Activate Windows
Go to Settings to activate Windows.
0T1 Otolaryngology Toronto Notes 2023
Head and Neck
Temporal branch
Zygomatic branch
/
Superficial temporal a. Buccal branch
Styloid process
Mastoid process
Stylomastoid foramen
Facial n.lCN VII)
Posterior belly of
digastric nt.
Parotid gland
Mandibular branch
Marginal mandibular
branch
Cervical branch
Maxillary a.
Angular a.
^
/
Lateral nasal a ./ %
Occipital a.
Posterior auricular a.
-
-
Ascendingpharyngeal a,
Superior labial a.
- ;
Internal carobd a.
barotd a.
Inferior labial a.-—-"
-^External
\
— Facial a s
"
y
Lingual a S
Superior thyroid a
- Common carobd a ?:
VI
0
Figure 7. Extratemporal segment of facial nerve
Branches of facial nerve (in order from superior to inferior)
To Zanzibar By Motor Car
Figure 8. Blood supply to the face
Branches of the external carotid artery (in order from inferior to superior)
Some Anatomists Like Freaking Out Poor Medical Students
Post,belly
digastric m.
— Common carotid
a.bifurcation
Sternocleidomastoid m.
Ant. belly
digastric m.
—'
Hyoid bone /
Sternohyoid m.'
Omohyoid m.
Anterior Triangle
•submental triangle
Posterior Triangle
occipital triangle *
(
•
or
submandibular
digastric) triangle
—
•carotid triangle -
•muscular triangle
Posterior triangle
Trapezius m
subclavian triangle *
Anterior triangle **
'
Lisa Qlu 2019. altor
Hyoid bone
•Thyrohyoid membrane External
carotid a *
Thyroid cartilage
Common
carotid a.
Internal
bifurcation
— jugularv.
Ant. belly
omohyoid m."
|i\ W
1)l
Median cricothyroid
ligament '
•
|
Si Sternocleidomastoid m.
Greater auricular n.
Lesser occipital n.
^
Ventral ramus (C2)
Ventral ramus IC3)
Accessory n.(CN XI)
Ventral ramus (C5)
Anterior scalene m.
Phrenic n.
V r Digastric m.
Hypoqlossal n.
(CN XII)
Superior root
ansa cervicalis
Inferior root /
ansa cervicalis /
*
1 / Sternocleidomastoid m.
!/
I
- km
Cricoid cartilage r T
Post, belly ,
omohyoidm.
L J
Thyroid gland Vagus n.
Sternohyoid m. Brachial plexus
Trache. Clavicle
© Kateryna Procunier 2014.after ©’J-'
W*
-
15
y
© Inessa Stanishevskaya 2012 after Subclavian
a. and v.
Figure 9. Anatomy of the neck
Activate Windows
Go to Settings to activate Windows.
0T5 Otolaryngology Toronto Notes 2023
Anatomical Triangles of the Neck Paired Parasympathetic Ganglia of the
Head and Neck
• Ciliary (supplied by CN III):pupillary
constriction
• Pterygopalatine (supplied by CN
VII):lacrimal gland,nasal mucosa
• Submandibular (supplied by CN
VII): submandibular, sublingual
glands
• Otic (supplied by CN IX):parotid
gland
Anterior triangle
• bound by anterior border of SCM, midline of neck, and lower border of mandible
• divided into:
.submental triangle: bound by both anterior bellies of the digastric muscles from the mentum to
the hyoid bone
digastric triangle: bounded by anterior and posterior bellies of the digastric muscles and Inferior
border of mandible
carotid triangle: bounded by SCM,anterior belly of the omohyoid muscles, and posterior belly of
digastric muscles
• contains: tail of parotid,submandibular gland, hypoglossal nerve, carotid bifurcation, and
lymph nodes
Posterior triangle
• bound by posterior border of the SCM, anterior border of trapezius, and middle third of clavicle
• divided into:
