Otolaryngology - Head & Neck Surgery
Otolaryngology - Head & Neck Surgery
Otolaryngology - Head & Neck Surgery
EARS
helical crus
antihelix
scapha tragus
antitragus
lobule
Stapes
Tympanic membrane
flaccid portion
Malleus (handle)
Tympanic membrane
tense portion
Annulus
Posterior Cone of light
Anterior
• in normally hearing individuals, sound travels down the auditory canal and vibrates the tympanic membrane
• these vibrations are amplified by the middle ear ossicles (malleus, incus, stapes) and are transmitted to the oval window of the cochlea
• varying pressure on the fluid in the cochlea causes movement of the basilar membrane
• hair cells housed within the organ of Corti (which rests on the basilar membrane) are stimulated by this movement
• the auditory signal is transduced to a neural code, which is passed along spiral ganglion neurons of the auditory nerve (CN VIII) and up to the
inferior colliculi (centers for auditory reflex) and via the medial geniculate body in the thalamus to the auditory cortex (Brodmann’s area 41).
Auditory Acuity
❏ mask one ear and whisper into the other
❏ tuning fork tests - see Table 1
• Rinne's Test
• 512 Hz tuning fork is struck and held firmly on mastoid process to test bone conduction (BC).
When it can no longer be heard it is placed close to ear to test air conduction (AC)
• if it can then be heard then AC > BC or Rinne positive
• a loss of approximately 15 dB is required to reverse the Rinne (BC > AC)
• Weber's Test
• vibrating fork is held on vertex of head and patient states whether it is heard centrally
(Weber negative) or is lateralized to one side (Weber right, Weber left)
• lateralization indicates ipsilateral conductive hearing loss or contralateral sensorineural
hearing loss
• place vibrating fork on patient’s chin while they clench their teeth,
or directly on teeth to elicit more reliable response
• a difference of approximately 5 dB is required for the Weber to lateralize
Table 1. The Interpretation of Tuning Fork Tests
Examples Weber Rinne
Right Sided Conductive Hearing Loss, Normal Left Ear Lateralizes to Right BC>AC (–) right
Right Sided Sensorineural Hearing Loss, Normal Left Ear Lateralizes to Left AC>BC (+) bilaterally
* a vibrating fork on the mastoid stimulates both cochleae, therefore in this case, the left cochlea is stimulated by the Rinne test
on the right, i.e. a false negative test
These tests are not valid if the ear canals are not free of cerumen (i.e. will create conductive loss)
NOSE
External Examination of Nose
❏ inspect nose
• look for swelling, trauma, congenital anomalies, deviation
• test patency of each nostril if deviation is suspected
❏ palpate sinuses
• tenderness over frontal and maxillary sinuses may indicate sinusitis
Internal Examination of Nose
❏ inspect with nasal speculum
• position of septum
• colour of nasal mucosa
• normally pink and moist with a smooth clean surface, blue/grey secondary to allergies, and red
secondary to inflammation
• size, colour and mucosa of inferior and middle turbinates
• possible abnormal findings
• septal deviation or perforation
• exudate, swelling, epistaxis
• nasal polyps
ORAL CAVITY
❏ ask patient to remove dentures
❏ lips
• colour of skin and mucosal surface, presence of lesions
❏ buccal mucosa
• use two tongue blades and slowly move around the mouth
• identify Stensen’s duct (parotid gland duct orifice) opposite upper
first or second molar
❏ gingivae and dentition
• 32 teeth in full dentition; colour and condition of gingiva
• look for malocclusion
❏ hard and soft palates
• examine for symmetry
• inspect for ulceration or masses
❏ tongue
• inspect for colour, mobility, masses, tremor, and atrophy
• use tongue depressor to manipulate tongue to examine undersurface
and sides Figure 4. Sagittal Section
• palpate tongue for any masses with Divisions of
• test cranial nerve XII Nasopharynx, Oropharynx,
❏ floor of mouth Hypopharynx
• palpate for any masses
• identify Wharton's ducts (submandibular gland ducts) on either side Figure from Essentials of Otolaryngology. 4th ed.
just lateral to frenulum of tongue Lucente FE and Har-EIG. (eds)
• bimanually palpate submandibular glands
Oropharynx
❏ anterior faucial pillars, tonsils, tonsillolingual sulcus
• depress middle third of tongue with tongue depressor and scoop tongue forward to visualize tonsils
• note size and inspect for tonsillar exudate or lesions
❏ posterior pharyngeal wall
NASOPHARYNX
Postnasal Mirror (Indirect)
❏ ensure good position of patient
• must sit erect with chin drawn forward (“Sniffing Position”)
• instruct patient to breathe through nose, allowing palate to depress and nasopharynx to open
❏ with adequate tongue depression, the warmed mirror is placed next to uvula and almost touches the
posterior pharyngeal wall
❏ rotate mirror to inspect the following areas
• choana
• posterior end of the vomer: should be in midline
• inferior, middle, and superior meatus
• may see pus dripping over posterior end of inferior meatus (sign of maxillary sinusitis)
• eustachian tubes
• adenoids (mostly in children)
Nasopharyngolaryngoscope (Direct)
❏ detailed view of nasal cavities and nasopharynx
HYPOPHARYNX AND LARYNX
Indirect Laryngoscopy
❏ ensure good position of patient
❏ while holding tongue with gauze, introduce slightly warmed mirror into mouth
and position mirror in oropharynx
❏ ask patient to breathe normally through mouth while mirror is pushed
upward against the uvula
• touching the uvula and soft palate usually does not elicit a gag reflex, unlike touching the back of
the tongue
• the gag reflex can be suppressed if patients are told to pant in and out
❏ image seen in mirror will be reversed (see Figure 5)
❏ inspect the following, noting any irregularity of the edges, nodules or ulcerations
• circumvallate papillae and base of tongue, lingual tonsils, valleculae epiglottis, aryepiglottic folds and
pyriform fossae, false vocal cords, true vocal cords
• note position and movement of cords
• quiet respiration
• cords are moderately separated
• inspiration
• cords abduct slightly
• ask patient to say "eeee"
• cords adduct to midline
• look for signs of paralysis or fixation
vestibule
thyroid cartilage
ventricular folds
(false cords)
vocal folds
(true cords)
trachea posterior
pyriform fossa
Posterior View arythroid cartilage
Figure 5. Anatomy of Normal Larynx
Illustration by Glen Oomen
Figure 6. The Dix-Hallpike Test of a Patient with Benign Positional Vertigo Affecting
the Right Ear
Source: Furman JM nad Cass SP. Benign Paroxysmal Positional Vertigo. The New England Journal of Medicine. Vol. 341 (21): 1590-1596. 1999.
