end at the apex of the nipple,
which consists of erectile tissue covered with pigmented skin, which also covers
the areola (Fig. 28.1B).
FIGURE 28.1A Surgical anatomy of breast.
FIGURE 28.1B Anatomy of breast.
Breasts have a very generous lymphatic drainage, mainly into two depots, the
axillary and internal mammary nodes. On an average, about 50 lymph nodes are
in the axilla arranged along the course of the arteries and veins, and the internal
mammary nodes averaging about 3 or 4 on each side lying along the internal
mammary vessels, usually in the first, second and the third intercostal spaces.
Lymph from the nipple and areola may drain into both the internal mammary
and the axillary nodes. The axillary lymph nodes are divided into six groups, at
three levels based on their relationship to pectoralis minor muscle, for operative
purposes (Fig. 28.2).
FIGURE 28.2 Lymphatic drainage of breast.
28.3 Physiology of breasts
The breasts undergo physiologic changes at seven phases of life (Table 28.1) as
they are hormone dependent.
TABLE 28.1
Physiological Changes of Breasts
Phase of Life Normal Physiological Changes

Neonatal Breasts contain lactiferous ducts with no alveoli
Prepuberty Ducts proliferate and their ends proliferate to form solid masses—future breast lobules
Puberty
Early adult life Alveoli appear during pregnancy which display lumen surrounded by secretory cells. Colostrum is
secreted during late pregnancy and milk after childbirth
Pregnancy
Late Glandular tissue atrophies, connective tissue becomes cellular and collagen decreases. Breasts shrink
premenopause in size
Menopause
Many aberrations and alterations of normal development and involution take

place, which are responsible for many disease states (Table 28.2). They all
comprise in the general classification, benign breast disease, the most common
cause of breast problems, and affect up to 30% of women. The classification is
given in Table 28.3.
TABLE 28.2
Aberrations and Alterations of Development of Breasts and Disease
States
Clinical
Phase Normal Process Aberration Disease
Presentation
Early reproductive Lobule formation Fibroadenoma Giant fibroadenoma Discrete lump or

period lumps
Active reproductive Cyclical changes Cyclical mastalgia, Painful breasts
period nodularity
Involutional period Lobular involution Cysts Discrete lumps
Ductal involution Periductal inflammation Periductal mastitis Nipple discharge
Ductal dilatation Ductal ectasia Nipple discharge
Periductal fibrosis Nipple retraction
Increased epithelial Epithelial hyperplasia Hyperplasia with Asymptomatic
turnover atypia
TABLE 28.3
Classification of Benign Breast Disease
Developmental Traumatic Inflammatory Dysplasia Benign Neoplasia

Supernumerary breast Haematoma Puerperal abscess Nodularity Fibroadenoma
Absent breast Fat necrosis Plasma cell mastitis Solitary cysts Lipoma
Asymmetric breasts Tuberculosis Epithelial hyperplasia Duct papilloma
Note
It should be noted that the male breast does not normally develop after
childhood, but slight temporary enlargement may occur at puberty.
28.4 Diseases and abnormalities of the breasts

The aetiological classification of diseases and abnormalities of breasts are given
in Table 28.4.
TABLE 28.4
Diseases and Abnormalities of the Breasts
Classification Female Breasts Male Breasts

Nipple and Breasts Nipples Breasts
areola and
areola
Congenital Athelia, Amazia, polymazia, small or large breasts Amazia,
polythelia, polymazia
retracted
nipple
Traumatic Cracked nipple Traumatic fat necrosis, haematoma Irradiation mastitis
Acute Eczema, Acute mastitis, plasma cell mastitis, acute Neonatal mastitis,
inflammatory extragenital abscess pubertal
chancre of mastitis
nipple
Chronic Antibioma, tuberculosis, actinomycosis Antibioma,
inflammatory tuberculosis
Benign Papilloma Epithelial: Duct papilloma, adenoma Papilloma Fibroadenoma,
neoplastic Connective: Lipoma, neurofibroma, lipoma
haemangioma, cystosarcoma phyllodes
Mixed: Fibroadenoma, papillary
cystadenoma
Malignant Paget’s disease Carcinoma, sarcoma, cystosarcoma phyllodes, Carcinoma,
Neoplastic of nipple, secondaries sarcoma
squamous
cell
carcinoma
Miscellaneous Cyst of gland of Fibroadenosis, cystic hygroma, galactocoele, Gynecomazia,
montgomery serocystic disease of Brodie, Mondor’s fibroadenosis
disease, duct ectasia, mamillary fistula
Amazia (amastia) and athelia

• Amazia or amastia is a condition where there is total absence of breasts in a
female
• Athelia is a condition in which nipples are absent
This is a rare condition and results when the mammary ridges fail to develop
or completely disappear
• There is total absence of breasts, nipples may be present or may be absent
totally (Fig. 28.3A)
• When associated with the absence of chest wall muscles, (Fig. 28.3B), 2–5
ribs, deformities of hands and vertebrae, it is known as Poland syndrome
FIGURE 28.3A Right amazia Source: (Courtesy Dr K. Sridhar).

FIGURE 28.3B Absence of right breast and chest wall
muscles Source: (Courtesy Dr K. Sridhar).
No specific investigations
are required, excepting hormonal studies to assess the female hormonal status
in the individual
Treatment
• Reconstruction of breasts with silicone implants (augmentation
mammoplasty) and the nipple and areolae by reconstructive surgery
• Usage of myocutaneous flaps have become very popular recently for breast
reconstruction
Polymazia (polymastia) and polythelia

The breasts are modified sweat glands, which develop from a cord of tissue
extending from the axilla to the groin on each side
• Instead of one breast on each side, many may develop giving rise to a
condition called polymazia
• Polythelia is a condition where multiple nipples are seen along the mammary
ridge
• More than one breast on each side (Fig. 28.4), sometimes secreting milk after
childbirth
• Occur along the milk line, usually underneath the normally located breasts or
nipples, rarely on the back or the buttock
FIGURE 28.4 Bilateral accessory breasts.
No specific investigation is required
Treatment
• Removal of extra breasts is necessary to reduce the inconvenience, as it may
respond to hormonal stimulation during menstrual cycles and secrete milk
during lactation
• Removal is justified for the fear of malignancy in future
Small or large breasts

• These are genetic problems and may run in families
• Idiopathic virginal hypertrophy is a known entity
Small (Fig. 28.5) or large breasts (Fig. 28.6), without any pathology
FIGURE 28.5 Right small breast Source: (Courtesy Dr K. Sridhar).

FIGURE 28.6 Bilateral large pendulous breasts.
No specific investigation may be necessary
Treatment
• Augmentation mammoplasty is done to increase the size of small breasts
• Reduction mammoplasty is done to reduce the size of big breasts
Traumatic fat necrosis

Associated with history of trauma such as seat belt injury during a road traffic
accident, or following a violent contraction of pectoralis muscles responding to a
blow
A hard painless lump in the breast resembling malignancy
Fine-needle aspiration cytology (FNAC) and mammography (Fig. 28.7) are
needed to rule out malignancy
FIGURE 28.7 Mammogram—fat necrosis.
Treatment
No treatment is necessary, unless malignancy is suspected
Haematoma of breast
Associated with history of trauma such as seat belt injury during a road traffic
accident, or following a violent contraction of pectoralis muscles responding to a
blow
Presence of bruise over the breast may be the contributory finding for diagnosis
FNAC and mammography
are needed to rule out malignancy
Treatment
Exploration and histopathological confirmation
Mastitis and cyclical mastalgia

Mastitis can occur at any age:
• In infants, it may be due to stimulation of neonatal breast tissue by maternal
hormones
• At puberty, hormonal changes can cause the same. Some viral infections such
as mumps can cause mastitis
• In lactating women, it may be due to local infection arising out of cracks in
the nipple
• Painful uniform enlargement of breasts, unilateral or bilateral, with or without
tender enlargement of axillary lymph nodes
• It may progress to suppuration forming an abscess
Treatment
Appropriate antibiotics and breast-supporting undergarments should suffice
Acute breast abscess

• Previous mastitis results in an abscess
• Common in lactating women
• Starts with dull ache, which proceeds on to throbbing pain
• Systemic manifestations such as fever and malaise may develop
• On examination:
• Superficial abscesses may show as fluctuant tender lumps
• Deep abscesses may show as severe cellulitis with oedema of breast (Fig.
28.8) without fluctuation
FIGURE 28.8 Acute breast abscess.
• Polymorphonuclear leucocytosis is generally present
• Diagnostic aspiration may confirm the presence of pus
Treatment
• Surgical drainage gives full relief
• Spontaneous or inadequate drainage may result in the formation of
antibioma, chronic abscess, mammary fistula with purulent or
serosanguinous discharge
Antibioma and chronic breast abscess
• Antibioma of the breast or chronic breast abscess results from:
• improperly or inadequately treated acute abscess
• inadequate drainage of acute abscess
• A hard painless lump, which may be fixed to the skin or the deeper structures
• May present with a sinus (Fig. 28.9)
• Mild pain and tenderness on deep palpation will be present in some cases
FIGURE 28.9 Sinus of chronic breast abscess.

• Ultrasound (US) and mammography may be required to rule out mastitis
carcinomatosa, in longstanding cases with induration
• FNAC or biopsy is needed for confirmation
Treatment
• Surgical drainage gives full relief
• Excision of lump is curative
Tuberculosis of breasts
Found in patients with pulmonary tuberculosis or cervical lymph node
tuberculosis
• Presents as chronic multiple abscesses of the breast without signs of acute
inflammation, which may progress to form sinuses
• Axillary lymph nodes are usually enlarged, which may be matted and firm,
may form cold abscesses, which may form sinuses or ulcers
• Mammography may be required in longstanding cases with induration
• FNAC or biopsy of the ulcer or lumps is needed for confirmation
Treatment
• Antitubercular treatment is mandatory and curative
• Aspiration or surgical drainage may be needed for some abscesses
Duct papilloma
• True benign neoplasm of the ductal epithelium of the breast
• Common in women between 35 and 55 years
• They are divided into:
• Central lesions arising from a main duct which is single
• Peripheral lesions arising from terminal duct lobular units and are multiple
• Peripheral lesions are more prone to become malignant than the central
lesions
• Bloodstained discharge through nipple limited to a single duct
• On examination
• A small, localized, well-defined swelling usually under the areola
• Application of pressure discharges bloodstained fluid
• Sono- and X-ray mammography may be conclusive
• Ductogram is confirmatory (Fig. 28.10)
FIGURE 28.10 Ductogram—duct papilloma.

Treatment
Excision of the diseased duct (mircrodochectomy) is the treatment of choice
Fibroadenoma
• Benign condition considered as an aberration, and not a neoplasm
• Common below the age of 30
• Usually hormone dependent and undergoes involution around menopause
• Some may undergo cystic degeneration to form cystadenoma
• A small firm or hard lump or lumps, usually ovoid or spherical in shape, very
mobile slipping to palpating fingers (called breast mouse or floating
tumour)
• The lump characteristically moves within the breast tissue
• They are neither attached to the skin nor to the deeper structures
• Some may be bilateral
• Sonomammography is useful in diagnosis
• X-ray mammography is diagnostic (Fig. 28.11)
FIGURE 28.11 Mammogram—large fibroadenoma.
Treatment
• Excision is advised for fibroadenomas over 4 cm in diameter, and in older
women to rule out malignancy
• If confirmed by cytology, smaller tumours in women below 30 years need
not be excised
Cystosarcoma phyllodes
• Relatively rare stromal tumour
• Most cases are benign
• Occasionally shows cystic degeneration, rarely the malignant features of a
true sarcoma
• Occurs in middle-aged or elderly women
• Rare below the age of 40
• It may grow rapidly and cause unilateral breast enlargement or ulceration of
overlying skin
• It is divided into:
• low grade (the majority)
• high grade (about 5%)
• Malignant phyllodes tumour, such as other stromal malignancies, tends to
metastasize to the lung
• A firm to hard lump, often larger than 2 cm in diameter, resembling a
fibroadenoma, ovoid in shape, with local infiltration
• Large tumours are common (Fig. 28.12)
• They tend to invade locally and recur after removal
• Axillary nodal spread is not common
FIGURE 28.12 Cystosarcoma phyllodes.

• Sonomammography and X-ray mammography (Fig. 28.13) are diagnostic
• FNAC demonstrates abnormal number of fibroblasts, with normal epithelial
elements, and extensive mitotic activity in malignant tumours
FIGURE 28.13 Mammogram—phyllodes tumour.
Treatment
• Low-grade tumours are treated in the same manner as fibroadenomas
• High-grade tumours are treated as for sarcoma and should undergo radical
excision with tumour-free margins
• Malignant tumours require quadrantectomy or simple mastectomy, with
regular follow up
Primary malignancy
• Most common malignancy in females
• Peak age incidence 50–70 years
• Increased incidence in higher socioeconomic groups
• Primary malignancy can arise (Fig. 28.14) from:
• Ducts (ductal carcinoma)
• Lobules (lobular carcinoma)
• Connective tissue (sarcoma)
• The incidence (Fig. 28.15) and histologic classification of breast malignancies
are:
A. Paget’s disease of nipple (1%)
B. Carcinoma of mammary ducts
a. Noninfiltrating (1%)
b. Infiltrating (88%)
1. Papillary carcinoma (1%)
2. Comedocarcinoma (1%)
3. Scirrhous carcinoma (80%)
4. Medullary carcinoma (5%)
5. Colloid carcinoma (1%)
C. Carcinoma of mammary lobules (10%)
a. Noninfiltrating
b. Infiltrating
D. Rare carcinomas
E. Sarcomas (very rare)
• History of previous breast cancer
• Early menarche (< 12 years)
• First pregnancy after 30 years of age
• Late menopause (> 55 years)
• Use of oral contraceptives and hormone replacement therapy
• Genetic and environmental factors. BRCA 1(17q) and BRCA 2(13q) gene
mutations are implicated in 2% of cases
• Breast cancer in first-degree relative, to a lesser extent in a second-degree
relative, the risk is particularly great if:
- the affected relative is on the maternal side
- two first-degree relatives are affected
- the relative has bilateral cancer
- the relative’s cancer was diagnosed before the age of 50 years
• The tumour can spread
• Locally into the breast tissue and underlying structures and skin
• Lymph to axillary, internal mammary, supraclavicular lymph nodes
• Blood to lungs, liver, brain and bones
• Lobular carcinoma has a very high propensity for bilaterality, multicentricity
and multifocality, and has a particular propensity to metastasize to the
peritoneum, pleura and meninges
• Sarcomas are fast-growing tumours with local infiltration
• The primary malignancy of the breast can affect the males also (Fig. 28.16),
but it is rare (< 1% of all breast cancers)
FIGURE 28.14 Anatomical origin of primary breast malignancies.
FIGURE 28.15 Incidence of various primary malignancies of breast.
FIGURE 28.16 Primary breast malignancy in a male Source: (Courtesy Dr R.
Rajaraman).
Symptoms
• Painless lump (commonest), mobile in the early stages (but it does not move
within the breast)
• Breast pain
• Changes in shape and size of breast
• Dimpling of skin
• Ulceration of the skin
• Inversion of nipple
• Bloody discharge from nipple
Signs
• Nontender irregular lump (early stages)
• By direct spread, it may locally invade the tissues producing
• dimpling of skin (due to fibrosis and contracture of Cooper’s ligament)
(Fig. 28.17)
• retraction of nipples (Fig. 28.18)
• peau d’orange (due to obstruction of cutaneous lymphatics and fixation of
hair follicles and sebaceous glands) (Fig. 28.19)
• infection and form an abscess
• ulceration (tumour cells replace the skin and break down) (Fig. 28.20)
• satellite nodules (Fig. 28.21)
• cancer en cuirasse (due to coalescion of skin nodules) (Fig. 28.22)
FIGURE 28.17 Dimpling of skin due to malignancy.

FIGURE 28.18 Nipple retraction due to cancer (right breast).
FIGURE 28.19 Peau d’orange.
FIGURE 28.20 Ulcerated breast malignancy.
FIGURE 28.21 Sarcoma breast with skin infiltration and fungation.
FIGURE 28.22 Cancer en cuirasse left breast.
The tumour may directly invade the muscles and chest wall
• Lymphatic spread occurs in the axillary nodes, supraclavicular and internal
mammary nodes. At later stages, axillary metastases produce oedema of the
arm
• Through blood the disease spreads to metastasize to the liver, lungs, bones,
brain, contralateral breast and ovaries (Krukenburg tumour) (Fig. 28.23)
FIGURE 28.23 Krukenburg tumour.
• Mammography (Fig. 28.24) is many times conclusive with accuracy of over
95%. Microcalcification is commonly seen in ductal carcinoma and not in
lobular carcinoma
• Ultrasonography has a specificity of 100% in distinguishing a solid mass
from a cystic lesion, confirmed by simple aspiration
• Scinti-mammography (using technetium Tc 99m sestamibi) is useful for
localizing the lump, especially in patients with dense breast tissue, where
mammography is not contributory (Fig. 28.25)
• MRI (Fig. 28.26) with contrast enhancement is gaining popularity
• FNAC has almost 100% specificity in the hands of experienced
cytopathologists
• Core-cut biopsy may be required to confirm the diagnosis, when FNAC is
equivocal
• Excisional or wedge biopsy is performed when diagnosis remains equivocal
in patients who have been investigated fully by FNAC and core-cut biopsy
• Sentinel node biopsy (sentinel node identified by using injection of a vital dye
or radioactive isotope bound to colloidal iodine, with a hand held γ-counter,
and the principle that if the sentinel node is negative, it is reasonable not to
explore the axilla any further, and if positive, to proceed to formal axillary
dissection)
• Serum CA 15-3 breast cancer tumour marker assay (persistently high after
surgery may suggest distant metastases)
• X-ray chest and US abdomen for lung and liver metastases respectively
• Isotope bone scan for bone metastases
FIGURE 28.24 Mammogram—malignant tumour.

FIGURE 28.25 Scinti-mammogram—infiltrating duct carcinoma with
axillary lymph node metastases Source: (Courtesy Dr K. M. Lakshmipathy).
FIGURE 28.26 MRI—malignancy of breast.
Treatment
For local control of tumour
• Surgery is the first modality of treatment (varying from wide excision to
radical mastectomy)
• Radiotherapy (for effective local control and prevent local recurrence in 80%
of operated women) for women with
• large primary tumour—poorly differentiated
• axillary node involvement and not undergone full axillary dissection
• involvement of pectoralis muscle
Adjuvant therapy to prevent or delay distant metastases
• Chemotherapy: Administration of cytotoxic drugs initiated close to the time
of surgery. The drugs used will depend on:
• Prognosis
• Patient’s co-morbidities
• Experience of treating of oncologist
• Hormone manipulation: For patients with ER, PR +ve cancers, and growth
factor receptor HER2-neu
• Antioestrogens (tamoxifen)
• Aromatase inhibitors (anastrozole, letrozole, exemestane) which block the
synthesis of oestrogen—medical adrenalectomy)
In some situations such as very advanced states, preoperative chemotherapy
(neoadjuvant chemotherapy) and or radiotherapy may be needed.
Recent advances
• Breast reconstruction is a good alternative
• Breast conservation techniques
• Intra operative or perioperative radiotherapy as alternative to 6 weeks
conventional postoperative radiotherapy
Treatment of metastatic disease

• Surgery—toilet mastectomy in symptomatic locally uncontrollable disease
• Radiotherapy—for painful bone metastases
• Hormone therapy (more effective in ER +ve patients)—tamoxifen, aromatase
inhibitors and progestogen, oophorectomy for premenopausal women
• Chemotherapy
• Immunotherapy—monoclonal antibody (trastuzumab) for HER2-neu positive
patients
Paget’s disease of breasts

Disease of menopausal women
• Eczematous reaction of the nipple and areola (Fig. 28.26), with an underlying
malignancy of the breast
• There is gradual destruction of the nipple
• This has to be differentiated from eczema (Table 28.5)
TABLE 28.5
Differentiating Features of Eczema and Paget’s Disease of Breasts
S. No. Features Eczema Paget’s Disease

1 Occurrence During lactation At menopause
2 Itching Present Absent
3 Vesicles Present Absent
4 Nipples Intact Destroyed
5 Palpable lump Absent Present
• Mammography is required to look for the underlying lump
• Scrapings from the excoriations may show malignant cells
Treatment
Treatment is the same as for ductal carcinomas
Fibroadenosis
An aberration occurring in the age group of 35–50 years
• Discrete multiple cystic lumps varying from 2–28 ml in volume
• Nipple discharge of varying colour (Fig. 28.27A) may be present
FIGURE 28.27 Paget’s disease of breast Source: (Courtesy Dr R. Rajaraman).
FIGURE 28.27A Dark brown discharge of fibroadenosis.
• Sonomammography and X-ray mammography (Fig. 28.28) are diagnostic
• Aspiration is performed for symptomatic cysts. The colour of the cyst fluid
may range from yellow to dark green, usually cytology of the fluid is not
required, unless it is bloodstained or there is a residual lump.
• Cytology may indicate an intracystic papilloma or rarely, a malignancy

FIGURE 28.28 Mammogram—fibroadenosis.
Treatment
• Aspiration itself is sufficient, in most cases
• Excisional surgery may be required if there is a residual lump
Galactocoele
Usually seen in a lactating or recently lactated breast, due to blockage of the
ducts resulting in accumulation of milk in lactiferous tubules
A nontender cystic swelling with or without a milky discharge (Fig. 28.29)
FIGURE 28.29 Whitish discharge (galactocoele).
• Aspiration will show milky fluid
• Sonomammogram shows a cystic swelling
Treatment
Therapeutic aspiration of the cystic swelling is the treatment of choice
Mammary duct ectasia

• Means dilatation of larger ducts of the breast, which occurs usually around
menopause, an exaggeration of normal cyclical changes
• This may contain green fluid or sterile pus
• When it ruptures, chronic inflammatory response is seen in the surrounding
tissue, plasma cells forming the histology, and hence called ‘plasma cell
mastitis’
• Patients present with a green discharge (Fig. 28.30), with a tender lump close
to the areola and nipple, with inversion of nipple
• The breasts may be lumpy to feel
• Occasionally, it may show signs of inflammation, usually settling to
antibiotics
FIGURE 28.30 Greenish discharge of duct ectasia.
• Mammography may be diagnostic
• FNAC needs to be done to exclude malignancy
Treatment
• Antibiotics and anti-inflammatory drugs are sufficient
• Surgical drainage should be avoided, as it may result in a mammary fistula
Mamillary fistula
Results due to:
• spontaneous and surgical drainage of a chronic abscess (commonly
tubercular)
• inflammatory reaction of duct ectasia
• Discharging sinus on the breast
• There is always a preceding history of an inflammatory reaction of the breast,
which has been surgically drained
Fistulogram is conclusive
Treatment
Excision of the fistula with the involved duct is curative
Gynecomastia
• Majority of them are idiopathic
• Other causes are:
• Congenital: Bilateral anorchism, bilateral cryptorchism, Klinefelter
syndrome (chromosomal abnormality with the genotype XXY)
• Traumatic: Bilateral orchidectomy, irradiation to testes
• Inflammatory: Orchitis due to tuberculosis, syphilis and leprosy
• Neoplastic: Choriocarcinoma of testis producing excessive gonadotraphin,
Sertoli tumours of testis, adrenal or pituitary carcinoma, bronchogenic
carcinoma
• Hormonal: Oestrogen therapy in carcinoma prostate, corticosteroid
therapy, chorionic gonadotrophins
• Nonhormonal drug use: Digitalis, isoniazid, spironolactone and steroids
• Diseases: Liver failure
• Uniform enlargement of one (Fig. 28.30A) or both breasts (Fig. 28.30B), and
may be tender
• Breast enlargement occurring due to stilboestrol therapy is soft, and is called
mammoplasia
FIGURE 28.30A Unilateral gynecomazia.
FIGURE 28.30B Bilateral gynecomazia.
Chromosomal analysis may be useful
Treatment
Subcutaneous mastectomy or liposuction
28.5 Symptoms of breast diseases

• Lump
• Pain
• Discharge
Lump
The commonest presentation of a breast disease is lump. The lumps can be:
• Solitary (e.g. fibroadenoma, malignancy)
• Multiple (e.g. fibroadenosis)
A lumpy feel of the breasts is commonly seen in fibroadenosis
The lump can be:
• Smooth, firm and globular (e.g. fibroadenoma)
• Hard and irregular (e.g. malignancy)
Pain
Pain in the breast can be:
• Generalized involving the entire breast (e.g. hormonal imbalances such as
mastitis)
• Localized to an area (e.g. abscess)
The intensity of pain can be:
• Severe (e.g. abscess)
• Moderate (e.g. mastitis)
• Dull (e.g. late stages of malignancy)
Discharge
Discharges from the nipple can be:
• Bright red blood (e.g. duct papilloma, duct malignancy)
• Bloodstained fluid (e.g. intracystic papilliferous carcinoma)
• Dark, altered blood. (e.g. duct papilloma obstructing the duct allowing stasis
of bloody discharge)
• Thick greenish discharge (e.g. duct ectasia, fibroadenosis)
• Milky discharge (e.g. galactocoele, rarely secreting prolactinoma of the
pituitary gland)
• Serous watery discharge (e.g. fibrocystic disease)
Eliciting history
General particulars
• Age: Malignancies such as carcinoma are more common in the elderly and
benign breast disease and sarcoma are common in the young
• Occupation: Nuns who remain unmarried, have a high incidence of
malignancy of breasts as they have never breast fed
Lump
acute pathology such as acute infections and the long duration indicates
chronic pathology such as benign tumours
Sudden origin indicates acute pathology such as infections and gradual
development indicates chronic pathology such as benign tumours. History of
trauma indicates traumatic pathology, e.g. traumatic fat necrosis which may
mimic malignancy clinically
Description of the size of the swelling will permit the examiner to compare
its growth, if any and can be correlated with the duration of the illness, which
may indicate acute or chronic pathologies. Likewise, decrease in size may
indicate resolving infections, e.g. resolving mastitis, resolving haematoma of
the breast
Pain
• Pain: Is there associated pain and if so is it localized to the lump or is it
generalized to the entire breast? What is the intensity of the pain?
The pain can be generalized, dull and cyclical (e.g. hormonal imbalances
such as mastitis), localized and severe pain (e.g. abscess especially in the
lactating woman), and dull and localized pain (e.g. malignancy)
Discharge
• Discharge from nipples: Is there any discharge from nipples?
The nature and quantity of discharges vary according to pathology
Related symptoms
cellulitis) or low-grade fever may indicate malignancies
• Menstrual history: This decides the treatment plan, as chemotherapy and
hormonal therapy are based on menstrual history and the menopausal status
of the patient. Early menarche and late menopause are relevant points related
to aetiology of breast cancer
• Personal history: Marital history is very important as many breast diseases
including malignancy are common in unmarried women. Likewise, they are
common in women who had not breast fed their children
• Family history: Eliciting this has great relevance, as majority of breast
diseases including malignancy are prevalent in certain families, following a
genetic pattern
• History of taking drugs: Special attention to this history, regarding the
intake of oral or parenteral contraceptives as it is associated with breast
malignancies
The symptoms of breast diseases are correlated in Table 28.6.
TABLE 28.6
Correlation of Symptoms with Diseases of Breast
Symptom
Lesion
Nipple Loss of
Duration Pain Fever Past history
discharge appetite/weight
Congenital Amazia Since birth Absent Absent Absent Absent Nil
Polymazia Since birth Absent Absent Absent Absent Nil
Small or large Since birth Absent Absent Absent Absent Nil
breasts
Traumatic Fat necrosis Short Usually Absent Absent Absent Rarely
duration absent
Haematoma Short May be Absent Absent Absent History of

duration present
Acute Acute mastitis Short Present May be Absent (may be Absent May be
inflammatory duration present lactating)
Abscess Short Present May be Pus Absent May be
duration present
Chronic Chronic mastitis Long Present May be Absent May be present May be
inflammatory duration present
Antibioma and Long Present May be Absent Absent History of

chronic duration present
abscess
Benign neoplastic Duct papilloma Short May be May be Blood May be present Absent
present present
Fibroadenoma Variable Absent Absent Absent Absent Absent
Benign/malignant Cystosarcoma Variable May be Absent Absent Absent Absent

phyllodes present
Malignant Duct carcinoma Short May be May be Blood May be present Absent
neoplastic present present
Paget’s disease Short May be May be May be present May be present Absent
present present
Miscellaneous Fibroadenosis Long May be Absent Absent Absent Absent

present
Galactocoele Short Present May be Milky Absent Recent
duration present
Duct ectasia Long Present May be Green Absent Absent

duration present
Mammary fistula Long May be May be Serosanguinous Absent May be
duration present present
Analyzing the symptoms in women with breast diseases can give a reasonable
diagnosis. The local physical examination will give further information, which
will guide the examiner to arrive at a clinical diagnosis.
Pre-requisites
The examiner should inspect both the breasts at the same time Position of the
examiner
1. Standing in front of the patient (Fig. 28.31A)
2. View from the side of the patient (Fig. 28.31B)
FIGURE 28.31A Inspection from front.

FIGURE 28.31B Inspection from sides.
Positions of the patient

1. Standing or sitting erect, with arms down and also arms up (Figs. 28.32A and
B)
2. With the hands pressing her hips—to assess the fixity of lesion to pectoral
muscles (Fig. 28.32C)
3. With the hands pressing a wall—to assess the fixity of lesion to serratus
anterior muscle (Fig. 28.32D)
4. Bending forwards—to assess the fixity to the chest wall (Fig. 28.32E)
FIGURE 28.32A Inspection of breasts with arms at the sides.
FIGURE 28.32B Inspection of breasts with arms elevated above head.
FIGURE 28.32C Inspection of breasts while pressing the hips.
FIGURE 28.32D Inspection of breasts while pressing the wall.
FIGURE 28.32E Inspection of breasts while bending forwards.
Breasts
This consists of two parts:
1. Inspection
2. Palpation
Inspection
The breasts are examined in a specific pattern. Each breast is divided into four
quadrants (Fig. 28.33). The breast is inspected quadrant by quadrant (upper inner
quadrant [UIQ], lower inner quadrant [LIQ], lower outer quadrant [LOQ], upper
outer quadrant [UOQ] in that order), including the nipple and areola region,
lastly the axillary tail, followed by the nipples and areolae. The following points
are to be noted:
FIGURE 28.33 Quadrants of breasts.
Size and symmetry

• Symmetrical enlargement
• No pathology
• Small lump or lumps which have not altered the size of the breast
• Congenital anomaly
• Hormonal aberration
• Idiopathic virginal hyperplasia (unilateral or bilateral)
• Large and unilateral (disease in the larger side) (Fig. 28.34)
• Asymmetrical enlargement
• Irregular (e.g. malignancy with (Fig. 28.35) or without skin involvement)
FIGURE 28.34 Large right breast due to large tumour.
FIGURE 28.35 Irregular enlargement (with skin involvement) of breast due
to breast malignancy.
Note
Large lumps nearer to the skin, especially of small breasts (Fig. 28.36A) may
be visible (small lumps in large breasts are not visible and do not alter the
contour of the breast when there is no skin involvement).
FIGURE 28.36A Irregular enlargement (without skin involvement) of
breast due to breast lump.
Visible lumps
The size, shape, surface, margins and the quadrant involved have to be described
for all visible lumps
Note
Remember to lift the breast and examine for lumps if the breast is large and
pendulous (Fig. 28.36B).
FIGURE 28.36B Lump visible on lifting the breast.
Skin over the breasts

• Redness and oedema—acute inflammatory disease or malignancy (Fig.
28.37)
• Orange peel appearance on the skin (peau d’orange)—(malignancy with skin
involvement) (Fig. 28.38)
FIGURE 28.38A Ulcer Source: (Courtesy Dr Usha Dorairajan).
• Ulceration or fungation (malignancy with skin involvement) (Fig. 28.22)

• Scar of previous surgery—local recurrence (Fig. 28.39)
• Dimpling of the skin over the swelling (malignancy with skin involvement)
(Fig. 28.40)
• Engorged veins—large fibroadenomas or malignancies
• Increased vascularity—sarcomas (Fig. 28.41)
FIGURE 28.37 Redness and oedema of skin over a malignant lump.
FIGURE 28.38 Peau d’orange.
FIGURE 28.39 Local recurrence.
FIGURE 28.40 Dimpling of skin due to cancer.
FIGURE 28.41 Increased vascularity due to underlying sarcoma.
(Few veins are usually visible on some breasts more so during pregnancy)
Nipples and areolae

• Level of nipples (generally lie in one horizontal plane)
• Small tumours with puckering raise the level of nipple (Fig. 28.42A)
• Large tumours push the nipple down (Fig. 28.42B)
• Discharge
• Blood—duct papilloma
• Milk—galactocoele
• Dark green—duct ectasia
• Pus—abscess
• Areola—(cracks, fissures, ulcers, eczema, swellings)—eczematous (probably
Paget’s disease)
FIGURE 28.42A Nipple pulled up by the lesion on the left breast.

FIGURE 28.42B Nipple pushed down by the lump in the right breast.
Note
Nipple retraction unilateral or bilateral may be congenital, but recent
retraction may be a manifestation of an underlying disease.
Arm and thorax

The arm and the thorax have to be seen with special attention, as there may be
secondary oedema of the arm due to lymph nodal enlargement and also rarely,
cancerous nodules may be seen on the thorax and arm to appear like an armour, a
condition called, “cancer en cuirasse” (Fig. 28.22)
Lifting the arms above the patient’s head may reveal the mobility of the
breast in the upward direction and also the submammary region will become
visible especially in women with larger breasts
Palpation
The breasts are palpated keeping the patient in three positions:
1. Sitting position (Fig. 28.43A)
2. Semi recumbent position (Fig. 28.43B)
3. Supine with arms above the head (Fig. 28.43C)
FIGURE 28.43A Palpation in sitting position.

FIGURE 28.43B Palpation in a semirecumbent patient.
FIGURE 28.43C Palpation in a recumbent patient with arms up.
Palpation of breasts
Normal breast is palpated first to get the feel of the texture in that particular
person, as it varies from woman to woman.
Each breast is divided arbitrarily into four quadrants. The hand is kept flat on
the breasts and the palpation is done with the flat of the hand (Fig. 28.44A), and
examined quadrant by quadrant (UIQ, LIQ, LOQ, UOQ in that order), including
the nipple and areola region, lastly the axillary tail. The axillary tail is examined
by holding it between finger and thumb as it extends into the axilla. In other
words, the breast should be considered as a face of a clock and each hour of the
clock should be examined carefully (Fig. 28.44B).
FIGURE 28.44A Feeling the breast with the flat of the hand.
FIGURE 28.44B Representation of clock for palpation of breasts.
Palpation of nipples
The nipple is held gently between the index finger and thumb and attempt should
be made to express any discharge (Figs. 28.45A and B)
FIGURE 28.45A Method of expressing the nipple for discharge.
FIGURE 28.45B Expressing the lump for nipple discharge.
Note
Examination of normal breast is done the same way.
The findings of physical examination and diseases of breasts are correlated in

Table 28.7.
TABLE 28.7
Correlation of Findings of Physical Examination and Diseases of
Breasts
Examination Pathognomonic Feature
Lesion
Inspection Palpation
Congenital Amazia Absence of Not applicable Total absence of breast tissue
breasts
Polymazia Multiple nipples Breasts can be palpated Multiple nipples on the milk line
with or if present
without
breasts
Small or large Normal but differ No specific pathology Absence of pathology
breasts in size to
normals
Traumatic Fat necrosis Enlarged breast Hard lump Rarely history of trauma
Mastitis Enlarged breast Firm and tender breast History of trauma
Acute Acute mastitis Enlarged breasts Firm and tender breasts Period of hormonal changes
inflammatory (bilateral)
Abscess Enlarged breast Localized tenderness Fluctuation may be present
Chronic Chronic mastitis Enlarged breasts Firm and tender breasts Associated pulmonary pathology
inflammatory (bilateral)
Antibioma and Enlarged breast Firm lump History of acute abscess with
chronic inadequate antibiotic intake or
abscess improper drainage
Benign neoplastic Duct papilloma Bloody nipple Palpable lump Discharge increasing after applying
discharge pressure over the lump
Fibroadenoma Normal Well-defined mobile Mobility of lump within breast
lump tissue
Benign/malignant Cystosarcoma Normal or Ill-defined lump with Restricted mobility
phyllodes enlarged restricted mobility
breast
Malignant Duct carcinoma Irregular shape Hard palpable lump Irregular edges of a hard infiltrative
neoplastic of the breast with or without lump with axillary
nipple discharge lymphadenopathy
Paget’s disease Excoriation of Lump may be palpable Unilateral disease (eczema is
nipple and bilateral)
areola
Miscellaneous Fibroadenosis Normal Lumpy feel of both Generalized lumpiness
breasts
Galactocoele Normal breasts Small solitary lump Associated milky discharge
Duct ectasia Retracted nipple, Nodular feel Greenish discharge per nipple
inflammatory
signs
Mammary fistula Discharge in Tenderness Serosanguinous and purulent
areolar discharge
region
If a lump is felt during the palpation of the breasts, the following are to be
noted carefully:
• Location—helps in treatment planning (e.g. carcinoma is more common in
UOQ)
• Number—single lumps are usually fibadenomas or malignancies, multiple
lumps are fibroadenosis
• Size and shape—globular indicate a benign tumour and irregularity indicates
a malignant tumour
• Surface—smooth surface indicates a benign tumour and irregular surface
indicates a malignant tumour
• Margins—well-defined smooth margin indicates a benign tumour and
irregular margin indicates malignant tumour
• Local temperature and tenderness—indicates an acute inflammatory lesion
such as abscess
• Consistency—soft and fluctuant swelling indicates a cyst or abscess, soft
swelling indicates fibroadenosis and hardness is a hallmark of malignancy
• Mobility (fixity to deeper structures) (Fig. 28.46)—fixity denotes local
infiltration of malignant tumours
• Move the lump when the patient presses her hips with her hands making
the pectoral muscles taut—restricted mobility denotes involvement of the
muscles
• Move the lump when the patient presses a wall making the serratus anterior
muscle taut—restricted mobility denotes involvement of the serratus
muscle
• Restricted mobility without the muscles put into action, denotes fixity to
chest wall including the muscles
FIGURE 28.46 Testing the mobility of the lump.
Note
Fibroadenoma is freely mobile within the breast tissue)
• Fluctuation—indicates cystic lesion and normal soft breasts themselves may

also show fluctuation
• Transillumination—indicates cystic lesion containing clear fluid
• Fixity to skin—may indicate inflammatory adherence or fixity of a malignant
tumour (peau d’orange—French term for orange peel)
Large breasts may require bimanual palpation, and when adequate
examination is not possible, mammography may be needed to screen them.
The lumps or the lumpy feel of the breasts are analyzed in Table 28.8.
TABLE 28.8
Analysis of Breast Lumps
Local
Temperature Trans-
Lesion Shape Surface Margins Consistency Mobility Fluctuation
and illumination
Tenderness
Fat necrosis Irregular Uneven Ill defined Normal Firm to hard May be Absent Absent
absent
Traumatic Irregular Uneven Ill defined May be raised Firm Present Absent Absent
mastitis
Acute mastitis Irregular Uneven Ill defined Raised Firm Absent Absent Absent
Acute abscess May be Even Well Raised Soft Absent Present Absent
regular defined
Chronic Irregular Uneven Ill defined May be raised Soft to firm Present Absent Absent
mastitis
Duct Irregular Uneven Ill defined Normal Firm May be Absent Absent
papilloma absent
Fibroadenoma Globular Even Well Normal Firm Present Absent Absent
defined
Cystosarcoma Irregular Uneven Ill defined Normal Firm Restricted Absent Absent
Duct Irregular Uneven Ill defined Normal a Firm to hard May be Absent b Absent
carcinoma absent
Paget’s Irregular Uneven Ill defined Normal Firm to hard May be Absent Absent
disease absent
Fibroadenosis Lumpy Uneven Ill defined Normal Soft to firm May be Present May be
feel present within positive
breast
Galactocoele Regular Even Well May be raised Soft Present Present Present
defined
Duct ectasia Irregular Nodular Ill defined May be raised Soft to firm Present Present in Present in
cysts cysts
a
Temperature may be raised in infected carcinomas.
b
Fluctuation may be present in malignancies, which have undergone cystic degeneration.
Axillae and supraclavicular areas

Inspection
Visibly enlarged lymph nodes may be seen as fullness in these areas
Palpation
Method of palpation of axillary group of lymph nodes(described in Ch. 12;
Figs. 12.28A–E)
Note
Examination of the symptomatic breast is done first, followed by the
examination of axilla on the same side. This should be followed by the
examination of the other breast and the axilla in the same manner.
Method of palpation of supraclavicular lymph nodes

Supraclavicular lymph nodes are best palpated from behind (Fig. 12.32C)
Abdomen
Examination of the abdomen has to be done systematically for liver enlargement,
as the malignancies of the breast are known to metastasize to the liver.
Chest
The chest should be examined for tracheal shift (e.g. shift to opposite side due to
pleural effusion) and auscultated for adventitious sounds (e.g. metastatic lung
disease) and absent breath sounds (e.g. malignant pleural effusion).
Skeletal system
The skull, vertebral column and long bones are to be examined systematically, to
rule out skeletal secondaries.
Pelvis
The pelvis should be examined per abdomen and by rectal examination in male
and vaginal and rectal examinations in females (for pelvic deposits). Bimanual
examination may have to be done in some cases (e.g. Krukenburg tumours).
CHAPTER 29
Spine and spinal cord

K.R. Suresh Bapu, S. Devaji Rao
CHAPTER OUTLINE
29.1. Development of spine and spinal cord 450
29.2. Surgical anatomy of spine and spinal cord 450
29.3. Disorders and diseases of spine 453
• Kyphosis 453
• Lordosis 453
• Scoliosis 454
• Wedge and hemivertebra 455
• Unsegmented bar, block vertebra 455
• Injuries to bony and ligamentous spine 455
• Tuberculosis of spine (Pott’s disease) 456
• Pyogenic infections 459
• Rheumatoid arthritis 459
• Ankylosing spondylitis 460
• Benign tumours of spine 461
• Malignant tumours of spine 461
• Degenerative diseases of disc and facet joints 462
• Spondylosis (osteoarthritis) 463
• Spondylolisthesis 463
29.4. Disorders of sacroiliac joints 465
• Sacroiliac ligamentous strain 465
29.5. Disorders and diseases of spinal cord 465
• Meningocoele and meningomyelocoele 465
• Spina bifida occulta and diastematomyelia 467
• Dermal sinus tracts 467
• Injuries of spinal cord 468
• Demyelinating diseases 469
• Acute infections 469
• Tuberculosis of spinal cord 469
• Cysticercosis of spinal cord 469
• Spinal cord tumours 469
• Vascular disorders 470
29.6. Abnormalities of craniovertebral junction 470
29.7. Symptoms of spine and spinal cord pathologies 471
• Back 478
• Special tests 482
29.1 Development of spine and spinal cord

The neurons and supporting glia of the brain, spinal cord and peripheral ganglia
are derivatives of the ectoderm. The nervous system begins as a proliferation of
ectodermal cells in the craniocaudal axis of the embryo dorsal to the notochord.
Growth proceeds in the neural plate so that a longitudinally oriented groove,
flanked on either side by a crest is formed on its dorsal aspect. The dorsal lips of
the groove meet and fuse to form a hollow tube extending the length of the
embryo. Normally, the neural tube which represents the primitive brain and
spinal cord completely separates from the cutaneous ectoderm which comes to
overlie it, from the underlying notochord around which the vertebral bodies are
formed. Spinal and peripheral ganglia are formed from the cells of the neural
crest.
The process of closure of the dorsal elements situated in the neural groove and
separation of the neural elements from the cutaneous ectoderm starts in its
midportion and progresses craniad and caudad, around the third week of
gestation. Incompleteness of this process leads to a series of anomalies, which
can occur anywhere in the midline, most commonly the extremes, namely the
lumbosacral and occipital regions (as part of various syndromes, e.g.
craniovertebral anomalies, spinal dysraphism).
29.2 Surgical anatomy of spine and spinal cord

The spinal column (Fig. 29.1) transmits body weight to the pelvis and through it
to both lower limbs. The intervertebral disc and the two apophyseal joints
between adjacent vertebrae permit movement of the spinal column, affected by
the paraspinal muscles. The bony spine, the disc, the attached ligaments and
muscles take part in the transmission of weight in various weight-bearing
postures and movements. The cervical and lumbar vertebrae are more mobile
than the thoracic vertebrae, explaining the increased incidence of injury and
degenerative diseases in these regions.
FIGURE 29.1 Spine and its curves.
A vertebra basically consists of:

• a body and
• a neural arch surrounding the vertebral canal
The neural arch is made up of a pedicle on either side, each supporting a
lamina, which meets its opposite posteriorly in the midline. The pedicle bears a
notch above and below which, with its neighbour, form the intervertebral
foramen. The arch bears a posterior spine, lateral transverse processes and upper
and lower articular facets (Fig. 29.2).
FIGURE 29.2 Typical thoracic vertebra.
The spinal canal contains the dural sac with cerebrospinal fluid (CSF) from
foramen magnum to S2 level housing the spinal cord and roots.
• The spinal cord is much shorter than the spinal column and ends at L1
vertebral level
• The descending roots below L1 are called ‘cauda equina’ (Fig. 29.3)
• Each root from the spinal cord travels down to and through its intervertebral
foramen and supplies specific muscle groups and dermatomes in the body
though there will be an overlap between adjacent spinal segments
FIGURE 29.3 Cauda equina roots.
Cervical spine has:

• Seven vertebrae, the atlas and the axis with odontoid are unique with more
than 60° rotary movement to either side.
• Atlas (C1) has no body but the lateral masses are prominent and can be felt
on either side below the tip of the mastoid process
• Axis (C2) has very prominent spinous process and can be felt up in the
neck
• From C3 to C7, the facet joints are more transversely oriented with 29°–40°
slope forwards and hence with flexion–distraction forces of trauma, one
vertebra can jump over the other without fracture of facet joints
• There are eight pairs of cervical roots:
• C1 to C7 exiting above the corresponding vertebra and
• C8 root exiting through the intervertebral foramen between C7 and T1
Hence, a posterolateral disc prolapse causes compression of the exiting root at
the same level. This is in contrast to the disc prolapse at the lumbar region where
the exiting root escapes and the traversing root is affected (see below).
• Cervical spine has wide range of movements:
• Nodding occurs at the atlanto-occipital joint
• Rotation of head (60° to either side) occurs at atlanto-axial joint
• Flexion of neck allows the chin to touch the sternum
Flexion–extension range is about 90° and lateral flexion to either side is about
29°.
Thoracic spine is the longest with twelve vertebrae
• Because of the relative paucity of movement and additional stability given by
the rib cage, the spinal column from T1 to T10 is less vulnerable to injury
• Thoracolumbar junction from T11 to L2, being the junction of fixed and
mobile part gets the brunt of trauma
• Spinal cord segments T1 to T12 are located behind the vertebral bodies of T1
to T10 and lumbar spinal cord segments L1 to L5 are located behind T11 and
T12 vertebral bodies
• Movements at thoracic spine are relatively less with very little rotation:
• By flexion of spine, one’s hands can reach below the knee with smooth
convexity of the back
• Lateral flexion enables one’s hand to reach up to the knee on either side
Lumbar spine has five vertebrae:
• The vertebral body is relatively large so as to transmit the increasing axial
load
• The body-pedicle junction is on the upper half of body and hence the exiting
root below the pedicle is well above the level of the disc. Hence, the
posterolateral disc prolapse compresses the traversing root and not the
exiting root, e.g. the posterolateral disc prolapse at L4-5 level compresses the
L5 root and not the exiting L4 root (Fig. 29.4)
• The spinal cord ends at L1 and hence spastic paraplegia (upper motor neuron
deficit) cannot be due to disease of lumbar spine
• All movements are permitted at lumbar spine—flexion–extension, lateral
flexion with rotation
FIGURE 29.4 Relationship of spinal nerves to the vertebrae.
Sacrum and coccyx have five and four fused vertebral segments,
respectively:
• The upper sacrum transmits body weight to the ilium through sacroiliac joints
• The sacral roots S3, 4 and 5 arising from the conus behind L1 vertebral body
travel all the way down to sacral canal to exit through the anterior sacral
foramina, form the sacral plexus and innervate the bladder and anorectal
region
Intervertebral discs are placed between the vertebral bodies. Each disc
consists of a peripheral annulus fibrosus, which adheres to the thin cartilage
plate on the vertebral body above and below. The annulus surrounds the
gelatinous semifluid nucleus pulposus (Fig. 29.5).
FIGURE 29.5A Anatomy of spine and the intervertebral disc.
Ligaments of the spine which support the spinal column (Fig. 29.5A) are:
• Ligamentum flavum links all the vertebral laminae
• Supraspinous and infraspinous ligaments link the spines
• Articular ligaments support the articular facets
• Anterior and posterior longitudinal ligaments run along the whole length of
the vertebral bodies along the anterior and posterior aspects
The spinal cord conducts the sensory and motor fibres from the periphery
(Fig. 29.5B).
FIGURE 29.5B Cross section of the spinal cord.
29.3 Disorders and diseases of spine

The disorders and diseases of the spine can be divided based on their aetiology
(Table 29.1).
TABLE 29.1
Aetiological Classification of Diseases and Disorders of Spine
Aetiology Diseases
Congenital Anomalies Wedge and hemivertebra
Unsegmented bar, block vertebra
Traumatic Injuries of bony and ligamentous spine
Inflammatory Infective Tuberculosis of spine
Pyogenic infections of spine
Noninfective Rheumatoid arthritis
Ankylosing spondylitis
Neoplastic Benign Haemangiomas, osteoblastoma, aneurysmal bone cysts
Malignant Metastatic tumours, lymphoma, multiple myeloma
Degenerative Prolapsed intervertebral disc
Spondylosis
Spondylolisthesis
Kyphosis
• Kyphosis denotes excessive posterior curvature of the spinal column due to
collapse of vertebral body
• It is a manifestation of an underlying disorder, such as:
• Tuberculosis of the spine
• Unreduced vertebral compression fracture
• Osteochondritis
• Ankylosing spondylitis
• Senile osteoporosis
• Tumour of spinal column
The curve (Fig. 29.6) can be:
• Knuckled: One spinous process becomes prominent indicating collapse of one
vertebra (e.g. tuberculosis)
• Acutely angulated: Collapse of two or three vertebrae (e.g. advanced
tuberculosis or malignant deposits)
• Rounded: Several vertebrae are affected (e.g. Schuermann’s osteochondritis)
FIGURE 29.6 Kyphosis lateral view. Source: (Courtesy Dr V. Thulasiraman)
• X-rays (Fig 29.7), CT and MRI are diagnostic
• Investigations should be related to the pathological conditions outlined
FIGURE 29.7 X-ray—kyphosis.
Treatment
• The treatment is that of the underlying condition
• In severe cases, deformity correction will be indicated
Lordosis
• Lordosis is the opposite deformity to kyphosis, denoting excessive anterior
curvature of the spinal column (Fig. 29.8)
• Usually, it is a postural deformity rather than an effect of a disease
FIGURE 29.8 Lordosis.
Patients present with the lordotic posture
X-rays, CT and MRI are diagnostic
Treatment
Often no treatment is required
Scoliosis
Scoliosis denotes lateral curvature of the spine. It is of four types:
• Primary or idiopathic scoliosis (unknown aetiology)—begins in childhood
and progresses till the cessation of skeletal growth—lumbar, thoracolumbar
or thoracic
• Secondary scoliosis—congenital (sharp angulation at the site of anomaly,
poliomyelitis (unequal pull of muscles) and neurofibromatosis (pathology
not clear)
• Sciatic scoliosis
• Compensatory scoliosis
Deformity is the only symptom (Figs. 29.9A and B)
FIGURE 29.9A Scoliosis anterior view. Source: (Courtesy Dr V. Thulasiraman)
FIGURE 29.9B Scoliosis posterior view. Source: (Courtesy Dr V. Thulasiraman)
X-rays, CT and MRI (Fig. 29.10) are diagnostic
FIGURE 29.10 MRI—scoliosis. Source: (Courtesy Dr V. Thulasiraman)
Treatment
• Mild to moderate deformities will need bracing
• Severe deformity will need surgical correction
Wedge and hemivertebra

• In this anomaly, the vertebral development fails in one part of the vertebral
body
• The defect can be anterior, posterior, on the right or left side
• The defect may occur at any level:
• Incomplete failure—wedge vertebra
• Complete failure—hemivertebra
The patient presents with:
• Kyphosis (due to anterior failure)
• Scoliosis (due to unilateral failure)
X-rays of spine are (Fig. 29.11) diagnostic
FIGURE 29.11 X-ray—hemivertebra. Source: (Courtesy Dr V. Thulasiraman)
Treatment
• No treatment is required in mild cases
• Severe cases need surgical correction
Unsegmented bar, block vertebra

Unsegmented bar (incomplete) and block vertebra (complete) result due to a
defect in segmentation of the vertebral bar, and may involve one or more regions
• Usually asymptomatic. In mild cases, unopposed growth on the opposite side
leads to spinal deformity, and the deformity is significant in severe cases
X-rays (Fig. 29.12), CT and MRI of spine are diagnostic
FIGURE 29.12 X-ray—block vertebra.

Treatment
• No treatment is required in mild cases
• Severe cases need surgical correction
Injuries to bony and ligamentous spine

• When an overwhelming force strikes and compresses the spine, the bone
crumbles resulting in fracture of spine
• The type of the vertebral fracture depends on the direction of an injuring force
and the curvature of spine at the time of injury
• With increasing force of injury, two or three columns of spine get injured
leading to instability and dislocation
• Generally compression forces cause fracture while distraction forces cause
ligament injury
Symptoms
• When the spinal cord is not affected, pain on movement, stiffness and
tenderness are the symptoms
• When the spinal cord is affected, neurological deficit occurs, depending on
the level and completeness of damage to the cord
• Limb paralysis such as paraplegia or quadriplegia may be the presenting
symptoms
• Respiratory, circulatory and urinary bladder dysfunctions may be
superadded
Signs
Clinical examination is to determine the level and type of injury
• External injuries give clue to the mechanism of injury (e.g. chin injury may
indicate hyperextension injury, occipital injury may indicate flexion–
distraction injury, vertex injuries may indicate vertical compression)
X-rays (Figs. 29.13A and B), CT (Fig. 29.13C) and MRI are essential to assess
the extent of injury
FIGURE 29.13A X–ray—fracture of the fifth sacral vertebra.
FIGURE 29.13B X–ray—compression fracture vertebra.
FIGURE 29.13C CT cervical spine—fracture body of C3 vertebra.
Treatment
• Rest to the injured area may be sufficient with analgesic support. Many of
them recover completely
• Surgical decompression and stabilization are mandatory for incomplete cord
injuries. Though, the procedures are useful for bony stability in complete
cord injuries, the neurologic recovery is poor
Tuberculosis of spine (pott’s disease)

• Caused by Mycobacterium tuberculosis, affecting any age and involves the
spine at any level, but more commonly the dorsal spine
• More common in persons with poor defence mechanisms—malnutrition,
diabetes, postpartum state, on steroid therapy and immunosuppressants and
patients with HIV
• The spread to the spine is haematogenous and affects two vertebral endplates
on either side of the disc (as developmentally they originate from the same
somite and have common blood supply)
• Spinal cord compression (in the form of paraplegia) is possible due to
• Presence of tuberculous granulation tissues with or without an abscess in
the epidural space
• Posterior displacement or pathological dislocation of a diseased vertebral
body or disc
• Anterior vertebral collapse leads to an angular kyphosis
• Rarely, thrombosis of veins and archnoiditis can cause ischaemic injury to the
spinal cord
• Pain in the back—related to movements of the spine (night pain and pain
persisting in lying down posture are characteristics)
• Stiffness of the back—due to reflex muscle spasm
• Visible deformity of the back—due to kyphosis (gibbus)
• Localized swelling—due to paraspinal cold abscess (Fig. 29.14A)
• Abscesses can track down along fasciomuscular or neurovascular planes and
become clinically palpable near or far from the vertebral lesion
• In the cervical region, it can present in the neck (Fig. 29.14B) or in the
retropharyngeal space
• In the thoracic region, pus collects around the spinal column, forming a
fusiform paraspinal abscess or it may track towards the surface between
ribs (Fig. 29.14C)
• From the lower thoracic and lumbar region, pus tracks down behind the
psoas sheath and burst into the compartment behind the iliacus fascia to
form a palpable abscess in the iliac fossa (psoas abscess) (Fig. 29.14D)
FIGURE 29.14F X-ray—tuberculosis of the thoracolumbar spine.
• Weakness of legs (Pott’s paraplegia) or visceral dysfunction—epidural cord

compression may be seen in caries spine
FIGURE 29.14A Paraspinal abscess with gibbus. Source: (Courtesy Dr V.
Thulasiraman)
FIGURE 29.14B Tuberculosis cervical spine with cold abscess in
neck. Source: (Courtesy Dr K. Dakshinamoorthy)
FIGURE 29.14C Tuberculosis spine with abscess between the
ribs. Source: (Courtesy Dr S. Devaji Rao)
FIGURE 29.14D Ileopsoas abscess with psoas spasm.
Concomitant tuberculosis elsewhere in the body, if present will give a clue to

the diagnosis.
• X-rays (Figs. 29.14E) show reduced disc space with parasternal shadow (Fig.
29.15)
FIGURE 29.14G X-ray—paraspinal abscess.
• CT and MRI (Figs. 29.15A, B, C and D) are diagnostic

• Lymphocytosis and raised sedimentation rate may be present
• Mantoux test may be positive
• Tubercle bacilli may be isolated from aspirated pus
• PCR test for M. tuberculosis may be positive
FIGURE 29.14E X-ray—tuberculosis of the cervical spine. Source: (Courtesy
Dr V. Thulasiraman)
FIGURE 29.15A MRI spine—paraspinal cold abscess. Source: (Courtesy Dr V.
Thulasiraman)
FIGURE 29.15B MRI—tuberculosis of spine (fracture C4 vertebra) with
cord compression. Source: (Courtesy Dr V. Thulasiraman)
FIGURE 29.15C MRI cervical spine—caries spine (C2, 3, 4) with
retropharyngeal abscess.
FIGURE 29.15D MRI—tuberculosis of spine (fracture T12 vertebra) with
cord compression. Source: (Courtesy Dr V. Thulasiraman)
Treatment
• Surgical decompressions are required in cases with progressive compression
of the spinal cord
• Stabilization will be indicated in selected cases
• Antitubercular treatment is mandatory
Pyogenic infections
• Pyogenic infections of the spine are uncommon
• Infections reach through the bloodstream, from a septic focus elsewhere
• Other modes of spread are through spinal venous plexus from a focus in
pelvis, or through lymphatics from a neighbouring focus
• Spinal cord compression or damage may occur due to pressure
Clinical features resemble that of tuberculosis and pyrexia is more pronounced
• X-rays show local rarefaction or erosion of bone with diminution of disc
space
• Marked leucocytosis and raised sedimentation rate are noted
Treatment
• Rest in bed is mandatory
• Abscesses require drainage
Rheumatoid arthritis
• The joint changes are such as those of rheumatoid arthritis elsewhere
• The changes begin in the upper cervical region
• The changes do not progress to bony ankylosis
• Pain in the back of a rather diffuse type, with impairment of spinal
movements
• The symptoms develop insidiously, without preceding injury
• Examination of the limbs usually reveal typical rheumatoid changes in several
joints
• X-ray (stress views) may show atlantoaxial subluxation. In longstanding
cases, rarefaction of the vertebrae with thinning of the intervertebral disc
spaces may be seen
• CT and MRI of spine are useful
Treatment
Treatment is in line recommended for rheumatoid arthritis of other joints
Ankylosing spondylitis
• In ankylosing spondylitis, there is chronic inflammation progressing slowly to
bony ankylosis of the joints of the spinal column
• Heredity is one of the important causes
• The disease begins in the sacroiliac joints, and extends upwards to involve the
lumbar, thoracic, and often the cervical spine
• The articular cartilages, synovium and ligaments show chronic inflammatory
changes and eventually become ossified (bamboo spine)
• Disease confined to men between the ages of 18 and 29
Complications: Fixed flexion deformity of spine, intercurrent respiratory
infections and iridocyclitis, which may lead to blindness
• Pain in the lower back and increasing stiffness (Fig. 29.16A)
• Later the pain migrates upwards, and radiates down to one or both lower
limbs
FIGURE 29.16A Ankylosing spondylitis producing stiff cervical
spine. Source: (Courtesy Dr V. Thulasiraman)
• X-rays (Figs. 29.16B, C and D) show fuzziness of sacroiliac joints, with poor
definition of joint outline. Bony ankylosis is seen in advanced cases
• Erythrocyte sedimentation rate (ESR) may be raised in an active phase
• CT (Fig. 29.17) and MRI are diagnostic
FIGURE 29.16B X-ray cervical spine—ankylosing
spondylitis. Source: (Courtesy Dr V. Thulasiraman)
FIGURE 29.16C X-ray thoracic spine—ankylosing
FIGURE 29.16D X-ray lumbar spine—ankylosing
FIGURE 29.17 MRI cervical spine—ankylosing spondylitis.
Treatment
• Activity rather than rest is encouraged
• Nonsteroidal anti-inflammatory drugs (NSAIDs) are useful
• Radiotherapy is useful in controlling the progression
• Severe flexion deformity can be corrected by wedge osteotomy of the spine
Benign tumours of spine
Vertebral haemangiomas, chondromas, osteoblastomas, aneurysmal bone cysts
are some benign tumours of the spine, but they are relatively uncommon
Constant back pain is the clinical presentation, sometimes with signs of cord
compression
Treatment
• Asymptomatic tumours need no treatment
• Patients with signs of cord compression need surgery to relieve the
compression
• En bloc vertebrectomy is indicated in certain situations
Malignant tumours of spine

• Metastatic tumours are usually from malignancy of lungs, breasts, kidneys
and prostate, and common in the elderly
• Multiple myeloma is common in the middle aged
• Lymphoma can occur at any age
Local bony destruction with oedema causes pain clinically similar to caries
spine
• Epidural spread of tumour, vertebral collapse and displacement can cause
cord compression similar to tuberculosis of spine
• Progressive back pain with or without signs of cord compression
• Tumours of cervical spine can present with obvious swelling in the neck (Fig.
29.18)
• Constitutional symptoms such as fever, loss of weight and appetite are
common
• Diagnosis is obvious when the primary is known
FIGURE 29.18 Malignant tumour of the cervical spine. Source: (Courtesy Dr V.

Thulasiraman)
X-rays of spine (Fig. 29.19), CT (Figs. 29.20A and B) and MRI are diagnostic,
which show erosion and collapse (disc space is characteristically normal in
contrast to tuberculosis)
FIGURE 29.19 X-ray—malignant tumour of the cervical

spine. Source: (Courtesy Dr V. Thulasiraman)
FIGURE 29.20A CT—spinal tumour. Source: (Courtesy Dr V. Thulasiraman)
FIGURE 29.20B CT—multiple metastases from carcinoma breast.
Treatment
• Chemoradiation is a useful adjunct to the primary therapy
• Measures should be taken to prevent pathological fractures and they can
precipitate cord compression and permanent damage to the cord
Degenerative diseases of disc and facet joints

Degenerative diseases of the spine are very common. They affect the lumbar,
cervical and thoracic regions in decreasing order of frequency.
• Lumbar degenerative disease:
• Prolapse of intervertebral disc: Discs between L5/S1 and L4/L5 are most
often affected. Part of the gelatinous nucleus pulposus protrudes through
the rent in the annulus fibrosus at its weakest part, which is posterolateral
and compress the nerve roots (compressive radiculopathy) (Fig. 29.21).
Occasionally, a large central disc prolapse at L5/S1 compresses the cauda
equina (cauda equina syndrome)
• Facet joint disease: Degenerative changes cause root compression
• Lumbar canal stenosis: Increasing wear and tear, bony overgrowth and
ligamentous hypertrophy can cause narrowing of the spinal canal
• Cervical degenerative disease: Pathogenesis is the same as in lumbar disease
FIGURE 29.21 Stages of prolapse of intervertebral disc.
• Lumbar degenerative disease: Back pain is the constant feature, but lower
limb pain varies according to the compression of the root
• Prolapse of intervertebral disc: Back pain radiating to:
- back of thigh and inner aspect of leg (L4 root compression–L3/L4
prolapse) or to
- outer aspect of the leg to the big toe (L5 root compression–L4/L5
prolapse) or to
- the sole of foot (S1 root–L5/S1 prolapse) is the presenting symptom
Acute radiating pain and inability to move, aggravated by coughing and
sneezing, are the symptoms of acute disc prolapse. Straight leg-raising (SLR)
test is positive on the affected side.
Cauda equina syndrome consists of back pain, bilateral sciatica and urinary
retention.
• Facet joint disease presents with pain similar to the synovial joint pain (more
after a period of rest such as early mornings and becomes less after
movement)
• Lumbar canal stenosis causes numbness and weakness of lower limbs on
walking
• Cervical degenerative disease: The presenting symptom is neck pain related
to movements with radiculopathy
CT and MRI (Fig. 29.21A) are diagnostic
FIGURE 29.21A MRI—prolapse of L5-S1 intervertebral disc.
Treatment
• Acute attacks require rest and analgesics, followed by physiotherapy
• Chronic, persistent or progressive symptoms require surgery to remove the
prolapsed disc or decompressive laminectomy
Spondylosis (osteoarthritis)
• Cervical spondylosis: Degenerative changes are common in the cervical
spine, commonly in the lowest three cervical joints
• Thoracic and lumbar spondylosis: Spondylosis of thoracic and lumbar
intervertebral joints is common in those used to heavy physical work, but it
is not necessarily accompanied by symptoms
• Previous injury to spinal joints
• Previous disease of the joints
• Intervertebral disc lesions
• Age-related changes
• In general, the changes affect the central intervertebral (body to body) joints
and the posterior intervertebral (facet) joints
• When symptomatic, pain in the affected area worsening on activity is the
presentation
• No objective findings are seen
• Spinal movements may be restricted moderately, especially flexion
• X-rays (Figs. 29.22A and B) are informative. In the central joints, the
intervertebral disc undergoes narrowing subsequent to degenerative changes,
with osteophyte formation. In the posterior joints, the articular cartilages
degenerate with osteophyte formation (spurring) at the joint margins
FIGURE 29.22A Cervical spondylosis.
FIGURE 29.22B Severe lumbar spondylosis.
Treatment
• Avoidance of heavy lifting and similar strains is recommended
• Corsets are useful in controlling pain
• Physiotherapy (radiant heat, short-wave diathermy, massage, traction and
exercises) is useful
• Laminectomy or decompression may be required, in exceptional cases
• Operative fusion may be required in cases where pain is bad enough to cause
serious hardship
Spondylolisthesis
• This term signifies slipping of one vertebra over the lower, which is usually
forwards, but may be backwards. In the normal spine, forward displacement
of a vertebral body is prevented by engagement of the articular processes
with those of the segment next below it, and this check mechanism is weak
in spondylolisthesis
• The displacement is most common in the fifth lumbar vertebra, and the
displacement may increase slowly over years, and reach a severe degree of
spondyloptosis
• Spondylolysis (a defect in the pars interarticularis of the neural arch)
• Osteoarthritis of the posterior (facet) joints (degenerative)
• Congenital malformation of the articular processes (rare)
• Chronic backache with or without sciatica
• Examination may reveal a step above the sacral crest
• Lumbar vertebral bodies may be felt per abdomen due to its forward
displacement
• SLR test may be positive.
• X-rays (Fig. 29.23A) and CT (Fig. 29.23B) are diagnostic
• MRI (Fig. 29.23C) is used to assess root compression
FIGURE 29.23A X-rays—spondylolisthesis.
FIGURE 29.23B CT—spondylolisthesis. Source: (Courtesy Dr V. Thulasiraman)
FIGURE 29.23C MRI spine—C4 C5 spondylolisthesis.
Treatment
• Asymptomatic patients require no treatment
• Mild cases require surgical corset
• Surgery is justified only when the disability is severe
29.4 Disorders of sacroiliac joints

The disorders and diseases of the spine can be divided based on their aetiology.
They are given in Table 29.2.
TABLE 29.2
Aetiological Classification of Disorders and Diseases of Sacroiliac
Joints
Aetiology Diseases
Traumatic Sacroiliac ligamentous strain
Inflammatory Infective Tuberculosis of sacroiliac jointsa
Pyogenic infections of sacroiliac joints a
Noninfective Rheumatoid arthritisa
Ankylosing spondylitisa
Degenerative Osteoarthritisa
a
The diseases are similar to those elsewhere in the body.
Sacroiliac ligamentous strain

Follows trauma, commonly in women
• Pain is localized to the sacroiliac joint, rarely as a diffuse ache in the thigh
• The pain is aggravated by twisting the trunk
• Examination reveals good range of movements with pain only at the extremes
• There are no neurological signs
X-rays are normal
Treatment
• Physiotherapy is useful
29.5 Disorders and diseases of spinal cord

The disorders and diseases of the spinal cord can be divided based on their
aetiology. They are given in Table 29.3.
TABLE 29.3
Aetiological Classification of Disorders and Diseases of Spinal Cord
Aetiology Diseases
Congenital Defects of posterior spinal elements Open neural defectsa Myeloschisis
Meningomyelocoele
Closed neural Meningocoele
defectsb
Spina bifida occulta,
diastematomyelia
Dermal sinus tracts
Dermoid tumours
Defects of dura and anterior spinal Neuroenteric cyst
elements
Anterior sacral meningocoele
Dural defects
Traumatic Complete and incomplete injuries
Inflammatory Demyelinations
Infective Tuberculosis
Parasitic Cysticercosis
Neoplastic Spinal cord tumours
Degenerative Spinal degenerative diseases
Vascular AV malformation, ischaemic
a
Open neural defects—spinal cord is exposed to the surface through a complete defect in the
dura, bone and skin.
b
Closed neural defects—spinal cord is covered by normal skin.
Meningocoele and meningomyelocoele

• Meningocoeles (protrusion of meninges through a defect in spine to form a
sac filled with cerebrospinal fluid) and meningomyelocoeles (protrusion of
meninges and spinal cord components through a defect in the spine to form a
sac filled with cerebrospinal fluid) are the most common of the defects of
dorsal components of the vertebrae
• Children with meningomyelocoeles have neurologic deficit, and majority
have hydrocephalus and many have associated congenital anomalies but they
are not only confined to the spinal cord
• In addition to spina bifida, other anomalies of the spine such as hemivertebrae
are often present
• Mental retardation occurs if hydrocephalus is untreated
• Most of the meningomyelocoeles occur in the dorsolumbar region
• A saccular swelling (Fig. 29.24) usually covered by the arachnoid and
occasionally by the skin
• The dysplastic cord may be seen through the membrane
• Neurologic deficit attributable to the spinal cord lesion is both motor and
sensory, its degree depends upon the site and severity of malformation. Most
have flaccid paralysis with the sensory level lower than the motor level
FIGURE 29.24 Meningomyelocoele. Source: (Courtesy Dr K. Dakshinamoorthy)
• X-ray demonstrates the bony defect, which usually extends over three or more
segments, and the spinal canal is often widened
• CT and MRI (Fig. 29.25) are diagnostic
FIGURE 29.25 MRI spine—lumbosacral meningocoele.
Treatment
• Meningocoeles require surgical intervention, emergent, if the sac is extremely
thin or ulcerated or leaking CSF
• Meningomyelocoeles need surgery (excision of the membranous sac,
replacement of the herniated spinal cord within the spinal canal and closure
of the dura, fascia and skin) whenever possible, and the surgery should be
done within few hours of life
Note
Long-term care is multidisciplinary.
Spina bifida occulta and diastematomyelia

• Spina bifida occulta is the incomplete fusion of the two halves of the neural
arch of one or two lumbar or sacral vertebrae with intact skin and meninges
and may be associated with cutaneous stigmata such as midline skin
angiomas, or pigmentation or tufts of hair (Fig. 29.26A)
• Diastematomyelia (split cord malformation—cord divided into two halves, by
a bony projection or fibrous band from the dorsal surface of the vertebral
bodies) is another abnormality of the spinal cord
FIGURE 29.26A Spina bifida with tufts of hair in the back.
• Spina bifida occulta is usually asymptomatic, but neurologic dysfunction or
with enuresis may be a presenting symptom in a child. Symptoms are seen
with a hamartoma, or lipomatous or a tethered filum terminale
• Diastematomyelia usually presents with sphincter dysfunction, difficulty in
walking and / or deformities of the feet
• Spina bifida is most commonly picked up in adults from an X-ray
examination (Fig. 29.26B)
• Diastematomyelia can be diagnosed from spinal column X-rays and CT (Fig.
29.26C)
FIGURE 29.26B X-ray—spina bifida.

FIGURE 29.26C CT—diastematomyelia—classical owl’s eye
appearance. Source: (Courtesy Dr V. Thulasiraman)
Treatment
• Spina bifida occulta needs no treatment
• Diastematomyelia requires surgery in infancy (removal of bony or fibrous
band)
Dermal sinus tracts

• This closure defect results from incomplete separation of the neural ectoderm
from either the cutaneous ectoderm or the entoderm
• These epithelial lined tracts may provide a direct communication between the
skin surface and the subarachnoid space
• The tract begins as low as the gluteal cleft but always upwards toward the
conus medullaris, which may end at or above the dura, or continue through
the subarachnoid space or even penetrate the nervous tissue
• Associated infections of the tract may cause meningitis
• An opening at the skin, which may be inconspicuous by the hair
• Fever and signs of meningitis may supervene
X-rays and sinograms are diagnostic
Treatment
Excision of sinus tracts is advised before the infant is 6 weeks of age
Note
The spinal cord can come out of the spinal canal and get tethered to the skin
directly or by fibrous bands or by a lipoma (lipomyelocoele).
Injuries of spinal cord

• During the injuries of the spinal cord, the neurons suffer primary damage on
impact and are prone to secondary injuries from hypoxia, hypotension,
haematoma and swelling
• When the damage is severe, spinal cord function at and below the level of the
lesion is abolished
• Spinal cord injuries are usually associated with injuries of the vertebral
column, usually fracture or fracture-dislocation
• The mechanisms of injury to the spinal cord / root are by:
• Primary injuries: The primary injuring force itself can cause violent
movement and stretching or disruption of cord with or without abnormal
bony displacements
• Secondary injuries: The fractured segments of vertebrae, extruded disc,
infolded ligaments and intraspinal haematomas can cause secondary
compression of cord or roots causing neurologic deficit
• Paralysis occurs below the level of the lesion, e.g. thoracic cord injury leads
to paraplegia and cervical cord injury leads to quadriplegia
• Flaccid paralysis with no sensation indicates complete lesion with a poor
prognosis
X-rays and CT are useful in diagnosis
Treatment
• The treatment should focus on maintaining stability of the vertebral column
either by external or internal fixation
• Recovery is variable and rehabilitation should start early for better results
Demyelinating diseases
They can be classified into primary and secondary:
• Primary—due to multiple sclerosis and neuromyelitis optica—are rare
• Secondary—post infectious and post vaccinial—are common
Acute or subacute paraplegia with very little back pain
MRI shows hyperintense signals in cord without cord expansion
Treatment
Medical—steroids and supportive care
Acute infections
Acute infections of the spinal cord generally result from:
• Entry of organisms through congenital dermal sinus or penetrating injuries
• Blood spread from infections elsewhere
The patient presents with fever, back pain and acute paraplegia
MRI is diagnostic and differentiates from demyelination, epidural metastases
and lymphoma
Treatment
• Abscesses require drainage
Tuberculosis of spinal cord

• Tuberculosis of the spinal cord is rare
• Tuberculous spinal archnoiditis occurs by spread from the cranial meninges,
and tuberculomas of spinal cord
Subacute progressive paraplegia
• MRI (Fig. 29.27) is diagnostic
• CSF analysis may be needed in select cases
• Biopsy may be needed in some cases

FIGURE 29.27 MRI—spinal cord tuberculoma.
Treatment
Antitubercular treatment is curative
Cysticercosis of spinal cord

Rare parasitic infection associated with central cysticercosis
Progressive paraparesis
MRI (Fig. 29.28) is diagnostic
FIGURE 29.28 MRI spine—giant intramedullary cysticercosis.
Treatment
Surgical excision through laminectomy is curative
Spinal cord tumours
• Spinal tumours are far less common than the brain tumours
• They are classified based on the anatomical location and the histological
appearance (Table 29.4)
TABLE 29.4
Classification of Spinal Tumours
Anatomical Location Histology

Extradural Metastatic tumours, lymphomas
Intradural Extramedullary Meningioma, neurofibroma
Intramedullary Astocytomas, ependymomas
Clinical presentation depends on the location of the tumours (Table 29.5)
TABLE 29.5
Clinical Presentation of Spinal Tumours
Anatomical Location Clinical Presentation
Extradural Nonspecific back pain, rarely radicular

Intradural Extramedullary Root pain, myelopathy in late stages, ascending type of deficit
Intramedullary LMN signs in upper limbs and UMN signs in lower limbs, early bladder involvement,
dissociated sensory loss, suspended sensory loss
Treatment
• Surgical removal is the only effective treatment
• Radiotherapy is useful for multiple or metastatic tumours to palliate pain
Vascular disorders
• Rare
• Congenital lesions occur in intramedullary locations as glomus lesion
• Acquired causes are dural arteriovenous (AV) fistula presenting after 50 years
due to venous reflux and venous hypertension
Paraplegia
MRI and spinal digital subtraction angiography (DSA) are characteristic (Figs.
29.29A and B)
FIGURE 29.29A CT spine—AV malformation of cord.
FIGURE 29.29B Angiogram—dural AV fistula.
Treatment
Surgery or interventional radiology
29.6 Abnormalities of craniovertebral junction

Anatomically these are divided into:
• Those which affect the basiocciput and
• Those which primarily involve the first and second cervical vertebrae:
• Atlantoaxial dislocation: The causes may be trauma, infection or
degenerative bone disease. This may be associated with the
maldevelopment of the atlas. The upper cervical spinal cord may get
compressed between the odontoid, and the posterior arch of the atlas
• Occipitalization of atlas: The atlas may be fused to the base of the occiput,
and the odontoid
• Condylar hypoplasia
• Chiari malformation and syringomyelia
• Many remain asymptomatic until adult life
• Minor trauma can precipitate symptoms (e.g. cranial nerve signs such as
dissociated sensory loss over the face (descending trigeminal tract) and
palatal and vocal cord weakness)
• Nystagmus and spastic weakness of extremities are common, and may have
loss of position sense, ataxia, bladder dysfunction and atrophy of shoulder
musculature and small muscles of the hand
• Local examination reveals a short neck with restriction of neck movements
• Condylar hypoplasia leads to torticollis
• X-rays are confirmatory
• CT and MRI (Fig. 29.30) give finer details of cord compression
FIGURE 29.30 MRI—craniovertebral anomaly (tonaillar descent and
syrinx in cervical spinal cord).
Treatment
• Minor degrees require bracing
• Severe dysfunction requires decompression of craniovertebral junction by
occipital craniotomy and laminectomy of the arches of C1 and C2
29.7 Symptoms of spine and spinal cord

pathologies
• Back pain
• Neck pain
• Root pain
• Neurologic deficit
• Spinal deformity
• Swelling
Back pain
The pain in the low back is of many types. They are:
• Lumbago: In a typical attack of acute lumbago, the patient is suddenly seized
with agonizing pain in the lumbar region, usually during the act of stooping,
lifting or coughing. The pain is usually relieved by rest, but sometimes it
may be succeeded by sciatica, suggesting irritation of lumbar roots
• Sciatica: Pain radiating along the back of lower limbs. If the pain is severe
and radiates in a well-defined course, and if it is accompanied by motor,
sensory and reflex impairment, it suggests mechanical pressure over the
lumbar and sacral roots / plexus / sciatic nerve. If it is vague in distribution,
it is more likely to be a referred pain originating from a disordered joint or
ligament
• Coccydynia: Any painful condition in the region of the coccyx, usually after
an injury—fall on the tail, causing strain of sacrococcygeal joint or contusion
of periosteum over the lower sacrum or coccyx
• Discogenic back pain: Pain aggravated by situations increasing the
intradiscal pressure, e.g. sitting, bending forward and lifting heavy weights.
Pain is generally less while standing or walking as the axis of weight
transmission is shifted posteriorly with lessened intradiscal pressure. In
nonweight bearing lying position, the intradiscal pressure is lowest and the
pain is negligible. Pain may get aggravated by coughing or sneezing,
indicating that the outer pain sensitive layers of the annulus are in touch with
the dural sac. When the disc totally extrudes, it compresses the nerve roots,
causing radiation of pain along the distribution of the roots but falling short
of foot
• Referred pain: Radiation of pain to proximal parts of the limbs can occur
without root involvement and is due to pain from sensitive structures such as
the annulus, dura, epidural tissue, bone, facet joint, ligaments and muscles
• Facet joint pain: The pain characteristically is more in the early mornings
and less on mobility
• Neurogenic claudication: The pain is chronic in nature, which progressively
increases in intensity on prolonged walking or even standing and compels
the patient to sit or lie down; but it takes some time to settle even after
sitting. Bending backwards precipitates the pain while bending forwards
relieves the pain due to increase in size of intervertebral foramen during
forward bending. For the same reason, climbing down the stairs will be more
difficult than climbing up. Pedal pulses will be normal.
• Pain of chronic instability: In addition to discogenic pain, facetal pain and
neurogenic claudication, sudden stabbing pain may occur with specific
movement more often while extending the back
• Myofascial pain: This pain is more localized and is aggravated by muscle
contraction, particularly isometric, i.e. contraction of muscles against
resistance preventing movement of spine. It is short-lived and responds well
to rest and analgesics and lasts 2–3 days.
• Psychogenic pain: This pain is ill-defined and often extends to the whole of
the spine and to all four limbs without conforming to any anatomical region.
The description is dramatic with high sounding words. Patients do not
comply with any exercise programme, and avoid working. Pain of this nature
does not prevent them from social activities or activities of daily life and is
not relieved by analgesics but subsides with antidepressants
• Referred pain from extrinsic disorders: Variety of extrinsic disorders can
cause back pain. They are given in Table 29.6
TABLE 29.6
Extrinsic Disorders Causing Back Pain
Region Pathology Nature of Pain
Abdomen Peptic ulcer infiltrating the pancreas Pain is relieved by food intake and also stooping forwards
Pancreatic pathology Pain is more on lying supine and relieved by lying prone or
stooping forwards
Visceroptosis Drag caused on the posterior abdominal muscles by
pendulous viscera, relieved by combined abdominal and
lumbosacral supports
Gallstones or cholecystitis Pain in the right back referred along the intercostal nerves
Pelvis Intrapelvic tumours Sciatica due to involvement of sacral plexus
Gynecological (menstruation) or Pain in the low back related to menstrual cycles or
obstetric (pregnancy) causes advancement of pregnancy
Retroperitoneum Renal colic Colicky pain in the loin often associated with urinary
symptoms
Tumours (renal, primary and secondary Constant pain due to nerve involvement
lymphatic malignancies) with nerve
involvement
Lower limb Arthritis of the hip Pain related to hip joint movements
Vascular system Occlusion of aorta, iliac arteries Claudication pain with changes in lower limb pulses
Note
• Retroperitoneal diseases such as lymphomas, secondary lymph nodes,
malignancy of prostate, pancreas and stomach with retroperitoneal
infiltration can present with back pain. Without retroperitoneal infiltration,
large tumours such as those of the kidneys and ovaries can cause back pain.
• In women, normal menstruation and pregnancy are common causes of back
pain.
Neck pain
• Pain localized in the neck: Pain of short duration precipitated by awkward
positioning or movement of the neck during sleep or following travel. This
pain is relieved by application of pressure by fingers or massage or physical
measures and relieved by simple analgesics. This pain is characteristically
localized and shows no radiation
• Spondylitic pain: Pain of cervical spondylosis is chronic or recurrent and
lasts for several months, and is aggravated by movements of the neck
• Radiculopathy: Pain of radiculopathy shows characteristic radiation along
the nerve root distribution
• Pain of anxiety: This pain is usually suboccipital or nuchal, lasting for
several months or years but will not restrict the movements of the neck.
Other features of anxiety such as tremors, palpitation, insomnia or poor relief
with analgesics will give clue to the diagnosis
• Meningitic pain: Pain due to meningitis is associated with headache,
vomiting, altered sensorium and neck stiffness
• Constant neck pain: Pain due to caries spine and malignant disease lasts
longer probably for over 3 weeks, and is more at night time in lying position
with limitation of movement in all directions
Root pain
When a nerve root is compressed, pain distributes proximo-distally, partly along
the distribution of the root. This pain often stops short of hand or foot and does
not correspond to the dermatomal mapping of the limbs. This pain is called
compressive radiculopathy, which can be acute (e.g. sciatica) or chronic (e.g.
neurogenic claudication of lumbar canal stenosis). This should be differentiated
from the pain of joint (e.g. arthritis) and joint-related structures (e.g.
periarthritis), which has maximum intensity over the joint with proximal and
distal spread, and is exaggerated by movements of the joint. The distribution of
pain due to compression of specific nerve roots is given in Table 29.7.
TABLE 29.7
Distribution of Pain Due to Compression of Specific Roots
Limb Nerve Root Area of Pain
Upper limb C5 Proximal lateral arm

C6 Anterolateral arm → radial forearm (+/− pectoral)
C7 Posterolateral arm → elbow (+/− forearm)
C8 and T1 Medial arm → medial forearm
Lower limb L2 Inguinal region
L3 Anterior thigh
L4 Anterolateral thigh → knee → medial leg, gluteal, posterior hip
L5 Posterolateral thigh → calf, gluteal
S1 Posterior thigh → calf, gluteal
S2 Proximal posterior thigh (+/− pelvic / genital)
Neurologic deficit
• Neurologic deficit can be due to:
• Compression of nerve roots (compressive radiculopathy)
• Compression of the spinal cord (compressive myelopathy)
• Compression of root / spinal cord is commonly due to traumatic,
degenerative, infective or neoplastic diseases of spinal column with
extradural extension. All these conditions have characteristic pain, in
addition to neurologic deficit
• When the neurologic deficit is not accompanied by pain, it is likely due to
noncompressive diseases (e.g. infective polyneuroradiculopathy—Gullian
Barre syndrome) or transverse myelitis, diabetes plexopathy, various
demyelinating diseases of cord-roots-plexus-peripheral nerves
• Neurologic deficit without significant pain or with mild pain only can occur
due to intradural extramedullary tumours such as ependymoma, astrocytoma,
dermoid and epidermoid. Clinically, they have characteristic features:
• Progressive deficit over weeks or months
• Asymmetric involvement of the limbs
• Definite segmental level of deficit above which there is no neurological
deficit
• Involvement of motor, sensory and other tracts at the same level
Note
Neurologic deficit without pain can also occur in congenital and
developmental diseases of the spinal cord such as meningomyelocoele, spinal
dysraphism, syringomyelia, intradural cysts, tethering or cord etc.
Compressive radiculopathy
Symptoms of root compression can be motor or sensory:
• Motor symptoms: Patients usually experience weakness of the whole limb
and express their inability to use the limb as before (e.g. inability to lift the
upper limb should indicate proximal muscle weakness and difficulty in the
acts such as mixing food, buttoning the shirt with the fingers should indicate
distal muscle weakness, likewise difficulty in getting up from the chair
indicates proximal muscle weakness and difficulty in holding the footwear
with the toes should indicate distal muscle weakness in the lower limb)
• Sensory symptoms: Distribution of sensory symptoms is fairly reliable to
specify the affected root only when the roots innervating the hands or feet are
affected. In proximal parts of the limbs, the normal overlap of dermatomes
masks sensory loss due to any one specific root. Numbness and tingling of
fingers in upper limbs is the usual symptom of cervical compressive
radiculopathy and that of the lower limbs are the usual symptoms of
lumbosacral compressive radiculopathy. They are tabulated in Table 29.8.
TABLE 29.8
Radiculopathy and the Corresponding Symptoms
Radiculopathy Nerve Root Area of Sensory Symptoms
Cervical C5 No specific area of numbness, sensory loss over deltoid insertion may be present
C6 Numbness / tingling over thumb and index finger
C7 Numbness / tingling over middle finger (and also index and / or ring finger)
C8 Over ring and little fingers and ulnar aspect of hand and forearm
T1 Over ulnar aspect of arm and elbow
Lumbosacral L1, L2, L3 No specific area of sensory loss because of dermatomal overlap
L4 Medial aspect of leg and ankle
L5 Over dorsum of foot, 1st and 2nd toes
S1 Over lateral foot and 5th toe
S2 Posterior thigh +/−
Compressive myelopathy
Weakness of limb muscles with stiffness (spasticity) of legs. Sensory deficit at
the level of spinal cord is of five patterns ( Figs. 29.31A–E). They are tabulated
in Table 29.9.
FIGURE 29.31A Complete cord section.
FIGURE 29.31B Left hemisection of cord.
FIGURE 29.31C Central cord lesion.
FIGURE 29.31D Posterior spinal syndrome.
FIGURE 29.31E Anterior spinal syndrome.
TABLE 29.9
Causes and Description of Compressive Myelopathy
Type of Deficit Description of Deficit Cause

Complete Hyperesthesia at the upper level with loss of Trauma, spinal cord compression by tumour, cervical
transverse all modalities a few segments below the spondylosis, transverse myelitis, multiple sclerosis
lesion lesion (Fig. 29.31A) (rarely—intraspinal tumours, spinal abscess,
infections)
Hemisection of Loss of joint position sense and vibration on -do-
the cord the same side as the lesion and pain and
(Brown- temperature on the opposite side a few
Sequard levels below the lesion (Fig. 29.31B)
syndrome)
Central cord Loss of pain and temperature sensations at Syringomyelia, intramedullary tumours, hyperextension
the level of the lesion, where the injury
spinothalamic tracts cross with other
modalities preserved (Fig. 29.31C)
Posterior spinal Loss of joint position and vibration senses Trauma, spinal cord compression by tumour, cervical
syndrome with intact pain and temperature (Fig. spondylosis, transverse myelitis, multiple sclerosis
29.31D) (rarely—intraspinal tumours, spinal abscess,
infections), subacute degeneration of cord, tabes
dorsalis
Anterior spinal Loss of pain and temperature below the Anterior spinal artery emboli or thrombosis
syndrome level with preserved joint position sense
and vibration sense (Fig. 29.31E)
Note
Spinal cord ends as conus medullaris at L1 level. Any lesion at or below L1
will affect the conus or cauda equina and will cause lower motor neuron
(LMN) type of motor deficit and radicular type of sensory loss. Lesions above
L1 will lead to LMN type of deficit at the level of compression and upper
motor neuron (UMN) type of deficit below the level of compression, e.g.
spastic paraplegia.
Spinal deformity
• Spinal deformity can be of various types:
• Torticollis—lateral tilt of the head
• Kyphosis—forward bending of the body—knuckle type, angular type or
round type
• Scoliosis—convexity to the lateral side (left or right)
• Kyphoscoliosis—rib hump on the convexity side or concavity side
• Lordosis—backward bending of the body
• Associated deformities can be:
• Secondary curvatures above and below
• Rib crowding or splaying
• Anterior chest wall deformity
• Pelvic tilts
• Neurofibromatosis
• The deformities can be fixed or mobile:
• Fixed deformities—not correctable
• Mobile deformities—partly correctable
• Deformities can occur in any region of the spine such as:
• Cervical
• Dorsal
• Dorsolumbar
• Consequences of the deformity:
• Neurologic—weakness or numbness of the limbs
• Cardiorespiratory—breathlessness, cough
• Cosmetic
Swelling
• Congenital: The commonest swellings over the spine are congenital (e.g.
meningocoele, meningomyelocoele). Intact skin over the swelling will
indicate a closed neural defect. In open neural defects, the open spinal cord
will be seen as a central elliptical area—raw or epithelialized with a
surrounding thin adherent abnormal skin representing the epithelialized
arachnoid
• Traumatic: Fractures and haematomas
• Infective: Tubercular cold abscess
• Neoplastic: Benign and malignant tumours of posterior elements of spine
Note
Kyphosis (angular kyphosis) itself may resemble a swelling.
The guidelines for localization of neurologic disorders by symptom analysis

are:
1. Distribution of neurologic deficit
• Upper limb only
• Lower limb only
• Upper and lower limbs
• Neck weakness
• Bladder and bowel disturbances
2. Unilateral or bilateral
3. UMN symptoms or LMN symptoms
4. Sensory symptoms ipsilateral or contralateral to motor deficit
5. Involvement of spinothalamic tract and posterior column
6. Bladder, bowel and sexual disturbances
7. Level of associated pain
The symptoms of spinal pathologies are shown in Table 29.10.
TABLE 29.10
Analysis of Symptoms of Spinal Pathologies
Root
Age at Pain at Increased by Root Cord
Disease Root Deficit Tension
Onset Rest Weight Bearing Pain Compression
Test
Lumbar / cervical > 40 Less ++ Negative Negative Negative Lumbar −ve
spondylosis years Cervical + /
−ve
Disc prolapse with > 25 Less ++ Positive Positive / Positive Lumbar −ve
radiculopathy years negative Cervical + /
−ve
Caries spine Any age ++ Positive Negative Positive / Negative Positive /
negative negative
Malignancy > 40 ++ Positive Negative Positive / Negative Positive /
years negative negative
Eliciting history
The clinical presentation of disorders and diseases of the spine and spinal
column have overlapping symptoms, a detailed history taking becomes
necessary before the physical examination, for perfect diagnosis.
• Age
• At birth: Spina bifida and menigocoele
• Young adults (between 15 and 29 years): Prolapse of intervertebral disc
• Elderly: Secondary malignant deposits
• Sex
• Males: Ankylosing spondylitis and prolapsed intervertebral disc
• Females: Osteomalacia and psychogenic pain
Pain over the spine (neck, back and low back) and
symptoms of cord compression
• Location: What is the location of pain?
The exact location of the pain should be questioned, so that the pathology to
a certain extent can be localized. The pain can be anywhere in the line of the
spine, neck, back or low back
• Duration: How long is the patient suffering from pain?
Short duration may indicate minor pathologies such as sprain, myofacial
pain, long duration may indicate caries spine, and recurrent attacks of pain
may indicate pain related to repeated strain (e.g. disc disease)
• Mode of onset: How did the pain start?
The pain may start after a major trauma (e.g. fall from a height) or after a
trivial trauma, or after a bout of fever (e.g. tuberculosis)
• Spread of pain: Does the pain spread or radiate and if so, where does it
originate and spread in which direction?
Short radiation to adjacent areas is referred pain and has no significance.
Root pain—cervical roots / thoracic roots / lumbar or sacral roots, tract pain
due to compression of sensory tracts in the spinal cord
• Precipitating factors: How did this pain become severe and was it following
any accident?
Severe trauma, lifting heavy objects can precipitate pain of the spine (e.g.
prolapsed intervertebral disc)
• Aggravating factors: When does the pain become more?
Acts such as movements of the spine, coughing, sneezing and turning in bed
can aggravate the pain (e.g. prolapsed intervertebral disc)
• Relieving factors: Does the pain become less at any time and if so, when?
Bed rest, lying position (supine or lateral), relief with analgesics are some of
the relieving factors of spinal pain
• Night pain: Does the pain disturb the sleep of the patient?
Patient waking up after falling asleep strongly suggests caries or malignancy
• Associated neurologic symptoms: Are there any symptoms like weakness of
limbs and if so describe them?
Numbness or weakness in the limbs may be present when the cord is
compressed, and they have a very characteristic distribution
Spinal deformity
• Duration: How long has the deformity of the spine been present?
This question will answer whether the deformity has been present since birth
(e.g. congenital kyphosis) or acquired during adolescence (e.g. kyphosis of
adolescence)
• Mode of onset: How did this deformity start?
Trauma causing fractures of spine, or infections such as tuberculosis and
pathological fractures can lead to deformity like kyphosis
• Progression: Since the onset, how has the deformity been, stationary or
progressive?
Kyphosis can progress during growth period and remains stationary after the
growth period
• Symptoms related to cord compression: Questions related to pain and cord
compression should be addressed
Spinal deformity can cause neurologic deficit (e.g. kyphosis can cause
stretch of spinal cord and resultant symptoms), and also the spinal or spinal
cord diseases per se can cause deformities (e.g. tumours of the spinal cord)
Swelling in the back

• Duration: How long has the swelling been present?
This question will answer whether the deformity been present since birth
(e.g. meningocoele) or acquired later (e.g. cold abscess)
• Mode of onset: How did this swelling start?
Trauma causing fractures of spine (e.g. haematoma), or infections such as
tuberculosis (e.g. cold abscess)
• Progression:Since the onset, how has the swelling been, stationary or
progressive?
Benign swellings (e.g. lipoma) may remain stationary, haematomas may
resolve and malignant swellings may progress
• Symptoms related to cord compression: Questions related to pain and cord
compression should be addressed
Swellings can cause neurologic deficit (e.g. spinal tumours causing cord
compression)

Association of high-grade fever with rigor may indicate an infective
pathology (e.g. pyogenic infections) and low-grade fever (e.g. tuberculosis,
lymphoma)
• Loss of appetite and weight:Is there any loss of appetite and weight during
and malignancies
give a clearer picture of diagnosis (e.g. recurrence of spinal tuberculosis)
• Personal history: Is the patient a smoker, consumes alcohol and is he a
diabetic?
History relating to personal habits such as smoking and consumption of
alcohol should be taken. History of diabetes and the medication he is on
should be enquired (e.g. diabetic neuropathy)
treatment?
such as recurrence of tuberculosis and recurrent malignancies
Diseases such as tuberculosis and demyelinating diseases occur in families
and the positive history may be a good indicator for the present diagnosis.
Family history of diabetes mellitus should be enquired
match the situation, like extramarital contact if the symptom is suspected to
be of syphilitic / HIV aetiology
Examination of back
Determine whether the patient can sit up comfortably, stand and walk. If the
pain is severe, examination is to be done in the lying position only.
Inspection
Posture and attitude of the spine

• As the patient walks in, the posture adopted by the patient has to be noted
• Head tilt (e.g. torticollis)
• Short neck with low hair line (e.g. basilar invagination)
• Levels of shoulders (e.g. varying levels in scoliosis)
• Stiffness of neck (e.g. sprain)
In spinal injuries, the patient adopts to a posture of comfort depending on the
level of injury. (e.g. C6 level—the arm is kept abducted (supraspinatus, deltoid)
and externally rotated (infraspinatus and teres minor) with the forearm flexed
and supinated (biceps), due to irritation of 5th cervical segment).
Note
Injuries of the spinal cord above C5 level cause phrenic nerve paralysis and
death.
Gait of the patient

Various gaits of patients with neurological illnesses are shown in Table 29.11
and some are shown in Figs. 29.32A and B.
FIGURE 29.32A Symmetrical gaits.
FIGURE 29.32B Hemiplegic gait.
TABLE 29.11
Gaits of Patients with Neurological Illnesses
Symmetry Gait
Symmetrical Small paces Stooped with reduced armswing (parkinsonian)
Upright with marked armswing (marche a petits pas)
Normal paces Feet broadly separated (broad based)
Incoordinated legs (cerebellar)
Crossing over, legs dragged (scissoring)
Marked rotation of pelvis and shoulder (waddling)
Asymmetrical Painful (antalgic)
Leg swinging outside (hemiplegic)
Deformities of the back

The patient should be viewed from all sides, front, back and both sides for:
• Kyphosis
• Scoliosis
• Kyphoscoliosis
• Hyperlordosis
Swellings or soft tissue contours

• Midline swelling (e.g. meningocoele)
• Lateral swelling (e.g. paraspinal cold abscess)
Wasting of muscles
• Wasting of muscles in the paraspinal region, e.g. erector spinae is quite
evident on inspection
Scars and sinuses

• The skin should be specifically inspected for scars (e.g. previous surgery scar)
and sinuses (e.g. tuberculous sinus)
Palpation
Deformity
The deformity is ascertained by running the fingers without pressure on the
spine.
Temperature
The local temperature on the spinal and paraspinal areas should be determined
with the back of the hand.
Tenderness
• Bony tenderness is elicited by:
• Application of pressure gently on the spine with the thumb (Fig. 29.33A)
• Tapping over the midline on the spinous processes (Fig. 29.33B) and over
the paraspinal areas (Fig. 29.33C)
• By applying gentle blows on the spine with the fist of the examining hand
(Fig. 29.34)
• Anvil test—by compressing or gently tapping the head over the spine in a
sitting patient (Fig. 29.35)
FIGURE 29.35B Tapping on the spine for eliciting tenderness.

FIGURE 29.35C Tapping on paraspinal areas for eliciting tenderness.
FIGURE 29.35E Method of performing Anvil test.
FIGURE 29.35D Applying gentle blows on the spine.
• Joint tenderness such as that on the sacroiliac joint can be elicited by pressing
over the dimple situated just medial to the posterior superior iliac spine with
the thumb while the patient is bending forwards (Fig. 29.36)
FIGURE 29.33A Application of pressure on the spine to elicit tenderness.
FIGURE 29.33B Tapping on the spine for eliciting tenderness.
FIGURE 29.33C Tapping on paraspinal areas for elicitng tenderness.
FIGURE 29.34 Applying gentle blows on the spine.
FIGURE 29.35A Application of pressure on the spine to elicit tenderness.
FIGURE 29.36 Method of eliciting sacroiliac joint tenderness.
Muscle spasm and wasting

The stiff paraspinal muscles can be palpated by running the fingers on the
paraspinal areas (Fig. 29.37). The wasting and flaccidity of the muscles should
be felt.
FIGURE 29.37 Method of palpating the paraspinal muscles for stiffness.
Swelling
If swelling is found, it is palpated in the usual lines to determine the warmth,
tenderness, consistency, plane of swelling, skin over swelling, transillumination
and impulse on coughing (described in Ch. 9).
Movements
Range of movements can be elicited in standing/sitting/lying positions. It should
be remembered that the joints of the spinal column must necessarily be
considered as a group, for it is impractical to study the movement of each joint
separately.
• Movements of cervical spine: By asking the patient to bend forwards,
backwards and sideways.
• Flexion: The patient is asked to bring his or her chin to the sternum and
this range is assessed (Fig, 29.38A). Normally it is possible to touch the
sternum with the chin
• Extension: The patient is asked to look up at the ceiling with full stretch of
the neck (Fig. 29.38B)
• Lateral rotation: Patients are asked to turn their head to the sides, and
normally they should be able to bring the chin in line with the line of the
shoulder on the same side (Figs. 29.38C and D)
• Lateral tilt: Patients are asked to tilt their head to one side after the other as
much as possible (Figs. 29.38E and F)
FIGURE 29.38 Movements of cervical spine—(A) Flexion. (B) Extension.

(C) Lateral rotation of cervical spine to left. (D) Lateral rotation of cervical
spine to right. (E) Lateral tilt of cervical spine to left. (F) Lateral tilt of
cervical spine to right.
The range of movements can be measured with a spoon or a spatula firmly
held between the teeth (Fig. 29.38G).
• Movements of dorsolumbar spine: Measured by asking the patient to bend
forwards, backwards and sideways. Rigidity of the spine is conspicuous in
ankylosing spondylitis, and tuberculosis. They are painful in tuberculosis.
• Flexion: Patients are asked to bend forwards, keeping their knees straight
and touch their toes (Fig. 29.39A). It is important to judge what proportion
of movement occurs at the spine and how much is contributed by a hip
flexion
• Extension: Patients are asked to look up at the ceiling with full stretch of
their back (Fig. 29.39B), which occurs predominantly at the lumbar spine
• Lateral rotation: Seated on a bench, the patients are asked to turn their
body to the sides (Figs. 29.39C and D)
• Lateral tilt: Patients are asked to tilt their body to one side and slide their
hand on the thigh downwards as much as possible (Fig. 29.39E). This is
repeated on the other side
FIGURE 29.38G Measurement of cervical spine movements with a

spatula in the mouth.

FIGURE 29.39 (A) Flexion of dorsolumbar spine. (B) Extension of
dorsolumbar spine. (C) Lateral rotation of dorsolumbar spine to left. (D)
Lateral rotation of dorsolumbar spine to right.
FIGURE 29.39E Lateral tilt of dorsolumbar spine to left.
Root tension tests

• Appropriate root tension test is done depending on the distribution of root
pain
Lower limb
• SLR test: This test is specific for determination of compression of L4, L5 and
sacral roots by prolapsed intervertebral disc
• Active SLR test: Method: The patient in supine position, with both legs
extended is asked to lift one leg without bending the knee and watched for
pain. The same is repeated for the other lower limb (Fig. 29.40A)
• Passive SLR test (Lassegue’s test): Method: The patient is asked to keep
the knee straight and the ankle is supported by the examiner and lifted
passively (Fig. 29.40B).
FIGURE 29.40A Active straight leg-raising test.

FIGURE 29.40B Passive straight leg-raising test (Lassegue’s test).
Positive: The test is positive if the patient experiences pain along the back of
the thigh and leg, and the pain becomes less on bringing down the leg by a few
degrees. Negative: If the pain experienced is limited only to the low back, it is
said to be negative.
• Lassegue’s sign: During the SLR test, at the angle where the patient
experiences pain, the ankle is passively dorsiflexed (Fig. 29.41). This is
considered positive if the pain is exaggerated as the sacral roots are further
compressed, and is negative if the pain is not exaggerated as the roots are not
compressed but suggests sacroiliac joint pathology
FIGURE 29.41 Eliciting Lassegue’s sign.
Alternate method of SLR

• SLR test can also be elicited in the sitting / standing position by asking
patients to touch their toes (Fig. 29.42)
FIGURE 29.42 Eliciting root tension pain by touching the toes.
Points to note:
• A normal person will be able to lift his or her leg up to 90° without pain.
However, the angle at which the pain is experienced is not important, but the
appearance of pain is important
• This test is first done on the normal side and then on the symptomatic side
• Disparity in different positions will give clue to the possible psychological
overlay
• Crossed SLR test: Passively lifting the straight leg towards the side
contralateral to the pain (Fig. 29.43) will indicate the severity of root
compression
• Femoral stretch test: This test is done when the pain is in the distribution of
L2, L3 roots
• Method: Patient in prone position, the leg is flexed at the knee or the whole
leg is extended at the hip (Fig. 29.44)
• Positive: The test is positive if the pain is experienced along the front of the
thigh as originally complained by the patient
• Naffziger’s test: Application of pressure on the jugular vein increases pain
due to an intervertebral disc prolapse
FIGURE 29.43 Crossed straight leg-raising test.

FIGURE 29.44 Femoral stretch test.
Upper limb
• Upper limb root tension test: This test is done when cervical radiculopathy
is suspected clinically.
• Method: With the neck extended and laterally flexed to the side of the pain,
gentle traction on the limb is applied (Fig. 29.45)
• Positive: The test is positive if the pain experienced is along the
distribution of root due to foraminal compression
• Lhermitte’s sign: Patients should be asked to flex their neck and the hip
simultaneously with their knees in full extension while sitting (Fig. 29.46). If
patients experiences sharp pain radiating down the spine and into the upper
or lower extremities, it suggests irritation of the spinal dura either by a
tumour or a protruded disc in the cervical spine
• Looking at the ceiling test: The patient is asked to look at the ceiling and
keep the neck in extension looking at the ceiling for a minute. If the patient
feels pain in the base of the neck, interscapular region or lateral aspect of the
shoulders or arms, it suggests degenerative changes either in the cervical
intervertebral discs or the facet joints (Fig. 29.47)
• Adson’s test: The patient is asked to turn the head to the affected side and
take a deep breath while the upper limb is pulled down and the radial pulse is
examined. The pulse will weaken or disappear, if there is compression at
thoracic outlet. Unfortunately, there are significant false positives for this test
(Ref Fig. 13.33)
• Phalen’s test: When the wrist is fully flexed and held for a few moments in
that position (Fig. 29.48), exacerbation of pain of the distribution of the
median nerve indicates positive test
FIGURE 29.45 Upper limb root tension test.
FIGURE 29.46 Eliciting Llhermitte’s sign.

FIGURE 29.47 Looking at the ceiling test.
FIGURE 29.48 Demonstrating Phalen’s test.
Tests for sacroiliac joint disorders

• Gillie’s test: The patient is should lie in prone position. While fixing the
pelvis by keeping the hand over the asymptomatic sacroiliac joint, the other
leg is hyperextended at the hip (Fig. 29.49). The test is positive for sacroiliac
arthritis, if the patient experiences pain
• Gaenslen’s test: The patient should lie on the symptomatic side, and the
pelvis is fixed by flexing the hip and knee of the affected side (Fig. 29.50).
The asymptomatic leg is hyperextended at the hip to produce rotational
strain. Occurrence of pain indicates sacroiliac disorder
• Pump handle test: With the patient lying supine, the limb is grasped just
below the knee and the hip and knee joint are fully flexed. Firm pressure is
applied directed towards the opposite shoulder so as to raise the pelvis off the
bed (Fig. 29.51). The test is positive if pain is experienced in the sacroiliac
joint
• SLR test: During this test, patients with sacroiliac disorder experience pain
on the sacroiliac region and not in the legs
FIGURE 29.49 Method of eliciting Gillie’s test.

FIGURE 29.50 Method of eliciting Gaenslen’s test.
FIGURE 29.51 Pump handle test.
Other systems
Neurological system
Tests to determine the muscle power (UMN type or IMN type)

• Upper limb
• Arm drift—for proximal muscles—C5 and C6
• Finger grip power—for long flexors of hand—C7 steadies and C8 prime
mover
• Finger spanning power—for small muscles of hand mostly dorsal
interossei T1
• Lower limb
• Stoop walking
• Squat walking
• Toe walking
• Heel walking
• Tandem walking
• Hopping with either leg
• Foot tapping
• Toe wriggling
Tests of motor deficits root or spinal cord segments

• Cervical radiculopathy
• C5—deltoid, supraspinatus, infraspinatus, biceps and brachialis
• C6—pectoralis major (clavicular head), brachioradialis (biceps and
brachialis with C5)
• C7—triceps, wrist extensors
• C8—finger flexors and extensors (interossei with T1)
• T1—intrinsic muscles of hand
• Lumbosacral radiculopathy
• L1 and L2—iliopsoas
• L3—quadriceps
• L4—tibialis anterior and tibialis posterior (quadriceps with L3, hip
abductors with L5)
• L5—extensor hallucis longus, extensor digitorum (hip extensors and knee
flexors with S1)
• S1—gastrocnemius, soleus, flexor digitorum hallucis (hip extensor and
knee flexors with S1)
• S2—toe flexors
Tests for sensory loss

The skin sensation is tested, segment by segment, by a wisp of cotton (touch
sensation), pin prick (pain sensation), a test tube of hot or cold water
(temperature sensation) and tuning fork (vibratory sensation) (Ch. 50).
Muscular system
The muscles of the limbs are examined for the following:
• Wasting and hypertrophy—by measuring the limb circumference with a tape
and compared with other side
• Fasciculation
Reflexes (ch. 50)

• Knee jerk (mainly L3 and L4)
• Ankle jerk (mainly S1)
• Plantar reflex
It is important to note only the presence or absence of the response, but also
any difference of intensity, by comparing to the other side.
Lymphatic system
Of drainage area
It is always mandatory to examine the area of lymphatic drainage, especially
when a lump is felt (e.g. tumours).

detail, e.g. tuberculosis and lymphoma. Examination of the liver and spleen
Neck
The neck should be systematically examined as neck lesions like abscess can
mimic lesions of the spine, or also, thyroid malignancies may present with spine
secondaries.
Chest wall
The chest wall should be examined for associated bony pathologies (e.g.
metastasis, tuberculosis, multiple myeloma), and also the breast should be
examined systematically (e.g. primary breast malignancy). Respiratory
excursions should be noted, especially in spinal injuries (e.g. lesions above T2
may cause paralysis of intercostal muscles and the respiration is abdominal).
Thorax
The chest should be examined for tracheal shift (e.g. shift to opposite side due to
pleural effusion) and auscultated for adventitious sounds, e.g. primary lung
disease—tubercular or malignancy) and absent breath sounds (e.g. tubercular or
malignant pleural effusion).
Abdomen
Examination of the abdomen has to be done for liver enlargement, and other
primary malignancies. Distended bladder and priapism may be seen in spinal
injuries. Iliac fossae and groins should be examined with attention (e.g. psoas
abscess originating from the lumbar spine).
Skeletal system
The skull, vertebral column and long bones are to be examined both by
inspection and palpation (e.g. multiple secondaries, multiple myeloma).
Pelvis (rectal and vaginal examinations)

The pelvis should be examined per abdomen and by rectal examination in males,
and vaginal and rectal examinations in females (for primary malignancies).
CHAPTER 30
Acute abdomen
N. Mohan
CHAPTER OUTLINE
30.2. Acute inflammatory conditions of abdomen 489
• Acute appendicitis 489
• Acute cholecystitis 492
• Acute diverticulitis 494
• Acute Meckel’s diverticulitis 494
• Acute ulcerative colitis 495
• Liver abscess 495
• Acute mesenteric lymphadenitis 496
• Acute salpingitis 496
30.3. Perforated bowel pathologies 496
• Acute abdominal catastrophes 496
30.4. Intestinal obstruction 498
30.5. Diseases causing intestinal obstruction 499
• Ascariasis 499
• Foreign bodies / bezoars 500
• Acute Intussusception 501
• Gallstone ileus 503
• Enteroliths / food bolus 503
• Strictures (tubercular or malignant) 503
• Bands and adhesions 503
• Volvulus 504
• Sigmoid volvulus 504
• Caecum volvulus 504
• Volvulus of the midgut 505
• Herniae (internal and external) 505
30.6. Adynamic lesion 505
• Paralytic ileus 505
30.7. Vascular conditions 506
• Ischaemic enteritis /Mesenteric vascular obstruction 506
30.8. Haemorrhagic conditions 506
• Ruptured ectopic gestation 506
• Acute haemorrhagic pancreatitis 507
• Leaking / dissecting aortic aneurysm 509
• Rupture of lutein cyst 509
30.9. Torsions 509
• Torsion of ovarian cyst 509
• Torsion of mesenteric cyst 510
• Torsion of omentum 510
30.10. Colics 511
30.11. Extra abdominal causes of abdominal pain 511
• Rupture of rectus abdominis muscle and rectus sheath
haematoma 511
30.12. Symptoms of patients with acute abdomen 511
• Acute abdominal pain 511
• Vomiting 513
• Alteration in bowel habits 513
• Urinary symptoms 514
• General 515
• Abdomen 516
• Pelvis 524
30.1 Introduction
Acute abdominal pain is a common symptom reflecting a variety of aetiologies.
The prevalence of the disease depends upon sex, age and country or the locality
where the patient lives.
The pain is usually due to the inflammation of an intra-abdominal organ or a
viscus. The pain is due to the involvement of the visceral peritoneum and is
referred to the abdominal wall, dependent on its origin from the fore-, mid- or
the hindgut. When the inflammation worsens, the parietal peritoneum gets
involved and the pain localizes accurately to the site of the disease.
Acute abdominal pain may be caused by a variety of diseases either from
inside the abdomen (intraperitoneal or retroperitoneal) and also from outside the
abdomen. They are tabulated in Tables 30.1 and 30.2.
TABLE 30.1
The Intra-abdominal Causes of Acute Abdominal Pain
Intraperitoneal Pathologies
Inflammatory conditions Acute appendicitis
Acute cholecystitis
Acute pancreatitis
Acute diverticulitis
Crohn’s disease
Ulcerative colitis
Liver abscess
Acute mesenteric lymphadenitis
Acute salpingitis
Subdiaphragmatic abscess
Perforated bowel pathologies (acute abdominal Duodenal ulcer
catastrophes)
Gastric ulcer
Typhoid ulcer
Diverticulitis
Meckel’s diverticulitis
Ulcerative colitis
Perforated appendicitis
Gastric malignancy
Perforation due to helminths
Obstructive lesions of the bowel
Dynamic
Intraluminal Ascariasis
Foreign bodies / bezoars
Intussusception
Gallstones
Enteroliths
Intramural Strictures (tubercular or malignant)
Extraluminal Bands
Adhesions
Volvulus
Herniae (internal and external)
Adynamic Paralytic ileus
Vascular pathologies Ischaemic enteritis
Mesenteric vascular obstruction (embolism or
thrombosis)
Intra-abdominal bleeding due to ruptures Ruptured ectopic gestation
Haemorrhagic pancreatitis
Acute leaking aortic aneurysm
Rupture of lutein cyst
Torsion of pedicled structure Torsion of ovarian cyst
Torsion of mesenteric cyst
Torsion of omentum
Colics Biliary / ureteric / intestinal, appendicular
Retroperitoneal Pathologies
Acute pyelonephritis
Retroperitoneal haematoma
Retroperitoneal lymphadenitis (filarial), lymphangitis
Leaking aortic aneurysm
Dissecting aneurysm
TABLE 30.2
Extra Abdominal Causes of Acute Abdominal Pain
Abdominal wall Cellulitis

Abscess
Rectus sheath haematoma
Rupture of rectus abdominis
Thorax Diaphragmatic pleurisy
Basal pneumonia
Inferior wall infarction
Angina pectoris
Pericarditis
Spine Herpes zoster of lower intercostal nerves
Pott disease
Gastric crisis
Tabes dorsalis
Intercostal neuralgia
General illnesses Typhoid fever
Malaria
Filariasis
Diabetic crisis
Sickle cell anaemia
Haemophilia
Purpura
Some illnesses which cause acute abdominal pain have greater preponderance
to the paediatric age group and need special consideration as the clinical
presentation may be different from those of adults. They are:
• Acute appendicitis
• Acute mesenteric adenitis
• Worm obstruction
• Intussusception
• Meckel’s diverticulitis
• Primary peritonitis
30.2 Acute inflammatory conditions of

abdomen
Acute appendicitis
• Commonest acute abdominal condition, occurring at any age
• Uncommon only below the age of 2
• Most commonly seen between the age of 18 and 35. The two varieties of
appendicitis are:
1. Catarrhal appendicitis—occurs due to acute inflammation of the
appendix, which produces oedema and even gangrene due to vascular
involvement in inflammatory process
2. Obstructive appendicitis—caused by obstruction of its lumen by
worms, faecoliths (Fig. 30.1A) or hypertrophied lymphoid follicles.
The appendix itself may be filled with pus (Fig. 30.1B)
FIGURE 30.1A Appendix with faecoliths.

FIGURE 30.1B Acute suppurative appendicitis (note the pus in the cup).
Complications
• When the adjacent tissues and omentum wall off the appendix or its
perforation, it forms a mass called ‘appendicular mass’ (see "33.8 Lumps in
the Iliac Fossae" in Ch. 33)
• When there is suppuration, it forms an abscess named ‘appendicular
abscess’, (see "33.8 Lumps in the Iliac Fossae" in Ch. 33) which may burst
into the peritoneal cavity to produce severe peritonitis and even death
Symptoms
• Pain—a dull continuous ache starting at the umbilical region (visceral pain)
and then localizing at the right iliac fossa (parietal pain)—catarrhal variety.
Obstructive appendicitis presents with colicky pain (appendicular colic) in
the right lower abdomen
• Nausea, vomiting and anorexia are usually present and are diagnostic
• Fever is the last to develop
(Pain, vomiting and fever in appendicitis is called Murphy’s syndrome)
Signs
• Hyperaesthesia over Sherren triangle
• Tenderness over McBurney point
• Guarding and rigidity in the right iliac fossa
• Rovsing sign (pain in the right iliac fossa on application of pressure in the left
iliac fossa) may be elicited
• Tender mass may be felt (appendicular mass / abscess)
• Dullness on percussion (if mass is already formed)
The signs and symptoms of appendicitis vary according to the position of the
appendix (Fig. 30.2). They are given in Table 30.3.
FIGURE 30.2 Various positions of appendix.
TABLE 30.3
Signs and Symptoms of Acute Appendicitis Related to the Position
of the Appendix
Retrocaecal and Paracaecal Pelvic and Subcaecal Pre- and Post-ileal

Symptoms and Signs
Appendicitis Appendicitis Appendicitis
Pain Right flank and back lateral to Right iliac fossa Right iliac fossa
sacrospinalis muscle
Diarrhoea Absent Absent May be present
Tenderness and Not marked Absent Present
guarding
Positive test Cope’s psoas test Obturator test Nil specific
Baldwing’s test
Tenderness in rectal Absent Present May be present
examination
Special situations
• In children
• Constitutional symptoms such as fever and tachycardia are more
predominant
• Use the child’s hand itself for palpation, and if there is tenderness in the
McBurney point, the child will withdraw its hand
• Percussion rebound is useful in diagnosing acute appendicitis
• Appendicular mass is rare as the omentum is small in size and does not
reach the appendix
• In the elderly
• Guarding and rigidity are not pronounced as the abdominal musculature is
weak
• Incidence of gangrene is more as there is associated atherosclerosis
• Peritonitis supervenes early
• In pregnant women
• The point of tenderness is shifted up, as the appendix itself is pushed up by
the enlarged gravid uterus
• Pyelitis and cystitis of pregnancy add to the difficulties in diagnosis of
appendicitis
• Accidental haemorrhage mimics acute appendicitis
Cardinal signs and symptoms of acute appendicitis are:
1. Periumbilical pain shifting to the right iliac fossa (very important)
2. Association of nausea
3. History of similar episodes in the past
4. Tenderness at McBurney point
5. Guarding and rigidity in the right iliac fossa
DD: Right ureteric colic (commonest), right ovarian pathology and acute
cholecystitis. The differentiating features of acute appendicitis and right ureteric
colic are given in Table 30.4.
TABLE 30.4
Differentiating Features of Acute Appendicitis and Right Ureteric
Colic
Sign and Symptom Pathology
Acute appendicitis Right ureteric colic

Pattern of pain Periumbilical pain shifting to right iliac Loin to groin radiation on the right side
fossa
Nature of pain Dull and continuous Very severe and colicky with pain-free
intervals
Onset of pain Slow and continuous Sudden onset
Relationship to body Aggravated Not related to movement
movements
Urinary symptoms Absent May be present
Rebound tenderness May be present Absent
Plain X-ray of abdomen Nonspecific Ureteric calculus
• US (Figs. 30.3A and B) may be contributory. The immobile swollen appendix
with free fluid in the right iliac fossa may be imaged. Mildly swollen
appendix is generally not seen in an ultrasound scan. The scan helps to
eliminate other lesions such as the ureteric calculus, ovarian pathology,
which can be imaged by US
• CT is useful in identifying inflamed appendix and appendicular mass (Fig.
30.3C). The signs of appendicitis are tabulated in Table 30.5
FIGURE 30.3A US: Inflamed appendix.
FIGURE 30.3B US: Appendicolith. Source: (Courtesy Dr V. Ganesan)
FIGURE 30.3C CT: Appendicular mass. Source: (Courtesy Bharat scans)
TABLE 30.5
CT Findings Associated with Acute Appendicitis
Appendiceal Signs Periappendiceal Signs
Appendix > 6 mm in anteroposterior diameter Increased fat attenuation (stranding) in the right lower
quadrant
Failure of appendix to fill with oral contrast or gas to its Caecal wall thickening
tip
Enhancement of appendix with IV contrast Phlegmon in the right lower quadrant
Appendicolith Abscess or extraluminal gas
Fluid in the right lower quadrant or pelvis
Treatment
• Emergency appendicectomy (laparoscopic or open) is the treatment of choice
• Conservative management is adopted for appendicular mass, subacute or
chronic appendicitis (Oschner Scherren regime), followed by
appendicectomy at a later date (interval appendicectomy)
Acute cholecystitis
• Common in fat, flatulent, fertile, female of fifty (five Fs)
• Caused by:
• infection by a variety of organisms
• obstruction caused by a calculus in the cystic duct
Complications
• Acute obstruction of the cystic duct causes distension and the bile can be
replaced by mucus (mucocoele) or pus (empyema) (Fig. 30.4A)
• Gangrene and perforation of gallbladder (p. 501) is common in diabetics
• Jaundice may occur due to the obstruction caused by an impacted stone in the
cystic duct (Mirizzi’s syndrome type 1)
FIGURE 30.4A Mucocoele or empyema of gallbladder.
Symptoms
• Severe colicky pain (biliary colic) in the right hypochondrium, radiating to the
inferior angle of the right scapula and the right shoulder
• Pain may be associated with vomiting
• Fever and jaundice are associated when there is associated cholangitis
• Symptom complex of pain, jaundice and fever with chills is called ‘Charcot’s
triad’.
Signs
• Tenderness at the tip of the right ninth costal cartilage (Murphy’s sign)
• There may be associated guarding and rigidity in the right hypochondrium
• The inflamed and distended gallbladder with or without the omentum may be
palpable
DD: Acute appendicitis, acute right pyelonephritis, duodenal ulcer
perforation, right basal pleurisy and myocardial infarction.
• US (Figs. 30. 4B and C) is diagnostic
• Rarely CT scan (Figs. 30.4D–F ) may be required
• Isotope scans (Fig. 30.4G) are contributory
FIGURE 30.4B US: Stone in the cystic duct of gallbladder. Source: (Courtesy
Dr V. Ganesan)
FIGURE 30.4C US: Acute oedematous cholecystitis.
FIGURE 30.4D CT: Stone in the gallbladder.
FIGURE 30.4E CT: oedematous gallbladder of acute cholecystitis.
FIGURE 30.4F CT: Ruptured empyema of gallbladder.
FIGURE 30.4G Isotope scan: Acute cholecystitis.

Treatment
• Acute cholecystitis is treated conservatively with antibiotics followed by
elective cholecystectomy (laparoscopic or open) (Figs. 30.5A and B)
• Common duct stones need to be removed by endoscopic retrograde
cholangiopancreatography (ERCP), sphincterotomy and basketing / stenting
or by open choledochotomy, to relieve cholangitis and jaundice followed by
cholecystectomy later
FIGURE 30.5A Gallbladder with single stone.

FIGURE 30.5B Gallbladder with multiple stones.
Acute diverticulitis
Inflammation of the diverticulum of:
• small bowel (jejunal diverticulits, Meckel’s diverticulitis)
• large bowel (colonic diverticulitis)
Complications: Perforation, paracolic abscess and peritonitis
• Meckel’s diverticulitis mimics acute appendicitis with right iliac fossa pain,
and differentiation clinically is difficult
• Colonic diverticulitis presents with colicky pain in the left flank
When perforated, it may form an abscess in the paracolic region and present
with high-grade fever and a palpable tender lump.
• Double contrast barium enema (Fig. 30.6A) is informative
• Colonoscopy(Fig. 30.6B) is diagnostic
• US and CT (Fig. 30.7) are useful in diagnosing abscesses
FIGURE 30.6A Barium enema: Diverticulitis of colon.

FIGURE 30.6B Colonoscopy: Acute diverticulitis. Source: (Courtesy Dr Mani
Veeraraghavan)
FIGURE 30.7 CT: Diverticulitis of sigmoid colon (Courtesy Bharat scans).
Treatment
• Uncomplicated diverticulitis needs to be treated with antibiotics
• Perforated diverticulitis with or without abscess formation needs surgical
intervention
Acute meckel’s diverticulitis

• Meckel’s diverticulum: An embryological remnant (Fig. 30.8) present as a
free diverticulum with a wide mouth, about 25–30 cm from the ileocaecal
junction; may contain ectopic gastric mucosa (reason not known)
• Occurrence follows rough rule of 2s:
• 2% of the population
• 2 feet from the ileocaecal junction
• 2 inches in length
• 2 times more common in males than in females
FIGURE 30.8 Meckel’s diverticulum.
Complications: Perforation and peritonitis
Clinical features similar to acute appendicitis
No investigation is useful
Treatment
• Acute diverticulitis warrants diverticulectomy
• Perforation and peritonitis need appropriate management
Acute ulcerative colitis

• A chronic inflammatory bowel disease with relapses and remissions
• Acute inflammation is one of its clinical presentations
Complications: Perforation and peritonitis
• Incessant diarrhoea, mixed with blood, mucus and pus with constitutional
symptoms
• They present an emaciated appearance
• Deep ulcers involving the entire colon is called toxic megacolon, presenting
as grossly distended abdomen
• Plain X-ray abdomen is diagnostic
• Colonoscopy is essential for diagnosis
Treatment
• Uncomplicated cases are treated medically
• Perforation and peritonitis need appropriate management
Liver abscess
• Amoebic liver abscess: Amoebic infections causing hepatitis and dysentery
may resolve into a liver abscess (usually in alcoholics) (Ch. 33)
• Pyogenic liver abscess: Septicaemic patients may present with pyemic
abscesses in the liver (Ch. 33)
• Constitutional symptoms with high-grade fever, tachycardia and sometime
shock
• Patients with amoebic aetiology may give history of preceding diarrhoea or
dysentery
• Intercostal tenderness is pathognomonic of a right lobar liver abscess.
DD: Lower thoracic lesions (basal pleurisy, pneumonia and lung abscess),
which irritate the diaphragm
• Plain X-ray of abdomen or X-ray chest will reveal elevation of the right
dome of the diaphragm (Fig. 30.9), right pleural effusion is common
• Fluoroscopy will show reduced mobility of the right dome
• US and CT (Fig. 30.10) are diagnostic
• Aspiration is confirmatory
• Stool examination is routine
• Isolation of organism in culture is required
• Serologic test (for amoebiasis) is positive in majority of cases
FIGURE 30.9 X-ray chest: Elevated right diaphragm due to liver abscess.

FIGURE 30.10 CT: Abscesses both lobes of liver. Source: (Courtesy Bharat
scans)
Treatment
• Anti-amoebic treatment is administered for small abscess and hepatitis of
amoebic aetiology
• Drainage under US guidance with broad-spectrum antibiotics and anti-
amoebic drugs is required for large abscess
• Growth of pyogenic organisms in culture of pus requires appropriate
treatment
Acute mesenteric lymphadenitis

• Acute infection and inflammation of the mesenteric lymph nodes, mostly of
the ileocolic group (Fig. 30.11)
• Seen commonly in the paediatric age group
• Commonly caused by viral infections
FIGURE 30.11 Mesenteric lymphadenitis.
• Periumbilical pain associated with high-grade fever
• On examination:
• The point of tenderness is usually in the right iliac fossa in the supine
position, and shifts to the left side, if the patient is made to lie on the left
side and vice versa (‘Klein’s sign’)—shifting tenderness
• Guarding is not predominantly present
• In thin children, enlarged lymph nodes may be felt
DD: Tubercular infection and acute appendicitis
• Clinical suspicion is important
• US (Fig. 30.12) and CT may show large lymph node swellings
FIGURE 30.12 US: Mesenteric lymphadenitis. Source: (Courtesy Dr V.

Ganesan)
Treatment
Medical management with antibiotics and supportive measures
Acute salpinigitis
• A disease of the sexually active female, sometimes after sexually transmitted
diseases, can confuse with acute appendicitis
• Usually associated with menstrual period, abortion or puerperium
• Common infective agents are Neisseria gonorrhoeae, coliforms and
chlamydiae
• Suprapubic pain, with or without white discharge per vagina (leucorrhoea)
• Localized tenderness is elicited in the hypogastrium
• Vaginal examination may reveal tender cervix and a bulky uterus
DD: Acute appendicitis is to be thought of in right-sided salpingitis
US is useful in diagnosing mass of the right ovary and the bulky uterus
Treatment
Treatment with antibiotics
30.3 Perforated bowel pathologies
Acute abdominal catastrophes

There are a variety of intra-abdominal pathologies, which are serious
emergencies, and also threaten life, if not recognized early and treated. Such
conditions are called ‘acute abdominal catastrophes’. Most of these conditions
are a result of infection of peritoneum called ‘peritonitis’, caused by the leakage
of infected intestinal contents into the peritoneal cavity. Since the peritoneum is
a semipermeable membrane, it allows the spread of infection systemically into
the blood to result in septicaemia, a fatal condition.
Peritonitis consists of three stages. They are:
1. Stage of peritonism: Occurs due to the chemical irritation of the peritoneum
caused by the leaked contents of the bowel, and the patient feels sudden
excruciating pain. Constitutional symptoms are not prominent, though
tenderness and guarding can be elicited
2. Stage of reaction: The contents of the bowel are neutralized by the peritoneal
exudates, and the pain becomes less. Muscle guarding may be present, and
shifting dullness may be elicited indicating the presence of free fluid in the
abdomen
3. Stage of spreading peritonitis: This is an ominous stage, as there are signs of
severe infection. They exhibit classic facies, called ‘facies Hippocratica’—
sunken eyes, hollow cheeks and anxious face. Severe tachycardia (fast
thready pulse) is present. Abdomen shows board such as rigidity, indicating
generalized peritonitis. Death becomes imminent if not attended to, surgically.
The signs and symptoms of perforations caused by various parts of the bowel
have certain indicative findings. They are given in the Table 30.6.
TABLE 30.6
Signs and Symptoms of Perforations Caused by Various Diseases
of the Bowel
Perforation due to
Duodenal or
gastric
Signs and Typhoid/tubercular Ulcerative Diverticular
ulcer Appendicitisb Cholecystitis
symptoms ulcers colitis disease
(benign/
malignant)a
Previous history Frequent use Nil or pain in Gallstones or Prolonged fever (high Repeated Repeated
of the right chronic grade in typhoid attacks of attacks of
antacids iliac fossa cholecystitis and low grade in diarrhoea constipation
in the tuberculosis) and and
past abdominal abdominal
(treated pain pain
or
untreated)
History of drug NSAIDs Nil Nil Treatment for typhoid Medical Medical
intake fever management management
Area of abdominal Upper Umbilical to Right Umbilical or lower Flanks and Umbilical or
pain abdominal start and hypochondrial abdominal hypogastric flanks
then in
the right
iliac fossa
Gastrointestinal Upper Nil Nil Lower Lower Lower
bleeds
Treatment Surgical
a
Leaks of gastric contents due to perforated gastric ulcer (posteriorly placed), into the lesser sac
may mask abdominal symptoms.
b
Clinical presentation of perforated Meckel’s diverticulitis is the same as that of perforated acute
appendicitis.
DD: Myocardial infarction, diaphragmatic irritation caused by lower lobar

lung lesions, acute pancreatitis and ruptured or dissecting aortic aneurysm
• Plain X ray of abdomen in the erect posture is confirmatory (gas under the
diaphragm) in most cases (Fig. 30.13A) and peritonitis gives the classic
‘ground glass appearance’ (Fig. 30.13B)
• CT (Fig. 30.13C) is useful
FIGURE 30.13A Air under the right dome of diaphragm duodenal ulcer
perforation.
FIGURE 30.13B X-ray abdomen: Ground glass appearance of peritonitis.
FIGURE 30.13C CT: Pneumoperitoneum.
Treatment
• Treatment is always surgical
• Closure of bowel perforation if it is simple and of benign cause
• Cholecystectomy (gallbladder perforations)/appendicectomy
(appendicular perforations)/appropriate bowel resections (benign or
malignant bowel perforations)
• Peritoneal toileting is mandatory and should be complete
• Malignancy needs relook surgery
30.4 Intestinal obstruction
General features
• Intestinal obstructions may be dynamic or adynamic.
• Dynamic obstruction is a physical or mechanical obstruction of the
intestinal lumen due to various causes. They are:
1. Intramural causes (e.g. faecal impaction, worms)
2. Mural causes (e.g. strictures or stenosis due to tuberculosis, malignancies)
3. Extramural causes (e.g. adhesions, obstructed hernia)
• Adynamic obstruction of the bowel is due to its neural (autonomic)
paralysis, commonly seen after abdominal surgery in the immediate
postoperative period, peritonitis or any other cause such as fractures, tight
bandages, injection, etc.
• Intestinal obstruction may be at different levels. They are:
• Small intestinal (high or low)
• Large intestinal (colonic or sigmoid)
• Causes of intestinal obstruction are different for different age groups (Table
30.7)
TABLE 30.7
Causes of Intestinal Obstruction in Different Age Groups
Newborn Infants Adolescents Adults Elderly Rare Causes
Duodenal atresia Helminths Bands Postoperative Growth Enteroliths

adhesions
Pyloric stenosis Intussusception Intussusception Intussusception Intussusception Foreign bodies
Meconium ileus Meckel’s Volvulus Obstructed or Gallstones
diverticulum strangulated
hernia
Hirschprung’s Obstructed or Growth, obstructed or Trichobezoar
disease strangulated strangulated hernia Phytobezoar
hernia
Symptoms and signs
1. Sudden episodic colicky abdominal pain
2. Vomiting
3. Constipation
4. Abdominal distension
(The symptoms vary according to the level of obstruction)
• Abdominal pain: It is sudden and squeezing, and the patient doubles up. It is
felt in the umbilical region, sometimes accompanied by the appearance of a
contracting loop. There may be pain-free intervals. Colonic pain presents in
the hypogastrium
• Vomiting: Vomiting is predominant in high obstructions. The vomitus
consists of gastric contents, followed by the duodenal and lastly the
intestinal, depending on the level of obstruction. In the late stages, the
vomitus becomes faeculent—ominous sign. Vomiting by itself is a late sign
of chronic intestinal obstruction
• Constipation: The patient evacuates his bowel (contents distal to obstruction)
once or twice, and constipation becomes a noticeable feature after 24 h
• Abdominal distension: Common feature of intestinal obstruction. Distension
is:
• centrally located (Fig. 30.14) in small bowel obstruction (ladder pattern)
• more on the flanks (Fig. 30.15) when distal colon is obstructed
(asymmetrical)
• more on the left flank in sigmoid volvulus
• Dehydration: When vomiting is pronounced as in high level obstructions,
dehydration is a presenting feature
FIGURE 30.15 Lateral distension of abdomen.
Note
• Diarrhoea can be a feature in certain situations such as intussusception (red-
currant jelly stools), Richter’s hernia, adynamic obstruction caused by
mesenteric vascular occlusion, pelvic abscess, etc.
• Early dehydration and less abdominal distension suggests duodenal or
jejunal obstruction whereas late dehydration and more abdominal distension
suggests distal ileal obstruction
• Vomiting and dehydration are usually not present in isolated acute colonic
obstruction.
General: Pulse rate and blood pressure are maintained at normal levels in the
initial stages. As dehydration becomes prominent, tachycardia and hypotension
result
Abdomen: Bowel sounds are not heard as obstruction worsens
The summary of signs and symptoms related to intestinal obstruction are
given in Table 30.8 (findings of clinical examination and treatment of individual
diseases are discussed at appropriate headings in the following pages).
TABLE 30.8
Signs and Symptoms Related to Intestinal Obstruction
Signs and Symptoms

Level of
Obstruction Duration of Pain-free Distension of
Vomiting Constipation Dehydration
colic interval abdomen
High Short Short More Minimal Not constant Severe

Low Long Long Less More Late feature Mild to
moderate
• Plain X-rays of abdomen in the erect posture will reveal multiple air fluid
levels (Fig. 30.16A) and colonic obstruction may also show distended colon
(Fig. 30.16B)
FIGURE 30.16A Multiple air fluid levels of small bowel obstruction.

