OT

Otolaryngology - Head and Neck Surgery

Jayant Ramakriabna and Rebecca Zener, chapter editors
Alaina Garbens and Modupe Oyewumi, associate editors Adam Gladwish, EBM editor Dr. Jonathan Irish and Dr. Blake Papsin, staff editors
Basic 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 Fractures
Toronto 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 Review

Ear
External Temporalis fascia and muscle Triangular fossa Middle Auditory ossicles Inner

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

Throat
Superior Viaw
- -E'piglottit

i
Trachea
j

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 belly
digllllric 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

poslerior
tD 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.t
of a nad (VI'Cflrw's node) lillY indical8 an abd11111i'llli i'ldicllll
allhll

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

(Milliwl) Anblior bellies of digl8tric

nuscles, tip of 111111dible, IDI hyoid bn

Rlor of mouth. antaior oral antaior mandiQar alveolar ridge, loww IIJ
Oral

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 nmcle
JJos1:!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 of
blliwB111111
roll
1111 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

CCA
IJV ITA RRLN

1t

I
F"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

I
0

.II

OT6 Otolaryngology

Differential Diagnoses of Common Preaenting Problems

Toronto Notes 2011

Differential Diagnoses of Common Presenting Problems

Dizziness

.....

.. ,
I
LIIIyrintitil

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

..

I True Vertigo I

I Dizzil I

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

aenign paroxysmal positional vartiaa IBPPVI

ev.tilulllr ....,..itis Mani6ra'a dileue

{Vestibularl

I Central I
disorders 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 I

Cardiac

..

I Non-Vertiginau1 I

.
Dapmsion
Arucilly

CannnDJia.IM

Anhytlrniu

It' 5 D's af VwtllbraiHIIIIar lllllllllcillncy Drop lrtbcks

Diplopia

Dysarthria

Dilzinass
Dysphll!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

Otalgia
1. Local Causes
Tabla 2. Differential Diagnosis of Otalgia - Local Cau11s
Etialagy

Infection

Exlamal Ear Pain a. Otitis axt1111111

b. Herpes simpl!!ll/loster c. Auricular cellulitis

Midlhand Inn Ear Pain

a. 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 abscess

Trauma
Othar 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)

Teeth
Tongue 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.. I
1

CommnCII-

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

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

s..sarineural 1

I Acquired I
"PI'elllvclllil
LllbyrintMis
Sudden 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:ed
Menii11a"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

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

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 Obstruction
Tabla 3. Differential Diagnosis of Naul Obstruction
Aaiuired 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

Hoarseness
Tabla 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.

Naupluia
Cylll
Sys!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

Functi11111l
Congenital

Toronto Notes 2011

Differential Diagnoses of Common Praenti1J8 Problemii!Hearing

Otolaryngology OT9

Neck Mass

lnllammatory}lnfec:tian.

NeckMau

[ Midlme

..

I Congenital I
I

...

[ l.aleral [

..
...

[ Malignant

..

I Neaplallic I
I

[ Benign [

..
...

Reactive lymphadenoplllhy
TB 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 hygrom11

Lymphoma Thyroid Sarcoma Salivary gland neoplasm Rhabdomyosarcoma Neuroblutoma

Salivary gland neopl8$m Lipom11 Fibroma

Vascular

lnfraci11Vicul8r primary Leukemia

HINid and nack primary

Figure 14. Differential Diagnosis of a Neck Mass

Hearing
Normal 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 Lobe
ltl

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 Loss

1. Conductive Hearing Loss (CHL) the conduction of sound to the cochlea is impaired can be caused by external and middle ear disease 2. Sensorineural Hearing Loss (SNHL) due to a defect in the conversion of sound into neural signals or in the transmission of those signals to the cortex can be caused by disease of the cochlea, acoustic nerve (CN 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

Hearing
Table 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 forl<. on the mastoid stimulates the cochlea bilaterally, therefore in this case, the left cochlea is stimulated by the Rinne test on the right, i.e. afalse negative test These tests are not valid Wthe ear canals are obstructed with cerumen {i.e. will create conductive lossI

.... .-------------------,
Range of Frequencies Audible to Human Ear: 20 to 20,000 Hz Most sensitive frequencies: 1,000 to 4,000 Hz Range of human speech: 500 to 2,000 Hz

'.,

Pure Tone Audiometry

a threshold is the lowest intensity level at which a patient can hear the tone 50% of the time thresholds are obtained for each ear for frequencies 250 to 8000 Hz air conduction thresholds are obtained with headphones and measure outer, middle, inner ear, and auditory nerve function bone conduction thresholds are obtained with bone conduction oscillators which bypass the outer and middle ear

....

' .-------------------, ,

Hearing loss most often occurs at higher frequencies. Noise-induced (occupationall HL is seen at 4000 Hz. HL associated with otosclerosis is seen at 2000 Hz (Carhart's notchl.

Degree of Hearing Loss

determined on basis of the pure tone average (PTA) at 500, 1000, and 2000 Hz
Audiogram Lagend for a Left Ear X = AC Unmasked > = BC Unmasked D = AC Masked I = BC Masked
250 500 1000 2000 4000 8000 10 0 10 20 30 40 50 60 70

--

- --- --......

250

500

:t z

:>::

.... .-------------------,
Air conduction thresholds can only be equal to or greater than bone conduction thresholds.
250 500

'.,

"'

A. Normal Audiogram
1000 2000 4000 8000 10 0 7' 10 ......... 20 30 40 / 50 60 70 80 90 100 110 120 250 500

9().2! 100 110 120

B. Conductive Hearing Loss (Otitis Media)

250 500

1000 2000 4000 8000 10 0 10 / 20 :>:: 30 40 50 60 70 80 90 .2! 100 110 120

"'

:t z

-.

1000 2000 4000 8000 10 0 10 20 30 40 50 60 70 80 90 100 110 120

.._

i.,

t -1-

--

-.....: ---

1000 2000 4000 8000 10 0 10 20 30 40 50 -.....;;-. 60 70 ........ 80 90 100 110 120

""

C. Conductive Hearing Loss (Otosclerosis)

D. Sensorineural Hearing Loss (Noise Induced)

E. Sensorineural Hearing Loss (Presbycusis)

....

' .-------------------, ,
Degree of Hearing Loss Normal Mild Moderate Moderate- Severe Severe Profound

Degree of Hearing Loss Decibel Loss Oto20dB 21 to 40 dB 41 to 55 dB 56 to 70 dB 71 to 90 dB dB

Figure 15. Types of Hearing Loss and Associated Audiograms of a Left Ear

PURE TONE PATTERNS

1. Conductive Hearing Loss (CHL) (Figure 15B and 15C) bone conduction (BC) in normal range air conduction (AC) outside of normal range gap between AC and BC thresholds >10 dB (an air-bone gap) 2. Sensorineural Hearing Loss (SNHL) (Figure 15D and 15E) both air and bone conduction thresholds below normal gap between AC and BC <10 dB (no air-bone gap)

3. Mixed Hearing Loss

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

Toronto Notes 2011

Hearing

Otolaryngology OTll

Speech Audiometry
Speech 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

ExceUent
Good
Fair

Speech Discrimination Test

percentage 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

Poor
Very poor

Impedance Audiometry
Tympanogram

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

the eustachian tube equalizes the pressure between external and middle ear tympanograms graph the compliance of the middle ear system against pressure gradient ranging from to -400 to +200 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 mmH20
High
rl

Type A

TypeB

TypeC

I
Law

A__
0
Ai 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-: deafness
occurring blfol'l
1111 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.

