1.

Thoracic outlet syndrome:

Definition:
Thoracic outlet syndrome is an umbrella term for conditions involving the
compression of neurovascular structures (e.g., the brachial plexus or the
subclavian artery or vein) as they exit the thoracic outlet (Scalene triangle bound
by scalene anticus, scalene medius and 1st rib).

Types:
1. Neurogenic TOS is the most common type and involves the compression of
the brachial plexus, leading to neck pain and numbness and tingling in the
fingers.
2. Arterial TOS involves compression of the subclavian artery and presents
with pain, pallor, coldness, and pulselessness in the affected arm, especially
during overhead activities.
3. Venous TOS results in pain, cyanosis, and swelling of the arm

Etiology:
- Cervical rib (MC)
- Scalene muscle hypertrophy.
- Scalene minimus.
- Abnormal bands and ligaments.
- Fracture clavicle or first rib.

Clinical Features:
Clinical features of TOS depend on the anatomic structure affected by
compression and are more pronounced during and after overhead activity.
1. Compression of parts of the brachial plexus:
- Sensory loss or paresthesia (follows the distribution of the ulnar nerve)
- Pain in the neck and arm
- Gilliatt-Sumner hand: atrophy of intrinsic hand muscles, including the thenar,
hypothenar, lumbrical, and interossei muscles

2. Compression of the subclavian vein:

- Swelling
- Diffuse hand or arm pain
- Risk of thrombosis of the arm

3. Compression of the subclavian artery:

○ Mild arm ache and fatigue
○ Pulselessness, pain, pallor, paresthesia, and poikilothermia
○ ↓ Blood pressure of > 20 mm Hg in the affected arm compared to the
contralateral arm
○ Ischemia can lead to ulcerations and gangrene of the affected arm.

Tests of TOS:
A) Adson’s test: palpate the radial pulse, ask patient to turn head to affected side
and take deep inspiration and feel for weakening of radial pulse
B) Allen’s test: For patency of radial and ulnar arteries

Investigations:
● X-Ray Neck & cervical spin
● CT Neck
● Nerve Conduction Studies/Electromyography
Treatment:
Conservative—if nerve velocity is > 60 m/second
Surgical—if nerve velocity is < 60 m/second

Conservative & Medical treatment for TOS

. Exercises—neck stretching, postural and breathing exercises
. Drugs—analgesics, muscle relaxants, antidepressants
. Avoid weight lifting
. Physiotherapy
 Surgical treatment of TOS
. Transaxillary (ROOS)—mainly for first rib excision and also
cervical rib
. Supraclavicular approach for cervical rib and soft tissue excision,
scalenotomy, neurolysis, arterial reconstruction
. Cervical sympathectomy may be needed

2. ARTERIOVENOUS FISTULA (AVF)

Introduction
It is an abnormal communication between an artery and vein.

Types
A. Congenital—is arteriovenous malformation.
B. Acquired (Trauma is common cause).

A. Congenital Arteriovenous Malformation (Fistula)

During the developmental period AV communications occur.

Sites
1. Limbs, either part or whole of the limb is involved. It may be localised to toes or fingers.
2. Lungs, liver, brain—in circle of Willis.

B. Acquired Arteriovenous Fistula (AVF)

Etiology
1. Trauma in (most common cause):
Sites
Femoral region
Popliteal region
Brachial region
2. Surgical- in patients with CKD
Pathophysiology
1. Physiological changes: Cardiac failure due to hyperdynamic circulation.

2. Structural changes:

Changes at the Level of Fistula

Blood flows from high pressure artery to low pressure vein causing diversion of most of the
blood.
Between the artery and vein, at the site of fistula, dilatation develops with formation of fibrous
sac called as aneurysmal sac.
This presents as warm, pulsatile, smooth, soft, compressible swelling at the site with continuous
thrill and continuous machinery murmur.

Changes Below the Level of the Fistula

Because of diversion of arterial blood distal part becomes ischaemic.
Because of high pressure arterialisation of veins and valvular incompetence occurs causing
varicose veins.

Changes Proximal to the Fistula

Hyperdynamic circulation causes cardiac failure. Cardiac failure may be very severe in traumatic
AVF (often resistant to drug therapy).

If pressure is applied to the artery proximal to the fistula, swelling will reduce in size, thrill and
bruit will disappear, pulse rate and pulse pressure becomes normal. This is called as
Nicoladoni’s sign or Branham’s sign.

