OT
Otolaryngology - Head and Neck SurgeryJayant Ramakriabna and
Rebecca Zener, chapter editorsAlaina Garbens and Modupe Oyewumi,
associate editors Adam Gladwish, EBM editor Dr. Jonathan Irish and
Dr. Blake Papsin, staff editorsBasic Anatomy Review
................... 2 Ear Nose Throat Head and Neck Anatomical
Triangles of the Neck Differential Diagnoses of Common Presenting
Problems ..................... 6 Dizziness Otalgia Hearing Loss
Tinnitus Nasal Obstruction Hoarseness Neck Mass Hearing
............................... 9 Normal Hearing Physiology Types
of Hearing Loss Pure Tone Audiometry Speech Audiometry Impedance
Audiometry Auditory Brainstem Response Otoacoustic Emissions Aural
Rehabilitation Vertigo ............................... 12
Evaluation of the Dizzy Patient Benign Paroxysmal Positional
Vertigo Meniere's Disease (Endolymphatic Hydrops) Vestibular
Neuronitis labyrinthitis Vestibular Schwannoma (Acoustic Neuroma)
Tinnitus .............................. 15 Diseases ofthe External
Ear ............. 16 Cerumen Impaction Exostoses Otitis Externa
(OE) Malignant (Necrotizing) Otitis Externa (Skull Base
Osteomyelitis) Diseases ofthe Middle Ear .............. 17 Acute
Otitis Media and Otitis Media with Effusion Cholesteato rna
Mastoiditis Otosclerosis Diseases of the Inner Ear ................
19 Congenital Sensorineural Hearing Loss Presbycusis Sudden
Sensorineural Hearing Loss Autoimmune Inner Ear Disease Drug
Ototoxicity Noise-Induced Sensorineural Hearing Loss Inner Ear
Diseases that cause Vertigo Temporal Bone FracturesToronto Notes
2011
Facial Nerve Paralysis . . . . . . . . . . . . . . . . . . . 22
Rhinitis ............................... 23 Allergic Rhinitis (Hay
Fever) Vasomotor Rhinitis Sinusitis ..............................
25 Acute Suppurative Sinusitis Chronic Sinusitis Epistaxis . . . .
. . . . . . . . . . . . . . . . . . . . . . . . . 27 Hoarseness
........................... 28 Acute Laryngitis Chronic laryngitis
Vocal Cord Polyps Vocal Cord Nodules Benign laryngeal Papillomas
Laryngeal Carcinoma Salivary Glands ........................ 30
Sialadenitis Sialolithiasis Salivary Gland Neoplasms Parotid Gland
Neoplasms Neck Masses .......................... 32 Approach to a
Neck Mass Evaluation Congenital Neck Masses in Detail . 33
Branchial Cleft Cysts/Fistulae Thyroglossal Duct Cysts Cystic
Hygroma (lymphangioma) Neoplasms of the Head and Neck ......... 34
Thyroid Carcinoma Pediatric Otolaryngology ................ 38
Acute Otitis Media (AOM) Otitis Media with Effusion (OME) Adenoid
Hypertrophy Sleep-Disordered Breathing in Children Acute
Tonsillitis Peritonsillar Abscess (Quinsy) Tonsillectomy Airway
Problems in Children Signs of Airway Obstruction Acute
laryngotracheobronchitis (Croup) Acute Epiglottitis Subglottic
Stenosis Laryn goma lacia Foreign Body Deep Neck Space Infection
Common Medications .................. 47 References . . . 48
Otolaryngology OTI
OT2 Otolaryngology
Basic Anatomy Review
Toronto Notes 2011
Basic Anatomy ReviewEarExternal Temporalis fascia and muscle
Triangular fossa Middle Auditory ossicles Inner
I
Semicircular canals
Antihelix
Scapha Facial nerve (CN VII) Cochlea Antiragus
Aarti lnamdar
Tympanic membrane
Eustachian tube Susan Park 2009
Figure 1. Surface Anatomy of the External Ear; Anatomy of Ear
Tympanic membrane viewed through speculum View into tympanic cavity
after removal of tympanic membrane
Tensor tympani tendon Tensor tympani muscle
Fossa of round-"'--illirc (cochlear) window
Tympanic Plexus (branch of CN IX) Hypotympanum...... _ _ _
Annulus Diana Dai 2006
--:::-'0----- Cone of light
Figure 2. Normal Appearance of Right Tympanic Membrane on
Otoscopy
....
,}----------,
Drainage into Nasal Cavity Superior meatus: sphenoid (via
sphenodethmoidal recess), posterior ethmoid sinuses Middle meatus:
frontal, maxillary, anterior ethmoid sinuses Inferior meatus:
nasolacrimal duct
Speculum View of Right Nostril
Opening for Eustachian tube _ _ _ _ _ _ _ _ _ _ _ __ j
Figure 3. Nasal Anatomy
'IbroDlo Nota 2011
Buic Anatomy Review
Otolaryngology OT3
Sepillbi'IIIChof aphanopalati1111 a.
111plrior llbillla.
Branch
Greatar palatin a.
Figure 4. Nasal Saptmn and its Altarill Supply (sea Epistaxis
sectiDII far dmilld bload siQIIIIy)
0rauynx: ...,._..lliUC criCCJila.tiiagll
Nllophar,nx; siUI baa to soft p*te 111ft palm to hyoid bone
hyoid bDnB'Io irlerior
ThroatSuperior Viaw- -E'piglottit
iTracheaj
J"' 0
Poslllrior View
Figure 6. Anatomy of 1 Normal larynx: SIJIIIriDr View of Llrvu
01 l1dirac:t
OT4 Otolaryngology
1'oroDio
2011
Haad and Nack
AftcJJiara.
l.etrnJ I'IUIII.
i. _... rl Fulll Nlml (in arder from 11411riar tD irlflriarj Ten
ZibiQ ..._My Car
!
i "' G
1. Ext111temporal Segmant al Facial Nane
Br11cha If the Extlrnll C.rd Arti1T (il onler from inferior tD
Some A'9'{ Lacty Figullld Dut PMS
Figura I. BIDad SIQIIIIy 1D th1 flea
mu..::le-.....
Ant bellydigllllric mlllcle _
..
F"llg11'8 9. Anlblmy crf thl Naclt
.....
',
Anatomical Triangles of the Neck anterior trlanJie: bounded by
anterior border ofsternocleidomastoid (SCM), midline of neck, and
lower border of mandible divided into: IUbmeDtal triangle: bounded
by both anterior bellies of digastrics and hyoid bone dipmic
triaJicle: bounded by anterior and posterior bellies of digastric,
and inferior border of mandlhle carotid triaDgle: bounded by
stemocleidOJD88toid, anterior belly ofomohyoid. and
l'lhd l'lruynlpdletlt . . . at the Head llld Neck Cilillf-
P14111ry canstrictiDII l'tllygepald!l -IIICrinal gland, 111111
mucoea ......IIi!... -libJllrdhllr.IItie - paratid alrd
It'
r-tiln at Facial Nlrw "EEn, ..... he.. n... E11111- mpedius
muacl T11111 - llcrimation !lacrimal gllrd) 11'11 881ivlltion
(parotid) F11ea - nucl11 of facial axprauian Tllll - sensory
enllrior 2/3 of tDngue (Vie choldll tympani)
- contains: tail ofparotid, submandibular gland, hypoglossal
nerve, carotid Wurcation, and lymph nodes
Toronto Nota 2011 posterior triaDBle:
Otolarynplolf OTS
bounded by posterior border ofsternocleidomastoid, anterior
border of trapezius, and middle third of clavicle divided into:
ocdpltal triangle: superior to posterior belly of the omohyoid
subclavian triangle: inferior to postmor belly of omohyoid
amt:ain8: spinal accessory nerve and lymph nodes
Table 1.lplphatic Dni111g1 of Nodal Gra-..s au AnatamiCIII
Tril1glas of Neck, . SID!cdpitlll (S)2. llaCrolllicullr (R)
Base of
posleriortD miiii:Did procasa
Posterior scalp temporalregilll, exL IUditoly 11111111s, post.
piiDI
3.f'lltJticl1ll'lllllric.-r(P)
In front of
of lnnaiiDI
Exlemalll.lditay meetua. nritr pinna. lOft tisllues n9ons, root
of nose, eyelids, palpabllll Uhid.tof a nad (VI'Cflrw's node) lillY
indical8 an abd11111i'llli i'ldicllllallhll
4. &mmllltal U.MIIA)5. S!DnrntibiB (l..evliiiB)6.
(Milliwl) Anblior bellies of digl8tricnuscles, tip of
111111dible, IDI hyoid bn
Rlor of mouth. antaior oral antaior mandiQar alveolar ridge,
loww IIJOral
Anterior belly II dgiJS!ric musde, ltytobycid 1111Sde, body of
l!lllldilil
rriiHic:e.
anteriorrlllllll cavity, soft lilliiEI II till!
glrnt
j.lgiAII' (L.evals IIA rntiiB)(LMIIIO
7. Midde
W bale to Rarior bordar of hyoid bone IIBSIII alongSCMITIISI:Ie
illynx. pnlid lnferiar bcldar II hyoid bn tD i'laritr Oral
naw'nbyprymc. '-Ynx bllder II c:ricoid Cllliage alcng SCM ITIISI:Ie
lnferiar bcldar of cricoid cartilage to clavicle alcng SCM
nmcleJJos1:!riur bcrderII SCM, nrior border NIISil!Jiaym rnt
c:ubnous s1Juclures of tnpazius, fnm skuI bale to diiYicle of the
pcstlrior scalp IDI neck (Milliwl) Hyoid bone tD IUJIRISIImBI notth
Thyroid PKt. glutlie subglatlic lllryror.ipll
ofblliwB111111roll1111 pllihyruidlllllllls
mlltiii'ICV IIII"'IIIK anl1111811181lt mav
.....node
meclallilum.lunp, or PG*rior
may ildiclte
B.
(Level IV}
9. Fomrior triqe"" (Lmls VA and VB) 10. AniBrior(l.ev8l VII
Clllllid.tariBI
pirifunn ain111.. csvi:lllllllplll!jJII
'Vn:flr.y nodi; laft lrMer IMIIV
""'n:UUas pralrldall.!lllftDd,STA
"lliild8llalll
TC
STA
CCAIJV ITA RRLN
1t
IF"11111re 10. Anatamy of 'lbyruid Gl1nll
SPG TG lPG VN (CN X) l.RLN -
cc
Superior thyrDid lrllly Carrman Clf1llid lft8fy Intimal iua* vem
Jnflrior thyroid rtarv Ri;rt recurrent laryngeal nerve - Thyroid
cartillg& - Cri1:0id eartilage - Suplllrior pntlryroid gland
Tll'jnlid gilnd
Ill
lnflriorPl/llflyroid gland Vllgua narw (CN X) Left rBC:Urrent
iaryng11l nerve
I0
i
.II
OT6 Otolaryngology
Differential Diagnoses of Common Preaenting Problems
Toronto Notes 2011
Differential Diagnoses of Common Presenting
ProblemsDizziness
.....
.. ,ILIIIyrintitil
Tru1 nystagmus and v.rtigo CIIIISid by a peripheral lesion wiD
never IIIII longer than a couple of weeks becausevartigo will
pu&.
..
I True Vertigo I
I Dizzil I
of comp--'ion. do not compenllllll, hance nyslllgmus and
aenign paroxysmal positional vartiaa IBPPVIev.tilulllr
....,..itis Mani6ra'a dileue
+
{Vestibularl
I
I Central Idisorders Verllbrobasiliar insufficiency Transient
ilch1111ic attacks Wallanballl'l syndrome Cnbullar infarction
Migrainaul vartiga Multiple ICie._ill T..norous CPAtumou11
Posterior fossa tJJmours Glomus tJJmours lnllammlllion Meningitis
Cnbullar abSCIIII$ Tra..na: cerebellar contusion Toxic: alcohol,
hypnotics, drugs
..
