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. or directly on teeth to elicit more reliable response . Weber left) can place vibrating fork on patient’s chin while they clench their teeth.

and frequency of nystagmus elicited by different stimuli Balance Testing • Romberg’s test: patient stands upright with feet together. usually = medullocervical localization (e. cornea (+). 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. 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. Arnold-Chiari) Electronystagmography (ENG) • electrodes placed around eyes • eye is a dipole.Otoneurological Examination • otoscopy • cranial nerve testing (II to XII inclusive) • cerebellar testing Nystagmus (see Opthalmology.g. amplitude. eyes closed. nystagmus may again be observed but the direction will be reversed . retina (–) • used to measure rate. 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. OP36) • assess nystagmus – describe quick phase. 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.

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. deviation. swelling. congenital anomalies. blue/grey secondary to allergies.Nose External Examination of Nose • inspect nose look for swelling. and red secondary to inflammation size. colour. and mucosa of inferior and middle turbinates possible abnormal findings septal deviation or perforation exudate. hematoma. trauma. epistaxis nasal polyps .

look at tonsillar crypts • posterior pharyngeal wall . symmetry. 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. ulceration. deformities. masses.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. overbite) • hard and soft palates note any asymmetry. tonsils. and retromolar trigone • lips note colour. masses. 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. oronasal fistulas • tongue inspect for colour. alveolus. texture. tonsillolingual sulcus note size and inspect for tonsillar exudate or lesions. mobility.

middle. inferior meatus eustachian tubes choana adeynoids oropharynx/hypopharynx/larynx • look for nodules. irregularity of circumvallate papillae. aryepiglottic folds.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. lingual tonsil. allowing palate to depress and nasopharynx to open • with adequate tongue depression. ulcerations. pyriform fossae. 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. base of tongue. 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. 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. valleculae epiglottis. false vocal cords. 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) .

Conductive Hearing Loss (CHL) • the conduction of sound to the cochlea is impaired • can be caused by external and middle ear disease 2. or other neurological symptoms • history of head trauma. Mixed Hearing Loss • the conduction of sound to the cochlea is impaired. Aminoglycosides) • other medical problems Physical • otoscopy. noise exposure. bilateral • associated symptoms: otorrhea. disequilibrium. character. or barotrauma • family history of hearing loss • medications (especially use of ototoxic drugs e. and progression of loss • unilateral vs. aural pressure visual. 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 . and cortex 3. duration. 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.g. brainstem. vertigo. as is the transmission through the cochlea to the cortex History • onset.Approach to the Patient with Hearing Loss TYPES OF HEARING LOSS 1. tinnitus. acoustic nerve (CN VIII). speech. ear surgery.

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. Sensorineural Hearing Loss (SNHL) (Figure 11D. and 2000 Hz PURE TONE PATTERNS 1. 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. 11E) • both air and bone conduction thresholds below normal • gap between AC and BC < 10 dB (no air-bone gap) 3. 1000. inner ear. middle.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. 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. 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 . 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. If not. Conductive Hearing Loss (CHL) (Figure 11B.

3 to 1. reflex likely absent • stimulating either ear causes bilateral and symmetrical reflexes • for reflex to be present.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. if hearing threshold > 85 dB.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. acoustic reflex thresholds = 25 to 60 dB • with retrocochlear hearing loss (acoustic neuroma) ^ absent acoustic reflexes or marked reflex decay (>50%) within 5 seconds . 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.

FM.Auditory Brainstem Response (ABR) • measures neuroelectric potentials (waves) in response to a stimulus in five different anatomic sites. or induction loop systems telephone. 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. 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 . television. physical. age. communicative requirements. 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. motivation. expectations.

