Otolaryngology – Toronto Notes

Abridged for the PDA

To be used only in conjunction with the printed Toronto Notes
Kristen Davidge and John de Almeida
Cagla Eskicioglu and Nadra Ginting, associate editors
Maja Segedi, EBM editor
Staff Editor: Dr. Jonathan Irish

Physical Examination
Head and Neck
Ear
Otoneurological Examination
Nose
Oral Cavity
Nasopharynx (NP)
Hypopharynx and Larynx

Approach to the Patient with Hearing Loss

Pure Tone Audiometry
Speech Audiometry
Impedance Audiometry
Auditory Brainstem Response
Aural Rehabilitation

Evaluation of the Dizzy Patient

Tinnitus

Presbycusis
Drug Ototoxicity
Noise-Induced Sensorineural Hearing Loss
Benign Paroxysmal Positional Vertigo
Menière’s Disease
Vestibular Neuronitis
Acoustic Neuroma (AN)

Allergic Rhinitis
Nasal Polyps
Septal Deviation

Epistaxis

Sinusitis
Acute Suppurative Sinusitis
Chronic Sinusitis

Acute Otitis Media (AOM)

Otitis Media with Effusion (OME)
Head and Neck
Inspection of Head and Neck
• look for scars, asymmetry, masses, enlarged thyroid or parotids, skin lesions

Palpation of Head and Neck

• lymph node: note size, mobility, consistency, tenderness, warmth, regular/irregular
border, fixation to surrounding structures
• salivary glands: tenderness, swelling, masses, nodules on stones

Thyroid Gland
• note any stigmata of thyroid disease (see Endocrinology, E20)
• inspection of gland symmetry, mobility
• palpation via anterior or posterior approach
note size, shape, consistency, nodularity, tenderness
• thyroid bruits on auscultation may suggestive of a toxic goiter

Ears – Anatomy
External Examination of Ear (see Figure 1)
• inspect external ear structures
note position of ear, deformities, nodules, inflammation, or lesions
potential findings
microtia or macrotia: congenitally small or large auricles
cauliflower ear: deformity of pinna due to subperichondrial
hematomas resulting from repeated mechanical trauma
preauricular pits: due to failure of fusion the first and second
branchial arches
tophi: sign of gout
• palpate external ear structure
examine for infection of external ear
pain elicited by pulling pinna up or down, or pressing on tragus
examine for infection of mastoid bone
tenderness upon pressure to mastoid tip

Otoscopic Examination (see Figure 2)

• inspect external canal
look for evidence of inflammation, foreign bodies, or discharge
• inspect tympanic membrane (TM)
normal membrane: intact, translucent, gray
white (pus)
red (erythema): AOM, OME
clear yellow: serous otitis media
dark black/red/brown: hemorrhage
• possible abnormal findings
acute otitis media: erythema of pars flaccida and tensa, malleus not
visualized due to inflammation, lack of motion of tympanic membrane,
absence of light reflex
otitis media with effusion: erythema of malleus, pars tensa injected,
prominent short process of malleus, limited motion, decreased light reflex,
yellow serous fluid behind tympanic membrane
tympanosclerosis: dense white plaques
membrane perforation

Auditory Acuity
• mask one ear and whisper into the other
• tuning fork tests (see Table 1) (audiogram of greater utility)
Rinne test
 512 Hz tuning fork is struck and held firmly on mastoid process to
test bone conduction (BC). The tuning fork is then placed beside the
pinna to test air conduction (AC)
Weber test
512 Hz tuning 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)
can place vibrating fork on patient’s chin while they clench
their teeth, or directly on teeth to elicit more reliable response
Otoneurological Examination
• otoscopy
• cranial nerve testing (II to XII inclusive)
• cerebellar testing

Nystagmus (see Opthalmology, OP36)

• assess nystagmus – describe quick phase, avoid examining in extremes of lateral
gaze
• horizontal nystagmus that beats in the same direction = peripheral vestibular
disorder
the fast phase component of nystagmus is directed away from the site of the
lesion
• horizontal nystagmus that changes direction with gaze deviation = central
vestibular disorder
• vertical upbeating nystagmus = brainstem disease
• vertical downbeating nystagmus, usually = medullocervical localization
(e.g. Arnold-Chiari)

Electronystagmography (ENG)
• electrodes placed around eyes
• eye is a dipole, cornea (+), retina (–)
• used to measure rate, amplitude, and frequency of nystagmus elicited by different
stimuli

Balance Testing
• Romberg’s test: patient stands upright with feet together, eyes closed, and arms
extended in front of chest
sway is associated with loss of either joint proprioception or peripheral
vestibular disturbance
the patient leans or tends to fall toward the side of the diseased labyrinth
• Unterberger’s test: marching on the spot with the eyes closed
peripheral disorders: rotation of body to the side of the labyrinthine lesion
central disorders: deviation is irregular