occipital triangle:superior to posterior belly of the omohyoid
subclavian triangle:inferior to posterior belly of omohyoid
• contains:spinal accessory nerve and lymph nodes
Functions of the Facial Nerve
“Ears. Tears, Face, Taste"
Ears: stapedius muscle, sensory around
concha of auricle,EAC. and TM
Tears:lacrimation (lacrimal gland)
and salivation (submandibular and
sublingual glands)
Face:muscles of facial expression
Taste: sensory anterior AS of tongue
Table1Lymphatic Drainage of Nodal Groups and Anatomical Triangles of the Neck (via chorda tympani)
Nodal Group/Level Location Drainage
1.Suboccipital (S)
2. Rclroauricular (R)
Base of skull,posterior
Superficial to mastoid process
Posterior scalp
Scalp,temporalregion, external auditory
meatus,posterior pinna
External auditory meatus, anterior pinna,soft
tissue ol frontal and temporal regions,root ol
nose,eyelids,palpebral conjunctiva
Lymphadenopathy
• Left-sided enlargement of a
supraclavicular node (Virchow's
node) may indicate an abdominal
malignancy or malignancy below the
clavicle
• Right-sided enlargement may
indicate malignancy of the
mediastinum, lungs,or esophagus
• Occipital and/or posterior auricular
node enlargement may indicate
rubella
3.Parotid-proauricular (P) Anterior to car
4.Submental(Level 1A) Anterior bellies (midline) of digastric muscles. Floor of mouth,anterior tongue,anterior
mandibular alveolar ridge,lower lip
Anterior belly of digastric muscles,stylohyoid Oral cavity,anterior nasal cavity,soft tissues
muscle,body of mandible
Skull base to inferior border of hyoid bone
along SCM muscle
Inferior border of hyoid bone to inferior border Oral cavity,naso/oro,
'
hypopharynx.larynx
of cricoid cartilage along SCM muscle
Inferior border of cricoid cartilage to clavicle
along SCM muscle
Posterior border of SCM, anterior border of
trapezius,from skull base to clavicle
Hyoid bone (midline) to suprasternal notch
betvreen the common carotid arteries
tip of mandible,and hyoid bone
S. Submandibular (levelI8)
ol the mid- face,submandibular gland
6.Upper jugular (levels IIA and MB) Oral cavity,nasal cavrty.naso/orof
hypopharynx.larynx,parotid glands
7. Middle jugular (LevelIII)
8. Lower jugular*(Level IV) Hypopharynx.thyroid,cervical esophagus,
larynx
Nasopharynx and oropharynx. cutaneous
structures of the posterior scalp and neck
Thyroid gland,glottic,and subglottic larynx,
apex of piriform sinus,cervical esophagus
4 Strap Muscles of the Neck
• Thyrohyoid
• Omohyoid
• Sternohyoid
• Sternothyroid
9.Posterior triangle"(levels VA and VB)
10. Anterior compartment"* (Level VI)
'Virchow's node:left lower jugular [levelIV) supraclavicular node
"Includes some supraclavicular nodes
'"Includes prclrachcal.precrlcold.paratracheal.and perllhyroldal nodus
- Superior thyroid artury
- Common carotid artery
- Internal lugularvem
- Inlenorthyrord artery
- Right recurrent laryngeal nBrve
- Thyroid cartilage
- Cricoid cartilage
- Supurior parathyroid gland
- Thyroid gland
- Inferior parathyroid gland
VNICNXI - Vagus nerve ICN XI
IAIN - Lett recurrent laryngeal nerve
*Thyroidea ima artery present m 3% af population,
arises from aortic arch or innominate anery +
Figure 10. Anatomy of the thyroid
gland
Activate Windows
Go to Settings to activate Windows.
