OT

Otolaryngology - Head and Neck SurgeryJayant Ramakriabna and Rebecca Zener, chapter editorsAlaina Garbens and Modupe Oyewumi, associate editors Adam Gladwish, EBM editor Dr. Jonathan Irish and Dr. Blake Papsin, staff editorsBasic Anatomy Review ................... 2 Ear Nose Throat Head and Neck Anatomical Triangles of the Neck Differential Diagnoses of Common Presenting Problems ..................... 6 Dizziness Otalgia Hearing Loss Tinnitus Nasal Obstruction Hoarseness Neck Mass Hearing ............................... 9 Normal Hearing Physiology Types of Hearing Loss Pure Tone Audiometry Speech Audiometry Impedance Audiometry Auditory Brainstem Response Otoacoustic Emissions Aural Rehabilitation Vertigo ............................... 12 Evaluation of the Dizzy Patient Benign Paroxysmal Positional Vertigo Meniere's Disease (Endolymphatic Hydrops) Vestibular Neuronitis labyrinthitis Vestibular Schwannoma (Acoustic Neuroma) Tinnitus .............................. 15 Diseases ofthe External Ear ............. 16 Cerumen Impaction Exostoses Otitis Externa (OE) Malignant (Necrotizing) Otitis Externa (Skull Base Osteomyelitis) Diseases ofthe Middle Ear .............. 17 Acute Otitis Media and Otitis Media with Effusion Cholesteato rna Mastoiditis Otosclerosis Diseases of the Inner Ear ................ 19 Congenital Sensorineural Hearing Loss Presbycusis Sudden Sensorineural Hearing Loss Autoimmune Inner Ear Disease Drug Ototoxicity Noise-Induced Sensorineural Hearing Loss Inner Ear Diseases that cause Vertigo Temporal Bone FracturesToronto Notes 2011

Facial Nerve Paralysis . . . . . . . . . . . . . . . . . . . 22 Rhinitis ............................... 23 Allergic Rhinitis (Hay Fever) Vasomotor Rhinitis Sinusitis .............................. 25 Acute Suppurative Sinusitis Chronic Sinusitis Epistaxis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27 Hoarseness ........................... 28 Acute Laryngitis Chronic laryngitis Vocal Cord Polyps Vocal Cord Nodules Benign laryngeal Papillomas Laryngeal Carcinoma Salivary Glands ........................ 30 Sialadenitis Sialolithiasis Salivary Gland Neoplasms Parotid Gland Neoplasms Neck Masses .......................... 32 Approach to a Neck Mass Evaluation Congenital Neck Masses in Detail . 33 Branchial Cleft Cysts/Fistulae Thyroglossal Duct Cysts Cystic Hygroma (lymphangioma) Neoplasms of the Head and Neck ......... 34 Thyroid Carcinoma Pediatric Otolaryngology ................ 38 Acute Otitis Media (AOM) Otitis Media with Effusion (OME) Adenoid Hypertrophy Sleep-Disordered Breathing in Children Acute Tonsillitis Peritonsillar Abscess (Quinsy) Tonsillectomy Airway Problems in Children Signs of Airway Obstruction Acute laryngotracheobronchitis (Croup) Acute Epiglottitis Subglottic Stenosis Laryn goma lacia Foreign Body Deep Neck Space Infection Common Medications .................. 47 References . . . 48

Otolaryngology OTI

OT2 Otolaryngology

Basic Anatomy Review

Toronto Notes 2011

Basic Anatomy ReviewEarExternal Temporalis fascia and muscle Triangular fossa Middle Auditory ossicles Inner

I

Semicircular canals

Antihelix

Scapha Facial nerve (CN VII) Cochlea Antiragus

Aarti lnamdar

Tympanic membrane

Eustachian tube Susan Park 2009

Figure 1. Surface Anatomy of the External Ear; Anatomy of Ear Tympanic membrane viewed through speculum View into tympanic cavity after removal of tympanic membrane

Tensor tympani tendon Tensor tympani muscle

Fossa of round-"'--illirc (cochlear) window

Tympanic Plexus (branch of CN IX) Hypotympanum...... _ _ _ Annulus Diana Dai 2006

--:::-'0----- Cone of light

Figure 2. Normal Appearance of Right Tympanic Membrane on Otoscopy

....

,}----------,

Drainage into Nasal Cavity Superior meatus: sphenoid (via sphenodethmoidal recess), posterior ethmoid sinuses Middle meatus: frontal, maxillary, anterior ethmoid sinuses Inferior meatus: nasolacrimal duct

Speculum View of Right Nostril

Opening for Eustachian tube _ _ _ _ _ _ _ _ _ _ _ __ j

Figure 3. Nasal Anatomy

'IbroDlo Nota 2011

Buic Anatomy Review

Otolaryngology OT3

Sepillbi'IIIChof aphanopalati1111 a.

111plrior llbillla.

Branch

Greatar palatin a.

Figure 4. Nasal Saptmn and its Altarill Supply (sea Epistaxis sectiDII far dmilld bload siQIIIIy)

0rauynx: ...,._..lliUC criCCJila.tiiagll

Nllophar,nx; siUI baa to soft p*te 111ft palm to hyoid bone hyoid bDnB'Io irlerior

ThroatSuperior Viaw- -E'piglottit

iTracheaj

J"' 0

Poslllrior View

Figure 6. Anatomy of 1 Normal larynx: SIJIIIriDr View of Llrvu 01 l1dirac:t

OT4 Otolaryngology

1'oroDio

2011

Haad and Nack

AftcJJiara.

l.etrnJ I'IUIII.

i. _... rl Fulll Nlml (in arder from 11411riar tD irlflriarj Ten ZibiQ ..._My Car

!

i "' G

1. Ext111temporal Segmant al Facial Nane

Br11cha If the Extlrnll C.rd Arti1T (il onler from inferior tD Some A'9'{ Lacty Figullld Dut PMS

Figura I. BIDad SIQIIIIy 1D th1 flea

mu..::le-.....

Ant bellydigllllric mlllcle _

..

F"llg11'8 9. Anlblmy crf thl Naclt

.....

',

Anatomical Triangles of the Neck anterior trlanJie: bounded by anterior border ofsternocleidomastoid (SCM), midline of neck, and lower border of mandible divided into: IUbmeDtal triangle: bounded by both anterior bellies of digastrics and hyoid bone dipmic triaJicle: bounded by anterior and posterior bellies of digastric, and inferior border of mandlhle carotid triaDgle: bounded by stemocleidOJD88toid, anterior belly ofomohyoid. and

l'lhd l'lruynlpdletlt . . . at the Head llld Neck Cilillf- P14111ry canstrictiDII l'tllygepald!l -IIICrinal gland, 111111 mucoea ......IIi!... -libJllrdhllr.IItie - paratid alrd

It'

r-tiln at Facial Nlrw "EEn, ..... he.. n... E11111- mpedius muacl T11111 - llcrimation !lacrimal gllrd) 11'11 881ivlltion (parotid) F11ea - nucl11 of facial axprauian Tllll - sensory enllrior 2/3 of tDngue (Vie choldll tympani)

- contains: tail ofparotid, submandibular gland, hypoglossal nerve, carotid Wurcation, and lymph nodes

Toronto Nota 2011 posterior triaDBle:

Otolarynplolf OTS

bounded by posterior border ofsternocleidomastoid, anterior border of trapezius, and middle third of clavicle divided into: ocdpltal triangle: superior to posterior belly of the omohyoid subclavian triangle: inferior to postmor belly of omohyoid amt:ain8: spinal accessory nerve and lymph nodes

Table 1.lplphatic Dni111g1 of Nodal Gra-..s au AnatamiCIII Tril1glas of Neck, . SID!cdpitlll (S)2. llaCrolllicullr (R)

Base of

posleriortD miiii:Did procasa

Posterior scalp temporalregilll, exL IUditoly 11111111s, post. piiDI

3.f'lltJticl1ll'lllllric.-r(P)

In front of

of lnnaiiDI

Exlemalll.lditay meetua. nritr pinna. lOft tisllues n9ons, root of nose, eyelids, palpabllll Uhid.tof a nad (VI'Cflrw's node) lillY indical8 an abd11111i'llli i'ldicllllallhll

4. &mmllltal U.MIIA)5. S!DnrntibiB (l..evliiiB)6.

(Milliwl) Anblior bellies of digl8tricnuscles, tip of 111111dible, IDI hyoid bn

Rlor of mouth. antaior oral antaior mandiQar alveolar ridge, loww IIJOral

Anterior belly II dgiJS!ric musde, ltytobycid 1111Sde, body of l!lllldilil

rriiHic:e.

anteriorrlllllll cavity, soft lilliiEI II till!

glrnt

j.lgiAII' (L.evals IIA rntiiB)(LMIIIO

7. Midde

W bale to Rarior bordar of hyoid bone IIBSIII alongSCMITIISI:Ie illynx. pnlid lnferiar bcldar II hyoid bn tD i'laritr Oral naw'nbyprymc. '-Ynx bllder II c:ricoid Cllliage alcng SCM ITIISI:Ie lnferiar bcldar of cricoid cartilage to clavicle alcng SCM nmcleJJos1:!riur bcrderII SCM, nrior border NIISil!Jiaym rnt c:ubnous s1Juclures of tnpazius, fnm skuI bale to diiYicle of the pcstlrior scalp IDI neck (Milliwl) Hyoid bone tD IUJIRISIImBI notth Thyroid PKt. glutlie subglatlic lllryror.ipll ofblliwB111111roll1111 pllihyruidlllllllls

mlltiii'ICV IIII"'IIIK anl1111811181lt mav

.....node

meclallilum.lunp, or PG*rior

may ildiclte

B.

(Level IV}

9. Fomrior triqe"" (Lmls VA and VB) 10. AniBrior(l.ev8l VII

Clllllid.tariBI

pirifunn ain111.. csvi:lllllllplll!jJII

'Vn:flr.y nodi; laft lrMer IMIIV

""'n:UUas pralrldall.!lllftDd,STA

"lliild8llalll

TC

STA

CCAIJV ITA RRLN

1t

IF"11111re 10. Anatamy of 'lbyruid Gl1nll

SPG TG lPG VN (CN X) l.RLN -

cc

Superior thyrDid lrllly Carrman Clf1llid lft8fy Intimal iua* vem Jnflrior thyroid rtarv Ri;rt recurrent laryngeal nerve - Thyroid cartillg& - Cri1:0id eartilage - Suplllrior pntlryroid gland Tll'jnlid gilnd

Ill

lnflriorPl/llflyroid gland Vllgua narw (CN X) Left rBC:Urrent iaryng11l nerve

I0

i

.II

OT6 Otolaryngology

Differential Diagnoses of Common Preaenting Problems

Toronto Notes 2011

Differential Diagnoses of Common Presenting ProblemsDizziness

.....

