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0T15 Otolaryngology Toronto Notes 2023

Acoustic Neuroma (Vestibular Schwannoma)

Definition

• schwannoma of the vestibular portion of CN VIII

Pathogenesis

• tumourstarts in the internal auditory canal and expands into CPA, compressing cerebellum and

brainstem

• when associated with type 2 neurofibromatosis: bilateral acoustic neuromas, juvenile cataracts,

meningiomas, and ependymomas

Clinical Features

• usually presents with unilateral SNHL (chronic) or tinnitus

• dizziness and unsteadiness may be present, but true vertigo is rare as tumour growth occurs slowly,

allowing for compensation to occur

• facial nerve palsy and trigeminal (V1) sensory deficit (corneal reflex) are late complications

• risk factors:exposure to loud noise, childhood exposure to low-dose radiation, history of parathyroid

adenoma

Acoustic

Oneuroma isthe most common

intracranial tumour causing SNHL and

the most common CPA tumour

In the elderly, unilateral tinnitus or

SNHL is acoustic neuroma until proven

otherwise

Diagnosis

• M RI of internal auditory canal with gadolinium contrast (gold standard)

• audiogram (to assess SNHL)

• poor speech discrimination relative to the HL

• stapedial reflex absent orsignificant reflex decay

• ABR: increase in latency of the 5th wave

• vestibular tests: normal or asymmetric caloric weakness (an early sign)

Treatment

• expectant management if tumour is very small or in elderly

• definitive management is surgical excision

• other options: gamma knife, radiation

Tinnitus K

Definition

• an auditory perception in the absence of an acoustic stimuli,likely related to loss of input into neurons

in central auditory pathways, that results in abnormal firing

History

• subjective vs. objective (see I

'

igurc 14, 0/7)

• pulsatile vs.nonpulsatile

• unilateral vs. bilateral

• associated symptoms: HL, vertigo, aural fullness, otalgia, otorrhea

Investigations

• physical examination:cranial nerve examination, otoscopy, auscultate for bruits over the neck,

mastoid, and preauricular areas for pulsatile tinnitus

• audiology

• if pulsatile

CT or magnetic resonance angiogram and venogram of the H&N to rule out vascular

abnormalities

• if nonpulsatile and unilateral

• non-contrast MRI

Treatment

• if a cause is found, treat the cause (e.g. drainage of middle ear effusion, embolization, or excision of

arteriovenous malformation)

• with no treatable cause: 15% will resolve, 20% will improve, 15% will worsen, 50% will remain the

same

• primary and secondary prevention for SNHL (e.g. avoid high-volume music through headphones,

ototoxic meds,smoking, high glvcemic load, and hypercholesterolemia)

• conservative management (e.g. cneck zinc levels, Improve sleep, reduce stress, reduce caffeine and

alcohol consumption)

• if cause is deemed benign, recognize distress that patient may be experiencing and provide

reassurance

• sound amplification (e.g. hearing aids, white noise,tinnitus instrument)

• pharmacotherapy (e.g.melatonin)

consider tricyclic antidepressants and SSR1 if comorbidities include anxiety and depression

• tinnitus retraining therapy

• surgical management (rare)

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0T16 Otolaryngology Toronto Notes 2023

Diseases of the External Ear

Cerumen Impaction Is the most common

cause of CHL for those15 50 y/o

Cerumen Impaction

Etiology

• ear wax:a mixture of secretionsfrom ceruminous and pilosebaceous glands,squames of epithelium,

dust, and debris

Syringing

Indications

• Totally occlusive cerumen with pain,

decreased hearing,or tinnitus

Contraindications

• Active Infection

• Previous ear surgery

• Only hearing car

• TM perforation

Complications

. OE

• TM perforation

. Trauma

. Pain

• Vertigo

• Tinnitus

• Otitis media

Method

• Establish that TM is intact

• Gently pull the pinna superiorly and

posteriorly

• Using lukewarm water, aim the

syringe nozzle upwards and

posteriorly to irrigate the car canal

Risk Factors

• hairy or narrow ear canals, in-the-ear hearing aids, cotton swab usage, osteomata

Clinical Features

• CHL,tinnitus, fullness, itching, otalgia, discharge, odour, and cough

Treatment

• observation, cerumenolytic agents (water dissolves cerumen better than over-the-counter

medications),irrigation,or manual removal

Exostoses

Definition

• bony protuberancesin the EAC composed of lamellar bone

Etiology

• possible association with swimming in cold water

Clinical Features

• usually an incidental finding

• can cause cerumen impaction or OE, if large

Treatment

• no Tx unless symptomatic (e.g. frequent OE, CHL)