– O + – O + – O +
normal pressure peak at 0 no pressure peak negative pressure peak
note that with otosclerosis the peak poor TM mobility indicative of middle ear indicative of chronic eustachian tube
is still at 0mm H2O but has a lower effusion (e.g. otitis media with effusion) insufficiency (e.g. serous or secretory
amplitude (an As Tympanogram) or perforated TM otitis media)
Static Compliance
❏ volume measurement reflecting overall stiffness of the middle ear system
❏ normal range: 0.3 to 1.6 cc
❏ negative middle ear pressure and abnormal compliance indicate middle ear pathology
Acoustic Stapedial Reflexes
❏ stapedius muscle contracts when ear is exposed to loud sound and results in increased stiffness or
impedance of middle ear system (TM and ossicles)
❏ acoustic reflex thresholds occur at 70-100 dB above hearing threshold
❏ if hearing threshold is greater than 85 dB, the reflex is likely to be absent
❏ stimulating either ear causes reflex to occur bilaterally and symmetrically
❏ reflex pathway involving vestibulocochlear cranial nerve, cochlear nucleus, trapezoid body, superior olivary
nucleus, facial nucleus, and facial nerve (i.e. a measure of central neural function)
❏ for reflex to be present, CN VII must be intact and there must be no conductive hearing loss in the monitored
ear. If reflex is absent without conductive loss or severe sensorineural loss, suspect CN VIII lesion
❏ acoustic reflex decay test: tests the ability of the stapedius muscle to sustain contraction for 10 s at
10 dB stimulation
❏ normally, little reflex decay occurs at 500 and 1000 Hz
❏ with cochlear hearing loss the acoustic reflex thresholds are typically 25-60 dB
❏ with retrocochlear hearing loss (e.g. acoustic neuroma) may find absent acoustic reflexes or significant reflex
decay (> 50%) within 5 second interval
AUDITORY BRAINSTEM RESPONSE (ABR)
❏ the patient is exposed to an acoustic stimulus while an electroencephalogram is recorded to assess any
changes in brain activity
❏ delay in brainstem response is suggestive of cochlear or retrocochlear abnormalities (for the latter think
tumour or multiple sclerosis (MS))
Clinical Pearl
❏ This objective test can be used in screening newborns or much more rarely to uncover
normal hearing in malingering patients.
HEARING LOSS
*common
Hearing Loss +less common
Conductive Sensorineural
MASTOIDITIS
❏ osteomyelitis (usually subperiosteal) of mastoid air cells, most commonly seen approximately two weeks after
onset of untreated (or inadequately treated) acute suppurative otitis media
❏ previously common but is now rare due to rapid and effective treatment of acute otitis media with antibiotics
Presentation
❏ pinna displaced laterally and inferiorly
❏ persistent throbbing pain and tenderness over mastoid process
❏ development of subperiosteal abscess, post-auricular swelling
❏ spiking fever
❏ hearing loss
❏ otorrhea with tympanic membrane perforation (late)
❏ radiologic findings: opacification of mastoid air cells by fluid and interruption of normal trabeculations of cells
Treatment
❏ IV antibiotics with myringotomy and ventilating tubes
❏ cortical mastoidectomy
• debridement of infected tissue allowing aeration and drainage
• requires lifelong follow-up with otolaryngologist
❏ indications for surgery
1. failure of medical treatment after 48 hours
2. symptoms of intracranial complications
3. aural discharge persisting for 4 weeks and resistant to antibiotics
OTOSCLEROSIS (see Figure 7)
❏ commonest cause of conductive hearing loss between 15 and 50 years of age
❏ autosomal dominant, variable penetrance approximately 40%
❏ female > male - progresses during pregnancy (hormone responsive)
❏ 50% bilateral
Presentation
❏ progressive conductive hearing loss first noticed in teens and 20s
(may progress to sensorineural hearing loss if cochlea involved)
❏ +/– pulsatile tinnitus
❏ tympanic membrane normal +/– pink blush (Schwartz's sign) associated with the neovascularization
of otosclerotic bone
❏ characteristic dip at 2,000 Hz (Carhart's Notch) on audiogram (Figure 7)
Treatment
❏ stapedectomy with prosthesis is definitive treatment
❏ hearing aid may be used, however usually not a good long term solution
CONGENITAL SENSORINEURAL HEARING LOSS
❏ genetic factors are being identified increasingly among the causes of hearing loss
Hereditary Defects
❏ non-syndrome associated (70%)
• often idiopathic
• autosomal recessive
❏ syndrome associated (30%)
• Waardenburg's - white forelock, heterochromia iridis, wide nasal bridge and increased distance
between medial canthi
• Pendred's - goiter
• Treacher-Collins - first and second branchial cleft anomalies
• Alport's - hereditary nephritis
Prenatal TORCH Infections
❏ Toxoplasmosis, Others (e.g. HIV), Rubella, Cytomegalovirus (CMV), Herpes simplex
Perinatal
❏ Rh incompatibility
❏ anoxia
❏ hyperbilirubinemia
❏ birth trauma (hemorrhage into inner ear)
Postnatal
❏ meningitis
❏ mumps
❏ measles
OT12 – Otolaryngology MCCQE 2002 Review Notes
HEARING LOSS . . . CONT.