Sequelae / Complications:
1. Haemorrhage
2. ™Thrombosis
3. ™Cardiac failure (CCF) -Because of the hyperdynamic circulation, there is increased
cardiac output

Clinical Features
1. Limb is lengthened due to increase in blood flow since developmental period.
2. Limb girth is also increased.
3. Limb is warm.
4. Continuous thrill and continuous machinery murmur all over the lesion.
5. Dilated arterialised varicose veins are seen due to increased blood flow and also due to
valvular incompetence.
6. Often there is bone erosion or extension of AVF into the bone as such
7. hyperdynamic circulation.
Investigations
1. CT/MR angiogram is ideal.
2. Doppler study.

Treatment
1. Conservative— compression, avoiding injury.
2. Minimally invasive surgery- sclerotherapy
3. Surgery—
Indications for surgery:
Absolute: Haemorrhage, ischaemia, CCF.
Relative: Pain, functional disability, cosmesis, limb asymmetry.
Emergency: Torrential bleeding usually after trauma (example—road traffic accidents).

A) Surgical ligation of feeding vessels and complete excision of the lesion. Often if
lesion is extending into deeper planes it is technically difficult; but with usage of
tourniquet, careful meticulous dissection and ligation of all vessels will lead into
successful excision of entire lesion.

B) Therapeutic embolisation/preoperative embolisation hasten the proper surgical

excision.

C) Occasionally when extensive AVM is present often involving the entire limb,
amputation is the final option left as a life-saving procedure.
 3. Endoscopic ultrasound:
INTRO - IT IS AN ENDOSCOPY WHERE A USG PROBE IS ATTACHED AT THE TIP OF ENSOSCOPE
THUS ALLOWING IMAGING OF GI TRACT LAYERS AND ADJACENT STRUCTURES.

TYPES -a) RADIAL ENDOSONOGRAPHY - CIRCULAR IMAGE FORMED WITH ENDOSCOPE AT

THE CENTRE
b) LINEAR ENDOSONOGRAPHY - A SECTORAL IMAGE FORMED. IT IS USED FOR
TAKING IMAGE GUIDED BIOPSY

INDICATIONS-
Diagnostic
1) T AND N STAGING OF GI CANCERS
2) TRUS WITH BIOPSY DONE FOR DIAGNOSIS OF PROSTATE CA
3) DIAGNOSIS OF GI WALL SUBMUCOSAL LEISIONS LIKE GIST(IMAGE GUIDED BIOPSY CAN BE
TAKEN)
4) ENDOSCOPIC USG with FNAC OF PERIAMPULLARY LESION- IN A OJ PATIENT- DETECTS LOWER
CBD BLOCK -TO FIND OUT THE ETIOLOGY OF LOWER CBD BLOCK.

Therapeutic:
1) EUS guided drainage of pancreatic pseudocysts
2) EUS guided pancreatic duct stenting
3) Celiac plexus block

Technique: Anesthesia- Sedation/GA

Endoscopy performed depending on target area (upper GI/Colonoscopy)
When site reached, USG mode is turned on
EUS image is visualized and diagnostic/therapeutic procedure done

Advantages: Minimally invasive, negligible complications

Disadvantages: Generally requires anesthesia, operator dependent, expensive
 4. Doppler Ultrasound:
A Doppler ultrasound is a non-invasive test that is used to estimate direction the blood
flow through blood vessels by bouncing high-frequency sound waves off circulating red
blood cells.

Principles

Ultrasound principle: high-frequency sound wave aimed at a target will be reflected back
and detected
Doppler principle: effect of changes in the sound pitch depending on the movement of
the object in relation to the detector (positive or negative shift)
Types
1. Color flow Doppler ultrasound
B-mode imaging, using colour in pulsated system to depict positive or negative
shifts, allowing simultaneous visualization of anatomy and flow dynamics. These
colours show the speed and direction of blood flow in real time.

2. Continuous wave Doppler ultrasound

continuous emissions from transducer enables the measurement of high velocity
blood flow (like in valve stenosis).

3. Duplex Doppler ultrasound

two modes of ultrasound are used - Doppler and B-mode. The B-mode
transducer obtains an image of the vessel being studied. The Doppler probe
within the transducer evaluates the velocity and direction of blood flow in the
vessel. This provides a 2-dimensional (2-D) image of the arteries so that the
structure of the arteries and location of an occlusion can be determined, as well
as the degree of blood flow.