Otitis Externa

Definition

•inflammation of EAC or auricle

Etiology

• bacterial (90% of OE): Pseudomonas aeruginosa, Pseudomonas vulgaris, Escherichia coli,

Staphylococcus aureus

• fungal: Candida albicans, Aspergillus niger

Risk Factors

• anatomic abnormalities:canal stenosis, exostoses, hairy ear canal

• canal obstruction: cerumen, foreign body,sebaceous cyst

• epithelial integrity: cerumen removal, earplugs, hearing aids, instrumentation/itching

• dermatologic conditions:eczema, psoriasis,seborrhea

• water in ear canal:swimming, other prolonged water exposures

Clinical Features

• acute

otalgia, itching, fullness, ± HL, ± ear canal pain on chewing

tenderness aggravated by traction of pinna or pressure over tragus

ear canal edema, erythema, ± otorrhea, ± regional lymphadenitis, ± cellulitis of the pinna

• chronic

pruritus of external ear ± excoriation of ear canal

atrophic and scaly epidermal lining, ± otorrhea, ± HL

wide meatus, but no pain with movement of auricle

TM appears normal

Pulling on the pinna is extremely painful

in OE, but is usually well tolerated in

otitis media

j

Treatment

• microdebridement

• topical antimicrobials, topical antibiotics ± topical corticosteroids

antipseudomonal agents (e.g. ciprofloxacin) or a combination therapy (e.g.Ciprodex*)

ototoxic topical agents (e.g. gentamicin, neomycin, neomycin/polymyxin B/hydrocortisone)

should not be used in a perforated TM

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0T17 Otolaryngology Toronto Notes 2023

• keep the EAC dry

• oral antibioticsif the infection hasspread beyond the ear canal

• ± analgesics for pain management

• chronic OE:treat the underlying cause (e.g. dermatologic conditions)

Malignant (Necrotizing) Otitis Externa (Skull Base

Osteomyelitis)

Gallium and Technetium Scans

6allium scans are used to show sites

of active infection.Gallium is taken up

by PMN. and therefore only lights up

when active Infection is present. It will

not show the extent of osteomyelitis.

Technetium scans provide information

about osteoblastic activity and, as a

result are used to demonstrate sites of

osteomyelitis.Technetium scans help

with Dx,whereas gallium scans are

useful in follow-up

Definition

• osteomyelitis of the mastoid or temporal bone

Epidemiology

• occurs in elderly patients with DM and immunocompromised patients

Etiology

• rare complication of OE

• most commonly caused by Pseudomonas aeruginosa

Clinical Features

• otalgia and purulent otorrhea that is refractory to medical therapy

• granulation tissue or necrotic tissue on the floor of the auditory canal

Complications

• cranial nerve palsy (most commonly CN V11>CN X>CN XI)

• systemic infection,death

Management

• imaging: high resolution temporal bone CT scan, gadolinium-enhanced MR!, technetium scan

• medical emergency: hospitalization, debridement, IV antibiotics

• may require OR for debridement of necrotic tissue/bone

Diseases of the Middle Ear

Acute Otitis Media and Otitis Media with Effusion

• see Paediatric Otolaryngology,OT39

Chronic Otitis Media

Definition

• an ear with TM perforation in the setting of recurrent or chronic ear infections

Benign

• dry TM perforation without active infection

Chronic Serous Otitis Media

• continuousserous drainage (straw-coloured)

Chronic Suppurative Otitis Media

• persistent purulent drainage through a perforated TM

Cholesteatoma

Definition

• a cyst composed of keratinized desquamated epithelial cells occurring in the middle ear, mastoid, and

temporal bone

• two types: congenital and acquired

Congenital

• presents as a “small white pearl” behind an intact TM (anterior and medial to the malleus) or as CHL

• believed to be due to aberrant migration of external canal ectoderm during development

• not associated with otitis media/Eustachian tube dysfunction

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Acquired (more common)

• primary cholesteatoma

frequently associated with retraction pocketsin the pars (laccida, pars tensa,or both

a sequela of the dysfunction of the regulation of middle ear pressure

often has crusting or desquamated debris on lateral surface

• secondary cholesteatoma

“pearly mass"

evident behind TM, frequently associated with marginal perforation

may appear asskin that has replaced the mucosa of the middle ear

• the associated chronic inflammatory process causes progressive destruction ofsurrounding bony

structures

Mechanisms of Cholesteatoma

Formation

• Epithelial migration through TM

perforation|2“ acquisition)