Hearing loss sensorineural loss due to direct cochlear injury conductive hearing loss secondary
to ossicular injury
Other features • intact external auditory meatus, tympanic membrane • torn tympanic membrane
+/– hemotympanum with hemotympanum
• spontaneous nystagmus • bleeding from external auditory canal
• CSF leak in eustachian tube to nasopharynx +/or • step formation in external auditory canal
rhinorrhea (risk of meningitis) • CSF otorrhea
• Battle’s sign = mastoid ecchymoses
• Raccoon eyes = periorbital ecchymoses
Diagnosis
❏ otoscopy
❏ do not syringe or manipulate external auditory meatus due to risk of inducing meningitis via TM perforation
❏ radiology
• CT
❏ facial nerve tests (for transverse fractures), EMG, Schirmer's test, gustometry, stapedial reflexes, ENG
Treatment
❏ hemotympanum signifies significant force sustained, therefore monitor hearing until it returns to normal
❏ medical - expectant, prevent otogenic meningitis
• IV antibiotics if suspect CSF leak (penicillin G for 7-10 days)
❏ surgical - explore temporal bone, indications are
1. early meningitis (mastoidectomy)
2. bleeding from sinus
3. CSF otorrhea
4. CN VII palsy (complete)
5. gunshot wound
6. depressed fracture of external auditory meatus
Complications
❏ acute otitis media +/– labyrinthitis +/– mastoiditis
❏ meningitis / epidural abscess / brain abscess
❏ post-traumatic cholesteatoma
AURAL REHABILITATION
❏ dependent on degree of hearing loss, communicative requirements and difficulties, motivation and
expectations, age, and physical and mental abilities
❏ factors affecting prognosis with hearing aid/device
• poor speech discrimination
• narrow dynamic range (recruitment)
• unrealistic expectations
• cosmetic
❏ types of hearing aids
• behind the ear - BTE
• all in the ear - ITE
• bone conduction
• contralateral routing of signals (CROS)
❏ assistive listening devices
• direct/indirect audio output
• infrared, FM, or induction loop systems
• telephone, television, or alerting devices
❏ cochlear implant
• electrode is inserted into the cochlea to allow direct stimulation of the auditory nerve
• for profound bilateral sensorineural hearing loss not rehabilitated with conventional hearing aids
• established indication: post-lingually deafened adults and children
DIZZINESS
Clinical Pearl
❏ True nystagmus and vertigo will never last longer than a couple of weeks if caused
by a peripheral lesion because compensation occurs; such is not true for a central lesion.
OTALGIA
Local Causes
❏ furuncle (boil), usually as a result of a Staph Aureus infection
❏ foreign body in external auditory canal/impacted cerumen
❏ infection
• otitis externa
• acute otitis media and its complications
• acute mastoiditis and its complications
❏ trauma to tympanic membrane and canal
❏ barotrauma
Referred (10 T's + 2)
❏ CN V and CN X refer to external canal and CN IX to middle ear
1) eustachian Tube
2) TMJ (tempromandibular joint) syndrome
3) Trismus (i.e. pterygoids, quinsy)
4) Teeth - impacted
5) Tongue
6) Tonsillitis, tonsillar cancer, post tonsillectomy
7) Tic (CN IX) - glossopharyngeal neuralgia
8) Throat - cancer of larynx, vallecula, pyriform fossa
9) Trachea - foreign body, tracheitis
10) Thyroiditis
11) Geniculate herpes and Ramsey Hunt Syndrome
12) +/– CN VII palsy
NASAL OBSTRUCTION
Table 4. Differentia1 Diagnosis of Nasal Obstruction
Acquired Congenital
Nasal Cavity
Rhinitis - acute/chronic Nasal dermoid
- vasomotor Encephalocele
- allergic Glioma
Polyps
Foreign bodies
Trauma
Enlarged turbinates
Tumour
- benign - inverting papilloma
- malignant - squamous cell carcinoma (SCC)
esthesioneuroblastoma
adenocarcinoma
nasal septum
Septal deviation Dislocated septum
Septal hematoma/abscess
nasopharynx
Adenoid hypertrophy Choanal atresia
Tumour - nasopharyngeal carcinoma
- benign - juvenile nasopharyngeal
angiofibroma
- malignant - nasopharyngeal carcinoma
ACUTE RHINITIS
❏ irritation of nasal mucosa due to any cause
❏ most common cause is common cold
❏ children < 5 years most susceptible
❏ spread by droplet contact from sneezing
Etiology
❏ viral (ususally rhinovirus), may have secondary bacterial infection
Presentation
❏ irritation/burning sensation in nasopharynx; sneezing
❏ serous nasal discharge, may be purulent if secondary bacterial infection
❏ nasal obstruction, mucosal swelling and erythema
❏ +/– fever and malaise
❏ symptoms subside in 4-5 days
Complications
❏ sinusitis
❏ otitis media
❏ bronchitis
❏ tonsillitis
❏ pneumonia
Treatment
❏ rest, fluids, normal diet
❏ oral decongestants for symptomatic relief
❏ +/– analgesics, antihistamine, corticosteroid spray (e.g. triamcinolone, fluticasone, betamethasone)
❏ no indication for antibiotics, unless secondary bacterial infection present
Clinical Pearl
❏ Congestion reduces nasal airflow and allows the nose to repair itself.
Treatment should focus on the initial insult rather than at this defense mechanism.