Vertigo
Evaluation 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

Cenlnl
lmbaln:e

Unsteadiness

Nanea and vamiting Audilllry svn.tams Neurologic symplllml Campanlltian

NysblgiiUI

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

Canditi111
Benig plfOllyllllilll

Duration
Seconds

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 Alllxia
CN 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

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 Neuronitis
Definition
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

Labyrinthitis
Definition
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 no
associated 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 SNHL

and 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

Tinnitus
Definition
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 Ear

Cerumen 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

SVrinlina
Indications: 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, osteomata
Clinical 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

Exostoses
Definition
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 Ear

Acute Otitis Madia (AOM) and Otitis Madia with Effusion (OME)
see Pediatric Otolaryngology, OT38

OTIS Otolaryngology

Diseues of the Middle Ear

Toronto Notes 2011

Cholesteatoma
Definition 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 dysfunction
uf Cha..IIIHIDma

....

Fonnmion
1. 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 Complications
Table 8. Complications of Cholesteatoma

LOCII Ossicular erosion: conductive helling loss

Inner ear erosion: SNHL, dizziness .,4'or labyrinthitis Tempcnl bone infection: mastoiditis, plllrositis
Facial 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

Otosclerosis
Definition 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 Ear

Congenital Sensorineural Hearing Loss
Hereditary 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

Presbycusis
Definition
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 Disease

Etiology

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 Loss

Pathogenesis 85 to 90 dB over months or years causes cochlear damage early-stage hearing loss at 4000 Hz (because this is the resonance frequency of the temporal bone), extends to 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 picture
T1bl1 9. Futul'll al Tampon! BDlle Fncb11'81l111 Figure 11)
Wo bony labyrinth ..d mmaiiiJditury meatus lniD middle ear
IOID20%

70ta 911%
IJdenll!kijtJauna

FnnaVocc.,illl1nuna CN VI P*v (511%)

SIIIIOiilalnlloll ciJa to dnct cachlllll' injury
Figure 1I. TvP of Tamparllla11

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

Rln

Fncbnes

VeslikB _ ., .,._.1

.... \

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

(V8IIigo.

ID

lmct axtamalllldiiDfy maetus.

ligM of a.Rr 1111111 fnlnn

miiDinlna SponlllniCIUS nystapJs

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

Racoon Eva
CSF

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 CSFOionhaa
Battle's sign = masiDid ecchymDses Rlcco111 ayes = pariarbitiiiiCCIIvm:J

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

Cranial NIMI invaMrlant !fllcilrl p!lby

numbness ... 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) Paralysis

Etiology supraouclear and nuclear (MS. poliomyelitis, cerebral tumours) intranuclear - see table below
Treatment
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 Palsy
Idiopathic, {HSV) irlectian af the facial nerve

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

Findings Hx: Acutu 011&81

1-'iglllions
Stapedial 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 loss
90% 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 face

Vesicles 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

Rhinitis
Definition inflammation of the lining (mucosa) of the nasal cavity
Tabla 11. Classification of Rhinitis
lnfllllllllatury
o o

Nonlnflllmmatury
o o

Peremial nun-allergic
0

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 Irritant
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 madications

for only &-7 day5 ill racommended.

o
o

Dust Chemicals Pollution

OT24 Otolaryngology

Rhinitis

Toronto Notes 2011

Table 12. Nasal Discharge: Character and Associated Conditions

Assac:iatlld Coldilions
Watery/mucoid Allergic, viral, vasamDtor, CSF leak (halo signl

Mucapurulent
Serosquinous

Bacterial, fureign body Neoplasia

Trauma, 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 <20 years more common in those with a personal or family history of allergies/atopy Clinical Features nasal: obstruction with pruritus, sneezing clear rhinorrhea (containing increased eosinophils) itching of eyes with tearing frontal headache and pressure mucosa - swollen, pale, lavender colour, and "boggy" seasonal (summer, spring, early autumn) pollens from trees lasts several weeks, disappears and recurs following year at same time perennial inhaled: house dust, wool, feathers, foods, tobacco, hair, mould ingested: wheat. eggs, milk, nuts occurs intermittently for years with no pattern or may be constantly present Complications chronic sinusitis/polyps serous otitis media Diagnosis history direct exam allergy testing Treatment education: identification and avoidance of allergen nasal irrigation with saline antihistamines e.g. diphenhydramine, fexofenadine oral decongestants e.g. pseudoephedrine, phenylpropanolamine topical decongestant may lead to rhinitis medicamentosa other topicals: steroids (fluticasone), disodium cromoglycate, antihistamines, ipratropium bromide oral steroids if severe desensitization by allergen immunotherapy

Congestion 18duces nQal airflow and allows1ha non to itnl.

Trntment should focus on111e

insult rather then tlrq8t this defense mechanism.

Vasomotor Rhinitis
neurovascular disorder of nasal parasympathetic system (vidian nerve) affecting mucosal blood vessels nonspecific reflex hypersensitivity of nasal mucosa caused by: temperature change alcohol, dust, smoke stress, anxiety, neurosis

Toronto Notes 2011

Rhinitis/SinUBitia

Otolaryngology OT25

endocrine - hypothyroidism, pregnancy, menopause parasympathomimetic drugs beware of rhinitis medic:amentosa: reactive vasodilation due to prolonged use (>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)

Sinusitis
Development 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.

Definition
o

inflammation of the mucosal lining of the sinuses

Classification
acute: <4 weeks subacute: 4 weeks to 3 months chronic: >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 Exllnsian
Saurce: 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 Sinusitis

Definition 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 if symptoms increase after 5 days or persist > 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

Acute Si-a Complcllions Consider hospitlllimion 111y of 1he

fDUowing 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, V1
hypoesthesial b. Olbitalapsx syndrome (as"4a" above, plus neuritis,

papilledema, decraasad acuityl

Chronic Sinusitis
Definition 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 sinusitis
Surgical Treatment functional endoscopic sinus surgery -+ open osteomeatal complex balloon sinoplasty

Epistaxis
Blood 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, fungal
Idiopathic

Bammstric changBB
NBSIII

mvness: dry ai& septal deformities

Saptal perforation

......

Chemical: cocaine, nasel sprays, ammonia, etc.

Systamic

CDagulopathies
Meds: anticDagularrts, NSAIDs

SpeciiiC... Adote.cent male with unilallnl

This is the most common benign tumour of the 11111.upharynx patilllll- use reSOibable piCks Ill avoid risk of
recwrent epistaxis consider juvenile nuopluuynglllll angiufibruma (JNA).

Hemophilias, von Willebrand's Hamatololjicalmalignancias

Uver failure. uremia Vascular: hypertension, atherosclerosis, Osler-

Weber-Rerdl (HHTI Others: Wegener's. Sl

Investigations 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 hemostasis

1. 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

EpistaxWHoarsenas
3. 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,

Hoarseness
Definitions
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, chronic >2 weeks.

.....

Vocal Cord Panlrsls

IJniiiQral: affected cord lies in the

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

permedilln position, inadsqusta glottic

ciOSIR during pllomdion bnl8thy voice.

Bii!Mral: cords rest in midline 1herefare voice 1"8mains good but respiratory function is compromislld 111111 may
pnlll8lll 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 Larynx
lntamll 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 Laryngitis
Definition 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 Polyps

Definition 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 Palyps

Unillltaral
asymmebic
Mll'f IHOIVB Often follow a spontaneously chronic course

Acute onset

Gradual onset

capillary breakage

Aculll:
h1111orrhage or edama

Chronic: hyalinization within submucous lesion

Aculll: small, discrelll noclllas Chronic: hard, white, thickened fibrosed noclllas

Soft, 8111oolh, fusifann,

paduncuhdlld

mass

Surqical Surqicalaxcisian a axcisian rafractory persistent or in presence of risk

fac!Drs for

laryngaal cancer

Vocal Cord Nodules

Definition 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 Papillomas

Etiology
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 Glands
Sialadenitis
Definition
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 Factors
oHIV 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, &BIIIorinaural

hearing loss, orchitis.