• Invagination of TM (1“ acquisition)

• Metaplasia of middle ear epithelium

or basal cell hyperplasia (congenital)

Clinical Features

• history of otitis media (especially if unilateral), ventilation tubes, ear surgery

• symptoms

progressive HL (predominantly conductive, although may get SNHL in late stage)

otalgia, aural fullness, fever

• signs

retraction pocket in TM, may contain keratinous debris

TM perforation

• granulation tissue, polyp visible on otoscopy

malodourous, unilateral otorrhea

Complications

Table 8. Complications of Cholesteatoma

Local Intracranial

Ossicular erosion:CHL

Inner ear erosion:SNHl.dizziness,and/or labyrinthitis

Temporal bone infection:masloidilis,pelrosilis

Facial paralysis

Meningitis

Sigmoid sinus thrombosis

Intracranial abscess (subdural, epidural,cerebellar)

Investigations

• audiogram and non-contrast CT of temporal bones

Treatment

• surgical: mastoidectomy ± tympanoplasty ± ossicular reconstruction

Mastoiditis

Definition

• infection (usually subperiosteal) of mastoid air cells, most commonly seen approximately two wk after

onset of untreated or inadequately treated AOM (suppurative)

• more common in children than adults Classic Triad

• Otorrhea

• Tenderness to pressure over the

mastoid

• Retroauricular swelling with

protruding ear

Etiology

• acute mastoiditis is caused by the same organisms as AOM:.S'

.pneumoniae, H. influenzae, M.

catarrltalis, S. pyogenes, S. aureus, P.aeruginosa,etc.

Clinical Features

• otorrhea

• tenderness to pressure over the mastoid

• retroauricular swelling with protruding ear

• fever, HL, ± TM perforation (late)

• CT radiologic findings:opacification of mastoid air cells by fluid and interruption of normal

trabeculations of cells (coalescence)

Complications of AOM are rare due to

rapid and effective treatment of AOM

with antibiotics

Treatment

• IV antibiotics with myringotomy and ventilation tubes- usually all that is required in acute cases

• may require additional incision and drainage of postauricular abscess

• cortical mastoidectomy

debridement of infected tissue allowing aeration and drainage

• indicationsforsurgery

failure of medical treatment after 48 h

symptoms of intracranial complications

aural discharge persisting for 4 wk and resistant to antibiotics

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0T19 Otolaryngology Toronto Notes 2023

Otosclerosis

Definition

• fusion of stapesfootplate to oval window such that it cannot vibrate

Etiology

• autosomal dominant, variable penetrance approximately 40%

• T>M, progresses during pregnancy (hormone responsive)

Otosclerosis is the 2nd most common

cause of CHL in 15-50 y/o(after cerumen

impaction)

Clinical Features

• progressive CHL first noticed in teens and 20s(may progress to SNHL if cochlea involved)

• ± nonpulsatile tinnitus

• TM normal ± pink blush (Schwartz’

s sign) associated with the neovascularization of otosderotic bone

• characteristic dip at 2000 Hz (Carhart’

s notch) on audiogram (see l

-igure 16C,OT10)

Treatment

• monitor with serial audiograms if coping with loss

• hearing aid (AC, BC, BAHA)

• stapedectomy orstapedotomy (with laser or drill) with prosthesisis definitive treatment

Diseases of the Inner Ear

Congenital Sensorineural Hearing Loss

Hereditary Defects

• non-syndrome associated (70%)

often idiopathic,autosomal recessive

connexin 26 (GJB2) most common

• syndrome associated (30%)

• Waardenburg:white forelock, heterochromia iridis (each eye different colour), wide nasal bridge,

and increased distance between medial canthi

Pendred:euthyroid goiter,SLC26A4 gene, enlarged vestibular aqueducts

Treacher-Collins:first and second branchial deft anomalies

Alport: hereditary nephritis

Risk Factors for Neonatal Sensorineural Hearing Loss

• family history of permanent HL

• craniofacial abnormality

• prenatal infections

TORCH: toxoplasmosis, other (syphilis, varicella-zoster, parvovirus B19), rubella, CMV, HSV

Zika

• postnatal infections

bacterial meningitis,mumps, measles

• neonatal intensive care unitstay >2 d

• extracorporeal membrane oxygenation at birth

• assisted ventilation at birth/perinatal anoxia, birth trauma (hemorrhage into inner car)