+ ...
I Organic Diseases I I Functional ICardiac
..
I Non-Vertiginau1 I
.DapmsionArucilly
CannnDJia.IM
+
+
Anhytlrniu
It' 5 D's af VwtllbraiHIIIIar lllllllllcillncy Drop lrtbcks
Diplopia
Dysarthria
DilzinassDysphll!lill
Recumant vaslibulopa:thy T1111poral bone fracture Suparior
sernicincular canal dahiscanca Ototoxic drug exposure Autoimmune
inner ear disease Perilymph fililula CholestBatoma
Aortic stenosis Vasovagal Orthostatic hypotension Anemia
Puripheral neuropa:thy Visual impainnant
Pmic disorder lhyp.varrtilationl Purwonality di&order Phobic
dizzin111
Figure 11. Differential Diagnosis of Dizziness
Otalgia1. Local CausesTabla 2. Differential Diagnosis of Otalgia
- Local Cau11sEtialagy
Infection
Exlamal Ear Pain a. Otitis axt1111111b. Herpes simpl!!ll/loster
c. Auricular cellulitis
Midlhand Inn Ear Paina. Aculll otitis media b. Otitis media with
ellusion c. Mastoiditis, skull base infections (mal9!ant in
diabetics! Traumatic perforation, barotrauma Neoplasm, Wegener's,
cholesteatoma
d. Extemal canal abscessTraumaOthar Frostbite, bums, hematoma,
lacerations Neoplasm Dl external c!llal, fureiiJl body, cerumen
impaction
prin-..iy madillld by TM mtdiing
2. Referred Pain (from CN V, IX and X) -Ten T's
+2
Eustachian Tube TMJ Syndrome (pain in front of the ears) Trismus
(spasm ofmasticator muscles; early symptom of tetanus)
TeethTongue Tonsil (tonsillitis, tonsillar cancer,
post-tonsillectomy) Tic (glossopharyngeal neura1gia) Throat (cancer
oflarynx) Trachea (foreign body; tracheitis) Thyroiditis Ramsay
Hunt syndrome (Geniculate Herpes) CN VII palsy (e.g. Bell's
palsy)
Toronto Notes 2011
Differential Diagnosea of Common Presenting Problems
Otolaryngology OT7
Hearing Loss
1 Conductive 1
IExternal Eer I"lmlllCllld Cll'l.._
I HAring Lo.. I1
CommnCII-
I Middle EBr I"Acuta Dlilil medii "Oiitia media with dulion wrM
plllflll'8liDnOialdlroaill Tympanasclerasis Eustachian tube
dysfunctian Cholestaalama Ossiwar melfurmlllians Oniwar
Hematympanum Middle earlunour
I Congenital IGtnetic Synnme assacillled lnlnluterine infections
{i.e. TORCH) Teratogans l'llrinlllll hypoxia l'r8malurily/low bi1h
weight Hyperbilirubinemia
s..sarineural 1
I Acquired I"PI'elllvclllilLllbyrintMisSudden SNHL Autoimmune
inner eer disease Ototaxic drug exposure Temporal bane1numa
lnfuctiou& Postmeningitis Syphilis Viral: mumps. CM\1, HSV
Neopla&tic Acoustic CPAlunours Vascular accklsiarVennboli
Auditory nuopathy
',The incidence of Merlin's disease has
decreased since 1he introduction of H. itrffuenzae and s.
pneUITJOtliee Vllcc:iniS.
"Otilia ......a"Farwign bally K!ntosis oblurans EKastoses.
ostllamas Tumcu al canal CanganitBI stanosi.tlnicrotia
"No_.,.._ -illled
"Noille-induc:edMenii11a"s disease
-rom
Figura 12. Differential Diagnosis of Hearing Loss
Tinnitus
Subj11ctive Only heard by patient {common)Otologic Presbycuais
Naiseinduced hearing lass Otitiis media with affusion Menilne"s
disease Otosclerosis Cerumen Fo111ign body agairl$t TM Drugs
+
I Tinnitus I
Objective Can be heard by others {rare)V.cular Benign
+
ea.mlll -
', ,Tinnitus is most commonly iiSSOCiated SNHL.
ArtariOVIII'IOUS mlllformlllion
ASA
NSAIDsAminCMJiycosides Antihyperlalsives Heavy metals Metabolic
Hyper/lhypathyroidism V"rtamin A. B. Zi1c daficiency NauroiCMJiC
Head trauma Multiple sclerosis Acoustic nauroma CPA tumours
PsychiatricAnxiety
Glomus tympanicum Glomus jugulare Arterial bruits: Higlt-riding
carotid artery V.cular loop Persistent stapedial artery Carotid
stenosis Vanous hum: High jugular bulb Hypertension
Hyperllhypathyroidism Mechanical 1'1\ulous eustachian tube
1'11111111 myoclonus Stapedius muscle spasm
',.. ,DID_. Tympank:UIIV"Jugulanl TumSigns and Symptams
Pulllllile tinnitus Hearing loss Blue mus behind 1M Brown's sign
{blanching of the 1M with pneumatic omscopy)
Deprenion
Figura 13. Differential Diagnosis of Tinnitus
OTB Otolaryngology
Differential Diagnoses of Common Preaenting Problems
Toronto Notes 2011
Nasal ObstructionTabla 3. Differential Diagnosis of Naul
ObstructionAaiuired Nasal Cavity Rhinitis Acu!Wclrunic Vasomator
Allergic Polyps Foreign bodies Enlarged turbinates Tumour Ben9J-
inverting papilloma Malignant Squamous cell carcinoma {SCCI
Esthesioneuroblastoma {olfactory newublaslllmal Adenocarcinoma
Nasal Septum Septal deviation Septal hematomll/abscess Dislocated
&&plum Cangenilll Nasal Cavity Nasal dennoid cyst
Encaphulocale Glioma Chounal atresia Nasal Septum Septal deviation
Septal hematomll/abscess Dislocated septum
N11ophlrynx Adenoid hypertrophy Tumour Ben9J-juVllllile
nasopharyngeal angiofibroma {JNAI Malignant- nasopharyngeal
carcinoma
Functi11111l
Tumel nose syndrome: absence of feeling in 1105e prevents 1he
sensa1ion of aeration 1hrough nosbils
HoarsenessTabla 4. Differential Diagnosis of Hoarseness
....
..}-----------------.
lnfactious lnfll11matory
Acutaichronic laryngitis Laryngotracheobronchitis {croupI
Gastro-esophageal reflux {GERDI Vocal cord polyps/nodules
Lifllstyle: smoking. chronic ETOH use Externellaryngeallnluma
Endoscopy and endolnlcheal tube {e.g. intubation granulomaI
LLilQ is the mort common cause of vocal cord 111111lv1is.
NaupluiaCylllSys!elliC
Benign tumour Papillomas {HPV infection! Retention cyslll
Endocrine
Malignant tumour Squamous cell carcinoma (SCC) Comectiw
ti&sue disease Rheumatoid 1rtluitis (RA) SLE
Hypothyroidism Virilization
Na1011logic (vocal cord paralysis due to superior :!:: recurrent
laryngeaiiii!M! injJryl
Central lesions CerebllMIScular accident (CVAI Head injury
Multiple sclerosis (MSI Skull bese tumours Amold-Chiari MaHormation
Peripheral lesions Unilateral Lung malignancy Iatrogenic injJry -
thyroid. parathyroid surgery, carotid endarterectomy, patent ductus
arteriosus {PDA) ligation Bilateral Iatrogenic injJry:
bilataral1hyroid surgery, forceps delivery Neuromuscular Myasthenia
gravis Psychogenic aphonia (hysterical aphonia) Laryngomalaciu
Laryngeal Well Laryngeal Atresia
Functi11111lCongenital
Toronto Notes 2011
Differential Diagnoses of Common Praenti1J8
Problemii!Hearing
Otolaryngology OT9
Neck Mass
lnllammatory}lnfec:tian.
1
l
NeckMau
[ Midlme
..
I Congenital II
l
...
[ l.aleral [
.....
[ Malignant
..
I Neaplallic II
.
[ Benign [
.....
Reactive lymphadenoplllhyTB or atypical mycobacteria Infectious
mononucleO&il Abscassas Cat scratch fever Sarcoidosis
Kawasaki's HIV
Thyrogl0$$al duct C\'$1: Thyroid blmour/goitra Pyramidal lobe of
thyroid gland R1111ula
IBranchial cleft CY$1: I Cystic hygrom11Lymphoma Thyroid Sarcoma
Salivary gland neoplasm Rhabdomyosarcoma Neuroblutoma
.
Salivary gland neopl8$m Lipom11 Fibroma
Vascular
lnfraci11Vicul8r primary Leukemia
HINid and nack primary
I
Figure 14. Differential Diagnosis of a Neck Mass
HearingNormal Hearing Physiology Conductive pathway (External
auditory canal to cochlea) - Air conduction of sound energy down
the EAC -+ Vibration ofthe tympanic membrane (area effect) -+
Sequential vibration of the middle ear ossicles: malleus, incus,
stapes (lever effect) -+ Transmission of amplified vibrations from
the stapes footplate in the middle ear to the oval window of the
cochlea in the inner ear -+ Pressure differential on Cochlear fluid
creates movement along the basilar membrane within the Cochlea from
base to apex Neural pathway (Nerve to brain) - Basilar membrane
vibration stimulates overlying hair cells in the Organ of Corti-+
Stimulation ofbipolar neurons in the spiral ganglion of the
cochlear division of CN VIII -+ Cochlear nucleus -+ Superior
Olivary Nucleus -+ Lateral lemniscus -+ Inferior colliculus-+
Sylvian Fissure of Temporal Lobeltl
Onler uf th Nlnl Pdlway (with Cotl'fliiCindinl w-on ABR) Eighlh
cranial nerve (1-11) Cochlear nucleus (UI) Superior Olivary
nucl111s Lidl!ralleminiscus (IV- V) Inferior colliculus
ECOU
Types of Hearing Loss1. Conductive Hearing Loss (CHL) the
conduction of sound to the cochlea is impaired can be caused by
external and middle ear disease 2. Sensorineural Hearing Loss
(SNHL) due to a defect in the conversion of sound into neural
signals or in the transmission of those signals to the cortex can
be caused by disease of the cochlea, acoustic nerve (CN Vlll),
brainstem, or cortex 3. Mixed Hearing Loss the conduction of sound
to the cochlea is impaired, as well as transmission through the
cochlea to the cortex
Auditory Acuity whispered-voice test: mask one ear and whisper
into the other tuning fork tests (see Table 5) (audiogram is of
greater utility) sensitivity depends on which tuning fork used (256
Hz, 512 Hz, 1024 Hz) Rinne test: 512Hz tuning fork is struck and
held firmly on mastoid process to test bone conduction (BC). The
tuning fork is then placed beside the pinna to test air conduction
(AC) If AC >BC -+ positive Rinne, which is normal Weber test:
512Hz tuning fork is held on vertex of head and patient states
whether it is heard centrally (Weber negative) or is lateralized to
one side (Weber right, Weber left) can place vibrating fork on
patient's chin while they clench their teeth, or directly on teeth
to elicit more reliable response will only lateralize if difference
in hearing loss between ears is >6 dB
....
,,
Weber 1i11t lataralillltion = lpailatsral conductive hearing
IO$$ or CCIIIIRiatsral sensorineural helring loss. Wh1n conducliw
hlaring loss is present. the Weber Ills! is more sensitive in
det8cting the CHL 1lw1 the Rinne test
....