.. ,ILIIIyrintitil

Tru1 nystagmus and v.rtigo CIIIISid by a peripheral lesion wiD never IIIII longer than a couple of weeks becausevartigo will pu&.

..

I True Vertigo I

I Dizzil I

of comp--'ion. do not compenllllll, hance nyslllgmus and

aenign paroxysmal positional vartiaa IBPPVIev.tilulllr ....,..itis Mani6ra'a dileue

+

{Vestibularl

I

I Central Idisorders Verllbrobasiliar insufficiency Transient ilch1111ic attacks Wallanballl'l syndrome Cnbullar infarction Migrainaul vartiga Multiple ICie._ill T..norous CPAtumou11 Posterior fossa tJJmours Glomus tJJmours lnllammlllion Meningitis Cnbullar abSCIIII$ Tra..na: cerebellar contusion Toxic: alcohol, hypnotics, drugs

..

+ ...

I Organic Diseases I I Functional ICardiac

..

I Non-Vertiginau1 I

.DapmsionArucilly

CannnDJia.IM

+

+

Anhytlrniu

It' 5 D's af VwtllbraiHIIIIar lllllllllcillncy Drop lrtbcks

Diplopia

Dysarthria

DilzinassDysphll!lill

Recumant vaslibulopa:thy T1111poral bone fracture Suparior sernicincular canal dahiscanca Ototoxic drug exposure Autoimmune inner ear disease Perilymph fililula CholestBatoma

Aortic stenosis Vasovagal Orthostatic hypotension Anemia Puripheral neuropa:thy Visual impainnant

Pmic disorder lhyp.varrtilationl Purwonality di&order Phobic dizzin111

Figure 11. Differential Diagnosis of Dizziness

Otalgia1. Local CausesTabla 2. Differential Diagnosis of Otalgia - Local Cau11sEtialagy

Infection

Exlamal Ear Pain a. Otitis axt1111111b. Herpes simpl!!ll/loster c. Auricular cellulitis

Midlhand Inn Ear Paina. Aculll otitis media b. Otitis media with ellusion c. Mastoiditis, skull base infections (mal9!ant in diabetics! Traumatic perforation, barotrauma Neoplasm, Wegener's, cholesteatoma

d. Extemal canal abscessTraumaOthar Frostbite, bums, hematoma, lacerations Neoplasm Dl external c!llal, fureiiJl body, cerumen impaction

prin-..iy madillld by TM mtdiing

2. Referred Pain (from CN V, IX and X) -Ten T's

+2

Eustachian Tube TMJ Syndrome (pain in front of the ears) Trismus (spasm ofmasticator muscles; early symptom of tetanus)

TeethTongue Tonsil (tonsillitis, tonsillar cancer, post-tonsillectomy) Tic (glossopharyngeal neura1gia) Throat (cancer oflarynx) Trachea (foreign body; tracheitis) Thyroiditis Ramsay Hunt syndrome (Geniculate Herpes) CN VII palsy (e.g. Bell's palsy)

Toronto Notes 2011

Differential Diagnosea of Common Presenting Problems

Otolaryngology OT7

Hearing Loss

1 Conductive 1

IExternal Eer I"lmlllCllld Cll'l.._

I HAring Lo.. I1

CommnCII-

I Middle EBr I"Acuta Dlilil medii "Oiitia media with dulion wrM plllflll'8liDnOialdlroaill Tympanasclerasis Eustachian tube dysfunctian Cholestaalama Ossiwar melfurmlllians Oniwar Hematympanum Middle earlunour

I Congenital IGtnetic Synnme assacillled lnlnluterine infections {i.e. TORCH) Teratogans l'llrinlllll hypoxia l'r8malurily/low bi1h weight Hyperbilirubinemia

s..sarineural 1

I Acquired I"PI'elllvclllilLllbyrintMisSudden SNHL Autoimmune inner eer disease Ototaxic drug exposure Temporal bane1numa lnfuctiou& Postmeningitis Syphilis Viral: mumps. CM\1, HSV Neopla&tic Acoustic CPAlunours Vascular accklsiarVennboli Auditory nuopathy

',The incidence of Merlin's disease has

decreased since 1he introduction of H. itrffuenzae and s. pneUITJOtliee Vllcc:iniS.

"Otilia ......a"Farwign bally K!ntosis oblurans EKastoses. ostllamas Tumcu al canal CanganitBI stanosi.tlnicrotia

"No_.,.._ -illled

"Noille-induc:edMenii11a"s disease

-rom

Figura 12. Differential Diagnosis of Hearing Loss

Tinnitus

Subj11ctive Only heard by patient {common)Otologic Presbycuais Naiseinduced hearing lass Otitiis media with affusion Menilne"s disease Otosclerosis Cerumen Fo111ign body agairl$t TM Drugs

+

I Tinnitus I

Objective Can be heard by others {rare)V.cular Benign

+

ea.mlll -

', ,Tinnitus is most commonly iiSSOCiated SNHL.

ArtariOVIII'IOUS mlllformlllion

ASA

NSAIDsAminCMJiycosides Antihyperlalsives Heavy metals Metabolic Hyper/lhypathyroidism V"rtamin A. B. Zi1c daficiency NauroiCMJiC Head trauma Multiple sclerosis Acoustic nauroma CPA tumours PsychiatricAnxiety

Glomus tympanicum Glomus jugulare Arterial bruits: Higlt-riding carotid artery V.cular loop Persistent stapedial artery Carotid stenosis Vanous hum: High jugular bulb Hypertension Hyperllhypathyroidism Mechanical 1'1\ulous eustachian tube 1'11111111 myoclonus Stapedius muscle spasm

',.. ,DID_. Tympank:UIIV"Jugulanl TumSigns and Symptams Pulllllile tinnitus Hearing loss Blue mus behind 1M Brown's sign {blanching of the 1M with pneumatic omscopy)

Deprenion

Figura 13. Differential Diagnosis of Tinnitus

OTB Otolaryngology

Differential Diagnoses of Common Preaenting Problems

Toronto Notes 2011

Nasal ObstructionTabla 3. Differential Diagnosis of Naul ObstructionAaiuired Nasal Cavity Rhinitis Acu!Wclrunic Vasomator Allergic Polyps Foreign bodies Enlarged turbinates Tumour Ben9J- inverting papilloma Malignant Squamous cell carcinoma {SCCI Esthesioneuroblastoma {olfactory newublaslllmal Adenocarcinoma Nasal Septum Septal deviation Septal hematomll/abscess Dislocated &&plum Cangenilll Nasal Cavity Nasal dennoid cyst Encaphulocale Glioma Chounal atresia Nasal Septum Septal deviation Septal hematomll/abscess Dislocated septum

N11ophlrynx Adenoid hypertrophy Tumour Ben9J-juVllllile nasopharyngeal angiofibroma {JNAI Malignant- nasopharyngeal carcinoma

Functi11111l

Tumel nose syndrome: absence of feeling in 1105e prevents 1he sensa1ion of aeration 1hrough nosbils

HoarsenessTabla 4. Differential Diagnosis of Hoarseness

....

..}-----------------.

lnfactious lnfll11matory

Acutaichronic laryngitis Laryngotracheobronchitis {croupI Gastro-esophageal reflux {GERDI Vocal cord polyps/nodules Lifllstyle: smoking. chronic ETOH use Externellaryngeallnluma Endoscopy and endolnlcheal tube {e.g. intubation granulomaI

LLilQ is the mort common cause of vocal cord 111111lv1is.

NaupluiaCylllSys!elliC

Benign tumour Papillomas {HPV infection! Retention cyslll Endocrine

Malignant tumour Squamous cell carcinoma (SCC) Comectiw ti&sue disease Rheumatoid 1rtluitis (RA) SLE

Hypothyroidism Virilization

Na1011logic (vocal cord paralysis due to superior :!:: recurrent laryngeaiiii!M! injJryl

Central lesions CerebllMIScular accident (CVAI Head injury Multiple sclerosis (MSI Skull bese tumours Amold-Chiari MaHormation Peripheral lesions Unilateral Lung malignancy Iatrogenic injJry - thyroid. parathyroid surgery, carotid endarterectomy, patent ductus arteriosus {PDA) ligation Bilateral Iatrogenic injJry: bilataral1hyroid surgery, forceps delivery Neuromuscular Myasthenia gravis Psychogenic aphonia (hysterical aphonia) Laryngomalaciu Laryngeal Well Laryngeal Atresia

Functi11111lCongenital

Toronto Notes 2011

Differential Diagnoses of Common Praenti1J8 Problemii!Hearing

Otolaryngology OT9

Neck Mass

lnllammatory}lnfec:tian.

1

l

NeckMau

[ Midlme

..

I Congenital II

l

...

[ l.aleral [

.....

[ Malignant

..

I Neaplallic II

.

[ Benign [

.....

Reactive lymphadenoplllhyTB or atypical mycobacteria Infectious mononucleO&il Abscassas Cat scratch fever Sarcoidosis Kawasaki's HIV

Thyrogl0$$al duct C\'$1: Thyroid blmour/goitra Pyramidal lobe of thyroid gland R1111ula

IBranchial cleft CY$1: I Cystic hygrom11Lymphoma Thyroid Sarcoma Salivary gland neoplasm Rhabdomyosarcoma Neuroblutoma

.