Procedure

1. Patient lies on examination table, exposing the area the body to be tested

2. Ultrasound gel is applied on the skin over the area.

3. A transducer is placed or moved over the area.

 4. The movement of blood cells causes a change in the pitch of the sound
waves.

5. The waves are recorded and turned into images or graphs on a monitor.

USES

1. Detection and characterization of blood flow

2. Ankle branchial pressure index

3. Localization of blood vessel occlusions

Emboli, DVT, Vasospasm, Stenosis, Aneurysms.

4. Detection of
 Site of incompetence in varicose veins
 heart valve defects
 congenital heart disease
 fetal heart beat

5. Wound Healing
Introduction:- Wound healing is a mechanism by which the body attempts to restore anatomical and
functional integrity of injured tissue.

Etiology:-

1) Primary Healing (First Intention) - Clean incised wound approximated by sutures.

2) Secondary Healing (Second Intention) - Extensive tissue loss with wide edges leading to fibrosis.
3) Tertiary Healing (Third Intention) - Secondary suturing following debridement/ infection control
(also called delayed primary).

Pathogenesis:-

 Phases:
Inflammatory  Proliferative.  remodelling
0-3 days. 3 days- 3 weeks. 3 weeks- 3 months
Hemostasis, Granulation tissue Collagen cross linking
Coagulation and formed, angiogenesis Reduced vascularity,
Chemotaxis occur. occurs. Type 3 collagen Type 1 collagen with 80%
Laid down of original strength formed

Factors Affecting Wound Healing

● Local
1) Infection
2) Necrotic tissue and foreign body
3) Vascularity
4) Tissue tension
5) Site of wound- wounds over face heal faster
6) Type of wound- incised heal better than lacerated
● General
1) Age
2) Nutrition Status/ Vitamin deficiency
3) Diabetes/ Metabolic syndrome
4) HIV/ Immunosuppression/ Steroids
5) Smoking/ Alcohol consumption
Gross Morphology:-

1) Clean incised wound

2) Laceration
3) Contusion
4) Penetrating wound
5) Avulsion/ Traction injury
6) Crush Injury

Sequelae:-

1) Wound Infection
2) Wound dehiscence
3) Contracture
4) Hypertrophic scar (Keloid)
5) Paraesthesia/ Ischemia/ Paralysis

Clinical Features:-

1) Active bleeding
2) Breach in continuity of skin
3) Fractures
4) Hematoma/ Internal Bleeding
5) Cardinal signs of inflammation (Rubor, Tumor, Dolor, Calor)

Management:-

Depending on site and size of wound, it can be a Surgical Emergency

Cleaning of wound-

1) Use aseptic technique

2) Clean with warm sterile normal saline
3) Excision of devitalised tissue and removal of exudates
4) Wound irrigation and lavage

Secondary survey and Head to Toe examination to reveal => Site, Extent and Severity of wound.

Specific Management
 1) Incision- Clean wound and Primary suturing
2) Laceration- Excise wound and delayed primary suturing
3) Infected wound- Debridement->allow granulation tissue to form->Skin graft/ Secondary sutures
4) Tense wound- Skin grafting/ cutaneous Flaps
5) Crush Injury- Debridement/ Wound excision + Delayed primary suturing

6. Burst abdomen
1)Intro:

 Disruption of the abdominal wound(incisions) resulting in prolapse of the intra-abdominal

contents.
 Occurs most commonly on the 6th – 8th day after surgery when the strength of the wound is the
weakest.

2)Etiology /Risk Factors:

5S

 Sepsis: Uncontrolled infection of wound leading to poor healing

 Surgery: Contaminated surgeries like Peritonitis, Pancreatic Surgeries, Faecal fistula, etc. More
common in surgeries involving longitudinal incisions
 Sutures: Absorbable sutures (eg catgut) lead to increased risk. Hence Non- abs sutures preferred
for abdominal wound closure (eg Polypropylene). Sutures done under tension have higher risk.
 Sick Patient: Poor general health, Immunocompromised conditions (Diabetes, Malignancy,
Treatment with steroids
 Straining: Conditions causing increase in Intra- Abdominal Pressure: COPD with coughing,
vomiting, abdominal distension etc.

3) Clinical Features:

 Earliest feature: Patients complain of Pink or Brownish Serosanguinous discharge from the
wound. (Pathognomic) Indicates Impending Burst Abdomen or that the abdominal contents are
lying extraperitoneally.
 When skin sutures are removed, Omentum or small bowel coils seen to be lying outside without
any evidence of shock or pain.