,,
OTl 0 Otolaryngology
HearingTable 5. The Interpretation of Tuning Fork Tests Examples
Normal or bilateral sensorineural hearing loss Right-sided
conductive hearing loss, normal left ear Right-sided sensorineural
hearing loss, normal left ear Right-sided severe sensorineural
hearing loss or dead right ear, normal left ear Weber Central
lateralizes to Right lateralizes to Left Lateralizes to Left
Rinne
Toronto Notes 2011
.... .-------------------,Frequency of Tuning Fork (Hzl 256 512
1024 Minimum hearing loss to have NEGATIVE Rinne (BC > ACI (dBI
15 30 45
'.,
AC > BC (+) bilaterally BC>AC (-)right AC > BC (+)
bilaterally BC>AC (-)right*
* avibrating tuning forl10 dB (an air-bone gap) 2. Sensorineural
Hearing Loss (SNHL) (Figure 15D and 15E) both air and bone
conduction thresholds below normal gap between AC and BC 10 dB (an
air-bone gap)
Toronto Notes 2011
Hearing
Otolaryngology OTll
Speech AudiometrySpeech Reception Threshold (SRT) lowest hearing
level at which patient is able to repeat 50% oftwo syllable words
which have equal emphasis on each syllable (spondee words) SRT and
best pure tone threshold in the 500 to 2000 Hz range (frequency
range ofhuman speech) usually agree within 5 dB. Ifnot, suspect a
retrocochlear lesion or functional hearing loss used to assess the
reliability of the pure tone audiometry
......
'S,..b DilcrimiMtion
'1o of words
identilild 80to90'1o 6011180% 401D60'1o
ExceUentGoodFair
Speech Discrimination Testpercentage of words the patient
correctly repeats from a list of 50 monosyllabic words tested at a
level35 to 50 dB> SRT, therefore degree of hearing loss is taken
into account patients with normal hearing or conductive hearing
loss score >90% score depends on extent of SNHL rollover effect:
a decrease in discrimination as sound intensity increases are
typical of a retrocochlear lesion (e.g. acoustic neuroma)
investigate further if scores differ more than 20% between ears
used as best predictor ofhearing aid response, as if patient has HL
and prior word discrimination, hearing aids may not be helpful
PoorVery poor
Impedance AudiometryTympanogram
--------------------------------------------
the eustachian tube equalizes the pressure between external and
middle ear tympanograms graph the compliance of the middle ear
system against pressure gradient ranging from to -400 to +200 mmH2
0 tympanogram peak occurs at the point of maximum compliance where
the pressure in the external canal is equivalent to the pressure in
the middle ear normal range: -100 to +50 mmH20Highrl
Type A
TypeB
TypeC
ILaw
A__0Ai Pressure
+
-
0 Air Pressure No pressure plllk PoorTM rmblty indicl1iva af
middle ear efMiiiiiOMEt or psdoratad 1M
+
-
0' Nagl1iw j)T8RUT11 palk
+
Normel JlT8aur& peak at o Note: v.ith !Osclerosis, peek is
still at 0mmH,O but hq 1 low8r NDII: v.ith 011i:ular c!UI
discantinuity. palk iuliht 0nmi,O but han higher amplitude
hlicativt af ulllehi11111Di dyslunctilll or ellly stave otitis
medii will! out elfusi111
Figure 16. Tymp1nogrems
Static Compliance volume measurement reflecting overall
stiffness of the middle ear system normal range: 0.3 to 1.6 cc
negative middle ear pressure and abnormal compliance indicate
middle ear pathology in a type B curve, ear canal volumes of
greater than 2 cc in children and 2.5 cc in adults indicate TM
perforation or presence of a patent ventilation tube
Acoustic Stapedial Reflexes stapedius muscle contracts 2 to loud
sound acoustic .rdln: thresholds = 70 to 100 dB greater than
hearing threshold; ifhearing threshold >85 dB, reflex likely
absent stimulating either ear causes bilateral and symmetrical
reflexes for reflex to be present. CN VII must be intact and no
conductive hearing loss in monitored ear if reflex is absent
without conductive or severe sensorineural loss -+ suspect CN Vlll
lesion acoustic reflex decay test= ability of stapedius muscle to
sustain contraction for 10 s at 10 dB normally, little reflex decay
occurs at 500 and 1000 Hz with cochlear hearing loss, acoustic
reflex thresholds = 25 to 60 dB with retrocochlear hearing loss
(acoustic neuroma) -+ absent acoustic reflexes or marked reflex
decay (>50%) within 5 seconds
OT12 Otolaryngology
Hearing LoasNertigo
Toronto Notes 2011
Auditory Brainstem Response (ABR) measures neuroelectric
potentials {waves) in response to a stimulus in five different
anatomic sites {refer to Order ofNeural Pathway sidebar on OT9).
This test can be used to map the lesion according to the site of
the defect delay in brainstem response suggests cochlear or
retrocochlear abnormalities {tumour or multiple sclerosis) does not
require volition or co-operation of patient
Otoacoustic Emissions objective test of hearing where a series
of clicks is presented to the ear and the cochlea generates an echo
which can be measured often used in newborn screening can be used
to uncover normal hearing in malingering patients
.....
...----------------.lll1d
Aural Rehabilitation dependent on degree ofhearing loss,
communicative requirements, motivation, expectations, age,
physical, and mental abilities negative prognostic factors: poor
speech discrimination narrow dynamic range (recruitment)
unrealistic expectations types of hearing aids: behind the ear all
in the ear bone conduction - bone anchored hearing aid (BAHA):
applied and attached to the skull contralateral routing of signals
(CROS) assistive listening devices: direct/indirect audio output
infrared, PM radio, or induction loop systems telephone,
television, or alerting devices cochlear implants: electrode is
inserted into the cochlea to allow direct stimulation of the
auditory nerve for profound bilateral sensorineural hearing loss
not rehabilitated with conventional hearing aids established
indication: post-lingually deafened adults, pre- and post-lingually
deaf children
....Ungaalullfn-: deafnessoccurring blfol'l1111 acquired.
Post.fingul dellfn-: dllfness occurring after speech and
lll1gUIIge 1111 acquired.
.....
,
Pre-lingually deaf infants are the best candidlllas far
linllllhlbilitltion because they have benefitted !rum nonnal
devalapmenlll pluticity.
VertigoEvaluation of the Dizzy Patient vertigo: illusion of
rotational, linear, or tilting movement of self or environment
vertigo is produced by peripheral (inner ear) or central
(brainstem-cerebellum) stimulation it is important to distinguish
vertigo from other disease entities that may present with similar
complaints of"dizziness" (e.g. cardiovascular, psychiatric,
neurological, aging)
.....
llifftrenlia ntw.en the Fallowing TVJIIII of DiDin Spiming
lighlhelldedness Giddiness
, ..----------------.
Table 6. Peripheral vs. Central Vertigo
Cenlnllmbaln:e
Unsteadiness
Nanea and vamiting Audilllry svn.tams Neurologic symplllml
CampanlltianNysblgiiUI
Mild-Moderate Severe Common Rare Rapid Unidiractional Horimnllll
or ruiB1ory
Severe Variable Rare CoiiiiiDn Slow Bidirectional HoriZIIIIlll
or vertical
Teble 7. Differential Diagnosis of Vertigo Based on History
Canditi111Benig plfOllyllllilll
DurationSeconds
lllluing Loa
Tinnitus
Other Featwas
politianal nrtigo IBPPV)Meniere's disease Minutes to hou18
Precedes altllck HallS to days Days Chronic Urilbikrtnl,
fluctuating Unilateral Unilateral Progressive
+Whistling
Ywlllular n111ranitis ubyridhitis Al:ousli:neurom1
+
RecentAOM AlllxiaCN VII palsy
Toronto Notes 2011
Vertigo
Otolaryngology OT13
Benign Paroxysmal Positional Vertigo (BPPV)Definition acute
attacks of transient vertigo lasting seconds to minutes initiated
by certain head positions, accompanied by torsional (i.e. rotatory)
nystagmus (geotropic= fast phase towards the floor) Etiology due to
canalithiasis (migration of free floating otoliths within the
endolymph of the semicircular canal) or cupulolithiasis (otolith
attached to the cupula of the semicircular canal) can affect each
of the 3 semicircular canals, although the posterior canal is
affected in >90% of cases causes: head injury, viral infection
(URTI), degenerative disease, idiopathic results in slightly
different signals being received by the brain from the two balance
organs resulting in sensation of movement Diagnosis history and
positive Dix-Hallpike maneuver Dix-Hallpike Positional Testing (see
website for video and illustrations) the patient is rapidly moved
from a sitting position to a supine position with the head hanging
over the end of the table, turned to one side at 45 holding the
position for 20 seconds onset of vertigo is noted and the eyes are
observed for nystagmus see sidebar for the 5 signs ofBPPV Treatment
reassure patient that process resolves spontaneously particle
repositioning maneuvers Epley maneuver (performed by MD)
Brandt-Daroff exercises (performed by patient) surgery for
refractory cases anti-emetics for nausea/vomiting drugs to suppress
the vestibular system delay eventual recovery and are therefore not
used
.....
,,.-------------------,
BPPV is the most common cause of episodic vertigo. Patients
often are symptomatic when rolling over in bed or moving their head
to a position of extreme posterior extension.
.....
,,}-------------------.
5 Signs of BPPV Sean with Dix-Hallpike Maneuver o Geotropic
rotatory nystagmus (nystagmus MUST be present for a positive test)
o Fatigues with repeated maneuver o Reversal of nystagmus upon
sitting up o latency of -20 seconds o Crescendo/decrescendo vertigo
lasting 20 seconds
.....
,,.-------------------,
Patients can wear Frenzel's magnifying eyeglasses during the
Dix-Hallpike Maneuver, which inhibit visual fixation and allow for
better visualization of the eyes.
Supine
5
A. Epley Maneuver Figure 17. Epley and Dix-Hallpike
Maneuvers
UT -Utricle PSC - Posterior Semicircular Canal
"' 5.!!!
B. Dix-Hallpike Maneuver
OT14 Otolaryngology
Vertigo
Toronto Notes 2011
Meniere's Disease (Endolymphatic Hydrops)
,,., ,,.,....
Definition episodic attacks of tinnitus, hearing loss, aural
fullness, and vertigo lasting minutes to hours
Proposed Etiology inadequate absorption of endolymph leads to
endolymphatic hydrops (over accumulation) that distorts the
membranous labyrinth
fMtllnll Clf Meni' DiNVertigo, Tmnitus, Alnl Fullnenlllld
Helling Loss
Epidemiology peak incidence 40 to 60 years bilateral in 35% of
cases
Drop AUacka (Tumlllkin'alltDIIIIIIc Crilill are sudden falls
occurring without warning and without LDC.
Clinical Features syndrome characterized by vertigo, fluctuating
low frequency sensorineural hearing loss (SNHL), tinnitus, and
aural fullness drop attacks (Thmarkin crisis), nausea and vomiting
vertigo disappears with time (minutes to hours), but hearing loss
remains early in the disease: fluctuating sensorineural hearing
loss (SNHL) later stages: persistent tinnitus and low-frequency
hearing loss attacks come in clusters and can be debilitating to
the patient may be triggered by stress
,.. ,
}-----------------,
Before proceeding with gentamicin 1rultmunt. perform a CT Head
tu rule out CPA tumour as the CIUSe of symptoms.
