Otolaryngology PDA

8/7/2019 Otolaryngology PDA

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Otolaryngology Toronto Notes

Abridged for the PDA

To be used only in conjunction with the printed Toronto Notes

Kristen Davidge and John de AlmeidaCagla Eskicioglu and Nadra Ginting, associate editors

Maja Segedi, EBM editorStaff Editor: Dr. Jonathan Irish

Physical ExaminationHead and Neck

EarOtoneurological ExaminationNoseOral Cavity

Nasopharynx (NP)Hypopharynx and Larynx

Approach to the Patient with Hearing LossPure Tone AudiometrySpeech Audiometry

Impedance AudiometryAuditory Brainstem ResponseAural Rehabilitation

Evaluation of the Dizzy Patient

Tinnitus

PresbycusisDrug OtotoxicityNoise-Induced Sensorineural Hearing LossBenign Paroxysmal Positional Vertigo

Menires DiseaseVestibular NeuronitisAcoustic Neuroma (AN)

Allergic Rhinitis

Nasal PolypsSeptal Deviation

Epistaxis

Sinusitis

Acute Suppurative SinusitisChronic Sinusitis

Acute Otitis Media (AOM)Otitis Media with Effusion (OME)


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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/irregularborder, 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 secondbranchial 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 notvisualized 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


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512 Hz tuning fork is struck and held firmly on mastoid process totest bone conduction (BC). The tuning fork is then placed beside thepinna to test air conduction (AC)

Weber test

512 Hz tuning fork is held on vertex of head and patient stateswhether it is heard centrally (Weber negative) or is lateralized to oneside (Weber right, Weber left)

can place vibrating fork on patients chin while they clenchtheir teeth, or directly on teeth to elicit more reliable response


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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 lateralgaze

horizontal nystagmus that beats in the same direction = peripheral vestibulardisorder

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 Rombergs 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

Unterbergers 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 30 to bring the horizontal semicircular

canal into a vertical position the direction of endolymph flow is changed by irrigating the labyrinthine capsule

with warm (30C or 44C) or cold (0) 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 Frenzels (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 45 holding theposition 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 thedirection will be reversed


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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/greysecondary 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


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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 Stensens 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 Whartons 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


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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 vocalcords, 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 andnasopharynx to open

with adequate tongue depression, the warmed mirror is placed next to uvula and almost touches the posteriorpharyngeal 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 upwardagainst 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)


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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


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Pure Tone Audiometry

threshold is the lowest intensity level at which a patient can hear the tone 50% ofthe 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 ofhuman speech) usually agree within 5 dB. If not, suspect a retrocochlear lesion orfunctional 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 aretrocochlear lesion (rollover effect)

investigate further if scores differ more than 20% between ears


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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 thepressure 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 2 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 inmonitored ear

if reflex is absent without conductive or severe sensorineural loss ^ suspect CNVIII 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 ormarked reflex decay (>50%) within 5 seconds


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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 thedefect (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 theauditory nerve

for profound bilateral sensorineural hearing loss not rehabilitated withconventional hearing aids

established indication: post-lingually deafened adults and children


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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 Rombergs test, Unterbergers step test, tandem and normal gait Dix-Hallpike test

Investigations electronystagmography with caloric stimulation audiology imaging (MRI/CT) as indicated


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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)


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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 ifpatient 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 dosingpresents 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


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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 Epleys 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


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Menires 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 (overaccumulation) 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 commonlyused)

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


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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 Bells palsy, sudden hearing loss, andacute 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, visualimpairment, 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 ofCN VIII, caf-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 tumourgrowth occurs slowly

facial nerve palsy and trigeminal (V1) sensory deficit (corneal reflex) are latecomplications

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


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Treatment expectant management if tumour is very small, in elderly, or in moribund

definitive management is surgical excision other options: gamma knife, radiation


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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


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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, Kartaganers syndrome, Churg-Strauss syndrome note: triad of polyps, aspirin sensitivity, asthma (Samters 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)


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Epistaxis

Blood Supply to the Nasal Septum1. superior posterior septum

internal carotid ^ ophthalmic ^ anterior/posterior ethmoidal2. posterior septum

external carotid ^ internal maxillary ^ sphenopalatine artery

^ nasopalatine3. 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 Kiesselbachs plexus, located at Littles area(anterior portion of the cartilaginous septum), where 90% of nosebleeds occur

bleeding from above middle turbinate is internal carotid, and from below isexternal carotid

Investigations CBC, PT/PTT (if indicated)

Xray, CT as needed

Treatment aim is to localize bleeding and achieve hemostasis

1. First-aid ABCs

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 septalperforation

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 nasalroof 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


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watch for complications: hypoxemia (naso-pulmonic reflex), toxic shocksyndrome (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 carotidartery

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


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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 toinflammation

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 decreasedciliary action ^ retention of secretions ^ 2 bacterial infection ^ acutesinusitis 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

Guidelines1. 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)


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3. with 2-3 of the above, sinus radiography is suggested; begin with Waters view andadd others if inconclusive

4. also do radiographic exam in patients with frontal headaches to rule out frontalsinusitis

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 ethmoidsLow 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


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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, Kartageners chronic inflammatory disorder e.g. Wegeners 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


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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

Downs syndrome (horizontal position of eustachian tube),Crouzons, and Aperts syndrome

disruption of action of: cilia of eustachian tube Kartageners 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 ^ negativepressure (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


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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-clavulinicacid (Clavulin)

cephalosporins: cefuroxime axetil (Ceftil), ceftriaxone IM(Rocephin), cefaclor (Ceclor), cefixime (Suprax)

AOM deemed unresponsive if clinical signs/symptoms and otoscopicfindings 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 (useventilation 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 AOMMcIsaac 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


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meningitis brain abscess facial nerve paralysis

other

mastoiditis labyrinthitis sigmoid sinus thrombophlebitis


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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 diseasefaster 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 orpostero-superior TM

retraction of tympanic membrane, atelectasis, ossicular fixation

Otolaryngology PDA

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