0T6Otolaryngology Toronto Notes 2023
Differential Diagnoses of Common
Presentation
Dizziness
( Dizziness ) True nystagmus and vertigo caused
by a peripheral lesion usually do not
last longer than a few wk,due to
compensation from the cerebellum
(unless there is a history of cerebellar
ischemiafstroke). Central lesions do not
compensate,therefore nystagmus and
vertigo will persist
[ True Vertigo J Non-Vortiginous )
T
( Peripheral (Vestibular) J ( Central ] ( Organic Diseases ] [ Functional ]
v jr
Cardiac
Arrhythmias
Aortic stenosis
Vasovagal
Orthostatic hypotension
Anemia
Peripheral neuropathy
Visual impairment
Cerebrovascular disorders
Vertebrobasilar insufficiency
Transient ischemic attacks
Wallenberg syndrome
Cerebellar infarction
Migrainous vertigo
Multiple sclerosis
Inflammation
Meningitis
Cerebellar abscess
Trauma:cerebellar contusion
Toxic:alcohol,hypnotics,drngs
Tumours
CPA tumours
Posterior fossa tumours
Glomus tumours
Depression
Anxiety
Panic disorder
(hypeiventilabon)
Personality disorder
Phobic dizziness
Benign paroxysmal positional
vertigo (BPPV)
Labyrinthitis
Meniere's disease
Vestibular neuronitis
Autoimmune inner ear disease
Cholesteatoma
Ototoxic drug exposure
Perilymph fistula
Recurrent vesbbulopathy
Superior semicircular canal dehiscence
Temporal bone fracture
Findings Suggestive of Central Vertigo
Acute onset and continuous
Normal head impulse test
Multidirectional nystagmus
Skew deviation present
5 Ds of Vertebrobasilar Insufficiency
Drop attacks
Diplopia
Dysarthria
Dizziness
Dysphagia
Common causes inbold
Figure 11. Differential diagnosis of dizziness
Otalgia
Otalgia -Referred Pain
Sensory innervation to the ear is
supplied by CN V,VII.IX and X resulting
in many sources of referred pain that can
cause otalgia
( Otalgia )
’
r
'
r
f
External Ear Middle/Inner Ear j
f
Referred Pain ]
The 10 Ts of Referred Pain which Cause
Otalgia
Teeth:Impacted wisdom teeth,caries,
infant teething
TMD: Temporomandibular Joint Disease
Tubal Area:Eustachian tube dysfunction,
nasopharynx (area behind the nose (rule
out tumour)
Tonsils:Infections,tumours
Throat: Infections,tumours of pharynx,
larynx (voice box)
Tongue:inflammation,tumour
Trachea:(windpipe).Larynx (voice box)
Thyroid Gland:infections,tumours
Tempora Arteritis:inflammation of the
artery above the ear
Trauma
Infection
Auricular cellulitis
External canal abscess
HSV/zoster
Infection
AOM
Mastoiditis
Myringitis
OME '
Skull base infections
Trauma
Barotrauma
Traumatic perforation
Other
Cholesteatoma
Neoplasm
Infection
Ramsay Hunt syndrome
Tonsillitis
Tracheitis
Trauma
Cervical arthritis
Thyroiditis
Trigeminal neuralgia
Dental disease
Sinusitis
Other
Glossopharyngeal neuralgia
Neoplasm of oral cavity,
larynx,pharynx
TMJ syndrome
Trismus
OE
Perichondritis
Trauma
Burns
Frostbite
Hematoma
Lacerations
Other
Cerumen impaction
Foreign body
Neoplasm ol external canal
GPA
Figure 12. Differential diagnosis of otalgia
r T
L J
+
Activate Windows
Go to Settings to activate Windows,
0T7 Otolaryngology Toronto Notes 21)23
Hearing Loss
[ Hearing Loss ]
T 1
(Conductive J (Sensorineural J
T I
( External Ear j ( Middle Ear ] ( Congenital ) ( Acquired J
. '
T
'
Impacted cerumen
Otitis externa
Foreign body
Keratosis obturans
Exostoses,osteomas
Tumour of canal
Congenital stenosis/microtia
Presbycusis
Noise-induced
Meniere'
s disease
Labyrinthitis
Idiopathic sudden SNHL
Autoimmune inner ear disease
Ototoxic drug exposure
Temporal bone trauma
Infectious
Postmeningitis
Syphilis
Viral:mumps,CMV,HSV
Neoplastic
Acoustic neuroma
CPA tumours
Vascular occlusion/emboli
Auditory neuropathy
Genetic
Non-syndrome associated
Syndrome associated
Intrauterine infections
le.g. TORCH!
Teratogens
Perinatal hypoxia
Prematurity/low birth weight
Hyperbilirubinemia
OME
TM perforation
Otosclerosis
Tympanosclerosis
Eustachian tube dysfunction
Cholesteatoma
Ossicular malformations
Ossicular discontinuity
Hemotympanum
Middle ear tumour
Congenital stenosis/microtia
Common causes inbold
Figure 13. Differential diagnosis of hearing loss
Tinnitus
f Tinnitus J
Tinnitus is most commonly associated
with SNHL
j 1
Subjective
Only heard by patient (common)
Objective
Can be heard by others (rare)
Glomus Tympanicum/Jugulare Tumour
Signs and Symptoms
• Pulsatile tinnitus
• HL
• Blue mass behind TM
• Brown's sign (blanching of the TM
with pneumatic otoscopy)
T
Otologic
Presbycusis
Noise-induced HL
OME
Meniere's disease
Otosclerosis
Cerumen
Foreign body against TM
Drugs
ASA
NSAIDs
Aminoglycosides
Antihypertensives
Heavy metals
Metabolic
Hyper/hypothyroidism
Hyperlipidemia
Vitamin A,B,Zinc deficiency
Neurologic
Head trauma
Vascular
Benign intracranial hypertension
Arteriovenous malformation
Glomus tympanicum
Glomus jugulare
Arterial bruits:
High-riding carotid artery
Vascular loop
Persistent stapedial artery
Carotid stenosis
Venous hum:
High jugular bulb
HTN
Hyper/hypothyroidism
Mechanical
Patulous Eustachian tube
Palatal myoclonus
Stapedius muscle spasm
MS
CPA tumours
Psychiatric
Anxiety
Depression
Common causes inbold
r“i
Figure 14. Differential diagnosis of tinnitus L J
+
Activate Windows
Go to Settings to activate Windows.