Caloric Stimulation Test

• with the patient supine, the neck is flexed 30º to bring the horizontal semicircular
canal into a vertical position
• the direction of endolymph flow is changed by irrigating the labyrinthine capsule
with warm (30ºC or 44ºC) or cold (0º) water for 35 seconds
• the change in direction of endolymph causes deflection of the cupula and
subsequent nystagmus through the vestibuloocular reflex (VOR)
• the extent of response indicates the function of the stimulated labyrinth

Dix-Hallpike Positional Testing with Frenzel’s (Magnifying) Eyeglasses

(See Figure 5)
• the patient is rapidly moved from a sitting position to a supine position with the
head hanging over the end of the table, turned to one side at 45º holding the
position for 20 seconds
• onset of vertigo is noted and the eyes are observed for nystagmus
• upon return to starting position, nystagmus may again be observed but the
direction will be reversed
Nose
External Examination of Nose
• inspect nose
look for swelling, trauma, congenital anomalies, deviation, hematoma,
saddle-nose deforming
• palpate sinuses
tenderness over frontal and maxillary sinuses may indicate sinusitis

Internal Examination of Nose

• inspect with nasal speculum (see Figure 6)
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
• anatomic boundaries of oral cavity
anterior: lips
lateral: buccal mucosa
posterior: anterior tonsillar pillars (junction of hard and soft palate)
superior: hard palate
inferior: floor of trigone
also includes: tongue anterior to circumvallate papillae, alveolus, and
retromolar trigone
• lips
note colour, symmetry, texture, and lesions
• buccal mucosa
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 (underbite, overbite)
• hard and soft palates
note any asymmetry, ulceration, masses, deformities, oronasal fistulas
• tongue
inspect for colour, mobility, masses, tremor, and atrophy
palpate tongue for any masses
test cranial nerve XII
• floor of mouth
palpate for any masses
identify Wharton’s ducts (submandibular gland ducts) on either side just
lateral to frenulum of tongue
bimanually palpate submandibular glands

Oropharynx
• anterior facial pillars, tonsils, tonsillolingual sulcus
note size and inspect for tonsillar exudate or lesions, look at tonsillar crypts
• posterior pharyngeal wall
Nasopharynx
Fibre-Optic Nasopharyngolaryngoscope (Direct)
• patient is prepared by administering topical anesthetic/decongestant
• the scope is used to visualize
nasal cavity/nasopharynx
nasal vestibule
superior, middle, inferior meatus
eustachian tubes
choana
adeynoids
oropharynx/hypopharynx/larynx
• look for nodules, ulcerations, irregularity of circumvallate papillae, base of tongue,
lingual tonsil, valleculae epiglottis, aryepiglottic folds, pyriform fossae, false vocal
cords, true vocal cords
• note position of cords
quiet respiration: cords are moderately separated
inspiration: cords abduct slightly
ask patient to say “eee”: cords should abduct to midline
look for cord paralysis and fixation

Postnasal Mirror (Indirect)

• the 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

Hypopharynx and Larynx

Indirect Laryngoscopy
• position the patient leaning slightly forward with the head slightly extended
• 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 8)
Approach to the Patient with Hearing Loss
TYPES OF HEARING LOSS

1. Conductive Hearing Loss (CHL)

• the conduction of sound to the cochlea is impaired
• can be caused by external and middle ear disease

2. Sensorineural Hearing Loss (SNHL)

• due to a defect in the conversion of sound into neural signals or in the transmission
of those signals to the cortex
• can be caused by disease of the cochlea, acoustic nerve (CN VIII), brainstem, and
cortex

3. Mixed Hearing Loss

• the conduction of sound to the cochlea is impaired, as is the transmission through
the cochlea to the cortex

History
• onset, character, duration, and progression of loss
• unilateral vs. bilateral
• associated symptoms:
otorrhea, tinnitus, vertigo, disequilibrium, aural pressure
visual, speech, or other neurological symptoms
• history of head trauma, ear surgery, noise exposure, or barotrauma
• family history of hearing loss
• medications (especially use of ototoxic drugs e.g. Aminoglycosides)
• other medical problems

Physical
• otoscopy, pneumatic otoscopy
• tuning fork tests: Rinne and Weber tests
• general head and neck exam as indicated

Investigations
• audiologic testing (see below)
• auditory brainstem response (ABR) if loss is unilateral
Pure Tone Audiometry
• threshold is the lowest intensity level at which a patient can hear the tone 50% of
the time
• thresholds are obtained for each ear for frequencies 250 to 8000 Hz
• air conduction thresholds are obtained with headphones and measure outer,
middle, inner ear, and auditory nerve function
• bone conduction thresholds are obtained with bone conduction oscillators which
bypass the outer and middle ear

Degree of Hearing Loss

• determined on basis of the pure tone average (PTA) at 500, 1000, and 2000 Hz

PURE TONE PATTERNS

1. Conductive Hearing Loss (CHL) (Figure 11B, 11C)

• bone conduction (BC) in normal range
• air conduction (AC) outside of normal range
• gap between AC and BC thresholds >10 dB (an air-bone gap)