Treatment
❏ identification and avoidance of allergen
❏ topical steroid sprays, e.g. fluticasone (Flonase) - effective for seasonal rhinitis
❏ nasal irrigation with saline
❏ oral decongestants
❏ antihistamines
❏ injection of long-lasting steroid if severe
❏ desensitization by allergen immunotherapy
VASOMOTOR RHINITIS
❏ neurovascular disorder of nasal parasympathetic system (vidian nerve) affecting mucosal blood vessels
❏ nonspecific reflex hypersensitivity of nasal mucosa
❏ caused by
• temperature change
• alcohol, dust, smoke
• stress, anxiety, neurosis
• endocrine - hypothyroidism, pregnancy, menopause
• parasympathomimetic drugs
• beware of rhinitis medicamentosa: reactive vasodilation due to prolonged use (> 2 days) of nasal drops
and sprays (Dristan, Otravin)
Presentation
❏ chronic intermittent nasal obstruction, varies from side to side
❏ rhinorrhea: thin, watery, worse with temperature changes, stress, exercise, EtOH
❏ nasal allergy must be ruled out
❏ mucosa and turbinates: swollen, pale between exposure
❏ symptoms are often more severe than clinical presentation suggests
Treatment
❏ elimination of irritant factors
❏ parasympathetic blocker (Atrovent nasal spray)
❏ decongestants (nose drops/oral)
❏ steroids (e.g. Beclomethasone)
❏ surgery: electrocautery, cryosurgery, laser treatment or removal of inferior or middle turbinates
❏ vidian neurectomy (rarely done)
❏ symptomatic relief with exercise (increased sympathetic tone)
ADENOID HYPERTROPHY (see Pediatric ENT section)
NASAL POLYPS (see Colour Atlas OT6)
❏ benign pedunculated/sessile masses of hyperplastic ethmoidal mucosa caused by inflammation
❏ antrochoanal polyps - (uncommon) arise from maxillary sinus and extend beyond the soft palate into
the nasopharynx
❏ may obstruct airway
Etiology
❏ mucosal allergy (majority)
❏ sinonasal rhinosinusitis
❏ note: triad of polyps, aspirin sensitivity, asthma (Samter’s triad)
❏ cystic fibrosis/bronchiectasis (child with polyps - cystic fibrosis until proven otherwise)
Presentation
❏ progressive nasal obstruction, hyposmia, snoring
❏ post-nasal drip, stringy colourless/purulent rhinorrhea
❏ solitary/multiple glazed, smooth, transparent mobile masses (often bilateral)
Treatment
❏ eliminate allergen
❏ steroids (preoperative prednisone) to shrink polyp
❏ polypectomy - treatment of choice, however, polyps have marked tendency to recur
Complications
❏ sinusitis
❏ mucocele
❏ nasal widening (pseudohypertelorism)
Clinical Pearl
❏ Bilateral nasal polyps virtually never occur in children in the absence of Cystic Fibrosis.
SEPTAL DEVIATION
Etiology
❏ developmental - unequal growth of cartilage and/or bone of nasal septum
❏ traumatic - facial and nasal fracture or birth injury
Presentation
❏ unilateral nasal obstruction (may be intermittent)
❏ anosmia, crusting, facial pain
❏ septum: S-shaped, angular deviation, spur
❏ compensatory middle/inferior turbinate hypertrophy on nasal space
Treatment
❏ if asymptomatic - expectant management
❏ if symptomatic - submucous resection (SMR) or septoplasty
Complications of Surgery
❏ post-op hemorrhage (can be severe)
❏ septal hematoma, septal perforation
❏ external deformity (saddle-nose)
❏ anosmia (rare but untreatable)
SEPTAL HEMATOMA
❏ most common in children - secondary to trauma, even mild trauma
Complications
❏ may lead to infection ––> abscess ––> cavernous sinus thrombosis
❏ septal perforation
❏ ischemic necrosis of septum and saddle deformity
Presentation
❏ nasal obstruction
❏ pain/tenderness
❏ occurs in anterior part of septum
❏ swollen nose
Treatment
❏ incision and drainage with nasal packing
❏ antibiotics
SEPTAL PERFORATION
Etiology
❏ trauma: surgery, physical, digital
❏ infection: syphilis, tuberculosis
❏ inflammatory: systemic lupus erythematosus (SLE)
❏ neoplasia: squamous/basal cell, malignant granuloma infection
❏ miscellaneous: cocaine sniffing, chromic gases
Presentation
❏ perforation seen on exam
❏ crusting
❏ recurrent epistaxis
❏ whistling on inspiration/expiration
Treatment
❏ refer suspected neoplasia for biopsy
❏ surgical closure for small perforations, occlusion with Silastic buttons, free fascial graft, mucosal flap
anterior ethmoid
posterior ethmoid
frontal sinus
sphenoidal sinus
Kiesselbach’s
plexus
septal branch of
sphenopalatine
branch from
superior labial greater palatine
Local Idiopathic
Injection (vestibulitis)
Trauma (digital, dry air)
Foreign body
Tumours
Benign - juvenile angiofibroma (occurs in adolescent males)
- polyps
Maligant - squamous cell carcinoma
Systemic Hypertension
Arteriosclerosis
Drugs (anticoagulants, e.g. aspirin and coumadin)
Bleeding disorders
Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu disease)
Treatment
❏ aim is to localize bleeding and achieve hemostasis
1. First-aid
❏ patient sits upright with mouth open (to prevent swallowing)
❏ firm pressure is applied for 5 minutes superior to nasal alar cartilages (not bony pyramid!)