0T8 Otolaryngology Toronto Notes 2023
Nasal Obstruction
Table 2. Differential Diagnosis of Nasal Obstruction
Acquired Congenital
Nasal Cavity Pyriform aperture stenosis
Choanal atresia
Rhinitis
Acute/chronic
Vasomotor
Allergic
Rhinosinusitis
Foreign bodies
Enlarged turbinates
tumour
Benign:polyps,inverting papilloma (can
become malignant)
Malignant
Dermoid cyst
Encephalocele
Glioma
see
Eslhesioneuroblastoma (olfactory
neuroblastoma)
Adenocarcinoma
Septal deviation
Septal dislocation
Septal hematoma/abscess
Adenoid hypertrophy
tumour
Benign:juvenile nasopharyngeal angiofibroma
(JHA).polyps
Malignant:nasopharyngeal carcinoma
GPA.diabetes,vasculitis
Nasal Septum Septal deviation
Septal dislocation
Septal hematoma/abscess
Nasopharynx
Systemic
Hoarseness
Table 3. Differential Diagnosis of Hoarseness
Infectious Acute/chronic laryngitis
LaryngDtracheobronchitis (croup)
GERD
Vocal cord polyps/nodules
lifestyle:smoking,chronic alcohol use
External laryngeal trauma
Endoscopy and endotracheal lube (c.g.intubation granuloma)
Benign tumour
Papillomas|HPVinfection)
Minor salivary gland tumours
Other
Retention cysts
Endocrine
Hypothyroidism
Vrriliialion
Central lesions
Lung malignancy is the most common
cause of extralaryngeal vocal cord
paralysis Inflammatory
traumatic
Neoplastic Malignant tumours (e.g.thyroid)
sec
Other
Cysts
Systemic Connective tissue disease
RA
SIE
Neurologic (vocal cord
paralysisdue to superiors
recurrent laryngeal nerve
injury)
Iatrogenic injury:thyroid,parathyroid surgery,carotid
endarterectomy,patent ductus arteriosus(PDA) ligation
Bilateral
Iatrogenic injury:bilateral thyroidsurgery,forceps
delivery
Neuromuscular
Myasthenia gravis
CVA
Head injury
I!
Skull base tumours
Arnold-Chiari malformation
Peripheral lesions
Unilateral
lung malignancy
Psychogenic aphonia (hysterical aphonia)
laryngomalacia
laryngeal web
laryngeal atresia
P t
Functional
Congenital
L J
+
Activate Windows
AL GRAWANY Go to Settings to activate Windows.