FIGURE 30.16B Distenstion of large bowel. Source: (Courtesy Bharat scans)
30.5 Diseases causing intestinal obstruction

Ascariasis
• Common problem of the paediatric age group
• Obstruction occurs due to conglomeration of adult roundworms, Ascaris
lumbricoides
• Helminths can perforate and create an abdominal catastrophe
Symptoms
• Severe colicky abdominal pain
• History of passing worms in stool or in the vomitus (helminthemesis)
Signs
• The child is anaemic and undernourished
• Examination of abdomen may show palpable mass of worms around the
umbilicus
• Barium meal (Fig. 30.17A) in nonobstructed cases are informative
• US abdomen (Fig. 30.17B) may show adult worms
• Stool examination will show the presence of ova of ascaris
FIGURE 30.17A Barium meal series: Roundworms in the small bowel.
FIGURE 30.17B US abdomen: Ascaris adult worms. Source: (Courtesy Dr V.
Ganesan)
Treatment
• Anthelminthics are to be administered
• Surgical removal of the bolus of worms is required, if the obstruction is not
relieved
• Surgery of larger magnitude is required for perforations with peritonitis
Foreign bodies/bezoars
• Foreign bodies are generally swallowed accidentally by children and
intentionally by psychiatrically disturbed adults
• Generally small objects, if they are not sharp, may get impacted at the
cricopharyngeus level, and beyond that they do not pose any problem
• Bezoars are conglomeration of foreign material
• Phytobezoar—vegetable matter
• Trichobezoar—hair
• Tricho phytobezoar—combination of both
• Chronic abdominal pain and vomiting may be present
• Acute pain may be predominant when obstruction occurs
Plain radiographs, US, barium meal (Fig. 30.18), and endoscopy (Fig. 30.19)
are diagnostic
FIGURE 30.18 Barium meal: Trichobezoar.
FIGURE 30.19 Gastroscopy: Phytobezoar.
Treatment
• Digestive agents may be tried to dissolve vegetable matter
• Endoscopic or surgical removal may be necessary for hairballs
Acute intussusception
• Intussusception is the telescoping of a segment of bowel into the distal
adjacent loop (proximal into the distal)
In children:
• 2 per 1000 infants are affected with male preponderance, commonly affecting
the age group of 3 months to 1 year
• Commonly, it is secondary to an enlarged Payer’s patch due to viral or
bacterial infections (Fig. 30.20)
• The other less common causes are:
- Meckel’s diverticulum
- Duplication cyst in the bowel wall
- Polyp
FIGURE 30.20 Ileo ileal intussusception (kind permission: Jaypee).
In adults:
• intussusception of small bowel is always secondary to a polypoid lesion, a
lipoma (Figs. 30.21A and B)
• in large bowel it is due to a malignant polypoid lesion (Figs. 30.22A and B)
FIGURE 30.21A Ileo ileal intussusception (kind permission: Jaypee).
FIGURE 30.21B Lipoma the cause of ileo ileal intussusception (kind
permission: Jaypee).
FIGURE 30.22A Colo colic intussusception (kind permission: Jaypee).
FIGURE 30.22B Malignant growth of colon cause for intussusception (kind
permission: Jaypee).
Complications: When the mesentery is drawn between the loops, it may result
in vascular compromise, leading to strangulation, gangrene and perforation.
Symptoms
• In children, there may a history of preceding gastroenteritis following a
change in diet (weaning from milk to solid food)
• Severe acute colicky pain, with abdominal distension
• Passing of frequent semisolid stools with bright red blood may be
predominant (red-currant jelly)
Signs
• During the attacks of pain, a sausage-shaped mass may be felt, which appears
during the time of colic and disappears after the colic disappears. The right
iliac fossa is empty—Sign de Dance
• Rectal examination may reveal bloodstain on the examining finger (red-
currant jelly)
• Colorectal intussusception may be felt by the examining finger on rectal
examination, or it may even present through anus, resembling a rectal
prolapse
• Plain X-ray abdomen—soft tissue shadow in the region of transverse colon
with empty distal colon. Multiple air fluid levels may be seen when
obstruction predominates
• Barium enema may show a filling defect called pincer-shaped filling defect
(caused by the intessusceptum with the intussuscipiens)
• Colonoscopy can identify colocolic and ileocolic intussusceptions (Fig.
30.23A)
• US and CT (Fig. 30.23B) will reveal the intussuscepting mass (target or
pseudokidney appearance)
FIGURE 30.23A Colonoscopy—intussusception of small
bowel Source: (Courtesy Dr Mani Veeraraghavan).
FIGURE 30.23B CT: Intussusception. Source: (Courtesy Bharat scans)
Treatment
• Barium enema and colonoscopy by themselves may reduce the colonic
intussusception
• Laparotomy is required to reduce the small bowel intussusception, and treat
the cause appropriately
• Bowel resections may be needed if the bowel segment is strangulated, and
nonviable
• Perforation and peritonitis need appropriate treatment
Gallstone ileus
• Gallstone enters the bowel through a perforated gallbladder (post
cholecystitis) adherent to the small bowel (cholecysto-enteric fistula)
• When the stone is big and reaches the ileocaecal junction, it causes small
bowel obstruction
• Features of intestinal obstruction
• Previous history of vague attacks of right upper quadrant pain, suggesting
frequent cholecystitis
• Plain X-ray abdomen (Fig. 30.24) almost always shows air in the biliary tree
as bowel gas passes through the cholecysto-enteric fistula. A gallstone may
also be seen in the right lower quadrant, if it is radio-opaque
• CT is more informative. Rarely a gallstone may also be seen in the small
bowel, and also in the gallbladder if there are many
FIGURE 30.24 X ray—Gallstone ileus (arrow indicates air in the biliary
system).
Treatment
• During laparotomy:
• Simple crushing of stone with finger from outside the bowel may be
enough if it is soft
• Simple surgical removal through an enterotomy is required if the stone is
hard and big
• Cholecystectomy must be performed with closure of fistula
Enteroliths/food bolus
Obstructions may be caused by enteroliths or food bolus, resulting from poor
chewing in an edentulous patient, high consumption of high fibre (e.g. orange
pith), usually at a pre-existing narrowing due to tuberculosis, Crohn’s disease
and stricture
Symptoms of subacute or acute intestinal obstruction
Plain X-ray abdomen (erect) shows air fluid levels. Diagnosis is more clinical
and is difficult
Treatment
Surgery is indicated for acute obstructions, and the bolus or enterolith can be
milked into the large intestine and rarely it is necessary to open the bowel to
remove it
Strictures (tubercular or malignant)

• Obstructions can be caused by strictures of:
• tuberculosis (healing lesions)
• malignant lesions
• Postoperative strictures are not uncommon
• Symptoms of subacute or acute intestinal obstruction
• History of weight loss, low-grade pyrexia, anaemia and vague abdominal pain
may be present
• Clinical examination may show a mass in the right iliac fossa (DD: Crohn’s
disease)
• Ascites may be present
• Plain X-ray abdomen (erect) shows air fluid levels
• X-ray chest may reveal a primary tubercular lesion
Treatment
• Laparotomy is needed for acute obstructions
• Stricturoplasty or bypass procedures or resections are done for tubercular
strictures
• Radical resections or bypass procedures are done for malignant strictures
Bands and adhesions

• Bands may be congenital, but adhesions are postsurgical
• The adhesions may be such as a small band or generalized, flimsy or dense,
single (Figs. 30.25A and B) or multiple
FIGURE 30.25A Band in the pelvis causing internal rotation of small
bowel.
FIGURE 30.25B Adhesions of small bowel to previous surgery scar.
Features of subacute or acute intestinal obstruction, months or years after
surgery
• Plain radiographs of abdomen are useful in diagnosis
• Diagnostic laparoscopy is conclusive
Treatment
• Release of adhesions by laparoscopy or by open surgery
• Open surgery and release of adherent bowel loops for dense adhesions
obstructing the bowel
• It is better to manage the acute obstructions by trial medical management
with gastric suction and intravenous fluids
Note
Surgery has the disadvantage of recurrence, especially in generalized
adhesions.
Volvulus
• Volvulus is defined as a twist of the bowel around its mesenteric axis
• It is more common in the large bowel (commonly the sigmoid colon) than in
the small bowel
• Rotation of more than 180° may result in strangulation
Sigmoid volvulus
• Disease of the middle aged and elderly
• Rotation of the sigmoid around its axis occurs when its mesentery is
unusually long
• Occurs anticlockwise
• Sudden severe pain, frequ0065ntly when straining to pass stool. The patient
retches and develops hiccoughs
• The patient may give history of attacks of abdominal pain with constipation,
relieved by passing watery stools and large volumes of flatus
• Abdomen rapidly distends, disproportionate to the duration of pain, and the
distension is confined more to the left flank
• Rectum is empty on examination
• Plain radiograph of the abdomen will reveal a distended sigmoid, coffee
bean appearance—Freeman Dahl sign (Fig. 30.26) (convergence of three
white lines towards the base of the pedicle)
FIGURE 30.26 X-ray: Sigmoid volvulus.
Treatment
• Untwisting of the colon clockwise and fixing the colon to parietal
peritoneum to prevent recurrence
• Sigmoidectomy is the treatment of choice in long redundant sigmoid colon
Caecal volvulus
This occurs in those whose entire right colon has a mesentery continuous with
that of the small bowel, and the caecum does not lie in the right iliac fossa
A distended, tense palpable resonant mass in the umbilical region, with an empty
right iliac fossa
Plain radiograph of the abdomen is diagnostic (caecal bubble is seen)
Treatment
Untwisting of the volvulus with or without resection of the segment of the
bowel and cecopexy is required
Volvulus of the midgut

• In children, this occurs due to malrotation and failure of fixation of midgut,
usually before one year of age, rarely in neonates
• In adults, a loop of bowel rotates around a point of adhesion (to the abdominal
wall or to an adjacent viscera)
Severe abdominal pain with evidence of intestinal obstruction
Contrast study shows ‘Cork-screw effect’
Treatment
Emergency laparotomy (Fig. 30.27) and correction of the defect with fixing of
the bowel
FIGURE 30.27 Torsion of midgut.
Herniae (internal and external)

Internal hernias may occur due to congenital and acquired reasons.
• Congenital: Herniation through the pockets under the superior mesenteric and
interior mesenteric vessels
• Acquired: External hernia such as strangulated inguinal or femoral hernia can
cause intestinal obstruction
• Internal hernia may present with features of intestinal obstruction (Fig. 30.28).
Symptoms depend on the level of obstruction
• External hernia is clinically evident and may show signs of obstruction or
strangulation
FIGURE 30.28 Internal herniation of small intestines (kind permission:

Jaypee).
Plain radiographs and CT are useful in diagnosis
Treatment
• Reduction of herniating bowel and closure of defects
• Strangulated bowel may need resection
30.6 Adynamic lesion
Paralytic ileus
• Prolongation of ileus after abdominal operations beyond the third
postoperative day and lasts for a week or more
• Usual cause being electrolyte imbalance in the postoperative period
• Retroperitoneal or intra-peritoneal haemorrhage and sepsis are the other
causes
• Trivial causes such as an injection, application of plaster of Paris bandage and
any injury anywhere, fractures, etc. (Table 30.9)
TABLE 30.9
Causes of Paralytic Ileus
Causes Pathology Mechanism
Sympathetic dysfunction Postoperative ileus Reflex inhibition

Spinal injury
Acute renal colic
Trauma Retroperitoneal haemorrhage
Acute pancreatitis
Retroperitioneal malignancy Malignant infiltration
Local causes Peritonitis Bacterial infection
Advanced mechanical obstruction Excessive distension of bowel
Pharmacological Anticholinergics Interference with smooth muscle contractility
Antidiarrhoeals
Ganglion blockers
Biochemical Hypokalaemia
Uraemia
Diabetic crisis
Hypoxia
• Abdominal distension without pain
• Vomiting is a predominant symptom
• On examination, the abdomen is resonant with the characteristic absence of
bowel sounds
• Serum electrolyte levels show abnormalities
• Plain radiographs of the abdomen will show ‘step ladder pattern’ of the
small bowel (Fig. 30.29) with distension of both small and large bowels
FIGURE 30.29 X ray—Step ladder pattern of paralytic ileus.
Treatment
• Correction of electrolyte imbalances
• Treatment of retroperitoneal or intraperitoneal causes such as haemorrhage
and sepsis
30.7 Vascular conditions
Ischaemic enteritis / mesenteric vascular
obstruction
It is usually due to occlusion of mesenteric artery due to:
• Thrombosis on an atheromatous plaque (e.g. origin of superior mesenteric
artery)
• Embolus following atrial fibrillation/myocardial infarction/ detached
atheromatous plaque
• Severe acute abdominal pain with copious vomiting
• Very fast deterioration of health
• Haematemesis and melena also occur in some cases
• The clinical signs are disproportionate to the symptoms, and rarely an area of
tenderness may be felt near the infarcted bowel
• ECG, plain X-Ray and US abdomen are useful
• Selective angiography is informative
Treatment
• Conservative management to stabilize the patient
• Laparotomy and resection of nonviable bowel will be necessary, if the
patient is stable
• Balloon angioplasty or bypass grafts may be feasible in select cases
Note
Outcome is guarded in most cases.
30.8 Haemorrhagic conditions
Ruptured ectopic gestation (see ch. 38 also)

Occurs in young women of child-bearing age
Symptoms
• Acute pain in the hypogastrium accompanied by shock
• Generalized abdominal pain and pain at the shoulders are noted due to
stimulation of the diaphragm
• History of missed periods is usually obtained
Signs
• Discolouration may be seen around the umbilicus (Cullen sign) (Fig. 30.30)
• Tenderness in the hypogastrium
• Rebound tenderness and shifting dullness may be elicited
• Vaginal examination reveals a soft and acutely tender cervix, especially on
movement. A soft mass is felt in the fornix
FIGURE 30.30 Cullen sign of ruptured ectopic gestation (kind permission:
Jaypee).
• Haematocrit will be low
• US of the pelvis is diagnostic
Treatment
Emergency surgical intervention (salpingo-oophorectomy) is mandatory, with
management of shock
Acute haemorrhagic pancreatitis

• Common in the third decade
• Common causes are (mnemonic: I get smashed)
• I: Idiopathic
• G: Gallstone (in the ampulla of Vater)
• E: Ethanol
• T: Trauma
• S: Steroids
• M: Mumps (paramyxovirus, Epstein Barr virus, cytomegalovirus)
• A: Autoimmune (polyarteritis nodosa, systemic lupus erythematosus)
• S: Scorpion sting (Tityus trinitatis), snake bite
• H: Hypercalcemia, hyperlipidemia, hypertriglyceridemia, hypothermia
• E: ERCP
• D: Drugs (SAND—Steroids and Sulfonamides, Azathioprine, NSAIDs,
Diuretics)
• Less common causes are:
• Pancreas divisum
• Long common duct
• Carcinoma of the head of pancreas, and other cancers
• Ascaris blocking pancreatic outflow
• Chinese liver fluke
• Ischaemia from bypass surgery
• Fatty necrosis
• Pregnancy
• Infections other than mumps, including varicella zoster
• Repeated marathon running
• Cystic fibrosis
• Most common causes of pancreatitis, by demography are as follows:
• Western countries: Chronic alcoholism and gallstones
• Eastern countries: Gallstones
• In acute pancreatitis, there is oedema, haemorrhage and necrosis of the organ
partly due to autodigestion. The inflamed pancreas may return to normal, but
may recur, and likely to occur under two circumstances:
• The initiating cause has not been removed (gallstones, alcohol
consumption)
• Major pancreatic necrosis, resulting in chronic pancreatitis or stricture of
main pancreatic duct
Complications:
Systemic complications
• Respiratory failure
• Renal failure
• Metabolic abnormalities
• Coagulation disorders
• Multiple organ failure
Local complications
• Pancreatic necrosis
• Infection of pancreatic necrosis
• Fungal infections
• Haemorrhage
• Pancreatic pseudocyst, pancreatic fistula, pancreatic abscess
Symptoms
• Very severe, unbearable constant epigastric pain radiating to the back,
relieved by sitting and bending forwards
• Nausea and vomiting are marked, frequent and persistent
Signs
• Shock and cyanosis are marked
• Elevated temperature, tachycardia, tachypnoea
• Epigastric tenderness but guarding and rigidity are not marked
• Retroperitoneal haemorrhage may lead to characteristic discolouration:
• around the umbilicus (Cullen sign) (Fig. 30.30)
• of the flanks (Grey Turner’s sign) (Fig. 30.31)
FIGURE 30.31 Grey Turner’s sign (kind permission: Jaypee).
( These signs are not pathognomonic of pancreatitis, as they can be seen with
ruptured ectopic pregnancy as well)
DD: Perforated peptic ulcer, leaking aortic aneurysm, myocardial infarction,
acute cholecystitis, acute hyperacidity
• Elevation of serum amylase over 400 Somogyi units is indicative and more
than 1000 Somogyi units is diagnostic (It usually rises 2–12 h from the onset
of symptoms, and normalizes within 48–72 h)
• Serum lipase levels are elevated (It rises 4–8 h from the onset of symptoms
and normalizes within 7–14 days)
Note
Serum amylase may be normal (in 10% of cases) for cases of acute on chronic
pancreatitis (depleted acinar cell mass) and hypertriglyceridaemia. Reasons
for false positive elevated serum amylase include salivary gland disease
(elevated salivary amylase) and macroamylasaemia.
• Plain X-rays of abdomen show characteristic features:

• ‘Sentinel loop sign’—duodenum—which represents a focal dilated jejunal
loop in the left upper quadrant
• ‘Cut off sign’—transverse colon (Fig. 30.32A)—inflammatory exudate of
acute pancreatitis extends into the phrenicocolic ligament directly
spreading through the lateral attachment of the transverse mesocolon
causing functional spasm and / or mechanical narrowing of the splenic
flexure at the level where the colon returns to the retroperitoneum.
FIGURE 30.32A X-ray: Colon cut off sign.
(Absence of gas under the diaphragm eliminates the diagnosis of perforated

duodenal ulcer)
• US may not be very useful at all times
• CECT is very useful in assessing the size of the pancreas (Fig. 30.32B), and
also in determining the causes such as the biliary or pancreatic duct calculi
(Fig. 30.33)
FIGURE 30.32B CT: Enlarged and oedematous pancreas (red arrow) with
a pseudocyst (yellow arrow)—acute pancreatitis.
FIGURE 30.33 CT: Pancreatic calculi Source: (Courtesy Bharat scans).
Predicting the severity of an attack of acute pancreatitis is made on Glasgow

or Imrie criteria (simplified Ranson criteria) in Table 30.10.
TABLE 30.10
Criteria to Assess the Severity of Acute Pancreatitis
P Arterial PaO2 <9 Kpa
A Albumin <32 g/L

N Urea Nitrogen >10 mmol/L
C Calcium <2 mmol/L
R Raised white cell count > 16 mmol/L
E Enzyme—lactate dehydrogenase >600 mmol/L
A Age > 55 years
S Sugar glucose > 10 mmol/L
Presence of three or more criteria reached before or at 48 h of admission predicts a severe attack
and two or less predicts a mild attack
APACHE II score (Acute Physiology And Chronic Health Evaluation) can be

applied at anytime but it is cumbersome as it requires 15 different or biochemical
criteria
Treatment
• Initial management is conservative in intensive care unit
• Continuous arterial and CVP monitoring
• Assisted ventilation if required
• Inotropic support
• Enteral feeding
• Parenteral feeding if required
• Haemodialysis of renal failure if warranted
• Endoscopic treatment
• ERCP sphincterotomy and extraction of stones followed by laparoscopic
cholecystectomy
• Pancreatic necrosectomy is the treatment of choice with questionable
outcome in a grave situation
Leaking or dissecting aortic aneurysm

• Aneurysm of aorta (> 4 cm diameter—normal 1.5–2.5 cm) is the disease of
elderly, and rupture is the deadly complication, with a mortality of more than
80%
• Only a third with rupture of aneurysm live to reach the hospital
• The rupture can occur into the retroperitoneum or into the peritoneal cavity
• Acute severe upper abdominal pain or in the lower chest
• Radiation to the back mimics acute pancreatitis
• Aneurysm may be felt per abdomen with guarding and rigidity
• Lower limb pulses are feeble or absent
• Dissecting aneurysms present with retrosternal pain, as the pathology starts at
the aortic arch
US and CT of the abdomen (Fig. 30.34) are conclusive
FIGURE 30.34 CT: Dissecting aneurysm (L) axial (R) reconstructed 3D

images.
Treatment
Emergency surgical intervention is necessary, along with correction of shock
Rupture of lutein cyst
A common condition in young females
• Acute abdominal pain associated with vomiting (right-sided pathology may be
confused with acute appendicitis)
• On examination:
• A firm mass may be felt adjacent to the midline or in one of the iliac fossae
• Guarding and rigidity may be present
• Vaginal examination may reveal a tender mass
US of the abdomen is diagnostic
Treatment
Emergency surgical intervention is mandatory
30.9 Torsions
Torsion of ovarian cyst

It can occur at any age, may follow major physical exertion, which can initiate
the torsion
• Severe pain in the lower abdomen, with signs of shock
• On examination:
• Guarding and rigidity may be present
• A tender lump may be palpable, whose lower border cannot be made out
US and CT or MRI of abdomen are diagnostic
Treatment
Emergency laparotomy (Fig. 30.35) is needed. The cyst should be removed
FIGURE 30.35 Torsion of ovarian cyst.
Torsion of mesenteric cyst

• Cystic lesions of mesentery are more common than solid tumours(2:1)
• Cystic tumours of mesentery are:
• Chylous cyst, serous cyst (developmental)—more common
• Lymphangioma (lymphatic tissue)—more common
• Traumatic cyst (trauma)
• Enteric cyst, dermoid (embryonic rests)
• Majority of cysts are benign (except lymphangiosarcoma, malignant teratoma)
• Solid tumours of mesentery are:
• Lipoma (more common) and liposarcoma
• Fibroma (more common) and fibrosarcoma
• Neurilemmoma, neurofibroma and malignant schwannoma
• Leiomyoma, fibromyoma and leiomyosarcoma, fibromyosarcoma
• Haemangioma and hemangiopericytoma
• Benign solid tumours are more common than the malignant ones
• Malignant solid tumours arise near the root of mesentery, whereas solid
benign tumours develop near the intestine
• Malignant tumours spread by local spread or peritoneal implants
• Patient presents with sudden acute abdominal pain
• On examination, the tenderness in present in the mid abdomen with guarding
and rigidity
US and CT of abdomen are diagnostic
Treatment
Emergency laparotomy is needed. The cyst should be removed
Torsion of omentum
• More common in fourth to fifth decades
• Equal sex incidence
• The omentum twists on its long axis to an extent causing vascular obstruction
• May vary from mild vascular obstruction producing oedema to complete
strangulation leading to infarction and gangrene
• The situations to cause torsion are:
• Redundant and mobile segment
• Fixed point around which the segment can twist
• Causes of omental torsion are:
• Primary: Always unipolar, cause is unknown
• Secondary: Usually bipolar, associated with adhesions (intra-abdominal
inflammation—tuberculosis, postsurgical adhesions, internal and external
herniae)
• The precipitating factors for torsion are:
• Anatomic variations (bifid omentum, accessory omentum, large and bulky
omentum)
• Venous redundancy
• More common in right side (due to increased bulk and mobility)
Symptoms
• Acute abdominal pain
• Pain usually is localized to right lower quadrant
• Movement increases the pain
• Nausea and vomiting are common
Signs
• Tenderness, rigidity and guarding of abdomen
• A vague tender mass may be felt in the upper abdomen
DD: Acute cholecystitis, acute appendicitis, torsion of right ovary
US and CT of abdomen are diagnostic
Treatment
• Emergency laparotomy is needed
• Twisted omentum needs to be excised with release of adhesions
• Associated hernia needs repair
30.10 Colics
A colic is defined as a sudden squeezing or griping pain lasting for about 3–5
minutes with pain-free intervals
• Nausea, vomiting and retching are common accompaniments
• The cause of a colic is partial obstruction of a tubular structure due to varied
causes
• The varieties of colic and their features are given in Table 30.11
TABLE 30.11
Clinical Features of Various Abdominal Colics
Appendicular
Feature Biliary Colic Ureteric Colic Intestinal Colic
Colic
Incidence Fat, fertile, flatulent, Younger age Any age Any age
female of 50
Aetiology Gallstones Ureteric calculus, Parasitic infestations (younger Faecoliths, worms
papilloma, clot, age), strictures (middle
stricture age), malignancy (old age)
Nature of pain Right hypochondrial Severe colicky pain Colicky pain in the umbilical Colicky pain in
pain, referred to radiating from loin region the right iliac
right scapula or to groin, testis or fossa
shoulder thigh
Associated Dyspepsia Urinary symptoms Constipation or diarrhoea Repeated attacks
symptom of dull pain in
right iliac
fossa
30.11 Extra abdominal causes of abdominal

pain
Rupture of rectus abdominis muscle and rectus

sheath haematoma
• Severe bouts of coughing
• Severe muscular efforts such as lifting heavy weights
• Anticoagulant therapy
• Some vascular pathologies
• Epileptic fits
• An exquisitely tender mass over the lower abdomen, with bluish red
discolouration of the skin
• The mass becomes prominent, when the muscle is contracted by leg raising
(leg raising test)
• It needs to be differentiated from appendicular mass when it occurs on the
right side, and strangulated spigelian hernia, by the absence of features of
intestinal obstruction
US and CT are conclusive
Treatment
Medical management should suffice on many occasions
30.12 Symptoms of patients with acute

abdomen
• Acute abdominal pain
• Vomiting
• Alteration in bowel habits
• Urinary symptoms
Acute abdominal pain
Acute pain often denotes the presence of a disease process or injury, which needs
to be treated with elimination of cause. It is a signal of ongoing or impending
tissue damage. Acute abdominal pain denotes similar intra-abdominal organ
disease or pathology, which warrants emergent care. Since the GI tract is a
midline structure embryologically, pain is referred to the midline
(a) Pain at epigastrium: Diseases of the foregut structures
(b) Pain at the umbilical region: Diseases of midgut structures
(c) Pain at the hypogastrium: Diseases of hindgut structure
The abdomen is divided into nine arbitrary regions for convenience of
understanding and localizing. The two lateral vertical planes pass from the costal
margin close to the tip of the ninth cartilage above to the femoral artery below.
Of the horizontal planes, the subcostal plane connects the lowest points on the
costal margins and the inter-iliac plane connects the tubercles of the iliac crests
(Fig. 30.36). Some consider the scrotum the tenth segment, as its contents can
present with abdominal pain. These divisions will help in localizing the diseases.
FIGURE 30.36 Regions of abdomen.
Nature of pain
(a) Sudden onset pain: Pain is sudden in otherwise healthy and asymptomatic
persons. It increases in a very short time (e.g. pain due to perforations of
duodenal ulcer and appendicitis)
(b) Sudden onset with pain-free intervals: The pain of quick onset can reach a
peak making the patient writhe in pain and buckle up, and also quickly recede
to absolutely pain-free period, only to recur again (e.g. colics)
(c) Dull continuous pain increasing in severity: A persistent pain may increase
in severity over a period of time (e.g. a dull pain of subacute appendicitis in
the right iliac fossa may become severe when the appendicitis becomes severe
and acute due to superadded infection and inflammation)
(d) Burning pain: The pain may be of burning nature occurring suddenly (e.g.
pain in acid peptic disease)
(e) Constant or continuous pain: Persistent pain without variation in intensity
(e.g. peritonitis)
(f) Agonising pain: Very severe pain which upsets the morale of the patient (e.g.
pancreatitis, torsion of pedicled organ)
(g) Throbbing pain: Continuous pain throbbing in nature (e.g. acute
cholecystitis—due to inflammation being inside closed confines of a
structure)
Shift, migration and referred pain

• Shifting pain: Shifting pain is defined as the pain, which originates in one
region and shifts totally to another region, without any pain at the point of
origin (e.g. pain in acute appendicitis originates at the umbilical region and
shifts to right iliac fossa later)
• Migrating pain: Migrating pain is that pain which originates at one region
and shifts to another region, but does continue to stay at a lesser degree at the
point of origin (e.g. pain in perforated duodenal ulcer is right hypochondrial
to start with, and spreads to the right iliac fossa due to the flow of the gastric
contents down the right paracolic gutter)
• Referred pain: The pathology and the area of the pain are different, since the
organ of pathology and the area of pain share the same nerve supply. The
examples are given in Fig. 30.37 and Table 30.12
FIGURE 30.37 Referred pain.
TABLE 30.12
Referred Pain of Various Intra-abdominal Pathologies
Area of Referred
Shared Nerve Supply Organ of Pathology
Pain
T5–T8 Stomach and duodenum Epigastrium

T9–T10 Ileum and appendix Umbilical region
T11, T12, L1, L2 Colon Hypogastrium
C3–C5 Undersurface of the diaphragm (gallbladder, perforated DU, rupture of Right or left
spleen shoulder
Genitofemoral nerve L1, Ureteric colic Loin to groin
L2
T7–T9 Gallbladder Right scapula
Basal pleurisy, inferior wall ischaemia, Herpes zoster of lateral Abdomen
abdominal wall
Note
Segmental nerve supply mentioned here is sympathetic supply of the viscus.
Parasympathetic supply is from the vagus nerve, excepting for the hindgut and
the urinary bladder, which is from the sacral segments.
Effects of movements, food or habits

The abdominal pain may be aggravated by certain factors such as movements,
food or habits. Some examples are given in Table 30.13. The pain may get
relieved by certain factors. Some examples are given in Table 30.14.
TABLE 30.13
Aggravating Factors of Abdominal Pain
Aggravating Factor Pathology
Physical movements such as jolting Appendicitis, peritonitis

Deep inspiration Pleurisy
Intake of fatty food Cholecystitis
Intake of spicy food, alcohol Acid peptic disease
Lying supine Pancreatitis
Drugs—Analgesics, NSAIDs Acid peptic disease
TABLE 30.14
Relieving Factors of Abdominal Pain
Relieving Factor Pathology

Vomiting Peptic ulcer pain
Intake of bland food Peptic ulcer pain
Local pressure Colicky pain
Leaning forward Pancreatitis
Drugs—antacids, H2 blockers Acid peptic disease
Vomiting
Vomiting is a very common feature associated with pain in acute abdominal
emergencies. The patient should be asked about the following details, as each
has its own significance. They are:
• Character of vomiting
• Projectile: Involuntary projectile ejection of large quantities of vomitus
(e.g. high intestinal obstruction)
• Regurgitative: Effortless involuntary regurgitation of intestinal contents
(e.g. peritonitis due to perforation)
• Frequency of vomiting
• Constant: Persistent vomiting even in the absence of food intake (e.g. acute
intestinal obstruction, acute pancreatitis)
• Periodical: Vomiting with some periodicity or following food intake
indicates bowel obstruction (e.g. acute peptic ulcer, gastric outlet
obstruction)
• Nature of vomitus
• Coffee ground vomitus (brown to dark brown colour)—gastric contents
with altered blood (e.g. bleeding duodenal ulcer)
• Bloody (red in colour) (e.g. bleeding oesophageal varices)
• Faeculent (yellowish green and foul smelling) (e.g. gastric contents
followed by duodenal and intestinal contents in intestinal obstruction)
• Quantity of vomitus
• Large quantities indicate distal bowel obstruction
• Small quantities indicate gastric outlet obstruction
• Relationship with pain
The pain may precede, accompany or follow abdominal pain. The examples
TABLE 30.15
Relationship of Vomiting with Abdominal Pain
Relationship of Vomiting with Abdominal Pain Pathology
Pain preceding vomiting Acute appendicitis, acute peptic ulcer, bilary and renal colic
Pain and vomiting occurring together High intestinal obstruction
Vomiting occurs much later than the pain Low intestinal obstruction
Note
• Abdominal pain due to acute peptic ulcer may get relieved by vomiting, but
gives temporary relief in colics
• Vomiting is not a constant feature in acute appendicitis as the stomach gets
empty after one bout, but nausea persists
• In peritonitis, vomiting is absent but appears at a later stage.
Alteration in bowel habits

• Obstipation—inability to pass faeces and flatus (absolute constipation) (e.g.
acute intestinal obstruction)
• Constipation—inability to pass stools but able to pass flatus (due to solidified
faecal mass impacted at the anal verge ) (e.g. acute fissure in ano)
• Tenesmus—a desire to evacuate but results in passage of flatus only (e.g.
acute appendicitis)
• Passage of bloodstained stools—Red-currant jelly stools in acute
intussusception, mesenteric vascular obstruction, mesenteric thrombosis,
malignancy
• Diarrhoea—passage of loose stools; rarely seen in illnesses requiring
emergency surgery (e.g. ulcerative colitis, Crohn’s disease, acute enteritis)
Urinary symptoms
Patients presenting with abdominal pain may have associated urinary symptoms.
• Frequency in micturition: Patients presenting with renal or ureteric colic,
may have associated urinary infections along with urolithiasis. Frequency is
one of the common symptoms
• Strangury: Frequent passing of urine with excruciating pain. (e.g. impacted
stones in the urinary tract, pelvic or retrocaecal appendicitis). Patient
succeeds in passing a small quantity of bloodstained urine
• Haematuria: Passing blood in the urine (e.g. stones in the urinary tract, rarely
retrocaecal or pelvic appendix lying close to the ureter)
Abdomen is a ‘pandora’s box’! It is a temple of surprises! There are a variety of
expressions given by various surgeons and they are True! Sometime or the other
every medical person shall realize the truth in these statements. It is very
important that one masters the art of clinical examination of the abdomen, which
is acquired by diligent practice and application.
The abdominal pathologies can present in various ways. They are:
1. Acute abdominal pain
2. Chronic abdominal pain
Abdominal conditions which cause acute pain are simply called, ‘acute
abdomen’. The urgency is very acute and requires quick treatment, but there is
little time given to the examiner to make a diagnosis. More than anything else,
the investigations he or she is going to ask for and the treatment he or she is
going to offer to this patient depends on the clinical diagnosis he or she is going
to make. Wrong diagnosis leads to wrong investigations and treatment and
ultimately it is disastrous both to the patient and the surgeon. In this context,
proper clinical examination becomes very important. History taking takes most
of the time in arriving at a diagnosis.
Eliciting history
Abdominal pain
• Site of pain: Where did the pain start?
The site of origin of pain must me clearly noted. The site indicates the
underlying cause, as it indicates the organ of pathology. The patient must be
asked to indicate the site of pain in the abdomen with his own finger— ‘pointing
sign’ (Fig, 30.38) (e.g. in acute appendicitis, the patient will indicate the
McBurney point—the junction of medial two thirds and the lateral one third of
an imaginary line drawn between the umbilicus and the right anterior superior
iliac spine). The patient will use his entire hand if the pain is diffuse or
generalized (e.g. generalized peritonitis) (Fig. 30.39)
• Time of onset of pain: What was the time when the pain started?
FIGURE 30.38 Finger pointing sign.
FIGURE 30.39 Diffuse sign.
Usually the appendicular pain is noted in the mornings, when there is

increased intraluminal pressure of the appendix due to increased peristalsis to
evacuate the faecal matter; whereas pain due to duodenal ulcer perforations start
at late evenings
• Period of pain: How long has the pain been present?
Duration of pain indicates the disease process (e.g. persistent pain of acute
appendicitis)
• Mode of onset / description of pain: Can you describe the pain?
The abdominal pain has a variety of presentations (e.g. throbbing—acute
cholecystitis, colicky—obstructive lesions of hollow organs).
• Change in character of pain: Has the pain changed in its character since
its onset?
A change in character of pain has its own significance, e.g. colicky pain
changes into constant pain in strangulation of bowel, lessening of pain may be
seen when gangrene supervenes, or when peritonism progresses to stage of
reaction
• Shift, migration or radiation of pain: Has the pain been changing its place
from the point where it started?
Pain may shift from its place of origin (e.g. acute appendicitis) or even
migrate to another region of the abdomen (e.g. perforated duodenal ulcer) and
may present at a distant place (e.g. referred pains)
• Effects of movements, food or habits: Is the pain related to movements or
food?
The abdominal pain gets aggravated by certain factors such as food or habits
(e.g. spicy food aggravates acidity, and bland food relieves pain of acidity).
Vomiting
• Character of vomiting: What is the nature of the vomiting?
Vomiting can be projectile (e.g., high intestinal obstruction, enteritis) or
regurgitative (e.g. peritonitis due to perforation)
• Frequency of vomiting: How frequent is the vomiting?
Vomiting may be constant—(e.g. acute intestinal obstruction, acute
pancreatitis) or periodical (e.g. acute peptic ulcer, gastric outlet obstruction)
• Nature of the vomitus: Can you describe the nature of vomitus, the colour
and contents?
Vomitus may be coffee ground (e.g. altered blood), fresh blood (e.g. bleeding
oesophageal varices) or feculent (e.g. intestinal obstruction)
• Quantity of vomitus: What is the quantity of each vomitus (roughly as one
tumbler full or in any other description)?
Quantity of vomitus is useful in determining the level of obstruction. (e.g.
large quantities indicate high intestinal obstruction)
• Relationship with abdominal pain: Is the vomiting associated to pain? If
so, whether it is before or after the pain?
Abdominal pain may precede vomiting (e.g. acute appendicitis) or may be a
very late feature (e.g. distal large bowel obstruction)
Bowel habits
• Bowel habits: Is there any change in bowel habits?
Constipation is common in intestinal obstructions and obstipation is common
in total obstruction of bowel
Urinary symptoms
• Urinary symptoms: Are there any urinary symptoms such as burning in
micturition, frequency in micturition?
Urinary symptoms such as dysuria and frequency are common in abdominal
pain related to urologic pathology (e.g. haematuria in ureteric colic due to stone)

• Association of fever: Is or was the present illness associated with fever?
peritonitis) and low grade (e.g. acute appendicitis)
The information of any treatment received for this illness will give a clearer
picture of diagnosis (e.g. administration of antibiotics, aspiration in abscesses)
Past history
• Loss of appetite and weight: Is there any loss of appetite and weight
preceding the illness?
Loss of appetite and weight are indicative of illnesses such as tuberculosis and
malignancies, which the patient may not be aware
treated will indicate the examiner to reconsider the diagnosis such as colics. The
patient might have had some treatment and the present acute episode may be an
acute presentation of a chronic illness (e.g. acute exacerbation of recurrent
appendicitis)
Family history
Urolithiasis and colics are known to occur in families due to living in an
endemic area
match the situation. History relating to trauma (part of fight or shooting
incident) should also be elicited.
Personal history
The following needs to be questioned:
• Consumption of alcohol (e.g. acute duodenal ulcer, acute gastritis, acute
pancreatitis)
• Tobacco smoking (acute gastritis)
• Intake of drugs such as analgesics (e.g., acute duodenal ulcer)
• Menstrual history in women (e.g. missed periods may be of use in diagnosing
ruptured ectopic gestation)
General
Attitude
• Rolling and tossing in pain: Colics
• Lying still and motionless: Peritonitis
• Face: Careful observation of the face gives a wealth of information
• ‘Facies Hippocratica’ anxious look, staring eyes (lifeless), sunken cheeks,
cold clammy periphery (typical feature of terminal stage of peritonitis)
• Sunken eyes, sunken cheeks and dry tongue (e.g. dehydration)
• Livid bluish face (e.g. haemorrhagic pancreatitis)
• Pale face with gasping for breath (e.g. ruptured tubal gestation)
• Eyes
• Sunken eyes indicate dehydration and undernutrition (e.g. intestinal
obstruction)
• Jaundice (e.g. cholangitis)
• Pallor, a feature of acute bleeding (e.g. acute haemorrhagic pancreatitis)
• Tongue
• Dry in dehydration
• Dry and brown in toxaemia
• Dry and pale in intra-abdominal bleeding
• Skin
• Dry scaly skin (e.g. dehydration)
• Scratch marks may indicate obstructive jaundice
Vital signs
• Tachycardia (e.g. increased pulse rate in infective pathologies, due to pain
and impending gangrene in noninfective pathologies)
• Elevated temperature (e.g. mild rise—acute appendicitis, moderate rise—
acute cholecystitis, high-grade fever with chills—cholangitis, intra-
abdominal abscess (in acute appendicitis, ‘pain first, vomiting next, fever
last of all—Murphy’s syndrome’)
• Breathing
• Tachypnoea: Increased ventilation is seen in upper abdominal painful
conditions such as acute cholecystitis or perforated duodenal ulcer, and
more commonly in thoracic lesions such as pleurisy, bronchopneumonia
Abdomen
The patient should lie comfortably on the examination couch, and be examined
in the supine position under proper lighting. The patient’s body should be
exposed fully starting from the nipples to mid thighs, exposing the genitalia, the
inguinal and femoral areas for complete examination (Fig. 30.40). Privacy of the
patient must be assured, and a nurse be kept by the side of the patient, especially
when the patient is a female.
FIGURE 30.40 Exposure of entire abdomen including genitalia for
examination.
The clinical examination of abdomen in acute emergencies consists of:

1. Inspection
2. Palpation
3. Percussion
4. Auscultation
Inspection
Abdomen should be inspected over the entire area with special attention to the
flanks and groins. The abdomen should be observed from different positions at
different angles (from the sides tangentially, and from the ends of the couch).
• Shape
• Generalized distension: Generally due to fat, fluid, faeces or fetus (Figs.
30.41 and 30.42)
• Localized distension
- Symmetrical distension:.The central part of the abdomen appears
symmetrically distended (Fig. 30.14) when distal small bowel is
obstructed. The peristaltic waves may be seen, especially during the
attacks of pain
- Asymmetrical localized distensions are seen in gross enlargement of
liver (Fig. 30.43A), spleen or ovary, urinary bladder (Figs. 30.43B and
C) and sigmoid volvulus
• Peripheral distension: The flanks may show distension (Fig. 30.44) due to
the distension of the colon, when the rectum is obstructed
• A scaphoid abdomen (Fig. 30.45) is seen in advanced cases of dehydration,
starvation and malignancy, especially of the oesophagus and stomach
• Umbilicus
FIGURE 30.41 Generalized distension due to intestinal obstruction.

FIGURE 30.42 Generalized distension of abdomen due to ascites.
FIGURE 30.14 Central distension of abdomen.
FIGURE 30.43A Upper abdominal distension due to hepatomegaly.
FIGURE 30.43B Distended urinary bladder anterior view.
FIGURE 30.43C Distended urinary bladder lateral view.
FIGURE 30.44 Right flank distension.
FIGURE 30.45 Scaphoid abdomen Source: (Courtesy Dr A. Chandrasekar Rao).
Normal umbilicus is slightly retracted and inverted. It gets everted, in

umbilical hernia, which can be confirmed by eliciting the cough impulse (Fig.
30.46).
• Skin
FIGURE 30.46 Everted umbilicus.
The skin has to be given special attention for colour, striae, scars, veins,
pigmentations and nodules.
• Colour: Red erythematous skin (erythema ab igne) may indicate application
of hot water bottle for pain relief and suggest location of the organ of
pathology (e.g. acute pancreatitis)
• Striae: Irregular white or pink wrinkled linear marks caused by gross
stretching of skin with rupture of elastic fibres (e.g. pregnancy—striae
gravidarum (Fig. 30.47), ascites). Pink-coloured striae may be a part of
steroid overdosage or Cushing’s syndrome
• Scars: Special attention should be given to the scars on the abdominal wall.
Nature of previous surgery may indicate the present pathology (e.g.
adhesions) or a muscular weakness below the scar (e.g. incisional hernia
—Fig 30.48). A depressed wide scar indicates postoperative infection and
delayed healing of the wound
• Pigmentation: In South India, it is common practice to apply the calcium
paste, Chunam or Namakatti over the area of pain
• Nodules: Nodules at the umbilicus are seen with intra-abdominal
malignancies especially of the stomach—‘Sister Mary Joseph’s nodules’
(Ref Fig. 31.26)
• Movements of the abdominal wall
• Respiratory excursions
FIGURE 30.47 Striae gravidarum.

FIGURE 30.48 Large incisinal hernia with previous operation scars.
Abdominal wall moves regularly and smoothly with respiration. When the
movements of the abdominal wall are normal, it indicates the absence of any
peritonitis. Restricted movements occur in certain conditions
• Restricted movements to certain localized areas indicate local peritonitis
- Restricted movement in the right lower abdomen (e.g. acute appendicitis
with local peritonitis)
- Restricted movement in the right upper abdomen (e.g. acute cholecystitis)
• Total absence of movements (e.g. generalized peritonitis)
Pulsations
Normal abdominal aortic pulsations may be visible in the epigastrium in very
thin patients
Peristalsis
Visible peristalsis of the bowel is observed in some situations. They are:
• Visible gastric peristalsis: When the pylorus is obstructed by pathologies
such as cicatrized duodenal ulcer or malignancy and congenital pyloric
stenosis of infancy, a slow wave passes across from the left to right
hypochondrium. When the stomach is grossly dilated, the wave is seen to
originate from the left hypochondrium, pass down to the hypogastrium and
ascend to the right hypochondrium.
• Visible intestinal peristalsis: When the distal small bowel or the large bowel
(with incompetent ileocaecal valve) is obstructed, the distended small bowel
may be seen on the surface, especially in thin patients. It has a characteristic
‘ladder pattern’ in the centre of the abdomen. Sometimes, in thin individuals,
even normal intestinal peristalsis can be observed
External genitalia
It is essential to inspect the genitalia, and ensure that the testes are in the
scrotum (e.g. orchitis of intra-abdominal testis will cause acute abdominal pain)
Palpation
Palpation forms the most important part of the clinical examination of the
abdomen.
Method of examination: The examiners should adhere to the following while
examining the abdomen of a patient.
• The examiners should be gentle in their approach in palpation. If this hurts the
patient, he or she will contract his or her muscles and give false information.
Moreover, the patient will lose confidence in his or her doctor, and no further
cooperation could be expected
• The examiner should explain what he or she intends to do and also the
experience the patient will have; and he or she should also assure him or her
that will not hurt
• The hands have to be warmed by rubbing each other, as cold hands will
produce contraction of abdominal muscles
• The examining hand should be flat on the abdomen with the wrist and forearm
in the same horizontal plane. The examiner may have to sit by the patient on
a chair or even kneel down, if necessary
• It is better to follow a sequence as a matter of routine, so that no area is left
unexamined, but, the area of pain should be the last to be examined
• As the process of palpation is going on region by region, the examiner should
run on his or her mental screen, all the underlying anatomical structures from
front to back, skin to skin. This helps in getting an idea of the underlying
pathology
• Local temperature
By the dorsum of the hand, any area of rise in local temperature over the
abdominal wall can be assessed. Increase in temperature may indicate local
inflammation (e.g. liver abscess)
• Hyperaesthesia
Hyperaesthesia is an important point to note. It is elicited by stroking the skin.
Increased sensitivity may be noticed over the ‘Sherren triangle’, the triangle
bounded by the lines connecting the umbilicus, anterior superior iliac spine and
the pubic symphysis (Fig. 30.49) (e.g. acute appendicitis). Hyperaesthesia
elicited over the space between the ninth and eleventh ribs posteriorly on the
right side— Boas’s sign (e.g. acute cholecystitis) (Fig. 30.50)
• Tenderness
FIGURE 30.49 Sherren’s triangle.
FIGURE 30.50 Eliciting Boas’s sign.
Tenderness is the pain felt by the patient when the examiner presses over the
inflamed area. This is mainly elicited by observing the patient’s face; pain makes
him or her wince the face
Some of the common areas of tenderness are:
• Tenderness at the tip of ninth cartilage at the lateral margin of the right
rectus abdominis muscle (Murphy’s sign)—acute cholecystitis (Fig. 30.51).
Method: The patient lies in supine position. The examiner should keep his or
her examining hand on the lateral border of the right rectus abdominis just
below the costal margin, and the patient is asked to take deep inspiration.
The inflamed gallbladder will descend and hit the examining fingers, and the
patient will wince with a catch. The same can be done in the sitting position
• Tenderness at McBurney point (point at the junction of the lateral one-third
and medial two-thirds of a line drawn between the umbilicus and the right
anterior superior iliac spine)—acute appendicitis (Figs. 30.52A and B)
FIGURE 30.51 Eliciting Murphy’s sign.

FIGURE 30.52A McBurney point.
FIGURE 30.52B Eliciting tenderness at McBurney point.
The degree and the intensity of tenderness should be noted as they indicate the
severity of the disease. They can be determined by adopting different positions
of the patient.
• Shaking the abdomen side to side or elevating the feet increases tenderness
(e.g. acute peritonitis (Fig. 30.53A)
• Turning the patient to the left and trying to elicit tenderness in the right iliac
fossa may be possible as the bowel moves away from the appendix (e.g.
acute retrocaecal appendicitis) (Fig. 30.53B)
FIGURE 30.53A Shaking the abdomen to increase pain in peritonitis.
FIGURE 30.53B Turning left and eliciting tenderness in RIF.
Some specific tests in acute appendicitis

• Rovsing sign: Application of pressure in the left iliac fossa produces pain in
the right iliac fossa due to the shift of the intestines towards the inflamed
appendix (e.g. severe form of acute appendicitis) (Fig. 30.54A), and to
differentiate from extra-abdominal causes of right iliac fossa pain
• Blumberg’s sign: Application of firm pressure in the right iliac fossa followed
by a sudden release causes severe contraction of abdominal muscles along
with the inflamed parietal peritoneum, which causes severe pain to the
patient (e.g. localized peritonitis in acute appendicitis) (Fig. 30.54B)
• Cope’s psoas test: The retrocaecal appendix lies on the right psoas major
muscle. By positioning the patient in the left lateral position and
hyperextending the right hip joint, the patient points to the right iliac fossa
for pain (Fig. 30.54C) as this creates a stretch of the psoas major muscle,
which irritates the inflamed appendix (e.g. retrocaecal appendicitis)
• Obturator test: The pelvic appendix lies in close proximity to the obturator
internus muscle. Internal rotation of the hip joint makes the patient point to
the right iliac fossa for pain (Fig. 30.54D), as this movement produces a
stretch of this muscle and irritates the appendix in pelvic position (e.g. pelvic
appendicitis)
• Baldwing’s test: When the patient is asked to lift the right lower limb with the
knee straight, the patient points to the right iliac fossa for pain (Fig. 30.54E),
as the psoas major muscle irritates the inflamed appendix in the retrocaecal
position (e.g. retrocaecal appendicitis)
• Muscular guard
FIGURE 30.54A Rovsing sign.

FIGURE 30.54B Blumberg’s sign.
FIGURE 30.54C Cope’s psoas test.
FIGURE 30.54D Obturator test.
FIGURE 30.54E Baldwing"s test.
This is an involuntary reflex phenomenon and is protective in function. It

indicates acute inflammation and that some kind of complication has
supervened. It is a definite indication for emergency laparotomy. This muscle
guarding is due to the irritation of the serous membrane overlying the pathology
Guarding and rigidity are almost synonymous, as ‘guarding’ indicates the
function of the rigid muscles and ‘rigidity’ is what the examiner elicits during
palpation
Some overanxious patients keep their muscles tight and rigid due to fear, and
this is called ‘voluntary guard’. This has to be differentiated from the involuntary
guard (Table 30.16).
TABLE 30.16
Differentiation Between Involuntary and Voluntary Muscle Guard
Involuntary Muscle Guard Voluntary Muscle Guard
It is reflex in occurrence It is voluntarily kept by the patient
Usually corresponds to the area of pathology It is generalized all over the abdomen
Distracting the patient does not abolish the guard Distracting the patient does abolish the guard
Some illnesses produce muscle guard in specific areas (Table 30.17).
TABLE 30.17
Some of the Areas of Muscle Guard
Pathology Area of Muscle Guard

Peptic perforation Upper abdomen (right hypochondrium and epigastrium)
Acute appendicitis Right iliac fossa
Retrocaecal appendicitis Paravertebral muscles or the right side of the back
Acute cholecystitis Right hypochondrium
Ruptured ectopic gestation Suprapubic area extending into both iliac fossae
Impending gangrene in intestinal obstruction, volvulus, Over the distended area
obstructed hernia
Basal pneumonia or pleurisy Upper abdomen near the costal margins which disappear on
deep inspiration
Note
Tenderness, guarding and rigidity may not be pronounced in retrocaecal and
pelvic appendicitis.
• Mass or lump
Common lumps during the examination of acute abdomen with their
characteristics are shown in Table 30.18.
• Hernial sites
TABLE 30.18
Illnesses Which Produce Palpable Lumps per Abdomen
Appendicular lump Felt in the right iliac fossa
Appendicular abscess Well noticeable lump with skin oedema

Intussusception Sausage-shaped mass with the concavity towards the umbilicus
Twisted ovarian cyst Lump in the lower abdomen and its lower limit in the pelvis
It should never be forgotten to examine the groins, as obstructed inguinal

hernia is the commonest cause of intestinal obstruction
External genitalia
It is essential to palpate the testes in a male and record the findings
Percussion
Normally the entire abdomen is equally resonant, excepting over the liver where
the note is dull. This is useful in confirming the presence of enlarged liver,
spleen and gas or fluid in perforated bowel pathology.
Air in the peritoneal cavity is pneumoperitoneum and is usually due to the
leakage of gas from the bowel (e.g. perforated duodenal ulcer, intestinal ulcer),
and the abdomen becomes hyper-resonant. Since air is light, it moves to the
upper most part of the abdomen close to the abdominal wall and obliterates the
liver. Method: This is elicited by starting the process of percussion in the mid-
axillary line on the right side in the upper part of the chest, proceeding
downwards. In the normal circumstances, this area is resonant till the fifth
intercostal space, where the upper border of the liver presents. Then the note
becomes dull. In the presence of pneumoperitoneum, the dullness of the liver
area cannot be elicited and there will be resonant note on the liver area also.
Note
• Liver dullness may be obliterated when there is emphysema of the lung, as
it may enclose the liver area
• Liver dullness may not be obliterated when the leak is small
• Obliteration of liver dullness is not related to the size of perforation, but is
related to the amount of air leak
If there is fluid in the peritoneal cavity, due to reasons such as perforated

bowel pathologies such as duodenal ulcer, appendicitis or ruptured ectopic
gestation, and when the fluid is in moderate quantities, it gravitates down to the
flanks making the resonance present only in the central part of the abdomen due
to the floating intestines. Change in position of the patient, shifts the resonant
area in accordance with the floating intestines. Shifting of this fluid is confirmed
by percussion, and the method of percussion is to start at the midline and
proceed to one flank. Then the patient is asked to turn to the other side by 45°
and wait for some time for the intestines to float to the side of percussion. The
area where it was dull to percussion will become resonant (Fig. 30.55). This is
called ‘ shifting dullness’. The same process is repeated on the other side too.
FIGURE 30.55 Method of eliciting shifting dullness.
Note
It should be remembered that the percussing fingers be kept undisturbed, till
the process is completed.
Percussion for the liver, spleen and fluid in peritoneal cavity is detailed in
Ch. 31, and percussion for urinary bladder is detailed in Ch. 36)
Auscultation
This is an important part of clinical examination of the abdomen. The sounds
created by the air and food in the intestines create a periodical sound, as clicks
and gurgles. Since all these sounds reach the right iliac fossa ultimately, it is
called ‘abdominal postbox’. The correct method of listening to the intestinal
sounds is by keeping the stethoscope on the right iliac fossa (Fig. 30.56), for 3
min by the clock. Normally, 2–3 bowel sounds are heard per minute.
• Absence of bowel sounds (silent abdomen) is characteristic of diffuse
peritonitis
• Increased peristalsis (noisy abdomen) is characteristic of intestinal
obstruction (borborygmi)
FIGURE 30.56 Auscultation for bowel sounds in the right iliac fossa.
When the bowel is obstructed, the sounds emitted are heard through the
stethoscope. The sounds are low-pitched gurgling and rapidly change to high-
pitched tinkling, which are due to the splashing of enteric fluid against the
resonant distended taught walls of the intestine. Eventually, the sound can be
heard without the aid of a stethoscope. This can be elicited by shaking the body (
succussion splash) (Fig. 30.57).
FIGURE 30.57 Eliciting succussion splash.
Abdominal girth
Measurement of the abdominal girth is very useful in determining the variation
of abdominal distensions. This is measured by tape, inserted behind the patient,
at the level of L2 vertebra. This point is marked and the tape should be taken
round the body, to measure the abdominal girth (Fig. 30.58). The measurements
should be made at the same level, subsequently. Increase in abdominal girth
indicates serious pathology, and may need surgical intervention.
FIGURE 30.58 Measurement of abdominal girth.
Note
Increase in abdominal girth need not be present in conditions such as acute
appendicitis, acute cholecystitis, perforated bowel pathology, and still surgery
will be mandatory, hence it is not a very reliable sign in certain conditions. It
is of significance when obstruction is suspected.
Pelvis
Digital examination of the rectum is mandatory in the examination of the acute
abdomen (see Ch. 34). The following are to be noted:
• Integrity and nature of rectal mucosa (e.g. growths and ulcers of the anus
and rectum)
• Tenderness on the rectal walls
• Tenderness in the right wall of the rectum (e.g. acute pelvic appendicitis)
• Tenderness in the anterior wall of the rectum with a bulge (e.g. pelvic
abscess, prostatitis)
• Roomy ballooning of the rectum (e.g. intestinal obstruction and sigmoid
volvulus
• Blood at the tip of examining finger (e.g. intussusception—red-currant jelly)
In women, vaginal examination has to be carried out (Ch. 38) and the
following are to be noted:
• Area of tenderness
• Soft and tender cervix painful on movement (e.g. ruptured ectopic
gestation)
• Tenderness in the fornix with a mass (e.g. torsion of ovarian cyst)
• Abnormal discharges (purulent discharge with tender fornices (e.g. acute
salpingitis)
It should be remembered that many extra-abdominal pathologies present with
abdominal emergencies. They are listed in Table 30.19.
TABLE 30.19
Extra-abdominal Pathologies Presenting as Abdominal
Emergencies
Region Lesion Presentation
Chest Basal pleurisy, pneumonia, angina pectoris, Epigastric pain sometimes with one or two evacuations
myocardial infarction
Middle and lower lobar pneumonia Right hypochondrial pain
Back, loin, Pott disease Hypochondrial pain
spine
Herpes zoster of lower thoracic nerves Loin to groin shooting pain (vesicles will appear in a
couple of days)
Scrotum Retroperitoneal lymphangitis due to filariasis Pain in the back (testis will be swollen with associated
Spermatic associated with orchitis and funiculitis funiculitis)
cord
Nervous Tabes dorsalis Gastric crisis with vomiting (history of tightening pain in
system the limbs with Argyl Robertson pupil is hallmark)
Others Diabetic crisis, porphyria, malaria, sickle cell Acute abdominal pain
anaemia, haemophilia
CHAPTER 31
Chronic abdominal illnesses

N. Mohan
CHAPTER OUTLINE
31.2. Diseases of oesophagus, stomach and duodenum 525
• Acid peptic disease 525
• Gastric carcinoma 527
31.3. Diseases of gallbladder 528
• Chronic cholecystitis 528
• Gallbladder polyps 530
31.4. Diseases of pancreas 530
• Chronic pancreatitis 530
• Pancreatic malignancy 531
31.5. Diseases of intestines 533
• Recurrent appendicitis 533
• Abdominal tuberculosis 533
• Crohn’s disease 535
• Ulcerative colitis 535
• Diverticulosis of small bowel 536
• Diverticulitis of colon 536
• Hirschsprung disease 537
• Colonic malignancy 537
31.6. Diseases of any part of gastrointestinal system 539
• Gastrointestinal stromal tumours 539
• Gastrointestinal lymphomas 539
31.7. Symptoms of patients with chronic abdominal illnesses 540
• General 543
• Abdomen 543
• Pelvis 551
31.1 Introduction
Chronic pain is defined as pain, continuous or intermittent discomforting pain
lasting for at least 6 months. The types, sites and causes of this pain are many
and varied, and arise from any system, gastrointestinal (GI), genitourinary and
gynaecological. This chapter details the GI causes. The initial step of any
physician is to achieve a diagnosis and treat the disease, as many of them may
indicate a life-threatening problem. The diagnosis needs a multifaceted
approach. There are situations where, no cause can be found or even if found,
may not find an adequate treatment. Such patients end up with the psychiatrists,
physiotherapists, pain management specialists and acupuncturists. Patients with
chronic abdominal pain have the advantage of giving the clinician adequate time
to examine, investigate and diagnose the illness. Clinical examination plays a
role at this point, as unnecessary investigations and the related expenditure can
be avoided.
31.2 Diseases of oesophagus, stomach and

duodenum
Acid peptic disease

• Acid peptic disease (APD) is a very general term representing a variety of
overlapping symptoms of the upper abdomen related to acid and pepsin
secretion in the stomach
• This may result due to:
• Reflux oesophagitis
• Gastritis
• Duodenitis
• Gastric and duodenal erosions
• Gastric ulcer
• Duodenal ulcer
• Gastric ulcer is common in the elderly and the duodenal ulcer in the young
• Excessive usage of nonsteroidal anti-inflammatory drugs (NSAIDs)
• Stress factors
• Helicobacter pylori infections
• Genetic factors
• Use of tobacco, alcohol and caffeine
• Blood group O
• Unchecked gastric secretion (Zollinger–Ellison syndrome)
The scenario of APD has changed recently due to changes in lifestyle, usage
of acid suppressants and eradication of H. pylori infections. Severe acid
suppression produces achlorhydria, which is a precursor of gastric malignancy.
Patients with APD present with the following symptoms (Table 31.1):
• Pain: Burning in nature, more in the epigastrium, intermittent and always
related to food
• Periodicity: Pain-free intervals is a characteristic feature
• Vomiting: Sometimes a feature and has influence on pain, blood-stained
vomiting (haematemesis) may occur
• Weight: Duodenal ulcer patients gain weight, and gastric ulcer patients lose
weight
• Dyspepsia: A feature of gastric ulcer and not that of duodenal ulcer
• Diet: Fried spicy foods aggravate the ulcer
• Anaemia: May be a feature of gastric ulcer (malignant), duodenal ulcer
(bleeding)
TABLE 31.1
Clinical Features of Acid Peptic Disease
Clinical Feature Pathology
Gastric ulcer Duodenal ulcer

Pain Upper abdominal pain (epigastric), Upper abdominal pain (epigastric or right hypochondrial) on
when penetrates the pancreas empty stomach (hunger pain), common at night (12MN to 2
develops back pain AM)—’Nocturnal cries’
Relationship to Food intake increases pain Food intake relieves pain
food
Appetite Normal or reduced Increased
Body weight Loss due to reduced intake of food Gain due to increased intake of food
Vomiting Spontaneous, relieves pain Occurs when gastric outlet obstruction occurs
Haematemesis or Not uncommon, bleeds are small Common in posterior ulcers, and bleeds are large, presents as
melena and leads to anaemia emergency
Perforation Not uncommon, and presents as Common in anterior ulcers, and presents as peritonitis
peritonitis
Clinical Tenderness in epigastrium on deep Tenderness in epigastrium and right hypochondrium on
examination palpation palpation
• Barium meal (Fig. 31.1) may be diagnostic
• Upper GI endoscopy (Figs. 31.2A and 31.2B) is conclusive
• Biopsy differentiates benign and malignant ulcers of the stomach, and also
helps in diagnosing H. pylori infection
• C14 breath test: To check for the presence of H. pylori. The bacteria convert
urea into carbon dioxide. The test involves swallowing an amount of
radioactive carbon (C14) and testing the air exhaled from the lungs. A
nonradioactive test can be used for children and pregnant women
• Serology: ELISA can detect both immunoglobulins, IgG and IgA antibodies
directed against H. pylori. The sensitivity of most serologic tests is
approximately 95%
• Faecal antigen test: The detection of H. pylori in faeces is emerging as a
noninvasive method of detection. This test has mainly been used in
paediatric settings
FIGURE 31.1 Barium meal—gastric ulcer.
FIGURE 31.2A Endoscopy—chronic duodenal ulcer Source: (Courtesy Dr Mani
Veeraraghavan).

FIGURE 31.2B Endoscopy—chronic gastric ulcer Source: (Courtesy Dr Mani
Veeraraghavan).
Treatment
• Medical management with acid suppressants (H2 blockers and PPIs) and
antacids is curative in many cases
• Associated H. pylori infections require adequate treatment
Gastric carcinoma
• More common in men
• Common above the age of 50
• More common in the antrum or on the lesser curve, and less frequent on the
corpus
• Achlorhydria and atrophic gastritis
• Use of preserved and packed food (especially preserved in salt)
• H. pylori infection of the stomach
• Tobacco smoking
• Previous gastroenterostomy
• Blood group A
• Macroscopically the gastric cancer is of four types. They are:
1. Polypoid fungating growth
2. Sessile lesion
3. Ulcerative
4. Diffuse infiltrative type (scirrhous)—linitis plastica (leather bottle
stomach)
• Microscopically, they are adenocarcinomas of columnar or cuboidal type
• Gastric cancer spreads by various routes:
• Longitudinally and circumferentially within the stomach
• Submucosal spread leads to diffuse infiltration of the whole stomach
leading to luminal narrowing and rigidity of the stomach (linitis plastica)
• Direct spread to contiguous structures such as pancreas, transverse colon,
left lobe of liver occurs when the muscle layer and serosa are invaded
• Lymphatic spread to celiac nodes and to left supraclavicular nodes
(Virchow’s nodes)
• Haematogenous spread to liver (commonest), lungs, and brain
• Transcoelomic spread (by peritoneal seedling) to ovaries (Krukenburg
tumour) (Fig. 31.4B) and peritoneum (as nodules and ascites)
• Retrograde spread to umbilicus (Sister Mary Joseph’s nodules)
FIGURE 31.4B Cross section of faceted gallstones showing the layers.
• Early lesions are without symptoms; however, loss of appetite and early
satiety are early symptoms of gastric cancer
• Symptoms and signs of cancer of the stomach are given in Table 31.2 in the
order of occurrence
TABLE 31.2
Symptoms and Signs of Gastric Malignancy
Symptom Sign
Appetite loss Weight loss

Weight loss Abdominal lump in the epigastrium or right hypochondrium (local
fixity indicates local invasion)
Nausea Abdominal tenderness
Vomiting (in cancers in the pyloric region Irregular hepatomegaly (due to liver metastases)a
producing gastric outlet obstruction)
Upper abdominal discomfort, early satiety, Rectal shelf mass—Blumer’s shelf (due to pelvic deposits in the
postprandial fullness after small feeds rectovesical or rectovaginal pouch—Pouch of Douglas)a
Upper gastrointestinal haemorrhage (ulcerative Troisier’s sign—cervical lymphadenopathy (Virchow’s nodes)a
lesions)
Upper abdominal pain (usually indicates local Ascites (due to peritoneal spread)a
infiltration)
Melena (ulcerative lesions) Umbilical nodules (Sister Mary Joseph’s nodules) due to retrograde
spreada
Dysphagia (tumours near OG junction) Lung secondariesa
Jaundice (liver metastases) a Pathological fracturesa
Migrating thrombophlebitis (Trousseau’s sign)a
a
Indicates advanced disease
Note
To diagnose cancer of the stomach in its early stage, high degree of suspicion
is needed.
• Upper GI endoscopy (Fig. 31.3A) is diagnostic
• Barium meal series (Fig. 31.3B) is useful in diagnosis but upper GI
endoscopy has replaced it almost in recent times
• Contrast enhanced computed tomography (CECT) of the abdomen (Fig.
31.3C) will show the filling defect in the stomach
• Ultrasound (US) and CECT abdomen are useful is diagnosing liver, lymph
nodal and peritoneal metastases
• X-rays and CT of chest are useful in diagnosing lung metastases
FIGURE 31.3A Endoscopy—malignant stomach growth Source: (Courtesy Dr
FIGURE 31.3B Barium meal—gastric malignancy.
FIGURE 31.3C CT—stomach carcinoma with liver metastases.
Treatment
• Radical (clearance) surgery depending on the location of the tumour is the
treatment of choice, followed by chemotherapy and sometimes
radiotherapy
• Radiotherapy has no curative role in the treatment
• Preoperative chemoradiation (CRT) is useful in advanced lesions
Palliative
• Surgery—gastrojejunostomy to relieve gastric outflow obstruction
• Radiotherapy—to relieve local symptoms such as obstruction, haemorrhage
and pain
• Chemotherapy—confers marginal survival advantage
• Endoscopic procedures—laser therapy (for bleeding tumours) and
endoprosthesis (for obstructive tumours) of oesophago-gastric junction
31.3 Diseases of gallbladder
Chronic cholecystitis
• Common in fat, flatulent, fertile, female of fifty (five Fs)
• Majority of the gallstones are of the mixed variety (cholesterol + bile
pigments (calcium bilirubinate) + calcium salts)
• The causes of gallstones are:
• The deposit of these material on a small core of bacteria (which enter
through the bloodstream or the reflux from the duodenum) at various
times gives rise to stones of different sizes in the same gallbladder (Figs.
31.4A and B)
• Gallstones seem to be precipitated by derangement of equilibrium of the
gallbladder contents and also the influence of progesterone, which has a
muscle relaxing property leading to delay in the emptying of the
gallbladder with resultant stasis
• An excess of cholesterol in relation to bile salts and lecithin is believed to
be the main factor for stone formation
• Precipitation of cholesterol is enhanced by bile stasis (e.g. fasting), due to
obstruction or decreased contractility (e.g. post vagotomy, pregnancy) and
congenital anomalies (e.g. Phrygian cap (Fig. 31.5))
• Gallstones are found when there is increased bilirubin secretion (e.g.
haemolytic diseases) or deconjugation (e.g. hepatic insufficiency), and
they are pigment stones
• Acalculous cholecystitis may occur due to dysfunctional, dyskinetic
gallbladder without stones and also due to infection with typhoid
organisms
• Acute attacks are common (Ch. 30)
FIGURE 31.4A Multiple faceted gallstones.
FIGURE 31.5 Phrygian cap of gallbladder.
Symptoms
• Feeling of abdominal distension and flatulence, more following a fatty meal
(qualitative dyspepsia), associated with belching
• Abdominal pain may be constant or colicky (biliary colic), radiating to the
back to the inferior angle of the right scapula and right shoulder. This may be
associated with vomiting
• Jaundice can occur when a gallstone obstructs the common bile duct (CBD)
(obstructive jaundice) (Ch. 7)
Signs
• Tenderness in the right hypochondrium
• The gallbladder is usually not palpable, as it gets contracted due to recurrent
inflammation (Courvoisier’s law)
DD: Chronic duodenal ulcer, APD
• Plain X-rays may be contributory (Fig. 31.6).
• Transabdominal US (Ref Fig 30.4B) has a sensitivity rate of 95–98%
• Endoscopic US (EUS) is able to detect even small stones missed by
transabdominal US
• MRI has a sensitivity rate of 95%
• CT (Ref Fig 30.4D) may be required rarely
• Isotope scan (Fig. 31.7): 99Tc–HIDA (technetium labelled analogue of
iminodiacetic acid) with gallbladder stimulation with fat, or intravenous
administration of cholecystokinin (CCK) can be used to calculate the
ejection fraction. Ejection fraction below 35% is considered abnormal
FIGURE 31.6 Plain X-ray—radio-opaque gallstones: (A) Single. (B)

Multiple.
FIGURE 31.7 Isotope scan—chronic cholecystitis Source: (Courtesy Dr K. M.

Lakshmipathy).
Treatment
• Surgical
• Gallbladder stones: Elective cholecystectomy (laparoscopic or open)
• Common duct stones
- Sphincterotomy (Ref Fig. 7.17A), endoscopic retrograde
cholangiopancreatography (ERCP) and basketing or balloon extraction
(Ref Figs. 7.17B and C)
- Open choledochotolithotomy, to relieve cholangitis and jaundice, and
thereafter by cholecystectomy
• Medical
Select patients who are unfit for surgery are managed by medical therapy:
• Bile acid treatment: Ursodeoxycholic acid for prolonged periods of time (>
2 years) is useful in dissolving small stones (works by forming liquid
cholesterol crystals), and chenodeoxycholic acid, which removes cholesterol
as micelles
• Extracorporeal shock wave lithotripsy (ESWL): Most effective in single
stone, of less than 2 cm in size in a normally functioning gallbladder with a
nonobstructed cystic duct
Gallbladder polyps
• Seen in about 5% of normal subjects undergoing abdominal sonography
• Solitary sessile polyps that are 5–10 mm are more likely to turn malignant
than are small multiple, pedunculated, hyperechoic polyps
• The risk factors which increase the chance of malignancy of polyps are:
• Size > 1 cm
• Presence of gallstones
• Age > 60 years
• Increase in size on interval imaging
• Most patients are asymptomatic
• Chronic upper abdominal biliary type of pain is not uncommon
• No clinical finding
• Transabdominal US is diagnostic in many cases
• EUS is more precise and more informative in differentiating benign and
neoplastic polyps
• CT is not useful in detecting polyps
Treatment
• Cholecystectomy is indicated for polyps:
• More than 1 cm in size
• Associated with gallstones
• In patients with biliary symptoms
• That show increase in size on serial imaging
• Observation with serial imaging is indicated for small polyps with low risk
(apparently benign) for malignancy
31.4 Diseases of pancreas
Chronic pancreatitis
A progressive inflammatory process leading to slow progressive destruction and
fibrosis of the functional acini.
• Sometimes calcification occurs
• Both exocrine and endocrine parts of the pancreas are affected
• More common in females between 31 and 40 years of age
• The classification and risk factors for chronic pancreatitis are tabulated in
Table 31.3
TABLE 31.3
Classification and Risk Factors of Chronic Pancreatitis
Classification Risk Factors

Toxic-metabolic pancreatitis •Alcohol consumption
•Tobacco smoking
•Hypocalcaemia
•Chronic renal failure
•Toxins and drugs
Idiopathic pancreatitis •Tropical pancreatitis
•Tropical calcific pancreatitis
Genetic pancreatitis •Autosomal dominant (mutation in PRSS1 gene)
•Autosomal recessive (CFTR mutation / SPINK 1 mutation)
Autoimmune pancreatitis •Isolated variety
•Associated with Sjögren’s syndrome, IBS, primary biliary cirrhosis
Recurrent pancreatitis •Post necrotic
•Ischaemic
•Post radiation
Obstructive pancreatitis •Pancreas divisum
•Sphincter of Oddi dysfunction
•Post traumatic
Complications: Exocrine and endocrine deficiencies, pseudocyst, pancreatic

ascites, pancreatic fistula, ductal adenocarcinoma
Symptoms
• Abdominal pain, in the epigastrium or on either sides of the midline, radiating
to the back. The pain may be continuous or intermittent. Recurrent attacks
are common
• Anorexia, weight loss and insulin-dependent diabetes mellitus (features of
endocrine deficiency) are commonly seen
• About 25% have steatorrhoea, weight loss, peptic ulcer due to loss of
bicarbonate secretion (features of exocrine deficiency)
Signs
• Tenderness in the epigastrium
• Jaundice due to biliary obstruction
• Vomiting due to duodenal obstruction
• Abdominal distension due to pancreatic ascites
• Upper GI haemorrhage due to gastric varices
• Massive intra-abdominal bleeding due to rupture of pseudo aneurysm
• Cachexia due to ductal adenocarcinoma
• Blood tests—increased amylase during acute attacks, autoantibodies in
autoimmune variety
• Stool examination—raised faecal elastase (< 200 mcg/g)
• Pancreatolauryl test is more accurate than faecal elastase
• Secretin test, the best functional test for chronic pancreatitis
• Plain X-ray will demonstrate calcification or calculi (Fig. 31.8A)
• EUS is highly sensitive for chronic pancreatitis
• CT and MRI demonstrate the ductal calculi (Ref Fig. 30.33), calcifications
(Fig. 31.8B) and enlargement of pancreas
• Magnetic resonance cholangiopancreatography (MRCP) (Fig. 31.8C) and
ERCP demonstrate the ductal pathology
• EUS-guided fine needle aspiration or Trucut biopsy are useful for making
tissue diagnosis
FIGURE 31.8A Plain X-ray—pancreatic calculi Source: (Courtesy Bharat
scans).

FIGURE 31.8B CT—calcific pancreatitis.

FIGURE 31.8C CT—dilated pancreatic duct with calcific pancreatitis.
Treatment
• Medical
• Elimination of alcohol consumption and tobacco smoking
• Pancreatic enzyme supplementation (especially lipase up to 8 lakh units)
• Proton pump inhibitors
• Treatment of diabetes, analgesics and psychological support
• Endoscopic
• Stenting of biliary tree
• Drainage of pancreatic pseudocysts
• Celiac plexus block under EUS guidance
• Surgical
• Bilateral thoracoscopic splanchnicectomy
• Pancreatic duct drainage procedures (lateral pancreato jejunostomy) with
removal of stones (Fig. 31.8D)
• Drainage of pancreatic pseudocysts
• Bypass procedures (choledochojejunostomy or choledochoduodenostomy
for bile duct strictures)
• Pancreatic resections (pancreatoduodenectomy, Frey procedure, distal
pancreatectomy, total pancreatectomy)
FIGURE 31.8D Pancreatic calculi.
Pancreatic malignancy
Commonly refers to ductal adenocarcinoma:
• Occurs in the elderly
• Equal in both sexes
• More common in the head (80%), body (15%) and tail (5%)
• 90% arises from the ducts and 10% from the glandular elements
• Tobacco smoking
• High-dietary fat and meat consumption
• High coffee and / or alcohol consumption
• Familial varieties:
- BRCA2 gene mutation
- Peutz–Jeghers syndrome
- Familial breast and ovarian cancer
- Ataxia telangiectasia
- Li-Fraumeni syndrome
- Familial adenomatous polyposis
• Macroscopically, it may be well circumscribed or diffusely infiltrating the
pancreas
• Microscopically, they are:
• Mucinous adenocarcinoma (majority)
• Signet ring cell carcinoma
• Adenosquamous carcinoma
• Anaplastic carcinoma
• Acinar cell carcinoma
• Pancreatoblastoma
• Lymphoma
• The tumour spreads in many ways. They are:
• Tumour infiltrates diffusely through the gland
• May grow along the pancreatic duct system, eventually reaching the CBD
• May breach the capsule and invade the stomach, duodenum and spleen
• Transcoelomic spread leads to peritoneal deposits and ascites
• Lymphatic spread involves the pancreaticoduodenal, gastroduodenal,
hepatic, superior mesenteric and celiac groups
• Distant metastases to the liver, lungs, skin and brain are common
Symptoms
• Painless jaundice (progressive or deep jaundice), as the CBD is obstructed.
This may be first presenting symptom in an otherwise asymptomatic patient
• Weight loss, anorexia, fatigue, constipation, vomiting due to duodenal
obstruction
• Steatorrhoea is common
• Abdominal pain is common, which is ‘boring’ in nature forcing the patient to
sit up most of the day and night
• Foul-smelling clay-coloured stools (due to obstruction of the CBD) is
common
Signs
• Jaundice, scratch marks of obstructive jaundice, multiple bruises due to
impaired coagulation
• Gallbladder may be palpably enlarged (Courvoisier’s law)
• Migrating thrombophlebitis can occur (Trousseau’s sign)
• Hepatomegaly may be present when liver is metastasized
Note
Carcinoma of the body and tail of the pancreas does not present with
obstructive jaundice, unless it is metastasized to the liver.
• Serum cancer antigen (CA 19/9) is elevated but not specific
• Plain X-rays of the abdomen show dilatation of the CBD and main pancreatic
duct (double duct sign)
• US identifies the dilated biliary radicles and pancreatic duct, and also liver
metastases
• Barium meal series may show widening of the duodenal ‘C’ loop
• CECT (Figs. 31.9A and B) is gold standard for diagnosis and staging for
resectability
• MRCP (Fig. 31.9C) enhances the diagnosis by revealing the double duct sign
• EUS is highly sensitive in detecting small tumours
• ERCP is useful for diagnosis as tissue for biopsy may be taken, if possible
• Percutaneous transhepatic cholangiography (PTC) is useful for determining
the upper limit of the tumour obstructing the CBD
• Laparoscopy is useful in diagnosing metastases in the liver and the
peritoneum
• Histopathology is possible with ERCP brushing, or fine needle aspiration
guided by EUS, CT or US
FIGURE 31.9A CT—pancreatic head malignancy.
FIGURE 31.9B CT—malignancy of body and tail of
pancreas Source: (Courtesy Bharat Scans).
FIGURE 31.9C MRCP—carcinoma of head of pancreas.
Treatment
• Pancreatoduodenectomy (Whipple’s operation) for head and neck region
tumours
• Partial or subtotal pancreatectomy for body and tail region cancers
• Total pancreatectomy is reserved for large tumours
• Adjuvant chemotherapy is useful in improving survival and tumour-free
periods
• Modern radiotherapy use is controversial
Palliative
• Bypass procedures (choledochojejunostomy or stenting to relieve jaundice
and gastrojejunostomy to relieve duodenal obstruction) are used for
inoperable cancers
31.5 Diseases of intestines
Recurrent appendicitis
Recurrent attacks of appendicitis caused by low-grade infections, sometimes
associated with faecoliths in the appendicular lumen
• Patients do not present with a classic picture of appendicitis, but have vague
upper abdominal discomfort (appendicular dyspepsia), with constipation,
dysuria, and mild pain radiating to the right testis or thigh
• Obstructed appendix may present with recurrent colicky pain (appendicular
colic) (Ch. 30)
• Tenderness may be felt on deep palpation
• Plain X-ray abdomen (Fig. 31.10A) may show appendicolith
• US and barium meal follow through may be informative, but remain normal
on many occasions
• CT abdomen (Fig. 31.10B) may show the appendicolith or be useful at least
in eliminating other pathologies
FIGURE 31.10A X-ray abdomen—appendicolith.
FIGURE 31.10B CT abdomen—appendicolith and dilated appendix.
Treatment
Elective appendicectomy (laparoscopic or open)
Abdominal tuberculosis
Very common disease, especially in the lower socio-economic group, affecting
any age and any sex. The route of entry of the organism Mycobacterium
tuberculosis is by ingestion or through blood and by transmigration. Abdominal
tuberculosis is of three types:
• Intestinal tuberculosis:
• Ulcerative type: After the swallowing of the sputum, the organisms reach
the small bowel and get concentrated in the terminal ileum (area of
excessive lymphatics), and cause mucosal ulcers, which are transverse or
circular (following the pattern of the lymphatics of the bowel). Healing of
these ulcers causes fibrosis and strictures. Strictures lead to obstruction of
the small bowel. Ulcers in the proximal distended bowel may lead to
perforations and peritonitis, or internal fistulae, but rare when compared to
Crohn’s disease
• Hyperplastic type: The bacilli reach the ileocaecal region, cause solitary or
multiple lesions and reside in the lymphoid follicles leading to thickening
of the intestinal wall and narrowing, which may lead to intestinal
obstruction
• Tuberculosis of the mesenteric lymph nodes: This is common in children
• Peritoneal tuberculosis: The bacteria enter the peritoneal cavity through
transmigration from the intestines, tuberculous salpingitis or through blood
(haematogenous spread) and present in two forms. They are:
• Moist form:Ascitic form
• Dry form: Ascites is absent, but forms tubercles on the peritoneum
Clinical features depend on the type of tuberculosis.
• Intestinal tuberculosis
• Ulcerative type:
- Abdominal pain, intestinal colic, loss of appetite and weight
- Active lesions cause diarrhoea and healed lesions cause constipation and
features of intestinal obstruction
• Hyperplastic type:
- In addition to the features of ulcerative type, the patients may present
with a lump in the right iliac fossa confusing with appendicular mass,
Crohn’s disease, amoeboma and carcinoma
• Tuberculosis of the mesenteric lymph nodes:
• Periumbilical abdominal pain is the common presentation
• General debility, loss of appetite and weight with evening rise of
temperature
• Enlarged lymph nodes can cause kinking of the small bowel and cause
intestinal obstruction
DD: Acute appendicitis
• Peritoneal tuberculosis
• Moist form: Abdominal pain and distension due to ascites, and general
malaise and weakness
• Dry form: Abdominal pain without abdominal distension
• Plain X-rays of the abdomen and CT without oral contrast are useful in
diagnosing obstructed bowel lesions and lymph node enlargements
• Barium meal series (Fig. 31.11A) or CT with oral contrast (Fig. 31.11B) is
diagnostic for mucosal lesions, abscess and fistulae. Ileocaecal junction is
pulled up in hyperplastic type of intestinal tuberculosis
• Colonoscopy (Fig. 31.11C) has characteristic findings
• Complete analysis and PCR test for ascitic fluid, and peritoneal biopsy are
diagnostic in peritoneal type of tuberculosis
FIGURE 31.11A Ba meal series—matted intestines of intestinal
tuberculosis.

FIGURE 31.11B CT—intestinal tuberculosis Source: (Courtesy Bharat scans).
FIGURE 31.11C Tuberculous ulcer caecum Source: (Courtesy Dr Mani
Veeraraghavan).
Treatment
• Antitubercular treatment is curative
• Surgical treatment is for complications such as obstructions, abscesses and
fistulae
Crohn’s disease
• An inflammatory bowel disease of uncertain aetiology affecting any part of
the GI tract, commonly the small and large intestines, but the rectum is
characteristically spared
• Usually, a disease of young adults of the second and third decades, and rarely
of the elderly
Complications: Internal fistulae
Clinical presentation depends on the stage of the disease.
• Inflammatory stage: Mass in the right iliac fossa with a long history
(contrasting with appendicular mass which has a short aetiology) (See Ch.
33)
• Colitis stage: Diarrhoea, fever, anaemia and loss of weight
• Stenosis stage: Vomiting and constipation (features of intestinal obstruction)
• Fistula stage: Discharges (external fistula), recurrent infections (internal
fistula)
Crohn’s disease has extra-intestinal manifestations. They are:
• Skin: Erythema multiforme, erythema nodosum, pyoderma gangrenosum
• Eyes: Iritis, uveitis, conjunctivitis
• Joints: Peripheral arthritis, ankylosing spondylitis
• Blood: Anaemia, thrombocytosis, phlebothrombosis, arterial thrombosis
• Liver: Nonspecific triaditis, sclerosing cholangitis
• Kidneys: Nephrotic syndrome, amyloidosis
• Pancreas: Pancreatitis
• General: Amyloidosis
• Barium meal study is diagnostic. It demonstrates the mucosal involvement
(cobblestone appearance), strictures (string sign of Kantor) (Fig. 31.12),
segmental involvement, fistulous communications to adjoining organs
• Barium enema demonstrates signs of inflammation in the colon
• CT with oral contrast is more informative
FIGURE 31.12 Barium meal—string sign of Kantor.
Treatment
• Medical (essentially symptomatic)
• Long-term antibiotics
• Steroids
• Immunosuppressants
• Surgical treatment is warranted for treatment of complications
• Fistulae—excision
• Abscess—drainage
• Strictures—stricturoplasty, excision, bypass
Ulcerative colitis
• An inflammatory bowel disease of uncertain aetiology with remissions and
acute exacerbations
• Occurs in both sexes between the age of 20 and 40
• Inflammation is said to occur due to:
• Altered mucosal metabolism
• Defective mucosal barrier
• Immune deficiencies
• Pathology involves mucosa and submucosa of the bowel, starting at the
rectum proceeding upwards to affect the entire colon
• Genetic
• Infections
• Low-fat diet
• Psychological stress
Complications:
• GI: Stricture, carcinoma, pseudopolyps, ischiorectal abscess, fistula in ano,
cirrhosis of liver
• Non-GI:
• Skin: Erythema nodosum, pyoderma gangrenosum
• Eye: Iritis, episcleritis
• Joints: Ankylosing spondylitis, rheumatoid type arthritis
• Kidneys: Glomerulonephritis, secondary amyloidosis
• Diarrhoea with pus, mucus and blood
• Abdominal discomfort and pain
• Raised body temperature in acute or fulminant attacks (p. 558)
• Muscle wasting, emaciation and anaemia due to chronic blood loss
• Abdominal distension due to supervening toxic megacolon (acute dilatation)
• Barium enema is diagnostic. It shows a dilated colon with loss of
haustrations and mucosal ulcerations. Pseudopolyps are seen as filling
defects
• CT abdomen with contrast gives clearer pictures
• Sigmoidoscopy and colonoscopy (Fig. 31.13) show hyperaemia of colonic
mucosa, diffuse haemorrhagic areas and ulcerations. Pseudopolyps may be
seen
FIGURE 31.13 Colonoscopy—ulcerative colitis Source: (Courtesy Dr Mani

Veeraraghavan).
Treatment
• Medical
• Symptomatic
• Anti-inflammatory: Salazopyrine, steroids
• Surgical treatment is warranted for complications (stricture, malignancy)
Diverticulosis of small bowel
• Uncommon disease of congenital origin, but the exact cause is unknown
• Diverticula appear as herniated pouches at the mesenteric border of the small
intestines, commonly in the jejunum (Fig. 31.14)
• Meckel’s diverticulum occurs at about 2 ft from the ileocaecal valve (p. 557)
and presents with acute inflammation
FIGURE 31.14 Jejunal diverticula.
Complications: Diverticulitis, perforation, peritonitis

• Majority of them are asymptomatic
• Vague dyspepsia, recurrent abdominal pain
• Peripheral smear may show macrocytic anaemia due to infection
• Barium meal series and CT with oral contrast are useful in diagnosis
Treatment
• No treatment is required as the diverticula are asymptomatic
• Emergency surgical treatment is required for perforation
Diverticulitis of colon
• Diverticula are of two types. They are:
• Congenital (rare)—walls of diverticula contain all the layers of colon
• Acquired (common)—serosa covered outpouchings of mucosa alone
through gaps in muscularis by increased intracolonic pressure (pulsion
diverticulum)
• Commonly affects the left-sided colon, especially the sigmoid colon
• Rare under the age of 35, but the incidence increases with age, 50% of
diverticula are found in the age of 80–90
• Consumption of low-fibre diet is a common factor associated with diverticular
disease of the colon
• There are of two stages:
• Diverticulosis stage—diverticula without inflammation
• Diverticulitis stage—inflammation of the diverticula, caused by
accumulated faeces within the diverticula
Complications: Perforation, peritonitis, pericolic abscess and internal fistulae
• Diverticulosis stage—asymptomatic
• Diverticulitis stage
• Left lower abdominal pain
• Irregular bowel habits
• Episodic diarrhoea or constipation
• Feeling of incomplete evacuation
• Rectal bleeding (rarely due to associated malignancy)
• On examination, mild tenderness over the descending colon
Patients with haemorrhage, perforations and peritonitis are febrile and present
as acute emergency.
• Barium enema is diagnostic (diverticula—pouch-like projections,
diverticulitis—’saw tooth’ appearance (Ref Fig. 30.6A)
• Colonoscopy (Ref Fig. 30.6B) is conclusive
Treatment
• Diverticulosis needs no treatment
• Diverticulitis can be managed conservatively
• Surgical management is for complications such as perforations and bleeding
lesions or those with malignancy
Hirschsprung disease
• Affects 1 in 5000 childbirths, caused by an aganglionic segment in the
rectum, affects 80% male children
• A number of abnormal genes have been identified in families with
Hirschsprung disease
• Presents at birth or within few days
• Usually the baby is unable to pass the meconium, which can be helped out by
a finger or a tube. Slowly abdominal distension develops with visible
peristalsis. Enterocolitis may supervene
• Rectal examination reveals a contracted empty rectum and a normal anus.
After the examination, usually the meconium and flatus are passed
• Barium enema is diagnostic, which shows a dilated normal rectosigmoid
proximal to a narrow distal aganglionic rectal segment
• Rectal biopsy confirms diagnosis
Treatment
• Needs surgical correction (Fig. 31.15), primary rectal pull through operation
(with a defunctioning stoma)
FIGURE 31.15 Congenital megacolon Source: (Courtesy Dr V. Srinivasan).
Note
Acquired megacolon is a disorder secondary to a pathology-like fissure in ano
and Chagas disease. In this condition, the rectum is dilated up to the anal
canal.
Colonic malignancy (chs. 8 and 33)

• Rare before the age of 50 (except in familial adenomatous polyposis [FAP])
• The incidence of colonic malignancy varies anatomically (Fig. 31.16)
• First-degree relatives of colonic cancer patients have a very high
preponderance
• Adenomas
• FAP
• Hereditary nonpolyposis colon cancer (HNPCC) accounts for about 20%
cases
• Peutz–Jeghers syndrome
• Turcot syndrome
• Macroscopically the tumours are:
• Polypoid (exophytic and protrude into the lumen)
• Ulcerative
• Annular
• A combination of the above
• Microscopically, they are adenocarcinomas of varying differentiations and are
staged conventionally by Duke’s classification:
• Stage A—neoplastic cells confined to the mucosa
• Stage B—tumour extension into all layers of the colon without lymph node
involvement
• Stage C—tumour extension into all layers of the colon with lymph node
involvement
- C1—local lymph nodes only
- C2—proximal lymph nodes
• Colonic carcinomas spread by:
• Direct extension to the wall extending into the serosa and neighbouring
structures (sacral plexus posteriorly, ureters laterally and bladder in the
males and uterus in the females anteriorly)
• Lymphatic spread first to mesocolic nodes and then to para-aortic nodes
• Haematogenous spread reaches first to the liver and uncommonly to the
lungs and bones
• Transcoelomic spread occurs by implantation into the peritoneal cavity to
produce ascites and also on the ovaries
• Direct implantation occurs when the exfoliated cells implant on a breached
mucosa
FIGURE 31.16 Incidence of colonic malignancy.
Malignancies of the colon on the right and left side have different clinical
presentations. This is due to two factors:
1. Right colon is capacious and its faecal matter is liquid or semisolid in
consistency, whereas, the left colon is narrow in caliber and faecal matter is
more solid
2. Clinical features of colonic malignancy are shown in Table 31.4
• The common clinical presentation is bleeding per rectum and mucous
discharge. The character of blood and its mixing with the stools depends on
the level of the lesion, which determines the consistency of the faecal mass
• Constipation is the symptom of tumours of the left colon, due to relatively
smaller diameter of the colon
• Stenosed lesions and perforations with pericolic abscess present as acute
abdomen
TABLE 31.4
Clinical Features of Colonic Malignancies
Malignancy
Feature
Right colon Left colon
Type of lesion Cauliflower like exophytic growth Annular or sclerosing type
Obstructive Late feature Early feature
symptoms
Associated Anaemia, malaise, abdominal pain
symptoms
Altered bowel habits usually absent Constipation, diarrhoea or alternating constipation and
diarrhoea
Clinical Lump in the right iliac fossa or Lump in the left lower abdomen with distended colon with
presentation right flank faecal matter
Hepatomegaly, if liver is involved
Ascites due to peritoneal metastases
• Low haematocrit is usually present
• Faecal occult blood may be positive
• Serum carcinoembryonic antigen (CEA) level is usually elevated and is a
useful tumour marker for follow up
• Barium enema shows ‘apple core appearance’ and is diagnostic (Fig. 31.17A)
• Colonoscopy (Fig. 31.17B) has the added advantage of obtaining the tissue
for histopathology
• Histopathology is conclusive
• CT abdomen is useful in assessing local invasion (Fig. 31.17C), lymph nodal
and hepatic metastases
FIGURE 31.17A Barium enema—apple core appearance.

FIGURE 31.17B Colonoscopy—malignancy colon Source: (Courtesy Dr Mani
Veeraraghavan).
FIGURE 31.17C CT—malignancy of descending colon.
Treatment
• Radical excision of tumour-bearing colon (radical colectomies)
• Postoperative chemotherapy and radiotherapy are administered in majority
of cases
• Preoperative CRT is administered in advanced lesions
Palliative
• Defunctioning colostomy for nonresectable, advanced and obstructed
malignancies
• Surgical excision (wedge resection to hepatectomy) of metastases limited to
a lobe of liver
• Chemotherapy for multiple diffuse metastases
31.6 Diseases of any part of gastrointestinal
system
Gastrointestinal stromal tumours

• Rare neoplasm
• Three per cent of all GI neoplasms
• GI stromal tumours (GISTs) are the most common mesenchymal tumours of
the GI tract (GIT)
• Approximately 60% occur in the stomach, 25% in the small intestine and 10%
in the colon and rectum. The remainder arises from other sites such as the
gallbladder, appendix, omentum or mesentery
• Most GISTs are benign, but malignant tumours can metastasize to liver and by
intra-abdominal dissemination
• Rectal GISTs metastasize to lungs.
DD: Smooth muscle tumours, nerve sheath tumours, fibromatosis
Symptoms are most representative of the site of origin.
• Oesophageal GISTs—dysphagia, odynophagia, weight loss, dyspepsia,
retrosternal burning, haematemesis
• Gastric GISTs—abdominal pain, anorexia, weight loss or GI haemorrhage
• Small intestine GISTs—abdominal pain, haemorrhage
• Colorectal GISTs—abdominal discomfort, haemorrhage, bowel obstruction
• CT and MRI (Figs. 31.18A and B) and PET scans are useful. Presence of
intratumural gas, fluid or calcification are useful determinants in diagnosis
• Histopathology determines malignancy by factors such as mitotic rate,
tumour size and site
• Immunohistochemistry:
• About 85 to 95% of GISTs express KIT (Stem cell receptor CD117),
regarded as a key confirmatory marker of diagnosis, though not specific
for GISTs
• Sixty per cent show expression of CD34 and 20–40% to small muscle actin
FIGURE 31.18A CT—GIST stomach.

FIGURE 31.18B CT—GIST jejunum.
Treatment
• Surgery is the mainstay of treatment. Wide resection or segmental resection is
adequate. Lymph node dissection is not necessary as they rarely metastasize
to lymph nodes
• Radiation has little role, as GISTs are radioresistant
• Chemotherapy is by imatinib mesylate
Gastrointestinal lymphomas
• Represent 5% of all GI malignancies
• Peak incidence is between 50 and 70 years
• Male predominance 2:1
• Malignant transformation of mucosa associated lymphatic tissue (MALT) is
important
• Atrophic gastritis
• H. pylori infections
• α-chain disease
• Celiac disease
• Dermatitis herpetiformis
• Autoimmune disorders
• Crohn’s disease
• Immunodeficiency syndromes including AIDS
• The staging of GI lymphomas is:
• Stage 1—tumour confined to GI organs
• Stage 2—tumour with intra-abdominal lymph node involvement
• Stage 3—extra-abdominal nodes or other organs are involved
• Stage 4—disseminated disease
• Pathologically, the three main types are:
• Non-Hodgkin’s lymphoma
• Primary lymphoma associated with celiac disease (T-cell lymphoma)
• Mediterranean lymphoma associated with α-chain disease
Symptoms
• Chronic abdominal pain
• Nausea
• Vomiting
• Weight loss
• Fatigue
• Symptoms of obstruction, perforation or haemorrhage
Signs
• Abdominal mass
• Anaemia
• Signs of obstruction and peritonitis
• Haematocrit levels lowered
• X-ray and CT of chest
• US and CT of abdomen are useful
• Endoscopy (upper and lower GI)
• EUS
• Contrast studies of GIT
• Laparotomy / laparoscopy
Treatment
Treatment depends upon the site, stage and histological subtype.
• Stage I and II: Surgical resection with regional lymph nodes. Post op CRT
• Stage III and IV: CRT, and surgery for obstruction, haemorrhage and
obstruction
31.7 Symptoms of patients with chronic

abdominal illnesses
• Abdominal pain
• Dyspepsia
• Nausea and vomiting
• Haematemesis and melena
• Jaundice
• Appetite and weight loss
• Fever
Chronic abdominal pain
Abdominal pain lasting for more than 6 months is referred to as chronic
abdominal pain. The pain has a particular pattern and has regional localization.
The abdomen is divided into ten arbitrary regions (Fig. 30.36) for convenience
of understanding and localization (p. 585).
So far as the GI tract is concerned, in a human embryo, it is a midline
structure and the pain arising from the GI tract is referable to the midline as
indicated below:
a) Pain at the epigastrium—diseases of the foregut (abdominal oesophagus,
stomach and proximal half of second part of the duodenum and their
offshoots such as liver, gallbladder, pancreas and spleen) (e.g. gastric and
duodenal ulcers)
b) Pain at the umbilical region—diseases of the midgut (distal half of second
part of the duodenum, small bowel, colon up to the proximal 2/3 of transverse
colon) (e.g. intestinal tuberculosis)
c) Pain at the hypogastrium—diseases of the hindgut (distal one-third of
transverse colon to the anorectal junction) (e.g. colorectal pathologies)
Nature of pain
a) Constant pain: Pain constantly present all through the day at one region (e.g.
epigastric pain of chronic pancreatitis)
b) Pain with pain-free intervals: This variety of pain has some periodicity and it
may coincide with the time of high gastric acid secretion or with periods of
intense physical and mental stress (e.g. pain of chronic duodenal ulcer)
c) Dull and recurrent pain: Pain can be dull and recurrent (e.g. subacute
appendicitis)
d) Dull continuous pain increasing in severity: Persistent pain may increase in
severity over a period of time (e.g. chronic gastric ulcer transforming into
malignancy)
e) Burning pain: Pain may be of burning nature (e.g. pain in APD or reflux
oesophagitis)
Shift, migration and referred pain

• Migrating or radiating pain: Migrating pain is that pain which originates at
one region and shifts to another region, but does continue to stay at a lesser
degree at the point of origin (e.g. pain of duodenal ulcer is epigastric to start
with, and spreads to the back due to its infiltration to pancreas)
• Referred pain: The pathology and the area of the pain are different as the
organ of pathology and the area of pain share the same nerve supply. The
examples are given in Table 30.12 (Fig. 30.37)
Effects of movements, food or habits

The pain may be aggravated and relieved by certain factors. Some examples are
given in Tables 30.13 and 30.14, respectively.
Dyspepsia
This is a very general term used for abdominal discomfort. This is seen in
various combinations in various illnesses.
• Dyspepsia and flatulence (e.g. chronic cholecystitis)
• Dyspepsia and early satiety (e.g. duodenal stenosis and gastric outlet
obstruction, gastric carcinoma)
• Feeling of fullness (e.g. chronic pancreatitis, obstructive jaundice)
Nausea and vomiting

Nausea and vomiting are present with many chronic abdominal conditions.
Inflammatory lesions (e.g. hepatitis, gastritis, pancreatitis, cholecystitis) and
malignancies (carcinoma stomach, pancreas and gallbladder) present with
nausea and vomiting.
• Character of vomiting
• Projectile: Involuntary projectile ejection of large quantities of vomitus
(e.g. high intestinal obstruction)
• Regurgitative: Effortless involuntary regurgitation of intestinal contents
(e.g. low intestinal obstruction)
• Frequency of vomiting
• Constant: Persistent vomiting even in the absence of food intake (e.g.
gastric outlet obstruction)
• Periodical: Vomiting with some periodicity or following food intake
indicating bowel obstruction (e.g. intestinal obstruction)
• Nature of vomitus
• Coffee ground vomitus (brown to dark brown colour): Gastric contents
with altered blood (e.g. chronic duodenal ulcer, gastritis, carcinoma of the
stomach)
• Fresh blood (red in colour) (e.g. bleeding oesophageal varices)
• Faeculent (yellowish green and foul smelling) (e.g. gastro-jejuno-colic
fistula)
• Greenish: Due to the presence of bile (e.g. high intestinal obstruction)
• White or colourless: Due to the absence of bile (e.g. gastric outlet
obstruction and pyloric or antral growth which prevent the bile reflux)
• Reddish: Due to large quantities of blood in the stomach (e.g. oesophageal
varices)
• Yellowish: Due to presence of faecal matter or decomposed material (e.g.
gastro-jejuno-colic fistula)
• Quantity of vomitus
• Large quantities indicate distal bowel obstruction
• Small quantities indicate gastric outlet obstruction
• Relationship with pain
The pain may precede, accompany or follow abdominal pain. The examples
Haematemesis and melena

Detailed in Chapter 8, Gastrointestinal Haemorrhage.
Jaundice
Detailed in Chapter 7, Jaundice.

• Constipation is one of the common complaints of a patient suffering from a
surgical illness (clinical evaluation of a patient with constipation is
discussed in detail in Ch. 6)
• Diarrhoea (e.g. ulcerative colitis, intestinal tuberculosis)
• Alternating diarrhoea and constipation (e.g. left-sided colonic tumours)
• Spurious diarrhoea (e.g. left-sided obstructing colonic tumours)
However, the colour of stools has its significance.
• Bloodstained hard stools (e.g., left-sided colonic malignancy)
• Bloodstained mucoid loose stools (e.g. Crohn’s disease, ulcerative colitis,
colorectal malignancy)
• Black-coloured stools (e.g. upper GI bleed proximal to ileocaecal junction)
• White clay-coloured stools (e.g. obstructive jaundice)
• Large, fatty, offensive frothy stools (e.g. chronic pancreatitis)
Appetite and weight loss

Appetite loss is a common feature and an early sign of GI malignancy. In
patients with recurrent appendicitis, food intake causes nausea and vomiting, and
there is a tendency to eat less. Qualitative dyspepsia is a feature of gallbladder
disease, where fatty food precipitates pain, and the patient loses weight.
Weight loss of 10% of basal weight in a period of 6 months is considered
pathological.
Fever
Fever is a feature of some chronic infective conditions. The fever is usually low
grade in majority of chronic pathologies.
• Evening rise of temperature (e.g. abdominal tuberculosis (tabes
mesenterica))
• Varying grades of temperature (e.g., appendicitis, ulcerative colitis)
• High-grade fever with chills (e.g. cholangitis)
Eliciting history
Abdominal pain
• Site of pain: Where is the pain?
The patients should be asked to show the region of pain in the abdomen.
When they are asked to point with their own finger, it may denote the anatomical
origin of pain— ‘pointing sign’ (e.g. pain in the right iliac fossa in recurrent
appendicitis)
• Duration of pain: How long is the patient suffering from pain?
If the patient has been suffering from pain for a very long period of time, it
indicates chronicity, possibly also indicates that it is not a malignant condition
(e.g. chronic cholecystitis), as patients with untreated malignancies do not
maintain good health
• Description of pain: Can you describe the pain?
Abdominal pain has a variety of presentations. Constant pain (e.g. chronic
pancreatitis), burning pain (e.g. reflux oesophagitis)
• Recent change in the quality, intensity of pain: Is there a change in its
quality, periodicity or intensity of pain or not?
Recurrent attacks of pain of chronic calculous cholecystitis may change to a
constant pain when there is malignant transformation
from its point where it started?
Some pains may shift its place (e.g. epigastric pain of chronic duodenal ulcer
may shift to the back when it infiltrates the pancreas)
• Effects of movements, food or habits: Is there any factor such as food,
which relieves or makes the pain worse?
The abdominal pain gets altered by certain factors such as food (e.g. spicy
food aggravates the pain of chronic duodenal ulcer, whereas bland food relieves
it)
Nausea and vomiting

• Nausea and vomiting: Does the patient have persistent nausea or episodes
of vomiting?
Nausea and vomiting are seen in many chronic abdominal conditions (e.g.
gastritis, gastric malignancy)
• Colour of vomitus: What is the colour of the vomitus?
The vomitus can be of different colours due to its contents
• Quantity of vomitus: What is the quantity of the vomitus?
Patients may be permitted to answer in their own terms such as cupful, large
vessel full, etc. so that the approximate quantity can be determined.
• Small quantity (e.g. reflux oesophagitis)
• Large quantity (e.g. gastric outlet obstruction, high intestinal obstruction)
• Contents of vomitus: What were the contents of the vomitus?
The vomitus may contain undigested or partly digested food particles
consumed even a day earlier indicating prolonged stasis in the stomach (e.g.
gastric outlet obstruction)
• Frequency: How frequently is the patient been vomiting?
Vomiting is a constant feature and always follows food intake in certain
situations such as pyloric obstruction and severe gastritis. Though not constant,
it is frequent with appendicular dyspepsia, cholecystitis and pancreatitis
• Relationship to food: Is vomiting related to food intake?
Some food items have a tendency to induce vomiting soon after food intake,
e.g. gastritis, and delayed vomiting after food intake occurs in pyloric stenosis.
Fatty food induces vomiting in cholecystitis. Food has no relationship with
vomiting in pancreatitis
• Relationship to abdominal pain: Does this vomiting relieve or aggravate
abdominal pain?
Vomiting gives relief from abdominal pain (e.g. gastric ulcer, carcinoma
stomach, pyloric obstruction, pancreatitis, gallbladder diseases and appendicitis).
Gastric ulcer pain is sometimes relieved by vomiting and hence patients resort to
induction of vomiting to get pain relief
Melena
• Melena: Did the patient pass blood or black-coloured stools?
Melena is common in bleeding lesions of the upper GI tract. This may be
associated with haematemesis. Passing fresh blood per rectum may be due to
rectal malignancies, haemorrhoids, etc.
Jaundice
• Jaundice: Did the patient suffer from jaundice during the illness?
Jaundice may manifest when the biliary system is obstructed (e.g. stone in the
CBD) and also gets relieved on its own. Jaundice may persist in malignancies of
the biliary tract (e.g. carcinoma of head of pancreas), fluctuation of jaundice is
seen in certain conditions (e.g. periampullary carcinoma)

• Alteration in bowel habits: Does the patient have any change in his bowel
habits?
Recent change in bowel habits is to be noted carefully. Recent constipation in
an otherwise normal individual especially in the elderly is to be noted (e.g.
colonic malignancy), alternating diarrhoea and constipation (e.g. left-sided
colonic malignancy)
Appetite and weight loss

• Appetite and weight loss: Is there any loss of appetite and weight in recent
months?
malignancies
Fever
• Fever: Does or did the patient have fever during the course of this illness?
Association of low-grade fever may be present (e.g. lymphomas,
malignancies), evening rise of temperature (e.g. tuberculosis)
Past history
treated will indicate the examiner to reconsider the diagnosis such as colics
Family history
Colonic malignancies are known to occur in families
match the situation
Personal history
Personal history should include the usage of:
• Alcohol (e.g. acute duodenal ulcer, acute gastritis, acute pancreatitis)
• Tobacco (e.g. acute gastritis)
• Drugs such as analgesics (e.g. acute duodenal ulcer)
Menstrual history is extremely important in women (e.g. menorrhagia in
uterine malignancies).
General
• General build: Patient’s build varies in different pathologies
• Normal (e.g. recurrent appendicitis, chronic duodenal ulcer)
• Subnormal (e.g. chronic inflammatory bowel disease, abdominal
tuberculosis)
• Emaciated (e.g. malignancies)
• Distended abdomen (e.g. ascites, large lumps)
• Eyes
• Sunken eyes indicate dehydration and undernutrition
• Jaundice may be an indicator of metastatic liver disease
• Pallor a feature of malignancy or any chronic bleeding in the GI tract
• Skin
• Scratch marks may indicate obstructive jaundice
• Generalized oedema (anasarca) may be seen in patients with hepatic
failure
• Examination of oral cavity
• Caries teeth, pyorrhoea
• Tongue—pale (e.g. anaemia of malignancy)
Vital signs
• Hypertension (e.g. chronic renal pathology)
• Elevated temperature (e.g. infective pathologies and malignancies)
Abdomen
in the supine position with the arms by the sides, under proper lighting. The
patient’s body should be exposed fully starting from the nipples to mid thighs,
exposing the genitalia, the inguinal and femoral areas for complete examination
(Ref Fig. 30.40). Privacy of the patient must be assured, and a nurse be kept by
the side of the patient, especially when the patient is a female.
The clinical examination of the abdomen in acute emergencies consists of:
1. Inspection
2. Palpation
3. Percussion
4. Auscultation
Inspection
The abdomen should be inspected over the entire area with special attention to
the flanks and groins. The abdomen should be observed from different positions
at different angles (from the sides tangentially, and from the ends of the couch).
Look for the following during inspection:
1. Shape
Distension of abdomen occurs depending on the intra-abdominal pathology.
Normal shape of the abdomen is flat.
• Scaphoid shape: Abdomen is scaphoid (boat like) in thin persons or in
emaciated individuals (Ref Fig. 30.45)
• Generalized distension: This is generally due to fat, fluid (Ref Fig. 30.42),
faeces or fetus or due to very large intra-abdominal swellings
• Localized distension:
• Distension of the central abdomen is caused (Fig. 31.19) when it is
occupied by the distended or floating small bowel (e.g. ileocaecal
tuberculosis)
• Asymmetrical localized distensions:
- Upper abdominal distension (right side) is seen in gross enlargement of
the liver (Ref Fig. 30.43A), and (left side) in splenomegaly (Fig. 31.20)
- Lower abdominal distension is seen when the urinary bladder is
distended (Ref Fig. 30.43B).
- Fullness of right iliac fossa may be seen in distended caecum in
obstructing colonic malignancies
- Distension of one of the flanks is seen with renal mass on that side (Ref
Fig. 30.44)
• Peripheral distension: Both flanks may show distension when the colon is
distended, due to obstructing rectal malignancies
2. Umbilicus
FIGURE 31.19 Distension of central abdomen.

FIGURE 31.20 Upper abdominal distension due to splenomegaly.
Normal umbilicus lies midway between the xiphoid process and pubic
symphysis in the midline, and is slightly retracted and inverted. It appears in
various shapes in various pathologies.
• Everted and transverse—ascites (Ref Fig. 30.46)
• Displaced downwards—ascites (Tanjot’s sign) (Fig. 31.21)
• Displaced upwards—pelvic masses, e.g. large ovarian cyst
• Pushed sideways—masses appearing from one side
• Everted and globular—umbilical hernia (Fig. 31.22)
• Everted with crescentic margin—paraumbilical hernia (Fig. 31.23)
3. Skin
FIGURE 31.21 Tanjot’s sign (A) is more than (B).

FIGURE 31.22 Umbilical hernia.
FIGURE 31.23 Paraumbilical hernia.
The skin has to be given special attention for colour, striae, scars, veins,
pigmentations and nodules.
• Colour: Red erythematous skin (erythema ab igne) may indicate application
of hot water bottle for pain relief and suggest location of the pain (e.g.
chronic pancreatitis)
• Striae: The irregular white or pink wrinkled linear marks caused by gross
stretching of skin with rupture of elastic fibres (e.g. pregnancy—striae
gravidarum (Fig. 31.24), ascites). Pink-coloured striae may be a part of
steroid overdosage or Cushing’s syndrome
• Scars: Special attention should be given to the scars on the abdominal wall.
Nature of previous surgery may indicate the present pathology (e.g.
recurrence of malignancy) (Fig. 31.25) or a muscular weakness below the
scar (e.g. incisional hernia) (Ref Fig. 30.48)
• Veins: There may be distended or prominent superficial veins visible on the
skin of the abdomen. Long dilated veins may be seen on the lateral sides of
the abdominal wall due to obstruction of the inferior vena cava. They
represent the communication between the superficial epigastric and
circumflex iliac veins below and the lateral thoracic veins above, diverting
blood flow from the saphenous vein to the axillary vein. Distended veins
around the umbilicus (caput medusae) are seen in portal hypertension. The
direction of flow of blood in the distended veins should be determined
• Nodules: Nodules at the umbilicus are seen with intra-abdominal
malignancies especially of the stomach – ‘Sister Mary Joseph’s nodules’
(Fig. 31.26)
4. Movements of the abdominal wall
FIGURE 31.24 Striae gravidarum.
FIGURE 31.25 Scars on the abdominal wall.
FIGURE 31.26 Sister Mary Joseph nodule of colonic malignancy.
The abdominal wall moves regularly and smoothly with respiration. When the
movements of the abdominal wall are normal, it indicates the absence of any
gross inflammation. Restricted movements to certain localized areas indicate
local pathology such as liver enlargement, e.g. liver metastases causing pain.
Pulsations
Normal abdominal aortic pulsations may be visible in the epigastrium in very
thin patients. Abnormal and prominent pulsations may be seen in the mid
abdomen—abdominal aortic aneurysm.
Visible peristalsis of the bowel is observed in some situations. They are:
• Visible gastric peristalsis—e.g. cicatrized duodenal ulcer or malignancy and
congenital pyloric stenosis of infancy
• Visible intestinal peristalsis—e.g. distal small bowel or the large bowel
External genitalia
scrotum (e.g. recurrent orchitis of intra-abdominal testis will cause chronic
abdominal pain).
Palpation
abdomen.
Pre-requisites:
• The patient should lie supine completely relaxed
• Hips are flexed to 45° and knees flexed to 90°
Method of examination: The examiner should adhere to the measures
explained in Ch. 30 (p. 518)
Palpation consists of two techniques:
Superficial palpation
This is carried out for the clinician to orient himself with the patient’s abdomen
and also to give confidence to the patient about the ensuing process of deep
palpation. During this process, the clinician should determine the warm and
tender areas by watching the patient’s face, who will wince if there are tender
areas. This will help the clinician not to hurt the patient during deep palpation.
Firstly, the patient is asked to point the area of pain by his finger, which may
indicate the place of diseased viscera (finger pointing test).
• Local temperature
By the dorsum of the hand, any area of raise in local temperature over the
abdominal wall should be assessed. Increase in temperature may indicate local
inflammation
• Tenderness
Tenderness is the pain felt by the patient when the examiner presses gently
over the inflamed area. The examination for tenderness should start at the side
opposite to the site of pain, and the area of pain should be examined last. This is
mainly elicited by observing the patient’s face; pain makes the patient wince the
face
Some of the common areas of tenderness in chronic abdominal illnesses are:
• Tenderness at McBurney’s point—recurrent appendicitis (Ref Figs. 30.52A
and B)
In children, who are too young to cooperate, the child’s right hand itself is
used for palpation. The child’s hand is taken over the abdomen by the examiner,
and the child will withdraw and cry when tenderness is felt (Grainger’s method)
Deep palpation
This is done when the abdominal muscles are relaxed fully, i.e. during expiration
or in the pause between inspiration and expiration.
Intra-abdominal organs
• It is better to follow a sequence as a matter of routine, so that no area is left
unexamined
• It is better to start the palpation in the left iliac fossa, and go anticlockwise to
end in the genitalia (Fig. 31.27A):
• Next is to feel the left kidney, and spleen
• Next is to feel the liver, gallbladder, right kidney
• Next is to feel the right colon, urinary bladder and the left colon
• Next is to feel the aorta, para-aortic lymph nodes
• Next is to feel the groins
• Lastly, the external genitalia
FIGURE 31.27 Paths for examination of intra-abdominal organs—(A) Path
1; (B) Path 2.
If a swelling is palpable, more time should be spent in examining the same,

and follow the steps described in Chs. 9 and 33.
Alternatively, the organs can be palpated in the order given below (Fig.
31.27B):
1. Liver and spleen
2. Left and right kidneys
3. Aorta and para-aortic nodes
4. Right iliac fossa
5. Left iliac fossa
6. Groins
7. Suprapubic region and
8. Genitalia
In general, in adults, intra-abdominal organs are not palpable unless they
are distended, dilated or enlarged. Pancreas is not palpable even when it is
enlarged.
1. Stomach
Normal stomach is not palpable. The following pathologies can make the
stomach palpable.
• Congenital pyloric stenosis—felt like a smooth ball
• Carcinoma stomach—irregular mobile or fixed lump
• Abscess in the prepyloric region following perforation—tender lump
Gross dilatations of stomach with pent up secretions can be confirmed by
making sudden tapping movements on the area of the stomach or by shaking the
patient gently from side to side, and at the same time, keeping the examiner’s ear
on the abdominal wall or a stethoscope. A splashing sound can be heard, which
is called ‘succussion splash’ (Ref. Fig. 30.57). Making the patient drink some
quantity of water will help in eliciting this sign better.
2. Liver
Normal liver is palpable up to the age of 3 due to small capacity of the
abdomen compared to the size of the liver, whereas the liver is not palpable in
an adult.
• Enlargement of liver may indicate pathology (normal liver may also be
palpable in some individuals)
• Upward enlargement or shift (e.g. amoebic abscess or hydatid cyst in the
upper part of liver)
• Dropping of entire liver (e.g. visceroptosis)
• Pushing down of entire liver (e.g. subphrenic abscess, hydrothorax)
Method of palpation of liver
• Step 1: Liver enlargement is assessed by starting to feel its lower border. This
is done with the flat of the right hand kept on the abdomen in the right groin
and advanced upwards towards the right subcostal region lateral to the rectus
with the fingers pointing towards the ribs. The patient is asked to take deep
inspiration during the whole process (liver moves well with respiration), and
when the resistance is encountered, the fingers are pressed firmly inwards
and upwards and the lower border is assessed (Fig. 31.28A). The entire
lower border of the palpable edge should be assessed, which passes upwards
to cross the right hypochondrium to the epigastrium
• Step 2: The pulps of the fingers then should glide over the surface of the liver
till the fingers reach the costal margin, and above this point the liver cannot
be felt. The findings are noted
FIGURE 31.28A Method of palpation of liver.
Note
The same procedure can be done with both hands, left over the right for a
better feel of the liver, especially the obese (Fig. 31.28B). Trying to feel the
liver for enlargement by keeping the hand below the costal margin should be
avoided, as it will give the impression of ‘liver not felt’.
FIGURE 31.28B Palpating the liver with both hands.
When the liver is palpable, the following points are to be noted:

• Extent of enlargement—expressed in inches or centimeters or fingerbreadths
below right costal margin
• Lower edge of the liver (shape)
• Rounded (e.g. secondary deposits, cirrhosis of liver)
• Sharp (e.g. hepatitis)
• Surface of liver
• Smooth (e.g. hepatitis, abscess, hydatid cyst, haemangioma)
• Irregular or nodular (e.g. secondary deposits, regenerating nodules of
cirrhosis)
• Consistency
• Soft (e.g. hepatitis, fatty liver)
• Firm (e.g. cirrhosis, portal hypertension, hepatoma)
• Hard (e.g. secondary deposits)
• Tenderness (e.g. amoebic hepatitis)
3. Gallbladder
Normal gallbladder is not palpable, as it lies well concealed by the lower
border of the liver.
• Distended gallbladder (e.g. mucocoele, empyema and carcinoma of
periampullary region and head of pancreas)
• Contracted gallbladder (e.g. chronic calculous cholecystitis)
• Hard gallbladder (e.g. carcinoma of gallbladder, porcelain gallbladder)
Courvoisier’s law: In a jaundiced patient, if the gallbladder is palpably
enlarged, the obstruction is not due to stones (because in a calculous disease, the
gallbladder remains contracted due to repeated attacks of inflammation, and does
not distend), but due to malignancy of distal biliary system (Figs. 31.29A and
B).
FIGURE 31.29 Courvoisier"s law—(A) Obstructive tumour. (B) Obstructive
gallstone.
Exceptions to Courvoisier’s law are:

• Double stones—stone in the CBD and stone in the cystic duct
• Pancreatic calculus or gallstone obstructing the ampulla of Vater
• Mucocoele of gallbladder due to a stone obstructing the cystic duct
Method of palpation of gallbladder
The gallbladder is palpated in the same way as the liver.
When the gallbladder is palpable, it is felt as a firm, smooth, globular
swelling, just lateral to the rectus abdominis near the tip of the ninth cartilage. It
moves well with respiration, along with the liver. The upper border of the
gallbladder cannot be felt and it is not bimanually palpable and lies just beneath
the anterior abdominal wall—distinguishing feature from right renal swelling.
4. Spleen
A normal spleen is not palpable, as it lies nicely tucked inside the ribcage
more posteriorly. Only when it is enlarged two to three times, it becomes
palpable.
• Splenomegaly (e.g. portal hypertension, haemolytic disorders)
The enlargement is superio-posterior before it is felt below the left costal
margin. This enlargement generally is towards the right iliac fossa. The examiner
should place his left hand over the lowermost part of the rib cage
posterolaterally, and the right hand below the costal margin.
Methods of palpation of spleen
• Method 1: As the patient is asked to take deep inspiration, the fingers of the
right hand are kept parallel to the left costal margin and the enlarged spleen
might hit the lateral border of the index finger (Fig. 31.30A)
• Method 2: As the patient is asked to take deep inspiration, the fingers of the
right hand are kept in the right iliac fossa and advanced towards the left
hypochondrium (Fig. 31.30B). In the process the spleen may be felt. If not,
the fingers are pressed in deeply beneath the costal margin. If the spleen is
not palpated, and if it is expected to be enlarged, from the history, it is better
to examine the patient in right semirecumbent position (Fig. 31.30C)
• Method 3: The left hand is placed over the lateral aspect of the left costal
margin and certain amount of even forward thrust is exerted, and in this
process the skin and subcutaneous tissues below the costal margin are pushed
downwards and forwards. The fingers of the right hand are pressed in deeply
beneath the costal margin to feel the spleen (Fig. 31.30D)
FIGURE 31.30A Palpation of spleen in supine position.
FIGURE 31.30B Paths of examination of liver and spleen.
FIGURE 31.30C Method of palpating the spleen in semirecumbent
position.

FIGURE 31.30D Method of palpating the spleen with both hands.
Note
If the spleen is not palpated, but if it is expected to be enlarged from the
history elicited, it is better to examine the patient in right semi-recumbent
position.
When the spleen is palpable, it is felt as a firm swelling with smooth, rounded
borders with notches, which is diagnostic. When there is considerable
splenomegaly, it appears as a firm swelling, moving well with inspiration, dull to
percussion, not bimanually palpable, and the upper border cannot be felt, but
with a notch in the lower border. (Renal swellings are bimanually palpable, and
one can reach the upper border by inserting the fingers between the costal
margin and the swelling but no notch is felt).
Note
Even if after all the attempts fail to feel the spleen and its borders riding over
the fingers, it cannot be concluded safely that the spleen is not enlarged.
Nonpalpability is not against splenic enlargement since the spleen can be felt
below the costal margin only when it is enlarged two to three times its normal
size.
5. Pancreas
Pancreas is totally inaccessible to physical examination even in its diseased
state and also when it is enlarged. The diseases are reflected indirectly in some
situations, e.g. obstructive jaundice caused by obstruction by carcinoma of the
pancreatic head. Lesions of the body and tail are not accessible to physical
examination and indirect evidences are also not possible.
6. Small bowel
Normal small bowel is not palpable. Small bowel may be felt only when it is
dilated due to obstructions, and they give a very vague soft feel, mostly in the
central abdomen.
7. Large bowel
Normal large bowel is not palpable. Distended large bowel due to
obstructions can be seen as fullness in the flanks depending on the level of
obstruction, but whatever is the level of obstruction, caecal distension is always
present. This is seen as fullness in the right iliac fossa and can be felt with a
gurgling on deep palpation.
It may be possible to feel a mass in the line of the colon, which may be a
growth or a faecal mass. Faecal mass is indentable by the examining fingers
whereas a growth cannot be indented. On second examination, the faecal mass
disappears whereas a growth stays at its place.
Mass in the region of transverse colon is mobile in the vertical direction. This
needs to be differentiated from a pyloric lump. Gurgling to the left of the lump is
due to pyloric stenosis (direction of flow—left to right) and to the right of the
lump is due to stenotic lesion of the transverse colon (direction of flow—right to
left).
8. Left kidney
Method of palpation of the left kidney
The right hand is placed anteriorly on the left lumbar region and the left hand
posteriorly in the left loin (see Ch. 37). The patient is asked to take deep breaths
and both the hands are brought together (bimanual palpation) to attempt to
palpate the left kidney (Ref Fig. 37.53). Normal kidney is not palpable. When
the left kidney is palpable, it is felt as a rounded firm swelling. If it can be
moved or tossed antero posteriorly and vice versa, and it is called ‘ballottement’
(to be differentiated from splenic enlargement).
9. Right kidney
The right kidney is felt the same way for the left. The examiner should place
the right hand horizontally in the right lumbar region anteriorly and the left hand
posteriorly. The patient is asked to take deep breaths and both the hands are
brought together (Ref Fig. 37.54) (Bimanual palpation) to attempt to palpate the
right kidney. Normal right kidney may be palpable in thin individuals. When the
right kidney is palpable, it is felt as a smooth rounded firm swelling. If it can be
moved antero posteriorly and vice versa, it is called ‘ballottement’ (Ch. 37).
Note
Normally kidneys are not palpable.
10. Urinary bladder

Normal urinary bladder is not palpable.
Urinary bladder becomes palpable, when it fills up. When it is full, it is felt as
a smooth oval-shaped swelling in the suprapubic region, and the dome may
reach the level of the umbilicus. It will not be possible to feel its lower border
(cannot get below the swelling). Application of pressure over the swelling gives
the patient a desire to micturate. In women, this needs to be differentiated from
the uterus or uterine swellings such as the fibroid.
11. Aorta and para-aortic region
In most adults the aorta is not palpable.
Aorta may be palpable in thin individuals especially with marked lumbar
lordosis. It is felt with the tips of the extended fingers of both hands, held side by
side in the midline. Lymph nodes in the para-aortic regions are palpable only
when the enlargement is considerable.
Lumps
Chronic abdominal pathologies can present in the form of lumps or swellings,
and they should be examined in the manner explained in the Chs. 9 and 33.
Hernial sites
It should never be forgotten to examine the groins, as there may be associated
herniae.
External genitalia
It is essential to palpate the testes in a male and record the findings (e.g. para-
aortic lymph node enlargement of testicular malignancy).
Percussion
the note is dull. This method is useful in confirming the presence of enlarged
liver, spleen and fluid in the peritoneal cavity (ascites).
Percussing the liver

When the liver is palpably enlarged, it can be confirmed by percussion.
Percussion should start considerably below the lower border of the liver and
move upwards towards the costal margin. Area of the enlarged liver gives a dull
note. The upper border of the liver can be determined only by percussion (not by
palpation as it hides in the thoracic cage). The percussion should start at the
fourth intercostal space (where it is resonant due to the presence of air-filled
lung) in the mid-axillary line and proceeded downwards. Once the upper border
of the liver is reached, the note becomes dull, usually at the fifth intercostal
space (Fig. 31.31).
FIGURE 31.31 Percussion for hepatomegaly.
Percussing the spleen

The dullness on percussion due to spleen is elicited in the posterior axillary line
on the left side from the 9th to 11th ribs (Fig. 31.32).
FIGURE 31.32 Percussion for splenomegaly.
Percussion for the presence for fluid in the peritoneal cavity

When the fluid is in large quantities (e.g. tense ascites) and encloses the
intestines, the entire abdomen is dull to percussion. This can be elicited by
tapping one flank with the right index finger and feeling the vibrations on the
other flank with the left hand (fluid thrill). The patient’s or a colleague’s hand
should be kept at the midline to obstruct the vibrations transmitted by the
subcutaneous fat (Fig. 31.33).
FIGURE 31.33 Eliciting fluid thrill.
When the fluid is in moderate quantities (e.g. moderate ascites), it gravitates

down to the flanks making the resonance present only in the central part of the
abdomen due to the floating intestines. Change in position of the patient, shifts
the resonant area in accordance with the floating intestines. Shifting of this fluid
is confirmed by percussion, and the method of percussion is to start at the
midline and proceed to one flank till the note is dull. Then the patient is asked to
turn to the other side by 45° and wait for some time giving time for the intestines
to float to the side of percussion. The area where it was dull to percussion will
become resonant. This is called ‘shifting dullness’. The same process is repeated
on the other side also (Fig. 30.55).
Note
It should be remembered that the percussing fingers be kept undisturbed, till
the process is completed.
When the fluid is in very small quantities (e.g. minimal ascites), it can be
confirmed by making the patient adopt knee–elbow position. After waiting for a
few minutes allowing the fluid to gravitate down, percussing the central
abdomen, will demonstrate dullness. This is called ‘puddle sign’ (Fig. 31.34).
FIGURE 31.34 Eliciting puddle sign.
Note
An ovarian cyst large enough to touch the anterior abdominal wall also gives
the fluid thrill, but shifting dullness is characteristically absent. Encysted
ascites also exhibits the same findings as a large ovarian cyst.
The common causes of ascites are portal hypertension, tuberculous ascites,
peritonitis, malignant ascites and congestive cardiac failure.
Auscultation
Auscultation has a very limited application in chronic abdominal conditions.
In general, the abdomen is auscultated:
• In the midline at and above the umbilicus—for bruits in the abdominal aorta
• Just lateral to midline above the umbilicus—for bruits in the renal arteries
• Over the liver—for rub
• Over the spleen—for rub and hum*
Dilated stomach: This can be identified by a combination of auscultation and
percussion ( auscultopercussion). The bell of the stethoscope is placed below
and to the left of the xiphoid process and held with the left hand. Gentle radial
strokes are made with the fingers of the right hand. The resonant note is heard in
the region of stomach and it changes beyond that. This point is marked. Several
such points are made and joining all of them will give the greater curvature of
the stomach (Fig. 31.35).
FIGURE 31.35 Eliciting auscultopercussion.

Pelvis
Pelvic organs can be examined from above (per abdomen) and below (rectal and
vaginal examinations).
Rectal examination
A digital examination of the rectum is mandatory during the examination of the
abdomen. The following are to be noted:
1) Perianal skin pathologies—fistula in ano (e.g. Crohn’s disease)
2) Integrity and nature of rectal mucosa (e.g. growths of anus and rectum)
3) Tip of the examining finger for blood and mucus (e.g. growths of anus and
rectum)
4) Proctoscopy for haemorrhoids (e.g. part of portal hypertension and rectal
malignancies) and growth
Vaginal examination
In women, vaginal examination has to be carried out, and the following are to be
noted:
1) Assessment of uterus and cervix (e.g. for malignancies)
2) Fornices (e.g. ovarian tumours, Krukenburg tumours)
3) Pouch of Douglas for pelvic metastases
Lymphatic system
detail, e.g. tuberculosis and lymphoma. Examination of the liver and spleen
Troisier’s sign: This is the enlargement of the left supraclavicular lymph
nodes (Virchow’s nodes) secondary to gastric (especially of the lesser curvature),
testicular or ovarian malignancies. This is a very important examination of
chronic abdominal illnesses which every student of surgery should remember
(Fig. 31.36).
FIGURE 31.36 Troisier’s sign.
Other systems
Examination of other systems becomes necessary as the symptoms mimic those
of abdominal pathologies. They are enumerated in Table 31.5.
TABLE 31.5
Extra Abdominal Causes of Abdominal Symptoms
Chest Basal pleurisy, pneumonia, unstable angina pectoris, Epigastric pain sometimes with one or two
myocardial ischaemia evacuations
Middle and lower lobar pneumonia Right hypochondrial pain
Back, loin, Pott’s disease Epigastric pain
spine
*
Kenawy’s sign (splenic enlargement with portal hypertension): The bell of the stethoscope is placed below
the xiphoid process and the patient is asked to take a deep breath. A venous hum is heard since there is
engorgement of the splenic vein as the spleen is compressed during inspiration.
CHAPTER 32
Abdominal injuries
N. Mohan
CHAPTER OUTLINE
32.2. Injuries of abdominal organs 553
• Injuries of liver 553
• Injuries of spleen 554
• Injuries of mesentery 555
• Injuries of duodenum 555
• Injuries of small intestine 556
• Injuries of large intestine 556
32.3. Symptoms of injuries of abdominal organs 556
• General 558
• Abdomen 558
• Pelvis 559
32.1 Introduction
Abdominal injuries can be of two varieties. They are:
• Closed injuries (caused by blunt injuries).
• Open injuries (caused by penetrating or stab injuries).
Closed injuries
Caused by a blunt force exerted suddenly on the abdomen, such as
• fall from a height
• blow with a fist
• injuries inflicted by heavy weapons such as crowbars, poles, sticks
• run over injuries in road traffic accidents; and
• hitting against the steering wheel during sudden deceleration or braking of a
speeding vehicle (in the absence of seat belt).
leading to compression of intra-abdominal organs against the vertebral column
causing rupture of
• solid organs
• hollow organs
• mesentery
• detachment of gut from the mesentery and
• contusion of abdominal wall.
Open injuries
• Caused by any sharp instrument such as knife, flying objects like bullets,
missiles, pieces of wood or glass.
• The incriminating agents enter the abdominal cavity taking with them some
infection resulting in peritonitis.
• The points of entry and exit of the agent will indicate the direction and the
possible organs injured.
• Hollow organs may perforate and infect the peritoneal cavity (due to
contamination by the contents of the organ—faeces, urine, intestinal or
gastric contents), or bleed (either into the organ or outside or both).
• Solid organs cause haemorrhage (inside the organ or outside or both), and
heavy bleeding can cause shock and sometimes death.
• General features
• Symptoms: Weakness, clouding of thoughts and speech, air hunger,
restlessness, decreased or absent urine output.
• Signs: Pallor, tachycardia, hypotension, subnormal temperature.
• Local features (depends on the organ involved and the severity of damage).
32.2 Injuries of abdominal organs
Injuries of liver
The liver ranks high on the list of intra-abdominal organs involved by injury
• Blunt injuries are more common than the penetrating injuries due to increase
in motor traffic moving at high speeds, and are associated with fracture of
lower ribs on the right side. The dome of the liver is involved with anterior–
posterior tears, more on the right lobe (7:1).
• Spontaneous rupture of liver is seen in
• primary carcinoma in adults and
• trauma during birth in children (postmature babies) being delivered per
vaginum.
Liver injuries (Fig. 32.1) are classified into three categories. They are as
follows:
• Transcapsular (blood and bile will seep into the peritoneal cavity).
• Subcapsular (collection of blood between the capsule and the liver
parenchyma mostly on the superior surface of liver).
• Central (interruption of liver parenchyma leading to intrahepatic haematoma,
abscess and haemobilia).
FIGURE 32.1 Liver injuries.
• Transcapsular: Symptoms and signs of shock and peritoneal irritation (pain
right upper abdomen with reference to the right shoulder, guarding and
rigidity of the right hypochondrium, absent bowel sounds, shifting dullness).
• Subcapsular: Local tenderness and increase in area of liver dullness.
• Central: Signs of shock may be present with haemobilia and haematemesis.
• Plain X-ray chest will demonstrate fracture of lower ribs on the right side.
• Plain X-ray abdomen may show haziness in the area of the liver with
elevation of right dome of diaphragm.
• CT (Ref. Fig. 27.3) and MRI are useful in localizing the damaged areas of
liver and collections of blood or bile.
• Peritoneal tap may be useful in identifying bile leaks.
• Colloidal gold Au198 or Technetium–sulphur colloid Tc99mscans are useful
during active bleeding.
Treatment
• Correction of shock.
• No surgical intervention is needed for small injuries.
• Early surgical intervention, sometimes amounting to hepatectomy, is needed
for large injuries associated with vascular or biliary tract injuries.
Injuries of spleen
• Spleen is the intra-abdominal organ most frequently injured by blunt trauma,
usually by thoraco abdominal injuries associated with fractures of left lower
ribs.
• The causes of splenic injuries are as follows:
• Blunt injuries of lower chest and abdomen (e.g., automobile accidents—
may be associated with rib fractures, lung injuries, fracture of spine, intra-
abdominal organs).
• Transabdominal and transthoracic penetrating injuries (e.g., gunshot or
knife injuries—may be associated with injuries to left kidney, colon,
pancreas, vascular structures of mesentery).
• Operative injuries (e.g., during operations on adjacent viscera—
gastrectomy).
• Spontaneous rupture or minor trauma (e.g., enlarged spleen of malaria).
• Splenic injuries may be
• Linear or stellate lacerations (due to excessive traction on the capsule
during operations).
• Capsular tears (due to excessive traction on the capsule during operations).
• Subcapsular haematoma (due to excessive traction on the capsule during
operations).
• Puncture wounds (caused by penetrating injuries).
• Intrasplenic haematomas (caused by penetrating injuries).
• Rupture of parenchyma (due to extreme friability and vascularity of the
organ).
The clinical presentation is of three types. These are
1. Acute: Immediate presentation of symptoms.
2. Delayed: A quiescent period of 7 days to less than 2 weeks, between the
injury and intraperitoneal bleeding (latent period of Baudet), probably related
to a temporary tamponade of a minor laceration or the presence of a slowly
enlarging subcapsular haematoma, which eventually ruptures.
3. Occult: Mild symptoms caused by rupture of organized intrasplenic or
parasplenic haematoma.
Symptoms
• Symptoms and signs of shock and peritoneal irritation.
Signs
• Pain left upper abdomen with reference to the left shoulder (Kher’s sign).
• Guarding and rigidity of the left hypochondrium.
• Absent bowel sounds.
• No shifting dullness.
• A mass of percussible area of fixed dullness in the left hypochondrium
(Ballance’s sign).
• Lacerations may be seen on the left lower chest (Ref. Fig. 27.1).
• X-Ray Chest will demonstrate fracture of ribs on the left side.
• Plain X-ray abdomen may show
• Haziness in the area of the spleen.
• Elevated immobile left dome of diaphragm.
• Medial displacement of gastric shadow with indentation
• Obliteration of psoas shadow.
• Widening of space between splenic flexure and the properitoneal pad of fat.
• CT (Fig. 32.2) and MRI are useful in localizing the damaged areas of spleen
and collections of blood.
• Peritoneal tap may be useful in identifying blood in the peritoneal cavity.
FIGURE 32.2 Splenic haematoma Source: (Courtesy Bharat scans).
Treatment
• Once the diagnosis is made, the operation should not be delayed.
• Splenectomy is the recommended treatment, regardless of the type and the
extent of the injury.
• Minor injuries can be treated by splenorrhaphy.
Injuries of mesentery
• Mesentery consists of its arteries and veins and they may be injured by either
penetrating or nonpenetrating abdominal trauma.
• In most cases, associated organ injuries are found.
• Isolated injury to mesenteric vessels is rare.
Symptoms
• Depending on the size of the vessel lacerated, the rapidity of bleeding and
associated organ injury, the patient will present with signs of shock,
abdominal pain and distension.
Signs
• On examination, tenderness is marked.
Note
When the bleeding occurs within the layers of mesentery, the clinical signs
evolve slowly and the viability of the bowel is threatened.
• Plain X-rays may show air under the diaphragm when the bowel is perforated
by the injury.
• Peritoneal tap may be useful in establishing the bleeding.
Treatment
• Repair of the torn mesentery is required.
• Resection and anastomosis is required for nonviable intestine.
Injuries of duodenum
• Duodenum can be injured both by penetrating and nonpenetrating abdominal
trauma.
• The duodenum can rupture
• intraperitoneally and cause immediate chemical irritation of the
peritoneum due to the highly alkaline duodenal content; and
• retroperitoneally (more common with blunt trauma such as steering wheel
injuries).
• Intraperitoneal rupture
• Abdominal pain, fever and distension with vomiting.
• Examination shows marked tenderness in the upper abdomen and later
signs of generalized peritonitis.
• Retroperitoneal rupture
• Pain in the epigastrium and back, with pronounced vomiting.
• Testicular pain is a common feature of retroperitoneal rupture of
duodenum.
• Plain X-ray of abdomen may show air under the domes of diaphragm
(intraperitoneal rupture) or large accumulation of air above the right kidney
(retroperitoneal rupture). Diagnostic accuracy can be increased by injecting
air in the Levine’s tube to increase the air collections. Water-soluble dye
injections in the tube can make the diagnosis more precise.
• CT with contrast is conclusive.
• Paracentesis may show bile-stained fluid, if the rupture is intraperitoneal.
Treatment
• Simple suturing may be adequate in many cases.
• Supplementary gastroenterostomy is required for large tears.
• Rarely, even a pancreato-duodenectomy may be necessary for extensive
trauma involving the periampullary region.
Injuries of small intestine

• Injuries to the small intestine are more common than injuries to the duodenum
and large intestine, the usual mechanism being the blunt trauma crushing the
bowel against the vertebral column, more commonly the duodeno—jejunal
flexure and the ileocecal junction, the fixed parts.
• Blunt injuries cause slow necrosis of bowel and leak occurs late.
• Signs and symptoms develop late—2 to 3 days later, depending on the size of
the damage and leak of contents.
• Penetrating injuries can also cause small bowel trauma, but less commonly,
probably due to its sliding away from a knife because of its great mobility.
• Associated mesenteric tears are common.
• Abdominal pain, distension and vomiting.
• Tenderness and guarding are pronounced around the damaged bowel and the
patient may point it (Pointing sign).
• Plain X rays may show air under the domes of the diaphragm.
• Paracentesis will show bile-stained fluid.
Treatment
• Simple suturing is done for simple tears.
• Resections are required for large tears with nonviable bowel.
• Peritoneal toileting is mandatory under cover of antibiotics.
Injuries of large intestine

• Large bowel injuries can be caused by penetrating and nonpenetrating
injuries.
• Ruptures may be
• extraperitoneal, for ascending and descending colon injuries, whereas
• intraperitoneal, when the injuries are of transverse and sigmoid colons.
• Patient develops septic complications quickly as the fluid leak is large, faecal
and infected.
• Delayed presentation is not uncommon as in small bowel injuries.
• Abdominal pain, vomiting and distension.
• High-grade fever occurs due to faecal contamination.
• Clinical examination will show signs of peritonitis.
• Plain X-rays may show air under the domes of the diaphragm (intraperitoneal
ruptures).
• Paracentesis will show feculent fluid.
Treatment
• Early laparotomy is required.
• Closure of tears with proximal diversion is necessary.
• Peritoneal toileting is mandatory under cover of broad spectrum antibiotics.
Injuries of kidneys and urinary bladder

(Discussed in Chapter 37, Urinary System)
32.3 Symptoms of injuries of abdominal organs

• Abdominal pain
• Passage of blood in vomitus (haematemesis)
• Passage of blood per rectum (melena)
• Passage of blood in urine
• Abdominal distension
• Symptoms of shock
Before questioning the patient or the relatives, the patient’s general condition
should be assessed.
• If the patient is in shock, should be mobilized to the intensive care unit for
immediate resuscitation and no time should be wasted in eliciting history.
• If the patient is stable, the history can be elicited.
• Cases of blunt injury of the abdomen should always be admitted in the
hospital and observed.
Eliciting history
The patient or the attendants should be allowed to describe the accident or
trauma in their own words. The following details should be elicited, by direct
questioning, if not already told by the patient. The relevant questions should
relate to the following:
• Type of injury: Penetrating (e.g., gunshot or knife injury) or nonpenetrating
injury (e.g., hit by a blow).
• Mechanism of injury (e.g., fall from a height, deceleration injury).
• Time of injury (e.g., time elapsed has relevance).
Abdominal pain
• Abdominal pain: Where does it hurt on the abdomen and point it with one
finger?
The patient should be asked to point the area of pain with one finger
(pointing sign) and this has great relevance in diagnosis (e.g., right
hypochondrial pain in liver injury).
• Radiation of pain: Does the pain radiate to any specific area?
Radiation of abdominal pain is characteristic in certain situations (e.g., right
shoulder pain in superior surface of liver injury, testicular pain in
retroperitoneal rupture of duodenum).
Passage of blood in vomitus (haematemesis)

• Vomiting: Has the patient vomited or has been continuously vomiting since
the incident?
Vomiting may indicate peritoneal irritation or peritonitis (e.g., bowel injury)
and persistent vomiting may indicate increasing soiling of the peritoneum
(e.g., large leaks causing peritonitis). Retroperitoneal ruptures cause
paralytic ileus and cause abdominal distension and vomiting.
• Haematemesis: Does the vomitus contain blood and if so in what quantities?
When was the last vomit?
Haematemesis may indicate hollow organ injury (e.g., gastric injury) and
large quantities of bleed may indicate major vessel injury (e.g., avulsion of
major vessels in the organ). The period between the last vomit and the
time of examination is important, as longer interval may indicate control
of bleeding.
Passage of blood per rectum (melena)

• Melena: Has the patient passed blood per rectum and if so what are the
colour and quantity? When was the last bleed?
Passing of blood after abdominal injury indicates lower gastrointestinal injury
(e.g., mesenteric, small bowel or large bowel injury), and this should alert the
clinician. Quantity of the bleed is not very relevant as the melena seen outside is
only an indication of the nature of injury and there may be a large quantity of
blood in the bowel. The period between the last bleed and the time of
examination is important, as longer interval may indicate control of bleeding.
Micturition and passage of blood in urine

• Micturition: Has the patient passed urine after the accident? Does he have
the desire to pass urine or not?
Passing of clear urine indicates integrity of the urinary system. If the patient
had not passed urine after the accident, if may indicate hypotension, or
extravasation of urine through injured bladder or urethra. More the time
interval more is the possibility. There may be intense desire, but not able to
pass urine in cases of extraperitoneal rupture of urinary bladder or
membranous urethra. Loss of desire to pass urine may indicate an empty
bladder, a symptom of hypovolemia or renal failure.
• Haematuria: Has the patient passed blood in the urine or frank blood per
urethra?
Passing of blood either separately or mixed with urine is a matter of concern,
as the possibility of urethral or bladder rupture becomes pronounced.
• Abdominal distension: Has the abdomen distended since the accident and if so,
is it progressive?
Abdominal distension may indicate leakage of contents of the bowel or urine
(e.g., bowel injury, intraperitoneal rupture of urinary bladder) or even paralytic
ileus (e.g., retroperitoneal rupture of duodenum).
Symptoms of shockl
Shock: Does or did the patient have any symptom related to shock?
Since the time of the accident, if the patient has had any symptom like
dizziness, loss of consciousness, which was managed by first aid, this point is to
be noted. This may be an indication of the severity of the trauma and damage to
the intra-abdominal organ (e.g., delayed presentation of symptoms as in splenic
injuries).