4)Complications: Incisional Hernia, Re- Dehiscence

5) Management: Emergency Closure surgery may be done under GA if burst abdomen is “non-
adherent” type.
  Procedure: Adequate exposure -> Protruded Bowel Loops are washed with saline and replaced
into peritoneal cavity-> Edges of wound are trimmed-> Single layer mass closure is done with
polypropylene sutures.
 Subsequent Re- dehiscence is uncommon.
 Post op care: The general condition is improved by transfusion, plasma and vitamins, and
infection is controlled by chemotherapy and antibiotics
Locally, the wound is supported by a firm corset of adhesive plaster and the stitches are
kept for 2 or 3 weeks, after which an abdominal binder or corset is used for several months.

7. ACUTE URINARY RETENTION

Definition of urinary retention-inability to voluntarily void

Acute urinary retention- sudden and painful inability to void despite of the bladder being full.

Etiology

1) Obstruction- ….a)in men- bep,phimosis and paraphimosis,severe ca prostate…….b)in

women- pelvic prolapsed,cystocele,rectocele……..c)in infants- meatal stenosis, posterior
urethral valve……….d)general- urethral stricture,foreign body,stones.
2) Infective/inflammatory-acute prostitis,urethritis,vulvovaginal candidiasis
3) Pharmacological-tricyclic antideppresssants,anticholinergics,antihistaminics
4) Neurologic- stroke,diabetes ,disc herniation ,spinal trauma,cord compression due to
tumor
5) Post surgical- rectal surgeries,total hip arthroplasty,gynecological surgeries

Clinical features
Depend on etiology
1) Pain and swelling in suprapubic region
 2) Difficulty in initiating urination(straining)
3) Dribbling of urine
4) Poor stream
5) Smooth,soft ,tender,swelling in hypogastric region which is dull on percussion
6) If cause is neurologic-lack of urge to urinate

Sequelae

1) Due to outlet obstruction- bladder distension>hydro

ureter>hydronephrosis>pyelitis>pyelonephritis>pyonephrosis>perinephric
abscess>fistula
2) Due to bladder distension ->hypertrophy of muscles>trabeculations>diverticuli
formation

Investigations

1. Urinary analysis - Normal

2. RFT- Normal

3. X Ray KUB - normal

4. IVU-nephrogram and pyelogram -normal

Cystogram -hypertrophy/diverticuli

If BEP ; MCU -elongated urethra

5.USG :TRUS with biopsy for BEP

6.Cystoscopy

7.Blood :S.PSA ( can be slightly elevated in BEP )

8.Urodynamic studies :

1.check post voidal urine :increased

2.In BEP :bladder pressure increased

Urinary flow rate is reduced .

3. classify neurogenic bladder

Management :

No medical management

Emergency management :

Mainstay of treatment :

Bladder decompression with foleys catheter

C/I :urethral injury suspected

When C/I to bladder decompression or failed catheterisation :

Emergency suprapubic catheterisation

After relief of urinary retention :Treatment of the underlying cause is the Definitive
management

BEP :TURP

Urethral stricture :minimal invasive :urethral dilation using listers urethral dilator

Urethroscopic :visual internal urethrotomy

Surgical :resection and anastomosis -> urethroplasty

8. Phimosis:
Introduction: Phimosis is defined as inability to retract the foreskin or prepuce of the
penis .
 Types:
- Congenital phimosis: children are born with tight foreskin at birth and separation
occurs naturally over time.
Phimosis is normal for the uncircumcised infant /child and usually resolves around 5-
7 years of age.

- Acquired phimosis: Phimosis that occurs due to scarring ,infection or inflammation.

Etiology :
1. Congenital- adhesions
2. Acquired:- Inflammatory- Balanitis/Posthitis (diabetics)
3. Malig- CA penis
4. Miscellaneous- Poor hygiene

Gross- Physiologic phimosis, the preputial orifice is unscarred and healthy

appearing.
In pathologic phimosis, a contracted white fibrous ring may be visible around the
preputial orifice.

Sequelae- Urethral obstruction-> Bladder obstruction-> Hydroureter->

Hydronephrosis
- Difficulty in hygiene- Risk of Ca penis
- Recurrent UTI
- Difficulty in intercourse

C/f: Inability to retract foreskin

- Forced retraction may lead to para-phimosis

Diagnosis: Clinical

Rx: Circumcision
STEPS OF CIRCUMSISION
ANESTHESIA- CHILDREN – GEN ANESTH
ADULT – LOCAL ANESTH – RING BLOCK at root of penis
POSITION – SUPINE
Techniques: 1. CONVENTIONAL (SAFER)
2. Guillotine method
3. Use of plasti-bell device

STEPS (conventional)
- Parts painted and draped
- Straight hemostat introduced at 12 o clock over prepuce
- All 3 rachets are fired – crushing the prepuce at 12 o clock
- Cut along that crushed edge ( less bleeding)
- Rest of prepuce is circumferentially excised after crushing, leaving some amount of
prepuce
- catgut / moncryl sutures are taken to approximate mucosa to foreskin.
- Hemostasis confirmed.