2. Assess Blood Loss (it can be a potentially fatal hemorrhage)
❏ pulse, blood pressure (BP), and other signs of shock
❏ IV NS, cross match for 2 units packed RBCs if significant
SINUSITIS
Development of Sinuses
❏ birth - ethmoid and small maxillary buds present
❏ age 9 - maxillary full grown, frontal and sphenoid cell starting
❏ age 18 - frontal and sphenoid cell full grown
Drainage of Sinuses
❏ frontal, maxillary, anterior ethmoids: middle meatus
❏ posterior ethmoid: superior meatus
❏ sphenoid: sphenoid ostium (at level of superior meatus)
Pathogenesis of Sinusitis
❏ inflammation of the mucosal lining of the paranasal sinuses
❏ anything that blocks air entry into the sinuses predisposes them to inflammation
PEDIATRIC OTOLARYNGOLOGY
ACUTE OTITIS MEDIA (AOM)
❏ inflammation of middle ear associated with pain, fever, irritability, anorexia, or vomiting
❏ 60-70% of children have at least 1 episode of AOM before 3 years of age
❏ 18 months to 6 years most common age group
❏ peak incidence January to April
❏ one third of children have had 3 or more episodes by age 3
Etiology
❏ S. pneumoniae - 35% of cases
❏ H. influenzae - 25% of cases
❏ M. catarrhalis
❏ S. aureus and S. pyogenes (all ß-lactamase producing)
❏ anaerobes (newborns)
❏ viral
MCCQE 2002 Review Notes Otolaryngology – OT25
PEDIATRIC OTOLARYNGOLOGY . . . CONT.
Predisposing Factors
❏ eustachian tube dysfunction/obstruction
• swelling of tubal mucosa
• upper respiratory tract infection (URTI)
• allergies/allergic rhinitis
• chronic sinusitis
• obstruction/infiltration of eustachian tube ostium
• tumour - nasopharyngeal CA (adults)
• adenoid hypertrophy (not due to obstruction but by maintaining a source of infection)
• barotrauma (sudden changes in air pressure)
• inadequate tensor palati function - cleft palate (even after repair)
• abnormal spatial orientation of eustachian tube
• Down's Syndrome (horizontal position of eustachian tube), Crouzon's, and Apert's syndrome
❏ disruption of action of
• cilia of eustachian tube - ?Kartagener's syndrome
• mucus secreting cells
• capillary network that provides humoral factors, PMNs, phagocytic cells
❏ immunosupression/deficiency due to
• chemotherapy
• steroids
• diabetes mellitus
• hypogammaglobulinemia
• cystic fibrosis
Risk Factors
❏ bottle feeding
❏ passive smoke
❏ crowded living conditions (day care/group child care facilities) or sick contact
❏ male
❏ family history
Pathogenesis
❏ obstruction of eustachian tube ––> air absorbed in middle ear ––> negative pressure
(an irritant to middle ear mucosa) ––> edema of mucosa with exudate ––> infection of exudate
Presentation
❏ triad of otalgia, fever (especially in younger children), and conductive hearing loss
❏ otorrhea if tympanic membrane perforated (see Colour Atlas OT4)
❏ pain over mastoid
❏ infants/toddlers
• ear-tugging
• irritable, poor sleeping
• vomiting and diarrhea
• anorexia
❏ otoscopy of tympanic membrane (see Colour Atlas OT1)
• hyperemia
• bulging
• contour of handle of malleus and short process disappear (middle ear effusion)
Treatment
❏ antibiotic treatment hastens resolution - 10 day course
• amoxicillin - 1st line
• trimethoprim-sulphamethoxazole (Bactrim) - if penicillin-allergic
• AOM deemed "unresponsive" if clinical signs/symptoms and otoscopic findings persist beyond
48 hours of antibiotic treatment
• change to broad spectrum: cefaclor (Ceclor), Clavulin, erythromycin + sulfisoxizole (Pediazole),
cefixime (Suprax)
• clarithromycin (Biaxin) for recurrent AOM
❏ antipyretics (e.g. acetaminophen)
❏ no role for decongestants in AOM
❏ myringotomy with tubes - indications (see Surgical Procedures section)
1. complications of AOM suspected
2. recurrent AOM (> 5 in a year)
3. immunologically compromised child
4. failure of 3 different antibiotics - fever and bulging of drum
❏ adenoidectomy
Complications of AOM
❏ extracranial
• chronic suppurative otitis media
• acute mastoiditis
• facial nerve paralysis
• febrile seizures
• nystagmus - bacterial labyrinthitis
• TM perforation
❏ intracranial
• meningitis
• extradural, subdural, cerebral abscess
• petrositis
• lateral sinus thrombosis
OT26 – Otolaryngology MCCQE 2002 Review Notes
PEDIATRIC OTOLARYNGOLOGY . . . CONT.