• Association of fever: Is or was there fever after the accident? Association
offever mayindicate an infection (e.g., peritonitis after bowel injury)
• Treatment for the injury: Has any treatment (first aid or surgical) been given
to the accident victim? The information of any treatment received at the
accident site or in a nearby hospital or clinic will give more information and
records should be obtained for further management and for medico-legal
purposes (e.g., suturing of a wound on the abdominal wall).
• Past history: Was there any illness in the past, which required any surgical
treatment? If the patient had any illness in the past, which required organ
removal (e.g., splenectomy or nephrectomy for previous accident or illness),
will help in the diagnosis. If the patient has been on medication (e.g., anti-
epileptics) in the past, the examiner will find it easy to relate this to the cause
and nature of injury (e.g., fall from a height).
match the situation (e.g., family problems, property matters etc., as shooting
incidents are not uncommon by relatives).
General
• General appearance
• Lying quiet (e.g., as in peritonitis)
• Restlessness (e.g., intraperitoneal haemorrhage)
• Air hunger (e.g., electrolyte disturbances, hypovolemia)
• Severe pain on respiratory movements (e.g., fracture ribs)
• Eyes
• Sunken eyes may indicate dehydration.
• Jaundice may be an indicator of hemobilia.
• Pallor (e.g., severe blood loss).
• Skin
• Dry skin may indicate dehydration and undernutrition.
• Oedema of skin may indicate local injuries like extravasation of blood,
urine, fractures
• Tachycardia, low volume pulse may indicate hypovolemia.
• Hypotension may indicate hypovolemia.
• Elevated temperature may indicate associated infection.
• Examination of head, neck and thorax
• Associated injuries should be evaluated (see Chapters 19 and 27).
Abdomen
exposing the genitalia, the inguinal and femoral areas for complete examination.
Privacy of the patient must be assured, and a nurse should be kept by the side of
the patient, especially when the patient is a female.
The clinical examination of abdomen in acute emergencies, consists of
• Inspection
• Palpation
• Percussion
• Auscultation
Inspection
Shape Distensions of abdomen have various characteristics depending on the
trauma of the intra-abdominal organ. Normal shape of the abdomen is flat.
• Scaphoid shape: Abdomen is scaphoid (boat-like) in thin persons or in
emaciated individuals and indicate that there is no large leaks (blood or
intestinal fluid).
• Generalized distension: This is generally due to leakage of large quantities
of fluid or paralytic ileus in late stages of peritonitis (Ref. Fig. 30.41).
• Peripheral distension: Both flanks may show distension when the colon is
distended, due to low rectal injuries or collection fluid or blood in the
pelvis. One of the flanks may be distended if there is injury in that area
(e.g., right flank distension in liver and duodenal injury) (Ref. Fig. 30.44).
Movements of the abdominal wall Respiratory excursions
In normal individuals, the abdominal wall moves regularly and smoothly
with respiration. When the movements of the abdominal wall are normal, it
indicates the absence of any gross collections.
• Generalized restriction is seen when the distension is generalized (e.g.,
peritonitis, hemoperitoneum).
• Localized restriction of movements are seen when the injury is localized
(e.g., liver injury).
Skin The skin has to be given special attention for colour, bruises, abrasions
and lacerations, tyre or belt marks, puncture wounds and scars.
• Colour: Red erythematous skin (e.g., hemoperitoneum or subcutaneous
extravasation of blood)
• Bruises, abrasions and lacerations: These marks may indicate the nature
of injury (bruises and abrasions—fall from a height, lacerations in injuries
may indicate a hit by an object).
• Tyre or seat belt marks: Runover accidents may indicate tyre marks of the
vehicle and seat belt marks indicate deceleration injuries. Impressions
made by clothes of the victim will indicate the nature of injury (London’s
sign).
• Puncture wounds: Puncture wounds like gunshot wounds indicate the
points of entry and exit (entry point appears more charred than the exit
point by the heat of the missile).
External genitalia and perineum It is essential to inspect the genitalia, and
ensure that the testes are in the scrotum, and the perineum should be
examined for injuries (e.g., extravasation of urine in urethral injuries).
Palpation
abdomen in trauma.
explained in Chapter 31.
Local temperature By the dorsum of the hand, any area of rise in local
temperature over the abdominal wall should be assessed. Increase in
temperature may indicate fresh bleeding in that area or infection or
inflammation.
Tenderness Tenderness is the pain felt by the patient when the examiner
presses over the inflamed area. The examination for tenderness should start
at the opposite side of the site of pain, and the area of pain should be
examined last. This is mainly elicited by observing the patient’s face; as pain
makes him wince his face. When the patient is asked to point the area of pain
by his finger and if it coincides with the point of tenderness, it should
indicate the place of injured viscera (finger pointing test).
Guarding and rigidity Localized guarding and rigidity are elicited in localized
collections of blood or over-injured viscera (e.g., liver injury) or in localized
peritonitis.
Intra-abdominal organs It is better to follow a sequence as a matter of
routine, so that no area is left unexamined (See Ch. 31). In a case of
abdominal trauma, the intra-abdominal organs are not palpable unless
they are distended, dilated or enlarged. Pancreas is not palpable even when
it is enlarged.
If a swelling is palpable, more time should be spent in examining the same,
and record the findings.
Lumps
In the process of palpation of abdomen, any lump felt should be examined in
the manner explained in the Chapters 9 and 33.
Percussion
the note is dull. This method is useful in confirming the presence of
• enlarged liver
• enlarged spleen
• distended urinary bladder and
• fluid or gas in the peritoneal cavity (hemoperitoneum or peritonitis).
Shifting dullness may be elicited when the fluid in the peritoneal fluid is in a
liquid state (e.g., intestinal fluid, fresh blood). When the blood is clotted
‘shifting dullness’ cannot be elicited. (e.g., Balance’s sign on the left side in
splenic injuries).
Auscultation
Bowel sounds are heard normally initially in any case of abdominal trauma, but
become absent at later stages (e.g., peritonitis, intraperitoneal haemorrhage,
retroperitoneal haemorrhage) and sometimes, intestinal sounds may be heard in
the chest (e.g., rupture diaphragm).
Pelvis
Rectal examination
Examination of the rectum is mandatory in the evaluation of abdominal trauma.
The following are to be noted
• Perianal skin oedema (e.g., urinary extravasation in urethral injuries)
• Integrity and nature of rectal mucosa (e.g., injuries of rectum)
• Tip of the examining finger for blood and mucus (e.g., injuries of rectum
and lower GIT)
• Proctoscopy (e.g., injuries of rectum and anus)
Vaginal examination
noted
• Assessment of uterus and cervix (e.g., injuries of uterus and cervix)
• Fornices (e.g., collection of fluid and blood)
• Pouch of Douglas (e.g., collection of fluid and blood)
Colpocentesis is useful.
Other systems
Examination of other systems becomes necessary especially in
thoracoabdominal, pelvic and spinal injuries, as a patient may have multiple
injuries in various parts of the body (see Ch. 50). They are enumerated in Table
32.1.
TABLE 32.1
Injuries of Organs Other Than Abdomen, and the Clinical
Presentations
Lesion Clinical Presentation

Region
Presenting symptoms Signs on examination
Chest Fracture ribs, Pain at fracture site or on Tenderness in the fracture area, shift of the trachea
hemothorax, respiratory movements. and apex beat towards other side, local crepitus,
Epigastric pain sometimes may pleural rub, alteration of breath sounds
predominate
Rupture of Respiratory embarrassment Shift of trachea and apex beat towards the other
diaphragm side, alteration of breath sounds, presence of
intestinal sounds in the chest
Back, loin, Spine fracture Pain on movements of spine Local tenderness
spine
Nervous Transection of Inability to use lower limbs Loss of power in lower limbs (paraplegia)
system spinal cord
Pelvis Fracture of Pain on movements of pelvis and Tenderness on compression, oedema of genitalia in
pelvic bones haematuria extraperitoneal ruptures of urinary bladder
CHAPTER 33
Abdominal lumps
N. Mohan
CHAPTER OUTLINE
33.2. Lumps of abdominal wall 561
• Cold abscess 561
33.3. Lumps in the right hypochondrium 561
• Hepatomegaly 561
• Amoebic hepatitis/liver abscess 561
• Pyogenic abscess of liver 562
• Hydatid cyst of liver 562
• Cysts of liver 563
• Benign liver tumours 564
• Hepatoblastoma 564
• Hepatocellular carcinoma 564
• Metastatic liver disease 565
• Cirrhosis of liver 565
• Mucocoele/pyocoele of gallbladder 566
• Carcinoma of gallbladder 566
33.4. Lumps in the left hypochondrium 567
• Splenomegaly 567
• Infections of spleen 568
• Rheumatoid arthritis and Felty’s syndrome 568
• Portal hypertension 569
• Haemoglobinopathies 570
• Idiopathic thrombocytopenic purpura 570
• Porphyrias 571
• Leukaemias and myeloproliferative disorders 571
• Lymphatic malignancies 571
• Splenic cyst and splenic abscess 572
33.5. Lumps in the epigastrium 572
• Gastric malignancy 572
• Congenital pyloric stenosis 573
• Malignancy of transverse colon 574
• Intussusception of colon 574
• Tuberculosis of omentum 574
• Solid tumours of omentum 574
• Pancreatic pseudocyst 575
• Adrenal tumours 575
• Aortic aneurysm 576
• Para aortic lymphadenopathy 576
33.6. Lumps in the lumbar regions 577
• Lumbar abscess 577
• Lumbar hernia 577
33.7. Lumps in the umbilical region 577
• Umbilical granuloma/enterotoma 577
• Rectus sheath haematoma 578
• Desmoid tumour 578
• Small bowel tumours 579
• Mesenteric cysts 579
• Retroperitoneal swellings 580
33.8. Lumps in the iliac fossae 580
• Appendicular mass/abscess 580
• Ileocaecal tuberculosis 582
• Amoeboma 582
• Actinomycosis 582
• Carcinoma caecum 582
• Solitary caecal diverticulitis 583
• Iliac lymphadenopathies 583
• Abscess of iliopsoas sheath 583
• Chondrosarcoma of iliac bone 584
• Pelvic abscess 584
33.9. Lumps in the hypogastrium 585
• Abdomen 586
• Pelvis 589
33.1 Introduction
Clinical evaluation of abdominal lumps becomes easy, if the examiner is
thorough with the anatomy of the abdomen and its structures. The abdomen is
divided into nine arbitrary regions and the genitalia as the tenth, for convenience
of communication (Ref Fig. 30.36). These divisions will help in localizing the
lumps.
Abdominal lumps are classified based on their anatomical location. It is
necessary to ascertain
• its geographical location (area or region of the abdomen)
• its presence either outside (extra-abdominal) or inside (intra-abdominal) the
abdominal cavity and
• its anatomical origin (structure from the skin of the anterior abdominal wall to
the skin of the posterior abdominal wall).
33.2 Lumps of abdominal wall

Variety of lumps arising from the skin, subcutaneous tissues can occur anywhere
on the abdominal wall (detailed in Ch. 9).
Cold abscess
It originates from the tuberculous disease of the ribs or spine, former being more
common. It can occur on any region of the abdominal wall.
• A soft fluctuant swelling, the inflammatory signs being absent, unless
secondary infection occurs (Fig. 33.1).
• Clinically, the ribs on the same side may show some irregularity or tenderness
on the spine.
FIGURE 33.1 Cold abscess of abdominal wall.
• X-ray of the spine is contributory.
• X-ray of the ribs is useful in the upper quadrant abscesses.
Treatment
• Nondependent aspiration is needed for large abscesses.
33.3 Lumps in the right hypochondrium
The lumps of the right hypochondrial region are tabulated in Table 33.1.
TABLE 33.1
Lumps of Right Hypochondrium
Extra-abdominal Intra-abdominal
Organ Pathology
Cold abscess Right lobe of liver Amoebic hepatitis/liver abscess
Pyogenic abscesses of liver
Hydatid cyst
Malignancy of liver
Cirrhosis of liver
Gallbladder Mucocoele/pyocoele
Malignancy
Stomach (pylorus) Malignancy
Perigastric abscess
Hepatic flexure colon Malignancy
Tuberculosis
Intussusception
Right kidney Hydronephrosis/malignancy
Peritoneal cavity Subphrenic abscess
Right suprarenal gland Tumours
Hepatomegaly
Liver is the most important organ of the right hypochondrium and its palpability
can be due to various causes. Palpability of the liver below the costal margin is
not always due to hepatomegaly, as the liver as a whole may be pushed down
and the causes are as follows:
• emphysema, bronchial asthma;
• subdiaphragmatic abscess;
• aberrant lobe of liver, e.g. Riedel’s lobe and
• visceroptosis.
True hepatomegaly occurs due to variety of causes. They are tabulated in
Table 33.2.
TABLE 33.2
Causes of Hepatomegaly and Their Mechanisms
Aetiology Disorder Mechanism

Cardiovascular Congestive heart failure Vascular congestion
Hepatic vein thrombosis
Obstructive Biliary cirrhosis Obstruction of biliary system
Infiltrative Leukaemia, lymphoma Lymphatic infiltration of liver
Alcoholism Fatty infiltration of liver
Diabetes mellitus
Amyloidosis Infiltration of liver parenchyma
Inflammatory Hepatitis Parenchymal inflammation
Cirrhosis Regenerative phase
Neoplastic Primary (HCC) Malignant infiltration of liver parenchyma
Secondary (metastatic)
Miscellaneous Simple cyst, hydatid cyst, polycystic disease Space occupying lesion
Amoebic hepatitis/liver abscess

Infection of the liver parenchyma secondary to the intestinal infection caused by
the parasite Entamoeba histolytica (see p. 495).
• Constitutional symptoms like fever, toxicity.
• Pain in the right upper abdomen referred to the right shoulder.
• History of diarrhoea or dysentery in the recent past may be present.
• On examination,
• mild icterus may be present;
• liver is enlarged and acutely tender;
• marked tenderness and pitting oedema are noted on application of pressure
on the lower intercostal spaces on the right side (intercostal tenderness).
• Rarely, the abscess can present as a visible swelling in the abdomen (Fig.
33.2).
FIGURE 33.2 Amoebic liver abscess Source: (Courtesy Dr N. Dakshinamoorthy).
• Plain X-ray of abdomen or X-ray chest will show elevation of the right dome
of diaphragm (Ref Fig 30.9). Right pleural effusion is common.
• Fluoroscopy will show reduced mobility of the right dome.
• US and CT (Ref Fig. 30.10) are diagnostic.
• Aspiration is confirmatory.
• Stool examination is routine.
• Serologic test is positive in majority of cases.
Treatment
• Anti-amoebic drugs (metronidazole or tinidazole) cure small abscess and
hepatitis.
• Drainage under US guidance, under cover of broad-spectrum antibiotics
and anti-amoebic drugs is curative for a large abscess.
• Growth of pyogenic organisms in culture of pus requires appropriate
treatment.
Pyogenic abscess of liver

• Pyogenic abscesses of the liver are caused by
• spread of infection (portal pyaemia) from GIT, following pyelephlebitis
(secondary to appendicitis, infected pile masses, diverticulitis) and
• ascending cholangitis (impacted stone in the CBD).
• These abscesses are usually multiple.
• High-grade fever, with chills and jaundice.
• Clinically, the liver may be palpable and tender.
• Plain X-ray of abdomen or X-ray chest will reveal elevation of the right
dome of diaphragm, with pleural effusion on right side.
• Fluoroscopy will show reduced mobility of the right dome of diaphragm.
• US and CT abdomen (Ref Fig. 30.10) are diagnostic.
• Aspiration is confirmatory.
Treatment
• Broad-spectrum antibiotics are curative for small abscesses.
• Therapeutic aspiration under US or CT guidance is needed for large
abscess.
• Open drainage may be rarely required.
• Abscesses in communication with biliary tree will require drainage by
endoscopic procedures.
Hydatid cyst of liver
• Parasitic infection caused by Echinococcus granulosus, with dog as the
primary host.
• Close handling of dogs in a contaminated environment leads to oral ingestion
of ova, which penetrate the bowel wall and through the portal circulation
reaches the liver and get trapped in the liver sinusoids and form cysts.
• Hydatid cyst has many daughter cysts (Fig. 33.3) within, and the fluid is
allergenic.
• Usually occupies the upper pole of the right lobe and are slow growing.
FIGURE 33.3 Hydatid cysts of liver.

Complications: Rupture (into peritoneal cavity or biliary tree), infection,
calcification.
• Constitutional symptoms and tenderness occur when cysts are infected.
• Hepatomegaly (upward enlargement), with a localized smooth rounded
swelling in the right hypochondrium.
• Jaundice and cholangitis results when cyst ruptures into the biliary tree.
• Plain X-rays (Fig. 33.4A) demonstrate the calcified cysts.
• US (Fig. 33.4B) and CT are diagnostic.
• Casoni’s test is positive.
FIGURE 33.4 (A) X-ray abdomen—calcified hydatid cyst of liver. (B) US—
hydatid cyst liver
Treatment
• Calcified cysts need no treatment, as they are dead.
• Excision is curative for large symptomatic cysts.
• Mebendazole or albendazole are useful for small cysts.
Cysts of liver
Cysts of the liver are classified as
• Simple cysts are found in 2% of population.
• Polycystic liver disease may occur in isolation or with polycystic kidney
disease. Sometimes entire liver may be replaced by cysts.
• Choledochal cysts is congenital cystic dilatations of the biliary tree with
congenital hepatic fibrosis (see Ch. 7).
• Simple cysts—most are asymptomatic, unless complicated by infection or
haemorrhage.
• Polycystic liver disease—most are asymptomatic, unless complicated by
infection or haemorrhage.
• Choledochal cysts—abdominal pain and jaundice.
• Simple cysts—US (Fig. 33.5A) appearance is characteristic as well-defined
echo-free lesion with posterior acoustic enhancement.
• Polycystic liver disease—US appearance is characteristic.
• Choledochal cysts—US and CT are useful.

FIGURE 33.5 (A) US: Simple liver cysts. (B) CT—haemangioma of liver.
Treatment
• Simple cysts—simple aspiration will suffice, though recurrences are common.
Surgical removal is alternative therapy.
• Polycystic liver disease—liver transplantation is the only choice, when the
liver parenchyma is replaced.
• Choledochal cysts—surgical excision.
Benign liver tumours

Common benign tumours of the liver are:
• Haemangioma—Most common benign focal lesion, occurring in 1% of
population.
• Focal nodular hyperplasia—Most frequently seen in women of reproductive
years, with weak association to oral contraceptives, without any risk of
malignant change.
• Adenoma—Rare liver tumours. Closely linked to oral contraceptives in
women and androgen therapy in men. Have a potential to grow, bleed and
rupture especially during pregnancy. Malignant transformation is a
possibility.
• Haemangioma—Majority are solitary and asymptomatic. Large lesions cause
hepatomegaly.
• Focal nodular hyperplasia—Vague abdominal pain in a small minority of
patients. Hepatomegaly may be present.
• Adenoma—Usually asymptomatic, but severe abdominal pain indicates
complications.
• Haemangioma—US, CT (Fig. 33.5B) and MRI have characteristic findings.
• Focal nodular hyperplasia—US, CT and MRI have characteristic findings.
• Adenoma—US, CT and MRI have characteristic findings.
Treatment
• Haemangioma—majority need no treatment. Embolization and surgery are
indicated for very large lesions.
• Focal nodular hyperplasia—needs no treatment.
• Adenoma—lesions >10 cm in size require surgical resection for fear of
malignant transformation.
Hepatoblastoma
• Most common primary hepatic malignancy in children.
• An aggressive tumour with poor prognosis.
• Abdominal swelling, weight loss and failure to thrive.
• Serum Alpha fetoprotein is almost always elevated.
• CT abdomen (Fig. 33.6A) is diagnostic.

FIGURE 33.6 (A) CT—hepatoblastoma. (B) CT—HCC Source: (Courtesy
Bharat scans).
Treatment
• Resection for small encapsulated tumours.
• Liver transplantation is the only option.
Hepatocellular carcinoma (hcc, hepatoma)

• HCC is a malignancy of the hepatocytes.
• Peak incidence between 40 and 60 years.
• Male predominance of 2:1.
• High incidence in Hepatitis B endemic areas.
• Men following use of androgenic anabolic steroid used for body building.
• cirrhosis of any aetiology;
• chronic liver diseases caused by Hepatitis B and C;
• haemochromatosis;
• aflatoxin (mycotoxin produced by fungus Aspergillus flavus) exposure and
• exposure to thorotrast (radiographic contrast).
• They are multifocal in origin and arise from liver parenchyma or cirrhotic
nodules.
• Microscopically, they are as follows:
• diffuse
• single
• encapsulated
• fibrolamellar.
• The tumour spreads by various routes.
• Direct spread—They grow through liver capsule, leading to invasion of
adjacent structures, viz., hepatic veins, portal vein, inferior vena cava,
right kidney and adrenal, stomach and transverse colon, peritoneum and
ascites.
• Lymphatic spread—Hilar lymph nodes at the base of liver and portal nodes
may be involved.
• Haematogenous spread—Metastases to lungs (common), bone, skin and
brain (uncommon).
• HCC may form a part of paraneoplastic syndromes.
• Malaise, appetite and weight loss, abdominal discomfort, pain and jaundice.
• Clinical examination may reveal hepatomegaly
HCC is difficult to diagnose until there is widespread involvement of the liver.
• Raised alpha-fetoprotein levels (>200 mg/mL) are highly suggestive of HCC
(30%–40% of HCC patients have normal AFP).
• Serology for virus A, B, C and D should be performed.
• US has a sensitivity of 50%.
• CT (Fig. 33.6B) has better sensitivity in diagnosis.
• MRI, angiography and PET may each provide additional information.
• Isotope scan (Fig. 33.7) may be informative.
• Biopsy (percutaneous or laparoscopic) is confirmatory.
FIGURE 33.7 Isotope scan showing a large HCC in the right lobe of
liver Source: (Courtesy Dr K. M. Lakshmipathy).
Treatment
• Surgical resection of the liver with the lesion is the primary treatment.
Palliative (inoperable tumours)
• Hepatic– dearterialization
• Hepatic artery embolization
• Chemotherapy (systemic and intra-arterial)
• Low-dose radiotherapy
• Percutaneous alcohol injection and cryotherapy
• Radioablation.
Many primary cancers like colon, breast, lungs, stomach and pancreas
metastasize to the liver.
• Large lesions may cause right upper quadrant pain, ascitis, jaundice and
anorexia.
• Liver may become palpable and hepatomegaly may be nodular and hard, with
a rounded edge.
• A search for the primary must be made.
• US and CT (Fig. 33.8) and MRI are diagnostic.
• Percutaneous guided needle biopsies are conclusive.
• Carcinoembryonic antigen estimations may be useful in colonic
adenocarcinoma.
• Detailed examination and investigations in relation to search for a primary
(e.g., gastroscopy, colonoscopy) will be necessary.

FIGURE 33.8 CT—multiple liver metastases.
Treatment
Surgical resection is the treatment of choice, if the tumour is resectable
(outcome depends on the micrometastases and recurrences).
Cirrhosis of liver
• Cirrhosis is a generic term that includes all forms of chronic liver disease
characterized by extensive loss of liver cells with extensive disorganization
of hepatic architecture with diffuse liver cell death and fibrosis.
• It is classified as
• Alcoholic (alcoholic fatty liver, alcoholic hepatitis, alcoholic cirrhosis)—in
alcoholics.
• Postnecrotic (postinfective)—in nonalcoholic young patients.
• Biliary (primary and secondary—due to unrelieved biliary obstructions.
• Haemochromatosis (iron storage disorder).
• Cardiac or congestive—(following right-sided cardiac failure).
• In the initial stages, anorexia, nausea and vomiting, malaise, weight loss,
abdominal distress, ascites and jaundice are present.
• Signs of liver failure may be present in late stages.
• Regenerative stage causes hepatomegaly.
• Elevation of liver enzymes (SGOT/SGPT) is common.
• Coagulation profile is altered.
• Liver biopsy is conclusive.
• Immunologic studies are useful.
Treatment
• Symptomatic treatment and management of complications.
• Removal of biliary obstructions at the earliest.
• In haemochromatosis, the excess iron should be removed by chelating and
frequent phlebotomies.
• Cardiac cirrhosis requires management of the cardiac pathology.
Mucocoele/pyocoele of gallbladder
• Obstruction of the cystic duct causes distension of gallbladder and the bile is
replaced by clear mucus (mucocoele) or pus (empyema/pyocoele).
• Sometimes, the bile is replaced by calcium salts, which produces a hazy
opacification of the gallbladder (porcelain gallbladder).
• Acute right hypochondrial pain, with fever and vomiting.
• Patients with pyocoele present with swinging fever and tachycardia.
• Distended gallbladder may be palpable.
• Plain X-ray, US and CT (Fig. 33.9) are useful in diagnosing porcelain
gallbladder.
FIGURE 33.9 CT—porcelain gallbladder.
Treatment
• Cholecystectomy is the treatment of choice.
• Percutaneous (under US guidance) or open cholecystostomy followed by
cholecystectomy at a later date, is for pyocoele.
Carcinoma of gallbladder
• Commonest biliary tract tumour
• Common between 60 and 80 years of age.
• Female predominance 3:1.
• The risk factors are as follows:
• Gallstones (most common; Fig. 33.10)
• Gallbladder polyps (Fig. 33.11)
• Porcelain gallbladder
• Choledochal cysts
• Chronic Salmonella type infection of gallbladder.
• In the gallbladder
• 80% occur in the fundus and neck.
• Macroscopically it presents as infiltrating mass.
• Microscopically, they are
• adenocarcinomas (90%) and
• squamous cell carcinoma (10%)
• The tumour spreads by
• direct spread to adjacent liver capsule and parenchyma;
• lymphatic spread to hilar nodes around the liver and
• haematogenous spread to liver and lungs.
FIGURE 33.10 Gallbladder malignancy with faceted gallstones.
FIGURE 33.11 Polyps of gallbladder.
Incidental finding of carcinoma in the gallbladder specimen after

cholecystectomy for a calculous disease is not uncommon (0.5%–1%).
Symptoms
• Right hypochondrial pain.
• Weight loss, appetite loss, nausea. and vomiting.
• Obstructive jaundice due to bile duct invasion, duodenal obstruction and
lymph node metastases in the porta hepatis.
Signs
• An irregular lump may be felt in the gallbladder region.
• Hepatomegaly due to liver metastases.
• Transabdominal US shows thickening and irregularity of gallbladder, with
loss of interface with the liver or invasion of liver, with a sensitivity of
>70%.
• CT (Fig. 33.12) is useful in staging to detect liver invasion, lymphadenopathy
and distant metastases.
• MRI and MRCP are useful in mapping the tumour, vascular encasement. and
lymphadenopathy.
• ERCP or PTC are done for biliary decompression but only after obvious
diagnosis.
• EUS is useful in staging and to differentiate the benign and malignant polyps.
FIGURE 33.12 Carcinoma gallbladder with liver secondaries.
Treatment
• Radical cholecystectomy with wedge resection of liver.
• Revision radical cholecystectomy is done for incidental diagnosis of cancer
during cholecystectomy.
Palliative
• Chemotherapy and radiation for unresectable tumours.
• Surgical or endoscopic procedures are done to relieve jaundice and bowel
obstruction.
33.4 Lumps in the left hypochondrium

The lumps in the left hypochondrial region are tabulated in Table 33.3.
TABLE 33.3
Lumps of Left Hypochondrium
Extra- Intra-abdominal
abdominal
Organ Pathology
Cold abscess Left lobe of liver Amoebic hepatitis/liver abscess
Hydatid cyst
Malignancy of liver
Cirrhosis of liver
Spleen Infections
Portal hypertension
Haemoglobinopathies
Idiopathic thrombocytopenic purpura
Porphyrias
Leukaemias and myeloproliferative disorders
Lymphatic malignancies
Splenic cyst, splenic abscess, cavernous haemangioma, aneurysm of splenic
artery
Stomach Carcinoma
Perigastric abscess
Splenic flexure of Malignancy
colon
Tuberculosis
Intussusception
Pancreas Pseudocyst
Left kidney Hydronephrosis/malignancya
Peritoneal cavity Subphrenic abscess
Left suprarenal gland Tumours
a
Discussed in Chapter 37.
The major organs present in the left hypochondrium are the spleen and the left
kidney. They feel alike during palpation and need to be distinguished by their
characteristic features. They are given in Table 33.4.
TABLE 33.4
Differentiating Features of Splenomegaly and Renal Enlargement
Clinical Feature Splenic Enlargement Renal Enlargement

Enlargement Downwards and forwards towards the Downwards and forwards towards the left
right iliac fossa iliac fossa
Lower border of the swelling Notches are present Notches are absent
Mobility with respiration Moves well with respiration Moves slightly with respiration
Location Superficial Deep
Insinuation of fingers below the Not possible Possible
costal margin
Getting above the swelling Not possible Possible
Percussion note Dull throughout A resonant note may be made anteriorly
caused by the colon
Renal angle Free Full and dull to percussion
Splenomegaly
Splenomegaly is enlargement of the spleen and can occur due to varied causes
(Table 33.5).
• Primary (unknown aetiology).
• Secondary to variety of disorders.
TABLE 33.5
Causes of Splenomegaly
Aetiology Mechanism Splenomegaly

Immunologic–inflammatory
Infections Subacute bacterial endocardiitis, brucellosis, tuberculosis, Direct or secondary Constant
infectious mononucleosis, syphilis, cytomegalovirus, to hepatic feature
malaria, kala-azar, schistosomiasis involvement
Connective Rheumatoid arthritis Felty’s syndrome Immunologic Constant
tissue feature
disorders
Congestive
Portal Cirrhosis of liver Portal vein thrombosis Budd–Chiari syndrome Increased splenic Constant
hypertension venous pressure feature
Haematologic
Non-neoplastic Haemoglobinopathies Abnormal Variable
disorders haemoglobin
production
Thromphocytopenic purpura Antibodies to Rare
platelets
Porphyria Large
Neoplastic Lymphocytic leukaemias, myeloproliferative diseases Direct or secondary Massive
disorders to hepatic
involvement
Lymphoreticular
Lymphatic Hodgkin’s lymphoma Non-Hodgkin’s lymphoma Direct or secondary Variable
malignancy to hepatic
involvement
Miscellaneous
Cyst, splenic abscess, cavernous haemangioma, aneurysm of splenic artery Direct involvement Variable
Hypersplenism is overactivity of spleen in one or more of its functions, which

may result in anaemia, leucopoenia, thrombocytopenia, or a combination of all
the three— pancytopenia.
Infections of spleen
Infections of the spleen can be caused by
• malaria
• subacute bacterial endocarditis
• brucellosis
• tuberculosis
• infectious mononucleosis
• cytomegalovirus, syphilis
• histoplasmosis
• malaria
• kala-azar and
• schistosomiasis.
• Anaemia
• Recurrent upper GI bleeding from oesophageal varices.
• Huge enlargement of spleen (secondary to portal fibrosis).
• Ascites may manifest in late cases.
• Haemogram indicates hypochromic anaemia, eosinophilia and leukopenia
and lymphocytosis.
• Complement fixation test, precipitin, immunoelectrophoresis are useful in
diagnosis.
Treatment
Splenectomy.
Rheumatoid arthritis and felty’s syndrome

• Felty’s syndrome is a combination of rheumatoid arthritis, splenomegaly and
neutropenia.
• Occurs in longstanding rheumatoid arthritis.
• Symptoms of rheumatoid arthritis, with anaemia and thrombocytopenia occur.
• Anorexia, loss of weight and lymph node enlargements are common.
• Leg ulcers occur due to vasculitis and peripheral neuropathy.
• Repeated infections may occur due to neutropenia.
• Spleen is enlarged in Felty’s syndrome.
• Neutropenia, raised ESR, disturbances of protein electrophoresis are
present.
• Investigations relevant to rheumatoid arthritis are necessary.
Treatment
Splenectomy is useful to improve neutropenia and repeated infections.
Though neutropenia may recur, the course of arthritis is not altered by
splenectomy.
Portal hypertension
• Portal hypertension is defined as increased portal pressure of over 30 cm of
saline when measured at surgery or a wedged hepatic vein pressure greater
than 4 mm Hg above the inferior vena caval pressure.
• Portal hypertension is caused by variety of causes. They are:
• Hepatic causes: Cirrhosis of liver.
• Posthepatic causes: Budd–Chiari syndrome.
• Prehepatic causes: Portal vein thrombosis.
Symptoms
• Upper and lower gastrointestinal bleeds (due to rupture of collaterals).
• Jaundice and signs hepatic failure (due to cirrhosis).
Signs
• Abdominal distension (due to ascites).
• Liver is enlarged in Budd–Chiari syndrome, not enlarged in cirrhosis and
portal vein thrombosis.
• Splenomegaly is a constant finding in all cases of portal hypertension.
• Pancytopenia indicates hypersplenism.
• Liver function tests to establish the liver disease.
• Endoscopy to establish the collaterals.
Treatment
• Splenectomy is needed in cases with hypersplenism and large spleens.
• Shunt procedures are needed to reverse the portal systemic flow of blood.
• Emergencies (acute upper GI bleeds) require blood replacement and
tamponade of collaterals.
• Liver transplantation provides cure for irreversible liver disorders.
Haemoglobinopathies
Splenomegaly may be caused by haemolytic anaemia, which is of two types:
• Congenital haemolytic anaemia
• Hereditary spherocytosis: Autosomal dominant disease caused by
increased permeability of the red blood cell membrane leading to
destruction of RBCs due to increased osmotic pressure and increased
fragility. Unconjugated bilirubinemia occurs (acholuric jaundice).
• Sickle cell anaemia: A hereditary disease of very young (common in
Negroes), HbF (foetal haemoglobin) is replaced by HbS (sickle cell
haemoglobin) with elongation of biconcave RBCs to rigid crescent shaped
or sickle-shaped cells, which obstruct capillary circulation.
• Acquired haemolytic anaemia: An autoimmune disease, where antibodies are
produced which destroy the RBCs, due to deficiencies of enzymes of
glycolytic pathway. It can be
• primary (idiopathic - childhood);
• secondary to a collagen disease (adults or elderly); and
• a drug reaction (e.g., antimalarials, sulfonamides).
• Congenital haemolytic anaemia
• Hereditary spherocytosis: Anaemia, jaundice and splenomegaly are
constant. Pigment stones also occur due to increased bile pigment
metabolism. Chronic leg ulcers occasionally occur.
• Sickle cell anaemia: Child presents with retarded growth, with general
failure to thrive. Repeated infections occur, with impaired splenic
function. Anaemia presents with vaso-occlusive phenomena with painful
crises of various parts of the body. When they reach adult life, almost all
organs have undergone damage.
• Acquired haemolytic anaemia: Anaemia, jaundice and splenomegaly are
constant. Pigment stones also occur due to increased bile pigment
metabolism.
• Coomb’s test is positive in acquired haemolytic anaemia.
• Faecal urobilinogen is increased.
• A reliable indicator, RBC fragility test is positive.
• Reticulocytosis is present.
• RBC labelling with radioactive chromium Cr51 is useful in deciding
treatment.
• US reveals gallstones (pigment stones).
Treatment
• Splenectomy is indicated depending on the situation.
Idiopathic thrombocytopenic purpura

• A chronic platelet disorder (thrombocytopenia) of autoimmune mechanism.
• Acute forms are not uncommon.
• Bleeding episodes of varying intensity, as purpuric rashes on the skin, mucous
membrane and skin, seen more commonly on dependent parts of the body.
• Epistaxis and menorrhagia are common presentations.
• GI bleeding, haematuria and haemarthrosis are rare.
• Splenomegaly is mild (a large spleen is against the diagnosis of ITP).
• Capillary fragility test (Tourniquet test)—increasing the pressure using a
sphygmomanometer tied to the upper arm and maintaining at just below the
systolic pressure causing venous engorgement, and petechial haemorrhages
occur (Fig. 33.13), indicating increased fragility of the veins.
• Low platelet count (with normal morphology), high sedimentation rate and
demonstration of platelet antibodies are diagnostic.
FIGURE 33.13 Petechial haemorrhages.
Treatment
• Medical management is with steroids and platelet transfusions.
• Splenectomy is the treatment of choice.
• Immunosuppression is required in splenectomy failed cases.
Note
Secondary purpura: Purpura can occur secondary to infections (e.g.,
septicaemia, tuberculosis, brucellosis, Boeck’s sarcoidosis), idiosyncrasy
(e.g., alkylating agents, quinine, arsenicals, extensive burns, malignancies
(e.g., leukaemia, osseous carcinomatosis) and irradiation.
Porphyrias
• Porphyrias occur due to inherited or acquired disturbances of heme synthesis,
and are divided into two main groups:
• Erythropoietic
• Hepatic
• The only pure erythropoietic form is the rare congenital erythropoietic
porphyria.
• Hepatic porphyrias are genetically transmitted as autosomal dominants.
• Congenital erythropoietic porphyria
• Patient passes pink or red urine.
• Cutaneous photosensitivity.
• Splenomegaly at later stages.
• Death may occur in childhood.
• Hepatic porphyries
• Abdominal pain occurs due to episodes of crisis (probably due to
autonomic neuropathy), which may last for several days, mimicking an
inflammatory bowel disease.
• Constipation is common.
• Neurological and mental aberrations also occur.
• Anaemia is present.
• Spleen is markedly enlarged.
• Jaundice is sometimes present.
• Urine contains high concentration of uroporphyrin.
• Normoblasts, reticulocytes and erythrocytes exhibit red fluorescence due to
high amounts of uroporphyrin.
• Excessive excretion of alpha-aminolevulonic acid (ALA) and
porphobilinogen (PBG) is characteristic during acute attacks.
Treatment
• Exposure to sunlight should be avoided.
• Splenectomy is useful in some cases.
• Large quantities of glucose is administered intravenously during acute
attacks.
Leukaemias and myeloproliferative disorders

Splenomegaly is a finding of leukaemias (lymophocytic and myeloid) and many
myeloproliferative disorders. They are:
• polycythemia rubra vera and
• melofibrosis.
• Dragging abdominal discomfort, exacerbated by pain due to splenic infarcts.
• Fatigue and dyspnoea (anaemia), recurrent infections (leukopenia) and/or
spontaneous bleeding episodes (thrombocytopenia) are common.
• Massive splenomegaly is the characteristic feature, especially of the myeloid
type.
• Haemogram and peripheral smear study are diagnostic.
• Bone marrow study is confirmatory.
• US and CT are useful to assess splenic infarcts.
Treatment
• Leukaemias require appropriate treatment.
• Role of splenectomy is questionable.

• Lymphomas are a group of primary malignant diseases of lymphoreticular
origin, with a wide spectrum of clinical and pathological features.
• They are widely classified as follows:
• Hodgkin’s lymphoma
• Non-Hodgkin’s lymphoma
• Majority of them originate in the lymph nodes, with differences in the cell of
origin.
• Aetiology is nonconclusive but its viral origin is widely accepted.
• Asymptomatic with discrete, painless rubbery enlargement of lymph nodes.
• Fever of cyclical nature (Pel-Ebstein fever) is characteristic of Hodgkin’s
lymphoma.
• Splenomegaly may be present either due to the disease process or secondary
to liver involvement.
• CT scan (Fig. 33.14) determines the extent of the disease.
• Bone marrow aspiration or biopsy is necessary to determine the extent.
• Immunologic tests and histopathology are diagnostic.
FIGURE 33.14 CT—gross splenomegaly in non-Hodgkin’s lymphoma.
Treatment
• Chemotherapy is effective.
• Multidisciplinary approach is effective.
Splenic cyst and splenic abscess

• Cyst of the spleen is a rare condition.
• They can be
• congenital
• parasitic (hydatid).
Splenic abscess is another uncommon condition usually associated with
severe systemic infection with a high mortality rate.
• Simple cyst is asymptomatic.
• Splenic abscess presents with constitutional symptoms with a previous history
of severe intra-abdominal sepsis.
• Splenomegaly may be present.
US and CT (Fig. 33.15) are diagnostic.

FIGURE 33.15 CT—splenic abscesses.
Treatment
• No treatment for simple cysts with mild splenomegaly.
• Splenectomy is done for large spleen with abscesses.
33.5 Lumps in the epigastrium

A variety of diseases present as a lump in the epigastrium. They are given in
Table 33.6.
TABLE 33.6
Lumps of Epigastrium
Extra-abdominal Epigastric hernia
Intra-abdominal
Organ Pathology
Left lobe of liver Amoebic hepatitis/liver abscess

Hydatid cyst
Malignancy of liver
Cirrhosis of liver
Stomach/duodenum Congenital pyloric stenosis
Perigastric abscess
Carcinoma of stomach
Transverse colon Intussusception
Diverticulitis
Tuberculosis
Malignancy
Omentum Tuberculosis
Malignant deposits
Retroperitoneum Pancreas Pseudocyst
Abdominal aorta Aneurysm
Lymph nodes Lymphadenopathy
Connective tissue Sarcoma/teratoma
Gastric malignancy

• Adenocarcinoma is the commonest tumour of stomach.
• More common in men.
• Common above the age of 50 years.
• More common in the antrum or on the lesser curve, and less frequent on the
corpus
• smoking
• alcohol consumption
• blood group A
• diet (high intake of salt and dried or pickled foods)
• H. pylori infection
• genetic (mutation of E-cadherin gene) and
• precancerous conditions are as follows:
- chronic gastritis and atrophy and
- Menetrier’s disease.
• Macroscopically the gastric cancer is of four types. They are as follows:
• polypoid fungating growth;
• sessile lesion;
• ulcerative and
• diffuse infiltrative type (scirrhous)—Linitis plastica (leather bottle
stomach).
• Microscopically they are adenocarcinomas.
• Tumour spreads in various directions (see Chapter 31).
• Early lesions are without any symptoms, however, loss of appetite and early
satiety are early symptoms of gastric cancer.
• Palpable lump in the epigastrium or right hypochondrium (local fixity
indicates local invasion).
• Upper GI endoscopy (Ref Fig. 31.3A) is diagnostic.
• Barium meal (Figs 33.16A and B) is useful in diagnosis but upper GI
endoscopy has replaced it almost in recent times.
• US and CT abdomen (Fig. 33.17) are useful is diagnosing liver, lymph nodal
and peritoneal metastases.
• X-ray and CT of chest are useful for diagnosing lung metastases.
FIGURE 33.16 Barium meal—(A) linitis plastica, (B) malignancy of
stomach.
FIGURE 33.17 CT—carcinoma stomach with liver metastases.
Treatment
• Radical (clearance) surgery depending on the location of the tumour is the
treatment of choice, followed by chemotherapy and sometimes radiotherapy.
• Preoperative chemoradiation is useful in advanced lesions.
Congenital pyloric stenosis

Congenital anomaly of babies of 2 to 4 weeks of age
• Projectile vomiting is a constant symptom.
• Clinical examination reveals
• dehydration and shrunken appearance;
• a palpable lump in the epigastrium and
• visible gastric peristalsis is prominent.
Barium meal (Fig. 33.18) and US are useful.

FIGURE 33.18 Barium meal—congenital pyloric stenosis.
Treatment
Pyloromyotomy or Ramstedt’s operation.
Malignancy of transverse colon
(See Chapters 8 and 31)
• Anaemia, anorexia, weight loss.
• Abdominal pain.
• Lump in the epigastrium, mobile in the vertical axis in the initial stages.
Treatment
• Radical transverse colectomy.
• Defunctioning ileostomy is done in nonresectable, advanced and obstructed
malignancies.
Intussusception of colon
Tuberculosis of omentum
Caused by tuberculous infection of the greater omentum, involving its
lymphatics.
• Chronic abdominal pain.
• A mobile lump in the epigastrium due to rolling up of omentum (Tabes
mesenterica), due to enlarged lymph nodes in it.
• The lump is firm to feel and is transversely placed, and the mobility is
transverse (in contrast to transverse colon malignancy, which is mobile
vertically).
• There may be associated ascites.
• There may be evidences of pulmonary and intestinal tuberculosis.
• US and CT (Fig. 33.19) are useful.
• Laparoscopy biopsy is diagnostic.
FIGURE 33.19 CT—tuberculosis of omentum.
Treatment
• Antitubercular treatment is mandatory.
• Omentectomy may be required.
• Adherent intestines need appropriate treatment such as adhesions release
and resections.
Solid tumours of omentum

• Most common solid tumour is metastatic carcinoma.
• Involvement occurs due to tumour implant.
• Primary sources: colon, stomach, pancreas and ovaries.
• Usually there is associated ascites.
• Primary solid tumours are exceedingly rare.
• May be benign or malignant.
• Most tumours are smooth muscle tumours and one third of them are
malignant.
• Benign tumours: lipoma, leiomyoma, fibroma, fibrosarcoma.
• Malignant tumours: leiomyosarcoma, fibrosarcoma, liposarcoma,
hemangiopericytoma.
Palpable lump in the epigastrium.
• US and CT abdomen (Fig. 33.20) are diagnostic.
• Laparoscopy biopsy is confirmatory.
FIGURE 33.20 CT—Metastatic deposits of omentum from ovarian
carcinoma.
Treatment
• Total omentectomy is for primary tumours (resection of adjacent organs may
be necessary).
• For metastatic deposits, adjuvant chemotherapy as for the primary tumour
is necessary, but it is palliative.
Pancreatic pseudocyst
• Active collections of fluid after acute pancreatitis may mature into
pseudocysts.
• They start either as sympathetic inflammatory collections (usually in the
lesser sac) or as a result of rupture of pancreatic duct or one of its tributaries.
• Cysts larger than 6-cm diameter that persist for more than 6 weeks are more
often in communication with a duct.
• A smooth rounded soft lump in the epigastrium.
• Cysts behind the stomach push the stomach and are impalpable.
Barium meal series, US and CT abdomen (Fig. 33.21) are diagnostic.
FIGURE 33.21 CT—pancreatic pseudocysts Source: (Courtesy Bharat scans).

Treatment
• Small cysts and those that result as sympathetic reaction resolve
spontaneously.
• Cysts in communication with pancreatic ductal system and large cysts,
especially those that persist for more than 6 weeks require internal drainage
procedures (cytsogastrostomy, cystojejunostomy).
• Percutaneous drainage procedures for pseudocysts are rarely done.
Adrenal tumours
• Adrenal gland is divided into two components: adrenal cortex and adrenal
medulla.
• Hyperplasia or neoplasia can occur in both and produce characteristic
syndromes (Table 33.7).
TABLE 33.7
Syndromes Associated with Adrenal Pathologies
Component Zones Hormones Syndromes
Adrenal cortex Zona glomerulosa Aldosterone Primary aldosteronism

Zona fasciculata Cortisol Cushing’s syndrome
Zona reticularis Androgens Virilism
Adrenal Chromaffin cells Adrenaline and Pheochromocytoma
medulla noradrenaline
Non-chromaffin Neuroblastoma, ganglioneuroma,
cells ganglioneuroblastoma
Adrenal cortex
• Idiopathic hyperaldosteronism: Bilateral adrenal hyperplasia or a single
benign tumour (Conn’s syndrome).
• Cushing’s syndrome: Glucocorticoid excess due to Adrenocorticotrophic
hormone (ACTH)-dependent hyperplasia or ACTH-independent adenoma or
carcinoma.
• Virilism: Sex steroid hormone excess due to congenital adrenal hyperplasia,
adrenocortical adenoma or carcinoma.
Adrenal Medulla
Tumours from adrenal medulla (see Table 33.8).
TABLE 33.8
Tumours of Adrenal Glands
Adrenal Cortex Adrenal Medulla

Benign Malignant Benign Malignant
Hyperplasia Carcinoma Pheochromocytoma Ganglioneuroblastoma
Adenoma Metastases Ganglioneuroma Neuoblastoma
Metastases
Symptoms and signs are tabulated in Tables 33.9 and 33.10.
TABLE 33.9
Symptoms of Adrenal Cortical Lesions
Clinical
Hyperaldosteronism Cushing’s Syndrome Virilism
Feature
Symptoms Vague or absent Facial or truncal obesity Pseudohermaphroditism

Lethargy, muscle Lethargy, muscle weakness
weakness
Menstrual irregularity
Hirsutism
Clinical Normal Moon face, buffalo hump, central obesity, striae, Male external genitalia
examination hirsutism. Lump may be palpable in adrenal in females
carcinomas.
Precocious sexual
maturity in males
Hypertension Hypertension
TABLE 33.10
Symptoms of Adrenal Medullary Lesions
Clinical Feature Pheochromocytoma Neuroblastoma
Symptoms Excessive spontaneous sweating, paroxysmal headache, palpitations Malaise and weight loss
Clinical examination Normal and abdominal lump occasionally palpable Abdominal mass is felt
Hypertension Rarely hypertension
• Determination of appropriate hormone levels will confirm the diagnosis.
• US, CT (Fig. 33.22) and selective venous sampling localizes the tumours.
FIGURE 33.22 CT—bilateral adrenal masses.
Treatment
• Adrenalectomy cures adenomas.
• In the treatment of virilizing tumours, surgical correction of abnormal
genitalia may be necessary.
Aortic aneurysm
• A rare condition, the dilatation of aorta, usually more than 3 cm is called an
aneurysm, which may be fusiform or saccular.
• Aneurysm is caused by
• atherosclerosis (commonest)
• trauma
• infection (mycotic) and
• connective tissue disorders, Marfan’s syndrome and Ehlers–Danlos
syndrome type IV.
Complications: Rupture, distal embolus, infection, gut ischemia, aortic-
intestinal fistula, arteriovenous fistula (erosion into inferior vena cava).
• Majority are asymptomatic and a smooth rounded lump may be palpable in
the epigastrium.
• Expansile pulsation is characteristic of aortic aneurysm.
• Peripheral pulses of the lower limbs may be less prominent.
• US and CT (Ref Fig. 13.12B) are diagnostic.
• Doppler studies are useful.
• Arteriography or MRA may be necessary to measure involvement of renal
arteries.
Treatment
• Small asymptomatic aneurysms (less than 5.5 cm) are followed up with
regular ultrasound.
• Abdominal aneurysmectomy with reconstruction is the treatment of choice.
Para aortic lymphadenopathy

The common causes of para aortic lymphadenopathy are as follows:
• primary lymphomas
• secondary deposits (e.g., testicular tumours) and
• tuberculosis.
• Many are asymptomatic.
• Palpable lump is usually a chance finding.
• Symptoms related to primary pathology may be prominent.
• US and CT abdomen (Fig. 33.23) are diagnostic.
FIGURE 33.23 CT—enlarged para aortic lymph nodes Source: (Courtesy

Bharat scans).
Treatment
Treatment is specific to the pathology.
33.6 Lumps in the lumbar regions
A variety of diseases present as a lump in the lumbar regions, and the pathology
of the organ on that side determine the characteristics of the lump. They are
given in Tables 33.11 and 33.12. The intra-abdominal diseases are detailed at
various pages already.
TABLE 33.11
Lumps of Right Lumbar Region
Intra-abdominal
Extra-abdominal
Organ Pathology
Cold abscess (lumbar abscess) Right kidney Hydronephrosis/malignancy
Lumbar hernia Ascending colon Intussusception
Malignancy
Liver (hepatomegaly) Amoebic hepatitis/liver abscess
Hydatid cyst
Malignancy of liver
Cirrhosis of liver
Gallbladder Mucocoele/pyocoele
Carcinoma
TABLE 33.12
Lumps of Left Lumbar Region
Extra-abdominal Intra-abdominal
Organ Pathology
Cold abscess (lumbar Left kidney Hydronephrosis/malignancy
abscess)
Lumbar hernia Descending Intussusception
colon
Malignancy
Spleen Infections
Portal hypertension
Haemoglobinopathies
Leukaemias and myeloprolifertive disorders
Splenic cyst, splenic abscess, cavernous haemangioma, aneurysm of
splenic artery
Lumbar abscess and lumbar hernia

Lumbar abscess (cold abscess) and lumbar hernia present as a lump in the
lumbar region, and they can be distinguished by their characteristic findings
(Table 33.13).
TABLE 33.13
Distinguishing Features of Lumbar Abscess and Lumbar Hernia
Clinical Feature Lumbar Abscess Lumbar Hernia
Cough impulse Present Present but expansile

Reducibility Partial Usually complete
Percussion Dull Resonant or dull
Examination of spine Deformed, tender with rigid muscles Normal
X-ray spine findings Narrowing of intervertebral space with destruction of adjoining vertebrae Normal
A variety of diseases present as a lump in the umbilical region. They are given
in Table 33.14.
TABLE 33.14
Lumps of Umbilical Region
Intra-abdominal
Abdominal Wall
Organ Pathology
Umbilical granuloma Small intestine/mesentery Tuberculosis

Umbilical herniaa Tumours
Paraumbilical herniaa Mesenteric cyst
a
Postoperative/incisional hernia Retroperitoneum Retroperitoneal cyst
Rectus sheath haematoma Lymphomas
Desmoid tumour Sarcomas
a
33.7 Lumps in the umbilical region
Umbilical granuloma/enterotoma
• These are moist granulations, pedunculated with irregular surface.
• This results due to
• sepsis of an infolded umbilical cicatrix and
• persistence of intestinal mucosa of a patent vitello-intestinal duct (Ref Fig.
37.32).
• Rarely, a persistent urachus (see Ch. 37) can present like a granuloma.
Sprouting granulation at the umbilicus (Fig. 33.24), discharging pus, stools or
urine.

FIGURE 33.24 Umbilical granuloma.
• Fistulogram is useful in localizing the fistulous communication between the
bowel or bladder.
• Laparoscopy is useful in diagnosis.
Treatment
• Granulomas may be cauterized with copper sulphate crystals or with silver
nitrate.
• Fistulae need excision with limited laparotomy.
Rectus sheath haematoma

• Haematoma of the rectus sheath occurs due to rupture of inferior epigastric
artery below the arcuate line behind the rectus abdominis muscle.
• This follows trauma to the anterior abdominal wall after
• convulsions after tetanus, epilepsy or strychnine poisoning and
• direct trauma.
• Very rarely, a violent cough or sneeze can cause a haematoma of the rectus
sheath.
• Painful lump in the lower end of the anterior abdominal wall lateral to the
midline.
• Bruising of the skin may be visible, and the lump is exquisitely tender.
• Lump becomes less prominent on lifting the legs in supine position.
US and CT (Fig. 33.25) abdomen are useful in diagnosis.
FIGURE 33.25 CT—rectus sheath haematoma.
Treatment
• Many of these haematomas resolve in due course of time, with anti-
inflammatory drugs.
• Evacuation (aspiration or open method) is rarely needed.
Desmoid tumour
An un-encapsulated fibroma arising from the muscle fibres of the rectus
abdominis, or may arise from the scar after surgery, or a haematoma may itself
initiate this tumour.
• Painful lump on the anterior abdominal wall lateral to the midline in the
muscle layer or anterior to it.
• Lump becomes more prominent of lifting the legs in supine position.
US and CT abdomen are useful in diagnosis.
Treatment
Wide excision with mesh repair is the treatment of choice and recurrences are
common (recurrent fibroid of Paget).
Small bowel tumours

• Small bowel tumours are rare.
• They can be benign or malignant.
• The benign tumours are as follows:
• adenomas
• endocrine tumours (carcinoids)
• stromal tumours
• lipoma (Ref Fig. 30.21B)
• vascular tumours (haemangioma)
• neurogenic tumours
• tumours of lymphoid tissue
• benign polyps (Peutz–Jeghers syndrome).
• The malignant tumours are as follows:
• Lymphomas of small intestine are uncommon but account for 30% of small
bowel malignancies.
• Adenocarcinomas of small intestine are much rarer than carcinoma of
stomach and large intestine.
- Periampullary region and duodenum are most common sites.
- Most cancers arise within a preexisting adenoma.
• Carcinoid tumours account for about one third of all small intestinal
tumours.
- More common in the duodenum and ileum.
- They are slow growing and produce narrowing.
• Malignant Gastrointestinal stromal tumours (GISTs) and vascular
tumours (angiosarcoma) are rare.
• Small bowel tumours are generally not palpable clinically (excepting large
GISTs).
• May present with intestinal obstruction.
• Rarely, may ulcerate and bleed insidiously.
• Major haemorrhage presenting as melena is not uncommon.
Note
Obstructions present as acute emergency, and diagnosis is during laparotomy.
• Capsule endoscopy is diagnostic (Fig. 33.26A and B).
• CT abdomen (Fig. 33.26C) is also diagnostic for large tumours.

FIGURE 33.26 (A) Capsule endoscope. (B) Capsule endoscopy—
carcinoid tumour. (C) CT—GIST Jejunum.
Treatment
• Excision with resection of bowel is required for symptomatic tumours.
• Adjuvant chemotherapy may be required for malignant tumours.
Mesenteric cysts
Cysts of the mesentery may be
• enterogenous;
• urogenital remnant;
• chylolymphatic;
• dermoid and
• reduplication.
Complications: Pain, haemorrhage, torsion and rupture.
• Smooth, tense, distension of abdomen.
• On examination, the mass is central, is mobile across the attachment of
mesentery, and dull to percussion with surrounding area of resonance
(Tillaux’s triad).
• If the bowel is overlying it, it may show a resonant band.
• Pain is a symptom of complication.
US and CT abdomen (Fig. 33.27A) with oral contrast is diagnostic.
FIGURE 33.27 (A) CT—lymphatic cyst of mesentery. (B) Large mesenteric
cyst.
Treatment
Excision (Fig. 33.27B) is the treatment of choice.
Retroperitoneal swellings
Retroperitoneal swellings can be
• Cysts: Usually Wollfian remnants or reduplication cysts.
• Lymph node swellings: Tuberculosis, primary lymphomas, metastatic
tumours (e.g., testicular tumours).
• Connective tissue tumours: Sarcoma.
• Cysts: They may reach enormous size and contain clear fluid, dermoid and
teratoma contain sebaceous material.
• Lymph node swellings: Firm swellings with no mobility.
• Connective tissue tumours: Solid firm to hard swellings.
US and CT abdomen (Fig. 33.28A and B) are diagnostic.
FIGURE 33.28 (A) CT—enlarged tuberculous necrotic nodes of
peripancreatic region. (B) CT—mesenchymal tumour of retroperitoneum.
Treatment
• Excision is advised for cystic tumours and connective tissue tumours.
• Tuberculosis and lymphomas require appropriate medical management.
33.8 Lumps in the iliac fossae

A variety of diseases present as a lump in the iliac fossa. They are given in
Tables 33.15, 33.16 and 33.17.
TABLE 33.15
Lumps of Right Iliac Fossa
Intra-abdominal
Extra Abdominal
Organ Pathology
Cold abscess Appendix Appendicular mass/abscess

Ileocaecal region Hypertrophic tuberculosis
Crohn’s disease
Caecum Amoebic typhlitis/amoeboma
Actinomycosis
Carcinoma
Solitary caecal diverticulitis
TABLE 33.16
Lumps of Left Iliac Fossa
Intra-abdominal
Extra Abdominal
Organ Pathology
Cold abscess Sigmoid and Descending colon Diverticulitis
Carcinoma
TABLE 33.17
Lumps of One or Both Iliac Fossae
Organ Pathology
Lymph nodes Tuberculosis, filariasis, Primary and secondary lymphatic malignancies

Iliac vessels Aneurysm
Retroperitoneum Retroperitoneal cyst, lymphoma, sarcoma
Ileopsoas sheath Pyogenic abscess, cold abscess
Iliac bone Chondrosarcoma
Uterus and adnexa Ectopic pregnancy, tubo-ovarian pathologies a
Kidney Pelvic kidney or nephroptosis b
Testis Undescended testis c
Urinary bladder Diverticulum
Peritoneum Pelvic abscess
a
Discussed in detail in Chapter 38.
b
c
Appendicular mass/abscess
• When the adjacent tissues and omentum wall off the appendix or its
perforation following infections, it forms a mass (Fig. 33.29) called
‘Appendicular mass (nature’s way of localizing the infection)’.
• When there is suppuration, it forms an abscess named ‘Appendicular
abscess’, which may burst into peritoneal cavity to produce severe peritonitis
and even death (see p. 489).
FIGURE 33.29 Appendicular mass.

• Pain in the right iliac fossa following central abdominal pain (see p. 489).
• Mass appears about the 3rd or 4th day in the right iliac fossa.
• On examination, the mass is irregular, firm, immobile and tender.
• Fever and toxicity are symptoms of appendicular abscess.
• Leucocytosis may be present.
• US and CT (Figs. 33.30A and B) are diagnostic.
FIGURE 33.30 CT—(A) Appendicular mass. (B) Appendicular
abscess Source: (Courtesy Bharat scans).
Treatment
• Appendicular mass is managed conservatively.
• Appendicular abscess by drained extraperitoneally.
• For both conditions, elective (interval) appendicectomy is performed.
Ileocaecal tuberculosis
• Very common disease, especially of the lower socio-economic group.
• Affects any age and any sex.
• The route of entry of the organism Mycobacterium tuberculosis is by
• ingestion
• through blood and
• transmigration.
• Ileocaecal tuberculosis can be
• Ulcerative
• Hyperplastic—The bacilli reach the lymphoid follicles leading to
thickening of the intestinal wall and narrowing, which may lead to
intestinal obstruction.
Hyperplastic type: In addition to the features of ulcerative type, the patients may
present with a lump in the right iliac fossa, to distinguish from Crohn’s disease
and amoeboma (see Ch. 31).
• Plain X-rays and CT abdomen without oral contrast are useful in diagnosing
obstructed bowel lesions.
• Barium enema or CT with rectal contrast is diagnostic for mucosal lesions.
• Colonoscopy (Fig. 33.31) is characteristic.
FIGURE 33.31 Colonoscopy—ileocaecal tuberculosis Source: (Courtesy Dr
Treatment
• Antitubercular treatment is curative.
• Right hemicolectomy or bypass procedures are done for obstructive lesions.
Amoeboma
• Inflammation of caecum (typhlitis) caused by amoebic infection (E.
histolytica) sometimes results in a mass (amoeboma).
• May coexist with malignancy.
Complications: Obstruction, perforation and pericolic abscess.
• Recurrent attacks of passing blood stained loose stools and pain in the right
lower abdomen.
• On examination, there may be gurgling (local ileus) in the right iliac fossa and
a lump becomes palpable.
DD: Appendicular mass.
• Stool examination and complement fixation test for amoebae are mandatory.
• Colonoscopy is useful in diagnosis.
Treatment
Anti-amoebic treatment is curative.
Actinomycosis
• Actinomycosis develops when a breach occurs in the mucous membrane, due
to disease or trauma, which permits the entry of Actinomyces israelii into the
deeper layers.
• Suppuration occurs and the disease spreads into the retroperitoneal tissues and
eventually, the abdominal wall becomes the seat of multiple sinuses.
• Liver may get affected through portal venous spread.
• Usually, a mass forms in the right iliac fossa following appendicectomy,
which discharges through sinuses.
• Sinus discharge is thin and watery to start with and later becomes thick and
foul smelling due to secondary infection. The discharge is granular and
yellowish (sulphur granules) or black in colour.
• Pus when allowed to trickle down the test tube, demonstrates sulphur
granules.
• Bacteriological examination of the pus is mandatory.
Treatment
• Prolonged intensive course of penicillin is curative.
• Appropriate antibiotic therapy is given for secondary infection.
Carcinoma caecum
• 5% of all colonic carcinomas.
• Bulky exophytic growths occur principally in the caecum.
• Tumour may invade the wall including the serosa and surrounding structures.
• Colonic carcinomas metastasize through lymphatics (first to mesenteric nodes
and then to para-aortic nodes) and blood stream (first to liver and
uncommonly to the lungs and bones).
• Anaemia may be predominant.
• Malaise and chronic pain in the right iliac fossa.
• An irregular nontender mass may be palpable.
• Barium enema, US and CT abdomen (Fig. 33.32) are diagnostic.
• Colonoscopy (Fig. 33.33) biopsy is confirmative.
FIGURE 33.32 CT—carcinoma caecum.
FIGURE 33.33 Colonoscopy—carcinoma caecum Source: (Courtesy Dr Mani
Veeraraghavan).
Treatment
Right radical hemicolectomy with adjuvant chemotherapy.
Solitary caecal diverticulitis

• Solitary diverticulum is common in the caecum.
• Inflammation of the diverticulum presents like acute appendicitis and mislead
the examiner.
• Pain in the right iliac fossa (similar to acute appendicitis).
• A lump may be felt in the right iliac fossa.
US and CT may be useful.
Treatment
Diverticulectomy or right hemicolectomy is the treatment of choice.
Iliac lymphadenopathies
Lymph node swellings in the iliac fossa can occur due to
• abdominal tuberculosis;
• filariasis and
• primary and secondary malignancy.
• Abdominal tuberculosis
• Discomfort and pain in the iliac region.
• Examination reveals nontender swelling or swellings matted as a nodular
mass.
• Other evidences of tuberculosis may be present.
• Filariasis
• Fever and rigor associated with pain in the lower abdomen.
• Examination may reveal palpable swellings in the iliac regions.
• Primary and secondary malignancy
• Pain and discomfort in the lower abdomen may be present.
• Examination reveals hard enlarged nodes more than 2 cm in diameter
mobile or multiple. There may be associated pedal oedema and varicosity
of lower limb veins due to pressure on the external iliac vein.
• US and CT are diagnostic.
• Investigations should be directed towards the above pathologies.
Treatment
Treatment specific to the diagnosis.
Abscess of iliopsoas sheath

The ileopsoas sheath in the pelvic regions may be a seat for
• pyogenic abscess (results due to infection of a haematoma from a muscle
tear);
• cold abscess (results gravitation of the inflammatory material from the
thoracolumbar vertebrae—Pott’s spine or sacroiliac tuberculosis).
• Pyogenic abscess: Pain is localized to the iliac fossa (mimics appendicitis and
appendicular mass on the right side, but origin of pain at the umbilical region
is absent). There may be a palpable, tender and soft lump.
• Cold abscess: Pain localized to the iliac fossa with pain in the back for a long
duration. A soft nontender mass may be felt in the iliac fossa, which may
also track down into the thigh behind the inguinal ligament (cross fluctuation
may be elicited). Kyphosis with paraspinal muscle spasm may be present.
In both situations, psoas spasm is present, and the patient is not able to
extend the thigh on the affected side Ref (Fig. 29.14D).
• US, CT and MRI abdomen (Fig. 33.34) are diagnostic.
• X-rays of chest and spine may be useful in identifying the tubercular lesions.
FIGURE 33.34 MRI—bilateral ileopsoas abscesses.
Treatment
• US or CT-guided aspiration of abscess with appropriate antibiotics.
• Tuberculosis needs antitubercular treatment.
Chondrosarcoma of iliac bone

• Occurs in the age group of 30–50 years.
• Commonly involves flat bones; scapula, ribs and pelvis.
• They may be well-differentiated or high-grade anaplastic in type.
A painless, hard bony swelling in the iliac fossa.
X-rays and CT (Fig. 33.35) are diagnostic.
FIGURE 33.35 X-ray—chondrosarcoma of left ileum.
Treatment
• Wide excision with bone grafting is the treatment of choice.
• It is radioresistant.
Pelvic abscess
Collection of pus in the pelvic cavity most often follows rupture of bowel in
• inflammatory bowel diseases;
• appendicitis;
• colonic diverticulitis
• or improperly drained upper abdominal collections or a result of generalized
peritonitis.
• Fever, lower abdominal pain, diarrhoea, and urinary symptoms (urgency,
frequency and dysuria).
• Large abscess presents as a tender hemispherical mass in the hypogastrium,
but presents as a tender bulge in the rectal examination.
DD: Pelvic inflammatory mass.
US and CT (Fig. 33.36) are diagnostic.
FIGURE 33.36 MRI—pelvic abscess.
Treatment
• Transrectal or transvaginal drainage is curative.
• Very large abscess needs suprapubic drainage.
33.9 Lumps in the hypogastrium

A variety of diseases present as a lump in the hypogastrium. They are given in
Table 33.18. They are already discussed in various chapters.
TABLE 33.18
Lumps of Hypogastrium
Intra-abdominal
Extra-abdominal
Organ Pathology
Urachal cyst Urinary bladder Distended bladder a
Postoperative hernia Uterus Pregnancy b
Pelvic bone swellings Fibroid b
Ovaries and adnexae Cyst, ectopic pregnancy, ovarian malignancy b
Peritoneum Pelvic abscess
a
b
General particulars
• Age: Malignancies like carcinoma are more common in the elderly and
sarcomas are common in the young.
• Sex : Testicular tumours in the males and uterus and ovaries related tumours
should be considered in the analysis of abdominal lumps in females.
• Race and religion: Jews and Muslims who perform religious circumcisions
have a low incidence of carcinoma of the penis.
• Place of residence: Certain areas show endemicity for certain illnesses like
filariasis.
Eliciting history
acute pathology (e.g., acute abscess) and the long duration indicates chronic
pathology (e.g., benign tumours). Patients with malignant lesions do not
preserve themselves in good health for a very long time if they have not had
any treatment.
Sudden origin indicates acute pathology (e.g., acute abscess) and gradual
development indicates chronic pathology (e.g., benign tumours). History of
trauma indicates traumatic pathology,.for example haematoma. Sometimes
the trauma might bring the attention of the patient to a preexisting swelling.
• Size at the time of onset: What was the size of the swelling when the patient
saw it first?
Description of the size of the swelling will permit the examiner to compare
its growth if any and can be correlated with the duration of the illness (e.g.,
malignant growths). Likewise decrease in size may indicate resolving lesions
(e.g., resolving rectus sheath haematoma).
• Association of pain: Was or is the swelling painful?
Lumps of acute infectious pathology (e.g., liver abscess) are associated with
pain of varying intensity and nature. Dull pain may indicate swellings due to
chronic pathologies like tuberculosis, or even malignancy.
Association of high-grade fever may indicate an infective pathology (e.g.,
liver abscess) or low-grade fever may indicate malignancies (e.g.,
lymphomas).
• Pressure effects: Is it producing any pressure effect on neighbouring
structures?
Association of pressure effects will indicate its local invasiveness and the
inward growth, which is not seen from the outside (e.g., pedal oedema due to
pressure on inferior vena cava by retroperitoneal swellings), and also
indicate the urgency of treatment required. It may also indicate the relevant
investigations to be performed to facilitate the correct treatment.
Ileopsoas abscess causes psoas spasm, and interferes with extension of the
hip.
course of illness?
Loss of appetite and weight are indicative of illnesses like tuberculosis and
malignancies.
give a clearer picture of diagnosis (failed treatment will help in the
elimination from differential diagnosis and success will help in confirmation
of the diagnosis and continuation of the treatment).
treatment?
Diseases like tuberculosis occur in families, which live in crowded areas and
a positive history may be a good indicator for the present diagnosis.
Personal habits like smoking and drinking alcohol may be the causative
factor for certain illness (e.g., pancreatic malignancy).
match the situation.
Abdomen
exposing the genitalia, the inguinal and femoral areas for complete examination
(Ref Fig. 30.40). Privacy of the patient must be assured, and a nurse be kept by
the side of the patient, especially when the patient is a female.
The clinical examination of abdomen, consists of
1. Inspection
2. Palpation
3. Percussion
4. Auscultation
Inspection
Shape
Distension of abdomen has various characteristics depending on the intra-
abdominal pathology. Lumps of the abdominal cavity distort the shape of the
abdomen due to localized distensions.
• Localized distension
• Distension of central abdomen (e.g., large retroperitoneal nodes).
• Asymmetrical localized distensions.
- Upper abdominal distension (right side) is seen in gross enlargement of
liver, and (left side) in splenomegaly.
- Lower abdominal distension (e.g., large tumours in lower abdomen)
(Fig. 33.37).
- Fullness of iliac fossa (e.g., appendicular mass) (Fig. 33.38).
- Distension of one of the flanks is seen with renal mass on that side.
FIGURE 33.37 Fullness of lower abdomen in large metastatic lymph nodal
swelling of pelvis.
FIGURE 33.38 Fullness of right iliac fossa in appendicular mass.
Movements of the abdominal wall
Some pathologies like inflammatory swellings (e.g., liver abscess) and
malignancies (e.g., secondaries liver) restrict the movements of the abdominal
wall in that region, due to stretch or pain.
Pulsations
• Normal abdominal aortic pulsations may be visible in the epigastrium in
very thin patients.
• Abnormal and prominent aortic pulsations may be seen in the mid abdomen
(e.g., abdominal aortic aneurysm).
Peristalsis
• Visible gastric peristalsis (e.g., obstructing gastric malignancy).
• Visible intestinal peristalsis (e.g., ileocaecal tuberculosis with obstruction).
• Visible colonic peristalsis (e.g., obstructing rectal malignancy).
Site of the swelling

The site of the swelling should be noted with reference to the region (Fig.
30.36).
Size and shape of the swelling
The exact size and shape of an intra-abdominal swelling is difficult to assess
by inspection. Vague fullness is caused by these swellings and a rough estimate
of the size may be possible (e.g., globular–distended urinary bladder).
Skin over the swelling
Changes are seen on the skin when the swelling is very large (e.g., stretch may
be caused by a large ovarian cyst, inflammatory changes may be caused by an
appendicular abscess). Veins may be seen prominently on the skin when the
swelling is very large. Scars may indicate previous surgery.
Movement of the lump on respiration

The lumps arising from the structures lying close to the diaphragm like the liver,
gallbladder, spleen and stomach will move well with respiration. The swellings
in the mid and lower quadrants do not move with respiration (e.g., malignancy of
the caecum). Retroperitoneal tumours (large) do not move with respiration.
Lump is intra-abdominal or extra-abdominal

This can be distinguished by three methods:
• Head raising test: The patient lying supine is asked to raise the head, which
makes the abdominal muscles of the upper abdomen contract. Intra-
abdominal lumps of the upper abdomen will become less prominent and the
extra-abdominal lumps or those in the abdominal wall will become more
prominent (Fig. 33.39).
• Leg raising test (Carnett’s test): The patient in the supine position is asked
to raise the legs without bending the knees, which will make the abdominal
muscles of the lower abdomen contract. Intra-abdominal lumps of the lower
abdomen will become less prominent and the extra-abdominal lumps or
those in the abdominal wall will become more prominent (Fig. 33.40).
• Kamath’s test: This method is utilized in very ill patients who will not be
able to cooperate for the above tests. The patient lying supine is asked to
strain (as if in the toilet), which will make all the abdominal muscles
contract. Intra-abdominal lumps will become less prominent and the extra-
abdominal lumps or those in the abdominal wall will become more
prominent.
FIGURE 33.39 Head raising test.

FIGURE 33.40 Leg raising test (Carnett s test).
Hernial sites
Inspecting the hernial sites in the groin should be an important step, as many
times, an obvious diagnosis may lie there (e.g., incarcerated groin hernia).
Left supraclavicular area

The left supraclavicular area gains importance because of the presence of lymph
node swellings in this area secondary to intra-abdominal pathology (e.g.,
malignancy of stomach, pancreas, etc.)—Troisier’s sign (enlargement of
Virchow’s nodes situated between the sternal and clavicular heads of
sternocleidomastoid, and indicates advanced malignancy commonly from
stomach and testis).
External genitalia
scrotum and assess any scrotal swelling.
Palpation
abdomen.
explained in Chapter 31.
Local temperature
By the dorsum of the hand, any area of raise in local temperature over the
abdominal wall, especially on the lump should be assessed. Increase in
temperature may indicate local inflammation (e.g., liver abscess, appendicular
abscess).
Site, size and shape of the swelling

Site, size, shape, surface and margin of the swelling give an indication of the
organ involved. The examples are given as follows:
• Site: e.g., swelling in the hypochondria–hepatomegaly (right side)
splenomegaly (left side).
• Size: e.g., large swelling in the hypochondria–hepatosplenomegaly or
splenomegaly, moderate size, e.g., renal swellings, small swellings, e.g.,
gallbladder tumours.
• Shape: e.g., shape of the kidney in renal swellings.
• Surface: e.g., smooth surface in splenic swellings, nodular or irregular
surface in malignant hepatomegaly.
• Margin: e.g., upper border is characteristically not felt in hepatomegaly and
splenomegaly (in contrast upper border is felt in renal swelling), notches are
felt in splenic swellings (absent in renal swellings).
Consistency
Consistency of the swelling is tested by application of mild pressure over the
swelling with the fingers. This is described as soft, firm and hard, depending on
the feel by the examining fingers.
• Soft: Fluid containing swellings are soft in consistency (e.g., mucocoele of
gallbladder, mesenteric cyst, ovarian cyst).
• Firm: Tensely distended hollow organs (e.g., carcinoma of gallbladder, lymph
node swellings).
• Hard: Malignant lumps (e.g., secondary deposits of liver), calcified masses
(e.g., calcified haematoma, tuberculous lymph nodes), bony swellings (e.g.,
chondrosarcoma of ileum).
Tenderness
Tenderness is the pain felt by the patient when the examiner presses over the
swelling. This is mainly elicited by observing the patient’s face; pain makes
patient wince (e.g., liver abscess).
Fluctuation
If the abdominal mass is soft, fluctuation may be tested (Figs 33.41A and B)
FIGURE 33.41 (A) Eliciting fluctuation with two fingers. (B) Eliciting
fluctuation with four fingers.
Pulsations
Is the mass pulsatile? There are two varieties of pulsations: expansile and
transmitted.
• Expansile pulsations: This property is exhibited by aneurysm and, this can be
tested by keeping both the index fingers as far possible on the swelling.
When the fingers show upward movement, but separate and diverge, it is
considered positive.
• Transmitted pulsations: The pulsation may be transmitted on the swelling
(e.g., lump on the aorta). This is tested by keeping the index fingers of both
hands on the swelling far apart. The fingers will show an equal upward
movement without separation. Knee elbow test: This can be further
confirmed by putting the patient in knee-elbow position. Swellings sitting on
the aorta will not show any pulsations as it gets separated from the aorta by
gravity, whereas a true aneurysm will continue to show pulsations.
Movement of the swelling

• Movement with respiration: The lumps related to the organs that are closely
related or situated close to the diaphragm, will show up and down movement
corresponding to expiration and inspiration respectively. Method of
examination: The examining hand is kept near the lower border of the
swelling, and the patient is asked to take deep inspiration. It will show a
downward movement and hit or lift the examining hand, and at the same
time, the expiratory movement will take the swelling back to its original
position. (e.g., mass arising from liver and spleen, stomach, gallbladder and
kidney).
• Side to side mobility: The mass if it is small can be held with the thumb and
other fingers of the examining hand (e.g., mucocoele of gallbladder) and
moved side to side. Mobility is a good indication that the lump is not fixed to
deeper structures.
• Ballottement: When the lump is large, it can be held with both hands, and
moved side to side and this movement is called Ballottement (e.g., large
ovarian cyst, renal swellings).
Abdominal organs
All abdominal organs should be palpated. It should also be remembered that the
intra-abdominal organs are not palpable unless they are distended, dilated or
enlarged. Pancreas is not palpable even when it is enlarged (see Ch. 32).
Hernial sites
It should never be forgotten to examine the groins, as there may be associated
herniae (see Ch. 35).
External genitalia
It is essential to palpate the testes in a male and record the findings (e.g., para
aortic lymph nodes of testicular malignancy).
Percussion
Percussion over solid abdominal lumps exhibit dullness (e.g., hepatomegaly)
unless there is a loop of bowel lies in front of it (e.g., transverse colon anterior to
renal swelling). Percussion of liver and spleen are detailed in Chapter 31.
Auscultation
• Bruit: Bruit may be heard over the abdominal aortic aneurysms.
• Bowel sounds: Bowel sounds may be exaggerated in chronic small bowel
obstructions caused by obstruction (e.g., caecal malignancy).
Pelvis
Rectal examination
Digital examination of the rectum is mandatory in the examination of abdomen.
The following are to be noted:
1) Perianal skin pathologies : fistula in ano (e.g., Crohn’s disease).
2) Integrity and nature of rectal mucosa (e.g., growths of anus and rectum).
3) Swellings in the para rectal areas (e.g., sigmoid colon growths, lymph
nodes).
4) Tip of the examining finger for blood and mucus (e.g., growths of anus and
rectum).
5) Proctoscopy for haemorrhoids (e.g., part of portal hypertension and rectal
malignancies) and growth.
Vaginal examination
noted:
1) Assessment of uterus and cervix (e.g., for malignancies).
2) Fornices (e.g., ovarian tumours, Krukenburg’s tumours).
3) Pouch of Douglas for pelvic metastases.
Lymphatic system
detail, for example tuberculosis and lymphoma. Examination of the liver and
spleen completes the lympho reticular system, which is useful in diagnosis.
Virchow’s nodes (enlarged left supraclavicular lymph nodes secondary to
intra-abdominal malignancy) should be looked for (Troisier’s sign).
Other systems
Examination of other systems becomes necessary as the symptoms mimic those
of abdominal pathologies. They are enumerated in Table 33.19.
TABLE 33.19
Extra Abdominal Diseases Presenting with Abdominal Symptoms

Chest Tuberculosis of ribs Cold abscess of upper abdomen
Back, loin, spine Pott’s disease Cold abscess of abdominal wall or ileopsoas sheath
Scrotum Malignancy of testis Para aortic lymphadenopathy
CHAPTER 34
Rectum and anal canal

N. Mohan, S. Devaji, Rao
CHAPTER OUTLINE
34.1. Surgical anatomy of rectum and anal canal 590
34.2. Aetiological classification of anorectal diseases 590
34.3. Anorectal diseases 590
• Anorectal malformations 590
• Post anal dermoid 591
• Sharp, blunt or penetrating injuries of rectum and anal canal
592
• Anorectal abscesses 592
• Fistula in ano 592
• Amoebic proctitis and ulcers 594
• Polyps 595
• Malignancy of rectum 595
• Malignancy of anal canal 595
• Haemorrhoids 596
• Perianal haematoma 597
• Anal fissures 598
• Prolapse of rectum 598
• Solitary rectal ulcer 599
• Sexually transmitted diseases of anus and rectum 599
34.4. Symptoms of anorectal pathologies 599
34.5. Rectal examination 601
• Indications 602
• Rectum 603
• Abdomen 607
• General 607
34.1 Surgical anatomy of rectum and anal

canal
The rectum is the final straight portion of the large intestine, which is about 12
cm long, and begins at the rectosigmoid junction (at the level of the third sacral
vertebra or the sacral promontory) and terminates at the level of the anorectal
ring (the level of the puborectalis sling) or the dentate line.
The dentate line (called for its resemblance to a row of teeth) is the line of
junction of anal and rectal mucosae, but the transition takes place gradually with
a transitional zone above the dentate line. This line is a watershed of lymphatic
drainage, above the dentate line into the inferior mesenteric nodes and below the
line to inguinal nodes.
The pelvic floor is funnel shaped and is formed by the levator ani muscles.
The puborectalis muscle envelopes the lower rectum on all sides, except
anteriorly. This continues as external anal sphincter. The external sphincter
forms three arbitrary bundles, subcutaneous, superficial and deep. The internal
anal sphincter is the direct continuation of the circular muscle fibres of the
rectum, which is felt like a tight band. Between the sphincters, lies the
intersphincteric space, containing anal glands.
The rectum is followed by the anal canal, before the GIT terminates at the anal
verge. The distal part of anal canal is lined by stratified, squamous, non-
keratinized epithelium, whereas the perineal skin is lined by stratified,
squamous, hairy and keratinized epithelium.
34.2 Aetiological classification of anorectal

diseases
The anorectal diseases can be divided based on its aetiology (Table 34.1).
TABLE 34.1
Aetiological Classification of Anorectal Diseases
Congenital Anorectal malformations

Sacrococcygeal teratoma
Post anal dermoid
Traumatic Sharp, blunt or penetrating injuries of rectum
Inflammatory Anorectal abscesses
Fistula in ano
Amoebic proctitis and ulcers
Benign neoplastic Benign tumours
Polyps
Malignant neoplastic Malignancy of rectum
Malignancy of anal canal
Miscellaneous Haemorrhoids
Perianal haematoma
Anal fissures
Prolapse of rectum
Solitary ulcer of rectum
Sexually transmitted diseases of anus and rectum
34.3 Anorectal diseases
Anorectal malformations
• An imperforate anus or anorectal malformations (ARMs) are birth defects
in which the rectum is malformed, with a spectrum of different congenital
anomalies, that varies from fairly minor lesions, to complex anomalies.
• Estimated incidence of 1 in 5000 births.
• It affects boys and girls with similar frequency. However, imperforate anus
will present as the low version 90% of the time in females and 50% of the
time in males.
• Cause of ARMs is unknown.
• The terminal part of hind gut enters into the cloaca, an endoderm lined cavity
in direct contact with surface ectoderm. The urorectal septum arises as a
transverse ridge in the angle between allantois and hind gut and grows
caudally dividing the cloaca into an anterior primitive urogenital sinus and a
posterior anorectal canal. The cloacal membrane gets divided into anterior
urogenital membrane and posterior anal membrane (Fig. 34.1). During this
course, the anal membrane is surrounded by mesenchymal swelling and by
about eighth weeks it is located at the bottom of the ectodermal depression
known as anal pit or proctodeum and by the ninth week, anal membrane
ruptures to form the anal opening. Any abnormality in the above process
leads to the various anorectal malformations.
FIGURE 34.1 Development of rectum and anal canal.
• A very obvious defect, probing will confirm the nonpatency.
• Associated anomalies should be assessed.
• US can determine the type of the anomaly.
• Wangensteen–Rice invertogram: X-ray of the child in inverted position 12–
24 hours after birth, when swallowed air has reached rectum and can act as a
natural contrast agent; will show the level of obstruction by cessation of air
level.
• MRI is a better method to assess the level of the atretic rectal cul-de-sac with
respect to the pubococcygeal line (the radiological landmark for the upper
border or the levator ani muscle).
• Contrast studies will confirm the level of obstruction precisely.
Treatment
• Imperforate anus usually requires immediate surgery to open a passage for
faeces unless a fistula can be relied on until corrective surgery takes place.
Depending on the severity of the imperforate, it is treated with a posterior
sagittal anorectoplasty with or without a colostomy.
• Complete rectal reconstruction is required where the anorectal system is
linked by fistulae into the urinary tract.
• Sometimes surgical treatment involves relocating the anal and rectal area into
their normal positions.
Post anal dermoid

• This congenital condition occurs in the potential space between the anal canal
and the coccyx.
• This is a form of teratoma.
• Contains ectodermal structures of hair and sebaceous glands in addition to
keratin.
• The patient may be asymptomatic and may be diagnosed during routine rectal
examination.
• The cyst may get infected and burst spontaneously and form a sinus in the
post anal skin.
• Large cysts may cause constipation.
• CT abdomen is diagnostic.
• Barium enema is useful.
Treatment
Excision of large and symptomatic cysts.
Sharp, blunt or penetrating injuries of rectum

The injuries of the anus and rectum can be
• self-inflicted;
• by erotic sex (anal sex);
• following trauma (accidental sitting on sharp objects, or part of road traffic
accidents) and
• a part of injuries inflicted by others (consequence of a fight or shooting
incident).
• Painful bleeding per rectum, with a preceding history of trauma.
• Rectal examination by finger will be diagnostic. The examining finger may
feel the rent or it may get stained by frank blood.
• Proctoscopy is necessary for assessment of anal and low rectal injuries.
• Variety of investigations like CT, barium enema are useful.
• US may be needed depending upon the seriousness of the injury.
Treatment
Primary repair of the injuries may be needed with or without defunctioning
colostomies, as per the situation.
Anorectal abscesses
• Acute infections of the anal intersphincteric glands caused by aerobic and
anaerobic organisms.
• They are of four types (Fig. 34.2):
(1) Pelvi rectal abscess
(2) Submucous abscess
(3) Ischiorectal abscess
(4) Perianal abscess
• The infection originating in the intersphincteric space may spread in three
directions:
(1) Upwards
(2) Downwards
(3) Horizontally and circumferentially
• When the infection spreads in the vertical direction, that is upwards and
downwards, and opens at two places, forming an internal opening in the
rectum and an external opening on the perianal skin, resulting in a fistula.
FIGURE 34.2 Anorectal abscesses.
• A painful lump in the perianal region (Fig. 34.3), associated with fever.
• Signs of acute inflammation in the perianal region.
• Fluctuation is difficult to demonstrate.
FIGURE 34.3 Perianal abscess - 3 O"clock position.
Treatment
• Incision and drainage of painful abscess under general anaesthesia, under
cover of antibiotics.
• Appropriate antibiotics are necessary based on culture examination of pus,
after drainage.
Fistula in ano
• A track lined by epithelium or granulation tissue with two openings, one at the
outside on the skin and the other inside the anal canal.
• This is the end product of anorectal sepsis.
• When the internal opening is
• above the anorectal ring it is called ‘high fistula’ and
• below the anorectal ring it is called ‘low fistula’.
• Anal fistulae are classified (Fig. 34.4) in relation to the anal musculature
(sphincters). They are as follows:
• Transsphincteric: primary track is across the external sphincter with the
internal opening above (high fistula) or below the levator ani muscle (low
fistula).
• Intersphincteric: the primary track is between the sphincters (usually high
fistula).
• Suprasphincteric: primary track with the internal opening above the
levator ani (high fistula).
• Extrasphincteric: primary track below the sphincters (low fistula).
• Recurrent and multiple fistulae are caused by infections like tuberculosis,
Crohn disease, ulcerative colitis and colloid carcinoma.
FIGURE 34.4 Anal fistulae.
Symptoms
• Intermittent anal discharge, purulent or blood stained.
• Pain may be present during discharge free intervals.
Signs
• A discharging opening in the perianal skin (Fig. 34.5A and B).
• The internal opening may be felt as an indurated nodule or a depression, seen
at proctoscopy.*
• Tuberculosis and Crohn disease may present with multiple external fistulous
openings (Fig. 34.6).
FIGURE 34.5 Fistula in ano—(A) 11 O’clock position and (B) 2 O’clock
position.
FIGURE 34.6 Multiple perianal fistulae of tuberculosis. Source: (Courtesy Dr K.
Sridhar)
*Goodsall’s rule (Fig. 34.7)

• When the external fistulous opening liesanterior to transverse anal line (an
imaginary line connecting both the ischial tuberosities), and is
• more than 3 cm away from the anal orifice, it takes a curved course to
open at posterior midline internally at 6 O’clock position, whereas
• within 3 cm from the anal orifice, it takes a direct course to open at its
corresponding position running radially.
• When the external fistulous opening liesposterior to transverse anal line,
whatever distance it is away from the anal orifice, takes a curved course and
opens at the posterior midline internally.
FIGURE 34.7 Goodsall’s rule.
Special investigations are necessary in recurrent fistulae.
• Fistulogram (Fig. 34.8) is useful for treatment planning.
FIGURE 34.8 Anal fistulogram.
Treatment
• Anal fistulectomy is the treatment of choice.
• Appropriate medical treatment is for recurrent fistulae caused by infections
like tuberculosis and Crohn disease.
Amoebic proctitis and ulcers

• Infection of the rectum and colon caused by Entamoeba histolytica.
• The cysts are consumed through contaminated food or water.
• Chronic or, mild to fulminant acute dysentery.
• Proctoscopy or sigmoidoscopy will be conclusive.
• Identification of the organisms in stool.
• Endoscopic (Fig. 34.9) biopsy of the ulcer.
• Serologic tests are conclusive.
FIGURE 34.9 Sigmoidoscopy—multiple amoebic ulcers of

rectum. Source: (Courtesy Dr Mani Veeraraghavan)
Treatment
Anti-amoebic treatment is curative.
Benign tumours
• Adenomas form the majority of benign tumours.
• Connective tissue tumours include lipomas, fibromas, and leiomyomas.
• These tumours fall into a new entity called ‘Gastrointestinal stromal tumours
(GIST)’.
Mucous diarrhoea with or without rectal bleed.
Proctoscopy, sigmoidoscopy (Fig. 34.10) and histopathology are conclusive.
FIGURE 34.10 Sigmoidoscopy—rectal lipoma. Source: (Courtesy Dr Mani

Veeraraghavan)
Treatment
Excision of these tumours is necessary as adenomas have very high malignant
potential.
Polyps
• Polyps of rectum are common, may be associated with those of the colon
(familial polyposis).
• Juvenile polyps occur in infants and children.
• They have a strong malignant potential.
• Rectal bleed.
• On examination they can be felt as sessile or pedunculated growths.
Total colonoscopy (Fig. 34.11) is necessary to rule out familial varieties (familial
adenomatous polyposis).
FIGURE 34.11 Sigmoidoscopy—rectal polyps. Source: (Courtesy Dr Mani
Veeraraghavan)
Treatment
• Excision of polyps by colonoscopy is the treatment of choice.
• Total colectomy with ileostomy or ileo-anal anastomosis with pouch
construction is done for familial polyposis and multiple polyposis.
Malignancy of rectum
• Malignancies of the rectum include
• adenocarcinoma (commonest)
• squamous cell carcinoma and
• lymphoma.
• The commonest spread is to the liver.
• Most patients present with rectal bleed, recent change in bowel habit like
constipation or overflow diarrhoea, mucous in nature.
• Sense of incomplete evacuation and tenesmus are also possible symptoms.
• Digital examination and proctoscopy confirm the clinical diagnosis in low
rectal tumours.
• Examination of the abdomen for hepatomegaly is essential in case of rectal
malignancies.
• Proctoscopy or sigmoidoscopy (Fig. 34.12A) is diagnostic.
• Punch biopsy and histopathology are conclusive.
• Contrast enhanced computerised tomogram (CECT) will show a filling
defect (Fig. 34.12B).
FIGURE 34.12 (A) Sigmoidoscopy—malignant growth Source: (Courtesy Dr
Mani Veeraraghavan). (B) ECT—malignant growth rectosigmoid.
Treatment
Appropriate radical surgery with adjuvant chemoradiation is the treatment of
choice.
Malignancy of anal canal

• Malignancies of the anal canal are uncommon.
• Affects the elderly.
• Linked to oncogenic types of human papilloma virus (HPV) types 16, 18, 32
and 33.
• genital warts
• homosexuality
• HIV infection
• chronic fistulae and
• pelvic radiation.
• Macroscopically, it appears as a
• nodule
• polyp and
• ulcer with everted edges.
• squamous cell carcinoma (90%)
• adenocarcinoma from mucous glands (10%)
• basal cell carcinoma (rare) and
• malignant melanoma (rare).
• circumferentially and longitudinally within the anus and invade perianal
skin
• laterally to sphincters, ischiorectal fossae, anteriorly to vagina and urethra
• lymphatically to inguinal nodes, iliac nodes and
• haematogenously to liver, lungs and skeleton (very rare).
Symptoms
• Discharge
• Irritation/discomfort
• Bleeding
• Tenesmus
Signs
• Distal anal tumours are evident on inspection, as warty growths (Fig. 34.13)
with ulcerations.
• Inguinal lymph nodes may be palpable.
FIGURE 34.13 Anal carcinoma.
• Endoanal US is very informative.
• CT abdomen is informative.
• Punch biopsy and histopathology is conclusive.
Treatment
• Radiotherapy with or without chemotherapy is the treatment of choice.
• Surgery is reserved for some tumours.
Palliative
• Defunctioning colostomy for inoperable tumours.
• Radiotherapy.
Haemorrhoids
• Haemorrhoids (piles) are the varicosities of the haemorrhoidal plexus of
veins.
• Haemorrhoids are caused by
• chronic constipation;
• purgation and
• malignancies.
• Haemorrhoids may occur in the late middle age or elderly, secondary to rectal
growths infiltrating or compressing the haemorrhoidal veins, called
‘symptomatic piles’ since it is a symptom of a condition more proximally.
• External piles are covered by skin and the internal piles are covered by
mucosa.
• Haemorrhoids are of four degrees:
• First degree: only bleeding (splash in the pan) and no mass.
• Second degree: masses prolapse on straining and reduce spontaneously
(Fig. 34.14A).
• Third degree: masses prolapse on straining and need manual reduction.
• Fourth degree: masses stay prolapsed at all times (Fig. 34.14B).

FIGURE 34.14 (A) Second-degree haemorrhoids. (B) Prolapsed
haemorrhoids. (C) Inflamed haemorrhoid,
Complications: Profuse haemorrhage, prolapse, strangulation, thrombosis,

infection (Fig. 34.14C), gangrene, ulceration and fibrosis.
Symptoms
• Majority of patients present with painless rectal bleed.
• Constipation is a common accompaniment.
• Mucous discharges and pruritus ani are commonly present.
• Pain is felt when the pile masses are thrombosed and strangulated.
On examination
• Lumps (3, 7 and 11 O’clock positions—primary piles) at the anal orifice.
• Digital examination to rule out associated sphincter spasms and tumours is
important.
• Proctoscopy is diagnostic.
Note
• Uncomplicated haemorrhoids are not felt by the examining finger.
• Thrombosed piles masses are firm to feel and visible on inspection, and
present with gross oedema and ulcerations.
No special investigation is required unless other pathologies like malignancies
are suspected.
Treatment
• Haemorrhoidal bleeds are usually self-limiting.
• Banding or infra-red coagulation controls acute bleeds.
• Venotonics control chronic recurrent rectal bleeds.
• Laxatives to manage constipation.
• Haemorrhoidectomy is curative.
Perianal haematoma
• It is sometimes called as ‘thrombosed piles’, but it is not related to
haemorrhoids.
• The cause is not exactly known.
• Occurs due to thrombosis of a subcutaneous vein below the transitional zone.
• A discrete painful swelling (Fig. 34.15).
• On examination it is tender and lies external to the anal canal.
FIGURE 34.15 Perianal haematoma (ulcerated).
• Proctoscopy to rule out associated haemorrhoids.
Treatment
• No treatment as most of them resolve.
• Incision and curettage gives quick relief from painful swellings.
• Since it opens up a vein, bleeding may be troublesome.
Anal fissures
• It is a tear in the anal skin, usually found in the 6 O’clock or 12 O’clock
positions, following a bout of constipation and passage of a large hard stool.
• Posterior fissures are common than the anterior due to following reasons:
• Anal canal is posteriorly angulated.
• Anal orifice is elliptical in shape.
• Posterior part of the anus is not supported by the muscles.
• Local ischaemia.
• Anal fissures are of two types. They are as follows:
• Acute fissures: tear in the anal skin due to forceful expulsion of hard faecal
matter.
• Chronic fissures: nonhealing of acute fissure due to repeated trauma
caused by hard faecal matter.
• Anal fissures can occur secondary to Crohn disease, ulcerative colitis, syphilis
and tuberculosis.
• Acute fissure is a very painful condition associated with fresh bleeding
(streak of blood on the hard faecal matter), presenting with a linear tear in
the anal skin (Fig. 34.16A).
• Chronic fissure has a swollen skin at its lowest part called ‘sentinel pile’
(Fig. 34.16B).
FIGURE 34.16 (A) Acute fissure in ano—6 O’clock position. (B) Chronic
fissure in ano.
No specific investigation is necessary, excepting a proctoscopy.
Treatment
• Acute fissure heals when constipation is taken care of, with probable anal
dilatation.
• Chronic fissure requires excision.
• Secondary fissures require appropriate management.
Prolapse of rectum
• Generally caused by chronic constipation and straining at stool and when the
pelvic floor is weak.
• Occurs at extremes of age.
• The rectum presents as a prolapsed mucosa, varying from partial to full
thickness (Fig. 34.17), appearing more during the act of defecation.
• It can reduce spontaneously or may need manual reduction.
• There may be associated mucous discharge, bleeding, pain and incontinence.
• Patient may have to strain to make it prolapse for clinical examination, in
most cases.
• On examination
• Prolapse upto 5 cm is considered to be partial and more than that is
considered complete.
• They can be differentiated by feeling the wall with the thumb and the index
finger.
FIGURE 34.17 Prolapse rectum. Source: (Courtesy Dr K. Dakshinamoorthy)
DD: Haemorrhoids, intussusception.
Proctoscopy and colonoscopy may be needed to rule out the causes of
constipation, and associated malignancy.
Treatment
Various operative procedures are available for the treatment of prolapse.
Solitary rectal ulcer

This occurs in patients who strain to pass stools, producing an internal
intussusception occasionally a prolapse, resulting in a solitary ulcer in the
rectum.
• Rectal bleed associated with mucus.
• Proctoscopy reveals a solitary ulcer usually on the anterior rectum just above
the anal canal.
• The ulcer may be polypoid or elevated.
DD: Carcinoma
• Defecography, transrectal ultrasound (TRUS) and anorectal manometry are
necessary.
• Proctoscopy or sigmoidoscopy (Fig. 34.18) is diagnostic.

FIGURE 34.18 Sigmoidoscopy—solitary rectal ulcer. Source: (Courtesy Dr Mani
Veeraraghavan)
Treatment
• Rectopexy for complete rectal prolapsed and internal intussusception.
Sexually transmitted diseases of anus and

rectum
• Anal intercourse is known to transmit the infections such as gonorrhoea,
syphilis and herpes simplex.
• Perianal warts is a condition caused by human papilloma virus.
• Gonorrhoea and herpes simplex present with constipation and mucous or
purulent discharge.
• Herpes simplex produces vesicular lesions in the perianal skin, which may
ulcerate.
• Syphilis presents with an ulcer (chancre), which may have to be differentiated
from a fissure. Syphilitic ulcers do not occupy the midline as fissures.
• Warts (condyloma accuminata) is another condition transmitted through
sexual contact (Ref Fig. 9.8).
Discharges may isolate the incriminating organism.
Treatment
• Antibiotics for gonococcal and syphilitic infections.
• Antiviral drugs for herpes simplex infection.
34.4 Symptoms of anorectal pathologies

• Bleeding per rectum
• Pain
• Discharge
• Mass per rectum
• Associated symptoms
Bleeding per rectum
• Bleeding due to anorectal malignancy is frank red in colour
(haematochezia).
• Passing altered blood or black coloured stool (melena) is due to causes
proximal to the ligament of Treitz and are discussed in detail in Chapter 8.
• Rectal bleed is a serious symptom and it indicates a definite pathology, and
they are listed in Table 34.2.
TABLE 34.2
Causes of Rectal Bleeding
Nature of Bleed Cause Region Disease
Frank blood Local Anal canal Injuries, haemorrhoids, anal fissures, anal malignancy,
(Haematochezia) perianal warts
Rectum Injuries, proctitis of varied causes, malignancy, prolapse
Frank or altered blood General Blood dyscrasias Diseases affecting blood coagulation
Drug-induced Analgesics, anticoagulants
conditions
Rectal bleeding has different characteristics. They are given in Table 34.3.
TABLE 34.3
Characteristics of Rectal Bleeding
Nature of
Characteristic of Rectal Bleed Disease
Pain
Bright red blood or fresh bleeding (haematochezia) No pain Haemorrhoids, polyps, diverticulosis, malignancy
mixed or independent of stools of rectum
Mixed with mucus, pus with offensive odour No pain Rectal malignancy, ischaemic colitis, Crohn"s
disease, ulcerative colitis
Streaks of blood on the faecal matter No pain Malignancy of rectum
Pain during Anal fissures
defecation
Variable bleeding Constant pain Anorectal abscess, infected fistula in ano,
endometriosis, malignancy of anal canal
Tenesmus Rectal polyps, rectal malignancy, diverticulitis,
ulcerative colitis
Note
In children, bleeding per rectum is usually due to a rectal polyp.
Pain
• The lesions above the dentate line (the line of junction of anal and rectal
mucosae) are painless and those below may be painful.
• Association of pain and rectal bleeding are shown in Table 34.4.
TABLE 34.4
Association of Pain and Rectal Bleeding
Painful anorectal Trauma, anal fissures, anorectal abscesses, infected sinuses or fistulae, anal malignancy,
conditions complicated haemorrhoids
Painless anorectal Uncomplicated haemorrhoids, rectal malignancy, stricture, rectal prolapse
conditions
Note
Rectal malignancy exhibits pain when it extends into the anal canal or
becomes infected.
The pain due to anorectal diseases has different characteristics. They are given
in Table 34.5. Pain may be associated with other features. They are shown in
Table 34.6.
TABLE 34.5
Characteristics of Pain due to Anorectal Diseases
Characteristic of pain Disease
Throbbing pain Perianal abscess, ischiorectal abscess

Sharp cutting pain (at the time of defecation and persists for hours after the act) Acute fissure in ano
Pain disappears after discharge of pus Fistula in ano
Associated with a mass Complicated haemorrhoids
Colicky pain of lower abdomen Obstructive malignancy of rectum
TABLE 34.6
Association of Pain and Other Symptoms of Anorectal Pathologies
Pain and Other Disease

Features
Pain alone Anal fissure, proctalgia fugax
Pain and bleeding Anal fissure, thrombosed piles, anal canal and rectal malignancy, anorectal abscess, fistula in
ano
Pain and swelling Perianal haematoma, perianal abscess, anal carcinoma
Pain and mass per anum Prolapse rectum, IV degree piles, intussusception, anal canal malignancy
Discharge
Patients may complain of some discharge and staining of the undergarments. It
can be
• mucous: rectal malignancy, inflammations of rectum.
• purulent: spontaneous burst of anorectal abscess.
• mucopurulent: rectal malignancy.
Note
Discharges may occur with or without pain, depending on the pathology.
Discharges may occur from fistulous openings in the perianal region. The
causes of perianal discharges are as follows:
• Fistula in ano
• Urinary fistulae
• Sinuses due to osteomyelitis of pelvic bones
• Pilonidal sinus
• Accidentally opened infected post anal dermoid

Alteration in bowel habits may be in the form of constipation, diarrhoea,
alternating constipation and diarrhoea or spurious diarrhoea.
• Constipation: Constipation dating back to childhood is habitual and needs no
special investigation, whereas constipation of recent onset or short duration,
and a change in the pattern of chronic constipation needs special attention,
especially in the elderly (e.g., annular growth of malignancy of pelvic colon).
• Diarrhoea: Diarrhoea per se is not a complication of a surgical illness, and
may indicate infective pathologies such as amoebic colitis, diverticulitis.
• Alternating constipation and diarrhoea: Partially obstructing growths of the
lower rectum may constipate the patient and the patient may not pass stools
for some days. After sometime, the colon distends and gives way to the
secretions and liquid faecal matter above the faecal mass and cause loose
stools causing diarrhoea.
• Spurious diarrhoea: Patients may present with a diarrhoea like symptom,
when they have growths which are partially obstructing and produce a
feeling of incomplete evacuation. The next morning the patient passes
offensive liquid stools containing blood, mucus and pus, mimicking
diarrhoea, called ‘spurious diarrhoea’ (e.g., proliferative growths of rectal
ampulla). There may be associated tenesmus.
Mass per rectum

Mass appearing from the anal opening may be due to
• external piles
• prolapse of internal piles
• prolapse of rectum
• polyp of rectum and
• intussusception.
Associated symptoms
There may be other symptoms, which may predominate and mask the original
symptom. They are:
• Pruritus ani: due to constant wetting due to the anal secretions and
discharges.
• Cachexia/loss of weight: rectal malignancies.
• Dyspepsia: rectal malignancies, constipation due to benign causes.
Causes of pruritus ani are shown in Table 34.7.
TABLE 34.7
Causes of Pruritus Ani
Causes Pathology
Rectum and anal canal Internal piles, fissures, fistula in ano, polyp, malignancy, condyloma acuminata
Vagina Trichomonal infections, monilial vaginitis, gonorrhoea, cervical erosions
Skin Tinea cruris, monilial dermatitis
Parasites Thread worm infestation, pinworm infestation
Old age Ichthyosis, poor hygiene, excessive intake of laxatives containing liquid paraffin
34.5 Rectal examination
Rectal examination gives a wealth of information in all abdominal illnesses,
more so in anorectal conditions. It is said, ‘If you don’t put your finger into it,
you will put your foot into it’, meaning that if this simple examination is not
done, crucial information is likely to be missed.
Indications
• Gastrointestinal problems: Acute abdomen, suspected pelvic pathology,
constipation, mucus or blood in stools.
• Genitourinary problems: Assessment of prostate in urinary problems.
• Miscellaneous problems: Unexplained backache, lumbosacral nerve root pain,
pyrexia of unknown origin.
Eliciting history
• Age: certain diseases affecting anorectum are common in certain age groups.
• Newborns and infants: sacrococcygeal teratoma, postanal dermoid.
• Small children: rectal polyps.
• Young adults: haemorrhoids, anal fistulae.
• Elderly: rectal malignancy.
Bleeding
• Bleeding per rectum: What is the nature of bleed? Is it red, dark red or
black and how long has it been present?
Bleeding from the rectum and anal canal is red is colour (e.g.,
haemorrhoids), from the colon is dark red (e.g., colonic malignancies) and
from upper gastrointestinal tract it is black (e.g., bleeding from duodenal
ulcer). Intermittent painless bleeding since young age indicates benign
pathology like haemorrhoids, and a recent onset of bleeding indicates a new
pathology like malignancy.
• Relationship of bleeding with faecal matter: Is the bleeding mixed with
faeces or is it separate?
• Blood mixed with faecal matter is seen in colonic pathologies as the stool
is soft and miscible (e.g., malignancies).
• Blood on the surface of the faecal matter when the faecal matter is more
solid as in rectal pathologies (e.g., rectal cancer).
• Bleeding independent of defecation is seen in low rectal pathologies (e.g.,
haemorrhoids).
Pain
• Association of pain: Is there pain either during defecation or at other
times?
• Pain is associated with fistulae due to pent up secretions when they are
closed and once the fistula starts discharging, the pain reduces. This is
independent of defecation.
• Acute pain during defecation is felt with acute fissures, especially the solid
faecal matter needs straining to evacuate.
• Dull constant pain is felt with thrombosed or strangulated haemorrhoids.
Discharge
• Association of discharge: Is or was there any other discharge? If so what is
the nature of discharge?
Anal fistulae may discharge serous or serosanguinous discharge in the
perianal region. Mucous discharges per rectum are seen in inflammatory
bowel diseases like Crohn disease and rectal malignancies, large
haemorrhoids, large polyps.
Bowel habits
• Bowel habits: Is the patient passing the stools without strain? If
constipated, is it of a recent onset or present for a long time?
Habitually constipated patients tend to develop haemorrhoids and bleed.
Constipation of a recent onset may cause acute fissures, and persistent
constipation tends to delay the healing process of acute fissures and chronic
fissures result. Constipation of a recent onset may itself be a result of an
obstructing lesion in the colon and rectum (e.g., malignancy). Some patients
may discharge large quantities of mucus with blood in the mornings, which
get accumulated above the level of the growth and evacuate it urgently
giving an impression of a loose stool (Spurious morning diarrhoea).
Mass per rectum

• Presence of lumps or mass in the anus: Is there any mass or lump
projecting at the anus? If so does it get reduced at any time with or without
a push?
Haemorrhoids may prolapse as masses in the anal orifice. Second degree
haemorrhoids may disappear once the act of defecation is complete, and the
third degree haemorrhoids may stay on even after the act of defecation and
may need to be pushed by the patient’s fingers. Prolapse of the rectal mucosa
may be a reason for a mass in the anal orifice. Anal malignancy is a
possibility.
Associated symptoms
Association of fever may indicate an infective pathology (e.g., anorectal
sepsis)
malignancies.

give a clearer picture of diagnosis (fistulae with previous history of surgery
may indicate a tuberculous pathology or Crohn disease).
treatment?
like recurrence of tuberculosis and Crohn disease. Even recurrent
malignancies should be considered. Previous history of dysentery or
diarrhoea is relevant as it may cause weakening of pelvic floor and result in
prolapse and intussusception, especially in children.
Diseases like fistulae due to tuberculosis occur in families and the positive
history may be a good indicator for the present diagnosis. Polyps, fissures,
haemorrhoids and malignancy have familial preponderance.
match the situation, like extramarital contact or anal intercourse if the lump
is suspected to be of syphilitic aetiology (e.g., condyloma). History relating
to trauma (part of fight or shooting incident) should also be elicited.
Explain to the patient
The patient should be explained about the procedure in detail and the sensation
patient may have during the procedure, and reassure that examiner will not hurt
the patient during the procedure. It should be explained that if the patient
experiences pain, should tell the examiner and not wriggle out of the
examination couch, as it will inconvenience the patient and hurt more. There are
instances of patients falling down from the couch as they are made to lie at the
edge of the couch.
Privacy of the patient must be assured, and a nurse be kept by the side of the
patient, especially when the patient is a female.
Examination of the anus and rectum can be done in any of the following
four positions:
1. Left lateral (Sims’ Position): The patient should lie in the left lateral position
across the examination table, with the buttocks at the edge of the table. The
hips and knees should be flexed and the heels clear of the perineum (Fig.
34.19A).
2. Dorsal position: The patient is in semi-recumbent position with the knees
flexed. The examiner passes his right hand below the right thigh of the patient
to introduce his finger in the anal orifice (Fig. 34.19B). This procedure is
useful in situations like spinal injuries, where the patient cannot be disturbed.
Inspection of the perineum and perianal area cannot be done in this position.
3. Knee elbow position: The patient should flex his thighs and knees, and also
his elbows to rest the body on the flexed knees and elbows (Fig. 34.19C), and
this position is useful for palpating the prostate and seminal vesicles.
4. Lithotomy position: The patient is put in lithotomy position, with the
buttocks projecting beyond the edge of the operating table, with the hips
flexing beyond right angles and the legs supported in stirrups outside the
poles (Fig. 34.19D). This position is useful for preoperative assessment, just
before surgery (Fig. 34.19E).
FIGURE 34.19 Positions for rectal examination—(A) Left lateral position.
(B) Dorsal position. (C) Knee elbow position. (D) Lithotomy position. (E)
Rectal examination in Lithotomy position.
Rectum
The examination of anus and rectum consists of
• inspection of perineum and anus;
• palpation of perianal region;
• digital examination of the anus and rectum and
• proctoscopy.
Inspection of perineum and anus

Examine the patient in left lateral position fully crouched, but the buttocks
should be separated well.
Normal anal orifice: The normal anal orifice looks like an antero-posterior
slit with a few skin folds radiating away from it (due to corrugator cutis ani).
What to look for?
• Soiling: incontinence, poor hygiene.
• Seepage or discharge (blood, mucus or pus) from the anus: haemorrhoids,
fistula, fissure, rectal polyp, prolapse or malignancy, postoperative status.
• Excoriation: scratch marks due to itching, pinworm infestation, primary skin
disorders like fungal infections (Fig. 34.20A), local allergy to toilet paper,
radiation (Fig. 34.20B), etc.
• Swellings
• Perianal haematoma.
• Thrombosed or prolapsed haemorrhoids.
• Skin tags (e.g., shrunk external piles, condyloma).
• Sentinel tags (e.g., chronic fissures in ano): note its position (common in 6
and 12 O’clock positions).
• Growths (e.g., anal carcinoma, condyloma): note the colour (black in
melanoma).
• Polyp protruding through the anal orifice (Fig. 34.21).
• Sinuses(e.g., openings of hydradenitis and pilonidal sinus)and fistulae(e.g.,
external openings of anal fistulae).
• Scars: scars of previous surgeries (e.g., anal fistulae).
• Ulcers (e.g., anal carcinoma).
• Others: Prolapse rectum or intussusception.
FIGURE 34.20A Fungal infections with multiple abscesses.
FIGURE 34.20B Excoration after radiation for anal cancer.
FIGURE 34.21 Rectal polyp.
Note
The anal orifice is imagined as a clock face, with the patient supine, and the
pathology is described in relation to positions of hour hand, for universal
understanding (Fig. 34.22).
FIGURE 34.22 Clock representation of anal opening.
Palpation of perianal region

Examination procedure
• The best position to palpate the perianal skin is the left lateral position.
• The examiner should wear a glove and run his fingers on the surface of the
perianal skin, and note the following:
• Acute fissure increases the perianal muscle spasm when the fingers are run
nearer to it, which is evidenced by increased skin rugosities radiating from
the anus.
• When an external opening of a fistula is seen, the finger should be run on
an imaginary line from it towards the anal orifice, and attempt should be
made to feel the fistulous tract (Goodsall’s rule: Ref Fig. 34.7).
• Perianal skin may be tender and show brawny oedema if there is an
underlying abscess (e.g., ischiorectal abscess).
• If there is rectal prolapse, it should be differentiated from intussusception
(in intussusception fingers can be inserted between the intussusception and
rectal wall, whereas in rectal prolapse it may not be possible).
Digital examination of anus and rectum

1. The best position to do the digital examination of the anus and rectum is the
left lateral position.
2. The gloved and generously lubricated pulp of the index finger should be kept
flat on the anal verge and slowly introduced into the anal canal with the pulp
facing posteriorly (Fig. 34.23A).
3. The pulp of the finger should be rotated circumferentially on all sides (360o)
(Fig. 34.23B and C).
4. After withdrawal of the finger, the examining finger should be examined for
stool colour, mucus and blood.
5. Small discharges could be examined by wiping on a clean white pad.
FIGURE 34.23 (A) Index finger pulp on the anal opening. (B) Entering the
anus and rectum. (C) Sweeping the finger 360°.
What to look for during digital examination?

As the finger enters the anal canal, record the tone of sphincters
• internal sphincter at rest and
• external sphincter while straining.
Once the finger enters the anal canal, feel and record the findings in the
following fashion.
• Inside the lumen
• Presence of faecal matter and their consistency (hard faecal matter needs
evacuation for further examination).
• Ballooning of rectum (seen in intestinal obstruction and sigmoid volvulus).
• Mass protruding into the lumen (e.g., polyp, rectal carcinoma, apex of
intussusception).
• In the rectal wall
• Integrity of the rectal mucosa: break in the mucosa may indicate an ulcer,
or internal opening of fistula in ano.
• Irregularity or elevated mucosa on underlying firm tissue may indicate a
malignancy.
• Strictures are felt as firm circumscribed thickening.
- Benign strictures feel like a diaphragm with a central hole with normal
mucosa (e.g., postoperative).
- Malignant strictures feel like hard irregular thickening fixed to deeper
layers with ulcerations.
- Strictures of lymphogranuloma venereum is tubular and rubbery in
consistency).
• Polyps of rectum (pedunculated polyps are pushed up by the finger and are
better felt when the finger is brought down, whereas sessile polyps move
along the finger when it is taken up and down and felt with equal ease).
• Growths of rectum: 75% are ulcerative or proliferative, 25% occur as
annular strictures (assess the extent, consistency, edges, fixity and
extension to surrounding structures).
• Outside the rectal wall
• Anteriorly,
- Prostate and seminal vesicles in males: the prostate is felt for its size,
tenderness, consistency and the presence of the median sulcus. and
seminal vesicles (detailed in Ch. 37) (Fig. 34.24A).
- Cervix in females: normal cervix may be felt projecting through the
anterior rectal wall (can be mistaken for a neoplasm by the
inexperienced; detailed in Ch. 38) (Fig. 34.24B).
- Rectovesical pouch (in males) and recto-uterine pouch of Douglas (in
females): for collections of pus, blood and secondary deposits etc.
• Posteriorly, Sacrum and coccyx, sacrococcygeal teratoma or post anal
dermoid are palpable.
• Laterally, the ischiorectal fossae for ischiorectal abscess, inflamed
appendix on the right side, tuboovarian pathology on both sides.
FIGURE 34.24 Diagrammatic representation of rectal examination—(A) in
male, (B) in female.
Note
• Only distal 10 cm of rectum can be examined digitally.
• Entry of examining finger may not be possible when acute fissures are
present and the procedure may have to be abandoned and not to be forced
upon.
• Normal rectum is usually empty and smooth-walled.
• Haemorrhoids are not felt unless thrombosed.
• In women, normal cervix and retroverted uterus are often palpable on the
anterior wall.
• Vaginal tampon may confuse the inexperienced examiner.
• Faecal masses may be mistaken for growths (faecal masses are movable and
can be indented).
• Pelvic metastases or colonic tumours may be mistaken for faeces and vice
versa.
Proctoscopy
1. The patient should lie in the left lateral position with the buttocks at the edge
of the couch, the knees drawn up well upto the chest and the heels clear of the
perineum. Knee elbow position can also be used.
2. The buttocks should be separated well with the left hand and a well-lubricated
proctoscope with the obturator (Fig. 34.25) should be inserted into the anus
directed towards the umbilicus and after the entry, it is tilted posteriorly, to
bring the scope in line with the lumen of rectum.
3. The obturator is withdrawn and removed (Fig. 34.26A), and the rectal mucosa
is visualized with good illumination (Fig. 34.26B).
4. The proctoscope should be withdrawn slowly, as it is visually examined up to
the exit.
FIGURE 34.25 Proctoscope.
FIGURE 34.26 (A) The obturator is removed. (B) Visualization of rectum.
What to see?
Normal rectal mucosa is pink in colour with uniform folds.
Pathologies to be looked for:
• Haemorrhoids
• Chronic fissures
• Internal openings of fistula in ano (If the internal opening is near the anal
papilla, the papilla looks hypertrophied).
• Ulcers and growths
Remember
After the completion of the examination, it should be remembered to wipe the
anal orifice with a gauze, so that the patient does not experience any
discomfort of the stickiness of the lubricant or the secretions.
Lymphatic system
Of drainage area
It is always mandatory to examine the area of lymphatic drainage of the rectum
and anus, i.e., para-aortic and inguinal lymph nodes, which will give useful
information (e.g., rectal malignancies metastasize to para-aortic nodes and anal
malignancies metastasise to inguinal nodes)

detail, e.g., tuberculosis. Examination of the liver and spleen completes the
lympho reticular system, which is useful in diagnosis.
Abdomen
Systemic examination of the abdomen should be performed, as haemorrhoids
can be due to intra-abdominal masses pressing the inferior vena cava or due to a
liver disease (e.g., haemorrhoids), likewise hepatomegaly may be an effect of
metastasis of rectal cancer.
General
General physical examination will give clues for diagnosis like evidence of
pulmonary tuberculosis as the cause for a recurrent fistula or even pulmonary
metastases secondary to rectal cancer.
CHAPTER 35
Herniae
K.S. Ravishankar
CHAPTER OUTLINE
35.2. Classification of herniae 608
35.3. General features of herniae 608
• Predisposing factors for hernia 608
• Anatomy of hernial sac 608
• Complications of hernia 609
35.4. Anatomical nomenclature 609
35.5. Groin herniae 609
• Inguinal hernia 610
• Femoral hernia 613
35.6. Ventral herniae 614
• Epigastric hernia 614
• Umbilical hernia 615
• Paraumbilical hernia 615
• Spigelian hernia 615
• Incisional hernia 616
35.7. Other herniae 616
• Obturator hernia 616
• Sciatic hernia 617
• Lumbar hernia 617
• Perineal hernia 618
35.8. Symptoms of hernia 618
• Hernia 619
• General (Abdomen, Chest) 624
35.1 Introduction
Hernia is a protrusion of an internal part of an organ through an aperture with the enclosing membrane.
– Oxford dictionary
Further, hernia may also be defined as a protrusion of a viscus or any other

structure beyond the normal coverings of the cavity in which it is present
(external hernia) or between two adjacent cavities like abdomen and thorax or
into any other subcompartment or cavity (internal hernia).
35.2 Classification of herniae
Herniae are classified as congenital and acquired.
Congenital hernia
Herniation occurs through a preformed sac resulting from incomplete
intrauterine development, e.g., persistent processus vaginalis forming indirect
inguinal hernia, incomplete obliteration of umbilicus forming umbilical hernia.
Acquired hernia
• Primary: Herniae occurring at the natural weak points such as umbilicus
(umbilical hernia), area of femoral vessels penetrating the abdominal wall
(femoral hernia).
• Secondary: Herniae occurring at the site where weakness is caused by factors
such as penetrating injury of the abdomen or surgery (incisional hernia).
35.3 General features of herniae
Predisposing factors for hernia

• Increased intracavitary pressure caused by lifting heavy weights, chronic
cough, sneeze, long-standing constipation, straining to pass urine.
• Weakened abdominal wall caused by advancing age, abnormal collagen
metabolism, previous surgery.
Anatomy of hernial sac

• The hernia sac consists of mouth, neck, body, and fundus (Fig. 35.1).
• The coverings of a hernia will vary according to its site, but commonly, will
be skin, subcutaneous fat, aponeurosis, muscle, endocavity fascia, and
endothelial lining (pleura or peritoneum).
• The contents will vary depending on its location (e.g., caecum, appendix,
small bowel, omentum and right ovary in the right groin hernia, and sigmoid
colon, left ovary in the left groin hernia). The contents of the hernia are
returnable into the cavity when it is uncomplicated, a property called
‘Reducibility’.
FIGURE 35.1 Anatomy of hernia.
Complications of hernia
• Irreducibility: When the contents cannot be returned into the cavity, it is
called irreducible. This may be due to the narrow neck of the sac (e.g.,
femoral, umbilical), or adhesions between the contents of the sac (e.g., long-
standing herniae).
• Obstruction: When the neck of the sac is totally obstructed due to the contents
of the hernia sac (e.g., distended bowel which forms a closed loop), without
vascular impedance, it is said to be ‘obstructed’.
• Strangulation:The venous and lymphatic occlusion distends the bowel further
secreting more fluid in the bowel, causing further increase in the swelling.
The tissues undergo ischaemic necrosis called ‘strangulation’. The tissues
may slough and become permeable to bacteria and bacteraemia results. It
may even perforate to cause septicaemia and septic shock.
• Inflammation: The sac may get inflamed if the contents of the sac like the
appendix or Meckel’s diverticulum is inflamed.
35.4 Anatomical nomenclature
Whatever be the cause, the hernia is named conveniently based on its anatomical
location (Fig. 35.2).
1. Groin hernia
• Inguinal
• Femoral
2. Ventral hernia
• Epigastric hernia
• Umbilical hernia
• Paraumbilical hernia
• Spigelian hernia
• Incisional hernia (postoperative)
• Divarication of recti
3. Others
• Obturator hernia
• Sciatic hernia
• Lumbar hernia
• Perineal hernia
FIGURE 35.2 Types of hernia.
To understand the pathology of each hernia, it is necessary to understand the

anatomy of that region.
35.5 Groin herniae
Anatomy of the inguinal region

The inguinal canal is a 4-cm-long space, running antero-inferiorly (in an oblique
direction) from the internal to external inguinal rings. This is the path taken by
the testis in males to reach the scrotum. So, inguinal canal contains the spermatic
vessels and the vas deferens in the male and the round ligament in the female.
• The internal (deep) ring lies about 2 cm above and 2 cm lateral to the mid-
inguinal point (mid-point between the anterior superior iliac spine and the
pubic symphysis). Clinically, this corresponds to a point 2-cm lateral and
above the upper most femoral pulse. The medial aspect of the internal ring is
bounded by the inferior epigastric vessels (branch of the femoral artery).
• The external (superficial) ring is just above the pubic crest and the pubic
tubercle (Fig. 35.3A and B).
FIGURE 35.3 (A) Anatomical landmarks of inguinal canal. (B) Palpation of
pubic tubercle.
In infants, the external and the internal rings lie one over the other, and as the
child grows the rings go apart.
Boundaries (Fig. 35.4):
FIGURE 35.4 Anatomy of inguinal canal.
The inguinal canal is bounded

• Anteriorly by external oblique aponeurosis and muscle in its entire and
internal oblique muscle laterally.
• Posteriorly it is bounded by the transversalis fascia and conjoint tendon.
• Medially, the roof is formed by arching fibres of the internal oblique muscle.
• The floor is formed by the gutter shaped inguinal ligament.
Inguinal hernia
Constitutes about 80% of all external herniae.
• Indirect inguinal hernia: The sac passes through the internal ring lateral to
the inferior epigastric vessel and enters the inguinal canal to exit at the
external ring, into the scrotum. There are three types of indirect inguinal
hernia (Fig. 35.5), classified depending on the location of the fundus of the
hernial sac. They are as follows:
• Bubonocoele: the fundus of the sac appears only upto the external ring.
• Incomplete (funicular) variety: when the fundus traverses the inguinal
canal but just touches the testis (Fig. 35.5A).
• Complete variety: when the fundus descends fully into the scrotum and
reaches its base (Fig. 35.5B).
• Direct inguinal hernia: The sac bulges through the posterior wall of the
inguinal canal medial to the inferior epigastric vessels (Hasselbach’s
triangle) (Fig. 35.6A), and is not covered by the layers of the cord. This
occurs usually due to increase in the intra-abdominal pressure due to various
causes, and usually at the older age, usually bilateral (Fig. 35.6B).
• Pantaloon hernia (dual hernia/saddle bag hernia): Combination of direct
and indirect varieties, the sacs saddling the inferior epigastric vessels.
• Congenital hernia: It is the herniation through the patent processus vaginalis
(Fig. 35.7), which normally closes after the testis reaches the scrotum during
development in normal persons.
FIGURE 35.5 Varieties of inguinal hernia.
FIGURE 35.5 (A) Incomplete indirect inguinal hernia. (B) Complete
indirect inguinal hernia.
FIGURE 35.6 (A) Left direct inguinal hernia. (B) Bilateral direct inguinal
herniae.
FIGURE 35.7 Right congenital hernia.
Symptoms
• A bulge in the groin with a cough impulse.
• Pain and vomiting indicate complications like obstruction (Fig. 35.8) and
strangulation.
FIGURE 35.8 Obstructed inguinal hernia.
Signs
• A bulge medial to the pubic tubercle is of the indirect variety and a direct
hernia is lateral to the pubic tubercle. The features differentiating the indirect
and direct varieties are shown in Table 35.1.
• Uncomplicated hernia can be reduced and is nontender.
• Oedema and reddening of the skin over the hernia with signs of intestinal
obstruction suggests strangulation.
TABLE 35.1
Differences between the Indirect and Direct Inguinal Herniae
Property Indirect Direct

Age Any age, usually young Old
Cause May be congenital Acquired
Shape Pyriform Globular
Neck of sac Narrow Wide
Reduction on lying down Slow Immediate
Deep ring occlusion test Positive Negative
Relationship to inferior epigastric vessels Lateral Medial
Strangulation Not uncommon Unusual
Clinically, obstruction and strangulation may be difficult to differentiate. An

inguinal hernia should be differentiated from other groin swellings (see Table
35.2).
TABLE 35.2
Salient Features of Groin Swellings
Groin Swelling Salient Features
Direct inguinal hernia Above inguinal ligament, lateral to pubic tubercle, cough impulse positive
Indirect inguinal hernia Above inguinal ligament, medial to pubic tubercle, cough impulse positive
Femoral hernia Below the inguinal ligament and lateral to pubic tubercle
Encysted hydrocoele of cord Traction test positive, transilluminant
Congenital hydrocoele Can get above the swelling, transilluminant
Lipoma of the cord Soft and irreducible
Torsion of ectopic testis Tender swelling,
Femoral artery aneurysm Expansile pulsations with bruit
Funiculitis Tender elongated swelling in the inguinal canal
Enlarged lymph node Usually multiple, firm to hard in consistency
Saphena varix Compressible, palpable thrill on coughing (Cruveilhier’s sign)
Psoas abscess Lateral to the femoral artery, fluctuant, small bowel or spine pathology
Hydrocoele of the canal of Nuck Irregular tense cystic swelling in the superficial ring of a young female
US has some role in clinically indeterminable hernial sacs.
Treatment
Treatment is always surgical
• Uncomplicated hernia: elective surgery
• In children: Herniotomy—removal of the sac and closure of its neck.
• In adults: Herniorrhaphy—removal of the sac and closure of its neck,
followed by restoration of anatomy and strengthening of the abdominal
wall.Hernioplasty—along with herniorrhaphy, reinforcements may be
given with a nonabsorbable mesh as onlay or inlay grafts.
• Complicated hernia: Emergency surgery. Nonviable parts of the viscus need
resection.
Special types of inguinal hernia

Richter’s hernia
In this type of hernia, only a part of the circumference of the wall of the bowel is
trapped in the sac (Fig. 35.9). Since the entire lumen of the bowel is not
involved, it may not present with the classical signs of intestinal obstruction, but
may present a morbid picture (e.g., in femoral hernia).
FIGURE 35.9 Richter’s hernia.

Sliding hernia (hernia en glissade)
In this type of hernia, a part of extraperitoneal structure itself forms a wall of the
hernia (Fig. 35.10A). In the right inguinal hernia, caecum and ascending colon
may get involved and in the left, the sigmoid, and descending colon (Fig.
35.10B). Urinary bladder may form a wall in direct inguinal hernia. Diagnosis
can be made only at operation.
FIGURE 35.10 (A) Sliding hernia. (B) Left-sided sliding hernia (sigmoid
colon).
Maydl’s hernia (hernia en W)

In this type of hernia, two loops of the bowel get trapped in the form of the
English letter ‘W’. The strangulation affects the loop inside the abdomen due to
the pressure imparted by the adjacent loops entering the hernia sac (Fig. 35.11).
FIGURE 35.11 Maydl’s hernia.
Anatomy of the femoral region

The femoral canal is a 1.25-cm gap lying medial to the femoral sheath and the
femoral vein. This contains fat and a lymph node (lymph node of Cloquet). The
femoral canal is about 2-cm long, and is (Fig. 35.12) bounded
• anteriorly by the inguinal ligament (Poupart’s ligament);
• medially by the crescentic edge of the lacunar part of the inguinal ligament
(Gimbernat’s ligament);
• posteriorly by the pectineal part of the inguinal ligament (Ligament of Sir
Astley Cooper) and
• laterally by the femoral vein.
FIGURE 35.12 Anatomy of femoral region.
Femoral hernia
• Femoral hernia is a downward protrusion of peritoneum into the potential
space of the femoral canal.
• When the femoral hernia enlarges, it passes through the saphenous opening of
the fascia lata, then up over the inguinal ligament superficial to the Scarpa’s
fascia, giving a retort shape (Fig. 35.13).
• It accounts for about 5% of all external herniae, but they are more common in
women.
• The contributory factors are wide female pelvis and laxity of ligaments after
repeated pregnancy and weight loss.
• Since the boundaries of the femoral canal are rigid and ligamentous,
strangulation is common, like Richter’s hernia.
• Bilateral femoral herniae occur in about 20%.
FIGURE 35.13 Femoral hernia.
• A bulge low in the groin lateral to the pubic tubercle (Fig. 35.14).
• It is difficult to elicit cough impulse in small herniae.
• Pain and vomiting are signs of strangulation (signs of small bowel
obstruction), which is common, and may itself be the first clinical
presentation.
• It may be difficult to differentiate a femoral hernia from other swellings of the
groin. See Table 35.2.
FIGURE 35.14 Right femoral hernia.
US has some role in demonstrating the clinically indeterminable hernial sacs.
Treatment
Treatment is always surgical.
• Early surgery is required to avoid complications.
• Complicated femoral hernia, such as strangulation, may need laparotomy to
relieve the trapped intestine and reconstructions if necessary.
Rare types of femoral hernia

Prevascular hernia
The sac passes in front of the femoral artery and sometimes associated with
congenital dislocation of hip (Narath’s hernia).
Pectineal hernia
The hernia sac passes behind the femoral vessels between the pectineus muscle
and its fascia (Cloquet’s hernia).
External femoral hernia

The hernia sac passes lateral to the femoral artery (Hasselbach’s hernia).
Lacunar hernia
The hernia sac passes through the lacunar ligament of Gimbernat (Langier’s
hernia).
35.6 Ventral herniae
Anatomy of the epigastric region

The linea alba is formed by the junction of the rectus sheaths and the decussation
of their fibres in the midline. The linea alba, about 3-cm wide, extends from the
xiphoid process to the symphysis pubis.
Epigastric hernia
Protusion of extraperitoneal fat through the attenuated fibres of linea alba in the
epigastrium is called epigastric hernia. The extraperitoneal fat may pull the
peritoneum along with it at later stages, which may contain the omentum.
• Asymptomatic bulge in the midline between the xiphoid and the umbilicus
(Fig. 35.15).
• If pain present, it is more with muscular movements and also may mimic the
pain of acid peptic disease.
FIGURE 35.15 Epigastric hernia.
US has some role in clinically indeterminable hernial sacs.
Treatment
Symptomatic herniae can be treated with surgery (Excision of fat and closure
of defect in the linea alba).
Anatomy of the umbilical region

Umbilicus is an irregular depression, the site at which the umbilical cord is
attached to the fetus. This scar is potentially weak and is a place for protrusion of
hernial sac, called adult umbilical hernia.
Umbilical hernia
• Protrusion of hernial sac through the umbilical scar, in the process everting
the umbilicus which forms the apex of the hernial sac.
• Caused by
• increased intra-abdominal pressure such as pregnancy
• obesity and
• large intra-abdominal tumours.
• Globular bulge at the umbilicus everting it (Fig. 35.16).
• The underlying cause should be determined.
FIGURE 35.16 Umbilical hernia.
• US may be useful in localizing small herniae and to determine the underlying
cause.
Treatment
Excision of sac and repair of the abdominal wall by overlapping (double
breasting) its layers (Mayo’s repair).
Paraumbilical hernia
• Protrusion of hernia through the weakest area of the umbilical scar, which is
the superior aspect between the umbilical vein and the upper margin of the
umbilical ring.
• As the hernia enlarges, the peritoneal sac cannot enlarge indefinitely because
of the fixation of the peritoneum about the umbilicus. It splits and the
contents, mostly the omentum, transverse colon and small bowel in large
herniae, become loculated and adherent. For these reasons, large
paraumbilical herniae are irreducible and strangulation is likely to occur.
• A painless swelling in the supra or infraumbilical region pushing and
distorting the umbilicus.
• Pain and vomiting indicate obstruction or strangulation.
• Examination reveals a swelling at the umbilical region giving the umbilicus a
crescent shape (Fig. 35.17A and B).
• Reducibility is common in uncomplicated cases.
• Tenderness and irreducibility indicate complications.
FIGURE 35.17 (A) Infraumbilical hernia. (B) Supraumbilical hernia.
It should be differentiated from

• cyst of the vitello-intestinal duct
• cyst of the urachus and
• metastatic tumour.
US may be useful to determine the underlying cause.
Treatment
• Excision of sac and repair of the abdominal wall by overlapping (double
breasting) its layers.
• Strangulations need appropriate attention.
Spigelian hernia
• An interparietal hernia occurring in the line of linea semilunaris (the lateral
margin of the rectus sheath, running from the tip of the ninth costal cartilage
to the pubic crest) (Fig. 35.18A).
• This results in the weak area where the aponeurosis is arranged in a way that
the transverses abdominis and internal oblique fuse together.
• There are three types of Spigelian hernia:
1. Properitoneal
2. Interstitial
3. Superficial
FIGURE 35.18 (A) Spigelian belt. (B) Spigelian hernia.
• A painful lump, above and lateral to the inguinal canal and deep inguinal ring
(Fig. 35.18B), with pain worsening on straining.
• There may be features of obstruction or strangulation.
• Tender lump may be felt in some cases.
• US may be useful to identify the hernial sac.
• CT is useful in diagnosing obstructed Spigelian herniae.
Treatment
Local surgical repair with or without a mesh is the treatment of choice.
Incisional hernia
• Forms about 10% of all external herniae.
• 1% of abdominal incisions are followed by hernia.
• Results due to partial dehiscence of the some or all layers of the abdominal
wall, following surgical closure.
• Causes for incisional hernia are classified as follows:
• Preoperative: Old age, sepsis, malnutrition, uraemia, jaundice, diabetes
mellitus, peritonitis.
• Operative: Type of incision, types of suture materials, surgical technique,
type of operation, drains.
• Postoperative: Wound infection, abdominal distension, severe cough.
• The anatomy of the incisional hernia varies considerably.
• Neck of the hernia is variable depending on the dehiscence.
• Contents vary according to the location.
• Usually develop within 1 year of surgery, and once formed, it enlarges due to
mechanical forces induced, and may even take a huge size almost like a
second abdominal cavity.
• When the recti muscles become weak even without previous surgery and
bulge out and gape, it is called ‘divarication’.
Complications: Obstru ction and strangulation.
• An apparent bulge at the site of incision, small when lying down and enlarge
when standing or coughing (Fig. 35.19A–C).
• The overlying thin skin in large herniae, sometimes show necrosis (Fig.
35.19D), ulcerate and rupture.
• Features of small bowel obstruction is a sign of obstruction or strangulation.
FIGURE 35.19 (A) Incisional hernia while lying down. (B) Incisional hernia
becoming prominent on coughing. (C) Incisional hernia becoming
prominent on standing. (D) Large hernia with skin changes. Source: (Courtesy
Dr N. Sivakataksham)
US may be useful to determine the intra-abdominal causes.
Treatment
• Surgery: Restoration of anatomy after reducing the contents of hernia into the
abdomen. The hernia sac is excised and the defect closed with reinforcement
using prosthetic mesh.
35.7 Other herniae
Obturator hernia
• Herniation occurs along the obturator canal, which carries the obturator nerve
and vessels out of the pelvis (Fig. 35.20).
• A loop of bowel may occupy the hernial sac.
FIGURE 35.20 Obturator hernia.
Complications: Obstruction and strangulation (common).
• Usually asymptomatic as these herniae lie deep to the pectineus muscle.
• When symptomatic, symptoms of intestinal obstruction is the clinical
presentation.
• Recurrent attacks of intestinal obstruction is common.
• Some patients complain of a radiating pain from the medial aspect of the thigh
to the knee.
• It is difficult to diagnose clinically, and rarely vaginal or rectal examinations
may show a swelling in the obturator foramen.
US or CT may be useful in diagnosis.
Treatment
• If diagnosed by laparotomy, the bowel should be reduced and repair done.
• Alternately, the repair can be done by retro-pubic or pre-peritoneal
approach.
Sciatic hernia
Protrusion of pelvic peritoneum through greater or lesser sciatic foramen (Fig.
35.21).
FIGURE 35.21 Sciatic hernia.
Complications: Herniation of ureters, strangulation.
• A swelling in the buttock with symptoms of sciatic nerve compression.
• Urinary symptoms when ureters herniate.
CT or MRI may be useful in diagnosis.
Treatment
Surgery is excision of sac and local repair by transabdominal or transgluteal
approach.
Lumbar hernia
Uncommon hernia occurs at the anatomical weak points in the lumbar region
(superior and inferior lumbar triangles). The contents are usually large bowel
and rarely kidney.
Complication: Strangulation (not uncommon).
A lump in the flank with cough impulse.
CT (Fig. 35.21A) or MRI may be useful in diagnosis.
FIGURE 35.21A CT—Left lumbar hernia.
Treatment
Primary herniae are surgically corrected by local repair with or without mesh.
Perineal hernia
Primary acquired perineal hernia occurs in middle-aged multiparous women
(Fig. 35.22).
FIGURE 35.22 Perineal hernia (diagrammatic representation).
• A swelling in the perineum causing discomfort while sitting.
• Clinical examination reveals a reducible soft mass in the perineum.
CT or MRI may be useful in diagnosis.
Treatment
Surgical repair is done with a combined abdomino-perineal approach.
35.8 Symptoms of hernia
• Swelling
• Pain
• Vomiting
• Abdominal distension
Swelling
The commonest symptom of hernia is a painless swelling. The swelling presents
as a bulge in the region of hernia, which disappears into the cavity of origin on
lying down, and indicates that it is not complicated. If the swelling does not
disappear on its own on lying down, and needs some manipulation it indicates
incarceration or obstruction.
Pain
A symptom of impending complications like incarceration, obstruction,
strangulation, or inflammation.
• Mild dragging pain: It is a common symptom when the hernia is
accommodating the omentum or loops of intestine, which creates a pull on
the mesentery. This pain may disappear when the hernia gets reduced on
lying down, and indicates that it is uncomplicated.
• Severe pain in the hernia swelling: This symptom is due to the complication
like obstruction, strangulation, and inflammation.
• Abdominal pain with abdominal distension: This symptom indicates a
serious complication like obstruction or strangulation, and needs immediate
attention.
• Abdominal pain with vomiting: This symptom indicates a serious
complication like obstruction or strangulation, producing intestinal
obstruction and needs immediate attention.
Vomiting
Vomiting associated with pain in the hernial sac should make the examiner
suspect that it is getting complicated.
Abdominal distension associated with pain in the hernial sac should make the
examiner suspect that it is getting complicated.
Eliciting history
• Age: certain herniae are common in certain age groups.
• Newborns, infants, and children: congenital inguinal hernia.
• Young adults and middle-aged: acquired inguinal hernia.
• Middle-aged women: incisional hernia, femoral hernia.
• Elderly: direct inguinal hernia.
• Occupation: manual workers are prone to get inguinal hernia.
Swelling
• Time of onset: When did the patient notice this swelling first?
This will indicate the duration of the illness. Special questioning should be
made regarding the presence of the hernia since childhood (e.g., congenital
hernia).
• Progression of hernia: What is the difference in size since it was noticed
first?
This will indicate the progression of the hernia.
• Extent of the swelling: Whether it started at the inguinal region and
descended into the scrotum or it was seen in the scrotum for the first time?
The former suggests an acquired inguinal hernia and the latter a congenital
hernia in a preformed sac.
• Presence of complication: Does the swelling disappear on lying down?
The spontaneous reduction indicates that it is not complicated.
Pain
Is the present pain always over the swelling or only when straining?
Presence of pain only during straining or standing may not be an indicator of a
complication, whereas persistent pain indicates a complication.
General symptoms
The patient should be enquired about symptoms related to the causes of
increased intra-abdominal pressure like chronic cough, chronic sneeze,
obstructive airway disease, obstructive urinary diseases like prostatic
enlargement and chronic constipation. These are common illnesses which cause
direct inguinal hernia, especially the bilateral direct variety (Fig. 35.6B).
Past history
The patient should be enquired about any previous surgery performed (e.g.,
incisional hernia) and for hernia on the same side and the method of repair
(usage of prosthetic mesh) performed (e.g., recurrent inguinal hernia).
Personal history
Chronic tobacco smokers suffer from chronic cough, and they should be asked to
quit smoking, as continuance is a risk factor for recurrence.
Hernia
This consists of four parts:
1. Inspection
2. Palpation
3. Percussion
4. Auscultation
Position of the patient: The patient should be asked to remove the clothes
adequately for the examination. The patient should be examined in two positions
(Fig. 35.19A and 35.19C).
• Standing: The uncomplicated hernia becomes evident while standing and
absence of pain indicates that it is not complicated. Association of pain
indicates impending complication.
• Supine: Uncomplicated hernia disappears on lying down.
Position of the examiner:When the patient is examined in standing position,
the examiner should sit comfortably and assess the findings.
Inspection
• Size and shape of the swelling: The shape of the swelling varies according to
the type of hernia.
• Globular shape (e.g., direct inguinal hernia) (Fig. 35.23A)
• Pyriform shape (e.g., indirect inguinal hernia) (Fig. 35.23B)
• Retort shape (e.g., femoral hernia)
• Globular shape (e.g., umbilical hernia) (Fig. 35.23C)
• Irregular shape (e.g., incisional hernia) (Fig. 35.23D)
• Extent of the swelling: The extent of the swelling indicate the type of hernia
to certain extent.
• Inguinal swelling descending into the scrotum (e.g., indirect inguinal
hernia).
• Swelling below the inguinal ligament ascending above (e.g., femoral
hernia).
• Skin over the swelling: The skin changes vary according to pathology.
• Normal skin: uncomplicated hernia.
• Loss of rugosity of skin: large and longstanding inguinoscrotal hernia.
• Reddened or dark-coloured skin: inflamed or strangulated hernia (Fig.
35.24A).
• Ulceration on the skin: repeated trauma (Fig. 35.24B).
• Scar on the skin: previous surgery (recurrent hernia) (Fig. 35.25).
• Visible peristalsis: When the hernia sac contains small bowel (enterocoele)
and not complicated, peristalsis may be visible.
• Cough impulse: The patient is asked to cough by turning his head to the
opposite side (to prevent infection to the examiner), the hernia will become
more prominent due to increased intra-abdominal pressure. If the hernia is
small and visible, it presents as a bulge while coughing. Large herniae
become very prominent (Fig. 35.26A and B).
FIGURE 35.23 (A) Globular shape of direct inguinal hernia. (B) Pyriform
shape of indirect inguinal hernia. (C) Globular shape of umbilical hernia.
(D) Irregular shape of incisional hernia.
FIGURE 35.24 (A) Dark skin of strangulated umbilical hernia. (B)
Ulceration on the skin of umbilical hernia due to repeated trauma.
FIGURE 35.25 Right recurrent inguinal hernia.
FIGURE 35.26 (A) Umbilical hernia. (B) Umbilical hernia on coughing.
Note
Cough impulse is often better seen than felt. Presence of cough impulse is
pathognomonic of a hernia, but absence does not rule out a hernia.
Obstruction of neck of hernia sac by adhesions or omental plug or
complications like strangulation will prevent a cough impulse.
Palpation
The points related to the examination of all swellings should be followed. The
specific points to note are as follows:
• Position of swelling: The position of the swelling should be noted.
• Above the inguinal ligament: inguinal hernia.
• Inguinal swelling lateral to pubic tubercle: direct inguinal hernia.
• Inguinal swelling medial to pubic tubercle: indirect inguinal hernia.
• Below the inguinal ligament: femoral hernia.
• At the umbilicus: umbilical hernia.
• Above or below the umbilicus: paraumbilical hernia.
• Swelling over a surgery scar: incisional hernia.
• Midline swelling in the epigastric region: epigastric hernia.
• Extent of swelling: The hernia can start at one place and extend into an
adjoining region.
• Inguinal swelling extending into the scrotum: inguinoscrotal hernia
• Swelling below the inguinal ligament extending into the inguinal region:
femoral hernia.
• Getting above the swelling: This is an important finding to differentiate a
inguinoscrotal hernia from a hydrocoele. The root of the scrotum is held with
the thumb and the other four fingers. If the approximation is possible, it
indicates a scrotal swelling, as the hydrocoele sac ends there (Fig. 35.27A).
This is not possible in inguinoscrotal herniae, as the sac and its contents
obstruct the approximation of the examiner’s fingers (Fig. 35.27B).
• Consistency: The consistency of the hernia varies according to its contents.
• Doughy feel: omentum (omentocoele)
• Elastic feel: intestine (enterocoele)
• Cough impulse: The examiner should place his thumb and the index finger of
the examining hand on the swelling and the patient is asked to cough (Fig.
35.28A and B). Presence of expansile cough impulse is indicated by a thrust
felt by the fingers and the fingers will separate.
• Presence of cough impulse: uncomplicated hernia
• Absence of cough impulse: complicated hernia
• Reducibility: Is the swelling reducible? Uncomplicated hernia with a wide
neck will reduce on its own, especially on lying down supine. When it does
not reduce spontaneously, an attempt should be made to determine its
reducibility. The patient should be made to lie down and relax his muscles,
and the hernia is reduced with the thumb and index gently pushing the sac
inside the abdominal cavity (Fig. 35.29A and B). In inguinal hernia, the thigh
should be flexed and internally rotated, which will relax the external ring and
also the abdominal wall muscles. The fundus of the swelling is held with the
fingers and gently squeezed towards the abdomen, whereas the fingers of the
other hand will guide the contents into the abdominal cavity. This procedure
is called ‘Taxis’ (Fig. 35.30).
• Easy reduction of contents in the beginning and difficulty later:
omentocoele.
• Difficulty in reduction of contents in the beginning and then later:
enterocoele.
• If the hernia cannot be reduced by the above procedure, it is called
obstructed.
• Determination of types of groin hernia: There are some specific tests to
differentiate groin herniae. They are:
• Internal ring occlusion test: After reducing the hernia, the examiner should
place his thumb at a point 2 cm above and lateral to the mid-inguinal point
(internal ring) and occlude the internal ring (Fig. 35.31). On straining,
indirect inguinal hernia will not be allowed to appear by this occlusion,
whereas the direct variety will show up.
• Finger invagination test: In a recumbent patient, after reducing the hernia,
the examiner should push his index or little finger through the scrotal skin
towards the pubic tubercle and then into the superficial inguinal ring. The
patient is asked to cough, and if the impulse hits the tip of the examining
finger, it is indirect inguinal hernia, and when it hits the pulp of the finger,
it is direct inguinal hernia (Fig. 35.32).
• Zieman test: In a recumbent patient, after reducing the hernia, the examiner
should place his index, middle and the ring fingers on the internal ring,
external ring and the saphenous opening, respectively. The patient is asked
to cough, and impulse hitting the index finger is indirect inguinal hernia,
the middle finger is direct inguinal hernia and the ring finger is the
femoral hernia.
• Relationship to the testis (in case of inguinal hernia): Its relationship
indicates the nature of hernia.
- Swelling lying anterior to the testis: Inguinoscrotal hernia (congenital
variety).
- Swelling above the testis: Inguinoscrotal hernia (acquired variety).
FIGURE 35.27 (A) Able to get above the swelling—hydrocoele. (B) Not
able to get above the swelling—see the bulge.
FIGURE 35.28 Methods of feeling the cough impulse.
FIGURE 35.29 (A) Method of reducing the hernia. (B) Umbilical hernia
after reduction.
FIGURE 35.30 Taxis.
FIGURE 35.31 Internal ring occlusion test.
FIGURE 35.32 Finger invagination test.
Percussion
This has no special significance in inguinal hernia, but in very large herniae like
the incisional herniae, resonant note may indicate the presence of gas-filled
bowel, and a dull note may indicate the presence of omentum.
Auscultation
Large herniae containing small bowel may show peristaltic sounds (Fig. 35.33).
FIGURE 35.33 Auscultation of hernia for bowel sounds.
Points to remember
• Never forget to examine the other side in case of groin hernia.
• Always examine the abdomen completely.
• When the patient’s description suggests a hernia and it is not found,
reexamine the patient after making the patient walk up and downstairs and
remain standing till examined. If nothing is found, recall the patient after a
period of time and examine till an abnormality is found or until the
symptoms disappear.
General examination
The examination should be centred round finding out the probable causative or
precipitating factor, as the treatment should include its management also, to
prevent a recurrence or postoperative complications.
1. Tone of abdominal muscles: Head raising test: The patient should lie supine
and raise his head to put the abdominal muscles under tension. Weakness of
abdominal muscles is exhibited as bulges in the lower abdomen called
‘Malgaigne’s bulgings’.
2. Mass in the abdomen or ascites: Special attention should be given to find out
the presence of any mass in the abdomen.
3. Examination for causes of urinary outflow obstruction: The external
genitalia should be examined for phimosis, meatal stenosis or urethral
strictures (see Ch. 36) and also a rectal examination to determine the
enlargement of prostate (see Ch. 37).
4. Examination of chest: The chest should be auscultated for chronic
obstructive airway diseases.
CHAPTER 36
Male genitalia
N. Anandan
CHAPTER OUTLINE
36.1. Development of male genitalia 625
36.2. Surgical anatomy of male genitalia 626
36.3. Diseases and abnormalities of penis 626
• Agenesis of phallus (Aphalia) 626
• Diphallia 626
• Phimosis 627
• Paraphimosis 628
• Hypospadias 628
• Epispadias 629
• Injury to penile skin 629
• Fracture penis 630
• Condylomata acuminata (Venereal warts) 630
• Venereal diseases 631
• Elephantiasis of penis 631
• Carcinoma penis 632
• Peyronie’s disease 633
• Priapism 633
36.4. Diseases and abnormalities of testis and epididymis 634
• Undescended testis 634
• Ectopic testis 635
• Retractile testis 635
• Hydrocele 635
• Traumatic orchitis 636
• Haematocele 636
• Pyocoele 637
• Acute epididymo orchitis 637
• Chronic epididymo orchitis 637
• Atrophic testis 638
• Testicular tumour 638
• Varicocele 639
• Torsion of testis 639
• Cysts of epididymis 640
36.5. Diseases of scrotum 641
• Penoscrotal transposition (Bifid scrotum) 641
• Ectopic scrotum 641
• Scrotal haemangioma 641
• Scrotal laceration 642
• Filarial scrotum 642
• Scrotal abscess 642
• Fournier’s gangrene 643
• Carcinoma of scrotum 643
• Sebaceous cysts 643
36. 6. Symptoms of diseases of male genitalia 644
• Penis 645
• Scrotum 646
• Testis 647
• Epididymis 648
• Cord structures 648
• Abdomen 649
• General 649
36.1 development of male genitalia
Penis develops from the genital tubercle. The genital tubercle elongates into a
cylindrical phallus. Mesenchyme in the genital tubercle condenses as the
primitive cavernous tissue. By 12 weeks, penis is well formed.
Urethra develops from the urogenital sinus, the phallic portion into bulbar and
penile urethra, and the pelvic portion into the prostatic and membranous urethra.
Scrotum develops from the genital swellings, which enlarge and migrate
posteriorly.
Testis arises from the germ cells of the genital ridge at the lower end of
abdomen. As the testis enlarges in size, it also undergoes a caudal migration and
descends into the scrotum, according to the following timetable.
• 3rd month of fetal life—reaches the iliac fossa.
• 7th month of fetal life—traverses the inguinal canal.
• 8th month of fetal life—reaches the external ring.
• 9th month of fetal life—descends into the scrotum.
This happens under the influence of testosterone, mullerian inhibiting factor
and gubernaculums. Failure to descend into the scrotum is called cryptorchism.
36.2 surgical anatomy of male genitalia

Penis is a male secondary sexual organ, which has special spongy tissue. This is
capable of trapping blood within the corpora cavernosa producing an erection
during sexual excitement. The urethra passes through the penis after leaving the
prostate. The urethra is firmly fixed to the pubic bone by puboprostatic
ligaments. Shearing of these ligaments during fracture pelvis causes rupture of
the prostatomembranous urethra (Fig. 36.1A and B).
FIGURE 36.1A Surgical anatomy of male genitalia.
FIGURE 36.1B Surgical anatomy of penis.
Scrotum is a sac, divided into right and left compartments by a septum. Scrotal
skin is thin, pigmented, rugose and endowed with sebaceous glands and marked
by a longitudinal median raphe. The subcutaneous tissue does not contain fat but
contain the involuntary dartos muscle.
Both testes and their cord structures (Fig. 36.2) are located within the
scrotum, the left lower than the right.
• Testis is located in the scrotum to have lower core temperature compared to
intra-abdominal organs. This is essential for spermatogenesis. Each testis is
contained by a firm fibrous capsule, tunica albuginea, and each testis
invaginates anteriorly into a double serous covering, the tunica vaginalis.
• Epididymis lies posterolateral to the testis, which is divided into head, body
and tail. The testis is supplied by the testicular artery, which arises from the
aorta. The venous drainage is in the form of a plexus called pampiniform
plexus, which forms a single vessel called testicular vein to drain into the
inferior vena cava on the right and into the renal vein on the left side.
• Vas deferens is a tube of about 45 cm and passes from the tail of the
epididymis to traverse the scrotum, inguinal canal, takes a devious course to
join the seminal vesicles to form the ejaculatory duct, which opens into the
prostatic urethra.
FIGURE 36.2 Structure of testis.
Testis retains its ability to produce sperms even beyond 60 years of age,
whereas ovaries fail to produce eggs beyond 40 years.
36.3 diseases and abnormalities of penis (table

36.1)
Agenesis of phallus (aphalia)

• Extremely rare anomaly.
• Occurs due to failure of development of genital tubercle.
• Also associated with many anomalies such as horseshoe kidney,
vesicoureteric reflux, renal agenesis and cardiopulmonary anomalies.
TABLE 36.1
Aetiological Classification of Diseases and Abnormalities of Penis
Aetiology Diseases
Congenital Agenesis of phallus Absent penis (Aphalia)

Duplication Diphallia
Phimosis
Paraphimosis
Hypospadias, epispadias
Traumatic Fracture penis
Infective Venereal infections Condyloma acuminata
Primary chancre, chancroid, lymphogranuloma venereum, granuloma inguinale
Chronic Elephantiasis
Neoplastic Malignant Carcinoma
Others Peyronie’s disease
Priapism
• Penile shaft is absent or rudimentary (Fig. 36.3).
• The scrotal sac is well developed with completely descended testes in it.
FIGURE 36.3 Rudimentary penis Source: (Courtesy Dr K. Sridhar).
Karyotyping and various studies to evaluate associated anomalies.
Treatment
Gender reassignment with orchidectomy and feminizing genitoplasty.
Diphallia
• Extremely rare.
• Several associated anomalies have been reported including agenesis of
kidney, hypospadias, bifid scrotum, anal and cardiac anomalies.
• It is variable from tiny rudimentary penis to complete duplication.
Radiologic imaging for complete urinary tract evaluation.
Treatment
Removal of poorly developed phallus and management of other associated
anomalies.
Phimosis
This condition can be congenital or acquired.
• Congenital: Concentric narrowing of the prepuce (Fig. 36.4) making the
retraction difficult, occurs due to congenital adhesions between the
undersurface of the prepuce and the glans penis.
• Acquired: It can occur due to
• repeated infections (balanoposthitis) especially in diabetics and
• underlying tumour of the glans penis.
FIGURE 36.4 Phimosis.
• Congenital: Child may cry during micturition with ballooning of prepuce,
caused by the accumulation of urine behind the tight foreskin. This is
followed by dribbling of urine.
• Acquired:
• Inability to retract the skin, with purulent or blood stained discharge
through the preputial orifice, and dysuria due to urinary infection.
• The edge of foreskin may be scarred in cases of balanoposthitis and in
Balanitis Xerotica Obliterans (BXO) (Lichen sclerosis) (Fig. 36.5).
• If there is a tumour covered by a tight foreskin, foul smelling discharge
may be seen from the preputial orifice due to secondary infection of
underlying tumour. The lump of tumour can be felt under the foreskin.
FIGURE 36.5 Balanitis xerotica obliterans.
Determination of blood sugar levels for diabetes.
Treatment
• Circumcision is the treatment of choice.
• If there is an underlying tumour it will require surgery or radiotherapy (see
Carcinoma penis, p. 636).
Paraphimosis
• Occurs due to forceful retraction of the foreskin with preexisting phimosis,
either by manipulation or during sexual intercourse.
• The fibrous band resulting from repeated infections, encircles the penis in the
subcoronal area to cause congestion of the glans penis.
• The patient unaware of phimosis, may develop this condition after the first
sexual intercourse, usually after marriage.
• Mild to moderate pain in the glans penis.
• On examination, the retracted foreskin just above coronal sulcus is swollen
and oedematous (Fig. 36.6).
FIGURE 36.6 Paraphimosis.
No specific investigation is required.
Treatment
• Immediate reduction of paraphimosis.
• Constricting band needs to be incised, when reduction is not possible.
• Circumcision should be done as an elective procedure after a couple of weeks,
to prevent a recurrence.
Hypospadias
• Common congenital condition affecting male urethra.
• Incidence around 1:300 births, with familial tendencies.
• Most common associated anomalies are undescended testis and inguinal
hernia.
• Hypospadias results from incomplete development of anterior urethra and
corpus spongiosum. The external urethral meatus opens on the undersurface
of penis or in the perineum. The inferior aspect of the prepuce is poorly
developed (hooded prepuce). The urethra and corpus spongiosum are absent
distal to the urethra, which is replaced by a fibrous band, which gives a
downward bend to the penis (chordee).
• The types of hypospadias are as follows:
• Glandular (commonest)
• Coronal
• Penile
• Penoscrotal
• Perineal (least common).
• The urethral opening is seen on the ventral aspect of the penis, at various
levels.
• Glandular: The urethral opening in the glans just proximal to normal
location at the level of frenulum or slightly above that (Fig. 36.7A).
• Coronal: The urethral opening at the level of the coronal sulcus.
• Penile: The urethral opening at some point on the undersurface of penile
shaft anywhere from coronal sulcus to penoscrotal level (Fig. 36.7B)
• Penoscrotal: The urethral opening at the junction of penis and scrotum
(Fig. 36.7C).
• Perineal: The opening at about 3 cm above the anus opening. The scrotum
is cleft in this type.
FIGURE 36.7A Glandular hypospadias.
FIGURE 36.7B Penile hypospadias.
FIGURE 36.7C Penoscrotal hypospadias. Source: (Courtesy Dr K. Sridhar).
Note
l Penile curvature is seen in all types of hypospadias except in the glandular
type
l There is excessive prepucial skin seen on the dorsum of penis.
Treatment
Surgical correction is aimed at straightening the penis by dividing all fibrous
tissue that holds the penis bent and bring the meatus to the tip (Urethroplasty).
This can be done in one or two stages.
Epispadias
• A rare anomaly.
• In penile epispadias, the opening is on the dorsal surface of the penis and the
penis is bent upwards.
• The external urethral opening may be seen at
• Glans
• Penile shaft
• Penopubic region.
• Total epispadias may be associated with diastasis of pubic symphysis and
deficiency of urinary continence mechanism or ectopia vesicae.
• Passes urine from the upper surface of penis, in different directions.
• Examination shows the meatus opening on the dorsal surface of penis, on the
glans, penile shaft or penopubic region with upward curvature of penis with
shortening (Fig. 36.8A).
• Urinary incontinence is present in penopubic type.
FIGURE 36.8A Ectopia vesicae with epispadias.
CT abdomen is done to rule out other congenital anomalies.
Treatment
Surgical treatment includes urethral reconstruction as well as bladder neck
reconstruction for urinary incontinence.
Injury to penile skin
• In adults, the injury to the penile skin occurs due to
• direct injury during a fall;
• assault or entrapment of clothing in machinery and
• in people who indulge in perverted sex or during masturbation with metal
objects.
• Children can injure the penis by pranky acts and cause damage to the penile
shaft and skin (Fig. 36.8B).
FIGURE 36.8B Gangrene of glans penis due to tying of hair around glans
penis Source: (Courtesy Dr N. Mohan).
The penile skin is lacerated in an irregular fashion (Fig. 36.8C) with profuse
bleeding.
FIGURE 36.8C Laceration penile skin.
Treatment
Immediate surgical repair is necessary.
Fracture penis
• Occurs due to direct injury to tunica albuginea or corpora cavernosa, when the
penis is in the erect state.
• The tear in the tunica albuginea leads to accumulation of blood outside the
corpora cavernosa.
• Fracture can occur during
• a fall;
• assault by the sexual partner and
• forceful manipulation by the patient himself.
• In about 10% of cases, urethral injury may be associated.
• Common in the young and middle aged.
• Erect penis becomes flaccid suddenly, followed by swelling of the penis and
scrotum with bluish discolouration (Fig. 36.9A).
• The patient is able to hear a click at the time of injury and hence the name
‘fracture penis’.
• There may be blood at the urethral meatus with difficulty in passing urine due
to associated urethral injury.
FIGURE 36.9A Fracture penis Source: (Courtesy Dr Ravisankar G Pillai).
• No specific investigation is necessary, however when in doubt,
cavernosogram can be done. This is done by injecting radiopaque contrast
into the corpora cavernosa, to visualize the corporal anatomy.
Treatment
• Immediate surgical repair to torn tunica albuginea is required to maintain
erectile function.
• Urethral injury, if present, can be repaired at the same time.
Condylomata acuminata (venereal warts)

• Also called genital warts, which are caused by human papilloma virus (HPV)
transmitted by sexual contact.
• These lesions can be confused with malignancy.
• The lesions can be present within the urethra in 5% of cases.
• Soft friable, reddish papillary lesions on the penis, commonly on the prepuce,
penile shaft and frenulum (Fig. 36.9B).
• The lesions
• can be single or multiple and
• moist and have peculiar odour.