Salivary gland neopl8$m Lipom11 Fibroma

Vascular

lnfraci11Vicul8r primary Leukemia

HINid and nack primary

I

Figure 14. Differential Diagnosis of a Neck Mass

HearingNormal Hearing Physiology Conductive pathway (External auditory canal to cochlea) - Air conduction of sound energy down the EAC -+ Vibration ofthe tympanic membrane (area effect) -+ Sequential vibration of the middle ear ossicles: malleus, incus, stapes (lever effect) -+ Transmission of amplified vibrations from the stapes footplate in the middle ear to the oval window of the cochlea in the inner ear -+ Pressure differential on Cochlear fluid creates movement along the basilar membrane within the Cochlea from base to apex Neural pathway (Nerve to brain) - Basilar membrane vibration stimulates overlying hair cells in the Organ of Corti-+ Stimulation ofbipolar neurons in the spiral ganglion of the cochlear division of CN VIII -+ Cochlear nucleus -+ Superior Olivary Nucleus -+ Lateral lemniscus -+ Inferior colliculus-+ Sylvian Fissure of Temporal Lobeltl

Onler uf th Nlnl Pdlway (with Cotl'fliiCindinl w-on ABR) Eighlh cranial nerve (1-11) Cochlear nucleus (UI) Superior Olivary nucl111s Lidl!ralleminiscus (IV- V) Inferior colliculus

ECOU

Types of Hearing Loss1. 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 Vlll), brainstem, or cortex 3. Mixed Hearing Loss the conduction of sound to the cochlea is impaired, as well as transmission through the cochlea to the cortex

Auditory Acuity whispered-voice test: mask one ear and whisper into the other tuning fork tests (see Table 5) (audiogram is of greater utility) sensitivity depends on which tuning fork used (256 Hz, 512 Hz, 1024 Hz) Rinne test: 512Hz 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) If AC >BC -+ positive Rinne, which is normal Weber test: 512Hz tuning fork is held on vertex of head and patient states whether it is heard centrally (Weber negative) or is lateralized to one side (Weber right, Weber left) can place vibrating fork on patient's chin while they clench their teeth, or directly on teeth to elicit more reliable response will only lateralize if difference in hearing loss between ears is >6 dB

....

,,

Weber 1i11t lataralillltion = lpailatsral conductive hearing IO$$ or CCIIIIRiatsral sensorineural helring loss. Wh1n conducliw hlaring loss is present. the Weber Ills! is more sensitive in det8cting the CHL 1lw1 the Rinne test

....

,,

OTl 0 Otolaryngology

HearingTable 5. The Interpretation of Tuning Fork Tests Examples Normal or bilateral sensorineural hearing loss Right-sided conductive hearing loss, normal left ear Right-sided sensorineural hearing loss, normal left ear Right-sided severe sensorineural hearing loss or dead right ear, normal left ear Weber Central lateralizes to Right lateralizes to Left Lateralizes to Left Rinne

Toronto Notes 2011

.... .-------------------,Frequency of Tuning Fork (Hzl 256 512 1024 Minimum hearing loss to have NEGATIVE Rinne (BC > ACI (dBI 15 30 45

'.,

AC > BC (+) bilaterally BC>AC (-)right AC > BC (+) bilaterally BC>AC (-)right*

* avibrating tuning forl10 dB (an air-bone gap) 2. Sensorineural Hearing Loss (SNHL) (Figure 15D and 15E) both air and bone conduction thresholds below normal gap between AC and BC 10 dB (an air-bone gap)

Toronto Notes 2011

Hearing

Otolaryngology OTll

Speech AudiometrySpeech Reception Threshold (SRT) lowest hearing level at which patient is able to repeat 50% oftwo 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. Ifnot, suspect a retrocochlear lesion or functional hearing loss used to assess the reliability of the pure tone audiometry

......

'S,..b DilcrimiMtion

'1o of words

identilild 80to90'1o 6011180% 401D60'1o

ExceUentGoodFair

Speech Discrimination Testpercentage of words the patient correctly repeats from a list of 50 monosyllabic words tested at a level35 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 rollover effect: a decrease in discrimination as sound intensity increases are typical of a retrocochlear lesion (e.g. acoustic neuroma) investigate further if scores differ more than 20% between ears used as best predictor ofhearing aid response, as if patient has HL and prior word discrimination, hearing aids may not be helpful

PoorVery poor

Impedance AudiometryTympanogram

--------------------------------------------

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 mmH2 0 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 mmH20Highrl

Type A

TypeB

TypeC

ILaw

A__0Ai Pressure

+

-

0 Air Pressure No pressure plllk PoorTM rmblty indicl1iva af middle ear efMiiiiiOMEt or psdoratad 1M

+

-

0' Nagl1iw j)T8RUT11 palk

+

Normel JlT8aur& peak at o Note: v.ith !Osclerosis, peek is still at 0mmH,O but hq 1 low8r NDII: v.ith 011i:ular c!UI discantinuity. palk iuliht 0nmi,O but han higher amplitude

hlicativt af ulllehi11111Di dyslunctilll or ellly stave otitis medii will! out elfusi111

Figure 16. Tymp1nogrems

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 in a type B curve, ear canal volumes of greater than 2 cc in children and 2.5 cc in adults indicate TM perforation or presence of a patent ventilation tube

Acoustic Stapedial Reflexes stapedius muscle contracts 2 to loud sound acoustic .rdln: thresholds = 70 to 100 dB greater than hearing threshold; ifhearing threshold >85 dB, reflex likely absent stimulating either ear causes bilateral and symmetrical reflexes for reflex to be present. CN VII must be intact and no conductive hearing loss in monitored ear if reflex is absent without conductive or severe sensorineural loss -+ suspect CN Vlll lesion acoustic reflex decay test= ability of stapedius muscle to sustain contraction for 10 s at 10 dB normally, little reflex decay occurs at 500 and 1000 Hz with cochlear hearing loss, acoustic reflex thresholds = 25 to 60 dB with retrocochlear hearing loss (acoustic neuroma) -+ absent acoustic reflexes or marked reflex decay (>50%) within 5 seconds

OT12 Otolaryngology

Hearing LoasNertigo

Toronto Notes 2011

Auditory Brainstem Response (ABR) measures neuroelectric potentials {waves) in response to a stimulus in five different anatomic sites {refer to Order ofNeural Pathway sidebar on OT9). This test can be used to map the lesion according to the site of the defect delay in brainstem response suggests cochlear or retrocochlear abnormalities {tumour or multiple sclerosis) does not require volition or co-operation of patient

Otoacoustic Emissions objective test of hearing where a series of clicks is presented to the ear and the cochlea generates an echo which can be measured often used in newborn screening can be used to uncover normal hearing in malingering patients

.....

...----------------.lll1d

Aural Rehabilitation dependent on degree ofhearing loss, communicative requirements, motivation, expectations, age, physical, and mental abilities negative prognostic factors: poor speech discrimination narrow dynamic range (recruitment) unrealistic expectations types of hearing aids: behind the ear all in the ear bone conduction - bone anchored hearing aid (BAHA): applied and attached to the skull contralateral routing of signals (CROS) assistive listening devices: direct/indirect audio output infrared, PM radio, or induction loop systems telephone, television, or alerting devices cochlear implants: 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, pre- and post-lingually deaf children

....Ungaalullfn-: deafnessoccurring blfol'l1111 acquired.

Post.fingul dellfn-: dllfness occurring after speech and lll1gUIIge 1111 acquired.

.....

,

Pre-lingually deaf infants are the best candidlllas far linllllhlbilitltion because they have benefitted !rum nonnal devalapmenlll pluticity.

VertigoEvaluation of the Dizzy Patient vertigo: illusion of rotational, linear, or tilting movement of self or environment vertigo is 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 of"dizziness" (e.g. cardiovascular, psychiatric, neurological, aging)

.....

llifftrenlia ntw.en the Fallowing TVJIIII of DiDin Spiming lighlhelldedness Giddiness

, ..----------------.

Table 6. Peripheral vs. Central Vertigo

Cenlnllmbaln:e

Unsteadiness

Nanea and vamiting Audilllry svn.tams Neurologic symplllml CampanlltianNysblgiiUI

Mild-Moderate Severe Common Rare Rapid Unidiractional Horimnllll or ruiB1ory

Severe Variable Rare CoiiiiiDn Slow Bidirectional HoriZIIIIlll or vertical

Teble 7. Differential Diagnosis of Vertigo Based on History

Canditi111Benig plfOllyllllilll

DurationSeconds

lllluing Loa

Tinnitus

Other Featwas

politianal nrtigo IBPPV)Meniere's disease Minutes to hou18 Precedes altllck HallS to days Days Chronic Urilbikrtnl, fluctuating Unilateral Unilateral Progressive

+Whistling

Ywlllular n111ranitis ubyridhitis Al:ousli:neurom1

+

RecentAOM AlllxiaCN VII palsy

Toronto Notes 2011

Vertigo

Otolaryngology OT13

Benign Paroxysmal Positional Vertigo (BPPV)Definition acute attacks of transient vertigo lasting seconds to minutes initiated by certain head positions, accompanied by torsional (i.e. rotatory) nystagmus (geotropic= fast phase towards the floor) Etiology due to canalithiasis (migration of free floating otoliths within the endolymph of the semicircular canal) or cupulolithiasis (otolith attached to the cupula of the semicircular canal) can affect each of the 3 semicircular canals, although the posterior canal is affected in >90% of cases 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 and positive Dix-Hallpike maneuver Dix-Hallpike Positional Testing (see website for video and illustrations) 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 the position for 20 seconds onset of vertigo is noted and the eyes are observed for nystagmus see sidebar for the 5 signs ofBPPV Treatment reassure patient that process resolves spontaneously particle repositioning maneuvers Epley 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

.....

,,.-------------------,

BPPV is the most common cause of episodic vertigo. Patients often are symptomatic when rolling over in bed or moving their head to a position of extreme posterior extension.

.....

,,}-------------------.

5 Signs of BPPV Sean with Dix-Hallpike Maneuver o Geotropic rotatory nystagmus (nystagmus MUST be present for a positive test) o Fatigues with repeated maneuver o Reversal of nystagmus upon sitting up o latency of -20 seconds o Crescendo/decrescendo vertigo lasting 20 seconds

.....

,,.-------------------,

Patients can wear Frenzel's magnifying eyeglasses during the Dix-Hallpike Maneuver, which inhibit visual fixation and allow for better visualization of the eyes.

Supine

5

A. Epley Maneuver Figure 17. Epley and Dix-Hallpike Maneuvers

UT -Utricle PSC - Posterior Semicircular Canal

"' 5.!!!

B. Dix-Hallpike Maneuver

OT14 Otolaryngology

Vertigo

Toronto Notes 2011

Meniere's Disease (Endolymphatic Hydrops)

,,., ,,.,....

Definition episodic attacks of tinnitus, hearing loss, aural fullness, and vertigo lasting minutes to hours

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

fMtllnll Clf Meni' DiNVertigo, Tmnitus, Alnl Fullnenlllld Helling Loss

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

Drop AUacka (Tumlllkin'alltDIIIIIIc Crilill are sudden falls occurring without warning and without LDC.

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

,.. ,

}-----------------,

Before proceeding with gentamicin 1rultmunt. perform a CT Head tu rule out CPA tumour as the CIUSe of symptoms.