Treatment acute management may consist ofbed rest, antiemetics,
antivertiginous drugs [e.g. betahistine (Sere)], and low molecular
weight dextrans (not commonly used) long term management may
include:
medical:low salt diet, diuretics (e.g. hydrochlorothiazide,
triamterene, amiloride) local application of gentamicin to destroy
vestibular end-organ, results in complete SNHL sere
prophylactically to decrease intensity of attacks
surgical: selective vestibular neurectomy or transtympanic
labyrinthectomy must monitor opposite ear as bilaterality occurs in
35% of cases
Vestibular NeuronitisDefinition acute onset of disabling vertigo
often accompanied by nausea, vomiting and imbalance without hearing
loss that resolves over daya leaving a residual imbalance that
lasts days to weeks
Etiology thought to be due to a viral infection (e.g. measles,
mumps, herpes zoster) -30% of cases have associated URTI symptoms
other: microvascular events, diabetes, autoimmune process
considered to be the vestibular equivalent of Bell's palsy; sudden
hearing loss, and acute vocal cord palsy
Clinical Features acute phase: severe vertigo with nausea,
vomiting. and imbalance lasting 1 to 5 days irritative nystagmus
(fast phase towards the offending ear) patient tends to veer
towards affected side convalescent phase: imbalance and motion
sickness lasting days to weeks spontaneous nystagmus away from
affected side gradual vestibular adaptation requires weeks to
months incomplete recovery likely with the following risk factors:
elderly, visual impairment, poor ambulation repeated attacks can
occur
Treatment acute phase: bed rest. vestibular sedatives (Gravol),
diazepam convalescent phase: progressive ambulation especially in
the elderly vestibular exercises: involve eye and head movements,
sitting, standing. and walking
Toronto Notes 2011
Vertigo/Tinnitus
Otolaryngology OTIS
LabyrinthitisDefinition acute infection of the inner ear
resulting in vertigo and hearing loss
Etiology may be serous (viral), or purulent (bacterial) occurs
as a complication of acute and chronic otitis media, bacterial
meningitis, cholesteatoma, and temporal bone fractures bacterial:
S. pneumoniae, H, influenzae, M. catarrhalis, P. aeruginosa, P.
mirabilis viral: rubella, CMV, measles, mumps, varicella zoster
Clinical Features sudden onset ofvertigo, nausea, vomiting,
tinnitus, and unilateral hearing loss, with noassociated fever or
pain meningitis is a serious complication
Investigations CThead if meningitis is suspected: lumbar
puncture, blood cultures
Treatment treat with IV antibiotics, drainage of middle ear
mastoidectomy
Vestibular Schwannoma (Acoustic Neuroma)Definition schwannoma
ofthe vestibular portion of CN VIII
Pathogenesis starts in the internal auditory canal and expands
into cerebellar pontine angle (CPA),
',...-----------------, ,Acoustic neuroma is thll most
common
compressing cerebellum and brainstem when associated with type 2
neurofibromatosis (NF2): bilateral acoustic neuromas, cafe-au-lait
skin lesions and multiple intracranial lesions
intJacranial tumour causing SNHLand 1111 most common
cllllballopontina angle rumour.
Clinical Features usually presents with unilateral SNHL or
tinnitus dizziness and unsteadiness may be present, but true
vertigo is rare as tumour growth occurs slowly facial nerve palsy
and trigeminal (V1) sensory deficit (corneal reflex) are late
complications
In the elderly, tinnitus ar SNHL is acoustic neuroma unti
proven
, ..----------------.
o1herwisl.
Diagnosis MRI with gadolinium contrast is the gold standard
audiogram - SNHL poor speech discrimination relative to the hearing
loss stapedial reflex absent or significant reflex decay acoustic
brainstem reflexes (ABR) - increase in latency of the 5th wave
vestibular tests: nonnal or asymmetric caloric weakness (an early
sign)
', ,Hilzalbllflllf sign: hypollsthesia of extErnal auditory
canal due to CN VII compression by an acoustic neuroma.
Treatment expectant management if tumour is very small. or in
elderly definitive management is surgical excision other options:
gamma knife, radiation
TinnitusDefinition an auditory perception in the absence of an
acoustic stimuli, likely related to loss of input to neurons in
central auditory pathways and resulting in abnormal firing
History subjective vs. objective (see Figure 13} continuous vs.
pulsatile (vascular in origin) unilateral vs. bilateral associated
symptoms: hearing loss, vertigo, aural fullness, otalgia,
otorrhea
OT16 Otolaryngology
Tinnitua/Diaeases of the External Ear
Toronto Notes 2011
Investigations audiology if unilateral: ABR, MRUCT to exclude a
retrocochlear lesion CT to diagnose glomus tympanicum (rare) MRI or
angiogram to diagnose AVM if suspect metabolic abnormality: lipid
profile, TSH
Treatment if a cause is found, treat the cause (e.g. drainage of
middle ear effusion, embolization or excision ofAVM) with no
treatable cause: 50% will improve, 25% worsen, 25% remain the same
avoid loud noise, ototoxic meds, caffeine, smoking tinnitus
workshops identify situations where tinnitus is most bothersome
(e.g. quiet times), mask tinnitus with soft music or "white noise"
hearing aid if coexistent hearing loss tinnitus instrument:
combines hearing aid with white noise masker trial of
tocainamide
....
,...----------------. ,,...----------------. ,
Diseases of the External EarCerumen Impaction
---------------------------------------Etiology ear wax is a
mixture of secretions from ceruminous and pilosebaceous glands,
squames of epithelium, dust, and debris
Cerumen impaction is tha most common caus. of conductive hearing
loss lor thOSIIged 15-50 'fiiiiiS-
....
Risk Factors
SVrinlinaIndications: Totally occlusive cerumen with pain,
diiCilllllld h111ring. or tinnitus Contraindications:
Nan-occlusi\18 ciiiUTlen Pravious ear surgllfY Only hearing aar 1M
perforation Complicl1ions:
hairy or narrow ear canals, in-the-ear hearing aids, cotton swab
usage, osteomataClinical Features hearing loss (conductive)
tinnitus, vertigo, otalgia, aural fullness
Treatment ceruminolytic drops (bicarbonate solution, olive oil,
glycerine, Cerumenol, syringing manual debridement (by MD)
Faiure Otitis IIX!IIma 1M perforation ll'lllml
ExostosesDefinition bony protuberances in the external auditory
canal composed oflamellar bone
Pail Vertigo limitus Otitis mudil
Method: Establish lhiii1M is inlllct Gendy pull the
pimuuperiorly and posteriorly Using warm wllllr, aim the syringe
nozzle upw!lrds and posteriorly to irrigata the eer canal
Etiology possible association with swimming in cold water
Clinical Features usually an incidental finding if large, they
can cause cerumen impaction or otitis externa
Treatment no treatment required unless symptomatic
Otitis Externa (OE)Etiology
-----------------------------------------------
bacteria (-90% of OE): Pseudomonas aeruginosa, Pseudomonas
vulgaris, E. coli, S. aureus fungus: Candida albicans, Aspergillus
niger
Risk Factors associated with swimming ("swimmer's ear")
mechanical cleaning (Q-tips), skin dermatitides, aggressive
scratching devices that occlude the ear canal: hearing aids,
headphones, etc.
Toronto Notes 2011
Diseases of the External Ear/Diseases of the Middle Ear""\ I
Otolaryngology OT17
Clinical Features acute: pain aggravated by movement of auricle
(traction of pinna or pressure over tragus) otorrhea (sticky yellow
purulent discharge) conductive hearing loss aural fullness 2 to
obstruction of external canal by swelling and purulent debris
post-auricular lymphadenopathy complicated OE exists if the pinna
and/or the periauricular soft tissues are erythematous and swollen
chronic: pruritus of external ear excoriation of ear canal atrophic
and scaly epidermal lining, otorrhea, hearing loss wide meatus but
no pain with movement of auricle tympanic membrane appears normal
Treatment clean ear under magnification with irrigation, suction,
dry swabbing, and C&S bacterial etiology antipseudomonal otic
drops (e.g. gentamicin, dprotloxadn) or a combination of antibiotic
and steroid (e.g. Garasone or Cipro He-) do not use aminoglycoside
if the tympanic membrane (TM) is perforated because of the risk of
ototoxicity introduction of fine gauze wick (pope wick) if external
canal edematous 3% acetic add solution to acidify ear canal (low pH
is bacteriostatic) systemic antibiotics if either cervical
lymphadenopathy or cellulitis fungal etiology repeated debridement
and topical antifungals (gentian violet, Mycostatin powder, boric
add, Locacorten, Viofonn drops) analgesics chronic otitis extema
(pruritus without obvious infection) -+ corticosteroid alone e.g.
diprosalic acid
9t-----------------,
Pulling Dn thl pima is lldr1ruly painful in otili1 IIXIBrna, but
ia U&uaUy wall
toleralld in otitis media.
Malignant (Necrotizing) Otitis Extarna (Skull Base
Osteomyelitis)Definition osteomyelitis of the temporal bone
Epidemiology occurs in elderly diabetics and immunocompromised
patients Etiology rare complication of otitis externa Pseudomonas
infection in 99% of cases
.....Clinical Features otalgia and purulent otorrhea that is
refractory to medical therapy granulation tissue on the floor ofthe
auditory canal Complications lower cranial nerve palsies systemic
infection, death Management imaging: high resolution temporal bone
CT scan, gadolinium scan, technetium scan requires hospital
admission, debridement, IV antibiotics, hyperbaric 0 2 may require
OR for debridement of necrotic tissue/bone
',
Gillum and TICbnltiiD Scans
Gallium scans are usad to show sites
not show 1lle extant of ostlomyalitis. Technulium scans provide
informlrlion about ostaoblastic activity llld as IUCh are uSid to
d1monslratl situ of osteomyelitis. Tachnetium scans halp with
diagnosis whereas gallilrn scans '" u1eful in follow-up.
of actiw infection. GaDium is tlklln up by PMNs and thlrtlfor.
only lights up when active infaction ia pment. It will
Diseases of the Middle EarAcute Otitis Madia (AOM) and Otitis
Madia with Effusion (OME) see Pediatric Otolaryngology, OT38
OTIS Otolaryngology
Diseues of the Middle Ear
Toronto Notes 2011
CholesteatomaDefinition a cyst composed of keratinizing squamous
epithelium occurring in the middle ear, mastoid and temporal bone
two types: congenital and acquired (see below) Congenital presents
as a "small white pearl" behind an intact tympanic membrane
(anterior and medial to the malleus) or as a conductive hearing
loss believed to be due to aberrant migration of external canal
ectoderm during development not associated with otitis
media/eustachian tube dysfunctionuf Cha..IIIHIDma
....
,
Fonnmion1. Epilhelial migrlltion through TM pllforalion (2"
acquinld) 2.1rMigirllltion of TM (1"acqund)
Acquired (more common} generally occurs as a consequence of
otitis media and chronic eustachian tube dysfunction frequently
associated with retraction pockets in the pars flaccida (1
acquired) and marginal
3. Metaplasia of middle ear epithelium (congenilll) 4. 8Qal eel
hyperplalia (congenital)
perforations (2" acquired) of the tympanic membrane the
associated chronic inflammatory process causes progressive
destruction of surrounding bony structures Clinical Features
symptoms: history of otitis media (especially if unilateral),
ventilation tubes. ear surgery progressive hearing loss
(predominantly conductive although may get sensorineural hearing
loss in late stage) otalgia, aural fullness, fever signs:
retraction pocket in TM, may contain keratin debris TM perforation
granulation tissue, polyp visible on otoscopy malodorous,
unilateral otorrhea ComplicationsTable 8. Complications of
Cholesteatoma
LOCII Ossicular erosion: conductive helling loss
Inner ear erosion: SNHL, dizziness .,4'or labyrinthitis Tempcnl
bone infection: mastoiditis, plllrositisFacial paraly&s
lnlnlcranill Meningitis Sigmoid sinus tlrumbosis Intracranial
abscess (1ubdural, spidural, cnbellar)
Investigations audiogram and CT scan Treatment there is no
conservative therapy for cholesteatoma surgical: mastoidectomy
tympanoplasty ossicular reconstruction
Mastoiditis
....