FIGURE 36.9B Venereal warts Source: (Courtesy Dr B. Loganathan).
• Biopsy and histological evaluation is essential.
• Cystourethroscopy will confirm the presence of lesions in the urethra.
Treatment
• Medical: Topical application of podophyllum, trichloro acetic acid and laser
therapy.
• Surgical: Circumcision may be indicated to remove the skin along with the
lesions.
Venereal diseases
See Table 36.2 and Figure 36.10A and B.
FIGURE 36.10A Primary chancre Source: (Courtesy Dr B. Loganathan).
FIGURE 36.10B Granuloma inguinale.
TABLE 36.2
Aetiology, Clinical Features and Treatment of Venereal Diseases
Lymphogranuloma
Chancroid (ref. Fig.
Features Primary Chancre Venereum (Ref Granuloma Inguinale
10.6)
Fig. 12.21)
Aetiology
Causative organism Treponema Haemophilus ducreyi Chlamydia Calymmatobacterium
pallidum trachomatis L1– (Donovania)
L3 granulomatis
Incubation period 9–90 days 3–7 days 3–12 days 3 days to 3 months
Genital Number Single Single or multiple Superficial, Ulceration
ulcers herpetiform ulcer
Induration Button like Absent Absent Marked
Pain Absent Present Absent Absent
Inguinal nodes Small, painless, Present Painful suppurative Gross nodes
discrete, nodes, may form
nontender, ulcer/sinus
rubbery
Investigations Dark ground Smear examination Frei’s test, Smear, PCR, HPE
illumination, (Gram’s stain, Complement
VDRL, Unna fixation test,
fluorescent Pappenheim’s electron
antibody stain, Wright’s microscopy, PCR
absorption stain), culture,
test ELISA, PCR, HPE
Treatment Benzathine Azithromycin, Doxycycline, Azithromycin,
penicillin G, ciprofloxacin, erythromycin, doxycycline,
doxycycline, erythromycin azithromycin tetracycline,
tetracycline, erythromycin, co-
erythromycin trimoxazole
Elephantiasis of penis
• Caused by Wuchereria bancrofti parasitic infection.
• Leads to obstruction of lymphatic channels followed by fibrosis of the tissue.
• Subcutaneous tissue of the penis is thickened and hard.
• Penis may look distorted due to unequal deposition of fibrous tissue, and the
condition is described as ‘Ram horn penis’ (ref. Fig. 12.18).
• Scrotum and penis may appear sunken under the hard thickened skin.
• Small and multiple vesicles over the scrotal skin may appear called lymph
varix and these can get secondarily infected.
• Blood smear particularly during the time of fever may demonstrate
microfilariae.
• US may show the presence of adult parasite in the inguinal lymph nodes and
in the lymphatics of cord structures.
Treatment
• Medical: Diethyl carbamazine citrate is helpful in killing microfilariae and
abolish microfilariae. Antibiotics are required for managing secondary
infection.
• Surgical: Excision of involved skin and skin grafting.
Carcinoma penis
• Uncommon in Jews and Muslims who practice routine circumcision, but
common in Hindus who do not practice circumcision. The social taboo
attached to the genitals and lack of genital hygiene is responsible for the
development of penile cancer.
• Excessive smegma in a patient with phimosis.
• Paget’s disease of penis (chronic red eczema like appearance in the glans or
undersurface of prepuce).
• Queyrat’s erythroplasia (dark red velvety lesion on the glans or
undersurface of prepuce).
• Leukoplakia (white patch).
• Macroscopically, it may be papilliferous or ulcerative on the shaft or glans
penis.
• Microscopically, it is a squamous cell carcinoma with degrees of
differentiation.
• The tumour spreads in many ways.
• Locally, invade the shaft of the penis.
• Lymphatically, to inguinal nodes.
• Hematogenously to lungs and liver (late).
Symptoms
• Local discharge and odour.
Signs
Penis
• In the initial stages, the prepuce is retractable and lesions can be either
papilliferous or ulcerative (Fig. 36.11A).
• Papilliferous lesions bleed from the surface and are associated with bad
odour when secondary infection supervenes.
• Ulcerative lesions are raised with rolled out margins and have indurated
base.
• After sometime, the prepuce cannot be retracted and patients are unaware of
the lesion until there is foul discharge coming under the prepucial sac.
• On clinical examination, the lesion may be felt under the skin and a dorsal
slit of the foreskin may be needed to visualize the lesion.
• Palpable inguinal nodes may suggest secondary deposits which may even
fungate (Fig. 36.11B).
FIGURE 36.11A Exophytic growth of carcinoma penis Source: (Courtesy Dr B.
Loganathan).
FIGURE 36.11B Carcinoma penis with bilateral inguinal lymph node
metastases Source: (Courtesy Dr B. Loganathan).
• US and CT abdomen to assess the lymph node enlargement.
• X-ray chest will assess the spread of tumour to the lungs.
• Biopsy of the penile lesion confirms the diagnosis.
Treatment
• Local excision by circumcision for small preputial tumours.
• Radiotherapy is indicated for very small lesions involving the glans penis.
• Partial or total amputation of penis (penectomy) along with ilio-inguinal
block dissection of the nodes will be required, when the lesion extends
beyond the shaft
(antibiotics to treat secondary infection).
Palliative
• Local irradiation for fixed inoperable inguinal nodes, locally advanced
disease or with distant metastases. Also useful to prevent local pain and
fungation.
Peyronie’s disease
• Occurs due to deposition of fibrous tissue over the covering of corpora
cavernosa of the penis.
• Exact aetiology is not known, however repeated trauma has been suggested to
precipitate this lesion.
• Common in middle age.
• Initially patient notices pain during erection.
• In the established lesion, there is a plaque palpable commonly over the
dorsum of the penis and less often on the ventral surface.
• The penis gets shortened with curvature to the opposite side of the plaque
(Fig. 36.12) during erection. No curvature in the flaccid state.
FIGURE 36.12 Peyronie’s disease. Source: (Courtesy Dr Ravisankar G Pillai)
US shows calcified plaque over tunica albuginea and corpora cavernosa.
Treatment
• Medical: (potaba, vitamin-E and verapamil, a calcium channel blocker) gives
slight improvement.
• Surgical: Incision of the plaque with skin or vein grafting.
Priapism
• In this condition there is persistent painful erection without any sexual desire.
• The causes include:
• Haematological disorders
- Leukaemia
- Sickle cell disease
- Thalassemia
• Neurological disorders
- Spinal cord lesions and trauma
• Secondary malignant deposits
• Drugs:
- Intracavernosal injection treatment with drugs (papaverine, alprostadil)
for erectile dysfunction (impotence)
- Antihypertensives
- Antipsychotics
- Antidepressants
- Anticoagulants
- Recreational drugs (e.g., alcohol, cocaine)
• If detumescence does not result in about 6 hours, permanent erectile failure
may result due to arterial and venous thrombosis and fibrosis of corpora.
Complications: Ischaemia, thrombosis, gangrene, impotence.
Persistent erection of penis for more than 6 hours accompanied by pain (Fig.
36.13).
FIGURE 36.13 Priapism.
Investigations towards the probable aetiology.
Treatment
• It should be treated as an emergency.
• The blood from the corpora cavernosa should be drained using a 18F butterfly
needle.
• If this fails, corporo-spongial shunt (anastomosing corpora cavernosa to
corpus spongiosum) or cavernoso-saphenous venous shunt may be required.
• The underlying pathology needs to be treated.
36.4 diseases and abnormalities of testis and

epididymis
The aetiological classification is shown in Table 36.3.
TABLE 36.3
Aetiological Classification of Diseases and Abnormalities of Testis
and Epididymis
Congenital Defects in descent Undescended testis

Ectopic testis
Retractile testis
Hydrocele
Traumatic Orchitis
Haematocele
Inflammatory Acute Pyocoele
Acute epididymo-orchitis
Chronic Filarial orchitis, tubercular orchitis
Atrophy of testis
Neoplastic Malignant Tumours
Others Varicocoele
Torsion testis
Cysts of epididymis
Spermatocoele
Undescended testis
• This is congenital.
• The incidence is about 3% during birth and 1% at 1 year in normal births.
• In premature infants, about 30% have bilateral undescended testes.
• In intrauterine life, the testis is located in the lower part of the abdomen and
descends into scrotum by various factors such as
• gubernacular contraction
• differential growth of testes and
• intra-abdominal pressure.
• Failure of any of these factors can lead to undescended testis.
Spontaneous descent after 1 year is very rare.
Complications: Infertility, susceptibility to trauma and torsion, malignancy of
intra-abdominal testis.
• The scrotum may be less developed and empty (Fig. 36.14).
• On palpation, testis is not palpable within the scrotum. Testis can be felt at the
level of superficial inguinal ring or within the inguinal canal, felt by rolling
the examining fingers over the area. It is more easily felt by examining the
patient standing.
• If the testis is purely intra-abdominal it cannot be felt anywhere.
• Vas deferens on the same side may be absent.
• They may present with signs of tumour, torsion, or hernia (complications of
undescended testis).
FIGURE 36.14 Left undescended testis.

• US is useful to locate inguinal testis.
• CT scan is useful for locating intra-abdominal testis.
• Diagnostic laparoscopy may be useful.
Treatment
• Surgery to bring and place the testis in the subdartos pouch of the scrotum is
the treatment of choice.
• However, in adults, orchidectomy will be needed if the testis is small and
atrophic.
Ectopic testis
• A rare condition.
• The testis descends into the scrotum due to contraction of gubernaculum
mostly attached to the scrotum. Sometimes the gubernaculum may be
attached at other areas and scrotal part of gubernaculum is poorly developed.
• In such a situation, abdominal descent is over but the testis does not enter the
scrotum but deviate from the normal line of descent and may lie in the
• superficial inguinal pouch in front of the penis
• perineum and
• thigh.
• The testis is actually of normal size and well developed but not located in the
scrotum, on the affected side.
• It may be located at superficial inguinal, suprapubic, perineal, femoral regions
or contralateral side of the scrotum.
US may be useful in identifying the testis.
Treatment
Surgery to bring down and fix the testis in the subdartos pouch is necessary.
Retractile testis
• When the lower abdomen, upper part of the thigh and scrotum touch each
other, the testis is pulled up into the superficial inguinal pouch.
• This is caused by contraction of cremaster muscle called cremasteric reflex.
This reflex is very brisk between the ages of 2 and 7 years.
• In this condition testis is actually present in the scrotum but gets pulled to the
external ring and lie between Scarpa’s fascia and external oblique
aponeurosis.
• The mother complains of testis not being present in the scrotum.
• Careful examination with warm fingers and gentle milking from the level of
inguinal canal toward scrotum will make the testes reach the scrotum (Fig.
36.15).
FIGURE 36.15 Bilateral retractile testes.
Treatment
Reassurance is all that is necessary.
Hydrocele
• There is accumulation of straw coloured fluid in tunica vaginalis.
• Hydrocele is of three types. They are as follows:
• Congenital hydrocele: occurs due to persistent processus vaginalis that
provides communication into the peritoneal cavity. The communicating
orifice is so small that the fluid alone comes into tunica vaginalis and not
the intra-abdominal contents (hernia).
• Primary hydrocele: no obvious reason for the accumulation of fluid. Also
called ‘vaginal hydrocele’.
• Secondary hydrocele: occurs secondary to epididymo orchitis and testicular
tumour.
• The presenting symptom is the swelling of the scrotum (Fig. 36.16).
• Congenital hydrocele: Typically the mother notices a swelling of scrotum
while bathing the child. The swelling is noted while the child is awake and
moving around and disappears when the child lies down, as the fluid
returns into the abdomen.
• Primary hydrocele: Typically occurs in adulthood with fluid all-round the
testis, the testis cannot be felt separately from the swelling. The scrotum is
tensely swollen with several millilitres of fluid.
• Secondary hydrocele: There is minimal hydrocele fluid and it is lax. There
is associated evidence of enlargement of epididymis, testis and thickening
of cord structures (epididymo-orchitis) or presence of nodular lump of
testis (testicular tumour).
FIGURE 36.16 Left-sided hydrocele.
In hydrocele, the fluid lies in front and above the body of testis.
Variants of hydocoele (Fig. 36.17):
• Infantile hydrocele: The hydrocele fluid collects in the persistent processus
vaginalis upto the internal ring. This can occur in infants and children as
well.
• Funicular hydrocele: This is rare and can be mistaken for hernia. The fluid is
collected only in the inguinal part of processus vaginalis. The testis can be
felt separately as there is no fluid around the testis.
• Encysted hydrocele of the cord: The fluid collection is only above the testis
but below the external ring. There is a swelling above the testis but separate
from it and when the testis is pulled down the swelling also moves down. It
may show side-to-side mobility.
FIGURE 36.17 Variants of hydrocele.
Getting above the swelling and transillumination are hallmark findings of

hydrocele.
• Blood smear for microfilaria.
• US of scrotum or blood for testicular tumour markers may be required, when
suspected.
Treatment
• Eversion or excision of hydrocele sac is the treatment of choice.
• Partial excision of scrotum if the scrotum is large.
• Antibiotic treatment in epididymoorchitis is needed.
Traumatic orchitis
• It is a common condition, an aseptic inflammation caused by direct trauma,
seen in sportsmen involved in contact sports like football.
• Any direct trauma to the testis causes this condition.
• Acute pain in the injured testis.
• Supporting or lifting the testis may give comfort (pain gets aggravated when
lifted if it is due to torsion).
• Mild hydrocele may be present.
Treatment
Scrotal support and analgesics would suffice.
Haematocoele
Occurs as a complication following:
• Any direct blunt trauma to scrotum.
• After needle aspiration of preexisting hydrocele.
• May be asymptomatic and can mimic a testicular tumour.
• Scrotal swelling becomes heavy and causes discomfort (Fig. 36.18).
• The testis may become atrophic following long standing pressure effect by the
haematoma.
FIGURE 36.18 Right haematocoele.
US is useful in diagnosing haematocele and the size of testis.
Treatment
Drainage of haematoma and excision of hydrocele sac.
Pyocoele
Can result following infection or after aspiration of hydrocele
• Severe pain and high-grade fever.
• Tenderness on pressing the swollen scrotum.
• Transillumination is characteristically absent.
• Leucocytosis may be pronounced.
• Diagnostic aspiration may reveal the presence of pus.
Treatment
• Needle drainage of pyocoele with antibiotic may be sufficient in early stages.
• Open drainage and or orchidectomy may be required in delayed cases.
Acute epididymo orchitis

Acute inflammation of testis and epididymis can be caused by
• viral infections (e.g., mumps).
• bacterial infections (e.g., Neisseria gonorrhoea, Escherichia coli and
Klebsiella, and Chlamydia):
• retrograde infection from prostate and seminal vesicle;
• blood borne infection from other focus and
• surgery of urinary tract (TUR).
• Pain and swelling of testis.
• Examination shows oedema of scrotal skin, cord structures very bulky and
thickened and epididymis is very much enlarged (Fig. 36.19).
• In addition the testis is also enlarged and tender.
FIGURE 36.19 Acute epididymo orchitis.
However, it is possible to make out the testis separate from epididymis

whereas this is not possible in torsion testis.
• Blood count: leucocytosis
• Blood culture: positive culture
• Urine culture is routinely requested.
• US will show enlarged epididymis and increased blood flow to the epididymis
(reduced in torsion).
Treatment
• Vigorous treatment with antibiotics is necessary.
• If the epididymoorchitis is not settling within 1 week of antibiotics then
tuberculosis or even tumour must be excluded.
Chronic epididymo orchitis

Chronic inflammations of the epididymis and testis are caused by
• filarial infections in tropics like India.
• tuberculosis.
• inadequate treatment for acute epididymo orchitis.
• often associated with chyluria and elephantiasis of legs.
• Chronic nagging pain in the testis.
• In long-standing cases of filarial aetiology, the testis is very large, heavy and
hard due to calcification. The scrotal skin is very much thickened and the
median raphe is very prominent.
• Presence of sinus in the posterior aspect of scrotum (ref. Fig. 11.26A) is
invariably caused by tuberculosis.
• Beading of vas deferens and grossly enlarged prostate and seminal vesicles,
point towards tuberculous pathology.
• Biopsy may be needed to differentiate from malignancy.
• Search for pulmonary lesion must be done, if tuberculosis is suspected.
• US may be useful.
Treatment
• Antitubercular drugs or antifilarial measures are required depending upon the
condition.
• Drainage, if an abscess develops.
• Orchidectomy may have to be performed in severe cases.
Atrophic testis
• It can be unilateral or bilateral, the commonest being unilateral.
• Unilateral atrophy can occur following:
• Torsion of testis.
• Epididymo-orchitis caused by mumps.
• Iatrogenic causes are:
• injury or ligation of testicular artery (during surgery for hernia, hydrocele,
undescended testis and varicocele).
• Bilateral atrophy can occur in Hansen’s disease and cirrhosis of liver.
The testis is very much reduced in size sometimes to the size of a pea.
US may be useful in confirming the diagnosis.
Treatment
No treatment is possible.
Testicular tumour
• Incidence is around 4 per 1,00,000 population.
• Rare before puberty.
• They are classified as:
• Teratomas (60%): common between 25 and 35 years of age.
- Teratoma differentiated (TD) (10%)
- Malignant teratoma intermediate (MTI) (24%)
- Malignant teratoma undifferentiated (MTU) (embryonal carcinoma)
(25%)
- Malignant teratoma trophoblastic (MTT) (choriocarcinoma) (1%)
• Seminomas (35%): common between 35 and 45 years of age.
• Mixed (treated as teratomas)
• Lymphomas (bilateral) (5%) common between 60 and 70 years of age.
• The incidence of testicular tumour is shown in Fig. 36.20.
• Higher incidence has been reported among twins, brothers and family
members.
• They are more common on the right side.
• The undescended testis is more prone to develop a testicular tumour.
FIGURE 36.20 Incidence of testicular tumours.

History
• History of previous orchidopexy may be present.
• Recent history of trauma merely to draw the patient’s notice.
Symptoms
• Painless swelling with a dragging sensation in the scrotum.
• Dull ache in the scrotum and lower abdomen may be present.
• Symptoms of secondaries: backache and neurological symptoms (spine
metastases), haemoptysis (lung metastases).
Signs
• Lump or swelling usually in the lower part or sudden increase in size of testis
(Fig. 36.21).
• Absence of tenderness on gentle squeezing of testis.
• Loss of testicular sensation.
• Cord structures may be thickened.
• Small and lax hydrocele may be present.
• Para-aortic and supraclavicular nodes may be enlarged.
• Gynaecomastia may be present in 5% of cases.
FIGURE 36.21 Enlarged right testis of testicular tumour.
• Tumour markers: good indicators for follow-up treatment.
• Serum alpha fetoprotein levels may be raised.
• Human chorionic gonadotrophin (beta HCG) levels may be raised.
• Lactic dehydrogenase (secreted by both seminomas and teratomas) may be
raised.
• Placental alkaline phosphatase (secreted by seminomas) may be raised.
• Radiology
• US of the testis may show nonhomogenous acoustic shadows with speckled
calcification (normal testis shown homogenous appearance).
• X-ray chest shows metastatic lung deposits.
• CT of abdomen and chest are necessary to stage the tumour
Treatment
• High orchidectomy (upto the level of internal ring) through inguinal route is
the treatment of choice.
• Biopsy of the contralateral testis is necessary (if it is small, atrophic with
history of subfertility), as 5% have carcinoma in situ is in the other testis.
• Radiotherapy, excision of retroperitoneal nodes and or chemotherapy will be
indicated in some cases, depending upon the type and spread of tumour.
Varicocele
• Varicocele is dilatation of pampiniform plexus of veins.
• The causative factors are as follows:
• Incompetence of veins draining into the renal vein on the left side and into
inferior vena cava on the right side.
• Pressure effect of loaded colon on the left side.
• Rarely, varicocele may occur due to a renal tumour causing blockage to
venous flow.
• Seen in 10% of normal population with the incidence of about 20% in patients
with primary infertility.
• It is common on the left side.
• Bilateral varicocele can occur in 5% to 10% cases.
• Presenting complaint may be pain in the scrotum.
• Infertility may be a presenting symptom, due to oligozoospermia caused by
increased intra-scrotal temperature by the varicocele.
• A soft lumpy mass is seen or felt loosely hanging (Fig. 36.22), which gives
the ‘feel of bag of worms’ to the examiner.
FIGURE 36.22 Left-sided varicocele.
• US shows veins of 3.5 mm or larger in diameter with reversal of venous flow
after Valsalva maneuver.
• Semen analysis is necessary in cases of infertility.
Treatment
Surgical ligation and excision (open or laparoscopic methods) is required for
severe pain or to improve the sperm count in infertile patients.
Torsion of testis
• The testis lies in the scrotum suspended by the cord structures, and the
testicular artery is a part of it. When the testis is twisted on the axis of the
cord, the blood supply can get impaired, which may lead to gangrene. This
twist is usually away from midline corresponding to contraction of cremaster
muscle (Torsion).
• Can be precipitated by horizontal lie of the testis or by the presence of a long
mesentery between epididymis and body of the testis (Clapper bell
deformity).
• Common in children at puberty, but can also occur in adults.
• Sudden onset of severe scrotal pain, usually following an act of physical
strain.
• Pain in the lower abdomen and suprapubic area, may be present.
• There may be mild fever.
• This is followed by swelling of the cord structures, and in the early stages, a
knot can be felt in the cord structure. There may be minimal hydrocele.
If not detected early, there will be swelling of testis and it cannot be separately
felt from epididymis.
Doppler studies will show decreased blood flow to the affected side (in
epididymo orchitis, blood flow is increased).
Treatment
It is a surgical emergency and no time should be wasted in treating this
condition. Delayed treatment will lead to loss of function of testis, atrophy or
gangrene.
• Surgery involves untwisting of the torsion to restore blood flow and fixing it.
• The opposite testis also needs fixation (orchidopexy), to prevent similar
problem occurring later.
• Gangrenous testis needs orchidectomy (Fig. 36.23).
FIGURE 36.23 Torsion of testis. Source: (Courtesy Dr Ravisankar G Pillai)
Note
Even if the diagnosis is in doubt, surgical exploration should be done.
Cysts of epididymis
There is collection of many cysts arising from the head of epididymis.
• Swelling in the scrotum.
• Swelling is generally small compared to hydrocele.
• It is located behind the body of testis and can be seen extending above the
testis (Fig. 36.24).
• It is transilluminant (Fig. 36.25) and gives a tessellated appearance.
FIGURE 36.24 Cyst of epididymis (left).
FIGURE 36.25 Transilluminant epididymal cyst Source: (Courtesy Dr S. Devaji
Rao).
DD: Spermatocele: It is soft and small and is not transilluminant. It can be

bilateral. It is rare.
US is diagnostic.
Treatment
• No treatment is needed and surgery can be detrimental in unmarried and in
men who have not completed the family. This is because surgical removal
can obstruct the sperm passage.
• Surgical removal is indicated in large and symptomatic cases.
36.5 diseases of scrotum
The diseases of scrotum can be classified based on its aetiology (Table 36.4).
TABLE 36.4
Aetiological Classification of Diseases of Scrotum
Aetiology Diseases
Congenital Penoscrotal transposition (Bifid scrotum)

Ectopic scrotum
Scrotal haemangioma
Traumatic Laceration
Inflammatory Abscess
Venereal diseases, Fournier’s gangrene
Neoplastic Carcinoma
Others Sebaceous cysts
Penoscrotal transposition (bifid scrotum)

• Very rare condition.
• Results from incomplete or complete failure of inferomedial migration of
labioscrotal swellings.
• It is often associated with perineal, scrotal or penoscrotal hypospadias with
chordee.
• Penis appears small and present posterior to the scrotum (Fig. 36.25A) or may
be surrounded by scrotal tissue (Fig. 36.25B)
FIGURE 36.25A Penoscrotal Source: (Courtesy Dr K. Sridhar).

FIGURE 36.25B Bifid scrotum Source: (Courtesy Dr K. Sridhar).
Treatment
Urethroplasty to reconstruct the urethra and scrotoplasty to bring the scrotum
below the penis is required.
Ectopic scrotum
• Extremely rare condition.
• Results from a defect in distal gubernacular formation that prevents migration
of labioscrotal swellings.
• Can be associated with cryptorchism, inguinal hernia, exystrophy and upper
urinary tract anomalies.
• One hemiscrotum is normally located and the other hemiscrotum is in an
anomalous position along with inguinal canal.
• Most often it is suprainguinal.
Complete evaluation of urinary tract to identify the anomalies may be needed.
Treatment
• Scrotoplasty is needed for the ectopic scrotum.
• Treatment for associated upper tract anomalies, undescended testis and
hernia.
Scrotal haemangioma
This rare congenital condition has an incidence of 1% in the population.
A strawberry type of swelling, which may resolve spontaneously.
Treatment
• No treatment for most lesions.
• Excision for ulcerated and bleeding lesions.
Scrotal laceration
Occurs commonly following
• blunt injury (road traffic accident)
• a fall and
• gunshot injuries.
• The laceration may be confined to a small area of the scrotum.
• Sometime, there may be loss of entire scrotal skin with exposure of the testis
(Fig. 36.26) due to machinery injury.
• The tunica albuginea of testis may be damaged with loss of testicular
substance.
• Intra-abdominal, chest and head injuries may be associated.
FIGURE 36.26 Laceration of scrotum.
Treatment
• Cleaning and primary repair of simple tears.
• Placing the exposed testis in the subcutaneous plane of the thigh, and
dressings for complex injuries.
• Skin grafting and or scrotal reconstruction may be needed at a later date.
• Any tear in the tunica albuginea needs repair to prevent loss of testicular
substance.
Filarial scrotum
In the tropics, filariasis remains the main cause of chronic lymphoedema of the
scrotum.
• Swelling of the scrotum, sometimes to massive proportions (Fig. 36.27)
burying the penile shaft, or may involve the penis itself (ref. Fig. 12.17).
• The skin becomes hyperkeratotic, and thick.
• There may be associated swelling of the lower limbs.
FIGURE 36.27 Filarial scrotum Source: (Courtesy Dr K. Sridhar).
Treatment
• Scrotoplasty is the treatment of choice.
• Sometimes, total excision of scrotum and implantation of the testes in the
thighs may be required.
Scrotal abscess
• Usually, a superadded infection of fungal infections.
• The incriminating organisms being Staphylococci.
• Minor trauma-like bruises and scratches are known to initiate this pathology.
• More common in diabetics.
• Sudden pain in the scrotum
• Pyrexia
• Tender swelling (Fig. 36.28)
FIGURE 36.28 Scrotal abscess.

• Screening for diabetes mellitus is useful.
• Diagnostic aspiration of pus and isolation of organism is necessary.
Treatment
• Broad spectrum antibiotics
• Incision and drainage of abscess
Fournier’s gangrene
• It is called a vascular disaster of infective origin.
• The incriminating organisms being haemolytic Streptococci, Staphylococci,
E. coli and Cl. Welchii.
• The three cardinal characteristics of Fournier’s gangrene are as follows:
1. Sudden appearance of scrotal inflammation.
2. Rapid onset of gangrene.
3. Predisposing factors
- Diabetes
- Local trauma
- Paraphimosis
- Periurethral extravasation of urine
- Perianal infection
- Surgery (circumcision/herniorrhaphy).
• Minor trauma-like bruises and scratches are known to initiate this pathology.
• Sudden pain in the scrotum
• Prostration
• Pallor
• Pyrexia
• When cellulitis spreads and scrotal coverings slough, the testes are exposed
(Fig. 36.29).
FIGURE 36.29 Fournier’s gangrene.
Culture of sloughed tissues or the overlying secretions is diagnostic.
Treatment
• Broad spectrum antibiotics and wide excision of slough, to stop the spread of
gangrene.
• Raw area needs split skin grafting.
Carcinoma of scrotum
• Was commonly seen in chimney sweepers in the past, and now, rare due to
improved. cleaning methods of chimney.
• Occurs due to irritant nature of the oil.
• Chronic ulcer of scrotum may turn malignant.
• It commences in a wart or an ulcer with raised and rolled edges.
• As it extends it may involve the underlying testis.
• Inguinal lymph nodes may be palpable.
Wedge biopsy is diagnostic.
Treatment
• Excision of growth (with wide margins).
• Orchidectomy, if testis is involved.
• Radical block dissection, if inguinal nodes are involved.
Sebaceous cysts
Obstruction of pores of sebaceous glands causes these cysts.
• They are either single or multiple in number (Fig. 36.30A and B).
• They discharge typical cheesy material, and when infected discharge pus.
FIGURE 36.30A Sebaceous cyst scrotum.
FIGURE 36.30B Large multiple sebaceous cysts of
scrotum Source: (Courtesy Dr N. Mohan).
Treatment
Surgical excision of the cyst is curative.
36.6 symptoms of diseases of male genitalia
• Pain
• Swelling
• Ulcer
• Sinus
• Discharge
Pain
• Acute attack of pain (e.g., torsion of testis and acute epididymoorchitis).
• Recurrent episodes of pain (e.g., intermittent torsion of testis).
• Dull constant pain (e.g., filarial and tubercular orchitis, malignancy).
Swelling
• Acute swelling of the scrotum (e.g., acute epididymoorchitis, acute torsion of
testis).
• Gradual increase in scrotal size (e.g., hydrocele).
• Multiple polypoid lesions on the penis (e.g., condyloma acuminata).
• Single or multiple globular swellings (e.g., sebaceous cysts).
Ulcer
• Painful multiple ulcers of short duration (e.g., chancroid).
• Painless solitary ulcer (e.g., chancre).
Sinus
• Sinus can occur and last for a long time in tuberculous aetiology.
Discharge
• Purulent discharge of short duration (e.g., burst scrotal or testicular abscess).
• Serous or serosanguinous discharge of long duration (e.g., tuberculous sinus).
Eliciting history
• Age: Certain diseases affecting male external genitalia affect certain age
groups.
• Newborns and infants: Phimosis, hypospadias and epispadias
• 1–5 years: Congenital hydrocele and phimosis
• 2 and 7 years: Retractile testis
• 10–15 years: Torsion testis
• Young adults and middle aged: Epididymo orchitis, filarial scrotum and
sexually transmitted diseases
• Newly married and youth: Paraphimosis
• Elderly: Cancer penis
• Occupation: Carcinoma scrotum is common in chimney sweepers.
• Race: Hindus are more prone to cancer of the penis. Jews and Muslims who
practice circumcision are almost immune to penile cancer.

• Duration of illness: For how long is the patient suffering from this illness?
Symptoms of short duration indicate acute pathology (e.g., torsion testis,
abscess) and long duration indicate chronic pathology (e.g., tuberculous orchitis,
malignancy).
Association of high-grade fever may indicate an acute infective pathology
(e.g., acute epididymoorchitis, acute filarial orchitis) and low-grade fever in
tuberculosis.
malignancies.
a clearer picture of diagnosis (e.g., sinuses with previous history of surgery may
indicate a tuberculous pathology).
treatment?
treated will indicate the examiner to reconsider the diagnosis like recurrence of
tuberculosis. Even recurrent malignancies should be considered.
• Family history: Has any other family member suffered from a similar illness
or had any treatment?
Diseases like sinuses due to tuberculosis occur in families living in close knit
style and the positive history may be a good indicator for the present diagnosis.
match the situation, like extramarital contact if the disease is suspected to be
of syphilitic aetiology. History relating to trauma (part of fight or direct
injury to genitalia as in active sports) should also be elicited.
Penis
Inspection
• Shape of the penis: Penis may be bent due to fibrous contracture associated
with hypospadias (Fig 36.7A and B). Thickened and deformed penis
(Ramhorn penis) may be seen in chronic filariasis.
• Skin surface: The skin over the penis should be examined for swellings (e.g.,
condylomata), ulcers (e.g., chancre) and urethral openings (e.g.,
hypospadias).
• Prepuce: Circumferential narrowing of the prepucial skin (e.g., phimosis) and
ballooning of prepuce may occur during micturition and urine may be passed
in trickles in tight phimosis. Adults may present with collection of smegma
under the prepuce with soft swelling associated with discharge. The
prepucial skin may show scarring due to chronic inflammation. This is
commonly seen in neonates and in adults as balanitis xeroticus obliterans
(BXO). The glans may be exposed with oedema of penis just at the coronal
sulcus in paraphimosis.
• Glans:
• Ulcers: Ulcers may be present over the glans, coronal sulcus. They may be
associated with pain, discharge and enlarged nodes in the groin. Hunterian
chancre is usually single without pain. Soft chancre is associated with
multiple painful ulcers.
• Growths: Papilliferous tumour or ulcer with everted and rolled edges is
usually suggestive of cancer of the penis.
• Premalignant conditions:
- Leukoplakia of the penis
- Paget’s disease of the penis: Chronic eczema-like condition over the
glans and inside prepuce
- Erythroplasia of Querat: Dark indurated patch over glans and inner
surface of prepuce (Fig. 31.31).
• Urethral meatus: It is seen in the ventral aspect in hypospadias and on the
dorsal aspect in epispadias. Oedema of the urethral opening indicates
urethritis. Foreign bodies are found in people who indulge in perverted
habits.
• Urethral discharges: Obvious discharges should be noted (e.g., White thick
discharge may be seen with gonococcal urethritis (Fig. 36.32).
FIGURE 36.31 Erythroplakia of penis Source: (Courtesy Dr R. Rjaraman).
FIGURE 36.32 Whitish discharge from the urethral meatus Source: (Courtesy
Dr B. Loganathan).
Note
Glans penis may not be visible in tight phimosis.
Palpation
The shaft of the penis is examined by running the pulps of the fingers (Fig.
36.33) for any tumour or lumps or stones (e.g., extension of malignant tumour of
glans penis along the shaft).
FIGURE 36.33 Palpation of penile shaft.
Scrotum
Inspection
Surface of skin
The normal scrotal skin has wrinkles (rugosity) and is freely mobile over the
testis.
• Rugosity of scrotal skin: Rugosity is lost in
• hydrocele, due to stretching of skin.
• In inflammatory conditions such as epididymoorchitis, the skin is fixed
over the testis and cord structures, due to inflammatory oedema.
• testicular tumours such as teratoma and seminoma.
• Thickening of scrotal skin:
• In filariasis, the skin is grossly thickened with increased pits. The scrotum
will be large and the penis may be buried in the scrotal swelling (e.g.,
filarial scrotum). Filarial scrotum should be distinguished from the
swollen scrotum of renal, hepatic, and cardiac pathologies, where the skin
is not thickened.
• Lumps over the skin
• Sebaceous cysts present as multiple lumps.
• Multiple small vesicles are seen in lymph varix.
• Pinkish strawberry shaped swellings may suggest haemangiomas.
• Ulcer on scrotal skin
• Presence of necrotic areas of skin with ulceration is seen in Fournier’s
gangrene These patients will have severe systemic symptoms.
• Single ulcer with raised rolled out edges will be seen in carcinoma of
scrotum.
Anteriorly placed ulcer on the scrotum may be malignant and posteriorly
placed ulcers are common in tuberculosis.
• Sinuses on the scrotal skin
• Sinus relating to posterior aspect of epididymis is due to tuberculosis.
• Multiple sinuses are seen in ‘Watering can perineum’ where patient passes
urine in small drips from these openings due to periurethral abscess
resulting from long standing urethral stricture.
Presence of the scrotal swelling
Small swellings such as epididymal cyst, spermatocele, cyst of the cord will
be noted on palpation of the scrotum. However, large swellings such as
hydrocele, epidymoorchitis are obvious during inspection
Impulse on coughing
The presence of visible impulse on coughing confirms the presence of hernia
(e.g., bubonocoele or large inguinal hernia) and is a differentiating feature from
other scrotal swellings.
Palpation
• Lumps, ulcers and sinuses on the scrotal skin: they are examined by palpation
as described in respective Chapters 9, 10 and 11.
• Swelling of the scrotal sac
Is the swelling confined to scrotum? If the thumb and index finger can feel
the upper limit of the swelling, i.e., getting above the swelling, then it is scrotal
and if not, it is inguinoscrotal (a differentiating point between hydrocele and
inguinoscrotal hernia) (ref. Fig. 35.27A and B).
The following are to be done during examination of scrotal swellings:
• Fluctuation test: In this test, the fluid is shifted from one point to another by
application of pressure and is felt by the fingers. Two things are to be done.
First thing is to steady the swelling with the thumb and other fingers of the
less dominant hand, and secondly, intermittent pressure applied by the
fingers of the other hand at the lower pole, and the pressure will be felt by
the upper end by the fingers of the less dominant hand. The positive test
confirms the presence of fluid in hydrocele (Fig. 36.34). Fluctuation must be
elicited in two planes at right angle to each other.
• Transillumination test: The test is done in a dark room. A good pen torch and
a dark paper rolled into a tube are required to do the test. The light is applied
from the side of the scrotum and a rolled paper or x ray plate (illuminoscope)
is placed over the scrotum on the opposite side and is looked through with
the eye placed over the other end of the rolled paper. Visibility of light
indicates positive transillumination (Fig. 36.35). This test is positive for
hydrocele and cyst of epididymis (ref. Fig. 36.25), but not so in pyocoele and
haematocoele. The hydrocele fluid being thin allows the light to pass
through.
• Reducibility: This test is done with the patient lying down. The swelling is
squeezed gently from the scrotum up into the external ring. If the swelling is
reducible it means the diagnosis is hernia or congenital hydrocele (swellings
which have communication with peritoneal cavity will exhibit reducibility).
• Impulse on coughing: When the patient is asked to cough, a swelling appears
in the inguinal region and is diagnostic of inguinal hernia, which is absent in
hydrocele (swellings. which have communication with peritoneal cavity will
exhibit impulse on coughing).
FIGURE 36.34 Method of eliciting fluctuation with the thumb and index
fingers of both hands.
FIGURE 36.35 Method of determining transillumination.
Testis
Palpation
Testis is palpated using the thumb and other fingers, for swellings and tenderness
(Fig. 36.36A and B).
• Position of testis: In undescended testis, retractile testis and in ectopic testis,
the testis is not felt in its normal position in the scrotum. It may be anteverted
when the epididymis lies anteriorly or completely inverted when the
epididymis lies at the lower part of the testis.
• Size of testis: The testis is very small in atrophic testis, following mumps
orchitis, in association with large varicocele, hypogonadotrophic
hypogonadism and in Klinefelter syndrome. Enlarged testis is seen in orchitis
and malignancies.
• Presence of lump: Localized lump in one of the poles is common in testicular
tumour.
• Presence of testicular sensation: There is normally a mild discomfort when
the testis is pressed. This may be absent in gumma of the testis, malignancy
of the testis and exaggerated in orchitis. One has to be gentle during this
examination.
FIGURE 36.36A Method of palpation of testis in an adult.

FIGURE 36.36B Method of palpation of testis in a child.
Epididymis
Palpation
Epididymis is palpated using the thumb and other fingers, for swellings and
tenderness (Fig. 36.37A) and with the thumb and index finger in a child (Fig.
36.37B).
• Size of epididymis: Normal epididymis lies above the posterior aspect of the
testis. Enlargement can occur in chronic epididymo orchitis of tuberculous
and filarial aetiology.
• Position of epididymis: It lies at the lower part of testis in completely
inverted testis. There may be presence of mesentery between testis and
epididymis and this condition predisposes to torsion of testis.
FIGURE 36.37A Method of palpation of epididymis in an adult.
FIGURE 36.37B Method of palpation of epididymis in a child.
Cord structures
Palpation
Cord is palpated using the thumb and other fingers, for swellings and tenderness
(Fig. 36.38A and B).
• Cord structures as a whole will be thickened in epididymoorchitis and
sometimes due to extension of a testicular tumour.
• Vas deferens is felt like a thick cord, which roles under the examining fingers.
Vas is absent in 10% of patients. Vas is beaded in tuberculosis.
• Venous plexus is felt as very soft tissues. A lax swelling of veins with the feel
of bag of worms is felt in varicocoele. Cough impulse is seen in varicocoele.
FIGURE 36.38A Method of palpation of cord structures in an adult.
FIGURE 36.38B Method of palpation of cord structures in a child.
Note
Examination in standing posture is essential to diagnose varicocoele.
Lymphatic system
Drainage area
It is always mandatory to examine the area of lymphatic drainage of the
genitalia, i.e., inguinal, iliac and para-aortic lymph nodes, which will give useful
information (e.g., penile malignancies metastasize to inguinal and iliac nodes,
testicular malignancies metastasize to para-aortic nodes).
• Inguinal lymph nodes: Felt with the flat of the fingers at or just below the
inguinal ligament.
• Iliac lymph nodes: Felt with the flat of the fingers just above the inguinal
ligament.
• Para-aortic lymph nodes Felt by deep palpation at the midline above the
umbilicus.
Other lymph nodes

detail. e.g., tuberculosis. Examination of the liver and spleen completes the
lympho reticular system, which is useful in diagnosis.
Abdomen
Systemic examination of the abdomen should be performed.
• Varicocoele can be due to intra-abdominal masses pressing veins draining into
the renal vein.
• Hepatomegaly may be an effect of metastasis of testicular tumours.
General
General physical examination will give clues for diagnosis like evidence of
pulmonary tuberculosis as the cause for orchitis or even pulmonary metastases
secondary to testicular cancer.
CHAPTER 37
Urinary system
M.G. Rajamanickam
CHAPTER OUTLINE
37.1. Development of urogenital system 651
37.2. Kidneys and renal pelvis 651
• Surgical anatomy 651
37.3. Diseases of kidneys and renal pelvis 651
• Renal injuries 654
• Acute pyelonephritis 655
• Pyonephrosis 655
• Carbuncle 655
• Perinephric abscess 655
• Chronic pyelonephritis 656
• Renal tuberculosis 656
• Wilms’ tumour (nephroblastoma) 657
• Renal cell carcinoma (hypernephroma, Grawitz tumuor) 657
• Transitional cell carcinoma/SCC of renal pelvis 659
• Renal calculi 660
37.4. Ureters6 61
37.5. Diseases of ureters 661
• Ureteric injuries 663
• Ureteric tumours 664
• Ureteric obstructions 664
• Ureteric calculi 666
37.6. Urinary Bladder 666
37.7. Diseases of urinary bladder 667
• Ectopia vesicae (bladder exstrophy) 667
• Bladder diverticulum 667
• Urachal abnormalities 667
• Bladder injuries 668
• Acute cystitis 669
• Chronic cystitis 669
• Papilloma 670
• Haemangioma 670
• Carcinoma 671
• Bladder calculi 672
37.8. Prostate 673
37.9. Diseases of prostate 673
• Acute prostatitis 673
• Chronic prostatitis 674
• Benign hypertrophy 674
• Carcinoma 675
• Prostatic calculi 676
37.10. Urethra 676
37.11. Diseases of urethra 676
• Meatal stenosis 677
• Posterior urethral valves 677
• Hypospadias 677
• Epispadias 678
• Urethral stricture 678
• Urethral duplication 678
• Urethral diverticulum 679
• Urethral injuries 679
• Acute urethritis 680
• Chronic urethritis 680
• Urethral caruncle 680
• Condyloma acuminata 680
• Urethral carcinoma 681
• Urethral calculi 681
37.12. Symptoms of urinary tract pathologies 681
• General 686
• Abdomen 686
• Rectal 689
37.1 Development of urogenital system
Kidneys and ureters

Mammals develop three kidneys in the course of intrauterine life. The embryonic
kidneys are the pronephros, the mesonephros and the metanephros in the order
of appearance—all developing from the intermediate mesoderm. The renal
parenchyma is derived from metanephros. The ureteric buds grow backward
from the lower end of mesonephric (Wolffian) duct in the sacral region, and
develop into ureters, their dilated upper ends, the renal pelvis. Repeated
bifurcation of the primitive renal pelvis from 6 to 8 months, form the calyces and
the collecting ducts. Ascent of each kidney in the posterior abdominal wall to its
normal position takes place between fifth and eighth weeks of embryonic
development and its rotation.
Urinary bladder and urethra

The vesicoureteric canal gives rise to the urinary bladder and the pelvic urethra.
The caudal urogenital sinus forms the phallic urethra in males and distal vaginal
vestibules in females. The trigone of the urinary bladder is formed from the
mesoderm of mesonephric ducts distal to ureteric buds (common excretory
ducts).
Prostate
Solid epithelial buds arise from the primitive urethra and get canalized. The
surrounding mesenchyme forms the muscular and connective tissue of the gland.
The homologue of prostate in females is the Skene’s tubules.
Epididymes and vas deferens

The Wolffian ducts become the epididymes and vas deferens.
Testes
Testes develop from the genital fold medial to the mesonephros in early fetal
life, lie in the retroperitoneum below the kidneys. Vasa efferentia are derived
from the mesonephric tubules that unite with the rete testis. Gubernaculum is a
peritoneal process that extends from its attachment to the vas and epididymis to
the region of developing phallus. The gubernaculum contains muscle fibres, but
its role in testicular descent is uncertain. The processus vaginalis starts as a
dimple of peritoneum at about the tenth week and precedes the testis in its
journey through the abdominal wall down to the scrotum. Maternal
gonadotrophins may play a role in testicular migration. The seminal vesicles
sprout from the distal mesonephric ducts.
37.2 Kidney and renal pelvis
Surgical anatomy
The kidneys lie well protected deep in the retroperitoneal space. Gerota’s fascia
surrounds the kidney and perinephric fat, an important anatomic barrier around
the kidney (Fig. 37.1). The renal hilum contains the renal vein, artery and the
renal pelvis, anterior to posterior. Renal artery arises from the aorta, and the
renal vein joins the inferior vena cava at the level of the body of L2 vertebra.
The main renal artery gives rise to four or five segmental vessels, which in turn
give rise to interlobar arteries, interlobular arteries and afferent arterioles. The
renal parenchyma drains into the seven calyces, three upper and two each,
middle and lower.
FIGURE 37.1 Anatomy of urological system.
37.3 Diseases of kidney and renal pelvis

The diseases of the kidneys and pelvis can be classified based on their
aetiologies (Table 37.1).
TABLE 37.1
Aetiological Classification of Diseases of Kidneys and Pelvis
Aetiology Diseases
Congenital Renal aplasia Absent kidney
Renal ectopia Pelvic kidney
Horseshoe kidney
Crossed ectopia
Cake kidney
Infantile polycystic kidney disease
Solitary renal cyst
Aberrant renal vessels Renal artery aneurysm
Multiple renal arteries and veins
Duplication Duplex kidney
Duplex renal pelvis
Duplex kidney and ureter
Dilatations Hydronephrosis
Traumatic Renal injuries
Infective Acute Acute pyelonephritis
Pyonephrosis
Carbuncle
Perinephric abscess
Chronic Chronic pyelonephritis
Renal tuberculosis
Neoplastic Malignant Wilms’ tumour
Renal cell carcinoma
Transitional cell carcinoma of renal pelvis
Squamous cell carcinoma of renal pelvis
Others Calculi
• Renal aplasia
• Total absence of renal tissue
• Rare in occurrence 1 in 1400
• An anomaly due to failure of mesonephric duct to bud, with or without the
development of ureter
• Many times discovered incidentally on radiological examination
• Renal ectopia
• Pelvic kidney: Kidney is present in the pelvis, but fails to ascend, more
commonly on the left side, may be associated with a contralateral kidney
in normal position (Fig. 37.2)
• Horseshoe kidney: Ectopic kidneys fused at the lower poles to give the
horseshoe appearance, fusion usually occurs in front of the fourth lumbar
vertebra, and the ascent prevented by the superior mesenteric artery.
Occurs due to the fusion of most medial subdivisions of mesonephric duct,
which impede normal ascent of the kidneys (Fig. 37.3)
• Crossed ectopia (unilateral fusion): Both kidneys are in one loin and the
ureter of the lower kidney crosses the midline to enter the urinary bladder
on the other side (Fig. 37.4)
• Cake kidney: Fused kidneys do not rise up but remain in the pelvis to form
an amorphous mass in front of the sacrum (Fig. 37.5)
• Polycystic kidney: Infantile form (autosomal recessive) is often fatal,
whereas the adult form (autosomal dominant) becomes symptomatic in
adult life (Fig. 37.6A)
• Solitary renal cysts (Fig. 37.6B) is not uncommon
• Hydronephrosis: Dilatation of renal pelvis due to functional obstruction
caused at the pelvi-ureteric junction by collagen and sparse muscular tissue
as a ring (Fig. 37.7)

FIGURE 37.2 Pelvic kidney.

FIGURE 37.3 Horseshoe kidney.

FIGURE 37.4 Crossed ectopia.

FIGURE 37.5 Cake kidney.
FIGURE 37.6A Polycystic kidney.
FIGURE 37.6B Solitary renal cyst.

FIGURE 37.7 Congenital hydronephrosis due to PUJ obstruction.
• Majority of congenital anomalies are identified incidentally and are
asymptomatic
• Crossed ectopic kidney and adult polycystic kidney may present as loin
masses
• Horseshoe kidneys present with urinary infection due to devious course of the
ureter
• Haematuria and hypertension may be presenting symptoms
• Patients with hydronephrosis present with pain with diuresis, fever, and rarely
a mass in thin individuals
• Ultrasound (US) and CT (Figs. 37.7A—D) are diagnostic
• Intravenous urography (IVU) gives excellent details of the urological
system, when the kidneys are functioning (Figs. 37.7E—G)
• Isotope scanning is useful in assessing the renal function
FIGURE 37.7A CT—pelvic kidney.

FIGURE 37.7B CT—bilateral polycystic kidneys.
FIGURE 37.7C CT—solitary cyst left kidney.
FIGURE 37.7D CT—horseshoe kidney.

FIGURE 37.7E IVU—horseshoe kidney.

FIGURE 37.7F IVU—crossed ectopia.

FIGURE 37.7G IVU—gross hydronephrosis left kidney due to PUJ
obstruction.
Treatment
• Division of horseshoe kidney may be indicated in some situations
• Deroofing may be done for symptomatic renal cysts
• Pyeloplasty is done for hydronephrosis
• Renal transplantation may be required when renal failure develops in
bilateral adult polycystic kidney disease
Renal injuries
• Kidneys are the most common organs to get injured in the urological system
• Injuries to the kidneys may be caused by:
• Closed blunt abdominal trauma such as road traffic accidents, during
active sports and may be associated with lower rib fractures
• Penetrating injuries by bullets, knives, etc.
• Renal trauma is of three types:
• Minor trauma (e.g. renal contusion, subcapsular haematoma)
• Major trauma (e.g. deep cortical lacerations, extravasation of urine)
• Renal vascular trauma (e.g. avulsion of renal pedicle)
• Haematuria is the commonest symptom
• Signs of shock may be seen in major trauma
Clinical examination may reveal bruising over the ribs posteriorly or
evidence of penetrating injury, tenderness and guarding in the loin and
expanding mass. Ecchymosis may be seen in renal angle (Fig. 37.8)
FIGURE 37.8 Ecchymosis over left renal angle in renal trauma.
• Plain X-rays may show fractures of lower ribs
• CT is the investigation of choice and accurate assessment is possible (Fig.
37.9)
• Renal arteriography may be needed in cases where CT is not contributory,
especially with renal vessel injuries
FIGURE 37.9 Contrast enhanced CT—left renal injury.
Treatment
• Any patient with renal injury should rest in bed and all urine samples
should be examined for blood
• Surgical exploration is warranted in closed injuries, when there is
retroperitoneal bleeding, expanding loin mass, urinary extravasation,
evidence of nonviable renal parenchyma and renal pedicle injuries
• Exploration of abdomen is required for penetrating injuries for assessment
of other injuries and kidneys should only be explored when the condition
warrants
Acute pyelonephritis
Acute infection of the renal parenchyma caused by Gram negative organisms
(less commonly Gram positive cocci), often associated with septicaemia
• High-grade pyrexia
• Loin pain with rigors
• Haematuria or pyuria
Significant leucocytosis, pyuria and bacteriuria (routine and culture) are
diagnostic
Treatment
Appropriate antibiotics are the mainstay of treatment
Pyonephrosis
Usually follows:
• attacks of acute pyelonephritis
• renal calculous disease (Fig. 37.10)
• infection of hydronephrosis
FIGURE 37.10 Calculous pyonephrosis.
• Triad of symptoms:
• Fever
• Anaemia
• Swelling in the loin
US and CT are diagnostic
Treatment
• Percutaneous aspiration of pyonephrosis is curative in many cases
• Nephrostomy gives good results
• Nephrectomy may be needed in bad cases
Carbuncle
• May result due to:
• haematogenous spread of infections caused by Staphylococcus aureus or
coliform organisms
• infection of a renal haematoma
• Commonly seen in diabetics and patients with HIV infection
Triad of symptoms:
• Fever
• Anaemia
US and CT are diagnostic
Treatment
Appropriate antibiotics and drainage of pus is curative
Perinephric abscess
May result from extension of:
• renal cortical abscess
• appendicular abscess
• infection of perirenal haematoma
• discharge of pyonephrosis into the perinephric fat or renal carbuncle
• spread through periureteral lymphatics and blood
Triad of symptoms
• Fever
• Anemia
US and CT (Fig. 37.11) are diagnostic
FIGURE 37.11 CT—left perinephric abscess.
Treatment
Appropriate antibiotics and open drainage of pus is curative (percutaneous
drainage is not effective due to loculations)
Chronic pyelonephritis
• Chronic inflammation of the kidneys is often associated with vesicoureteric
reflux (reflux nephropathy), and is a common cause of end-stage renal
disease
• There is interstitial inflammation and scarring of renal parenchyma; renal
tubules are atrophic and dilated
• Glomeruli retain normal structure till the end
• Most patients present with hypertension and uraemia
• May present with signs of end-stage renal disease, fatigue, lassitude, nausea,
weight loss, polyuria and nocturia
• Diagnosis is not straightforward
• White blood cell casts in the urine suggest diagnosis
• Renal biopsy may be useful
Treatment
• Surgically correctable lesions should be dealt with at the earliest
• Antibiotic therapy may be useful
• Hypertension needs to be controlled effectively
• Chronic dialysis and/or renal transplantation is for end-stage renal disease
Renal tuberculosis
• Usually secondary to pulmonary tuberculosis
• May cause obstructive lesions of the urinary tract
• Dysuria, frequency and haematuria
• Sterile pyuria is very common
• Constitutional symptoms are usually present
• IVU is useful in diagnosing early disease (Fig. 37.12A)
• Urinalysis for acid-fast bacilli (three consecutive early morning specimens of
urine) and their growth (culture test) are useful
• PCR for tuberculosis in urine is contributory
• US and CT (Fig. 37.12B) demonstrate obstructive lesions
FIGURE 37.12A IVU—GU TB showing dilatations of the upper tract with
contracted bladder.
FIGURE 37.12B CT—renal tuberculosis.
Treatment
• Surgery is reserved for obstructive lesions and it should be conservative
Wilms’ tumour (nephroblastoma)

• Commonest abdominal tumour in children
• A total of 80% of renal tumours of childhood
• Usually found in the first 4 years of life
• Uncommon in the first 6 months of life and children older than 6 years
• Association with congenital anomalies (e.g. cryptorchidism, hypospadias)
• Has a very poor prognosis
• Trisomy 18
• Deletion on the short arm of chromosome 11 (11p13)
• Macroscopically, it may be lobular and surrounded by pseudocapsule
• Microscopically, there is a variety such as
• Areas of primitive mesenchymal cells that may show differentiation into
fat, muscle or cartilage, and embryonal glomerular and renal tubular
elements are seen within
• The tumour spreads by:
• Local invasion into the renal pelvis and renal vein
• Blood to lungs and liver
• Lymph is relatively infrequent
Symptoms
• Abdominal pain
• Haematuria
• Unexplained fever
• Cough or dyspnoea indicate pulmonary metastases
Sign
• Abdominal mass with distension (Fig. 37.13)
FIGURE 37.13 Wilms’ tumour.
• Haematology—anaemia, uraemia
• Urine test—blood and protein
• X-ray chest—lung metastases
• IVU (Fig. 37.13A), US and CT (Fig. 37.13B) are diagnostic
FIGURE 37.13A IVU—Wilms’ tumour (right).
FIGURE 37.13B CT—Wilms’ tumour (right).
Treatment
• Nephroureterectomy and regional lymph node dissection
• Contralateral kidney should be carefully inspected for bilateral tumours
• Postoperative radiotherapy and chemotherapy
Palliative
• Chemotherapy
• Local radiotherapy
Renal cell carcinoma (hypernephroma, grawitz

tumour)
• Malignancy arising from renal tubular cells (Fig. 37.14)
• Exclusively a cancer of adults, increasing with age
• Common in the sixth decade
• More common in males
• Smoking
• Exposure to industrial toxins
• Association with von Hippel-Lindau disease
• Autosomal dominant polycystic kidney disease
• Tuberous sclerosis
• Usually, the tumour is solid, expanding the renal tissue with a central area of
necrosis or cystic degeneration and other haemorrhagic areas
• The tumour spreads in many ways:
• Local spread—extends into the lumen of renal vein and inferior vena cava,
and embolise
• Blood spread—metastasizes to lungs, liver and bones
• Lymphatic spread—renal hilar nodes and para-aortic lymph nodes

FIGURE 37.14 Renal cell carcinoma.
Symptoms and signs
• Triad
• Haematuria
• Flank pain (due to enlargement of tumour or haemorrhage within the
tumour)
• Abdominal mass
• Others
• Fever, hypertension (due to excess renin production)
• Polycythaemia (due to excess erythropoietin)
• Hypercalcaemia (due to ectopic production of parathormone-like protein)
• Anaemia and other paraneoplastic syndrome
Note
Chance finding during routine investigation is not uncommon, and notorious
for presenting as metastatic carcinoma of unknown primary (pathological
fracture).
• Blood tests—polycythaemia and hypercalcaemia
• US (Fig. 37.14A) is diagnostic
• Contrast enhanced computed tomography (CECT) (Fig. 37.14B) and MRI
(Fig. 37.14C) give additional information such as renal vein/IVC invasion
• CT angiography (Fig. 37.14D) is useful for planning surgery
• IVU is informative
• X-ray and CT of chest are required to detect lung secondaries (cannon ball
appearance)
• Isotope bone scan (Fig. 37.15) and skeletal survey are useful for assessing
bone metastases
• Fine needle aspiration cytology (FNAC) or biopsy is confirmative
FIGURE 37.14A US—renal cell carcinoma.
FIGURE 37.14B CT—renal cell carcinoma (right) Source: (Courtesy Dr G.
Ravisankar Pillai).
FIGURE 37.14C MRI—left renal cell carcinoma.
FIGURE 37.14D CT angiography—large right-sided vascular renal tumour.

FIGURE 37.15 Isotope scan—right renal tumour.
Treatment
Radical nephrectomy
Palliative
• Radiotherapy for bone and brain metastases
• Biological therapies—interferon and interleukin 2 (IL2) show some response
Transitional cell carcinoma/squamous cell

carcinoma of renal pelvis
• Less common malignancies of the kidney
• Most common in older individuals
Transitional cell carcinoma arises in the pelvicalyceal system
• Tends to involve the renal parenchyma
• Industrial carcinogens (rubber, cable, dye and printing industries)
• Smoking
• Phenacetin abuse
Distant spread is common
Squamous cell carcinoma of the renal pelvis
• A total of 10% of renal pelvic tumours
• Calculi
• Chronic infection
• They metastasize early and have a poor prognosis
Haematuria is the presenting symptom
• Urine cytology may help in diagnosis
• US (Fig. 37.16A) and IVU (Fig. 37.16B) or retrograde pyelography (RGP)
are diagnostic
• CECT is diagnostic
FIGURE 37.16A US—carcinoma of renal pelvis.
FIGURE 37.16B IVU—carcinoma of renal pelvis.
Treatment
• Transitional cell carcinoma
• Nephroureterectomy with a cuff of urinary bladder wall excision
• Radical nephrectomy (Fig. 37.17)

FIGURE 37.17 Carcinoma of renal pelvis.
Renal calculi
• Renal calculi are common in the age group of 30–50 years with a strong
family history
• The predisposing factors for formation of stones are given in Table 37.2
• The stones have their own characteristics (Fig 37.18). They are given in Table
37.3
FIGURE 37.18 Varieties of renal stones.
TABLE 37.2
Predisposing Factors and the Mechanism of Formation of Renal
Calculi
Factor Mechanism
Dietary Increased intake of calcium, oxalate and uric acid rich food
Dehydration Solute solvent imbalance
Calcium deposition Decreased citrate excretion in urine
Renal infection Caused by urea-splitting organisms
Obstructions of Urinary stasis
urinary tract
Prolonged Skeletal decalcification favours urinary calcium
immobilization
Metabolic causes Hyperparathyroidism, hypervitaminosis, myeloma, disseminated malignant disease, sarcoidosis,
milk alkali syndrome, hyperthyroidism, Cushing’s disease
Cystinuria, Increase in urinary solutes
xanthinuria,
oxaluria, gout
TABLE 37.3
Characteristics of Renal Stones
Radio-
Composition Incidence Colour Appearance
opacity
Calcium oxalate 80% Yellow Irregular with sharp projections Radio-
brown opaque
Calcium phosphate or calcium magnesium 10% Dirty Smooth (may form staghorn Radio-
ammonium phosphate white calculi) opaque
Uric acid or urate 3% Light Hard and smooth, often Radiolucent
brown multiple, multifaceted
Cystine 2% Pink or Hard and multiple Radio-
yellow opaque
Xanthine Rare Brick red Smooth rounded, lamellation on Radiolucent
cross section
Note
When the stones take the shape of the renal pelvis with projections, they are
known as "staghorn" calculi (Fig. 37.19).
FIGURE 37.19 Staghorn calculi.
• Many remain asymptomatic
• Pain in the renal angle may be present, when infection occurs
• Severe pain (renal colic) may be present in stones at the pelvi-ureteric
junction
• Haematuria may be present
• Crystalluria may cause strangury due to impaction at the intramural ureter or
urethra
• Plain X-rays (Fig. 37.20A) can localize radio-opaque stones
• IVU (Fig. 37.20B) can define the anatomy of urinary tract and localize
radiolucent stones
• US will define obstructions and dilatations
FIGURE 37.20A X-ray KUB showing stones (staghorn calculi).
FIGURE 37.20B IVU—right staghorn calculus Source: (Courtesy Bharat
Scans).
Treatment
• Conservative management is enough for stones of less than 0.5 cm size, as
they are likely to pass out spontaneously
• Removal is warranted for larger stones, especially those which are obstructing
and compromising on the renal function
• Stones can be removed either by open surgery (pyelolithotomy,
nephrolithotomy) or by percutaneous nephrolithotomy
• Stones can be fragmented by extracorporeal shock wave lithotripsy
(ESWL) and allowed to pass in urine
• Antibiotics are required to treat associated infections
37.4 Ureters
Surgical anatomy
The ureter on each side runs from the pelvi-ureteric junction to the urinary
bladder. It runs along the psoas major muscle, enters the pelvis anterior to the
sacroiliac joint at the common iliac bifurcation. It descends to the level of ischial
spine where it turns forwards and medially to enter the urinary bladder. It lies
relatively close to the lateral fornix of vagina in females.
37.5 Diseases of ureters
The diseases of the ureters can be classified based on their aetiology (Table
37.4).
TABLE 37.4
Aetiological Classification of Diseases of Ureters
Aetiology Diseases
Congenital Ureteric atresia Absent ureter
Duplications Ureteric duplication
Duplication of renal pelvis
Duplication of kidneys and ureters
Dilatations Congenital megaureter
Ureterocoele
Abnormal position Postcaval ureter (retrocaval ureter), circumcaval ureter
Traumatic Ureteric injuries
Neoplastic Ureteric tumours
Obstructive Extramural/intramural/intraluminal causes
Others Calculi
• Ureteric atresia (Fig. 37.21)
• Ureter is partly or totally absent, due to failure of development of ureteric
bud, or its arrest before coming into contact with the metanephric blastema.
Kidney is absent or multicystic, and contralateral vesicoureteric reflux may
be present

FIGURE 37.21 Ureteric atresia.
• Duplications of ureter (Fig. 37.22)

• Ureteric duplications: May be incomplete ‘Y’ type, or complete as two
ureters
• Duplication of renal pelvis: Most common anomaly of upper renal tract,
usually unilateral, more common on the left
• Duplication of kidneys and ureters: Two ureters and two kidneys on each
side
• Dilatations of ureter
• Congenital megaureter: Dilated ureter due to functional obstruction at the
lower end (Fig. 37.23)
• Ureterocoele: Cystic enlargement of intramural portion of ureter probably
due to congenital atresia of ureteric orifice (Fig. 37.24)
• Abnormal position
• Retrocaval ureter: Right ureter passes behind the inferior vena cava
instead of lying to its right (Fig. 37.25)
FIGURE 37.22 Ureteric duplications.

FIGURE 37.23 Congenital megaureter.
FIGURE 37.24 Ureterocoele.

FIGURE 37.25 Retrocaval ureter.
• Most of these patients remain asymptomatic
• Patients with hydronephrosis present with repeated episodes of urinary
infection especially in vesicoureteric reflux or uretero-ureteric reflux (two
ureters on one side)
• In females, when one of the two ureters opens into the vagina, the patient has
urinary incontinence
• Calculus formation is common due to recurrent infections
• IVU (Fig. 37.25A), micturating cystourethrogram (MCU) (Fig. 37.25B), US
and CT (Figs. 37.25C and D) are informative
• Cystoscopy and RGP (Fig. 37.25E) are conclusive, when kidneys are absent
or nonfunctioning
FIGURE 37.25A IVU—left duplicated ureter.

FIGURE 37.25B MCU—bilateral parauretric diverticulae.
FIGURE 37.25C US—ureterocoele.
FIGURE 37.25D CT—retrocaval ureter.
FIGURE 37.25E RGP—retrocaval ureter.
Treatment
• No treatment is required for asymptomatic anomalies
• Antibiotics are required for treating recurrent infections
• Refashioning and reimplantation (ureteroneocystostomy) are done for
grossly dilated ureters with functioning kidneys to prevent vesicoureteric
reflux
Ureteric injuries
• Commonest cause of ureteric injuries is during abdominal and pelvic
operations
• The operations associated with ureteric injuries are given in Table 37.5
TABLE 37.5
Causes of Ureteric Injuries
Operations
Gynaecology General surgery Urology

Hysterectomy (abdominal or vaginal)—open or Sigmoid colectomy Excision of bladder
laparoscopic diverticula
Ovarian cystectomy Abdomino perineal Ureterolithotomy
resection
Anterior colporrhaphy Surgery for aortic aneurysm Ureteroscopy
Nature of injuries
• Complete ligation of one or both ureters, leads to increase in intraureteric
pressure, with resultant dilatation of pelvis, kidneys stop secreting urine, and
kidney atrophies
• If bilateral ligation is not recognized during surgery, it manifests as uraemia
• When the obstruction is incomplete (inclusion in a stitch), secretion continues
to be normal, hydronephrosis and infection occur
• When the ureter is divided or suffers crushing injury, urine leaks into the
retroperitoneum or peritoneal cavity which may result in a urinary fistula
• The injury may be recognized at the time of surgery
• Urinary leak occurs around the fifth postoperative day
• The clinical presentation varies according to the nature of injury (Table 37.6)
TABLE 37.6
Ureteric Injuries and Their Clinical Presentations
Injury Clinical Presentation

Bilateral ligation Anuria in the immediate postoperative period
Unilateral ligation No symptoms/loin pain/fever
Division Urine leak through the drain/wound/vagina
Retroperitoneal urine leak Abdominal distension and paralytic ileus
Intraperitoneal urine leak Abdominal distension and paralytic ileus with peritonitis and sepsis
IVU or CECT will demonstrate the nature of obstruction and urinary leak
Treatment
• If injury is recognized during surgery, it should be rectified immediately
• Spatulation and end-to-end anastomosis is done, when the length is not
lost
• Incomplete damages to the ureter may be treated by stenting and
spontaneous healing may be expected
• Surgical corrections (ureteroureterostomy, ureteroneocystostomy) are
necessary to restore the anatomy, before renal function is compromised
(Fig. 37.26)
FIGURE 37.26 Surgeries for ureteric injuries.
Ureteric tumours
• They are rare and behave like tumours of renal pelvis
• They are transitional cell carcinomas
Haematuria is the presenting symptom
• IVU and CECT are diagnostic
• US (Fig. 37.27) is useful as preliminary investigation especially in obstructive
lesions
FIGURE 37.27 US—ureteric tumour projecting into urinary bladder.
Treatment
Nephroureterectomy is the treatment of choice
Ureteric obstructions
The ureters can get obstructed due to various causes (Table 37.7)
TABLE 37.7
Causes of Ureteric Obstructions
Extramural Cause Intramural Cause Intraluminal Cause

Retroperitoneal fibrosis Pelvi-ureteric junction obstruction Stones
Neoplasms Ureterocoele Renal papillary necrosis in diabetics
Strictures (tubercular) Blood clot
Schistosomal stricture Fungal balls
Surgical damage Ureteric tumours
• Colicky pain (severe, griping and spasmodic), radiating from loin to groin
• Fever with rigour and abdominal pain are commonly seen
• Grossly dilated pelvis and kidney due to chronic obstruction, may be palpated
per abdomen
• US can identify the stones of reasonable size, but dilated ureters proximal to
the obstruction can be identified without difficulty (Fig. 37.27A)
• IVU (Fig. 37.27B) and CECT with contrast enhancement are diagnostic in
identifying the cause of obstruction (Fig. 37.27C)
• RGP (Fig. 37.27D) and ureteroscopy are useful in localizing the lesions
FIGURE 37.27A US—right ureteric dilatation due to obstruction.
FIGURE 37.27B IVU—obstructive hydroureteronephrosis (megaureter).
FIGURE 37.27C CT—retroperitoneal fibrosis.
FIGURE 37.27D RGP—Rt hydronephrosis.
Treatment
Excisional surgery or plastic reconstructive procedures
are performed to relieve obstructions and to treat the cause
Ureteric calculi
• Ureteric calculi originate always in the kidney
• It may get impacted at five sites of anatomic narrowing:
• ureteropelvic junction
• iliac artery crossing
• juxtaposed vas deferens or broad ligament
• the vesicoureteric junction
• ureteric orifice
• Many of them remain asymptomatic
• Impacted stones produce colicky pain (ureteric colic) radiating to the groin,
external genitalia and anterior surface of thigh
• Haematuria may also be present
• Clinical examination may reveal tenderness and rigidity over the course of the
ureter
• Plain X-ray of kidney, ureter, bladder (KUB) may show the radio-opaque
stones (Fig. 37.28)
• IVU may show dilatation due to obstruction (Fig. 37.28A), and also
radiolucent (uric acid) stones, as filling defect
• Noncontrast enhanced spiral CT is diagnostic (Fig. 37.29)
• Cystoscopy is useful in identifying the stones impacted at the ureteric orifice
• Diagnostic ureteroscopy is conclusive
FIGURE 37.28 X-ray KUB showing stones in right kidney and
ureter Source: (Courtesy Bharat Scans).
FIGURE 37.28A IVU—left ureteric calculus with proximal
obstruction Source: (Courtesy Bharat Scans).
FIGURE 37.29 CT—ureteric calculus.
Treatment
• Small stones pass on their own by good hydration
• Stones need to be removed by surgery, when they are large, enlarging,
causing complete obstruction, with infections and in bilateral obstructions
• Ureteroscopy, basketing and lithotripsy are the minimally invasive methods
of removal
37.6 Urinary bladder
Surgical anatomy
In an adult, the urinary bladder when empty lies behind the pubic symphysis. It
lies anterior to seminal vesicles, vas deferens, ureters and rectum in the male and
uterus and vagina in the female. The normal capacity of the urinary bladder is
about 400–500 ml. Majority of the bladder is extraperitoneal although the dome
which expands on filling has a peritoneal covering. The ureters enter the urinary
bladder posteroinferiorly in an oblique manner. The ureteric orifices are situated
at the extremities of the interureteric ridge and are 2.5 cm apart. The triangular
area formed by the interureteric ridge and the bladder neck is known as trigone.
• Arterial supply of the bladder is from the superior and inferior vesical arteries
from the anterior trunk of internal iliac artery, branches of obturator and
inferior gluteal arteries and branches of uterine and vaginal arteries in the
female
• Venous drainage forms as a plexus on the lateral and inferior surfaces of the
bladder, which drains into internal iliac vein
• Lymphatics accompany the veins and drain into lymph nodes along the
internal iliac nodes, obturator and external iliac chains
• Nerve supply: Urinary bladder has a combination of nerve supply.
Parasympathetic innervation is from S2, S3, S4 through the pelvic
splanchnic nerves to inferior hypogastric plexus and from it to the bladder.
Sympathetic innervation is from the eleventh thoracic to second lumbar
segments, via presacral hypogastric nerves and sympathetic chains to inferior
hypogastric plexus. From there, the fibres are distributed to the bladder.
Somatic innervation to the distal sphincter is via pudendal nerves and fibres
that pass through the inferior hypogastric plexus without synapsing to the
distal sphincter
37.7 Diseases of urinary bladder

The diseases of urinary bladder are classified based on their aetiology (Table
37.8)
TABLE 37.8
Aetiological Classification of Diseases of Urinary Bladder
Aetiology Diseases
Congenital Ectopia vesicae
Bladder diverticulum
Urachal abnormalities
Traumatic Bladder injuries
Inflammatory Acute Cystitis
Chronic Interstitial cystitis, tuberculosis
Neoplastic Benign Papilloma, haemangioma
Malignant Carcinoma
Others Calculi
Ectopia vesicae (bladder exstrophy)

• Anomaly occurs due to incomplete closure of the lower abdominal wall in the
midline associated with incomplete development of anterior wall of urinary
bladder
• In males, the penis is epispadiac, with bilateral inguinal herniae, rudimentary
seminal vesicles and prostate, but with normally descended testes
• Umbilicus is absent
• Pelvic bones may stay separated and connected only by a strong ligament
The patient presents with the urinary bladder everted on the anterior abdominal
wall (Ref Fig. 36.8A)
X-ray of pelvis, IVU and CT give the details of the associated congenital
anomalies
Treatment
Treatment is always surgical, aiming to close the bony pelvic ring (by iliac
osteotomy), urinary bladder and posterior urethra and the abdominal defect
Bladder diverticulum
• Projections formed by herniation of mucosa through a defect in the muscular
wall, usually associated with:
• bladder outlet obstruction in adults
• congenital urethral valves in children
• Calculus and tumour formation can occur in the diverticulum
Recurrent attacks of urinary infections
• US (Fig. 37.30A) and CT (Fig. 37.30B) are useful in diagnosis
• Cystography (Fig. 37.31A) and cystoscopy are diagnostic

FIGURE 37.30 (A) US—urinary bladder diverticulum. (B) CT—urinary
bladder diverticulum.
FIGURE 37.31 Cystogram—urinary bladder diverticulum.
Treatment
Symptomatic diverticula need excision
Urachal abnormalities
• During fetal development, the urogenital sinus communicates with the
allantois via the urachus
• This tract closes before birth
• Occasionally, this tract may persist, as a fistula (urachal fistula) between
the urinary bladder and the umbilicus, but remains closed till adulthood
• When the tract closes at the urinary bladder and remains open at the
umbilicus, it is known as urachal sinus
• When both ends of the tract close and a localized collection occurs, it is
known as urachal cyst (Fig. 37.32)
FIGURE 37.32 Urachal abnormalities.
• Patient presents with an opening in the lower anterior abdominal wall close to
the umbilicus or at the umbilicus, discharging urine, or seropurulent material,
recurrently
• Fever may be associated
• Sinogram through the sinus opening
• Cystography and CT with sinogram or fistulogram are useful in diagnosis.
Treatment
• Appropriate antibiotics heal small fistulae
• Excision of sinus or fistula is curative
Bladder injuries
• Urinary bladder is mostly extraperitoneal and is also partially covered by the
parietal peritoneum, and because of this anatomy it can rupture
• extraperitoneally (80%)
• intraperitoneally (20%)
• Common in patients with abdominal trauma, who have a full bladder and are
in a drunken state. The aetiologies of these types vary. They are tabulated in
Table 37.9
TABLE 37.9
Aetiologic Factors of Bladder Injuries
Aetiology (trauma)
Extraperitoneal rupture Intraperitoneal rupture
Fracture pelvis Blunt abdominal trauma with full bladder

Prostatic surgery Penetrating injury
Difficult pelvic surgery Injuries during therapeutic and surgical endoscopy
• Severe lower abdominal pain with anuria
• Passage of bloodstained urine is a common symptom
• Clinical examination reveals a distended abdomen with or without signs of
peritonitis
• Catheterization is easy but no urine is drained, as there is leak
• Extraperitoneal leak is associated with pelvic fracture and causes tender
suprapubic thickening
• Plain X-ray of abdomen will show ground glass appearance of the lower
abdomen
• IVU, retrograde cystography or CT cystography are helpful in identifying the
rupture and leak
Treatment
• Intraperitoneal rupture of bladder requires surgical exploration and repair
• Extraperitoneal rupture is managed by drainage of retropubic space with
suprapubic drainage of bladder
Acute cystitis
• Infection of urinary bladder can occur alone or with infections of urethra, or
with upper urinary tract
• Females are more susceptible due to its proximity to the urethra which is only
about 3–4 cm long, and also from the perineum during sexual intercourse
• Stasis of urine as in incomplete emptying (diverticulum, bladder neck
obstructions) predispose to repeated infections
• The common infecting organism is coliform
• Schistosoma is a parasite, which commonly infects urinary bladder in Middle
East countries
• Typical symptoms are dysuria, frequency, urgency and sensation of
incomplete emptying
• Lower abdominal pain and fever are common
• Microscopic examination of urine for red blood cells, pus cells (WBCs) is
diagnostic, (more than 100,000 organisms per ml of urine is diagnostic)
• Urine is cultured to identify the organism and its antibiotic sensitivity
Treatment
• Appropriate antibiotics
• In recurrent infections (associated with calculi, diverticula), the causative
pathology should be treated surgically for permanent relief
Chronic cystitis
• Repeated episodes of acute cystitis result in chronic cystitis
• Eosinophilic cystitis occurs in immunocompromised patients
• Chronic interstitial cystitis (Fig. 37.33) is uncommon
• Mycobacterium tuberculosis is a common organism to cause chronic
cystitis, and is almost always associated with tuberculosis of rest of the
urinary tract. Small capacity, noncompliant bladder is a sequel (Fig.
37.34A) of treatment for tuberculosis
FIGURE 37.33 Cystoscopy—interstitial cystitis.
FIGURE 37.34A IVU—thimble bladder of GU tuberculosis.
• Continuous and constant abdominal pain, frequency, urgency and dysuria
• Haematuria is not uncommon
• Urinalysis for acid-fast bacilli (three consecutive early morning specimens of
urine) and their growth (culture test) are useful
• Sterile acid pyuria is diagnostic for tuberculosis
• PCR for tuberculosis in urine is contributory
• Cystoscopy shows changes of chronic cystitis, biopsy will show cystitis
follicularis or glandularis (Fig. 37.34B) or both. In tuberculosis, the bladder
mucosa is red (Fig. 37.34C), and rarely tubercles are seen. The ureteric
opening will show a characteristic ‘golf hole’ meatus (Fig. 37.34D)
FIGURE 37.34B Cystitis with bullous oedema—tuberculosis.

FIGURE 37.34C Cystoscopy—tuberculous cystitis with ulceration.
FIGURE 37.34D Golf hole ureteric meatus.
Treatment
• Antitubercular treatment is mandatory for tuberculosis
• All other forms of cystitis require empirical treatment
• Surgical corrections are needed for contracted bladders of interstitial cystitis
• Contracted thimble bladder needs augmentation
Papilloma
• This is a rare entity
• Existence of this entity is disputed (by definition, it has a single layer of cells,
with no cytological features of malignancy with intact basement membrane)
It seldom causes haematuria and is a chance finding during cystoscopy
Cystoscopy is diagnostic (smooth, pale and papillary lesion)
Treatment
Resection is necessary, and it should be regarded with suspicion and requires
follow-up
Haemangioma
This is a rare condition, occurs in varying sizes
Clinical presentation is profuse haemorrhage
Cystosopy is diagnostic (angry-looking collections of veins, confined to one area
of bladder)
Treatment
• Diathermy or laser coagulation is the treatment of choice
• Rarely, partial cystectomy may be required
Carcinoma
• Most tumours are from transitional epithelium, but are prone to undergo
metaplasia to squamous or columnar epithelium, and squamous cell
carcinoma and adenocarcinoma are also seen
• Industrial carcinogens such as naphthylamines and benzidine (rubber,
cable, dye and printing industries)
• Tobacco smoking
• Chronic irritation (infection, calculi, bilharziasis can give rise to
metaplasia)
• Bladder cancer spreads in many ways:
• Direct spread to perivesical fat, prostate, anterior vaginal wall or rectum
• Urine-borne spread to urethra
• Lymphatic spread to internal iliac nodes and para-aortic nodes
• Haematogenous spread to lung and bones
• Painless haematuria is a constant presentation
• Seldom there is any clinical finding
• Urine cytology is useful
• IVU (filling defects and ureteric obstruction) (Fig. 37.35), US (Fig. 37.35A)
and CT (Fig. 37.35B) are diagnostic
• Cystoscopy (Fig. 37.35C) and biopsy are conclusive
• Virtual cystoscopy is a useful investigation when cystoscopy is impossible
• CT is useful in assessing the spread and staging the tumour
FIGURE 37.35 IVU—irregular filling defect in the urinary bladder—tumour.
FIGURE 37.35A US—urinary bladder tumour Source: (Courtesy Dr G.
Ravisankar Pillai).
FIGURE 37.35B CT—urinary bladder tumour.
FIGURE 37.35C Cystoscopy view of bladder tumour.
Treatment
• Resection by transurethral route is done for superficial tumours
• Total cystectomy with urinary diversion is reserved for larger invasive
tumours without lymph node metastases
• Systemic or intravesical chemotherapy is required
• Intravesical immunotherapy (BCG, interferon, interleukin-2) is practiced by
many for superficial tumours
• Radiotherapy is used as postop adjuvant in larger tumours
Palliative
• Local radiotherapy for haematuria, local pain
• Chemotherapy
Bladder calculi
• Usually a manifestation of:
• underlying voiding dysfunction
• foreign body
• lower urinary tract obstruction
• The stones are commonly ammonium urate, uric acid and calcium oxalate
(Fig. 37.36)
FIGURE 37.36 Urinary bladder stones.
• Irritative voiding symptoms
• Intermittent urinary stream
• Urinary tract infections, haematuria and pelvic pain
• Plain X-rays identify radio-opaque stones (Figs. 37.36A and B)
• US identifies radiolucent stones, which characteristically move with the
change in body position, differentiating from bladder tumours
• CT is useful in identifying bladder stones (Fig. 37.36C)
• Cystoscopy (Fig. 37.36D) is diagnostic
FIGURE 37.36A X-ray KUB—vesical calculus.

FIGURE 37.36B X-ray KUB—multiple stones in the urinary bladder.
FIGURE 37.36C CT—urinary bladder stones.
FIGURE 37.36D Cystoscopy view of bladder stones.
Treatment
• Cystolitholapaxy allows most stones to be broken mechanically and removed
through a cystoscope
• Large hard stones are removed by cystolithotomy
37.8 Prostate
Surgical anatomy
In an adult, the prostate is of the size of a chestnut, weighing 10–15 g. The gland
encircles the urethra, which bends slightly as it passes through the gland. Most
of the normal prostate lies behind the urethra. Cranial to the prostate are the
trigone, ureters and base of urinary bladder. The two layers of Denonvillier’s
fascia separate the prostate and seminal vesicles from the rectum behind.
Anteriorly lie the deep veins of penis and symphysis pubis (Fig. 37.37A).
FIGURE 37.37A Anatomic relations of prostate.
The prostate is separated by the entry of ejaculatory ducts into three zones
(McNeal’s zones) (Fig. 37.37B)
• Peripheral zone: This lies posteriorly. This zone contains glands lined by
columnar epithelium and has long and branched ducts that open on either
side of verumontanum. Carcinomas arise from this zone
• Central zone: This zone lies posterior to the urethral lumen and above
ejaculatory ducts
• Periurethral transitional zone: Benign hyperplasia occurs from this zone.
Glands of central zone and transitional zone are shorter and unbranched
FIGURE 37.37B McNeal’s zones of prostate.
All these ducts, the common ejaculatory ducts and the prostatic utricle open
into the prostatic urethra. The process of benign prostatic hypertrophy (BPH)
may compress the outer peripheral zone of the prostate forming the false
capsule.
• Arterial supply to prostate is from both superior vesical branches of the
internal iliac artery
• Venous network is profuse and drains into plexus of Santorini in the pelvis,
which communicates with the obturator and internal iliac veins, as well as
with the bones of pelvis, vertebrae and upper third of each femur, so
providing an easy access for malignancies of prostate to bones and vertebrae
• Nerve supply is both sympathetic and parasympathetic
37.9 Diseases of prostate
The diseases of prostate are classified based on their aetiology (Table 37.10).
TABLE 37.10
Aetiological Classification of Diseases of Prostate
Aetiology Diseases
Inflammatory Acute Acute prostatitis
Chronic Chronic prostatitis, tuberculous prostatitis
Neoplastic Benign Hypertrophy
Malignant Carcinoma
Others Calculi
Acute prostatitis
• Usually caused by infection of urinary tract by Escherichia coli, klebsiella or
pseudomonas
• Dental and upper respiratory infections are known causes of acute prostatitis
• Epididymo-orchitis may follow due to retrograde spread of infection
• Untreated prostatitis may form prostatic abscess, which may rupture into
rectum to form a fistula
• Recurrent acute prostatitis is not uncommon
• Malaise, fever sometimes with rigour and pain in perineum, sometimes with
urinary retention
• Rectal examination will show tender and swollen prostate
Leucocytosis and pyuria may be present
Treatment
• Empirical antibiotics can be curative
• Acute retention of urine due to abscess needs suprapubic cystostomy with
antibiotics
• Abscess requires drainage per urethra to avoid iatrogenic fistula formation
Chronic prostatitis
• Chronic infection of prostate is commonly seen after urethral surgery,
prolonged catheterization
• Tuberculosis of prostate is often associated with tuberculosis of seminal
vesicles, epididymes and vasa
• Symptoms are nonspecific
• Some have relapsing episodes of frequency and dysuria
• Rectal examination reveals a boggy prostate with tenderness
• Tuberculous prostatitis may present as a cold abscess pointing in the perineum
or form a fistula into the rectum
• Calculi may be seen in plain radiographs
• Culture of urethral discharge after prostatic massage may grow the
organisms
Treatment
• Antibiotics which can penetrate the alkaline tissue of prostate (trimethoprim
and tetracyclines) are useful
• Antitubercular treatment is mandatory for tuberculous prostatitis
Benign hypertrophy
• Disease of men above 50 years of age
• Affects mainly the submucous group of glands in the transitional zone.
Involvement of subcervical central zone glands leads to the development of a
middle lobe
• May be caused by increased oestrogenic effect, and also secretion of
intermediate peptide growth factors
• Chronic enlargements may give rise to obstructive features such as bladder
trabeculae and diverticula, hydroureteronephrosis and calculi
Symptoms
• Many of them are asymptomatic
• Some show signs of bladder outlet obstruction
• Acute or chronic retention with overflow and haematuria are common
Signs
• Rectal examination has characteristic features:
• Smooth, convex, elastic and firm feel, the rectal mucosa moves over the
prostate
• Residual urine may be felt as a fluctuating swelling above the prostate
• US (abdominal or transrectal) is diagnostic (Figs. 37.38A and B)
• Uroflowmetry is useful in deciding on treatment (residual urine volume of
more than 150–200ml and flow rate of less than 10ml/s needs treatment)
• IVU and US are useful in assessing the upper urinary tract
• Cystourethroscopy is necessary to assess the prostate (Fig. 37.38C), urethra,
bladder diverticula and vesical calculi
FIGURE 37.38A TRUS—intravesical enlargement of prostate.
FIGURE 37.38B US—benign enlargement of prostate Source: (Courtesy Dr V.
Ganesan).
FIGURE 37.38C Urethroscopy—enlargement of both lobes of prostate.
Treatment
• Transurethral resection of prostate is gold standard
• Open prostatectomy is reserved for very large glands
• Medical management with alpha-blockers such as tamsulosin, alfuzosin and
5 alpha reductase inhibitors are used as preoperative preparation or in
patients who are unfit for surgery
• Decompression of bladder by catheterization or suprapubic cystostomy, is
done for acute retention
Carcinoma
• Most common malignant tumour in Western men over 65 years of age
• It has a variety of presentations—occult to advanced disease
• Prostatic intraepithelial neoplasia
• Primary atypical hyperplasia
• Large acinar dysplasia
• Acinar-ductal dysplasia
• An adenocarcinoma of varying differentiation
• Spread can occur in many ways:
• Local spread—to seminal vesicle, urinary bladder and rectum
• Haematogenous spread—spine and other parts of skeleton
• Lymphatic spread—pelvic nodes (less frequent)
Symptoms
• Many remain asymptomatic
• Advanced disease may present as bladder outlet obstruction (retention), pelvic
pain, haematuria
• Renal failure is a late feature
• Bone pain, malaise, arthritis, anaemia and pancytopenia are other
presentations
Signs
• Rectal examination is characteristic:
• Prostate is irregular, indurated, stony hard (in part or whole of the gland)
with obliteration of medial sulcus
• Nodularity is suggestive
• US (abdominal or transrectal) (Fig. 37.39A) and CT (Fig. 37.39B) are
diagnostic
• Serum PSA levels of more than 10 ng/ml is suggestive, more than 35 ng/ml is
diagnostic
• Prostatic biopsy (transrectal or perineal), with ultrasound guidance is useful in
confirming the diagnosis
• Chest X-ray and skeletal radiographs and isotope bone scan (Fig. 37.39C)
are needed to screen for lung and bone secondaries
• US and CT abdomen identifies liver secondaries
• MRI—investigation of choice for staging
FIGURE 37.39A TRUS—nodule prostate.

FIGURE 37.39B CT—carcinoma prostate with local infiltration.
FIGURE 37.39C Isotope scan showing bone secondaries from carcinoma
prostate.
Treatment
• Open or laparoscopic radical prostatectomy and radiotherapy are done for
localized lesions
Palliative (hormone ablation)
• Antiandrogen drugs (flutamide, bicalutamide or cyproterone acetate)
• Gonadotrophin releasing hormone (GnRH) analogue drugs (goserelin,
leuprorelin)
• Scrotal orchidectomy (for permanent androgen deprivation)
Prostatic calculi
• Prostatic calculi are rare in children, infrequent below age 40, and common in
males over 50
• Prostatic stones represent calcification of corpora amylacea and precipitation
of prostatic secretion
• The causes are:
• Pathologies producing acinar obstruction
• Infection
• They are composed of calcium phosphate
• They may be solitary but usually occur in clusters (Fig. 37.40A)
• Are associated with some other disease process (nodular hyperplasia, prostatic
carcinoma, metabolic abnormalities)
FIGURE 37.40A Prostatic calculi.

• Often asymptomatic
• Rarely, reduction of the urinary stream, prostatism and intense lower back and
perineal pain
Plain X-rays (Fig. 37.40B) demonstrate stones
FIGURE 37.40B X-ray KUB—prostatic calculi.
Treatment
Transurethral resection of prostate
37.10 Urethra
Surgical anatomy
The male urethra is an elastic tube capable of doubling in length during
erection. From bladder neck, it is lined by transitional epithelium up to the bulb,
from where it is squamous for the rest of its length. Paraurethral glands enter the
urethra in its entire length, Cowper’s glands lie within the levators and their
ducts open into the bulbar urethra. Paired glands of Littre open on either side of
the external urethral meatus. The urethra is surrounded by the spongy tissue,
corpus spongiosum, which is continuous with the glans penis.
The female urethra is lined by transitional epithelium above and squamous
epithelium below. The urethra is surrounded by the spongy tissue, which is
continuous with the gland of clitoris. Numerous paraurethral glands open into
the urethra.
37.11 Diseases of urethra
The diseases of urethra are classified based on their aetiology (Table 37.11)
TABLE 37.11
Aetiological Classification of Diseases of Urethra
Aetiology Diseases
Males Females
Congenital Meatal stenosis
Posterior urethral
valves
Hypospadias,
epispadias
Urethral stricture Urethral stenosis
Urethral
duplication
Urethral Urethral diverticulum
diverticulum
Traumatic Urethral injuries Urethral injuries
Inflammatory Acute Acute urethritis Acute urethritis
Chronic Chronic Chronic urethritis
urethritis
Neoplastic Benign Condyloma Urethral caruncle (prolapse of urethral mucosa, venereal warts,
acuminata condyloma acuminata, haemangioneurofibroma)
Malignant Carcinoma Carcinoma
Others Calculi Calculi
Meatal stenosis
Congenital stenosis of external urinary meatus is associated with phimosis
• When reduced to a pinhole (Fig. 37.41), chronic urinary retention and back
pressure changes ensue
• Lesser degrees of stenosis lead to loss of normal urinary stream with spraying
or dribbling
• Acquired: Meatal stenosis as a complication of circumcision (ammoniacal
urethritis)
FIGURE 37.41 Meatal stenosis.
US or IVU will show back pressure changes
Treatment
• Meatotomy is the treatment of choice
• Recurrent stenosis requires meatoplasty
Posterior urethral valves

• These are symmetrical folds of urothelium (usually distal to verumontanum)
causing obstruction to urine flow in male children
• This anomaly can be diagnosed by antenatal ultrasound in the last trimester of
pregnancy
• Since urine is continuously secreted in utero to make amniotic fluid, the child
may develop chronic retention, hydrouretero-nephrosis, and distended
bladder which may prevent normal development of abdominal wall
• Retention of urine is the presentation
• Presenting with uraemia is not uncommon
MCU (Fig. 37.42) can demonstrate the valves
FIGURE 37.42 Micturating cystourethrogram showing the posterior

urethral valve.
Treatment
Transurethral resection of the valves with a paediatric resectoscope after
stabilizing the patient with suprapubic urinary diversion
Hypospadias
Epispadias
Urethral stricture
• Urethral strictures can be due to varied causes (Table 37.12)
TABLE 37.12
Causes of Urethral Stricture
Inflammatory (postgonococcal)
Congenital
Traumatic
Instrumental (indwelling catheter, urethral endoscopy)
Postoperative (open prostatectomy, penile amputation)
(Mentioned in the order of incidence)
Complications: Retention of urine, urethral diverticulum, periurethral abscess,

urethral fistula, and hernia, haemorrhoids and rectal prolapse due to straining to
pass urine
• Strains to pass urine or splitting of urinary stream
• Ascending urethrography (Figs. 37.43 and 37.44) or micturating
urethrography is diagnostic
• Urethroscopy is confirmatory
FIGURE 37.43 Ascending urethrogram—stricture of
urethra Source: (Courtesy Bharat Scans).
FIGURE 37.44 Ascending urethrogram—long stricture of penile and
bulbar urethra.
Treatment
• Dilatation with urethral dilators
• Internal visual urethrotomy using endoscopic urethrotome is useful
• Rigid strictures require urethroplasty (excision and end-to-end
anastomosis/patch urethroplasty)
Urethral duplication
• Usual type of duplication is incomplete—a double-barrelled urethra (second
channel inferior to normal urethra)
• The second channel distends with urine and obstructs the normal urethra—
known as anterior urethral valve
• The child has a poor stream, strains to pass urine, which empties the second
urethra and the child looks incontinent
• Clinical examination reveals a translucent swelling in the midline
• In adulthood, the sac may present with a stone due to repeated infections
Urethrography and US of perineum are diagnostic
Treatment
Division of anterior leaf of the valve by endoscope is curative
Urethral diverticulum
• Usually congenital and represents a partial urethral duplication
• Acquired causes are urethral stricture, longstanding urethral calculus or
foreign bodies
Dysuria, swelling of undersurface of penis (Fig. 37.45A) or penoscrotal area
(Fig. 37.45B)
FIGURE 37.45A Large calculus in a urethral diverticulum Source: (Courtesy Dr
N. Mohan).
FIGURE 37.45B Urethral diverticulum.
Urethrography (Fig. 37.45C) is confirmative
FIGURE 37.45C Ascending urethrography showing a urethral
diverticulum.
Treatment
• Excision of diverticulum
• Where possible, the cause should be removed
Urethral injuries
• Male urethra is more prone to injury, and is commonly caused by
instrumentation
• Pelvic fracture is another cause of urethral injuries
• Treated or untreated, urethral injuries may end in strictures
• Urinary incontinence and impotence are other complications
• Urethral injuries present clinically with blood at urethral meatus, haematuria
and/or anuria
• Physical examination reveals a distended bladder with tenderness on pelvic
bones at the region of fracture, with perineal haematoma
• In rupture of membranous part of urethra, prostate is high riding
Retrograde urethrography (Fig. 37.46) will be informative (catheterization
should be avoided)
FIGURE 37.46 Retrograde urethrography showing leak of contrast
through urethral fistula.
Treatment
• Anterior urethral injuries
• Complete: Primary repair
• Incomplete: Catheterization and allow it to heal spontaneously
• Posterior urethral injuries: Suprapubic drainage and delayed perineal end-to-
end urethroplasty
Acute urethritis
• Acute inflammation of paraurethral glands caused usually by gonococcal
infections, and rarely by chlamydia
• Urethritis can lead to periurethral abscesses, and healing urethritis can lead to
stricture, due to scarring
• White urethral discharge (Fig. 36.32) with severe pain
• History of extra or premarital contact is available
• Isolation of organism in the discharge or urine
• Urethroscopy is diagnostic (Fig. 37.47)
FIGURE 37.47 Urethroscopy—acute urethritis.
Treatment
Appropriate antibiotics
Chronic urethritis
• Usually associated with prolonged catheterization, and associated with
inflammation of urinary bladder
• Tuberculosis is one of the causes
Dull constant ache with urethral discharge
Isolation of organism in the discharge or urine
Treatment
• Appropriate long-term antibiotics
• Tuberculosis requires antitubercular treatment
Urethral caruncle
A condition specific to female urethra, urethral caruncle is a term collectively
applied to a variety of conditions
• Prolapse of urethral mucosa: Analogous to haemorrhoids
• Venereal warts and condyloma acuminata: Caused by papilloma virus
• Haemangioneurofibroma: Rare benign condition
All the above conditions present as a painful bright red cherry-like swelling at
the external meatus
Biopsy is required to distinguish the lesions
Treatment
Excision of lesions with diathermy is curative
Condyloma acuminata
Condyloma acuminata of urethra is caused by a papilloma virus and resembles
those on the penis and vulva
They are polypoid and occur from time to time near the verumontanum and
cause obstruction and present with retention of urine
Urethroscopy is diagnostic
Treatment
• Transurethral coagulation with or without laser is curative in many
• Intraurethral instillation of thiotepa, 5-flurouracil or mitomycin is effective
Urethral carcinoma
• Urethral carcinomas usually are transitional cell carcinomas downstream of a
recurrent bladder tumour
• Squamous cell carcinomas occur upstream of chronic stricture
• Inguinal nodes are involved early
• Systemic spread is rare
• In females, cancer of external meatus spreads to inguinal nodes, and that of
the rest of the urethra to internal iliac nodes
• May present with retention of urine, resembling prostatic enlargement
• When a longstanding stricture presents with a periurethral abscess or a
watering-can perineum, malignancy should be suspected
Urethroscopy (Fig. 37.48) and biopsy is diagnostic
FIGURE 37.48 Urethroscopy—urethral tumour.

Treatment
• Partial or radical resection of urethra with reconstructions where necessary,
combined with radiotherapy and or chemotherapy
• Bilateral inguinal block dissection may be justified in some cases
Urethral calculi
• Common in men, mostly seen in prostatic or bulbous region of urethra
• In females, it is associated with urethral diverticula
• Symptoms similar to bladder calculi, may present with dribbling of urine,
acute retention of urine or severe pain radiating to the tip of the penis
• Palpation may reveal the stone
Plain X-rays (Fig. 37.49) and urethrography are diagnostic
FIGURE 37.49 X-ray—urethral calculi in urethral diverticulum.
Treatment
• Small stones can be extracted in full or in fragments
• Large stones are removed through urethrotomy
37.12 Symptoms of urinary tract pathologies

• Abdominal pain
• Haematuria (passage of blood in urine)
• Dysuria (pain associated with micturition)
• Frequency, urgency and hesitancy (disorders of act of micturition)
• Retention of urine
• Incontinence (loss of control of micturition)
• Dribbling of urine
• Mass per abdomen
• Pain, haematuria and frequency (triad of urinary system diseases)
Abdominal pain
Abdominal pain is not a very reliable symptom of urinary disease. Most urinary
tract lesions cause symptoms referable to the urinary tract. When associated with
abdominal pain, it is useful in diagnosis (Table 37.13). Urinary disorders can
also present as abdominal pain without urinary symptoms
TABLE 37.13
Urological Causes of Abdominal Pain
Diseases
Symptom
Kidneys Ureters Bladder Prostate
Abdominal pain Calculi Malignancy Polycystic kidney Pyelonephritis Calculi Cystitis, calculi Obstructive uropathy
Renal pain
Caused by distension of renal capsule and pelvis or stretch of the peritoneum by
large renal swellings.
• Nature of pain
• Pain localized to renal angle (posterior space between the twelfth rib and
the sacrospinalis muscle) (Fig. 37.50A) (e.g. acute pyelonephritis, renal
tuberculosis)—described by putting the hand on the waist with his fingers
on the renal angle and thumb pointing the umbilicus (Fig. 37.50B)
• Pain radiating to umbilicus (e.g. renal tuberculosis)
• Intensity of pain
• Severe (e.g. acute pyelonephritis)
• Dull and persistent (e.g. renal stones, polycystic disease and malignancy)
• Acute obstruction of the upper ureter can give a severe colicky pain in the
loin known as ‘renal colic’
FIGURE 37.50A Renal angle.

FIGURE 37.50B Expression of left renal pain.
Ureteric pain
Caused by obstruction of the ureter commonly by a stone or a clot, and may
correspond to the level of obstruction
• Nature of pain
• When the stone is lodged in the upper ureter, the pain radiates to the
testicle (T11-12)
• When the stone is lodged in the mid ureter, the pain may be in the
McBurney’s point on the right side and simulate diverticulitis on the left
side (T12-L1)
• When the stone is lodged in the distal ureter, the pain resembles vesicular
pain or may radiate to the genitalia or inner side of thigh (L1-L2)
• Dull pain in the side of abdomen (e.g. chronic obstruction of ureter with
calculi)
• Severe colicky pain—(loin pain radiating to the groin, genitalia or inner
thigh—genitofemoral nerve) in acute obstructions of ureter known as
‘ureteric colic’ (Fig. 37.51)
FIGURE 37.51 Ureteric colic (A) base of penis (B) genitalia (C) medial
side of thigh.
Urinary bladder pain

Pain is usually caused by distension or mucosal irritation
• Nature of pain
• Localized to the suprapubic area (e.g. cystitis)
• Referred to penis or vulva if the bladder trigone is involved
• May vary from mild discomfort to intense pain (e.g. cystitis)
• Severe pain: Painful desire to micturate combined with inability to
completely empty the bladder is known as ‘strangury’ (described as
stinging pain in the tip of the penis indicated by screaming and pulling of
prepuce, especially in children)
Prostatic pain
Prostatic pain is caused by inflammations
• Nature of pain
• Felt more as a vague discomfort or fullness in the perineal or rectal area
(S2-4) (e.g. prostatitis)
• Throbbing pain (e.g. prostatic abscess)
• Pain at the end of micturition (e.g. acute prostatitis)
Urethral pain
Urethral pain occurs usually during micturition
• Nature of pain
• Pain usually localized to the area of the urethra but associated with act of
micturition
• Scalding pain (e.g. acute urethritis, meatal ulcer)
• Colicky pain (e.g. obstruction by urethral calculus)
• Urethral pain is associated with dysuria and usually referred to the tip of
the penis in males
Note
Many urologic diseases (e.g. cancer, chronic pyelonephritis, tuberculosis,
polycystic kidney, hydronephrosis) do not cause pain because of the slow
progress, and there is no sudden capsular distension.
Haematuria (passage of blood in urine)

Passing of blood in the urine is known as haematuria
• Frank haematuria: Presence of frank blood or blood clots in the urine
• Microscopic haematuria: Presence of blood discovered by microscopy or
dipstick
• Whatever the cause, haematuria is usually episodic
• Haematuria (painless) (e.g. tumours of urological system)
• Haematuria with dysuria (e.g. urological infections)
• The causes of haematuria are given in Table 37.14
TABLE 37.14
Causes of Haematuria
Diseases
Aetiology
Kidneys Ureters Bladder Prostate Urethra
Congenital Polycystic kidney AV

malformation
Traumatic Trauma Trauma Trauma
Inflammatory Glomerulonephritis Cystitis Prostatitis Acute
Tuberculosis Schistosomiasis urethritis
Neoplastic Malignancy Urothelial Malignancy Malignancy Malignancy
tumours
Others Calculi Calculi Calculi Benign Calculi
enlargement
Nonurological Coagulation and haematological disorders
Note
Microscopic hematuria may represent a significant lesion in the urinary tract
and should be taken seriously, though in about 5% of cases, no cause can be
found.
Dysuria (pain associated with micturition)

Dysuria is the pain or discomfort associated with micturition, which is described
as ‘scalding’ or ‘burning’, the common causes being infections and
inflammations.
Frequency, urgency and hesitancy (disorders of

micturition)
Frequency—defined as passage of small quantities of urine at frequent intervals
but the total daily output is normal
• The causes of frequency are:
• Irritation of urinary bladder—infections
• Incomplete emptying of urinary bladder—prostatic enlargement,
neurogenic bladder
• Unstable bladder—detrusor instability—bladder outflow obstruction
• Small bladder—postsurgery, tuberculosis, schistosomiasis,
postradiotherapy
Urgency—defined as a sudden desire to micturate
• Bladder neck irritation as in cystitis and prostatic enlargement
Hesitancy—defined as difficulty in initiating the act of micturition
• The common cause is:
• Prostatic enlargement
Retention of urine
Defined as the inability to micturate even when the bladder is full
• This occurs when the sphincter is unable to relax or with proximal urethral
obstruction like in prostatic enlargement
• Retention can be of two types:
• Acute retention is of short duration and the bladder distension is painful
• In chronic retention, micturition is incomplete and a residue of urine stays
back in the bladder (residual urine). When the residual urine reaches the
bladder capacity, micturition occurs only by overflow, and bladder tends to
be distended abnormally without pain. Chronic retention can give rise to
dilatation of urinary tract with uremia and creatininaemia
• At any stage, acute-on-chronic obstruction can occur
The causes of acute retention of urine are given in Table 37.15.
TABLE 37.15
Causes of Acute Retention of Urine
Males Females Both Sexes
Prostatic enlargement Multiple sclerosis Clot retention

Urethral stricture Urethral stenosis Urethral calculus
Phimosis/meatal Retroverted gravid Rupture of urethra
stenosis uterus
Acute urethritis Cervical fibroid Spinal anaesthesia
Postoperative Neurogenic
Faecal impaction
Anal pain (posthaemorrhoidectomy)
Drugs (antihistamines, antihypertensives, anticholinergics,
antidepressants)
Urinary incontinence (loss of control of micturition)

Urinary incontinence—defined as involuntary passage of urine
• It may occur with a variety of structural and functional abnormalities of the
bladder or sphincter mechanisms
• Nocturnal incontinence is known as enuresis
• The causes of incontinence may be classified as urological and nonurological
(Tables 37.16 and 37.17)
TABLE 37.16
Urological Causes of Urinary Incontinence
Males Females Both Sexes
Chronic retention with Stress incontinence Fistulae

overflow
Prostatic enlargement Small bladder (interstitial cystitis) Idiopathic detrusor overactivity
Urethral stricture Ectopic ureter in females (opening in Old age
vagina)
Bladder neck obstruction Congenital (ectopia vesicae, severe
epispadias)
Postprostatectomy Trauma
Small bladders (tuberculosis)
Infections
Tumours with fistula formation
TABLE 37.17
Nonurological Causes of Urinary Incontinence
Cause Condition
Neurological Myelodysplasia
Multiple sclerosis
Spinal cord injuries
Cerebral dysfunction (CVA, dementia)
Parkinson’s disease
Radiotherapy Radiation cystitis
Drugs Phenothiazines
Dribbling of urine
Dribbling of urine—defined as leakage of urine without any effort
This usually happens in vaginal fistulae (vesicovaginal or ureterovaginal
fistulae), which occur with untreated obstructed labour, gynaecologic surgery,
infiltration by pelvic neoplasms and radiotherapy. It occurs also in congenital
ectopic ureteric opening into vagina.
Mass per abdomen

Main causes of enlargement of kidney are hydronephrosis, polycystic disease,
renal cell carcinoma in adults and Wilms’ tumour in children. Tenderness is not
common in noninfective conditions.
Eliciting history
• Age: Certain diseases affecting urological system are common in certain age
groups.
• Newborns and infants—phimosis, hypospadias, epispadias
• 1 to 5 years—Wilms’ tumour
• 2 and 7 years—posterior urethral valves
• 10 to 15 years—acute pyelonephritis
• Newly married and youth—paraphimosis, sexually transmitted diseases
• Young adults and middle aged—carbuncle of kidney, calculous disease
• Elderly—benign enlargement of prostate, prostatic malignancy
• Sex: Acute pyelonephritis and cystitis are common in females due to short
urethra and adenocarcinoma of kidneys has male preponderance
• Occupation: Carcinoma urinary bladder is common in industrial (printing
industry) workers
• Residence: Vesical calculus is common in Rajasthan and Punjab in India and
schistosomiasis is common in Africa, Iran, etc.

Since most urological illnesses present with symptoms related to the system, the
questions relating to other symptoms of the urinary tract illnesses
Abdominal pain
The site indicates the underlying cause, as it indicates the organ of pathology.
Patients must be asked to indicate the site of pain in the abdomen with their
own finger (e.g. renal pain in the loin and ureteric pain in the lower
abdomen)
Pain of hydronephrosis may be more before micturition in the morning and
be relieved once micturition starts
• Period of pain: How long has the pain been present? Duration of pain
indicates the disease process (e.g. short history in infections, and long history
may be in calculous disease)
• Mode of onset/description of pain: Can you describe the pain?
Abdominal pain has a variety of presentations (e.g. acute pain in acute
pyelonephritis, chronic pain in malignancies. Renal and ureteric colics are
common)
• Change in character of pain: Has the pain changed in its character since
its onset?
A change in character of pain has its own significance (e.g. colicky pain
changes into constant or lessening of pain may be seen calculous
hydronephrosis)
from the point where it started?
Pain may shift from its place of origin (e.g. ureteric colic to dull renal pain in
calculous hydronephrosis) or even migrate to another region of the abdomen
(e.g. ureteric calculus migrating to the urinary bladder) and may present at a
distant place (e.g. referred pains)
Haematuria
• Passage of blood in urine: What is the nature of bleed? Is it frank blood,
bloodstained or clots?
Bleeding from the urinary tract is usually episodic. The bleeding could be as:
• Frank blood replacing the urine (e.g. bladder tumours)
• Bloodstained (e.g. infections, tumours)
• Clots (e.g. renal malignancy as the bleeding becomes evident after a
longtime)
• Relationship of bleeding with pain: Is haematuria associated with pain? If
so, describe the nature of pain?
Haematuria associated with abdominal pain is common. They can be of
different types.
• Dull constant loin pain (e.g. hypernephroma, polycystic disease)
• Colicky pain.renal colic (e.g. renal calculi), ureteric colic (e.g. ureteric
calculi).
• Lower abdominal pain (e.g. cystitis)
• Pain in the perineum (e.g. prostatic pathology)
• Pain in the genitalia (e.g. urethral pathology)
• Pain associated with micturition is dysuria, commonly seen in infections
Disorders of act of micturition

• Frequency in micturition: Does the patient pass urine frequently, and how
many times does the patient wake up to pass urine in the night?
Passing urine at frequent intervals is seen with infections of urinary tract,
prostatic enlargement
• Urgency in micturition: Does the patient have to rush to the toilet to pass
urine?
Urgency is seen in patients with bladder neck irritation (e.g. cystitis and
prostatic enlargement)
• Hesitancy: Is there a delay in initiating the act of micturition?
Hesitancy is seen in patients with prostatic enlargement
Disorders of urine flow

• Thickness of urinary stream: Is the urine flow of the same thickness as
before or has it thinned out? Does the urine fall away as before?
The urinary stream will become thin and tend to have less projectile force
and tend to fall close to the person. It may also tend to stop and start
repeatedly (e.g. prostatic enlargement)
• Retention of urine: Was or is there inability to pass urine?
Inability to pass urine can be of short duration (acute retention), but is always
associated with pain. Patients with chronic retention do not feel any
discomfort (e.g. prostatic enlargement)
• Dribbling of urine: Does the patient complaint of dribbling of urine? Is it
associated with acts such as cough or any physical strain?
Constant dribbling of urine especially in women may be due to vesicovaginal
fistulae or disorders of sphincters (bladder is empty). Physical acts such as
coughing and sneezing can give rise to incontinence (stress incontinence) in
cystocoele in women. Distended bladders can give rise to overflow
incontinence. Nocturnal incontinence is such as enuresis

Association of high-grade fever with rigour may indicate an infective
pathology (e.g. urinary infections) and low grade (e.g. hypernephroma)
and malignancies
give a clearer picture of diagnosis (e.g. recurrences of fistulae, tuberculosis,
malignancy, stricture urethra)
treatment?
such as recurrence of tuberculosis and malignancies, strictures or stone
disease
• Personal history: Does the patient smoke tobacco and for how long?
Chronic tobacco smoking is associated with malignancies of urinary bladder
Diseases such as polycystic kidneys, posterior urethral valves occur in
families and the positive history may be a good indicator for the present
diagnosis
match the situation, such as extramarital contact if the symptom is suspected
to be of syphilitic/gonococcal aetiology. History relating to trauma (part of
fight or shooting incident) should also be elicited
General
• Sunken eyes indicate dehydration and undernutrition, seen in uraemia
• Jaundice may be an indicator of metastatic liver disease
• Pallor a feature of hypernephroma or any chronic bleeding in the urinary
tract
• Scratch marks may indicate uraemia
• Generalized oedema (anasarca) may be seen in patients with renal failure
• Recording of pulse and blood pressure Hypertension (e.g. pyelonephritis,
glomerulonephritis, renal artery stenosis, polycystic kidneys or
hypernephroma)
• Recording of temperature Elevated temperature (e.g. infective pathologies
and malignancies)
Abdomen
Inspection
The patient should be inspected in three positions:
• Supine (from the front)
• Left lateral
• Sitting (from behind)
What to observe?
• From the front:
• Abdomen
- Distension of abdomen: In chronic distension of bladder, there will be
localized distension at the suprapubic area (Ref Figs. 30.43B and C)
- Symmetry: Abdomen is asymmetrically enlarged and seen as fullness
due to renal masses as in polycystic kidneys in an adult or
nephroblastoma in a child
• External genitalia: All parts of external genitalia should be inspected (e.g.
phimosis, meatal stenosis, tumours of penis or vulva, fistulous openings)
• From behind:
• Examination of loins: Subtle fullness may be visible in renal masses such
as hypernephroma or perinephric abscess (Fig. 37.52), bruises in case of
trauma
FIGURE 37.52 Fullness of left loin due to renal mass.
Palpation
I. Kidneys
(a) Supine position on a hard bed
• Left kidney: The right hand is placed anteriorly on the left lumbar region
and the left hand posteriorly in the left loin (Fig. 37.53). The patient is
asked to take deep breaths and both the hands are brought together
(bimanual palpation) attempting to palpate the left kidney
• Right kidney: The right kidney is felt the same way for the left. The
examiner should place the right hand horizontally in the right lumbar
region anteriorly and the left hand posteriorly (Fig. 37.54). The patient is
asked to take deep breaths and both the hands are brought together
(bimanual palpation) attempting to palpate the right kidney
Note
When the kidney is palpable, it is felt as a smooth rounded firm swelling. If it
can be moved anteroposteriorly and vice versa, it is known as ‘ballottement’.
FIGURE 37.53 Method of palpation of left kidney.

FIGURE 37.54 Method of palpation of right kidney.
What to palpate:
• Size of the kidney swelling: Large enlargements are seen in polycystic
disease, hypernephroma in adults and Wilms’ tumour in children
• Shape of the kidney swelling: Irregular enlargement is seen in polycystic
disease and hypernephroma, and smooth enlargement is seen in
hydronephrosis
• Surface of the kidney swelling: Irregular surface is seen in polycystic
disease and hypernephroma, and smooth surface is seen in hydronephrosis
• Mobility with respiration: Renal mass will usually move with respiration
due to its proximity to the diaphragm
• Tenderness: Infective pathologies and acute obstructions may show
tenderness of varying intensities
(b) Examiner standing behind the seated patient
(c) Patient lying on one side allowing the upper most part of the kidney to
drop down
Murphy’s kidney punch test: Jabbing the kidney area under the ribs will
elicit tenderness in infective pathology (Fig. 37.55)
FIGURE 37.55 Murphy’s kidney punch test.
Note
Normal kidneys are not palpable except in very thin individuals, more so in
men due to increased abdominal tone and more fixed kidney. Enlarged kidney
is characteristically mobile, smooth, moves with respiration, palpable
bimanually and can get above (differentiates from enlarged spleen).
II. Urinary bladder

Normal urinary bladder is not palpable. When it is full, it is felt as a smooth
oval-shaped swelling in the suprapubic region (Fig. 37.56), and the dome may
reach the level of the umbilicus. It is not possible to feel its lower border (cannot
get below the swelling). Application of pressure over the swelling gives the
patient a desire to void. In women, this needs to be differentiated from the
ovarian or uterine swellings such as the fibroid, ovarian cyst and in men colonic
tumours, large bladder tumours
FIGURE 37.56 Palpation of urinary bladder.
Note
A suprapubic mass in the male is usually due to distended bladder whereas in
a female, ovarian masses and fibroids are more common than the distended
bladder.
III. External genitalia and urethra

The external genitalia should be palpated in detail. The prepuce should be
retracted well (Fig. 37.57) and the urethra should be palpated from behind to the
tip (Fig. 37.58), for any irregularities (e.g. urethral calculi) and tenderness (e.g.
urethritis) and discharges on milking the urethra (e.g. gonorrhoea). Cord
structures, epididymes and the testes should also be palpated for enlargement
(e.g. testicular tumours, epididymo-orchitis) and tenderness (e.g. orchitis). If
there is associated scrotal swelling, it should be evaluated (Ch. 36)
FIGURE 37.57 Retraction of prepuce.
FIGURE 37.58 Palpation of urethra.
Tansillumination: Distended bladder or a cystic mass will transilluminate,

especially in children
Percussion
1. Over the renal areas: Overlying area of resonance is present as the bowel
lies over this retroperitoneal structure
2. Over the suprapubic area: The percussion is done downwards starting from
above the umbilicus downwards (Fig. 37.59), and the distended bladder is
dull to percussion
FIGURE 37.59 Percussing for the distended bladder.
Note
For the urinary bladder to be percussible, it should contain at least 150 ml of
urine in it. It needs to be differentiated from pregnant uterus, fibroid uterus,
ovarian cyst in women. When in doubt, examination should be repeated after
emptying the bladder by catheterization.
Auscultation
Bruit over the lumbar area is of value when auscultated along the twelfth rib
posteriorly, which may indicate renal artery stenosis or even very vascular
tumours
IV. Prostate
Prostate is felt through the rectum. This can be done in any of the following four
positions (Ref Figs. 34.19A–D):
• Left lateral (Sims’) position
• Dorsal position
• Knee elbow position
• Lithotomy position
Rectal examination related to urological illness

It includes:
• Palpation or digital examination of prostate
• Palpation of rectal mucosa
Palpation or digital examination

Examination procedure (Ref Figs. 34.23A–C)
• The best position to do the digital examination of the anus and rectum is the
left lateral position
• Patients should be explained about the procedure and the sensation they may
have during the procedure
• The gloved and generously lubricated pulp of the index finger should be kept
flat on the anal verge and slowly introduced into the anal canal with the pulp
facing posteriorly
• The pulp of the finger should be rotated circumferentially on all sides (360
degrees)
What to palpate?
• Size of the prostate: Normal prostate is about 3cm in diameter and weighs
about 10–15 g. It is said to be moderately enlarged when it weighs about 30–
40 g, and greatly enlarged when it weighs more than 100 g (e.g. prostatic
hypertrophy)
• Surface: Normal prostate is smooth surfaced and divided into two halves by a
groove in the midline. In benign hypertrophy, the surface is smooth and the
midline groove is maintained. In malignant prostate, the surface is irregular
and asymmetrical and hard nodules may be felt
• Consistency: Normal prostate has rubbery firm consistency. Benign
enlargements do not alter the consistency, whereas malignancy makes the
prostate hard
• Tenderness: Application of pressure on the prostate determines the presence
of tenderness. Tenderness is seen in prostatitis and prostatic abscess
• Rectal mucosa: Rectal mucosa is normal in benign hypertrophy and can be
moved over the prostate gland. It becomes adherent or may even be breached
in advanced malignancy of prostate
Note
Rectal examination may be performed last for not inconveniencing the patient
by frequent change in positions.
Remember
After the completion of the rectal examination, it should be remembered to
wipe the anal orifice with a gauze, so that the patient does not experience any
discomfort of the stickiness of the lubricant or the secretions.
Lymphatic system
Of drainage area
urological system, i.e. para-aortic and inguinal lymph nodes, which will give
useful information (e.g. renal malignancies to para-aortic nodes and
malignancies of genitalia to inguinal nodes)

(e.g. tuberculosis and lymphoma). Examination of the liver and spleen completes
the lymphoreticular system, which is useful in diagnosis
CHAPTER 38
Female genital system

Chitra Subramanian, Lakshmi, Nagarajan
CHAPTER OUTLINE
38.1. Development of female genital tract 690
38.2. Surgical anatomy of female genital tract 690
38.3. Physiology response of female genital tract 692
38.4. Diseases of female genital tract 692
• Mullerian duct anomalies 692
• Genetic disorders 693
• Androgen insensitivity 693
• Coital injuries 693
• Injuries during childbirth 694
• Foreign bodies in the genital tract 694
• Tuberculosis of genital tract 694
• Pelvic inflammatory disease 694
• Sexually transmitted diseases 695
• Miscellaneous infections 696
• Uterine myomas 696
• Benign ovarian tumours 697
• Polyps of uterine cervix and endometrium 697
• Dysplasia of uterine cervix 697
• Carcinoma of uterine cervix 698
• Carcinoma of endometrium 699
• Carcinoma of vulva 699
• Carcinoma of ovaries 700
• Uterine prolapse 701
• Endometriosis 701
• Dysfunctional uterine bleeding 702
• Ectopic pregnancy 702
• Polycystic ovarian disease 703
• Asherman’s syndrome 703
38.5. Symptoms of diseases of female genital tract 703
• General 707
• Breasts 707
• Thyroid 707
• Abdomen 707
• Pelvis 707
38.1 Development of female genital tract

The external genitalia in females develop from the tubercle that is derived from
the mesoderm.
• The urogenital sinus gives rise to the labia minora and vestibule.
• The sino-vaginal bulbs of urogenital sinus give rise to lower one-fourth of
vagina.
• The Mullerian ducts are derived from the mesothelium of the coelomic cavity
on either side. They fuse in the midline to form the uterus, cervix and upper
three fourths of vagina.
• The unfused portion gives rise to fallopian tubes.
• Ovary develops from the genital ridge and contains primordial germ cells,
which develop into ova.

FIGURE 38.27 (A) Sim’s speculum. (B) Cusco’s speculum.
38.2 Surgical anatomy of female genital tract

The vulva comprises of the external genitalia and perineum.
• External genitalia comprise the external fold of labia majora that enclose the
two inner folds of labia minora. Anteriorly they join to form the prepuce
enclosing the clitoris and posteriorly the fourchette. The cleft between the
two is divided anteriorly into the vestibule and posteriorly the introitus. The
Bartholin’s gland is placed at the lower third of the minora. The vagina is a
hollow flask shaped organ that is longer posteriorly and lined by stratified
squamous epithelium. The upper part is divided into four fornices (anterior,
posterior and two lateral) by the cervix and the posterior is the deepest (Fig.
38.1)
• Uterus is a pyriform-shaped muscular organ, containing
• outer perimetrium,
• middle and thickest, myometrium and
• inner functional endometrium.
• The cervix is the lower part of the uterus and the demarcation between the
two is called the isthmus.
- Cervix is further divided into the endocervical canal lined by columnar
epithelium and outer ectocervix lined by squamous epithelium. The
demarcation between the two is called the ‘transformation zone’.
• In most women, the cervix points downwards or posteriorly (anteverted)
and the uterus flexed anteriorly over the cervix (anteflexed). Occasionally,
the cervix points upwards or anteriorly (retroverted) and the uterus is bent
backwards (retroflexed). However, the term ‘anteverted’ is used to denote
both anteversion and anteflexion (Fig. 38.2A and B).
• Upper part of the uterus has two ostia that open out into fallopian tubes.
Each tube is divided from medial to lateral into four parts. They are as
follows:
- Interstitial
- Isthmus
- Ampulla
- Fimbria
FIGURE 38.1 Anatomy of female external genitalia.
FIGURE 38.2A CS of female genital organs.
FIGURE 38.2B LS of female genital organs.
The longest part of the fimbria, called ovarian fimbriae, is in contact with the
ovary. The ovary is placed in the fossa between the bifurcation of common iliac
artery and the ureter. The ovary has an outer cortex and inner medulla.
The pelvic support is from the pelvic musculature and the tri-radiate ligament.
The pelvic musculature consists of the pelvic diaphragm made up of two
levator ani muscles and the urogenital diaphragm and superficial muscles of
pelvic diaphragm.
38.3 Physiological response of female genital

tract
An intact hypothalamo–pituitary–ovarian axis is essential for a normal menstrual
cycle. The cycle has three phases.
Menstrual phase is the first phase and lasts about four days and the first day
of the menses is taken as day 1 of the cycle.
Proliferative or follicular phase, follows the menstrual phase, which is
characterized by a gradual rise in levels of follicle stimulating hormone (FSH)
followed by oestrogen. Subsequently, there is a sudden rise in the levels of
luteinising hormone (LH) called ‘ LH surge’.
Luteal or secretory phase heralded by ovulation occurs 12–24 hours after the
LH surge, and is marked by increase in the levels of progesterone secretions by
corpus luteum.
In the absence of fertilization, exactly fourteen days after ovulation, there is
withdrawal of progesterone, which results in menses and a menstrual cycle (Fig.
38.3).
FIGURE 38.3 Physiology of menstruation.
38.4 Diseases of female genital tract

The diseases of female genital tract can be classified based on its aetiology (see
Table 38.1).
TABLE 38.1
Classification of Diseases of Female Genital Tract
Aetiology Diseases
Congenital Mullerian duct anomalies Genetic disorders Androgen insensitivity
Traumatic Coital injuries Injuries during childbirth Foreign bodies in the genital tract
Inflammatory Infectious diseases Pelvic inflammatory disease Sexually transmitted diseases
Benign Uterine myomas Dermoid cysts Mucinous cystadenoma Polyps of uterine cervix and endometrium
neoplastic
Malignant Dysplasia of uterine cervix Carcinoma of uterine cervix Carcinoma of endometrium Carcinoma of
neoplastic vulva Carcinoma of ovaries
Miscellaneous Uterine prolapse Endometriosis Dysfunctional uterine bleeding Ectopic pregnancy Polycystic ovarian
disease Asherman syndrome
Mullerian duct anomalies

These anomalies occur due to incomplete or defective fusion of Mullerian ducts
or failure of canalization (Fig. 38.4A).
FIGURE 38.4A Mullerian duct anomalies.
Most patients remain asymptomatic till puberty, and present with primary
amenorrhoea or infertility.
• US or CT is useful.
• Hysterosalpingography (Fig. 38.4B) is useful in diagnosing most lesions.

FIGURE 38.4B Hysterosalpingogram—bicornuate uterus.
Treatment
• Plastic reconstructive procedures are required.
• Excepting for imperforate hymen, other disorders require extensive plastic
reconstructive procedures, though results are not promising.
Genetic disorders
This variety of disorders occur due to chromosomal abnormalities, e.g., Turner
syndrome, Kallman syndrome.
Most common presentation is primary amenorrhoea.
Karyotyping can identify the genetic abnormalities.
Treatment
Cyclical hormonal therapy is useful, provided Mullerian structures are normal.
Androgen insensitivity
Patients are genetically male with normal testosterone levels. However, the
hormone is not able to act due to receptor defects.
• Presents with female phenotype with normal secondary sexual characters but
absent Mullerian structures.
• The most common presentation is primary amenorrhoea.
Normal circulating testosterone level and karyotyping will show male genotype
46XY.
Treatment
• Administration of female sex hormones to maintain the secondary sexual
characters.
• Gonads should be removed at puberty to prevent malignant transformation.
Coital injuries
Injuries commonly occur during forced intercourse and sometimes at the time of
first intercourse.
• Vulval or vaginal bleeding.
• Local examination reveals irregular abrasions in the vulva or vagina.
Local examination is conclusive and no specific investigation is necessary.
Treatment
• Application of pressure with gauze pack is effective in controlling most
bleeds.
• Suturing is done for larger bleeds.
• Uncontrolled bleeding should prompt a search for coagulation disorders.
Injuries during childbirth

Injuries of the genital tract occur during childbirth, especially due to
• delivery of large babies or
• deliveries conducted with the aid of instruments.
• Bleeding from the wound.
• Local examination reveals a laceration.
Treatment
Primary repair of the tear with correct approximation of layers is mandatory as
healing by secondary intention weakens the area resulting in anal or urinary
incontinence or uterine prolapse.
Foreign bodies in the genital tract

Foreign bodies may be inserted in the genital tract
• accidentally by children or
• sometimes by adults to induce abortion or as a part of perverted sexual act.
• Bleeding or discharge per vagina.
• Local examination will reveal the foreign body in the vagina.
X-ray or US may be required to diagnose, foreign bodies inserted in the uterine
cavity as a part of abortive procedure.
Treatment
• Removal of the foreign body is mandatory.
• Antibiotics and local treatment are required if there is associated infection.
Tuberculosis of genital tract

• Female genital tuberculosis affects all parts of genital tract.
• Silent tuberculous infection is still common in developing countries.
• Ectopic pregnancy is common with tubal tuberculosis.
• Menstrual disturbances and infertility.
• Constitutional symptoms accompany the active stages of infections.
• Biopsy of accessible lesions is conclusive.
• Curettage and biopsy is useful in endometrial lesions.
• Diagnostic laparoscopy is useful in identifying adhesions.
Treatment
Appropriate anti tubercular treatment is necessary, which is curative.
Pelvic inflammatory disease
• Collective term for a group of genital infections that includes cervicitis,
endometritis, salpingitis and tubo-ovarian abscess (Fig. 38.5).
• Most common organisms are Neisseria gonorrhoeae, Chlamydia trachomatis.
FIGURE 38.5 Right tuboovarian mass.
• Triad of symptoms
• lower abdominal pain;
• adnexal tenderness and
• cervical motion tenderness.
• Other symptoms are fever and cervical discharge.
• Smear taken from discharge may identify the organism.
• US and CT are diagnostic in identifying masses and abscesses (Fig. 38.6A
and B).
• Diagnostic laparoscopy is useful (Fig. 38.6C).
• Culture and sensitivity of discharge.
FIGURE 38.6A US—tuboovarian mass.