9. Adamantinoma/Ameloblastoma/Eve’sdisease (MULTILOCULAR CYSTIC DISEASE OF

JAW)
Intro: Adamantinoma is a rare bone cancer(<1% of bone tumors).Almost always
Occurs in bones of lower limb and involves both epithelium and osteo-fibrous tissue.
Ameloblastoma is Adamantinoma of jaw (most common molars)
It is a multilocular cystic disease of jaw arising from dental epithelium probably from
enamel or dental lamina.

Risk Factors: Preexisting dentigerous cyst, #mandible, #maxilla, # base of skull

Males, 40-50years
 Pathology
Types: Multilocular(mostcommon),unilocular
Histology: Ameloblast like cells

Clinical features:
-Often u/l, gradually progressive painless swelling-smooth, hard, inner part intact
(enlarges externally)
-Eggshell crackling, swelling in mandible-near the angle which attains a large size,
extending to vertical ramus

Spread: Locally malignant tumor, No LN or Hemat. spread, but recurrent

Adamantinoma can spread to lungs

Investigations: Orthopantogram- multiloculated (honeycomb appearance)

CT jaw, Biopsy from swelling

Treatment: Segmental resection of mandible or Hemi-mandubelectomy with

reconstruction of mandible
10. Epulis (above gums)

Intro/def : It is a painless swelling arising from the mucoperiosteum of the gums(gingiva).

Etio : -congenital

-pregnacy

-chronic irritation from an ill-fitting denture

-caries tooth

pathogenesis :

gingival mucosal irritation due to dental causes/any of the above risk factors leads to > ulceration of the
mucosa

Gross : types of epulis:

1) congenital epulis(Neumann's tumour)

-rare condition; more common in girls

-benign condition arising from gum pads

2) fibrous epulis-

-commonest type

-fibroma arising from periodontal membrane

3) pregnancy epulis-

-occurs in pregnant women d/t inflammatory gingivitis

-usually resolves after delivery

4) epulis fissuratum-

-It is benign hyperplasia of fibrous tissue d/t chronic irritation from an ill-fitting dentures

5) myelomatous epulis-

-seen in leukemic pts

c/f :

- painless, well localized, hard/firm, non-tender swelling in the gum which bleeds on touch

-colour of the swelling same as surrounding gingiva :- fibrous epulis

-deep red :- pyogenic/ pregnancy epulis

- purple blue :- giant cell epulis

Investigation:

-Orthopantomogram:- well localised lesion

-Biopsy from the swelling- gingival tissue lined by stratified squamous epithelium with acanthosis and
para keratosis

- X-ray

Treatment

-No medical treatment

-Surgery

* Surgical excision of lesion 1) removal by scalpel 2) electrocautery

* Fabrication of complete denture

- Pregnancy epulis usually resolves after delivery

- Myelomatous epulis treat the underlying cause (leukemia)

11. Non-Healing Ulcer LAQ: Etiology, Clinical Features and Management

Introduction:
An ulcer is a break in the continuity of the epithelium of the skin or mucous membrane
due to molecular death.
Non-healing Ulcer: Chronic ulcers or non-healing ulcers are defined as spontaneous or
traumatic ulcers, typically in lower extremities that are unresponsive to initial therapy or
that persist despite appropriate care and do not proceed towards healing in a defined
time period

Aetiology:
1. Local Causes:
a. Recurrent infection
b. Trauma/Foreign body/sequestrum
c. Absence of rest/immobilization
d. Oedema of the part (interstitium)
e. Poor blood supply, hypoxia (artery)
f. Loss of sensation (nerve)
g. Lymphatic Disease (lymphatic)
h. Fibrosis of surrounding soft tissues (soft tissues)
i. Periostitis or osteomyelitis of underlying bone (bone)

2. General/Specific Causes:
a. Anaemia, hypoproteinaemia
b. Vitamin Deficiencies
c. TB, Leprosy
d. DM, HTN
e. Chronic Liver Diseases, CKD
f. Steroid Therapy: locally or systematically
g. Cytotoxic Chemotherapy or Radiotherapy
h. Malignancy
Another etiological classification
1. Infections
2. Ischemic conditions - arterial insufficiency, venous hypertension, pressure
injuries,
3. Metabolic conditions - DM, Malnutrition, Anaemia,
4. Immunosuppression - systemic immunosuppression
5. Radiation