2. Sensorineural Hearing Loss (SNHL) (Figure 11D, 11E)

• both air and bone conduction thresholds below normal
• gap between AC and BC < 10 dB (no air-bone gap)

3. Mixed
• both air and bone conduction thresholds below normal
• gap between AC and BC thresholds > 10 dB (an air-bone gap)

Speech Audiometry
Speech Reception Threshold (SRT)
• lowest hearing level at which patient is able to repeat 50% of two syllable words
which have equal emphasis on each syllable (spondee words)
• SRT and best pure tone threshold in the 500 to 2000 Hz range (frequency range of
human speech) usually agree within 5 dB. If not, suspect a retrocochlear lesion or
functional hearing loss
• used to assess the reliability of the pure tone audiometry

Speech Discrimination Test

• percentage of words the patient correctly repeats from a list of 50 monosyllabic
words
• tested at a level 35 to 50 dB > SRT, therefore degree of hearing loss is taken into
account
• patients with normal hearing or conductive hearing loss score > 90%
• score depends on extent of SNHL
• a decrease in discrimination as sound intensity increases is typical of a
retrocochlear lesion (rollover effect)
• investigate further if scores differ more than 20% between ears
Impedance Audiometry
Tympanogram
• the eustachian tube equalizes the pressure between external and middle ear
• tympanograms graph the compliance of the middle ear system against pressure
gradient ranging from to –400 to +200 mm H2O
• tympanogram peak occurs at the point of maximum compliance where the
pressure in the external canal is equivalent to the pressure in the middle ear
• normal range: -100 to +50 mm H2O

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 2º to loud sound
• acoustic reflex thresholds = 70 to 100 dB > hearing threshold; if hearing threshold
> 85 dB, reflex likely absent
• stimulating either ear causes bilateral and symmetrical reflexes
• for reflex to be present, CN VII must be intact and no conductive hearing loss in
monitored ear
• if reflex is absent without conductive or severe sensorineural loss ^ suspect CN
VIII lesion
• acoustic reflex decay test = ability of stapedius muscle to sustain contraction for
10 s at 10 dB
• normally, little reflex decay occurs at 500 and 1000 Hz
• with cochlear hearing loss, acoustic reflex thresholds = 25 to 60 dB
• with retrocochlear hearing loss (acoustic neuroma) ^ absent acoustic reflexes or
marked reflex decay (>50%) within 5 seconds
Auditory Brainstem Response (ABR)
• measures neuroelectric potentials (waves) in response to a stimulus in five different
anatomic sites. This test can be used to map the lesion according to the site of the
defect (anatomic sites : ECOLI) (see side bar)
• delay in brainstem response suggests cochlear or retrocochlear abnormalities
(tumour or multiple sclerosis (MS))
• does not require volition or co-operation of patient

Aural Rehabilitation
• dependent on degree of hearing loss, communicative requirements, motivation,
expectations, age, physical, and mental abilities
• negative prognostic factors
poor speech discrimination
narrow dynamic range (recruitment)
unrealistic expectations
cosmetic concerns
• types of hearing aids
behind the ear (BTE)
all in the ear (ITE)
bone conduction – bone anchored hearing aid (BAHA):
applied to the skull and attached to the skull
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
Evaluation of the Dizzy Patient
• vertigo: an illusion of rotary movement of self or environment, made
worse in the absence of visual stimuli
produced by peripheral (inner ear) or central (brainstem-cerebellum)
stimulation
• it is important to distinguish vertigo from other disease entities that may present
with similar complaints (e.g. cardiovascular, psychiatric, neurological, aging)

History
• diagnosis is heavily dependent upon an accurate history
description of rotary movement
onset
acute vs. insidious
associated with body position, head movement
duration
course of illness
repeated acute attacks vs. single major attack that slowly improves
frequency of attacks
symptomatic vs. asymptomatic between attacks
exacerbating/relieving factors
effect of dark/eye closing
worse with head movement
associated symptoms (and temporal relationship to dizziness)
hearing loss, tinnitus, aural fullness, otorrhea, otalgia, nausea,
vomiting
neurological symptoms
eye movement (nystagmus) noted by observer
alcohol and drug history (antihypertensives, aminoglycosides)
medical history (vascular disease, anxiety disorder)
degree of disability caused by dizziness

Physical Examination (see Physical Exam, OT2)

• otoscopy
• cranial nerve exam (II-XII)
• extraocular motility (nystagmus) assessment
• balance testing – Romberg’s test, Unterberger’s step test, tandem and normal gait
• Dix-Hallpike test

Investigations
• electronystagmography with caloric stimulation
• ± audiology
• ± imaging (MRI/CT) as indicated
Tinnitus
Definition
• an auditory perception in the absence of an acoustic stimuli, often very annoying to
the patient