FIGURE 38.6B CT—right tuboovarian mass.
FIGURE 38.6C Laparoscopy—pyosalpinx.
Treatment
Medical treatment
• Regimen A: antibiotics: Cefoxitin (1 g) with Probenecid and Doxycycline
(200 mg per day) with or without Metronidazole or for a period of 2 weeks
on out-patient basis.
• Regimen B: Patients not responding to treatment can be treated as inpatient,
with injectable Cefoxitin (2 Gm i.v. 6 hrly) and oral Doxycycline (1.5 mg/kg
12 hrly) or Clindamycin (900 mg i.v. 8 hrly) with Gentamycin (2 mg/kg stat
followed by 1.5 mg/kg 8 hrly).
• Once constitutional symptoms abate, oral Doxycyline–Metronidazole
combination should continue for 2 weeks.
Sexually transmitted diseases

• These diseases are transmitted by sexual contact.
• The incriminating organisms are:
• Neisseria gonorrhoeae (gonorrhoea)
• Treponema pallidum (syphilis)
• Haemophilus ducreyi (Chancroid)
• Trichomonas vaginalis
• Herpes simplex
• Human papilloma virus
• Chlamydia trachomatis (Lymphogranuloma venereum)
• Klebsiella granulomatis
• Mixed infections are common.
• Purulent or white-coloured foul smelling discharge per vagina (Fig. 38.7A).
• The chancre is characteristic of primary syphilis (Fig. 38.7B), anywhere on
the lower genital tract, which heals spontaneously.
• Secondary and tertiary stages may follow.
• Other lesions have their own characteristic features (Fig. 38.7C) (see also Ch.
36).
FIGURE 38.7A White mucopurulent discharge.
FIGURE 38.7B Vulval chancre.
FIGURE 38.7C Chancroid of vulva.
• Identification of the incriminating organism.
• Screening for HIV is to be considered.
Treatment
Treatment is directed with appropriate specific antibiotics.
Miscellaneous infections
Variety of infections affect the genital tract, like
• bacterial vaginosis (Gardenerella vaginalis) and
• candida vaginitis (Candida albicans—most common).
• Colourless vaginal discharge with fishy odour.
• Candida causes a curdy white discharge (Fig. 38.8) associated with pruritus.
FIGURE 38.8 Vaginal candidiasis.
• Smear examination of the discharges will usually identify the organism in
candida vaginitis.
• The pH is usually alkaline (>5) and the KOH test (Whiff test) will be positive
in Bacterial vaginosis, but negative in Candidiasis.
Treatment
• Oral and local metronidazole are effective in Bacterial vaginosis.
• Locally applied antifungals (Clotrimazole, Miconazole) or oral single dose of
150 mg of Fluconazole.
• Recurrent infections need careful assessment and drugs in higher doses and
change of line of management.
Uterine myomas
• Benign tumours of the uterine wall.
• Arise from the smooth muscle (also called ‘fibroid’) (Figs 38.9A and B).
• Commonest tumour to affect female genital tract.
• Precise aetiology is unknown.

FIGURE 38.9 (A) Single fibroid. (B) Multiple fibroids (P indicates a
pedunculated fibroid).
• Many patients remain asymptomatic.
• Menstrual disturbances and dysmenorrhea.
• Large tumours may present with infertility or obstruct the urinary or
gastrointestinal tracts.
On clinical examination,
• irregularly enlarged palpable uterus per abdomen, which can be confirmed by
vaginal examination.
• US is diagnostic.
• CT is rarely necessary (Fig. 38.10).
FIGURE 38.10 CT—uterine fibroid.
Treatment
Treatment depends on three factors:
• Follow up without any treatment is suggested for asymptomatic patients with
small fibroids.
• Myomectomy/Myolysis (myomas alone may be removed) in patients whose
uterus need to be conserved due to young age and/or infertility.
• Hysterectomy with or without bilateral salpingo-oophorectomy is for
patients of older age.
Benign ovarian tumours

• These are cystic tumours commonly occurring in the ovaries.
• The two common tumours are:
• Benign cystic teratoma (dermoid cyst) and
• Mucinous cystadenoma.
• Majority of patients remain asymptomatic.
• Large tumours may undergo torsion and present as acute pain of the lower
abdomen.
US and CT (Fig. 38.11) are useful in diagnosis.
FIGURE 38.11 CT—ovarian dermoid.
Treatment
• Removal of cyst is the treatment of choice.
• Other ovary should be explored for similar pathology.
Polyps of uterine cervix and endometrium
Benign tumours of uterine cervix and endometrium.
Menstrual irregularities or postmenopausal bleeding.
• US (Fig. 38.12A) is informative
• Hysteroscopy (Fig. 38.12B) and biopsy are diagnostic.
FIGURE 38.12A Endoscopic ultrasound of endometrial polyp.

FIGURE 38.12B Hysteroscopic appearance of endometrial polyp.
Treatment
• Direct removal of cervical polyps.
• Hysteroscopic removal of endometrial polyps.
• Endocervical and endometrial curettage are mandatory.
Dysplasia of uterine cervix

• Human papilloma virus is considered to be the cause of dysplasia,
predominantly the strains 16 and 18.
• This is a premalignant condition.
• Many of these patients remain asymptomatic.
• Some present with vaginal discharge.
• Post coital bleeding.
• Most are picked up during a routine pap smear.
• Clinical examination is not contributory.
Colposcopy and biopsy are diagnostic.
Treatment
• If the biopsy conclusively rules out invasive disease, conservative therapies
like cryotherapy, laser application, loop electro excision procedure (LEEP),
cone biopsy.
• Invasive lesions are to be treated as carcinoma cervix.
• Follow up is essential.
Carcinoma of uterine cervix

• Common between 40 and 50 years age.
• Women with multiple partners.
• Virus infections (herpes simplex type 2 and human papilloma virus types
16 and 18).
• Macroscopically, it presents as
• proliferative growth at the cervix with surface ulcerations.
• diffusely infiltrating tumour with intact mucosa (Fig. 38.13).
• squamous cell carcinomas (95%) and
• adenocarcinomas (5%).
• The tumour spreads in all directions.
• Locally to parametrium, rectum.
• Through lymph to paracervical nodes to internal and external iliac,
presacral and obturator nodes, and para-aortic nodes.
• Through blood to lungs, liver and bones.
FIGURE 38.13 Carcinoma cervix.
Symptoms
• Many are asymptomatic.
• Irregular/intermenstrual/post coital bleeding per vagina.
• Vaginal discharge.
• Haematuria or rectal bleeding due to local spread.
• Low back pain and sacral pain due to pelvic lymphadenopathy.
• General symptoms like anorexia, malaise and weight loss.
Signs
• Pelvic examination—lesion and spread can be assessed.
• Rectal examination—to assess spread to parametrium or rectal mucosa.
• Colposcopy (Fig. 38.14) and biopsy is confirmatory.
• US or CT may be needed to rule out the local infiltration and metastases.
FIGURE 38.14 Colposcopy of carcinoma cervix.

Treatment
• Modified radical hysterectomy and radiotherapy for early lesions.
• Chemoradiation is used for advanced lesions.
Palliative
• Radiotherapy to control bleeding and pelvic pain.
Carcinoma of endometrium
• Common between 55 and 65 years of age.
• Uncommon below the age of 40.
• oestrogen replacement therapy and
• nulliparity.
• Macroscopically, it presents as
• polypoid mass and
• Diffuse or multifocal growth.
• Microscopically, they are adenocarcinomas of varying grades.
• Locally to myometrium and cervix, tubes and ovaries, occasionally to
parametrium bladder or rectum.
• Through lymph to pelvic nodes.
• Through blood to lungs and bone.
Symptoms
• Postmenopausal bleeding.
• Heavy/irregular periods in premenopausal women.
• Vaginal discharge.
• Endometrial biopsy or fractional curettage is diagnostic.
• US and CT (Fig. 38.15) are required to rule out metastases.
• Hysteroscopy is useful.
FIGURE 38.15 CT—carcinoma endometrium.
Treatment
• Staging laparotomy with total abdominal hysterectomy (Fig. 38.16), and
lymph node dissection should be done and can be followed by radiotherapy
if required.
FIGURE 38.16 Carcinoma endometrium.
Palliative
• Radiotherapy for locally advanced tumours and painful bone metastases.
• Hormone therapy: medroxyprogesterone acetate or megestrol, GnRH
analogues.
• Chemotherapy(cisplatin and adriamycin) for younger fit patients with
advanced disease.
Carcinoma of vulva
• Only 5% of all gynaecological cancers.
• Common in the middle aged and elderly.
• Lichen sclerosus and
• HPV types 16, 18, 31, 33, 35, 38, 45 and 52.
• Macroscopically, the tumour is
• typically papilliferous growth
• an ulcer
• bilateral tumours (Kissing cancer).
• squamous cell carcinomas (commonest)
• basal cell carcinoma
• melanoma
• sarcoma.
• Vulvar cancers spread by
• Local invasion to surrounding soft tissues and pubic bones.
• Lymph to inguinal nodes and pelvic nodes.
• Blood to lungs (very late event).
Symptoms
• Symptoms of skin dystrophy and local irritation.
• A lump may be obvious to the patient.
• Vaginal discharge, pruritus vulvae, pelvic pain, dysuria and dyspareunia.
Signs
• Growths or ulcers of vulva (Fig. 38.17).
• Inguinal nodes may be palpable.
FIGURE 38.17 Carcinoma vulva Source: (Courtesy Dr A. Chandrasekhar Rao).
DD: Condyloma, lymphogranuloma inguinale, lymphogranuloma venereum
• Biopsy is conclusive.
• CT abdomen for pelvic nodes.
• X-ray chest for lung metastases.
Treatment
• Vulvectomy (simple/radical) with bilateral femoral and inguinal node
dissection.
• Radiotherapy for some lesions.
Palliative
• Combined chemoradiation may be useful, but toxic.
• Diverting colostomy for extensive posterior infiltration.
• Radiotherapy to relieve local pain, discharge and bleeding.
Carcinoma of ovaries
• More common in women over 40.
• genetic factor: BRCA 1 and BRCA 2 gene mutation
• Macroscopically, it appears as cystic enlargement of ovary, of two types:
• Mucinous cyst (large, multiloculated tumour mass with mucinous material)
• Serous cyst (clear fluid within a thin walled cyst containing papillary
structures)
(solid masses may be formed by teratomas)
• Epithelial adenocarcinomas (commonest)
• Germ cell tumours (teratoma, dysgerminoma, endodermal sinus tumours)
• Sex cord stromal tumours (granulosa cell tumours, theta cell tumours)
• Gonadoblastomas
• Unclassified tumours
• Locally within the ovary, breaking the tumour wall onto the surface.
• Transcoelomically, across peritoneal cavity as seedlings on the peritoneal
surfaces, involve omentum and produce ascites.
• Lymphatically, to para-aortic nodes.
• Haematologically to liver and lungs.
• Meig’s syndrome is pleural effusion accompanying ovarian malignancy,
which has features of a transudate and is cytologically negative for malignant
cells.
Symptoms
• They remain asymptomatic and present late clinically.
• The symptoms are vague and nonspecific like feeling of a mass in the
abdomen, loss of appetite, feeling of bloatedness.
• Advanced lesions may present with obstruction of adjacent structures like the
ureter and colon, or as ascites (Fig. 38.18A).

FIGURE 38.18A Ascites of carcinoma ovaries Source: (Courtesy Dr R.
Rajaraman).
Signs
• Not specific unless the tumour is fairly big in size.
• Ascites may be present.
• Vaginal examination may reveal an ovarian mass.
• Chest examination, may show pleural effusion.
• US is helpful in localizing lesions.
• CT (Fig. 38.18B) may be needed to assess the spread of the disease.
• Serum CA 125 is a valuable marker for diagnosis and response to treatment.
• Tissues can be obtained for biopsy by ultrasound or CT guidance.
FIGURE 38.18B CT—ovarian carcinoma.
Treatment
Curative
• Total abdominal hysterectomy, bilateral salpingo-oophorectomy and
omentectomy. Careful examination of para-aortic nodes, liver and peritoneal
surfaces including subdiaphragmatic surfaces and their biopsy are required to
stage the disease.
• In patients who have undergone hysterectomy earlier, the mass along with
the ovary is excised (Fig. 38.19).
• Adjuvant chemotherapy is mandatory and is effective.
FIGURE 38.19 Ovarian carcinoma in a patient who has undergone

hysterectomy.
Palliative
• Chemotherapy for relapses and response is better for those after remission
(>1 year).
• Radiotherapy for symptomatic pelvic mass, vaginal bleeding and bone
metastases.
Uterine prolapse
• Uterus prolapses due to loss of pelvic supports leading to relaxation of
muscles, mostly in multiparous women.
• It is graded into four degrees:
• I degree: descent with cervix lying short of the introitus.
• II degree: descent with cervix upto the level of introitus.
• III degree: descent with cervix below the level of introitus.
• IV degree: prolapse of whole of the uterus outside the vulva (procedentia).
• Neighbouring structures may prolapse along with uterine prolapse. They are:
• Anteriorly
- Urinary bladder – cystocoele (due to weakness in pubocervical fascia)
and
- Urethra – urethrocoele (due to weakness of triangular ligament)
• Posteriorly
- Rectum – rectocoele (due to break in investing vaginal fascia)
Symptoms
• A sensation of swelling or fullness in the vagina or a dragging discomfort in
the lower abdomen and pelvis are presenting symptoms.
• Urinary symptoms may be present in patients with cystocoele (Fig. 38.20A)
and urethrocoele, and incomplete emptying of rectum in patients with
rectocoele.
• The patient presents with a mass descending per vagina.
FIGURE 38.20A Large cystocoele.
Signs
• Local examination will reveal the prolapsed structures (Fig. 38.20B).
• Totally prolapsed uterus may present with ulcerations on the uterine cervix
(decubitus ulcers).
FIGURE 38.20B Utreine prolapse.
• Pap smear or biopsy may be needed to rule out associated malignancy of
cervix.
Treatment
• Surgical procedures that support the uterus (sling operations, e.g.,
Purandare’s operation, Shirodkar’s operation) are useful in young
patients,
• Vaginal hysterectomy with pelvic floor reconstruction are for older patients
• Conservative management with pessaries and pelvic floor exercises, is
reserved for patients with poor surgical risk
Endometriosis
• Presence of ectopic endometrium outside the endometrial cavity.
• Presence of endometrial tissue in the myometrium is called ‘adenomyosis’.
• Most patients present with the triad of symptoms.
• Dysmenorrhoea
• Menstrual disturbances
• Abdominal pain
• Infertility is common.
• US of abdomen may reveal chocolate cysts in the abdominal cavity.
• Laparoscopy is diagnostic.
Treatment
Treatment depends on the severity of symptoms.
• Medical: Administration of oral contraceptives, progesterone or
gonadotrophin releasing hormone agonist analogues are useful in the
management of symptoms.
• Surgical: May be required in very symptomatic patients. They are as follows:
• Excision of endometriotic areas and chocolate cysts.
• Hysterectomy with bilateral salpingo-oophorectomy is usually curative.
Dysfunctional uterine bleeding

The bleeding may be
• anovulatory due to lack of progesterone.
• ovulatory due to imbalance of prostaglandins.
• Patient presents with a variety of bleeding disorders. They can be
• Menorrhagia: irregular and more than normal quantities.
• Oligomenorrhoea: less than normal quantities.
• Amenorrhoea: complete absence of vaginal bleeding.
• Metrorrhagia: irregular bleeding.
• Meno-metrorrhagia: irregular bleeding associated with increased flow.
• The cycles can be
• infrequent with reduced menstrual flow (hypomenorrhea).
Anovulatory bleeds are irregular and usually painless. Ovulatory cycles are
regular with increased flow and dysmenorrhea.
• US is useful to rule out causes like fibroids, endometriosis and polycystic
ovarian disease.
• Endometrial biopsy is done to differentiate whether it is ovulatory or
anovulatory in its aetiology, but it is not required in all cases.
Treatment
• Combined oral contraceptives or progesterone only pills are used to
regularize the menstrual cycles.
• NSAIDs are useful in the management of dysmenorrhea.
• Hysterectomy is curative in refractory cases.
Ectopic pregnancy
This is pregnancy outside the endometrial cavity, most commonly in the
fallopian tube (Fig. 38.21).
FIGURE 38.21 Tubal pregnancy.
• Unruptured ectopic pregnancy presents with amenorrhea and spotting.
• Ruptured ectopic pregnancy presents with amenorrhoea, spotting and severe
lower abdominal pain and vomiting (see Ch. 30).
• Circulatory collapse may be a presenting symptom.
• Vaginal examination is characteristic, with severe tenderness in one or both
vaginal fornices with or without positive cervical excitation test (CET).
• US (Fig. 38.22) is confirmative.
FIGURE 38.22 US—ectopic pregnancy.
Treatment
• Emergency laparotomy and salpingectomy with quick circulatory support for
ruptured ectopic pregnancy.
• Medical termination (with methotrexate) or surgery and conservation of the
tube, if possible, for unruptured ectopic pregnancy.
Polycystic ovarian disease

• A common condition characterized by anovulation.
• Hyperandrogenism with hyperinsulinism and obesity with altered FSH/LH
ratio may be associated.
Clinically, they may be obese and may show signs of virilisation and hirsutism.
• Determination of hormone levels (raised testosterone, insulin levels and
altered FSH/LH ratio) is useful in the management.
• US (Fig. 38.23) is useful in determining the cystic nature of ovaries, but not
necessary for diagnosis.
FIGURE 38.23 US—polycystic ovarian disease.
Treatment
• Measures to reduce weight are to be advised in all patients.
• Oral contraceptives and progesterone for regulation of periods in young
unmarried girls.
• Clomiphene and HCG for infertile women.
• Spironolactone or flutamide can be used in patients with hirsutism.
• Metformin is used in all cases if deemed necessary.
Asherman’s syndrome
Vigorous scraping of the endometrium at the time of curettage with formation of
adhesions inside the cavity.
Patients present with secondary amenorrhoea.
• Hysterosalpingogram shows honeycomb appearance.
• US is another alternative.
Treatment
Hysteroscopic removal of adhesions with placement of an intrauterine
contraceptive device for about three months along with administration of
hormones.
38.5 Symptoms of diseases of female genital

tract
The diseases of female genital tract have various clinical presentations. They are
given in Table 38.2.
TABLE 38.2
Clinical Presentations of Diseases of Female Genital Tract
Symptom Diseases
Discharge per vagina Physiological Pelvic inflammatory disease Carcinoma cervix Cervical erosions
Irregular vaginal bleeding Dysfunctional uterine bleeding Uterine fibroids Polyps Endometriosis
Amenorrhoea Primary Mullerian duct anomalies Genetic disorders Androgen insensitivity
Secondary Pregnancy Polycystic ovarian disease Virilising tumours CNS disorders Asherman’s
syndrome
Postmenopausal bleeding Endometrial atrophy Endometrial hyperplasia Carcinoma of endometrium Hormone
replacement therapy (HRT) Polyps
Mass descending per vagina Uterine prolapse Pedunculated polyp Vaginal tumours
Abdominal mass Uterine tumours Ovarian tumours
Infertility Endometriosis Congenital anomalies of genital tract Polycystic ovarian disease
Dysmenorrhoea Physiological Endometriosis Uterine fibroids
Pruritus Vulval dysplasia Vaginal infections
Abdominal pain (not related to Tubo-ovarian pathology (tubo-ovarian mass) Uterine fibroids Endometriosis Genital
menstruation) malignancies
Eliciting history
• Age: Certain diseases affecting gynaecological system are common in certain
age groups.
• Newly married and adolescents: ectopic gestation, sexually transmitted
diseases.
• Young adults and middle aged: fibroids, dysfunctional uterine bleeding.
• Elderly: uterine malignancy, ovarian malignancy.

Since most gynaecological illnesses present with symptoms related to the
system, detailed history taking starts with the presenting symptom, followed by
questions relating to other symptoms. It should be remembered that
gynaecological illnesses can present with symptoms unrelated to the system,
such as frequency in micturition, e.g., cystocoele.
Discharge per vagina

• Amount, consistency and duration: What is the amount and consistency of
discharge and how long it is been present?
Thick scanty discharge is commonly seen with Candidiasis, and also
normally presents in the luteal phase. Copious white discharge can be present
normally in follicular phase and also in infections-like trichomoniasis.
• Exact colour:What is the exact colour of the discharge?
Curdy white discharge is seen in candidiasis, greenish colour in
trichomoniasis and colourless discharge is seen in bacterial vaginosis.
• Odour: Does the discharge have any odour?
Under normal physiological conditions, the discharge is odourless. Fishy
odour is characteristic of bacterial vaginosis, and other infections tend to
give a foul smell to the discharge.
• Association of fever: Is or was the discharge associated with fever?
Association of fever may indicate an infective pathology.
Bleeding per vagina

• Menstrual cycle: Has the menstrual cycle been regular?
First, the patient should be asked to describe her menstrual cycle. The day of
appearance of blood flow is the first day of the menstrual cycle. This is
usually mentioned in a standard format, namely, number of days of blood
flow/the frequency of cycle. e.g., 3/30 (denominator includes the number of
days of bleeding also). Irregular menstrual cycles are seen in DUB, polyps.
The actual date of last menstrual period (LMP) is very important, e.g., in
diagnosing ectopic gestation and its complications. It is necessary to know
the age at menarche.
• Amount of bleeding: What is the quantity of bleeding during each episode?
Is it the same or varies in quantity?
Determination of quantity of bleeding is very important, e.g., small amounts
of bleeding (spotting) is common in DUB, polyp, while passage of large
amounts with clots is seen in fibroids, endometriosis, DUB. Number of pads
used indicate the amount of bleeding, and can be compared with the previous
episodes easily.
• Association of pain (Dysmenorrhoea): Is there pain during or preceding
menstruation?
Description of pain is very important, as there are two varieties of pain,
which are associated with menstruation.
• Congestive dysmenorrhoea: Pain in the second half of luteal phase which
is relieved by the onset of menses, e.g., fibroids, endometriosis.
• Spasmodic dysmenorrhoea: Pain is severe and colicky starts at the onset of
menses and is relieved in about 12–24 hours. It is considered physiological
and is present in ovulatory cycle. Severe pain may be associated with
giddiness.
• Bleeding per vagina between menstrual periods (intermenstrual
bleeding): Is there bleeding between menstrual periods?
The usual description is that there is no vaginal bleeding for 4–5 days,
followed by variable amounts of bleed, for the duration of the cycle. The
bleeding is usually irregular and unpredictable (e.g., endometriosis, cervical
or endometrial polyp, patients on hormonal medication).
• No bleeding per vagina (amenorrhoea): Was the patient’s periods regular
previously before the present episode of no bleeding? A person who has
been having fairly regular periods and has not had a period recently has
secondary amenorrhoea (due to underlying cause). Pregnancy is the
commonest cause of secondary amenorrhoea and pregnancy test is
mandatory.
Mass descending per vagina

• Duration: For how long the patient been suffering from the complaint of
mass descending per vagina?
The patient may describe the presence of it at all times or only on straining.
She may also describe the measures taken by her in reducing it. If the details
are not given spontaneously, leading questions are to be addressed to the
patient, e.g., irreducible prolapse is associated with complications like
oedema, decubitus ulcer etc.
• Association of discharge: Is there any discharge associated with the
symptom of prolapse?
Bloody or purulent discharges are seen in decubitus ulcers or associated
malignancy of cervix.
• Association of urinary symptoms: Does the patient have any urinary
symptom associated with the uterine prolapse?
Variety of urinary symptoms like, dysuria, urgency, incomplete emptying of
bladder and retention of urine may be associated with prolapse (e.g.,
cystocoele or urethrocoele). Urinary infection is a common accompaniment.
• Association of bowel disturbances:Is the patient passing the stools without
strain? If constipated, is it of a recent onset or present for a longtime?
Habitually constipated patients are at risk for uterine prolapse especially who
have undergone surgery in the perineal region. Requirement of manual
reduction to relieve constipation or sense of incomplete evacuation of stools
may indicate associated rectocoele.
• Association of chronic cough:Does the patient have chronic cough?
Patients with chronic cough as in chronic obstructive pulmonary disease tend
to develop prolapse of uterus.
• History of previous childbirth or surgery: Did the patient have a difficult
childbirth or undergo any surgery in the past in the perineal region?
History of instrumentation during previous childbirth and any surgery of the
perianal region weaken the pelvic floor, and predispose to a uterine prolapse.
Likewise, repeated childbirths also weaken the pelvic floor.
Postmenopausal bleeding
• Duration of menopause: When did the patient attain menopause?
If the bleeding occurs after a minimum period of one year of amenorrhoea, it
is considered post-menopausal bleeding, but bleeding after 6 months of
amenorrhoea also needs investigations.
• Amount and type of bleeding: What is the quantity of bleeding during each
episode? Is it the same or varies in quantity?
Small bleeds especially after several years after menopause is seen in
atrophy, and large amounts of continuous or recurrent bleed in varying
quantities are characteristic of hyperplasia or malignancy.
Pruritus vulvae
• Duration of pruritus: How long has the patient been suffering from
pruritus?
Pruritus of short duration may be seen in local dermatological lesions, and
longstanding pruritus is seen in dysplasia. In postmenopausal women, vulvar
dermatoses is the commonest cause and in the reproductive age group,
infections can cause pruritus.
Abdominal pain
The site of origin of pain must me clearly noted. Ovarian and tubal pain is
felt low in the abdomen, just above the inguinal ligament. Pain of uterine
origin is diffuse and hypogastric in site, sometimes referred to the inner
aspects of the thighs but not extending below the knees. Backache of pelvic
origin is midline, never higher than S1.
This will answer the duration of pain. Acute pain is caused by events like
torsion of ovarian cyst, ruptured ectopic gestation.
• Mode of onset/description of pain: Can you describe the pain?
The abdominal pain of gynaecological reasons has a variety of
presentations.
a) Sudden onset pain without pain-free intervals: Sudden pains are seen
in otherwise healthy and asymptomatic persons. It can have quick
onset and increase in a very short time as if it is starting instantly (e.g.,
ruptured ectopic gestation).
b) Sudden onset with pain-free intervals: The pain of quick onset can
reach a peak making the patient writhe in pain and buckle up, and also
quickly recede to absolutely pain-free period, only to recur again (e.g.,
colics of tuboovarian pathology-like torsion).
c) Dull and continuous pain: The pain can be dull and continuous (e.g.,
malignancy).
d) Dull continuous pain increasing in severity: A persistent pain may
increase in severity over a period of time (e.g., acute on chronic
torsion of ovarian cyst).
e) Burning pain: The pain may be of burning nature (e.g., urinary
infection or cystitis).
f) Radiation of pain: Has the pain been radiating from its point where it
started? The pain of uterine origin may be referred to the inner aspects
of the thighs never below the knees.
g) Period of pain: How long has pain been present? Repeated episodes
of similar pain for months or years (e.g., salpingitis).
Infertility
Many times, infertility is a presenting symptom of a gynecological pathology.
• Duration of married life and methods of contraception used: How long is
the patient married and does the couple use any method of contraception?
Failure to produce children after a year’s unprotected sex is defined as
primary infertility. Secondary infertility is the inability to conceive after two
years of unprotected sex following the first conception.
• Husband’s fertility status: Has the patient’s husband been investigated?
It is always easy to assess the fertility status in a male by a simple semen
analysis. If azoospermia or any other abnormality is found in the semen
analysis, it should be treated first. A semen analysis is an essential first step
in the management of infertility.
• Menstrual history: Has the patient been having regular menstrual cycles
with normal discharges?
This will help in eliciting history about the cycles whether ovulatory or not.
Even infrequent cycles are considered ovulatory if they are spontaneous.
• Frequency of intercourse: How frequently does the couple have
unprotected intercourse?
Sexual intercourse at least three times in a week at fairly equal intervals is
considered optimum and essential to effect pregnancy.
• Association of pain during sexual intercourse (dyspareunia):Does the
patient experience pain during intercourse?
Association of superficial pain during sexual intercourse is suggestive of
psychological causes (e.g., fear) and local infective and inflammatory
pathologies. Deep seated pain may be due to pelvic inflammatory disease or
endometriosis.
• Awareness of fertile period: Is the couple aware of a period called fertile
period?
The fertile period is the period when the ovulation is expected to happen.
This is calculated to be about 2 weeks from the expected date of the next
menses. Sexual intercourse during this period have higher chance of
conception.
• Personal history: What is the nature of job commitments does the couple
have? Do any of the partners use tobacco?
Partners who are working in high stress jobs with irregular working
schedules and do not have time and energy to have planned sexual
intercourses are common candidates for infertility. Cigarette smoking has a
direct correlation to infertility.
• Past medical history: Has the partner been on any treatment for the same
illness in the past?
Thorough scrutiny of the previous medical records should be scrutinized for
the investigations and treatment undertaken, which will give an idea, as to
how to go about in the case. Mumps in the past (e.g., mumps orchitis) is
directly correlated with infertility.
• History of drug intake and allergies: Has or is the patient’s partner on a
prolonged drug intake?
Men who have consumed drugs (e.g., anabolic steroids, chemotherapeutic
agents, spironolactone, tetracycline, etc.,) for prolonged periods in the past
are prone to be infertile, due to the drugs’ effect on spermatogenesis.
Dyspareunia
Pain with intercourse is called dyspareunia. All gynecological patients should
be specifically questioned about this symptom.
• Onset and duration:How long has the pain been present?
Recent onset pain can be due to vaginal infections or trauma. Longstanding
pain is however due to chronic diseases like endometriosis.
• Location of pain: Where is the pain located?
Superficial dyspareunia refers to pain with entry and is localized to vestibule
and is due pathology at the introitus. Deep dyspareunia refers to pain during
intercourse and is due to diseases of the upper vagina and pelvis including
retroverted uterus.
• Severity of pain: How severe is the pain?
Lack of adequate lubrication can result in discomfort rather than pain (e.g.,
atrophic vaginitis). Severe pain usually results from diseases like
endometriosis.
• Frequency of pain: Is pain present with every intercourse?
Sporadic pain is usually due to isolated episodes of infection or trauma and
will resolve when the disease resolves. Consistent deep pain is usually due to
chronic diseases.
Vomiting
Vomiting is a very common feature associated with abdominal pain in acute
gynecological emergencies, like torsion of ovarian cysts, ruptured ectopic
gestation.

malignancies.
• Treatment for the present illness: Has any treatment (medical or surgical)
been given to the present illness?
The information of any treatment received in the recent past for this illness
will give a clearer picture of diagnosis (may indicate incompleteness of
treatment and will help in finalizing the management).
treatment?
like recurrence of tuberculosis. Even recurrent malignancies should be
considered.
Diseases like tuberculosis occur in families and the positive history may be a
good indicator for the present diagnosis. Breast cancer and uterine or ovarian
cancers run in families.
• Questions specifically related to gynecological illnesses:
1. Use of contraception and other hormonal medications
2. Marital/sexual history
3. Obstetric history
General
General physical examination should be directed towards the evidences of
• anaemia
• dehydration
• body mass index (BMI) and
• features of hirsutism.
Breasts
Examination of the breast is mandatory, as it may be useful in excluding
tumours, especially in those on oral contraceptives and hormone replacement.
Thyroid
Thyroid is examined for swelling
Abdomen
Omission to examine the abdomen before pelvic examination may lead to many
errors. A systematic examination of abdomen needs to be carried out, both by
inspection and palpation (see Ch. 32).
Pelvis
Pelvic organs should be assessed, both by vaginal and or rectal examinations.
Vaginal examination
Pre-requisites
• Presence of a nurse or relative.
• Proper explanation of procedure and consent.
• Empty urinary bladder.
• Preferably empty rectum (for rectal examination).
• Good illumination.
Examination of the pelvis can be done in any of the following three positions:
1. Dorsal position (most commonly used): Patient is in semirecumbent position
with the knees flexed. The examiner passes index and middle fingers of the
examining hand into the vagina (Fig. 38.24). This procedure is useful in
examining the vulva and for bimanual palpation of uterus and appendages.
2. Left lateral (modified Sims’) position: The patient should lie in the left lateral
position across the examination table, with the buttocks at the edge of the
table. The hips and knees should be flexed and the heels clear of the perineum
(ref. Fig. 34.19A). Used in conjunction with the speculum examination, it is
good for examining the anterior vaginal wall and cervix, as when the introitus
is opened, the vagina balloons with air. Bimanual examination is not possible
in this position, as the examiner will not be able to reach the abdomen.
3. Lithotomy position: Described in Chapter 34 (ref. Fig. 34.19D). This
procedure is useful for preoperative assessment, just before surgery.
FIGURE 38.24 Dorsal position for vaginal examination.
Each position has certain merits and strict adherence to one position is
not necessary.
Each part of the genital tract should be examined in logical sequence: vulva,
vagina, cervix, body of uterus, appendages and pouch of Douglas.
Local examination
• Inspection of genitalia and perineum.
• Speculum examination of vagina.
• Digital examination of vagina and bimanual palpation.
Inspection of genitalia and perineum

What to inspect?
1. Labia majora and minora: skin discolourations, growths, malformations (Fig.
38.25A–D)
2. Clitoris: enlargement especially in patients with amenorrhoea and virilization.
3. Pubic hair (distribution): normally appears as inverted triangle with the base
on mons pubis, hairline may extend into the lower abdomen.
4. Bartholin’s gland area: swelling (Fig. 38.26), discharge, redness.
5. Mass descending per vagina: if present, assess grade of prolapse, state of
cervix, vaginal rugosities.
6. Introitus: discharge and its nature.

FIGURE 38.25 Examination of labia—(A) Oedema of labia majora. (B)
Oedema of labia minora. (C) Herpes simplex of labia. (D) Warts.
FIGURE 38.26 Bartholin’s cyst.
Speculum examination of vagina and cervix

See Table 38.3 for common types of vaginal speculums used for examination.
TABLE 38.3
Common Types of Vaginal Speculums Used for Examination
Type of Speculum Advantages Disadvantages

Sim’s speculum Can be used to assess vaginal Not self-retaining An assistant is needed to retract Another
(single blade) walls, and also its prolapse retractor may be needed to retract anterior wall Patient
(Fig. 38.27A) should be at the edge of the table
Cusco’s speculum Self-retaining Patient can be Vaginal wall and its prolapse cannot be satisfactorily assessed
(bi-valve examined in a couch Ideal for
speculum) (Fig. obtaining smear samples
38.27B)
• Patient should be explained about the procedure in detail, its requirement and
its simplicity.
• Speculum of required length should be chosen for examination.
• Speculum should be well lubricated with lukewarm water.
• Cusco’s speculum: Patient is positioned in dorsal position, and the
speculum is introduced gently through the introitus, with both blades
positioned mediolaterally. Once inserted to its full length, it is rotated
through 90° so that it is positioned anteroposterior. Once positioned well,
it is opened until the cervix is clearly visualized and it is screwed in
position (Fig. 38.27C).
FIGURE 38.27C Method of using Cusco’s speculum.

Note
• Enlarging the introitus using a finger helps in easy insertion of the speculum.
• Separating the labia majora with the other hand can help easy insertion and
avoid pulling on the pubic hair.
• Sim’s speculum: Patient is positioned in the lateral position or lithotomy
position and the speculum is introduced gently through the introitus.
Retracting the posterior vaginal wall exposes the urethral meatus,
anterior vaginal wall and bladder base. The cervix is visualized and the
level noted. The posterior vaginal wall is viewed by retracting the
anterior wall by rotating the speculum through 180° (Fig. 38.28A and
B).

FIGURE 38.28A Examination of anterior vaginal wall.

FIGURE 38.28B Examination of posterior vaginal wall.
What to see?
1. Vaginal walls
• Signs of inflammation
• Redness
• Discharge
2. Cervix
• Bleeding/discharge from cervix
• Redness
• Erosion
• Growth (position is expressed with the face of clock, and growth should
be described as it is done for any lump)
3. Vaginal walls (assessed while withdrawing the speculum)
• Posteriorly the first bulge that appears in the upper third is an
enterocoele, and lower half is the rectocoele.
• Anteriorly, the first bulge that appears is a cystocoele (ref. Fig. 38.20A)
and the second bulge is a urethrocoele.
Obtaining pap smears: Taking a PAP smear (smear for Papanicolou
staining) is an integral part of the pelvic examination and should always
precede the digital examination. This is indicated in
• sexually active women every year and
• postmenopausal women on hormone replacement therapy (HRT).
Method of obtaining the smear: Patient should be in lithotomy position.
The introitus is cleaned with plain water (no lubricant should be used). The
Cusco’s or Sim’s speculum can be used to visualize the cervix adequately.
To obtain samples,
• a spatula (Fig. 38.29A) is placed firmly in the cervical os, and rotated
through 360° to allow the removal of surface cells from the whole of the
squamocolumnar junction.
• a cytobrush (Fig. 38.29B) is used for the endocervix similarly.
FIGURE 38.29A Method of taking a smear with a spatula.
FIGURE 38.29B Method of taking a smear with the cytobrush.
A kit is available commercially for the above purpose (Fig. 38.29C).

FIGURE 38.29C Pap smear kit.
The smear is spread on the glass slides (Fig. 38.29D) and treated with a
fixative solution or spray.
FIGURE 38.29D Method of making smears with a spatula (i) and
cytobrush (ii).
Note
While collecting samples for Pap smear, the spatula/brush should be used in
a full circle, so that the transformation zone and squamocolumnar junctions
are included.
Digital examination of vagina and bimanual palpation

Procedure
• Patient in dorsal position.
• The patient should be explained about the procedure and the sensation she
may have during the procedure.
• The gloved and generously lubricated pulp of the index and middle fingers of
the right hand should be slowly introduced into the introitus (Fig. 38.30A
and B) with the left hand over the lower abdomen, to bring the various
organs within comfortable reach (Fig. 38.30C and D).
• Full length of the fingers is introduced, assessing the vaginal walls in transit
until the cervix is encountered.
• Uterine cervix is identified (it is approximately 3 cm in diameter with a
dimple in the middle, the cervical os, which is directed posteriorly when the
uterus is anteflexed and anteverted).
• Anterior lesions are usually elevated by the vaginal fingers and palpated
bimanually, whereas the posterior structures are assessed by the fingers in the
vagina and correlated with the rectal examination.
FIGURE 38.30A Palpation of anterior vaginal wall.

FIGURE 38.30B Palpation of posterior vaginal wall.
FIGURE 38.30C Diagramatic explanation of bimanual palpation.
FIGURE 38.30D Method of bimanual examination.
Note
The fingers should be inserted and withdrawn slowly to minimize discomfort.
What to feel?
1. Vagina: Lesions-like erosions and inflammations (vaginitis).
2. Uterine cervix: determine
• Consistency (firm/hard)
• Swellings (growth or polyps)
• Friability (malignancy)
• Position (retroversion/anteversion)
• CET (ectopic gestation, pelvic inflammation, endometriosis)
3. Uterine body and fundus: To feel the uterus, the vaginal fingers should move
the cervix as far backwards as possible to rotate the fundus downwards and
forwards. The abdominal hand is then placed just below the umbilicus (not
suprapubically) and gradually moved lower until the fundus is caught and
pressed against the fingers in the anterior fornix. Normal anteverted uterus is
felt as a firm, globular swelling Determine
• Size (expressed in terms of gravid uterus, e.g., 16 weeks size)
• Enlargement (uniform e.g., adenomyosis, irregular, e.g., fibroids)
• Position (anteverted or retroverted)
• Presence of tenderness (adenomyosis)
• Mobility ( loss of mobility is seen in pelvic endometriosis)
4. Adnexa: felt through lateral fornices
• Mass (ovarian cysts, tumours)
• Tenderness (pelvic inflammation, ruptured ectopic gestation and
endometriosis)
5. Pouch of Douglas: assessed through posterior fornix
• Mass or nodules (malignant deposits)
Remember
• Normal tubes are never palpable, even in the anesthetized patient.
• Palpation of ovaries is not always possible and if they are not felt it can be
taken that they are not enlarged.
• If one of the ovaries is felt in a postmenopausal woman, a cyst or a tumour
should be considered.
• CET: the mobility of the cervix is about 1–2 cm in all directions and testing
this movement should produce mild discomfort only. Severe pain indicates
positive CET.
Speculum examination of the vagina should precede bimanual
examination for the following reasons:
1. Vaginal discharge can be seen and taken for examination before it is
contaminated by lubricant.
2. Cellular debris from cervix and uterus remains undisturbed which is good
tissue for cytological examination.
3. Some lesions of vagina and cervix may bleed and obscure the visibility during
speculum examination.
Rectal examination
Rectal examination is useful when vaginal examination is not possible especially
in babies and children. It can be used as an adjunct to vaginal examination and is
the best approach for feeling the uterosacral ligaments, pouch of Douglas and
other parts of broad ligaments, and also to assess the extent of growth arising
from the uterine cervix.
Rectovaginal examination
The index finger is introduced into the vagina, and the middle finger into the
rectum. This procedure is useful to assess a retrodisplaced uterus and
parametrium (Fig. 38.31A).
FIGURE 38.31A Rectovaginal examination.

Remember
After the completion of the examination, it should be remembered to wipe the
vaginal introitus/anal orifice with a gauze, so that the patient does not
experience any discomfort of the stickiness of the lubricant or the secretions.
If there is a history or a labial swelling, Bartholin’s glands should be palpated
(Fig 38.31B)
FIGURE 38.31B Palpation of Bartholin’s glands.
Lymphatic system
genitalia, i.e., para-aortic and inguinal lymph nodes, which will give useful
information.
CHAPTER 39
General orthopaedics
V. Thulasiraman
CHAPTER OUTLINE
39.2. Diseases of bones 713
• Osteogenesis imperfecta 713
• Diaphyseal aclasis (multiple exostoses) 714
• Dyschondroplasia (multiple chondromata, Ollier disease) 715
• Achondroplasia 715
• Myositis ossificans progressiva 716
• Fractures 716
• Joint injuries 719
• Acute septic osteomyelitis 719
• Chronic pyogenic osteomyelitis 720
• Tuberculous osteomyelitis 721
• Syphilitic osteomyelitis 721
• Osteoma 722
• Chondroma 722
• Osteochondroma 722
• Giant cell tumour (osteoclastoma) 723
• Osteosarcoma 724
• Chondrosarcoma 725
• Fibrosarcoma of bone 726
• Ewing’s tumour 726
• Multiple myeloma 727
• Metastatic tumours 728
• Infantile scurvy 729
• Rickets 729
• Osteomalacia 730
• Granulomatosis 730
• Parathyroid osteodystrophy 730
• Hyperpituitarism 731
• Polyostotic fibrous dysplasia 731
• Osteitis deformans (Paget disease) 732
• Senile osteoporosis 733
• Osteochondritis juvenilis 733
• Solitary bone cyst 733
• Localized fibrous dysplasia 734
• Osteoid osteoma 734
39.3. Symptoms of pathologies of bones 734
• Bones 736
• Joints 736
• General 736
39.1 Introduction
The word orthopaedic is derived from Greek words. It was originally applied to
the art of correcting deformities. The orthopaedic surgeon is concerned with
diseases and injuries of the trunk and limbs.
Orthopaedic treatment falls into three categories. They are as follows:
1. No treatment—reassurance and advice
2. Nonoperative treatment
3. Operative treatment
More than half of the patients attending orthopaedic outpatient clinics
(excluding fracture) do not require operative treatment. A good trial of
nonoperative treatment may be required before surgery is contemplated.
Based on the aetiology, the lesions of bones and joints are classified as given
in Table 39.1.
TABLE 39.1
Aetiological Classification of Lesions of Bones and Joints
Aetiology Diseases
Congenital Osteogenesis imperfecta Diaphyseal aclasis Dyschondroplasia Achondroplasia Myositis
ossificans progressiva
Traumatic Fractures Dislocations Soft tissue injuries
Inflammatory Acute Acute osteomyelitis
Chronic Chronic osteomyelitis Tuberculous osteomyelitis Syphilitic osteomyelitis
Neoplastic Benign Osteoma Chondroma Osteochondrma Giant cell tumour
Malignant Osteosarcoma Chondrosarcoma Fibrosarcoma of bone Ewing’s tumour Multiple
myeloma Metastatic tumours
Nutritional Infantile scurvy Infantile rickets Osteomalacia Granulomatosis
Endocrine Parathyroid osteodystrophy Hyperpituitarism Cretinism
Unknown General Polyostotic fibrous dysplasia Osteitis deformans Senile osteoporosis
aetiology affections
Local Osteochondritis juvenilis Solitary bone cyst Localized fibrous dysplasia Osteoid
affections osteoma
39.2 Diseases of bones
Osteogenesis imperfecta
• Congenital and inheritable condition.
• Dominant mutant gene.
• Impairment of type I collagen maturation due to heterozygosity of mutation in
COLIA 1 on 17 and COLIA 2 on 7.
• Bones are abnormally soft and brittle.
• Fractures occur after trivial violence but unite and result in malunion.
• Pain after trivial injury.
• Child may be crippled (Fig. 39.1A).
FIGURE 39.1A Osteogenesis imperfecta.
X-rays (Fig. 39.1B) demonstrate fractures and deformities.
FIGURE 39.1B X-ray—osteogenesis imperfecta.
Treatment
• Conventional management of fractures.
• Protective appliances like walking callipers are required to prevent injuries.
• Alandronate group of drugs.
Diaphyseal aclasis (multiple exostoses)

• Congenital illness.
• Transmitted by a dominant mutant gene.
• Characterized by formation of multiple exostoses (osteochondromata) at the
metaphyseal regions of long bones.
• Cartilage cells become displaced giving bony outgrowths, which are capped
by proliferating cartilage.
• The exostoses constitute a type of benign tumour.
• The number of outgrowths varies, from 10 and 20.
• Rarely malignant change occurs in the cartilaginous cap leading to
chondrosarcoma.
• Localized swelling.
• Marked deformity may be seen in the limb.
• Rapid enlargement of the swelling suggest malignant change.
X-rays (Fig. 39.2) show bony outgrowths, in severe cases, the bones appear
remodelled but badly.
FIGURE 39.2 X-ray—multiple familial exostoses.
Treatment
Excision is advised for trouble causing outgrowths.
Dyschondroplasia (multiple chondromata, ollier

disease)
• Congenital disease.
• Heredity does not play any part.
• Masses of unossified cartilage persist within the metaphysis of long bones.
• Bone growth is retarded.
• Cartilage cells are displaced from the epiphyseal plate into the metaphysis,
and persist as enchondromata.
• Common sites are: lower end of femur and upper end of tibia, small long
bones of hands and feet.
• Growth may be affected when long bones are affected.
• Rarely malignant change occurs leading to chondrosarcoma.
• The limb is short and markedly deformed.
• Hands may be enlarged with multiple swellings.
X-rays show multiple areas of translucency.
Treatment
• Osteotomy may be required to correct deformities.
• Leg equalization procedures may be required for correction of discrepancies
in length.
Achondroplasia
• Congenital anomaly.
• Inherited by dominant mutant gene.
• Failure of normal ossification of long bones.
• Growth of the trunk is slightly impaired.
• Strikingly dwarfed (Fig. 39.3).
• Short limbs disproportionate to the trunk.
• Hands are short and broad, the central three fingers equal in length (trident
hand).
• Head is larger than normal but no mental impairment.
FIGURE 39.3 Achondroplasia.
X-rays (Fig. 39.3A) show deformities.
FIGURE 39.3A X-ray—achondroplasia.
Treatment
Multiple bone lengthening by Ilizarov method over 10-year period.
Myositis ossificans progressiva

• A congenital condition.
• Heredity plays a small part.
• Starts in early childhood.
• Metaplasia of connective tissue cells to form bones.
• Characterized by formation of masses of bone in the soft tissues.
• Movements are limited.
• Swellings appear in the neck and trunk (Fig. 39.4A).
• Soft to start with, later become hard masses.
• Movements of spine and ribs are reduced progressively leading to total
immobility.
• Great toe is generally short, thumbs and other fingers may also be short.
FIGURE 39.4A Swellings of the body.
X-rays show plates of bone is soft tissues (Fig. 39.4B).
FIGURE 39.4B X-ray—myositis ossificans progressiva.
Treatment
No effective treatment is possible.
Fractures
General principles
Definition
A fracture is defined as a break in the continuity of a bone, which may be
complete or incomplete.
Classification
Fractures may be subdivided according to their aetiology, into three groups.
1. Fractures caused solely by sudden injury.
2. Fatigue fractures.
3. Pathological fractures.
Fractures caused solely by sudden injury
• By far, the largest group.
• Occurs through a normal bone.
• Caused by
• Direct injury: fracture caused at the site of impact (e.g., fall of heavy object
on foot causing metatarsal fracture).
• Indirect injury: fracture caused at a site different from the site of impact
due to transmission of force (e.g., fracture of radius or clavicle due to fall
on outstretched hand).
Fatigue or stress fractures
• Occurs due to oft-repeated minor stress—‘stress fractures’, causing fatigue of
bones ‘fatigue fractures’ (e.g., metatarsal fracture after prolonged walking,
fracture of tibia and fibula after prolonged running or dancing).
• No single specific cause of injury noted.
• Apparently normal bones are affected.
• Usually confined to lower limb bones.
• Majority of them are metatarsals.
• Pain is insidious (seldom abrupt), increased by activity and relieved by rest.
• Examination reveals marked local tenderness, swelling may appear.
• X-ray may not show fracture line, but demonstrate callus formation.
• Displacement of fragments extremely rare.
• May be mistaken for a sarcoma.
Pathological fractures
• Fracture in a diseased bone (local or systemic disease—Table 39.2).
• Caused by trivial violence.
• Spontaneous fractures are not uncommon.
TABLE 39.2
Causes of Pathological Fractures
Local pathology Systemic pathology

Infections Congenital
Chronic osteomyelitis Osteogenesis imperfecta
Osteolytic form of syphilitic infection Diffuse rarefactions of bone
Benign tumours Senile osteoporosis
Enchondroma Parathyroid osteodystrophy
Osteoclastoma Rickets (infantile and celiac)
Malignant tumours Renal osteodystrophy
Osteosarcoma Nutritional osteomalacia
Ewing’s tumour Cushing syndrome
Metastastatic carcinoma and sarcoma Disseminated tumours
Miscellaneous Multiple myeloma
Simple bone cyst Diffuse metastatic carcinoma
Monostotic fibrous dysplasia Miscellaneous
Eosinophilic granuloma Paget disease
Tabes dorsalis Polyostotoic fibrous dysplasia
Post radiation brittle state Gaucher disease
Types of fracture
• The fractures are of two types (Fig. 39.5).
• Open or compound fracture (fracture site communicates with the exterior
of the body).
• Closed fracture (fracture site does not communicate with the exterior of the
body).
• Open fracture is liable to be contaminated by foreign body and or organisms
introduced from exterior, whereas closed fracture is free from this risk.
FIGURE 39.5 Types of fracture.
Note
Even when the wound is well away from the site of fracture, it should be
considered ‘open’ until proved otherwise.
Patterns of fracture
The patterns of fracture describe the shape of fracture (Fig. 39.6). They are:
• Transverse fracture (fracture line is horizontal to axis of bone)
• Oblique fracture (fracture line is oblique to axis of bone)
• Spiral fracture (fracture line is curved and oblique to axis of bone)
• Comminuted fracture (multiple fracture lines with more than two fragments)
• Compression or crush fracture (crushed bone fragments usually multiple and
devitalised)
• Greenstick fracture (crumpled fracture site, without an obvious crack or
displacement)
• Impacted fracture (fragments driven firmly together and interlocked without
any movement)
FIGURE 39.6 Types of fracture.
The pattern of fracture may indicate

• the nature of causative violence.
• Transverse fracture (angulation force)
• Oblique fracture (angulation force with pull of fragments by muscles
acting on them)
• Spiral fracture (twisting force)
• Comminuted fracture (heavy direct violence)
• Compression or crush fracture (heavy direct violence crushing the spongy
bone)
• Greenstick fracture (longitudinal compression force causes crumpling,
angulation force causing bend and break of one of the cortices of bone)
• Impacted fracture (strong pull of fragments by muscles acting on them)
Healing of fractures
Healing of a fracture starts as soon as the bone is broken, and if the conditions
are favourable, healing proceeds through a number of stages until the bone is
consolidated. However, the processes of healing vary considerably between the
tubular and cancellous bones.
Healing of cortical (tubular) bone fracture

The healing of tubular bone fracture is considered to pass through five stages
(Fig. 39.7). They are as follows:
1. Stage of hematoma: Blood seeps out of torn blood vessels to form a
haematoma between the fractured surfaces, which is limited by soft tissues
(periosteum and muscles), which by themselves get stripped to a varying
extent. A few millimetres of fractured segments become ischaemic due to
complete tear of capillaries which run longitudinally in the long bone.
2. Stage of periosteal and endosteal cellular proliferation: The cells from
deeper surface of periosteum proliferate, which are the precursors of
osteoblasts, which will later lay down the intercellular substance. There is
associated cellular activity within the medullary canal, due to proliferation of
cells from endosteum and marrow of each fragment. The tissues from both
fragments blend with each other.
3. Stage of callus: The cellular tissue matures to give rise to osteoblasts and
chondroblasts. The osteoblasts lay down an intercellular matrix of collagen
and polysaccharide, which is impregnated with calcium salts to form the
immature bone of callus or woven bone. The callus gives stability to the
fractured site and indicates healing (Fig. 39.7A).
4. Stage of consolidation: Osteoblasts soon transform the woven bone into more
mature bone with a typical lamellar structure.
5. Stage of remodelling: The medullary canal is blocked by the bulbous collar,
developed from the newly formed bone, indicating completeness of healing.
In the following months, the bone is gradually strengthened along the lines of
stress, but excess bone outside the lines of stress is slowly removed. This
remodelling process goes on constantly throughout life, but falls short of the
indistinguishability in adults, but in children, the repair is perfect that the site
of fracture becomes indistinguishable in radiographs.
FIGURE 39.7 Healing of tubular bone fracture.

FIGURE 39.7A-B X-ray—(A) callus formation, (B) malunion.
Healing of cancellous bone fracture

The structure of cancellous bone is different from that of the tubular bone. It has
uniform spongy texture and has no medullary canal, and there is much wider
area of contact between the fragments of a fractured bone, and union occurs
between the bony surfaces and not through the medium of external callus and
endosteal callus as in a tubular bone.
The stages of healing are:
1. Formation of haematoma
2. Stage of proliferation of osteogenic cells
3. Stage of consolidation
Rate of union
• The time taken for union of fracture varies considerably between individuals.
• Young children show faster union compared to older children and more so in
adults.
• Average time of complete union is 3 to 6 months.
• Large bones take more time for complete union than their smaller
counterparts.
Factors influencing union
• Age of the patient (younger the patient, union is faster).
• Type of bone (cancellous bone unites faster than the tubular bone).
• Blood supply (good blood supply favours faster union).
• Immobility (immobility favours faster union, with few exceptions like rib and
clavicle fractures).
• Infection (clean wounds heal faster).
• Interposition of soft tissues (interposed soft tissues hamper healing).
• Tumour at fracture site (tumour hampers healing).
• Fracture inside a joint (synovial fluid of the joint hampers healing due to
hindrance to granulation tissue).
• Calcium content (optimum calcium content favours good healing,
osteoporotic or fluorotic bones delay healing).
• Nutritional status (Vitamin D deficiency, hypoproteinemia, etc., delay
healing).
Complications of fractures
Although great majority of fractures heal as expected, complications are not
uncommon. The complications can be
• related to fractures themselves and
• related to injury to neighbouring structures.
Complications related to fractures themselves.
• Infection (common in compound fractures due to connection with exterior)
• Delayed union: union occurring after the expected period (see Table 39.3)
• Non-union: remaining ununited for ever (see Table 39.3)
• Avascular necrosis
• Mal-union (imperfect union due to imperfect position of fragments) (Fig.
39.7B)
• Shortening (due to overlap of fragments, loss of bone fragments, interference
with the growing epiphysis)
TABLE 39.3
Causes of Delayed Union or Nonunion
Infection of bone
Inadequate blood supply
Excessive movement between fragments
Loss of apposition of fragments
Interposition of soft tissue between fragments
Dissolution of haematoma by synovial fluid
Presence of corroding material near fracture site
Pathological fractures
Complications related to injuries to neighbouring structures

• Injury to major blood vessels (e.g., brachial artery injury in supracondylar
fracture of humerus).
• Traumatic aneurysm
• Impaired blood supply and gangrene
• Injury to nerves (e.g., ulnar nerve injury in medial epicondylar fracture of
humerus).
• Injury to tendons (e.g., rupture of extensor pollicis longus tendon in fracture
of lower end of radius).
• Injury to joints (e.g., fracture of head of radius extending into joint surface).
• Injury to viscera (e.g., bladder injury in pelvic fracture).
• Posttraumatic pathologies
• Intra-articular and peri-articular adhesions
• Posttraumatic ossification (e.g., myositis ossificans of fracture dislocation
of elbow)
• Sudeck’s osteodystrophy
• Osteoarthritis
• Fat embolism.
Joint injuries (detailed in appropriate chapters)

The joint injuries are classified as
• Dislocation or luxation denotes that the articular surfaces of the joint are
displaced wholly from one another, so that all apposition between them is
lost.
• Subluxation denotes that the articular surfaces are partly displaced but retain
some contact with one another. It can be
• Congenital (e.g., Developmental dysplasia of hip)
• Spontaneous (e.g., infectious pathologies)
• Traumatic (commonest, may be associated with fractures)
• Recurrent (e.g., patellofemoral subluxation)
• Strain is an incomplete rupture of a ligament. It may be acute or chronic.
• Contusion is a local inflammatory reaction involving the soft tissues around
the joint.
Acute septic osteomyelitis

• One of the important diseases of childhood; may also occur in adults.
• Common bones affected are tibia, femur and humerus.
• Caused by pyogenic organisms—usually the staphylococcus, less commonly
streptococcus and pneumococcus.
• Organisms reach the bone through
• blood from a septic focus elsewhere in the body or
• directly from an open wound.
• Metaphysis is involved first, pus is formed, finds its way out through ‘cloaca’
as subperiosteal abscess, then to soft tissues and skin.
• Blood supply is cut off by septic thrombosis, resulting in ischemic bone,
which separates from the living bone (sequestrum).
• New bone is laid beneath the stripped periosteum, forming an investing layer
(involucrum).
• Epiphyseal cartilage acts as a barrier preventing the spread of infection, but if
the metaphysis lies within the joint, the joint is liable to infection (acute
pyogenic arthritis)—e.g., upper metaphysis of humerus, all the metaphysis at
elbow, upper and lower metaphyses of femur).
Complications: Septicemia or pyemia, pyogenic arthritis, retardation of
growth, chronic osteomyelitis.
• Child feels ill.
• Pain over the affected bone.
• Not able to walk.
• History of recent boil or direct injury may be present.
• On examination, the child is pyrexic (high fever).
• Overlying skin is warm, soft tissues are indurated.
• Severe tenderness over the affected bone.
• Neighbouring joint may be swollen, fluctuant and immobile
(pseudoparalysis).
DD: Pyogenic arthritis, acute poliomyelitis, rheumatic fever, scurvy, syphilitic
metaphysitis, haemophilic arthritis in males).
• Leucocytosis (polymorphs), raised ESR.
• CRP is raised.
• Blood culture may grow the incriminating organism.
• X-rays are normal in the early stages, after 2–3 weeks, changes occur (diffuse
rarefaction and new bone outlining the periosteum). Oedema around the
muscle may be shown as a fine line called ‘Muscle sign’ indicating bone
infection.
• CT and MRI are useful in localizing abscesses.
• Tc99 Bone scan localizes infected areas.
Treatment
• General: rest in bed, systemic broad spectrum antibiotics.
• Local: if pus is suspected, it should be drained.
Chronic pyogenic osteomyelitis

• Nearly always follows acute osteomyelitis.
• Caused by staphylococcus, streptococci, pneumococci, typhoid organisms.
Complications: Pathological fracture, chronic nonhealing sinus, Brodie’s
abscess (an aborted infection in metaphyseal region), limb length discrepancy,
Amyloidosis, malignancy (rare).
• Purulent discharge (continuous or intermittent) from a sinus adherent to the
underlying bone.
• Pain in the affected area.
• ‘Flare up’—pain, fever and abscess is common.
• On examination,
• Limb appears swollen (Fig. 39.8).
• Scars and sinuses are seen on the limb (Fig. 39.8A).
• Bone is palpably thickened.
FIGURE 39.8 Chronic pyogenic osteomyelitis of right femur.
FIGURE 39.8A Chronic pyogenic osteomyelitis (sinus) with lengthening of
femur Source: (Courtesy Dr C.T. Alagappan).
• X-rays show thickening of bone, irregular and patchy sclerosis. Sequestrum
appears as a dense loose fragment, with irregular but sharply demarcated
edges, lying within a cavity in the bone (Fig. 39.8B).
• Isotope scan (Fig. 39.8C) can localize the lesion.
• Sinogram (Fig. 39.8D) is useful defining the abscess cavity and sequestrum.
FIGURE 39.8B X-ray—chronic osteomyelitis of femur.

FIGURE 39.8C-D (C) Isotope scan—chronic osteomyelitis of upper end of
left tibia (right), (D) Sinogram—chronic suppurative osteomyelitis.
Treatment
• Rest and antibiotics will help acute flare ups.
• Drainage of abscess.
• Sequestrectomy for sequestrum.
• Deroofing of Brodie’s abscess.
• Saucerization
Tuberculous osteomyelitis
• Caused by Mycobacterium tuberculosis.
• Uncommon except in the vertebral bodies and joints.
• Isolated lesion in a bone is rare.
• Common in immunocompromised patients (e.g., AIDS).
• Tubercle bacilli reach the bone through blood, adjacent focus in joint or soft
tissue.
• Tuberculous abscess (cold abscess) is commonly formed.
• May burst outside to form sinuses, may be multiple in number.
• Tuberculous dactalitis in phalanges may mimic a tumour.
• Pathological fractures are common.
• Constitutional symptoms.
• Pain and swelling at the affected area.
• On examination,
• Bone may be thickened, tenderness may not be prominent.
• Sinus may discharge watery fluid containing sandy granules.
• X-rays show typical findings (Fig. 39.9).
• Diffuse rarefaction around the site of infection.
• Erosion of bone without sclerosis.
• Soft tissue shadow suggesting a cold abscess.
• Sequestrum may be seen.
FIGURE 39.9 X-ray—tuberculous osteomyelitis of ulna.
Treatment
• General: adequate rest, good diet.
• Local: drainage or aspiration of pus.
• Surgery: for pathological fractures and complications.
• Systemic antitubercular chemotherapy is mandatory.
Syphilitic osteomyelitis
• Rare
• Two forms are recognized:
• Syphilitic metaphysitis of infants
• Osteo-periostitis of children and adults
• Syphilitic metaphysitis of infants: Severe local pain, inability to use the limb.
On examination, the metaphyseal region is thickened and tender.
• Osteo-periostitis of children and adults: Deep boring pain, more at nights,
and swelling. On examination, a swelling (localized or diffuse) is felt on the
bone.
• Wassermann reaction is positive.
• X-rays show
• Syphilitic metaphysitis of infant: Sclerosis of metaphysis adjacent to
epiphyseal cartilage.
• Osteo-periostitis of children and adults: Widespread subperiosteal new
bone, localized area of bone destruction, diffuse sclerotic thickening of the
overlying cortex.
Treatment
Intense anti-syphilitic treatment.
Osteoma
• Most common benign tumour of bone.
• More common in males.
• More common in second decade of life.
• Can affect any long (proximal femur) or flat bone (skull).
• There are two types:
• Ivory osteoma (hard compact bone)
• Cancellous osteoma (spongy bone)
• Gardner syndrome (autosomal dominant disease): Polyostotic osteoma,
colonic polyposis, soft tissue fibromas.
• Dull aching pain.
• Smooth rounded bony prominence on the surface of a long bone or a flat
bone.
X-rays: a mass of dense bone of varying size protruding from the outer surface
with extensive reactive sclerosis.
Treatment
• No treatment is necessary, in general.
• Excision may be done for unsightly swellings.
Chondroma
• Tumour arising from the cartilaginous component of bone
• There are two forms. They are:
• Ecchondroma (tumour growing outwards from the bone): common in flat
bones like scapula or ilium.
• Enchondroma (tumour growing within the bone): common in bones of
hands and feet.
• Chondromata of long bones occur in dyschondroplasia (multiple
chondromatosis or Ollier disease).
• Malignant change is not uncommon, usually of the major bones.
DD: Chondrosarcoma, fibrous dysplasia, chondroblastoma, giant cell tumour.
• Ecchondroma: hard swelling on the affected bone.
• Enchondroma: expansion of affected bone (Fig. 39.10).
FIGURE 39.10 Enchondroma middle finger.
X-rays are diagnostic.
• Centrally or eccentrically placed medullary osteolytic tumour.
• Stippled or punctate matrix calcification is seen throughout the lesion in 50%
of cases.
• Ecchondroma: bony outgrowth from the bone (Fig. 39.11).
• Enchondroma: lesion inside the bone expanding the cortex.
FIGURE 39.11 X-ray—chondroma of humerus.
Treatment
• No treatment is necessary, in general.
• Excision may be done for unsightly swellings.
• Follow up is required for patients with Ollier disease for fear of malignancy.
Osteochondroma
• The commonest benign tumour of bone.
• Arises from the growing epiphyseal cartilage plate, but gets left behind at the
centre as the bone grows.
• Grows outwards like a mushroom, and it is capped by a cartilage.
• Usually single.
• Multiple in diaphyseal aclasis (multiple exostoses).
• May affect several bones at a time.
• Malignant change is more common in multiple familial exostoses (15%).
• A circumscribed hard swelling near a joint (Fig. 39.12A).
• Retarded growth and dwarfism are seen in diaphyseal aclasis.

FIGURE 39.12A-B (A) Exostosis of humerus, (B) X-ray—exostosis
humerus.
X-rays show pedunculated or sessile bony tumour (Fig. 39.12B). The capping
cartilage is not seen.
Treatment
Excision when required. Surgical margin should include the entire cartilaginous
cap to prevent malignant change.
Giant cell tumour (osteoclastoma)

• Potentially malignant tumour.
• Behaves like a malignant tumour by recurrence and metastasizing through
blood.
• Common in young adults (third decade).
• Common sites are: lower end of femur, upper end of tibia, lower end of
radius, upper end of humerus.
• Originates at the metaphyseal region, extends into epiphyseal cartilage and
reach the joint surface, destroying the bone and expands eccentrically.
• Histologically, the tumour consists of abundant oval or spindle shaped cells
interspersed with giant cells containing as many as 50 nuclei (hence called
giant cell tumour).
• Pathological fracture is common.
• Pain at the site of swelling.
• Gradually increasing local swelling (Fig. 39.13).
• Pathological fracture can be the first presentation.
• Examination reveals a bony swelling which may be tender on firm palpation
and gives the feel of ‘eggshell crackling’.
FIGURE 39.13 Osteoclastoma radius.
• X-rays show (Fig. 39.13A and B) destruction of bony substance, with
expansion of cortex (soap-bubble appearance).
• CT is diagnostic (Fig. 39.14A and B).
FIGURE 39.13A X-ray—osteoclastoma of lower end of radius.
FIGURE 39.13B X-ray—osteoclastoma of calcaneum.
FIGURE 39.14A CT—osteoclastoma of lower end of femur.
FIGURE 39.14B CT—osteoclastoma of calcaneum.
Treatment
• Excision of the part or entire bone if it can be dispensed with (e.g., clavicle,
scapula, fibula).
• Curettage with packing with bone grafts or bone cement, for bone which
cannot be sacrificed, but recurrence is a possibility.
• Excision of entire bone is necessary for recurrent tumour. Reconstruction is
done with auto/allograft or custom prosthesis.
• Radiotherapy and or chemotherapy may be useful in some instances.
Osteosarcoma
• Primary malignancy of bone.
• Most common malignant tumour of bone.
• 20% of all primary malignancies of bone.
• Arises from primitive bone forming cells.
• Predominantly a tumour of childhood and early adulthood.
• Genetic factors suggested.
• In later life, it is a complication of Paget disease.
• Common sites are:
• Lower end of femur (30%)
• Upper end of tibia (15%)
• Upper end of humerus (10%)
• Macroscopically, it originates in the metaphysis (seldom crosses the physeal
cartilage into the epiphysis), grows by expanding the cortex and raises the
periosteum at its edges and also along the medulla. Areas of haemorrhage
and necrosis are seen within the tumour
• Microscopically, there are two components:
• A background stroma of spindle-shaped sarcomatous cells containing a
matrix (myxoid, cartilaginous and osteoid tumour).
• Multinucleate giant cells.
• Local spread within the bone, typically the medullary cavity, eventually
infiltrates the soft tissues.
• Blood to lungs and other bones.
• Lymph is not predominant.
Symptoms
• Local pain.
• Gradually increasing swelling.
• Severe pain followed by swelling.
Signs
• A swelling near the end of a bone, close to the joint (Fig. 39.15).
• The skin over the swelling is warm, dilated veins may be seen.
• The swelling is diffuse as firm thickening and highly vascular.
FIGURE 39.15 Osteosarcoma ulna Source: (Courtesy Dr R. Rajaraman).
DD: Osteomyelitis, other bone tumours.
• X-rays show (Fig. 39.16) irregular destruction of the metaphysis, evidence of
new bone formation under the corners of the raised periosteum (Codman’s
triangle). Occasionally, the new bone formation is seen as radiating spicules
within the bone (sun-ray appearance).
• CT and MRI are useful to determine the extent and treatment planning.
• Chest X-ray may show lung secondaries.
• Isotope bone scan is useful to identify bone secondaries.
FIGURE 39.16 X-ray—osteogenic sarcoma of upper end of humerus.
Treatment
• Preoperative chemotherapy (methotrexate, doxorubicin, cisplatin and
ifosfamide).
• Limb sparing surgery with wide resection and reconstruction with
prosthesis, for extremity osteosarcoma.
Palliative
• Local irradiation for painful tumours.
• Chemotherapy for metastatic disease.
• Amputation if limb salvage is not possible.
Chondrosarcoma
• Malignant tumour derived from cartilage cells.
• Low-grade tumour.
• More common in men.
• Common in middle age.
• Pelvis and femur are most common locations.
• Extremely rare in small bones.
• There are two types:
• Central chondrosarcoma (develops in the inside of bone—femur, tibia and
humerus, may arise denovo or as malignant change of chondroma)
• Peripheral chondrosarcoma (develops on the surface of bone—
innominate, scapula, sacrum, usually as malignant change of
osteochondroma)
• Grows slowly and metastasize late even after 15 years.
• Prognosis is very good.
Pain and local swelling (Fig. 39.17).
FIGURE 39.17 Chondrosarcoma of left humerus.
X-rays show
• Central chondrosaroma is seen to grow inside the bone and may burst
through the cortex (Fig. 39.17A).
• Peripheral chondrosarcoma is seen as a soft tissue shadow growing outwards
from the surface of the bone with speckled calcification.
• CT (Fig. 39.17B) and angiography (Fig. 39.17C) and biopsy are diagnostic.
FIGURE 39.17A X-ray—chondrosarcoma of humerus.
FIGURE 39.17B CT—chondrosarcoma of humerus.
FIGURE 39.17C Angiogram—chondrosarcoma of humerus.
Treatment
• Radical excision.
• Radiotherapy for inoperable tumours.
Fibrosarcoma of bone
• Uncommon malignancy.
• Tumour arising from fibroblastic connective tissue.
• Common in fourth decade.
• Common sites are distal femur and proximal tibia.
Pain and swelling at the site of tumour.
• X-rays show destruction of bone.
Treatment
• Wide local excision is sufficient for low-grade malignancy.
• Amputation is advised for high-grade malignancy.
Ewing’s tumour
• Uncommon but highly malignant sarcoma arising in the bone marrow.
• Believed to be representing an undifferentiated member of neural tumours
distinct from neuroblastoma.
• Genetic factor—reciprocal translocation in chromosomes 11 and 22.
• Common between 5 and 25 years.
• Males are more affected and have a worse prognosis.
• Commonest in the shaft of femur, tibia or humerus.
• Macroscopically, it is soft and vascular and arises in the diaphysis and grows
subperiosteally.
• Microscopically, it is composed of sheets of small round cells which are rich
in glycogen.
• local growth to considerable size;
• blood to lungs or
• lymph is not predominant.
Symptoms
• Local pain and fever.
Signs
• A diffuse or fusiform swelling (Fig. 39.18), the skin over it is warm and the
swelling firm to feel.
FIGURE 39.18 Ewing’s sarcoma of scapula Source: (Courtesy Dr R.

Rajaraman).
• X-rays show destruction of bone substance and concentric layers of
subperiosteal new bone (onion-peel appearance), bone forming along the
periosteal vessels which run perpendicularly between the cortex and elevated
periosteum (hair-on-end appearance) (Fig. 39.19).
• CT and MRI are useful in getting details of tumour.
• Isotope scan (Fig. 39.20) is contributory.

FIGURE 39.19 Ewing’s tumour tibia.
FIGURE 39.20 Isotope scan—Ewing’s sarcoma of left tibia.
Treatment
Curative
• Multidrug chemotherapy.
• Radiotherapy (after 2–3 months of chemotherapy).
• Surgery is reserved for tumours of fibula or rib.
• Resection of lung metastases, if possible improves survival.
Multiple myeloma
• Tumour of bone marrow.
• Affects adults past middle age.
• Affects axial skeleton (spine, pelvis) more than extremities.
• Probably arises from plasma cells.
• Disseminates easily through blood.
• Bone is simply replaced by tumour tissue.
• Pain at tumour site.
• On examination, the patient is anaemic and pale.
• Local tenderness over the affected bones.
• X-rays show multiple small areas of transradiance, with rarefaction (Fig.
39.21A–D).
• ESR is raised.
• Bence Jones protein is present in urine.
• Serum globulin is increased reversing the A G ratio.
• Bone marrow biopsy is confirmatory.
FIGURE 39.21A X-ray skull—multiple myeloma.
FIGURE 39.21B X-ray pelvis—multiple myeloma.
FIGURE 39.21C X-ray—multiple myeloma with pathological fracture.
FIGURE 39.21D X-ray spine—multiple myeloma with compression
fracture of vertebra.
Treatment
• Chemoradiation
• Stem cell therapy is the recent advance.
Metastatic tumours
• Secondary malignant tumours are more common than primary tumours in
bone.
• Metastatic tumours are more common in old age.
• The tumours, which metastasize to bone are lung, breast, prostate, thyroid and
kidney.
• Metastases occur most commonly in parts of skeleton that contain bone
marrow (e.g., vertebral bodies, ribs, pelvis and upper ends of femur and
humerus).
• Pain is the main symptom.
• Disability occurs due to pathological fracture.
• X-ray shows circumscribed area of translucency, without any reaction in
surrounding bone (Fig. 39.22A) (in spine, the intervertebral disc is not
involved).
• Isotope bone scan (Fig. 39.22B) is diagnostic.
FIGURE 39.22A X-ray—multiple metastases right humerus.
FIGURE 39.22B Isotope scan—multiple bone metastases.
Treatment
• Radiotherapy is the treatment of choice.
• Radioiodine is useful for metastasis due to thyroid malignancies.
• Hormone therapy is useful for metastasis due to breast and prostate
malignancies.
• Local splinting and internal fixation are useful for pathological fractures.
Infantile scurvy
• A haemorrhagic disease caused by deficiency of Vitamin C.
• Affects infants.
• Lack of osteoblastic activity in epiphyseal growth cartilage.
• Haemorrhage, at the epiphyseal cartilage extends beneath the periosteum,
which may be raised from the bone.
• Haemorrhage may occur from the gums or within the orbit.
• Pain the limb causes difficulty in movement (pseudoparalysis).
• On examination,
• The limb is swollen and tender.
• The gums are spongy and bleed.
• X-rays show dense line at the junction between epiphyseal cartilage and
metaphysis, with clear band of rarefaction on the diaphyseal side.
Subperiosteal haematoma may be seen.
• Investigations to rule out bleeding disorders in children.
Treatment
Administration of vitamin C is curative.
Rickets
• Usually a disease of children, less than a year old.
• Caused by disturbed calcium—phosphorus metabolism.
• Caused by deficiency of Vitamin D in diet and inadequate exposure to
sunlight, which is necessary for synthesis of Vitamin D in the body.
• Deficiency of Vitamin D leads to inadequate absorption of calcium and
phosphorus.
• To maintain the blood levels of calcium, bone calcium moves into the blood.
• Lack of calcium deposit causes proliferating osteoid tissue in the growing
epiphysis to remain uncalcified, resulting in general softening of bones
already formed.
• The child’s general health is impaired.
• The child has a large head, retarded skeletal growth, enlarged epiphyses and
curved long bones with deformity of chest.
X-rays (Fig. 39.23A–C) show a general loss of density of bones, with marked
loss in the epiphyses. The vertical length of physes are increased and also
widened, and the ends of shafts are hollowed out or cupped. Bending of bones is
prominent.

FIGURE 39.23A X-ray hand—rickets.
FIGURE 39.23B X-ray chest—rickets ribs.
FIGURE 39.23C X-ray legs—rickets.
Treatment
• Administration of Vitamin D is curative.
• Surgery (osteotomy) may be needed for severe bony deformities.
Osteomalacia
• Adult counterpart of rickets.
• Common in elderly females.
• Dietary deficiency and inadequate absorption of Vitamin D lead to resorption
of calcium from bones.
• Intake of drugs (prolonged used of anticonvulsants).
• In the bones, osteoid tissue is poorly calcified with abundant fibroid tissue in
the marrow.
DD: Fanconi syndrome, renal rickets, celiac rickets.
• Pain in the bones and deformity.
• X-rays (Fig. 39.24) show rarefaction of whole skeleton. The bony cortices are
thin. The bones are curved. Multiple spontaneous fractures (Looser’s zones)
may be seen in ribs, pubic rami and other parts of skeleton.
• Serum calcium is normal or low.
• Serum alkaline phosphatase is increased.
FIGURE 39.24 X-ray—osteomalacia.
Treatment
• Administration of calcium and Vitamin D is curative.
• Surgery (osteotomy) may be needed for severe bony deformities.
Granulomatosis
• Uncommon disorders of reticuloendothelial system.
• Deposits of granulomatous tissue occur in the bones or elsewhere.
• Common in children and young adults.
• They are of two types:
• Lipoid granulomatoses
- Gaucher disease: Inborn error of lipoid metabolism.
• Nonlipoid granulomatoses
- Eosinophilic granuloma: Solitary lesion
- Hand–Schuller–Christian disease: Multiple lesions, progresses slowly
and fatal eventually.
- Letterer Siwe disease: A condition where histiocytes proliferate in the
body. Most serious form (sometimes classified as a form of Langerhans
cell histiocytosis or a disseminated form of histiocytosis X), progresses
rapidly and fatal eventually, involves lymph nodes also.
• Gaucher disease: Hepatosplenomegaly
• Eosinophilic granuloma: Usually asymptomatic, bone pain and pathological
fracture are known.
• Hand–Schuller–Christian disease: Retarded growth, diabetes insipidus and
exophthalmos.
• Letterer Siwe disease: Lymphadenopathy, hepatosplenomegaly and
seborrhoea-like lesions on the skin.
• Gaucher disease
• Sternal puncture: Gaucher cells can be demonstrated.
• X-ray: Irregular cyst-like spaces in bones.
• Eosinophilic granuloma
• Eosinophilia
• X-ray: Punched out bone (usually a rib, skull bone, pelvic bone, vertebra,
femur or humerus).
• Hand–Schuller–Christian disease: Resembles bone cysts in X-ray.
• Letterer Siwe disease: Resembles bone cysts in X-ray.
Treatment
• Gaucher disease: Splenectomy relieves local discomfort but is not curative.
Radiotherapy may be useful to regress the lesions.
• Eosinophilic granuloma: Lesions heal spontaneously. Surgical curettage is
useful.
• Hand–Schuller–Christian disease: Radiotherapy may be helpful.
• Letterer Siwe disease: No effective treatment is available, 50% die in spite of
treatment.
Parathyroid osteodystrophy
(hyperparathyroidism)
• Common in adults.
• Caused by excessive secretion of parathormone, usually from parathyroid
adenoma.
• Parathormone affects calcium metabolism, causes resorption of bones, draws
calcium into blood (hyperkalaemia) with reduced renal clearance of calcium.
• The bone loses it density, becomes spongy and cortices become thin.
• Cystic changes develop in the long bones (Osteitis fibrosa cystica) - Von
Recklinghausen Disease of Bone.
• Pathological fractures are common.
• Hyperkalaemia causes renal stones.
• Lassitude, dyspepsia and bone pain.
• Deformities may be seen due to bending of bones.
• Brown tumours seen in the end of long bones (lower femur common).
• X-rays of
• long bones (Fig. 39.25A and B) and vertebrae show rarefaction of entire
skeleton. Early lesion is cortical erosion of phalanges of fingers.
• skull shows uniform fine granular mottling, with some cystic areas.
• KUB may show renal stones.
• Scintigraphy (using Technetium Tc99m Sestamibi) (Fig. 39.25B) is useful for
localizing the parathyroid adenoma.
• US of neck to localize parathyroid adenoma.
FIGURE 39.25A X-ray—parathyroid bone lesion.

FIGURE 39.25B Isotope scan—parathyroid adenoma.
Treatment
• Parathyroid adenoma should be searched for and removed.
• Pathological fracture may be surgically stabilized in long bones.
Hyperpituitarism
• Caused by excess of pituitary hormone ‘growth hormone’.
• Usually due to hyperactivity of anterior pituitary adenoma.
• Excessive growth is seen in the epiphyseal cartilages.
• Despite this overactivity, epiphyseal fusion occurs at the normal time.
• Patient grows to a height of seven feet or more (Gigantism).
• Increase in height is due to length in limb increase.
• Hands and feet show enlargement.
• Sexual development and mental status are impaired.
X-rays show marked enlargement of hands and feet, and mandible. Vertebral
bodies are also enlarged, especially in the antero-posterior plane.
Treatment
Excision of pituitary adenoma is curative, but changes are not reversible.
Polyosteotic fibrous dysplasia

• Parts of several bones are replaced by fibrous tissue, without any evidence of
hyperparathyroidism.
• Cause is unknown.
• More than one bone is affected at a time.
• Commonest is the femur.
• Skull bone is also commonly affected.
• Affected bones bend and break easily (pathological fractures).
• Can be a part of Albright syndrome (skin pigmentation and sexual precocity
in females).
• Deformity is prominent due to enlargement and bending (Fig. 39.26A).

FIGURE 39.26A-B (A) Fibrous dysplasia, (B) X-ray—fibrous dysplasia.
X-rays (Fig. 39.26B) show well-defined transradiant areas, which have a
characteristic ‘groundglass’ appearance. Advanced lesions show ‘honeycomb’
appearance.
Treatment
• Curettage and bone grafting for painful lesions, but recurrence rates are high.
• Corrective osteotomy for deformities.
Osteitis deformans (paget disease)

• A slowly progressive disorder of one or many bones.
• Common after the age of 40.
• Common bones affected: pelvis, vertebrae, femur, tibia and skull.
• Affected bones lose the normal compact density and becomes spongy, and are
liable to bend.
• At the same time, new bone formation takes place and bones are thickened.
• The marrow spaces are filled with fibrous tissue.
• Pathological fractures may occur.
• Rarely, osteosarcoma can develop.
• Thickening and deformity are the presentations.
• Thickening of skull is obvious for the patient.
• Bending of tibia is noticeable.
• X-rays (Fig. 39.27A) show thickening of bone due to widening of cortex,
diminished density of cortex giving a spongy or honeycombed texture,
marked coarsening of trabeculae and in later stages, general increase in
density of affected bones.
• Isotope scan (Fig. 39.27B and C).shows increased uptake due to increased
vascularity.
FIGURE 39.27A X-ray—Paget’s disease with pathological fracture of tibia.

FIGURE 39.27B-C Isotope scan—(B) increased bone density of Paget
disease; (C) increased uptake with bending deformities of lower limbs.
Treatment
• Usually symptomatic.
• Bisphosphonates and calcitonin injections are effective In symptomatic
patients.
Senile osteoporosis
• Affects older age, above 60.
• Generalized reduced density of bones.
• May have endocrine aetiology.
• Pathological fractures are known to occur.
• Upper thoracic vertebrae tend to collapse resulting in kyphosis.
DD: Osteoporosis due to parathyroid diseases, Cushing syndrome,
carcinomatosis, multiple myeloma or leukaemia.
• Back pain.
• Kyphosis may be predominant.
• X-rays show (Fig. 39.28) reduced density of vertebral bodies and wedging of
one or more of vertebral bodies. Loss of bone trabeculae in the metaphysis is
characteristic.
• Bone densitometry may show reduced bone density.
FIGURE 39.28 X-ray—senile osteoporosis.
Treatment
• Regular exercises like walking.
• Calcium supplements.
• Analgesics for back pain.
Osteochondritis juvenilis
• A bony centre becomes temporarily softened.
• Deformation occurs due to pressure.
• Common sites are:
• ring epiphyses of vertebral bodies (Scheuermann disease);
• upper epiphysis of femur (Perthe disease) and
• nucleus of navicular bone (Kohler disease)
Complication: osteoarthritis.
• Local pain
• Painful joint movements
X-rays taken serially can assess the changes (patchy increase in density of bony
nucleus → fragmentation and increased density → return to normal bone texture.
Treatment
• Prevention of weight bearing by bed rest in early cases.
• Corrective surgery in late cases.
Solitary bone cyst

• Affects mostly the long bones of children and adolescents.
• Commonly the proximal end of humerus.
• Occasionally in the scaphoid and lunate.
• Starts as a spherical lesion, and enlarges in the long axis of bone expanding
the cortex.
• Cyst contains clear fluid.
• Pain develops if pathological fracture occurs.
• X-ray will show (Fig. 39.29) circumscribed area of transradiance without
surrounding zone of sclerosis. The cyst may appear loculated and the cortex
may be distended or fractured
• CT is diagnostic.
FIGURE 39.29 X-ray—solitary bone cyst second metatarsal.
DD: Bone abscess, eosinophilic granuloma, localized fibrous dysplasia,

tumour.
Treatment
• Aspiration and hydrocortisone injection is required for small cysts.
• Curettage and packing with bone chips is suggested for large cysts and
recurrent cysts.
• Internal fixation may be an added procedure to the above in some cases.
Localized fibrous dysplasia

A solitary area of bone is partly replaced by fibrous tissue, in which scanty bone
trabeculae may persist.
• Long bones are affected.
• Pathological fracture is not uncommon.
• Local pain in the affected bone.
X-ray shows a clear zone of transradiance within the bone.
Treatment
Curettage of affected bone and replacement with bone graft.
Osteoid osteoma
• A benign circumscribed lesion of bone.
• Aetiology is unknown.
• Deep boring pain, worst at night, relieved by aspirin.
• On examination, thickening and local tenderness at the affected site.
• X-ray (Fig. 39.30A) shows a central nidus of bone tissue surrounded by dense
sclerosis.
• CT (Fig. 39.30B) is diagnostic.
FIGURE 39.30A X-ray—osteid osteoma.

FIGURE 39.30B CT—osteoid osteoma.
Treatment
Excision of nidus with a margin of surrounding bone.
39.3 Symptoms of pathologies of bones

• Pain
• Swelling
• Deformity
• Limitation of movements
• Loss of function
• Shortening and lengthening of part of limb
Pain
The threshold of pain varies in individuals. It is a very subjective, and of varying
descriptions.
• Mild
• Boring
• Dull
• Throbbing
• Vague
• Severe
Pain caused by fracture is severe and is aggravated by movements, and pain of
neuropathic pathology is disproportionate to the lesion.
Swelling
Swellings caused by bone pathologies vary in shape.
• Globular (e.g., head of femur in posterior dislocation of hip)
• Fusiform (e.g., osteosarcoma of lower femur)
• Irregular (e.g., osteochondroma, chondosarcoma)
Deformity
Deformities of bony pathologies result due to
• diseases (e.g., tumours);
• fractures(e.g., displaced and malunited fractures) and
• peripheral nerve injuries (e.g., clawing of hand).
Limitation of movements
The long bones take part in the movements of the adjacent joints, hence bony
pathologies may can limitation of movements of the joint. If the fracture
involved the articular surface, it limits the movements due to pain, and in later
life due to osteoarthritis. The muscles attached to the bones go into severe spasm
and limit the movements of the joint further.
Loss of function
Loss of function becomes evident when there are:
• Deformities
• Muscle spasm
• Shortening or lengthening of limb
• Paralysis of muscles due to peripheral nerve injuries or nerve root
compression.
Shortening and lengthening of part of limb

The limb may get
• shortened (e.g., displaced fractures, malunited displaced fractures—
trochanteric fracture) and
• lengthening (e.g., congenital, epiphyseal acceleration of growth in
metaphyseal region).
Eliciting history
• Onset of pain:When did the pain start, was it slow in onset or sudden?
This question will answer the duration of pain, and its mode of onset (e.g.,
acute onset pains are generally due to trauma and insidious onset pain are
usually due to inflammatory pathology/tumours)
• Relationship to trauma: Is this pain preceded by a direct injury, an accident,
or sport or a fall?
This will answer the act following which the pain has appeared, and
description of the fall or accident will indicate the severity of injury (e.g.,
small slips may cause soft tissue injuries, and fall during active sports or road
traffic accidents may cause fractures). Fracture pain is severe and starts
almost instantly, whereas soft tissue injury pain starts late. Sometimes,
trauma draws the attention of the patient towards the tumour pathology.
• Relationship of pain and swelling: Did the patient notice pain first or
swelling first?
Pain is experienced for a brief period at the site of osteosarcoma, and
swelling develops later
• Position during the fall: What was the position of the limb or body during
the time of injury?
Fall on outstretched hand may result in Colles’s fracture or fracture of
scaphoid (indirect injury), and fall on the point of wrist may result in Smith’s
fracture (direct injury). Fall on the back may produce injury to spine, and on
the side may lead to trochanteric fracture. Severe muscular contraction is an
important factor producing (indirect) injury to the bone (e.g., convulsions—
avulsion fracture of patella and dislocation of shoulder, violent cough—
fracture of vertebra, rib).
• Intensity of pain: How bad is this pain?
Pain is of various natures (e.g., dull pain in tumours).
• Relationship to movements: Is this pain related to movements?
Pain related to movements with the preceding history of trauma may indicate
fractures, and nontraumatic situations, may indicate arthritis. Pain while
rolling in bed is characteristic of sacro-iliac arthritis.
• Treatment: Was any treatment or first aid given to this pain?
This will answer about the first aid or hospital admissions (e.g., aspirations
of joints) and the radiographs have to be scrutinized if available. Recurrences
have to be thought of, when a disease reappears after treatment (e.g.,
recurrent giant cell tumour, infection).

Association of high-grade fever may indicate infective pathology like
pyogenic arthritis, and low-grade prolonged fever may indicate lesions like
tuberculous arthritis, Ewing’s sarcoma.
malignancies.
give a clearer picture of diagnosis (e.g., tuberculosis/tumour).
treatment?
Diseases like tuberculosis and haemophilia can occur in families and the
positive history may be a good indicator for the present diagnosis.
Pre-requisites
• Patient should be undressed so that the limb to be examined is exposed well.
Undressing
What to watch during undressing:
• How clumsy is he in his movements (e.g., nerve injuries causing motor
paralysis of small muscles of hand).
• How protective is he during the act (e.g., denotes pain).
The examination should follow the standard pattern of look, feel, move,
strain and investigate.
The examination should be done from close quarters and also from at a
distance.
• Position of patient: Sitting or standing with both upper limbs side by side (for
upper limb pathology).
• Position of examiner: The examiner should view the limbs from all sides,
from the front, back, and sides.
Inspection
What to look for?
• Attitude of the patient (e.g., patients with fracture dislocation, are seen
supporting the limb with the other hand).
• Change in contour of the limb (e.g., tumours change the contour).
• Deformities (e.g., Dinner fork deformity in Colles’s fracture, Spade deformity
in Smith’s fracture, Ulnar drift in rheumatoid hand).
• Skin—shiny skin (e.g., tumours stretch the overlying skin), ecchymosis (e.g.,
direct injury).
• Abnormal swellings (e.g., ganglion, rheumatoid nodule, hematoma, tumours).
• Wasting of muscles, nails and pulps of fingers.
• Vascularity.
Palpation
Palpation of the painful area (described by the patient) is done last.
Swellings are examined as described in Ch. 9.
Bones
• Temperature—Felt with the back of the hand (e.g., acute osteomyelitis).
• Thickening—Malunited fractures, involucrum in bone infections.
• Irregularity and crepitus—Crackling sensation is felt in fractures and in
tenosynovitis.
• Tenderness—Tenderness is elicited in fractures and infective conditions.
• Abnormal movements or deformity—Ununited fractures.
Bones and bony points
• Examination of the bones and bony points are detailed in appropriate chapters
(Chs 40–42 and 44–46 ).
Soft tissue swellings
• The swellings should be examined in lines with the examination of the
swellings in general (Ch. 9).
Sinus
• A sinus should be examined in line with the examination of any sinus (see Ch.
11).
Note
Sinus adherent to the underlying bone is suggestive of osteomyelitis below the
sinus.
Joints
• The joint lines, movements and the laxity of joints are examined as detailed in
appropriate chapters.
Muscles and Tendons
• The methods of examination of muscles and their actions on the bones are
detailed in appropriate chapters.
Nerves
Tests of sensory and motor functions of the nerves are detailed in Chapter 49.
Circulation
Warmth, colour, capillary return and cutaneous sensibility should be
determined as detailed in Chapter 13.
Movements
• The movements of the adjacent joints should be evaluated, as the lesions
nearer the joint can affect them.
Note
If the patient can by himself reproduce the pain (e.g., subluxation of shoulder)
or sounds (e.g., clicks and crackling due to loose bodies in knee joint) by
performing certain movements, it should be noted carefully.
Measurements
• Measurements of bones and the joints is mandatory and the methods of
determination are detailed in appropriate chapters.
Lymphatic system
Examination of the regional lymph nodes and all other groups is essential (e.g.,
tuberculosis, malignancies).
General
General survey of other parts of the body, should be undertaken, as the local
symptoms may be only one manifestation of a widespread disease (e.g.,
malignancy with pathological fractures).
CHAPTER 40
Shoulder and arm

V. Thulasiraman
CHAPTER OUTLINE
40.1. Shoulder joint 737
• Anatomy 737
• Movements 738
40.2. Traumatic lesions (fractures) 740
• Fractures of the shoulder girdle 740
• Fractures of clavicle 740
• Fractures of scapula 740
• Fractures of upper end of humerus 740
40.3. Nonfracture lesions of shoulder joint 741
• Acromioclavicular disorders 741
• Strain, subluxation and dislocation 741
• Acromioclavicular osteoarthritis 742
• Subacromial disorders 742
• Impingement syndrome 742
• Rotator cuff injuries 743
• Calcific supraspinatus tendinitis 743
• Frozen shoulder (periarthritis) 743
• Glenohumeral disorders 744
• Acute dislocations 744
• Recurrent anterior dislocation 744
• Osteoarthritis 745
40.4. Nontraumatic lesions of shoulder joint 745
• Pyogenic arthritis 745
• Tuberculous arthritis 746
• Villonodular synovitis 746
40.5. Fracture shaft of humerus 746
40.6. Symptoms of shoulder joint pathologies 747
• Shoulder and arm 748
• General 753
40.1 Shoulder joint
Anatomy
Shoulder joint is formed by the glenoid cavity of the scapula and the head of the
humerus. The shoulder girdle comprises the clavicle and scapula on each side.
The disproportionate sizes of the head of the humerus and the small, shallow
glenoid cavity (glenohumeral joint), combined with a lax articular capsule give
this joint a wide range of movements but make the joint inherently unstable. This
instability is overcome by the surrounding strong muscles and is attached to the
capsule, but displacement of the humeral head occurs at the lower part of the
capsule, which is inadequately supported by the long head of triceps. Long head
of biceps originates from supraglenoid tubercle and passes through the bicipital
groove and straps the humerus firmly to the glenoid cavity.
FIGURE 40.2 (A) Flexion. (B) Extension. (C) Adduction. (D) Abduction. (E)
Internal rotation. (F) External rotation. (G) Internal rotation in abduction. (H)
External rotation in abduction. (I) Circumduction.
Articular capsule (outer fibrous membrane and inner synovial membrane) is

attached to the margin of the glenoid cavity and to the anatomical neck of the
humerus mostly, with a redundant fold, and the axillary nerve lies close to it.
Subscapular and infraspinatus bursae are extensions of synovial membrane,
through the rents in the fibrous capsule. Coracohumeral ligament and three
glenohumeral ligaments (superior, middle and inferior) as thickened parts of the
capsule give additional strength to the joint (Fig. 40.1).
FIGURE 40.1 Anatomy of shoulder joint.
Related joints:
• The outer end of the clavicle is attached to the coracoid process of the scapula
by coracoclavicular ligament (conoid and trapezoid parts) which helps in
suspending and stabilizing the arm, and to the acromion process of the
scapula by coracoacromial ligament and forms the acromioclavicular joint.
The subacromial bursa protects the humeral head from impingement against
the acromial process and liable to undergo degenerative inflammation.
• Medial end of the clavicle is attached to the sternum by sternoclavicular joint
—the only articulation of an upper limb bone with a bone of the trunk. The
clavicle acts as a strut, which prevents the scapula and the shoulder from
sagging downwards and medially under the weight of the limb. Scapula lies
posterior to the axilla and is covered with strong muscles, which attach the
scapula to the humerus or hold it to the thorax and allows sliding
movements, which are limited only by the sternoclavicular joint.
Nerve supply is by the axillary, suprascapular and lateral pectoral nerves.
Movements
The movements of the shoulder joint (Table 40.1) is the sum total of all the
movements at different points of the shoulder girdle.
TABLE 40.1
Movements at the Shoulder Joint (Figs. 40.2A–I)
Movement Procedure Range of

Movement
Flexion Arm is carried forward and medially 0–165°
Extension Arm is carried backward and laterally 0–60°
Adduction Arm is carried backward and inward 0–75°
Abduction Arm is carried forward and outward 0–180°
Internal rotation Arm by the side of the chest, elbow flexed to 90°, hand is moved to the opposite 70°
side of chest
External rotation Arm by the side of the chest, elbow flexed at 90°, forearm supinated and 70°
extended wrist moved outwards
Internal rotation in Arm abducted to 90°, the elbow is flexed to 90°, the forearm lowered in 70°
abductiona horizontal plane
External rotation in Arm abducted to 90°, the elbow is flexed to 90°, the forearm lifted in horizontal 70°
abductiona plane
Circumduction Upper limb extended at the elbow and wrist, and a full circle is completed 360°
starting from the adducted position
a
After 90° abduction by deltoid, the scapulothoracic movements take place and further abduction
of 90° is possible. In 180° the shoulder is so stable that it takes maximum load.
The complex movements of shoulder joint are described in three phases:

• Phase 1: The first 60° of flexion or 30° of elevation of humerus involves
about 15° of movement of the clavicle at the sternoclavicular joint. The
scapula does not elevate significantly but rotates to allow the elevation of the
clavicle
• Phase 2: This consists of subsequent 90° of flexion or abduction. Now, the
scapula and clavicle elevate about 5° for every 10° of glenohumeral
movement
• Phase 3: This phase completes the movement of the humerus to the fully
elevated position
The rotator cuff is made of the musculotendinous attachments to the greater
tuberosity (teres minor, supraspinatus and infraspinatus), lesser tuberosity
(subscapularis) and the fibrous capsule of the shoulder joint.
Muscles acting on the shoulder joint are tabulated in Table 40.2.
TABLE 40.2
Muscles Acting on the Shoulder Joint
Abductors Supraspinatus, deltoid, seratus anterior

Adductors Pectoralis major, latissimus dorsi
Flexors Pectoralis major, coracobrachialis, deltoid (anterior fibres)
Extensors Teres major, latissimus dorsi, deltoid (posterior fibres)
Internal rotators Pectoralis major, latissimus dorsi, teres major, deltoid (anterior fibres), subscapularis
External rotators Infraspinatus, teres minor, deltoid (posterior fibres)
Note
• The rotators (medial and lateral), can work only after stabilization of the
joint by supraspinatus muscle.
• The neurovascular structures lie at the anterior–inferior part of the shoulder
joint, medial to coracoid process.
40.2 Traumatic lesions (fractures)
Fractures of the shoulder girdle

Fractures of the clavicle are common and they are caused by indirect injury,
whereas the fractures of scapula are uncommon and they are caused by direct
injury.
Fractures of clavicle
• Most fractures of clavicle are caused by a fall on the outstretched hand
• The commonest site is at the junction of the middle and lateral one third
• When displacement occurs, the distal fragment is pushed downwards and
medially
• Commonest fracture in children
• Pain over the clavicle or the shoulder joint
• Tenderness on the clavicle
• Restriction of shoulder movements
• Rarely, neurovascular compression by fracture ends
• Plain X-ray (Fig. 40.3) is diagnostic
FIGURE 40.3 Fracture right clavicle.
Treatment
• Figure of 8 bandage application is useful
• After 3 weeks, it is discarded and active movements are encouraged
• Strapping for 1 week will suffice in children
• Ununited fractures need surgery
Fractures of scapula
• Fractures of scapula are uncommon
• Caused by direct injury
• Displacements are seen in fractures of acromion and coracoid processes
• The varieties of fractures of scapula (Fig. 40.4) are:
1. Fracture of neck
2. Fracture of body
3. Fracture of acromion process
4. Fracture of coracoid process
FIGURE 40.4 Fractures of scapula.
Severe pain and swelling with extensive extravasation of blood into the tissues,
with ecchymosis
• X-ray (Fig. 40.5A) is useful
• CT scan (Fig. 40.5B) is diagnostic
FIGURE 40.5A X-ray—fracture scapula.
FIGURE 40.5B CT—fracture of scapula.
Treatment
• Conservative with early active mobilization for undisplaced fractures
• Surgery for displaced acromion and fracture of glenoid
Fractures of upper end of humerus

• It consists of:
• Fracture of head of humerus
• Fracture of anatomical neck of humerus
• Fracture of surgical neck of humerus
• Fracture of greater tuberosity
• Caused by fall on the shoulder or the limb, usually in the elderly with
osteoporosis
• Impaction is common in fractures of neck of humerus and separation of
fragments is seen in greater tuberosity fractures
Pain may be absent or mild, but skin bruising may be seen in fractures of the
neck
X-rays (Figs. 40.6 and 40.7) are diagnostic
FIGURE 40.6 X-ray—fracture neck of humerus with displacement.

FIGURE 40.7 X-ray—fracture greater tuberosity.
Treatment
• Immobilization for impacted fractures for sometime
• Internal fixation is required for displaced and unimpacted fractures
40.3 Nonfracture lesions of shoulder joint

The nonfracture lesions of the shoulder joint are tabulated in Table 40.3.
TABLE 40.3
Nonfracture Lesions of the Shoulder Joint
Disorder Pathology
Acromioclavicular disorders Strain, subluxation and dislocation Acromioclavicular osteoarthritis

Subacromial disorders Impingement Rotator cuff injuries Calcific supraspinatus tendinitis Frozen shoulder
Glenohumeral disorders Synovitis Dislocation Osteoarthritis
Acromioclavicular disorders
Strain, subluxation and dislocation
They are caused by falls on the outer prominence of the shoulder, tending to
force the acromion downwards, as in football players:
• Strain: Strain of the joint capsule with no bony injury
• Subluxation: Joint capsule is torn and the acromion is displaced slightly
downwards from the lateral end of clavicle, but total displacement is
prevented by the intact coronoid and trapezoid ligaments
• Dislocation: In addition to the damage in the process of subluxation, the
conoid and trapezoid ligaments are also torn displacing the acromion
markedly downwards (or clavicle upwards, reflecting more severe injury
• Severe pain and swelling on the shoulder joint
• Compression between the clavicle and the flexed elbow may produce pain in
the acromioclavicular joint (pathognomonic of acromioclavicular joint
subluxation and dislocation)
• In strains, the X-ray is normal
• In others, X-ray (Fig. 40.8) is diagnostic
FIGURE 40.8 X-ray—acromioclavicular dislocation.
Treatment
• Strains recover spontaneously, and slings may be of help in controlling the
pain
• Slight displacement (subluxation) may be accepted and support of limb with
a sling for 2 weeks and early active shoulder exercises is recommended
• Dislocations require operative treatment
Acromioclavicular osteoarthritis
Occurs almost invariably secondary to trauma with or without dislocation of the
joint
• Pain felt on the top of the shoulder, aggravated by lifting the arm above the
head
• On clinical examination
• Acromioclavicular joint is prominent, with supraspinatus muscle wasting
• Localized tenderness with crepitus at the joint is characteristic
• The pain gets aggravated on lifting the arm passively
Treatment
• Fusion of acromioclavicular joint gives relief, but some muscle weakness
results. Surgery is indicated only when medical management such as local
steroid injections and physiotherapy fail
Subacromial disorders
Impingement syndrome
Occurs due to repetitive compression or rubbing of the tendons of supraspinatus
and subscapularis under the coracoacromial arch
Normally, when the arm is abducted, at 90°, the natural tendency is to rotate
externally for further abduction:
• In impingement syndrome, at this position (60–120°), the rotator cuff comes
in contact with the coracoacromial ligament and the acromion process,
causing severe pain (painful arc) (Fig. 40.9)
• Tenderness over the anterior edge of the acromion may be elicited
FIGURE 40.9 Painful arc.
X-ray may not show any significant finding, excepting osteoarthritis of
acromioclavicular joint with osteophytes
Treatment
• Medical treatment with nonsteroidal anti-inflammatory drugs (NSAIDs)
should suffice
• Local steroid injections may be useful
• Wedge excision of the undersurface of the acromion may be necessary in
refractory cases
• Arthroscopic shaving is beneficial in some cases
Rotator cuff injuries

• Rotator cuff: The rotator cuff is an anatomical term given to the group of
muscles and their tendons that hold the head of the humerus (ball) in the
glenoid fossa (socket), and act to stabilize the shoulder (supraspinatus,
infraspinatus, teres minor and subscapularis). Subscapular and infraspinatus
bursae permit smooth gliding between bone, muscle, and tendon. They
cushion and protect the rotator cuff from the bony arch of the acromion.
• Rotator cuff injuries may be acute or chronic
• They are caused by:
• Acute: Trauma
• Chronic: Degenerative lesions within the rotator cuff secondary to previous
dislocation
• Pathologically, the rotator cuff may suffer from impingement to small
abrasions to full thickness tears
• Muscle wasting especially of supraspinatus may be evident
• Tenderness over the lateral border of the acromion may be elicited
• Active movement, particularly abduction is reduced, but passive movements
are full
US and MRI of shoulder are useful in identifying the tears
Treatment
• Active shoulder exercises after acute pain subsides are useful
• In the young, especially when the tear is thought to be complete, surgical
repair with sutures may be required
• Reconstructive procedures are done for neglected large tears
Calcific supraspinatus tendinitis

• Occurs due to deposition of calcium hydroxyapatite within the supraspinatus
tendon, producing a severe inflammatory reaction
• Aetiology is not known
• Diabetes mellitus usually coexists
• Very severe pain around the joint and movements are avoided
• There is a typical history of pain at the shoulder in a certain arc of abduction
(60–120°)
• Tenderness may be diffuse or below the subacromial area and over the greater
tuberosity
• X-rays and MRI (Figs. 40.10A and B) may show calcific deposits above the
greater tuberosity of humerus
FIGURE 40.10A X-ray—calcific supraspinous tendinitis.

FIGURE 40.10B CT—calcific greater tuberosity.
Treatment
• Rest and anti-inflammatory drugs should suffice
• Local anaesthetic injections may help
• In refractory cases, incising the tendon releases the calcific deposit, which
can be squeezed out and the pain relief is immediate
Frozen shoulder (periarthritis)

• May be related to pericapsular adhesions following minor trauma to the
degenerated rotator cuff
• Aetiology is unknown
• Affects usually the middle aged
• Common in diabetics
• Diffuse pain over the shoulder with radiation to the middle of the upper arm
• Tenderness may be elicitable at the subacromial region
• Abduction and external rotation will be restricted
X-ray may not show any significant finding
Treatment
• Disease is usually self-limiting (usually within 2 years, the shoulder returns
to normal)
• Physiotherapy is useful to maintain the movements
• Manipulation under anaesthesia is useful when recovery is slow
• Focal sepsis if present should be attended to
Glenohumeral disorders
Acute dislocations
There are two types of dislocation, anterior and posterior, the former being more
common
• Anterior dislocation always follows a fall on the outstretched hand or on the
region of the shoulder itself. The humeral head gets displaced through a rent
in the capsule and comes to lie in the infraclavicular fossa below the
coracoid process (subcoracoid dislocation). This is common in the young
• Posterior dislocation occurs due to direct blow. This occurs consequent to
electric shock or epileptic convulsions, perhaps due to violent medial
rotation
Dislocations in general can give rise to complications like injury to axillary
nerve, brachial plexus, axillary artery. Both may be associated with fracture of
greater tuberosity of humerus
• Anterior dislocation
• Pain is severe, and patient does not allow movements
• On examination, the convex contour of the humeral head is seen and felt in
the infraclavicular fossa but it is flattened at the region below the tip of
acromion (Fig. 40.11)
• Posterior dislocation
• Pain is severe, and patient does not allow movements
• On examination, the area anterior and below the front of acromion is
flattened and the rounded bulge is lost
• The classical sign is the fixed internal rotation of the arm, which cannot be
rotated outwards
FIGURE 40.11 Anterior dislocation of shoulder.

• Anterior dislocation: X-rays show that the outline of the humeral articular
surface is not congruous with the articular surface of the glenoid fossa (Fig.
40.12)
• Posterior dislocation: Lateral projection of the shoulder joint, rays directed
upwards from the axilla with the arm abducted, is diagnostic (Fig. 40.13)
FIGURE 40.12 X-ray—anterior dislocation of shoulder.

FIGURE 40.13 X-ray—posterior dislocation of shoulder.
Treatment
• Manual reduction under anaesthesia is possible and effective in both types
• Surgery is indicated when closed reduction is not possible
Recurrent anterior dislocation

• Recurrent dislocations occur due to:
• Stripping of the capsule from the anterior margin of the glenoid rim
(Bankart lesion)
• Lateral denting of the articular surface of the humeral head (Hillsack’s
lesion)
• Recurrent dislocations occur when the arm is abducted, extended and rotated
laterally
• Some patients show hypermobile joints as in Ehlers–Danlos syndrome
• ‘Luxatio in erecta’ is acute dislocation of the head towards the chest with an
upright humerus (very rare)
Features as described under the heading ‘dislocations’ (p. 848), with similar
previous histories
CT demonstrates the deformities of the head of humerus and glenoid cavity
Treatment
Surgery gives effective cure
Note
Habitual or voluntary dislocations are seen in psychiatric patients and
children.
Osteoarthritis
Uncommon but usually secondary to trauma
Pain at the front of the joint and may radiate posteriorly
• X-rays may show osteoarthritic changes (Fig. 40.14)
• Arthroscopy is diagnostic (Fig. 40.15)
FIGURE 40.14 X-ray—osteoarthritis of shoulder joint.
FIGURE 40.15 Arthroscopy—severe osteoarthritis right shoulder.
Treatment
• Anti-inflammatory drugs and steroid injections are useful
• Arthroscopy to wash out and remove the loose bodies may give relief
• Arthroplasty with prosthesis is useful in refractory cases
• Arthrodesis is done as a salvage procedure after failed joint replacement
40.4 Nontraumatic lesions of shoulder joint

Pyogenic arthritis
It is rare, but common in children, especially in neonates, the infection spreading
from a focus of osteomyelitis in the upper metaphysis of the humerus
High grade pyrexia with swelling of the joint, with restriction of movements
• X-ray may not be contributory
• US is very useful
• Leucocytosis and raised ESR may be present
• Diagnostic aspiration and isolation of organism is confirmatory
Treatment
• Administration of broad-spectrum antibiotics with aspiration of pus from
the joint
• Open drainage may be needed in some cases
• Less commonly affected when compared to other joints
• Often associated with polyarticular involvement, more common in females
• Local pain and morning stiffness
• Increased warmth
• Swelling due to synovial thickening
• Moderate impairment of movements
• X-ray (Fig. 40.16) may show juxta-articular osteoporosis
• Biochemical parameters are useful
FIGURE 40.16 X-ray—rheumatoid arthritis of shoulder joint.
Treatment
• Medical management
• Late cases may need joint replacement surgery
Tuberculous arthritis
• It occurs less commonly than the tuberculosis of spine, hip and knee, with the
primary focus in the lung
• Some show no synovial thickening or fluid (Caries sicca)
• Axillary lymphadenitis is more significant
Pain in the shoulder joint with restriction of movements
• X-ray shows diffuse rarefaction throughout glenohumeral area, with
narrowing of cartilage space and erosion of underlying bones
• Synovial biopsy is conclusive
Treatment
• Arthrodesis reduces pain in severely damaged joints
Villonodular synovitis
• A rare form of synovial inflammation of unknown aetiology
• Inflamed synovium form villi which erode the bones
Pain in the shoulder with restriction of movements
• X-ray demonstrates huge soft tissue shadow
• Arthroscopy biopsy is confirmatory
Treatment
Total or subtotal excision of diseased synovium
Note
Haemophilic, neuropathic, alkaptonuric and gouty arthritis are rare in shoulder
joint.
40.5 Fracture of shaft of humerus

• The shaft of humerus is fractured usually in its middle third
• Common in adults of any age, rare in children
• The injury can be:
• indirect (causing spiral fracture)
• direct (causing transverse, short oblique or comminuted fractures)
• Marked angulation or overlapping can occur
• Proximal half is commonly affected in pathological fractures (e.g. metastatic
deposits)
Complications: Injury to radial nerve, nonunion
• Pain and swelling in the arm
• Severe tenderness on palpation
• Abnormal movements at shaft of humerus
X-rays (anteroposterior (AP) and lateral views) (Fig. 40.17) are diagnostic

FIGURE 40.17 X-ray—fracture shaft of humerus.
Treatment
• Undisplaced fracture requires an upper arm plaster cylinder including the
elbow, or extended to include the forearm with the elbow flexed to a right
angle
• Displaced fracture requires internal fixation with an intramedullary nail or
plate and screws
• Comminuted fracture requires internal fixation with bone grafting
40.6 Symptoms of shoulder joint pathologies

• Pain
• Swelling
• Deformity
• Restriction of movements
Pain
• True shoulder pain: True shoulder joint pain is generalized and is difficult to
pinpoint. The patient tends to apply his or her entire palm over the joint to
show the area of pain (palm sign) (Fig. 40.18). True shoulder pain radiates
down to the insertion of deltoid, and if it is severe, can radiate down to the
radial side of the wrist, but never to the fingers. Radiation to the fingers
should indicate a cervical spine pathology
• Acromioclavicular pain: Pain of acromioclavicular joint is specific, and the
patient is able to show the point of pain with his or her fingertip (finger sign)
(Fig. 40.19). This pain can radiate to the neck or anywhere in the C4 nerve
root distribution
• Sternoclavicular joint pain: This classically radiates along the course of the
clavicle
• Referred pain: Visceral referred pain occurs in angina pectoris to the left
shoulder and gall bladder to the right shoulder
FIGURE 40.18 Palm sign.
FIGURE 40.19 Finger sign.
Swelling
• Swelling around the shoulder joint: Generalized swelling of the shoulder
joint may be seen in infective pathologies (e.g. pyogenic arthritis), and
anteriorly dislocated head of the humerus can cause fullness in the
infraclavicular area close to the joint
• Swelling of the acromioclavicular and sternoclavicular joints:
Displacements of the joints and benign hypertrophy of medial end of clavicle
may present with swellings
• Swelling of bones: Swellings are caused by displaced fractures (e.g. fracture
of clavicle, fracture of acromion) and tumours of scapula (Fig. 40.18) or
head of humerus (Fig. 40.17) (e.g. osteoclastoma, chondrosarcoma)
Deformity
Deformities are caused by localized pathologies (e.g. malunited fracture of shaft
of humerus)
Restriction of movements
Movements of the shoulder joint are restricted to traumatic, inflammatory,
neoplastic and degenerative conditions
• Traumatic (e.g. dislocations, fracture dislocations)
• Inflammatory (e.g. septic arthritis)
• Neoplastic (e.g. chondrosarcoma, osteosarcoma of upper end of the humerus)
• Degenerative (e.g. osteoarthritis of shoulder joint)
Eliciting history
• Onset of pain: When did the pain start, was it slow or sudden in onset?
This question will answer the duration of pain, and its mode of onset. (e.g.
sudden onset of pain is generally due to trauma and insidious onset pain is
usually due to inflammatory pathology). Fracture pain is severe and starts almost
instantly, whereas rotator cuff tear pain starts late
• Relationship to trauma: Is this pain preceded by an injury, an accident, or
sport or a fall or even long hours of working?
description of the fall or accident will indicate the severity of injury (e.g. small
slips may cause soft-tissue injuries such as rotator cuff injuries, and fall during
active sports or road traffic accidents may cause fractures). Long hours of
working such as painting as in painters, can cause microtrauma and cause pain
(e.g. supraspinatous tendonitis)
• Position during the fall: What was the position of the hand during the fall?
Fall on outstretched hand may result in anterior dislocation of shoulder, and
fall on the outer prominence may result in acromioclavicular dislocations
Very severe pain may indicate fractures, and crescendo pain is seen in calcific
tendinitis. Referred pain from the neck often has a burning nature. Acute
exacerbations and remissions are seen in rheumatoid arthritis
Painful arc may be worse during abduction in rotator cuff pathologies and
acromioclavicular disorders. Acromioclavicular pain may be exacerbated by
cross body adduction and full internal rotation
This will answer about the first aid or hospital admissions and the radiographs
have to be scrutinized if available

See Chapter 39, General Orthopaedics.
Pre-requisites
• Patient should be undressed up to the waist. Ladies should keep their bra for
their privacy and decorum
• Opposite shoulder should be exposed for comparison
• Adequate knowledge and orientation of the shoulder and its related joints is
mandatory
Undressing
• Can the elbow be taken sideways
• How clumsy is he or she in his or her movements
• How protective is he or she during the act
• Any trick movement—shrugging of shoulders
Note
Watching the act of undressing gives abundant information of movements of
the shoulder.
The examination should follow the standard pattern of look, feel, move, strain
and investigate
The examination should be done from close quarters and also from a
distance
• Position of patient: Sitting or standing
• Position of examiner: The examiner should view the shoulder from all sides,
from the front, back, side, above and also through the axilla where possible
(A–E)
FIGURE 40.20A Inspecting the shoulder joints from the front.

FIGURE 40.20B Inspecting the right shoulder joints from the side.
FIGURE 40.20C Inspecting the shoulder joints from the back.
FIGURE 40.20D Inspecting the shoulder joints from above.
FIGURE 40.20E Inspecting the shoulder joints through axilla.
Inspection
What to look for?
• Attitude of the patient (e.g. patients with fracture clavicle and dislocation of
the shoulder are seen supporting the elbow with the other hand)
• Change in contour of the shoulder (e.g. contour of the shoulder is lost in
anterior dislocation of the shoulder joint)
• Deformities (e.g. bone deformity may be seen in fracture clavicle)
• Abnormal swellings (e.g. undue prominence may be seen in the subcoracoid
region in anterior dislocation)
• Shortening of arm (e.g. arm itself may look shortened in fracture of the upper
end of the humerus)
• Lengthening of arm (e.g. anterior dislocation of shoulder)
From the front:
Abnormal swelling along the shaft of clavicle (e.g. fractures and dislocations
of sternoclavicular joint)
1. Contour of shoulder and greater tuberosity (e.g. contour of shoulder is lost in
anterior dislocation of shoulder joint, joint is swollen in synovitis)
2. Deltoid prominence (e.g. lost in anterior dislocation, deltoid muscle atrophy)
3. Anterior axillary fold (e.g. lower than the noninjured side in anterior
dislocation) (Bryant’s sign)
4. Coracoid process
5. Scar, sinus, pigmentation (e.g. previous surgery (Fig. 40.21), tuberculosis)
6. Wasting of muscles (e.g. periarthritis of shoulder)
FIGURE 40.21 Attitude of the patient and scar of previous surgery.
Note
Bony prominences are seen without difficulty in thin individuals, and in the
obese, acromioclavicular joint alone is clearly visible.
From behind:
1. Spine of scapula, acromion process, winging of scapula
2. Contour of shoulder
3. Undescended scapula in children
Note
Since the back of the individual is covered by various muscles, clinical
examination by inspection is not a very good contributor, excepting in
swellings of the body of scapula.
From side:
1. Deltoid muscle prominence (e.g. lost in anterior dislocation, deltoid muscle
atrophy)
2. Drooping of shoulder (e.g. brachial plexus injury)
Note
The upper arm is not at right angles to the body, but at 30° forward.
From above:
1. Lumps anterior to the joint
2. Lumps posterior to the joint
3. Deltoid prominence
4. Rotated arm (e.g. internally rotated arm in posterior dislocation)
Through axilla (arm abducted):
1. Normal depth of the axilla
2. Abnormal swellings
3. Abnormal pulsations
4. Sinus openings
Note
Axilla is a three sided pyramidal space, narrow when adducted and opens up
and the floor (base) rises on abduction.
Palpation
Palpation of the painful area (described by the patient) is done last
Bones
What to look for:
• Temperature—warmth (e.g. infective conditions like septic arthritis) (Fig.
40.22)
• Thickening—thickening may be felt in malunited fracture of clavicle
• Irregularity and crepitus—crackling sensation is felt in fractures
• Tenderness—tenderness is seen in fractures and infective conditions (e.g.
marked tenderness in subacromial region is seen in fracture of greater
tuberosity or rupture of supraspinatus tendon) (Fig. 40.23)
• Abnormal movements or deformity (e.g. fractures and nonunion of fractures)
FIGURE 40.22 Feeling the shoulder for warmth.

FIGURE 40.23 Feeling the shoulder for tenderness.
Methods of examination
• Clavicle: The clavicle is palpated by the surgeon standing behind the seated
patient and by running the fingers from the sternoclavicular joint to the
acromioclavicular joint (e.g. fractures and dislocations alter the continuity of
the bone, and it may be tender. Abnormal movements and crepitus should be
noted) (Fig. 40.24)
• Upper end of humerus: The surgeon should stand behind the seated patient
and the greater tuberosity of the humerus is identified as a prominence below
the acromion (Fig. 40.25) (e.g. abnormal depression or loss of resistance may
be felt in cases where glenoid becomes empty as in anterior dislocation).
Greater tuberosity is better identified by rotating the arm internally by
rotating the flexed elbow inwards (Fig. 40.26)
• Scapula
• Spine of scapula is felt by running the finger (Fig. 40.27) starting at the
acromion process (Fig. 40.27A) towards the midline
• Vertebral border can also be felt easily though it is covered by muscles
(Figs. 40.27B and C)
• Inferior angle of scapula is felt easily (Fig. 40.27D)
• Axillary border of scapula is palpated with some difficulty (e.g. tenderness
of any of these may indicate fractures)
• Neck of scapula is the most difficult to palpate and to elicit tenderness (e.g.
fracture neck of scapula and it can be mistaken for fracture of the upper
end of the humerus)
• Coracoid process is situated half inch below the clavicle at the junction of
the medial two thirds and lateral one third. This is identified as a dimple
seen in front of the shoulder below the clavicle (Fig. 40.28)
• Position of bony points: The tip of coracoid process, acromial end of clavicle
and the greater tuberosity of the humerus should be compared with the other
side (e.g. in acromioclavicular dislocation, the acromial end of the clavicle
becomes prominent and comes nearer to the greater tuberosity, whereas the
distance between the coracoid process and the acromial end of the clavicles
becomes more)
• Muscles and tendons: The biceps tendon is palpated at the bicipital groove,
between the two tuberosities. (e.g. in traumatic rupture of biceps muscle, it
cannot be palpated in the groove, as it gets detached from its insertion and
coils in the middle of the arm) (Fig. 40.29)
• Examination of axilla: The axilla should be examined for the following:
• Fullness of the joint (e.g. fullness caused by effusion)
• Head of the humerus (e.g. displaced in dislocations)
• Axillary arterial pulsations (this artery is easily palpated near the anterior
axillary fold during abduction of the shoulder to 90°)
• Lymph node enlargement
FIGURE 40.24 Palpating the clavicle.
FIGURE 40.25 Palpating the upper end of humerus.
FIGURE 40.26 Palpating the greater tuberosity.
FIGURE 40.27 Palpating the spine of scapula.
FIGURE 40.27A Palpating the acromion process.
FIGURE 40.27B Palpating the superior angle of scapula.
FIGURE 40.27C Palpating the vertebral border of scapula.
FIGURE 40.27D Palpating the inferior angle of scapula.
FIGURE 40.28 Palpating the coracoid process.
FIGURE 40.29 Palpating the bicipital groove.
Movements
A full range of movement of the shoulder joint usually rules out the possibility of
fractures in and around the joint. Abnormal movements should be determined by
moving the arm in more than two directions (anteroposterior and mediolateral)
and also rotation. Voluntary subluxation is seen in Ehlers–Danlos syndrome
Measurements
• Length of the arm: This is measured with a tape from the acromion to the
lateral epicondyle (Fig. 40.30) (e.g. the length is shortened in fracture of the
shaft of the humerus, whereas it is increased in subglenoid dislocation)
• Calloway’s sign: Vertical circumference of axilla is measured with a tape
taking it round the axilla. This is compared with the other side (Fig. 40.31)
(e.g. increased in all dislocations of the shoulder)
FIGURE 40.30 Measuring the upper arm length.
FIGURE 40.31 Measuring the vertical circumference of axilla.
Special tests
• Hamilton’s ruler test: Normally, the acromion process and the lateral
epicondyle are not in a straight line and cannot be touched with the ruler at
the same time, as the greater tuberosity pushes the ruler away (Fig. 40.32)
(e.g. in dislocation of the shoulder, the greater tuberosity does not come in
the way, and the ruler can touch the acromion and the lateral epicondyle at
the same time)
• Dugas test: Normally a person should be able to touch the opposite shoulder.
In anterior dislocations, the patient will not be able to do this, but after
successful and proper reduction he should be able to do so (Fig. 40.33)
FIGURE 40.32 Hamilton ruler test (normal individual).
FIGURE 40.33 Dugas test.
Lymphatic system
Examination of the regional lymph nodes and all other groups is essential (e.g.
tuberculosis)
General
symptoms may be the only manifestation of a systemic disease (e.g.
tuberculosis)
CHAPTER 41
Elbow and forearm

V. Thulasiraman
CHAPTER OUTLINE
41.1. Elbow joint 754
• Movements 755
41.2. Surgical anatomy of forearm bones 755
41.3. Deformities of elbow 755
• Cubitus valgus 755
• Cubitus varus 756
41.4. Traumatic lesions of elbow joint 756
• Fractures of lower end of humerus 756
• Supracondylar fracture 756
• Fractures of condyles 757
• Intercondylar fracture 757
• Fractures of epicondyles 757
• Fracture of capitulum 758
• Fractures of upper end of ulna 758
• Fracture of olecranon process 758
• Monteggia fracture dislocation 759
• Posterior dislocation of elbow joint 759
• Myositis ossificans 760
• Fractures of upper end of radius 761
• Fracture head of radius 761
• Fracture neck of radius 761
41.5. Nontraumatic lesions of elbow joint 761
• Haemophilic arthritis 763
• Neuropathic arthritis 763
• Osteochondritis dissecans 763
• Loose bodies 764
• Pulled elbow 764
41.6. Extra-articular disorders of elbow 764
• Tennis elbow 764
• Golfer’s elbow 765
• Olecranon bursitis 765
• Friction neuritis of ulnar nerve 765
• Congenital radioulnar synostosis 766
41.7. Fractures of shafts of forearm bones 766
• Fractures of shafts of ulna and radius 766
41.8. Symptoms of elbow joint pathologies 767
• Elbow and forearm 767
• General 773
41.1 Elbow joint
Surgical anatomy
The elbow joint is a complex joint (Figs. 41.1 A and B) formed between the
lower end of the humerus and the upper end of radius and ulna, involving three
separate articulations, which share a common synovial cavity.
FIGURE 41.1A Anatomy of elbow joint (AP view).