Treatment acute management may consist ofbed rest, antiemetics, antivertiginous drugs [e.g. betahistine (Sere)], and low molecular weight dextrans (not commonly used) long term management may include:

medical:low salt diet, diuretics (e.g. hydrochlorothiazide, triamterene, amiloride) local application of gentamicin to destroy vestibular end-organ, results in complete SNHL sere prophylactically to decrease intensity of attacks

surgical: selective vestibular neurectomy or transtympanic labyrinthectomy must monitor opposite ear as bilaterality occurs in 35% of cases

Vestibular NeuronitisDefinition acute onset of disabling vertigo often accompanied by nausea, vomiting and imbalance without hearing loss that resolves over daya 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: microvascular events, diabetes, autoimmune process considered to be the vestibular equivalent of Bell's palsy; sudden hearing loss, and acute vocal cord palsy

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

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

Toronto Notes 2011

Vertigo/Tinnitus

Otolaryngology OTIS

LabyrinthitisDefinition acute infection of the inner ear resulting in vertigo and hearing loss

Etiology may be serous (viral), or purulent (bacterial) occurs as a complication of acute and chronic otitis media, bacterial meningitis, cholesteatoma, and temporal bone fractures bacterial: S. pneumoniae, H, influenzae, M. catarrhalis, P. aeruginosa, P. mirabilis viral: rubella, CMV, measles, mumps, varicella zoster

Clinical Features sudden onset ofvertigo, nausea, vomiting, tinnitus, and unilateral hearing loss, with noassociated fever or pain meningitis is a serious complication

Investigations CThead if meningitis is suspected: lumbar puncture, blood cultures

Treatment treat with IV antibiotics, drainage of middle ear mastoidectomy

Vestibular Schwannoma (Acoustic Neuroma)Definition schwannoma ofthe vestibular portion of CN VIII

Pathogenesis starts in the internal auditory canal and expands into cerebellar pontine angle (CPA),

',...-----------------, ,Acoustic neuroma is thll most common

compressing cerebellum and brainstem when associated with type 2 neurofibromatosis (NF2): bilateral acoustic neuromas, cafe-au-lait skin lesions and multiple intracranial lesions

intJacranial tumour causing SNHLand 1111 most common cllllballopontina angle rumour.

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

In the elderly, tinnitus ar SNHL is acoustic neuroma unti proven

, ..----------------.

o1herwisl.

Diagnosis MRI with gadolinium contrast is the gold standard audiogram - SNHL poor speech discrimination relative to the hearing loss stapedial reflex absent or significant reflex decay acoustic brainstem reflexes (ABR) - increase in latency of the 5th wave vestibular tests: nonnal or asymmetric caloric weakness (an early sign)

', ,Hilzalbllflllf sign: hypollsthesia of extErnal auditory canal due to CN VII compression by an acoustic neuroma.

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

TinnitusDefinition an auditory perception in the absence of an acoustic stimuli, likely related to loss of input to neurons in central auditory pathways and resulting in abnormal firing

History subjective vs. objective (see Figure 13} continuous vs. pulsatile (vascular in origin) unilateral vs. bilateral associated symptoms: hearing loss, vertigo, aural fullness, otalgia, otorrhea

OT16 Otolaryngology

Tinnitua/Diaeases of the External Ear

Toronto Notes 2011

Investigations audiology if unilateral: ABR, MRUCT to exclude a retrocochlear lesion CT to diagnose glomus tympanicum (rare) MRI or angiogram to diagnose AVM if suspect metabolic abnormality: lipid profile, TSH

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

....

,...----------------. ,,...----------------. ,

Diseases of the External EarCerumen Impaction ---------------------------------------Etiology ear wax is a mixture of secretions from ceruminous and pilosebaceous glands, squames of epithelium, dust, and debris

Cerumen impaction is tha most common caus. of conductive hearing loss lor thOSIIged 15-50 'fiiiiiS-

....

Risk Factors

SVrinlinaIndications: Totally occlusive cerumen with pain, diiCilllllld h111ring. or tinnitus Contraindications: Nan-occlusi\18 ciiiUTlen Pravious ear surgllfY Only hearing aar 1M perforation Complicl1ions:

hairy or narrow ear canals, in-the-ear hearing aids, cotton swab usage, osteomataClinical Features hearing loss (conductive) tinnitus, vertigo, otalgia, aural fullness

Treatment ceruminolytic drops (bicarbonate solution, olive oil, glycerine, Cerumenol, syringing manual debridement (by MD)

Faiure Otitis IIX!IIma 1M perforation ll'lllml

ExostosesDefinition bony protuberances in the external auditory canal composed oflamellar bone

Pail Vertigo limitus Otitis mudil

Method: Establish lhiii1M is inlllct Gendy pull the pimuuperiorly and posteriorly Using warm wllllr, aim the syringe nozzle upw!lrds and posteriorly to irrigata the eer canal

Etiology possible association with swimming in cold water

Clinical Features usually an incidental finding if large, they can cause cerumen impaction or otitis externa

Treatment no treatment required unless symptomatic

Otitis Externa (OE)Etiology

-----------------------------------------------

bacteria (-90% of OE): Pseudomonas aeruginosa, Pseudomonas vulgaris, E. coli, S. aureus fungus: Candida albicans, Aspergillus niger

Risk Factors associated with swimming ("swimmer's ear") mechanical cleaning (Q-tips), skin dermatitides, aggressive scratching devices that occlude the ear canal: hearing aids, headphones, etc.

Toronto Notes 2011

Diseases of the External Ear/Diseases of the Middle Ear""\ I

Otolaryngology OT17

Clinical Features acute: pain aggravated by movement of auricle (traction of pinna or pressure over tragus) otorrhea (sticky yellow purulent discharge) conductive hearing loss aural fullness 2 to obstruction of external canal by swelling and purulent debris post-auricular lymphadenopathy complicated OE exists if the pinna and/or the periauricular soft tissues are erythematous and swollen chronic: pruritus of external ear excoriation of ear canal atrophic and scaly epidermal lining, otorrhea, hearing loss wide meatus but no pain with movement of auricle tympanic membrane appears normal Treatment clean ear under magnification with irrigation, suction, dry swabbing, and C&S bacterial etiology antipseudomonal otic drops (e.g. gentamicin, dprotloxadn) or a combination of antibiotic and steroid (e.g. Garasone or Cipro He-) do not use aminoglycoside if the tympanic membrane (TM) is perforated because of the risk of ototoxicity introduction of fine gauze wick (pope wick) if external canal edematous 3% acetic add solution to acidify ear canal (low pH is bacteriostatic) systemic antibiotics if either cervical lymphadenopathy or cellulitis fungal etiology repeated debridement and topical antifungals (gentian violet, Mycostatin powder, boric add, Locacorten, Viofonn drops) analgesics chronic otitis extema (pruritus without obvious infection) -+ corticosteroid alone e.g. diprosalic acid

9t-----------------,

Pulling Dn thl pima is lldr1ruly painful in otili1 IIXIBrna, but ia U&uaUy wall

toleralld in otitis media.

Malignant (Necrotizing) Otitis Extarna (Skull Base Osteomyelitis)Definition osteomyelitis of the temporal bone Epidemiology occurs in elderly diabetics and immunocompromised patients Etiology rare complication of otitis externa Pseudomonas infection in 99% of cases

.....Clinical Features otalgia and purulent otorrhea that is refractory to medical therapy granulation tissue on the floor ofthe auditory canal Complications lower cranial nerve palsies systemic infection, death Management imaging: high resolution temporal bone CT scan, gadolinium scan, technetium scan requires hospital admission, debridement, IV antibiotics, hyperbaric 0 2 may require OR for debridement of necrotic tissue/bone

',

Gillum and TICbnltiiD Scans

Gallium scans are usad to show sites

not show 1lle extant of ostlomyalitis. Technulium scans provide informlrlion about ostaoblastic activity llld as IUCh are uSid to d1monslratl situ of osteomyelitis. Tachnetium scans halp with diagnosis whereas gallilrn scans '" u1eful in follow-up.

of actiw infection. GaDium is tlklln up by PMNs and thlrtlfor. only lights up when active infaction ia pment. It will

Diseases of the Middle EarAcute Otitis Madia (AOM) and Otitis Madia with Effusion (OME) see Pediatric Otolaryngology, OT38

OTIS Otolaryngology

Diseues of the Middle Ear

Toronto Notes 2011

CholesteatomaDefinition a cyst composed of keratinizing squamous epithelium occurring in the middle ear, mastoid and temporal bone two types: congenital and acquired (see below) Congenital presents as a "small white pearl" behind an intact tympanic membrane (anterior and medial to the malleus) or as a conductive hearing loss believed to be due to aberrant migration of external canal ectoderm during development not associated with otitis media/eustachian tube dysfunctionuf Cha..IIIHIDma

....

,

Fonnmion1. Epilhelial migrlltion through TM pllforalion (2" acquinld) 2.1rMigirllltion of TM (1"acqund)

Acquired (more common} generally occurs as a consequence of otitis media and chronic eustachian tube dysfunction frequently associated with retraction pockets in the pars flaccida (1 acquired) and marginal

3. Metaplasia of middle ear epithelium (congenilll) 4. 8Qal eel hyperplalia (congenital)

perforations (2" acquired) of the tympanic membrane the associated chronic inflammatory process causes progressive destruction of surrounding bony structures Clinical Features symptoms: history of otitis media (especially if unilateral), ventilation tubes. ear surgery progressive hearing loss (predominantly conductive although may get sensorineural hearing loss in late stage) otalgia, aural fullness, fever signs: retraction pocket in TM, may contain keratin debris TM perforation granulation tissue, polyp visible on otoscopy malodorous, unilateral otorrhea ComplicationsTable 8. Complications of Cholesteatoma

LOCII Ossicular erosion: conductive helling loss

Inner ear erosion: SNHL, dizziness .,4'or labyrinthitis Tempcnl bone infection: mastoiditis, plllrositisFacial paraly&s

lnlnlcranill Meningitis Sigmoid sinus tlrumbosis Intracranial abscess (1ubdural, spidural, cnbellar)

Investigations audiogram and CT scan Treatment there is no conservative therapy for cholesteatoma surgical: mastoidectomy tympanoplasty ossicular reconstruction

Mastoiditis

....

,

Definition complication of AOM infection (usually subperiosteal) of mastoid air cells, most commonly seen approximately two weeks after onset of untreated or inadequately treated acute suppurative otitis media Etiology acute mastoiditis caused by the same organisms as AOM: S. pneumoniae, S. pyogenes, S. aureus, H. influenzae Clinical Features clasaic: triad otorrhea tenderness to pressure over the mastoid retroauricular swelling with protruding ear fever, hearing loss, TM perforation (late) CT radiologic findings: opacification of mastoid air cells by fluid and interruption of normal trabeculationsofcells

Mastoiditis is now rar8 dua to rapid and elleclive 1rell1menl of acute otitis media with antibiotics.