Investigations
• audiology
• if unilateral
ABR, MRI/CT to exclude a retrocochlear lesion
• if suspect metabolic abnormality: lipid profile, TSH

Treatment
• if a cause is found, treat the cause (e.g. drainage of middle ear effusion)
• with no treatable cause, 50% will improve, 25% worsen, 25% remain the same
• avoid: loud noise, ototoxic meds, caffeine, smoking
• tinnitus workshops
• identify situations where tinnitus is most bothersome (e.g. quiet times),
mask tinnitus with soft music or “white noise”
• hearing aid if coexistent hearing loss
• tinnitus instrument
combines hearing aid with white noise masker
• trial of tocainamide

Presbycusis
Definition
• sensorineural hearing loss associated with aging (5th and 6th decades)

Etiology
• hair cell degeneration
• age related degeneration of basilar membrane
• cochlear neuron damage
• ischemia of inner ear

Clinical Features
• progressive, gradual bilateral hearing loss initially at high frequencies, then middle
frequencies (see Figure 11E, OT9)
• loss of discrimination of speech especially with background noise present - patients describe people as mumbling
• recruitment phenomenon: inability to tolerate loud sounds
• tinnitus

Treatment
• hearing aid if patient has difficulty functioning, hearing loss > 30-35 dB
• ± lip reading, auditory training, auditory aids (doorbell and phone lights)
Drug Ototoxicity
Aminoglycosides
• toxic to hair cells by any route: oral, IV, and topical (only if the TM is perforated)
• destroys sensory hair cells – outer first, inner second
• high frequency hearing loss develops earliest
• ototoxicity occurs days to weeks post-treatment
• streptomycin and gentamycin (vestibulotoxic), kanamycin and tobramycin
(cochleotoxic)
• must monitor levels with peak and trough levels when prescribed, especially if
patient has neutropenia, history of ear or renal problems
• q24h dosing, with amount determined by creatinine clearance not serum creatinine
• aminoglycoside toxicity displays saturable kinetics therefore once daily dosing
presents less risk than divided daily doses
• duration of treatment is the most important predictor of ototoxicity
• treatment: immediately stop aminoglycosides

Salicylates
• hearing loss with tinnitus, reversible if discontinued

Antimalarials (Quinine)
• hearing loss with tinnitus
• reversible if discontinued but can lead to permanent loss
• others: antineoplastics, loop diuretics

Chemotherapy
• many agents one ototoxic
Noise-Induced Sensorineural Hearing Loss
Pathogenesis
• 85 to 90 dB over months or years causes cochlear damage
• early-stage hearing loss at 4000 Hz (because this is the resonance frequency of the
temporal bone), extends to higher and lower frequencies with time (see Figure 11D,
OT9)
• speech reception not altered until hearing loss > 30 dB at speech frequency,
therefore considerable damage may occur before patient complains of hearing loss
• difficulty with speech discrimination, especially in situations with competing noise

Phases of Hearing Loss

• dependent on intensity level and duration of exposure
• temporary threshold shift
when exposed to loud sound, decreased sensitivity or increased threshold
for sound
may have associated aural fullness and tinnitus
with removal of noise, hearing returns to normal
• permanent threshold shift
hearing does not return to previous state

Treatment
• hearing aid
• prevention
ear protectors: muffs, plugs
machinery which produces less noise
limit exposure to noise with frequent rest periods
regular audiologic follow-up

Benign Paroxysmal Positional Vertigo (BPPV)

Definition
• acute attacks of transient vertigo lasting seconds to minutes initiated by certain
head positions, accompanied by nystagmus

Etiology
• due to migration of an otolith (cupulolithiasis) into posterior semicircular canal
where it stimulates one of the semicircular canals
causes: head injury, viral infection (URTI), degenerative disease, idiopathic
results in slightly different signals being received by the brain from the two
balance organs resulting in sensation of movement

Diagnosis
• history
• positive Dix-Hallpike maneuver (see Otoneurological Examination, OT7)

Treatment
• reassure patient that process resolves spontaneously
• particle repositioning maneuvers
Epley’s maneuver (performed by MD)
Brandt-Daroff exercises (performed by patient)
• surgery for refractory cases
• anti-emetics for nausea/vomiting
• drugs to suppress the vestibular system delay eventual recovery and are therefore
not used
Menière’s Disease (Endolymphatic Hydrops)
Definition
• episodic attacks of tinnitus, hearing loss, aural fullness, and vertigo lasting minutes
to hours

Etiology
• inadequate absorption of endolymph leads to endolymphatic hydrops (over
accumulation) that distorts the membranous labyrinth

Epidemiology
• peak incidence 40 to 60 years
• bilateral in 35% of cases

Clinical Features
• syndrome characterized by vertigo, fluctuating hearing loss, tinnitus, and aural
fullness
• ± drop attacks (Tumarkin crisis), ± nausea, and vomiting
• vertigo disappears with time (minutes to hours), but hearing loss remains
• early in the disease, fluctuating sensorineural hearing loss
• later stages are characterized by persistent tinnitus and low-frequency hearing loss
• attacks come in clusters and may be very debilitating to the patient
• may be triggered by stress