Mumps ulllllly pmllll1s

Sialolithiasis
Definition ductal stone (mainly hydroxyapatite) leading to chronic sialadenitis 80% in submandibular gland, <20% in parotid gland, -1% in sublingual gland Risk Factors any condition causing duct stenosis or a change in salivary secretions (e.g. dehydration, diabetes, EtOH, hypercalcemia) Clinical Features pain and tenderness over involved gland intermittent swelling related to meals digital palpation reveals presence of calculi Investigations sialogram Treatment may resolve spontaneously encourage salivation to clear calculus remove calculi by dilating duct and orifice or excision through floor of mouth if calculus is within the gland parenchyma, then the whole gland must be excised

... , ,
Billlleral emrgement of the parotid glands may be a manifutlltion of a &yS!emic dil811511, auch u Sjiigran'1

or an aeting disorder [i.e. anorexia,

bulimia).

Mlllll-nt of Sialolthiait
Masslgl Analgesia ll1d Antibiotics Sialogoguas {e.g. Ieman wedgn, sour

MASH

lemon candies}
Heat (wann compress}

Salivary Gland Neoplasms

Etiology anatomic distribution parotid gland: 70 to 85% submandibular gland: 8 to 15% sublingual gland: 1% minor salivary glands, most concentrated in hard palate: 5 to 8% malignant (see Table 16 and Table 17) benign benign mixed (pleomorphic adenoma): 80% Warthin's tumour (5 to 10% bilateral, M>F): 10% cysts, lymph nodes and adenomas: 10% oncocytoma: <1% Epidemiology 3 to 6% of all head and neck neoplasms in adults mean age at presentation: 55 to 65 M=F

A mns sitting above an imaginary line drawn between the mastoid process
and engle of the mandible is 1 parotid neoplasm proven olharwise.

Parotid Gland Neoplasms

Clinical Features 80% benign (pleomorphic adenoma most common), 20% malignant (mucoepidermoid most common) painless slow-growing mass ifbilateral, suggests benign process (Warthin's tumour, Sjogren's, bulimia, mumps) or possible lymphoma

OT32 Otolaryngology

Salivary GlancWNeck Muses

Toronto Notes 2011

Investigations
fine needle aspiration (FNA) biopsy CT or MRI to determine extent of tumour

.....

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

Treatment
treatment of choice is surgery for all salivary gland neoplasms - benign and malignant benign tumours are excised due to risk of malignant transformation pleomorphic adenoma -+ carcinoma ex-pleomorphic adenoma superficial tumour superficial parotidectomy above plane of CN VII, radiation incisional biopsy contraindicated deep lesion near-total parotidectomy sparing as much ofCN VII as possible if CN VII involved then it is removed and cable grafted complications of parotid surgery hematoma, infection, salivary fistula, temporary facial paresis, Frey's syndrome (gustatory sweating)

DDx Pllrotid Tumo

Benign 1. Pleomorphic adenDIIIil Z. Warthin"&lumour (mont common

in men) 3. Cy$1:
Mallgnllllt 1. Mucoepidermoid can;inoma

2. Adenoid cystic carcinoma 3. Acinic cell can;inoma

Prognosis
benign: excellent, <5% of pleomorphic adenomas may recur malignant: dependent on stage and type of malignancy (see OT36)

Neck Masses
Approach to a Neck Mass
.....

ensure that the neck mass is not a normal neck structure (hyoid, transverse process of C 1 vertebra)
Tabla 15. Acquired Causes of Neck Lumps According to Aga

:ZO.. of lnjurr to the Nick

Clavicle -+ inferior border of cricoid

Au (ynl
<ZO

Poaibla C... af Nac:k Lump

Cong1111ital: lateral (branchial cleft cyst. blyngocels. cystic hygrornal, midline (thyrogiDSSal duct cyst) lnflammiiiDry neck nodes (tonsillitis, infectious mnmucleosis, ICawasaki'sl Lymphoma
HIV

Injuries he111 hav1 highlst mortality Angiography, a&aphagoscopy

Cricoid .... angle of 111111"1dibla

Most common site, lower mortality due to good cc-ibility To OR for SIJI1Iical apia ration
Angle Df mandible -+ skull base Angiognlphy

Z0-40

infection, tumourl Thyroid [goitre, infliction, tumour) Granulomatous disease (lB. sarcoidosis)
Salivary

>40

Primary or sacondary malignant diSBIISs

.....

llule of 7s for Duration of Symptoms

.,

.----------------.

Evaluation
Investigations
history and physical (including nasopharynx and larynx) laboratory investigations WBC - infection vs.lymphoma Mantoux TB test thyroid function tests and scan imaging neckU/S CTscan angiography - vascularity and blood supply to mass radiologic exam of stomach, bowel and sinuses biopsy - for histologic examination fine needle aspiration (FNA) -least invasive needle biopsy open biopsy- for lymphoma identification of primary tumour panendoscopy: nasopharyngoscopy, laryngoscopy, esophagoscopy, bronchoscopy with washings, and biopsy of suspicious lesions biopsy of normal tissue of nasopharynx, tonsils, base of tongue, and hypopharynx primary identified 95% of time -+ stage and treat primary occult 5% oftime - excisional biopsy of node for histologic diagnosis -+ manage with radiotherapy and/or neck dissection (squamous cell carcinoma)

1 days: ilfllmnwrtory 1 months: neoplastic 1 yan: congenital

ofaNeckMIII

.....

, ...----------------.
N N N

liltllry

y Pailful H&Ninf1lction y

...,...
Age

Wllight lou N CA risk filc:tn N

Fwar

y y

Yatmger

Old
N
y

Tender

Mobil! Size

Rubbery Rocthlnl

y y y

Occ.

<2cm

>Zcm

fixad

Toronto Notes 2011

Congenital Neck Maasea in Detail

Otolaryngology OT33

Congenital Neck Masses in Detail

Branchial Cleft Cysts/Fistulae
Embryology
at 6th week of development. the 2nd branchial arch grows over the 3rd and 4th arches and fuses with the neighbouring caudal pre-cardia! swelling forming the cervical sinus 3 types of malformations: 1. branchial fistula - persistent communication between skin and GI tract 2. branchial sinus - blind-ended tract opening to skin 3. branchial cyst - persistent cervical sinus with no external opening

Clinical Features
2nd branchial cleft malformations most common fistulas present in infancy as a small opening anterior to the sternocleidomastoid muscle cysts present as a smooth, painless, slowly enlarging lateral neck mass, often following an URTI 1st branchial groove malformations present as pre-auricular pit/sinus

Treatment
surgical removal of cyst or fistula tract if infected - allow infection to settle before removal

l.'ti71ffi'1!l!'l'---=--- Hyoid
Thyrohyoid membrana

Thyroid cartilage

A. First Branchial Anomaly

B. Second

Anomaly

Internal carotid a. - l . , - - - -++11 External carotid . Hyoid Thyroid cartilage ----1,....-----.1-1-l-

Cricoid cartilage Left common carotid a.

Left subclavian a.

Arch of aorta

C. Dird Figura 19. Branchial Claft Cysts

Anomaly

D. Fourth

Anomaly

OT34 Otolaryngology

Congenital Neck Muses in DetaWNeopllllllDJl of the Head and Neck

Toronto Notes 2011

Thyroglossal Duct Cysts

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

Embryology thyroid originates as ventral midline diverticulum of floor of pharynx caudal to junction of 3rd and 4th branchial arches (foramen cecum) thyroid migrates caudally along a tract then curves underneath and down to cricoid thyroglossal duct cysts are vestigial remnants of tract Clinical Features usually presents in the 2nd to 4th decades as a midline cyst that elevates with swallowing and tongue protrusion Treatment pre-operative antibiotics to reduce inflammation potential for neoplastic transformation so complete excision of cyst and tract up to foramen cecum at base of tongue with removal of central portion of hyoid bone (Sistrunk procedure)

Cystic Hygroma (Lymphangioma)

Definition lymphatic malformation arising from vestigial lymph channels of neck Clinical Features usually presents by age 2 thin-walled cyst extending from floor of mouth to mediastinum, usually in posterior triangle or supraclavicular area usually painless, soft. compressible infection causes a sudden increase in size Treatment surgical excision if it fails to regress - difficult dissection due to numerous cyst extensions

.....