FIGURE 41.1B Anatomy of elbow joint (lateral view).
It is made up of three distinct articulations, which are:

1. Humeroulnar, between the trochlea of humerus and the trochlear notch of the
ulna (a hinge joint)
2. Humeroradial, between the capitulum and the upper concave surface of the
radial head (a ball and socket joint)
3. Superior radioulnar, between the head of the radius and radial notch of the
ulna, head being held in place by the tough annular ligament (a pivot joint)
Articular capsule of the elbow joint is closely applied around this complex
articular arrangement; the nonarticular medial and lateral epicondyles are outside
the capsule. The capsule is thin and loose anteriorly and posteriorly to allow
flexion and extension, whereas it is very thick on either side to form the medial
and lateral collateral ligaments. The lateral ligament is attached distally to the
annular ligament around the radial head.
Blood supply
The elbow joint derives its blood supply from a network of vessels derived from
collateral and recurrent branches of the brachial, profunda brachii, radial and
ulnar arteries.
Movements
Two sets of movements take place at the elbow:
1. Flexion and extension at the humeroulnar and humeroradial joints
2. Pronation and supination at the proximal radioulnar joint (in conjunction with
the distal radioulnar joint)
Various muscles act on the elbow joint to produce the movements (Table
41.1).
TABLE 41.1
Muscles Acting on the Elbow and Their Action
Flexors Bicepsa, brachialis, brachioradialis, forearm flexors

Extensors Triceps, anconeus
Pronators Pronator teres, pronator quadratus, flexor carpi radialis
Supinators Bicepsa, supinator
41.2 surgical anatomy of forearm bones

The forearm bones are ulna and radius. Ulna, which is relatively straight, acts
as an axis around which the laterally bowed radius rotates. Radial shaft fractures
with loss of lateral curvature cause loss of supination and pronation movement.
The interosseous membrane which spans between the radius and ulna is 3.5 cm
wide in the central band which runs obliquely from distal ulna to proximal
radius. Division of central band alone reduces the stability by 70%.
Fracture location dictates deforming forces:
• Radius fracture distal to supinator insertion but proximal to pronator teres
insertion tend to result in supination of proximal fragment due to unopposed
pull of supinator and biceps brachii
• Radius fracture distal to supinator and pronator teres results in neutral
rotational alignment of the proximal fragment
• Radius fracture proximal to pronator quadratus results in pronation of distal
fragment and supination of proximal segment 41.3 DEFORMITIES OF
ELBOW
Cubitus valgus
• Normally, in an extended elbow, the arm and the forearm are in a position of
slight valgus—usually 10° in males and 15° in females, which is called
‘carrying angle’
• If this angle is increased it is called cubitus valgus (Fig. 41.2)
• Common causes are:
• Previous fracture of neck radius and lateral condyle, with malunion
• Interference with epiphyseal growth on the lateral side, from injury or
infection
FIGURE 41.2 Cubitus valgus (right) normal carrying angle (left).
Complications: Ulnar nerve irritation, fibrosis of ulnar nerve trunk due to

repeated friction (tardy ulnar nerve palsy), osteoarthritis
Visible deformity is the only presentation
X-rays will show the cause of deformity
Treatment
• No treatment is offered for slight deformity
• Osteotomy near the lower end of humerus is justified, if angulation is severe
• Transposition of ulnar nerve (from its posthumeral groove to a new bed at
the front of the elbow), if the function of ulnar nerve is impaired
Cubitus varus
• Deformity of the elbow opposite to valgus deformity (Fig. 41.3)
• The causes are:
• Previous fracture of the lower end of humerus (supracondylar fracture) with
malunion (common)
• Interference with epiphyseal growth on the medial side, from injury or
infection (rare)
FIGURE 41.3 Cubitus varus (left).
Visible deformity is the only presentation
• X-rays will show the cause of deformity (Fig. 41.4)
FIGURE 41.4 X-ray—cubitus varus.
Treatment
• No treatment is offered for slight deformity
• Correction by osteotomy near the lower end of humerus is justified, if
angulation is severe
41.4 Traumatic lesions of elbow joint
Fractures of lower end of humerus

Supracondylar fracture
• One of the most common and most important fractures of childhood, and it is
seldom seen in adults
• Regarded as potentially dangerous fracture because of the risk of injury to the
brachial artery
• Caused by a fall on the outstretched hand
• It is of two types:
• Extension type
• Flexion type
• When displacement occurs, it is characteristic; the lower fragment is displaced
backwards and tilted (extension type), and the flexion type is rare
Complications: Brachial artery injury (severed or contused) and Volkmann’s
ischemic contracture of hand, median nerve injury, malunion
• Severe pain, swelling, deformity and restricted movements of the elbow joint
• The patient holds the elbow in flexion after injury
• Clinical examination: Acute injury does not reveal any disturbance of the
triangular relationship of the bony prominences, medial epicondyle, lateral
epicondyle and the olecranon
• Radial and ulnar pulses should be examined for the fear of injury to the
brachial artery
• X-rays of the elbow joint (anteroposterior (AP) and lateral views) (Fig. 41.5)
are diagnostic
• Doppler studies may be required to rule out vascular injury
FIGURE 41.5 X-ray—supracondylar fracture of humerus (extension type).
Treatment
• Undisplaced fractures need immobilization with an above-elbow (AE) slab
• Displaced fractures need open surgery and fixation, or closed reduction and
pinning
Fractures of condyles
• Fractures of condyles of the humerus are relatively uncommon, and are
common in children, the usual cause being a fall
• The lateral condyle is fractured more commonly than the medial condyle
• The lateral fracture extends obliquely so that the fractured fragment includes
the epiphysis of capitulum, and the displacement is seldom severe, but even
moderate displacement is important because the fracture involves the joint
surface. Since common extensors take origin here, displacement is rotated
downward and outward
Complications: Nonunion, tardy ulnar nerve palsy, radial nerve entrapment,
malunion and valgus deformity with restriction of movements
Pain, swelling and tenderness over the lateral aspect of the elbow
X-rays of the elbow joint (AP and lateral views) are diagnostic
Treatment
• Undisplaced fractures need immobilization with an AE slab
• Displaced fractures always need open surgery and fixation
Intercondylar fracture
• Common in adults
• Usual cause being a fall on the point of the elbow so that the olecranon is
driven into the distal humerus, splitting the two humeral condyles apart
• The fracture lines take the shape of ‘T’ or ‘Y’ and involve the articular surface
• Pain, swelling, ecchymosis around the elbow
• Crepitus is felt
• The intercondylar distance is increased and the relationship between the
three bony landmarks is altered
X-rays of the elbow joint (AP and lateral views) (Figs. 41.6 A and B) are
diagnostic

FIGURE 41.6A-B X-ray—(A) intercondylar with supracondylar fracture of
humerus, (B) intercondylar fracture of humerus.
Treatment
• Displaced fractures need open surgery and fixation
Fractures of epicondyles
• Most condylar fractures affect the lateral side, whereas epicondylar fractures
affect the medial side
• More common in children and adolescents
• Caused by direct violence, but more often an avulsion injury
• The epicondyle is pulled off by the attached flexor muscles during a fall,
which may be associated with dislocation or momentary subluxation of the
elbow
• There may be associated ulnar nerve injury
• Pain, swelling and restriction of movements of the elbow
• Tenderness over the medial aspect of the elbow
• Signs of ulnar nerve injury should be elicited
X-rays of the elbow joint (AP and lateral views) (Fig. 41.7) are diagnostic

FIGURE 41.7 X-ray—fracture of medial epicondyle of humerus.
Treatment
• Displaced fractures need open surgery and fixation
• Ulnar nerve if entrapped, should be released
Fracture of capitulum
• Fracture of the capitulum is rare
• It is always intra-articular
Pain and swelling over lateral aspect of the elbow with restricted movements of
elbow
• X-rays of the elbow joint (AP and lateral views) (Fig. 41.8) are useful but
sometimes fragments are not visible in the X-rays
FIGURE 41.8 X-ray—fracture of capitulum.
Treatment
• If possible they can be fixed with small screws
Fractures of upper end of ulna
Fracture of olecranon process
• Olecranon is fractured by a fall on the point of the elbow
• It may take three forms:
1. Crack without displacement
2. Clean break with separation of fragments (avulsion type)
3. Comminuted variety
Complications: Nonunion, late osteoarthritis of elbow
• Pain and swelling of the elbow
• Tenderness is present on the point of the elbow
• Crepitus or a gap between the fragments may be palpable
• Active extension of the elbow is not possible
FIGURE 41.9 X-ray—fracture olecranon process.
Treatment
• Undisplaced fractures need immobilization with AE slab in 30° flexion
• Displaced fractures need open surgery and fixation (tension band wiring in
avulsed injuries)
Monteggia fracture dislocation

• Fracture of the upper end of the ulna with dislocation of the head of radius
• The displacement is characteristic; the ulna is angled forwards and the head of
the radius is dislocated forwards
• Rarely, the reverse deformity occurs
• Usually caused by:
• A fall associated with forced pronation of the forearm
• A direct blow on the back of the forearm
Complications: Nonunion of ulna, nerve injury (radial / median / anterior or
posterior interosseous)
• Pain, swelling and deformity
• Severe loss of elbow movements and forearm movements (supination and
pronation)
• Head of the radius may become palpable easily
• X-rays of the elbow joint (AP and lateral views) (Figs. 41.10 A and B) are
diagnostic
• CT (Fig. 41.11) is diagnostic

FIGURE 41.10A X-ray—Monteggia fracture dislocation (AP view).
FIGURE 41.10B X-ray—Monteggia fracture dislocation (lateral view).
FIGURE 41.11 CT—Monteggia fracture dislocation with olecranon
fracture.
Treatment
Open surgery is required, since accurate reduction is not possible, especially in
adults
Posterior dislocation of elbow joint

• Common in both children and adults
• Caused by a heavy fall on the outstretched hand
• Dislocation is always posterior or posterolateral, that is the ulna and radius are
displaced backwards, or backwards and laterally, relative to the humerus
• There may be associated fracture of the coronoid process, or of the radial
head, the capitulum or the medial epicondyle, and mostly the fracture is of
the minor degree
Complications: Injury to brachial artery, injury to major nerve trunks,
persistence or irreducibility of dislocation, myositis and joint stiffness
• Elbow is swollen with the prominence of the olecranon with a depression just
above it due to forward placement of the distal end of the humerus
• The three bony prominences are disturbed
X-ray (Fig. 41.12) is confirmatory
FIGURE 41.12 X-ray—posterior dislocation of the elbow joint.
Treatment
• Closed reduction under general anaesthesia, as soon as possible. Reduction
should be confirmed by radiographs and should be rested in plaster in 90°
flexion for 3 weeks, followed by mobilizing exercises
• Open reduction is required for neglected cases
Myositis ossificans
• This is posttraumatic ossification, occurs following a severe injury to a joint,
in which the capsule and periosteum have been stripped from the bones by
violent displacement of fragments
• Blood collects below the stripped soft tissues, forming a large haematoma.
Instead of being absorbed, the haematoma is invaded by osteoblasts and
become ossified
• If a large mass of bone is formed, the joint movements are restricted
• It occurs commonly following a fracture dislocation of the elbow joint, more
commonly in children as the periosteum is easily stripped
• It can also happen following vigorous massage of the contused elbow
• Warmth is felt in the early stages due to increased vascularity of reparative
process
• Movements, especially flexion gets restricted and a hard lump may become
palpable in front of the elbow, as the myositis matures into bone
• History of oil massage of haematoma is elicitable in some cases
X-rays (Fig. 41.13) are diagnostic
FIGURE 41.13 X-ray—myositis ossificans.
Treatment
• Immobilization is useful during early stages
• Removal of the mass of bone blocking the movement is useful in late stages
Fractures of upper end of radius

Fracture head of radius
• One of the commonest fractures of the upper limb in young adults
• Caused by a fall on the outstretched hand, the force being transmitted axially
along the shaft of the radius
• It can be of three types:
1. Crack with no displacement
2. Disc-shaped head is broken away and depressed below the plane of the
articular surface (sectoral fracture)
3. Comminuted variety
Complications: Joint stiffness, cubitus valgus, osteoarthritis
• Pain, swelling and localized tenderness over the head of radius, which is
located distal to the lateral condyle of humerus
• Rotations (pronation and supination) of forearm are painful
• Extension of the elbow is restricted
FIGURE 41.14 X-ray—fracture head of radius (sectoral fracture).
Treatment
• Undisplaced fractures need immobilization for 2 weeks with an AE slab in
90° flexion and forearm in midpronation
• Severe damage to head warrants excision of the entire head in adults and in
children, head should not be excised, because as growth occurs the radius is
liable to ride up towards the humerus, with consequent disturbance of its
relationship to the ulna
Fracture neck of radius

• Common in children
• Occurs due to valgus injury of the elbow
• Pain and swelling over the lateral aspect of the elbow
• Supination and pronation are painful
FIGURE 41.15 X-ray—fracture of neck of radius.
Treatment
• Undisplaced fractures need immobilization for 3 weeks with an AE slab
• Severe angulation requires ‘K’ wire fixation
• Excision of head of radius is done in selected cases in adults
41.5 Nontraumatic lesions of elbow joint
Pyogenic arthritis
• Infection of the elbow joint with suppuration, which can be:
• Acute
• Subacute
• Chronic
• Infection reaches through three routes:
• Through blood (haematogenous spread)
• Through a penetrating wound
• From an adjacent focus of infection of osteomyelitis of humerus, radius or
ulna
• Common organism being Staphylococcus aureus, and the inflammatory
reaction causes exudation of fluid into the joint; the fluid is turbulent or
frankly purulent
Complications: Total destruction of joint with fibrous or bony ankylosis and
growth arrest in children
• Constitutional symptoms with pyrexia, and restricted joint movements
• Clinical examination reveals:
• Elbow swollen with overlying warmth and red skin
• All movements are restricted by pain and muscle spasm
• Leucocytosis and raised erythrocyte sedimentation rate (ESR) may be
present
• X-rays are normal at first, may later show diffuse rarefaction and loss of
cartilage space
• Ultrasonography (US) is useful
• Diagnostic aspiration and isolation of organism is confirmatory
Treatment
Aspiration or surgical drainage with systemic and local antibiotics, with
immobilization
• One or both elbows are commonly affected, usually in conjunction with
several other joints
• The pathological changes are such as those of rheumatoid arthritis (RA)
elsewhere
• A female preponderance is seen
• Main symptoms are pain, swelling due to synovial thickening, abnormal
warmth of the overlying skin
• Movements are impaired
• X-rays show rarefaction of joint (Fig. 41.16). In longstanding cases the
cartilage space is lost with erosion of both ends, with subluxation of joint
• Biochemical parameters are useful
• RA factor positive
• ESR is raised
FIGURE 41.16 X-ray—rheumatoid arthritis of elbow.
Treatment
• Medical treatment is along the lines suggested for RA in general
• Surgical treatment: If extensive destruction of the articular cartilage leads to
persistent and disabling pain, synovectomy, excision arthroplasty and
replacement surgery are useful
Tuberculosis is much less common in the elbow than it is in the large weight-
bearing joints such as the hip and knee
• Marked swelling of the elbow with severe wasting of muscles around the joint
with restriction of joint movements
• Multiple sinuses may be seen
• Regional lymph nodes are swollen and matted
• Lymphocytosis, raised ESR, positive Mantoux and polymerase chain
reaction (PCR) tests are contributory
• X-rays show generalized rarefaction and erosion of articular surface with
narrowing of joint space
• Synovial biopsy is confirmatory
• IgA, IgG and IgM antibody estimations are useful
Treatment
• Aspiration, immobilization in plaster for 3–6 weeks supported by
antitubercular treatment
• Synovectomy is useful for neglected cases
Osteoarthritis
• Seldom seen in a normal elbow joint
• Occurs in patients with damaged articular surface from previous fractures or
from osteochondritis dissecans of trochlea
• Slowly increasing pain worsening on activity
• Sudden locking suggests presence of loose bodies
• Clinical examination may show:
• Thickening of joint margins due to osteophytes
• Flexion and extension are impaired
• Crepitus may be felt
X-rays are diagnostic with osteophytes. Loose bodies may be present
Treatment
• Conservative treatment such as exercises and physiotherapy are advised
• Loose bodies require removal
• Arthroplasty may be advised, when the disability is severe
Haemophilic arthritis
• Haemophilic arthritis affects elbow more often than any other joint except the
knee
• There is intra-articular haemorrhage, with irritation and later degeneration of
joint
• Swollen joint with restriction of movements
• Clue to diagnosis is bleeding tendency with positive family history
• Prolonged clotting time is contributory to diagnosis
• Diagnostic aspiration of blood may be confirmatory, but should be done with
adequate precaution
• US is safe
Treatment
• General treatment is that of haemophilia
• Local treatment is by firm bandaging and rest in plaster for 3–4 weeks,
followed by gentle mobilizing exercises
Neuropathic arthritis
• Rare in the elbow joint
• More commonly idiopathic
• Usual cause is syringomyelia
• The protective ligaments become insensitive to pain and the joint is liable to
injury. The joint surfaces undergo degeneration and attrition with coincident
massive hypertrophy of bone at the joint margins
• Pain over the joint is disproportionate to the swelling of the joint with feeling
of instability and weakness
• Examination will show:
• Marked thickening and irregularity of bone ends (Fig. 41.17)
• Joint becomes abnormally lax and lateral movements are pronounced
FIGURE 41.17 Neuropathic arthritis right elbow.
X-rays will show grossly disorganized joint with destruction of bones (Fig.
41.18)
FIGURE 41.18 X-ray—neuropathic joint elbow.
Treatment
• If the elbow is severely disorganized, it should be protected by a right-angled
splint of plastic or leather
• Rarely, arthroplasty is justified
Osteochondritis dissecans
• After the knee, the elbow is the most common site of osteochondritis
dissecans
• This is characterized by necrosis of part of articular cartilage and the
underlying bone, which ultimately separates to form an intra-articular loose
body
• Initially, the symptom is mild ache and intermittent swelling
• Examination shows little swelling with slight limitation of flexion and
extension
• Painful locking occurs when loose bodies are formed
• X-rays may show an area of irregularity on the articular surface, usually the
capitulum. Loose body is seen
• Arthroscopy is diagnostic
Treatment
• Medical management is advisable
• Loose bodies require surgical removal
Loose bodies
There are four important causes of loose bodies in the elbow joint:
1. Osteochondritis dissecans (1–3 bodies)
2. Osteoarthritis (1–3 bodies)
3. Fracture with separation of fragment (1–3 bodies)
4. Synovial chondromatosis (50–500 bodies)—numerous synovial villi become
pedunculated and transformed into cartilage, which eventually detach to form
loose bodies
• Many are silent and asymptomatic
• Swelling of the elbow may be predominant in some cases
• Sudden locking of the joint is common
• Recurrent attacks occur
• X-rays are diagnostic
• Arthroscopy is confirmatory
• MRI (Fig. 41.19) is helpful
FIGURE 41.19 MRI—synovial chondromatosis.
Treatment
• Silent loose bodies may be left alone
• Recurrent locking warrants surgical removal of loose bodies
• Synovectomy is the treatment of choice in synovial chondromatosis
Pulled elbow
• Occurs in children between 2 and 5 years
• The radial head slides partly out of the annular ligament, when a child is lifted
by its wrist
• The child starts crying and is unable to move the affected limb and a mild
swelling may be seen
• The forearm is kept in pronation and supination is restricted
X-rays are required to rule out bony injuries.
Treatment
• The head is reduced by applying direct pressure over the head of the radius
keeping the forearm fully supinated
• A sudden click is felt as the head goes back to its place and pain disappears
immediately
41.6 Extra-articular disorders of elbow
Tennis elbow
• Also called lateral epicondylitis
• Caused by strain (incomplete rupture) of forearm extensor muscles at the
point of their origin from the bone
• Pain at the lateral aspect of the elbow, often radiating down the back of the
forearm
• Pain is aggravated by putting the externsor muscles on stretch—by flexing the
wrist and fingers with the forearm pronated
• There may be a history of recent excessive activity involving the elbow, e.g.
sweeping, painting, playing tennis
• Localized tenderness on the epicondyle
X-ray shows no abnormality
Treatment
• Symptoms may subside spontaneously or may persist for many years
• Medical management:
• Analgesics are to be tried first
• Physiotherapy in the form of short-wave diathermy, deep massage and
ultrasound therapy are useful
• Injection of steroid at the point of tenderness is useful
• Surgical treatment
• Stripping the extensor origin (allows it to fall back into place) is reserved
for cases with severe disability
Golfer’s elbow
• Also called medial epicondylitis
• Common between 35 and 50 years
• Common in golf players
• Occurs due to nonspecific inflammation or strain of the common flexor origin
• Pain at the medial aspect of the elbow, often radiating down the back of the
forearm
• Pain is aggravated by putting the flexor muscles on stretch
• Localized tenderness on the medial epicondyle is present
X-ray shows no abnormality
Treatment
• Symptoms may subside spontaneously or may persist for many years
• Medical management
• Analgesics are to be tried first
• Physiotherapy in the form of short-wave diathermy, deep massage and
ultrasound therapy are useful
• Injection of steroid at the point of tenderness is useful
• Stripping the flexor origin (allows it to fall back into place) is reserved for
cases with severe disability (very rarely done)
Olecranon bursitis
• Inflammation of the bursa behind the olecranon may occur due to:
• trauma
• infection
• gout
• Traumatic bursitis is common in students due to constant friction caused by
the skin over the olecranon (student’s elbow)
• A swelling on the olecranon
• On examination:
• In traumatic bursitis, bursa is swollen and the fluid is clear (Fig. 41.20A)
• In septic bursitis, bursa is red and inflamed and contains pus (Fig. 41.20B)
• In gouty bursitis, the bursa is mildly swollen and whitish deposits of
sodium biurate (tophi) may be visible through the walls of the bursa
FIGURE 41.20A Traumatic olecranon bursitis.
FIGURE 41.20B Septic olecranon bursitis.
• Serum uric acid is increased in gouty bursitis
• X-rays are normal in early stages
Treatment
• Traumatic bursitis needs simple aspiration
• Septic bursitis needs incision and drainage
• Gouty bursitis needs anti-gout drugs such as allopurinol
Friction neuritis of ulnar nerve

• Ulnar nerve lies in the groove behind the medial epicondyle of the humerus
and its function may be interfered by:
• Constriction (secondary to osteoarthritis with encroachment of osteophytes
upon the ulnar groove)
• Recurrent friction
• Friction under tension occurs when the carrying angle is increased. The ulnar
nerve undergoes fibrosis unless the fault is relieved
• Numbness and tingling in the ulnar distribution with clumsiness in performing
fine finger movements
• On examination:
• Sensory loss in the little finger and medial half of the ring finger
• Wasting and weakness of ulnar innervated small muscles
• Sweating is impaired in its distribution
Ulnar nerve conduction studies are useful
Treatment
Transposition of ulnar nerve to a new bed in front of the joint, where it will lie
free of friction
Congenital radioulnar synostosis

Common in children
Restriction in supination and pronation movements
X-rays (Fig. 41.21) show synostosis of superior radioulnar joint
FIGURE 41.21 X-ray—superior radioulnar synostosis Source: (Courtesy Dr T.
V. Raja).
Treatment
Severe cases require surgical correction
41.7 Fractures of shafts of forearm bones
Fractures of shafts of ulna and radius

• A fracture may involve either the radius alone or ulna alone or both may be
fractured
• The cause may be either:
• Indirect force (fall on the outstretched hand)
• Direct force (blow on the forearm)
• The fracture may be:
• Closed or open
• Displaced, angulated or rotated
• Comminuted (segmental or multifragmented)
• Greenstick fractures are common in children
Complications: Compartment syndrome, Volkmann’s ischaemia, infection,
delayed union, nonunion and malunion
• Pain and swelling of forearm
• Tenderness at the fracture site is dominant
• Loss of hand and forearm function
• In severe cases, closed fractures produce compartment syndrome whereas
open fracture produces neurovascular damage
X-rays of forearm (AP and lateral views) (Fig 41.22A–C) are diagnostic. It is
wiser to add the elbow and wrist to determine the respective joint involvement

FIGURE 41.22A-C X-ray—(A) fracture shaft of radius, (B) fracture shaft of
ulna, (C) fracture both bones of forearm.
Treatment
• Undisplaced and greenstick fractures may be managed with full-length arm
plaster with the elbow fixed at right angle and the forearm in a position
midway between pronation and supination
• Displaced fractures, especially in adults require operative treatment with a
metal plate with screws
41.8 Symptoms of elbow joint pathologies

• Pain
• Swelling
• Deformity
Pain
Pain due to elbow joint pathology is localized to the elbow area. However, there
are extrinsic sources of pain. They are:
• From shoulder (from tip of acromion to the middle of arm, but it does not
extend below the elbow)
• From the neck when brachial plexus or roots are involved (extends
throughout the length of arm and forearm into the hand and fingers,
sometimes with paresthesia)
Swelling
The swellings around the elbow joint can be generalized or localized.
• Generalized (e.g. arthritis)
• Localized (e.g. posterior dislocation)
Deformity
Deformities are caused by localized pathologies (e.g. malunited fracture of head
of radius, epiphyseal injury of radius, supracondylar fracture of humerus)
Movements of elbow joint are restricted due to traumatic, inflammatory,
neoplastic and degenerative conditions:
• Neoplastic (e.g. osteoclastoma of lower end of humerus, osteosarcoma of
lower end of humerus)
• Degenerative (e.g. osteoarthritis of the elbow joint)
Eliciting history
• Onset of pain: When did the pain start, was it slow in onset or sudden?
This question will answer the duration of pain, and its mode of onset (e.g.
sudden onset pains are generally due to trauma and insidious onset pain is
instantly, whereas soft tissue injury pain starts late
sport or a fall?
slips may cause soft tissue injuries, and fall during active sports or road traffic
accidents may cause fractures)
• Position during the fall: What was the position of the hand during the fall?
Fall on outstretched hand may result in posterior dislocation of the elbow
joint, and fall on the point of the elbow may result in olecranon fractures
Very severe pain may indicate fractures
fractures, and nontraumatic situations, may indicate arthritis
have to be scrutinized if available. History related to needle aspiration of joint
(arthrosynthesis) and massage (massage worsens myositis ossicifans) should be
questioned
Pre-requisites
• Patient should be undressed so that both the upper limbs are exposed
Undressing
• Can the elbow be taken sideways (e.g. may indicate pain of shoulder or elbow
pathology)
• How clumsy is he or she in his or her movements (e.g. nerve injuries causing
motor paralysis of small muscles of hand)
• How protective is he or she during the act (e.g. denotes pain)
Note
the elbow.
distance.
• Position of patient: Sitting or standing
• Position of examiner: The examiner should view the elbow from all sides,
from the front, back, sides
Inspection
What to look for:
• Attitude of the patient (e.g. patients with fracture dislocation of the elbow, are
seen supporting the elbow with the other hand)
• Change in contour of the elbow (e.g. contour of the elbow is disturbed in
fractures of elbow)
• Deformities (e.g. bone deformity may be seen in supracondylar fracture of
humerus)
• Abnormal swellings (e.g. undue prominence may be seen in the posterior
aspect in posterior dislocation)
• Shortening of the arm (e.g. supracondylar fracture) or forearm (e.g. posterior
dislocation of the elbow)
From the front
• Carrying angle (Cubitus valgus, Cubitus varus)
Note
Normally, carrying angle disappears on flexion.
• Swelling (e.g. Myositis ossificans)

From behind
• Swelling (e.g. olecranon bursitis)
• Olecranon process (e.g. prominent in posterior dislocation)
• Hollows on both sides of olecranon (e.g. full in synovitis, haemarthrosis)
• Bony landmarks (medial condyle, lateral condyle and the tip of olecranon lie
in straight line when the elbow is extended, they form an isosceles triangle
when the elbow is flexed)
From side
• Olecranon process (e.g. undue prominence in posterior dislocation)
From all sides
• Discolouration (e.g. haematoma, cellulites)
• Swelling (e.g. callosity)
• Sinus and discharge (e.g. tuberculous arthritis)
• Scars (e.g. surgical wounds)
AP widening is seen in posterior dislocation of olecranon and supracondylar
fracture
Palpation
Palpation of the painful area (described by the patient) is done last.
Bones
What to look for:
• Temperature: Elbow is felt with the back of the hand for warmth (e.g.
infective conditions such as septic arthritis) (Fig. 41.23A)
• Thickening: Thickening is felt in malunited fractures
• Irregularity and crepitus: Irregularity and crackling sensation is felt in
fractures
• Tenderness: Tenderness is elicited in fractures and infective conditions (e.g.
tenderness over the medial epicondyle—golfer’s elbow, lateral epicondyle—
tennis elbow, olecranon process—olecranon bursitis). Joint line tenderness
should be elicited (e.g. synovitis)
• Abnormal movements or deformity: Abnormal movements are seen in
ununited fractures
FIGURE 41.23A Feeling the elbow for warmth.
• Lower end of humerus: The surgeon should stand in front of the seated
patient and should gently run the examining hand on the humerus (Fig.
41.23B) above, downwards, all round (e.g. abnormal depression or
prominence may be felt in cases of displaced supracondylar fractures, the
lower end of humerus is widened in intercondylar fracture).
• Upper end of ulna: The upper end of ulna is felt by running the finger
starting at the mid forearm and run upwards towards the elbow (Fig. 41.23C)
and looked for undue prominences (e.g. olecranon is prominent in posterior
dislocation of ulna) and depressions (e.g. displaced fractures of ulna).
• Upper end of radius:
• The upper end of the radius is felt by running the finger starting at the mid
forearm and run upwards towards the elbow and looked for undue
prominences (e.g. dislocation of radial head) (Fig. 41.24A).
• The head of the radius is palpated 3 cm distal to the lateral epicondyle and
appreciated by supination and pronation movements of the forearm (Fig.
41.24B) (e.g. head of radius is displaced anteriorly in Monteggia fracture,
and posteriorly in reverse Monteggia fracture)
• Position of bony points: In extension, the tip of olecranon process and the
condyles make a straight line, and in flexion, they form a triangle (Figs.
41.25 A and B). Intercondylar distance is determined in relation to the other
side (e.g. intercondylar fracture)
• Swellings: The swellings should be examined in lines with the examination of
the swellings in general (Ch. 9)
• Sinus: Should be examined in line with the examination of any sinus (Ch.
11).
FIGURE 41.23B Palpating the lower end of humerus.
FIGURE 41.23C Palpating the upper end of ulna.
FIGURE 41.24A Palpating the upper end of radius.
FIGURE 41.24B Palpating the head of radius.
FIGURE 41.25A Bony points of elbow forming a triangle in flexion.
FIGURE 41.25B Bony points of elbow forming a line on extension.
Note
sinus.
• Laxity of the joint: The joint should be moved with the fingers and tested for
abnormal laxity (Fig. 41.26)
• Muscles and tendons: The triceps tendon is palpated in the posterior aspect
of the elbow (e.g. displaced backwards in posterior dislocation).
FIGURE 41.26 Examining the elbow for laxity.
Power of each muscle group (Ch. 49) should be tested by:

• Shoulder and elbow movements
• Wrist movement
• Thumb and finger movements
• Gripping
• Nerve function: Tests of sensory and motor functions, sweating in
distribution of median, ulnar and radial nerves should be performed (Ch. 49)
• Circulation: Radial pulse and ulnar pulse (Ch.13) should be felt (e.g. absent
in application of tight bandages, supracondylar fracture). Warmth, colour,
capillary return and cutaneous sensibility should be determined
• Examination of cubital fossa: The cubital fossa should be examined for the
following:
• Fullness of the fossa (e.g. fullness caused by effusion)
• Biceps tendon (e.g. tendinitis)
• Brachial artery pulsation (this artery is easily palpated medial to the biceps
tendon) (Fig. 41.27)
• Examination of posterior aspect of elbow
• Ulnar nerve: This is palpated behind the medial epicondyle by rolling the
nerve over the bone by the examining index finger, and looked for
swellings or thickenings (e.g. Hansen’s disease) (Fig. 41.28A)
• Supratrochlear lymph node: This is felt above the medial epicondyle (Fig.
41.28B)
FIGURE 41.27 Feeling the brachial artery pulse medial to biceps tendon.
FIGURE 41.28A Palpating the ulnar nerve behind the medial epicondyle.
FIGURE 41.28B Feeling for the supratrochlear nodes above the medial
epicondyle.
Movements
A full range of movement of the elbow joint usually rules out the possibility of
moving the forearm in various directions. The normal range of movements of the
elbow and the methods of determination (Figs. 41.29 A–D) are given in Table
41.2.
FIGURE 41.29 (A) Flexion of elbow. (B) Extension of elbow. (C) Pronation
of forearm. (D) Supination of forearm.
TABLE 41.2
Normal Range of Movements at the Elbow and the Methods of
Determination
Movement Method Normal Range

Flexion Fingertips are brought up to touch the shoulder on the same side 0–145°
Extension The arm and forearm are made to lie in a straight line 0°
Hyperextension The arm is taken behind beyond the neutral position 10–15°
a
Rotation movements
Pronation In the elbow in neutral position, the palm is turned downwards 0–75°
Supination In the neutral position, the palm is turned upwards 0–80°
Note
To determine the range of pronation and supination accurately, the patient’s
elbows must be flexed at right angle in order to eliminate rotation at the
shoulder.
Measurements
• Length of the arm: Measured with a tape from the angle of the acromion to
the lateral epicondyle of the humerus (e.g. shortened in displaced lower
humeral fractures) (Fig. 41.30)
• Length of the forearm: Measured with a tape from the tip of olecranon to the
ulnar styloid, and from the lateral condyle of humerus to radial styloid (e.g.
the length is shortened in posterior dislocation of elbow) (Figs. 41.31 A and
B)
• Bony points: The distance between the three bony points, the epicondyles
and the olecranon are measured with a tape. Normally, they are equidistant
forming an isosceles triangle (e.g. altered in posterior dislocation of
olecranon, intercondylar fracture of humerus)
FIGURE 41.30 Measuring the upper arm length.
FIGURE 41.31A Measuring the length of ulna.
FIGURE 41.31B Measuring the length of radius.
Note
While taking the above measurements, the elbow should be flexed at right
angle so that the epicondyles become prominent.
• Circumference of the elbow: This is measured with a tape taken round the
elbow. This is compared with the other side (e.g. this is increased in all
dislocations of elbow, effusions of the joint) (Fig. 41.32)
FIGURE 41.32 Measuring the circumference of elbow.
Special tests
• Thomsen’s test: The patient is asked to clench the fist, dorsiflex the wrist and
extend the elbow. If the patient is forced to flex the wrist by the examiner
and while the patient resists, severe pain is felt over the lateral epicondyle in
Tennis elbow (Fig. 41.33).
• Mills manoeuvre: With the elbow flexed and forearm pronated, the flexed
elbow is extended against resistance, and pain over the lateral condyle
suggests Tennis elbow (Fig. 41.34)
• Test of Golfer’s elbow: When the elbow flexed and forearm supinated, elbow
is passively extended by the examiner, and pain over the medial condyle
suggests Golfer’s elbow (Fig. 41.35)
FIGURE 41.33 Performing Thomsen’s test for tennis elbow.
FIGURE 41.34 Performing Mill’s manoeuvre for tennis elbow.
FIGURE 41.35 Performing test for golfer’s elbow.
Lymphatic system
tuberculosis).
General
General survey of other parts of the body should be undertaken, as the local
symptoms may be the only manifestation of a systemic disease (e.g.
tuberculosis).
CHAPTER 42
WRIST, hand and fingers

V. Thulasiraman
CHAPTER OUTLINE
42.1. Wrist joint 774
• Anatomy 774
• Movements 775
42.2. Bones of the hand 775
42.3. Joints of the hand 775
42.4. Traumatic articular lesions of wrist and hand 776
• Fractures of lower end of forearm bones 776
• Colles fracture 776
• Smith fracture (Barton fracture, reversed Colles fracture) 777
• Fracture separation of lower radial epiphysis 777
• Fracture of radial styloid process (Chauffeur’s fracture) 778
• Galleazzi fracture dislocation 778
• Fracture of lower end of ulna 778
42.5. Traumatic lesions of carpal bones 779
• Fractures of carpal bones 779
• Fracture of scaphoid 779
• Dislocation of lunate 779
42.6. Traumatic lesions of metacarpal bones 780
• Fracture of base of first metacarpal bone 780
• Fractures of metacarpal bones 780
42.7. Traumatic lesions of phalanges 781
• Fractures of phalanges 781
• Mallet finger (baseball finger) 781
• Dislocations of metacarpophalangeal and interphalangeal joints
782
42.8. Nontraumatic articular lesions of wrist and hand 782
• Madelung’s deformity 782
• Kienbock’s disease 784
42.9. Extra-articular disorders of wrist and hand 784
• Simple ganglion (palmar / dorsal) 784
• Compound palmar ganglion 785
• Volkmann’s ischaemic contracture 785
• Sudeck’s atrophy (reflex sympathetic osteodystrophy) 786
42.10. Symptoms of pathologies of wrist, hand and fingers 786
• Wrist, hand and fingers 787 •
Entire upper limb 792
• General 792
42.1 Wrist joint
Anatomy
Wrist joint is a synovial joint of the ellipsoid variety between the lower end of
the radius, the articular disc overlying the distal end of the ulna and the scaphoid,
lunate and triquetral. The articular disc of the inferior radioulnar joint covers the
head of the ulna and is attached to the base of the ulnar styloid process. This
disc, along with the distal end of the radius, forms the proximal surface of the
wrist joint. The distal surface is made by the proximal articular surfaces of
scaphoid, lunate and triquetral bones (Fig. 42.1A).
FIGURE 42.1A Anatomy of joints of wrist and hand.
The articular capsule surrounds the wrist joint. It is attached above to the
lower ends of the radius and ulna, and below to the proximal row of carpal
bones. The capsule is reinforced by the following ligaments:
1. Palmar radiocarpal ligament—it is a broad band and begins from the anterior
margin of the lower end of the radius and its styloid process, runs downwards
and medially and attaches to the anterior surfaces of the scaphoid, lunate and
triquetral bones
2. Palmar ulnocarpal ligament—it is a rounded fasciculus, and begins above
the base of the ulnar styloid and anterior margin of the articular disc, runs
downwards and laterally and attaches to the lunate and triquetral bones
3. Dorsal radiocarpal ligament—it is attached above to the posterior border of
the lower end of the radius, its fibres are directed obliquely downward and
medialward and is attached to the dorsal surface of scaphoid and lunate and
continues with intercarpal ligaments
4. Ulnar collateral ligament—it extends from the tip of the ulnar styloid process
to the triquetral and pisiform bones
5. Radial collateral ligament—it extends from the tip of the radial styloid
process to the scaphoid bone
Relations of the WRIST joint

• Anteriorly: Long flexors with their synovial sheaths, flexor retinaculum,
median and ulnar nerves
• Posteriorly: Extensor tendons of the wrist and fingers with their synovial
sheaths, and extensor retinaculum
• Laterally: Radial artery and its branches
Movements
It is a condyloid joint meaning that it allows flexion, extension, abduction,
adduction and circumduction, the last being a combination of all other four
movements, occurring at the radiocarpal joint. Flexion and extension are
increased by associated sliding movements of the intercarpal joints, but the range
of flexion is actually less than that of the extension at the wrist.
The muscles acting on the wrist are tabulated in Table 42.1.
TABLE 42.1
Muscles Acting on the Wrist
Flexors All long muscles crossing the anterior aspect of the wrist joint (flexor carpi radialis, flexor carpi ulnaris,
palmaris longus, flexor pollicis longus)
Extensors All long muscles crossing the posterior aspect of the wrist joint (extensor carpi radialis longus, extensor carpi
radialis brevis, extensor carpi ulnaris)
Adductors Flexor carpi ulnaris, extensor carpi ulnaris
Abductors Flexor carpi radialis, extensor carpi radialis longus, xtensor carpi radialis brevis, abductor pollicis longus,
extensor pollicis brevis and longus
The inferior radioulnar joint aids the movements of the wrist joint with its
movements, pronation and supination.
42.2 Bones of the hand

Carpal bones are eight in number arranged in two rows of four each:
• Proximal row: Pisiform, triquetral, lunate and scaphoid
• Distal row: Hamate, capitate, trapezoid and trapezium
The proximal row excepting the pisiform, forms a convex curve, which
articulates with the concave radial articular surface. The carpal bones are
supplied by dorsal and palmar carpal arterial arcades.
Metacarpals are five and articulate proximally with the distal carpal row, and
distally with the proximal phalanges of the respective fingers. First metacarpal is
in a more palmar plane than the others. This helps to oppose the thumb against
the fingers. It articulates with the trapezium as a specialized saddle joint. This
carpometacarpal joint is the most important joint for hand function.
Phalanges: There are three phalanges in each finger, excepting in the thumb,
where there are two.
42.3 Joints of the hand

Joints between the individual carpal bones allow gliding movement, and increase
the extension and more particularly flexion of the wrist.
The ranges of movement at various joints of the hand (Fig. 42.1B) are
tabulated in Table 42.2 and the muscles acting on the fingers are tabulated in
FIGURE 42.1B Movements.
TABLE 42.2
Range of Movement at Various Joints of Hand
Joints Movements Range

First carpometacarpal joint (saddle Flexion and extension (in a plane parallel to the palm of the hand) 15°
shaped)
Abduction and adduction (in a plane perpendicular to the palm of 20°
the hand)
Opposition (thumb is brought in contact with the little finger)
Second and third carpometacarpal Gliding movement of second and third metacarpals Few
joint degrees
Fourth and fifth carpometacarpal joint Flexion and extension of fourth and fifth metacarpals Small
range
M/p joint of thumb Flexion 55°
Extension 50°
Other m/p joints Flexion 90°
Extension 90°
Hyperextension 10°
Abduction 20°
Adduction 25°
Circumduction (index finger only) 360°
All interphalangeal joints Flexion 90–100°

Extension 0-5°
TABLE 42.3
Muscles Acting on the Fingers
Flexors Flexor digitorum profundus, flexor digitorum superficialis, lumbricals (profundus tendon pierces that of
superficialis over the proximal phalanx)
Extensors Extensor digitorum longus, extensor indicis, extensor digiti minimi
Adductors Palmar interossei
Abductors Dorsal interossei
TABLE 42.4
Muscles Acting on the Thumb
Long Flexor pollicis longus, extensor pollicis longus, extensor pollicis brevis, abductor pollicis longus
Short Adductor pollicis, flexor pollicis brevis, abductor pollicis brevis, opponens pollicis
Note
The flexors and extensors of the wrist play an important role in movements of
the hand for maximum efficiency.
42.4 Traumatic articular lesions of WRIST and

hand
Fractures of lower end of forearm bones
Colles fracture
• Fracture of the distal end of the radius occurring at about 2.5 cm above the
articular surface of the radius
• The lower segment is displaced slightly backwards and laterally and is tilted
backwards so that the articular surface, instead of pointing downwards,
points slightly upwards. The lower fragment is also driven upwards and
impacted into the upper fragment
• Nearly always caused by a fall on the outstretched hand
• Common in adults above 40 years of age
• Common in women due to associated osteoporosis (postmenopausal women)
Complications: Malunion, subluxation of inferior radioulnar joint, stiffness of
fingers, rupture of tendon of extensor pollicis longus, Sudeck’s atrophy of the
bones of the wrist and hand, median nerve injury
• Pain and swelling near the wrist
• Clinical examination reveals:
• Hollow depression is seen in the lowest third of the forearm (proximal to
the fracture), but immediately below this is a marked prominence caused
by the lower fragment’s being carried backwards along with the carpus
and hand. This deformity is termed the ‘dinner fork deformity’—
described by Abraham Colles (Fig. 42.2)
• The styloid process of the radius comes to lie in line with that of the ulnar
styloid
• Palmar flexion is severely restricted and painful
FIGURE 42.2 Colles fracture left (dinner fork deformity).
X-rays of the wrist
with the lower end of the forearm (anteroposterior (AP) and lateral views)
(Fig. 42.3) are diagnostic
FIGURE 42.3 X-ray—Colles fracture.
Treatment
• Undisplaced fractures need immobilization in plaster cast for 6 weeks
• Displaced fractures need manipulation reduction under anaesthesia, followed
by immobilization in a cast in the position of palmar flexion and ulnar
deviation for 6 weeks
• Severely comminuted fractures need surgical stabilization
Note
Abraham Colles was an Irish surgeon and described this deformity in 1814
much before the X-rays were invented.
Smith fracture (barton fracture, reverse colles fracture)

• When the distal fragment of the lower end of the radius fracture is displaced
and tilted forwards, it is termed Smith fracture
• Usually caused by a fall on to the back of the hand, which at the time of
impact is flexed at the wrist
• Pain and swelling near the wrist
• Clinical examination reveals the classical ‘spade deformity’
X-rays of the wrist
with the lower end of the forearm (AP and lateral views) (Fig. 42.4) are
diagnostic
FIGURE 42.4 Smith fracture.
Treatment
• Undisplaced fractures need immobilization in a plaster cast for 6 weeks
by immobilization in an above elbow cast in the position of dorsiflexion and
supination for 6 weeks
• Severely comminuted fractures require open surgery and fixation
Fracture separation of lower radial epiphysis

• Seen in young children, in which, the epiphysis is separated through the
epiphyseal line, but a small fragment from the metaphysis is carried with it
• Can be a counterpart of a severely displaced Colles fracture in adults
Complications: Disturbance of epiphyseal growth (may occur in spite of
adequate treatment)
Deformity is similar to that of Colles fracture
X-rays of the wrist
diagnostic. X-ray of the normal side is essential for comparison
FIGURE 42.5 X-ray—fracture separation of lower radial epiphysis.
Treatment
• Undisplaced fractures need immobilization in a plaster cast for 6 weeks
by immobilization in a cast in the position of palmar flexion and ulnar
deviation for 3–6 weeks
• Severely comminuted fractures require open surgery and internal fixation
Fracture of radial styloid process (chauffeur’s fracture)

• An oblique fracture of the radial styloid process, which is intra-articular
• Occurs following an attempt to start a car with a starting handle, which recoils
to hit the styloid process
• Usually undisplaced
• Pain and swelling over the radial styloid, with a typical history of attempting
to start a car with a starting handle
• Clinical examination reveals tenderness over the anatomical snuffbox
X-rays of the wrist
diagnostic
FIGURE 42.6 X-ray—fracture of radial styloid.
Treatment
Immobilization in below elbow plaster cast for a period of 3–4 weeks
Galleazzi fracture dislocation

• Analogous to Monteggia fracture dislocation
• The shaft of the radius is fractured near the middle and lower thirds, the
ligaments of the inferior radioulnar joint are ruptured and the head of the
ulna is displaced from the ulnar notch of the radius
• Caused by:
• Direct trauma over the bone
• Indirect trauma such as a fall on the outstretched hand
Complications: Ulnar nerve injury, malunion, nonunion
• Pain, swelling and deformity
• Tenderness is remarkable
• Movements at elbow and wrist are painful and restricted
X-rays of the wrist and forearm (AP and lateral views) (Fig. 42.7) are diagnostic
FIGURE 42.7 X-ray—Galeazzi fracture dislocation.
Treatment
Open surgery and fixation of radial fragments with reduction of dislocation of
inferior radioulnar joint
Fracture of lower end of ulna

• Common fracture in adults
• Caused by a fall on the outstretched hand or a direct blow or injury over the
subcutaneous border of the ulna
• May be associated with inferior radioulnar dislocation
• Pain and swelling near the wrist joint
• Tenderness is remarkable on the fracture site
X-rays of the wrist
diagnostic
FIGURE 42.8 X-ray—fracture of lower end of ulna.
Treatment
• Stable fracture needs immobilization in a cast for 6 weeks
• Unstable fracture needs open reduction and internal fixation
42.5 Traumatic lesions of carpal bones

Fractures of carpal bones
Apart from the scaphoid bone, the carpal bones are seldom the site of serious
fractures, and the principles of treatment are like those for uncomplicated
fractures of scaphoid bone
Fracture of scaphoid
• Usually caused by a fall on the outstretched hand
• The fracture is usually through the middle or waist of the scaphoid; so the
proximal and distal fragments are of about equal size
• Displacement of the fragments occurs when the violence is severe
Complications: Delayed union, nonunion, avascular necrosis and
osteoarthritis
• Pain in the wrist (very slight and the diagnosis may be missed)
• Tenderness in the scaphoid region (anatomical snuffbox) is elicitable
• X-rays of the wrist with the lower end of the forearm (AP and lateral views,
and oblique views) (Fig. 42.9) are useful
• CT is useful in doubtful cases
FIGURE 42.9 X-ray—scaphoid fracture.
Treatment
Immobilization of the wrist in a plaster cast (scaphoid cast) for 2–3 months
Dislocation of lunate
In spite of the strong ligamentous attachments, the lunate bone is liable for
dislocation through a fall on the hand
• The displacement is characteristic, it lies at the front of the wrist and it is
rotated through 90° or more on a horizontal axis so that its concave lower
articular surface faces forwards, which occurs due to the tear of its posterior
attachments
Note
When X-rays are normal, repeat X-rays are required after 1 week for
confirmation
Complications: Avascular necrosis, osteoarthritis, injury to median nerve
• Pain and swelling around the wrist joint
• The concave articular surface of the lunate may be palpable
X-rays of the wrist
(AP and lateral views) (Fig. 42.10) are diagnostic
FIGURE 42.10 X-ray—dislocation of lunate.
Treatment
• Manipulation under anaesthesia is the treatment of choice, followed by
immobilization
• Rarely, surgical excision of the lunate bone is required in neglected cases
42.6 Traumatic lesions of metacarpal bones
Fracture of base of first metacarpal bone

• Caused by longitudinal violence applied by a blow, as in boxing
• It is of two types:
1. Transverse or short oblique fracture across the base of metacarpal,
but not entering the joint
2. Oblique fracture entering the carpometacarpal joint at about middle of
articular surface (Bennett’s fracture)—more serious as this can result
in displacement proximally and laterally on trapezium due to pull of
the abductor pollicis longus
• Swelling and pain over the base of the thumb
• Severe tenderness on movement of the thumb
X-rays of the wrist
(AP and lateral views) (Fig. 42.11) are diagnostic
FIGURE 42.11 X-ray—Bennet fracture.
Treatment
Internal fixation after reduction of fracture in Bennett’s fracture dislocation
Fractures of metacarpal bones

• Fairly common at all ages
• Commonest cause being a fall on the hand and a blow upon the knuckles as in
boxing
• The types of fracture are:
• Fracture through the base of metacarpal
• Oblique fracture of shaft
• Transverse fracture through the neck of the bone
• Slight displacement does not interfere with functional recovery of hand
• Marked angulation at fracture site is uncommon
Pain at fracture site of the metacarpal bone
X-rays of the wrist and hand
(AP, lateral and oblique views) (Figs. 42.12A and B) are diagnostic
FIGURE 42.12A X-ray—fracture of head of fourth and base of fifth

metacarpal bone.
FIGURE 42.12B X-ray—fracture of third, fourth, fifth metacarpal bones.
Treatment
• Undisplaced fractures need no treatment excepting analgesics. If the swelling
is severe, rest in plaster slab for 3 weeks is sufficient
• Displaced fractures need fixation with K wire. Fractures through the neck
may need surgery to improve the function of the metacarpophalangeal joint
42.7 Traumatic lesions of phalanges
Fractures of phalanges
• Varieties of fractures occur in phalanges, usually caused by:
• Direct injury (fall of heavy objects, crush injury)
• Industrial accidents in functioning hands
• They are:
• Long spiral fracture of shaft
• Transverse fracture of shaft
• Oblique fracture of base
Pain and swelling over the fracture site of the finger
X-rays of the finger
(AP and laterwal views) (Figs. 42.13A–C) are diagnostic
FIGURE 42.13A X-ray—fracture of proximal phalanx.
FIGURE 42.13B X-ray—fracture of middle phalanx index finger.
FIGURE 42.13C X-ray—fracture of terminal phalanx.
Treatment
• Undisplaced fractures: The fingers may be bound to the adjacent normal
finger with adhesive strapping
• Displaced fractures: K-wire fixation and splintage
• Comminuted fractures: Need external fixation for 6 weeks
Mallet finger (baseball finger)
• Tearing of the extensor tendon at the base of distal phalanx, usually due to
sudden flexion violence
• A fragment of bone may also get avulsed with the tendon, in most cases
• Pain and swelling at the base of terminal phalanx of the finger, with severe
pain on movement
• Flexion deformity of terminal phalanx at 20° and is unable to extend
• Passive extension is possible
X-rays of the finger (AP and lateral views) are diagnostic if bone is avulsed
(Fig. 42.14)

FIGURE 42.14 X-ray—mallet finger.
Treatment
• Immobilization of the finger for 3 weeks, in a position of flexion of proximal
interphalangeal joint and extension of distal interphalangeal joint
• If a large fragment of bone is avulsed, wire fixation is warranted
Dislocations of metacarpophalangeal or
interphalangeal joints
• Usually caused by forced hyperextension
• The distal fragment is usually displaced backwards from the proximal
• They may be associated with fractures
• Swelling and pain at the dislocated site, with inability to move the finger joint
X-rays of the finger
(AP and lateral views) (Figs. 42.15A and B) are diagnostic
FIGURE 42.15A X-ray—metacarpophalangeal dislocation.

FIGURE 42.15B X-ray—dislocation of proximal interphalangeal joint.
Treatment
• Reduction under anaesthesia or finger blocks
• Fractures need fixation
Note
The fibrocartilage plate is torn in the dislocation of the second
metacarpophalangeal joint and closed reduction is not usually successful and
requires open surgery.
42.8 Nontraumatic articular lesions of wrist and

hand
Madelung’s deformity
• Congenital subluxation or dislocation of the lower end of the ulna
• The deformity varies in degree from a slight prominence of the lower end of
the ulna at the back of the wrist to complete dislocation of the inferior
radioulnar joint with marked radial deviation of the wrist
• Severe types may be associated with congenital absence of the radius
DD: Radial club hand—congenital absence (total or partial) of the radius with
deformity of wrist
Deformity is characteristic (Fig. 42.16A)

FIGURE 42.16A Madelung’s deformity 2 (right).
X-rays of the wrist
(AP and lateral views) (Fig. 42.16B) are diagnostic

FIGURE 42.16B X-ray—Madelung’s deformity.
Treatment
• If disability justifies surgery, lower end of the ulna may be excised
• When the radius is dysplastic and the deviation is very marked, it is better to
correct the lower end of the radius by surgery
Pyogenic arthritis
• Pyogenic arthritis of the wrist is uncommon
• Infection is haematogenous or by direct penetrating trauma
Clinical presentation, investigations and treatment are those like pyogenic
arthritis of elbow(Ch. 41)
• Rheumatoid arthritis is common in the joints of the wrist and hands
• Starts in a single joint and involves more joints
• The affected joints are swollen due to synovial thickening and movements are
restricted
• In the later stages, articular cartilage and the underlying bones are eroded, and
the fingers tend to deviate medially (ulnar drift)
The joints are swollen and the movements are painful giving a typical
appearance ‘rheumatoid hand’ (Fig. 42.17)
FIGURE 42.17 Rheumatoid hand.
Investigations (Fig. 42.18) and treatment are those like rheumatoid arthritis of
elbow (Ch. 41).
FIGURE 42.18 X-ray—rheumatoid arthritis of wrist and hand.
Tuberculosis is much less common in the wrist than it is in the large weight-
bearing joints such as the hip and knee
Clinical presentation, investigations and treatment are those like
tuberculous arthritis of elbow (Ch. 41)
Osteoarthritis
• Osteoarthritis of the wrist is common because of its tendency to get injured
and also due to high incidence of nonunion of scaphoid fractures. The
changes are degenerative and damage the articular cartilage lining the joint
surfaces
• Osteoarthritis of the metacarpophalangeal and interphalangeal joints,
though common are relatively unimportant, excepting the osteoarthritis of
trapeziometacarpal joint (carpometacarpal joint of the thumb)
• Osteoarthritis of the wrist: Increasing pain and stiffness of the wrist,
worsening on activity. Movements are markedly limited and painful when
forced
• Osteoarthritis of trapeziometacarpal joint seriously impairs the function of
the thumb
X-rays
are diagnostic (Fig. 42.19), with narrowing of cartilage space and sharpening
or spurring of the bone at the joint margins
FIGURE 42.19 X-ray—osteoarthritis wrist.
Treatment
• Physiotherapy is useful in most cases
• Osteoarthritis of the wrist: Operative treatment is reserved for worst cases,
and arthrodesis of wrist joint is the only reliable method
• Osteoarthritis of trapeziometacarpal joint, in worst situations, require
arthroplasty (excision of trapezium) or arthrodesis of trapeziometacarpal
joint
Kienbock’s disease
• Osteochondritis of lunate bone characterized by temporary shortening,
fragmentation and liability to deformation, and later osteoarthritis
• Exact cause is not known
• Pain in the wrist, most marked at the centre of the lunate area, which is worse
during active use
• On examination, there is discomfort on pressure and movements of the wrist
are limited
X-rays
are diagnostic (Fig. 42.20). Lunate bone appears fragmented with small areas
of scattered density. Late stages show signs of osteoarthritis

FIGURE 42.20 X-ray—Kienbock’s disease.
Treatment
Established cases require excision of the lunate bone or the inclination of the
lower radius may be changed by surgery
42.9 Extra-articular disorders of wrist and hand
Simple ganglion (palmar / dorsal)

• A localized, tense (often painless), cystic swelling containing clear gelatinous
fluid
• It often communicates with the tendon sheath or the capsule or joint
• The origin is uncertain, but it is believed to arise as mucoid degeneration of
connective tissue or possibly as a consequence of leakage of synovial fluid
through the capsule of a joint or tendon sheath
• Most commonly found on the dorsum of the wrist
• A tense nontender cystic swelling on the wrist, showing mobility
perpendicular to the axis of the tendon sheath (Fig. 42.21)
• Transillumination is positive
FIGURE 42.21 Simple ganglion of wrist Source: (Courtesy Dr K. Sridhar).
No special investigation
is necessary
Treatment
• Some disappear spontaneously
• Injection of hyaluronidase into the cyst and local compression is curative
• Excision for recurrent ganglia
Compound palmar ganglion

• Chronic tenosynovitis of flexor muscles causing effusion
• Usually caused by tubercle bacilli
• Effusion presents as ‘melon-seed bodies’, which resemble grains of boiled
sago, which are fibrous loose bodies composed of fibrin, cellular debris and
occasional tubercle bacilli
• A soft painless swelling above and below the flexor retinaculum (Fig. 42.22),
with cross fluctuation between compartments
• There may be associated wasting of muscles of the hand
FIGURE 42.22 Compound palmar ganglion (left wrist).

• X-ray wrist to rule out bony pathology
• US may be informative
Treatment
• General measures with use of antitubercular drugs and application of
appropriate plaster cast to immobilize the involved flexor sheath is advisable
• If the condition progresses, careful dissection and removal of the tendon
sheath is indicated
Volkmann’s ischaemic contracture

• Flexion deformity of the wrist and fingers due to fixed contracture of the
flexor muscles in the forearm
• It is the ischaemic necrosis of structures contained within the volar
compartment of the forearm (Fig. 42.23A), especially muscle fibres of
forearm flexors (flexor digitorum profundus and flexor pollicis longus)
• Common cause is injury or obstruction of brachial artery near the elbow (see
supracondylar fracture)
• Often associated with ischaemic paralysis of median nerve
• Rarely, a tight plaster or bandage is a cause
• Common in children
FIGURE 42.23A Mechanism of Volkmann’s ischaemic contracture.
• In the incipient stage, the fingers are blue or white, and cold, with absent
radial pulse (Fig. 42.23B). Movements are weak and painful. Anaesthesia of
the hand and paralysis of small muscles of the hand may be evident (Table
42.5)
• In late stages. there is a striking flexion contracture of the wrist and fingers
(Fig. 42.23C). Sensory and motor paralysis of hand may be present. The
wrist can be partly extended if the fingers are flexed, and the fingers can be
partly extended if the wrist is flexed, but shortened flexors prevent extension
of the wrist and fingers together (Volkmann’s sign) (p. 796).
FIGURE 42.23B Ischaemic limb in incipient stage.

FIGURE 42.23C Volkman’s ischaemic contracture.
TABLE 42.5
Clinical Features of Volkmann’s Ischaemia (Six ‘P’s)
Pain
Pallor
Paraesthesia
Paralysis
Pulselessness
Positive passive stretch test of flexor digitorum profundus
Doppler studies of brachial artery
may be useful
Treatment
• In the incipient stage, all plasters, splints should be removed quickly, and the
vascularity should be established
• In the acute stage:
• Brachial artery should be explored and repaired by excision and end-to-end
anastomosis or by a vein graft
• In late stages:
• Muscle sliding and tendon transfer operations are required
• Nerve injuries need appropriate repair
Sudeck’s atrophy (reflex sympathetic

osteodystrophy)
• Otherwise called, posttraumatic painful osteoporosis, is an occasional cause of
prolonged disability after fractures or other injuries of limbs
• Exact cause is not known
• Commonly seen in hypertensives
• Pain, swelling and marked joint stiffness in the hand of the injured limb
• The symptoms are noticed about 2 months after injury, or when the plaster is
removed and the function is not regained
• On examination:
• In acute stage:
- The extremity is swollen and hyperaemic
• In the late stages:
- Obliteration of skin creases and the nails and hair become atrophic (Fig.
42.24)
- Palmar aponeurosis may be thickened
- Joint movements are severely impaired and result in ‘frozen hand’

FIGURE 42.24 Sudeck’s atrophy.
X-rays
show spotty osteoporosis, often of severe degree
Treatment
• Active exercises and conservative treatment is fruitful
• Patience and encouragement are required and adequate recovery is usually
gained in 2–4 months
42.10 Symptoms of pathologies of wrist, hand

and fingers
• Pain
• Swelling
• Deformity
Pain
Pain due to wrist joint pathology is localized to the wrist area. The causes may
be related to:
• Bones and joints (e.g. arthritis)
• Soft tissues (e.g. carpal tunnel syndrome)
Swelling
The swellings around the wrist joint can be generalized or localized:
• Generalized (e.g. arthritis)
• Localized (e.g. ganglion, osteoclastoma of lower end of radius)
Deformity
Deformities are caused by localized pathologies (e.g. malunited Colles fracture,
Madelung’s deformity)
Movements of wrist joint are restricted due to traumatic, inflammatory,
neoplastic and degenerative conditions:
• Neoplastic (e.g. osteoclastoma of lower end of the radius)
• Degenerative (e.g. osteoarthritis of wrist joint)
Eliciting history
1. Onset of pain: When did the pain start, was it slow in onset or sudden?
2. Relationship to trauma: Is this pain preceded by an injury, accident, or
sport or a fall?
This will answer the act following which the pain has appeared, and the
slips may cause soft tissue injuries, and fall during active sports or road traffic
accidents may cause fractures)
3. Position during trauma: What was the position of the hand during the fall?
A fall on outstretched hand may result in Colles fracture or fracture of
scaphoid (indirect injury), and a fall on the point of wrist may result in Smith
fracture (direct injury)
4. Intensity of pain: How bad is this pain?
Very severe pain may indicate fractures
5. Relationship to movements: Is this pain related to movements?
fractures, and nontraumatic situations, may indicate arthritis
6. Treatment: Was any treatment or first aid given to this pain?
have to be scrutinized if available

Note
It should be remembered that the symptoms in the hand are often caused by
disorders of the neck (with involvement of brachial plexus) and also by
disorders at the elbow. Enquiry should be made to any previous injury or any
trouble with the neck or with the upper limb as a whole, more so in
neurological involvement.
wrist, hand and fingers
Pre-requisites
• Patient should be undressed so that the entire upper limb is exposed
Undressing
• How clumsy is he or she in his or her movements (e.g. nerve injuries causing
motor paralysis of small muscles of the hand)
strain and investigate. It should be done from close quarters and also from at a
distance:
• Position of the patient: Sitting or standing with both hands side by side
• Position of the examiner: The examiner should view the hands from all sides,
from the front (palmar aspect), back (dorsal aspect) and sides
Inspection
What to look for?
• Attitude of the patient (e.g. patients with fracture dislocation of wrist are seen
supporting the wrist with the other hand)
• Change in contour of the shoulder (e.g. contour of the shoulder disturbed in
fractures of the wrist, due to adaptation by the patient—shoulder-hand
syndrome)
• Deformities (e.g. dinner-fork deformity in Colles fracture, spade deformity in
Smith fracture, ulnar drift in rheumatoid hand)
• Skin—shiny (e.g. Sudeck’s atrophy), ecchymosis (e.g. direct injury)
• Abnormal swellings (e.g. ganglion, rheumatoid nodule, haematoma)
• Wasting of muscles, nails and pulps of fingers
From the front:
• Angular deformities of the wrist (e.g. manus valgus deformity in inferior
radioulnar instability, ulnar drift in rheumatoid arthritis)
• Swelling (e.g. ganglion)
From behind:
• Ulnar styloid process (e.g. less prominent in fractures of the lower end of
ulna)
• Radial styloid process (e.g. prominent in fracture of radial styloid)
• Bony landmarks (normally the radial styloid is 1.3 cm lower than the ulnar
styloid (Fig. 42.25), but they come to lie in straight line in Colles fracture)
FIGURE 42.25 Normal positions of radial (red arrow) and ulnar (black
arrow) styloid processes.
From sides:
• Swelling of the wrist (e.g. synovial proliferative effusion)
• Deformities.(e.g. mallet finger deformity / boutonniere deformity)
From all sides: Note for discolouration (e.g. haematoma), sinus and discharge
(e.g. tuberculous arthritis)
Palpation
Palpation of the painful area (described by the patient) is done last
Bones
What to look for:
• Temperature—wrist is felt with the back of the hand for warmth (e.g.
infective conditions such as septic arthritis) (Fig. 42.26)
• Thickening—malunited fracture in Colles fracture
• Irregularity and crepitus—crackling sensation is felt in fractures and in
tenosynovitis
• Tenderness
• Joint line tenderness (e.g. osteoarthritis, synovitis) (Fig. 42.27)
• Tenderness is elicited in fractures and infective conditions
• Tenderness over the styloid processes (e.g. radial styloid in de Quervain’s
tenovaginitis, fracture of ulnar styloid)
• Tenderness over the scaphoid in the anatomical snuffbox
• Tenderness on the lower end of the forearm bones (e.g. fractures).
Springing the radius is done by squeezing the radius and ulna together at
the lower part of the forearm (Fig. 42.28), and this can induce pain at the
fracture site on the bones of the forearm
• Abnormal movements or deformity—unnited fractures
FIGURE 42.26 Feeling the wrist joint for warmth.
FIGURE 42.27 Eliciting tenderness on the wrist.
FIGURE 42.28 Method of springing the forearm bones.
• Lower end of radius: The surgeon should stand in front of the seated patient
and should gently run the examining hand on the radius above, downwards,
all round (e.g. abnormal depression on the dorsal aspect may be felt in Colles
fracture, on the ventral aspect in Smith fracture, and thickening in malunited
fractures) (Fig. 42.29)
• Lower end of ulna: The surgeon should stand in front of the seated patient
and should gently run the examining hand on the ulna above, downwards, all
round (e.g. abnormal depression on the ulna in fracture dislocations of its
lower end) (Fig. 42.30)
• Position of bony points (styloid processes): The examiner should feel both
the styloid processes together at the same time with the index fingers of both
hands (Fig. 42.31). (Normally the radial styloid is 1.3 cm lower than the
ulnar styloid (Fig. 42.25), but they come to lie in straight line in Colles
fracture)
• Carpal bones: The examiner should run the examining fingers on the carpal
bones, both on the palmar and dorsal aspect (e.g. dislocated lunate bone may
be palpable) (Figs. 42.32A and B)
• Swellings: The swellings should be examined in lines with the examination of
the swellings in general (Ch. 9)
• Sinus: Sinus should be examined in line with the examination of any sinus
(Ch. 11)
FIGURE 42.29 Palpating the shaft and lower end of radius.
FIGURE 42.30 Palpating the shaft and lower end of ulna.
FIGURE 42.31 Palpating the styloid processes.
FIGURE 42.32A Palpating the carpal bones on the palmar aspect.
FIGURE 42.32B Palpating the carpal bones on the dorsal aspect.
Note
sinus.
• Laxity of the joint: The wrist joint should be moved anteroposteriorly and
tested for abnormal laxity (e.g. Ehlers–Danlos syndrome) (Fig. 42.33). The
general laxity should also be determined
• Muscles and tendons: The muscles of the hand should be felt (e.g. wasting
may be felt in Dupuytren’s contracture, shortening of flexors in Volkmann’s
ischaemic contracture). Power of each muscle group should be tested by:
• Wrist movement
• Thumb and finger movements
• Gripping (denotes combined action of the flexors and extensors of the wrist
and the flexors of the fingers and thumb)
distribution of median, ulnar and radial nerves should be performed (Ch. 49)
• Circulation: Radial pulse and ulnar pulse should be felt (e.g. absent in
application of tight bandages, Volkmann’s ischaemic contracture). Warmth,
colour, capillary return and cutaneous sensibility should be determined (Ch.
13)
FIGURE 42.33 Determining the laxity of wrist joint.
Movements
A full range of movement of the wrist joint usually rules out the possibility of
the moving the wrist in various directions.
Both the components of the wrist joint, the radiocarpal joint and the inferior
radioulnar joint are to be examined independently.
The normal range of movements of radiocarpal joint is given in Table 42.6.
TABLE 42.6
Normal Range of Movements of the Radiocarpal Joint and the
Methods of Determination
Normal
Movement Method
Range
Flexion In a supinated forearm, the fingers are taken upwards from its neutral 80°
position
Extension In a supinated forearm, the fingers are taken downwards from its neutral 90°
position
Adduction or ulnar In a supinated forearm, the hand is taken medially 35°
deviation
Abduction or radial In a supinated forearm, the hand is taken laterally 25°
deviation
Note
It is impractical to measure the movements of the intercarpal joints
individually, and it is better to regard them as integral parts of the radio-carpal
joint.
The normal range of movements of inferior radioulnar joint and the
methods of determination (Ref Figs. 41.29C and D) are given in Table 42.7.
TABLE 42.7
Normal Range of Movements of the Inferior Radioulnar Joint and
the Methods of Determinationa
Pronation In the elbow in neutral position, the palm is turned downwards 90°
Supination In the neutral position, the palm is turned upwards 90°
aIf the range of rotation (pronation and supination) is restricted, possible causes must be
sought in the forearm and the wrist as well as in the elbow.
Note
To determine the range accurately, the patient’s elbows must be flexed at right
angle in order to eliminate rotation at the shoulder.
Measurements
• Length of the forearm: This is measured with a tape from the tip of olecranon
to the ulnar styloid, and from the lateral condyle of humerus to radial styloid
(Figs. 42.34A and B) (e.g. the length is shortened in displaced fracture of
forearm bones, such as Colles fracture)
FIGURE 42.34A Measuring the length of ulna.

FIGURE 42.34B Measuring the length of radius.
Note
While taking the measurements, the elbow should be flexed at right angle so
that the epicondyles become prominent.
• Circumference of the forearm and the wrist: This is measured with a tape
taking it around the forearm and the wrist. This is compared with the other
side (e.g. this is increased in all effusions of the joint) (Fig. 42.35)
FIGURE 42.35 Measuring the circumference of wrist.
Special tests
• Finkelstein’s test: The patient is asked to flex the elbow at right angle, make a
fist over the examiners thumb. Then the patient’s hand is bent to ulnar
deviation. This will give pain on the lateral border of the distal end of the
radius, as the abductor pollicis longus and extensor pollicis brevis tendons
are put on stretch. This is positive in de Quervain’s disease (Fig. 42.36)
• Phalen’s test: The patient’s wrist is passively flexed and kept in that position
for some time. Presence of pain and paraesthesia in the area of distribution of
median nerve is indicative of carpal tunnel syndrome (Fig. 42.37)
• Maisonneuve’s sign: The patient is asked to flex the elbow at right angle, and
keep the forearm pronated. When he or she is asked to extend the wrist joint,
the wrist will get hyperextended in malunited Colles fracture
• Tinel’s sign: A gentle percussion is done over the median nerve at the
compression site. Feeling of paraesthesia in the area of distribution of
median nerve is an indication of carpal tunnel syndrome (Fig. 42.38)
• Volkmann’s sign: Wrist can be partly extended if the fingers are flexed, and
the fingers can be partly extended if the wrist is flexed, as shortened flexors
prevent extension of the wrist and fingers together (Fig. 42.39). This is
characteristic of Volkman’s ischaemic contracture
FIGURE 42.36 Demonstrating Finkelstein’s test.

FIGURE 42.37 Demonstrating Phalen"s test.
FIGURE 42.38 Demonstrating Tinel’s sign.
FIGURE 42.39 Eliciting Volkmann’s sign.
Entire upper limb

Examination of the entire limb is essential, as the disorders of any part of the
upper limb can manifest as a clinical finding in the wrist and hand (e.g.
Volkmann’s ischaemic contracture secondary to malunited supracondylar
fracture).
Lymphatic system
tuberculosis).
General
symptoms may be only one manifestation of a widespread disease (e.g.
tuberculosis).
CHAPTER 43
Hands (soft tissues)

K. Sridhar
CHAPTER OUTLINE
43.1. Development of hands 793
43.2. Surgical anatomy of hands 793
43.3. Diseases of hands 795
• Congenital lesions 795
• Failure of formation (absent fingers) 795
• Failure of differentiation (syndactyly) 796
• Duplication (supernumerary fingers, polydactyly) 797
• Overgrowth (gigantism, macrodactyly) 797
• Undergrowth (hypoplasia) 798
• Congenital constriction ring syndrome 798
• Injuries of hands 798
• Lymphangitis 800
• Cellulitis 801
• Abscess 801
• Infection of dorsum and dorsal spaces 801
• Carbuncle 801
• Acute paronychia 802
• Apical space infection 802
• Terminal pulp space infection 802
• Infection of volar spaces 802
• Infection of web space 803
• Deep palmar abscess 803
• Subungual haematoma 803
• Chronic paronychia 804
• Carpal tunnel syndrome 804
• Pronator syndrome 804
• Anterior interosseous syndrome 805
• Cubital tunnel syndrome 805
• Guyon’s canal syndrome 806
• Injuries to tendons 806
• Simple tenosynovitis 806
• Acute suppurative tenosynovitis 806
• Stenosing tenosynovitis 807
• Dupuytren’s contracture 807
• Implantation dermoid 807
• Palmar warts 808
• Epithelioma (squamous cell carcinoma) 808
• Benign giant cell synovioma 808
• Glomus tumour 809
43.4. Symptoms of pathologies of hands 810
• Hands 812
• Entire upper limb 813
• General 813
43.1 Development of hands
• At about 26 days, when the embryo is 4 mm long, the arm buds can be
recognized. These buds grow rapidly in length during the subsequent week
• At about fourth week, when the embryo is about 7.5 mm long, they become
paddle shaped from which the hands develop. Bone formation can be
recognized at this stage itself and is almost entirely cartilaginous. Nerves
grow into this from C4-T2 segments and so also muscles develop in the arm
• At about 6th week, the embryo reaches 17 mm in size and the fingers appear
in the hand and in 2 weeks’ time they show separation into individual
fingers. By now the embryo has grown to 25 mm
• Joints appear as clefts in between, and become subdivided by constrictions
into arm, forearm and hand. Ossification centres for radius, ulna and terminal
phalanges also appear
43.2 Surgical anatomy of hands

Hand should be considered as a specialized organ capable of performing the
prehensile function and also sensory function. It is represented in the cerebral
cortex over a wider area than most of the parts of the human body.
Skin
The dorsal skin is thin with very little subcutaneous fat and can be made to move
freely over the tendons and bones. It can stretch considerably to accommodate
the range of full flexion as we see in making a tight fist. On the other hand the
palmar skin is thicker, attached to deeper aponeurosis and septae with multiple
fibrous strands. It is made to withstand pressure and does not have hair follicles
or sebaceous glands. Palmar skin is hairless and is called ‘glabrous skin’.
Normally, keloids do not develop in glabrous skin but corns and callosities are
common.
Bones and joints

Carpal bones are eight in number arranged in two rows of four each. They form
a concave gutter on the volar (palmar) side. The scaphoid, pisiform, trapezium
and hamate give attachment to the flexor retinaculum which stretches across this
gutter converting it into a canal called carpal tunnel. The flexor tendons and the
nerves pass through the carpal tunnel from the forearm into the palm. The
proximal row excepting the pisiform, form a convex curve, which articulates
with the concave radial articular surface. The carpal bones are supplied by dorsal
and palmar carpal arterial arcades.
Muscles and tendons

The movements of the hand are produced by both extrinsic and intrinsic
muscles.
• Extrinsics are the long flexors and extensors of fingers, thumb and wrist
• Intrinsics are the thenar muscles, hypothenar muscles, lumbricals and
interossei. The palmar aponeurosis divides the palm into various
compartments, namely:
• Thenar
• Hypothenar
• Mid palmar (contains the flexor tendons and neurovascular bundles)
• Metacarpophalangeal joints are flexed by the intrinsic muscles and extended
by extrinsic muscles (extensor digitorum and extensor pollicis longus)
• The interphalangeal joints are flexed by extrinsic muscles (sublimis,
profundus and flexor pollicis longus) and extended by intrinsics. The flexor
digitorum sublimis gets inserted into the base of middle phalanx and is
responsible for flexion of proximal interphalangeal (PIP) joint. The flexor
digitorum profundus (FDP) gets inserted to the base of terminal phalanx and
is responsible for flexion of distal joint (Fig. 43.1). The flexor pollicis longus
flexes the interphalangeal joint of thumb
• The long extensors namely extensor digitorum communis and proprious
tendons extend the metacarpophalangeal joints. They form part of an
intricate extensor apparatus. These long tendons are joined by the interrossei
and lumbricals, which emerge at the sides of fingers from the palmar side.
Together they proceed distally and divide into one central and two lateral
slips. The central slip gets inserted into the dorsal aspect of the base of the
middle phalanx and is responsible for extending the PIP joint. Injury to this
central slip produces boutonniere deformity (inability to extend PIP joint).
The two lateral slips proceed distally and join together and get inserted into
the base of the terminal phalanx and is responsible for extending the distal
joint. Division of this part in any injury causes mallet deformity
FIGURE 43.1 Flexors and extensor apparatus of finger.
Tendon sheaths
• The extensor tendons are covered by a thin layer of connective tissue which is
called as paratenon
• The flexor tendons of the little finger are covered by a synovial sheath which
extends from the forearm into the palm called ulnar bursa. The sheath for
the thumb flexor is separate and is called radial bursa
• There are many variations in its arrangement
The importance of these bursae is the fact that they can swell in chronic
inflammatory conditions and can crowd the carpal tunnel. Cross fluctuation can
be elicited across the wrist when it is inflamed. The sheath becomes thick as the
fibrous flexor sheath in the distal palm and extends into fingers forming multiple
annular and cruciform pulleys keeping the tendon down preventing
bowstringing.
Vascular supply
• Both radial and ulnar arteries supply the hand. The ulnar artery is usually
dominant but rarely it can be radial
• The ulnar and radial arteries join to form the superficial and deep palmar
arches
• The superficial and deep palmar arches give off multiple branches to supply
the hand
• Three common digital arteries arise from the superficial palmar arch, and each
divides into two at the level of distal palm crease and supply the adjacent
sides of middle three fingers
• Apart from these, arteries are given off which supply the ulnar side of little,
radial side of index and the thumb
• Vena comitantes accompany these arteries
• The dorsal veins are more dominant and form dorsal venous arches, which
ultimately give rise to the cephalic and basilic veins at the radial and ulnar
sides, respectively
Lymphatics
They are mainly in the subdermal area of dorsum running along the veins and
drain most of hand. They predominantly drain into axillary nodes. Very few end
up at cubital nodes.
Nerves
• Ulnar nerve supplies:
• The skin of ulnar one and half fingers
• Extrinsic: Flexor carpi ulnaris and medial half of FDP
• Intrinsic: All interrossei and the medial two lumbricals, hypothenar
muscles, adductor pollicis, deep head of flexor pollicis brevis
• Median nerve supplies:
• The skin of radial three and half fingers
• Extrinsic: Lateral half of FDP, sublimis, flexor pollicis longus, flexor carpi
radialis and palmaris longus, pronator quadratus
• Intrinsic: Lateral two lumbricals, adductor pollicis brevis and one head of
flexor pollicis brevis
• Radial nerve supplies:
• The skin of dorsal aspect of hand thumb and parts of fingers*
• All extensors of wrist and hand
43.3 Diseases of hands
Congenital lesions
• Congenital lesions of hand are classified with regard to the embryological
failure
• There are seven such categories:
• Failure of formation (absent fingers)
• Failure of differentiation or separation (syndactyly)
• Duplication (polydactyly)
• Overgrowth (gigantism or hyperplasia)
• Undergrowth (hypoplasia)
• Congenital constriction ring syndrome
• Generalized skeletal abnormality
*Note: Ulnar and median nerves supply the distal part of fingers to a variable
extent.
Failure of formation (absent fingers)

• Occurs due to arrest in development in part or parts (Fig. 43.1A)
• May occur in an entire ray including the metacarpal and finger
• The absence may be seen in:
• Radial ray (Fig. 43.1B)
• Ulnar ray (Fig. 43.1C)
• Central ray (Fig. 43.1D)
• Complete absence of thumb or any of the other fingers can happen
• Lobster hand has only two rays with a wide cleft in between (Fig. 43.1E)
FIGURE 43.1A Hypoplasia of fingers.
FIGURE 43.1B Absence of radial ray.
FIGURE 43.1C Absence of ulnar ray.
FIGURE 43.1D Absence of central ray.

FIGURE 43.1E Lobster hand.
These children get used to using the available fingers for daily activities,
surprisingly effectively with dexterity, unless all the fingers are absent
X-rays are contributory and also in evaluating associated bony abnormalities in
the adjoining bones
Treatment
• No treatment is required if the function is good
• If the thumb is entirely absent, a finger may be used to reconstruct the thumb
(pollicization)
• Whatever be the reconstruction, the aesthetic appearance is not good
• If appearance is the only concern then only prosthesis is advisable
Failure of differentiation (syndactyly)

• One of the most common anomalies of hand with an incidence of about 1 in
2000–3000 births
• It occurs due to failure of differentiation or separation
• Syndactyly can present in isolation or in association with other malformations
or as part of a recognized syndrome
• Can present with only fusion of soft tissue (simple) to bony fusion
(compound). The entire length of the finger may be fused or only part of its
length (Fig. 43.2)
• When the fingers are almost fused together distally and small tunnels remain
in the web, it is called as acrosyndactyly (Fig. 43.3). This is common in
syndrome of craniofacial anomalies such as Apert syndrome
• Fusion also can manifest in hypoplastic fingers, supernumerary fingers and
also in short fingers and among the remaining fingers with absence of rays.
The growth of the longer finger will be restricted by the smaller one and may
deviate towards the smaller finger
• Function may be good in partial simple syndactyly between two fingers,
which have grown normally and compromised in compound syndactyly
FIGURE 43.2 Syndactyly.
FIGURE 43.3 Acrosyndactyly.
X-rays demonstrate associated bony abnormalities especially the bony fusion
Treatment
• Separation of syndactyly is done by modified ‘Z’ plasty in stages, if all
fingers are involved. Marginal fingers are released first
• Thumb requires early release in very bad syndromic syndactyly, so that the
child can use the thumb against the fused fingers to hold objects
Duplication (supernumerary fingers,

polydactyly)
• One of the most common congenital anomalies of hand
• The incidence is about 1 in 3000 births
• Among the coloured races, the little finger duplication and in Whites, thumb
duplication is common
• May present with floating little finger or thumb with otherwise normally
developed hand (Fig. 43.4)
• Duplication of central ray is rare and sometimes it manifests as a sixth finger
• Mirror hand: Three fingers on ulnar and three on the radial side with absence
of thumb and radius. The metacarpals can duplicate, especially the third
giving rise to two fingers instead of one
• Thumb duplication is common. It can manifest in different ways from just
bifid tip to two completely duplicated thumbs. The two thumbs may have
grown equally but both remain smaller than normal size or grow unequally,
one being more hypoplastic than the other
FIGURE 43.4 Floating little finger.
X-Rays will show the bony abnormalities
Treatment
Treatment depends on the extent of duplication:
• If it is just a floating supernumerary digit with other normally developed
digits, then it requires only simple removal
• If it is a complicated duplication of thumb, then it requires extensive
procedures of thumb reconstruction
Overgrowth (gigantism or macrodactyly)

• Occurs due to overgrowth of fingers, and local gigantism is one of the rare
malformations affecting the hands
• Normally, there is abundant amount of fat in the gigantic digit, but neural
elements are also said to form the basic pathological tissue
• The fingers are very large in size with total asymmetry (Fig. 43.5)
• Commonly, the central digits are affected, and the thumb being the next
common
• Little fingers are the least affected
• Deviation or curvature of fingers is common due to unequal affection of both
sides of the digit
FIGURE 43.5 Gigantism.
X-Rays will show the bony abnormalities
Treatment
Treatment is difficult
• Reduction of the soft tissues, shortening of bones both in transverse and
vertical height have to be tried
• Stapling of epiphysis has been tried to arrest the growth of the bones with
unsatisfactory results
• Correction osteotomy can be done for deviations
Undergrowth (hypoplasia)
• Hypoplasia occurs due to undergrowth of finger or fingers, commonly the
thumb
• Thumb hypoplasia (Fig. 43.6) along with radial club hand is a common and
important anomaly
• When radial side is affected, it is called ‘radial ray hypoplasia’ and when the
ulnar side is affected it is called ‘ulnar ray hypoplasia’
• Can exist along with other anomalies and duplications
FIGURE 43.6 Hypoplasia of thumb.
• The fingers are short and undeveloped
• In radial ray hypoplasia, the radius is hypoplastic or even absent and the hand
is deviated to the radial side. Elbow joint may be involved
• Abnormalities of radioulnar joints also may be noticed
• Short metacarpals with hypoplastic fingers can occur along with or without
syndactyly
X-rays are important to assess the condition of bones including the epiphysis
Treatment
Treatment depends on the degree of hypoplasia.
• In radial club hand, which is one of the common conditions, the hand is
centralized or radialized over the ulna and the index finger along with its
neurovascular bundle is shifted to a new position as thumb
• Deviations and curvatures may require osteotomy
Congenital constriction ring syndrome

Rare and complex congenital anomaly
• The limb presents with grooves, furrows or bands in the limb (Fig. 43.7),
which form constrictions and in severe cases, amputation
• Lower limbs may also be affected in some cases
• Distal to the constriction, lymphoedematous thickening may be noticed
FIGURE 43.7 Constriction ring syndrome.
X-rays are required to assess the skeletal involvement
Treatment
Early treatment consists of relieving the constriction by performing ‘Z’ plasty of
the deep grooves, so that the distal oedema subsides and there is no progression
of the constricting defect
Injuries of hands
• Hand injuries form nearly one third of all injuries to human body
• They can be:
• Open
• Closed
• Acute injuries can be classified depending on the nature of force and on
contamination as tidy, untidy and indeterminable injuries.
• Tidy injuries: Clean cuts and incised wounds, usually resulting from sharp
force
• Untidy injuries: Ragged skin wounds, may be with associated fractures,
usually resulting from crush or avulsion force
• Indeterminable injuries: Injuries where it is difficult to determine the
extent of injury and the viability of tissues, usually caused by very severe
force
• Injuries to the vessels, nerves, bones and joints may be present in any of the
above injuries
Complications: Posttraumatic deformities such as contractures, neurovascular
deficit
The patient presents to the surgeon either in the acute or late stage.
• In acute injuries (Figs. 43.8 and 9), the pain is excruciating, and assessment
is difficult, unless pain is alleviated by analgesics.
• Nail injury—avulsion of nail (complete or partial) (Fig. 43.10)
• Skin damage —loss of skin, especially degloving
• Nerve damage—sensory or motor loss depending on the nerve affected
• Damage to arteries—suspected by profuse haemorrhage (incomplete
tears), gangrene (complete injuries) (Fig. 43.11)
• Damage to tendon sheaths and tendons—lack in active movement
• Damage to bones and joints—pain, deformity, tenderness and loss of
movement
FIGURE 43.8 Traumatic amputation of tip of middle finger.

FIGURE 43.9 Penetrating injury of three fingers.
FIGURE 43.10 Avulsion of nails by crush injury Source: (Courtesy Dr S. Devaji
Rao).

FIGURE 43.11 Gangrene of fingertip following crush injury.
In acute injuries, for assessment of damage, surgical exploration may be

necessary when in doubt and it should be done meticulously. The structures
should be considered divided until otherwise proved.
When patients arrive late, infection gets superadded, and result in
posttraumatic sequelae
• In late posttraumatic cases, detailed examination of movements and
sensation can be done with ease, and damage assessed completely
• Skin injuries: Necrosis of skin may manifest as raw area, when very late
can present with contracture due to secondary healing. Scars can
hypertrophy or break down due to instability
• Vascular injuries: Gangrene and necrosed skin exposing deeper structures
• Extensor tendon injuries: Dropped finger (if injury is at dorsum or
proximal to it), boutonniere deformity (when injury is at proximal finger
level) (Fig. 43.12A) and mallet finger (when injury is at distal finger level)
(Fig. 43.12B) and neglected or untreated mallet fingers may progress to
swan neck deformity (Fig. 43.12C)
• Flexor tendon injuries: Lack of movement at PIP joint suggests flexor
digitorum superficialis (FDS) injury and distal interphalangeal (DIP) joint
suggests FDP injury.
• Nerve damage: Wasting of muscle groups (motor), lack of sweating,
trophic changes (sympathetic) and lack of sensation
• Bone or joint injuries: Malunion and nonunion of fractures
FIGURE 43.12A Boutonniere deformity of little finger.

FIGURE 43.12B Mallet finger.
FIGURE 43.12C Swan neck deformity.
Note
• In most hypermobile Indian hands, especially those of women, injury to
flexor digitorum sublimis can produce a swan neck deformity (DIP
hyperflexion and PIP hyperextension) due to associated extensor apparatus
derangement.
• Other than trauma, rheumatoid arthritis and familial causes produce swan
neck deformity.
• X-rays (in various views) are necessary to assess bone injuries
• Doppler studies are required to assess vascular damage
Treatment
• Bleeding can be controlled by elevating the limb or by applying pressure
directly over the site with pads
• In acute cases:
• Skin injuries—primary repair wherever possible
• Vascular injuries—primary microvascular repair
• Bone and joint injuries—proper debridement and splinting, reduction of
dislocations and immobilization
• Nerve injuries—primary repair under magnification where possible
• Tendon injuries—primary repair in clean wounds
• In late posttraumatic cases:
• Skin injuries—wound healing by secondary intention cause severe fibrosis
and contractures, and may need release and repair and skin grafting or flap
cover in some cases
• Vascular injuries—grafts wherever required
• Bone and joint injuries—malunion or nonunion should be treated
accordingly
• Nerve injuries—nerve grafts
• Tendon injuries—tendon transfers or grafts
Note
Dirty wounds should be debrided well and converted into a clean wound and
further treatment is carried out.
Lymphangitis
• The common infecting organism is Streptococcus, which gains entry through
an abrasion, which may be microscopic
• Common in manual workers and housewives
• Hand becomes swollen with considerable elevation of temperature. Later red
streaks characteristic of lymphangitis occur
• Epitrochlear, axillary or supraclavicular lymph nodes enlarge in ulnar, mid
and lateral areas of hand, respectively
• Blisters may appear and serous fluid may ooze
Polymorphonuclear leucocytosis is present
Treatment
Penicillin G 12 lac units sixth hourly is necessary to control infection
Cellulitis
• Spreading inflammation along the subcutaneous and fascial planes
• Streptococcus pyogenes is the commonest organism to infect, usually through
an abrasion of a prick, commonly in diabetics
• The condition depends on the virulence of the organism, and gangrene may
follow with widespread necrosis of tissues
• Generalized swelling of hand with a small infected (redness and itching)
wound at the site of inoculation
• Swelling, induration and localized tenderness (triad called brawny swelling)
may be present
• Polymorphonuclear leucocytosis
• Erythrocyte sedimentation rate (ESR) is elevated
Treatment
• Broad-spectrum antibiotics are necessary to control infection
• Incision and drainage for localized abscesses
Abscess
• Localized abscesses can be of many types:
• Intraepidermal abscess
• Intradermal abscess
• Subcutaneous abscess
• Superficial part of collar stud abscess
Localized tender swelling in the hand
Isolation of organisms from the pus is necessary
Treatment
Incision and drainage is curative under cover of appropriate antibiotics
Infection of dorsum and dorsal spaces

Commonest cause being:
• an abscess of the skin penetrating the dorsal space
• a penetrating wound
• Swelling of the dorsum of the hand and / or corresponding space of fingers
(Fig. 43.13)
• Induration and redness are cardinal signs, and fluctuation may not be present
FIGURE 43.13 Abscess dorsum of middle finger.
Polymorphonuclear leucocytosis is present with elevation of ESR
Treatment
Incision and drainage under cover of appropriate antibiotics is curative
Carbuncle
• Carbuncle is common on the dorsal aspect of a proximal segment of a digit,
infection acquired from the mouth or nose while wiping with the back of the
hand
• More common in males as these areas are hairy
• May extend into the extensor tendon
• Causative organism being Staphylococcus aureus
• Common in diabetics
• Commences as a painful swelling with marked induration
• Skin becomes red and oedematous, with the appearance of pustules on it
• They burst to form multiple discharging sinuses like a sieve, a characteristic
feature of carbuncle (Fig. 43.14)
FIGURE 43.14 Carbuncle middle finger.
• Culture of the pus and identifying the causative organism is necessary
• Determination of blood sugar levels is mandatory
Treatment
• Control of diabetes is necessary
• Drainage of pus and excision of slough under cover of appropriate
antibiotics is curative
Acute paronychia
• Most common infection of the hand affecting anyone, infancy to old age
• Arises from a hangnail, careless nail cutting or a manicurist’s infected
instruments
• Causative organism being Staphylococcus aureus
• Infection is subcuticular in nature
• The infection starts beneath the eponychium with consequent suppuration,
and the pus tracks around the cutaneous margin
• Yellowish discolouration and swelling of the cutaneous margin of the nail
(Fig. 43.15), with exquisite pain
• Tenderness is predominant
FIGURE 43.15 Acute paronychia of finger.
Treatment
• Incision and drainage under cover of appropriate antibiotics is curative
• When pus is found below the nail, that part of the nail may have to be
removed
• Floating nail is to be excised totally
Apical space infection

Occurs usually following a prick beneath the nail (a splinter), causing infection
of the space between the subungual epithelium and the periosteum
Exquisite pain beneath the nail, and remarkable tenderness on application of
pressure on the free edge of the nail
Treatment
Excision of small ‘V’ from the free edge of the nail lets out the pus and is
curative
Terminal pulp space infection

• Second most common infection of the hand
• Affects commonly the index finger and thumb
• Origin of infection is usually a prick
• Dull pain, worse on dependent position in the early stages
• Pain becomes throbbing and interferes with sleep as the infection becomes
severe
• The tip of the finger may be swollen and appear red (Fig. 43.16)
• Tenderness is remarkable even on slight pressure
FIGURE 43.16 Terminal pulp space infection of index finger.
Treatment
Incision and drainage under cover of appropriate antibiotics is curative
(without waiting for fluctuation)
Infection of volar spaces

• Infection of volar spaces is relatively rare, and the presentation of middle and
proximal volar spaces are different due to its anatomical considerations
• Middle volar space is shut off below and above, whereas the proximal volar
space communicates with the web space
DD: Acute tenosynovitis
Tender induration over the involved space (Fig. 43.17)
FIGURE 43.17 Infection of middle volar space of ring finger.
Treatment
Incision and drainage with appropriate antibiotics is curative
Infection of web space

• The web spaces are between the dorsal and volar skins filled with loose fat,
which bulge between the divisions of the palmar fascia
• When filled with pus, although most of the pus is volar, the abscess points
dorsally
• The infection arises from:
• A skin crack
• Purulent blister beneath a callosity
• Lumbrical canal from an abscess in a proximal volar space
• At the initial stages, the dorsum is oedematous with severe pain and elevated
temperature
• As the localization occurs, after administration of antibiotics, the base of the
finger gets swollen and the fingers get separated
• Maximum tenderness is found in the web
• Polymorphonuclear leucocytosis
• Elevated ESR
Treatment
Incision and drainage through the palmar surface of the web space under
cover of appropriate antibiotics is curative
Deep palmar abscess

• Infection and formation of abscess beneath the palmar fascia, though rare, is a
serious condition
• Usually seen in manual workers
• The infection arises from:
• A penetrating wound
• Infection of a haematoma
• Complication of suppurative tenosynovitis
• In the early stages, there is intense throbbing pain with deep tenderness of the
palm of the hand, with oedematous swelling of the dorsum of the hand
• The hand is kept in flexion as the palmar fascia is relaxed in this posture
• Extension of metacarpophalangeal joints is very painful, but extension of
interphalangeal joints is painless and free
• When the collection of pus increases, the concavity of the hand is lost
• Polymorphonuclear leucocytosis is present with elevation of ESR
• MRI is useful in localizing pus
• Diagnostic aspiration is confirmative
Treatment
Incision and drainage under general anaesthesia is curative
Subungual haematoma
It is a collection of blood below the nail following injury, usually a crush injury
of the terminal phalanx
Painful blackish discolouration of the finger nail, following an injury (Fig.
43.18)
FIGURE 43.18 Subungual haematoma of finger.

Treatment
• Evacuation of haematoma through drill holes made in the nail
• It is easy to use a needle which is made red hot in a spirit lamp
Chronic paronychia
• The history usually runs for months and has insidious onset
• The infection is usually fungal or mixed organisms
• Usually found in women who use their fingers in water for prolonged hours
such as washerwomen and housewives
• Superadded infections can make it acute
Nails (Fig. 43.19) and the paronychium are deformed
FIGURE 43.19 Chronic paronychia of fingers (arrows).
Microscopic examination of scrapings or cultures for fungi is useful
Treatment
• Antifungal drugs are useful in controlling infections
• Wearing of protective gloves is necessary
Carpal tunnel syndrome

• The carpal tunnel is formed by the flexor retinaculum anteriorly and by the
distal row of the carpus posteriorly. The median nerve and the flexor tendons
pass through it (Fig. 43.20)
• The median nerve is compressed by increased bulk due to causes such as
flexor synovitis due to:
• rheumatoid arthritis
• trauma
• myxedema
• carpal dislocation
• ganglion
• pregnancy causing fluid retention
• Computer professionals who use the keyboard for long periods of time in a
day, suffer from this due to the abnormal posture of wrist
FIGURE 43.20 Carpal tunnel.

• Hyperaesthesia or paraesthesia in the distribution of median nerve
• Symptoms get aggravated on usage of hand, especially the grasp
• Waking up from sleep with numbness of radial fingers and palm is
characteristic
• Pain in fingers and clumsiness in movement is present, especially of the
thumb
• The symptoms of numbness are reproduced on percussion over median nerve
in carpal tunnel and on acutely flexing the wrist (positive Phalen’s test)
• The pain may radiate proximal to wrist, or even to the arm
Median nerve conduction studies are useful
Treatment
• Conservative
• Splinting the wrist in neutral position along with anti-inflammatory and
analgesic medication
• Surgical
• Simple decompression of the tunnel by longitudinal incision of the flexor
retinaculum yields good result, when conservative management fails
Pronator syndrome
• The median nerve can also get compressed proximally in the lower part of the
arm or upper forearm at specific locations (levels). This entity is called as
pronator syndrome
• Compression can occur at:
1. about 5 cm above the epicondyle
2. the level of elbow where the lacertus fibrosis crosses the elbow from
bicipital aponeurosis
3. in between the two heads of pronator teres
4. where the nerve is crossed by the arch of flexor digitorum sublimis
muscle mass
• Pain in the flexor side of lower arm, forearm, and hand
• Paraesthesia as in carpal tunnel syndrome is noticed in radial three and half
fingers but Phalen’s test will be negative
• Symptoms get aggravated on:
1. Flexion of elbow against resistance if the compression is proximal
(level 1)
2. Pronation and flexion of elbow keeping wrist in flexion (to relax
sublimis) (level 2 and 3)
3. Flexion of sublimis of mid finger (level 4)
Treatment
Release of the compression after exploration
Anterior interosseous syndrome

This is similar to pronator syndrome but the compression is distal
There are no sensory symptoms but there is weakness of profundus of index,
flexor pollicis longus and pronator quadratus
Treatment
Release as in pronator syndrome
Cubital tunnel syndrome

• The cubital tunnel is located behind the medial epicondyle. The ulnar nerve in
the arm passes on to the medial head of triceps after piercing the medial
intermuscular septum, then, it passes behind the medial epicondyle, then
between the two heads of flexor carpi ulnaris
• It can be compressed at all these three places
• In India, where Hansen’s disease is prevalent, the nerve gets compressed
commonly at these places
• Excruciating pain radiating to medial and volar forearm with paraesthesia of
ulnar one and half fingers and hand
• There may be weakness of ulnar-innervated intrinsic muscles (Fig. 43.21A)
• Crossing of fingers will not be possible due to intrinsic muscle weakness (Fig.
43.21B)
• Flexion of elbow and percussion will exaggerate the symptoms
• There may be abnormal mobility and subluxation of nerve in non-Hansen’s
cases, whereas in Hansen’s disease, the nerve is thickened and loses its
mobility due to inflammation
FIGURE 43.21A Wasting and contracture of small muscles distributed by
ulnar nerves in leprosy Source: (Courtesy Dr S. Devaji Rao).
FIGURE 43.21B Crossing of fingers to test ulnar nerve weakness.
Treatment
• Release of the intermuscular septum, cubital tunnel and flexor carpi ulnaris
• Medial epicondylectomy and anterior transposition of nerve are useful,
when there is subluxation
Guyon’s canal syndrome (ulnar tunnel

syndrome)
Guyon’s canal is a fibro-osseous tunnel formed by the volar carpal ligament and
pisohamate ligament as the roof and the flexor retinaculum forming the floor
The common causes of compression are:
• Constant trauma
• Fracture of hamate
• Fracture of base of fifth metacarpal bone
• Lipoma or ganglion, ulnar artery disease (rare causes)
• Pain is characteristically in the distribution of the ulnar nerve
• Wasting of intrinsic muscles may be present depending on the level of
compression, either before or after the division into superficial and deep
branches
Treatment
Simple decompression of the tunnel by longitudinal incision of the flexor
retinaculum cures the condition, often in a dramatic fashion
Injuries to tendons
• Injuries to tendons are usually a part of injuries to the hand
• Isolated tendon injuries are extremely rare
• Rupture of tendons occur at special situations (Ch. 49)
Tendon injuries when complete present with loss of function related to that
particular tendon
MRI is useful in assessing injuries to tendon and tendon sheaths
Treatment
• Primary repair should be done wherever possible
• Tendon grafting is done when there is loss of tissue
Note
In the hand, extensor tendons are highly elastic and vascular and play very
minor role in the movement of fingers and primary repair gives excellent
results.
Simple tenosynovitis
• Follows excessive or improper or unaccustomed use
• Commonly the extensor tendons are affected
• Pain and local swelling
• A rustling noise (soft crepitus) may be palpable on finger movement
Treatment
Complete rest for 3 weeks on a splint is required, followed by a period of gentle
activity
Acute suppurative tenosynovitis

• Infection of tendon sheath usually occurs:
• when the sheath is penetrated by a sharp object
• by extension of infection from its terminal pulp space (rare)
• The infecting organism is usually Staphylococcus aureus or Streptococcus
hemolyticus
Complications: Spread of infection into forearm, suppurative arthritis of
related joint, stiff digit, median nerve paralysis due to compression by swollen
radial or ulnar bursa
• Symmetrical swelling of entire finger
• Flexion deformity with exquisite pain on extension (Hook sign)
• Tenderness over the infected sheath
Infection of ulnar bursa is characterized by:
• Oedema of entire hand
• Painful resistance to extension of flexed fingers
• Kanavel’s sign is positive. It consists of four components:
1. The affected finger is held in slight flexion
2. A fusiform swelling over the affected tendon
3. Tenderness over the affected tendon
4. Pain on passive extension of the affected finger
Infection of radial bursa is characterized by:
• Distal phalanx of thumb is held in flexion
• Painful resistance to extension of interphalangeal joint of thumb
• Normal extension of other fingers
• Tenderness over the sheath of flexor pollicis longus
• Polymorphonuclear leucocytosis is present with elevation of ESR
• MRI is useful in localizing pus
• Diagnostic aspiration is confirmatory
Treatment
Incision and drainage is curative with appropriate antibiotics
Stenosing tenosynovitis
• Tendon sheath thickens and entraps the tendon
• Unknown aetiology
• Commonly affects the:
• tendon sheath of abductor pollicis longus and extensor pollicis brevis (de
Quervain’s disease)
• the retinaculae of the flexor tendons of the fingers and thumb in the palm
(trigger finger)
• de Quervain’s tenosynovitis
• Pain in the region of radial styloid aggravated on grasp
• Thickening and tenderness may be felt over the radial aspect of lower
forearm
• Finkelstein test: The thumb is kept flexed into palm and the fingers closed
to form a fist and the hand is grasped and ulnar deviated. This will
produce the typical pain
• Trigger finger
• The stenosis is commonly found in the region of the proximal annular
flexor pulley called as A1 pulley
• Flexion of finger or thumb is easy but extension becomes difficult and
occurs with a click
• In established disease of longer duration, the click may disappear and the
digit is kept flexed with absence of active extension
• Can occur also as a congenital condition of thumb where the child keeps
the interphalangeal joint in flexion
Treatment
• Surgical division of the constricting portion of sheath is curative
• Injection of triamcinolone in the region of sheath gives good results
Dupuytren’s contracture
• It is a localized thickening of the palmar fascia
• The fascia eventually contracts to draw the fingers into flexion, with flexion
deformity of metacarpophalangeal and PIP joints
• The overlying skin adheres to the palmar fascia. The pathology starts usually
near the base of the little finger. Later it involves the ring finger and rarely
the other fingers
• It is common in men with some familial tendency, but the exact aetiology is
unknown
The deformity is characteristic (Fig. 43.22)
FIGURE 43.22 Dupuytren’s contracture.
Treatment
• Exercises and gentle stretching may be useful in early stages or subcutaneous
fasciotomy is useful
• Surgical excision of the involved fascia is useful in late stages
Implantation dermoid
• Typically they occur in areas of old injury. But often there is no positive
history of trauma
• It is postulated that some epithelium gets buried at the site of injury and gets
converted into a cyst. Hence, this is more common in men such as tailors,
gardeners and manual workers who are more prone to get finger injuries.
A round or oval-shaped cystic and firm swelling commonly on the volar aspect
of fingers or palm (Fig. 43.23)
FIGURE 43.23 Implantation dermoid Source: (Courtesy Dr V. Srinivasan).
Treatment
Excision
Palmar warts
• It is a rough excrescence of skin, can occur in any part of the palm, commonly
in fingers and thumb
• This has a viral aetiology
• They are like warts elsewhere (Figs. 43.24A and B)
• The surrounding skin is thickened
• There is always tenderness on pressure over the wart
FIGURE 43.24A Palmar wart.

FIGURE 43.24B Periungual warts.
DD: Callosities (warts occur anywhere, whereas the callosities occur only
over points of pressure)
Treatment
• Curettage under local anaesthetic is curative
• Application of liquid nitrogen is an alternative
• Electrocauterization and radiofrequency ablations are very effective
Callosity or corn
• Callosity is a raised patch of hyperkeratosis, increased thickening of the
epidermis, particularly of stratum corneum and the granular layer, commonly
seen in areas of excessive pressure or repeated trauma
the surface and the apex deep inside. This is composed of keratin masses
with intact basal layers
• Callosity presents as a thick skin in the areas of excessive pressure, commonly
on the head of distal phalanx of thumb
• Corn presents as a thickened tissue anywhere in the palm
Treatment
• Removal of the pressure points will help in the treatment
• Urea-containing creams soften the skin
• Callosity disappears / decreases when the causative factor is removed
Epithelioma (squamous cell carcinoma)

Described in Chapter 9, Lumps and Swellings.
Malignant melanoma
Described in Chapter 9, Lumps and Swellings.
Benign giant cell synovioma

• One of the more common tumours of the hand
• Consists of foreign body giant cells, foam cells, spindle cells and
macrophages laden with pigments
• Macroscopically, they are yellowish or yellowish-brown swelling with grayish
stripes
• Even though they are benign, if inadequately removed, recurrence is high
(10–40%), because of its extensive nature
• Appear as rounded firm swelling (Fig. 43.25)
• More commonly they arise in fingers
• They can occur both on the dorsum or the palmar side of a finger or thumb
• They are soft to firm in consistency and are less mobile
• They seem to be adherent to the underlying tendon sheath
• When it occurs on the volar side of fingers they tend to go deeper to flexor
tendon to lie on the bone
FIGURE 43.25 Benign giant cell synovioma.
Treatment
• Wide excision is the treatment of choice
Glomus tumour
• These tumours comprise an artery, a vein, shunt and fine spirals of vessels in
between, forming red or bluish round mass
• The artery is surrounded by glomus cells, fine nerve fibres, Pacinian
corpuscles
• Excruciating pain disturbing sleep is the main symptom, and it may require
strong analgesics or opiates
• On examination, the tumour is so small that it is not possible to clinically see
it (Fig. 43.26)
• Commonly it is found under the nail bed or at the tip of the finger
• The pain can be elicited by pressure with a pencil tip and can be precisely
located
FIGURE 43.26 Glomus tumour.
No special investigation is necessary treatmen t
• Exploration under magnification with tourniquet control
• If it is under the nail bed, the nail has to be removed for adequate exposure
Other benign tumours

• Lipoma (Fig. 43.27A), fibroma, haemangioma, neurofibroma and
schwannoma also can arise from connective tissues of hand like other parts
of the body
• Similarly, benign tumours of bones such as osteoma, ecchondroma,
enchondroma, aneurysmal bone cyst and giant cell tumours are also
encountered in metacarpals and phalanges (Fig. 43.27B)
FIGURE 43.27A Lipoma of hand.

FIGURE 43.27B Giant cell tumour of phalanx Source: (Courtesy R.
Rajaraman).
Other malignant tumours

• Fibrosarcoma, malignant synovioma and rhabdomyosarcoma can arise but are
rare
• These arise as a firm fleshy mass and show rapid growth
• They arise in young adults
• They metastasize to lymph nodes and lungs
• Treatment consists of wide excision or amputation
43.4 Symptoms of pathologies of hands

• Pain and paraesthesia
• Swelling
• Ulcer
• Sinuses
• Deformity
Pain and paraesthesia
• Pain and paraesthesia may be a presenting symptom of compression or
entrapment neuropathies (e.g. carpal tunnel and Guyon’s canal syndromes),
but they have a very definite distribution (e.g. carpal tunnel syndrome—
lateral three and half fingers, Guyon’s canal syndrome—medial one and half
fingers). So also, entrapment of nerves at a high level such as the elbow can
cause symptoms similar to the above syndromes (e.g. cubital tunnel and
pronator syndromes)
• Pain may also indicate localized inflammatory pathologies (e.g. apical space
abscess) and certain noninflammatory pathologies (e.g. corns and callosities)
Swelling
A generalized swelling may be seen in sprains, fractures and haematomas, or at
specific sites (e.g. ganglion, implantation dermoid)
Ulcer
The hand being an actively used organ and is liable to many varieties of stress,
especially in the population who are manual workers, ulcers are common. Ulcers
can be due to various causes (Ch. 10)
Sinuses
Sinuses occur in pathologies such as tuberculosis, osteomyelitis (Ch. 11)
Deformity
Deformities occur in some pathologies of hand:
• Congenital conditions—developmental anomalies
• Acquired conditions—Dupuytren’s contracture, nerve injuries (e.g. wrist
drop, claw hand)
Eliciting history
Pain in the hand

• Site of pain: In which part of the hand does the patient complain of pain?
Pain may be present in the fingers (e.g. ischaemia, corns and callosities), or
have a definite distribution (e.g. medial one and half fingers in ulnar nerve
lesions)
duration may indicate acute pathology (e.g. deep palmar infections) and long
duration (e.g. entrapment neuropathies)
Nature of trauma and severity of it will indicate the pathology (e.g. strains and
fractures)
• Precipitating factors: Does the pain become severe and if so when?
Working can aggravate ischaemic pain and arthritic pain. Entrapment
neuropathic pain is aggravated on use of hands in particular postures as in
computer professionals, who use the keyboard and mouse excessively
the relief the patient had with the intake of drugs. Recurrence of pain after
previous surgical procedures will give an idea about the diagnosis (e.g.
entrapment neuropathies)
Swelling of hands
If swelling is present in the hand, the nature of the swelling should be
questioned. The questions should be in line with any swelling in general (Ch. 9).
Some of the examples are:
• Generalized swelling
• one hand (e.g. local infective pathology such as abscess, fracture) (Fig.
43.28A)
• both hands (e.g. part of hypoproteinaemia) (Fig. 43.28B)
• Localized swelling (e.g. ganglion, implantation dermoid)
FIGURE 43.28A Swollen hand in metacarpal fracture.

FIGURE 43.28B Generalized swelling of both hands.
Ulcer on dorsum of hand

• Duration of ulcer: For how long the ulcer has been present?
those of longer duration are due to repetitive trauma or chronic infections such
as tuberculosis
• Site of the ulcer: In which part of the limb is the ulcer present?
Ulcers occur at pressure points, and ischaemic ulcers occur at the terminal part
of the fingers
Chronic ulcer may be painless, and acute ischaemic ulcers are painful.
Infection is the commonest cause of association of pain in the ulcer
Application of strong chemicals and native medicines can delay healing, and
also detailed history regarding the treatment taken will give an idea about the
chronicity of the ulcer
Sinuses
If the patient is complaining of discharge through sinus openings, the
questioning should be in line with the examination of any sinus (Ch. 11). Some
of the examples of sinuses of hands are:
• Multiple sinuses occur in osteomyelitis
• The nature of discharge varies according to pathology, e.g. bone chips in
osteomyelitis, caseous material in tuberculosis
Deformity
• Duration of deformity: For how long the deformity been present?
Deformities may be present since birth (e.g. congenital conditions—absent
fingers or accessory fingers) or may be acquired later in life (e.g. traumatic
deformities) (Fig. 43.29A)
FIGURE 43.29A Absent little finger (post amputation).

Association of high-grade fever may indicate infective pathology such as
cellulitis of hand, palmar abscess, and low-grade prolonged fever may indicate
lesions such as tuberculosis
malignancies
given for the illness?
a clearer picture of diagnosis (e.g. tuberculosis, leprosy)
treatment?
If the patient had suffered from a similar illness in the past, which was
successfully treated will indicate the examiner to reconsider the diagnosis such
as recurrence of tuberculosis
Diseases such as Dupuytren’s contracture can occur in families and the
positive history may be a good indicator for the present diagnosis
Hands
• The hand should be exposed well
• Opposite hand should be exposed for comparison
• Adequate knowledge and orientation of the hand and its anatomy are
mandatory
Inspection
Deformity
• Absent fingers (e.g. congenital or amputations)
• Polydactyly
• Syndactyly
• Congenital deviations (Fig. 43.29B)
FIGURE 43.29B Congenital swan neck deformities.
Dorsum of the hand

Skin
• Texture of skin—dry skin (e.g. eczema)
• Reddish colour—cellulitis
• Red streaks—lymphangitis
• Absence of veins—oedema and cellulitis
Swelling
• Generalized swelling—one hand (e.g. cellulitis, fractures)
• Localized swelling—simple ganglion
• Red streaks due to lymphangitis and thrombophlebitis
Ulcers and sinuses on the dorsum (Chs. 10 and 11)
• Site of ulcer—ulcers on the dorsum and palm (e.g. trauma)
• Nature—margin, floor and edge of the ulcer
• Surrounding skin—features of cellulitis and prominent veins
• Number of sinuses—multiple sinuses occur in mycosis, osteomyelitis and in
buried foreign bodies
• Nature of discharge—bone chips in osteomyelitis and fungal granules in
mycosis
Fingers
• Colour—reddish (e.g. haematoma, cellulitis), yellow (e.g. paronychia), black
(e.g. gangrene)
• Swelling—cellulitis, haematoma, wart (Fig. 43.30), pyogenic granuloma (Fig.
43.31)
• Ulcer—trophic ulcer (Fig. 43.32)
FIGURE 43.30 Wart on the dorsal aspect of finger Source: (Courtesy Dr Ramji
Gupta).
FIGURE 43.31 Pyogenic granuloma of finger.
FIGURE 43.32 Trophic ulcer finger.
Nails
• Nail changes—fungal lesions
• Overhanging lateral skinfold of the nail—ingrowing nail
• Discolouration—subungual haematoma, fungal lesions
Palm
The palm is inspected for pressure points, corns and injuries by sharp objects.
Lateral borders of hand

Lateral and medial borders—corns, callosities
Palpation
The following signs are elicited on palpation:
• Temperature and site of maximum tenderness
• Arterial pulsations
• Venous and nail bed filling
• Discharge from sinuses on pressure
• Abnormal mobility of joints
• Induration in the base of ulcers
• Assess the degree of sensation (touch, pain and joint and position sense)
A swelling in the hand is palpated in line with any swelling in general (Ch. 9).
Movements of all joints in the hand

The patient should be asked to make all the movements of the joints of the hand:
1. Movements of all joints of thumb individually
2. Flexion and extension of all joints individually
• Ulnar three fingers share common FDP muscle belly and thus in a normal
individual, when fingers adjoining the testing finger are held firmly in
extension, the FDP of the testing finger is prevented from contracting (DIP
flexion not possible) and only FDS will act (flexion at PIP possible), when
patient is asked to flex. This act eliminates FDP action while testing for FDS
(Fig. 43.33). Inability to flex the PIP joint indicates FDS disruption
• Index finger functions more independently as the muscle belly of FDP of
index is separate. To test the FDS of the index finger, the patient must be
asked to flex the PIP of the index finger while his own thumb keeps the DIP
of the index finger extended (FDP inaction) (Fig. 43.34)
• FDS to the small finger may be absent in some individuals
FIGURE 43.33 Method of testing flexor digitorum sublimis.

FIGURE 43.34 Method of testing the FDS of index finger.
Entire upper limb

Examination of the entire limb is essential, as the disorders of any part of the
upper limb can manifest as a clinical finding in the hand (e.g. wrist drop after
fracture of humerus, tardy ulnar palsy, etc.)
Lymphatic system
Lymph from the ulnar aspect of the hand drains to the epitrochlear node while
the thumb and index fingers predominantly drain to the axillary nodes. The
lymph of the middle finger sometimes drains directly into the supraclavicular
node. It should be remembered to examine the above lymph nodes
General
Detailed general examination is essential to rule out systemic illnesses such as
tuberculosis.
CHAPTER 44
Pelvis, hip and thigh

V. Thulasiraman
CHAPTER OUTLINE
44.1. Hip joint 814
• Anatomy 814
• Movements 815
44.2. Deformities of hip 816
• Coxa vara 816
44.3. Congenital lesions 816
• Congenital dislocation of hip 816
44.4. Traumatic lesions of pelvis and hip 817
• Fractures of pelvis 817
• Isolated fractures 817
• Fractures with disruption of pelvic ring 817
• Fractures of bones of hip joint 818
• Fracture of neck of femur 818
• Fracture of trochanteric region 819
• Fracture of head of femur 819
• Dislocations and fracture dislocations 820
• Posterior dislocation and fracture dislocation 820
• Anterior dislocation 820
• Central fracture dislocation 821
• Epiphyseal injury of head of femur 821
44.5. Nontraumatic lesions of hip joint 822
• Transient synovitis of hip in children 822
• Pyogenic arthritis (septic arthritis) 822
• Osteochondritis (Perthe"s disease) 824
• Slipped upper femoral capital epiphysis 824
44.6. Extra-articular disorders of hip 825
• Trochanteric bursitis 825
• Snapping hip 825
44.7. Fracture of shaft of femur 825
44.8. Symptoms of hip joint pathologies 826
• Pelvis, hip and thigh 828
• General 837
44.1 Hip joint
Anatomy
Hip joint is the most perfect example of a ball and socket joint in the human
body (Fig. 44.1). The hip joint is formed by the acetabular cavity of the iliac
bone and the head of the femur. Though the range of movements it permits is
less than that at the shoulder joint, the strength and stability it provides are much
greater. These features are attributed to:
• The depth of the acetabulum, which is increased by the labrum acetabulare
• The strength of the ligaments and the surrounding muscles
FIGURE 44.19C Flexion of the left hip joint.
FIGURE 44.19D Extension of the right hip joint.

FIGURE 44.19E Abduction of the right hip joint.
FIGURE 44.19F Adduction of the right hip joint.
FIGURE 44.19G Internal rotation of the left hip joint.
FIGURE 44.19H External rotation of the left hip joint.
FIGURE 44.1 Anatomy of hip joint.
The acetabulum faces an angle of 30° outwards and anteriorly. The normal
neck shaft angle of femur is 125° and anteversion of the neck is 15–20° (forward
inclination). The neck is made up of spongy bone with aggregation of bony
trabeculae along the lines of stress.
Articular capsule is exceedingly strong anteriorly, and surrounds the joint on
all sides. Proximally, it is attached to the margin of the acetabulum and its
transverse ligament. Distally, it is attached anteriorly to the whole length of the
intertrochanteric line and to the root of the greater trochanter. Posteriorly, it falls
short of the intertrochanteric crest by about a finger-breadth, and its attachment
to the neck of the femur is weak. The fibre bundles which form the fibrous
capsule run in two different directions. The majority run obliquely from the
acetabulum to the femur. Other bundles encircle the capsule more or less parallel
to the margin of the acetabulum to form the zona orbicularis.
The fibrous membrane has three thickenings. They are:
• Iliofemoral ligament is the thickest and most powerful part of the articular
capsule and lies in front of the joint, requiring about 500–750 lb to rupture it.
Proximally, it is attached to the inferior part of the anterior inferior iliac spine
and to the surface of the ilium immediately lateral to the spine. Distally, it
widens to be attached to the intertrochanteric line of the femur. It is thicker at
the sides than in the middle and gives the appearance of an inverted Y
• Pubofemoral ligament arises from the pubic bone and the obturator
membrane and lies in the lower and anterior part of the fibrous capsule
• Ischiofemoral ligament is a weak band, which arises from the ischium below
the acetabulum. It passes upwards and laterally into the fibrous capsule
Transverse ligament of acetabulum is a strong band of fibre, which bridges
the acetabular notch. It completes the rim of acetabulum and converts the notch
into a foramen through which vessels and nerves enter the acetabular fossa and
the ligament of the head of femur
Labrum acetabulare is a fibrocartilaginous ring attached to the acetabular rim
and the transverse ligament and deepens the acetabular cavity
Ligament of head of the femur is a relatively weak band of connective tissue
surrounded by synovial membrane. Its narrow, cylindrical end is implanted into
the pit on the head of the femur and its broad, flattened end is attached to the
transverse ligament and the adjacent margins of the acetabular notch. It is tensed
when the thigh is flexed and slightly adducted
A mass of fat occupies the nonarticular fossa of the acetabulum. It is covered
by synovial membrane, which extends to the inner margin of the lunate surface
and is reflected onto the ligament of the head of femur at the acetabular notch. It
lines the inner surface of the fibrous capsule and covers the neck of the femur as
far as the margin of the articular cartilage of the head
Blood supply is derived from an anastomosis formed around the neck by:
• ascending branches of the medial and lateral circumflex arteries
• acetabular branches of the obturator and medial circumflex arteries
• branches of superior and inferior gluteal arteries
The nerve supply is from:
• the nerve to quadratus femoris
• femoral, through the nerve to rectus femoris
• anterior division of obturator nerve
• occasionally, the accessory obturator nerve
Movements
The movements of the hip joint and the muscles acting on it are shown in Table
44.1.
TABLE 44.1
Movements and Muscles Acting on the Hip Joint
Muscles Normal
Movement Range of
Prime movers Accessory muscles Movement
Flexion Iliopsoas, iliacus Rectus femoris, sartorius, tensor fascia lata, 0°–120°
pectineus, adductor brevis and longus and
oblique fibres of adductor magnus
Extension Gluteus maximus Semimembranosus, semitendinosus, long head of 0°–15°
the biceps
Adduction Adductor magnus, adductor brevis, 0°–30°
adductor longus, pectineus, gracilis
Abduction Gluteus medius Gluteus minimus, tensor fascia lata, upper fibres 0°–40°
of gluteus maximus
Internal Gluteus minimus, tensor fascia lata Gluteus medius, semitendinosus, 0°–25°
rotation semimembranosus
External Obturator externus and internus, Sartorius 0°–65°
rotation piriformis, superior and inferior
gemelli and gluteus maximus
Movements at the hip joint are restricted by various factors. They are shown
in the Table 44.2.
Table 44.2
Factors Restricting the Movements of the Hip Joint
Movement Restricting Factor

Flexion Thigh coming into contact with the anterior abdominal wall
Extension Iliofemoral ligament
Adduction Bony pelvis
Abduction Lateral part of iliofemoral ligament and upper part of fibrous capsule
Medial rotation Ischiofemoral ligament
Lateral rotation Pubofemoral ligament and lateral part of iliofemoral ligament
For normal walking, 30° of flexion, 10° of adduction and 9° of external

rotational movements are necessary at the hip joint. While standing, the line of
gravity passes posterior to hip joint through the centre of S2 vertebra. The
posterior tilt is compensated by the anterior ligaments.
The movements at the hip occur around various axes. They are:
• Flexion and extension—transverse axis
• Adduction and abduction—anteroposterior axis
• Medial rotation and lateral rotation—vertical axis
• Circumduction—combination of axes
44.2 Deformities of hip
Coxa vara
• It includes any condition in which neck-shaft angle of the femur is less than
the normal of about 120–140°, and the name coxa vara indicates angle less
than 120°
• The deformity is caused by the stress of the body weight acting on the femur,
which is defective or abnormally soft
• It is caused by:
• Congenital causes (e.g. congenital or infantile coxa vara)
• Acquired causes:
- Capital coxa vara (e.g. Perthes disease, chondro osteodystrophy)
- Epiphyseal coxa vara (e.g. slipped upper femoral epiphysis)
- Cervical coxa vara (e.g. traumatic—fracture with malunion, pathological
—softening of bone, e.g. osteomalacia, parathyroid osteodystrophy)
- Malunited trachanteric fracture
• Shortening of limb and resultant limp
• Hip abduction is impaired
X-rays (Figs. 44.2A and B) indicate the underlying pathology
FIGURE 44.2A Capital coxa vara (right).
FIGURE 44.2B X-ray—epiphyseal coxa vara (right).
Treatment
• Treatment is that of the underlying cause
• Osteotomy is done to correct the neck-shaft angle
44.3 Congenital lesions
Congenital dislocation of hip (developmental

dysplasia of hip)
• Dislocation of the hip joint occurring either before or during birth or shortly
afterwards
• Commonly seen in firstborn female children, five times as often as boys
• In one third of all cases both hips are affected
• The possible causes are:
• Genetically determined ligamentous laxity
• Hormonal laxity of ligaments
• Breech presentation at birth
• The bony nucleus of femoral head appears late and its development gets
retarded, and the femoral head is dislocated upwards and laterally from the
acetabulum. The femoral neck is anteverted beyond the normal angle for the
infants, which is 25°. The ossific centre of acetabulum also is late in
developing, and the acetabular socket assumes a shallow contour with
steeply sloping roof. The fibrocartilaginous labrum is often folded into the
acetabular cavity, which may impede complete reduction of acetabulum. The
capsule is gradually elongated as the femoral head is displaced upwards
(intracapsular dislocation)
• Unless specially looked for, the abnormality may not be noticed till the child
begins to walk. Walking is often delayed, and there is a limp or a waddling
gait
On examination:
• In unilateral cases, the gluteal folds are asymmetrical and the affected limb
is shortened. This is determined by noting the levels of knee joints, with
reference to a horizontal line, when the child lies supine with the hips and
knees in flexion (Galeazzi or Allen sign)
• In bilateral cases, the perineum is widened with marked lumbar lordosis. The
range of movement is full except for abduction, which is characteristically
slightly restricted. Abnormal telescopic movement of the trochanter is seen
in all cases
• X-rays (Figs. 44.3 and 44.4) are diagnostic with three characteristic features.
They are:
• Retarded development of capital epiphysis
• Steeply sloping acetabular roof
• Lateral and upward displacement of the upper end of femur
• US is useful for diagnosis and confirmation
FIGURE 44.3 X-ray—congenital dislocation of hip (right) in a child.
FIGURE 44.4 X-ray—bilateral congenital dislocation of the hip joint in an
adult.
Treatment
The earlier the dislocation is reduced the better the prognosis:
• The treatment varies according to the age of the patient when the advice is
sought:
• Neonates (up to 6 months): Reduction of dislocation and maintenance of
abduction by a splint or a plaster for 3 months, with follow-up radiographs
for at least 1 year
• 6 months to 1 y ear: Closed reduction and hip spica application
• More than 2 y ears: Surgical management is useful (acetabuloplasty,
capsular arthroplasty and osteotomy of innominate bone)
44.4 Traumatic lesions of pelvis and hip
Fractures of pelvis
Fractures of pelvis are not very serious injuries in themselves but may be so by
reason of their complications. They are caused by direct injury, or violence
transmitted through the femur.
Isolated fractures
• Isolated fractures can affect any part of the pelvis
• Fracture through the superior or inferior ischiopubic ramus or both rami
• Fracture of wing of ilium
• Fracture of anterior inferior iliac spine caused by violent contraction of
rectus femoris
Local pain
FIGURE 44.5 X-ray—fracture of pubic ramus (right).
Treatment
• No special treatment is required, excepting analgesics
• Rest in bed for 3 weeks is usually sufficient
Fractures with disruption of pelvic ring

• The pelvic ring is composed of sacrum and two innominate bones. Disruption
of the ring can occur only if there are fractures or dislocations at two points
approximately opposite to each other
• In most such cases:
• Anterior injury takes the form of a fracture through both ischiopubic rami
with separation, or of disruption of the symphysis pubis
• Posterior injury is usually a subluxation of sacroiliac joints or a fracture
through the ilium or the ala of the sacrum near the sacroiliac joint
Associated injuries: Extraperitoneal rupture of urinary bladder (Ch. 37),
injury to the rectum, injury to the blood vessels (common iliac artery and its
branches), injury to the nerves (lumbosacral trunk)
Complication: Osteoarthritis, lower back pain
• Severe pain on movement
• Complications like injury to urinary bladder and rectum may present with
abdominal distension
FIGURE 44.6 X-ray—fracture pelvis with disruption of ring.
Treatment
• If displacement is minimal, rest in bed for 4–6 weeks, with lower limb
exercises
• Displaced fractures need open surgical management
Fractures of bones of hip joint

Fracture of neck of femur
• Fracture of neck of the femur is common in persons over the age of 60, more
in women, when the fragility is increased due to osteoporosis
• The causative injury is usually slight—a fall or a stumble
• The fracture is caused by a rotational force, causing marked displacement of
fragments, the shaft being rotated laterally moderately (limited by the
iliofemoral ligament and fracture being intracapsular) and displaced
upwards. In a small minority, the fragments impact with each other
Complications: Avascular necrosis of head, nonunion
• In displaced fractures:
• The history is typical that the patient is unable to get up unaided after a
fall, and unable to take weight on the injured limb
• On examination, the most striking feature is the marked lateral rotation of
the limb (patella and foot point laterally almost to 90°) and the limb is
shortened by about 2–3 cm
• In impacted fractures:
• The patient may be able to get up and walk for some distance but with
pain
• On examination, there may not be any shortening or rotational deformity
• There may be local tenderness and all hip joint movements are painful
X-rays (Figs. 44.7A and B) are diagnostic in identifying the fractures and
complications (Fig. 44.7C)
FIGURE 44.7A X-ray—undisplaced fracture of the neck of femur.
FIGURE 44.7B X-ray—displaced fracture of the neck of the femur (left).
FIGURE 44.7C X-ray—avascular necrosis of the head of the femur (left).
Treatment
• Irrespective of displacement, all fractures of neck of femur need appropriate
surgical intervention
Fracture of trochanteric region

• Fracture of trochanteric region means any fracture in the region that lies
approximately between the greater and lesser trochanter
• They are:
• Intertrochanteric fracture
• Fracture of greater trochanter
• Fracture of lesser trochanter
• Subtrochanteric fracture
• This fracture is common in very old patients, above the age of 75
• Common in women
• Almost always after a fall
Complications: Malunion
The history is almost the same as that of a displaced fracture of neck and the
clinical findings are also similar, but the lateral rotation is complete, so that the
lateral border of foot touches the couch, as the fracture is extracapsular, but the
pain and tenderness are marked on the trochanteric region
X-rays (Fig. 44.8A and B) are diagnostic in identifying the fractures, but careful
scrutiny is required

FIGURE 44.8A X-ray—intertrochanteric fracture.
FIGURE 44.8B Comminuted trochanteric fracture.
Treatment
• Unstable variety requires internal fixation by a nail plate
• Stable variety may be managed conservatively
Fracture of head of femur

• Motor vehicle accidents form the major cause
• Often these fractures are associated with hip dislocations
• They complicate 10% of posterior hip dislocations
• Injury to sciatic nerve may occur
• Pain in the affected hip
• Clinical evaluation should focus on looking for other potential life-threatening
injuries considering the nature of injuries
• Careful neurovascular evaluation is needed
• X-rays of pelvis in anteroposterior (AP) and oblique views (Fig. 44.9) are the
first investigations
• CT scans of pelvis are needed to assess fracture pattern and to formulate
treatment plans
• Other investigations are needed considering the general condition of the
patient
FIGURE 44.9 X-ray—fracture of the head of the femur (left).
Treatment
• Hip dislocations are almost always present, and closed reduction is attempted
• If the reduction is satisfactory, frequent follow-up is required with X-rays
• If not adequate, open reduction and internal fixation (ORIF) by posterior
approach is needed
• When associated with fracture of neck of the femur, emergent ORIF is
performed
• In older individuals, prosthetic replacement is indicated
• Primary ORIF is indicated when there is an associated acetabular fracture
Dislocations and fracture dislocations

• There are four varieties of dislocations of hip joint
• They are:
• Posterior dislocation
• Anterior dislocation
• Central fracture dislocation
• Inferior dislocation (rare)
Posterior dislocation and fracture dislocation

• The commonest type of dislocation of hip joint
• The femoral head is forced out of the back of acetabulum by violence applied
along the shaft of the femur while the hip is flexed or semiflexed, usually in
an occupant of a car or in a motorcycle crash
• In about half the cases, this type of dislocation is associated with a fracture of
the fragment of acetabular rim
Associated injuries: Sciatic nerve injury
Complications: Avascular necrosis of femoral head, osteoarthritis, myositis
ossificans
• Pain, swelling of hip region with the entire limb kept internally rotated with
significant shortening of the limb (Fig. 44.10), when iliofemoral ligament is
intact (regular type), whereas, when the iliofemoral ligament also ruptures,
the deformity disappears (irregular type)
• Femoral artery pulsation is feebly palpable at the mid-inguinal point, as the
supporting femoral head is displaced from its socket (Narath’s sign)
• Sciatic nerve integrity should always be assessed
FIGURE 44.10 Posterior dislocation of the right hip.
• X-rays (Fig. 44.10A) are diagnostic, and show associated fracture
• CT (Fig. 44.10B) is diagnostic
FIGURE 44.10A X-ray—posterior dislocation of the femur (left).
FIGURE 44.10B CT—posterior dislocation of the femur (posterior view).
Treatment
Dislocation should be reduced under anaesthesia as soon as possible. It is
done by pulling longitudinally upon the femur while the hip is held flexed to a
right angle and rotated laterally. Post reduction, the limb should be kept at slight
traction for 3–6 weeks
Anterior dislocation
• Anterior dislocation of the hip is uncommon
• It is caused by forced abduction and lateral rotation of the limb, usually in a
violent injury like motorcar or aircraft crash
• This is not usually associated with a fracture of acetabular margin
Complications: Osteoarthritis, avascular necrosis
• Pain, swelling of hip region with the entire limb kept externally rotated with
significant lengthening of the limb
• Movements are restricted

FIGURE 44.11 X-ray—anterior dislocation of the femur (right).
Treatment
Closed reduction under anaesthesia is effected by traction upon the flexed
limb combined with medial rotation
Central fracture dislocation

• Caused by:
• a heavy lateral blow upon the femur, as in a fall from a height on to the side
• a longitudinal force acting upon the femur while the hip is abducted
• The severity varies with the force
• It differs from the anterior and posterior dislocations in that the capsule
remains intact, and a comminuted fracture of acetabulum is invariably
present
• High-velocity injury can cause pubic bone fractures
• The fracture of acetabulum may be of various types. They are:
• Undisplaced fracture of acetabulum
• Fracture acetabulum with intact weight-bearing part
• Superior rim fracture
• Comminuted displaced fracture (bag of bones)
Complications: Osteoarthritis, low back pain
• Pain, swelling and limitation of abduction and rotations
• Rectal examination reveals smooth bulge which rotates with the movement of
femur over the lateral wall of rectum, which is diagnostic
X-rays (Fig. 44.12A) and CT (Fig. 44.12B) are diagnostic
FIGURE 44.12A X-ray—central dislocation of the femur with acetabular

fracture.
FIGURE 44.12B CT—central dislocation of the femur with acetabular
fracture.
Treatment
• Skeletal traction for 4–6 weeks with 30° abduction
• Surgical fixation of acetabulum is necessary, if reduction is not satisfactory
Epiphyseal injury of head of femur

• Rare injury seen in children, generally caused by high-energy trauma
• Child abuse and difficult labour are the causes in infants
• In adolescents, attempted closed reduction of hip dislocation may cause this
injury. It should be differentiated from slipped capital femoral epiphysis,
which is chronic in nature
• Older children may complain of pain in the hip
• Pseudoparalysis and high index of suspicion are the keys to diagnosis in
younger children
• X-ray of pelvis in AP view (Fig. 44.12C) is the initial investigation
• US and MRI also have a role in selected cases, since ossification centre may
not have appeared
• Bone scan may be useful in doubtful cases
• Aspiration of hip joint will help to differentiate from other causes of hip pain
such as septic arthritis or synovitis

FIGURE 44.12C X-ray—traumatic slip of epiphysis of the head of the
femur.
Treatment
• In toddlers, fractures without displacement are treated with hip spica in mild
abduction
• In toddlers with displaced fractures and in older children, ORIF is done
44.5 Nontraumatic lesions of hip joint

Transient synovitis of hip in children
(observation hip)
It is short-lived arthritis of the hip in children, especially boys, with uncertain
etiopathology
• Pain, limp and limitation of movements
• It is diagnosed only after the hip has recovered and not while the symptoms
and signs are present, as it closely resembles the earliest stages of
tuberculous arthritis or of Perthes disease
X-rays may show increased joint space
Treatment
Rest in bed until the pain has settled and full movements are restored is the only
treatment required
Pyogenic arthritis (septic arthritis)

• Pyogenic arthritis of the hip is not uncommon
• There is an acute inflammatory reaction in the joint tissues, with an effusion
of turbid fluid or pus In children:
• Usually secondary to osteomyelitis of upper end of the femur
• The joint is restored to normal in some cases, and in others, the joint is
permanently destroyed or damaged, leading to bony ankylosis, especially
in older children and adults
• The femur shortens due to destruction of the upper femoral growth
cartilage, and due to dislocation (Fig. 44.13)
In infants:
• Usually secondary to umbilical sepsis
• The joint may get permanently destroyed, bony ankylosis does not occur
because the femoral head and the acetabulum are composed almost
entirely of cartilage rather than of bone, but pathological dislocation
occurs, because ossification of the head of the femur occurs at 11–12
months of age. This type of pyogenic arthritis is called Tom Smith’s
arthritis
FIGURE 44.13 Postpyogenic arthritis (right hip).
Symptoms
• Onset is acute
• Umbilical sepsis may be present in infants
• Pain in the hip made worse by attempted weight bearing movement and
severe limp results
• Pyrexia is usually present
Signs
• On examination, there is a fullness in the hip region with markedly restricted
movements of the hip
• An abscess may point at the skin surface of the thigh or buttock, only in late
stages, as the thick capsule and the deep position may delay this
• X-rays show increase in space between the femoral head and acetabulum due
to distension of the joint with pus. At later stages, destruction of the bones
and narrowing of the cartilage space become evident. In infants, destruction
of capital epiphysis of the femur with the failure of appearance of ossific
nucleus may be seen. Pathological dislocation can be made out
• Polymorphonuclear leucocytosis and raised erythrocyte sedimentation rate
(ESR) are present
• Aspiration may yield pus, from which causative organism needs to be
identified
Treatment
• Arthrotomy and joint clearance under the cover of appropriate antibiotics is
curative
• Definitive surgical treatment for crippling conditions should be done at a
later date
• Hip joints often escape rheumatoid arthritis, but when they are involved, the
disability is serious
• A variant is seen in children and adolescents
• Rheumatoid arthritis associated with pyrexia, lymphadenosis and
hepatosplenomegaly is called ‘Still’s disease’
• Pain and limitation of movement aggravated by activity
• On examination:
• Local findings are not contributory as the joint is deeply situated, but the
movements are grossly impaired and painful
• The gluteal and thigh muscles may be wasted
Investigations (Fig. 44.14) and treatment are those like rheumatoid arthritis in
general (Ch. 41)
• If extensive destruction of the articular cartilage leads to persistent and
disabling pain, cup arthroplasty or replacement surgery are useful
FIGURE 44.14 X-ray—rheumatoid arthritis of the hips.
• Hip is one the most commonly affected joints by tuberculosis
• Usually children and young adults are affected
• The disease passes through three stages:
1. Synovitis
2. Arthritis
3. Destructive stage
The clinical presentation varies according to the stage of disease. They are given
in Table 44.3.
TABLE 44.3
Clinical Features of Tuberculous Arthritis of Hip
Stage of Restriction of
Pathology Position of Limb
Disease Movements
Synovitis Effusion Abduction and external rotation with pelvic tilt causing apparent At extremes
lengthening
Arthritis Inflammation of Flexion, adduction and internal rotation, which causes upward tilt All movements
cartilages causing apparent shortening
Destructive Destruction of Exaggeration of flexion, adduction and internal rotation with true All movements
bones shortening
A cold abscess is sometimes palpable in the upper thigh or buttock

DD: Transient synovitis, Perthes’ disease, low-grade pyogenic arthritis and
rheumatoid arthritis
Investigations (Fig. 44.15) and treatment are those such as tuberculous
arthritis in general (Ch. 41)
FIGURE 44.15 X-ray—tuberculous arthritis of the left hip joint.
Osteoarthritis
• Osteoarthritis of the hip is a common entity
• Osteoarthritis of the hip is more common in the West
• It can be primary or secondary:
• Primary osteoarthritis is caused by wear and tear (e.g. old age)
• Secondary osteoarthritis is caused by diseases, which damage the joint
surfaces. They are:
- Fractures of acetabulum
- Fracture of the head of the femur
- Perthes disease
- Slipped upper femoral epiphysis
- Dislocation (congenital or traumatic)
- Avascular necrosis of the neck of the femur after fracture
- Infection
- Rheumatoid arthritis
• Hypertrophy of bone at the joint margins gives rise to the formation of
osteophytes
• Pain in the hip and thigh, and also in the knee
• Pain gets worse by walking and relieved by rest
• Symptoms increase progressively
• On examination, all movements in the hip joint are painful
• Fixed deformity of various combinations is common
X-rays show diminution of cartilage, with a tendency to sclerosis of bone
surface. Hypertrophic spurring of bone is seen at joint margins (Fig. 44.16)
FIGURE 44.16 Perthe’s disease (right).
Treatment
• Mild cases require no treatment
• Moderate cases are treated with relative rest, analgesics and physiotherapy
• Arthroscopic treatment can be done
• Total hip replacement is a good alternative
• Haemophilic arthritis of the hip joint is not uncommon
• Initially, there is simple haemorrhage in the joint (haemarthrosis) and by
repeated attacks, degenerative changes occur in the articular cartilage and
forms fibrous thickening of the synovial membrane due to deposition of iron
in the articular surface
Clinical presentation, investigations and treatment are those like haemophilic
arthritis in general (Ch. 41).
Osteochondritis (perthe’s disease)

• It is osteochondritis of the epiphysis of the femoral head
• Common in male children of 5–10 years
• Common in the west coast of India
• Affects only one hip (rarely bilateral)
• Femoral head is temporarily softened and may become deformed
• Aetiology is not clearly understood, but disturbance of local blood supply is a
suggested cause
• Bony nucleus of the epiphysis undergoes necrosis and loses its trabecular
structure, gets flattened due to weight-bearing stress. Eventually, it gains its
vascular supply but the misshapen bone never gets back to normal. Growth
at the epiphyseal cartilage is impaired, which leads to shortening of the
femoral neck, though the head is usually enlarged (coxa magna)
Complication: Osteoarthritis
• Pain and limp are the presenting features
• On examination, the movements in the hip joint are limited especially to
abduction and external rotation
X-rays (Fig. 44.17) show slight decrease in the ossific nucleus of the femoral
head, whereas the clear cartilage space is often increased in depth. The nucleus
becomes denser than the normal side, later it takes on a fragmented or granular
appearance. In severe cases, the nucleus becomes more flattened, with deformed
femoral head
FIGURE 44.17 X-ray—osteoarthritis of both hip joints.
Treatment
Treatment is aimed to prevent deformity and promote containment of femoral
head inside the acetabulum
• In the early stages, traction for 3–4 weeks with analgesics will suffice
• In late stages, osteotomy of the femur is useful
Slipped upper femoral capital epiphysis
• An affection of late childhood, between the age of 10 and 15
• Upper femoral epiphysis is displaced from its normal position upon the
femoral neck
• The displacement occurs insidiously at the epiphyseal line
• Aetiology is not known, but it is common in obese children or with growth
hormone disturbances
• Weight bearing displaces the epiphysis downwards and backwards, so that the
epiphysis comes to lie at the back of the femoral neck. Left unrecognized,
the epiphysis fuses with the femoral neck in the abnormal position
Complications: Avascular necrosis, osteoarthritis, deformity of limb
• Gradual onset of pain and limp are the usual symptoms
• Pain is aggravated by exercise and relieved by rest
• The limb is shorter and lies externally rotated and adducted
• Elevation of greater trochanter limits abduction and internal rotation
• Axis deviation occurs (normally, when the hip is flexed, the knee will point
towards the opposite shoulder. But, in this condition, due to the
displacement, the knee points to the shoulder on the same side or lateral to it)
X-rays (Fig. 44.18) especially the lateral view is useful
FIGURE 44.18 X-ray—slipped femoral epiphysis.
Treatment
• Acute slip—only surgery, closed reduction and pin fixation
• Chronic slip—no reduction, pin fixation in situ
• Severe slip needs osteotomy
44.6 Extra-articular disorders of hip
Trochanteric bursitis
• The inflammation of the large bursa between the greater trochanter and the
gluteal aponeurosis, and it is rare
• It is usually caused by:
• posttraumatic bleeding
• fracture of trochanter
• protruding metal splint
• tuberculosis
• tumoural calcinosis
• Pain and swelling in the trochanteric region are common symptoms
• On examination, the trochanteric bursa is thickened, warm and red
• Often there is a palpable abscess or a discharging sinus
• Movements of the hip are not impaired
• X-rays may show superficial roughening or erosion of the lateral aspect of
greater trochanter
• ESR may be raised in tuberculosis
• Biopsy of the bursa is useful in tuberculosis
Treatment
• Excision of bursa is curative
• In tuberculosis, antitubercular treatment is mandatory
Snapping hip
• Harmless condition of no significance
• The snap may occur due to slipping of iliotibial band, a tendinous aponeurosis
over the bony prominence of the greater trochanter
• Patient complains of a distinct snap heard and felt on certain movements of
the hip joint
• It is not generally reproduced by passive movement with the muscles relaxed
US is useful
Treatment
• Usually not required
• Severe cases may benefit by iliotibial band divisioning
44.7 Fracture of shaft of femur

• Can occur at any age
• Caused by:
• High-energy trauma (road traffic accidents in adults, fall from height)
• Pathological fractures in children
• Stress factors in military recruits or marathon runners
• Equally common in upper, middle or lower thirds of the shaft
• Pattern of fracture is variable (transverse, oblique, spiral, comminuted or
greenstick in children)
• Displacements (angulation or overlap) are common
• Common in metastatic deposit (upper third is common)
Complications: Infection, injury to femoral artery, injury to sciatic nerve,
delayed union, nonunion, malunion, stiffness of knee, fat embolism
• Pain and swelling at fracture site
• Variable deformity
• Shortening of limb
• Neurovascular instability
• Severe blood loss into thigh muscles
X-rays of thigh (AP and lateral views) (Fig. 44.19) are conclusive. It is wise to
add hip and knee joints in the radiographs
FIGURE 44.19 X-ray—fracture shaft of the femur.
Treatment
• The best first aid is Thomas splint
• For upper-third fracture (subtrochanteric level) internal fixation with
dynamic hip screw and plate system or condylar plate are used. Proximal
femoral nails such as gamma nails are available now
• For middle-third fracture, intramedullary nailing for transverse and broad
plate screws for oblique unstable fractures
• For distal third fracture, ORIF with angled blade plate is indicated. Recently,
dynamic condylar screw and plates are used
44.8 Symptoms of hip joint pathologies

• Pain
• Limp
• Abnormal gait
• Swelling
• Deformity
Pain
• True hip pain: Hip joint pain can be generalized and localized to one area,
which is usually felt in the groin, front and inner side of the thigh or rarely in
the knee. Occasionally knee pain can be a presenting symptom of hip
pathology, due to common nerve supply. Hip pain can get aggravated by
movements, and relieved by rest (e.g. arthritis)
• Referred hip pain: The pain can get referred from spine, but the pain is in
the gluteal region, radiating to the back, outer side of the thigh, back of the
thigh and leg and is aggravated by stooping, sneezing or lifting weights and
decreased by walking
• Night pain or night cry: Night pain occurs due to lack of protective spasm
around the hip joint at nights, which when present at day times immobilizes
the joint and prevents contact between eroded articular surfaces (e.g.
tuberculous arthritis)
Types of pain
• Dull pain—arises from deeper structures due to inflammation or tumour
• Shooting pain—indicates neurogenic pathology
• Pain with remissions and exacerbations (e.g. rheumatoid arthritis)
• Rest pain—seen in vascular and inflammatory pathology (e.g. avascular
necrosis of neck of the femur)
• Pain with movements (e.g. arthritis or fractures)
• Pain in terminal range of movement (e.g. synovitis)
Extrinsic sources of pain in the hip
• From the spine (e.g. sciatic pain from a prolapsed intervertebral disc)
• From the abdomen and pelvis (e.g. periappendicular abscess, pyosalpinx)
• From lower aorta (e.g. occlusive vascular disease)
Note
If satisfactory explanation is not found in the hip for hip pain, the examination
should extend to the spine.
Limp
Limp is one of the most common symptoms of hip pathology and usually occurs
due to pain. The limp may be noticed by a relative or a friend than by the patient
himself. The limp may be due to a variety of causes. They are:
• Painful limping (e.g. tuberculosis, osteoarthritis, rheumatoid arthritis)
• Painless limping (e.g. congenital dislocation of hip, coxa vara, fused hip)
• Limp due to lengthening (e.g. malunion of the shaft of the femur) or
shortening (e.g. malunited intertrochanteric fracture of the femur)
Gait
Gait cycle has two phases. They are:
• Stand phase—it forms 60% of a gait cycle and is divided into 5 phases:
1. Contact
2. Loading
3. Midstance
4. Terminal stance
5. Preswing
• Swing phase—forms 40% of a gait cycle and occurs in the process of forward
swing
The normal gait is symmetric, brought out by a good relationship between
swing and stance phases of each leg in a consistent manner (Fig. 44.19A).
Abnormal gaits are:
FIGURE 44.19A Phases of gait (Whittle’s circular illustration).
• Antalgic gait—the stand phase is shortened on the affected side and the
weight is quickly transferred to the normal limb (e.g. painful hip conditions)
• Stiff hip gait—the patient elevates the pelvis on the affected side and swings
the pelvis along with the leg in circumduction
• Unstable hip gait—the pelvis dips on the affected side while walking due to
deficiency of abductor mechanism (e.g. ununited fracture of the neck of the
femur, posterior dislocation of hip)
• Quadriceps gait—the terminal locking of knee joint in extension is lost and
the patient brings his hand to push the knee back called ‘hand knee gait’ (e.g.
poliomyelitis)
• High stepping gait—the patient lifts his or her foot unusually high for
clearing the foot off the ground (e.g. foot drop—paralysis of dorsiflexor
muscles)
• Short limb gait—the patient compensates the shortening of one limb by a
pelvic tilt, or of the foot or flexion of opposite knee (e.g. shortened limb after
malunited fractures)
• Scissoring gait—the limbs cross the midline due to severe adductor spasm
(e.g. cerebral palsy)
Swelling
Swelling of the hip can be either diffused or localized.
• Diffused (e.g. inflammations). A diffuse swelling of the hip can arise from
three fundamental causes:
• Thickening (e.g. synovial, bone)
• Fluid (e.g. effusion)
• Tumours (e.g. bony tumours)
• Localized—callus formation, e.g. myositis ossificans, benign growths—
neurfibromas, multiple exostoses)
Deformity
The hip can adapt to many deformities. They may be the end result of disease
processes. The types of deformities are:
• Flexion deformity (common)
• Extension deformity (uncommon)
• Abduction deformity
• Adduction deformity
• Rotational deformity
The movements are restricted due to various causes (e.g. inflammatory,
traumatic or degenerative)
Age: certain hip conditions are common in particular age groups
• 0–2 years: Congenital dislocation of hip
• 2–5 years: Tuberculosis of hip
• 8–10 years: Perthe’s disease
• 10–20 years: Slipped capital femoral epiphysis
• 20–40 years: Secondary osteoarthritis, traumatic
• Over 40 years: Primary arthritis
Eliciting history
usually due to inflammatory pathology). Fracture pain is severe and starts
sport or a fall?
description of the fall or accident will indicate the severity of injury (e.g.
small slips may cause soft tissue injuries, and fall during active sports or road
traffic accidents may cause fractures)
• Position during trauma: What was the position of the hip during the fall or
trauma?
Injury to the hip when it is flexed and adducted, can cause posterior
dislocation as in motorcar accidents
Very severe pain may indicate fractures or septic arthritis
• Relationship to movements: Is this pain related to movements and are
there any relieving factors?
fractures, and nontraumatic situations, may indicate arthritis. Morning
stiffness is common in rheumatoid arthritis and reduction of pain on
movements may indicate osteoarthritis
This will answer about the first aid or hospital admissions and the
radiographs have to be scrutinized if available. History related to needle
aspiration of joint (arthrocentesis) should be questioned

Pelvis, hip and thigh
Pre-requisites
• Patient should be undressed except for a pelvic slip or underpants, and in
women, a brassiere, so that both the lower limbs are fully (from pelvis to
toes) exposed
• Both lower limbs should be examined simultaneously
• Patient should lie on a hard couch
• Knee joint and ankle joint should also be examined
• The patient should be examined first on the couch lying and afterwards
standing and walking
Getting onto the examination couch

What to watch when the patient gets onto the examination couch:
• How clumsy is he or she in his or her movements (e.g. taking support onto
something indicates severe pain in the joint and not willing to put weight on
the joint)
• Any trick movement to avoid pain
The examination should follow the standard pattern of look, feel, move, strain
and investigate. The examination should be done from close quarters and also
from a distance.
• Position of patient: Lying supine on a hard flatbed (abdomen, pelvis, both
hips and limbs should be exposed with a ‘T’ Bandage), lying prone, standing
and walking
• Position of examiner: The examiner should view the hips from all sides;
from the front, back and sides
Inspection
• While lying on the couch: Exaggerated lumbar lordosis
• While standing: Positional deformity in spine/hip, limb shortening is more
obvious, compensatory contractures of knee and ankle
• While walking: Stiff hip/mobile hip, painful hip/painless short limb/stable
joint/unstable joint
• While sitting: Restriction of flexion of hip
• While squatting: Restriction of abduction and external rotation
What to look for?

From the front:
Lying down
Standing
• Trunk—hip alignment
• Position of pelvis and set it square with the limbs if possible
• Deformities (e.g. coxa vara), rotational deformities (e.g. marked external
rotation in extracapsular fracture of neck of femur and less external rotation
in intracapsular fracture of the neck of the femur as the intact capsule
prevents full rotation)
• Shortening of thigh or limb (e.g. intertrochanteric fracture of the femur,
malunited fracture of the femur)
• Bone contours
• Soft tissue contours (e.g. muscle wasting) (Fig. 44.19B)
• Patella and patellar ligament (rotational deformities)
• Localized swelling (e.g. haematoma, tumour)
• Skin (e.g. colour changes, abrasions, lacerations—injuries, sinuses—
tuberculosis and scars—previous surgery)
FIGURE 44.19B Wasting of the left thigh muscles.
From behind:
• Skin (colour—haematoma, scars—previous surgery, sinuses—tuberculosis)
• Abnormal gluteal crease and widening of perineum (e.g. congenital
dislocation of hip)
• Swellings (e.g. haematoma, mass)
• Soft tissue contours (e.g. wasting of gluteal muscles)
From sides:
• Exaggerated lumbar lordosis (e.g. fixed flexion deformity of the hip joint)
• Swelling on the lateral side of the hip joint
• Position of greater trochanter
• Supra- and infra-trochanteric hollow
From all sides: Note for discolouration (e.g. haematoma), sinus and discharge
(e.g. tuberculous arthritis). Special attention should be given to scars—surgical
wound.
Palpation
• Temperature: Warmth (e.g. infective conditions such as septic arthritis)
• Bones
- Anterior superior iliac spine on both sides
- Ischial tuberosities—tip of the examining finger is insinuated at the gluteal
fold
- Trochanters
• Abnormal—bony mass (e.g. myositis, fracture dislocation of the hip)
• Tenderness
• Bitrochanteric tenderness—elicited by compressing both trochanters
towards the hip (e.g. fracture neck of the femur)
• Tenderness over Scarpa’s triangle (e.g. arthritis hip)
• Tenderness over the origin of adductor longus may be elicited in sports
injuries causing strain of that muscle
• Tenderness over the lesser trochanter during external rotation occurs in
the strain of iliopsoas
• Tenderness over the ischial tuberosity occurs in strain of hamstrings
• Tenderness over the sacroiliac (SI) joint (e.g. SI arthritis)
• Bi-iliac compression test produces pain in SI joint disease
• Crepitus: Method: The fingers of the left hand are placed over the head of
the femur below the inguinal ligament, lateral to the femoral artery. The leg
is rotated medially and laterally with the right hand. In thin individuals,
crackling sensation is felt with the left hand (e.g. fractures, degenerative
arthritis)
• Swelling of the joint
Swelling of the joint can be determined by deep palpation.
• Muscles and tendons
• Tone, texture and contractive pliability, spasms, contractures of each
muscle around the hip should be tested
• Power of each muscle group should be tested by
• Hip and knee movements
• Nerve function Tests of sensory and motor functions, sweating in distribution
of femoral nerve and sciatic nerve should be performed
• Circulation Femoral, popliteal, posterior tibial and dorsalis pedis pulses
should be felt (Ch. 13). Warmth, colour, capillary return and cutaneous
sensibility should be determined.
Movements
A full range of movement of the hip joint usually rules out the possibility of
fractures in and around the joint. The accurate determination of hip movement is
easily masked by the movement of the pelvis, and it is essential to place one
hand upon the pelvis to detect any movement in the hip while the other guides
and supports the limb.
The normal range of movements of the hip and the methods of determination
(C–H) are given in Table 44.4.
TABLE 44.4
Normal Range of Movements of the Hip and the Methods of
Determination
Flexion The patient should lift his knee towards his chest, and asked to pull it up as much as 0°–120°
he can without pain (Fig. 44.19C) but only till the lumbar lordosis is obliterated
Extension The patient should lie prone with his legs straight and take the leg backwards (Fig. 0°–15°
44.19D)
Abduction in Lying supine, the patient should take his lower limb away from his body (Fig. 44.19E) 0°–30°
hip
extension
Abduction in The patient should flex his hip and knee by drawing the heel towards the buttock. (Adult) 0°–75°
hip Then he should allow the knee to fall away from one another towards the couch (Newborn)
flexion 0°–90°
Adduction The limb should be taken inwards to cross over the other limb (Fig. 44.19F) 0°–30°
Gross rotation The patient lying supine with the limb flat on the bed should rotate the foot outwards 0°–40° each
or inwards from neutral position. The patella is kept as a marker
Internal The patient lying prone (Fig. 44.19G) or supine, with the knees flexed, and take the 0°–25°
rotation feet outwards
(accurate)
External The patient lying prone (Fig. 44.19H) or supine, with the knees flexed, and take the 0°–65°
rotation feet inwards
(accurate)
Measurements
Setting the pelvis square:

This is an important preliminary step: From the position of the anterior
superior iliac spines, it should be determined whether the pelvis is lying square
with the limbs (both anterior superior iliac spines should be perpendicular to the
midline) (Fig. 44.20A). If it is not, attempt should be made to set it square (Figs.
44.20B and C). The fact that the hip is tilted should be borne in mind during
subsequent steps of examination.
FIGURE 44.20A Normal square pelvis.
FIGURE 44.20B Squaring the pelvis.

FIGURE 44.20C Setting the pelvis square in a child.
Measuring the length of the lower limbs
Measurement of discrepancy of true length

• Since there is no landmark for the centre of the femoral head, anterior
superior iliac spine is the nearest convenient bony landmark for measurement
proximally. Distally, the medial malleolus is chosen
• In normal persons, the anterior superior iliac spine is lateral to the axis of hip
movement and an adducted lower limb will increase the length, whereas an
abducted limb will decrease the length. The rule is, therefore, to obtain an
accurate comparison of their true length by surface measurement and
the two limbs must be placed in identical positions relative to the pelvis.
Thus, if one limb is adducted, the other limb also should be adducted to the
same angle before measurements are made (Fig. 44.21) Method of
measurement (Fig. 44.22)
• At the anterior superior iliac spine: The flat end of the tape is placed
immediately at the anterior superior iliac spine (defined as the first bony
prominence when the inguinal ligament is palpated mediolaterally) and
pushed against its lower end, to give a rigid fixation of the tape against the
bone
• At the medial malleolus: The tip of the index finger is placed immediately
distal to the medial malleolus and pushed against it. The thumbnail is
brought down against the tip of the index finger so that the tape is pinched
between them. The point of measurement is indicated by the thumbnail
FIGURE 44.21 Measuring the true length of the lower limb in adduction.
FIGURE 44.22 Measuring the true length of the lower limb.
Alternate method: True shortening of the limbs can also be measured by

blocking up the short leg until both anterior superior spines and iliac crests lie
horizontal, and the natal cleft is vertical. The height of the block used is the
measure of shortening
Determining the site of true shortening
Tests for shortening above the trochanteric level

• Palpating the bony points: Begin by hooking the thumbs under the anterior
superior iliac spines. The greater trochanters are felt with the fingers. If the
distance between the thumb and the fingers is shorter on one side, this
suggests the pathology lies above the trochanters (Fig. 44.23) on that side
• Measurement of Bryant’s triangle: This compares the distance between the
greater trochanter and the wing of the ilium on both sides. With the patient
lying supine, a perpendicular line is dropped from the anterior superior iliac
spine to the couch. A second line is projected upwards from the tip of the
greater trochanter to meet the first line at a right angle. The third line joining
the two points forms the Bryant’s triangle but this line measures longer or
shorter depending on the position of the trochanter. The second line is
measured and compared on two sides. This gives a comparison between
the pelvis to trochanter distance on each side. Relative shortening indicates
that the femur is displaced upwards due to lesion in or near the hip (Figs.
44.24A and B). Squaring of pelvis, if possible gives accurate measurement
• Measurement of Nelaton’s line: With the patient lying on one side, a
measuring tape is stretched on the affected side from the ischial tuberosity to
the anterior superior iliac spine. Normally, the trochanter lies on or below
that line. If the trochanter lies above this line, the femur is considered
displaced upwards (Figs. 44.25A and B)
• Measurement of Shoemaker’s line: A line is projected on each side of the
body from the greater trochanter through and beyond the anterior superior
iliac spine. Normally, the two lines meet in the midline above the umbilicus.
If one femur is displaced upwards, the lines will meet at a point away from
the midline on the opposite side. If both femurs are displaced upwards, the
lines will meet at or near the midline but below the umbilicus (Figs. 44.26A
and B)
• Chiene’s test: A measuring tape is placed joining the two anterior superior
iliac spines and another tape is placed joining the two greater trochanters.
Normally they lie parallel to each other (Fig. 44.27A). When a trochanter is
raised as in fracture the neck of the femur, the tapes converge towards the
affected side (Fig. 44.27B)
FIGURE 44.23 Method of palpating the bony points.
FIGURE 44.24A Bryant’s triangle.
FIGURE 44.24B Bryant’s triangle.
FIGURE 44.25A Nelaton’s line.
FIGURE 44.25B Nelaton’s line left hip (trochanter above the line).
FIGURE 44.26A Shoemaker’s lines.
FIGURE 44.26B Shoemaker’s lines.
FIGURE 44.27A Chiene’s test (normal).
FIGURE 44.27B Chiene’s test (abnormal left side).
Tests for shortening below the trochanteric level

• To estimate the shortening below the trochanteric level, individual
measurements should be made of the femur (tip of greater trochanter to line
of knee joint) and of the tibia (line of knee joint to medial malleolus) on each
side (Fig. 44.27C). This type of shortening can be seen in conditions like
congenital defects, impaired epiphyseal growth or overlapped fracture
segments
FIGURE 44.27C Measuring the length of the femur.
Measurement of ‘apparent’ discrepancy of length

• This is entirely due to incorrectable sideways tilting of the pelvis, usually due
to a fixed adduction deformity of the hip, giving an appearance of shortening
on that side or a fixed abduction deformity giving an appearance of
shortening
Method of measurement: To measure apparent discrepancy, the limbs must
be placed parallel to one another and in line with the trunk. Measurement is
made from any fixed point in the midline of the trunk (e.g. xiphisternum) to each
medial malleolus (Fig. 44.28)
FIGURE 44.28 Measuring the apparent length.
Note
Measuring the lengths of the lower limbs has to be accurate, as corrective
operations and adjustments to the shoes are to be contemplated. Apparent
discrepancy is measured only when there is a compensated pelvic tilt.
Test for medial or lateral displacement of trochanter

Morris’ bitrochanteric test: The distance between the outer border of the
greater trochanter to the symphysis pubis is measured on both sides and
compared. It will reveal any medial or lateral displacement of the trochanter
Determination of fixed deformity

The neutral position of the hip may be disturbed by fixed deformities caused by
contracture of the joint capsule or of muscles. The fixed deformities can be:
• Fixed flexion deformity: With this deformity, the patient compensates by
arching the spine and pelvis resulting in exaggerated lordosis (Fig. 44.29A).
One hand is placed behind the lumbar spine (between the back and the
couch) to assess lordosis. If there is no lordosis, when the affected limb lies
flat on the couch there can be no fixed flexion deformity and there is no need
to proceed with the test Method: If there is excessive lordosis, it is corrected
by flexing the sound hip and pushing it further, thereby rotating the pelvis on
a transverse axis until the arching of the spine is completely obliterated.
During this procedure, the affected limb will automatically get lifted from
the couch. The angle through which the thigh is raised from the couch is the
angle of fixed flexion deformity (Fig. 44.29B). This is known as Thomas’s
hip flexion test
• Fixed adduction deformity: This is detected by judging the relationship
between the pelvis and limbs. In this deformity, the transverse line joining
the anterior superior spines cannot be set at right angles to the affected limb,
but lies at an acute angle with it
• Fixed abduction deformity: The angle between the transverse axis of the
pelvis and the limb is greater than the normal of 90° (Fig. 44.30)
• Fixed rotation deformity: The most reliable way to determine this deformity
is the position of patella. The patella points 5–10° laterally and the angle by
which it falls short of the neutral when rotated medially is the angle of fixed
lateral rotation deformity and vice versa (Gross method)
FIGURE 44.29A Excessive lordosis.