• ototoxic drug use

• hyperbilirubinemia requiring exchange transfusion

Treatment

• presence of any risk factor: ABR study performed before leaving NICU and at 3 mo adjusted age

• early rehabilitation improvesspeech and school performance

Presbycusis

Definition

• SNHL associated with aging (starting in 5th and 6th decades)

Etiology

• hair cell degeneration

• age-related degeneration of basilar membrane, possibly genetic etiology

• cochlear neuron damage

• ischemia of inner ear

Presbycusis is the most common cause

of SNHL n

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+ Clinical Features

• progressive, bilateral hearing deterioration initially at high frequencies, followed by middle and lower

frequencies

• loss of discrimination of speech, especially with background noise present

- patients describe people

as mumbling

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OT20 Otolaryngology Toronto Notes 2023

•recruitment phenomenon:inability to tolerate loud sounds

•tinnitus

Treatment

•hearing aid if patient has difficulty functioning, HL >30-35 dB, and good speech discrimination

•± lip reading, auditory training,auditory aids (doorbell and phone lights)

Sudden Sensorineural Hearing Loss

Etiology

• usually idiopathic (80-90% of cases); rule out other causes

autoimmune

infectious (e.g.EBV,group A Streptococcus, HSV, herpes-zoster virus, HIV, Lyme disease,

meningitis,syphilis)

• trauma

vascular (e.g. cerebrovascular disease)

neoplastic (e.g.angioma, meningioma, neurofibromatosis 2,schwannoma)

other (e.g. ototoxins, pregnancy)

Sudden SNHL may easily be confused

with ischemic brain events.It is

important to leep a high index of

suspicion especially with elderly patients

presenting with sudden SNHL.as well

as vertigo

Clinical Features

• presents as a sudden onset ofsignificant SNHL (usually unilateral) ± tinnitus,vertigo, aural fullness

Treatment

• treat the underlying cause

• MRI to rule out tumour and/orCl'

to rule out ischemic/hemorrhagic stroke if associated with any

other focal neurological signs (e.g. vertigo, ataxia, abnormality of CN V or VII, weakness)

• if idiopathic, intratympanic or oral corticosteroids (prednisone I mg/kg/d for 7-14 d ). Start within 3 d

(most ideal) up to 14 d after onset

Clinical Practice Cnideline:Sudden Hearingtoss

Otolaryngol Head Keek Surg 201$ »ug:1H

(

^

commendations Based onFindings

• Confirm HL issensorineuralwilt aadioMlrit

testing (loss of at least30 dB affectingthree

consecutive frequencies)

.. Cl. or HRI not required unless

indicated by history and physical

• Initiate steroidtreatment within 14 dolsymptom

Prognosis

• depends on degree of HL

• 70% resolve within 10-14 d

• 20% experience partial resolution

• 10% experience permanent HL onset

Autoimmune Inner Ear Disease

Etiology

• idiopathic

• may be associated with systemic autoimmune diseases(e.g. RA,SLE), vasculitides(e.g.GPA,

polyarteritis nodosa), and allergies

Epidemiology

• most common between ages 20-50

Clinical Features

• rapidly progressive or fluctuating bilateral SNHL

• ± tinnitus, aural fullness,vestibularsymptoms(e.g. ataxia, disequilibrium, vertigo)

Investigations

• autoimmune workup:CBC, ESR, ANA, rheumatoid factor

Treatment

• high-dose corticosteroids; treat early for at least 30 d

• consider cytotoxic medication for steroid non-responders

Drug Ototoxicity

Aminoglycosides

• streptomycin and gentamicin (vestibulotoxic), kanamycin,and tobramycin (cochleotoxic)

• toxic to hair cells by any route:oral, IV, and topical (if theTM is perforated)

• destroys sensory hair cells: outer first, inner second (therefore, otoacoustic emissions arc lost first)

• high frequency HL develops earliest

• ototoxicity occurs d-wk post-treatment

• must monitor with peak and trough levels when prescribed, especially if patient has neutropenia and/

or history of ear or renal problems

• q24 h dosing recommended (with amount determined by creatinine clearance)

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•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

Analgesics and Antipyretics

•acetaminophen, NSA1DS, and salicylates

•HL with tinnitus, reversible if discontinued

Others

•antineoplastic agents (e.g. bleomycin)