OTy Otolaryngology Toronto Notes 2023
Neck Mass
( Neck Mass J
*
\
’ 4
f Congenital J f Inflammatory/lnfectioiis J
f Neoplastic J
£ I I
( Lateral J ( Malignant ^
Midline f Benign J
4 4 4
Reactive lymphadenopathy Thyroglossal duct cyst Branchial cleft cyst
TB or atypical mycobacteria Thyroid tumour/goitre Cystic hygroma
Infectious mononucleosis Pyramidal lobe — Abscesses ol thyroid gland
Cat scratch fever Ranula
Sarcoidosis
Kawasaki disease
Salivary gland neoplasm
Lipoma
Fibroma
Vascular
T
j
Lymphoma
Thyroid
Sarcoma
Salivary gland neoplasm
Rhabdomyosarcoma
Neuroblastoma
Head and neckprimaiy
Infraclavicular primary
Leukemia
HIV
Figure 15. Differential diagnosis of a neck mass
Hearing
Normal Hearing Physiology
• conductive pathway (EAC to cochlea): AC ofsound down the EAC -> vibration of TM -> sequential
vibration of middle ear ossicles (malleus, incus,stapes) > transmission of amplified vibrationsfrom
stapes footplate to the oval window of the cochlea > vibrations transmitted via cochlear lluid create
movement along the basilar membrane within the cochlea
• neural pathway (nerve to brain):basilar membrane vibration stimulates overlying hair cells in the
organ of Corti-> stimulation of bipolar neurons in the spiral ganglion of the cochlear division of CN
VIII propagates the signal through > cochlear nucleus -> superior olivary nucleus -> lateral lemniscus
> inferior colliculus > Sylvian fissure of temporal lobe
Order of the Neural Pathway (with
Corresponding Waves on ABR)
ECOLI
Eighth cranial nerve (I-II)
Cochlear nucleus (III)
Superior Olivary nucleus
Lateral lemniscus (IV - V)
Inferior colliculus
Types of Hearing Loss
1. Conductive Hearing Loss
• conduction ofsound to the cochlea is impaired
• can be caused by external and middle ear disease
2. Sensorineural Hearing Loss
• defect in the conversion of sound into neuralsignals or in the transmission of those signals to the
cortex
• can be caused by disease of the inner ear (cochlea), acoustic nerve (CN VIII), brainstem, or cortex
3. Mixed Hearing Loss
• combination of CHL and SNHL
Auditory Acuity
• whispercd-voice test: mask one ear and whisper into the other
• tuning fork tests (see Table 4, OTIO; audiogram is of greater utility)
Rinne test
512 Hz tuning fork is struck and held firmly on mastoid process to test BC; the tuning fork is
then placed beside the pinna to test AC
ifAOBC > positive Rinne (normal)
if BC > AC > negative Rinne (abnormal)
• Weber test
512 Hz tuning fork is held on vertex of head and patient states whether it is heard centrally
(Weber negative/does not lateralize) or islateralized 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 HL between ears is >6 dB
Weber
e
test lateralization -ipsilateral
CHL or contralateral SNHL
The Weber test is more sensitive in
detecting CHL than the Rinne test
r T
L J
+
Activate Windows
Go to Settings to activate Windows.
OTIO Otolaryngology Toronto Notes 2023
Table 4. The Interpretation of Tuning Fork Tests
Examples Weber Rinne
Normal or bilateral SNHL
Right-sided CHL.normal left car
Right-sided SNHl.normal left car
Right-sided severe SNHL or dead right ear, Lateralizes left
normal left ear
Central
lateialnes right
Lateralizes left
ACvBC (*
) bilaterally
SC -AC (-)right
AOBC I*
) bilaterally
BOACI-) right*
Frequency ol Tuning Minimum Hearing
loss forRinneto
Reverse|BC»AC,
NEGATIVE Rinne) (dB)
Fork (Hz)
256 15
512 30
'A vibrating tuningIoik onlilt.
- mastoid stimulates the cochlea bilaterally,then-lore,In thiscase,the left cochlea Is stimulated by the Rinne test on
the light (eg.a false negative test),these tests are not valid it theear canals are obstructed with cerumen (eg.will cieate conductive loss)
1024 45
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 at frequencies of 250,500, 1000, 2000, 4000, and 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
Range of Frequencies Audible to
Human Ear
• 20 to 20000 Hz
• Most sensitive frequencies:1000 to
4000 Hz
• Range of human speech:500 to
Degree of Hearing Loss 2000 Hz
•determined on basis of the pure tone average (PTA) at 500, 1000, and 2000 Hz
FREQUENCY (Hzl
Audiogram Legend 250 500 1000 2000 4000 8000
for a Left Ear
x - AC Unmasked
> v BC Unmasked
- AC Masked
) = BC Masked
250 500 1000 2000 4000 8000
- 10 10
0 0 HL occurs most often at higher
frequencies. Noise-induced
(occupational) HL is classically seen
at 4000 Hz (Boilermak er's notch).Ht
associated with otosclerosis is seen at
2000 Hz (Carhart’s notch)
10 <10
20 20
30 m 30
40 §
50 2
«
TO
|
§
W 5
90 Z>
40
50
60
70
60
90
M
10
20
A. Normal Audiogram B. Conductive Hearing
Loss (Otitis Motlia)
250 500 1000 2000 4000 6000
10
- 0
250 500 1000 2000 4000 6000 250 500 1030 2000 4000 6003
10 10
0 0
+
2 10 •
20
10 10
20 20
/
30 30 30
* 40 4,1 — 40
50 50 50
60 60 . 60
70 70 70
80 > SO
90 .
too
no .