,
Definition complication of AOM infection (usually subperiosteal)
of mastoid air cells, most commonly seen approximately two weeks
after onset of untreated or inadequately treated acute suppurative
otitis media Etiology acute mastoiditis caused by the same
organisms as AOM: S. pneumoniae, S. pyogenes, S. aureus, H.
influenzae Clinical Features clasaic: triad otorrhea tenderness to
pressure over the mastoid retroauricular swelling with protruding
ear fever, hearing loss, TM perforation (late) CT radiologic
findings: opacification of mastoid air cells by fluid and
interruption of normal trabeculationsofcells
Mastoiditis is now rar8 dua to rapid and elleclive 1rell1menl of
acute otitis media with antibiotics.
Toronto Notes 2011
Diseases of the Middle Ear/Diseases of the Inner Bar
Otolaryngology OT19
Treatment IV antibiotics with myringotomy and ventilation tubes
- usually all that is required acutely cortical mastoidectomy:
debridement of infected tissue allowing aeration and drainage
indications for surgery: failure of medical treatment after 48
hours symptoms of intracranial complications aural discharge
persisting for 4 weeks and resistant to antibiotics
OtosclerosisDefinition fusion of stapes footplate to oval window
so that it cannot vibrate Etiology autosomal dominant, variable
penetrance approximately 40% female> male, progresses during
pregnancy (hormone responsive) Clinical Features progressive
conductive hearing loss first noticed in teens and 20's (may
progress to sensorineural hearing loss if cochlea involved)
pulsatile tinnitus tympanic membrane normal pink blush (Schwartz's
sign) associated with the neovascularization of otosclerotic bone
characteristic dip at 2,000 Hz (Carhart's notch) on audiogram (see
Figure 15) Treatment monitor with serial audio grams if coping with
loss hearing aid (air conduction, bone conduction, BAHA)
stapedectomy or stapedotomy (with laser or drill) with prosthesis
is definitive treatment..._. I
caus1 of conductiw hearing loss i1 1511150 yaar olds (eftar
cerumen in1)aclion).
Dlllsclllnllil illhe zo most common
Diseases of the Inner EarCongenital Sensorineural Hearing
LossHereditary Defects non-syndrome associated (70%): often
idiopathic, autosomal recessive connexin 26 (G]B2) most common
syndrome associated (30%): Waardenburg's - white forelock,
heterochromia iridis, wide nasal bridge and increased distance
between medial canthi Pendred's - deafness associated with thyroid
gland disorders, SLC26A4 gene, enlarged vestibular aqueducts
Treacher-Collins - first and second branchial cleft anomalies
Alpert's - hereditary nephritis Prenatal TORCH Infections
toxoplasmosis, rubella, cytomegalovirus {CMV), herpes simplex,
others (e.g. HIV; syphilis) Perinatal Rh incompatibility anoxia
hyperbilirubinemia birth trauma (hemorrhage into inner ear)
Postnatal meningitis mumps measles High Risk Registry (for Hearing
Loss in Newborns) risk factors: low birth weight/prematurity
perinatal anoxia (low APGARs) kernicterus- bilirubin >25 mgldL
craniofacial abnormality famlly history of deafness in
childhood
..._. I
Congenilzll SNHL is decreasing in
.
vacciles and improved neonatal care.
incidence due to the availability Df
OT20 Otolaryngology
Diseases of the Inner Ear
Toronto Notes 2011
1st trimester illness - TORCH infections neonatal sepsis
ototoxic drugs perinatal infection, including post-natal meningitis
consanguinity 50-75% of newborns with sensorineural hearing loss
have at least one of the above risk factors, and 90% of these have
spent time in the NICU presence of any risk factor: auditory
brainstem response (ABR) study performed before leaving NICU and at
3 months adjusted age early rehabilitation improves speech and
school performance
PresbycusisDefinition sensorineural hearing loss associated with
aging (staging in 5th and 6th decades)
Etiology hair cell degeneration age related degeneration
ofbasilar membrane cochlear neuron damage ischemia of inner ear
Clinical Features progressive, gradual bilateral hearing loss
initially at high frequencies, then middle frequencies loss of
discrimination of speech especially with background noise present -
patients describe people as mumbling recruitment phenomenon:
inability to tolerate loud sounds tinnitus
Treatment hearing aid if patient has difficulty functioning,
hearing loss >30-35 dB, and good speech discrimination lip
reading, auditory training, auditory aids (doorbell and phone
lights)
Sudden Sensorineural Hearing Loss....
,
Clinical Features presents as a sudden onset of significant SNHL
(usually unilateral) tinnitus, aural fullness usually idiopathic,
rule out other causes: autoimmune causes - ESR, rheumatoid factor,
ANA MRI to rule out tumour and/or CT to rule out
ischemic/hemorrhagic stroke if associated with any other focal
neurological signs (e.g. vertigo, ataxia, abnormality of CN V or
VII, weakness)
Sudden sensorineural hearing loss may Blsily ba confused with
ischemic bnlin BYBIIII. It ia ""'artmt ta ksep a high ildex of
suspicion aspecially with 1lder1y petilnts p11santing with sudden
s.nsariniUilll hBIR!g lou as wall as Vlrtigo.
Treatment treat with oral corticosteroids within 3 days of
onset: prednisone 1-2 mg/kg/day, tapering over 2 weeks
Prognosis depends on degree ofhearing loss 70% resolve
spontaneously within 10 to 14 days 20% experience partial
resolution 10% experience permanent hearing loss
Autoimmune Inner Ear DiseaseEtiology
may be associated with systemic autoimmune diseases (ie.
rheumatoid arthritis, SLE),vasculitides (i.e. Wegener's,
polyarteritis nodosa) and allergies
idiopathic
Epidemiology most common between ages 20-50
Clinical Features rapidly progressive or fluctuating bilateral
SNHL tinnitus, aural fullness, vestibular symptoms (ie. ataxia,
disequilibrium, vertigo)
Toronto Notes 2011
Diseases of the Inner Ear
Otolaryngology OT21
Investigations autoimmune work-up: CBC, ESR, ANA, rheumatoid
factor Treatment high-dose corticosteroids: treat early for at
least 30 days consider cytotoxic medication for steroid
non-responders
Drug Ototoxicity
----------------------------------------
Aminoglycosides toxic to hair cells by any route: ora]. IY, and
topical (ifthe TM is perforated) destroys sensory hair cells- outer
first, inner second (therefore O.AEs are lost first) high frequency
hearing loss develops earliest ototoxicity occurs days to weeks
post-treatment streptomycin and gentamicin {vestibulotoxic),
kanamycin and tobramycin (cochleotoxic) must monitor with peak and
trough levels when prescribed, especially if patient has
neutropenia and/or history of ear or renal problems q24h dosing
recommended. with amount determined by creatinine clearance, not
serum creatinine aminoglycoside toxicity displays saturable
kinetics therefore once daily dosing presents less risk than
divided daily doses duration oftreatment is the most important
predictor of ototoxicity treatment: immediately stop
aminoglycosides Salicylates hearing loss with tinnitus, reversible
if discontinued Antimalarials (Quinine) hearing loss with tinnitus
reversible if discontinued but can lead to permanent loss
Others many antineoplastics agent are ototoxic (weigh risks vs.
benefits) loop diuretics
Noise-Induced Sensorineural Hearing LossPathogenesis 85 to 90 dB
over months or years causes cochlear damage early-stage hearing
loss at 4000 Hz (because this is the resonance frequency of the
temporal bone), extends to nigher and lower frequencies with time
(see Figure lSD) speech reception not altered until hearing loss
>30 dB at speech frequency, therefore considerable damage may
occur before patient complains ofhearing loss difficulty with
speech discrimination, especially in situations with competing
noise Phases of Hearing Loss dependent on: intensity of sound and
duration of exposure temporary threshold sliift: when exposed to
loud sound. decreased sensitivity or increased threshold for sound
may have associated aural fullness and tinnitus with removal of
noise, hearing returns to normal permanent threshold shift: hearing
does not return to previous state Treatment hearing aid prevention:
ear protectors: muffs, plugs machinery which produces less noise
limit exposure to noise with frequent rest periods regular
audiologic follow-up
....
,,
Limita Ill' NDiH C.ning Dllm... Continuous sound pressu18 >85
dB Single toUnd impulse > 135 dB
Inner Ear Diseases that cause Vertigo see Vertigo, OT12 benign
paroxysmal positional vertigo (BPPV} Meniere's disease
{endolymphatic hydrops) vestibular neuronitis
labyrinthitis acoustic neuroma (AN), (vestibular schwannoma)
OT22 Otolaryngology
Dileasel of the IDDer Bari.Fadal Nerve (CN VII) Paral.}'lis
1'oroDio
2011
Temporal Bona Fractures rarely are temporal bbone fractures
purely transwrse or longitudinal, often it is a mixed pictureT1bl1
9. Futul'll al Tampon! BDlle Fncb11'81l111 Figure 11)Wo bony
labyrinth ..d mmaiiiJditury meatus lniD middle earIOID20%
70ta 911%IJdenll!kijtJauna
FnnaVocc.,illl1nuna CN VI P*v (511%)SIIIIOiilalnlloll ciJa to
dnct cachlllll' injuryFigure 1I. TvP of Tamparllla11
CN VII palsy (10 to 20%) Condul:liva hlollsacmryto Ollic.-r
ijuyRln
Fncbnes
VeslikB _ ., .,._.1
.... \
,
Sudllen onut vastib.-r direct semk:icullw c-.al !pllntln!DUS
nysblgnDI)
(V8IIigo.
u
ID
lmct axtamalllldiiDfy maetus.
ligM of a.Rr 1111111 fnlnn
miiDinlna SponlllniCIUS nystapJs
Battla' Sign: er;chymo of the maloid prollal af 1ha lllmplnl
bonaRacoon EvaCSF
CSF leak il euslldlian die to nasophar,m:t rhioonhea (risk of
meningitis)
Blaeding tom axtama1 auiiDry Cllllll Slap famlltiCII in IXIImal
aucllary c:anal CSFOionhaaBattle's sign = masiDid ecchymDses
Rlcco111 ayes = pariarbitiiiiCCIIvm:J
Clllssic twas llllldlnesm .-rrnan with moclall irfny IMVA/;
ollln QmlidJnel
Cranial NIMI invaMrlant !fllcilrl p!lbynumbness ... CN VI-o CN
Vll nyslagltkls -o CN VI. fal:ial
Diagnosis otoscopy
.... \
,
lhe halo lign il the ..,., mgad ppnn:a af CSF ft.lid on whilll
filbr ...,.... it ......... aut from blaad.
do not syringe or manipulate external auditory meatus due to
r.IBk ofinducing meningitis via TM perforation Cfhead aurliol.ogy,
fuci.al nerve testa (for transverse fractures), Schirmer's teat (of
lacrimation), stapedial refleua ifCN vn palsy lf suspecting CSF
leak: look for halo sign (see sidebar), send fluid for
beta-2-transferrin
Treatment ABC's medical - expectant. prevent otogenic meningitis
surgical - explore temporal bone, indi.cati.Ollll: CN VII palsy
(immediate and complete) gunshot wound depressed fracture of eDemal
auditory meatus early meningitis (mastoidectomy) bleeding
lnt:rac:ranially from sinus CSF otorrhea (may resolve
spontaneous]y)Compliartions BCUte otitis media labyrinthitis
mastoiditis .meningitis!epidural abacesslbraln abscess
post-traumatic cholesteatoma
H_llrulau... FeciiiiNGrumg lydanr lhdll: Normal facial mDtllr
functicm lhdlll: Mid dyliunetion -SI9rl-kn111
Facial Nerve (CN VII) ParalysisEtiology supraouclear and nuclear
(MS. poliomyelitis, cerebral tumours) intranuclear - see table
belowTreatment treat acccrding to etiology plus provide corneal
protection with artificial tears, nocturnal lid taping.