Treatment
• acute management may consist of bed rest, antiemetics, antivertiginous drugs
(e.g. betahistine (Serc™)), and low molecular weight dextrans (not commonly
used)
• longterm management may be
medical
low salt diet, diuretics (e.g. HCTZ, triamterene, amiloride)
local application of gentamicin to destroy vestibular end-organ
Serc™ prophylactically to decrease intensity of attacks
surgical – selective vestibular neurectomy or transtympanic labyrinthectomy
• may recur in opposite ear after treatment
Vestibular Neuronitis
Definition
• acute onset of disabling vertigo often accompanied by nausea, vomiting and
imbalance without hearing loss that resolves over days leaving a residual
imbalance that lasts days to weeks

Etiology
• thought to be due to a viral infection (e.g. measles, mumps, herpes zoster)
• ~30% of cases have associated URTI symptoms
• other possible etiologies: microvascular events, diabetes, autoimmune process
• considered to be the vestibular equivalent of Bell’s palsy, sudden hearing loss, and
acute vocal cord palsy

Clinical Features
• acute phase
severe vertigo with nausea, vomiting, and imbalance lasting 1 to 5 days
irritative nystagmus (fast phase towards the offending ear)
patient tends to veer towards affected side
• convalescent phase
imbalance and motion sickness lasting days to weeks
spontaneous nystagmus away from affected side
gradual vestibular adaptation requires weeks to months
• incomplete recovery likely with the following risk factors: elderly, visual
impairment, poor ambulation
• repeated attacks can occur

Treatment
• acute phase
bed rest, vestibular sedatives (dimenhydrinate (Gravol™), diazepam)
• convalescent phase
progressive ambulation especially in the elderly
vestibular exercises: involve eye and head movements, sitting, standing,
and walking

Acoustic Neuroma (AN)

Definition
• schwannoma of the vestibular portion of CN VIII

Pathogenesis
• starts in the internal auditory canal and expands into CPA, compressing cerebellum
and brainstem
• when associated with type 2 neurofibromatosis (NF2): bilateral tumours of
CN VIII, café-au-lait lesions, multiple intracranial lesions

Clinical Features
• usually presents with unilateral sensorineural hearing loss or tinnitus
• dizziness and unsteadiness may be present, but true vertigo is rare as tumour
growth occurs slowly
• facial nerve palsy and trigeminal (V1) sensory deficit (corneal reflex) are late
complications

Diagnosis
• MRI with gadolinium contrast is the gold standard
• audiogram – sensorineural hearing loss
• poor speech discrimination and stapedial reflex absent or significant reflex decay
• acoustic brainstem reflexes (ABR) – increase in latency of the 5th wave
Treatment
• expectant management if tumour is very small, in elderly, or in moribund
• definitive management is surgical excision
• other options: gamma knife, radiation
Allergic Rhinitis (Hay Fever)
Definition
• rhinitis characterized by an IgE mediated hypersensitivity to foreign allergens
• acute and seasonal or chronic and perennial
• perennial allergic rhinitis often confused with recurrent colds

Etiology
• when allergens contact the respiratory mucosa, specific IgE antibody is produced
in susceptible hosts
• concentration of allergen in the ambient air correlates directly with the rhinitis
symptoms

Epidemiology
• age at onset usually < 20 years
• more common in those with a personal or family history of allergies/atopy

Clinical Features
• nasal: obstruction with pruritus, sneezing
• clear rhinorrhea (containing increased eosinophils)
• itching of eyes with tearing
• frontal headache and pressure
• mucosa – swollen, pale, lavender color, and “boggy”
• seasonal (summer, spring, early autumn)
pollens from trees
lasts several weeks, disappears and recurs following year at same time
• perennial
inhaled: house dust, wool, feather, foods, tobacco, hair, mould
ingested: wheat, eggs, milk, nuts
occurs intermittently for years with no pattern or may be constantly present

Complications
• chronic sinusitis/polyps
• serous otitis media

Diagnosis
• history
• direct exam
• allergy testing

Treatment
• education: identification and avoidance of allergen
• nasal irrigation with saline
• antihistamines e.g. diphenhydramine, terfenadine
• oral decongestants e.g. pseudoephedrine, phenylpropanolamine
• topical decongestant may lead to rhinitis medicamentosa
• other topicals: steroids (fluticasone), disodium cromoglycate, anti-histamines,
ipatropium bromide
• oral steroids if severe
• desensitization by allergen immunotherapy
Nasal Polyps
Definition
• benign pedunculated/sessile masses of hyperplastic sinus mucosa caused by
inflammation
• antrochoanal polyps – (uncommon) arise from maxillary sinus and may extend
into the nasopharynx obstructing airway