Toronto Notes 2011

Diseases of the Middle Ear/Diseases of the Inner Bar

Otolaryngology OT19

Treatment IV antibiotics with myringotomy and ventilation tubes - usually all that is required acutely cortical mastoidectomy: debridement of infected tissue allowing aeration and drainage indications for surgery: failure of medical treatment after 48 hours symptoms of intracranial complications aural discharge persisting for 4 weeks and resistant to antibiotics

OtosclerosisDefinition fusion of stapes footplate to oval window so that it cannot vibrate Etiology autosomal dominant, variable penetrance approximately 40% female> male, progresses during pregnancy (hormone responsive) Clinical Features progressive conductive hearing loss first noticed in teens and 20's (may progress to sensorineural hearing loss if cochlea involved) pulsatile tinnitus tympanic membrane normal pink blush (Schwartz's sign) associated with the neovascularization of otosclerotic bone characteristic dip at 2,000 Hz (Carhart's notch) on audiogram (see Figure 15) Treatment monitor with serial audio grams if coping with loss hearing aid (air conduction, bone conduction, BAHA) stapedectomy or stapedotomy (with laser or drill) with prosthesis is definitive treatment..._. I

caus1 of conductiw hearing loss i1 1511150 yaar olds (eftar cerumen in1)aclion).

Dlllsclllnllil illhe zo most common

Diseases of the Inner EarCongenital Sensorineural Hearing LossHereditary Defects non-syndrome associated (70%): often idiopathic, autosomal recessive connexin 26 (G]B2) most common syndrome associated (30%): Waardenburg's - white forelock, heterochromia iridis, wide nasal bridge and increased distance between medial canthi Pendred's - deafness associated with thyroid gland disorders, SLC26A4 gene, enlarged vestibular aqueducts Treacher-Collins - first and second branchial cleft anomalies Alpert's - hereditary nephritis Prenatal TORCH Infections toxoplasmosis, rubella, cytomegalovirus {CMV), herpes simplex, others (e.g. HIV; syphilis) Perinatal Rh incompatibility anoxia hyperbilirubinemia birth trauma (hemorrhage into inner ear) Postnatal meningitis mumps measles High Risk Registry (for Hearing Loss in Newborns) risk factors: low birth weight/prematurity perinatal anoxia (low APGARs) kernicterus- bilirubin >25 mgldL craniofacial abnormality famlly history of deafness in childhood

..._. I

Congenilzll SNHL is decreasing in

.

vacciles and improved neonatal care.

incidence due to the availability Df

OT20 Otolaryngology

Diseases of the Inner Ear

Toronto Notes 2011

1st trimester illness - TORCH infections neonatal sepsis ototoxic drugs perinatal infection, including post-natal meningitis consanguinity 50-75% of newborns with sensorineural hearing loss have at least one of the above risk factors, and 90% of these have spent time in the NICU presence of any risk factor: auditory brainstem response (ABR) study performed before leaving NICU and at 3 months adjusted age early rehabilitation improves speech and school performance

PresbycusisDefinition sensorineural hearing loss associated with aging (staging in 5th and 6th decades)

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

Clinical Features progressive, gradual bilateral hearing loss initially at high frequencies, then middle frequencies 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, and good speech discrimination lip reading, auditory training, auditory aids (doorbell and phone lights)

Sudden Sensorineural Hearing Loss....

,

Clinical Features presents as a sudden onset of significant SNHL (usually unilateral) tinnitus, aural fullness usually idiopathic, rule out other causes: autoimmune causes - ESR, rheumatoid factor, ANA MRI to rule out tumour and/or CT 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)

Sudden sensorineural hearing loss may Blsily ba confused with ischemic bnlin BYBIIII. It ia ""'artmt ta ksep a high ildex of suspicion aspecially with 1lder1y petilnts p11santing with sudden s.nsariniUilll hBIR!g lou as wall as Vlrtigo.

Treatment treat with oral corticosteroids within 3 days of onset: prednisone 1-2 mg/kg/day, tapering over 2 weeks

Prognosis depends on degree ofhearing loss 70% resolve spontaneously within 10 to 14 days 20% experience partial resolution 10% experience permanent hearing loss

Autoimmune Inner Ear DiseaseEtiology

may be associated with systemic autoimmune diseases (ie. rheumatoid arthritis, SLE),vasculitides (i.e. Wegener's, polyarteritis nodosa) and allergies

idiopathic

Epidemiology most common between ages 20-50

Clinical Features rapidly progressive or fluctuating bilateral SNHL tinnitus, aural fullness, vestibular symptoms (ie. ataxia, disequilibrium, vertigo)

Toronto Notes 2011

Diseases of the Inner Ear

Otolaryngology OT21

Investigations autoimmune work-up: CBC, ESR, ANA, rheumatoid factor Treatment high-dose corticosteroids: treat early for at least 30 days consider cytotoxic medication for steroid non-responders

Drug Ototoxicity

----------------------------------------

Aminoglycosides toxic to hair cells by any route: ora]. IY, and topical (ifthe TM is perforated) destroys sensory hair cells- outer first, inner second (therefore O.AEs are lost first) high frequency hearing loss develops earliest ototoxicity occurs days to weeks post-treatment streptomycin and gentamicin {vestibulotoxic), kanamycin and tobramycin (cochleotoxic) must monitor with peak and trough levels when prescribed, especially if patient has neutropenia and/or history of ear or renal problems q24h dosing recommended. 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 oftreatment 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 many antineoplastics agent are ototoxic (weigh risks vs. benefits) loop diuretics

Noise-Induced Sensorineural Hearing LossPathogenesis 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 nigher and lower frequencies with time (see Figure lSD) speech reception not altered until hearing loss >30 dB at speech frequency, therefore considerable damage may occur before patient complains ofhearing loss difficulty with speech discrimination, especially in situations with competing noise Phases of Hearing Loss dependent on: intensity of sound and duration of exposure temporary threshold sliift: 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

....

,,

Limita Ill' NDiH C.ning Dllm... Continuous sound pressu18 >85 dB Single toUnd impulse > 135 dB

Inner Ear Diseases that cause Vertigo see Vertigo, OT12 benign paroxysmal positional vertigo (BPPV} Meniere's disease {endolymphatic hydrops) vestibular neuronitis

labyrinthitis acoustic neuroma (AN), (vestibular schwannoma)

OT22 Otolaryngology

Dileasel of the IDDer Bari.Fadal Nerve (CN VII) Paral.}'lis

1'oroDio

2011

Temporal Bona Fractures rarely are temporal bbone fractures purely transwrse or longitudinal, often it is a mixed pictureT1bl1 9. Futul'll al Tampon! BDlle Fncb11'81l111 Figure 11)Wo bony labyrinth ..d mmaiiiJditury meatus lniD middle earIOID20%

70ta 911%IJdenll!kijtJauna

FnnaVocc.,illl1nuna CN VI P*v (511%)SIIIIOiilalnlloll ciJa to dnct cachlllll' injuryFigure 1I. TvP of Tamparllla11

CN VII palsy (10 to 20%) Condul:liva hlollsacmryto Ollic.-r ijuyRln

Fncbnes

VeslikB _ ., .,._.1

.... \

,

Sudllen onut vastib.-r direct semk:icullw c-.al !pllntln!DUS nysblgnDI)

(V8IIigo.

u

ID

lmct axtamalllldiiDfy maetus.

ligM of a.Rr 1111111 fnlnn

miiDinlna SponlllniCIUS nystapJs

Battla' Sign: er;chymo of the maloid prollal af 1ha lllmplnl bonaRacoon EvaCSF

CSF leak il euslldlian die to nasophar,m:t rhioonhea (risk of meningitis)

Blaeding tom axtama1 auiiDry Cllllll Slap famlltiCII in IXIImal aucllary c:anal CSFOionhaaBattle's sign = masiDid ecchymDses Rlcco111 ayes = pariarbitiiiiCCIIvm:J

Clllssic twas llllldlnesm .-rrnan with moclall irfny IMVA/; ollln QmlidJnel

Cranial NIMI invaMrlant !fllcilrl p!lbynumbness ... CN VI-o CN Vll nyslagltkls -o CN VI. fal:ial

Diagnosis otoscopy

.... \

,

lhe halo lign il the ..,., mgad ppnn:a af CSF ft.lid on whilll filbr ...,.... it ......... aut from blaad.

do not syringe or manipulate external auditory meatus due to r.IBk ofinducing meningitis via TM perforation Cfhead aurliol.ogy, fuci.al nerve testa (for transverse fractures), Schirmer's teat (of lacrimation), stapedial refleua ifCN vn palsy lf suspecting CSF leak: look for halo sign (see sidebar), send fluid for beta-2-transferrin

Treatment ABC's medical - expectant. prevent otogenic meningitis surgical - explore temporal bone, indi.cati.Ollll: CN VII palsy (immediate and complete) gunshot wound depressed fracture of eDemal auditory meatus early meningitis (mastoidectomy) bleeding lnt:rac:ranially from sinus CSF otorrhea (may resolve spontaneous]y)Compliartions BCUte otitis media labyrinthitis mastoiditis .meningitis!epidural abacesslbraln abscess post-traumatic cholesteatoma

H_llrulau... FeciiiiNGrumg lydanr lhdll: Normal facial mDtllr functicm lhdlll: Mid dyliunetion -SI9rl-kn111

Facial Nerve (CN VII) ParalysisEtiology supraouclear and nuclear (MS. poliomyelitis, cerebral tumours) intranuclear - see table belowTreatment treat acccrding to etiology plus provide corneal protection with artificial tears, nocturnal lid taping. tarsorrhaphy, gold welgbting of upper lid

- Normll 8'jllllletJy and tone

atrMI 11'1' lhdllll: Modnl8 dysfunction - Obvioua waakn111 Grade IV! Modarately WV818 dysfunc:tion - Obvioua waakn111 diqriv ll'flllmiCry

- h:omplate 11'1' clolura- No forahlllld mDiicn

- Moutll asymmlllric mcrtion lhdl V: Slwra dyJhllction - Barely pan:apliblll motion of moutll - Asymmllric at l1lt Grads VI: TaiBI - No mDVImanl

fildal paralysis that does not resolve with time or with medical treatnwrt will often be referred for possible reanimation tecbnlques to restore function common reanimation techniques Include: direct facial nerve anastomosis interpositi.onal grafts anastomosis to other motor nerves muscle transpositions