tarsorrhaphy, gold welgbting of upper lid
- Normll 8'jllllletJy and tone
atrMI 11'1' lhdllll: Modnl8 dysfunction - Obvioua waakn111 Grade
IV! Modarately WV818 dysfunc:tion - Obvioua waakn111 diqriv
ll'flllmiCry
- h:omplate 11'1' clolura- No forahlllld mDiicn
- Moutll asymmlllric mcrtion lhdl V: Slwra dyJhllction - Barely
pan:apliblll motion of moutll - Asymmllric at l1lt Grads VI: TaiBI
- No mDVImanl
fildal paralysis that does not resolve with time or with medical
treatnwrt will often be referred for possible reanimation
tecbnlques to restore function common reanimation techniques
Include: direct facial nerve anastomosis interpositi.onal grafts
anastomosis to other motor nerves muscle transpositions
Toronto Notes 2011
Facial Nerve (CN VII) Paralysis/Rhinitis
Otolaryngology OT23
Table 10. Differential Diagnosis of Peripheral Facial Paralysis
(PFP)Etialagy
llllrs PalsyIdiopathic, {HSV) irlectian af the facial nerve
lncidn:e 80 to 90% at PFP Rill! hcturs:
Findings Hx: Acutu 011&81
1-'iglllionsStapedial refti!X absent Audiology normal (or
basalina) 811Ctrcmyugram (EMG)- bll&t measure for prognosis
Topognoslic testing MRI with gadolinium- enhancemsnt CN VII VIII
H1gh resolution CT
TRIItlllnt. Foll-..p.and l'rlvtoli (Px)Rx:
Diab818s Pr&gnancy Diagnosis uf lllll:lusion Viral prodrome
(50%)
Nwnbness af aar Schinner's test Recurnnce {12%1 + FHx{14%)
Hyperacusis {30%1
Prutact the 8Y8 to prevent eJIPU&Ura kllratitis with
patx:hing ortarsorraphy Systemic steroids may lessen degeneration
and hasten recovery Consider antiviral (acyclovir)
FJll:Spontaneous remission should begin withil 3 weeks of onset
Delayed (3 to 6 months) recovery portends at least some functional
loss90% racovar spontaneously and ovaral; >90% n!covary
pan!lysis was incomplete Poorer hyperacusis, > 60 vrs. diabetes,
HTN, severe pain
Piny$is or pai'Biii& af all mU&cle groups on one side at
thll face Absence af signs at CNS disease Absence at signs at ear
or CPA diseases
PIE:
Px:
Rlmlatllunt
Synlhm (Hirpea Zllltlr Oticus)Varicella zo51er infection at
CNVIWIII
4.5 to !1% of PFP Rill! hcturs:lf11lilirad immunity Cane
Radiathllrapy Chemotherapy (see OT22}
>60'(81111
Hyperacusis SNHL Severe pain of pinna, mouth, or faceVesicles on
pinna, ext. canal (enupt 3-7 days after onset of pain) Associated
herpes mster uphthalmicus (uveitis, lantacunjunctivitis, optic
neuritis, or glaucoma)
Hx:
PIE:
Stapedial refti!X absent Audiology- SNHL Villll EUSA studies to
cunfinn MRI with gadolinium (86% at facial neMJS enhance)
Rx: Pt should avoid lesions to prevent spraad of infection
Systemic steroids can raliM pain, vertigo, avoid postherpetic
nauralgia Acyclovir may lessen pain, aid healilg of vesicles
Poorer prognosis than Belrs palsy; 22% recover coqJietEiy, 66%
paralysis, 111% coqJiete paralysis Skull XofliYS CT head
FJll: 2to 4W88b Px:
Tampanl Bona Fnclunl Langitudi111l (911%) 211% have PFP
Blow to side at head Trauma to side of head Neuro findings
consistEnt with epiduraVsubdural bleed
Hx:
PIE:
Injury usually due tu stratch or impingBI'nent; may recover with
time
Px:
r..nna(10%)
40%have PFP
Blow to frontal or occipital area
Hx:
Skull XofliYS CT head
Nerve 1nlnsection
Px:
lmaganic
Trauma to front or back of haad Variable (depending on level at
injury) Wait lor lidocaine to weer off
PIE:
EMG
Rx:
if nerve pa.aysis No exploration if any movement present
RhinitisDefinition inflammation of the lining (mucosa) of the
nasal cavityTabla 11. Classification of Rhinitislnfllllllllaturyo
o
Nonlnflllmmaturyo o
Peremial nun-allergic0
Asthma, MA SIIISitivity
Allgic o Seasonal o Peremial o Atrophic o Primary: (especially
in eldelly) o Acquired: post-slJ'IIerv if too 1111ch mucosa or
bllilinate has been resected o Infectious o Viral: e.g. lhinovirus,
influelllll, parailfluiiiJZII, etc. o Bacterial: e.g. S.IIUIIlUS o
Fungal o Granulomatous: TB, syplilis, leprosy o Non-infactious o
Sarcoidosis o Wegane(s gnmulomatosis o Irritanto
o
Rhinitis medicamentosa o Topical decungssllmts Honnonal o
Pr&gnancy o Estrogens 0 Thyroid Idiopathic vasomotor
.....
}-----------------,medicllltlentou is rebound
congestion due to 1he owruse of int1'81111SIII
VIIIOCDnstriciDrs. For uu of theu madicationsfor only &-7 day5
ill racommended.
oo
Dust Chemicals Pollution
OT24 Otolaryngology
Rhinitis
Toronto Notes 2011
Table 12. Nasal Discharge: Character and Associated
ConditionsAssac:iatlld ColdilionsWatery/mucoid Allergic, viral,
vasamDtor, CSF leak (halo signl
MucapurulentSerosquinous
Bacterial, fureign body NeoplasiaTrauma, nBOplasia, blaeding
disaniBr, hyp&rta1siorl"vasculll" diseass
Bloody
Allergic Rhinitis (Hay Fever)Definition rhinitis characterized
by an IgE-mediated hypersensitivity to foreign allergens
acute-and-seasonal or chronic-and-perennial perennial allergic
rhinitis often confused with recurrent colds
.....
,...----------------. ,
Etiology when allergens contact the respiratory mucosa, specific
IgE antibody is produced in susceptible hosts concentration of
allergen in the ambient air correlates directly with the rhinitis
symptoms Epidemiology age at onset usually 5 days) of nasal drops
and sprays (Dristan, Otrivin)
Clinical Features chronic intermittent nasal obstruction, varies
from side to side rhinorrhea: thin, watery nasal allergy must be
ruled out mucosa and turbinates: swollen, pale between exposure
symptoms are often more severe than clinical presentation
suggests
Treatment elimination of irritant factors nasal spray)
parasympathetic blocker o steroids (e.g. beclomethasone,
fluticasone) o surgery (often of limited lasting benefit):
electrocautery, cryosurgery, laser treatment or removal of inferior
or middle turbinates o vidian neurectomy (rarely done) o
symptomatic relief with exercise (increased sympathetic tone)
SinusitisDevelopment of Sinuses sinus pneumatization begins in
3rd-4th month of fetal life o maxillary sinus first to develop
neonate - clinically significant ethmoid and maxillary buds present
age 9 - maxillary full grown; frontal and sphenoid cells starting
age 18 - frontal and sphenoid cells full grown
....Pathogenesis of Sinusitis inflammation of the mucosal lining
ofthe paranasal sinuses anything that blocks mucus from exiting the
sinuses predisposes them to inflammation all sinuses drain to a
common prechamber under the middle meatus called the osteomeatal
complex
,EildPCOpic Sinua
FESS = Surprr
Opening of the entire amorneabll campiBK in ardar to facilitate
drainaQII while sparing 111e sinus mucosa.
Definitiono
inflammation of the mucosal lining of the sinuses
Classification acute: 3 months
Table 13. Etiologies of Sinusitis
Ollill Obltruc:lion
Inflammation Mechanical
URTI
Septal deviation Turbinate hypellrophy Polyps Tumours Adenoid
hypertrophy
Foreign body Cangenital abnormalities i.e. cleft palate
Immune
Wegener's g11111lomatosis
Dii'ICI ExllnsianSaurce: Dr. J. Cl'lpnik.
Dental Trawna
Lyrl1lhoma. leukemia lmm.mosuppressed patients (e.g.
neutropenics, diabetics, HIV) CVstic fibrosis lmmotile cilia
(Kartagener'sl Infection
Facial fractures
OT26 Otolaryngology
Sinuaitia
Toronto Notes 2011
Acute Suppurative SinusitisDefinition acute infection and
inflammation of the paranasal sinuses clinical diagnosis requiring
at least 2 major symptoms or 1 major and 2 minor symptoms minor
symptoms major symptoJDS facial pain/pressure headache facial
fullness/ congestion halitosis nasal obstruction fatigue
purulent/discoloured nasal discharge dental pain hyposmia/anosmia
cough fever ear pressure/fullness Etiology viral vs. bacterial
(viral etiology is more common) children are more prone to a
bacterial etiology, but viral is still more common maxillary sinus
most commonly affected must rule out fungal causes (mucormycosis)
in immunocompromised hosts (especially if painless, bloodless
mucosa on examination) organisms viral: rhinovirus, influenza.
parainfluenza bacterial: S. pneumoniae (35%), H. influenzae (35%),
M. cata"halis, anaerobes (dental) Clinical Features sudden onset of
nasal blockage/congestion and/or nasal discharge/posterior nasal
drip facial pain or pressure, hyposmia signs more suggestive of a
bacterial etiology are erythematous nasal mucosa, mucopurulent
discharge, pus originating from the middle meatus and the presence
of nasal polyps or a deviated septum acute viral rhinosinusitis
lasts 10 days, consider bacterial etiology Management anterior
rhinoscopy x-ray/CT scan not recommended unless complications are
suspected (ie. sub-periorbital abscess or intracranial spread-
Pott's Puffy tumour) symptoms improving within 5 days: symptomic
relief and expectant management moderate symptoms that worsen or
persist beyond 5 days: institute an intranasal corticosteroid spray
and continue for 14 days if symptomic relief is noted within 48 hrs
severe symptoms that worsen or persist beyond 5 days and are
refractory to intranasal corticosteroid (INCS): clarithromycin or
Clavulin therapy INCS referral to a specialist surgery if medical
therapy fails: FESS
I
Acute Si-a Complcllions Consider hospitlllimion 111y of
1hefDUowing ar.suspactld 1. Olbital (Chandler's classifil:lllionl
a. Periorbilll celulitis b. Olbilll c. SubpariostlllllbsciSI d.
OlbillllbiCIIIS a. Cavem011s sintJS 1hrombosis 2.1ntnacranial a.
Meningitis b.Absc111
3. Bony a. Subperiost11l frontal bona abscess ("Pott's Puffy
Tumour'"l b. Osteomyelitis 4. N111.1rologic a. Superior olbital
fissura syndroma CN IIVIVM palsy, immobile globe, dilatad pto$is,
V1hypoesthesial b. Olbitalapsx syndrome (as"4a" above, plus
neuritis,
papilledema, decraasad acuityl
Chronic SinusitisDefinition inflammation ofthe paranasal sinuses
lasting >3 months
....