120 -
60
90
100 100
110 110
120 120 C. Conductive Hearing
Loss (Otosclerosis)
E. Sensorineural
Hearing Loss
(Presbycusis)
D. Sensorineural
Hearing Loss
(Noise Induced)
Figure 16. Types of hearing loss and associated audiograms of a left ear
PURE TONE PATTERNS
1. Conductive Hearing Loss (see Figures 16B and 16C)
• BC in normal range
• AC outside of normal range
• gap between AC and BC thresholds >10 dB (an air-bone gap)
2. Sensorineural Hearing Loss (see Figures 16D and 16E)
• 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)
r T
L J
+
Activate Windows
Go to Settings to activate Windows.
0T11 Otolaryngology Toronto Notes 2023
Speech Audiometry
Speech Reception Threshold
• lowest hearing level at which patient is able to repeat 50% of two syllable words which have equal
emphasis on each syllable (spondee words)
• speech reception threshold (SRT) and best pure tone threshold in the 500 to 2000 Hz range (frequency
range of human speech) usually agree within 5 dB; if not,suspect a retrocochlear lesion or functional
HL
• used to assess the reliability of the pure tone audiometry
Speech Discrimination Test
• percentage of words the patient correctly repeats from a list of 50 monosyllabic words
• tested at 40 dB above the patients SRT, therefore degree of HL is taken into account
• patients with normal hearing or CHL score >90%
• rollover effect: a decrease in discrimination assound intensity increases; typical of a retrocochlear
lesion (c.g. acoustic neuroma )
• investigate further ifscores differ more than 20% between ears, as asymmetry may indicate a
retrocochlear lesion
• best predictor of hearing aid response:a poor discrimination score indicatessignificant neural
degeneration and hearing aids may not be the best option for the patient
Impedance Audiometry
Tympanogram
• the Eustachian tube equalizesthe pressure between the external and middle ear
• tympanograms graph the compliance of the middle ear system against a pressure gradient ranging
from -400 to +200 mmH 20
• 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 mmHiO
( High
Type A Type B
s
Jl
Low
0 D - 0 -
Air Pressure
• Normal pressure peakatOmmHO
• Note: with otosclerosis,peak is still at
0 mmH ,0 but has a lower amplitude
• Note: with ossicular chain discontinuity,
peak is still at 0 mmHi0 buthas a
higher amplitude
Air Pressure
* No pressure peak
• Poor TM mobility indicative of
MEE or perforated TM
Air Pressure
• Negative pressure peak
•Indicative ol Eustachian tube dysfunction
or early stage otitis media without effusion
Figure 17. Tympanograms
Static Compliance
• volume measurement reflecting overall stiffness of the middle ear system
• normal range: 0.3-1.6 cc
• negative middle ear pressure and abnormal compliance indicate middle ear pathology
• in a type B curve, ear canal volumes of >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 in response to loud sound
• acoustic reflex threshold = 70-100 dBgreater than hearing threshold; if hearing threshold >85 dB,
reflex likely absent
stimulating either ear causes bilateral and symmetrical reflexes
for reflex to be present, CN VII must be intact with no CHL in monitored ear
• if reflex is absent without CHL or severe SNHL,suspect CN VII 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 HL, acoustic reflex thresholds are 25-60 dB
• with retrocochlear HL (acoustic neuroma), absent acoustic reflexes or marked reflex decay (>50%)
within 5s
r-»
u
+
Activate Windows
Go to Settings to activate Windows.