•loop diuretics (e.g.furosemide) and antimalarials (e.g.quinine)

reversible by decreasing orstopping medications

Noise-Induced Sensorineural Hearing Loss

Pathogenesis

• 85-90 dB over mo or yr,single sound impulses >135 dB,or repetitive vibratory insults (e.g.

jackhammer) can cause cochlear damage

• bilateral SNHL initially and most prominently at 4000 Hz (resonant frequency of the temporal bone),

known as “boilermaker'

s notch" on audiogram, extendsto higher and lower frequencies with time

(see Figure 16D,0770)

• speech reception not altered until HL >30 dB at speech frequency, therefore considerable damage may

occur before patient complains of HL

• difficulty with speech discrimination, especially in situations with competing noise

Phases of Hearing Loss

• dependent on:intensity ofsound 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

hearing returns to normal with removal of noise

permanent threshold shift

hearing does not return to previousstate

Treatment

• hearing aid

• prevention

ear protectors: muffs, plugs

limit exposure to noise with frequent rest periods

regular audiologic follow-up

Temporal Bone Fractures

Table 9. Features of Temporal Bone Fractures

Otic Capsule Involving (1) Otic Capsule Sparing (2)

Extension

Incidence

Etiology

CN Pathology

Hearing Loss

Into hony labyrinth and internal auditory meatus

10-20%

Fronla l/occipital trauma

Into middle ear

70-90%

Laleral skull trauma

CN VII palsy|50%) '

SNHL due to direct cochlearinjury

Vestibular Symptoms Sudden onset vestibular symptoms due lodirectsemicircular Rare

canal injury (vertigo,spontaneous nystagmus)

Intact external auditory meatus,1M t hemotympanum

Spontaneous nystagmus

CSF leak In Eustachian tube to nasopharynx

t rhinorrhea (risk ol meningitis)

CN VII palsy (10-20%)

CHL 2°toossicular injury

Other Features TornTM or hemotympanum

Bleeding from EAC

Step formation in EAC

CSF otorrhea

Battle'ssign'mastoid ecchymosis

Raccoon eyes

- periorbital ecchymosis

S Teddy Cameron 2002^

Figure18.Types of temporal bone

fractures iJ

• characterized aslongitudinal or transverse relative to the long axis of the petrous temporal bone

• temporal bone fractures are rarely purely transverse or longitudinal (often a mixed picture)

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Diagnosis

• otoscopy

• do not syringe or manipulate external auditory meatus due to risk of inducing meningitis via TM

perforation

• CT of temporal bones

• audiology, facial nerve tests (for transverse fractures),Schirmer'

s test (of lacrimation),stapedial

reflexes if CN VII palsy

• ifsuspectingCSF leak:look for halo sign,send fluid for P-2 transferrin or p-trace protein

(prostaglandin D synthase)

Treatment

. ABCs

• medical: expectant, prevent otogenic meningitis

• surgical: explore temporal bone; indications:

• CN Vll palsy (immediate and complete)

gunshot wound

depressed fracture of external auditory meatus

• early meningitis (mastoidectomy)

bleeding intracranially from sinus

CSF otorrhea (may resolve spontaneously)

Signs ol Basilar Skull Fracture

• Battle’ssign (bruising over mastoid)

• Racoon eyes(periorbital ecchymosis)

• CSF rhinorrheafotorrhea

• Cranial nerve involvement:

• facial palsy

- CN Vll:

• nystagmus »CN VI;

• facial numbness » CN V

Complications

• AOM ± labyrinthitis ± mastoiditis

• meningitis/epidural abscess/brain abscess

• post-traumatic cholesteatoma

Facial Nerve (CN Vll) Paralysis

Central Facial Paralysis

• (see Neurology. N4)

<§)

Peripheral Facial Paralysis (PFP)

• mononeuropathy of the facial nerve characterized by weakness in the muscles of facial expression

• classified as primary if idiopathic or secondary if ascribed etiology

KITTENS acronym for DDx of Facial

Nerve Palsy

( K) Congenital

Infection/Idiopathic

Trauma/toxins

Tumour

Endocrine

Neurologic

Systemic

Etiology

• congenital

• infection (e.g. otitis media, mastoiditis, HSV, varicella-zoster virus)

• idiopathic (Bell'

s Palsy)

• trauma

• toxins/drugs

• tumour

• endocrine (diabetes, preeclampsia, hyperthyroidism)

• neurologic (e.g. Guillain-Barre syndrome, myasthenia gravis,stroke, multiple sclerosis)

• systemic (e.g.sarcoidosis, amyloidosis, hyperostoses)

Think neoplasm rather than Bell's

palsy If:

• Slow, progressive onset

• Involvement of other cranial nerves

or presence of lateralizing signs(e.g.