cardiovascular. neurological.g. insidious associated with body position.Evaluation of the Dizzy Patient • vertigo: an illusion of rotary movement of self or environment. otorrhea. otalgia. aural fullness. tinnitus. psychiatric. OT2) • • • • • otoscopy cranial nerve exam (II-XII) extraocular motility (nystagmus) assessment balance testing – Romberg’s test. Unterberger’s step test. 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. aminoglycosides) medical history (vascular disease. asymptomatic between attacks exacerbating/relieving factors effect of dark/eye closing worse with head movement associated symptoms (and temporal relationship to dizziness) hearing loss. single major attack that slowly improves frequency of attacks symptomatic vs. anxiety disorder) degree of disability caused by dizziness Physical Examination (see Physical Exam. vomiting neurological symptoms eye movement (nystagmus) noted by observer alcohol and drug history (antihypertensives. head movement duration course of illness repeated acute attacks vs. tandem and normal gait Dix-Hallpike test Investigations • electronystagmography with caloric stimulation • ± audiology • ± imaging (MRI/CT) as indicated . aging) History • diagnosis is heavily dependent upon an accurate history description of rotary movement onset acute vs. nausea.

drainage of middle ear effusion) with no treatable cause. gradual bilateral hearing loss initially at high frequencies. treat the cause (e. 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. 50% will improve.patients • recruitment phenomenon: inability to tolerate loud sounds • tinnitus describe people as mumbling Treatment • hearing aid if patient has difficulty functioning. hearing loss > 30-35 dB • ± lip reading. OT9) • loss of discrimination of speech especially with background noise present . then middle frequencies (see Figure 11E. auditory training. often very annoying to the patient Investigations • audiology • if unilateral ABR. 25% remain the same avoid: loud noise.Tinnitus Definition • an auditory perception in the absence of an acoustic stimuli. TSH Treatment • • • • • if a cause is found. caffeine. smoking tinnitus workshops identify situations where tinnitus is most bothersome (e.g.g. ototoxic meds. quiet times). MRI/CT to exclude a retrocochlear lesion • if suspect metabolic abnormality: lipid profile. auditory aids (doorbell and phone lights) . 25% worsen.

Drug Ototoxicity Aminoglycosides • • • • • • • • • • toxic to hair cells by any route: oral. IV. 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. kanamycin and tobramycin (cochleotoxic) must monitor levels with peak and trough levels when prescribed. and topical (only if the TM is perforated) destroys sensory hair cells – outer first. reversible if discontinued Antimalarials (Quinine) • hearing loss with tinnitus • reversible if discontinued but can lead to permanent loss • others: antineoplastics. especially if patient has neutropenia. loop diuretics Chemotherapy • many agents one ototoxic . inner second high frequency hearing loss develops earliest ototoxicity occurs days to weeks post-treatment streptomycin and gentamycin (vestibulotoxic).

therefore considerable damage may occur before patient complains of hearing loss • difficulty with speech discrimination. 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. degenerative disease. decreased sensitivity or increased threshold for sound may have associated aural fullness and tinnitus with removal of noise. 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 . 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.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). 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. OT9) • speech reception not altered until hearing loss > 30 dB at speech frequency. 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. viral infection (URTI). hearing returns to normal • permanent threshold shift hearing does not return to previous state Treatment • hearing aid • prevention ear protectors: muffs. extends to higher and lower frequencies with time (see Figure 11D.

HCTZ.g. antiemetics. 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. triamterene. 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.Menière’s Disease (Endolymphatic Hydrops) Definition • episodic attacks of tinnitus. ± nausea. and vomiting • vertigo disappears with time (minutes to hours). and low molecular weight dextrans (not commonly used) • longterm management may be medical low salt diet. but hearing loss remains • early in the disease. fluctuating hearing loss. betahistine (Serc™)). and aural fullness • ± drop attacks (Tumarkin crisis). antivertiginous drugs (e. diuretics (e. 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 .g. hearing loss. tinnitus. aural fullness.

café-au-lait lesions. measles. multiple intracranial lesions Clinical Features • usually presents with unilateral sensorineural hearing loss or tinnitus • dizziness and unsteadiness may be present. diazepam) • convalescent phase progressive ambulation especially in the elderly vestibular exercises: involve eye and head movements. vestibular sedatives (dimenhydrinate (Gravol™).g. diabetes. sitting. 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. and acute vocal cord palsy Clinical Features • acute phase severe vertigo with nausea. 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 . 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. poor ambulation • repeated attacks can occur Treatment • acute phase bed rest. visual impairment.Vestibular Neuronitis Definition • acute onset of disabling vertigo often accompanied by nausea. vomiting. 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. mumps. compressing cerebellum and brainstem • when associated with type 2 neurofibromatosis (NF2): bilateral tumours of CN VIII. autoimmune process considered to be the vestibular equivalent of Bell’s palsy. sudden hearing loss. herpes zoster) ~30% of cases have associated URTI symptoms other possible etiologies: microvascular events. standing.