.. ,

Neoplasms of the Head and Neck

Pre-Malignant Disease leukoplakia hyperkeratosis risk of malignant transformation 5 to 20% erythroplakia red superficial patches adjacent to normal mucosa commonly associated with epithelial dysplasia associated with carcinoma in situ or invasive tumour in 40% of cases dysplasia histopathologic presence of mitoses and prominent nucleoli involvement of entire mucosal thickness = carcinoma in situ associated progression to invasive cancer in 15 to 30% of cases Investigations initial metastatic screen includes chest x-ray scans of liver, brain, and bone only if clinically indicated TNM (tumour, nodes, metastases) classification varies slightly depending on the specific type of head and neck tumour (see online tables) TNM classification widely used for staging in order to: guide treatment indicate prognosis evaluate results oftreatment facilitate accurate exchange of information cr scan is superior to MRI for the detection ofpathologic nodal disease and bone cortex invasion MRI is superior to discriminate tumour from mucus and to detect bone marrow invasion PET scans Treatment treatment depends on: histologic grade of tumour stage physical and psychological health ofpatient facilities available expertise and experience of the medical and surgical oncology team

All p.tienbl p,...,.q with . . . . and llllllk - l b o l j d be allkad if ....., .... upi-ing th fvllawm1 ollltnlctill'l,l'llferred loCI! qmptoma: 1. Dyspn11 or stridor (positional VI. non-politio1111l) 2. Hoar18118111 or Dysphonia 3. Otalgia 4. Aural fulln8111 5. Dysphllgill

.....

,
nodes on

Detection of phy$ic:al 8XIImilllllion:

Fals1 to 311% False posiliw 111111 3D to 4D'lla

.....

,
cantral necrosis

l'llhologicallymphadiiiiOpatl!y dalilllld mliographicaUy as: 1. A node > 1.5 em in diamatar

2. Anode of any siza whic:t1 conlllins

.....

.. ,

Common silas of dillllnt mlllaslllsas for hAd and nack naoplasms: lungs > liver > bones

Toronto Notes 2011

Neoplasms of the Head and Neck

Otolaryngology OT35
Acc8111D PET IICII'IIIIC!llll c-dl il millil&111d 111111111 MliirQ inlficlti011111g11rding its USI il 1118 field of hllld llld II8Ci PET m,:.diagnolisllld ll'llllllllnt rJ pllilnll wiillr1111d 1laid - dMop iiiC!IUid 1111111 111y!oglabill without ewidlla rJ reC111181Ce on convenliorll CTMRL tlllft is illy pplicltion iltht kllowing liniCII Detedianalm.a-mprirllly llulllnnililg the exlrlnl rJ DclltiltJue D8l8l:tioa alllli!UI d..... lfllrtllltmllll

in general: 1o surgery for malignant oral cavity tumours with radiotherapy reserved for salvage or poor prognostic indicators 1o radiotherapy for nasopharynx. oropharynx, hypopharynx. larynx malignancies with surgery reserved for salvage palliative chemotherapy for metastatic or incurable disease concomitant chemotherapy or alternating chemoradiotherapy may increase survival in resectable!unresectable disease chemotherapy has a role as induction therapy prior to surgery and radiation panendoscopy to detect primary disease when lymph node metastasis is identified anti-EGFR treatment (cetuximab, panitumumab) has a role as concurrent therapy with radiation (for advanced local and regional disease)

Prognosis
synchronous tumours occur in 9 to 15% of patients late development of 2nd primary most common cause of post-treatment failure after 36 months

Soiml: C.IICII C.. Ontario. '1'ET SCAN I'Rir.tll: 1PJe 1D tile Gl pgsilron emission 11:1mognp11yimlgilg il Onmio. rJ thl Onlario PET Slllrilg CarmiUu. Dill: Aug
31,2008

Tabla 16. Quick Look-Up Summary of Head and Neck Malignancies - Etiology and Epidemiology
Efialagy OI'IIICMy 95%SCC athe111: sarcoma, mlllanomu, minor salivary gland tumour Nau ud PIIIMIII Si1111 75to 80%SCC than adanoCA and mucoupidBmJoid 99% in maxillary/ethmoid sinus 1ll% arise 1rom minor salivary glands Epidamiolagy
50% on antErior 2/3 of tongue Millin age; 50 to 60 M>F Most common site of H&N cancers

""'9}-----------------, I

Risk Fac:bn

Trvmnent of locoregionaU advam:ed y hHd lll1d neck canc1r with concomilllnt

highdon radiothe111py plus celuximab improves locoregional control end

Poor oral hygiene Leukoplakia, erythroplakia uv light -lip Oral HPV infection WootVsholl/lllxtile ildustry Hlldwood Ml (nasaVathmoid sinus) Nickel, chromium (maxillary sinus) Air pollution Chronic sinusitis HPV infection - role undell'

reduces mortality without increasing lhe common toxic lfltlcts associlltld with llldiotherapy to the head lll1d neck.
Bonnll
)ils Cllaillllb far Cminonll ct1be Held llld NKk.

Millin age: 50 to 70 Raretumou111 "" incidence in last 5to 10years

NEJIIZOOI; 354l6):587-57l

""' I

c.dnDmi ul th11 Phlrynx- Subtyplls (NiiiiUphiUJIUI. Oraphlrynx. Hypophlrynx 11d Lirynx) Naaphuynx: 91l%SCC lncidance 0.8 par 100,000 Epsteii-Barrvirus (EBV) -1D%1ymphoma 1OOx increased incidence in southern Salted fish Chinese Nickel elCJIDSUre Poor Drill hygiene M:F=2.4:1 Mean age: 50 to 59 Southern Chinese
Orapharynx 95% sec - poorly differentiated
lfvpaphlrynx 95%SCC

IIi* FactD,. far Head and Nack

!.Smoking
2. EtOH !this i& &yneflli&tic with #1) 3. Radiation

5. 01111 HPV iln.ction (indtipllldlllt of

4. Occupational/Enviromlentlll exposuras smoking and EtOH exposure)

M:F =4:1 Mean age: 50 to 70 M>F Mean age: 50 to 70 8 to 1ll% of all H&N cancer

Oral HPV Infection

.....

',
',

3 sites:

1. piriform sinus (60%) 2. post-cricoid (30%) 3. post pharyngeal wall ( 10%)

HPV-16 accounts for over 90'llo of HPV positive held and neck squamous cell carcinoma.

sec most common

3 sites:
1. (30 to 35%) 2. glottic (60 to 65%) 3. subglottic (1%)

Urynll

.....
45% of all H&N cancer M:F = 10:1 Mean age: 45 to 75 Oral HPV Infection

Th1 smalllr th1 salivary gland till grellter the likelihood that a mass in the
gland is mllignlllt.