Hemiparesthesias. hcmiparalysis.

aphasia)

• Sparing of frontalis(central palsy) vs.

involvement of frontalis(peripheral

palsy)

• Palpable mass over parotid gland in

middle ear

• Adult with unilateral middle ear

effusion

Treatment

• treat according to etiology;provide corneal protection with artificial tears, nocturnal lid taping,

tarsorrhaphy, upper eyelid weighted implants

• if idiopathic, corticosteroids ± antivirals in patients with severe to complete paresis

• facial paralysisthat does not resolve with time or with medical treatment will often be referred for

reanimation techniquesto restore function

common reanimation techniques include:

• direct facial nerve anastomosis

interpositional grafts

anastomosis to other motor nerves

• muscle transpositions

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OT23 Otolaryngology Toronto Notes 2023

Table 10. Bell’s Palsy vs. Ramsay Hunt Syndrome

Etiology Incidence Findings Investigations Treatment, Follow-up, and

Prognosis (Px)

Bell's Palsy

Idiopathic,possible

(HSV)infection involving

CN VII

80 -90% olPfP

Risk Factors:

Stapedial reflex absent

Audiology normal (or

baseline)

EMC -best measure for

prognosis

Topognostic testing

MRI with gadolinium -

enhancement of CN VII

and VIII

High resolutionCl

Hs Rx

Prevent exposure keratitis with

patching ortarsorrhaphy

Systemic steroids may lessen

degeneration and hasten

recovery

Consider antiviral (acyclovir)

Acute onset

tviral-like prodrome

Postauricular pain

Hyperacusis (30%)

Oecteased lacrimation

DM

Pregnancy

Past history

Diagnosis olexclusion

P/E

Paralysis or paresis of all

muscle groups on one side

olthe face

Absence of signs oICNS

disease,upper motor

neuron lesion or CVA

F/ll

Spontaneous remission should

begin within 3 wk of onset

Delayed (3- 6 mo) recovery

portends at least some

functional loss

Px

»90%’

no voluntary EMC

motor unit potentials - consider

surgical decompression

Poorer if hyperacusis,»60 yr,

DM, HIN. severe pain,complete

facial paralysis

4.5-9% olPFP

Risk Factors:

Stapedial reflex absent

Audiology -SNHL

Viral ELISA studies to

confirm

Ramsay Hunt

Syndrome Herpes Zoster

Olicus)

Varicella cosier infection of Impaired immunity

Cancer

Hx Rx

Hyperacusis

SNHL

Severe pain of pinna,

mouth,or face

Avoid touchinglesions to prevent

spread of infection

Systemic steroids can relieve

MRI with gadolinium (86% pain, vertigo,avoid postherpetic

ol facial nerves enhanced) neuralgia

60 yr

CN VII/VIII

Radiotherapy

Chemotherapy

P/E

Vesicles on pinna,external

canal(erupt 3-7 d after

onset of pain)

Associated herpes coster

ophthalmicus (uveitis,

keratoconjunctivitis,optic

neuritis,or glaucoma)

Acyclovir may lessen pain,aid

healing of vesicles

F/U: 2- 4 wk

Px

Worse prognosis than Bell's

palsy;22% recover completely.

66% incomplete paralysis.10%

complete paralysis

Iatrogenic Variable (depending on

level of injury)

Wait for lidocaine to

wear off

Rx

Exploration ilcomplete nerve

paralysis

No exploration if any movement

present

EMG

Rhinitis

Definition

• inflammation of the lining (mucosa ) of the nasal cavity

Table 11. Classification of Rhinitis

Inflammatory Noninflammatory Rhinitis medicamentosa:rebound

congestion due to the overuse of

intranasal vasoconstrictors:limit use to

no more than 3-5 d.Treat with saline

irrigations and intranasal steroid

Perennial non-allergic

Asthma.ASA sensitivity

Allergic (seasonal vs.perennial)

Atrophic

Primary:Klebsiella ocena (especially in elderly)

Acquired:post-surgery if too much mucosa or turbinatehas been

resected

Infectious

Viral:rhinovirus,influenza,parainfluenza, etc.