in elderly. or in moribund • definitive management is surgical excision • other options: gamma knife. radiation .Treatment • expectant management if tumour is very small.

foods. phenylpropanolamine topical decongestant may lead to rhinitis medicamentosa other topicals: steroids (fluticasone). disodium cromoglycate. ipatropium bromide • oral steroids if severe • desensitization by allergen immunotherapy .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. feather. milk. spring. terfenadine oral decongestants e. early autumn) pollens from trees lasts several weeks. and “boggy” seasonal (summer.g. disappears and recurs following year at same time • perennial inhaled: house dust. sneezing clear rhinorrhea (containing increased eosinophils) itching of eyes with tearing frontal headache and pressure mucosa – swollen. anti-histamines. wool.g. pseudoephedrine. eggs. mould ingested: wheat. pale. lavender color. tobacco. 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. hair. diphenhydramine. 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.

snoring. smooth. stringy colorless/purulent rhinorrhea • solitary/multiple glazed. facial pain septum: S-shaped. Churg-Strauss syndrome note: triad of polyps. angular deviation.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. crusting. hyposmia. asthma (Samter’s triad) Clinical Features • progressive nasal obstruction. transparent mobile masses (often bilateral) Treatment • eliminate allergen • steroids (preoperative prednisone) to shrink polyp • polypectomy is treatment of choice. 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. aspirin sensitivity. epiphora • post-nasal drip. 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. Kartaganer’s syndrome. however. septal perforation external deformity (saddle-nose) anosmia (rare but untreatable) .

PT/PTT (if indicated) • Xray. Assess Blood Loss (can be potentially fatal hemorrhage) • pulse. 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. and from below is external carotid Investigations • CBC. 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 . Determine site of bleeding • insert cotton pledget of 4% topical lidocaine ± topical decongestant cocaine. where 90% of nosebleeds occur • bleeding from above middle turbinate is internal carotid. located at Little’s area (anterior portion of the cartilaginous septum). cross match for 2 units packed RBCs if significant 3. and other signs of shock • IV NS.Epistaxis Blood Supply to the Nasal Septum 1. 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. 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. blood pressure.e. superior posterior septum internal carotid ^ ophthalmic ^ anterior/posterior ethmoidal 2. coagulation studies 4. 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. anterior hemorrhage treatment if fail to achieve hemostasis with cauterization anterior pack with half inch Vaseline™ and ribbon gauze strips or absorbable packing (i. CT as needed Treatment • aim is to localize bleeding and achieve hemostasis 1. posterior hemorrhage treatment if unable to visualize bleeding source. then usually posterior source different ways of placing a posterior pack with a Foley catheter. visualize nasal cavity with speculum and aspirate excess blood and clots • anterior/posterior hemorrhage defined by location in relationship to bony septum • if suspicion. Control the bleeding • first line topical vasoconstrictors (Otrivin™.

or topical ointments • avoidance of irritants • medical management of hypertension and coagulopathies . 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. pharyngeal fibrosis/ stenosis. aspiration C. saline spray. toxic shock syndrome (Rx: remove packs immediately).watch for complications: hypoxemia (naso-pulmonic reflex). alar/septal necrosis. Prevention • prevent drying of nasal mucosa with humidifiers.

sinusitis can be ruled in (likelihood ratio > 6. occipital or parietal headaches • systemic: fever. Maxillary sinus 1st to develop neonate – clinically significant ethmoid and maxillary buds present age 9 – maxillary full grown. chills.5) 2. pneumonia (35%). influenza. roof of orbit sphenoid – vertex. with fewer than 2/5 of the above. catarrhalis.4) . anaerobes (dental) Viral: rhinovirus. maxillary.Sinusitis Development of Sinuses • • • • sinus pneumatization begins in 3-4th month fetal life. H. influenzae (35%). M. with 4 or more of the above. frontal and sphenoid cells starting age 18 – frontal and sphenoid cells full grown Drainage of Sinuses • frontal. 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. sinusitis can be ruled out (likelihood ratio < 0. retroorbital pain frontal – supraorbital ridge. 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. malaise • • • • • Guidelines 1.