Slliwry Glud (11111 Slliftry Gland]

40'lo ll'l!CoapidBITIIDid

3D% adenoid cystic

5% acinic cell 5% malignant mixed

Rate of malignancy: Parotid 15 to 25% Submandibular 37 to 43% Minor salivary >Bil% J to 6% of all H&N cancer Mean age: 55 to 65 M=F
Children AcUts <30 or >60 Nodules more common in females Mali!J"Iancy more common il mules Radiation exposure Fanily history- papillary CA or multiple Endocrine neoplasia- MEN II Older age Male Papillary- Gardner's, Cowden's, familial adenOillillous polypo&is (FAPJ

Thyroid ( 90% blnig1 - 1O'lo 60 to 70% papillary 15 to 20% follicular 2to 5% anaplastic 2to 5% medullary 1to 5% Hurthle cell
1to 2% msta&tatic
l'lnthyraid

Rare tumour Mean age: 44 to 55 '/8818

OT36 Otolaryngology

Neoplasms of the Head and Neck

Toronto Notes 2011

Table 17. Quick Look-Up Summary of Head and Neck Malignancies- Diagnosis and Treatment
Clinical Flllum
Oral Cavity AsvnlJ!amatic neck mass (30%1 Non-healing ulcer bleedilg Dysphagia. sialonh811, Oral fetur, allllgia leukllplakia or el"flhroplakia (pre-malignant changes or CISI

Investigations Biopsy

Tl'lllment
1 surgi!IY local resection neck dissection 5 yell': - T1tr2: 75% -13/r4: 30 to 35% Poor prognostic ildicators: Depth of invasion. clasa surgical margins location (tongue worse than floor of mouthI CeiVicel nodes, extra spread 5 yell': 30 to 60% Poor prognosis 2 to late IJ8S6fllalion

CT

reconstruction
"l' radiation

N01elllll Plnnlllll Si1111

E'a'IJ
Unilllhnll nasal obstruction Epistaxis, rhinai'Thea

CTJMRI
Biopsy

Surgery and radiation

Chemoradiotherapy lor unesec:table disease

late symptoms:
"l' to ilvasion of nose, orbit, nenres, oral cavity, skin, skull base, cribriform plats

Naqhlrynx CIIIVical nodes (60 to 90%1 Nasal obstruction. epistaxis Unilatl!ral AOM :!:: h&nlg loss CN Ill to VI, IX to XII (25%1 Proptosi&, voice change, dy&phagia
Oruphuynx Odynophagia, atalgia Ulcelli'I!!Q/enlarged tonsil Fixed tonguaftrismll&'dysarlhia llnll fator, bloody sputum Cervicel (60%1 Distal mets: lunWbane/liver (7%1

Nasapharyngascopy Biopsy

1"radiation "l' surgary

5 yell' survival:
I: 79% -11:72% -Ill: 50 to 60% -IV: 36 to 42% Base of tongue - control rates T1: >90% T4: 13to 52% T1/T2: 90to 100% T4: 15 to 33% Hl"/iiositive tumours have an approximately 20% improved overall survival rate T2/T3 wre rate: 60% T4J5 year survival: 251D 40%

CTJMRI

Biopsy

CT

1"radiation "!' surgi!IY local niSac:tian neck dissection

Tonsils - cure rata

reconstruction

Hypopharynx
Dyspha(ja, odynophagia Otlllgia. hoarsanass Cervicel

Pturyngoscopy
Biopsy CXR r/o lung mats

1"radiation "l' surgary

CT
L..ynx
Dyspha(ja, odynophagia, globus Otlllgia. hoarseness, Dyspnllll/rtridor CougMlemoptysis Cervicel nodes (rare wJ glottic CAl Salivary Gland PlliniBS& maa CN VII- paratid mass Cervicel Rapid growth Invasion of skin Constitutional signs/symptoms L!ryngoscapy 1"radiation "!' surgi!IY 1 surgi!IYfor bulky T4 5 year T4 > 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 IV
Rewrrances occur within 5yean; Need Vu: clinical exam, thyroglobulin

Thyroid
Thyroid 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 Carcinoma
Tabla 18. Cytology results of FNA Samples

.....

CateuaiY
Nan-diagnostic Benign

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

SU5piciau& or indetllrminate
Malignant

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

Medullary
Anaplllslic

Lymphoma Plpilluy Follicular

1(1'1(,

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

AniiPiatic
Zta5%

Lymphoma <1% 2% of exlnlnodal lymphomas

70to 75% Incidence (% of all thyroid cancersI

Route vi
Spraad Histology

Lymphatic
Orphan Annie nuclei Psammoma bodies

Hematogenous Capsulaublaod Vessel ilvasian Influences prognosis

L'f'1111hatic !lid hematogenous

Amyloid May secrete calcitonin,. ACTH, serotorin, kallikrein or bntdykinil M's- medullary cancer Multiple endocrine neoplasia (MEN IIa or llbl aMyloid Median node dissection

Giant ellis
Spinllecells

Other

P's - papilary cancer Popular (most commonl Palpable lyn'flh nodes Positive !1 31 uptake Po&itiva prapsis 131 Post-op 1 scan to diagnose treatments

rs- follicular cancer Fari!Nifll/mels Female (3:11 NOT FNA (can't be diagno5ed by FNAI Favourable prognosis

MD18 common in elderly 70% in women 20 to 30% haveHxof dilfarantiated thyroid Ca {mostly papilaryl or nodular goitres mass Rapilly enlargilg neck

Usually non-Hodgkins Rapidly enlarging goitre Hashimlllo's thyroiditis lncraased risk 60x 4:1 famala predominanca dysphagia, dyspnea, stridar,haamness, neck pain, facial edema accompanied by "II" symptoms *

Prognlllil

98% at 10years

92% at 10years

detected when dinicaly palpable

50% at 10years 20% at 1ayears if

20 to 35% at 1 year 13%at10years

5 year Stage IE 55%-80% Stage liE 20%-50% Stage IIW 15%-35%

Nart-surgical Combined radiation Chamotharapy (CHOP"* I

Tlllltmlnt

SmalltumoLn: Near tutal thyroidectDrny or lobectomy Diffus.-b ilateral: Total thyroidectomy

Post-<lp 1131 lx

Small turnouB: Near total thyroidectomy/ lobectomy/ isthmectomy Large/diffuse tumours: Total thyroidectomy

Tallll thyroidectomy Small twnauB: median lymph node Total thyroidectomy Dissection lataral axlllmal cervical nodas +ve modified neck dissection Post-op thyroxile Tracheostomy Screen asymptomatic rallllives
......

8..,..., =

r-. nighl-'5,

lo >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 procedure
Tabla 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 (hyperfunctioningl
CD111J1011ents: 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 Thyrokl

AsiOCiltion Mlnlgsment Nalllr,foid No!Ues d llillmrtillld lbynJid C.CIIt 1I( I 1):1 167-214.

'IW lildings: cystic: riltofm-ncy <1%. sold: risk of

OT38 Otolaryngology

Pediatric Otolaryngology

Toronto Notes 2011

Pediatric Otolaryngology
Acute Otitis Media (AOM)
Definition
acute inflammation of middle ear

Epidemiology
60 to 70% of children have at least 1 episode of AOM before 3 years of age 18 months to 6 years most common age group peak incidence January to April one third of children have had or more episodes by age 3
S. pneumoniae- 35% of cases (incidence decreasing due to pneumococcus vaccine) H. influenzae - 25% of cases M. catarrluzlis- 10% of cases S. aureus and S. pyogenes (all beta-lactam.ase producing) anaerobes (newborns) Gram-negative enterics (infants)

Etiology

viral

Predisposing Factors
eustachian tube dysfunction/obstruction: swelling of tubal mucosa: upper respiratory tract infection (URTI) allergies/allergic rhinitis chronic sinusitis obstruction/infiltration of eustachian tube ostium: tumour- nasopharyngeal carcinoma (adults) adenoid hypertrophy (not due to obstruction but by maintaining a source of infection) barotrauma (sudden changes in air pressure) inadequate tensor palati function- cleft palate (even after repair) abnormal eustachian tube: Down syndrome (horizontal position of eustachian tube), Crouzon's, and Apert's syndrome disruption of action of: cilia of eustachian tube - Kartagener's syndrome mucus secreting cells capillary network that provides humoral factors, PMNs, phagocytic cells immunosuppression/deficiency due to chemotherapy, steroids, diabetes mellitus, hypogammaglobulinemia, cystic fibrosis

Risk Factors
bottle feeding, pacifier use second-hand smoke crowded living conditions (day care/group child care facilities) or sick contacts male family history