FIGURE 44.29B Flexing the left thigh (normal), the right leg (affected)
goes up.
FIGURE 44.30 Fixed abduction deformity.
Special tests
Examination for abnormal mobility

• Telescopic test: In hips with marked instability, a longitudinal movement may
be seen, especially in children (e.g. congenital dislocation).
• Method: The limb is grasped firmly in one hand and alternately pushed
and pulled in its long axis, the trunk being steadied by the examiner’s
other hand upon the iliac crest (Figs. 44.30A and B)
• Ortolani’s test:
• Method: The surgeon should face the child’s perineum, and grasp upper
part of each thigh between fingers behind and thumb in front, the child’s
knees being fully flexed and the hips flexed to a right angle. While each
thigh in turn is steadily abducted towards the couch, the middle finger
applies forward pressure behind the greater trochanter (Fig. 44.31)
• Inference: An easily palpable click caused by the femoral head slipping
into the acetabulum denotes that the hip was dislocated
• Barlow’s provocative test: The pelvis is fixed between symphysis and
sacrum with one hand. With the thumb of the other, attempt is made to
dislocate the hip by gentle but firm backward pressure, which results in a
click. Release of pressure brings the hip to its normal position, which is
called a dislocatable hip. Both sides are checked similarly (Fig. 44.32)
• Barlow’s test: With the above procedure, if the head of the femur is felt to
sublux backwards, its reduction should be achieved by forward finger
pressure or wider abduction. The movement of reduction should also be
appreciated with the fingers (Fig. 44.33)
FIGURE 44.30A Telescopic test (pull).

FIGURE 44.30B Telescopic test (push).
FIGURE 44.31 Ortolani’s test.

FIGURE 44.32 Method of performing Barlow’s provocative test.
FIGURE 44.33 Method of performing Barlow’s test.
Examination for postural stability

Trendelenburg test: This is a test for the stability of the hip, and particularly of
the hip abductors (gluteus medius and gluteus minimus) to stabilize the pelvis
upon the femur Principle of the test: Normally, for example, when right leg is
raised from the ground by standing on the left leg, the pelvis tilts upwards,
through the action of the hip abductors of the left limb. If the abductors are not
efficient, they are unable to sustain the pelvis against the body weight and it tilts
downwards (instead of rising)
Method: The examiner should stand behind the patient. The patient is asked
to stand upon the sound limb and to raise the other from the ground (Fig.
44.34A). Having understood as to what he should do, he is asked to stand on the
affected limb and lift the sound leg from the ground. By inspection of the dimple
of Venus or by palpation with a hand upon the iliac crest, it is observed whether
the pelvis is rising or falling on the lifted side (Fig. 44.34B)
FIGURE 44.34A Patient standing on the sound lower limb (right).
FIGURE 44.34B Patient standing on the affected lower limb (left).
Inference: If the pelvis rises from the opposite side (normal) the test is
negative, and if it falls, it is positive
Causes of positive Trendelenburg test are:
• Paralysis of abductor muscles (e.g. poliomyelitis)
• Origin and insertion of muscles are too close as in upward displacement of
greater trochanter (e.g. severe coxa vara, congenital dislocation of hip)
• Absence of stable fulcrum (e.g. ununited fracture of the neck of the femur)
Duchenne’s sign: While walking the patient with unstable hip will lurch to
one side. This is due to the patient trying to reduce pain by shifting his or her
body weight over the hip. It is often associated with positive Trendelenburg sign
but not invariably
Examination of other hip

Examination of the other hip has to be done in detail
Examination of entire limb on both sides
It should be remembered that both the lower limbs should be examined
thoroughly
Lymphatic system
Examination of the regional lymph nodes (inguinal and external iliac) and all
other groups is essential (e.g. tuberculosis)
General
symptoms may be only one manifestation of a widespread disease (e.g.
tuberculosis). Rectal examination should be included to rule out pelvic abscess
in association with tuberculous arthritis and dislocation of hip joint (central type)
CHAPTER 45
Knee and leg

V. Thulasiraman
CHAPTER OUTLINE
45.1. Knee joint 838
• Anatomy 838
• Movements 840
45.2. Deformities of knee 840
• Genu valgum and genu varum 840
• Genu recurvatum 842
45.3. Traumatic lesions of knee joint 842
• Fracture of patella 842
• Fracture of femoral condyles 843
• Fracture of tibial condyles 843
45.4. Soft tissue injuries of knee joint 844
• Dislocations of patella 844
• Collateral ligament injuries 844
• Cruciate ligament injuries 845
• Meniscal injuries 845
• Dislocation of knee joint 846
• Haemarthrosis of knee joint 846
45.5. Nontraumatic lesions of knee joint 846
• Neuropathic arthritis 848
• Ochronotic arthritis 848
• Chondromalacia of patella 848
• Osteochondritis dissecans 849
• Loose bodies 849
45.6. Extra-articular disorders of knee 850
• Rupture of quadriceps apparatus 850
• Apophysitis of tibial tubercle 850
• Prepatellar bursitis 851
• Popliteal cysts 851
• Pellegrini–Stieda disease 851
45.7. Fractures of shafts of leg bones 852
• Fracture of shafts of tibia and fibula 852
45.8. Symptoms of knee joint pathologies 853
• Knee and leg 854
• General 861
45.1 Knee joint
Anatomy
Knee joint is the largest hinge joint of the body, formed by two articulations
between
• femur and tibial condyle and
• patella and the patellar surface of the femur.
Articular capsule is very thin and is attached to the margins of the above
articular surfaces but communicates with the suprapatellar bursa, posteriorly
with the bursa under the medial head of gastrocnemius and often with the bursa
under semimembranosus, and also with the bursa under the lateral head of
gastrocnemius. The capsule is also perforated by popliteus, similar to the long
head of biceps in the shoulder joint.
Outside the joint, the capsule is reinforced by
• Medial (tibial) and lateral (fibular) collateral ligaments, on the sides of the
joint, the latter passes to the head of the fibula but lies free from the capsule.
• Medial ligament is attached to medial epicondyle of femur just below the
adductor tubercle. Inferiorly, it divides into two parts, anterior and
posterior.
- Anterior part is attached to the medial border and posterior part of the
medial surface of the tibial shaft below.
- Posterior part is short and blends with the capsule and the medial
meniscus. Morphologically, it represents the degenerated tendon of
adductor magnus.
• Lateral ligament is strong and cord like, and is attached to lateral condyle
of femur just above the popliteal groove, and is attached to the head of
fibula below. Morphologically, this represents the femoral attachment of
peroneus longus. Iliotibial band strengthens the capsule on the lateral side
and the tendons of sartorius and semimembranosus on the medial side.
• Ligamentum patellae,the common tendon of insertion of quadriceps femoris,
strengthens the capsule on the anterior side, and on each side of the patella,
by the medial and lateral patellar retinacula, the expansions from vastus
medialis and lateralis. Ligamentum patellae is 7.5-cm long and 2.5-cm wide
and is attached to the margins and rough posterior surface of the apex of
patella above and upper part of tibial tuberosity below.
• Oblique popliteal ligament (arcuate ligament) supports the capsule
posteriorly and it arises from an expansion from the insertion of
semimembranosus and blends with the capsule.
• Arcuate popliteal ligament is a posterior expansion from the short lateral
ligaments.
Inside the joint, the structures (Fig. 45.1A and B) which give stability to the
joint are:
• Cruciate ligaments give strong connections between the femur and tibia, and
arise from the anterior and posterior intercondylar areas of superior aspect of
tibia, pass obliquely upwards to attach to the intercondylar notch of the
femur. They are named anterior and posterior based on their tibial origins.
The anterior ligament is taut during the extension of knee joint, and posterior
ligament is taut during the flexion.
• Transverse ligament connects the anterior ends of the medial and lateral
menisci.
• Menisci (semilunar cartilages) are crescent-shaped fibrocartilaginous
structures and triangular in cross section, the medial being larger and less
curved than the lateral.
• The extremities of the menisci are attached to the tibial intercondylar areas,
anterior ends are connected by the transverse ligament and the posterior
ends are attached to the femur through two meniscofemoral ligaments.
• The periphery of the menisci are attached to the capsule of the joint.
Lateral cartilage is intervened by the popliteus tendon, at its attachment
with the capsule.
• Surfaces: The upper surface is concave for articulation with femur. The
lower surfaces are flat and rest on the peripheral part of the tibial condyle.
• Vascularity: The peripheral part is thick and vascular whereas the inner part
is avasular and nourished by synovial fluid.
• Functions: Menisci function as shock absorbers, help in smooth movement
of the joint and give rise to proprioceptive impulse to the higher centre.
• Infrapatellar pad of fat fills the space between the ligamentum patellae and
the femoral intercondylar notch.
• Synovial membrane lines the capsule all around the knee joint except
posteriorly. In front, it is prolonged upwards to form the suprapatellar bursa.
FIGURE 45.1A Interior view of knee joint(Patella reflected downwards).
FIGURE 45.1B Knee joint (inner view).
Structures related to the knee joint are shown in Table 45.1.
TABLE 45.1
Structures Related to the Knee Joint
Anterior Posterior Medial Lateral
Prepatellar bursa Popliteal fossa Sartorius Biceps femoris

Ligamentum Popliteal vessels Semimembranosus Tendon of popliteus origin
patellae
Patellar plexus of Common popliteal Inferior medial genicular vessels and Inferior lateral genicular vessels and
nerves nerve nerves nerves
Blood supply is derived from

1. Five genicular branches of popliteal artery.
2. Descending genicular branch of femoral artery.
3. Descending branch of lateral circumflex femoral artery.
4. Two recurrent branches of anterior tibial artery.
5. Circumflex fibular branch of posterior tibial artery.
The nerve supply is from
1. Femoral nerve: through its branches to vastus medialis.
2. Sciatic nerve: through genicular branches.
3. Obturator nerve: posterior branch.
A number of bursae are present around the knee joint. They are shown in
Table 45.2.
TABLE 45.2
Bursae Around the Knee Joint
Anterior Posteromedial Posterolateral
Subcutaneous Bursa deep to medial head of gastrocnemius Bursa deep to lateral head of
prepatellar gastrocnemius
bursa
Subcutaneous Anserine bursa (separates the tendons of sartorius, gracilis and Bursa between fibular
infrapatellar semitendinosus from one another from the tibia and from tibial collateral ligament and
bursa collateral ligament) biceps femoris
Deep Bursa deep to the tibial collateral ligament Bursa between fibular
infrapatellar collateral ligament and
bursa tendon of popliteus
Suprapatellar Bursa deep to semimembranosus Bursa between the tendon of
bursa popliteus and lateral
condyle of tibia
Bursa between the tendons of semimembranosus and semitendinosus
Popliteal fossa is a diamond shaped depression behind the knee joint. The
boundaries are shown in Table 45.3.
TABLE 45.4
Causes of Loose Bodies of Knee Joint
Nontraumatic Traumatic
Tuberculous arthritis Intra-articular fracture

Rheumatoid arthritis Meniscal injuries
Osteoarthritis Detached articular cartilage
Synovial chondromatosis Foreign body
Roof of the popliteal fossa is formed by deep fascia, the Floor is formed by
capsule of knee joint and strong fascia covering the popliteus muscle.
Contents of popliteal fossa are as follows:
1. Popliteal artery
2. Popliteal vein
3. Tibial nerve
4. Popliteal lymph node
5. Fat
Movements
Three sets of movements take place at the knee.
1. Flexion and extension are the chief movements, which occur at the upper
compartment joint above the menisci. These movements occur at the
transverse axis, which is not fixed, i.e., the axis moves forwards and upwards
during extension and backwards and downwards during flexion. They are
accompanied by rotation.
2. Medial and lateral rotation: Medial rotation of femur occurs during the last
30° of extension, and lateral rotation during the initial stages of flexion. When
the foot is off the ground, tibia rotates instead of the femur, but in the opposite
direction. Rotatory movements take place around a vertical axis, and occur in
the lower compartment of the joint, below the menisci.
3. Gliding movement of patello femoral articulation.
Muscles Acting on the Knee and Their Action
Flexors Biceps femoris, semitendinosus, semimembranosus

Extensors Quadriceps femoris
Locking and unlocking of the knee joint

Locking is a mechanism that allows the knee to remain in position of full
extension for weight bearing and occurs as a result of medial rotation of the
femur during the last stage of extension. Locking is produced by quadriceps
femoris. When locked, the ligaments remain taut. The knee can be flexed only
when the knee is unlocked by a reversal of medial rotation, brought about by the
action of popliteus.
45.2 Deformities of knee
Genu valgum and genu varum

• Common in childhood, with no underlying cause (physiological).
• Genu valgum (knock knee): 3 to 5 years
• Genu varum (bow leg): 1 to 3 years
• They can occur due to injury or disease.
• Common causes are as follows:
• Malunited fractures of lower end of femur or upper part of tibia.
• Rarefying diseases like rickets, osteomalacia.
• Bone softening diseases like Paget disease.
• Uneven growth of epiphyseal plates in children, after injury or
osteomyelitis or dyschondroplasia.
• Genu valgum: knee and leg are bowed inwards (Fig. 45.2A).
• Genu varum: knee and leg are bowed outwards (Fig. 45.2B).
FIGURE 45.2A Genu valgum (congenital).

FIGURE 45.2B Genu varum.
X-rays (Fig. 45.2C and 45.2D) show underlying cause.
FIGURE 45.2C X-ray—Genu valgum.

FIGURE 45.2D X-ray—Genu varum.
Treatment
• In early childhood, treatment is unnecessary, as it is physiological.
• If rickets is the cause, medical management is required.
• In genu valgum,
• Fitting a wedge in the shoe in the medial aspect for genu valgum and lateral
aspect for genu varum about 3- to 5-mm deep, to shift the line of weight
bearing.
• Deformity persisting beyond 10 years requires active treatment by
supracondylar osteotomy of the femur with excision of suitable wedge
from the medial side.
• After cessation of growth, osteotomy is the only hope to correct the
deformity.
Genu recurvatum
• Bending backwards (reverse of flexion) of the knee.
• Physiological or familial in aetiology.
• Can occur due to
• instability of the ligaments
• epiphyseal arrest after an old injury and
• post poliomyelitis paralysis.
Knee and leg are bowed backwards (Fig. 45.3).
FIGURE 45.3 Genu recurvatum.
X-rays show underlying cause.
Treatment
Corrective surgery may be needed after the cessation of skeletal growth.
45.3 Traumatic lesions of knee joint
Fracture of patella
• Patella may be fractured by direct or indirect forces.
• Direct force: Fall on the flexed knee or blow on the anterior part of the
knee joint.
• Indirect force: Forceful sudden contraction of quadriceps muscle.
• Patellar fractures are classified into
• Undisplaced fracture
• Displaced transverse fracture
• Upper and lower polar fractures
• Comminuted fracture
• Pain, swelling and tenderness over the anterior aspect of knee, with inability
to extend the knee joint actively (extensor lag). Passive extension is possible.
• Crepitus is felt in comminuted fractures.
• Skin abrasion is telltale evidence in direct injuries.
• Haemarthrosis may be present.
X-rays(AP and lateral) (Fig. 45.4A and B) are conclusive.
FIGURE 45.4A X-ray—fracture patella.
FIGURE 45.4B X-ray—comminuted fracture patella.
Treatment
• Undisplaced fractures: Conservative treatment.
• Displaced fractures: The fragments are fixed with a screw or by tension band
wiring. If the fracture is comminuted and reconstruction is not possible,
patella is excised and the expansion sutured.
Fracture of femoral condyles

• Fractures of femoral condyles are uncommon, but common in young adults
after high-energy trauma or in the elderly with osteoporosis.
• Three types of fracture occur:
• Supracondylar fracture: due to hyperextension injury.
• Unicondylar (medial or lateral) fracture: due to varus or valgus injury.
• Intercondylar fracture: T- or Y-shaped fracture: due to direct injury.
• The fractures may be undisplaced or displaced.
Associated injury: Injury to popliteal artery and nerve.
Complications: Stiffness of knee, osteoarthritis, deformity, shortening.
• Pain and swelling in the knee region.
• Examination may reveal
• tenderness and abnormal mobility
• haemarthrosis may be present
• varus or valgus deformity or shortening of the limb may occur and
• intercondylar distance is increased.
• X-rays (Fig. 45.5A and B) are diagnostic.
• CT is useful to rule out intra-articular extension.
• MRI is useful to localize injuries to the ligaments, anterior cruciate ligament
tear, meniscal tear.
FIGURE 45.5A X-ray—supracondylar fracture.
FIGURE 45.5B X-ray—fracture lateral condyle femur.
Treatment
• Undisplaced fractures are treated by immoblization in a long leg plaster for 8
weeks.
• Displaced fractures need surgical fixation for accurate apposition.
• Incomplete or fracture in osteoporotic bones require traction, reduction, cast
brace and early mobilization in 3 to 6 weeks.
Fracture of tibial condyles
• Fracture of lateral condyle of tibia is caused by a force that abducts the tibia
upon the femur while the foot is fixed on the ground.
• Usually seen when the bumper of a car strikes the outer side of the knee
of a pedestrian (Bumper fracture).
• There are three types of fractures of tibial condyles. They are as follows:
1. Compression fracture with fragmentation.
2. Depressed plateau type of fracture.
3. Oblique shearing fracture.
• Pain, swelling and bruising of the knee region.
• Examination may reveal tenderness and abnormal mobility.
• Haemarthrosis may be present.
• Injury to the popliteal artery should be ruled out, if bruising is seen on the
posterior aspect.
• X-rays (Fig. 45.6) are diagnostic.
• CT is useful to rule out intra-articular extension.
• MRI is useful to localize injuries to the ligaments.
FIGURE 45.6 X-ray—fracture tibial condyles.
Treatment
• Compression fracture with fragmentation: Hinged cast brace with early
mobilization after skeletal traction for 4 to 6 weeks.
• Depressed plateau type of fracture: Open surgery to align the articular
surfaces.
• Oblique shearing fracture: Open surgery and fixation.
45.4 Soft tissue injuries of knee joint
Dislocations of patella
The patella is dislocated laterally, and are of three types:
• Acute dislocation: single isolated injury when the knee is flexed or semi-
flexed.
• Recurrent dislocation: usually seen in girls with congenital laxity of the joint,
congenital defect in lateral femoral condyle, small or high lying patella, with
the first episode during adolescence.
• Habitual dislocation: due to shortening of quadriceps muscle (vastus lateralis
component) following repeated intramuscular injections during infancy.
• Acute dislocation: The patient is unable to straighten the knee, unless the
reduction is spontaneous. Later the knee swells due to effusion. Marked local
tenderness on the anteromedial part is prominent.
• Recurrent dislocation: Repeated dislocations occur when the knee is being
flexed from extended position.
• Habitual dislocation: Lateral dislocation occurs every time the knee is flexed.
X-rays (skyline view) (Fig. 45.7) are useful.
FIGURE 45.7 X-ray—skyline view—lateral dislocation of patella (both

sides).
Treatment
• Acute dislocation: Closed reduction under anaesthesia with firm bandaging
and immobilization for 3 weeks followed by quadriceps exercises.
• Recurrent dislocation: Surgery, detaching the bony insertion of patellar
tendon and transposing it to a new bed on the tibia, so as to change the line
of pull of the quadriceps.
• Habitual dislocation: Release of tight muscle or band by dividing to permit
full flexion of knee without displacement of patella.
Collateral ligament injuries

Tear of the medial collateral ligament is more common than the lateral.
• Medial ligament injury: Caused by an injury that abducts the tibia upon the
femur. The joint gets momentarily subluxated but undergoes spontaneous
reduction.
• Lateral ligament injury: Caused by an injury that adducts the tibia upon the
femur.
Common peroneal nerve palsy may be present.
Cruciate ligaments also may be torn when the force is high and subluxation is
severe.
• Medial ligament injury
• Pain and swelling of the medial side of the knee joint.
• On examination,
- Tenderness is elicited on the medial side of the joint and the femoral
condyle.
- Haemarthrosis may be present.
- Valgus stress test is positive at 30° flexion of the knee.
• Lateral ligament injury
• On examination, tenderness is elicited on the lateral side of the joint and the
femoral condyle.
• X-rays are necessary to rule out fractures.
• MRI is useful in diagnosing intra-articular ligament injuries.
Treatment
• Conservative treatment is to support in long leg plaster, with aspiration of
joint if necessary.
• Ligament repair may be necessary, if stability is compromised.
Cruciate ligament injuries

Cruciate ligaments may get torn in isolation or along with the collateral ligament
injuries.
• Anterior ligament is torn by a force driving the upper end of tibia forwards
relative to the femur, or by hyperextension of the knee.
• Posterior ligament is torn by a force driving the upper end of tibia backwards.
• Diffuse pain in the knee joint, with haemarthrosis.
• Anterior drawer test and Lachmann test are positive in anterior cruciate
ligament tear.
• Posterior drawer test is positive in posterior cruciate ligament tear.
• MRI (Fig. 45.8A) is useful in diagnosis.
• Arthroscopy (Fig. 45.8B) is confirmative.
FIGURE 45.8A MRI—anterior cruciate ligament tear.
FIGURE 45.8B Arthroscopy—anterior cruciate ligament tear.
Treatment
Repair of torn ligaments (open or arthroscopic) is curative.
Meniscal injuries
• Common in men under 45 years.
• The tear is usually caused by a twisting force with the knee semi-flexed or
flexed, as in football players.
• Medial meniscus is torn more commonly than the lateral.
• There are three types of meniscal tears (Fig. 45.9):
1. Bucket handle tear: a longitudinal split of the meniscus with the ends
intact.
2. Posterior horn tear: the tear emerges at the concave border and the
pedunculated tag is attached at its posterior horn.
3. Anterior horn tear: the tear emerges at the concave border and the
pedunculated tag is attached at its anterior horn.
FIGURE 45.9 Medial meniscal tears.
• History is characteristic. A twisting injury on a flexed or semiflexed knee, and
he is unable to continue with the activity. He is unable to straighten the knee
and this episode is followed by swollen knee.
• There is spontaneous recovery of symptoms only to recur during a twisting
movement.
• Locking is characteristic.
• X-rays are normal.
• Arthroscopy is diagnostic.
Treatment
Meniscal repair (Arthroscopic) is warranted since torn menisci do not heal
spontaneously, as they are almost avascular.
Note
• Lateral meniscus injury presents with symptoms similar to medial meniscus
injuries.
• Lateral meniscus can be discoid in shape, rarely.
• Discoid feature can be present in lateral menisci of both knees as a
congenital anomaly.
• Discoid meniscus is more prone for injuries.
Dislocation of knee joint

• Dislocation of knee is a rare phenomenon, in spite of its flat articular surfaces.
• Dislocations are possible only when some or all of the ligaments are ruptured.
• The tibia is displaced backwards, forwards, laterally or medially upon the
femur.
Associated injury :Popliteal artery and nerve injuries.
Complications: Osteroarthritis, ligamental instability.
Pain, swelling and deformity.
• X-ray (Fig. 45.10) is diagnostic.
• Doppler study of popliteal artery is useful.
• US may demonstrate massive soft tissue damage.
FIGURE 45.10 Fracture dislocation of knee.
Treatment
• Reduction by traction and manipulation, with support in full-length lower
limb plaster cast for 6 to 8 weeks.
• Surgery may be needed if instability is demonstrated.
Haemarthrosis of knee joint

Blood in the knee joint (haemarthrosis) may occur due to
• bony injury
• ligament injury or
• synovial injury.
In children, haemophilia should be ruled out (see Haemophilic arthritis).
Painful swelling of the knee joint.
• X-rays may be normal or may show fractures of bones of the joint.
• Diagnostic aspiration will show unclotted blood.
Treatment
• Therapeutic aspiration may be carried out, with compression bandage.
• Underlying cause should be determined and treated.
45.5 Nontraumatic lesions of knee joint
Pyogenic arthritis
• Pyogenic arthritis is commoner in the knee probably because of its
vulnerability to injuries and also to its close relationship of the joint cavity to
the lower metaphysis of femur, one of the commonest sites of acute
osteomyelitis.
• Common infecting organisms are as follows:
• Staphylococcus aureus (commonest)
• Streptococci
• Escherichia coli
• Klebsiella
• Septic arthritis is seen in neonates also.
• Seen in immunocompromised adults.
• Pain, swelling and loss of function.
• Constitutional symptoms may be present.
• X-rays are normal in the initial stages.
• US is most useful.
• Leucocytosis and raised ESR may be present.
• Diagnostic aspiration and isolation of organism is confirmatory.
Treatment
• Appropriate antibiotics and rest in plaster is necessary.
• Pus if present should be aspirated or drained.
• Most frequently affected joints in rheumatoid arthritis, which may lead to
permanent disability.
• They may be affected simultaneously with several other joints in the same
person.
• Female preponderance is seen.
rheumatoid arthritis in general (Ch. 41).
After the hips, knee is the most commonly affected joint by tuberculosis,
especially in children and young adults.
• Knee is painful, diffusely swollen due to synovial thickening and warm to
feel.
• Movements are restricted, thigh muscles are wasted and abscess and sinus
formation occur.
• Constitutional symptoms may be present.
• Triple deformity (flexion, external rotation and posterior subluxation due to
unopposed action of biceps femoris) is seen in early stages).
Investigations and treatment are those like tuberculous arthritis in
general (Ch. 41).
Osteoarthritis
• Osteoarthritis affects the knee joint more often than any other joint in the
body, which is usually due to wear and tear.
• Previous diseases, fractures and overweight are predisposing factors.
• The changes affect predominantly the femoro-tibial joint or the patello-
femoral joint, but usually the whole joint is affected.
• Pain in both the knees increasing on activity.
• Sudden locking suggests presence of loose bodies.
• Clinical examination may show
• slightly swollen joint (Fig. 45.11A) with varus/valgus deformity;
• palpation may show thickening of synovium;
• joint line tenderness;
• restriction of joint movements and
• positive patellar tap.
FIGURE 45.11A X-ray—osteoarthritis knee joint.
• X-rays () are diagnostic, which show reduced joint space and ‘spiking’ of the
joint margins. Loose bodies may be seen. Stress X-rays (standing on the
affected side) are contributory.
FIGURE 45.11B X-ray—lateral view - Osteoarthritis knee.
FIGURE 45.11C X-ray—skyline view—osteoarthritis of knee.
Treatment
• Conservative treatment like exercises and physiotherapy are advised.
Hydrocortisone injections are useful.
• Surgery is indicated depending on the circumstances. The operations are as
follows:
• Removal of loose bodies
• Upper tibial osteotomy
• Patellar maltraching (surgery to release soft tissue)
• Arthroplasty
• Knee joint (total or partial) replacement
• Arthrodesis (rare)
• Haemophilic arthritis affects the knee more often than any other joint.
• Initially, there is simple haemorrhage in the joint (haemarthrosis) and by
repeated attacks, degenerative changes occur in the articular cartilage and
forms fibrous thickening of the synovial membrane due to deposition of iron
in the articular surface.
haemophilic arthritis in general (Ch. 41).
Neuropathic arthritis
• One of the most commonly affected joints (Charcot’s osteoarthropathy).
• Commonest cause is tabes dorsalis.
• Diabetes mellitus and Hansen’s disease are other causes.
• The articular cartilage and the parts of underlying bones show signs of
wearing away, and there is associated hypertrophy of bone at the joint
margins. The ligaments become lax and the joint is unstable.
• Single joint presentation.
• Slight pain may be present.
• Bones are thickened.
• Movements are restricted in flexion, but there is severe lateral laxity
sometimes giving a severe bow-leg deformity.
X-rays show severe destructive changes with some new bone formation at the
joint margins (findings disproportionate to pain).
Treatment
• Splinting may be useful.
• Severely damaged joints require replacement.
Ochronotic arthritis
• Degenerative arthritis caused by accumulation of oxidized homogentisic acid
pigment in connective tissue (ochronosis).
• Results from a rare disorder of tyrosine metabolism in which deficiency of the
enzyme homogentisic acid oxidase leads to excretion of large amounts of
homogentisic acid in urine (alkaptonuria).
• Inherited as autosomal recessive trait.
• Pigmentation of heart valves, larynx and tympanic membrane and skin are
also seen.
• Pain, stiffness and limitation of movement of hips, knees and shoulder,
resembling rheumatoid arthritis.
• Darkening of urine to blackness on standing, degenerative arthritis and
ochronotic pigmentation forms the diagnostic triad.
• Urine analysis: Presumptive tests of urine for the presence of homogentisic
acid.
• Purple black colour on addition of ferric chloride.
• Brown colour on addition of Benedict’s reagent.
• Black colour on addition of saturated silver nitrate.
• Biochemistry: Confirmation by chromatography, enzymatic and
spectrophotometric tests.
• X-rays of spine are virtually pathognomonic (degeneration and dense
calcification of the intervertebral discs and narrowing of intervertebral
spaces).
Treatment
• No specific treatment is available.
• Treatment is symptomatic as in osteoarthritis.
• Dietary restriction of phenylalanine and tyrosine may be of use.
• Ascorbic acid is used as it curbs the oxidation and polymerization of
homogentisic acid.
• In severe cases, total knee replacement is advised.
Chondromalacia of patella
• Common disorder of young adults of unknown aetiology, where the cartilage
of the articular surface of the patella is roughened and fibrillated. This is
defined as a blistering cystic change of the patellar cartilage and is
commonly associated with vastus medialis tendonitis.
• This condition predisposes to osteoarthritis.
• Pain deep in the knee, behind the patella, which is aggravated by climbing or
descending stairs.
• Clinical examination may reveal
• Effusion in the joint and tenderness on palpating the deep surface of patella
after displacing it to one side.
• There may be a point of marked tenderness over the front of the medial
femoral condyle.
• Zohler’s test: Patient in supine position with extended knees. The patella is
pushed towards the foot and the patient is asked to lift the leg to make the
quadriceps to contract. The test is positive if there is appearance of pain
(behind the patella).
• X-rays are normal.
• MRI and arthroscopy are useful.
Treatment
• Spontaneous improvement is seen on application of elastic bandage with
restriction of activities.
• Surgery is indicated in select cases (shaving of retro-patellar surface by
arthroscopy).
Osteochondritis dissecans
• Most common site of osteochondritis dissecans.
• Characterized by necrosis of part of articular cartilage and the underlying
bone, which ultimately separates to form an intra-articular loose body.
• May affect several joints in one patient and also several members in one
family.
• The lesion commonly affects the articular surface of medial femoral condyle.
• Initially, the symptom is mild ache and intermittent swelling.
• Locking may be a symptom when loose bodies have formed.
• Examination shows
• little swelling due to effusion;
• movements are not usually impaired;
• quadriceps is wasted and
• tibial spine may be prominent.
• X-rays (tangential PA projection) (Fig. 45.12) may show area of clearcut
deformity on the articular surface of medial condyle of femur. Loose body is
seen.
• Arthroscopy (Fig. 45.13) is diagnostic.

FIGURE 45.12 X-ray—osteochondritis dissecans knee.

FIGURE 45.13 Arthroscopy—osteochondritis dissecans.
Treatment
• Medical management is advisable.
• Surgery is required to remove loose bodies.
Loose bodies
• Loose bodies commonly form inside the knee joint.
• Causes may be traumatic or nontraumatic, as shown in Table 45.4.
TABLE 45.5
Causes of Thickening of Bone
Generalized Thickening Localized Thickening
Infection of bone Osteophytes
Expanding tumour Exostoses
Expanding cyst Aneurysmal bone cyst
Injury to knee Healing callus
• A sense of giving way may be felt by the patient.
• A feeling of something moving within the joint is also felt (Joint mouse).
• Intermittent locking of the joint due to interposition of loose bodies between
the joint surfaces.
• Severe pain accompanies locking.
• The joint gets swollen.
• Clinical examination reveals a swollen joint and sometimes the loose bodies
can be felt.
• X-rays (Fig. 45.14A) demonstrate the loose bodies.
• Arthroscopy (Fig. 45.14B) is diagnostic.
FIGURE 45.14A X-ray—loose bodies knee joint.

FIGURE 45.14B Arthroscopy—loose bodies knee joint.
Treatment
Removal of loose body (arthroscopic or open) is curative.
45.6 Extra-articular disorders of knee
Rupture of quadriceps apparatus

• Quadriceps muscle is inserted into the tibia through the medium of the patella
(a sesamoid bone) and the patellar tendon.
• Complete rupture of the muscle can occur at three points. They are as follows:
1. At the point of attachment of quadriceps tendon to the upper pole of
patella (avulsion from patella).
2. Through the patella and the quadriceps expansion (disruption through
patella).
3. At the attachment of patellar tendon to the tibial tubercle (avulsion at
tibial tubercle).
• In all cases, the injury is caused by an unexpected flexion force, resisted
automatically with a sudden contraction of quadriceps muscle.
• Pain, swelling and tenderness over the anterior aspect of knee.
• Inability to extend the knee joint in the last 15° (Extensor lag).
X-rays in AP, lateral views (Fig. 45.15) are conclusive.
FIGURE 45.15 X-ray—pulled up patella due to rupture of tendon.
Treatment
• Avulsion from patella: The tendon is reattached by sutures.
• Disruption through patella: The fragments are fixed with a screw or by
tension band wiring. If the fracture is comminuted and reconstruction is not
possible, patella is excised and the quadriceps expansion sutured.
• Avulsion at tibial tubercle: The tendon is reattached by sutures.
Apophysitis of tibial tubercle (osgood–schlatter

disease)
• Apophysitis of tibial tubercle affects adolescents
• Usually boys of 10 to 14 years of age are affected.
• The tibial tubercle is enlarged and painful, due to pull of the patellar tendon.
• Pain in front and below the knee, worsening on strenuous activity.
• On examination,
• Tibial tubercle is unduly prominent and tender.
• Straight leg raising against resistance is painful.
• Joint movements are normal.
X-rays (fig. 45.16) may show enlargement and sometimes fragmentation of the
tubercle.
FIGURE 45.16 X-ray—apophysitis tibial tubercle.
Treatment
• NSAIDs may give relief.
• Local steroid injections are useful.
• Cylinder cast may be necessary for 6 weeks.
Prepatellar bursitis (housemaid’s knee,

clergyman’s knee)
The bursa that lies in front of the lower half of patella and upper part of patellar
tendon is prone to inflammation. These are of two types:
• Irritative type: caused by repeated friction, like in the people who kneel for
long hours (housemaid, clergymen).
• Infective or suppurative type: infection by pyogenic organisms directly from
a puncture wound or through lymphatics from the infection of leg.
• Irritative: Painless soft fluctuant swelling in front of the knee, without joint
involvement (Fig. 45.17).
• Suppurative: Painful swelling in front of the knee with pyrexia. Swelling is
tender with erythematous and oedematous skin over it. Inguinal
lymphadenitis may be present. Extension is painful though the joint is not
involved.

FIGURE 45.17 Prepatellar bursitis (left knee).
Diagnostic aspiration is informative.
Treatment
• Irritative: Aspiration and avoidance of friction, hydrocortisone injection in
some cases.
• Suppurative: Drainage of pus with appropriate antibiotics is curative.
Popliteal cysts
Most cystic swellings in the knee are of irritative variety.
The common cysts are as follows:
• Inflamed semimembranosus bursa.
• Baker’s cyst (herniation of the synovial membrane).
• Cyst secondary to degeneration of tendon sheath (ganglion).
• Semimembranosus bursitis: Presents as a soft nonreducible cystic swelling at
the back of the knee, close to the medial condyle of the femur.
• Baker’s cyst: Presents as a soft cystic bulge near the midline behind the knee
and upper calf. May be reducible in communicative variety (Fig. 45.18).
FIGURE 45.18 Baker’s cyst left knee.
DD: Popliteal artery aneurysm.
X-rays may demonstrate signs of osteoarthritis.
Treatment
• Semimembranosus bursitis: No treatment is necessary.
• Baker’s cyst: The primary condition should be treated, and if the cyst is very
large and discomforting, it may be excised, with subtotal synovectomy, and
repair of capsular rent.
Pellegrini–stieda disease
Ossification of subligamentous hematoma after partial avulsion of the medial
ligament from the medial femoral condyle.
• Persistent discomfort at the medial side of the knee after any injury to the
medial ligament.
• Clinical examination reveals thickening and tenderness over the site of
attachment of the ligament to the medial femoral condyle.
X-rays show a thin plaque of new bone close to the medial condyle.
Treatment
Active mobilization and muscle-strengthening exercises.
45.7 Fractures of shafts of leg bones
Fracture of shafts of tibia and fibula

• Most of the injuries of leg involve both the shafts of tibia and fibula.
• Isolated fracture of tibia is relatively uncommon.
• Isolated fracture of fibula is caused by direct blow over the bone.
• Motorcycle accidents are the commonest cause.
• May occur following
• angulatory force (causing transverse or short oblique type of fracture) and
• rotational force (causing spiral fractures at different levels of two bones).
• Tibial fracture is common at the junction of middle and lower thirds, whereas
fibular fracture is near the junction of middle and upper thirds.
• Displacement of fragments is considerable.
• Undisplaced crack fractures are seen in children.
• Most tibial fractures are compound due to its proximity to surface and poor
protection by muscles.
• Rarely, fatigue or stress fracture of tibia may occur.
Associated injury: Popliteal artery and nerve injuries.
Complications: Infection, delayed union, nonunion, mal-union, leg
shortening.
• Pain and swelling at the fracture site.
• Loss of function of knee joint.
X-rays of leg(AP and lateral views) (Fig. 45.18A-D) are diagnostic.
FIGURE 45.18 (A) X-ray—fracture of tibia. (B) X-ray—comminuted
fracture of tibia. (C) X-ray—fracture shaft of fibula. (D) X-ray—fracture
both bones of leg.
Treatment
Tibial fracture treatment should be concentrated when both bones are fractured,
as fibular fracture unites readily as it is a bone of secondary importance in the
leg.
• Undisplaced fracture is immobilized in full-length plaster with the knee
slightly flexed and the ankle at a right angle for 6 weeks.
• Displaced fractures are internally fixed with intramedullary nailing or
transfixion screws or metal plate with screws.
45.8 Symptoms of knee joint pathologies
• Pain
• Swelling
• Deformity
Pain
• Knee pain: Knee joint pain is generalized and localized to one area. The
patient tends to apply his entire palm over the joint to show the area of pain
when it is generalized as in arthritis. Localized knee pain may be due to
ligament tears. Knee pain can get aggravated by movements, and relieved by
rest (e.g., arthritis).
Extrinsic sources of pain in the knee
• From hip (e.g., arthritis, slipped upper femoral epiphysis).
• From the spine (e.g., sciatic pain from a prolapsed intervertebral disc).
Note
If satisfactory explanation is not found in the knee for knee pain, the
examination should extend to the hip, spine and abdomen.
Swelling
Swelling of the knee can be either diffuse or localized, and arise from three
fundamental causes. They are as follows:
1. Thickening of bone: general or localized (Table 45.5).
2. Fluid within the joint (Table 45.6) and thickening of synovial membrane.
3. Cysts around knee (Table 45.7).
TABLE 45.6
Characteristics of Various Effusions of Knee Joint
Characteristic Nature Of Fluid
Blood Serous fluid Pus

History Haemophilia Arthritic pain Constitutional symptoms
Trauma Synovitis
Time duration of appearance Within 1 or 2 hours 12 to 24 hours More than 24 hours
Clinical examination Tense appearance Not tense appearance Redness of overlying skin
Mildly tender Nontender Severely tender
TABLE 45.7
Varieties of Cystic Swellings Occur Around the Knee
Location In Relation To The Knee Joint

Anterior Posterior Lateral Medial
Suprapatellar bursa Morrant Baker’s cyst Biceps bursa Bursa anserine
Prepatellar bursa Semimembranosus bursa Cyst of lateral meniscus Cyst of medial meniscus
Infrapatellar bursa Popliteal aneurysm Tumour fibular head Ganglion of semimembranosus tendon
Patellar tumour Enlargement of popliteal nodes Cold abscess Haemangioma of vastus medialis
Schwannoma of popliteal nerve
TABLE 45.8
Age Preponderance in Knee Joint Pathologies
Age Groups Males Females

0–12 Discoid lateral meniscus Discoid lateral meniscus
12–18 Osteochondritis dissecans Recurrent dislocation of patella
Osgood–Schlatter disease Osgood–Schlatter disease
18–30 Longitudinal meniscal tears Recurrent dislocation of patella
Chondromalacia patellae
30–50 Rheumatoid arthritis Rheumatoid arthritis
>50 Osteoarthritis Osteoarthritis
Fluid within the joint: The fluid within the joint can be in varying quantities.
Distinctions between effusions of blood, serous fluid and pus are made partly
from history and clinical examination and confirmed by aspiration. The
characteristics of various effusions are shown in Table 45.6.
Thickening of synovial membrane: It is a predominant feature of chronic
inflammatory arthritis, and synovitis (e.g., Rheumatoid, tuberculosis, traumatic
synovitis).
Deformity
Deformities are caused by localized pathologies (e.g., malunited fracture of
lower end of femur or upper end of tibia, Paget disease of bone, rickets).
Movements of knee joint are restricted due to traumatic, inflammatory,
neoplastic and degenerative conditions.
• Traumatic (e.g., dislocations, fracture dislocations)
• Inflammatory (e.g., septic arthritis)
• Neoplastic (e.g., osteoclastoma of upper end of tibia, osteosarcoma of lower
end of femur)
• Degenerative (e.g., osteoarthritis of knee joint)
Age and sex of the patient should be borne in mind as some diseases are
preponderant in certain age groups (see Table 45.8).
TABLE 45.3
Boundaries of Popliteal Fossa
Boundaries
Superolateral Superomedial Inferolateral Inferomedial
Biceps femoris Semitendinosus Lateral head of gastrocnemius Medial head of gastrocnemius

Semimembranosus
Gracilis
Eliciting history
This will answer the duration of pain, and its mode of onset (e.g., sudden
onset pains are generally due to trauma and insidious onset pain is usually
due to inflammatory pathology).
• Relationship to trauma: Is this pain preceded by an injury, an accident,
or sport or a fall?
small slips may cause soft tissue injuries, and fall during active sports or
road traffic accidents may cause fractures). Fracture pain is severe and
starts almost instantly, whereas soft tissue injury pain starts late.
• Position during the fall:What was the position of the knee during the fall?
Fall on flexed knee may result in fracture of patella.
Very severe pain may indicate fractures or septic arthritis.
• Relationship to movements: Is this pain related to movements and are
there any relieving factors?
fractures, and nontraumatic situations, may indicate arthritis. Morning
stiffness may indicate rheumatoid arthritis and reduction of pain on
movements may indicate osteoarthritis. History of locking is common in
patients with loose bodies, or meniscal tears.
radiographs have to be scrutinized if available. History related to needle
aspiration of joint (arthrosynthesis) should be questioned.

Knee and leg
Pre-requisites
• Patient should be undressed so that both the lower limbs are fully (from pelvis
to toes) exposed.
• Both knees should be examined simultaneously.
• Patient should lie on a hard couch.
• Hip joint and ankle joint should also be examined.

What to watch when the patient gets on to the examination couch:
• Can the knee be flexed (e.g., may indicate pain of knee pathology)?
• How clumsy is the patient during movements (e.g., taking support onto
the joint)?
• How protective is the patient during the act (e.g., denotes pain)?
distance.
• Position of patient: Sitting, standing, lying supine, lying prone and while
walking.
• Position of examiner: The examiner should view the knee from all sides,
from the front, back and sides.
Inspection
What to look for?
• Attitude of the patient (e.g., patients with fractures of knee, are seen
supporting the knee with both hands).
• Change in contour of the knee (e.g., quadriceps prominence is seen in
suprapatellar injuries, wasting of muscles).
• Deformities (e.g., bone deformity may be seen in supracondylar fractures of
femur).
• Abnormal swellings (e.g., undue prominence may be seen in the posterior
aspect in Baker’s cyst).
• Shortening of thigh or limb (e.g., supracondylar fracture of femur).
From the front:
• Deformities (e.g., Genu valgum, Genu varum).
• Patella (size, shape and location and compare with opposite side).
• Patellar ligament.
• Suprapatellar and parapatellar regions (e.g., fullness is seen in bursitis,
effusion).
• Tibial tubercle and shin of leg.
• Swelling
• Generalized [e.g., synovitis (Fig. 45.19A)].
• Localized [e.g., hematoma (Fig. 45.19B), bursa anserine (Fig. 45.19C)].
• Skin (e.g., colour changes, abrasions, lacerations—injuries, sinuses—
tuberculosis and scars—previous surgery).
FIGURE 45.19A Synovitis left knee.

FIGURE 45.19B Haematoma of knee.
FIGURE 45.19C Bursa anserine.
From behind:
• Popliteal fossa (e.g., full in synovitis, haemarthrosis, Baker’s cyst).
• Skin (colour—haematoma, scars—previous surgery, sinuses—tuberculosis
and veins—varicose veins).
• Pulsation of swelling (e.g., aneurysm).
From sides:
• Contour (e.g., changed in effusions, genu recurvatum).
• Vastus lateralis, iliotibial band.
• Fibular neck depression.
• Swelling on the lateral side of knee joint.
From all sides: Note for discolouration (e.g., haematoma), sinus and
discharge (e.g., tuberculous arthritis). Special attention should be given to scars
—surgical wound.
Palpation
• Temperature: Warmth (e.g., infective conditions like septic arthritis).
• Bones
• Lower end of femur: The surgeon should gently run the examining hand
on the femur above downwards all round (Fig. 45.20) (e.g., abnormal
depression or prominence may be felt in cases of displaced supracondylar
fractures).
• Upper end of tibia is felt by running the finger starting at the midleg and
running it upwards towards the knee joint. When the knee is kept in 90°
flexion, the articular surfaces can be palpated (Fig. 45.20A) and looked for
thickening and undue prominences (e.g., exostoses) and depressions (e.g.,
fractures). Inferior joint linecan be felt by insinuating the finger on the
sides of ligamentum patellae with side to side rolling movements of
patella (Fig. 45.20B).
• Upper end of fibula: The upper end of fibula is felt by running the finger
starting at the midleg and running it upwards towards the knee joint and
looked for thickening and undue prominences (e.g., fractures, tumours,
exostoses) (Fig. 45.21).
• Patella: The patella is felt when the patient keeps his knee extended and
relaxes his quadriceps muscle. The surface of patella is felt by the
examiner with the flat of his hand (Fig. 45.22A), and later it is held with
the thumb and the index finger and moved side to side (Fig. 45.22B).
• Tenderness: Tenderness is elicited in fractures and infective conditions (e.g.,
tenderness over the medial condyle—medial ligament tear, lateral epicondyle
—lateral ligament injury. Joint line tenderness should be elicited (e.g.,
synovitis) all round the joint.
• Crepitus: Crackling sensation is felt in fractures, degenerative arthritis.
• Swelling of joint
FIGURE 45.20 Method of palpating the lower end of femur.
FIGURE 45.20A Method of palpating the shaft and upper end of tibia.
FIGURE 45.20B Method of palpating of joint line.
FIGURE 45.21 Method of palpating the shaft and upper end of fibula.
FIGURE 45.22A Palpation of surface of patella.
FIGURE 45.22B Moving the patella over the femur.
A diffuse swelling of the knee can arise from three fundamental causes. Each
one can be determined by deep palpation.
1. Thickening of bone: Thickening of bone can be detected without difficulty by
deep palpation, but should be compared with the opposite side.
2. Fluid within the joint: Since the quantity varies according to pathology,
different methods have to adopted to confirm its presence.
• Small quantity: Presence of small quantity of fluid in the joint manifests as
obliteration of suprapatellar fossa. Compression of this fossa will displace
the fluid into the joint, but the fossa slowly refills after release of pressure.
• Moderate quantity: Moderate quantity of fluid in the joint will obliterate
the parapatellar fossae.
- Patellar tap is one of the methods to identify this. Method: The patient
keeps the knee extended. The examiner pushes the contents of the
suprapatellar bursa into the joint with his left hand, which will lift the
patella and make it float. The conjoint fingers of the right hand should
push the patella downwards and tap. The tapped patella hits the anterior
surface of the femur and rebounds to its floating position on release of
pressure (Fig. 45.23). This characteristic tap is called ‘Patellar tap’ or
‘Ballottement of patella’.
- Fluctuation test: Method: Palm of the left hand is placed over the
suprapatellar fossa, and the other hand is placed over the patella.
Application of pressure by one hand will displace the fluid the other
way, and the other hand will feel the hydraulic impulse.
• Large quantity: Large quantity will be visible and will not allow both the
above tests, but will give a boggy feel of the joint and the patella can be
felt without difficulty floating on it.
3. Thickening of synovial membrane: The thickening of the synovial
membrane is best felt above the patella, by running the four fingers of the
examining hand (ref. Fig. 45.20), where the reflected membrane forms the
suprapatellar pouch. It has a characteristic boggy feel on palpation, as if a
sheet of sponge has been placed between the skin and the underlying bone.
Thickened synovial membrane will show warmth of the overlying skin due to
its high vascularity.
• Transillumination: This test is done only when the fluctuation is positive.
Knee joint that contains clear serous fluid is transilluminant (e.g.,
rheumatoid arthritis). This test is done in a dark room, the light transmitted
by a beam of torch, is seen through a fine tube prepared by folding a card
board or a X-ray film called ‘illuminoscope’. The light may be passed on
one side of the patellar tendon and viewed from the other side.
FIGURE 45.23 Method of eliciting patellar tap.
Note
The torch should have a unidirectional beam. If the synovial thickening is
considerable, it may not be transilluminant.
• Muscles and tendons: Tone, texture and contractive pliability of each muscle
around the knee should be tested.
Power of each muscle group should be tested by
• hip and knee movements;
• ankle movement and
• foot and toe movements.
distribution of popliteal nerve should be performed.
• Circulation: Popliteal, posterior tibial and dorsalis pedis pulses should be felt
(e.g., aneurysm, cut injuries of back of knee). Warmth, colour, capillary
return and cutaneous sensibility should be determined.
Movements
A full range of movement of the knee joint usually rules out the possibility of
moving the leg in various directions. The normal range of movements of the
knee and the methods of determination (Figs. 45.24 and 45.25) are given in
Table 45.9.
FIGURE 45.24 Flexion of knee joint.

FIGURE 45.25 Extension of knee joint.
TABLE 45.9
Normal Range of Movements of the Knee and the Methods of
Determination
Flexion From zero position (full extension of knee) to the heel touching the thigh 0°–120°/130°
Extension From fully flexed position to zero position 120°/130°–0°
Hyperextension From zero position the leg lifted 0°–10°
Adduction and abduction Lateral and medial deviation Small degree
Rotation Knee partially flexed Medial rotation 0°–10°
Lateral rotation 0°–15°
Note
Accurate assessment of the range of movement is important in the knee,
because a slight impairment of movement is significant.
• Flexion may be restricted in fat individuals.

• Range of sound knee must be taken as normal or yardstick for that individual.
• Hyperextension is possible in women than in men.
• Note whether the movements are painful and accompanied with abnormal
sounds.
Varieties of abnormal sounds (crepitations) may be heard or felt during
movements of the knee joint. They are as follows:
• Fine crepitations: Chondromalacia patellae.
• Coarse crepitations: Osteoarthritis, Neuropathic arthritis.
• Click: Meniscal tear, Meniscal cyst.
• Thud sound: Discoid lateral meniscus.
Measurements
• Length of the thigh: This is measured with a tape from the tip of greater
trochanter to the medial point on the joint line of the knee (e.g., the length is
shortened in supracondylar fracture) (ref. Fig. 44.27C).
• Length of the leg: This is measured with a tape from a point on the medial
joint line to the medial malleolus (e.g., the length is shortened in old
epiphyseal injury, malunited fracture of the shaft of tibia) (Fig. 45.26).
FIGURE 45.26 Measuring the length of the leg.
Note
While taking the above measurements, the knee should be flexed at right angle
so that the condyles become prominent.
• Circumference of knee: This is measured with a tape taking it round the

knee. This is compared with the other side (e.g., this is increased in all
dislocations of knee, effusions of the joint) (Fig. 45.27).
• Circumference of muscles acting on the knee: This is measured with a
tape taking it round the muscles. This is compared with the other side
(e.g., this is decreased when the muscles are wasted) (Fig. 45.28).
FIGURE 45.27 Measuring the circumference around knee joint.
FIGURE 45.28 Measuring the circumference of thigh.
Note
All measurements are to be taken at identical places on both sides to get
accuracy and comparison.
Special tests
Tests for integrity of collateral ligaments

The knee should be fully extended and quadriceps relaxed, and only in this
position the medial and lateral ligaments are taut.
• Valgus (abduction) stress test for medial collateral ligament integrity: The
left hand of the examiner is used as a fulcrum at the side of the knee, the
ankle is supported by the right hand (Fig. 45.29). An abduction force is
applied to the knee, which will open the medial ligament. If the joint opens
out medially without pain, it indicates a complete tear. If there is pain
without opening the joint, it indicates strain.
• Varus (adduction) stress test for lateral collateral ligament integrity: The
knee should be fully extended and quadriceps relaxed, and only in this
position the lateral ligament is taut. Method: The left hand of the examiner is
used as a fulcrum at the side of the knee, the ankle is supported by the right
hand (Fig. 45.30). An adduction force is applied to the knee, which will open
the lateral ligament. If the joint opens out laterally without pain, it indicates
a complete tear. If there is pain without opening the joint, it indicates strain.
• Apley’s distraction test: Patient should lie prone with knee flexed to 90°.
The clinician should hold the foot and pull the leg and rotate internally (Fig.
45.31). Pain during this movement indicates lateral collateral ligament injury.
Likewise, when the leg is pulled and rotated externally, pain indicates medial
collateral ligament injury.
FIGURE 45.29 Valgus stress test.
FIGURE 45.30 Varus stress test.
FIGURE 45.31 Apley distraction test.
Tests for integrity of cruciate ligaments

The patient lying supine, knee kept flexed at 90°, the foot fixed on the couch and
the quadriceps relaxed. The anterior cruciate ligament prevents the anterior glide
of the tibia on the femur and the posterior ligament prevents the posterior glide.
Anterior cruciate ligament

• Anterior drawer test: Method: With the knee flexed at 90°, the fingers of the
examiner should sling behind the upper end of tibia, and clasp the sides of
the leg between thenar eminences. The tips of thumbs should be placed on
the femoral condyles. A pull–push movement is given on the tibia to
determine the anterior-posterior movement (Fig. 45.32). Normally, the glide
is about half a centimetre. Excessive glide in the anterior direction indicates
damage to the corresponding ligament.
FIGURE 45.32 Anterior drawer test.
Note
This should be compared with the normal side.
• Lachman’s test: The patient lying supine and knee is flexed to 20° with the
foot resting on the couch. The examiner should grasp the thigh and lower leg
with each hand, a forward translational force is applied to the tibia while the
femur is pushed backwards (Fig. 45.33). An increase in movement is
suggestive of rupture of anterior cruciate ligament.
• Pivot shift test: The patient should lie supine with the hip in neutral rotation
and slightly flexed. The knee is held extended initially. The examiner should
hold the foot internally rotated in one hand and apply valgus stress to the
knee with the other hand. This causes forward subluxation of tibia on the
femur when there is rupture of anterior cruciate ligament. The knee is then
smoothly flexed from full extension. The pivot test is considered positive, if
a clunk is palpated at about 20° to 30° as the tibia reduces into its normal
position.
FIGURE 45.33 Lachman test.
Posterior cruciate ligament

• Posterior drawer test: Both knees of the patient are flexed to 90° with both
feet placed together. When the knees are observed from the sides, posterior
sag of the tibia on the femur indicates a rupture of posterior cruciate
ligament. A pull–push movement is given on the tibia to determine the
anterior-posterior movement, as in the anterior drawer test. Excessive glide
in the posterior direction indicates damage to the corresponding ligament.
Note
This should be compared with the normal side.
Tests for integrity of semilunar cartilages or menisci

• McMurray’s test: The tibia is rotated upon the femur with the knee in
various positions of flexion and extension. This is done to demonstrate
mobile pedunculated tags of meniscus, and maneuvering the joint it is hoped
that the pedunculated tag would jam the bone ends temporarily, and a click
sound will be heard when the tag is disengaged. Method: The limb is grasped
firmly at the ankle with the right hand of the examiner so that he has a full
control of flexion-extension and rotatory movements. The left hand is kept
on the knee to feel the click (Fig. 45.34). Step 1: The knee is fully flexed and
the tibia is rotated laterally upon the femur to the full extent. Maintaining this
position, the knee is extended and felt for a click. Step 2: The same is
repeated with medial rotation, and findings are noted. Step 3: Same steps are
repeated in varying degrees of flexion, i.e., 120°, 105°, 90°, 75° and 60°. A
loud click suggests a tear (not in bucket handle tear). Inference: When the
test is done with knee abducted, and if the posterior part of medial meniscus
is torn, the patient will experience pain in the initial stages of extension. If
middle part is torn, pain is experienced in the middle of extension. If the
anterior part is torn, the pain will be experienced at full extension. Similar
test is done with adducted knee, and similar findings will appear for lateral
meniscus injury.
FIGURE 45.34 McMurray test.
Note
Loud clicks may be produced in a normal knee, mostly from the movements of
patella.
• Apley’s grinding test: The patient should lie prone on the couch. The knee
is flexed at right angle. The clinician should hold the foot and apply
compressive force (Fig. 45.35) and rotate the leg laterally. Inference: Pain
indicates tear in medial meniscus. Likewise, medial rotation causes pain if
the lateral meniscus is torn.
FIGURE 45.35 Apley grinding test.
Tests for arcuate ligament complex

• External rotation recurvatum test: With the patient supine, the legs are
elevated from the examining table by grasping the great toes and lifting
them. The test is positive if the knee falls into a varus angulation, with
hyperextension and if the tibia rotates externally.
• Posterolateral drawer test: The knee is flexed to 90°. The tibia is pushed
posteriorly (Fig. 45.36) and the test is positive when the lateral side of the
tibia plateau is subluxed posteriorly in relation to the femoral condyle. The
medial side of the tibial plateau remains stationary.
FIGURE 45.36 Posterolateral drawer test.
Lymphatic system
tuberculosis).
General examination
tuberculosis).
CHAPTER 46
Ankle, foot and toes

V. Thulasiraman
CHAPTER OUTLINE
46.1. Ankle joint 862
• Anatomy 862
• Movements 863
46.2. Anatomy of foot 863
46.3. Deformities of foot 864
• Club foot (Talipes equino-varus) 864
• Talipes calcaneo-valgus 865
• Flat foot (Pes planus) 865
• High arch foot (Pes cavus) 865
• Hallux valgus 866
• Hallux rigidus 866
• Hammer toes 867
• Claw toes 867
46.4. Traumatic lesions of ankle joint 867
• Fracture dislocation about the ankle 867
46.5. Soft tissue injuries of ankle joint 869
• Rupture of lateral ligaments 869
• Recurrent subluxation of ankle 869
• Strain of lateral ligament 869
• Rupture of calcaneal tendon 870
46.6. Injuries to the tarsal bones 870
• Fractures of talus 870
• Fractures of calcaneum 871
• Fractures of metatarsals 871
• Lisfranc fracture dislocation 872
• Fractures of phalanges 872
46.7. Nontraumatic lesions of ankle and foot 872
• Gouty arthritis 873
• Haemophilic and neuropathic arthritis 874
46.8. Extra-articular disorders of ankle and foot 874
• Osteochondritis of navicular bone 874
• Osteochondritis of talus 874
• Calcaneal paratendinitis 874
• Calcaneal apophysitis 874
• Freiberg’s disease 875
• Tarsal tunnel syndrome 875
• Dislocation of peroneal tendon 876
46.9. Symptoms of ankle and foot pathologies 876
• Ankle, foot and toes 877
• General 879
46.1 Ankle joint
Anatomy
Ankle joint is a synovial joint of modified hinge variety with great strength. Its
stability is ensured by
• the powerful ligaments and tendons around it;
• the insertion of the trochlea tali into the deep socket between the medial and
lateral malleoli.
Articular capsule is attached to articular margins of all three bones except the
anterior part of talus, where it is fixed to the neck. The synovial membrane lines
the inside of the capsule.
Ligaments
Because this joint is a hinge joint, the main ligaments are lateral and medial.
• Medial (deltoid) ligament is very strong and triangular in shape. This radiates
from the medial malleolus to the medial side of the talus, sustentaculum tali,
medial edge of the spring ligament, navicular bone and neck of talus. The
ligament not only strengthens the ankle joint, but also holds the calcaneus
and the navicular against the talus. This attachment helps to maintain the
medial longitudinal arch of foot.
• Lateral ligament consists of three bands, of which the anterior and posterior
are thickenings of fibrous capsule.
• Anterior talofibular ligament: anteromedially to the neck of talus.
• Posterior talofibular ligament: medially backwards to the posterior
tubercle of talus.
• Calcaneofibular ligament: a round cord runs posteromedialy from the
distal end of lateral malleolus to lateral surface of calcaneus.
Blood supply is derived from
• anterior and posterior tibial artery and
• peroneal artery.
Nerve supply is from
• peroneal nerve and
• tibial nerve.
Subtalar joint is formed by talus and calcaneum. Inversion and eversion are
the movements in the joint.
• Inversion (raising the medial border of foot) is produced by tibialis anterior
and tibialis posterior.
• Eversion (raising the lateral border of foot) is produced by peroneus group of
muscles.
Movements
The only two significant movements of ankle joint are as follows:
1. Plantar flexion: by the action of gastrocnemius, soleus and tibialis posterior
assisted by flexors of toes.
2. Dorsiflexion: by the action of tibialis anterior and extensors of toes.
The surfaces of trochlea tali, which articulate with the malleoli are wider apart
anteriorly, and the socket is also broader in front. Thus, the talus fits snugly into
the socket when the foot is dorsiflexed, whereas it is slightly loose when plantar
flexed. Maximum stability is achieved in the standing position.
46.2 Anatomy of foot
Bones
The superior surface is the dorsum and the inferior surface is the sole (planta).
The foot is divided into tarsus and metatarsus (Fig. 46.1A).
• Tarsus is the posterior half formed by the tarsal bones, which are arranged in
two rows.
• The proximal row consists of two large bones set one (talus) above the
other (calcaneus), which is the largest of the tarsal bones and forms the
bone of the heel.
• The distal row consists of the cuboid bone laterally and the three wedge-
shaped cuneiform bones, set side by side, medially. The cuboid articulates
proximally with the calcaneus and distally with the lateral two metatarsals.
The cuneiforms articulate distally with the medial three metatarsals but are
separated by the navicular bone, which lies between the two rows. The
navicular articulates proximally with the talus and distally with the three
cuneiforms. Between the tarsal bones are the intertarsal joints.
• Metatarsus consists of metatarsals set side by side and are numbered 1 to 5
from the medial side. The proximal ends (bases) articulate with the tarsal
bones (tarso-metatarsal joints) and with each other in the case of the lateral
four (intermetatarsal joints). The distal end of each metatarsal articulates
with the proximal end (base) of the phalanx (metatarso-phalangeal joint).
The toes are numbered from the medial side, the first is the big toe or hallux
and the fifth is the little toe or digitus minimus.
• Phalanges are the bones of the toes. The big toe has two phalanges and the
other toes three each, proximal, middle, and distal phalanges. The phalanges
articulate at interphalangeal joints. There are several sesamoid bones in the
foot, two of them constantly present on the plantar surface of the metatarso-
phalangeal joint of the big toe.
FIGURE 46.1A Bones of foot.
Muscles
• First layer: abductor hallucis, flexor digitorum brevis and abductor digiti
minimi.
• Second layer: tendons of flexor hallucis longus, flexor digitorum longus,
flexor digitorum accessories and lumbricals.
• Third layer:flexor hallucis brevis, flexor digiti mini brevis and adductor
halluces.
• Fourth layer: dorsal and plantar interossei.
Arches
The arches of the foot are formed by the tarsal and metatarsal bones and
strengthened by ligaments and tendons, which allow the foot to support the
weight of the body in the erect posture with the least weight. The arches are
categorized as longitudinal and transverse (Fig 46.1B).
• Longitudinal arch: It is an anteroposterior arch contributed by medial and
lateral arches, and consists of the calcaneus, cuboid, lateral cuneiform and
third metatarsal. The arch is maintained by the stretched plantar aponeurosis,
which acts like a bowstring. The tendon of flexor hallucis longus, assisted by
the tendons of flexor digitorum longus and the short muscles of foot, play a
significant role in maintaining the medial part; whereas, the tendons of flexor
digitorum longus and muscles of first layer, flexor digitorum brevis and
adductor digiti minimi maintain the lateral part.
• Transverse arch: The arches are complete at the posterior part of the
metatarsals and the anterior part of the tarsus. In between, at the middle of
the tarsus, the arches are incomplete and present the characters of half-
domes, and complete the dome when the feet are kept together. The
transverse arches are strengthened by the interosseous, plantar and dorsal
ligaments, by the short muscles of the first and fifth toes (especially the
transverse head of the Adductor hallucis), and by the Peronæus longus,
whose tendon stretches across between the piers of the arches.
FIGURE 46.1B Arches of foot.
46.3 Deformities of foot
Club foot (talipes equino varus)

• Developmental defect.
• May have familial tendency (Fig. 46.2).
• Common in male children.
• The soft tissues at the medial side of the foot are underdeveloped and shorter
than normal. The foot is adducted and inverted at the subtalar, midtarsal, and
anterior tarsal joints and is held in equinus (plantar flexion) at the ankle.
• The deformity consists of three parts:
1. Inversion of the foot (twisting inwards).
2. Adduction of the forefoot relative to the hindfoot (inward deviation).
3. Equinus (plantar flexion).
FIGURE 46.2 Familial tendency of club foot.
• The foot is turned inwards so that the sole is directed medially.
• The criterion for diagnosis is that the deformity cannot be readily corrected or
overcorrected to bring the foot into eversion and dorsiflexion (Fig. 46.2A and
B).

FIGURE 46.2A-B Talipes equinovarus—(A) anterior view; (B) posterior
view.
X-rays (Fig. 46.2C) are required to rule out associated bony deformities.
FIGURE 46.2C X-ray—Club foot.
Treatment
• Closed manipulation by serial correction using cast (Ponseti method).
• Surgical correction if conservative management fails.
Talipes calcaneo valgus

• This congenital deformity is opposite to talipes equino-varus, and is less
common.
• The foot is everted and dorsiflexed.
• The cause is not known, it is suggested that it may be a postural deformity in
the intra-uterine life.
The foot rests in a position of eversion and dorsiflexion, so that its dorsum lies
almost in contact with the shin.
Treatment
• In most cases, manual stretching of tissues is enough to correct the
deformity.
• Surgery is indicated in those which do not respond to conservative measures.
Flat foot (pes planus)

In this congenital condition, the longitudinal arch of the foot is reduced so that,
on standing, the medial border of the foot is close to, or in contact with the
ground (Fig. 46.3).
• Usually associated with some degree of twisting outwards of the foot on its
longitudinal axis.
• In late life, osteoarthritis of the tarsal joints may occur due to mal-alignment.
FIGURE 46.3 Flat foot.
• Usually symptomless.
• Rarely, they suffer from foot strain and pain in the midfoot.
X-ray of foot in standing position will show medial arch collapse.
Treatment
• In children over 3 years of age, the treatment is to tilt the shoe slightly to the
lateral side by inserting a wedge, base medially, between the layers of the
heel.
• In adults, physiotherapy is useful to alleviate pain.
• Surgery may be needed in late cases when arthritis develop.
High arch foot (pes cavus)

• In this congenital condition, the longitudinal arch of the foot is accentuated.
• It is rarely familial.
• It may be associated with some underlying neurological sorders like spina
bifida and may also follow poliomyelitis.
• The soft tissues are abnormally shortened hastening the deformity.
• The deformity is characteristic
• The longitudinal arch is high
• The toes appear clawed, which are hyperextended at the metatarso-phalangeal
joints and flexed at the proximal and distal interphalangeal joints (Fig 46.4).
The toes are almost functionless due to defective action of interossei and
lumbricals
• The excessive weight bearing occurs at the metatarso-phalangeal joints
leading to callosities on the skin.
• Spine should be examined for congenital anomalies
FIGURE 46.4 Pes cavus.
X-rays are required to rule out associated bony deformities.
Treatment
The treatment should start in childhood since correction of this deformity in
adult life is virtually impossible.
• First step is to encourage exercises for the intrinsic muscles.
• If exercises fail, mildest cases are treated by subcutaneous fasciotomy.
• Bony correction operation is the last resort.
Hallux valgus
• In this deformity, the great toe is deviated laterally at the metatarso-
phalangeal joint and is common in middle-aged women.
• Cause is usually acquired due to the use of narrow pointed footwear.
• The effects of hallux valgus are as follows:
• An exostosis on the medial side of the head of first metatarsal.
• A bunion (inflamed adventitious bursa over the head of first metatarsal.
• A bunionette (adventitious bursa over the lateral aspect of the head of fifth
metatarsal.
• Osteoarthritis of the first metatarso-phalangeal joint.
• Overriding or under-riding of second toe by the first (Fig. 46.5A).
FIGURE 46.5A Hallux valgus with overriding of second toe Source: (Courtesy
Dr T. V. Raja).
• The deformity is obvious at a glance (Fig. 46.5B).
• Pain may occur due to osteoarthritis of the joint.
FIGURE 46.5B Hallux valgus (left).
X-rays (Fig. 46.6) are diagnostic.
FIGURE 46.6 X-ray—Hallux valgus.
Treatment
Surgery is very effective in moderate to severe cases.
Hallux rigidus
• In this condition, the metatarso-phalangeal joint of the great toe is stiff and
painful
• They are of two types:
1. Adolescent type: Due to synovitis of the metatarso-phalangeal joint
following trauma, with muscular spasm. There are no radiological
changes.
2. Adult type: It is mono-articular osteoarthrosis, sometimes precipitated
by injury. Capsular fibrosis, deformation of the articular surfaces and
interlocking of osteophytes cause the stiffness.
Stiff great toe without any movement associated with pain (Fig. 46.7).
FIGURE 46.7 Hallux rigidus Source: (Courtesy Dr T. V. Raja).
X-ray changes (Fig. 46.8) are seen in adult type.
FIGURE 46.8 X-ray—Hallux rigidus Source: (Courtesy Dr T. V. Raja).

Treatment
Surgery (arthrodesis of metatarsophalangeal joint) is very useful.
Hammer toes
This denotes hyperextension of the metatarso-phalangeal and distal
interphalangeal joints, and flexion of the proximal interphalangeal joints.
• They may affect the second, third and fourth toes.
• Can occur due to overcrowding of toes, either by small or pointed shoes, or
there is no obvious cause.
Deformity is obvious and callosities may develop over the bony prominence on
the dorsum of proximal interphalangeal joint (Fig. 46.9).
FIGURE 46.9 Hammer toes.
X-rays to demonstrate any bone abnormality.
Treatment
• Treatment is correcting any predisposing cause and wearing a corrective
splint or a corn plaster.
• Established deformities require open surgery (arthrodesis of proximal
interphalangeal joint with extensor tenotomy and dorsal capsulotomy of
metatarso-phalangeal joint).
Claw toes
• This condition is similar to hammer toes, but the distal interphalangeal joints
are flexed and not extended. Hence the toe pads do not touch the ground
when the patient stands
• Rheumatoid arthritis is a common cause
The deformity is obvious (Fig. 46.10).

FIGURE 46.10 Claw toes Source: (Courtesy Dr T. V. Raja).
X-rays demonstrate any bone abnormality.
Treatment
• Exercises for the intrinsic muscles of the foot if the metatarso-phalangeal
joints are mobile.
• Established deformities require open surgery (arthrodesis of proximal
interphalangeal joint with extensor tenotomy and dorsal capsulotomy of
metatarso-phalangeal joint).
46.4 Traumatic lesions of ankle joint
Fracture dislocation around the ankle

The bones forming the ankle joint are injured more often than any other bone
except lower end of radius. Many varieties of fractures and fracture dislocations
are recognized, and they are grouped together as ‘Pott’s fracture’ (Fig. 46.11).
FIGURE 46.11 Pott’s fracture.
Mechanism of injury
Malleolar fractures with or without subluxation or dislocation of the talus may
occur from three types of injury. They are as follows:
• An abduction or lateral rotation force or a combination of both (commonest
type).
• An adduction force.
• A vertical compression force.
Seven varieties of fracture and fracture dislocation are considered in the group
of ankle injuries. They are as follows:
• Isolated lateral malleolar fracture: caused by abduction or lateral rotation
force or avulsed by an adduction force.
• Isolated medial malleolar fracture: caused by an adduction force or avulsed
by an abduction force. Very often it is displaced with loss of smooth articular
contour of ankle mortise. A fringe of periosteum and tibialis posterior tendon
may intervene the bone fragments preventing union.
• Lateral malleolar fracture with lateral displacement of talus: caused by
abduction or lateral force. Medial malleolus is intact but the medial ligament
is torn (otherwise lateral displacement could not occur).
• Fractures of both malleoli with displacement of talus: caused by abduction
or lateral rotation force, the medial malleolus is avulsed and the ligament is
intact.
• Diastasis of inferior tibio-fibular joint: occurs due to rupture of tibiofibular
ligament caused when lateral malleolus withstands the abduction injury of
ankle, and talus is displaced laterally with the lower end of fibula, and fibula
may fracture at its upper end.
• Posterior marginal (posterior malleolar) fracture of tibia: caused by the
carrying of momentum forwards at the time of injury.
• Vertical compression fracture of tibia: caused by a fall from a height, but it is
relatively uncommon, may have associated calcaneal fracture
Complications: Nonunion, stiffness of ankle, osteoarthritis.
• Severe pain and swelling of ankle.
• Tenderness at the fracture site (entire length of fibula should be carefully
palpated).
• Fibular spring test is positive.
• X-rays (AP, lateral and mortise views) are diagnostic (Fig. 46.11A–F).
• CT is useful for delineating bony injuries.
• MRI is useful for delineating soft tissue injuries.
FIGURE 46.11 (A) Isolated fracture of lateral malleolus. (B) Fracture
medial malleolus. (C) Fracture of lateral malleolus with lateral
displacement. (D) Fracture of both malleoli with displacement. (E) Tibio-
fibular diastasis and fracture of fibula. (F) Posterior marginal fracture of
tibia.
Treatment
Principles of treatment
• Undisplaced fractures require below knee walking plaster for 3 to 6 weeks.
• Displaced fractures need to be reduced by manipulation under anaesthesia and
plaster for about 8 to 10 weeks.
• The reduction should ensure.
• Talus is restored to its normal relationship with tibio-fibular mortise.
• Tibia and fibula are in normal relationship with one another at their lower
ends.
• When reduction is not satisfactory, fixation of fragments with screws and
wires is necessary.
• Additional protection with a below knee plaster for 8 to 10 weeks in
osteoporotic patients.
Treatment
• Isolated lateral malleolar fracture: Immobilisation is essential to union, pain
is relieved if in plaster for 3 weeks.
• Medial malleolar fracture: Undisplaced fracture requires immobilization in
plaster, and displaced fracture requires surgery.
• Lateral malleolar fracture with lateral displacement of talus: Accurate
reduction is necessary, and is achieved by screw fixation of lateral malleolus
with below knee plaster for 8 weeks.
• Fractures of both malleoli with displacement of talus: Fixation of medial
malleolus with screw is sufficient as it automatically holds the talus and
lateral malleolus in intact positions as the ligaments are intact. Plaster
immobilization is necessary for 10 weeks.
• Diastasis of inferior tibio-fibular joint: Reduced under direct vision and
screw transversely across two bones (to be removed before walking).
• Posterior marginal fracture of tibia: open reduction with fixation by a screw.
• Vertical compression fracture of tibia: open reduction with bone grafting and
fixation by a screw or a plaster.
Note
Epiphyseal injury of lower tibia is common in children—grade II of Salter and
Harris type.
46.5 Soft tissue injuries of ankle joint
Rupture of lateral ligaments

• Rupture of talo-fibular and calcaenofibular ligaments is caused by a severe
adduction force.
• Rupture can be complete with subluxation of talus in the tibio-fibular mortise.
• Rapid swelling of the lateral aspect of ankle with severe pain.
• Walking may be difficult or impossible.
• History of adduction injury.
• Examination shows a swollen and tender lateral aspect of ankle.
• X-ray AP view taken while an adduction force is applied to heel, which will
show the talus tilted medially in the tibio-fibular mortise (a tilt of more than
20° is abnormal).
• US of the ankle is useful in identifying the tears (complete or incomplete).
Treatment
• Below knee plaster for 6 weeks.
• Suturing of torn capsule and ligaments with correct opposition is done for
recurrent dislocations.
Recurrent subluxation of ankle

Recurrent subluxation with medial tilt of talus results due to persistent instability
caused by tear of lateral ligaments.
• Giving way feeling especially when there is a tilt, sometimes causing a fall.
• Oedema of the ankle, with tenderness over the lateral ligaments.
• Heel can be inverted passively beyond the normal range, and during this
movement, a dimple may appear on the skin due to sucking of the soft
tissues between the tibia and talus.
• Generalized ligament laxity may be ruled out.
X-ray AP view taken while an adduction force is applied to heel, which will
show the talus tilted medially in the tibio-fibular mortise (a tilt of more than 20°
is abnormal).
Treatment
• Slight disability is treated with strengthening of evertors (peronei) by
exercises.
• Severe disability is treated by operation.
Strain of lateral ligament

• Strains of lateral ligaments is fairly common
• Caused by adductor force insufficient to cause a rupture
• Pain and swelling at the lateral aspect of the ankle, with difficulty in walking.
• Tenderness immediately below and anterior to lateral malleolus.
• Plantar flexion and dorsiflexion are comfortable, but attempted adduction
causes pain.
X-ray is required to exclude a fracture.
Treatment
• No treatment is required, if pain is mild.
• Severe pain and swelling requires a walking plaster for 2 to 3 weeks.
Rupture of calcaneal tendon (tendoachilles)

Rupture occurs about 3-5 cm proximal to the insertion of the tendon
• Severe pain at the back of the ankle felt during walking or running
• Walking is with a limp
• Tenderness at the site of rupture
• A gap is usually felt in the tendon (Fig 46.12)
• Plantar flexion is greatly weakened
• Patient will be unable to stand on the affected limb while lifting the other
from the ground
• Tip-toe standing or walking is not possible or painful
FIGURE 46.12 Rupture tendoachilles (arrow) compared with normal foot

(below).
• US of tendoachilles may be useful to assess the gap between torn ends
(partial or total).
• MRI (Fig. 46.12A) of ankle is diagnostic.
FIGURE 46.12A MRI—Rupture of calcaneal tendon.
Treatment
Surgical repair of the tendon is necessary, with immobilizing the knee in 90°
flexion and moderate ankle plantar flexion for 3 weeks, followed by below knee
plaster with foot in neutral position for 3 weeks.
46.6 Injuries of tarsal bones
Fractures of talus
• 2% of lower limb injuries.
• Most injuries are caused by a fall from a height on to the feet (talus fractures
are less common than calcaneus fractures).
• The fracture can be of two types. They are as follows:
• Major (fracture through neck): common in aircraft crash, where the rudder
bar is driven up against the middle of the foot or forced dorsiflexion.
• Minor(chip fracture from the margin of one of the articular surfaces).
Complications: Nonunion, avascular necrosis, osteoarthritis, compression of
posterior structures (tibial nerve and artery).
• Severe foot pain with diffuse swelling of hind foot.
X-rays (AP, lateral and mortise views) of ankle (Fig. 46.13) are diagnostic.
Canale view provides optimum view of the neck of talus.
FIGURE 46.13 X-ray—Fracture talus.
Treatment
• Minor fractures are treated with immobilization in below knee walking
plaster for three to four weeks.
• Undisplaced fractures require short leg cast for 8 to 12 weeks and kept
nonweight bearing for 6 weeks.
• Displaced fractures require immediate closed reduction, if not possible,
surgery is planned.
• Open and irreducible fractures are corrected by open surgery.
• Compression of posterior structures need emergency surgery.
Fractures of calcaneum
• Most injuries are caused by a fall from a height on to the heel.
• Both heels may be injured at the same time, and usually associated with
vertebral fracture during vertical landing.
• The fractures are
• crack or minor fracture without displacement;
• crush injury and
• associated with avulsion of tendoachilles.
Type of fracture depends on the severity of force, i.e., height of the fall.
Displaced intra-articular fracture forms the majority.
Complications: Heel pain, malunion, limping gait, stiffness of subtalar and
midtarsal joints, osteoarthritis, Sudeck’s atrophy.
• Pain and swelling of heel and unable to bear weight.
• On examination,
• Minor fracture: Small soft tissue swelling with severe tenderness over the
tuberosity, without any palpable deformity, movements are not restricted.
• Crush injury: The heel looks short and widened, marked local tenderness,
with marked restriction of inversion-eversion movement at the subtalar
and midtarsal joints.
X-rays (lateral view) (Fig. 46.14) are diagnostic. The upper surface of calcaneus
is flattened, so that the subtalar joint may form almost a straight line with the
upper surface of the tuberosity. The ‘tuberosity-joint angle’ (normal about 35° to
40°) has been used as an index of severity of compression, in severe case, the
angle is reduced to zero or it may be even inverted.
FIGURE 46.14 X-ray—Fracture calcaneum.
Treatment
• Undisplaced fractures are managed conservatively with bulky dressings.
• Displaced, open and dislocated fractures require surgical intervention.
Fractures of metatarsals
Caused by
• Direct violence from a heavy object falling upon the foot—any metatarsal.
• Muscular violence in a twisting injury—commonly base of fifth metatarsal
(Jone’s fracture—avulsion of peroneus brevis attachment).
• Repeated stress without any injury (stress or fatigue fractures).
• Pain and swelling at the fractured site.
• Walking is difficult.
• Marked local tenderness at the fractured site.
X-rays (Fig. 46.15A and B) are diagnostic. Stress views are taken to assess
stability.
FIGURE 46.15A X-ray—Fracture 3rd, 4th and 5th metatarsals.
FIGURE 46.15B Jones fracture.
Treatment
• Below knee walking plaster for 3 weeks to relieve pain and swelling.
Lisfranc fracture dislocation

It is a rare injury.
• Base of second metatarsal is recessed between the medial and lateral
cuneiforms. Middle three cuneiforms are trapezoidal and prevent plantar
displacement. Lisfranc ligament attaches medial cuneiform to second
metatarsal.
• Dorsalis pedis artery may get pinched.
Caused by
• Metatarsal displacement.
• Pain and swelling in the foot with deformity (valgus).
• High index of suspicion is necessary to diagnose.
FIGURE 46.16 Lisfranc fracture dislocation.
Treatment
• Undisplaced fractures are treated with short-legged plaster cast. Weight
bearing is allowed if pain permits.
• Displaced fractures are surgically managed—correction of fracture
dislocation.
Fractures of phalanges
• Most fractures are caused by direct crushing injuries, like a fall of a heavy
object.
• Great toe is commonly affected.
• Fracture is usually comminuted.
Pain and swelling at fractured site.
FIGURE 46.17 X-ray—Fracture of phalanges.
Treatment
No operative treatment is generally required, excepting for Mallet toe deformity
due to rupture of extensor hallucis longus.
46.7 Nontraumatic lesions of ankle and foot
Pyogenic arthritis
• Pyogenic arthritis of ankle is not uncommon in children.
• Staphylococcus aureus is the commonest organism.
• Organisms reach through blood or through penetrating wound.
• Local spread from a focus of osteomyelitis of tibia or fibula is rare, as the
metaphyses are extracapsular.
Clinical presentation, investigations and treatment are those pyogenic
arthritis in general (Ch. 41)
• One or both ankles may be affected.
• Common with other joints.
Clinical presentation (Fig. 46.18A), investigations (Fig. 46.18B) and
treatment are those like rheumatoid arthritis in general (Ch. 41).
FIGURE 46.18A Rheumatoid arthritis of foot and ankle.
FIGURE 46.18B X-ray—Rheumatoid arthritis of foot.
Much less common in the ankle than in the hip and knee.
tuberculous arthritis in general (Ch. 41)
Osteoarthritis
• Primary degenerative osteoarthritis is less common than in the knee.
• Commonest cause is mal-alignment of joint surfaces after a fracture.
Clinical presentation, investigations (Fig. 46.19) and treatment are those
like osteoarthritis in general (Ch. 41)
FIGURE 46.19 X-ray—Osteoarthritis ankle.
Gouty arthritis
• Clinical manifestation of a disturbed purine metabolism.
• Characterized by deposition of uric acid salt (sodium biurate) in connective
tissue like cartilage joints.
• Disease may be inherited.
• Common in men over the age of 40.
• May progress to chronic gout.
• Permanent disability is inevitable.
• Joints of great toe are most often affected, especially in the first attack.
• Sudden onset joint pain in the great toe.
• History of previous attacks with symptom-free intervals.
• On examination,
• The toe is swollen, red and extremely tender.
• Joint movements are extremely painful.
• Deposits of urate crystals in and around the joints of great toe.
• Serum uric acid levels may be raised.
• X-rays are normal in early stages, and deposits of sodium biurate in the
subchondral bone (appear transradiant) in chronic gout.
• Synovial aspiration may show urate crystals.
Treatment
• Acute attacks: respond well to allopurinol.
• Chronic gout and frequent attacks: Drugs to reduce plasma urate levels
(probenecid, allopurinol). Surgical fusion may be needed if there is severe
destruction.
Haemophilic arthritis and neuropathic arthritis

Though much less common in the ankle joint, it should be remembered that they
can affect the ankle joint. The clinical presentation and treatment are the same
described for knee joint.
46.8 Extra articular disorders of ankle and foot
Osteochondritis of navicular bone (kohler’s

disease)
• Common in the age group of 4 to 7 years.
• Exact cause is not known, but disturbance of blood supply is a possible cause.
• The developing nucleus of navicular bone is temporarily softened and
compressed by mechanical forces while walking.
• The bone may lose its trabecular structure and get fragmented.
• Pain in the mid tarsal part of foot.
• Walks with a limp.
• On examination,
• Mild swelling in the midtarsal region.
• Tenderness on deep palpation of navicular bone.
• Antalgic gait may be seen.
X-rays (Fig. 46.20) are diagnostic (bony nucleus of navicular bone appears
squashed from before backwards).
FIGURE 46.20 Kohler’s disease.
Treatment
• Mainly symptomatic.
• Mild cases can be treated with restriction of activities.
• Severe cases warrant immobilization or longitudinal arch support in short leg
cast for 3 to 4 weeks.
Osteochondritis of talus
• More common in sportspersons.
• Young are more commonly affected.
• May be due to repeated trauma.
Unexplained pain and slight limitation of movements of foot.
X-rays are diagnostic (small bony separation from the anteriomedial or
posterolateral aspect of superior surface of talus).
Treatment
• Mild cases warrant only immobilization.
• Severe cases require arthroscopic drilling or resection.
Calcaneal paratendinitis
The calcaneal tendon is surrounded by loose connective tissue or paratenon,
which allows gliding movements.
• Excessive friction can cause inflammation of this tissue.
• Affects young active adults.
• Pain in the region of calcaneal tendon, worse on running or dancing.
• On examination,
• Tenderness over the deep part of tendon.
• Mild tightness of tendoachilles may be seen.
MRI may exhibit tendon thickening.
Treatment
• Raising the heels in footwear helps to reduce pain by shortening the
tendoachilles.
• Ultrasound therapy.
• Local hydrocortisone injection will suffice.
• Below knee walking plaster for 4 weeks will help in some cases.
• Persistent pain warrants excision of loose connective tissue surrounding and
deep to the tendon.
Calcaneal apophysitis (sever’s disease)

• Self-limiting condition of growing children (between 8 and 13 years).
• Occurs during active growth of calcaneal apophysis.
• Most common overuse syndrome.
• Pain behind the heel with a limp.
• On examination, tenderness over the lower posterior part of calcaneal
tuberosity.
X-rays show signs of osteosclerosis/fragmentation of calcaneal apophysis (Fig.
46.21).
FIGURE 46.21 X-ray—Calcaneal apophysitis.
Treatment
• No surgical treatment is required.
• If the pain is severe, rest for a few weeks in a below knee walking plaster will
give quick relief.
Freiberg’s disease of a meatatarsal head

(metatarsal osteochondritis)
• Usually affects between 14 and 18 years old
• Nearly always affect the heads of 2nd and 3rd metatarsals
• Partial necrosis and fragmentation of metatarsal head, which may become
deformed under the pressure of weight bearing
• The articular surface of the metatarsal head loses its normal dome-shaped
contour and becomes flat
• Though the texture of the bone returns to normal, the articular surface remains
flat and causes osteoarthritis
• Pain in the affected joint, worse on standing or walking
• On examination
• Slight thickening in the region of the metatarsal head.
• Movements of metatarso-phalangeal joint are restricted and painful.
DD: Metatarsal neuralgia—side compression of metatarsal will produce pain.
X-rays (Fig. 46.22) are diagnostic (metatarsal head is flattened, and the end of
the bone appears square-cut instead of round).
FIGURE 46.22 Freiberg’s disease.
Treatment
The goal of treatment is to obtain healing of the aseptic necrosis.
• Initial treatment is symptomatic with decreased activities and using metatarsal
pads.
• More acute symptoms require short walking cast.
• Surgical treatment is for failed medical treatment, in the form of removal of
loose fragments and fusion of metatarsophalangeal joint.
Tarsal tunnel syndrome

Occurs when the posterior tibial nerve is compressed within the fibrosseous
tunnel, posterior and inferior to medial malleolus.
• Pain along the distribution of posterior tibial nerve.
• Medial calcaneal nerve may be involved.
• Percussion over the affected nerve elicits Tinel’s sign.
Nerve conduction studies may show reduced velocity of conduction of nerve.
Treatment
• Surgical decompression by release of flexor retinaculum and perineural
fibrosis when conservative treatment fails.
Dislocation of peroneal tendon

• Occurs in older children.
• Cause not known.
• Can be bilateral.
• May be due to shallow groove in fibula.
Sensation of snap and feeling of instability.
US (dynamic study) is useful.
Treatment
• Deepening the groove behind the lateral malleolus by sliding bone graft.
• Creating restraint by retinacular reconstruction using Achilles tendon.
46.9 Symptoms of ankle, foot and toe
pathologies
• Pain
• Swelling
• Deformity
Several causes influence the disorders of ankle, foot and the toes. They are as
follows:
• Hereditary: Consequence to man’s adoption to walking on feet, has a great
influence on the efficiency of the mechanism of movements of feet.
• Posture: Overweight is an important factor, which influences the ankle and
feet, by the weight bearing property.
• Footwear: The type of footwear has a great influence on the feet, especially
the high heel and pointed shoe of the ladies.
Majority of the symptoms of the leg, foot and toes are explained by a local
abnormality, and only rarely they are referred from a distant lesion.
Pain
• Pain is generalized and localized to one area. The patient has a relationship to
the movements of the ankle and foot. The pain may be more on standing, on
walking or running. It may have relationship to certain movements of the
ankle.
• Ankle pain can get aggravated by movements, and relieved by rest (e.g.,
arthritis).
• Referred pain from spine (S1 segment pain in lateral foot).
Swelling
Swelling of the ankle can be either
• diffuse (e.g., osteoarthritis) or
• localized (e.g., TB synovitis).
Deformity
• Heel—valgus or varus deformity due to subtalar disease.
• Forefoot—valgus deformity due to Lisfranc dislocation.
• Toes—Hallux valgus—gouty arthritis.
• Arthritis of subtalar joints. Pain is more or unlevel ground than on level
ground.
Eliciting history
• Onset of pain:When did the pain start, was it slow in onset or sudden? This
question will answer the duration of pain, and its mode of onset (e.g., sudden
onset pains are generally due to trauma and insidious onset pain is usually
due to inflammatory pathology). Fracture pain is severe and starts almost
instantly, whereas soft tissue injury pain starts late.
sport or a fall? This will answer the act following which the pain has
appeared, and description of the fall or accident will indicate the severity of
injury (e.g., small slips may cause soft tissue injuries, and fall during active
sports or road traffic accidents may cause fractures).
• Position during trauma:What was the act of the patient during the fall?
Landing on the ground from a height can produce bilateral calcaneal
fractures.
• Intensity of pain: How bad is this pain? Very severe pain may indicate
fractures or septic arthritis.
• Relationship to movements: Is this pain related to movements and are there
any relieving factors? Pain related to movements with the preceding history
of trauma may indicate fractures, and nontraumatic situations, may indicate
arthritis. Morning stiffness and reduction of pain on movements may indicate
osteoarthritis.
• Treatment:Was any treatment or first aid given to this pain? This will answer
about the first aid or hospital admissions and the radiographs have to be
scrutinized if available. History related to needle aspiration of joint
(arthrosynthesis) should be questioned.
Ankle, foot and toes
Pre-requisites
• Patient should be undressed so that both the lower limbs are fully exposed.
• Both ankles should be examined simultaneously.
• Patient should lie on a hard couch.
• Knee joint should also be examined.
• Spine should be examined in all ankle and foot disorders.

What to watch when the patient gets on to the examination couch:
• Can the patient lift his limb to get on to the couch (e.g., calcaneal tendon
tear)?
• How clumsy the patient is during movements (e.g., taking support onto
the joint).
• How protective the patient is during the act (e.g., denotes pain).
distance.
• Position of patient: Standing, walking and on the bed.
• Position of examiner: The examiner should view the ankle from all sides,
from the front, back and sides.
Inspection
What to look for?
• Attitude of the patient (e.g., patients with fractures of ankle, are seen limping
and hopping and avoid putting on the body weight on the affected side).
• Change in contour of the ankle (e.g., sprain, fractures).
• Deformities (e.g., fracture of lower end of tibia).
• Abnormal swellings (e.g., callosities).
From the front:
• Deformities (e.g., flat foot, high arched foot)
• Localized swelling (e.g., haematoma)
• Skin (e.g., colour changes, abrasions, lacerations—injuries, sinuses—
tuberculosis and scars—previous surgery)
From behind:
• Calcaneal tendon (e.g., full in synovitis, haemarthrosis)
• Skin (colour—hematoma, scars—previous surgery, sinuses—tuberculosis and
veins—varicose veins)
From sides:
• Contour (e.g., changed in effusions)
From all sides:
• Note for discolouration (e.g., haematoma), sinus and discharge (e.g.,
tuberculous arthritis). Special attention should be given to scars—surgical
wound.
Sole of foot
• Look for corns, callosities, ulcers (see Ch. 47).
Palpation
• Temperature: Warmth (e.g., infective conditions like septic arthritis).
• Bones
• Lower end of tibia: The surgeon should gently run the examining hand on
the tibia above downwards to the ankle (e.g., tenderness may be elicited in
medial malleolar fracture).
• Lower end of fibula: The surgeon should gently run the examining hand
on the fibula above downwards to the ankle (e.g., tenderness may be
elicited in lateral malleolar fracture).
• Bones of tarsus: The surgeon should gently run the examining hand on the
foot near the ankle all round, calcaneus is the best felt of tarsal bones (e.g.,
tenderness may be elicited in fractures).
• Metatarsals: The surgeon should gently run the examining hand on the
foot from ankle towards toes (e.g., tenderness is elicited in fractures). The
first and fifth metatarsals are better felt.
• Phalanges: The surgeon should gently run the examining hand on the
phalanges all round (e.g., tenderness is elicited in fractures and dislocations).
• Tenderness: Tenderness is elicited in fractures and infective conditions (e.g.,
tenderness over the medial condyle—medial ligament tear, lateral epicondyle
—lateral ligament injury). Joint line tenderness should be elicited (e.g.,
synovitis) all round the joint.
• Crepitus: Crackling sensation is felt in fractures, degenerative arthritis.
• Swelling of joint: Thickness of synovial membrane is best palpated in the
anterolateral aspect of ankle.
• Muscles and tendons: Tone, texture and contractive pliability of each muscle
around the ankle should be tested (see Ch. 48). Power of each muscle group
should be tested.
distribution of popliteal nerve should be performed (see Ch. 49).
• Circulation: Popliteal, posterior tibial and dorsalis pedis pulses should be felt
(e.g., aneurysm, cut injuries of back of knee). Warmth, colour, capillary
return and cutaneous sensibility should be determined (see Ch. 13).
Movements
A full range of movement of the ankle joint usually rules out the possibility of
the moving the foot in various directions.
Since the ankle and tarsal joints are close to each other, movement at the tarsal
joints is easily mistaken for movement at the ankle, and vice versa. Each
individual joint should be carefully examined.
Ankle joint movements

The normal range of movements of the ankle and the methods of determination
(Fig. 46.23A–D) are given in Table 46.1.
FIGURE 46.23 (A) Dorsiflexion of ankle joint. (B) Plantar flexion of ankle
joint. (C) Foot inversion. (D) Foot eversion.
TABLE 46.1
Normal Range of Movements of the Ankle and the Methods of
Determination

Dorsiflexion The foot is lifted upwards from zero position 0°–25°
Plantar flexion The foot taken downwards from zero position 0°–35°
Method of examination: The lower leg is supported by the left hand of the
examiner. With the other hand the foot is grasped from the heel. The patient is
instructed to move the foot plantar and dorsalwards invert and evert the foot, the
range through which the foot moved is noted.
Subtalar and midtarsal joint movements

In normal conditions, the subtalar and talar joints work together as a single unit.
The movements at these joints are:
• combined inversion and adduction (supination) and
• combined eversion and abduction (pronation)
Movements at subtalar joints
Movement at Subtalar Joint Method Normal Range

Foot inversion Foot is taken inwards from the vertical 0°–20°
Foot eversion Foot is taken outwards from the vertical 0°–30°
Note: Talotibial movement should be blocked by dorsiflexing the ankle during subtalar movements
are examined.
Method of examination: The lower leg is supported by the left hand of the
examiner. With the other hand the calcaneus is grasped from below and ankle
dorsilfexed (Fig. 46.24). The patient is instructed to invert and evert the foot, the
range through which te heel rocks is noted or passively the subtalar movement is
associated by moving the calcaneus.
FIGURE 46.24 Method of examining the subtalar joints.

Movements at midtarsal joints
Movement At Midtarsal Joints Normal Range

Mediolateral movements 5°–10°
Method of examination: The lower leg should grasp the calcaneus by the left
hand of the examiner. With the other hand the midfoot is grasped firmly from
below near the bases of metatarsals (Fig. 46.25). The patient is instructed to twist
the foot inwards and outwards into inversion and eversion, and compared with
the sound foot.
FIGURE 46.25 Method of examining the midtarsal joints.
Note
The range should be judged from the movement of hindfoot rather than the
forefoot, so that any contribution from the tarsal joints is disregarded. The
testing of movements at passive stage, should be controlled form the heel.
Toe movements
The active and passive range of metatarso-phalangeal and interphalangeal joints
should be assessed. The normal range of flexion is nearly 90°. Limitation to less
than 60° is considered pathological.
Varieties of abnormal sounds (crepitations) may be heard or felt during
movements of ankle joint. They are as follows:
• Fine crepitations: Tenosynovitis, subluxation of joints.
• Coarse crepitations: Osteoarthritis, neuropathic arthritis.
Measurements
• Circumference of ankle: This is measured with a tape taking it round the
knee. This is compared with the other side (e.g., this is increased in all
dislocations of knee, effusions of the joint) (Fig. 46.26).
• Circumference of muscles acting on the ankle: This is measured with a tape
taking it round the muscles (e.g., calf muscles). This is compared with the
other side (e.g., this is decreased when the muscles are wasted) (Fig. 46.27).
• The dimensions of the triangle made by joining the medial malleolus,
calcaneum and the head of first metatarsal and comparing with the other side
will help in diagnosing lesions in the hind food (Fig. 46.28).
FIGURE 46.26 Measuring the circumference of ankle joint.
FIGURE 46.27 Measuring the circumference of calf muscles.
FIGURE 46.28 Triangle made by the medial malleolus, calcaneum and the
head of first metatarsal.
Note
All measurements are to be taken at identical places on both sides to get
accuracy and comparison.
Feet under weight bearing stress

The patient is asked to stand evenly on both feet. Observe the following:
• Shape of the ankle, foot and toes
• Shape of longitudinal arch
• Shape of transverse arch
• Gait
The patient should be asked to stand on the affected leg and raise the heel
from the ground.
• To see formation of arch in mobile flat foot.
• The patient is asked to stand on toes, which will create the medial plantar arch
or the big toe should be actively dorsiflexed to get the same effect.
Footwear
The examination is not complete until the patient’s footwear is inspected and
compared on the two sides.
Lymphatic system
tuberculosis).
General
tuberculosis).
CHAPTER 47
Feet (soft tissues)

G. Sivakumar
CHAPTER OUTLINE
47.1. Development of feet 880
47.2. Surgical anatomy of foot 880
47.3. Diseases of the feet 881
• Injuries of soft tissues of foot 881
• Pyogenic infections of dorsum of foot 882
• Maduramycosis (Madura foot) 882
• Leprosy 883
• Infection of web space 883
• Epithelioma (squamous cell carcinoma, epidermoid carcinoma)
883
• Trophic ulcer of foot 884
• Dry and wet gangrene 884
• Simple ganglion 884
• Adventitious bursa 884
• Plantar warts 885
• Terminal pulp space infection 885
• Deep plantar abscess 885
• Infection of heel space 886
• Diabetic foot 886
• Plantar fasciitis 887
• Ingrowing toe nail 887
• Onychogryposis 887
• Subungual haematoma 887
• Acute paronychia 887
• Fungal infection (Tinea pedis and Tinea unguium) 888
• Subungual exostoses 888
47.4. Symptoms of pathologies of feet 889
• Feet 890
• Lower limbs and spine 892
• General 892
47.1 Development of feet
The limb buds are paddle-shaped outgrowths that arise from the sidewall of the
embryo at the beginning of the second month of intrauterine life. The hindlimb
bud is formed opposite the segments L2, L3, L4, L5, S1 and S2. The forelimb
buds appear a little earlier than the hind limb buds. As each hindlimb bud grows,
it becomes subdivided by constrictions into thigh, leg and foot. The foot itself
shows outlines of digits, which separate from each other.
47.2 surgical anatomy of foot

The foot extends from the point of the heel to the roots of the toes. The human
foot is a highly specialized structure containing 26 relatively small bones and
more than 150 ligaments with an intricate network of muscles, nerves and blood
vessels.
The foot has many features in common with the hand in its structure, but
differs in its function of mechanical support and carry static loads during
standing and other movements like kicking, landing etc. Strength and resilience
are the major hallmark features of the foot. Strength is obtained from the bones
and the resilience from various joints articulating in a special pattern, and the
plantar aponeurosis, which acts like a tie-beam. The intrinsic muscles provide
good grip for the foot, and the arches help in walking with grace and yet
maintain the equilibrium of the biped man.
While standing, the weight is supported on the heel and on the heads of
metatarsals (mainly the first metatarsal). The weight bearing normal foot evenly
distributes body weight to the sole.
The ‘human gait’ consists of two phases (p. 826) called the
• stance and
• swing.
The structures in the sole of the foot are large in number and are not clearly
separated from one another by fascial planes. From superficial to deep, the
layers consist of:
• abductor hallucis, flexor digitorum brevis, abductor digiti minimi and planter
digital vessels and nerves distally;
• the medial and lateral plantar nerves and vessels;
• the long flexor tendons;
• flexor hallucis brevis, adductor hallucis and flexor digiti minimi brevis;
• the deep parts of the lateral plantar artery and nerve and their branches;
• the bones (p. 996) and ligaments of the foot, the interossei.
These layers have no significance beyond that of description.
47.3 Diseases of the feet

The diseases of feet are tabulated in Table 47.1.
TABLE 47.1
Diseases of Feet
Feet and Toes
Aetiology Diseases
Congenital Club foot or Talipes equino-varusa
Talipes calcaneo-valgusa
Flat foot or Pes planusa
High arch foot or Pes cavusa
Hallux valgusa
Hallux rigidusa
Hammer toesa
Claw toesa
Traumatic Injuries of foot
Infective Dorsum Paronychia
Pyogenic infections of dorsum of foot
Madura foot
Leprosy
Sole Infection of web space
Infection of plantar interdigital space
Infection of heel space
Deep plantar abscess
Diabetic foot
Tuberculous arthritisa
Osteomyelitisb
Neoplastic Epithelioma
Malignant melanoma
Degenerative Osteoarthritisa
Charcot’s jointa
Trophic Trophic ulcer of foot
Ischaemic Dry and wet gangrene
Others Dorsum Ganglion
Adventitious bursa
Sole Plantar warts
Corn or callosity
Plantar fasciitis
Nails
Congenital Ingrowing toe nail
Onychogryposis
Traumatic Subungual haematoma
Inflammatory Acute Paronychia
Chronic Fungal infection (Tinea pedis and unguium)
Others Subungual exostoses
a
Discussed in Chapter 46 - Ankle, Foot and Toes.
b
Discussed in Chapter 39 - General Orthopaedics.
Injuries of soft tissues of foot

• Foot injuries form a considerable number.
• They can be
• open or
• closed.
• Acute injuries can be classified depending on the nature of force and on
contamination as tidy, untidy and indeterminable injuries.
• Tidy injuries: Clean cuts and incised wounds, usually resulting from sharp
force.
• Untidy injuries: Ragged skin wounds, may be with associated fractures,
usually resulting from crush or avulsion force.
• Indeterminable injuries: Injuries where it is difficult to determine the
extent of injury and the viability of tissues, usually caused by very severe
force.
Injuries to the vessels, nerves, bones and joints may be present in any of the
above injuries.
Complications: Posttraumatic deformities like contractures, neurovascular
deficit.
The patient presents to the surgeon either in the acute stage or late stage.
In acute injuries (Fig. 47.1), the pain is excruciating, and assessment is
difficult, unless pain is alleviated by analgesics.
• Skin damage: Look for obvious loss of skin, especially degloving as the
viability is questionable due to total detachment.
• Nerve damage: Accurate sensory testing is difficult, motor testing is not
possible.
• Damage to arteries: Suspected by profuse haemorrhage (incomplete tears),
gangrene (complete injuries). Colour of toes, nails and capillary refill are to
be tested. Warmth should be tested along with the presence of peripheral
pulsations.
• Damage to tendon sheaths and tendons: Lack in active movement, and by
exploration of wound.
• Damage to bones and joints: Pain, deformity, tenderness and loss of
movement.
FIGURE 47.1 Laceration of foot.
When patients arrive late, infection gets superadded, and result in

posttraumatic sequelae.
In late post traumatic cases, detailed examination of movements and
sensation can be done with ease, and damage assessed completely.
• Vascular injuries: Necrosed skin and deeper tissues.
• Tendon injuries: Deformities.
• Nerve damage: Wasting of muscle groups, lack of sweating and trophic
changes.
• Bone or joint injuries: Fractures with or without dislocations of joints.
X-rays (in various views) are necessary to assess bone injuries, and Doppler
studies are required to assess vascular damage.
Treatment
Bleeding can be controlled by elevating the limb or by applying pressure
directly over the site with pads.
In acute cases:
• Nail avulsion: nail removal.
• Skin damage: primary repair wherever possible. Wounds healing by
secondary intention cause severe fibrosis and contractures, and may need
release and repair and skin grafting in some cases.
• Vascular injuries: primary microvascular repair.
• Bone and joint injuries: proper debridement and splinting, reduction of
dislocations and immobilization.
• Nerves: primary repair under magnification where possible.
• Tendons: primary repair in clean wounds and delayed in contaminated
wounds.
In posttraumatic cases:
• Skin damage: contracture release and skin grafting.
• Vascular damage: grafts if viability can be restored.
• Bone and joint injuries: malunion or nonunion should to be treated.
• Nerve damage: nerve grafts.
• Tendon damage: tendon grafts or transfers.
Note
Dirty wounds should be debrided well and converted into a clean wound and
further treatment is carried out.
Pyogenic infections of dorsum of foot

The dorsal subcutaneous space is infected by extension from a subcutaneous
interdigital or web space, while the dorsal subaponeurotic space is infected either
from a direct puncture or from deep plantar space.
• Pain and swelling of the dorsum of foot (Figs 47.2).
• History of penetrating injury may be available.
FIGURE 47.2 Pyogenic infection of dorsum of foot.
• Diagnostic aspiration may be needed to confirm the presence of pus.
• Isolation of organism in culture for appropriate antibiotics.
Treatment
Incision and drainage with appropriate antibiotics is curative.
Maduramycosis (madura foot)

• The infection caused by Nocardia madurae.
• Entry gained through a prick in the foot in people who walk barefoot.
• First manifestation is a firm, pale and painless nodule.
• Vesicles develop on the nodules (Fig. 47.3), which burst to form sinuses,
which discharge watery fluid, containing yellow, red or black granules.
• There is no lymphatic involvement.
FIGURE 47.3 Madura foot Source: (Courtesy Dr Ramji Gupta).
Biopsy is conclusive.
Treatment
• Wide spectrum antibiotic to control the secondary infection followed by a
prolonged course of Dapsone is useful.
• Amputations are necessary for severe infections with deformity.
Leprosy
• Infection caused by Mycobacterium leprae, an acid fast bacillus.
• The basic lesion is a granulomatous infiltration of the superficial tissues of the
body.
• The deformities of leprosy are divided into two types:
1. Primary: those which are caused by leprosy and its reactions—posterior tibial
nerve is involved at the ankle giving rise to clawing of toes and anaesthesia of
the sole of foot. When the lateral popliteal nerve is involved, it causes foot
drop.
2. Secondary: those which result from anaesthesia and consequent misuse—
trophic ulcers develop due to anaesthesia, infections supercede leading to
contraction of foot.
Ulcers on the sole of the foot with or without deformities of the foot (Fig. 47.4).
FIGURE 47.4 Leprosy foot.
Biopsy of ulcers.
Treatment
Treatment of leprosy.
Infection of web space

• The web space between the great toe and the second toe is the largest of the
four web spaces.
• The infection arises from
• a skin crack,
• a blister or from beneath a callosity and
• secondary to fungal infections of foot.
• Constitutional symptoms with pain between toes.
• As the symptoms become severe, there is oedema of the dorsum of foot (Fig.
47.5).
• On examination, maximum tenderness is found in the web space and along
the sides of proximal segments of the toes related to the infected web.
FIGURE 47.5 Severe infection of second inderdigital space.
Aspiration of pus and isolation of organism.
Treatment
Incision and drainage is curative.
Squamous cell carcinoma (epidermoid

carcinoma)
Described in Chapter 9, Lumps and swellings.
Malignant melanoma
Described in Chapter 46 - Ankle, Foot and Toes.
Trophic ulcer of foot

Described in Chapter 10, Ulcers.
Dry and wet gangrene

Clinically, the gangrene is classified into dry and wet gangrene.
• Dry gangrene: Occurs when the tissues are desiccated by gradual slowing of
the blood stream (e.g., atherosclerosis, trauma, frost bite).
• Wet gangrene: Occurs when venous as well as arterial obstruction occurs
suddenly as in embolus. Infection and putrefaction follow and gas producing
organisms may invade the tissues.
• Dry gangrene: The toes or foot is dry and wrinkled, discoloured from
disintegration of haemoglobin (Fig. 47.6A).
• Wet gangrene: The affected part is swollen, discoloured and blebs appear
(Fig. 47.6B).
FIGURE 47.6 (A) Dry gangrene little toe. (B) Abscess of dorsum and
gangrene little toe due to diabetes mellitus.
• Doppler studies are required to establish the vascularity of the limb.
• Status of diabetes should be determined.
Treatment
• Medical management: Control of diabetes, vasodilators and appropriate
antibiotics form the mainstay of treatment to create a zone of demarcation.
• Surgical management: Amputations are required to remove the gangrenous
toes (disarticulation of toes) or foot (Syme’s amputation or below knee
amputation) at a level of good vascularity.
Ganglion
• A localized, tense (often painless) cystic swelling containing clear gelatinous
fluid.
• It often communicates with the tendon sheath or the capsule or joint.
• The origin is uncertain, but they are believed to arise as mucoid degeneration
of connective tissue or possibly as a consequence of leakage of synovial fluid
through the capsule of a joint or tendon sheath.
• It is seen on the dorsum of the foot.
A tense nontender cystic swelling on the dorsum of the foot, showing mobility
perpendicular to the axis of the tendon sheath (Fig. 47.7).
FIGURE 47.7 Ganglion foot.
Treatment
• Some disappear spontaneously.
• Injection of hyaluronidase into the cyst and local compression is curative.
• Recurrent ganglia require excision.
Adventitious bursa
• Adventitious bursae form as a result of prolonged pressure over bony
prominences, due to shearing motion of the tissue.
• In the ankle, it is common on the lateral epicondyle of the tibia, and in the
foot over the medial aspect of the head of the first metatarsal in hallux valgus
(bunion) and over the head of fifth metatarsal (bunionette).
• A soft nontender cystic swelling occurs at the site (Fig. 47.8).
• Infection causes pain and shows signs of inflammation.
FIGURE 47.8 Adventitious bursa of foot.
Treatment
• Asymptomatic bursa may be left alone.
• Suppurative bursitis requires incision and drainage.
Plantar warts
• It is a rough excrescence of skin, can occur in any part of the sole of foot,
including the undersurface of the heel.
• This has viral aetiology.
• They are like warts elsewhere, but they do not project beyond the skin
surface, due to the pressure of weight bearing.
• The surrounding skin is thickened.
There is always tenderness on pressure over the wart.
DD: Warts occur anywhere, whereas the callosities occur only over points of
pressure.
Treatment
• Curettage under local anaesthetic is curative.
• Application of liquid nitrogen is an alternative.
Terminal pulp space infection

• Common infection of the toe affecting commonly the great toe.
• The origin of infection is usually a prick.
• Dull pain, worse on dependant position in the early stages.
• Pain becomes throbbing and interferes with sleep as the infection becomes
severe.
• The tip of the toe may be swollen and appear red.
• Tenderness is remarkable even on slight pressure.
• A pustule may develop (Fig. 47.9).
FIGURE 47.9 Terminal pulp space infection of great toe.
Treatment
Incision and drainage under cover of appropriate antibiotics is curative.
Deep plantar abscess

• The central plantar space situated deep to the plantar fascia is arranged like a
compartment with four divisions, each occupied by the muscles that
constitute the flexors of the toes.
• Common cause of infection is penetrating injury.
• Common in diabetics.
Pain in the midfoot with constitutional symptoms.
Treatment
Infection of heel space

• The infection of fat pad of heel is intradermal.
• The infection arises from
• A blister or from beneath a corn.
• Penetrating injury—thorn prick.
• Constitutional symptoms with pain under the heel.
• As the symptoms become severe, there is oedema of the ankle.
• On examination, maximum tenderness is found in the heel.
Treatment
Diabetic foot
In diabetes, the neuropathic factor impairs sensation of the foot, and minor
injuries are neglected, which results in callosities on the sole, through which
infections gain entry.
• Trophic changes result from peripheral neuritis, atheroma of the arteries
resulting in ischaemia and excess of sugar in the tissues lower the resistance
to infection.
• Infections involving the fascia, tendon and bone can spread rapidly upwards
via the subfascial planes.
• Diabetic gangrene may occur due to the above factors.
• Swollen foot with discharge of pus from the callosity or a crack in the foot
(Fig. 47.10).
• Pain is not a predominant feature.
• Constitutional symptoms appear.
• Gangrene of toes, commonly the great toe occurs (Fig. 47.11).
FIGURE 47.10 Cracked foot.

FIGURE 47.11 Diabetic foot with gangrene great toe.
Blood sugar levels are elevated when diabetes is not under control.
Treatment
• Medical treatment: Strict control of diabetes, appropriate antibiotics.
• Incision and drainage is mandatory (The fascial planes need
decompression to prevent upward spread of pus).
• Disarticulation or amputation is required for gangrenous toes.
• Below knee amputation is required for gangrene of foot.
Callosity or corn
• Callosity is a raised patch of hyperkeratosis, increased thickening of the
epidermis, particularly of stratum corneum and the granular layer, commonly
seen in areas of excessive pressure or repeated trauma.
the surface and the apex deep inside, commonly seen in soles of the feet due
to ill-fiting footwear. This is composed of keratin masses with intact basal
layers.
• Callositypresents as a thick skin in the areas of excessive pressure (ref. Fig
9.24B), commonly beneath the metatarsal heads.
• Corn presents as a thickened tissue mostly in the soles (ref. Fig 9.24B).
Treatment
• Callosity: Wearing properly fitting footwear and removal of the pressure
points will help in the treatment and urea containing creams soften the skin.
• Corns can be treated with local salicylic acid and some will require excision.
Plantar fasciitis
• Aetiology is uncertain.
• It is suggested that it may be due to a tear in the attachment of the plantar
fascia to the calcaneum.
Pain and localized tenderness occur under the heel.
Treatment
• Soft padding of the insole of the footwear is useful.
• Hydrocortisone injections bring relief when the pain is severe and
conservative measures are ineffective.
Ingrowing toe nail

• It is common in the big toe.
• The causative factors are:
• incorrect cutting of nail.
• pressure on the nail wall by tight fitting footwear.
• Dirt and sweat accumulate in the crevice created by the skinfold and infection
is likely to supercede (Paronychia).
• The skin fold is inflamed with local suppuration in the fold of skin
overhanging the nail (Fig. 47.12).
• Pain is predominant.
FIGURE 47.12 Ingrowing nail with infection.
Treatment
A strip of the nail along with corresponding germinal matrix should be
removed to let out the pus and also to relieve the crevice.
Onychogryposis
A congenital deformity otherwise called ‘hooked nail’.
The nail is enormously thickened and curved resembling a small ox-horn.
Treatment
• Simple removal is adequate, but it is a temporary remedy, since the nail bed is
defective, the new nail will also regrow in the same fashion.
• Ablation of nail bed and germinal matrix will give permanent cure.
Subungual haematoma
It is a collection of blood below the nail following injury, usually a crush injury
of the terminal phalanx.
Painful blackish discolouration of the toe nail, following an injury of the toe
(Fig. 47.13).
FIGURE 47.13 Subungual haematoma great toe.
Treatment
• Evacuation of haematoma will relieve the pain.
• Removal of entire nail may be necessary for loose hanging nail.
Acute paronychia
Infection of the eponychium, resulting in suppuration, which is caused by
careless cutting of toenail using contaminated scissors.
• The pus tends to track around the cutaneous margin and also it extends below
the nail.
• Incriminating organism is Staphylococcus aureus. Escherichia coli infections
can superadd.
• Ingrowing toenail is a common cause.
• Pain and swelling around the nail (Fig. 47.14).
• Suppuration is evident at the side of the nail, in some cases.
• Pus may discharge from the edge of the nail.
FIGURE 47.14 Acute paronychia.
Treatment
• Early administration of antibiotics may subside the inflammatory process.
• Spontaneous rupture is common.
• Incision and drainage of pus is curative.
Fungal infections (tinea pedis and tinea
unguium)
• Fungal infections of the nail are caused by species of trichophyton,
microsporum, epidermophyton, which are called dermatophytes, which grow
and remain confined to the keratinous structures.
• The infection is acquired from
• minor trauma
• maceration and
• poor hygiene.
• It can infect the skin (Tinea pedis) or the nails (Tinea unguium).
• Tinea pedis presents as fissuring of the foot webs, scaling of the plantar
surfaces, or vesicles around the toe webs (Fig. 47.15) and soles.
• Tinea unguium (Onychomychosis) presents as white discoloured thickened
nails, with peeling and fissuring of perinychia or keratotic debris under the
nail edge may also be seen (Fig. 47.16).
FIGURE 47.15 Tinea pedis.
FIGURE 47.16 Tinea unguium of great toes.
KOH smear and culture of fungus of debris under infected nails are useful.
Treatment
• Oral antifungal drugs are needed for treatment. Cutting or removal of nails
and cleaning interdigital webs can expedite cure.
• Antibioticsare needed for secondary bacterial infections.
Subungual exostoses
It is a bony outgrowth from the dorsal surface of the distal phalanx of a toe—
usually great toe. It projects upwards and forwards between the tip of the nail
and the terminal pulp.
• The nail is lifted and deformed, and the skin of the pulp overlying the
outgrowth is thickened and hard.
• Sharp pain when pressure is applied over the nail or terminal pulp.
X-rays demonstrate the exostosis best seen in lateral projection.
Treatment
Excision of exostosis through a terminal incision just beyond the tip of the nail.
47.4 Symptoms of pathologies of feet

• Pain in the foot
• Swelling
• Ulcer in the foot
• Sinuses
• Deformity
• Gigantism
Pain in the foot
Being the weight bearing parts of the human body, pain is the commonest
symptom of many pathologies of the feet. The common causes of pain in adult
foot are given in Fig. 47.17.
FIGURE 47.17 Causes of pain.
Swelling
Swellings can be another presentation of foot problems.
• A generalized swelling may be seen in sprains, fractures and hematomas or in
cardic, hepatic and renal pathologies.
• Localized swelling at specific sites (e.g., ganglion, adventitious bursa) (Fig.
47.18).
FIGURE 47.18 Infected callosity lateral border of foot.
Ulcer in foot
The foot being in contact with the ground and is liable to many varieties of
stress, especially in the population who walk barefoot, ulcers are common.
Ulcers can be due to various causes (see Ch. 10).
Sinuses
Sinuses occur in pathologies like tuberculosis, madura foot, osteomyelitis (see
Ch. 11).
Deformity
Deformities occur in some pathologies of foot.
• Congenital conditions—club foot, flat foot.
• Acquired conditions—hallus valgus due to improper footwear, amputations
after trauma and surgery.
Gigantism
Gigantism is seen in large arterio-venous malformations of the foot.
Eliciting history
Pain in the foot

• Site of pain: In which part of the foot does the patient complain of pain?
Pain may be present in the forefoot (e.g., ischaemia, metatarsalgia, corns and
callosities under the metatarsal heads due to pes cavus), or may be in the middle
of the foot (e.g., flat foot) or in the heel (e.g., plantar fasciitis).
duration may indicate acute pathology (e.g., deep plantar infections) and long
duration (e.g., plantar fasciitis).
Nature of trauma and severity of it will indicate the pathology (e.g., strains
and fractures).
• Precipitating factors: Does the pain become severe on walking or standing
Walking can aggravate ischaemic pain of the foot and standing for a long time
may precipitate pain of venous origin. Exercise relieves pain of venous origin
due to venous return of blood.
the relief he had with the intake of drugs.
Swelling of feet
If a swelling is present in the foot, the nature of swelling should be questioned.
The questions should be in line with any swelling in general (see Ch. 9).
Note
Generalized swellings of the foot reduce on elevation of the limb in venous
and lymphatic pathologies.
Ulcer on dorsum of foot
• Duration of ulcer: For how long the ulcer been present?
Ulcers that are present for a short duration are generally due to trauma, and
those of longer duration, are due to repetitive trauma and trophic ulcer like
those due to diabetes mellitus.
Trophic ulcers occur at pressure points, and ischaemic ulcers occur at the
terminal part of the toes, where the vascularity is minimum.
Trophic ulcers are painless, and acute ischaemic ulcers are painful. Infection
is the common cause of association of pain in the ulcer.
Applications of strong chemicals and native medicines can delay healing, and
also detailed history regarding the treatment taken will give an idea about the
chronicity of the ulcer.
Sinuses
If the patient is complaining of discharge through sinus openings, the
questioning should be in line with the examination of any sinus (see Ch. 11).
Some of the examples of sinuses of feet are as follows:
• Multiple sinuses occur in osteomyelitis and in mycetoma.
• The nature of discharge varies according to pathology, e.g., bone chips in
osteomyelitis, caseous material in tuberculosis
Deformity
Deformities occur in some pathologies of foot.
• Congenital conditions: club foot, flat foot.
• Acquired conditions: hallus valgus due to improper footwear, amputations
after trauma and surgery.

Association of high-grade fever may indicate infective pathology like
cellulitis of foot, plantar abscess, and low-grade prolonged fever may indicate
lesions like tuberculous lesions.
malignancies.
a clearer picture of diagnosis (e.g., tuberculosis, leprosy).
treatment?
treated will indicate the examiner to reconsider the diagnosis like recurrence of
tuberculosis.
Diseases like tuberculosis can occur in families living in crowded
environment and the positive history may be a good indicator for the present
diagnosis.
Feet
Pre-requisites for physical examination:
• Patient should be undressed up to the knee.
• Adequate knowledge and orientation of the foot and its anatomy is mandatory.
In general, the patient should be examined in the following positions:
• Standing: Patient is requested to stand evenly on a flat surface and both feet
are examined from the front, back and sides and compared
• Walking: When the patient walks, his swing, the stance. and the contact of the
feet with the floor are noted (e.g., arches of the feet) (Fig. 47.19).
• Lying: When he lies down the soles are inspected.
FIGURE 47.19 Arches of feet.
Inspection
Deformity
• Club foot: congenital talipes equino varus (usually bilateral).
• Flat foot: congenital low longitudinal arch.
• High or flat arch foot: Pes cavus.
• Abnormal positions: Charcots’ joint (insensate joint).
• Missing toes: amputations (Fig. 47.20).
• Deformities of toes (e.g., Hallux valgus).
FIGURE 47.20 Missing second toe (amputated for diabetic gangrene).
Dorsum of the Feet

1. Skin
• Texture of skin: dry skin (e.g., eczema)
• Reddish colour: cellulitis
• Red streaks: lymphangitis
• Absence of veins: oedema and cellulitis
2. Swelling
• Generalized swelling: one foot (e.g., filariasis, cellulitis, postoperative,
both feet (e.g., medical conditions).
• Localized swelling: simple ganglion, bunion, bunionette.
3. Ulcers and sinuses on the dorsum (see Chs. 10 and 11)
• Site of the ulcer: ulcers on the dorsum (e.g., trauma from footwear) on the
sole (e.g., diabetes mellitus).
• Nature: Margin, floor and edge of the ulcer.
• Surrounding skin: Features of cellulitis and prominent veins.
• Number of sinuses: Multiple sinuses occur in mycosis, osteomyelitis and
in buried foreign bodies.
• Nature of discharge: Bone chips in osteomyelitis and fungal granules in
mycosis.
4. Toes
• Colour: reddish (e.g., haematoma, cellulitis), yellow (e.g., paronychia),
black (e.g., gangrene).
• Swelling: cellulitis, haematoma.
5. Nails
• Nail changes: Onychogryposis, fungal lesions.
• Overhanging lateral skinfold of the nail: Ingrowing toe nail.
• Discolouration: Subungual haematoma, fungal lesions.
6. Sole of foot
• The sole is inspected for pressure points, trophic ulcers, hyperkeratotic
plaques, corns and impalement by sharp objects.
7. Lateral and posterior borders of foot
• Lateral and posterior borders: corns, warts, cracks, callosities
8. Movements of all joints in the foot
• The patient should be asked to make all the movements of the joints of the
foot.
- Flexion and extension of all joints.
- Inversion and eversion of subtalar joints.
- Fore foot adduction and abduction.
Note
Inspection of the footwear the patient uses maximum is important as many
clues are obtained for diagnosis (Fig. 47.21).
FIGURE 47.21 Foot ulcer with incriminating footwear.
Palpation
• Temperature and site of maximum tenderness.
• Foot arterial pulsations.
• Venous and nail bed filling.
• Discharge from sinuses on pressure.
• Abnormal mobility of joints.
• Induration in the base of ulcers.
• Assess the degree of sensation (touch, pain and joint and position sense).
A swelling in the foot is described in line with any swelling in general (Ch. 9).
Lower limbs and spine
Both the lower limbs are to be examined along with the spinal column, as there
may be associated abnormalities (e.g., genu valgum and pes planus, pes cavus
and spina bifida).
Lymphatic system
Lymph from the lateral aspect of the foot and 4th and 5th toes drain to the
popliteal nodes while the foot predominantly drains to the inguinal vertical
chain. It should be remembered to examine the above lymph nodes.
General
Detailed general examination is essential to rule out foot changes due to cardiac,
renal, hepatic and neurological diseases. Primary pathologies of the external
genitalia can cause lymph nodal involvement, which can in turn cause swelling
of the foot, and hence examination of external genitalia is very important.
Note
Diabetes mellitus may produce foot changes like deformed arches and ulcers.
‘Examination of the foot is not complete without the examination of

neurological and vascular status of the limb’.
CHAPTER 48
Muscles, tendons and fasciae

S. Devaji Rao
CHAPTER OUTLINE
48.3. Diseases of muscles, tendons and fasciae 893
• Hamartomas 893
• Haematomas of muscles 894
• Rupture of tendons and fasciae 894
• Intramuscular abscess 895
• Chronic inflammations of tendons and fasciae 895
• Fibroma 895
• Rhabdomyoma 896
• Fibromatosis 896
• Fibrosarcoma 896
• Rhabdomyosarcoma 896
48.4. Symptoms of pathologies of muscles, tendons and fasciae
897
• Lesion 898
• Neurological system 899
• Vascular system 899
• General 899
48.1 Introduction
Muscle tissue is composed predominantly of cells that are specialized to shorten
in length on contraction, which results in movement. Muscle tissue is made up
basically of cells called myocytes, which are elongated in one direction called as
muscle fibres. Histologically, muscles are divided into three types. They are:
• Skeletal muscle: striated, has very close relationship to the bones, present
mainly in the limbs and body wall, and under voluntary control.
• Smooth muscle: nonstriated, present mainly in relation to viscera, and not
under voluntary control.
• Cardiac muscle: striated, present exclusively in the heart, has inherent
rhythmic contractility.
Skeletal muscle is made up essentially of long, cylindrical fibres, with variable
lengths. The longest being as much as 30 cm in length. Within a muscle, the
muscle fibres are arranged in the form of bundles or fasciculi, the numbers of
both vary. Many muscle fasciculi constitute a muscle belly. The muscles end in
tendons, which serve to concentrate the pull of a muscle on a relatively small
area of bone. Tendons also allow the muscle mass to be placed at a convenient
distance away from its site of action.
The nerve supplying a muscle enters it (along with the main blood vessels) at
an area called the neurovascular hilus, which is usually situated nearer the
origin of the muscle than its insertion. The junction between a muscle fibre and
the nerve terminal that supplies it is highly specialized and is called a motor end
plate. The contractions of the muscle depend on the number of motor units that
are activated.
48.3 Diseases of muscles, tendons and fasciae

Diseases of muscles, tendons and fasciae are tabulated in Table 48.1.
TABLE 48.1
Diseases of Muscles, Tendons and Fasciae
Aetiology Diseases
Congenital Hamartomas
Traumatic Haematomas of muscles
Rupture of tendons and fasciae
Inflammatory Acute Intramuscular abscess
Chronic Supraspinous tendinitis
Plantar fasciitis
Achilles tendinitis
Stenosing tenosynovitis
Neoplastic Benign Fibroma
Rhabdomyoma
Potentially malignant Fibromatosis
Malignant Fibrosarcoma
Rhabdomyosarcoma
Ischaemic Volkman’s ischaemic contracture
Hamartomas
Rare soft tissue swellings present from birth, which are benign.
Swellings of variable consistency.
Biopsy reveals a heterogenous mixture of all the tissues from which they are
derived.
Treatment
Excision is curative.
Haematomas of muscles
• Results after a blunt injury of the muscle or as an association of other injuries.
• Postsurgical haematomas result due to improper haemostasis.
• Family history of bleeding disorders may be present.
Complications: Abscess, calcification.
• Red brawny diffuse swelling at the injured site (Fig. 48.1A)
• Clotted and longstanding haematomas give a dark discoloration.
FIGURE 48.1 (A) Intramuscular haematoma forearm. (B) CT—
Intramuscular haematoma forearm.
• Blood coagulation profile may be useful.
• X-rays will document associated fracture.
• CT (Fig. 48.1B) or MRI will delineate the lesion.
Treatment
• Most haematomas resolve spontaneously.
• Diffuse haematomas need medical management.
• Infected haematomas require aspiration or drainage.
• Calcified haematomas may have to be excised if they are large, painful and
unsightly.
Rupture of tendons and fasciae

• Tendons and fasciae usually rupture due to
• overactivity(e.g., tendoachilles rupture)
• degeneration (e.g., patellar tendon rupture) and
• spontaneously (e.g., rupture of extensor pollicis longus, supraspinatus
tendon rupture, long head of biceps brachii rupture).
• Ruptures occur at the
• junction of the muscle mass and the tendon (e.g., tendoachilles rupture) and
• where the tendon takes an acute turn over a bony prominence (e.g., rupture
of extensor pollicis longus).
• Rupture of ligaments close to the joints may be accompanied by subluxation
or dislocation of the joint (e.g., rupture of lateral ligaments of knee and ankle
joints).
• Ruptures may occur after seizures or vigorous contraction of muscles.
• Severe pain at the site of rupture.
• If ignored, they cause chronic pain sometimes restricting the movements.
• On examination, local swelling (Fig. 48.2A) and tenderness (Fig. 48.2B) and
sometimes a depression may be seen and felt.
FIGURE 48.2 (A) Rupture of biceps brachii (right) Source: (Courtesy Dr V.
Thulasiraman). (B) Eliciting tenderness on a tendon.
MRI is diagnostic in many cases.
Treatment
• Tendon ruptures require suturing for restoration of function.
• Ruptures of ligaments when small heal spontaneously.
Intramuscular abscess
• This pyogenic abscess results after an intramuscular injection under nonsterile
conditions.
• Common in diabetics.
Painful swelling at the injection site.
Isolation of organisms in culture is necessary.
Treatment
Chronic inflammations of tendons and fasciae

• Chronic inflammations of the tendons and fasciae occur due to overstretching
during active exercises, but the exact aetiology is not certain.
• The common conditions are:
• Supraspinous tendinitis
• Plantar fasciitis
• Achillis tendinits
• Stenosing tenosynovitis.
• Severe pain on overstretching of the tendon or fascia.
• Clinical examination may reveal point tenderness over the area of stretch.
No specific investigation is contributory.
Treatment
• Most inflammations resolve spontaneously.
• Local administration of steroid has beneficial effect.
Fibroma
• Benign tumour of the fibrous connective tissue.
• They are hyperplastic fibrous tissue rather than true neoplasms.
• True fibromas are rare, and combinations with other mesenchymal tissue
elements are more frequent, e.g., neurofibroma, fibromyoma, etc.
• Histologically three types of fibromas are distinguished. They are as follows:
1. Fibroma durum: benign, often pedunculated and well circumscribed
tumour on the body surface or mucous membrane.
2. Fibroma molle or fibrolipoma (soft fibroma): mixture of mature
fibrous connective tissue with adult type fat.
3. Elastofibroma: benign fibrous tumour in the subscapular region.
Soft to firm swelling anywhere on the body surface (ref. Fig. 9.14A).
Excision biopsy is confirmatory.
Treatment
Excision of unsightly tumours is curative.
Rhabdomyoma
• Benign tumour of skeletal muscle
• Occurs in the head and neck, most often in the upper neck, tongue, larynx and
pharynx
• Per se, these tumours are extremely rare
A firm nontender mass.
Biopsy is confirmatory.
Treatment
Excision is curative.
Fibromatosis
• Fibromatosis denotes tumour-like lesions of fibrous tissue, which continue to
proliferate actively and resemble sarcomas, with a tendency to invade locally
and recur after surgical excision.
• They are divided into two groups:
1. Infantile or juvenile type
2. Adult type
• Aggressive fibromatosis have very high potential to recur at the same site.
Tumour-like lesions on various parts of the body [(e.g., juvenile aponeurotic
fibroma, adult type penile fibromatosis (Peyronie disease)].
• MRI (Fig. 48.3) has characteristic features.
• Excision biopsy is confirmatory.
FIGURE 48.3 MRI - Fibromatosis Source: (Courtesy Dr R Rajaraman).
Treatment
Excision is required but need follow up after surgery.
Fibrosarcoma
• A slow growing malignant tumour.
• Affects adults between the fourth and seventh decades of life.
• They metastasize through bloodstream.
• A grey-white lobulated circumscribed mass.
• Commonly seen in the thigh and around the knee, upper extremity, trunk,
head and neck and retroperitoneum (Fig. 48.4).
FIGURE 48.4 Fibrosarcoma of leg Source: (Courtesy Dr R. Rajaraman).
Biopsy is confirmatory.
Treatment
Three dimensional excision is curative.
Rhabdomyosarcoma
• A highly malignant tumour arising from rhabdomyoblasts in varying degrees
of differentiation.
• No known aetiology.
• Depending on the growth pattern, they are differentiated into four types. They
are as follows:
1. Embryonal rhabdomyosarcoma: Most common type, occur in
children below 12 years of age, commonly in the head and neck,
urogenital tract and retroperitoneum.
2. Botryoid rhabdomyosarcoma: A variant of the embryonal type in
children below 10 years, most frequently in the vagina, urinary
bladder and nose.
3. Alveolar rhabdomyosarcoma: More commonly in older children and
young adults, more common in the extremities.
4. Pleomorphic rhabdomyosarcoma: Common in adults above 40 years,
most common in the extremities particularly in the lower limbs.
• Macroscopically, they appear as pink fleshy masses.
• Microscopically, in embryonal variety, embryonal cells are rich in glycogen
and within which myofibrils can be demonstrated, distinct from alveolar
type.
• local infiltration rapidly infiltrating the surrounding tissues;
• blood to lungs, liver and bones and
• lymphto draining lymph nodes.
Symptoms
• Enlarging painless lump.
• Nasal obstruction and epistaxis (tumours of nasopharynx).
• Haematuria (tumours of urinary tract).
• Vaginal bleeding (tumours of vagina and uterus).
• Visual disturbances (tumours of orbit).
Signs
• A firm solid nontender swelling (Fig. 48.5)
FIGURE 48.5 Rhabdoyosarcoma of arm Source: (Courtesy Dr V. Srinivasan).
• X-ray chest for lung metastases.
• CT and MRI of affected site may show extent and resectability.
• Bone marrow aspiration for metastases.
• Isotope scan for skeletal metastases.
Treatment
• Radical excision where possible.
• Pre- and postoperative chemotherapy (vincristine, actinomycin D and
cyclophosphamide).
Palliative
• Chemotherapy
• Radiotherapy
48.4 Symptoms of pathologies of muscles,

tendons and fasciae
• Pain
• Swelling
Eliciting history
Pain
1. Onset of pain: When did the pain start, was it slow in onset or sudden?
This question will answer the duration of pain, and its mode of onset (e.g.,
usually due to inflammatory pathology).
2. Relationship to injury: Is this pain preceded by an injury, an accident or
sport or a fall?
small slips may cause minor ruptures of muscle fibres, and fall during active
sports or road traffic accidents may cause severe muscle ruptures with
haematomas or fractures, e.g., rupture of Achilles tendon).
3. Position of limb during injury: What was the position of the limb during
the fall?
Sudden stopping movement during active run is known to cause severe muscle
ruptures (e.g., tendoachilles rupture).
4. Intensity of pain: How bad is this pain?
Very severe pain may indicate associated fractures.
5. Onset of pain after injury: Did this pain start immediately or after a period
from the time of injury?
Pain may become severe after sometime if there is formation of haematoma.
6. Remedy: What was done to the pain to reduce it?
Supporting the limb may reduce the pain indicating a muscle injury with
dislocation or a fracture.
7. Relationship to movement: Is this pain related to movements?
associated fractures, and nontraumatic situations, may indicate fasciitis or
abscesses.
8. Treatment: Was any treatment or first aid given to this pain?
radiographs have to be scrutinized if available.
Swelling
Questions should be asked in line with those in Chapter 9.

Association of high grade fever may indicate infective pathology like
abscess, and low-grade prolonged fever may indicate lesions like
malignancy.
Loss of appetite and weight are indicative of illnesses like malignancies.
a clearer picture of diagnosis (e.g., aggressive fibromatosis).
treatment?
like recurrence of aggressive fibromatosis.
Diseases like muscular dystrophies can occur in families and the positive
Note
It should be remembered that the symptoms of muscular pathologies may
overlap with those of other neighbouring tissues including bones.
Pre-requisites
• Patient should be undressed so that the entire limb is exposed.
Act of undressing
• How clumsy is he in his movements (e.g., associated nerve injuries causing
motor paralysis of small muscles of hand).
• How protective is he during the act (e.g., denotes pain).
Note
limb.
distance.
• Position of patient: Sitting or standing with both limbs side by side, with the
area to be examined bare.
• Position of examiner: The examiner should view the concerned area from all
sides.
Lesion
Inspection
Swelling
The following should be determined (in line with examination of any swelling—
see Ch. 9).
• Plane of swelling.
• Consistency of swelling (e.g., fibrous swellings are firm, rapidly growing
tumours have variable consistency due to degeneration).
• Fluctuation (e.g., ganglion).
• Cross fluctuation (e.g., compound palmar ganglion).
• Attachment to muscles and tendons (e.g., fibroma).
• Fixity to bone (e.g., fibrosarcoma adherent to underlying bone).
Deformity
• Bowstringing of tendons occur in contractures (e.g., Dupuytren’s contracture
—the palmar fascia to the ring and little fingers are affected).
Muscle wasting
• Muscle wasting is seen is nerve lesions (e.g., median nerve palsy, carpal
tunnel syndrome). This is confirmed by measurement of circumference and
comparing it with the same spot in the other side.
• Individual nerves must be examined for both motor and sensory loss.
Examination of contralateral side: Bursae are usually bilateral over bony
points.
Movements
Full range of movements of the joints proximal and distal to the tumour must be
assessed.
Palpation
Point of tenderness
The point of tenderness should be determined by application of pressure (e.g.,
application of pressure on tendon (e.g., rupture of tendoachilles) (Ref Fig. 48.2)
or by appropriate movement (e.g., keeping the wrist flexed 90° (60 seconds) can
trigger the pain in Carpal tunnel syndrome—Phalen’s sign) (Fig. 43.40).
Swelling
The swelling should be palpated in line with any swelling (see Ch. 9).
• Mobility of the swelling (e.g., mobility is restricted in ganglions in tensing the
tendon, and also in the axis of the tendon).
• Crepitus (e.g., compound palmar ganglion).
Deformity
Extent of the deformity is assessed by measuring the movements in the relevant
joints, which reflect the muscle function.
Muscle power
The muscles of the hand should be felt with the fingers for their bulk (e.g.,
wasting may be felt in Dupuytren’s contracture, shortening of flexors in
Volkmann’s ischaemic contracture). Power of each muscle group should be
tested by
• joint movement and
• gripping in the case of upper limb pathologies.
Neurological system
Nerve function: Tests of sensory and motor functions (see Ch. 49), sweating in
distribution of individual nerves (e.g., median, ulnar and radial nerves in case of
upper limb pathologies) should be performed.
Vascular system
Circulation: All pulses should be felt (e.g., absent in application of tight
Volkmann’s ischaemic contracture). Warmth, colour, capillary return and
cutaneous sensibility should be determined (see Ch. 13).
Lymphatic system
(e.g., tuberculosis and malignancy). Examination of the liver and spleen
completes the lympho reticular system, which is useful in diagnosis.
General
General survey of other parts of the body, particularly the lymphatic system
should be undertaken, as the local symptoms may be only one manifestation of a
widespread disease (e.g., tuberculosis). Haemoptysis may denote lung
metastases from soft tissue sarcomas.
CHAPTER 49
Peripheral nerves
R. Priya, A.V. Srinivasan
CHAPTER OUTLINE
49.1. Surgical anatomy of nerves of upper limb 900
• Brachial plexus 900
• Peripheral nerves of brachial plexus 900
• Musculocutaneous nerve 900
• Axillary nerve 901
• Radial nerve 901
• Ulnar nerve 902
• Median nerve 902
• Cutaneous supply of upper limb 902
49.2. Surgical anatomy of nerves of lower limb 902
• Lumbar plexus 902
• Peripheral nerves of lumbar plexus 902
• Femoral nerve 902
• Obturator nerve 903
• Sacral plexus 903
• Peripheral nerves of sacral plexus 903
• Pudendal nerve 903
• Sciatic nerve 903
• Cutaneous supply of lower limb 904
49.3. Causes of peripheral nerve disorders 904
49.4. Injuries of peripheral nerves 904
• Injuries of peripheral nerves of upper limb 905
• Brachial plexus injuries 905
• Axillary nerve injuries 905
• Radial nerve injuries 906
• Ulnar nerve injuries 906
• Median nerve injuries 907
• Injuries of peripheral nerves of lower limb 908
• Femoral nerve injuries 908
• Sciatic nerve injuries 908
• Tibial nerve injuries 908
• Common peroneal nerve injuries 908
• Leprosy 908
49.5. Symptoms of peripheral nerve pathologies 909
49.1 Surgical anatomy of nerves of upper limb

The nerves of upper limb are derived from the brachial plexus.
FIGURE 49.10 Clenching of teeth.
FIGURE 49.11 Clenching of fists.