Bacterial:S.aureus

Fungal

Granulomatous:T8.syphilis,leprosy

Hon-infectious (eg.sarcoidosis,GPA)

Irritant (e.g. dust,chemicals,pollution)

Rhinitis medicamentosa

Topical decongestants

Hormonal

Pregnancy

Estiogens

thyroid

Idiopathic vasomotor

Table 12. Nasal Discharge: Character and Associated Conditions

Character Associated Conditions P1

L J

Walcty/Mucoid

Mucopurulent

Serosanguinous

Bloody

Allergic,viral,vasomotor. CSF leak (halo sign)

8acterial.foreign body

Neoplasia

Trauma,neoplasia,bleeding disorder.HTN/vascular disease +

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Allergic Rhinitis (i.e. Hay Fever)

Definition

• rhinitis characterized by an IgE-mediated hypersensitivity to foreign allergens

• acute-and-seasonal orchronic-and-perennial

• perennial allergic rhinitis often confused with recurrent colds

Etiology

• IgK antibody mediated hypersensitivity reaction of the respiratory mucosa upon exposure to allergen

• concentration of allergen in the ambient air correlates with the rhinitis symptoms

Epidemiology

• age at onset usually <20 yr

• personal or family history of atopic disease

Clinical Features

• nasal congestion, nasal itch, watery rhinorrhea,sneezing, and hyposmia

• ± allergic conjunctivitis(redness, tearing, itching of the eyes)

• seasonal

caused by pollen from trees, grass, and ragweed

occurs during a specific season

• perennial

caused by airborne dust mite fecal particles,cockroach residues,animal dander, moulds, and

tobacco smoke

• occurs throughout the yr

Complications

• chronic sinusitis/polyps

• serous otitis media

Congestion reduces nasal airflow and

allows the nose to repair itself (i.e.

washes away the irritants). Treatment

should focus on the initial insult rather

than target this defense mechanism

Diagnosis

• history

• physical exam

congested gray/blue turbinates

• nasal tip transverse crease

• reversible obstruction with topic decongestant

• allergy testing

Treatment

• allergen identification and avoidance

• nasalsaline irrigation

• oral antihistamine (e.g.desloratadine, fexofenadine,loratadine, cetirizine)

• intranasal corticosteroid (mainstay of treatment)

• combination intranasal corticosteroid/antihistamine spray

• leukotriene receptor antagonist

• allergen immunotherapy

• other therapies: decongestants (risk of rhinitis medicamentosa ), oral corticosteroids, eye drops

Vasomotor Rhinitis

Definition

• rhinitissecondary to changes in vascular permeability caused by dysregulation of nociceptors and

autonomic nerves

Etiology

• temperature change

• alcohol, dust,smoke

• stress, anxiety, neurosis

Clinical Features

• chronic intermittent nasal obstruction, varies from side to side

• similar to allergic rhinitis

• nasal allergy must be ruled out

«. J

+

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OT25 Otolaryngology Toronto Notes 2023

Treatment

• elimination of irritant factors

• congestion-predominant:

intranasal antihistamine

1NCS

combination INCS/antihistamine

• ± oral decongestant (risk of rhinitis medicamentosa)

• rhinorrhea-predominant:

• intranasal anticholinergic (e.g. ipratropium)

• ± intranasal corticosteroid,intranasal antihistamine

• symptomatic relief with exercise (increased sympathetic tone)

Rhinosinusitis

Definition

• inflammation of the mucosal lining of the sinuses and nasal passages

Pathogenesis of Rhinosinusitis

• ostial obstruction or dysfunctional cilia permit stagnant mucous and, consequently, infection

• all sinuses drain into a common area under the middle meatus called the osteomeatal complex

Classification

• acute:<4 wk

• chronic: >12 wk

Table 13. Etiologies of Rhinosinusitis

Ostial Obstruction Inflammation URTI

Allergy

Septal deviation

Turbinate hypertrophy

Polyps

Tumours

Adenoid hypertrophy

Foreign body

Congenital abnormalities (e.g.cleft palate)

Mechanical

Immune GPA

Lymphoma,leukemia

Immunosuppressed patients (e.g.neutropenics. diabetics,HIV)

Cystic fibrosis

Immotile cilia (e.g. Kartagener'

s syndrome)

Infection

Facial fractures

Systemic

Direct Eitension Dental

Trauma

Acute Bacterial Rhinosinusitis

Definition

• bacterial infection of the paranasal sinuses and nasal passageslasting >7 d

• clinical diagnosis requiring >2 majorsymptoms, and at least one of the symptoms is either nasal

obstruction or purulent/discoloured nasal discharge

• can confirm diagnosis with CT of paranasal sinuses and/or endoscopically

Acute Rhinosinusitis Complications

Consider hospitalization if any of the

following are suspected:

Orbital (Chandler'

s classification)

• I Preseptal cellulitis

• II Orbital cetluftis

• III Subperiosteal abscess

• IVOrbital abscess

• V Cavernoussinusthrombosis

Intracranial

• Meningitis

. Abscess

Major Symptoms (at least 2 of PODS.1must

be 0 or D)

Minor Symptoms

P FacialPain/Pressure/fuHness Headache

Halitosis

Fatigue

Dental pain

Cough

Ear pam.fullness

0 Nasal Obstruction

Purulentfdiscoloured nasalDischarge

Hyposmia/anosmia (Smell)

D

S

Bony

• Subperiosteal frontal bone abscess

("Pott'

s puffy tumour"

)

• Osteomyelitis

Neurologic

• Superior orbital fissure syndrome (CN

Ill/lVrVI palsy,immobile globe, dilated

pupils, ptosis.VI hypoesthesia)

• Orbital apex syndrome (as above.

Etiology

• bacteria:S. pneumoniae (35%), H.influenzae (35%),M.catarrhalis, S.aureus, anaerobes (dental)

• children are more prone to a bacterial etiology, but viral isstill more common

• the maxillary sinusis the most commonly affected sinus

• must rule out fungal causes (mucormycosis) in immunocompromised hosts (especially if painless

black or pale mucosa on examination)

L J

+

plus neuritis, papilledema, decreased

visual acuity)

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Clinical Features

• sudden onset of:

nasal blockage/congestion and/or purulent nasal discharge/posterior nasal drip

• ± facial pain or pressure, ihyposmia, ±sore throat

• persistentsymptoms >10 d or worsening symptoms >5 d or presence of purulence for 3-4 d with high

fever (>39°C)

• speculum exam: erythematous mucosa, mucopurulent discharge, pus originating from the middle

meatus

• predisposing factors: viral URT'

l, allergy, dental disease, anatomical defects

• differentiate from acute viral rhinosinusitis(course: <10 d, peaks by day 3)

SystemicCorticosteroid Thfrajjloticate

Sinusitis

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corticosteroids associated wSt maturedtfuwal

outcomes

*

petestswithacute ssusitrscasoaredto

placebo orUStlDs?

Coadasioa:0*

al cortcosterods cosbraedarts

antibioticsaajbe associated withmodest beseht w

short-terra relief of sjnrptoots ia adults with seiere

symptoms of acutesinusitiscomparedart:aabbiotes

alone.Oral corticosteroids as monotherapy art act

asscratedrttiraptured chocaloattosesia adahs

irtir clinically diagnosed acutessasnts.

Management

• depends on symptom severity (i.e. intensity/duration ofsymptoms, impact on quality'of life)

• mild-moderate:1NCS

• if no response within 72 h, add antibiotics

• severe:1NCS + antibiotics

• antibiotics

1st line: amoxicillin x 10 d (TMP-SMX or macrolide if penicillin allergy7

)

• if no response to 1st line antibiotics within 72 h,switch to 2nd line

2nd line:fluoroquinolones or amoxicillin-clavulanic acid

• adjuvant therapy (saline or hypochlorous acid (paediatric sinusitis) irrigation, analgesics,oral/topical

decongestant) may provide symptomatic relief

CT indicated only if complications are suspected

Chronic Rhinosinusitis

Definition

• inflammation of the mucosa of paranasalsinuses and nasal passages >12 wk

• diagnosis requires >2 major symptoms for >12 wk and >1 objective finding of inflammation of the

paranasalsinuses(CT/endoscopy)

Major Symptoms (similar to acute, but less

severe)

Minor Symptoms

C Facial Congestion /fullness

Facial PainfPressure/fullness

Chronic nasal Obstruction

Purulent anterior/posterior nasal Discharge

Hyposmia/anosmia $ anell)

Halitosis

Chronic cough

Maxillary dental pain

P

0

D

S

Etiology

• unclear etiology7

but the following may contribute or predispose

inadequate treatment of acute rhinosinusitis

untreated dental disease

anatomic factors(lost ostium patency, deviated septum)

local physiologic factors

ciliary disorder (e.g.cystic fibrosis,Kartagenersyndrome, primary ciliary dyskinesia)

bacterial colonization/biofilms ( S.aureus,hnterobacteriaceae spp.. Pseudomonasspp.,.S

'

.