Pathogenesis
obstruction of eustachian tube -+ air absorbed in middle ear -+ negative pressure (an irritant to middle ear mucosa) -+ edema of mucosa with exudate/effusion -+ infection of exudate from nasopharyngeal secretions

Clinical Features triad of otalgia, fever (especially in younger children), and conductive hearing loss rarely tinnitus, vertigo, and/or facial nerve paralysis
otorrhea if tympanic membrane perforated pain over mastoid process infants/toddlers ear-tugging hearing loss, balance disturbances (mild) irritable, poor sleeping vomiting and diarrhea anorexia

Toronto Notes 2011

Pediatric Otolaryngology

Otolaryngology OT39
,......,.,,.. Otitilll..lil Cli... Codnne Dlfllllse of_,.Reviews 2004;1 ltudy: MRnlyU lllndallizad Contrullad TrillsiRCTsl on ciUI1111 (>6moj with ICidtotitis medii lllf llllibiotic regime to Pacebo.

otoscopy of tympanic membrane (TM) hyperemia bulging, pus may be seen behind TM loss oflandmarks: handle and long process of malleus not visible

Treatment
antibiotic treatment hastens resolution - 10 day course 1st line: amoxicillin 80-90 mglkg!day divided into two doses - safe, effective, and inexpensive if penicillin allergic: macrolide (clarithromycin, azithromycin), trimethoprimsulphamethoxazole (Bactrim) 2nd line (for amoxicillin failures): double dose of amoxicillin (80 mg/kglday), amoxicillin-clavulinic acid (Ctavu!in) cephalosporins: cefuroxime axetil (Ceftin), ceftriaxone IM(Rocephin), cefaclor (Cedar), cefixime (Suptax-) AOM deemed unresponsive if clinical signs/symptoms and otoscopic findings persist beyond 48 hours of antibiotic treatment symptomatic therapy: antipyretics/analgesics (e.g. acetaminophen) decongestants - may relieve nasal congestion but does not treat AOM prevention: parent education about risk factors (see above) antibiotic prophylaxis - amoxicillin or macrolide shown effective at half therapeutic dose pneumococcal and influenza vaccine surgery: choice of surgical therapy for recurrent AOM depends on whether local factors (eustachian tube dysfunction) are responsible (use ventilation tubes), or regional disease factors (tonsillitis, adenoid hypertrophy, sinusitis) are responsible

IIIIIS.U.: Codl11111 Clnlnll Raaist1r rA Canllaled Trills {2003 issue 1), MllliNE (Jirlu.y 2000to MR1120031,1111d IMIIASE {Jirulry 1111 to March 2003) wMhout QUIQe ltSiriclions. . . . . . . . .:1ll'llinlll24hoP.n.lllld27 drtL 21 Haaring mnuad by \ympll1omlllyllll ..t31111111h1. l'llillll: Pain: 24 41111di (n=717l; 2-1 dris 9sUiies la=22871. Helling: 1rrri. 3 lllfi (n=472); 3 manltl, Zltllbs [n=l701. lllnlll: Tlllllmentwilh lllllibiolicshad 111 lignificlnti-on painll24 iWL J)lillt27 days was iDwlf in 1hunlili:Jtic 1JGU115 with 111 NHT rA 16 (p<D.IXDI11. Anliiaticl had no lignificlnt llltct Cll Mlli'Q. CIIICbiu: The rol8 of ntibDtics is illglly mtri:tad 'II JMin coroul. Tlil CI!UIIo buclliawd byllllignict. TilerefR, pBIIIIIs sllould be Cllllllllad tlllllllilll nlgaaics IIIII\' ba alllfw

apliml.

Indications for Myringotomy and Tympanostomy Tubes in Recurrent AOM and OME (tubes are more commonly inserted for OME, rarely for AOM)
persistent effusion >3 months (OME)

....

,,

lack of response to >3 months of antibiotic therapy (OME)

persistent effusion for 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!ots
Alilxlldi1 (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 allergies
Pharyngeai11Jnsl lllllinlid)

- '".;_, t Jr
I

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 nose
TWa! 1111111 (x2)

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

Flllhllile

lllhar....

...

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 Children

Definition 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 Tonsillitis
Etiology 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 1he

muse'- 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 <2 years old
'' I
DDx SDnl Throat Sbvptococclll phatyngilil Viral pharyngitis Infectious mononucleoais Tonsilitis PeriiDnsiUar abscass Foreign body/lrllume Leukemia Hodgkin' di88Q8

OT42 Otolaryngology

Pediatric Otolaryngology

Toronto Notes 2011

.....

'.. ,

Camplicltia of TOIIIillitia Rhaullllllic heart diSBIIS8

Arttvitis

SCIIIIutfvvar Paritonsillar abseass (Ouinsyl.

intratonsillar Cup nack space infaction

Sepsis Glomerulonephritis

Treatment bed rest, soft diet, ample fluid intake gargle with wann saline solution analgesics and antipyretics antibiotics: only after appropriate swab for C&S 1st line penicillin or amoxicillin (erythromycin if penicillin allergy) x 10 days rheumatic fever risk emerges approximately 9 days after the onset of symptoms: antibiotics are utilized mainly to avoid this serious sequela and to provide earlier symptomatic relief no evidence for the role of antibiotics in the avoidance ofpost-streptococcal glomerulonephritis see sidebar for complications

Peritonsillar Abscess (Quinsy)

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

Definition cellulitis of space behind tonsillar capsule extending onto soft palate leading to abscess Etiology bacterial: Group A strep (GAS) (50% of cases), S. pyogenes, S. aureus, H. injluenzae, and anaerobes Epidemiology can develop from acute tonsillitis with infection spreading into plane of tonsillar bed unilateral most common in 15 to 30 year old age group Clinical Features fever and dehydration sore throat, dysphagia and odynophagia extensive peritonsillar swelling but tonsil may appear normal edema of soft palate uvular deviation involvement of motor branch of CN V -+ can lead to increased salivation and trismus dysphonia with "hot voice (edema -+ failure to elevate palate) 2 to CN X involvement unilateral referred otalgia cervical lymphadenitis Complications aspiration pneumonia 2 to spontaneous rupture of abscess airway obstruction lateral dissection into parapharyngeal and/or carotid space bacteremia retropharyngeal abscess Treatment secure airway surgical drainage (incision or needle aspiration) with C&S warm saline irrigation IV penicillin G x 10 days if cultures positive fur GAS add oral/IV metronidazole or clindamycin x 10 days if culture +ve fur Bacteroides possible tonsillectomy 6 weeks later with interim oral antibiotic prophylaxis for high risk individuals Other Parapharyngeal Space Infection pharyngitis parotitis (see Salivary Gland, OT30) otitis mastoiditis (Bezold's abscess) odontogenic infection

.....

'..,

Ouin1y Trild Trismus

Uvular deviation
Hot po111to wicu

Toronto Notes 2011

Pediatric Otolaryngology

Otolaryngology OT43

Tonsillectomy
Absolute Indications

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

acute airway obstruction cor pulmonale suspected malignancy, especially if unilateral tonsillar hypertrophy {lymphoma/squamous cell carcinoma or an unusual infection such as Mycobacterium tuberwlosis, atypical mycobacteria, fungal organism or actinomycosis) acute hemorrhage (rare)

Relative Indications
age 1 to 4 years: tonsillar hypertrophy leading to: sleep apnea -+ cor pulmonale chronic nasal obstruction or mouth breathing -+ malocclusion difficulty swallowing -+ FTT speech abnormalities severe orofacial/dental abnormalities tonsilolithiasis (small cylindrical calcific inclusions within the tonsillar crypts) recurrent/chronic otitis media school age: chronic recurrent tonsillitis if 4-7 episodes in 1 year, >5 episodes/year over 2 consecutive years or >3 episodes/year over 3 consecutive years any complication of tonsillitis: quinsy, parapharyngeal abscess, retropharyngeal abscess strep bacteremia: rheumatic heart disease, nephritis, arthritis