Presentation
❏ any age, most commonly 1-4 years
❏ rapid onset
❏ toxic-looking, fever, anorexia, restless
❏ cyanotic/pale, inspiratory stridor, slow breathing, lungs clear with decreased air entry
❏ prefers sitting up, open mouth, drooling, tongue protruding, sore throat, dysphagia
Presentation
❏ fever and dehydration
❏ sore throat and dysphagia
❏ extensive peritonsillar swelling but tonsil may appear normal
❏ edema of soft palate
❏ uvula deviated across midline
❏ “hot potato” voice (edema->failure to elevate palate->hot potatoe voice)
❏ increased salivation and trismus (trigeminal nerve disturbance with spasm of masticatory muscles and
lockjaw)
❏ unilateral referred otalgia
❏ cervical lymphadenopathy
Complications
❏ may dissect inferiorly and rupture into airway or penetrate mediastinum
❏ may extend laterally and weaken wall of carotid artery
❏ may ascend and penetrate skull base
Treatment
❏ surgical drainage (incision or needle aspiration) - do C&S
❏ possible tonsillectomy at presentation or 6 weeks later
❏ IV antibiotics (clindamycin)
❏ warm saline irrigation
RETROPHARYNGEAL ABSCESS
❏ most commonly in young infants/children < 2 years old
❏ in children
• due to accumulation of pus between posterior pharyngeal wall and prevertebral fascia
• pus is from breakdown of lymph node in retropharyngeal tissue
• often secondary to posterior pharyngeal trauma
(e.g. endotracheal tube (ETT) or suction in neonate, popsicle stick abrasion in child)
❏ in adults
• secondary to spread from parapharyngeal space due to an abscess or trauma of posterior
pharyngeal wall
Presentation
❏ child
• acute throat pain, difficulty swallowing, loss of appetite, speech change
• unexplained high fever post URTI
• stiff neck, stridor
❏ adult
• dysphagia
• odynophagia
• symptoms of airway obstruction
• pain and swelling in neck
Diagnosis
❏ lateral soft tissue radiograph showing increased soft tissue between pharyngeal airway and cervical vertebral
bodies +/– trapped air
❏ barium swallow (rarely necessary)
Treatment
❏ IV antibiotics
❏ surgery: incision and drainage with airway secured
LUDWIG'S ANGINA
❏ cellulitis/inflammation of submandibular, sublingual, and submental spaces
❏ causes firmness of floor of mouth, tongue protrudes upward and back causing airway obstruction
Etiology
❏ most commonly secondary to a dental infection
(multiple organisms involved usually - including anaerobic bacilli)
❏ suppurative lymph node in submaxillary space
Treatment
❏ incision through midline and prepare for possible tracheostomy because of the difficulty in intubation
❏ IV penicillin + metronidazole/clindamycin
ACUTE TONSILLITIS and TONSILLECTOMY
(see Pediatric ENT and Surgical Procedures section)
ACUTE LARYNGITIS
Etiology
❏ viral +/– URTI - influenza, adenovirus, GAS
❏ voice abuse
❏ toxic fume inhalation
Presentation
❏ URTI symptoms and hoarseness, aphonia, cough attacks, +/– dyspnea
❏ indirect laryngoscopy shows true vocal cords erythematous and edematous with vascular injection and normal
cord mobility
Treatment
❏ self-limited
❏ voice rest with humidification to prevent further irritation of inflamed cords
❏ removal of irritants (e.g. smoking)
❏ if bacterial - treat with antibiotics
CHRONIC LARYNGITIS
❏ long standing inflammatory changes in laryngeal mucosa
Etiology
❏ repeated attacks of acute laryngitis
❏ exposure to irritating dust/smoke
❏ voice abuse
❏ esophageal disorders: Zenker's diverticulum/hiatus hernia/GERD
❏ systemic: allergy, hypothyroidism, Addison's
Presentation
❏ longstanding hoarseness and vocal weakness - rule out malignancy
❏ indirect laryngoscopy - cords erythematous, thickened with normal mobility
Treatment
❏ remove offending cause
❏ treat related disorders
❏ speech therapy with voice rest
❏ +/– antibiotics, +/– steroids to decrease inflammation
SALIVARY GLANDS
❏ major salivary glands: paired parotid, submandibular, and sublingual glands
SIALOADENITIS
❏ sialoadenitis: inflammation of salivary glands
Etiology
❏ obstructive vs. non-obstructive
❏ bacterial: (commonly S. aureus) patient prone to bacterial infection when salivary flow is decreased
or obstructed
❏ viral: most common infectious cause
Presentation
❏ acute onset of pain and edema of parotid or submandibular gland that may lead to marked swelling
❏ +/– fever
❏ +/– leukocytosis
❏ +/– suppurative drainage from punctum of the gland
❏ mumps usually presents with bilateral parotid enlargement, +/– sensorineural hearing loss, +/– orchitis
Diagnosis
❏ imaging with U/S employed to differentiate obstructive vs. non-obstructive sialoadenitis
Treatment
❏ bacterial: treat with cloxacillin +/- abscess drainage
❏ viral: no treatment
SIALOLITHIASIS
❏ ductal stone with chronic sialadenitis
❏ 80% occurs in the submandibular gland, <20% in parotid gland, ~1% in sublingual gland
❏ predisposing factors:
• any condition causing duct stenosis or a change in salivary secretions
(e.g. dehydration, diabetes, EtOH,hypercalcemia)
Presentation
❏ pain and tenderness over involved gland
❏ intermittent swelling related to meals
Diagnosis
❏ by digital palpation of calculi
❏ sialogram
Treatment
❏ remove calculi by dilating duct and orifice or excision through floor of mouth
❏ if calculus is within the gland parenchyma then the whole gland must be excised
SALIVARY GLAND MANIFESTATIONS OF SYSTEMIC DISEASE
❏ Sjögrens syndrome: chronic disorder characterized by immune-mediated destruction of exocrine glands
(triad of conjunctivitis sicca, xerostomia, parotidenlargement) diffuse non-tender, asymptomatic
enlargement of the parotid glands and occasionally other salivary glands
❏ bulemia nervosa: bilateral swelling of parotid glands, approximately 30% of patients will have resolution
with control of bulemia
OT36 – Otolaryngology MCCQE 2002 Review Notes
NECK MASSES
Submental triangle
Digastric
(anterior belly)
Digastric triangle
Trapezius
Posterior triangle
Occipital triangle
Omohyoid
(inferior belly)
Omohyoid
(superior belly) Subclavian triangle
Sternocleidomastoid
Figure 11. Anatomical Triangles of the Neck
Illustration by Evan Propst
I II
VI III
V
IV
Figure 12. Lymphatic Drainage of the Neck Figure 13. Zones of the Neck
Reproduced with permission from Churchill Livingston, Dhillon, R.S, East, C.A. Ear, Nose and Throat and Head and Neck Surgery. Churchill Livingston, UK, 1994.