FIGURE 49.12A Determining the tone of forearm muscles by alternating
supination and pronation.
FIGURE 49.12B Determining the tone of arm muscles by alternating
flexion and extension of elbow.
FIGURE 49.13 Rolling the knee to determine the hip tone.
FIGURE 49.14 Determination of knee tone by flexion and extension of
knee.
FIGURE 49.15 Determination of ankle tone by planar flexion and
dorsiflexion.
FIGURE 49.16 Testing the deltoid by shoulder abduction.
FIGURE 49.17 Testing the biceps brachii by elbow flexion.
FIGURE 49.18 Testing the triceps brachii by elbow extension.
FIGURE 49.19 Testing the flexors of wrist by wrist flexion against

resistance.
FIGURE 49.20 Testing the wrist extensors by extension of wrist against
resistance.
FIGURE 49.21 Testing the flexors of fingers against resistance.
FIGURE 49.22 Testing the extensors of fingers against resistance.
FIGURE 49.23 Testing the dorsal interossei by abduction of fingers
against resistance.
FIGURE 49.24 Card test—Testing the adductors of fingers.
FIGURE 49.25 Testing the abductors of thumb against resistance.

FIGURE 49.26 Card test for adductors of thumb.
FIGURE 49.27 Testing the serratus anterior.
FIGURE 49.28 Testing the rhomboids on right side.
FIGURE 49.29 Testing the supraspinatus (right) against resistance.
FIGURE 49.30 Testing the infraspinatus (Rt) against resistance.
FIGURE 49.31 Testing the brachioradialis.
FIGURE 49.32 Method of testing the flexor digitorum profundus.
FIGURE 49.33 Ochsner’s clasp test for medial half of flexors of wrist.
FIGURE 49.34 Froment’s sign—paralysed adductors of left
thumb Source: (Courtesy Dr K. Sridhar).
FIGURE 49.35 Method of testing the supinator.
FIGURE 49.43 Testing the gluteus maximus by hip extension.

FIGURE 49.44 Testing gluteus medius and minimus by hip abduction.
FIGURE 49.45 Testing adductors by hip adduction.

FIGURE 49.46 Testing quadriceps femoris by knee extension.
FIGURE 49.47 Testing hamstrings by knee flexion.
FIGURE 49.48 Testing tibialis anterior by dorsiflexion of foot.
FIGURE 49.49 Testing gastrocnemius by plantar flexion.
FIGURE 49.50 Testing the tibialis posterior by foot inversion against
resistance.
FIGURE 49.51 Testing the peronei by foot eversion against resistance.
FIGURE 49.52 Testing the extensor hallusis longus by big toe extension
against resistance.
FIGURE 49.53 Testing the extensor of toes by extension against
resistances.
FIGURE 49.54 Testing the intrinsic muscles of foot by flexing the toes
against resistance.
FIGURE 49.55 Eliciting biceps reflex.
FIGURE 49.56 Eliciting triceps reflex.
FIGURE 49.57 Eliciting supinator reflex.
FIGURE 49.58 Eliciting finger reflex.
FIGURE 49.59 Eliciting knee reflex.
FIGURE 49.60 Eliciting ankle reflex—method 1.
FIGURE 49.63 Eliciting abdominal reflex.
FIGURE 49.64 Eliciting plantar reflex.
TABLE 49.5
Various Muscle Tones and Their Causes
Tone Explanation Cause
Normal Slight resistance through the whole range of

movement
Decreased Loss of resistance through movement (Marked Lower motor neuron paralysis (common), myopathies,
tone loss is called spinal shock
Increased Tone increases suddenly Upper motor neuron lesion
tone
Increased tone through entire movement Extrapyramidal syndromes, e.g., Parkinson’s disease,
phenothiazines
Regular intermittent break in tone
Deliberate opposition by the patient Bilateral frontal lobe damage, e.g., cerebrovascular
disease
TABLE 49.6
Grades of Muscle Power (Medical Research Council Scale)
Grade Power
5 Normal power
4+ Submaximal movement against resistance
4 Moderate movement against resistance
4− Slight movement against resistance
3 Moves against gravity but not resistance
2 Moves with gravity eliminated
1 Flicker
0 No movement
TABLE 49.7
Grades of Tendon Reflexes
Grade Observation Reason

0 Absent Generalized: peripheral neuropathy Isolated: a peripheral nerve, a root lesion
a
+/− Present only with reinforcement
1+ Present but depressed Peripheral neuropathy, muscle disease, cerebellar disease
2+ Normal
3+ Increased Upper motor neuron lesion
4+ Clonusb
a
Reinforcement:This manoeuvre is performed to obtain the reflex when it is unobtainable. The
patient is asked to clench his teeth as the hammer is swung (Fig. 49.10). Otherwise, the patient is
asked to make a fist, or link hands across his chest and pull one against the other (Fig. 49.11), as
the hammer is swung.
b
Clonus:Rhythmic contractions seen after a brisk movement is called ‘Clonus’. At the knee, the leg
is held straight, and the patella is brought down briskly downwards, and rhythmic contractions
may be noted (Always abnormal). At the ankle, the ankle is dorsiflexed briskly and the foot held in
that position, and rhythmic contractions may be noted (more than three beats is abnormal).
Brachial plexus
Brachial plexus (Fig. 49.1) is formed as follows:
• Five roots, derived from the anterior primary rami of C5, C6, C7, C8, and T1
link upto form
• Three trunks formed by the union of
Present only with reinforcement
• C5 and C6 (upper),
• C7 alone (middle) and
• C8 and T1 (lower),
FIGURE 49.1 Brachial plexus.
which split into

• Six divisions, formed by each trunk dividing into anterior and posterior
divisions, which link to form
• Three cords
• A lateral, from the fused anterior divisions of the upper and middle trunks;
• A medial, from the anterior division of the lower trunk and
• A posterior, from the union of all three posterior divisions.
• Cordscontinue distally to form the main nerve trunks of the upper limb.
• Lateral cord continues as musculocutaneous nerve.
• Medial cord continues as ulnar nerve.
• Posterior cord as the radial and axillary nerves.
• Cross communication between the lateral and medial cords forms the
median nerve.
The derivatives of brachial plexus (Fig. 49.2) are given in Table 49.1.
FIGURE 49.2 Derivatives of brachial plexus.

TABLE 49.1
Derivatives of Brachial Plexus
Cords
Roots Trunk
Lateral Medial Posterior
n. to Rhomboids Suprascapular n. Musculocutaneous n. Medial pectoral n. Suprascapular nn.
n. to Subclavius Lateral pectoral n. Ulnar n. Axillary nerve
n. to Serratus Lateral antebrachial Medial antebrachial n. to Latissimus
anterior cutaneous nerve cutaneous nerve dorsi
Lateral root of median n. Medial brachial cutaneous
nerve
Medial root of median n. Radial n.
Peripheral nerves of brachial plexus

Musculocutaneous nerve
Musculocutaneous nerve (C5, C6, C7) continues from the lateral cord of
brachial plexus. It pierces coracobrachialis, then runs between biceps and
brachialis. The branches and innervation are as follows:
• Muscular branches: coracobrachialis, biceps and brachialis.
• Cutaneous branch: skin of the lateral forearm.
Axillary nerve
Axillary nerve (circumflex) nerve (C5, C6) arises from the posterior cord of
brachial plexus, winds round the surgical neck of humerus accompanied by the
circumflex humeral vessels. Its branches are as follows:
• Muscular branch: deltoid and teres minor.
• Cutaneous branch: to a palm-sized area over the deltoid (‘regimental badge’
area).
Radial nerve
Radial nerve (C5, C6, C7, C8, T1) is the main branch of posterior cord of
brachial plexus. It lies behind the axillary artery, then, passes backwards between
the long and medial heads of triceps brachii to lie in the spiral groove of the
humerus between the medial and lateral heads of triceps. At the lower end of
humerus, the radial nerve pierces the lateral intermuscular septum to enter the
anterior compartment of the arm between the brachialis and brachioradialis. At
the level of lateral epicondyle, it gives off its posterior interosseous nerve
(supplies extensor muscles of forearm except those supplied by main radial
nerve*), which winds round the radius within the supinator muscle and sprays
out to innervate the extensor muscles of forearm. The radial nerve itself
continues into superficial radial nerve, lying deep to brachioradialis.
Above the wrist, it emerges posteriorly from beneath the brachioradialis to
end by dividing into cutaneous nerves to posterior aspects of the radial three and
half digits.
The branches of radial nerve and their innervation are as follows:
• Main trunk innervates triceps and anconeus (proximal to spiral groove),
brachioradialis and externor carpi radialis longus* (distal to spiral groove).
• Posterior interosseous nerve: part of supinator, extensor carpi radialis brevis
(before it enters the supinator tunnel), rest of supinator (in the supinator
tunnel) and extensor digitorum, extensor digiti minimi and indicis, extensor
carpi ulnaris, abductor pollicis longus, extensor pollicis longus and brevis
(after leaving the supinator tunnel).
Cutaneous branches: back of the arm and forearm (posterior cutaneous
branch) and radial side of dorsum of hand (superficial radial branch or terminal
part of radial nerve).
Ulnar nerve
Ulnar nerve (C7, C8, T1) is a branch of the medial cord of brachial plexus. It
descends medially in the upper arm medial to brachial artery. At elbow, it lies in
the condylar groove, behind the medial epicondyle and then enters the cubital
tunnel. At the wrist, ulnar nerve passes between the pisiform bone and hook of
hamate through Guyon’s canal. It bifurcates in the Guyon’s canal into superficial
sensory and a deep motor branch. The palmar cutaneous nerve and dorsal
cutaneous branches arise in the distal forearm and do not pass through Guyon’s
canal and their innervations are as follows:
• Muscular: flexor carpi ulnaris and medial half of flexor digitorum profundus
(in the forearm), the hypothenar muscle, the interossei, third and fourth
lumbricals and adductor pollicis (in the hand), deep head of flexor pollicis
brevis.
• Cutaneous: ulnar side of both aspects of hand and both surfaces of the ulnar
1½ fingers.
Median nerve
Median nerve (C6, C7, C8, T1) arises from the medial and lateral cord of
brachial plexus. The nerve lies lateral to the brachial artery, then crosses
anteriorly the artery at the mid humerus level and continues down the forearm
between the heads of pronator teres. Here it gives off its anterior interosseous
nerve (supplies flexor pollicis longus, half of flexor digitorum profundus to the
index and middle fingers, and pronator quadratus). The main nerve descends
down and passes through carpal tunnel. Proximal to carpal tunnel, it gives a
sensory branch, palmar cutaneous branch supplying the thenar eminence.
Its branches and innervation are as follows:
• Muscular: all the muscles of flexor aspect of forearm except the flexor carpi
ulnaris and ulnar half of flexor digitorum profundus, muscles of thenar
eminence, radial two lumbricals (in the hand) (except adductor pollicis and
deep head of flexor pollicis brevis).
• Cutaneous: to the skin of the radial side of the palm, the palmar and a
variable degree of the dorsal aspect of the radial three and half fingers.
Cutaneous supply of upper limb (fig. 49.3)

In spite of interlacing complex of the nerve roots, the skin of the upper limb has
a perfect regular segmental nerve supply, which is derived from C4 to T2
segments.
• C4: skin over the shoulder tip.
• C5: lateral side of upper arm up to elbow.
• C6: lateral side of forearm including thumb and index.
• C7: over triceps, midforearm and middle finger.
• C8: medial side of forearm including little finger.
• T1: medial side of upper arm, axilla down to olecranon.
• T2: skin of axilla.
FIGURE 49.3 Cutaneous supply of body.
49.2 Surgical anatomy of nerves of lower limb

The nerves of lower limb are derived from the lumbar and sacral plexuses.
Lumbar plexus
The lumbar plexus (Fig. 49.4) is formed from the anterior primary rami of L1–
L4. The nerves originating in the lumbar plexus are as follows:
• Ilio hypogastric nerve (T12–L1)
• Ilioinguinal nerve (L1)
• Genitofemoral nerve (L1, L2)
• Lateral femoral cutaneous nerve (L2, L3)
• Femoral nerve (L2–L4)
• Obturator nerve (L2–L4)
FIGURE 49.4 Lumbar plexus.
The femoral nerve and the obturator nerves are the principal nerves of lower
limb from lumbar plexus.
Peripheral nerves of lumbar plexus

Femoral nerve
The femoral nerve (L2–L4) arises from the posterior divisions of anterior rami
of L2–L4 in the substance of psoas muscle. It runs in the groove between the
psoas and the iliacus (the flexors of thigh, both of which it supplies) and
descends beneath the inguinal ligament and separates into anterior and posterior
divisions.
Its branches are as follows:
• Muscular: to the anterior compartment of the thigh (quadriceps, sartorius and
pectineus).
• Cutaneous: the medial and intermediate cutaneous nerves of thigh and
saphenous nerve, to supply the skin of the medial side of the thigh, leg, ankle
and foot to great toe.
• Articular: to the hip and knee joints.
Note
Lateral aspect of the thigh is supplied by the lateral cutaneous nerve of the
thigh, a branch from the lumbar plexus.
Obturator nerve
The obturator nerve (L2–L4) emerges from the medial aspect of the psoas, runs
deep to the internal iliac vessels, travels downwards to reach the obturator
foramen, then in company with the obturator vessels enters the thigh. Its
branches are as follows:
• Muscular: to obturator externus, adductor muscles and gracilis.
• Cutaneous: to an area of the skin over the medial aspect of the thigh.
• Articular: to the hip and knee joints.
Sacral plexus
The sacral plexus (Fig. 49.5) originates from the anterior primary rami of L4,
L5, S1–S4. L4 is shared by both plexuses, a branch from it joining L5 to form the
lumbosacral trunk. Its branches are as follows:
• Superior gluteal nerve (L4–S1)
• Inferior gluteal nerve (L5–S2)
• Sciatic nerve (L4–S3)
• Posterior femoral cutaneous nerve (S1–S3)
• Pudendal nerve (S2–S4)
FIGURE 49.5 Sacral plexus.
They supply the pelvic muscles, muscles of the hip, skin of the buttock and
the back of thigh, the perineum.
Sacral plexus itself terminates as:
• pudendal nerve and
• sciatic nerve.
Peripheral nerves of sacral plexus

Pudendal nerve
The pudendal nerve (S2–S4) innervates the perineum. It arises as the lower
main division of sacral plexus and leaves the pelvis through the greater sciatic
foramen below the piriformis muscle, crosses the dorsum of ischial spine and
disappears through the lesser sciatic foramen into the perineum. It traverses the
lateral wall of ischiorectal fossa with the internal pudendal vessels and lies in
pudendal canal (Alcock’s canal). In the canal, it gives off the inferior rectal
nerve, which supplies the external sphincter and perianal skin, and divides into
perineal nerve and dorsal nerve of penis (or clitoris).
• Perineal nerve
• Superficial branch supplies skin of the posterior aspect of scrotum or
vulva.
• Deeper branch supplies sphincter urethrae and muscles of anterior
perineum.
• Dorsal nerve of penis (or clitoris): traverses the deep perineal pouch, pierces
the perineal membrane to supply the dorsal aspect of penis (or clitoris).
Sciatic nerve
The sciatic nerve (L4, 5, S1–S3) is the largest nerve of the body. It emerges from
the greater sciatic foramen distal to piriformis and under cover of gluteus
maximus, crosses the posterior surface of ischium and obturator internus, and
descends on adductor magnus, lying deep to hamstrings. The trunk supplies
hamstrings (biceps, semimembranosus and semitendinosus) and also adductor
magnus (also supplied by obturator nerve). The sciatic nerve teminates into
• tibial (medial popliteal) nerve and
• common peroneal (lateral popliteal) nerve.
Tibial nerve (medial popliteal nerve)

The tibial (medial popliteal) nerve (L4, 5, S1–S3) traverses the popliteal fossa
superficial to the popliteal artery and vein. Its branches are as follows:
• Muscular: to gastrocnemius, soleus and popliteus. It also supplies flexor
hallucis longus, flexor digitorum longus and tibialis posterior. Its terminal
plantar branches (medial plantar and lateral plantar) supply the intrinsic
muscles and skin of sole of the foot.
• Cutaneous: the sural nerve (with common peroneal nerve) supplies the lateral
side of the leg, foot and fifth toe.
• Articular: to the knee joint.
Common peroneal nerve (lateral popliteal nerve)

The common peroneal (lateral popliteal) nerve (L4, L5, S1, S2), the smaller of
the two terminal branches of sciatic nerve enters the upper part of the popliteal
fossa, passes along the medial border of biceps tendon, then curves round the
neck of fibula, and here in the substance of peroneus longus, gives its terminal
branches, the superficial and deep peroneal nerves.
Superficial peroneal nerve

The superficial peroneal nerve runs in the lateral compartment of the leg. Its
branches are as follows:
• Muscular: muscles of lateral compartment of leg (peroneus longus and
brevis).
• Cutaneous: to skin of the distal two-third of lateral aspect of the leg and to
the dorsum of foot (excepting the area specified below*).
Deep peroneal nerve

The deep peroneal nerve pierces extensor digitorum longus, then descends with
the anterior tibial vessels over the interosseous membrane and then over the
ankle joint. Medial to it lies the tibialis anterior, while laterally lies first extensor
digitorum longus, and extensor hallucis longus. Its branches are as follows:
• Muscular: muscles of anterior compartment of leg (extensor digitorum
longus, extensor hallucis longus, tibialis anterior, peroneus tertius and
extensor digitorum brevis)
• Cutaneous: to small area of skin in the web between the 1st and 2nd toes*.
Cutaneous supply of lower limb (fig. 49.3)

In spite of interlacing complex of the nerve roots, the skin of the lower limb, has
a perfect regular segmental nerve supply, which is derived from L1 to S4
segments.
• L1, L2, and L3: anterior aspect of thigh from above down.
• L4: Medial aspect of the leg.
• L5: Lateral aspect of the leg but also extends onto the medial side of the foot.
• S1: lateral side of the foot and the sole.
• S2: posterior surface of the leg and thigh.
• S3 and S4: buttocks and perianal region.
Note
To remember easily, L5 supplies the first toe and S1 supplies the fifth toe. S3
supplies the posterior part of scrotum (or vulva), L1 supplies the anterior part
of these structures via the ilioinguinal nerve.
49.3 Causes of peripheral nerve disorders

Peripheral nerve disorders are classified based on their aetiologies (Table 49.2).
TABLE 49.2
Aetiological Classification of Peripheral Nerve Disorders
Aetiology Single Nerve Disorder Multiple Nerve Disorder (Mononeuropathy Multiplex)

(Mononeuropathy)
Traumatic Closed and open injuries
Inflammatory Herpes zoster Herpes zoster
Leprosy Leprosy
Diphtheria Lyme
Neoplastic Neurofibroma Neurofibromatosis
Neurofibrosarcoma
Metabolic Vasculitis
Diabetes mellitus Diabetes mellitus
Sarcoidosis Sarcoidosis
Radiation Porphyria
Miscellaneous Tunnel syndrome Lead poisoning, multifocal motor neuropathy with conduction
block, MADSAM
49.4 injuries of peripheral nerves

The peripheral nerves are prone to get injured at certain situations. According to
the extent of damage, they are classified into three types. Their details are listed
in Table 49.3.
TABLE 49.3
Pathophysiology and Clinical Presentations of Peripheral Nerve
Injuries
Type Cause Pathophysiology Clinical Recovery

Presentation
Neuropraxia (no Minor stretching, Physiological paralysis of Temporary sensory Complete in a
damage to nerve torsion or conduction, no loss, paresthesia, few weeks or
or sheath) vibration degeneration muscle weakness months
Axonotmesis (partial Stress, traction or Partial loss of conduction Loss of sensation, Recovery is
division of nerve compression of with Wallerian tone and muscle almost
in an intact nerve (as in degeneration in distal part power and reflex complete
sheath) closed fracture) of broken axon activity
Neurotmesis (partial Open injuries of Complete loss of conduction Complete loss of Recovery is
or complete nerve with retrograde motor, sensory incomplete
division of nerve regeneration in the and reflex (worse in
and sheath) proximal segment activity mixed
nerves)
Injuries of peripheral nerves of upper limb

Brachial plexus injuries
Brachial plexus injuries can be
• complete (occur due to severe accidents) or
• incomplete (stab injuries or cuts).
The injuries can involve
• upper brachial plexus (occurs when the angle between the shoulder and the
neck is widened. e.g., fall of weight on shoulder in adults and difficult labour
in children) or
• lower brachial plexus (occur during forceful abduction of shoulder joint in
adults, or breech presentation with arms above head during labour in
children).
The clinical presentation varies according to the lesion.
• Complete lesions: Patients present with anaesthesia of the entire upper limb
(except upper part of arm supplied by C3, C4 and C5). Complete paralysis of
arm is the presentation (Fig. 49.6).
• Incomplete lesions:
• Upper brachial plexus injuries (Erb-Duchenne paralysis), affect C5 and
C6 nerve roots, and affects deltoid, biceps, brachioradialis and supinator
muscles. The limb gets internally rotated, elbow is extended and pronated
to a specific posture called ‘Policeman’s tip’. There may be sensory loss
over the outer side of arm and upper part of lateral aspect of forearm.
• Lower brachial plexus injuries (Klumpke’s paralysis), affect C8 and T1
nerve roots and affects intrinsic muscles of the hand producing a classical
‘claw hand’. There may be anaesthesia of medial side of forearm, hand,
and inner 1½ fingers due to ulnar and median nerve injuries. Horner’s
syndrome (ptosis, enophthalmos, constriction of pupil and anhydrosis of
affected side of face) may coexist.
FIGURE 49.6 Complete injury of right brachial plexus Source: (Courtesy Dr V.

Thulasiraman).
Neuralgic amyotrophy (Parsonage–Turner syndrome) is characterized by

acute severe pain in the shoulder radiating into arm, neck and back and arm is
held in flexion at elbow, adduction at shoulder to prevent pain. Pain is followed
by weakness of shoulder and predominantly of proximal arm muscles.
Thoracic outlet syndromes: Results from compression of brachial plexus or
subclavian vessels in the space between the first rib and the clavicle often
associated with vascular signs and symptoms. Usually lower trunk of brachial
plexus is involved. Pain is the most common sensory symptom and referred to
radial border of hand, medial forearm and arm. Paresthesias and sensory loss
occur in same distribution. Thenar wasting and paresis are more prominent,
while muscles supplied by ulnar nerve may be spared (see Ch. 13).
Axillary nerve injuries

The axillary nerve may be injured in fractures of head of humerus or shoulder
dislocations.
The injury causes weakness of shoulder abduction, wasting of deltoid and a
small patch of anaesthesia over the deltoid (Fig. 49.7)—regimental badge area.
FIGURE 49.7 Sensory loss of axillary nerve injuries.
Radial nerve injuries

Radial nerve may be injured at various levels. They are as follows:
• Main trunk
• In the axilla
- Pressure due to crutches (Crutch palsy).
- Pressure due to the back of a chair (Saturday night palsy).
- Fracture dislocation of upper end of humerus.
- Improper reduction of fracture dislocations.
• In the radial groove
- Fracture of shaft of humerus.
- Extraneous pressure as in operating tables, or tight tourniquets.
• Posterior interosseous nerve
• In the upper forearm
- Fracture dislocation of upper end of radius.
- Iatrogenic injuries during operations of upper forearm.
The patient presents with paralysis of muscles depending on the site of injury,
but ‘wrist drop’ is the classical presentation.
• Injuries in the axilla: Paralysis of all muscles supplied by the nerve with loss
of sensation of the areas supplied by the cutaneous branches of radial nerve.
• Injuries in the radial groove: Paralysis of all muscles supplied by the nerve
(Fig. 49.8) with loss of sensation of the areas supplied by the cutaneous
branches of radial nerve, excepting triceps and posterior cutaneous nerve
supply.
• Injuries to the posterior interosseous nerve: Loss of extension of wrist joint
and metacarpo-phalangeal joints1.
FIGURE 49.8 Wrist drop of radial nerve injury in radial groove (fracture of
shaft of humerus) Source: (Courtesy Dr K. Sridhar).
By clinical examination, the integrity of radial nerve is tested by determining

the power of the following muscles (see pages 918–920):
• Triceps
• Supinator
• Brachioradialis
• Extensor muscles of wrist joint (extensor carpi radialis longus, extensor carpi
radialis brevis, Extensor carpi ulnaris)
• Extensor digitorum.
And, also the cutaneous sensation on the back of the arm, forearm and radial
side of dorsum of hand, depending on the level of lesion (Fig. 49.8A).
FIGURE 49.8A Sensory loss of radial nerve injuries.
Ulnar nerve injuries

• The ulnar nerve may be injured at various levels. They are as follows:
• In the axilla
- Trauma
- Other lesions in this area.
• At the level of medial epicondyle
- Ulnar neuritis due to local friction, pressure or stretching as may occur in
cubitus valgus and osteoarthritis.
• Distal to the elbow
- By compression as it passes between the heads of flexor carpi ulnaris.
• At the wrist
- Lacerations
- Occupational trauma
- Ganglion
• In the ulnar tunnel: where the nerve passes between the pisiform and the
hook of hamate (Ulnar tunnel syndrome; see Ch. 43 Hands).
• Wasting of muscles depending on the site of injury and ulnar claw hand (Fig.
49.8B and C).
• The first dorsal interosseous muscle is almost always the first to become
noticeably affected, and the hollowing of the skin over the dorsal aspect of
the first web space is often most striking.
• Forearm muscle wasting indicates lesion proximal to the wrist.
• The nerve is inspected for abnormal mobility during the movements of elbow
(e.g., deficiency in anchoring tissues in traumatic ulnar neuritis).
• The nerve should be palpated and rolled at above the medial epicondyle, and
also at the wrist, for local thickening (Hansen’s disease), tenderness (e.g.,
neuritis) and unusual paresthesia.
FIGURE 49.8B Tardy ulnar nerve palsy (left) Source: (Courtesy Dr K. Sridhar).
FIGURE 49.8C Ulnar nerve palsy Source: (Courtesy Dr K. Sridhar).
The integrity of ulnar nerve is tested by determining the power of the

following muscles (see p. 919):
• Flexor carpi ulnaris
• Interossei
• First palmar interosseous and adductor pollicis
And, also the cutaneous sensation on the ulnar side of the both aspects of hand
and both surfaces of the ulnar 1½ fingers (Fig. 49.8D).
FIGURE 49.8D Sensory loss of median and ulnar nerve injuries.
Median nerve injuries

• The median nerve may be injured at various levels.
• In the arm or above the elbow
- Fracture of shaft of humerus
• At the elbow
- Supracondylar fracture
- Dislocation of elbow joint
- Inadvertent application of tourniquet
• Just distal to the elbow
- Entrapment between the heads of pronator teres (pronator syndrome—
see Ch. 43).
• In the forearm
- Forearm bone fractures
• At the wrist
- Lacerations and cut injuries
• In the carpal tunnel
- Compression of median nerve (Carpal tunnel syndrome—see Ch. 43)
Wasting of muscles of thenar eminence (atrophy of the pulp of index finger) and
trophic ulcers (e.g., cigarette burns) on the index due to local sensory loss.
• At or above the elbow
• Wasting of lateral aspect of forearm, and the index finger is held in
extension (Benediction attitude).
• Paralysis of all the muscles of flexor aspect of forearm except the flexor
carpi ulnaris and ulnar half of flexor digitorum profundus, muscles of
thenar eminence, radial two lumbricals.
• At the wrist: Paralysis of muscles of thenar eminence, radial two lumbricals.
The integrity of median nerve is tested by determining the power of the
following muscles (see p. 920):
• Flexor digitorum superficalis and profundus (lateral half)
• Flexor pollicis longus
• Flexor carpi radialis
• Muscles of thenar eminence
• Abductor pollicis brevis
• Opponens pollicis
And also the cutaneous sensation on the radial side of the palm, the palmar
and the dorsal aspect of the radial 3½ fingers (Fig. 49.8D).
Injuries of peripheral nerves of lower limb

Femoral nerve injuries
• Closed injuries of femoral nerve are rare.
• Damage may occur when a haematoma is formed in the iliopsoas muscle
causing local pressure. This is seen in haemophilia and in extension injuries
of the hip.
Weakness or paralysis of iliopsoas (weakness in flexion of hip) and quadriceps
(weakness of extension of knee).
Sciatic nerve injuries

• Complete lesion of this nerve is very rare, but incomplete lesion occurs
commonly during subtrochanteric fracture of femur and posterior dislocation
of hip.
• Almost always involves the common peroneal part of the nerve.
Complete lesion–complete paralysis of the hamstring and all the muscles below
the knee.
Tibial nerve injuries

These injuries are rare and occur in
• ischaemic lesions of calf (e.g., posterior compartment syndrome from tight
plasters), diabetic neuropathy;
• fractures of medial malleolus and
• tarsal tunnel syndrome.
Paralysis of the plantar flexors of ankle joint, leading to a deformity ‘talipes
calcaneo valgus’, where the patient will not be able to plantar flex and invert the
foot.
Common peroneal nerve injuries

These injuries occur during fracture of neck of fibula
• Paralysis of extensors and peroneal muscles of the leg leading to a deformity
‘talipes equino varus’, where the patient will not be able to dorsiflex and
evert the foot.
• Patient will walk with undue lifting of the foot to clear the ground—‘drop
foot’ deformity (Fig. 49.9).
FIGURE 49.9 Drop foot deformity (left) Source: (Courtesy Dr K. Sridhar).

Note
Individual sensory deficit is commonly seen in the injuries of individual
nerves of lower limb (Fig. 49.9A–D).
FIGURE 49.9A Sensory loss in femoral nerve injury.

FIGURE 49.9B Sensory loss in sciatic nerve injury.
FIGURE 49.9C Sensory loss in lateral cutaneous nerve of thigh injury.
FIGURE 49.9D Sensory loss in common peroneal nerve injury.
Leprosy
• An infectious disease caused by Mycobacterium leprae, spread by direct
contact for prolonged periods of time, from the nasal secretions of the
infected patient.
• A systemic disease that involves the skin, respiratory tract and peripheral
nerves.
• It is classified into two types:
• lepromatous leprosy and
• tuberculoid leprosy.
• Skin lesions.
• Swelling or thickening of certain nerves, e.g., great auricular, supraorbital,
radial cutaneous, and ulnar nerves (at the elbow) and rarely common
peroneal nerve (at the neck of fibula), tibial nerve (behind the medial
malleolus), median nerve (at the wrist).
• Patches of anaesthesia occur on the skin due to involvement of peripheral
nerves.
Biopsy and histopathology of skin lesion is confirmative.
Treatment
Anti-leprosy drugs cure the disease.
49.5 Symptoms of peripheral nerve pathologies

• Motor changes (paralysis, palsies)
• Sensory changes (anaesthesia, hyperesthesia)
• Deformities
Motor changes
Motor function of a nerve is assessed by evaluating the following:
• Tone: defined as resistance of muscle to passive movement at a joint.
• Power: strength of muscle measured by the ability to contract the muscle
against force or gravity.
• Reflexes: A deep tendon reflex is the reaction of a muscle being passively
stretched by percussion on the tendon, and it is a measure of the integrity
both of the afferent and efferent peripheral nerves and of their central
inhibitory controls.
• Wasting and fasciculations.
There are five patterns of muscular weakness. They are tabulated in Table
49.4.
TABLE 49.4
Patterns of Muscular Weakness
Muscle Tone (Table Muscle Power (Table Reflexes (Table

Pattern of Paralysis Wasting
49.5) 49.6) 49.7)
Upper motor neuron Increased Pyramidal pattern of Increased Absent
(UMN) weakness
Lower motor neuron Decreased Decreased Absent Present with
(LMN) fasciculations
Muscle disease Decreased Decreased Impaired or Present
absent
Neuromuscular junction Normal or decreased Fatigable weakness Normal
Functional weakness Normal Erratic Normal Absent
A tendon reflex results from the stimulation of a stretch-sensitive afferent

from a neuromuscular spindle, which via a single synapse, stimulates a motor
nerve to contract a muscle.
• Tendon reflexes are increased in upper motor neuron lesions.
• Tendon reflexes are decreased in lower motor neuron lesions and muscle
abnormalities.
The reflexes are graded and shown in Table 49.7.
The level of nervous system affected can be determined by the distribution
and pattern of weakness and by associated findings. See Table 49.8.
TABLE 49.8
Various Patterns of Muscle Weaknesses
Muscle Weakness Examples of Lesions
Generalized weakness (limbs and cranial nerves)

Diseases of nerves Polyradiculoneuropathy
Diseases of neuromuscular junction Myasthenia gravis
Diseases of muscles Myopathy
Weakness of all four limbs
Upper motor neuron Cervical cord lesion Brainstem lesions Bilateral cerebral lesions
Lower motor neuron Polyradiculopathy Peripheral neuropathy
Mixed (UMN and LMN) Motor neuron disease
Unilateral and leg weakness
Upper motor neuron Hemisection of spinal cord Brainstem lesion Cerebral lesion
Weakness of both legs
Upper motor neuron Spinal cord lesion
Lower motor neuron Cauda equina lesion
Weakness of single limb
Upper motor neuron Lesion above highest involved level
Lower motor neuron Single nerve: mononeuropathy Single nerve root: radiculopathy
Patchy weakness
Upper motor neuron Multiple CNS lesions
Lower motor neuron Polyradiculopathy
Sensory changes
Changes in sensory function are evaluated by assessing the following
• Touch
• Pain Spinothalamic tract
• Temperature
• Position Posterior column
• Vibration
Light touch and pin prick loss are usually symptomatic. Vibration sense,
position sense and temperature are often lost without prominent symptoms.
The sensory examination is used
• as a screening test;
• to assess a symptomatic patient and
• to test hypothesis generated by motor examination.
Differentiating peripheral neuropathy from radiculopathy

Radiculopathy is recognized by a group of symptoms and signs caused by
lesions of nerve root. Radicular pain and paresthesias are accompanied by
sensory loss in the dermatome, weakness in the myotome and diminished
reflexes at a segmental level (see p. 473).
Some common radiculopathies that resemble peripheral lesions are as follows:
• C7 root and radial nerve:
• C7 root lesion causes weakness of shoulder abduction, extension, wrist
extension and wrist flexion.
• Radial nerve lesion, in contrast, cannot affect shoulder abduction or wrist
flexion and will affect the brachioradialis muscle.
• C5 root and axillary nerve:
• C5 root lesion weakens all 180° of shoulder abduction; whereas
• axillary nerve lesion affects only the second 90° movement.
• L5 root and common peroneal nerve:
• L5 radiculopathy causes back pain and leg pain, weakness of hip
abduction, weakness of foot inversion, positive root stretch signs and
depression of the medial hamstring reflex.
• Common peroneal nerve lesion causes foot drop or calcaneus
equinovalgus.
• S1 radiculopathy and tibial nerve:
• S1 radiculopathy is characterized by weakness of plantar flexion of foot
and toes, eversion of foot, hip extension and knee flexion.
• Tibial neuropathy causes paresis of plantar flexors of foot and toes and
inversion of foot.
Distribution of weakness
• Bilateral symmetrical distal weakness is always neurogenic (exceptions—
distal myopathy, myotonic dystrophy).
• Bilateral symmetric proximal muscle weakness if of myopathic causes
(exception—Guillian Barre syndrome, proximal spinal muscular atrophy).
Segmental localization in spinal cord lesions

In a case of paraparesis or quadriparesis, localization of spinal cord segment is
by detecting motor, sensory and reflex levels. They are tabulated in Table 49.9.
TABLE 49.9
Localization of Spinal Cord Segment in Paraparesis and
Quadriparesis
Action Involved Segment

Motor level
Neck flexion C1–C4
Shoulder abduction C5
Elbow flexion C5, C6
Elbow extension C7
Small muscles C8, T1
Hip flexion L1, L2
Knee extension L3
Ankle dorsiflexion L4, L5
Dorsiflexion of great toe L5
Ankle plantar flexion S1
Knee flexion S2
Anal sphincter S3, S4, S5
Sensory Level
Areas to be tested
Nape of neck C2
Midpoint above clavicle C3
Midpoint below clavicle C4
Over the deltoid C5
Thumb C6
Middle finger C7
Little finger C8
Inner arm T1
Axilla T3
Nipple T4
Lower costal margin T7
Umbilicus T10
Inguinal ligament L1
Front of thigh (pocket region) L2
Front of knee L3
Medial side of leg L4
Great toe L5
Little toe S1
Back of thigh S2
Perianal region S3, S4, S5
Reflex level
Reflex
Biceps reflex C5, C6
Supinator reflex C5, C6
Triceps reflex C6, C7
Finger flexion reflex C7–T1
Abdominal reflex T8–T12
Cremasteric reflex L1
Adductor reflex L2, L3, L4
Knee jerk L2, L3, L4
Ankle jerk S1
Anal reflex S2, S3, S4
Deformities
Deformities like claw hand, wrist drop, occur due to over action of a group of
muscles over the opposite group of muscles, which are paralysed due to loss of
motor function.
Eliciting history
Motor changes (paralysis and palsies)
• Duration of paralysis: When did he first notice the difficulty in using the
limb?
This will give the duration of present illness (e.g., shortest duration in
injuries of nerve, short duration in malignancies, long duration in muscular
paralysis).
there any trauma preceding the paralysis?
Incidence like complete nerve injuries of trauma may precipitate the event
(e.g., fractures, operative injuries).
Sensory changes
• Duration of sensory changes: When did he first notice the changes in
sensation?
This will give the duration of present illness (e.g., shortest in nerve injuries,
short duration in malignancies, long duration in peripheral neuropathy).
there any trauma preceding change in sensation?
Incidence like complete nerve injuries of trauma may precipitate the event
(e.g., fractures, operative injuries).
Deformity
• Duration of deformity: When did he first notice the deformity?
This will give the duration of present illness (e.g., short duration like
Saturday night palsy, long duration of Tardy ulnar palsy).
there any trauma preceding the deformity?
Incidence like drunkenness may precipitate the event (e.g., Saturday night
palsy) or a trauma can precipitate this (e.g., fracture shaft of humerus causing
wrist drop due to radial nerve injury).

course of illness?
Loss of appetite and weight are indicative of illnesses like malignancies.
give a clearer picture of diagnosis (failed treatment will help in the
elimination from differential diagnosis and success will help in confirmation
of the diagnosis and continuation of the treatment if necessary).
treatment?
like neuropathy and malignancies and eliminate diagnosis like viral
infections.
Diseases like leprosy occur in families (closed communities) and the
presence of it may be a good indicator for the present diagnosis.
• Personal history: Questions regarding personal habits? Personal habits like
drinking alcohol have direct relationship with peripheral nerve disorders.
match the situation, like extramarital contact if the disease is suspected to be
of aetiology like syphilis and HIV.
Pre-requisites
• Patient should be undressed so that the entire limb is exposed.
Act of undressing
• How clumsy is the patient during the movements (e.g., nerve injuries causing
motor paralysis of small muscles of hand).
• How protective is the patient during the act (e.g., denotes pain).
Note
the wrist and fingers.
Inspection
What to look for?
• Attitude of the patient (e.g., patients with paralysis of upper limb muscles are
seen supporting with the other hand).
• Deformities (e.g., wrist drop in radial nerve paralysis, foot drop in lateral
popliteal nerve paralysis, winging of scapula in long thoracic nerve paralysis,
claw hand in ulnar nerve paralysis).
• Skin—shiny skin (e.g., complete paralysis), dry skin (e.g., sympathetic
paralysis).
• Change in colour of skin (e.g., pallor, cyanosis due to vasomotor changes).
• Abnormal swellings (e.g., neurofibromata).
• Scars or wounds (e.g., traumatic or postoperative—infected wounds in the
past are more the cause).
• Wasting of muscles (e.g., longstanding paralysis), fasciculations.
Note
Always compare with the other side.
Palpation
1. Temperature: The temperature should be felt with the back of the hand and
compared with the other side (e.g., paralyzed parts are usually cold).
2. Skin: The skin has to be tested for areas of anaesthesia (e.g., paralysis of
cutaneous branches of affected nerve) or paresthesia or hyperesthesia (e.g.,
indicate regeneration of injured nerve)—detailed on p. 926.
3. Scars: The scar has to be palpated for tenderness or adherence to underlying
structures (e.g., adherence of scar to nerve).
4. Thickening of nerve: the nerve is palpated behind the medial epicondyle
(e.g., Hansen disease).
Motor function
Muscles: The muscles are to be palpated (e.g., long-standing paralysis of
muscles make them soft and flabby). Furthermore, the muscles are to be tested
for:
• tone
• power and
• reflexes.
Tone
Testing muscle tone is a very important indicator of the presence and site of
pathology.
Pre-requisites
• Patient should be totally relaxed, and may be distracted by conversation.
The methods of examination to determine the muscle tone is given in Table
49.10.
TABLE 49.10
Methods of Determination of Tone in Various Muscles
Part to be
Method of Examination
Examined
Arms Supporting the forearm with left hand, the patient’s right hand is held in shake hand position by the
examiner, it is pronated and supinated, then the arm is moved through full range of flexion and
extension of elbow (Fig. 49.12A and B).
Hips Patient lying supine, the knee is rolled side to side (Fig. 49.13).
Knee Knee is lifted by putting the hand behind the knee and the heel is watched. The knee is held with the left
hand and the ankle with the right hand, and knee is flexed and extended (Fig. 49.14).
Ankle The ankle is held with left hand and the foot is flexed and dorsiflexed by right hand (Fig. 49.15).
Power
Upper limb
While determining the power of upper limb muscles, remember the following:
• Upper motor neuron or pyramidal weakness predominantly affects finger
extension, elbow extension and shoulder abduction (elbow flexion and grip
are relatively preserved).
• Muscles are innervated by more than one root, and exact distribution varies
between individuals.
• The three nerves of greatest clinical importance in the upper limb are as
follows:
• Radial nerve (supplies extensors in the upper limb)
• Ulnar nerve (supplies all intrinsic muscles except LOAF)
• Median nerve (supplies LOAF)
- L: Lateral two lumbricals
- O: Oppenens pollicis
- A: Abductor pollicis brevis
- F: Flexor pollicis brevis
The method of determining the power of individual muscles of the upper limb
TABLE 49.11
Methods of Determining the Power of Muscles of Upper Limb
Movement Method Muscle Nerve Root

Shoulder Patient should lift his elbow outside against Deltoid Axillary nerve C5
abduction resistance (Fig. 49.16).
Elbow With the elbow extended (forearm supinated), the Biceps brachii Musculo C5, C6
flexion hand should be brought towards the face cutaneous
against resistance (Fig. 49.17). nerve
Elbow With the elbow flexed (forearm supinated), the Triceps brachii Radial nerve (C6),
extension hand should be taken away from the face C7,
against resistance (Fig. 49.18). (C8)
Wrist flexion With the forearm supinated, the fingers are held All long muscles Median and ulnar C7
with the examiner’s fingers and patient asked crossing the nerves
to lift the fingers upwards (Fig. 49.19). anterior aspect of
the wrist joint
Wrist With the forearm pronated, the patient is asked to All long muscles Radial nerve (C6),
extension lift the fingers upwards against resistance crossing the C7,
(Fig. 49.20). posterior aspect of (C8)
the wrist joint
Finger The fingers of patient should be closed and Flexor digitorum Median and ulnar C8
flexion fingers should be taken towards the palm superficialis and nerves
pulling the examiner’s resisting fingersa (Fig. profundus
49.21).
Finger Hand held in neutral position, the fingers should Extensor digitorum Posterior C7, (C8)
extension push the examiner’s resisting fingers (Fig. interosseous
49.22). nerve
Finger The fingers should be spread out against Dorsal interossei Ulnar nerve T1
abduction resistance (Fig. 49.23).
Finger The fingers should be brought together against Palmar interossei Ulnar nerve T1
adduction resistance (Card Test) (Fig. 49.24).
Thumb With the flat palm with a supinated forearm, Abductor pollicis Median nerve T1
abduction thumb is moved towards nose right angle to brevis
the palm (Fig. 49.25).
Thumb The patient is asked to grasp a book or a card Adductor pollicis and Ulnar nerve T1
adduction with the thumb and other fingersb (Fig. first palmar
49.26). interosseous
Arm power Patient should press the wall with both his hands Serratus anterior Long thoracic C5, C6,
(arms straight at the level of shoulder) (Fig. nerve C7
49.27).
Patient should press on his hips and asked to Rhomboids Nerve to C4, C5
bring elbows backwards against resistance rhomboids
(Fig. 49.28).
Patient is asked to lift his arm from the side Supraspinatus Suprascapular C5, C6
against resistance (Fig. 49.29). nerve
Patient should turn the forearm outwards with the Infraspinatus Suprascapular C5, C6
elbow flexed (Fig. 49.30). nerve
Examiner should hold the semipronated forearm Brachioradialis Radial nerve C6
of patient and should be asked to take it
towards his face (Fig. 49.31).
Patient should grip the examiner’s fingers and Flexor digitorum Ulnar nerve C8
extension of distal interphalangeal joints of profundus
little and ring fingers should be attempted
(Fig. 49.32).
a
When the median nerve is injured, if the patient is asked to clasp his hands, the index finger of
the affected side fails to flex and remains as a pointing ‘index’. This test is called Ochsner’s
clasping test (Fig. 49.33.)
b
If the ulnar nerve is injured, the muscles will be paralyzed, and the patient holds the book by
flexing the thumb with the help of Flexor pollicis longus supplied by median nerve (Froment’s sign)
(Fig. 49.34).
Clinical tests for specific nerve injuries of upper limb

These tests are performed by putting the muscles supplied by the nerve into
action.
Axillary nerve injuries

Deltoid: The patient is asked to abduct his shoulder by lifting the arm with the
elbow flexed at right angle against resistance. With the other hand the clinician
feels the deltoid muscle (ref. Fig. 49.16).
Radial nerve injuries
Triceps: The patient is made to keep the shoulder extended, and he is asked to
extend the elbow against resistance (ref. Fig. 49.18). Weakness of triceps
suggests a lesion at mid-humeral level or an incomplete high level; loss of
triceps activity suggests a high (plexus) lesion.
Supinator: The elbow must be extended to eliminate the supinating action of
biceps. The patient is asked to turn his hand while counter-force is applied by the
examiner (Fig. 49.35).
Brachioradialis: The patient is asked to keep the forearm in midprone
position and flex the elbow against resistance. The muscle becomes prominent
and shows up which can be seen or palpated (ref. Fig. 49.31).
Extensor muscles of wrist joint: The patient is asked to extend the wrist joint
against resistance. Complete paralysis leads to ‘wrist drop’ (Fig. 49.36).
FIGURE 49.36 Wrist drop Source: (Courtesy Dr K. Sridhar).
Extensor digitorum: The patient is asked to extend the joints of the hand
against resistance. Paralysis of this muscle will lead to inability of extension of
metacarpo-phalangeal joints, but not the interphalangeal joints (extension of
interphalangeal joints are unaffected as the extensors of the these joints are
interossei (through extensor expansion), which are supplied by ulnar nerve) (ref
Fig. 49.22).
Ulnar nerve injuries

Flexor carpi ulnaris: The patient is asked to flex the wrist joint against
resistance, the hand tends to deviate towards the radial side (as the other flexors
are supplied by median nerve).
Interossei: Dorsal interossei are responsible for abduction of fingers and
palmar interossei for adduction.
• The patient is asked to abduct the fingers against resistance, which will
indicate the power of dorsal interossei (abductors of fingers) (ref. Fig.
49.23).
• The patient is asked to hold a card tightly between the fingers, which will
determine the power of palmar interossei (adductors of fingers)—Card test
(ref. Fig. 49.26).
Interossei and lumbricals: These muscles along with extensor expansion
take care of extension of proximal and terminal interphalangeal joints. To
determine the power of these muscles together, the proximal phalanx has to be
steadied by the examiner and the finger has to be extended against resistance
(Fig. 49.37).
FIGURE 49.37 Testing the interossei and lumbricals.
First palmar interosseous and adductor pollicis: The patient is asked to grasp
a book between the extended thumb and other fingers. When the ulnar nerve is
paralyzed, first palmar interosseous and adductor pollicis are paralyzed, but the
patient will hold the book with a flexed thumb (due to flexor pollicis longus
supplied by median nerve) —Froment’s sign (ref. Fig. 49.34).

Flexor pollicis longus: The patient is asked to bend the terminal phalanx of
thumb against resistance with the examiner steadying the proximal phalanx with
the finger of the other hand. This is not possible when the muscle is paralyzed
due to median nerve injury at the level of elbow (Fig. 49.38).
FIGURE 49.38 Testing flexor pollicis longus.
Flexor digitorum superficialis and profundus (lateral half): The patient is

asked to clasp his hands, and if these muscles are paralyzed, the index finger of
the affected side fails to flex and remains as a ‘pointing index’ — Ochsner’s
clasping test (ref. Fig. 49.33).
Abductor pollicis brevis: This muscle abducts the thumb (moving right angle
to the palm when the hand is laid flat). The patient is asked to touch a pen held at
a slightly higher level ( Pen test). If the muscle is paralyzed he will not be able
to touch it (Fig. 49.39).
FIGURE 49.39 Pen test for abductor pollicis brevis.
Opponens pollicis: This muscle helps in swinging of the thumb across all the
fingertips. When this muscle is paralyzed, he will not be able to do this
movement (Fig. 49.40).
FIGURE 49.40 Testing the opponens pollicis by swinging the thumbs
across the tips of other fingers.
Pronator teres: The elbow must be kept extended, and the patient is asked to
pronate his forearm against resistance. The contraction of pronator teres should
be felt by the examiner during the movement (Fig. 49.41). Accompanying pain
and tenderness over the muscle is found in pronator syndrome.
FIGURE 49.41 Method of testing the pronator.
Lower limb
While determining the power of lower limb muscles, remember the following:
• Upper motor neuron or pyramidal weakness predominantly affects hip
flexion, knee flexion and foot dorsiflexion.
• Muscles are innervated by more than one root, and exact distribution varies
between individuals.
• The two nerves of greatest clinical importance in the lower limb are:
• Femoral nerve supplies knee extension.
• Sciatic nerve supplies knee flexion.
- Posterior tibial branch provided plantar flexion, inversion.
- Common peroneal branch supplies dorsiflexion and eversion of ankle.
The method of determining the power of individual muscles of the lower limb
TABLE 49.12
Methods of Determining the Power of Muscles of Lower Limb
Movement Method Muscle Nerve Root

Hip flexion The patient should lift his knee towards chest, and asked to Ileopsoas Lumbar sacral L1, L2
pull it up as hard as he can, against resistance (Fig. plexus
49.42).
Hip extension The patient should lie flat with his legs straight and push the Gluteus Inferior L5, S1
examiner’s hand kept under the heel (Fig. 49.43). maximus gluteal
nerve
Hip abduction Lying supine, the patient should take lower limb away from Gluteus Superior L4, L5
his body against resistance (Fig. 49.44). medius and gluteal
minimus nerve
Hip adduction Lying supine, the patient should resist the examiner who is Adductors Obturator L2, L3
trying to pull the lower limb away from his body (Fig. nerve
49.45).
Knee extension The patient should straighten the flexed knee against Quadriceps Femoral nerve L3, L4
resistance (Fig. 49.46). femoris
Knee flexion The patient should bend his knee against resistance (Fig. Hamstrings Sciatic nerve L5, S1
49.47).
Foot The patient should dorsiflex his ankle against resistance Tibialis Deep peroneal L4, L5
dorsiflexion (Fig. 49.48). anterior nerve
Foot flexion Lying supine, the patient should push the hand of the Gastocnemius Posterior tibial S1
examiner with his toes (Fig. 49.49). nerve
Foot inversion With the ankle at 90°, the patient should turn his foot Tibialis Tibial nerve L4, L5
inwards against resistance (Fig. 49.50). posterior
Foot eversion With the ankle at 90°, the patient should turn his foot Peroneus Superficial L5, S1
outwards against resistance (Fig. 49.51). longus and peroneal
brevis nerve
Big toe The patient should pull his big toe towards his face against Extensor Deep peroneal L5
extension resistance (Fig. 49.52). hallucis nerve
longus
Extension of The patient should pull all his toes towards his face against Extensor Deep peroneal L5, S1
toes resistance (Fig. 49.53). digitorum nerve
brevis
Flexion of toes The patient should fold his toes towards the sole of his foot Intrinsic Tibial nerve L4, L5
against resistance (Fig. 49.54). muscles of
foot
Clinical tests for specific nerve injuries of lower limb

These tests are performed by putting the muscles supplied by the nerve into
action.
Femoral nerve injuries

Iliopsoas: The patient is asked to flex the hip against resistance (ref. Fig.
49.42).
FIGURE 49.42 Testing the ileopsoas by hip flexion against resistance.
Quadriceps femoris: The patient is asked to extend the knee against

resistance (ref. Fig. 49.46).
Common peroneal nerve injuries

Extensors and peroneals of leg: The patient presents with visible deformity
of foot drop and talipes equinovarus. The patient will not be able to overcome
this deformity due to the paralysis of these muscles.
Medial peroneal nerve injuries

Calf muscles: The patient is asked to plantar flex the foot, which he will not
be able to do, due to paralysis of calf muscles.
Reflexes
The tendon reflex is determined using a knee hammer. The whole length of the
hammer should be used, the hammer should be allowed to swing well, and the
patient should be relaxed. The methods of eliciting reflexes in the upper and
lower limbs are given in .
TABLE 49.13
Reflexes of Upper Limb and Methods of Eliciting Them
Reflex Method Tendon Nerve Root

Biceps reflex The patient’s hand should be kept on his abdomen. The Biceps brachii Musculo C5 (C6)
examiner should place his left index finger on the biceps cutaneous
tendon, the hammer is given a full swing to hit the left nerve
index finger, and the biceps muscle should be watched
(Fig. 49.55).
Triceps The arm is drawn across the chest, the examiner should hold Triceps brachii Radial nerve C7
reflex the wrist with the elbow at 90°. The triceps is struck with
the hammer, and the triceps muscle should be watched
(Fig. 49.56).
Supinator The arm is kept on the abdomen flexed. The examiner should Brachioradialis Radial nerve C6 (C5)
reflex place his left index on the radial tuberosity, and it is
struck with the hammer, and the brachioradialis is
watched (Fig. 49.57).
Finger reflex The patient should hold his hand in neutral position, the Flexor Median and C8
examiner should place his hand opposite the fingers, the digitorum ulnar
back of the examiner’s fingers are struck (Fig. 49.58). profundus nerves
and
superficialis
TABLE 49.14
Reflexes of Lower Limb and Methods of Eliciting Them
Reflex Method Tendon Nerve Root
Knee With the patient lying, the examiner should place his left hand below Quadriceps Femoral L3, L4
reflexa the knee so that it is slightly flexed. The point below the patella is nerve
stuck with the hammer, watching the quadriceps (Fig. 49.59).
Ankle The foot is held dorsiflexed at 90°, with the medial malleolus facing Muscles of Tibial nerve S1, S2
reflexb the ceiling. The knee should be flexed and lie to the side. The calf
hammer is stuck on the Achilles tendon directly, watching the calf
muscles (Fig. 49.60).
With legs straight, the left hand is placed on the ball of the foot with
the ankles at 90°. The hammer is stuck on the hand, watching the
calf muscles (Fig. 49.61).
The patient should kneel on a chair with the ankle hanging loose over
the edge. The Achilles tendon is stuck with the hammer, watching
the calf muscles (Fig. 49.62).
a
When the knee continues to swing for several beats following the hit by the hammer, it is called
pendular reflex (e.g., cerebellar disease).
b
Relaxation phase may be increased (Slow relaxing reflex) in ankle jerk (e.g., hypothyroidism).
TABLE 49.15
Other Reflexes
Reflex Method Observation Interpretation Reason

Abdominal The abdominal wall is scratched with a small stick Absent Obesity,
from the sides towards the midline, which will previous
contract the abdominal muscles (Fig. 49.63). surgery,
Segmental nerves Above umbilicus: T8, T9 Below pyramidal
umbilicus: T10, T11 tract above
the level
Plantar A stick is gently drawn along the lateral border of the All toes flex Negative sign Normal
response foot starting near the heel and go across the foot (flexor
(Babinski pad, the great toe is watched (Fig. 49.64). plantar
sign) response)
Hallux Positive sign UMN lesion
extends,
other toes
spread
Hallux Withdrawal Needs
extends, response repetition
other toes
extend
and ankle
flexes
No movement No response Profound UMN
weakness,
sensory
abnormality
Sensory function
For effective sensory testing, it essential to
• teach the patient about the test:
• perform the test:
• check that the patient has understood and
• move from areas of sensory loss to areas of normal sensation.
Note
Sensory signs are softer than reflex or motor change, and therefore less weight
is generally given to them while computing the findings.
The relevant sensory losses of individual nerves in the upper and lower limbs
are shown in Figs 49.7, 8A, 8D, 9A–D.
Touch sensation
• Demonstrate: With the patient’s eyes open, the patient should be shown that
the examiner will be touching an area of skin, and should be asked to say
‘yes’ every time he/she is touched.
• Test: The patient is asked to close his eyes, and the areas are touched (dab)
with the cotton wool at random intervals (Fig. 49.65A) or a fine brush (Fig.
49.65B).
FIGURE 49.65A Method of eliciting touch sensation with cotton wool.

FIGURE 49.65B Method of eliciting touch sensation with a soft brush.
Note
Avoid dragging the cotton wool on the skin or tickle the patient.
Pain sensation
• Demonstrate: The patient should be told that he will be pricked gently with a
pin, and also an unaffected area of his skin will be touched with the sharp
and blunt ends of the pin, and that he is expected to tell whether the pin is
sharp or blunt.
• Test: The patient should be asked to close his eyes and the sharp and blunt
tips of the pin are applied randomly on the skin and the patient’s response
noted (Fig. 49.65C).
FIGURE 49.65C Eliciting pain sensation.
Note
Use a pin, neurological pin or dressmaker’s safety pin.
Temperature sensation
• Demonstrate: Explain that he will be touched at random with hot and cold
tubes.
• Test: Hot and cold tubes are applied at random to hands, feet and areas of
interest (Fig. 49.65D).
FIGURE 49.65D Method of eliciting temperature sensation.
Note
Two tubes, one with warm and the other with cold water are used.
Vibration sense
• Demonstrate: The patient should be explained that he will feel a vibration,
when a tuning fork is placed on the sternum or chin.
• Test: The patient is asked to close his eyes. A vibrating tuning fork is placed
on the bony prominences and he should be asked for the vibrations. It is
placed initially on toe tips, metatarsophalangeal joint, medial malleolus,
tibial tuberosity, anterior superior iliac spine, in the arms, on the fingertips,
each interphalangeal joint, metacarpophalangeal joint, the wrist, elbow and
the shoulder in that order (Fig. 49.65E).
FIGURE 49.65E Method of eliciting vibration sense.
Note
If the sensation is normal distally there is no point in proceeding proximally.
Use a 128 Hz tuning fork. Those of higher frequency (256 or 512 Hz) are not
adequate.
Joint position sense
• Demonstrate: Explain the procedure with the patient eyes open.
• Test: With the patient’s eyes closed, hold the distal phalanx between your two
fingers, and move the finger up and down and ask the patient whether the
finger is up or down (Fig. 49.65F).
FIGURE 49.65F Method of eliciting joint sensation.
Note
The procedure is done individually for the joints.
Nerve
The whole course of the nerve should be palpated for
• thickening due to infections (e.g., nerve may be thickened in leprosy);
• localized thickening due to nerve injuries—may be suggested by bone
injuries or scars near the course of the nerve (e.g., supracondylar fracture of
humerus);
• signs of regeneration can also be made by palpation. A sensation of ‘pins and
needles’ or hyperesthesia may be felt by the patient on tapping the nerve
(Tinel’s sign).
Movements
Movements of joints are controlled by muscles. Active movements are less than
passive movements when muscles are paralyzed.
Note
Severe scarring in the muscles and tendons and ankylosis of joints interfere
with active and passive movements equally.
Deformity
Deformity results due to paralysis of one group of muscles and the overactivity
of the opposing group of muscles, e.g., wrist drop or foot drop.
1
Extension of interphalangeal joints are unaffected as the extensors of these
joints are interossei (through extensor expansion) which are supplied by ulnar
nerve.
PA R T I V
Polytrauma
OUTLINE
50. Polytrauma
CHAPTER 50
Polytrauma
S. Devaji Rao
CHAPTER OUTLINE
50.2. Preparation 930
50.3. Receiving the patient 931
50.4. Primary survey and resuscitation 931
• Airway and cervical spine control 931
• Breathing 931
• Circulation and haemorrhage control 931
• Disability 932
• Exposure 932
50.5. Secondary survey 932
50.7. Conclusion 934
50.1 Introduction
Management of a patient with polytrauma depends on proper and systematic
clinical evaluation, which identifies immediate and potentially life-threatening
conditions before the limb threatening ones, but does not omit the latter. This
usually starts with a call from ambulance control.
The first couple of hours following injury are critical, as the patient is very
vulnerable. This critical time period is called ‘golden hour’, which is usually
spent in the place of accident or in the emergency department, making this
period extremely crucial.
The trauma life support programme consists of
• preparation
• primary survey and resuscitation
• secondary survey and
• continuous monitoring and evaluation.
50.2 Preparation
Pre-hospital communication
A warning from the ambulance control ideally from the scene of accident
provides essential information so that receiving personnel are ready to receive
the patient of trauma, which provides assessment and treatment without delay.
The essential pre-hospital information are as follows:
• Nature of injury.
• Mechanism of injury.
• Number, age and sex of the casualties.
• Consciousness level of the casualties.
• Airway, breathing and circulatory status of casualties.
• Treatment provided.
• Estimated time of arrival.
• Treatment options required.
Trauma reception team

The makeup of this team varies between hospitals depending upon the resources
and the time of the day. The trauma team should consist of
• trained medical personnel
• supportive trained paramedical personnel and
• a team leader who should assign specific tasks to each person.
The trauma reception team undertakes the following tasks:
Team leader
• Coordinates the tasks assigned to the team members.
• Questions ambulance personnel.
• Assimilates clinical findings.
• Determines investigations in order of priority.
• Liaises with relatives and provide information to trauma team.
• Liaises with specialists who are called.
Team members
• Manage the airway.
• Clear the secretions and intubate if necessary.
• Manage circulation.
• Establish infusion line quickly.
• Takes blood for investigations.
• Supportive measures.
• Connect to monitors.
• Urinary catheterization.
• Jugular vein catheterization where necessary.
50.3 Receiving the patient

Receiving and transferring the patient is very crucial and requires five people to
do the job, which should be a well-practiced procedure in order to protect the
spinal cord if it is intact, and to prevent further injury if it is already
compromised. During the transfer, the patient’s head and neck are stabilized by
one member of the team, three others lift from the side and the fifth member
replaces the ambulance trolley with the resuscitation trolley.
50.4 Primary survey and resuscitation

The activities listed below are carried out simultaneously if there are enough
personnel, if not should be done in alphabetical order (ABCDE).
• Airway and cervical spine control
• Breathing
• Circulation and haemorrhage control
• Disability
• Exposure
Airway and cervical spine control
A cervical spine injury should be assumed if the patient has been the victim of
significant blunt trauma or if the mechanism of injury indicates that the cervical
region may have been damaged. One member of the team needs manually to
immobilize the cervical spine while talking to the patient, which also assesses
the airway.
• If the patient is able to give a logical answer in a normal voice, the airway is
assumed to be patent and the brain adequately perfused.
• If the patient gives an impaired or fails to reply, the airway could be
obstructed, immediate measures should be taken immediately.
• A simple chin lift will help in relieving the obstructing soft tissue usually
the tongue.
• Saliva, blood, vomitus, tooth or other foreign bodies should be removed.
• Suction through rigid suction tube is necessary to remove secretions.
• In patients who vomit and regurgitate, head end of the bed should be
dropped 20 degrees, allowing the secretions to drip down and facilitate
removal by suction.
• A nasogastric tube may be inserted to aspirate the stomach contents and
prevent further vomiting.
When it is established that the airway is clear and patent, 100% oxygen is
provided via mask or by endotracheal intubation. Pulse oxymeter is connected to
maintain good SaO2, if needed with ventilatory support.
The neck should be examined for the following five signs, which could
indicate the presence of immediately life-threatening thoracic conditions. See
Table 50.1.
TABLE 50.1
Signs of Life-Threatening Thoracic Conditions
Sign Condition
1 Swellings and wounds Vascular and airway injury
2 Distended neck veins Cardiac tamponade, tension pneumothorax
3 Tracheal deviation Tension pneumothorax
4 Subcutaneous emphysema Pneumomediastinum
5 Laryngeal crepitus Fracture of laryngeal cartilage
When the above signs are checked, the neck may be immobilized with
appropriate collar if the patient is not restless, in a restless patient, semirigid
collar is accepted.
Note
All multiply injured patients, particularly those who have injuries above the
clavicle or a change in level of consciousness, should be treated as though
they have a cervical spine injury, until it is ruled out.
Breathing
The clinical examination of chest consists of
• Inspection
• Marks and wounds
• Respiratory rate
• Inspiratory effort
• Symmetry of chest movements
• Percussion
• Assess ventilation at the periphery.
• Auscultation
• Assess defects in air movement.
Note
The respiratory rate and effort are sensitive indicators of underlying lung
pathology, and requires to be monitored and recorded at frequent intervals.
Circulation and haemorrhage control

Bleeding can result due to
• fractures of long bones
• vascular injuries and
• soft tissue injuries.
Application of pressure is the best way of management of haemorrhage, as
tourniquets increase intraluminal pressure of the vessels, distal ischaemia and
tissue necrosis. Application of tourniquet is undertaken in select situations, and
when used the time of application of tourniquet has to be noted so that
neighbouring soft tissue is not jeopardized.
Recognition and assessment of hypovolemia

The assessment of hypovolemia has to be done in a systematic manner.
• Skin: colour, clamminess and capillary refilling
• Vital signs: heart rate, blood pressure and pulse volume
• Consciousness level
Note
Isolated determinations of above parameters is unreliable as various organs try
to compensate at early stages, especially at extremes of age.
Common sites of occult bleeding are as follows:

• Chest
• Abdomen and retroperitoneum
• Pelvis
• Long bone fractures
• External bleed into splints and dressings
Fluid resuscitation
Once any overt bleeding is controlled, it is necessary to maintain the circulatory
volume. This is done by administering a warm crystalloid followed by blood
transfusions, maintaining the radial pulse and blood pressure. This
administration of fluids is done by peripheral venous cannulation, and when not
possible done through central venous catheterization.
Note
• Vital signs return to normal after less than 2 L of fluid are administered,
when the lost blood is less than 20% of the blood volume.
• Transient responders who are actively bleeding or recommence bleeding
during the resuscitation, and the improved vital signs deteriorate indicating
loss of over 30% of the blood volume.
• Little or no response indicates that the loss is more than 40% or no
hypovolemia.
Disability
Disabilities when occur in a patient with trauma shows seriousness. It can occur
in
• hypoxia
• hypovolemia
• hypoglycaemia and
• increased intracranial pressure.
Exposure
The patient’s clothes have to be removed by cutting through the seams so that
there is minimal patient movement. All clothes are removed only after adequate
intravenous access is established, as a rapid removal of tight trousers can
precipitate sudden hypotension due to the loss of the tamponade effect in a
hypovolemic patient.
Once stripped, trauma victims should be kept warm with blankets when not
being examined. Now the patient is rolled on and the spine examined from base
of skull to the coccyx, with a rectal examination.
What to look for during rectal examination in a trauma victim?
• Is the sphincter tone present?
• Is the rectal wall breached?
• Is the prostate in normal position?
• Is there blood on the examiner’s finger?
50.5 Secondary survey
Once the immediately life-threatening conditions are recognized and treated, the
whole of the patient is assessed. This requires head to toe, front to back
assessment along with detailed medical history and appropriate investigations.
Note
If the patient deteriorates at any stage, the airway, breathing and circulation
must be immediately re-assessed as described in the primary survey.
Eliciting history
The history is elicited quickly and in concise manner, concentrating on
• nature of injury
• mechanism of injury
• treatment provided and
• medical history.
• Five important points should be remembered while eliciting medical
history. They are as follows:
- A: allergies
- M: medicines
- P: past medical history
- L: last meal
- E: events leading to the incident.
The physical examination should be done in a systematic manner.
Scalp
The scalp is examined for
• lacerations
• swellings and
• depressions.
The examination is carried out by inspection and palpation (by running the
fingers on the scalp).
Note
• It should be remembered to examine the occipital region, which is usually
missed out.
• Blind probing should be avoided as it may further damage the underlying
structures.
• In children, bleeding from scalp lacerations can cause hypotension and
efforts to stop bleeding (application of pressure, applying self-retaining
retractors) have to be taken immediately.
Neurological state
The neurological state of the patient by the Glasgow Coma Score, the papillary
responses and the presence of lateralizing signs should be assessed. This
examination should be done frequently so that any deterioration is detected early.
Base of skull
Since the skull base lies along a diagonal line running from the mastoid to the
eye, the signs of a fracture in this region are also found along this line.
Signs of a base of skull fracture:
• Bruising over the mastoid (Battle’s sign)
• Panda’s eyes
• Blood and CSF rhinorrhoea
• Blood and CSF otorrhoea
• Hemotympanum
• Scleral haemorrhage with no posterior margin
• Sub-hyoid haemorrhage.
Note
Battle’s sign and Panda’s eyes appear after about 12 to 36 hours, and is not a
reliable sign in a resuscitation room. CSF rhinorrhoea may be missed as it is
invariably mixed with blood.
Neck
If any deformity is found, it is necessary to splint the neck preferably with a
collar.
Eyes
• Haemorrhage
• Foreign bodies (including contact lenses)
• Papillary response and corneal reflexes (in unconscious patient)
• Visual acuity (in conscious patient).
Face
The face is examined by systematic inspection and palpation, and look for:
• Soft tissue injuries
• Fractures of mid face
• Fractures of mandible
• Missing or lost teeth.
Note
• Midface fractures may be associated with fractures of base of skull.
• Mandibular fractures can cause airway obstruction due to loss of stability of
tongue.
Thorax
The thorax is examined for
• soft tissue injuries
• fractures of clavicles and ribs
• crepitus (e.g., surgical emphysema) and
• movements of chest (e.g., flail chest).
Abdomen
The abdomen is examined in a very systematic manner, without forgetting to
examine the pelvis and perineum. Percussion is an ideal way to determine the
injuries of liver and spleen. In penetrating injuries, if bowel is exposed, it should
be covered immediately with sterile cloth.
Urine output measurement is a good indicator in a shocked patient, and this
requires catheterization for accurate measurement. Transurethral catheterization
without any difficulty may indicate that there is no severe urethral disruption. If
the patient is not able to urinate, and catheterization is not possible, severe
urethral injury should be suspected, and suprapubic catheterization should be
done. The signs of urethral injury in a male are as follows:
• Bruising around the scrotum
• Blood at the urethral meatus
• High-riding prostate.
Note
• Intra-abdominal bleed should be suspected if the patient is hemodynamically
unstable, especially if the lower six ribs are fractured or there are marks on
the abdominal surface.
• In unexplained hypotension, pelvic bone injuries should be suspected.
Compression or distraction test is useful.
• Clinical examination may not be reliable in neurologically unstable patients,
and investigations like ultrasound and CT or MRI may be needed.
Diagnostic peritoneal lavage may be relied upon in certain situations like
massive hemoperitoneum.
Extremities
The limbs are examined in the traditional manner of inspection, palpation and
active and passive movement.
• The fractures should be assessed and the blood loss estimated.
• Distal loss of arterial pulsation may be due to profound shock or arterial
injury.
Definitive care
Once the patient is adequately assessed and successfully resuscitated, he is
moved to the next stage for definitive care, but they are vulnerable during
transfers as monitoring becomes difficult during this time.
Before transfer, it is necessary to
• close an open wound with sterile pads and
• correct the deformity and splint the limb.
50.7 Conclusion
In polytrauma, clinical examination is crucial and important, but has to be done
with agility without wasting time for the definitive care. The questions have to
be asked in quick succession in an organized manner, as primary care itself has
to be done instantaneously. Investigations are to be ordered in a judicious
manner, without wasting time and money.
Index
Page numbers followed by f, t, and b indicate figures, tables, and boxes,
respectively.
A
Abdomen, 448
Abdominal aortic aneurysm, 153
Abdominal distension, 556 , 618
Abdominal pain, 540 , 556
Abdominal postbox, 524
Abdominal tuberculosis, 533–534
Abducent (VI) nerve, 203–204
Abduction and external rotation manoeuvre (90° AER), 161
Abnormal gaits, 827
Abnormalities of craniovertebral junction, 470–471
Abnormalities of tympanic membrane, 319–320
Abscess, 394 , 801
Abscess of iliopsoas sheath, 583–584
Absent fingers, 795–796
Achalasia (cardiospasm), 25
Achondroplasia, 715
Acid peptic disease, 525–527
Acoustic neuroma, 309
Acquired arterio venous fistula, 167
Acquired haemolytic anaemia, 570
Acquired hernia, 608
Acromioclavicular disorders, 741–742
Acromioclavicular osteoarthritis, 742
Acrosyndactyly, 796
Actinomycosis, 582–583
Actinomycosis of right iliac fossa, 114
Acute abdominal catastrophes, 496–498
Acute abdominal pain, 511
Acute appendicitis, 489–492
Acute breast abscess, 430
Acute cholecystitis, 492–494
Acute cystitis, 669
Acute dislocations, 744
Acute diverticulitis, 494
Acute empyema, 397
Acute epididymo orchitis, 637
Acute epiglottitis, 331
Acute extradural haematoma, 214
Acute fissures, 598
Acute haemorrhagic pancreatitis, 507–509
Acute infections, 469
Acute infections and inflammations, 51
Acute inflammatory conditions of abdomen, 489–496
Acute intussusception, 501–503
Acute ischaemia, 144–146
Acute laryngitis, 328
Acute laryngotracheobronchitis, 331
Acute lymphadenitis, 133–134
Acute lymphangitis, 130–131
Acute mastoiditis, 306–307
Acute Meckel’s diverticulitis, 494–495
Acute mediastinitis, 408
Acute mesenteric lymphadenitis, 496
Acute otitis media, 304–305
Acute paronychia, 802 , 887–888
Acute prostatitis, 673–674
Acute pyelonephritis, 655
Acute pyogenic abscess, 72
Acute respiratory distress syndrome (ARDS), 407
Acute retropharyngeal abscess, 324–325
Acute salpinigitis, 496
Acute septic osteomyelitis, 719–720
Acute sinusitis, 285–286
Acute subdural haematoma, 214
Acute suppurative sialadenitis, 337–338
Acute suppurative tenosynovitis, 806–807
Acute tonsillitis, 324
Acute tracheitis and laryngotracheobronchitis (croup), 400
Acute ulcerative colitis, 495
Acute urethritis, 680
Acute viral parotitis (epidemic parotitis, mumps), 337
Adenoidal hypertrophy, 283–284
Adenoma, 355
Adiposis dolorosa, 74
Adjuvant therapy to prevent or delay distant metastases, 436
Adrenal cortex, 575
Adrenal medulla, 575
Adrenal tumours, 575–576
Adson’s test, 161 , 485
Adventitious bursa, 884–885
Aetiological classification of anorectal diseases, 590
Aetiological classification of diseases and abnormalities of penis, 627t
Aetiological classification of diseases and abnormalities of testis and epididymis,
634t
Aetiological classification of diseases of kidneys and pelvis, 652t
Aetiological classification of diseases of scrotum, 641t
Aetiological classification of diseases of ureters, 661t
Aetiological classification of diseases of urethra, 677t
Aetiological classification of diseases of urinary bladder, 667t
Aetiological classification of disorders of oral cavity, 223–224t
Aetiological classification of lesions of bones and joints, 714t
Aetiological classification of lesions of the face, 222t
Age preponderance in knee joint pathologies, 854t
Agenesis of phallus (aphalia), 626
Airway and cervical spine control, 931
Allen’s test, 158
Allergic rhinitis, 281–282
Alteration in bowel habits, 511 , 540
Alveolar sinus, 103
Amalgam tattoo, 228
Amazia (amastia) and athelia, 426–427
Ameloblastoma, 236–237
Amoebic hepatitis/liver abscess, 561–562
Amoebic proctitis and ulcers, 594
Amoeboma, 582
Ampulla of Vater, 507
Anal fissures, 116 , 593 , 598
Analysis of pain, 9t
Analysis of symptoms, 410–411 , 439
Anaplastic carcinoma, 357
Anatomic relations of prostate, 673f
Anatomical nomenclature of hernia, 609
Anatomy of biliary system, 34
Anatomy of female external genitalia, 691f
Anatomy of foot, 863–864
Anatomy of hernial sac, 608–609
Anatomy of hip joint, 815f
Anatomy of joints of wrist and hand, 775f
Anatomy of oral cavity, 222f
Anatomy of salivary glands, 336
Anatomy of shoulder joint, 738f
Anatomy of skin, 180
Anatomy of the epigastric region, 614
Anatomy of the femoral region, 612
Anatomy of the inguinal region, 609–610
Anatomy of the umbilical region, 614
Anatomy of urological system, 651f
Androgen insensitivity, 693
An ephelis, 250
Aneurysms, 152–153
Angiofibroma, 284–285
Angioneurotic oedema, 231
Angular cheilitis, 229
Ankle joint, 862–863
Ankyloglossia, 227
Ankylosing spondylitis, 460
Ankylosis, 228–229
Ann Arbor staging of lymphoma, 137
Anomalies in structure of teeth, 260t
Anomalies of sternum, 393
Anorectal abscesses, 592
Anorectal diseases, 590–599
Anorectal malformations, 590–591
Anosmia, 288
Antalgic gait, 827
Anterior dislocation, 820
Anterior drawer test, 860
Anterior horn tear, 845
Anterior interosseous syndrome, 805
Anterior rhinoscopy, 293–295
Antibioma, 430–431
Antrochoanal polyps, 283t
Aortic aneurysm, 576
Apache II score, 509
Aphthous ulcers, 230–231
Apical space infection, 802
Apley’s distraction test, 859–860
Apley’s grinding test, 861
Apophysitis of tibial tubercle, 850–851
Appendicular abscess, 489 , 581
Appendicular mass, 489 , 581
Appendicular mass/abscess, 581–582
Appetite and weight loss, 540
Apraxic gait, 212
Arachnoid cyst, 191
Arches of feet, 863–864 , 891f
Arm drift, 210
Arterial (ischemic) ulcers, 91–92
Arterial supply of ears, 298t
Arterial system, 144–161
Arteriovenous malformations, 193
Ascariasis, 499–500
Ascites, 624
Asherman’s syndrome, 703
Aspiration pneumonia, 403
Assessment of hearing, 320–321
Atrophic rhinitis, 282
Atrophic testis, 638
Attic or marginal perforations, 306
Aural dressing forceps, 316
Aural speculum, 315
Auscultopercussion, 551
Autophony, 311
Axillary nerve, 901
Axillary nerve injuries, 905
Axillary vein thrombosis, 171
B
Back pain, 471
Balance’s sign, 559
Balanitis xerotica obliterans, 627
Baldwing’s test, 521
Ballottement, 550 , 687
Ballottement of patella, 857
Bands and adhesions, 503–504
Bankart lesion, 744
Barber’s hand, 116
Barlow’s provocative test, 836
Barrett’s oesophagus, 21
Barton fracture, 774
Basal cell carcinoma, 66–67 , 92
Basal ganglia, 210
Basilic vein, 164
Battle’s sign, 317
Bazin’s ulcer (erythema induratum), 94
Bell’s phenomenon, 206
Benign breast disease, 426
Benign giant cell synovioma, 808–809
Benign hypertrophy, 674–675
Benign liver tumours, 564
Benign ovarian tumours, 697
Benign positional vertigo, 309–310
Benign strictures, 38
Benign swelling, 56t
Benign tumors, 22–23 , 286 , 401 , 594–595 , 810
Benign tumors of small bowel, 50
Benign tumours of ribs, 395
Benign tumours of spine, 461
Berry aneurysm, 152
Berry’s sign, 369–370
Bidigital palpation, 347
Biliary atresia, 35
Bilirubin metabolism, 34
Bird’s beak appearance, 25
Bladder calculi, 672–673
Bladder diverticulum, 667
Bladder injuries, 668–669
Blanching, 83
Bleeding per vagina, 704–705
Blocked sensation in ear, 313
Blue leg, 170
Blumberg’s sign, 522
Blunt injuries, 553–554
Boas’s sign, 519
Bohn’s nodules, 227
Bones of foot, 863f
Bones of hand, 775
Borborygmi, 86
Boutonniere deformity, 799
Bowen’s disease, 64
Brachial plexus, 900
Brachial plexus injuries, 905–906
Brain, 188–213
Brain abscess, 191–192
Brain injury, 214
Branchial cyst, 380
Branchial fistula, 106
Branham Nicoladoni’s sign, 161
Brodie Trendelenberg’s test for perforator incompetence, 177
Brodie Trendelenberg’s test for saphenofemoral incompetence, 176–177
Bronchiectasis, 400–401
Broncho-pleuro-cutaneous fistula (thoracic region), 107–108
Bryant’s triangle, 832–833
Bubonocoele, 610
Buccal mucosa, 255–256
Bucket handle tear, 845
Buerger’s disease, 148
Buerger’s test, 158–160
Burns, 180–187 , 228
Bursae, 840t
Burst sublingual dermoid, 106
C
Caecal volvulus, 505
Cake kidney, 652
Calcaneal apophysitis, 874–875
Calcaneal paratendinitis, 874
Calcific supraspinatus tendinitis, 743
Callosity, 71 , 808 , 886–887
Calloway’s sign, 752
Caloric testing (Hallpike and Dix test), 207
Capillary malformation, 165
Carbuncle, 72–73 , 655 , 801–802
Carcinoma, 67 , 671 , 675
Carcinoma caecum, 582
Carcinoma head of pancreas, 40
Carcinoma larynx, 329–330
Carcinoma of endometrium, 699
Carcinoma of gallbladder, 566–567
Carcinoma of hypopharynx, 327
Carcinoma of nose, 279
Carcinoma of ovaries, 700–701
Carcinoma of postnasal space, 285
Carcinoma of scrotum, 643
Carcinoma of uterine cervix, 698–699
Carcinoma of vulva, 699–700
Carcinoma penis, 632–633
Card test, 920
Caroli disease, 37
Carotid artery tortuosities and aneurysm, 381
Carotid body tumour, 381
Carpal tunnel syndrome, 804–805
Carrying angle, 755
Catarrhal, 489
Cauda equina, 451
Cauda equina syndrome, 463
Cauliflower ear, 299
Causes of acute retention of urine, 684t
Causes of haematuria, 683t
Causes of peripheral nerve disorders, 904–909
Causes of ureteric obstructions, 665t
Causes of urethral stricture, 678t
Cavernous haemangioma, 58
Cellulitis, 71–72 , 301 , 801
Central fracture dislocation, 820 , 821
Central perforation, 306
Central ray, 795
Cephalic vein, 164
Cerebellar gait, 212
Cerebellar haemangioblastoma, 196
Cerebellar vermis, 210
Cerebral haemorrhage, 193–194
Cerebral infarcts, 193–194
Cerebral metastases, 197
Cerumen spud, 315
Cervical degenerative disease, 463
Cervical radiculopathy, 487
Cervical rib, 382–383
Cervical spine, 451
Cervical spondylosis, 463
Cervico-facial actinomycosis, 103–105 , 235
Chancroid, 91 , 631t
Change of voice, 332
Characteristics of renal stones, 661t
Charcot’s triad, 492
Chemical burns, 180
Chest pain, 410
Chest wall, 390
Chiene’s test, 834
Choanal atresia, 280
Cholangiocarcinoma, 39–40
Choledochal cyst, 36–38 , 36f
Choledocholithiasis, 41
Chondrodermatitis nodularis helicis, 303–304
Chondroma, 722
Chondromalacia of patella, 848–849
Chondrosarcoma, 725–726
Chondrosarcoma of iliac bone, 584
Choreic gait, 212
Chronic abscess or antibioma, 73
Chronic breast abscess, 430–431
Chronic cholecystitis, 528–530
Chronic cystitis, 669–670
Chronic epididymo orchitis, 637–638
Chronic fissures, 598
Chronic granulomatous rhinitis, 282
Chronic inflammations of tendons and fasciae, 895
Chronic laryngitis, 328–329
Chronic lower limb ischaemia, 146–148
Chronic mediastinitis, 408
Chronic osteomyelitis of jaws, 235
Chronic osteomyelitis of mandible, 105
Chronic osteomyelitis of metatarsals, 117
Chronic pancreatitis, 530–531
Chronic paronychia, 804
Chronic prostatitis, 674
Chronic pyelonephritis, 656
Chronic pyogenic osteomyelitis, 720–721
Chronic recurrent parotitis, 338
Chronic retropharyngeal abscess, 325
Chronic sinusitis, 286
Chronic subdural haematoma, 198
Chronic submandibular sialadenitis, 338–339
Chronic suppurative otitis media, 305–306
Chronic tonsillitis, 324
Chronic upper limb ischaemia, 149
Chronic urethritis, 680
Circulation and haemorrhage control, 931–932
Cirrhosis of liver, 565–566
Clapper bell deformity, 639
Classification of burns, 181–182
Classification of diseases of female genital tract, 693t
Classification of fistulae, 102–103
Classification of sinuses, 101
Claudication distance, 154–155
Claw toes, 867
Clawhand, 905
Clefts, 224–225
Clergyman’s knee, 851
Clinical evaluation of facial injuries, 268–273
Clinical features of Volkmann’s ischaemia, 786t
Clinical presentation of intraoral malignancies, 240t
Clinical tests for specific nerve injuries of lower limb, 923–926
Clinical tests for specific nerve injuries of upper limb, 918–921
Clonus, 911t
Closed injuries, 553
Club foot (talipes equino varus), 864
Cobblestone appearance, 535
Coccydynia, 471
Coffee bean appearance—Freeman Dahl sign, 504
Coital injuries, 693–694
Cold abscess, 73 , 135 , 561
Cold exposure test, 161
Colics, 511
Collar stud abscess, 135
Collateral ligament injuries, 844
Colles fracture, 776–777
Colloid cyst, 196
Colocutaneous fistulae of right iliac fossa, 114–115
Colocutaneous fistulae of the loins, 113
Colonic malignancy, 537–539
Colorectal polyps, 51–52
Coloured lesions of lip, 247t
Coloured lesions on the oral mucosa, 249t
Combined malformation, 167
Common lesions of the palate, 258
Common peroneal nerve, 904
Communicating hydrocephalus, 190
Communicating veins, 163
Complete hernia, 610
Complicated hernia, 612
Complications of fractures, 719
Compound palmar ganglion, 785
Compressibility, 82
Compressive myelopathy, 473–475
Compressive radiculopathy, 473
Concussion, 214
Conductive deafness, 312t
Condyloma acuminata, 61 , 630–631 , 680–681
Confrontation testing, 202
Congenital anomalies – ears, 298–299
Congenital anomalies – nose, 276
Congenital arteriovenous malformation, 166
Congenital constriction ring syndrome, 798
Congenital dislocation of hip (developmental dysplasia of hip), 816–817
Congenital haemolytic anaemia, 570
Congenital hernia, 608 , 610
Congenital lesions of hand, 795
Congenital pyloric stenosis, 573–574
Congenital radioulnar synostosis, 766
Congenital renal anomalies, 651–654
Congenital swellings, 54
Congenital ureter anomalies, 662
Congenital vascular malformations, 165–167
Coning, 188
Constant neck pain, 473
Constipation, 31–33
Contusions, 214
Coomb’s test, 570
Cope’s psoas test, 522
Cork screw appearance, 25
Cork screw collaterals, 148
Corn, 71 , 808 , 886–887
Cottle’s test, 292
Cotton buds, 316
Cough impulse, 82 , 621
Cough impulse test (Morrissey’s sign), 176
Cough with expectoration, 410
Courvoisier’s law, 41 , 532 , 548
COWS (cold opposite warm same) response, 207
Coxa vara, 816
Cranial nerves, 202–208 , 203t
Craniopharyngioma, 196
Craniosynostosis, 191
Crepitus, 82
CREST syndrome, 152
Crile’s method, 367
Crohn’s disease, 535 , 551 , 600t
Cross bite, 242
Cross fluctuation, 81
Crossed ectopia (unilateral fusion), 652
Crossed haemiplegia, 189
Crossed SLR test, 484
Crowding, 242
Cruciate ligament injuries, 845
Crutch palsy, 906
CSF fistulae, 215–216
CSF otorrhea, 215
CSF rhinorrhea, 215
Cubital tunnel syndrome, 805–806
Cubitus valgus, 755–756
Cubitus varus, 756
Cullen sign, 507
Cut off sign, 509
Cutaneous supply of lower limb, 904
Cutaneous supply of upper limb, 902
Cystic fibrosis, 403
Cystic hygromas, 166 , 236
Cysticercosis of spinal cord, 469
Cystosarcoma phyllodes, 432
Cysts of epididymis, 640
Cysts of liver, 563–564
Cysts of newborn, 227–228
D
Dalrymple’s sign, 371
Dark field microscopy, 90
De Quervain’s thyroiditis, 354
Deafness, 310–311
Deciduous teeth, 259t
Deep bite, 242
Deep cervical lymph nodes, 125t
Deep palmar abscess, 803
Deep peroneal nerve, 904
Deep plantar abscess, 885
Deep vein thrombosis, 169–170
Deep venous system, 163
Deformities of elbow, 755–756
Deformities of foot, 864–867
Deformities of hip, 816
Deformities of knee, 840–842
Degenerative diseases of disc and facet joints, 462–463
Demyelinating diseases, 469
Dental caries, 262
Dental cyst, 235
Denture stomatitis, 228
Dercum’s disease, 74
Derivatives of brachial plexus, 901f
Dermal sinus tracts, 00038 s0485
Dermis, 180
Dermoid cyst, 56–58
Desmoid tumour, 578–579
Determination of fixed deformity, 835–836
Determination of tone in various muscles, 914t
Developmental dysplasia of hip, 816–817
Development of brain, 188
Development of breasts, 425
Development of ear and auditory canal, 296–297
Development of face, 221f
Development of face and oral structures, 220–221
Development of feet, 880–881
Development of female genital tract, 690
Development of hands, 793
Development of male genitalia, 625
Development of pharynx and larynx, 322
Development of respiratory tract, 389–390
Development of salivary glands, 336
Development of spine and spinal cord, 450
Development of thyroid, 349
Development of urogenital system, 651
Diabetic foot, 886
Diabetic ulcer, 93
Diaphragmatic injuries, 421
Diaphyseal aclasis (multiple exostoses), 714–715
Diarrhoea, 514
Differentiating peripheral neuropathy from radiculopathy, 910–912
Diffuse axonal injury, 214
Diffuse lipoma, 74
Diffuse oesophageal spasm, 25
Digital examination of vagina and bimanual palpation, 710–711
Dinner fork deformity, 776
Diphallia, 626–627
Diplacusis, 311
Direct inguinal hernia, 610
Direct laryngoscopy, 334 , 335t
Discharge - ear, 312
Discharge per vagina, 704
Discogenic back pain, 471
Discolourations of intraoral pathologies, 243t
Discolourations of teeth, 260t
Discolourations on the oral mucosa, 250t
Discrepancy of length, 834–835
Diseases and abnormalities of the breasts, 426–439
Diseases of any part of gastrointestinal system, 539–540
Diseases of bones, 713–734
Diseases of chest wall, 392–395
Diseases of face, 221
Diseases of feet, 881
Diseases of female genital tract, 692–703
Diseases of gallbladder, 528–530
Diseases of hands, 795–810
Diseases of inner ear, 308–309
Diseases of intestines, 533–539
Diseases of kidney and renal pelvis, 651–661
Diseases of larynx, 328
Diseases of larynx in adults, 328–331
Diseases of larynx in children, 331–332
Diseases of lymphatic system, 129t
Diseases of mediastinum, 408–410
Diseases of middle ear, 304–308
Diseases of muscles, tendons and fasciae, 893–897
Diseases of oesophagus, stomach and duodenum, 525–528
Diseases of oral cavity, 223–241
Diseases of pancreas, 530–533
Diseases of prostate, 673–676
Diseases of salivary glands, 337t
Diseases of trachea and bronchi, 399–403
Diseases of ureters, 661–666
Diseases of urethra, 676–681
Diseases of urinary bladder, 667–673
Dislocation of knee joint, 846
Dislocation of lunate, 779–780
Dislocations and fracture dislocations, 820–821
Dislocations of metacarpophalangeal or interphalangeal joints, 782
Dislocations of patella, 844
Distended bladdera, 585t
Divarication, 616
Diverticula, 26–27
Diverticulitis of colon, 536–537
Diverticulosis of small bowel, 536
Dizziness, 312–313
Doll eye movement, 218–219
Doll’s head maneuver, 204
Dorsal position, 707
Dorsal radiocarpal ligament, 774
Drop foot, 908
Dropped finger, 799
Dry and wet gangrene, 884
Duchenne’s sign, 837
Duct papilloma, 431
Ducts, 41–42
Dugas test, 753
Dupuytren’s contracture, 807
Dyschondroplasia (multiple chondromata, ollier disease), 715
Dysmetria, 208
Dyspareunia, 706
Dyspepsia, 18 , 19t , 540
Dysphagia, 18–30
Dysplasia of uterine cervix, 697–698
Dyspnoea (breathlessness), 410
Dystrophic gait, 212
Dysuria, 683
E
Ears, 296–322
Echinococcus granulosus, 562
Ectopia vesicae (bladder exstrophy), 667
Ectopic pregnancy, 702–703
Ectopic scrotum, 641
Ectopic testis, 635
Edge of the ulcer, 97
Effects of movements, food or habits, 513
Effort vein thrombosis, 171
Effusions of knee joint, 854t
Elastofibroma, 895
Elbow joint, 754–755
Electrical burns, 180
Elephantiasis, 131
Elephantiasis of penis, 631–632
Elevated arms stress test (EAST), 161
Ellis S curve, 396
Empyema, 492
Encephalocele, 190 , 280
Endometriosis, 701–702
Eosinophilic granuloma, 730
Epidermis, 180
Epidermoid carcinoma, 67
Epigastric hernia, 614
Epiphyseal injury of head of femur, 821
Epispadias, 629 , 678
Epistaxis, 288–289
Epstein’s pearls, 228
Epulis, 232
Erb-Duchenne paralysis, 905
Erysipelas, 60
Ethmoidal polyps, 283t
Ewing’s tumour, 726–727
Examination - external auditory canal, 317
Examination - external ear, 316
Examination - postaural area, 316–317
Examination - preauricular area, 316
Examination - tympanic membrane, 317–320
Examination for abnormal mobility, 835
Examining a child, 9
Expansile pulsations, 82
External angular dermoid, 56
External biliary fistula, 112–113
External fistula, 100
External hernia, 608
Extra-abdominal causes of abdominal pain, 511
Extra-articular disorders of ankle and foot, 874–876
Extra-articular disorders of elbow, 764–766
Extra-articular disorders of hip, 825
Extra-articular disorders of knee, 850–852
Extra-articular disorders of wrist and hand, 784–786
Extrasphincteric fistulae, 593
Extrinsic sources of pain in the hip, 826
F
Face, 244–246
Facet joint pain, 471
Facial (VII) nerve, 205–207
Facial nerve loss, 207
Facial palsy, 246 , 313
Facial skeleton, 265f
Facies Hippocratica, 497
Factors restricting the movements of the hip joint, 816t
Fasciae, 893–899
Fast flow anomalies, 167
Features of diseases of jaws, 263t
Feel of bag of worms, 639
Feet under weight bearing stress, 879
Fegan’s test, 179
Felty’s syndrome, 568–569
Female genital system, 690–713
Female genital tract infections, 696
Femoral hernia, 613–614
Femoral nerve, 902–903
Femoral nerve injuries, 908
Femoral stretch test, 484
Fibrin cuff theory of browse, 172
Fibroadenoma, 431–432
Fibroadenosis, 436–437
Fibroma, 64 , 895–896
Fibroma durum, 895
Fibroma molle or fibrolipoma (soft fibroma), 895
Fibromatosis, 896
Fibrosarcoma, 896
Fibrosarcoma of bone, 726
Filarial lymphadenitis, 134
Filarial scrotum, 642
Finger grip power, 211
Finger invagination test, 623
Finger spanning power, 211
Finger-tapping or toe-tapping test, 208
Finkelstein test, 791–792 , 807
Fistula, 100–101
Fistula in ano, 592–594
Fistula test, 320
Fixed abduction deformity, 835
Fixed flexion deformity, 835
Fixed rotation deformity, 835–836
Flail chest, 415–417
Flat foot, 865
Floor of mouth, 254–255
Floor of ulcer, 97t
Fluctuation, 79–81
Fluctuation test, 646
Fluid thrill, 86 , 550–551
Follicular carcinoma, 355
Foot tapping, 212
Fordyce’s granules, 225
Foreign bodies, 285 , 303 , 402–403
Foreign bodies in the genital tract, 694
Foreign bodies of larynx, 332
Foreign bodies of pharynx, 327–328
Foreign bodies, bolus obstruction, 29
Foreign bodies/bezoars (intestinal obstruction), 500–501
Foreign body granuloma, 232
Fournier’s gangrene, 643
Fracture dislocation, 820
Fracture dislocation around the ankle, 867–869
Fracture head of radius, 761
Fracture neck of radius, 761
Fracture of base of first metacarpal bone, 780
Fracture of capitulum, 758
Fracture of femoral condyles, 843
Fracture of head of femur, 819–820
Fracture of lower end of ulna, 778–779
Fracture of neck of femur, 818
Fracture of olecranon process, 758–759
Fracture of patella, 842
Fracture of radial styloid process (chauffeur’s fracture), 778
Fracture of scaphoid, 779
Fracture of shaft of femur, 825–826
Fracture of shaft of humerus, 746
Fracture of shafts of tibia and fibula, 852–853
Fracture of tibial condyles, 843–844
Fracture of trochanteric region, 819
Fracture penis, 630
Fracture separation of lower radial epiphysis, 777–778
Fractures, 716–719
Fractures of bones of hip joint, 818–820
Fractures of calcaneum, 871
Fractures of carpal bones, 779
Fractures of condyles, 757
Fractures of epicondyles, 757–758
Fractures of facial skeleton, 264
Fractures of lower end of forearm bones, 776–779
Fractures of lower end of humerus, 756–758
Fractures of mandible, 265
Fractures of maxilla, 265f
Fractures of metacarpal bones, 780
Fractures of metatarsals, 871–872
Fractures of mid face, 264–265
Fractures of pelvis, 817–818
Fractures of phalanges, 781 , 872
Fractures of scapula, 740
Fractures of shafts of forearm bones, 766–767
Fractures of shafts of leg bones, 852–853
Fractures of shafts of ulna and radius, 766–767
Fractures of skull, 214–215
Fractures of talus, 870–871
Fractures of the shoulder girdle, 740
Fractures of upper end of humerus, 740–741
Fractures of upper end of radius, 761
Fractures of upper end of ulna, 758–759
Fractures with disruption of pelvic ring, 817–818
Freckle, 250
Free field speech assessment, 321
Freiberg’s disease of a meatatarsal head (metatarsal osteochondritis), 875
Frequency in micturition, 514
Frequency, urgency and hesitancy, 683–684
Friction neuritis of ulnar nerve, 765–766
Frog face deformity, 284
Froment’s sign, 915–916t , 920
Frozen shoulder (periarthritis), 743–744
Fungal infections, 405–406 , 888
Fungal infections of oesophagus, 21–22
Furuncle, 60–61
Furunculosis, 281
G
Gaenslen’s test, 486
Gag reflex, 207–208
Galactocoele, 437
Gallbladder polyps, 530
Galleazzi fracture dislocation, 778
Gallstone ileus, 503
Gallstones in bile ducts, 41
Ganglion, 884
Gastric carcinoma, 527–528
Gastric lymphoma, 49
Gastric malignancy, 572–573
Gastrointestinal haemorrhage, 46–53
Gastrointestinal lymphomas, 539–540
Gastrointestinal stromal tumours, 539
Gaucher disease, 730
General physical examination, 15–16
General system examination, 11–15
Genetic disorders of female genital tract, 693
Genu recurvatum, 842
Genu valgum, 840–842
Genu varum, 840–842
GERD, 21
Giant cell arteritis (temporal arteritis), 152
Giant cell tumour (osteoclastoma), 723–724
Gifford’s sign, 371
Gillie’s test, 486
Gingiva, 256–257
Gingival cyst, 227
Gingivitis, 229–230
Glasgow coma score, 218t
Glenohumeral disorders, 744–745
Gliding test, 78
Glomus tumour, 809
Glossopharyngeal (IX) nerve, 207–208
Glue ear, 305
Golden hour, 146
Golfer’s elbow, 765
Goodsall’s rule, 594 , 605
Gouty arthritis, 873–874
Grades of muscle power, 911t
Grades of tendon reflexes, 911t
Grainger’s method, 546
Granuloma inguinale, 631t
Granuloma pyogenicum, 70
Granulomatosis, 730–731
Graves’ disease, 359
Grawitz tumour, 657–659
Great saphenous vein, 162
Grey Turner’s sign, 507
Grissinger sign, 317
Groin herniae, 609–614
Gummatous ulcer, 90
Guyon’s canal syndrome (ulnar tunnel syndrome), 806
Gynecomastia, 438–439
H
Haemangioma, 58–59 , 168t , 670
Haemarthrosis of knee joint, 846
Haematemesis, 46
Haematemesis and melena, 540
Haematochezia, 46 , 600 , 600t
Haematocoele, 636–637
Haematoma, 59–60
Haematoma auris, 299–300
Haematoma of breast, 429–430
Haematomas of muscles, 894
Haematuria, 514 , 683
Haemiplegic gait, 212
Haemoglobinopathies, 570
Haemophilic arthritis, 763 , 824 , 847–848 , 874
Haemoptysis, 410–411
Haemorrhage, 46–48
Haemorrhoids, 596–597
Haemothorax, 418–419
Hairy mole, 62
Halitosis, 288
Hallux rigidus, 866
Hallux valgus, 866
Hamartomas, 62 , 893–894
Hamilton’s ruler test, 753
Hammer toes, 867
Hand gigantism, 797
Hand knee gait, 827
Hand–Schuller–Christian disease, 730
Hard chancre, 90
Hashimoto thyroiditis, 354
Head injuries, 213–219
Head raising test, 587
Head, neck and abdomen, 424
Headache, 199
Healing of cancellous bone fracture, 718–719
Healing of cortical (tubular) bone fracture, 718
Healing of fractures, 718–719
Hearing loss, 321t
Heartburn, 18
Heel knee shin test, 210
Heller’s operation, 25
Hepatoblastoma, 564
Hepatocellular carcinoma, 39 , 564–565
Hepatoma, 564–565
Hepatomegaly, 561
Hereditary spherocytosis, 570
Herniae (internal and external), 505
Herpetic lesions, 229
Hiatus hernia, 27
High arch foot, 865–866
High fistula, 592
High grade gliomas, 196–197
High stepping gait, 827
Hillsack’s lesion, 745
Hip joint, 814–815
Hirschsprung disease, 537
Histiocytoma (dermatofibroma), 70–71
History, 6–9
Hodgkin’s lymphoma, 137 , 571
Hollow organs, 553
Homan’s sign, 169 , 176
Hopping with either leg, 212
Horner syndrome, 210 , 365
Horseshoe kidney, 651
Hospital acquired pneumonia, 403–404
Housemaid’s knee, 851
Hutchison’s freckle, 63
Hydatid cyst of liver, 562–563
Hydrocele, 635–636
Hydrocephalus, 190–191
Hypernephroma, 657–659
Hyperpituitarism, 731
Hypertrophic scar, 69–70
Hypoglossal (XII) nerve, 208
Hypoplasia, 798
Hyposmia, 288
Hypospadias, 628–629 , 677
I
Ice-caloric test, 218
Idiopathic thrombocytopenic purpura, 570–571
Ileocaecal tuberculosis, 582
Iliac lymphadenopathies, 583
Impacted tooth, 258
Impacted wax, 303
Imperforate anus, 590
Impingement syndrome, 742–743
Implantation dermoid, 59 , 807–808
Incisional hernia, 616
Incomplete (funicular) hernia, 610
Indirect inguinal hernia, 610
Indirect laryngoscopy, 333–334 , 335t
Infantile haemangioma, 168
Infantile scurvy, 729
Infection of costal cartilages, 393–394
Infection of dorsum and dorsal spaces, 801
Infection of heel space, 886
Infection of volar spaces, 802
Infection of web space, 803 , 883
Infections of spleen, 568
Inferior dislocation, 820
Infertility, 706
Inflammation, 609
Inflammatory swellings, 55
Ingrowing toe nail, 887
Inguinal hernia, 610–612
Injuries during childbirth, 694
Injuries of abdominal organs, 553–556
Injuries of chest wall, 415–418
Injuries of duodenum, 555–556
Injuries of face, 264–273
Injuries of hands, 798–800
Injuries of kidneys and urinary bladder, 556
Injuries of large intestine, 556
Injuries of liver, 553–554
Injuries of lung parenchyma, 419
Injuries of mediastinal structures, 419–421
Injuries of mesentery, 555
Injuries of myocardium, 420
Injuries of nose, 276
Injuries of peripheral nerves, 905
Injuries of peripheral nerves of lower limb, 908
Injuries of peripheral nerves of upper limb, 905–908
Injuries of pleura, 418–419
Injuries of small intestine, 556
Injuries of soft tissues of foot, 881–882
Injuries of spinal cord, 468
Injuries of spleen, 554–555
Injuries of tarsal bones, 870–872
Injuries of thoracic aorta, 419–420
Injuries to bony and ligamentous spine, 455–456
Injuries to tendons, 806
Injury to penile skin, 629
Injury to the earlobe, 300
Innominate tortuosity and aneurysm, 383
Inspection of genitalia and perineum, 708
Intercondylar fracture, 757
Intercostal tenderness, 561
Interior view of knee joint, 839f
Internal fistula, 101
Internal hernia, 608
Internal ring occlusion test, 623
Intersphincteric fistulae, 593
Intervertebral discs, 452
Intestinal tuberculosis, 533–534
Intracranial aneurysms, 193
Intracranial lesions, 190–199
Intramuscular abscess, 895
Intussusception of colon, 574
Inverted papilloma, 284
Involucrum, 720
Irreducibility, 609
Irwin Moore sign, 324
Isolated fractures, 817
J
Jaundice, 34
Jaws, 263
Jeep driver’s bottom, 116
Jerky nystagmus, 210
Jobson Horne probe, 316
Joffroy’s sign, 371
Joint injuries, 719
Joint mouse, 849
Joints of the hand, 775–776
Juvenile laryngeal papillomatosis, 331
K
Kahn tests, 90
Kamath’s test, 587
Kasai operation, 35
Keloid, 69–70
Kenawy’s sign, 551
Keratinized epithelium, 590
Keratoacanthoma (molluscum sebaceum), 63
Keratosis obturans, 302
Kidney and renal pelvis, 651
Kienbock’s disease, 784
Killian’s speculum, 291
Klatskin tumour, 39
Klein’s sign, 496
Klippel Trenaunay syndrome, 167
Klumke’s paralysis, 905
Knee elbow test, 588
Knee joint (inner view), 839f
Knee joint, 838–840
Krukenburg tumour, 527 , 552
Kyphoscoliosis, 475
Kyphosis, 453 , 475
L
Laceration, 214
Lachman’s test, 860
Lahey’s method, 367
Langerhans cells, 180
Laryngocele, 378
Laryngomalacia, 331
Laryngoscope, 334
Larynx, 322–335
Lassegue’s sign, 483
Lateral popliteal nerve, 904
Lateral swellings of neck, 385t , 388t
Layers of epidermis, 181t
Le fort classification, 264–265
Leaking or dissecting aortic aneurysm, 509
Left lateral (modified sims’) position, 707
Leg raising test (carnett’s test), 587
Length of the lower limbs, 832
Lentigo, 63
Leprosy, 883 , 908–909
Lerische’s syndrome, 146
Lesions of larynx, 328t
Lesions of nose, nasal cavity and paranasal sinuses, 277t
Lesions of oral cavity presenting as swellings, 242t
Lesions of pharynx, 323t
Lesions of subcutaneous tissues, 78t
Lesions presenting with bad breath, 244t
Letterer Siwe disease, 730
Leukaemias, 571
Lhermitte’s sign, 485
Lichen sclerosis, 627
Ligaments of the spine, 452
Lilly technique, 38
Lingual thyroid, 351
Linitis plastica, 527
Lipoma, 73–74
Liposarcoma, 74–75
Lips, 246–248
Lisfranc fracture dislocation, 872
Liver abscess, 495–496
Low fistula, 592
Lobster hand, 795
Localized fibrous dysplasia, 734
Localized lesions of the labial mucosa, 247t
Locking and unlocking of the knee joint, 840
Looking at the ceiling test, 485
Loose bodies, 764
Lordosis, 453–454 , 475
Low grade gliomas, 195
Lucid interval, 216
Ludwig’s angina, 231
Lumbago, 471
Lumbar abscess and lumbar hernia, 577
Lumbar degenerative disease, 462–463
Lumbar hernia, 617–618
Lumbar plexus, 902
Lumbar spine, 452
Lumbosacral radiculopathy, 487
Lumps, 54–86
Lumps in the epigastrium, 572–577
Lumps in the hypogastrium, 585
Lumps in the iliac fossae, 580–585
Lumps in the left hypochondrium, 567–572
Lumps in the lumbar regions, 577
Lumps in the right hypochondrium, 561–567
Lumps in the umbilical region, 577–580
Lumps of abdominal wall, 561
Lung abscess, 404
Lung contusion/laceration, 419
Lungs, 391
Lupus vulgaris, 89–90 , 278
Luxatio in erecta, 745
Lymph cyst (cystic hygroma), 132–133
Lymph node swelling, 141t , 143t , 379–380
Lymph nodes, 124–125 , 126t , 139–143
Lymph nodes of neck, 276t
Lymph varix, 632
Lymphadenitis due to AIDS, 136–137
Lymphadenitis due to venereal infections, 136
Lymphadenopathy, 125 , 129t
Lymphangioma, 132 , 166 , 236
Lymphangiosarcoma, 132
Lymphangitis, 800–801
Lymphatic drainage, 125 , 127t , 128t
Lymphatic drainage of the ears, 298t
Lymphatic malformation, 166
Lymphatic malignancies, 571–572
Lymphatic system, 140t, 414
Lymphatics, 124
Lymphoedema of the tropics, 131–132
Lymphogranuloma, 631t
Lymphoma, 357
M
Macrochelia, 236
Macrodactyly, 797
Madelung’s deformity, 782–783
Madura foot, 117 , 882–883
Maduramycosis,, 117 , 882–883
Maisonneuve’s sign, 792
Malgaigne’s bulgings, 624
Malignancies of salivary glands, 341t
Malignancies of tonsils, 326–327
Malignancy of anal canal, 595–596
Malignancy of rectum, 595
Malignancy of transverse colon, 574
Malignant fistula of umbilical region, 110
Malignant lesions of oral structures, 238–239
Malignant otitis externa, 302
Malignant primary salivary tumours, 340–341
Malignant sinuses of chest wall, 108–109
Malignant swelling, 56t
Malignant tumors of small bowel, 50–51
Malignant tumours, 286–287 , 302–303 , 401–402
Malignant tumours of jaws, 240–241
Malignant tumours of ribs, 395
Malignant tumours of spine, 461–462
Mallet finger (baseball finger), 781
Mallory Weiss tears, 48
Mamillary fistula, 438
Mammary duct ectasia, 437–438
Mammary ridge or milk line, 425
Mandible examination, 272–273
Marjolin’s ulcer, 92
Martorell’s ulcer, 94
Mass descending per vagina, 705
Mastitis and cyclical mastalgia, 430
Match-stick test, 80
Maydl’s hernia (hernia en W), 612
Mayo’s repair, 615
McBurney point, 520
McMurray’s test, 860–861
McNeal’s zones, 673
Meatal stenosis, 677
Mechanism of formation of renal calculi, 660t
Mechanism of Volkmann’s ischaemic contracture, 785f
Meckel’s diverticulum, 609
Medial meniscal tears, 845f
Medial or lateral displacement of trochanter, 834
Medial popliteal nerve, 904
Median dermoid, 378–379
Median mental sinus, 105–106
Median nerve, 902
Median nerve injuries, 907–908
Mediastinal tumours, 408–410
Mediastinum, 391–392
Medullary carcinoma, 357
Medulloblastoma, 197–198
Melanocytes, 180
Melena, 46
Meleney’s ulcer, 91
Membranous lesions of tonsils, 325t
Membranous tonsillitis, 324
Menetrier’s disease, 573
Ménière’s disease, 310
Meningioma, 194
Meningitic pain, 473
Meningocele, 190 , 280
Meningocoele and meningomyelocoele, 465–466
Meniscal injuries, 845–846
Merciful anosmia, 288
Merkel’s cells, 180
Mesenteric cysts, 579–580
Metabolic effects of burns, 182
Metastatic liver disease, 40 , 565
Metastatic lung disease, 406
Metastatic lymph nodes, 40–41
Metastatic tumours, 341–343 , 728–729
Methods of determining the power of muscles of lower limb, 921t
Methods of determining the power of muscles of upper limb, 915–916t
Midface examination, 268–272
Midline swellings of neck, 375–379
Midline swellings of the neck, 384t , 387t
Mikulicz’s disease, 343
Mills manoeuvre, 773
Mirizzi’s syndrome, 492
Mobility of tympanic membrane, 318–319
Modified Rinne’s test, 321
Moebius’s sign, 371
Moles or naevi, 62–63
Mondor’s disease, 169
Mononeuropathy, 904t
Mononeuropathy multiplex, 904t
Monteggia fracture dislocation, 759
Morris’ bitrochanteric test, 834
Motor coordination, 208–210
Motor function, 210–212
Motor symptoms, 473
Movements of the hip joint, 815
Movements of the shoulder joint, 738
Mucocoele, 492
Mucocoele/pyocoele of gallbladder, 566
Mullerian duct anomalies, 692–693
Multiple myeloma, 727–728
Multiple tourniquets test, 178
Murphy’s kidney punch test, 688
Murphy’s sign, 492 , 521
Murphy’s syndrome, 490
Muscle power, 212
Muscle tone, 210–212 , 910t
Muscles, 893–899
Muscles acting on the elbow and their action, 755t
Muscles acting on the fingers, 776t
Muscles acting on the hip joint, 815t
Muscles acting on the shoulder joint, 740t
Muscles acting on the thumb, 776t
Muscles acting on the wrist, 775t
Muscular guard, 522
Musculocutaneous nerve, 900–901
Mycobacterium tuberculosis, 533–534
Myeloproliferative disorders, 571
Myofascial pain, 472
Myositis ossificans, 760
Myositis ossificans progressiva, 716
N
Naevi, 62–63
Naffziger’s sign, 371
Naffziger’s test, 485
Nasal cavities, 275
Nasal fractures, 277
Nasal glioma, 280
Nasal packing forceps (tilley’s forceps), 291
Nasal septal deviation, 279
Nasal septal haematoma and abscess, 280–281
Nasopharyngolaryngoscopy, 334
Nasopharyngoscopy, 295
Nature, 513–514
Nausea and vomiting, 540
Neck pain, 471
Necrotizing sialometaplasia, 234–235
Nelaton’s line, 832
Neoplasms, 355
Neoplastic, 476
Neoplastic swellings, 56
Nerve supply of ears, 297t
Neural tube, 189t
Neurocysticercosis, 192–193
Neurofibroma, 65
Neurogenic claudication, 471–472
Neurologic deficit, 471
Neurological illnesses, 200t
Neuropathic arthritis, 763 , 848 , 874
Noma/gangerene (cancrum oris), 231–232
Non-Hodgkin’s lymphoma, 137 , 571
Non-specific aortoarteritis, 148–149
Nonallergenic eosinophilic rhinitis, 282
Nonfracture lesions of shoulder joint, 741–745
Nontoxic goitre, 358
Nontraumatic articular esions of wrist and hand, 782–784
Nontraumatic lesions of ankle and foot, 872–874
Nontraumatic lesions of elbow joint, 761–764
Nontraumatic lesions of hip joint, 822–825
Nontraumatic lesions of knee joint, 846–850
Nontraumatic lesions of shoulder joint, 745–746
Nonurological causes of urinary incontinence, 684t
Normal pressure hydrocephalus, 198–199
Normal range of movements at the elbow, 771t
Normal square pelvis, 831f
Nose, 275
O
Obstipation, 513
Obstruction, 609
Obstructive appendicitis, 489
Obstructive jaundice, 34
Obturator hernia, 616–617
Obturator nerve, 903
Obturator test, 522
Occlusion of dental arches, 262–263
Ochronotic arthritis, 848
Ochsner’s clasping test, 915–916t , 920
Oculomotor (III) nerve, 203–204
Oesophageal injuries, 420–421
Oesophageal malignancy, 23–24
Oesophageal varices, 48
Olecranon bursitis, 765
Olfactory (I) nerves, 202
Onychogryposis, 887
Open bite, 242
Open injuries, 553
Optic (II) nerves, 202–203
Oral candidiasis, 234
Oral hygiene, 262
Oral manifestation of anaemia, 241
Oral mucosa, 248–250
Oral submucous fibrosis (OSMF), 233–234
Oriental sore (delhi boil), 91
Ortolani’s test, 836
Oschner Scherren regime, 492
Osgood–Schlatter disease, 850–851
Osophageal atresia, 19
Osteitis deformans (Paget disease), 732–733
Osteoarthritis, 762–763 , 783–784 , 823–824 , 847 , 873
Osteochondritis (Perthe’s disease), 824
Osteochondritis dissecans, 763–764 , 849
Osteochondritis juvenilis, 733–734
Osteochondritis of navicular bone (Kohler’s disease), 874
Osteochondritis of talus, 874
Osteochondroma, 722–723
Osteogenesis imperfecta, 713–714
Osteoid osteoma, 734
Osteoma, 302 , 722
Osteomalacia, 730
Osteomyelitis of ribs, 108
Osteomyelitis of sternum, 394
Osteosarcoma, 724–725
Otitic labyrinthitis, 309
Otitis externa, 301–302
Otitis media with effusion, 305
Otosclerosis, 307–308
Otoscope, 315
P
Paget Shroetter syndrome, 150 , 171
Paget’s disease of breasts, 436
Paget’s disease of penis, 632
Paget’s recurrent fibroid, 64
Paget’s test, 80
Pain, 618
Pain in the ear, 312
Pain in the throat, 332
Pain localized in the neck, 472
Pain of anxiety, 472–473
Pain of chronic instability, 472
Palate, 257–258
Palmar radiocarpal ligament, 774
Palmar ulnocarpal ligament, 774
Palmar warts, 808
Palpation of lip lesion, 248
Pancreatic malignancy, 531–533
Pancreatic pseudocyst, 575
Pantaloon hernia (dual hernia/saddle bag hernia), 610
Papillary carcinoma, 356
Papilloma, 61–62 , 670
Papilloma larynx, 329
Para aortic lymphadenopathy, 576–577
Paracusis of Willis, 311
Paralytic ileus, 505–506
Paranasal sinuses, 275–276
Parapharyngeal abscess, 325
Paraphimosis, 628
Paraplegia, 559t
Paraplegic gait, 212
Parasitic diseases, 42–43
Parathyroid osteodystrophy (hyperparathyroidism), 730
Paraumbilical hernia, 615
Parkinsonian gait, 212
Parosmia, 288
Parotid fistula, 103
Parsonage–Turner syndrome, 905
Passage of blood in urine, 556
Passage of blood in vomitus (haematemesis), 556
Passage of blood per rectum (melena), 556
Passage of bloodstained stools, 514
Patellar tap, 857
Patent vitello-intestinal duct, 109
Paterson-Kelly syndrome, 25–26
Pathophysiology of burns, 181
Patterns of fracture, 717–718
Patterns of muscle weaknesses, 911t
Patterns of muscular weakness, 910t
Peau d’orange, 433
Pectus carinatum, 393
Pectus excavatum (funnel chest, cobbler’s chest), 393
Pel-Ebstein fever, 137 , 571
Pellegrini–Stieda disease, 851–852
Pelvic abscess, 584–585
Pelvic inflammatory disease, 694–695
Pelvis square, 830
Pemberton’s sign, 365
Pen test, 920
Pendular reflex, 925t
Penis, 625
Penoscrotal transposition (bifid scrotum), 641
Perforations, 306
Perforations of tympanic membrane, 319f
Perforators, 163–164
Periampullary carcinoma, 40
Perianal haematoma, 597–598
Perichondritis, 300
Perineal hernia, 618
Perinephric abscess, 655–656
Peripheral (labyrinthine) vertigo, 313t
Peripheral nerves, 900–929
Peripheral nerves of brachial plexus, 900–902
Peripheral nerves of lumbar plexus, 902–903
Peripheral nerves of sacral plexus, 903–904
Peristalsis, 82 , 519
Peritonsillar abscess, 326
Permanent teeth, 259t
Perthe’s test, 179
Pes cavus, 865–866
Pes planus, 865
Peyronie’s disease, 633
Phalen’s test, 486 , 792
Pharyngeal fistula, 106–107
Pharyngeal pouch, 323 , 377–378
Pharyngitis, 323–324
Pharynx, 322–335
Pharynx and larynx, 258
Phimosis, 627
Phlegmasia alba dolens, 170
Phlegmasia cerulea dolens, 170
Physiological response of female genital tract, 692
Physiology of breasts, 426
Physiology of menstruation, 692f
Phytobezoar, 500
Pierre Robin’s syndrome, 224
Pilonidal sinus, 116
Pinching test, 79
Pituitary adenoma, 194
Pivot shift test, 860
Plantar fasciitis, 887 , 895
Plantar warts, 885
Plaque, 256
Pleomorphic adenoma, 339–340
Pleura, 389
Pleural effusion, 396–397
Pleural space, 390
Pleural tumours, 397–399
Pleurisy, 395–396
Plexiform or cirsoid haemangioma, 58
Plummer-Vinson syndrome, 25–26
Plunging ranula, 378
Pneumothorax, 397 , 418
Poland syndrome, 427
Polycystic kidney, 652
Polycystic ovarian disease, 703
Polydactyly, 797
Polymazia (polymastia) and polythelia, 427–429
Polyosteotic fibrous dysplasia, 731–732
Polyps, 595
Polyps of uterine cervix and endometrium, 697
Polytrauma, 929–934
Popliteal aneurysm, 153–154
Popliteal cysts, 851
Porphyrias, 571
Portal hypertension, 569
Portwine stain, 58
Positions of vocal cords, 331t
Post anal dermoid, 591–592
Post auricular dermoid, 56
Post operative lymphoedema, 130
Post phlebitic syndrome, 170–171
Posterior dislocation, 820
Posterior dislocation of elbow joint, 759–760
Posterior drawer test, 860
Posterior horn tear, 845
Posterior rhinoscopy, 295f
Posterior urethral valves, 677
Postmenopausal bleeding, 705
Postnasal mirror, 291
Postoperative gastrointestinal fistulae, 110–112
Postoperative sinus (mesh), 114
Postoperative sinus (midline), 110
Postoperative sinus (sternal region), 107
Postoperative urinary fistulae, 112
Pott’s disease, 552t
Pott’s fracture, 867
Pouch of douglas, 527t , 552 , 589
Pratt’s test, 179
Pre-hospital communication, 930
Preauricular sinus, 103
Predisposing conditions of intraoral malignancies, 238t
Predisposing factors for hernia, 608
Prepatellar bursitis, 851
Presbycusis, 309
Pressure from extrinsic pathologies, 28–29
Primary chancre, 631t
Primary lymphatic malignancies, 137–138
Primary lymphoedema, 129–130
Primary malignancy, 432–436
Primary sclerosing cholangitis, 38–39
Proclination, 242
Proctoscopy, 606
Prolapse of rectum, 598–599
Pronator syndrome, 804
Prostate, 673
Prostatic calculi, 676
Prostatic pain, 682–683
Pruritus vulvae, 705
Pseudoclaudication, 155
Pseudotumour cerebri, 198
Pseudotumours, 62
Psychogenic pain, 472
Puddle sign, 551
Pudendal nerve, 903
Pulled elbow, 764
Pulmonary agenesis/hypoplasia, 403
Pulmonary embolism, 407–408
Pulmonary tuberculosis, 404–405
Pulp vitality tests, 262
Pulsations, 157t , 158f , 159f
Pulseless disease, 149
Pump handle test, 486
Punctum, 68
Pupillary reactions, 218f
Pyocoele, 637
Pyogenic abscess of liver, 562
Pyogenic arthritis, 745 , 761–762 , 783 , 822 , 846 , 872–873
Pyogenic infections, 459
Pyogenic infections of dorsum of foot, 882
Pyonephrosis, 655
Pyramidal lobe, 349
Q
Quadrants of tympanic membrane, 318f
Quadriceps gait, 827
Queyrat’s erythroplasia, 632
Quinsy, 326
R
Raccoon eyes, 268
Radial collateral ligament, 775
Radial nerve, 901–902
Radial nerve injuries, 906
Radial ray, 795 , 798
Radiation burns, 180
Radiation enterocolitis, 49–50
Radiculopathy, 472
Ramhorn penis, 134 , 632
Ramstedt’s operation, 574
Range of movement at various joints of hand, 776t
Range of movements of the hip, 831t
Range of movements of the inferior radioulnar joint, 791t
Range of movements of the knee, 858t
Range of movements of the radiocarpal joint, 791t
Ranula, 225–226
Raynaud’s phenomenon, 155
Raynaud’s syndrome, 161
Rebound test, 208
Recognition of emergency situations, 219
Rectal examination, 601–602
Rectovaginal examination, 712
Rectus sheath haematoma, 578
Recurrent anterior dislocation, 744–745
Recurrent appendicitis, 533
Recurrent subluxation of ankle, 869
Red lesions of the tongue, 251t
Red-currant jelly, 502
Reducibility, 83 , 609f , 621–623
Reed Sternberg cell, 137
Referred pain, 471
Referred pain from extrinsic disorders, 472
Reflexes of lower limb and methods of eliciting them, 925t
Reflexes of upper limb and methods of eliciting them, 924t
Reflux oesophagitis, 21
Regimental badge area, 901 , 906
Reinforcement, 911t
Reinkie’s oedema, 328
Relative afferent pupillary defect, 218
Renal aplasia, 651
Renal calculi, 660–661
Renal cell carcinoma, 657–659
Renal ectopia, 651–652
Renal injuries, 654–655
Renal pain, 682
Renal tuberculosis, 656–657
Respiratory tract, 391
Rest pain, 147 , 155
Retention of urine, 684
Retractile testis, 635
Retroperitoneal swellings, 580
Retrosternal ectopic/accessory thyroid, 352
Retrosternal goitre, 379
Reverse colles, 774
Rhabdomyoma, 896
Rhabdomyosarcoma, 896–897
Rheumatoid arthritis, 459–460 , 568–569 , 746 , 762 , 783 , 822–823 , 846–847 ,
873
Rhinitis, 281
Rhinolith, 285
Rhinophyma, 278
Rhinosporidiosis, 282–283
Rib anomalies, 392
Rib fractures, 415
Richter’s hernia, 612
Rickets, 729–730
Riedel’s thyroiditis, 355
Rinne’s test, 321
Rodentulcer, 66 , 92
Romberg test, 207
Root pain, 471
Rotator cuff injuries, 743
Rovsing sign, 521–522
Rule of hand, 186
Rupture of calcaneal tendon, 870
Rupture of lateral ligaments, 869
Rupture of lutein cyst, 509–510
Rupture of quadriceps apparatus, 850
Rupture of rectus abdominis muscle and rectus sheath haematoma, 511
Rupture of tendons and fasciae, 894–895
Ruptured ectopic gestation, 506–507
S
Sacral plexus, 903
Sacroiliac ligamentous strain, 465
Salivary calculi, 343–344
Salivary fistulae, 344
Salivary gland neoplasms, 339
Salivary gland tumours, 237
Salivary glands, 336–348
Salmon patch, 58
Sarcoidosis, 406–407
Sarcoma, 68
Saturday night palsy, 906
Scalp injuries, 216
Schatzki’s ring, 27–28
Schirmer’s test, 206
Schwannoma, 65–66
Schwartz test (percussion or tap sign), 177
Sciatic hernia, 617
Sciatic nerve, 903–904
Sciatic nerve injuries, 908
Sciatica, 471
Scissoring gait, 827
Scleroderma, 24–25 , 152
Scoliosis, 454 , 475
Scrotal abscess, 642–643
Scrotal haemangioma, 641–642
Scrotal laceration, 642
Scrotum, 625 , 626
Sebaceous cyst, 68–69 , 643–644
Seborrhoic wart (seborrhoic keratosis), 71
Secondary metastatic lymphadenopathy, 138–139
Seizures, 199
Senile osteoporosis, 733
Sensorineural deafness, 311t
Sensory symptoms, 473
Sensory-ataxic gait, 212
Sentinel loop sign, 508
Sentinel pile, 598
Sequestration dermoid, 56
Sequestrum, 105 , 720
Sever’s disease, 874–875
Sexually transmitted diseases, 695–696
Sexually transmitted diseases of anus and rectum, 599
Sharp, blunt or penetrating injuries of rectum, 592
Sherren triangle, 520–521
Shift, migration and referred pain, 512
Shifting dullness, 86 , 551f
Shoemaker’s lines, 833f , 834
Short limb gait, 827
Short saphenous vein, 163
Shortening below the trochanteric level, 834
Shoulder joint, 737–738
Sialadenosis/sialosis, 343
Sialectasis, 338
Sickle cell anaemia, 570
Siegalization, 319
Siegel’s speculum, 315
Sigmoid volvulus, 504–505
Sign de dance, 502
Signs of life-threatening thoracic conditions, 931t
Simple ganglion, 784
Simple nasal polyps, 283
Simple tenosynovitis, 806
Sims’ position, 603
Sinus, 100
Sinus due to retained foreign body, 117–118
Sinuses and fistulae, 100–121
Sister Mary Joseph’s nodules, 527 , 545
Site of true shortening, 832–834
Sjögren’s syndrome, 343
Skeletal system, 448
Skin discolourations, 11t
Skin tag, 61–62
Sliding hernia (hernia en glissade), 612
Slip sign, 74
Slipped upper femoral capital epiphysis, 824–825
Slow flow anomalies, 167
SLR test, 482 , 486
Sluder neuralgia, 279
Small bowel tumours, 579
Small intestinal fistulae of right iliac fossa, 114
Small or large breasts, 429
Smith fracture, 774
Smooth mole, 62
Snapping hip, 825
Soft chancre (chancroid), 91
Soft palate, 258
Soft tissue injuries of ankle joint, 869–870
Soft tissue injuries of knee joint, 844–846
Solar keratosis (intra epidermal carcinoma), 63–64
Solid organs, 553
Solid tumours of omentum, 574–575
Solitary bone cyst, 734
Solitary caecal diverticulitis, 583
Solitary rectal ulcer, 599
Spacing, 242
Speech discrimination score, 321
Speech reception threshold, 321
Spider naevus, 58
Spigelian hernia, 615–616
Spina bifida occulta and diastematomyelia, 467
Spinal accessory (XI) nerve, 208
Spinal column, 450–451
Spinal cord, 451
Spinal cord tumours, 469–470
Spinal deformity, 471
Splenic abscess, 572
Splenic cyst, 572
Splenomegaly, 567
Spondylitic pain, 472
Spondylolisthesis, 463–465
Spondylosis (osteoarthritis), 463
Spontaneous rupture, 554
Squamous cell carcinoma (epidermoid carcinoma), 67
Squamous cell carcinoma, 92
Squamous cell papilloma, 61–62
Stance and gait, 212
Steeple’s sign, 331
Stellwag’s sign, 371
Stenosing tenosynovitis, 807 , 895
Steoarthritis, 745
Steppage gait (foot drop), 212
Sternal fracture, 417–418
Sternomastoid tumour, 381
Stiff hip gait, 827
Strain, 741–742
Strain of lateral ligament, 869–870
Strangulation, 609
Strangury, 514
Strawberry angioma, 58
Striae gravidarum, 518
Strictures (tubercular or malignant), 503
Strictures of oesophagus, 19–20
Stridor, 332 , 369
String sign of Kantor, 535
Stroboscopy, 334
Structure of skin, 181f
Structure of testis, 626f
Structures related to the knee joint, 839t
Subacromial disorders, 742–744
Subacute lymphocytic thyroiditis and postpartum thyroiditis, 354
Subcapsular, 554
Subclavian aneurysm, 383
Subclavian steal syndrome, 151
Subglottic stenosis, 331
Subhyoid bursa, 376
Sublingual dermoid, 56
Subluxation, 741–742
Submandibular salivary fistula, 105
Submental lymph node, 375–376
Subungual exostoses, 888–889
Subungual haematoma, 803–804 , 887
Succussion splash, 547
Sudeck’s atrophy (reflex sympathetic osteodystrophy), 786
Sunset sign, 191
Superficial peroneal nerve, 904
Superficial phlebitis migrans, 168–169
Superficial thrombophlebitis, 168–169
Superficial venous system, 162–163
Supernumerary fingers, 797
Suppurative thyroiditis, 353
Supracondylar fracture, 756–757
Suprasphincteric fistulae, 593
Supraspinous tendinitis, 895
Surgical anatomy of arterial system, 144
Surgical anatomy of brain, 188–190
Surgical anatomy of breast, 425–426
Surgical anatomy of ear and auditory canal, 297
Surgical anatomy of face, 221
Surgical anatomy of facial skeleton, 264
Surgical anatomy of female genital tract, 690–692
Surgical anatomy of foot, 880–881
Surgical anatomy of forearm bones, 755
Surgical anatomy of hands, 793–795
Surgical anatomy of male genitalia, 626
Surgical anatomy of neck, 375
Surgical anatomy of nerves of lower limb, 902–904
Surgical anatomy of nerves of upper limb, 900–902
Surgical anatomy of oral structures, 222–223
Surgical anatomy of penis, 626f
Surgical anatomy of pharynx and larynx, 322–323
Surgical anatomy of rectum and anal canal, 590
Surgical anatomy of spine and spinal cord, 450–452
Surgical anatomy of thorax, 390–392
Surgical anatomy of thyroid, 349
Surgical anatomy of venous system, 162–164
Surgical emphysema, 418
Surgical jaundice, 34
Swan neck deformity, 799
Swelling, 54–87 , 471 , 618
Swellings of gingiva, 233t
Swellings of the floor of the mouth, 254t
Swellings of the skin, 77t , 85t
Swellings of the subcutaneous plane, 86t
Symptoms of ankle, foot and toe pathologies, 876
Symptoms of anorectal pathologies, 599–601
Symptoms of breast diseases, 439
Symptoms of chest injuries, 421
Symptoms of diseases of female genital tract, 703
Symptoms of diseases of male genitalia, 644
Symptoms of elbow joint pathologies, 767
Symptoms of hernia, 618–619
Symptoms of hip joint pathologies, 826–828
Symptoms of injuries of abdominal organs, 556
Symptoms of knee joint pathologies, 853
Symptoms of oral cavity pathologies, 241–243
Symptoms of pathologies of bones, 734–735
Symptoms of pathologies of chest, 410–411
Symptoms of pathologies of feet, 889
Symptoms of pathologies of hands, 810
Symptoms of pathologies of pharynx and larynx, 332
Symptoms of pathologies of wrist, hand and fingers, 786–787
Symptoms of patients with acute abdomen, 511–514
Symptoms of patients with chronic abdominal illnesses, 540–541
Symptoms of peripheral nerve pathologies, 909–912
Symptoms of salivary gland diseases, 344
Symptoms of shock, 556
Symptoms of shoulder joint pathologies, 747–748
Symptoms of urinary tract pathologies, 681–685
Syndactyly, 796–797
Syphilitic osteomyelitis, 721–722
Syphilitic ulcer, 90
T
Talipes calcaneo valgus, 865 , 908
Tandem hopping, 210
Tandem walking, 210 , 211
Tanjot’s sign, 544
Tarsal tunnel syndrome, 875
Taxis, 621–623
Teeth, 258–263
Tendoachilles, 870
Tendons, 893–899
Tenesmus, 514
Tennis elbow, 764–765
Terminal pulp space infection, 802 , 885
Testicular sinus, 115
Testicular tumour, 638–639
Testis, 625
The external (superficial) ring, 609
The internal (deep) ring, 609
Thermal burns, 180
Thomsen’s test, 772
Thoracic actinomycosis, 108
Thoracic and lumbar spondylosis, 463
Thoracic outlet syndrome, 149–151 , 382–383
Thoracic spine, 452
Thorax, 389–414
Three finger tap test, 81
Thrombosed piles, 597
Thudicum’s nasal speculum, 291
Thymic swelling, 379
Thyroglossal cyst/sinus/fistula, 106 , 350
Thyroglossal cyst, 376
Thyroid cork phenomenon, 365
Thyrotoxicosis, 359
Tibial nerve, 904
Tibial nerve injuries, 908
Tietze’s syndrome, 394
Tillaux’s triad, 580
Tinea pedis, 888
Tinea unguium, 888
Tinel’s sign, 792
Tinnitus, 313
Toe wriggling, 212
Tongue, 250–254
Tongue depressor, 291
Torsion of mesenteric cyst, 510
Torsion of omentum, 510–511
Torsion of ovarian cyst, 510
Torsion of testis, 639–640
Torticollis, 475
Torus, 227
Tourniquet test, 570
Toynbee manoeuvre, 319
Trachea, bronchi and lungs, 389–390
Tracheal stenosis, 399
Tracheo-oesophageal fistula, 399–400
Tracheobronchial tree, 391
Transcapsular, 554
Transient synovitis of hip (observation hip), 822
Transillumination, 81
Transillumination test, 646
Transitional cell carcinoma/squamous cell carcinoma of renal pelvis, 659–660
Transmitted pulsations, 82
Transsphincteric fistulae, 593
Trauma reception team, 930–931
Trauma to tympanic membrane, middle ear and temporal bone, 304
Traumatic articular lesions of wrist and hand, 776–779
Traumatic diseases - inner ear, 308–309
Traumatic fat necrosis, 429
Traumatic lesions (fractures), 740–741
Traumatic lesions of ankle joint, 867–869
Traumatic lesions of carpal bones, 779–780
Traumatic lesions of elbow joint, 756–761
Traumatic lesions of knee joint, 842–844
Traumatic lesions of metacarpal bones, 780
Traumatic lesions of pelvis and hip, 817–821
Traumatic lesions of phalanges, 781–782
Traumatic orchitis, 636
Traumatic swellings, 55
Trendelenburg test, 836–837
Triangles of the neck, 376t
Tricho phytobezoar, 500
Trichobezoar, 500
Trigeminal (V) nerve, 204–205
Triple a syndrome, 25
Trochanteric bursitis, 825
Trochlear (IV) nerve, 203–204
Troisier’s sign, 552 , 552f , 587 , 589
Trophic ulcer, 93–94
Tropical ulcer, 94
Trousseau’s sign, 527t , 532
Tuberculoma of brain, 192
Tuberculosis, 232
Tuberculosis of breasts, 431
Tuberculosis of genital tract, 694
Tuberculosis of omentum, 574
Tuberculosis of spinal cord, 469
Tuberculosis of spine (pott’s disease), 456–457
Tuberculous arthritis, 746
Tuberculous arthritis of hip, 823t
Tuberculous lymphadenitis, 134–136
Tuberculous osteomyelitis, 721
Tuberculous sinus (Pott’s spine), 113–114
Tuberculous sinus, 107
Tuberculous sinus of chest wall, 108
Tuberculous ulcer, 88–89
Tumours of muscles, 381–382
Tuning fork tests, 321
Tuning forks, 315
Types of dentition, 259t
Types of discharges from intraoral pathologies, 242t
Types of fracture, 716–717 , 717f
U
Ulcerative colitis, 535–536
Ulcers, 87–99
Ulcers on the labial mucosa, 248t
Ulnar collateral ligament, 775
Ulnar nerve, 902
Ulnar nerve injuries, 907
Ulnar ray, 795
Ulnar ray hypoplasia, 798
Ulnar tunnel syndrome, 907
Umbilical granuloma/enterotoma, 577–578
Umbilical hernia, 615
Umbilical sinus, 109
Uncomplicated hernia, 611–612
Unconsciousness, 213
Undescended testis, 634–635
Unsegmented bar, block vertebra, 455
Unstable hip gait, 827
Unterberger test, 207
Upper limb root tension test, 485
Urachal abnormalities, 667–668 , 668f
Urachal sinus and fistula, 109
Ureteric calculi, 666
Ureteric colic, 682
Ureteric duplications, 662
Ureteric injuries, 663–664
Ureteric obstructions, 664–666
Ureteric pain, 682
Ureteric tumours, 664
Ureters, 661
Urethra, 625 , 676
Urethral calculi, 681
Urethral carcinoma, 681
Urethral caruncle, 680
Urethral diverticulum, 679
Urethral duplication, 678
Urethral fistula, 115–116
Urethral injuries, 679
Urethral pain, 683
Urethral stricture, 678
Urinary bladder, 666–667
Urinary bladder pain, 682
Urinary fistulae of loins, 112
Urinary incontinence, 684
Urinary symptoms, 511
Urinary system, 650–689
Urological causes of urinary incontinence, 684t
Uterine myomas, 696–697
Uterine prolapse, 701
V
Vagus (X) nerve, 207–208
Valgus (abduction) stress test, 859–860
Valsalva manoeuvre, 319
Van der Woude’s syndrome, 224
Variants of hydrocele, 636f
Varicocele, 639
Varicose veins, 171–172
Varieties of malocclusion, 262t
Varus (adduction) stress test, 859–860
Vascular disorders, 470
Vascular injuries, 216
Vascular malformation, 49 , 168t
Vasculitis, 151–152
Velo-cardio-facial syndrome, 224
Venereal diseases, 631
Venereal warts, 630–631
Venereum, 631t
Venous (varicose) ulcers, 92
Venous gangrene, 170
Venous haemodynamics, 164–165
Venous malformation, 165
Venous system, 162–179
Venous thrombosis, 168–171
Venous ulcer, 172–173
Ventral herniae, 614–616
Verrucous carcinoma, 239–240
Vertebra, 451
Vertical nystagmus, 210
Vestibular neuronitis, 310
Vestibulitis, 281
Vestibulo-cochlear (VIII) nerve, 207
Video endolaryngoscopy, 334
VIII nerve schwannoma, 195
Villonodular synovitis, 746
Virchow’s nodes, 23 , 527 , 552 , 587 , 589
Virchow’s triad, 169
Visible gastric peristalsis, 519
Visible intestinal peristalsis, 519
Visual field defects, 203t
Vocal cord paralysis, 330–331
Vocal nodules, 330
Volkmann’s ischaemic contracture, 785–786
Volkmann’s sign, 785 , 792
Volvulus, 504
Volvulus of the midgut, 505
Vomiting, 511 , 513–514 , 618
Von Graefe’s sign, 371
Von Recklinghausen’s disease, 65
W
Wallace’s rule of nine, 186
Wangensteen–Rice invertogram, 591
Wart, 61
Warthin’s tumour (adenolymphoma), 340
Wassermann reaction, 90
Weber test, 321
Wedge and hemivertebra, 455
Werner’s classification, 371–372
Whipple’s procedure, 39 , 533
White cell trapping theory, 172
White leg, 170
White lesions, 233
Whittle’s circular illustration, 827f
Wilms’ tumour (nephroblastoma), 657
Wrist drop, 906
Wrist joint, 774
Z
Zenker’s diverticulum, 26
Zieman test, 623–624

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Clinical

S. Devaji Rao MS MNAMS FICS

2.4 Doctor-patient relationship

2.5 Examination of the patient

2.6 Frank communication

2.8 Management of patients in the hospital

2.9 Maintenance of records

2.10 Surgical ethics

2.11 Informed consent

3.2 Chief complaint*

3.3 History of present illness

3.4 Previous history of present complaint

3.5 Past medical history

3.6 History of drug intake and allergies

3.7 Social and personal history

3.8 Family history

3.9 History of immunization

3.10 Analysis of symptoms

3.11 Examining a child

3.12 Difficulties in history taking

4.2 At the time of patient’s entry or separately

4.3 Eliciting history

4.4 Height and weight measurements

4.5 Examination of the patient on the couch

4.6 General system examination

4.7 Method of general physical examination

2. Symptoms and Signs

5.2 Surgical anatomy of oesophagus

5.3 Causes of dysphagia

5.4 Diseases of oesophagus

5.5 Clinical evaluation

6.2 Pathophysiology of constipation

6.3 Etiology of constipation

6.4 Organic causes of constipation

6.5 Clinical evaluation

7.3 Anatomy of biliary system

7.4 Obstructive jaundice

7.5 Causes of obstructive jaundice

7.6 Clinical evaluation

8.2 Causes of gastrointestinal haemorrhage

8.3 Pathological conditions

8.4 Clinical evaluation

9. Lumps and swellings

9.3 Swellings of skin

9.4 Swellings of subcutaneous tissue

9.5 Clinical evaluation

10.2 Parts of ulcer

10.3 Classifications of ulcers

10.4 Traumatic ulcers

10.5 Inflammatory ulcers

10.6 Vascular ulcers

10.8 Miscellaneous ulcers

10.9 Clinical evaluation

11. Sinuses and fistulae

11.2 Aetiological classification of sinuses

11.3 Aetiological classification of fistulae

11.4 Regional classification of sinuses and fistulae

11.5 Sinuses and fistulae of parotid region

11.6 Sinuses and fistulae of mandibular and submandibular regions