Etiology
• mucosal allergy (majority)
• chronic rhinosinusitis
• associated with cystic fibrosis, Kartaganer’s syndrome, Churg-Strauss syndrome
• note: triad of polyps, aspirin sensitivity, asthma (Samter’s triad)

Clinical Features
• progressive nasal obstruction, hyposmia, snoring, epiphora
• post-nasal drip, stringy colorless/purulent rhinorrhea
• solitary/multiple glazed, smooth, transparent mobile masses (often bilateral)

Treatment
• eliminate allergen
• steroids (preoperative prednisone) to shrink polyp
• polypectomy is treatment of choice; however, polyps tend to recur
Complications
• sinusitis
• mucocele
• nasal widening (pseudohypertelorism)

Septal Deviation
Etiology
• developmental – unequal growth of cartilage and/or bone of nasal septum
• traumatic – facial and nasal fracture or birth injury

Clinical Features
• unilateral nasal obstruction (may be intermittent)
• anosmia, crusting, facial pain
• septum: S-shaped, angular deviation, spur
• compensatory middle/inferior turbinate hypertrophy

Treatment
• if asymptomatic – expectant management
• if symptomatic – septoplasty

Complications of Surgery
• post-op hemorrhage (can be severe)
• septal hematoma, septal perforation
• external deformity (saddle-nose)
• anosmia (rare but untreatable)
Epistaxis
Blood Supply to the Nasal Septum
1. superior posterior septum
internal carotid ^ ophthalmic ^ anterior/posterior ethmoidal
2. posterior septum
external carotid ^ internal maxillary ^ sphenopalatine artery
^ nasopalatine
3. lower anterior septum
external carotid ^ facial artery ^ superior labial artery ^ nasal branch
external carotid ^ internal maxillary ^ descending palatine
^ greater palatine

• these arteries all anastomose to form Kiesselbach’s plexus, located at Little’s area
(anterior portion of the cartilaginous septum), where 90% of nosebleeds occur
• bleeding from above middle turbinate is internal carotid, and from below is
external carotid

Investigations
• CBC, PT/PTT (if indicated)
• Xray, CT as needed

Treatment
• aim is to localize bleeding and achieve hemostasis

1. First-aid
• ABC’s
• patient leans forward to minimize swallowing blood
• firm pressure applied for 20 min on soft part of nose (not bony pyramid)

2. Assess Blood Loss (can be potentially fatal hemorrhage)

• pulse, blood pressure, and other signs of shock
• IV NS, cross match for 2 units packed RBCs if significant

3. Determine site of bleeding

• insert cotton pledget of 4% topical lidocaine ± topical decongestant cocaine,
visualize nasal cavity with speculum and aspirate excess blood and clots
• anterior/posterior hemorrhage defined by location in relationship to bony septum
• if suspicion, coagulation studies

4. Control the bleeding

• first line topical vasoconstrictors (Otrivin™, cocaine)
• if first line fails and bleeding adequately visualized, cauterize with silver
nitrate
• do not attempt to cauterize both sides of the septum due to risk of septal
perforation
A. anterior hemorrhage treatment
if fail to achieve hemostasis with cauterization
anterior pack with half inch Vaseline™ and ribbon gauze strips or
absorbable packing (i.e. Gelfoam™) layered from nasal floor toward nasal
roof extending to posterior choanae for 2 to 3 days (see Figure 19)
can also attempt packing with Merocel™ or nasal tampons of different shapes
B. posterior hemorrhage treatment
if unable to visualize bleeding source, then usually posterior source
different ways of placing a posterior pack with a Foley catheter, gauze pack
or Epistat™ balloon
bilateral anterior pack is layered into position
antibiotics for any posterior pack or any pack in longer than 48 hours
admit to hospital with packs in for 3 to 5 days
 watch for complications: hypoxemia (naso-pulmonic reflex), toxic shock
syndrome (Rx: remove packs immediately), pharyngeal fibrosis/
stenosis, alar/septal necrosis, aspiration
C. if anterior/posterior packs fail to control epistaxis
selective catheterization and embolization of branches of external carotid
artery
± septoplasty
vessel ligation of
anterior/posterior ethmoid artery
internal maxillary
external carotid

5. Prevention
• prevent drying of nasal mucosa with humidifiers, saline spray, or topical ointments
• avoidance of irritants
• medical management of hypertension and coagulopathies
Sinusitis
Development of Sinuses
• sinus pneumatization begins in 3-4th month fetal life. Maxillary sinus 1st to develop
• neonate – clinically significant ethmoid and maxillary buds present
• age 9 – maxillary full grown; frontal and sphenoid cells starting
• age 18 – frontal and sphenoid cells full grown

Drainage of Sinuses
• frontal, maxillary, anterior ethmoids: middle meatus (osteo-meatal complex)
• posterior ethmoid: superior meatus
• sphenoid: sphenoethmoidal recess
Pathogenesis of Sinusitis
• inflammation of the mucosal lining of the paranasal sinuses
• anything that blocks mucous from exiting the sinuses predisposes them to
inflammation