0T12 Otolaryngology Toronto Notes 2023
Auditory Brainstem Response
• measures neuroelectric potentials (waves) in response to a stimulus in live dilTerent anatomic sites (see
Order of the Neural Pathway sidebar,OT9; thistest can be used to determine the site of lesion)
• delay in brainstem response suggests cochlear or retrocochlear abnormalities
• does not require volition or co-operation of patient (therefore, value retained in children and
malingerers)
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
• signals come from outer hair cells which are a proxy for the inner hair cells which facilitate hearing
• often used in newborn screening
• can be used to uncover normal nearing in malingering patients
• absence of emissions can be due to HL, fluid in the middle ear, or narrow EACs
Prelingual deafness:deafness
occurring before speech and language
are acquired
Postlingual deafness:dealness
occurring after speech and language
are acquired
Aural Rehabilitation
• dependent on degree of H L, communicative requirements, motivation, expectations, and physical and
mental abilities
• negative prognostic factors
• poor speech discrimination
narrow dynamic range (recruitment)
• unrealistic expectations
• types of hearing aids
• BTE:behind-the-ear (with occlusive mould or open fit which allows natural sound to pass -for
lesssevere hearing loss)
1TE:in-the-ear, placed in concha
ITC: in-the-canal, placed entirely in ear canal
• C1C: contained-in-canal. placed deeply in ear canal
BAHA: bone-anchored hearing aid: attached to skull (bone conduction)
• CKOS: contralateral routing ofsignals
• assistive listeningdevices
direct/indirect audio output
infrared, EM 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 SNHL refractory to conventional hearing aids
• established indication: postlingually deafened adults, pre and postlingually deaf children
Prelingually deaf Infants are the best
candidatesfor aural rehabilitation
because they have maximal benefit from
ongoing developmental plasticity
BAHAs function based on bone
conduction and arc indicated primarily
for patients with CHI. unilateral
HL.and mired HL who cannot wear
conventional hearing aids.BAHAs
consist of an osseointegrated titanium
implant an external abutment and a
sound processor.The sound processor
transmits vibrations through the external
abutment to the titanium implant and
then directly to the cochlea
Vertigo
Evaluation of the Dizzy Patient
• vertigo: illusion of rotational, linear, or tilting movement of self or environment
produced by peripheral (inner ear) or central (brainstem-cerebellum) stimulation
important to distinguish vertigo from other potential causes of “dizziness" (see Pigure 11,OT6 )
Table 5. Peripheral vs. Central Vertigo
Symptoms Peripheral Central
Imbalance
Nausea and Vomiting
Auditory Symptoms
Neurologic Symptoms
Compensation
Nystagmus
Moderate-severe
Severe
Common
Mild-moderate
Variable
Rare
Rare Common
Rapid
Unidirectional
Horizontal or rotatory
Slow r -t
Bidirectional
Horltonlalor vertical
+
Activate Windows
Go to Settings to activate Windows.
0T13 Otolaryngology Toronto Notes 2023
Table 6. HINTS (Head Impulse-Nystagmus-Test of Skew) Exam
Test Central Peripheral (Vestibular Neuritis) (Infarct)
Sattade present
Nystagmus dominantly vertical,torsional or Unidirectional,horizontal nystagmus
gaze-evoked directional
Abnormal
Head Impulse
Nystagmus
No saccades
Test of Skew Normal
Table 7. Differential Diagnosis of Vertigo Based on History
Condition Time Course Hearing loss Tinnitus Aural Fullness Other Features
Benign Paroxysmal Seconds,recurrent
Positional Vertigo
(BPPV)
Menitre's Disease Mm to h,episodic Unifbilaleral.
fluctuating
Unilateral
Onsetwithchange in
position
Prcssurc/watmlh
Labyrinthitis/
Vestibular Neuronitis
H tod t Whistling May have recent AOM
Acoustic Neuroma Chronic Progressive Ataxia
CN VII palsy
Suspect if vascular
risk factors
Brainstem/
cerebellar infarct
Prolonged
Benign Paroxysmal Positional Vertigo
Definition
• acute attacks of transient rotatory vertigo lasting less than I min, initiated hv certain head positions,
accompanied by torsional (i.e. rotatory) nystagmus (geotropic = fast phase towards the floor)
• most common form of positional vertigo (50% of patients with peripheral vestibular dysfunction have
BPPV)
BPPV is the most common cause of
episodic vertigo: patients are often
symptomatic when rolling over in bed
or moving their head to a position of
extreme posterior extension (such as
looking up at a tall building or getting
their hair washed at the hairdresser)
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
caused by: head injury', viral infection (URT1), 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 (time course, provoking factors, associative symptoms)