Relative Contraindiccrtions
repaired cleft palate hemophilia epidermolysis bullosa retrognathia

Airway Problems in Children

DIFFERENTIAL DIAGNOSIS BY AGE GROUP Neonates (obligate nose breathers)

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

extralaryngeal: choana! atresia (e.g. CHARGE syndrome) nasopharyngeal dermoid, glioma, encephalocele glossoptosis- Pierre-Robin sequence, Down syndrome, lymphangioma, hemangioma laryngeal: laryngomalacia - most common cause of stridor in children laryngocele vocal cord palsy (Amold-Chiari malformations) glottic web subglottic stenosis laryngeal cleft tracheal: tracheoesophageal fistula tracheomalacia vascular rings

2to3 Months
congenital: laryngomalacia vascular: subglottic hemangioma (more common), innominate artery compression, double aortic arch laryngeal papilloma acquired: subglottic stenosis - post intubation tracheal granulation - post intubation tracheomalacia - post tracheotomy and tracheoesophageal fistula (TEF) repair

OT44 Otolaryngology

Pediatric Otolaryngology
Infants- Sudden Onset foreign body aspiration croup bacterial tracheitis caustic ingestion epiglottitis Children and Adults infection: Ludwig's angina peritonsillar-parapharyngeal abscess retropharyngeal abscess neoplastic: squamous cell carcinoma (SCC) (adults): larynx, hypopharynx retropharyngeal: lymphoma. neuroblastoma nasopharyngeal: carcinoma. rhabdomyosarcoma allergic: angioneurotic edema polyps (suspect cystic fibrosis in children)

Toronto Notes 2011

trauma:
laryngeal fracture. facial fracture burns and lacerations post-intubation caustic ingestion congenital: lingual thyroid/tonsil

Signs of Airway Obstruction

....

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

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

Symptoms and signs of airway obslruclion raquira a fuiiiiSSBISII'IanttD diagnose potentially seriou5 causes.

Stridor note quality, timing body position important: lying prone: subglottic hemangioma. double aortic arch lying supine: laryngomalacia. glossoptosis site of stenosis: vocal cords or above: inspiratory stridor subglottis and extrathoradc trachea: biphasic stridor distal tracheobronchial tree: expiratory stridor Respiratory Distress nasal flaring supraclavicular and intercostal indrawing sternal retractions use of accessory muscles of respiration tachypnea cyanosis altered LOC Feeding Dlfftculty and Aspiration supraglottic lesion laryngomalacia vocal cord paralysis post laryngeal cleft -+ aspiration pneumonia tracheoesophageal fistula

Acute Laryngotracheobronchitis (Croup)

Signs of Croup- th 3 S's
Stridor Subglottic awelling Seel balk cough

inflammation oftissues in subglottic space tracheobronchial tree swelling of mucosal lining and associated with thiclc, viscous, mucopurulent exudate which compromises upper airway (subglottic space narrowest portion of upper airway) normal function of ciliated mucous membrane impaired

Etiology viral: parainfluenzae I (most common), II, III, influenza A and B, RSV

Toronto Notes 2011

Pediatric Otolaryngology

Otolaryngology OT45

Clinical Features age 4 months to 5 years preceded by URTI symptoms generally occurs at night biphasic stridor and croupy cough (loud, sea-lion bark) appear less toxic than epiglottitis supraglottic area normal rule out foreign body and subglottic stenosis "steeple-sign" on AP x-ray of neck if recurrent croup, think subglottic stenosis Treatment racemic epinephrine via nebulizer q1 to 2h, prn systemic corticosteroids (e.g. dexamethasone, prednisone) adequate hydration close observation for 3 to 4 hours intubation if severe hospitalize if poor response to steroids after 4 hours and persistent stridor at rest consider alternate diagnosis ifpoor response to therapy (e.g. bacterial tracheitis)

Acute Epiglottitis
acute inflammation causing swelling of supraglottic structures of the larynx without involvement ofvocal cords

Etiology H. influmzae type B relatively uncommon condition due to HiB vaccine Clinical Features any age, most commonly 1 to 4 years rapid onset toxic-looking, fever, anorexia, restlessness cyanotic/pale, inspiratory stridor, slow breathing, lungs clear with decreased air entry prefers sitting up, open mouth, drooling, tongue protruding, sore throat, dysphagia Investigations and Management investigations and physical examination may lead to complete obstruction, thus preparations for intubation or tracheotomy must be made prior to any manipulation stat ENT/anesthesia consult(s) lateral neck radiograph - cherry-shaped epiglottic swelling ("thumb sign") - only if stable WBC (elevated), blood and pharyngeal cultures after intubation Treatment secure airway IV access with hydration antibiotics - IV cefuroxime, cefotaxime, or ceftriaxone moist air extubate when leak around tube occurs and afebrile watch for meningitis

... , ,
Wh111

may precipitate complete obstruction.

111ialottilis, it is important nat to agiblte 1he chid, as 1his

Subglottic Stenosis
Congenital diameter of subglottis <4 mm in neonate (due to thickening of soft tissue of subglottic space or maldevelopment of cricoid cartilage) Acquired following nasotracheal intubation due to: long duration trauma of intubation large tube size infection Clinical Features biphasic stridor respiratory distress recurrent/prolonged croup Diagnosis laryngoscopy CT

... , ,
and secure tapinv to prevent mDvement.
du1 to 1h1 UH af l/lllll11; softlr blbn

Acquired subglottic stenosis is now rare

OT46 Otolaryngology

Pediatric Otolaryngology

Toronto Notes 2011

Treatment if soft tissue -laser and steroids if cartilage -laryngotracheoplasty (LTP) balloon dilatation

Laryngomalacia
elongated omega-shaped epiglottis, short aryepiglottic fold. pendulous mucosa caused by indrawing of supraglottis on inspiration

....

..

Clinical Features
high-pitched crowing inspiratory stridor at 1 to 2 weeks constant or intermittent and more pronounced supine US\Ullly mild but when severe can be associated with feeding difficulties, leading to failure to thrive

Llryngomllacia is the most common cause of ttridor in inflnts.

Treatment observation is usually sufficient as symptoms spontaneously subside by 12 to 18 months in >90% of cases in the case of severe laryngomalacia, division of the aryepiglottic folds provides relief

Foreign Body
....

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

..

Ingested usually stuck at cricopharyngeus coins, toys presents with drooling, dysphagia, stridor if very large Aspirated usually stuck at right mainstem bronchus peanuts, carrot, apple core, popcorn, balloons presentation stridor iflodged in trachea unilateral "asthma if bronchial, therefore often misdiagnosed as asthma if impacts to totally occlude airway: cough, lobar pneumonia, atelectasis, mediastinal shift, pneumothorax Diagnosis and Treatment inspiration -expiration chest x-ray (if patient is stable) bronchoscopy and esophagoscopy with removal rapid onset, not necessarily febrile or elevated WBC

Foreign body inhalation is the mast common cause of acc:idanbll d8111h in

childr8n.

....

_._______________

Batteries MUST be ruled out as a foreign body (VI. cains) u they 11111lllthlll and c111 erode into the aorta.

Deep Neck Space Infection

TrismJs ma111s the pterygoids 11111 invatv.d and airway will bacom increasingly hard to ICC&ss.

most commonly arise from an infection ofthe mandibular teeth, tonsils, parotid gland. deep cervical lymph nodes, middle ear, or the sinuses often a rapid onset and may progress to fatal complications

......

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

Etiology
usually mixed aerobic and anaerobes that represent the flora of the oral cavity, upper respiratory tract, and certain parts of the ears and eyes

These investigations should be obtained carufuly and the IIUrgaan should consider accompanying the patient for the x-r11y as the worst place to lose an airway is during imaging.

Clinical Features
sore throat or pain and trismus dysphagia and odynophagia stridor and dyspnea late findings may include dysphonia and hoarseness swelling of the face and neck, erythema asymmetry of the oropharynx with purulent oral discharge lymphadenopathy

......