Definition
• inflammation of the mucosal lining of the sinuses

Classification
• acute: < 4 weeks
• subacute: 4 weeks to 3 months
• chronic: > 3 months

Acute Suppurative Sinusitis

Definition
• acute bacterial infection of the paranasal sinuses

Etiology
• inflammation of nasal and paranasal cavities ^ mucosal edema and decreased
ciliary action ^ retention of secretions ^ 2º bacterial infection ^ acute
sinusitis
• maxillary sinus most commonly affected

• organisms
Bacterial: S. pneumonia (35%), H. influenzae (35%), M. catarrhalis, anaerobes (dental)
Viral: rhinovirus, influenza, parainfluenza

Clinical Features
• facial pain or pressure
• nasal obstruction
• purulent nasal discharge
• hyposmia
• tenderness over involved sinus
maxillary – over cheek and upper teeth
ethmoids – medial nose, retroorbital pain
frontal – supraorbital ridge, roof of orbit
sphenoid – vertex, occipital or parietal headaches
• systemic: fever, chills, malaise

Guidelines
1. with fewer than 2/5 of the above, sinusitis can be ruled out (likelihood ratio < 0.5)
2. with 4 or more of the above, sinusitis can be ruled in (likelihood ratio > 6.4)
3. with 2-3 of the above, sinus radiography is suggested; begin with Waters view and
add others if inconclusive
4. also do radiographic exam in patients with frontal headaches to rule out frontal
sinusitis

Investigations
• 4-view radiographic exam (used infrequently):
Waters (occipitomental) view – maxillary sinuses; Caldwell (occipitofrontal)
view – ethmoid and frontal sinuses; lateral view (all); and submentovertex
view (sphenoid and ethmoid)
radiographic findings: air-fluid level (80% PPV, 60% sensitive), complete
opacification of sinus (100% PPV, 60% sensitive), mucosal thickening
(90% sensitive, 36-76% specific)
• CT provides superior detail and is more sensitive, but often shows mucosal
changes in normal individuals (more commonly used)
not cost-effective for routine diagnosis
indications: chronic refractory sinusitis, suspected malignancy or extrasinus
involvement, pre-op asessment
• MRI tends to overdiagnose sinus opacification

Treatment
• antibiotics although 40% recover spontaneously
amoxicillin 500 mg tid x 10 days is standard first-line therapy
numerous alternatives (TMP/SMX, clarithromycin, azithromycin) all equally
effective
failure of Rx= no improvement after 72 hrs
• adjunctive therapy
decongestants may be useful to reduce symptoms (weak evidence)
saline irrigation may reduce symptoms and prevent mucosal damage
no evidence for steroids
antihistamines may interfere with mucus clearance (contraindicated)
• surgery if medical therapy fails
FESS (functional endoscopic sinus surgery) (surgical procedure of choice)
traditional approaches (rarely used):
maxillary – antral puncture and lavage x max of 3, then antrostomy
ethmoid – external (Lynch incision), transantral or intranasal
ethmoidectomy
frontal– Lynch incision at medial orbital rim, irrigate, and drain
sphenoid – drain via posterior ethmoids
Low DE, Desrosiers M, McSherry J, et al: A practical guide for the diagnosis and treatment of acute sinusitis. CMAJ 1997;156(Suppl 6):S1-14
Chronic Sinusitis
Definition
• inflammation of the paranasal sinuses lasting > 3 months

Etiology
• can result from any of the following:
inadequate treatment of acute sinusitis
untreated nasal allergy
anatomic abnormality e.g. deviated septum
underlying dental disease
ciliary disorder e.g. cystic fibrosis, Kartagener’s
chronic inflammatory disorder e.g. Wegener’s
fungal allergy
• organisms
bacterial: S. pneumoniae, H. influenzae, M. catarrhalis, S. pyogenes, S. aureus,
anaerobes
fungal: Aspergillus

Clinical Features (similar to acute, but less severe)

• chronic nasal obstruction
• purulent nasal discharge
• pain over sinus or headache
• halitosis
• yellow-brown post-nasal discharge
• chronic cough
• maxillary dental pain

Treatment
• antibiotics for 3 to 6 weeks
augmented penicillin (Clavulin™), macrolide (clarithromycin),
fluoroquinolone (levofloxacin), clindamycin, Flagyl
• topical nasal steroid, saline spray
• surgery if medical therapy fails or fungal sinusitis

Surgical Treatment
• removal of all diseased soft tissue and bone, post-op drainage and obliteration of
pre-existing sinus cavity
• functional endoscopic sinus surgery
Retropharyngeal Abscess
Acute Otitis Media (AOM)
Definition
• acute inflammation of middle ear

Epidemiology
• 60 to 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 – 10% of cases
• S. aureus and S. pyogenes (all -lactamase producing)
• anaerobes (newborns)
• Gram negative enterics (infants)
• viral