Toronto Notes 2011

Facial Nerve (CN VII) Paralysis/Rhinitis

Otolaryngology OT23

Table 10. Differential Diagnosis of Peripheral Facial Paralysis (PFP)Etialagy

llllrs PalsyIdiopathic, {HSV) irlectian af the facial nerve

lncidn:e 80 to 90% at PFP Rill! hcturs:

Findings Hx: Acutu 011&81

1-'iglllionsStapedial refti!X absent Audiology normal (or basalina) 811Ctrcmyugram (EMG)- bll&t measure for prognosis Topognoslic testing MRI with gadolinium- enhancemsnt CN VII VIII H1gh resolution CT

TRIItlllnt. Foll-..p.and l'rlvtoli (Px)Rx:

Diab818s Pr&gnancy Diagnosis uf lllll:lusion Viral prodrome (50%)

Nwnbness af aar Schinner's test Recurnnce {12%1 + FHx{14%) Hyperacusis {30%1

Prutact the 8Y8 to prevent eJIPU&Ura kllratitis with patx:hing ortarsorraphy Systemic steroids may lessen degeneration and hasten recovery Consider antiviral (acyclovir)

FJll:Spontaneous remission should begin withil 3 weeks of onset Delayed (3 to 6 months) recovery portends at least some functional loss90% racovar spontaneously and ovaral; >90% n!covary pan!lysis was incomplete Poorer hyperacusis, > 60 vrs. diabetes, HTN, severe pain

Piny$is or pai'Biii& af all mU&cle groups on one side at thll face Absence af signs at CNS disease Absence at signs at ear or CPA diseases

PIE:

Px:

Rlmlatllunt

Synlhm (Hirpea Zllltlr Oticus)Varicella zo51er infection at CNVIWIII

4.5 to !1% of PFP Rill! hcturs:lf11lilirad immunity Cane Radiathllrapy Chemotherapy (see OT22}

>60'(81111

Hyperacusis SNHL Severe pain of pinna, mouth, or faceVesicles on pinna, ext. canal (enupt 3-7 days after onset of pain) Associated herpes mster uphthalmicus (uveitis, lantacunjunctivitis, optic neuritis, or glaucoma)

Hx:

PIE:

Stapedial refti!X absent Audiology- SNHL Villll EUSA studies to cunfinn MRI with gadolinium (86% at facial neMJS enhance)

Rx: Pt should avoid lesions to prevent spraad of infection Systemic steroids can raliM pain, vertigo, avoid postherpetic nauralgia Acyclovir may lessen pain, aid healilg of vesicles

Poorer prognosis than Belrs palsy; 22% recover coqJietEiy, 66% paralysis, 111% coqJiete paralysis Skull XofliYS CT head

FJll: 2to 4W88b Px:

Tampanl Bona Fnclunl Langitudi111l (911%) 211% have PFP

Blow to side at head Trauma to side of head Neuro findings consistEnt with epiduraVsubdural bleed

Hx:

PIE:

Injury usually due tu stratch or impingBI'nent; may recover with time

Px:

r..nna(10%)

40%have PFP

Blow to frontal or occipital area

Hx:

Skull XofliYS CT head

Nerve 1nlnsection

Px:

lmaganic

Trauma to front or back of haad Variable (depending on level at injury) Wait lor lidocaine to weer off

PIE:

EMG

Rx:

if nerve pa.aysis No exploration if any movement present

RhinitisDefinition inflammation of the lining (mucosa) of the nasal cavityTabla 11. Classification of Rhinitislnfllllllllaturyo o

Nonlnflllmmaturyo o

Peremial nun-allergic0

Asthma, MA SIIISitivity

Allgic o Seasonal o Peremial o Atrophic o Primary: (especially in eldelly) o Acquired: post-slJ'IIerv if too 1111ch mucosa or bllilinate has been resected o Infectious o Viral: e.g. lhinovirus, influelllll, parailfluiiiJZII, etc. o Bacterial: e.g. S.IIUIIlUS o Fungal o Granulomatous: TB, syplilis, leprosy o Non-infactious o Sarcoidosis o Wegane(s gnmulomatosis o Irritanto

o

Rhinitis medicamentosa o Topical decungssllmts Honnonal o Pr&gnancy o Estrogens 0 Thyroid Idiopathic vasomotor

.....

}-----------------,medicllltlentou is rebound

congestion due to 1he owruse of int1'81111SIII VIIIOCDnstriciDrs. For uu of theu madicationsfor only &-7 day5 ill racommended.

oo

Dust Chemicals Pollution

OT24 Otolaryngology

Rhinitis

Toronto Notes 2011

Table 12. Nasal Discharge: Character and Associated ConditionsAssac:iatlld ColdilionsWatery/mucoid Allergic, viral, vasamDtor, CSF leak (halo signl

MucapurulentSerosquinous

Bacterial, fureign body NeoplasiaTrauma, nBOplasia, blaeding disaniBr, hyp&rta1siorl"vasculll" diseass

Bloody

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 5 days) of nasal drops and sprays (Dristan, Otrivin)

Clinical Features chronic intermittent nasal obstruction, varies from side to side rhinorrhea: thin, watery nasal allergy must be ruled out mucosa and turbinates: swollen, pale between exposure symptoms are often more severe than clinical presentation suggests

Treatment elimination of irritant factors nasal spray) parasympathetic blocker o steroids (e.g. beclomethasone, fluticasone) o surgery (often of limited lasting benefit): electrocautery, cryosurgery, laser treatment or removal of inferior or middle turbinates o vidian neurectomy (rarely done) o symptomatic relief with exercise (increased sympathetic tone)

SinusitisDevelopment of Sinuses sinus pneumatization begins in 3rd-4th month of fetal life o maxillary sinus first 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

....Pathogenesis of Sinusitis inflammation of the mucosal lining ofthe paranasal sinuses anything that blocks mucus from exiting the sinuses predisposes them to inflammation all sinuses drain to a common prechamber under the middle meatus called the osteomeatal complex

,EildPCOpic Sinua

FESS = Surprr

Opening of the entire amorneabll campiBK in ardar to facilitate drainaQII while sparing 111e sinus mucosa.

Definitiono

inflammation of the mucosal lining of the sinuses

Classification acute: 3 months

Table 13. Etiologies of Sinusitis

Ollill Obltruc:lion

Inflammation Mechanical

URTI

Septal deviation Turbinate hypellrophy Polyps Tumours Adenoid hypertrophy

Foreign body Cangenital abnormalities i.e. cleft palate

Immune

Wegener's g11111lomatosis

Dii'ICI ExllnsianSaurce: Dr. J. Cl'lpnik.

Dental Trawna

Lyrl1lhoma. leukemia lmm.mosuppressed patients (e.g. neutropenics, diabetics, HIV) CVstic fibrosis lmmotile cilia (Kartagener'sl Infection

Facial fractures

OT26 Otolaryngology

Sinuaitia

Toronto Notes 2011

Acute Suppurative SinusitisDefinition acute infection and inflammation of the paranasal sinuses clinical diagnosis requiring at least 2 major symptoms or 1 major and 2 minor symptoms minor symptoms major symptoJDS facial pain/pressure headache facial fullness/ congestion halitosis nasal obstruction fatigue purulent/discoloured nasal discharge dental pain hyposmia/anosmia cough fever ear pressure/fullness Etiology viral vs. bacterial (viral etiology is more common) children are more prone to a bacterial etiology, but viral is still more common maxillary sinus most commonly affected must rule out fungal causes (mucormycosis) in immunocompromised hosts (especially if painless, bloodless mucosa on examination) organisms viral: rhinovirus, influenza. parainfluenza bacterial: S. pneumoniae (35%), H. influenzae (35%), M. cata"halis, anaerobes (dental) Clinical Features sudden onset of nasal blockage/congestion and/or nasal discharge/posterior nasal drip facial pain or pressure, hyposmia signs more suggestive of a bacterial etiology are erythematous nasal mucosa, mucopurulent discharge, pus originating from the middle meatus and the presence of nasal polyps or a deviated septum acute viral rhinosinusitis lasts 10 days, consider bacterial etiology Management anterior rhinoscopy x-ray/CT scan not recommended unless complications are suspected (ie. sub-periorbital abscess or intracranial spread- Pott's Puffy tumour) symptoms improving within 5 days: symptomic relief and expectant management moderate symptoms that worsen or persist beyond 5 days: institute an intranasal corticosteroid spray and continue for 14 days if symptomic relief is noted within 48 hrs severe symptoms that worsen or persist beyond 5 days and are refractory to intranasal corticosteroid (INCS): clarithromycin or Clavulin therapy INCS referral to a specialist surgery if medical therapy fails: FESS

I

Acute Si-a Complcllions Consider hospitlllimion 111y of 1hefDUowing ar.suspactld 1. Olbital (Chandler's classifil:lllionl a. Periorbilll celulitis b. Olbilll c. SubpariostlllllbsciSI d. OlbillllbiCIIIS a. Cavem011s sintJS 1hrombosis 2.1ntnacranial a. Meningitis b.Absc111

3. Bony a. Subperiost11l frontal bona abscess ("Pott's Puffy Tumour'"l b. Osteomyelitis 4. N111.1rologic a. Superior olbital fissura syndroma CN IIVIVM palsy, immobile globe, dilatad pto$is, V1hypoesthesial b. Olbitalapsx syndrome (as"4a" above, plus neuritis,

papilledema, decraasad acuityl

Chronic SinusitisDefinition inflammation ofthe paranasal sinuses lasting >3 months

....

,..}-----------------. ,

Allergic fungallhinosinusitis is a chronic sinusitis affee1ing mostly young, immunocompetent, lllopic individuals. Tllllllmant options include FESS intranasallllpical steroids, antifungals and immuno1harapy.

.....