The stemocleidomastoid divides the neck into two triangles (see Figure 11)
❏ Anterior triangle
• bounded by anterior border of sternocleidomastoid, midline of neck and lower border of mandible
• divided into
• submental triangle: bounded by both anterior bellies of digastrics and hyoid bone
• digastric triangle: bounded by anterior and posterior bellies of digastric, and inferior border
of mandible
• carotid triangle: bounded by sternocleidomastoid, anterior belly of omohyoid, and posterior
belly of digastric
• contains tail of parotid, submandibular gland, hypoglossal nerve, carotid bifurcation and lymph nodes
❏ Posterior triangle
• bounded by posterior border of sternocleidomastoid, anterior border of trapezius, and middle third of
clavicle
• divided into
• occipital triangle: superior to posterior belly of the omohyoid
• subclavian triangle: inferior to posterior belly of omohyoid
• contains spinal accessory nerve and lymph nodes
Neck Mass
❏ reactive lymphadenopathy
❏ Tb or atypical mycobacteria
❏ infectious mononucleosis Midline Lateral Malignant Benign
❏ abscesses
❏ cat scratch fever
❏ sarcoidosis • thyroglossal duct cyst • branchial cleft cyst • salivary gland
• thyroid tumour/goitre • cystic hygroma neoplasm
• pyramidal lobe of (pleomorphic
thyroid gland adenoma,
• midline dermoid cyst Warthin’s tumour)
• thymus cyst • lipoma
• fibroma
• vascular
• paragangliomas
• neurofibromas
• schwannomas
Primary Metastatic
• lymphoma • head and neck
(Hodgkin’s or primary
NHL: see • infraclavicular primary
Hematology • leukemia
Chapter)
• thyroid
• sarcoma
• salivary gland
neoplasm
(mucoepidermoid,
adenoid cystic,
acinic cell)
EVALUATION
Investigation
❏ history and physical (including nasopharynx and larynx)
❏ indirect tests - supply information about physical characteristics of mass
• WBC - infection vs. lymphoma
• Mantoux TB test
• thyroid function tests and scan
• neck U/S
• CT scan
• angiography - vascularity and blood supply to mass
❏ direct test - for histologic examination
• fine needle aspiration (FNA) - less invasive
• needle biopsy
• open biopsy-for lymphoma
• radiologic exam of stomach, bowel and sinuses
• search for the primary tumour (panendoscopy: nasopharyngoscopy, laryngoscopy, bronchoscopy with
brushings, esophagoscopy)
• biopsy of normal tissue of nasopharynx, tonsils, base of tongue and hypopharynx
❏ if primary found (95%), stage and treat
❏ if primary still occult (5%) - excisional biopsy of node for diagnosis,
manage with radiotherapy or neck dissection (squamous cell carcinoma)
CONGENITAL NECK MASSES IN DETAIL
Branchial Cleft Cysts/Fistulae (see Colour Atlas OT11)
❏ at 6th week of development, the second branchial arch grows over the third and fourth arches and fuses with
the neighbouring caudal pre-cardial swelling forming the cervical sinus
❏ branchial fistula formed by persistence of external opening of sinus while persistent parts of the cervical sinus
without an external opening cause branchial cysts
❏ 2nd branchial cleft cysts most common
❏ clinical presentation
• fistulas with an internal or external communication usually manifest during infancy as a small opening
anterior to the sternocleidomastoid muscle
❏ branchial cysts that do not have an external or internal opening present in teens and twenties as a smooth
painless slowly enlarging lateral neck mass, often following an acute URTI infection
❏ treatment
• surgical removal of cyst or fistula tract
❏ if infected - allow infection to settle before removal
Thyroglossal Duct Cysts (see Colour Atlas OT10)
❏ thyroid originates as ventral midline diverticulum of floor of pharynx caudal to junction of 1st and 2nd
branchial arches (foramen cecum)
❏ thyroid migrates caudally along a tract ventral to hyoid then curves underneath and down to cricoid with
thyroglossal duct cysts being vestigial remnants of tract
❏ clinical presentation
• usually presents in the second to fourth decades as a midline cyst that elevates with swallowing and
tongue protrusion
❏ treatment
• consists of pre-operative antibiotics to reduce inflammation followed by complete excision of cyst and
tract up to foramen cecum at base of tongue with removal of central portion of thyroid (Sistrunk
procedure)
Cystic Hygroma
❏ lymphangioma arising from vestigial lymph channels of neck
❏ clinical presentation
• usually presents by age 2 as thin-walled cyst in tissues from floor of mouth down to mediastinum,
usually in posterior triangle or supraclavicular area
• infection causes a sudden increase in size
❏ treatment
• surgical excision if it fails to regress - difficult dissection due to numerous cyst extensions
Prognosis
❏ benign: excellent, although pleomorphic adenomas may recur (< 5%)
❏ mucoepidermoid: good if low grade - 80% 5-year survival
❏ others: fair, but tend to recur - 40% 5-year survival
❏ if neck nodes involved: 20% 5-year survival
History
❏ F > M for nodules but in males a nodule is more likely to be malignant
❏ history of head and neck irradiation
❏ occupational/environmental radiation exposure associated with papillary carcinoma
❏ local compressive neck symptoms - hoarseness, dysphagia, dyspnea, and aspiration
❏ family history of multiple endocrine neoplasia type II (MEN II) (medullary cancer)
❏ nodule in patient with a history of Hashimoto's - at risk for lymphoma
❏ rapid increase in size of nodule - may indicate malignancy
Physical Findings
❏ palpation of thyroid - solitary, hard, irregular nodule is suggestive of malignancy, multinodular suggestive
❏ benign indirect laryngoscopy - vocal cord paralysis increases suspicion of malignancy
❏ cervical lymphadenopathy - deep cervical chain suggestive of metastatic disease
❏ signs of hypo/hyperthyroidism
THYROID CARCINOMA
Papillary Follicular Medullary Anaplastic