,..}-----------------. ,
Allergic fungallhinosinusitis is a chronic sinusitis affee1ing
mostly young, immunocompetent, lllopic individuals. Tllllllmant
options include FESS intranasallllpical steroids, antifungals and
immuno1harapy.
.....
,..}-----------------. ,
Etiology can result from any of the following: inadequate
treatment of acute sinusitis untreated nasal allergy allergic
fungal rhinosinusitis anatomic abnormality e.g. deviated septum
(predisposing factor) underlying dental disease dliary disorder
e.g. cystic fibrosis, Kartagener's chronic inflammatory disorder
e.g. Wegener's organisms: bacterial: S. pneumoniae, H. influenzae,
M. catarrhalis, S. pyogenes, S. aureus, anaerobes fungal:
Aspergillus Clinical Features (similar to acute, but less severe)
chronic nasal obstruction purulent nasal discharge pain over sinus
or headache
C DIIic lin11litit Complication .. 1.PolYIJ'
2. Mucocele
Toronto Notes 2011 halitosis yellow-brown post-nasal discharge
chronic cough maxillary dental pain
Sinusitis/Epistaxis
Otolaryngology OT27
Treatment antibiotics for 3 to 6 weeks for infectious etiology
augmented penicillin (Clavulin), macrolide (clarithromycin),
tluoroquinolone (levofloxacin), clindamycin, Flagyl topical nasal
steroid, saline spray surgery if medical therapy fails or fungal
sinusitisSurgical Treatment functional endoscopic sinus surgery -+
open osteomeatal complex balloon sinoplasty
EpistaxisBlood Supply to the Nasal Septum (Figure 4) 1. Superior
posterior septum: internal carotid -+ ophthalmic -+
anterior/posterior ethmoidal 2. Posterior septum: external carotid
-+ internal maxillary -+ sphenopalatine artery-+ nasopalatine 3.
Lower anterior septum: external carotid -+ facial artery-+ superior
labial artery -+ nasal branch external carotid -+ internal
maxillary -+ descending palatine -+ greater palatine these arteries
all anastomose to form Kiesselbach's plexus, located at Little's
area (anterior portion ofthe cartilaginous septum) bleeding from
above middle turbinate is internal carotid, and from below is
external carotid Tabla 14. Etiology of Epistaxis
Type
Caulea
Trauma (most commonl fnlctures: faciaL 11111111 Self-induced:
digital foreign body latmgenic: nasal. sinus. orbit surgery
Tumours Banign: polyps, ilvarting papiloma, angilllibmma
Malignant: squamous cell carcinoma. esthesioneuroblastoma
lnllammation Rhinitis: allergic, non-allergic Infections:
bacterial, viral, fungalIdiopathic
Bammstric changBBNBSIII
mvness: dry ai& septal deformities
Saptal perforation
......
,
Chemical: cocaine, nasel sprays, ammonia, etc.Systamic
CDagulopathies Meds: anticDagularrts, NSAIDs
SpeciiiC... Adote.cent male with unilallnlThis is the most
common benign tumour of the 11111.upharynx patilllll- use
reSOibable piCks Ill avoid risk ofrecwrent epistaxis consider
juvenile nuopluuynglllll angiufibruma (JNA).
Hemophilias, von Willebrand's Hamatololjicalmalignancias Uver
failure. uremia Vascular: hypertension, atherosclerosis, Osler-
Weber-Rerdl (HHTI Others: Wegener's. SlInvestigations CBC,
PT/PTT (if indicated) x-ray, CT as needed
ra-bleeding caused by pulling out the removable pack
Treatment aim is to localize bleeding and achieve hemostasis1.
First-aid ABC's patient leans forward to minimize swallowing blood
constant firm pressure applied for 20 min on soft part of nose (not
bony pyramid) 2. Assess Blood Loss (can be potentially fatal
hemorrhage) pulse, blood pressure, and other signs of shock IV NS,
cross match for 2 units packed RBCs if significant IV NS if
hypovolemic, or signs of shock
OT28 Otolaryngology
EpistaxWHoarsenas3. Determine Site of Bleeding
Toronto Notes 2011
anterior/posterior hemorrhage defined by location in
relationship to bony septum insert cotton pledget of 4% topical
lidocaine topical decongestant (ie. Otrivin), visualize nasal
cavity with speculum and aspirate excess blood and clots if
suspicion of bleeding disorder, coagulation workup
4. Control the Bleeding first line topical vasoconstrictors
(Otrivin) if first line fails and bleeding adequately visualized,
cauterize with silver nitrate do not cauterize both side& of
the septum at one time due to risk of septal perforation from loss
of septal blood supply A. Anterior hemorrhage treatment if fail to
achieve hemostasis with cauterization: place anterior pack with
half inch Vaseline-soaked ribbon gauze strips or absorbable packing
(ie. Gelfoam) layered from nasal floor toward nasal roof extending
to posterior choanae for 2 to 3 days can also attempt packing with
Merocel or nasal tampons of different shapes can also apply Floseal
(hemostatic matrix consisting topical human thrombin and cross
linked gelatin) if other methods fail
B. Posterior hemorrhage treatment if unable to visualize
bleeding source, then usually posterior source: place posterior
pack using a Foley catheter, gauze pack or balloon subsequently,
layer anterior packing bilaterally antibiotics for any posterior
pack or any pack in >48 hours admit to hospital with packs in
for 3 to 5 days watch for complications: hypoxemia (naso-pulmonic
reflex), toxic shock syndrome (Rx: remove packs immediately),
pharyngeal fibrosis/stenosis, alar/septal necrosis, aspiration
C. Ifanterior/posterior packs fail to control epistuis arterial
ligation of anterior/posterior ethmoid, branches of internal
maxillary, external carotid artieriesselective embolization of
branches of external carotid artery septoplasty
5. Prevention prevent drying of nasal mucosa with humidifiers,
saline spray; or topical ointments avoidance of irritants medical
management of hypertension and coagulopathies
.....
,t-----------------, ' ,..,weak,
HoarsenessDefinitions hoarseness: change in voice quality,
ranging from voice harshness to voice weakness reflects
abnormalities anywhere along the vocal tract from oral cavity to
lungs dysphonia: a general alteration in voice quality aphonia: no
sound emanates from vocal folds
If hollrsan.s p!allll far > 2 woks in a smoker, laryngoscopy
must be done to
rule out malignancy. Acute 2 weeks.
.....
Vocal Cord PanlrslsIJniiiQral: affected cord lies in the
Acute LaryngitisEtiology viral: influenza, adenovirus bacterial:
Group A Streptococcus acute voice strain -+ submucosal hemorrhage
-+ vocal cord edema -+ hoarseness environmental: toxic fume
inhalation
permedilln position, inadsqusta glotticciOSIR during pllomdion
bnl8thy voice.
Bii!Mral: cords rest in midline 1herefare voice 1"8mains good
but respiratory function is compromislld 111111 maypnlll8lll as
abidor.
r-tmlllt options: voicathsrapy,injection laryngoplasty
(collagen. fat),
cord madilllilalion.
....
,. ,
URTI symptoms, hoarseness, aphonia. rough attacks, dyspnea true
vocal cords erythematous/edematous with vascular injection and
normal mobility
Clinical Features
Treatment usually self-limited, resolves within -1 week voice
rest humidification hydration avoid irritants (e.g. smoking) treat
with antibiotics if there is evidence of coexistent bacterial
pharyngitis
Innervation of Larynxlntamll brancb of III'JII...I nern: Mnsory
to larynx abova cords.
Ext.nel branch of superior lery1111ul nern: motor to
crico1hyroid muscle. bcurnnt laryngul 1111rn: all motor to larynx
axcapt far cricothyroid muscle; sensory to larynx below cords.
Toronto Notes 2011
Hoarseness
Otolaryngology OT29
Chronic LaryngitisDefinition longstanding inflammatory changes
in laryngeal muooaa Etiology repeated attacks of acute laryngitis
chronic irritants (dust. smoke, chemical fumes) chronic voice
strain chronic sinusitis with postnasal drip (PND) chronic alcohol
use esophageal disorders: GERD, Zenker's diverticulum, hiatus
hernia systemic: allergy, hypothyroidism, Addison's Clinical
Features chronic dysphonia - rule out malignancy cough, globus
sensation, frequent throat clearing 2o to GERD laryngoscopy: cords
erythematous, thickened with ulceration/granuloma formation and
normal mobility Treatment remove offending irritants treat related
disorders e.g. antisecretory therapy for GERD speech therapy with
voice rest antibiotics, steroids to decrease inflammation
laryngoscopy to rule out malignancy
Vocal Cord PolypsDefinition structural manifestation of vocal
cord irritation acutely, polyp forms 2 to capillary damage in the
subepithelial space during extreme voice exertion Etiology most
common benign tumour of vocal cords voice strain (muscle tension
dysphonia) laryngeal irritants (GERD, allergies, tobacco)
Epidemiology 30 to 50 years of age M>F Clinical Features
hoarseness, aphonia, cough attacks dyspnea pedicled or sessile
polyp on free edge of vocal cord typically polyp asymmetrical, soft
and smooth more common on the anterior 1/3 of the vocal cord polyp
are intermittent respiratory distress with large polyps Treatment
avoid irritants endoscopic laryngeal microsurgical removal if
persistent or if high risk of malignancy
....
,,Noduli Bilateral
Vacal Cords: Palyps vs. Nodulel PalypsUnillltaralasymmebicMll'f
IHOIVB Often follow a spontaneously chronic course
Acute onset
Gradual onset
capillary breakage
Aculll:h1111orrhage or edama
Chronic: hyalinization within submucous lesionAculll: small,
discrelll noclllas Chronic: hard, white, thickened fibrosed
noclllas
Soft, 8111oolh, fusifann,paduncuhdlld
mass
Surqical Surqicalaxcisian a axcisian rafractory persistent or in
presence of riskfac!Drs for
laryngaal cancer
Vocal Cord NodulesDefinition vocal cord callus aka "screamer's
or singer's Etiology early nodules occur 2 to submucosal hemorrhage
mature nodules result from hyalinization which occurs with long
term voice abuse chronic voice strain URTI, smoke, alcohol
Epidemiology frequently in singers, children, bartenders, and
school teachers F>M
OT30 Otolaryngology
Hoarseness/Salivary Glands
Toronto Notes 2011
Clinical Features hoarseness worst at end of day on
laryngoscopy: red. soft nodules often bilateral at the junction of
the anterior 1/3 and posterior 2/3 of the vocal cords - point of
maximal cord vibration chronic nodules may become fibrotic, hard,
and white
Treatment voice rest hydration speech therapy avoid irritants
surgery rarely indicated for refractory nodules
Benign Laryngeal PapillomasEtiology human papilloma virus (HPV)
types 6, 11 possible hormonal influence, possibly acquired during
delivery
Epidemiology biphasic distribution - I) birth to puberty (most
common laryngeal tumour) and 2) adulthood
Clinical Features hoarseness/"frog voice" and airway obstruction
can seed into tracheobronchial tree highly resistant to complete
removal some juvenile papillomas resolve spontaneously at puberty
papillomas in adults may undergo malignant transformation
laryngoscopy shows wart-like lesions in supraglottic larynx and
trachea
Treatment C02 laser and microsurgery adjuvants under
investigation: interferon, cidofovir, acyclovir Gardasil HPV
vaccine may prevent/decrease the incidence but more research is
needed
Laryngeal Carcinoma see Neoplasms of the Head and Neck, OT34
Salivary GlandsSialadenitisDefinition inflammation of salivary
glands
Etiology viral most common (mumps) bacterial causes: S. aureus,
S. pneumoniae, H. influenzae obstructive vs. non-obstructive
obstructive infection involves salivary stasis and bacterial
retrograde flow
Predisposing FactorsoHIV anorexialbulimia Sjogren's syndrome
Cushing's, hypothyroidism, DM hepatic/renal failure meds that
increase stasis: diuretics, TCAs, beta-blockers, anticholinergics,
antibiotics sialolithiasis (can cause chronic sialadenitis)
Toronto Notes 2011
Salivary Glands
Otolaryngology OT31
Clinical Features acute onset of pain and edema of parotid or
submandibular gland that may lead to marked swelling fever
leukocytosis suppurative drainage from punctum of the gland
Investigations U/S imaging to differentiate obstructive vs.
non-obstructive sialadenitis Treatment bacterial: treat with
cloxacillin abscess drainage viral: no treatment
...