Pathogenesis:

Stages of Normal Ulcer Healing:

1. Stage of extension:
a. Correlates to Inflammatory Phase in wound healing
b. Ulcer floor is covered with slough, purulent discharge and inflamed edge and
margin

2. Stage of Transition:
a. Correlates to Proliferative Phase in wound healing
b. Floor shows separated slough, health granulation tissue and serous discharge

3. Stage of Repair:
a. Correlates to Remodelling Phase in wound healing
b. Fibrosis, collagen deposition, scar formation occur
Stages of Normal Ulcer Healing Any of the aetiology/risk factors for non-healing of
ulcers  Interrupts the normal healing process by creating a hostile healing
environment  Non-healing of Ulcers/Chronic Ulcers

Pathology:
Gross
- Non-Healing Ulcer:
- Edge is usually inflamed and oedematous
- Edge type depends on cause
- Punched out in Trophic Ulcers
- Undermined in TB Ulcers
- Rolled Out in Carcinomatous Ulcers
- Beaded in rodent Ulcer
- Floor
- Has unhealthy and pale granulation tissue and slough
- And serosanguinous/purulent/bloody discharge

- Regional Draining LNs may be enlarged but non-tender

- Callous ulcer/stationary ulcer/chronic non-healing ulcer: A clinical type of non-

healing ulcer characterised by its “callousness’ to healing.
- Ulcer:
- Floor:
- Has pale, unhealthy, flabby, whitish-yellow granulation tissue
- Also has thin scanty serous discharge or rarely copious serosanguinous discharge
- Edge
- Indurated, non-tended, often fixed
- Surrounding area:
- Induration and pigmentation
- Discharge: None/less
- Regional LNs: Enlarged, firm/hard and non-tender
-
Sequelae:
1. Infection
2. Osteomyelitis - due to infection spreading to the bone
3. Tissue Necrosis and Gangrene (esp. In PVD)
4. Periwound Dermatitis
5. Dehiscence
6. Neoplastic Transformation In chronically inflamed wounds eg. Marjolin’s ulcers
in chronic burn scars leading to SCC
.

Clinical Features:
1. Symptoms
a. Non-healing ulcer
b. h/o or symptoms of underlying cause: eg. diabetes, PVD, TB, trauma etc

2. On examination of ulcer:
a. Increased blanching erythema in the area surrounding the wound
b. Induration surrounding the wound
c. Wound drainage - especially thick, purulent discharge
d. Foul odour
e. Increased tenderness

Investigations:
Largely a clinical diagnosis. Investigations are for aetiology and complications of the non-
healing ulcer.
1. Blood investigations
a. HbA1C level - for diabetes
b. Albumin levels
c. CBC, CRP, ESR levels
2. Imaging
a. Xray of extremity for Osteomyelitis
b. Arterial duplex scan for arterial insufficiency
3. Cultures and biopsy of ulcer - for AST and cancer

Treatment:
1. Treatment of ulcer
a. Wound debridement
i. Mechanical
ii. Chemical - Hydrogen peroxide/ Acriflavine/ EUSOL(Edinburgh University Solution
of Lime)
iii. Biological - Maggots (Cultured, live and disinfected)

b. Wound cleaning -- every day 2-3 times with normal saline

c. Wound dressing
i. Gauze - Cotton
ii. Paraffin
iii. Polyurethane
iv. Alginate
v. Type 1 collagen
vi. Foam
vii. Transparent films
viii. Topical antimicrobial agents like Framycetin/Silver sulfadiazine/mupirocin (Add
to above only in infected ulcers)
d. Adjunctive therapies
i. Hyperbaric oxygen therapy
ii. Topical growth factors
iii. Vacuum-assisted closure(VAC) therapy
iv. Infrared/ short wave/ ultraviolet rays
e. Surgical procedures - if ulcer is too deep or large
i. Options:

1. Grafts
a. Split thickness
b. Full-thickness
c. Tissue flap reconstructions

2. Revascularization - endovascular or open vascular reconstruction.

ii. Postoperative Care to ensure proper healing:
1. Place extremity involved in non-weight bearing status.
2. Graft site should be inspected to see if graft has taken

2. Treatment of the underlying condition

a. Glycemic control
b. Nutritional support