Adenocarcinoma Adenocarcinoma Carcinoma
Incidence 60-70 % 10% 2-5% 5%
(% of all thyroid cancers) (10% familial, 90% sporadic)
Route of Spread Lymphatic Hematogenous Lymphatic and
Orpan Annie nuclei hematogenous
Histologic Findings Psammoma bodies Capsular or blood vessel Amyloid Giant cells, spindle cells
invasion delign malignancy secrete calcitonin
Other P’s of papillary F’s of follicular cancer M’s of medullary cancer
adenocarcinoma - Faraway mets - MEN (associated with
- Papillary cancer - Female (3:1) MEN II)
- Popular - FNA, NOT (can’t be - Multiple endocrine
(most common) diagnosed by FNA) neoplasia
- Palpable lymph nodes - Favourable prognosis
- Positive 131I uptake
- Positive prognosis
- Post-op 131I scan to
diagnose treatments
10 yr survival rate 95% 90% - 50%
- 20% if detected when - Survival past 2 years is
clinically palpable rare
Treatment - Small tumours: - Small tumours: - Total thyroidectomy - Small tumours:
(see Surgical Procedures - Near total - Near total and median lymph node - Total thyroidectomy
section) thyroidectomy thyroidectomy/lobectomty dissection ± external beam
or/thyroid lobectomy /isthemectomy - Modified neck dissection, - Airway compromise:
- Diffuse/bilateral - Large/diffuse tumours if lateral cervical nodes are debulking surgery and
- Total thyroidectomy total thyroidectomy positive tracheostomy
Thyroid Nodule
warm = increased 131I
Hx, Px, TSH, T4, ± thyroglobulin ± antithyroid antibody ± U/S* or 99mT uptake
= functioning/
FNA (if do U/S still must do a FNA) hyperfunctioning
nodule
benign inflammatory cells papillary follicular or indeteminant Cold = decreased 123I
or indeterminant (false postive < 1%) (high false negative) or 99mT uptake
= nonfunctionting
nodule
T4 suppression repeat OR U/S
cystic solid
TRACHEOSTOMY
❏ tracheotomy is a temporary alternative airway, whereas tracheostomy is a permanent or semi-permanent
tracheocutaneous fistula. In practice, the two are often used interchangeably
❏ indications
• airway obstruction
• long-term ventilatory support
• prevention of aspiration by allowing suctioning of excessive airway secretions
❏ tracheostomy
• open surgical tracheostomy
• first incision is horizontal, midway between the sternal notch and cricoid cartilage
(~2 fingerbreadths above the sternal notch)
• this incision is continued down through skin, subcutaneous tissue, and platysma
• separate the sternohyoid and sternothyroid muscle pairs with a midline vertical dissection
• these muscles are pulled away from midline with retractors, revealing the thyroid isthmus
• isthmus is transected vertically and each side is suture-ligated
• a cricoid hook (placed between the cricoid cartilage and the 1st tracheal ring) is used to pull the
trachea superiorly while the tracheal incision is placed at the level of 2nd tracheal ring
• removal of circular window of cartilage
• placement of double lumen tracheostomy tube
• percutaneous dilatational tracheostomy
• frequently used within many ICU settings
• translaryngeal tracheostomy
• the most recent technique
❏ complications
• hemorrhage
• tube obstruction
• mortality rate is < 2%
Reference
MacCallum PL et. al. Comparison of open, percutaneous,and translaryngeal tracheostomies. Otolaryngol Head Neck Surg 2000;122:686-90.
Weissler MC. Tracheotomy and Intubation. Chapter 57. In Bailey BJ (ed). Head & Neck Surgery - Otolaryngology 2nd ed. Loppincott-Raven Publishers. Philadelphia. 1998.
TONSILLECTOMY
❏ excision of tonsils
❏ indications
• most common reason: obstructive tonsillar hyperplasia
• absolute
• obstructive sleep apnea or cor pulmonale
• malignancy or suspected malignancy
• tonsillitis resulting in febrile convulsions
• persistent or recurrent tonsillar hemorrhage
• relative
• recurrent acute or chronic tonsillitis
• peritonsillar abcess
• eating or swallowing disorders
• tonisllolithiasis
• haletosis
• orofacial or dental abnormalities
• contraindications
• blood dyscrasias
• uncontrolled systemic diseases (diabetes, etc.)
• cleft palate
• acute infections
❏ technique: electrocautery (hot) vs. “cold steel” (uncommon)
❏ complications
• bleeding
• airway obstruction
• velopharyngeal insufficiency (VPI)
• pulmonary edema
• dehydration and weight loss
THYROIDECTOMY
❏ excision of the thyroid gland
• can be total, subtotal, lobectomy and isthmusectomy
• neck dissection with preservation of sternodedomastoid if lymph nodes clinically involved
• radical neck dissection of extensive infiltrating tumour
❏ indications
• any thyroid abnormality in a patient with previous irradiation of neck
• a solitary nodule in patient less than 20 years old
• a solitary nodule in male patient
• a nodule associated with signs suggestive of malignancy, inducing recurrent nerve paralysis,
palpable nodes in the neck, extreme hardness, or extension into adjacent tissues
• a solitary thyroid nodule in a patient over 60 years of age
• most (solitary) nodules
• a normal thyroid gland in a patient with proven metastatic thyroid cancer
• a patient with an abnormal calcitonin stimulation test
❏ complications
• damage to recurrent laryngeal nerves (hoarseness if unilateral, airway obstruction if bilateral)
• damage to superior laryngeal nerve (deeper and quieter voice)
• damage to parathyroid glands = hypoparathyroidism (signs of hypocalcemia)
• excessive bleeding
REFERENCES
Becker W, Naumann HH and Pfaltz CR. Ear, Nose and Throat Diseases. 2nd edition. 1994. Thieme Medical Publishers, Inc. New
York.
Furman JM and Cass SP. BPPV. 1999. NEJM. 341 (21): 1590-1596.
MacCallum PL et al. Comparison of open, percutaneous and translaryngeal tracheostomies. Otolaryngology Head Neck Surgery.
2000. 122: 686-690.
Mente FE and Har-El G (eds). Essentials of Otolaryngology. 4th edition. 1999. Lippincott Williams and Wilkins. USA.