Ludwig's angina is the prototypiclll

infection of lha IIUbmandibular and

sl.l)lingual space.

Diagnosis lateral cervical view of the plain radiograph

cr

MRI

Treatment secure the airway surgical drainage maximum doses of IV systemic antimicrobials regimens according to the site of infection

Toronto Notes 2011

Common Medications

Otolaryngology OT47

Common Medications
Table 21. Antibiotics
Generic Nlme(BI'IIIII Nna) Dosing Schedule amoxicillin (Amoxil18, Amoxi 18, lndiCIIians

Cam1111111s
In patients with infectious mononucleosis. may cause rash

Aillt: 500 mg PO tid S!nlp!Dcoccus, Pneumococcus, Chilcnn: H. inffuenzle, l'nlll!Us coverage 80-90 mg/kg/day in 2 divided doses 3gPOq6h Gram1Josiliva and negative aii!OOBI and anaerobes plus Pseudomonas
CDVInQe

pipe111cillin

(losynJ

tazobactam

May causa psaudcmamb111nous colitis

ciproftoxacin (Cipro18, Ciloxan18) etythromycin (Erytlvocin18, Staticin, &ybid3 , Novo!Yihro Encap18J

500 mg PO bid

Pseuclomones, SlrepiDctx:ci, MRSA, and most Gram-negative; no anaerobic coverage

Do not give quinolones til children

SDD mgPO qid

Altl!rnative to penicilin

Ototoxic

Table 22. Otic Drops

Ganaric Nlma(BI'IIId Nna) ciprutloxacin (Ciprodex8 )

DOll
4 gtt in affected ear bid

Indications I Nates For Dlitis extema and ccmplications of otitis media Pseudomonas, Streptococci, MRSA, and most Gramoflegativa; no anaerobic coverage For otitis extema Used for inflammatory which are cunently infected or at risk of bacterial ilfections May cause hearing loss placed in inner ear Bactericidal by lowering pH For chronic suppurative media Risk of vestibular or cochlear toxicity

neomycin, polymyxil Bsulfate, and hyd'ocortisone (Cartisporin Otic]

5 gtt in lllfectad ear tid

hydrocortisone and acetic acid (VoSol He) tobranycin and dexamethasone (TobraDax18)

S.10 gtt in affected ear tid

5-1 Dgtt in aftected ear bid

Tabla 23. Nasal Sprays

Generic Name (BI'IIId Nne) Steroid ftunisolide (Rhinalar) bud&lonids (Rhinocort) biamcinolonoe (Nasacort) beclomethBIDne (Beconase18) mometasone furoate, monohydrate (Nasonax) ftuticasona furoate (Avamys18) Altihislami11 levocamastine (Livostin411) Allergic rhinitis Immediate elfect If no aftact by 3 days than discontinue U1e during allergy season Allergic rhinitis Clronic sinusitis Requires up to four weeks of consistent use to have effect long term use Dries nasal mucosa; get minor bleeding Patient should stop epistaxis May sting and Nasolli!X" not absomed systamically

Natn: General

Dacangllllnt
xytometazoline (Otrivin] axymataZDiina {Dristan8 ) li!enylephrine (Neosyneplrile8 )

Acute sinusitis Rhinitis

Careful Wpatient has hypertension Short term usa (<5 days) If long term use, can cause decongestant addiction (i.e. rhinitis medicamentosa)

Altibialir/Decongaatant
fnlnycetin, gramicidin. phenylephrine (Soframycin18) Acute sinusitis

Altichalinergic
ipl'lllrapium bromide (Atrovent] Vasomotor rhinitis Careful not to spray into eyas lnc11111sed rate of epistexis when combined nasal steroids Usepm Rhinari&18 and Sscaris3 may cau&e stinging topical

LubriclliiJ
saline, Rhinaris18, Secaris18, Polysporin8 , Vll581ina18 Dry nasalrrucosa

OT48 Otolaryngology

References

Toronto Notes 2011

References
Tllllloaa lllilvy BJ. Head l1ld NIIC:k 2nd ad. Uppincotl Wilimns n Wilins. 1918. Becker W, Naumann HH, Phllz Cll. Ell. Nose, and llroat Diseases. 2nd ed. New Vorl. Thieme Mecbl f'Wiililell. 1994.
IM:Jo RS, East CA. Eat N01e, and llmlll, n Head and Nact&l1911V: an 2nd ad. NawYorl. &l.ivingllllll. 1919. pl22. Jilek BW, Murraw BW.INT Sec:nlls. 2nd ed. l'llillde_,liL HIT'iey &Belfus. 2001. p608. Lla ltJ {Ill]. Elllllllill Olaluyngology: lllld and Nact ad. MI:Grlw-Hil. New York. 2003. pl136. LLI:ants FE, H11-EI G.{eds{. Essantiallllf Dbilaryngology. 4th ad. Uppincott Wiliams IIIII Wilins. 11119. p48t l.aylllld MK ledl. oblllryngology UppincottWIIilms andWilins. 2003. pl87. Pallia R. Dtliiryngology Helland Neck SllrgeTY Ciii:al ReOOn::e Qlide. 2nd ed. San Diego. Plural Mlililing. 2006.

.lllrniiArti:l Birman S. Clll'an!CancaptJ: Otitis Medii in CYdllll. NEJM. 1995; 332{231: 1560-1565. lll:wlner JA. H111ri PM, at CetJ.oamsbfor Sq.lllmous-Cell Cllcinoma of111e Hllld and Nect. NEJM. 2006; 3$4:567-578Coopar DS, Doheny GM, HIJIIIII BR,IIal. llwisad American Thyraid Asaocillilrl Manag1111ant Guidelines for l'ltiants with Tlriroid Noclilas l1ld llffartntillld Jlriroid Thyroid.2008; 19:1167-1214. II'SCIIla G, Kreirne1 AR, ViKili R, et al. CaseCantral Study of lbnan PapibniMNS and Canl:lif_ NEJM. 'lltrl; 356:1944-56. Faklry C, W8lbl Wll US.llal.lmprlllllld Sul'lilll af l'ltiants 1\ith Human Papilknvirus-Fasiiva Head and Nick Sq.lllmaus Clll Carcinoma ila Praspactivl Clinic:al Triii.J Nltl Cancar lnrt 2008; 100:261-t. Koc:l1 W, TIO!Ii A, Sidranet:yD. Head l1ld NackC.cer. tJM. 2001;345: 1890-1900. FurmlliJM. Cass SP. Benign I'IAixy!mall'olitionaiVartigo. NEJM. 1999; 341:m0-1596. Hillun M, Pindar D. The Epley {t:anaith ntp011itioningl mall1UV81'for benign Wltigo. Cochnma Eat N01e, and llmlat Dilonlln Cochrane Dmbase of Syslemlltic A !Maws. 2004; Issue 4. Jackson CG, van o.m&n PG. The Facial NIM: Cu111nt Trtnds in Dilgnosis, Tr111:rnant. and Rahabilllion. Dtaaryngologyfor lha 1999; 83:17!1-195. Urtl Dasros&ll M. McShanyJ. etai.Ap!ICii:al glidafor111edi11Qr10$il andnmnent ohc:ute siaitis. CWJ. 1197; 156:$1-14. MIICCallum PL. Parnes LS, Slarpe MO. Harris C. rJ open, percutaneous and trlnsl1ryngeal trlc'-!umies. OlolllrynQOiogy Head Neck Surgery. 2000; 122:686-&BD. Mclsuc WJ, Cuyte PC. Cruxford R, et 1L Dtliiryngologisl$' rJ the indiclltions furtypanos1umy tube insertion in children. CWJ. 2000; 162:1285-1288. Sraffunj NO, Wilda A. Panltid Clllm Surgicel Onc:ology. 1197; 6:21l!l-211