,bilateral
pmid Bllillrgemllllt, &BIIIorinauralhearing loss,
orchitis.
Mumps ulllllly pmllll1s
SialolithiasisDefinition ductal stone (mainly hydroxyapatite)
leading to chronic sialadenitis 80% in submandibular gland, F): 10%
cysts, lymph nodes and adenomas: 10% oncocytoma: 40% (surgery with
radilltionl Control rate ear1y lesions >90% (rediationl 10 to
12% Ill small lesions fail radiotherapy
CTJMRI
Fine n811dle aspirate
Surgery:Benign and malignant Lymph node sampling Postop
radiotherapy Cherne if unresectabla
CT
Pll'utid 10-yearsurvival 85, 69, 43, and 14% for stages Ito IV
Submandibular 2 yell': 82%, 5year: 69% Minor salivary glilld 10
year: 83, 52. 25, 23% for stages I to IVRewrrances occur within
5yean; Need Vu: clinical exam, thyroglobulin
ThyroidThyroid mass, ciiiVical nodes Vocal card paralysis
Hypeuhypothyroidism Dyspha(ja
U/S
FNA
1 surgary 1131 for metastatic deposits port-op TSH
suppression
Plnrthyraid lncreBSed serum Ca
Neck mas&Bone disease, renal disease Pllncreatitis
Wide surgical excision Port-op monitoring of serum Ca
Rewrrence rates: 1-year 27% 5-year82% 1G-year91% Mean survival:
6to 7 yell'S
Toronto Notes 2011
Neoplasms of the Head and Neck
Otolaryngology OT37
Thyroid CarcinomaTabla 18. Cytology results of FNA Samples
.....
CateuaiYNan-diagnostic Benign
CharacterilliclMacrofollicular or colloid adanomas. chronic
autoimmune {Hashimota'l thyroiditis Microfollicular or cBiular
naophtsm
,
SU5piciau& or indetllrminateMalignant
Typea Clf Thyroid Clncllr (from most CO!Mion 1o least common)
Papillary Follicular
MedullaryAnaplllslic
Lymphoma Plpilluy Follicular1(1'1(,
Tabla 19. Thyroid Carcinoma Medullary 3ta5% {1 0% familial 90%
sporadicI
AniiPiaticZta5%
Lymphoma 10'J. il 6-
" CHOP =cydophosphlnidt, lldrilrTtcin, vil"ll:ri5tine,
P'Cini50118
Approach to Thyroid Nodule Recommendation A: all patients with
thyroid nodules require evaluation of serum TSH and ultrasound any
nodule >5 mm. with suspicious sonographic features (hypoechoic.
microcalcifications, increased nodular vascularity, infiltrative
margins, height > width on transverse view) should undergoFNA
when performing repeat FNA on initially non -diagnostic nodules,
US-guided FNA should be employed Recommendation B: nonpalpable,
mostly cystic. or posteriorly located nodules should undergo
US-guided FNA as the initial evaluative procedureTabla 20.
Management of the Thyroid Nodule Radioiodine tharapy Chemotherapy
and I or radiotherapy Surgical excision Hyperthyroid suspicious
solid mass. that is HOT on thyroid SCM
,...----------------. ,t-----------------,
A minimum of hamilllyroidectomy is required to confirm captldar
invasion for diagnosing fallic._.ll" or Hiirlhla cllll CA.
......
,
ln.uc.ti- for pollt-op
iodine ua.tian-1 111
Adjuvant lhnpymortality RAIIharapy -1nat parsistant
cancer......
,t-----------------, ,
Anaplastic CA or thyroid lymphoma Recument cyst that is
"suspicious an FNA or if patient is extremely anxious Malignancy
othll" than anaplastic CA or thyroid lymphoma Solid "tuspicious
mass that is "cold" on thyroid acan (excise to r/o capsular
invasionI Hyperthyroid suspicious solid mass, that is HOT on
thyroid scan (hyperfunctioninglCD111J1011ents:
riskol111111ill1Wicvsameashold
RAI ablation should be offar11d to patienlll with distant
metastases (Mil. gross axtrathyroidal axtansion, primary size >4
em 11!Q8rdless of patient age (Evidence Grade 8 and above).
COO!* DS. et Ill. Reviled Amllican ThyroklAsiOCiltion Mlnlgsment
Nalllr,foid No!Ues d llillmrtillld lbynJid C.CIIt 1I( I 1):1
167-214.
'IW lildings: cystic: riltofm-ncy 3 months (OME)
....
,,
lack of response to >3 months of antibiotic therapy (OME)
persistent effusion for months after episode of AOM (OME) recurrent
episodes of AOM (>7 episodes in 6 months) bilateral conductive
hearing loss of>20 dB (OME) chronic retraction of the tympanic
membrane or pars fl.accida (OME) bilateral OME lasting >4 to 6
mas craniofacial anomalies predisposing to middle ear infections
(e.g. cleft palate) (OME) complications of AOM (see below) WJ.
CaytB PC. Crald'vnl R. Ale he CV. Friacllerg J. W. Otuluyngolouim'
pii!Csptilmi of lila inliclliCII& for tymplliOIIDmyU!e
inlarlilll in chidran.21XXJ Mil\' 2. tubaL In: 200IJ dinicll
inllin!otsAlilxlldi1 (VAl: Amarican Acadamy rA
,....EaJiy
Complicno Gf TymJ1811.-Iomy
..... Myringosclerosia
Exlrulion Blockage Psrli$hlrll otorrhea Pmistant 1M perforation
Choleslelrtoma
CMAJ. MyringatDmy and
1111d Nd.
1999.
Complications of AOM otologic: TM perforation chronic
suppurative OM
ossicular necrosis cholesteatoma persistent effusion (often
leading to hearing loss)
CNS: meningitis
brain abscess facial nerve paralysis other: mastoiditis
labyrinthitis sigmoid sinus thrombophlebitis
Otitis Madia with Effusion (OME)Definition presence of fluid in
the middle ear without signs or symptoms of ear infection
Epidemiology not exclusively a pediatric disease follows AOM
frequently in children middle ear effusions have been shown to
persist following an episode of AOM for 1 mo in 40% of children, 2
mo in 20% and 3+ mo in 10%
OT40 Otolaryngology Risk Factors sameasAOM
1'oroDio
2011
Clinical Features fullness - blocked ear hearing loss t:!nnitus
confum with audiogram and tympanogram (flat) (see Figure 15B and
Figure 16B) pain, low grade fever o!Dscopy of tympanic membrane:
discolou.ration - amber or dull grey with "'glue'" ear meniscus
fluid level behind TM air bubbles retraction pocket&ITM
atelectasis most reliable 1indlng with pneumotoscopy Is Immobility
Treatment expectant - 9096 resolve by 3 months document hearing
lo&a no statistical proof that antihistamine&, antibiotia
clear disease faster surgery: myringotomy ventilation tubes
adenoidectomy (ifenlarged) ventilation tubes to equalize pressure
and drain ear
Complications of Otitis Media with Effusion (OME) hearing loss,
speech delay, learning problems in young children chronic
mastoiditis cholesteatoma espedally when retraction pockets involve
pars flacdda or postero-superior TM retraction of tympanic
membrane, atelectasis, oasicular fixation oasicular erosion
Adenoid Hypertrophy s1ze peaks at age 5 and resolves by 12 yean
of age increase in size with repeated URTI and
allergiesPharyngeai11Jnsl lllllinlid)
- '".;_, t JrI
ln......,...
Clinical Features nasal obstruction: adenoid facies (open mouth,
flat midface, dark circles under eya;) history ofhypernasal voice
and snoring long term mouth breather: minimal air escape through
noseTWa! 1111111 (x2)
IDnsil (x2)dGIIIP..,..lhllr ,....,.. ..
Flllhllile
lllhar....
...
2
choanal obstruction: chronic sinusitis/rhinitis obstructive
sleep apnea chronic lnfl.ammatlon: nasal discharge, post-nasal
drip, and cough
cervicallymphadenopathy
Liraual111nsl
:::>
polllltll' 1/3 of to..,a
..... 0
Figure 2D. Wllldeyer's Ring An iiDnujDd cirde of protective
lyqftoid 1issua attha uppar !lids af1ha 1811JiRIIDry and
_.inantllly traclll
Diagnosis enlarged adenoids on direct/indirect nasopharyngeal
exam enlarged adenoid shadow on lateral soft tissue x-ray lateral
view of the nasopharynx may show a large pad ofadenoidal tissue
Complications eustachian tube obstruction leading to serous otitis
media interference with l1ll58l breathing, nece!lllitating
mouth-breathing malocclWiion
sleep apnea/respiratory disturbance orofadal developmental
abnormalities
Indications for Adenoidectomy chronic upper airway obstruction
with sleep distu.rbencelapnea cor pulmonale chronic nasopharyngitis
resistant to medical treatment chronic serous otitis media and
chronic suppurative otitis media (after 2-3 sets oftubea) recurrent
acute otitis media resistant to antibiotics suspicion of
nasopharyngeal malignancy persistent rhinorrhea
Toronto Notes 2011
Pediatric Otolaryngology
Otolaryngology OT41
Contraindications for Adenoidectomy bleeding disorders recent
pharyngeal infection short or abnonnal palate (cleft or false
palate, zona pellucldum) Complications of Adenoidectomy bleeding,
infection velopharyngeal insufficiency with speech defect nasal
regurgitation scarring of Eustachian tube orifice
Sleep-Disordered Breathing in ChildrenDefinition comprises of a
spectrum of sleep-related breathing abnormalities ranging from
snoring to obstructive sleep apnea (OSA) Epidemiology peak
incidence between 2 and 8 years when tonsils and adenoids are the
largest relative to the pharyngeal airway Etiology due to a
combination of anatomic and neuromuscular factors: adenotonsillar
hypertrophy craniofacial abnormalities neuromuscular hypotonia
(i.e. cerebral palsy, Down syndrome) obesity Clinical Features
heavy snoring, mouth breathing, pauses or apnea. enuresis,
excessive daytime sleepiness, behaviouralJleaming problems, morning
headache, failure to thrive Investigations flexible
nasopharyngoscopy for assessment of nasopharynx and adenoids
polysomnography Treatment surgical management 1st line:
adenotonsillectomy nonsurgical: behavioural modification, CPAP
Acute TonsillitisEtiology Group A beta-hemolytic streptococci
and Group G streptococci S. pneumoniae, S. aureus, H. influenzae,
M. catarrhalis Epstein-Barr virus (EBV) Clinical Features..._'
I
Trillnus: motor disturbance of the trigeminal nerve, leading to
spasm of 1hemuse'- of masticlllion, with difliculty in apenilg the
mouth [lockjaw).
symptoms: sore throat dysphagia. odynophagia. trismus malaise,
fever otalgia (referred) signs: tender cervical lymphadenopathy
especially submandibular, jugulodigastric tonsils enlarged,
inflammation exudates/white follicles strawberry tongue,
scarletiniform rash (scarlet fever) palatal petechiae (infectious
mononucleosis) Investigations CBC swab for C&S latex
agglutination tests Monospot -less reliable children