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
• immunosuppression/deficiency due to chemotherapy, steroids, diabetes mellitus.
hypogammaglobulinemia, cystic fibrosis

Risk Factors
• bottle feeding, pacifier use
• passive smoke
• crowded living conditions (day care/group child care facilities) or sick contacts
• 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

Clinical Features
• triad of otalgia, fever (especially in younger children), and conductive hearing loss
• rarely, tinnitus, vertigo, and/or facial nerve paralysis
• otorrhea if tympanic membrane perforated
• pain over mastoid
• infants/toddlers
 ear-tugging
hearing loss, balance disturbances (mild)
irritable, poor sleeping
vomiting and diarrhea
anorexia
• otoscopy of tympanic membrane
hyperemia
bulging
loss of landmarks: handle and short process of malleus not visible

Treatment
• antibiotic treatment hastens resolution – 10 day course
1st line:
amoxicillin 40mg/kg/day divided into two doses – safe, effective,
and inexpensive
if penicillin allergic: macrolide (clarithromycin, azithromycin),
trimethoprim-sulphamethoxazole (Bactrim™)
2nd line (for amoxicillin failures):
double dose of amoxicillin (80mg/kg/day), amoxicillin-clavulinic
acid (Clavulin™)
cephalosporins: cefuroxime axetil (Ceftil™), ceftriaxone IM
(Rocephin™), cefaclor (Ceclor™), cefixime (Suprax™)
AOM deemed unresponsive if clinical signs/symptoms and otoscopic
findings persist beyond 48 hours of antibiotic treatment
• symptomatic therapy
antipyretics/analgesics (e.g. acetaminophen)
decongestants – may relieve nasal congestion but does not treat AOM
• prevention
parent education about risk factors (see above)
antibiotic prophylaxis – amoxicillin or macrolide shown effective at half
therapeutic dose
pneumococcal and influenza vaccine
surgery
choice of surgical therapy for recurrent AOM depends on whether
local factors (eustachian tube dysfunction) are responsible (use
ventilation tubes), or regional disease factors (tonsillitis, adenoid
hypertrophy, sinusitis) are responsible

Indications for Myringotomy and Tympanostomy tubes in Recurrent AOM and OME (tubes are more
commonly inserted for OME, rarely for AOM)
• persistent effusion > 3 months (OME)
• lack of response to > 3 months of antibiotic therapy (OME)
• persistent effusion for ? 3 months after episode of AOM (OME)
• recurrent episodes of AOM ( > 7 episodes in 6 months)
• bilateral conductive hearing loss of > 20 dB (OME)
• chronic retraction of the tympanic membrane or pars flaccida (OME)
• bilateral OME lasting > 4 to 6 mos
• craniofacial anomalies predisposing to middle ear infections (e.g. cleft palate) (OME)
• complications of AOM
McIsaac WJ. Coyte PC. Croxford R. Asche CV. Friedberg J. Feldman W. Otolaryngologists’ perceptions of the indications for tympanostomy tube
insertion in children. CMAJ. 162(9):1285-8, 2000 May 2.
Myringotomy and tympanostomy tubes. In: 2000 clinical indicators compendium. Alexandria (VA): American Academy of Otolaryngology-Head
and Neck Surgery; 1999.

Complications of AOM
• otologic
TM perforation
chronic suppurative OM
ossicular necrosis
cholesteatoma
persistent effusion (often leading to hearing loss)
• CNS
 meningitis
brain abscess
facial nerve paralysis
• other
mastoiditis
labyrinthitis
sigmoid sinus thrombophlebitis
Otitis Media with Effusion (OME)
Definition
• presence of fluid in the middle ear without signs or symptoms of ear infection

Epidemiology
• not exclusively a pediatric disease
• follows AOM frequently in children:
middle ear effusions have been shown to persist following an episode of
AOM for 1 mos in 40% of children, 2 mos in 20% and 3+ mos in 10%

Risk Factors
• same as AOM

Clinical Features
• fullness – blocked ear
• hearing loss ± tinnitus
confirm with audiogram and tympanogram (flat) (see Figure 11B, OT9)
• ± pain, low grade fever
• otoscopy of tympanic membrane
discoloration – amber or dull grey with “glue” ear
meniscus fluid level
air bubbles
retraction pockets/TM atelectasis
most reliable finding with pneumotoscopy is immobility
Treatment
• expectant – 90% resolve by 3 months
• document hearing loss
• no statistical proof that antihistamines, decongestants, antibiotics clear disease
faster than without
• surgery: myringotomy ± ventilating tubes ± adenoidectomy (if enlarged)
• ventilating tubes to equalize pressure and drain ear

Complications of Otitis Media with Effusion (OME)

• hearing loss, speech delay, learning problems in young children
• chronic mastoiditis
• ossicular erosion
• cholesteatoma especially when retraction pockets involve pars flaccida or
postero-superior TM
• retraction of tympanic membrane, atelectasis, ossicular fixation