• positive Dix-Hallpike maneuver (sensitivity 82%,specificity 71%)
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°, and neck extended 20" holding the position for 20 s
• onset of vertigo and rotatory nystagmus indicate a positive test for the dependent side
• other diagnostic testing is not indicated in posterior canal BPPV
Signs of BPPV Seen with Dix-Hallpike
Maneuver
• latency of
-20 s
• Crescendo/decrescendo vertigo
lasting 20 s
• Geotropic rotatory nystagmus
(nystagmus MUST be present for a
positive test)
• Reversal of nystagmus upon sitting
up
• Fatigability with repeated stimulation Treatment
• reassure patient that process resolvesspontaneously
• particle repositioning maneuvers
• Epley maneuver (performed by physician or by patient with the help of devices such as the
DizzyllX"
)
Brandt-Daroff exercises (performed by patient)
• anti-emeticsfor N/V
• posterior semicircular canal occlusion or singular neurectomy for refractory cases
• drugs to suppress the vestibular system delay eventual recovery and are therefore not used
Diagnostic Criteria for Meniere's
Disease
Definite Meniere'
s Disease
• Two or more spontaneous episodes
of vertigo lasting from 20 min to12 h
• Audiometric confirmation of SNHL
(low to mid frequency)
• Fluctuating tinnitus and/or aural
fullness
Probable Meniere'
s Disease
• Two or more spontaneous episodes
of vertigo or dizziness lasting from
20 min to 24 h
• Fluctuating tinnitus and/or aural
fullness
Meniere’s Disease (Endolymphatic Hydrops)
r T
LJ
Definition
• episodic attacks of tinnitus, HL, aural fullness, and vertigo lasting min to h
Proposed Etiology
• inadequate absorption of endolymph leads to endolymphatic hydrops (over accumulation) that
distorts the membranous labyrinth
+
Activate Windows
Go to Settingsto activate Windows. |
OTM Otolaryngology Toronto Notes 2023
Epidemiology
• peak incidence 40-60 yr
• bilateral in 35% of cases
Clinical Features
• episodic vertigo,fluctuating low frequency SNHL, tinnitus, and aural fullness, ± drop attacks
(Tumarkin crisis), ± N/V
• vertigo disappears with time (min to h), but HL remains
• early in the disease:fluctuating SNHL
• laterstages:persistent tinnitus and progressive HL
• attacks come in clusters and can be debilitating to the patient
• triggers: high salt intake, caffeine,stress, nicotine, and alcohol
Treatment
• acute management may consist of bed rest, antiemetics, antivertiginous drugs (e.g. betahistine (Sere*),
meclizine, diphenhydramine), and anticholinergics(e.g.scopolamine)
• long-term management may include
medical
low salt diet, diuretics (e.g. hydrochlorothiazide, triamterene, amiloride)
Sere’prophylactically to decrease intensity of attacks
« inlratympanic gentamicin to destroy vestibular end-organ, results in complete SNHL
intratympanic glucocorticoids (e.g. dexamethasone) may improve vertigo symptoms
surgical
selective vestibular neurectomy or laby rinthectomy
potential benefit for endolymphatic sac decompression orsacculotomy
must monitor opposite ear, 35% of cases are bilateral
Vestibular Neuronitis (Labyrinthitis)
Definition
• acute onset of disabling vertigo often accompanied by N/V and imbalance without HL that resolves
over days, leaving a residual imbalance that lasts d to wk
• vestibular neuronitis: inflammation of the vestibular portion of CN VIII
• labyrinthitis:inflammation of both vestibular and cochlear portions
Etiology
• thought to be due to a viral infection (e.g. measles, mumps, herpes zoster) or post-viralsyndrome
• only ~30% of cases have associated URT'
I symptoms
• labyrinthitis may occur as a complication of acute and chronic otitis media, bacterial meningitis,
cholesteatoma,and temporal bone fractures
Clinical Features
• acute phase
severe vertigo with N/V and imbalance lasting 1-5 d
irritative nystagmus (fast phase towards the offending ear)
ataxia: patient tends to veer towards affected side
tinnitus and HL in labyrinthitis
• convalescent phase
imbalance and motion sicknesslasting d-wk
spontaneous nystagmus away from affected side
gradual vestibular adaptation requires wk-mo
DropAttacks (Tumarkin'
s Otolithic
Crisis) are sudden falls occurring
without warning and without loss
ol consciousness, where patient
experiencesfeeling of being pushed
down into the ground
Treatment
• acute phase
bed rest, antivertiginous drugs
corticosteroids (methylprednisolone) ± antivirals
bacterial infection:treat with IV antibiotics, drainage of middle ear, ± mastoidectomy
• convalescent phase
progressive ambulation, especially in the elderly
vestibular exercises:involve eye and head movements,sitting,standing, and walking
Before proceeding with gentamicin
treatment, perform a gadoliniumenhanced MRI to rule out CPA tumour as
the cause of symptoms
rt
t
_ j
I
No comments:
Post a Comment
اكتب تعليق حول الموضوع