,..}-----------------. ,

Etiology can result from any of the following: inadequate treatment of acute sinusitis untreated nasal allergy allergic fungal rhinosinusitis anatomic abnormality e.g. deviated septum (predisposing factor) underlying dental disease dliary disorder e.g. cystic fibrosis, Kartagener's chronic inflammatory disorder e.g. Wegener's 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

C DIIic lin11litit Complication .. 1.PolYIJ'

2. Mucocele

Toronto Notes 2011 halitosis yellow-brown post-nasal discharge chronic cough maxillary dental pain

Sinusitis/Epistaxis

Otolaryngology OT27

Treatment antibiotics for 3 to 6 weeks for infectious etiology augmented penicillin (Clavulin), macrolide (clarithromycin), tluoroquinolone (levofloxacin), clindamycin, Flagyl topical nasal steroid, saline spray surgery if medical therapy fails or fungal sinusitisSurgical Treatment functional endoscopic sinus surgery -+ open osteomeatal complex balloon sinoplasty

EpistaxisBlood Supply to the Nasal Septum (Figure 4) 1. Superior posterior septum: internal carotid -+ ophthalmic -+ anterior/posterior ethmoidal 2. Posterior septum: external carotid -+ internal maxillary -+ sphenopalatine artery-+ nasopalatine 3. Lower anterior septum: external carotid -+ facial artery-+ superior labial artery -+ nasal branch external carotid -+ internal maxillary -+ descending palatine -+ greater palatine these arteries all anastomose to form Kiesselbach's plexus, located at Little's area (anterior portion ofthe cartilaginous septum) bleeding from above middle turbinate is internal carotid, and from below is external carotid Tabla 14. Etiology of Epistaxis

Type

Caulea

Trauma (most commonl fnlctures: faciaL 11111111 Self-induced: digital foreign body latmgenic: nasal. sinus. orbit surgery

Tumours Banign: polyps, ilvarting papiloma, angilllibmma Malignant: squamous cell carcinoma. esthesioneuroblastoma lnllammation Rhinitis: allergic, non-allergic Infections: bacterial, viral, fungalIdiopathic

Bammstric changBBNBSIII

mvness: dry ai& septal deformities

Saptal perforation

......

,

Chemical: cocaine, nasel sprays, ammonia, etc.Systamic

CDagulopathies Meds: anticDagularrts, NSAIDs

SpeciiiC... Adote.cent male with unilallnlThis is the most common benign tumour of the 11111.upharynx patilllll- use reSOibable piCks Ill avoid risk ofrecwrent epistaxis consider juvenile nuopluuynglllll angiufibruma (JNA).

Hemophilias, von Willebrand's Hamatololjicalmalignancias Uver failure. uremia Vascular: hypertension, atherosclerosis, Osler-

Weber-Rerdl (HHTI Others: Wegener's. SlInvestigations CBC, PT/PTT (if indicated) x-ray, CT as needed

ra-bleeding caused by pulling out the removable pack

Treatment aim is to localize bleeding and achieve hemostasis1. First-aid ABC's patient leans forward to minimize swallowing blood constant 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 IV NS if hypovolemic, or signs of shock

OT28 Otolaryngology

EpistaxWHoarsenas3. Determine Site of Bleeding

Toronto Notes 2011

anterior/posterior hemorrhage defined by location in relationship to bony septum insert cotton pledget of 4% topical lidocaine topical decongestant (ie. Otrivin), visualize nasal cavity with speculum and aspirate excess blood and clots if suspicion of bleeding disorder, coagulation workup

4. Control the Bleeding first line topical vasoconstrictors (Otrivin) if first line fails and bleeding adequately visualized, cauterize with silver nitrate do not cauterize both side& of the septum at one time due to risk of septal perforation from loss of septal blood supply A. Anterior hemorrhage treatment if fail to achieve hemostasis with cauterization: place anterior pack with half inch Vaseline-soaked ribbon gauze strips or absorbable packing (ie. Gelfoam) layered from nasal floor toward nasal roof extending to posterior choanae for 2 to 3 days can also attempt packing with Merocel or nasal tampons of different shapes can also apply Floseal (hemostatic matrix consisting topical human thrombin and cross linked gelatin) if other methods fail

B. Posterior hemorrhage treatment if unable to visualize bleeding source, then usually posterior source: place posterior pack using a Foley catheter, gauze pack or balloon subsequently, layer anterior packing bilaterally antibiotics for any posterior pack or any pack in >48 hours admit to hospital with packs in for 3 to 5 days watch for complications: hypoxemia (naso-pulmonic reflex), toxic shock syndrome (Rx: remove packs immediately), pharyngeal fibrosis/stenosis, alar/septal necrosis, aspiration

C. Ifanterior/posterior packs fail to control epistuis arterial ligation of anterior/posterior ethmoid, branches of internal maxillary, external carotid artieriesselective embolization of branches of external carotid artery septoplasty

5. Prevention prevent drying of nasal mucosa with humidifiers, saline spray; or topical ointments avoidance of irritants medical management of hypertension and coagulopathies

.....

,t-----------------, ' ,..,weak,

HoarsenessDefinitions hoarseness: change in voice quality, ranging from voice harshness to voice weakness reflects abnormalities anywhere along the vocal tract from oral cavity to lungs dysphonia: a general alteration in voice quality aphonia: no sound emanates from vocal folds

If hollrsan.s p!allll far > 2 woks in a smoker, laryngoscopy must be done to

rule out malignancy. Acute 2 weeks.

.....

Vocal Cord PanlrslsIJniiiQral: affected cord lies in the

Acute LaryngitisEtiology viral: influenza, adenovirus bacterial: Group A Streptococcus acute voice strain -+ submucosal hemorrhage -+ vocal cord edema -+ hoarseness environmental: toxic fume inhalation

permedilln position, inadsqusta glotticciOSIR during pllomdion bnl8thy voice.

Bii!Mral: cords rest in midline 1herefare voice 1"8mains good but respiratory function is compromislld 111111 maypnlll8lll as abidor.

r-tmlllt options: voicathsrapy,injection laryngoplasty (collagen. fat),

cord madilllilalion.

....

,. ,

URTI symptoms, hoarseness, aphonia. rough attacks, dyspnea true vocal cords erythematous/edematous with vascular injection and normal mobility

Clinical Features

Treatment usually self-limited, resolves within -1 week voice rest humidification hydration avoid irritants (e.g. smoking) treat with antibiotics if there is evidence of coexistent bacterial pharyngitis

Innervation of Larynxlntamll brancb of III'JII...I nern: Mnsory to larynx abova cords.

Ext.nel branch of superior lery1111ul nern: motor to crico1hyroid muscle. bcurnnt laryngul 1111rn: all motor to larynx axcapt far cricothyroid muscle; sensory to larynx below cords.

Toronto Notes 2011

Hoarseness

Otolaryngology OT29

Chronic LaryngitisDefinition longstanding inflammatory changes in laryngeal muooaa Etiology repeated attacks of acute laryngitis chronic irritants (dust. smoke, chemical fumes) chronic voice strain chronic sinusitis with postnasal drip (PND) chronic alcohol use esophageal disorders: GERD, Zenker's diverticulum, hiatus hernia systemic: allergy, hypothyroidism, Addison's Clinical Features chronic dysphonia - rule out malignancy cough, globus sensation, frequent throat clearing 2o to GERD laryngoscopy: cords erythematous, thickened with ulceration/granuloma formation and normal mobility Treatment remove offending irritants treat related disorders e.g. antisecretory therapy for GERD speech therapy with voice rest antibiotics, steroids to decrease inflammation laryngoscopy to rule out malignancy

Vocal Cord PolypsDefinition structural manifestation of vocal cord irritation acutely, polyp forms 2 to capillary damage in the subepithelial space during extreme voice exertion Etiology most common benign tumour of vocal cords voice strain (muscle tension dysphonia) laryngeal irritants (GERD, allergies, tobacco) Epidemiology 30 to 50 years of age M>F Clinical Features hoarseness, aphonia, cough attacks dyspnea pedicled or sessile polyp on free edge of vocal cord typically polyp asymmetrical, soft and smooth more common on the anterior 1/3 of the vocal cord polyp are intermittent respiratory distress with large polyps Treatment avoid irritants endoscopic laryngeal microsurgical removal if persistent or if high risk of malignancy

....

,,Noduli Bilateral

Vacal Cords: Palyps vs. Nodulel PalypsUnillltaralasymmebicMll'f IHOIVB Often follow a spontaneously chronic course

Acute onset

Gradual onset

capillary breakage

Aculll:h1111orrhage or edama

Chronic: hyalinization within submucous lesionAculll: small, discrelll noclllas Chronic: hard, white, thickened fibrosed noclllas

Soft, 8111oolh, fusifann,paduncuhdlld

mass

Surqical Surqicalaxcisian a axcisian rafractory persistent or in presence of riskfac!Drs for

laryngaal cancer

Vocal Cord NodulesDefinition vocal cord callus aka "screamer's or singer's Etiology early nodules occur 2 to submucosal hemorrhage mature nodules result from hyalinization which occurs with long term voice abuse chronic voice strain URTI, smoke, alcohol Epidemiology frequently in singers, children, bartenders, and school teachers F>M

OT30 Otolaryngology

Hoarseness/Salivary Glands

Toronto Notes 2011

Clinical Features hoarseness worst at end of day on laryngoscopy: red. soft nodules often bilateral at the junction of the anterior 1/3 and posterior 2/3 of the vocal cords - point of maximal cord vibration chronic nodules may become fibrotic, hard, and white

Treatment voice rest hydration speech therapy avoid irritants surgery rarely indicated for refractory nodules

Benign Laryngeal PapillomasEtiology human papilloma virus (HPV) types 6, 11 possible hormonal influence, possibly acquired during delivery

Epidemiology biphasic distribution - I) birth to puberty (most common laryngeal tumour) and 2) adulthood

Clinical Features hoarseness/"frog voice" and airway obstruction can seed into tracheobronchial tree highly resistant to complete removal some juvenile papillomas resolve spontaneously at puberty papillomas in adults may undergo malignant transformation laryngoscopy shows wart-like lesions in supraglottic larynx and trachea

Treatment C02 laser and microsurgery adjuvants under investigation: interferon, cidofovir, acyclovir Gardasil HPV vaccine may prevent/decrease the incidence but more research is needed

Laryngeal Carcinoma see Neoplasms of the Head and Neck, OT34

Salivary GlandsSialadenitisDefinition inflammation of salivary glands

Etiology viral most common (mumps) bacterial causes: S. aureus, S. pneumoniae, H. influenzae obstructive vs. non-obstructive obstructive infection involves salivary stasis and bacterial retrograde flow

Predisposing FactorsoHIV anorexialbulimia Sjogren's syndrome Cushing's, hypothyroidism, DM hepatic/renal failure meds that increase stasis: diuretics, TCAs, beta-blockers, anticholinergics, antibiotics sialolithiasis (can cause chronic sialadenitis)

Toronto Notes 2011

Salivary Glands

Otolaryngology OT31

Clinical Features acute onset of pain and edema of parotid or submandibular gland that may lead to marked swelling fever leukocytosis suppurative drainage from punctum of the gland Investigations U/S imaging to differentiate obstructive vs. non-obstructive sialadenitis Treatment bacterial: treat with cloxacillin abscess drainage viral: no treatment

...