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. 60% sensitive). begin with Waters view and add others if inconclusive 4. 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. Caldwell (occipitofrontal) view – ethmoid and frontal sinuses. then antrostomy ethmoid – external (Lynch incision). lateral view (all). CMAJ 1997. and drain sphenoid – drain via posterior ethmoids Low DE. irrigate. et al: A practical guide for the diagnosis and treatment of acute sinusitis. 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.156(Suppl 6):S1-14 . but often shows mucosal changes in normal individuals (more commonly used) not cost-effective for routine diagnosis indications: chronic refractory sinusitis. complete opacification of sinus (100% PPV. and submentovertex view (sphenoid and ethmoid) radiographic findings: air-fluid level (80% PPV. McSherry J. transantral or intranasal ethmoidectomy frontal– Lynch incision at medial orbital rim.3. with 2-3 of the above. mucosal thickening (90% sensitive. 36-76% specific) • CT provides superior detail and is more sensitive. clarithromycin. sinus radiography is suggested. suspected malignancy or extrasinus involvement. Desrosiers M. 60% sensitive).

H. anaerobes fungal: Aspergillus Clinical Features (similar to acute. S. S. saline spray • surgery if medical therapy fails or fungal sinusitis Surgical Treatment • removal of all diseased soft tissue and bone. M. fluoroquinolone (levofloxacin). clindamycin. deviated septum underlying dental disease ciliary disorder e.g. pneumoniae.g. macrolide (clarithromycin). 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™).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. Kartagener’s chronic inflammatory disorder e. pyogenes. post-op drainage and obliteration of pre-existing sinus cavity • functional endoscopic sinus surgery Retropharyngeal Abscess . aureus.g. cystic fibrosis. influenzae. Flagyl • topical nasal steroid. Wegener’s fungal allergy • organisms bacterial: S. catarrhalis.

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. and/or facial nerve paralysis otorrhea if tympanic membrane perforated pain over mastoid infants/toddlers . catarrhalis – 10% of cases S. influenzae – 25% of cases M. pneumoniae – 35% of cases H. PMNs. aureus and S. fever (especially in younger children). tinnitus. cystic fibrosis Risk Factors • • • • • bottle feeding. phagocytic cells • immunosuppression/deficiency due to chemotherapy.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. 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. hypogammaglobulinemia. and conductive hearing loss rarely. 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). steroids. diabetes mellitus. vertigo.

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. Coyte PC. Alexandria (VA): American Academy of Otolaryngology-Head and Neck Surgery. 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. Asche CV. In: 2000 clinical indicators compendium. Croxford R. 162(9):1285-8. adenoid hypertrophy. effective. 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). Feldman W. 2000 May 2. Otolaryngologists’ perceptions of the indications for tympanostomy tube insertion in children. amoxicillin-clavulinic acid (Clavulin™) cephalosporins: cefuroxime axetil (Ceftil™).ear-tugging hearing loss. trimethoprim-sulphamethoxazole (Bactrim™) 2nd line (for amoxicillin failures): double dose of amoxicillin (80mg/kg/day). or regional disease factors (tonsillitis. 1999. ceftriaxone IM (Rocephin™). sinusitis) are responsible Indications for Myringotomy and Tympanostomy tubes in Recurrent AOM and OME (tubes are more commonly inserted for OME.g. CMAJ. Friedberg J.g. balance disturbances (mild) irritable. Myringotomy and tympanostomy tubes. and inexpensive if penicillin allergic: macrolide (clarithromycin. cefaclor (Ceclor™). cleft palate) (OME) • complications of AOM McIsaac WJ. Complications of AOM • otologic TM perforation chronic suppurative OM ossicular necrosis cholesteatoma persistent effusion (often leading to hearing loss) • CNS . azithromycin). cefixime (Suprax™) AOM deemed unresponsive if clinical signs/symptoms and otoscopic findings persist beyond 48 hours of antibiotic treatment • symptomatic therapy antipyretics/analgesics (e.

meningitis brain abscess facial nerve paralysis • other mastoiditis labyrinthitis sigmoid sinus thrombophlebitis .

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. 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. ossicular fixation • • • • . 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. atelectasis.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. 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.

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