,bilateral

pmid Bllillrgemllllt, &BIIIorinauralhearing loss, orchitis.

Mumps ulllllly pmllll1s

SialolithiasisDefinition ductal stone (mainly hydroxyapatite) leading to chronic sialadenitis 80% in submandibular gland, F): 10% cysts, lymph nodes and adenomas: 10% oncocytoma: 40% (surgery with radilltionl Control rate ear1y lesions >90% (rediationl 10 to 12% Ill small lesions fail radiotherapy

CTJMRI

Fine n811dle aspirate

Surgery:Benign and malignant Lymph node sampling Postop radiotherapy Cherne if unresectabla

CT

Pll'utid 10-yearsurvival 85, 69, 43, and 14% for stages Ito IV Submandibular 2 yell': 82%, 5year: 69% Minor salivary glilld 10 year: 83, 52. 25, 23% for stages I to IVRewrrances occur within 5yean; Need Vu: clinical exam, thyroglobulin

ThyroidThyroid mass, ciiiVical nodes Vocal card paralysis Hypeuhypothyroidism Dyspha(ja

U/S

FNA

1 surgary 1131 for metastatic deposits port-op TSH suppression

Plnrthyraid lncreBSed serum Ca

Neck mas&Bone disease, renal disease Pllncreatitis

Wide surgical excision Port-op monitoring of serum Ca

Rewrrence rates: 1-year 27% 5-year82% 1G-year91% Mean survival: 6to 7 yell'S

Toronto Notes 2011

Neoplasms of the Head and Neck

Otolaryngology OT37

Thyroid CarcinomaTabla 18. Cytology results of FNA Samples

.....

CateuaiYNan-diagnostic Benign

CharacterilliclMacrofollicular or colloid adanomas. chronic autoimmune {Hashimota'l thyroiditis Microfollicular or cBiular naophtsm

,

SU5piciau& or indetllrminateMalignant

Typea Clf Thyroid Clncllr (from most CO!Mion 1o least common) Papillary Follicular

MedullaryAnaplllslic

Lymphoma Plpilluy Follicular1(1'1(,

Tabla 19. Thyroid Carcinoma Medullary 3ta5% {1 0% familial 90% sporadicI

AniiPiaticZta5%

Lymphoma 10'J. il 6-

" CHOP =cydophosphlnidt, lldrilrTtcin, vil"ll:ri5tine, P'Cini50118

Approach to Thyroid Nodule Recommendation A: all patients with thyroid nodules require evaluation of serum TSH and ultrasound any nodule >5 mm. with suspicious sonographic features (hypoechoic. microcalcifications, increased nodular vascularity, infiltrative margins, height > width on transverse view) should undergoFNA when performing repeat FNA on initially non -diagnostic nodules, US-guided FNA should be employed Recommendation B: nonpalpable, mostly cystic. or posteriorly located nodules should undergo US-guided FNA as the initial evaluative procedureTabla 20. Management of the Thyroid Nodule Radioiodine tharapy Chemotherapy and I or radiotherapy Surgical excision Hyperthyroid suspicious solid mass. that is HOT on thyroid SCM

,...----------------. ,t-----------------,

A minimum of hamilllyroidectomy is required to confirm captldar invasion for diagnosing fallic._.ll" or Hiirlhla cllll CA.

......

,

ln.uc.ti- for pollt-op

iodine ua.tian-1 111

Adjuvant lhnpymortality RAIIharapy -1nat parsistant cancer......

,t-----------------, ,

Anaplastic CA or thyroid lymphoma Recument cyst that is "suspicious an FNA or if patient is extremely anxious Malignancy othll" than anaplastic CA or thyroid lymphoma Solid "tuspicious mass that is "cold" on thyroid acan (excise to r/o capsular invasionI Hyperthyroid suspicious solid mass, that is HOT on thyroid scan (hyperfunctioninglCD111J1011ents: riskol111111ill1Wicvsameashold

RAI ablation should be offar11d to patienlll with distant metastases (Mil. gross axtrathyroidal axtansion, primary size >4 em 11!Q8rdless of patient age (Evidence Grade 8 and above).

COO!* DS. et Ill. Reviled Amllican ThyroklAsiOCiltion Mlnlgsment Nalllr,foid No!Ues d llillmrtillld lbynJid C.CIIt 1I( I 1):1 167-214.

'IW lildings: cystic: riltofm-ncy 3 months (OME)

....

,,

lack of response to >3 months of antibiotic therapy (OME) persistent effusion for 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 fl.accida (OME) bilateral OME lasting >4 to 6 mas craniofacial anomalies predisposing to middle ear infections (e.g. cleft palate) (OME) complications of AOM (see below) WJ. CaytB PC. Crald'vnl R. Ale he CV. Friacllerg J. W. Otuluyngolouim' pii!Csptilmi of lila inliclliCII& for tymplliOIIDmyU!e inlarlilll in chidran.21XXJ Mil\' 2. tubaL In: 200IJ dinicll inllin!otsAlilxlldi1 (VAl: Amarican Acadamy rA

,....EaJiy

Complicno Gf TymJ1811.-Iomy

..... Myringosclerosia

Exlrulion Blockage Psrli$hlrll otorrhea Pmistant 1M perforation Choleslelrtoma

CMAJ. MyringatDmy and

1111d Nd.

1999.

Complications of AOM otologic: TM perforation chronic suppurative OM

ossicular necrosis cholesteatoma persistent effusion (often leading to hearing loss)

CNS: meningitis

brain abscess facial nerve paralysis other: mastoiditis labyrinthitis sigmoid sinus thrombophlebitis

Otitis Madia 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 mo in 40% of children, 2 mo in 20% and 3+ mo in 10%

OT40 Otolaryngology Risk Factors sameasAOM

1'oroDio

2011

Clinical Features fullness - blocked ear hearing loss t:!nnitus confum with audiogram and tympanogram (flat) (see Figure 15B and Figure 16B) pain, low grade fever o!Dscopy of tympanic membrane: discolou.ration - amber or dull grey with "'glue'" ear meniscus fluid level behind TM air bubbles retraction pocket&ITM atelectasis most reliable 1indlng with pneumotoscopy Is Immobility Treatment expectant - 9096 resolve by 3 months document hearing lo&a no statistical proof that antihistamine&, antibiotia clear disease faster surgery: myringotomy ventilation tubes adenoidectomy (ifenlarged) ventilation 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 cholesteatoma espedally when retraction pockets involve pars flacdda or postero-superior TM retraction of tympanic membrane, atelectasis, oasicular fixation oasicular erosion

Adenoid Hypertrophy s1ze peaks at age 5 and resolves by 12 yean of age increase in size with repeated URTI and allergiesPharyngeai11Jnsl lllllinlid)

- '".;_, t JrI

ln......,...

Clinical Features nasal obstruction: adenoid facies (open mouth, flat midface, dark circles under eya;) history ofhypernasal voice and snoring long term mouth breather: minimal air escape through noseTWa! 1111111 (x2)

IDnsil (x2)dGIIIP..,..lhllr ,....,.. ..

Flllhllile

lllhar....

...

2

choanal obstruction: chronic sinusitis/rhinitis obstructive sleep apnea chronic lnfl.ammatlon: nasal discharge, post-nasal drip, and cough

cervicallymphadenopathy

Liraual111nsl

:::>

polllltll' 1/3 of to..,a

..... 0

Figure 2D. Wllldeyer's Ring An iiDnujDd cirde of protective lyqftoid 1issua attha uppar !lids af1ha 1811JiRIIDry and _.inantllly traclll

Diagnosis enlarged adenoids on direct/indirect nasopharyngeal exam enlarged adenoid shadow on lateral soft tissue x-ray lateral view of the nasopharynx may show a large pad ofadenoidal tissue Complications eustachian tube obstruction leading to serous otitis media interference with l1ll58l breathing, nece!lllitating mouth-breathing malocclWiion

sleep apnea/respiratory disturbance orofadal developmental abnormalities

Indications for Adenoidectomy chronic upper airway obstruction with sleep distu.rbencelapnea cor pulmonale chronic nasopharyngitis resistant to medical treatment chronic serous otitis media and chronic suppurative otitis media (after 2-3 sets oftubea) recurrent acute otitis media resistant to antibiotics suspicion of nasopharyngeal malignancy persistent rhinorrhea

Toronto Notes 2011

Pediatric Otolaryngology

Otolaryngology OT41

Contraindications for Adenoidectomy bleeding disorders recent pharyngeal infection short or abnonnal palate (cleft or false palate, zona pellucldum) Complications of Adenoidectomy bleeding, infection velopharyngeal insufficiency with speech defect nasal regurgitation scarring of Eustachian tube orifice

Sleep-Disordered Breathing in ChildrenDefinition comprises of a spectrum of sleep-related breathing abnormalities ranging from snoring to obstructive sleep apnea (OSA) Epidemiology peak incidence between 2 and 8 years when tonsils and adenoids are the largest relative to the pharyngeal airway Etiology due to a combination of anatomic and neuromuscular factors: adenotonsillar hypertrophy craniofacial abnormalities neuromuscular hypotonia (i.e. cerebral palsy, Down syndrome) obesity Clinical Features heavy snoring, mouth breathing, pauses or apnea. enuresis, excessive daytime sleepiness, behaviouralJleaming problems, morning headache, failure to thrive Investigations flexible nasopharyngoscopy for assessment of nasopharynx and adenoids polysomnography Treatment surgical management 1st line: adenotonsillectomy nonsurgical: behavioural modification, CPAP

Acute TonsillitisEtiology Group A beta-hemolytic streptococci and Group G streptococci S. pneumoniae, S. aureus, H. influenzae, M. catarrhalis Epstein-Barr virus (EBV) Clinical Features..._' I

Trillnus: motor disturbance of the trigeminal nerve, leading to spasm of 1hemuse'- of masticlllion, with difliculty in apenilg the mouth [lockjaw).

symptoms: sore throat dysphagia. odynophagia. trismus malaise, fever otalgia (referred) signs: tender cervical lymphadenopathy especially submandibular, jugulodigastric tonsils enlarged, inflammation exudates/white follicles strawberry tongue, scarletiniform rash (scarlet fever) palatal petechiae (infectious mononucleosis) Investigations CBC swab for C&S latex agglutination tests Monospot -less reliable children