Flashcards

Question
Amplitude of sound
Intensity of sound
Frequencies heard by human ear
Complex sound
Noise
White noise
Narrow band noise
Speech noise
Formula for decibel
0 dB sound pressure level (SPL)
0 dB hearing level (HL)
0 dB sensation level (SL)
Difference between sound pressure
level (SPL), hearing level (HL), and
sensation level (SL)
Difference between 0 dB HL and 0 dB
SPL in normal ear in speech
frequencies
Dimensions of external auditory canal
Decibel levels of common sounds
Answer
Extent of vibratory movement from rest to furthest point from rest in compression/rarefaction
Amount of sound energy through an area per unit time
20 20,000 Hz
Sound of more than one frequency (as opposed to pure tone)
Aperiodic complex sound
Noise containing all frequencies of audible spectrum (20 20,000 Hz)
Noise containing frequencies in a narrow band
Noise containing frequencies of speech spectrum (300 3,000 Hz)
dB=10 log (Io/Ir)
dB=20 log (po/pr)
20 Pa
Lowest intensity of sound perceived by normal ear 50% of the time
Lowest intensity of sound perceived by the patient 50% of the time
SPL is in reference to absolute reference point (20 Pa)
HL is in reference to a normal ear
SL is in reference to patients own ear
Approximately 10 dB
Length = 2.5 cm
Radius = 0.3 cm
Volume = 2 cm3 (?)
Soft whisper = 30 dB
Conversational speech = 60 dB
Pinna is more helpful for what kind of

sounds
Dimensions of middle ear
Mass of ossicles
Speech frequencies
Factors causing impedance matching
in middle ear
Dimensions of tympanic membrane
and oval window
Amplification achieved by middle ear
Bekesys traveling wave theory

Cochlear amplifier
Auditory pathway
Factory = 90 dB
Car horn = 120 dB
Jet plane = 150 dB
High-frequency (as opposed to low-frequency)
Height = 15 mm
Width = 2-4 mm
Depth = 6 mm
Volume = 1-2 cm3
Malleus = incus
Stapes = x malleus or x incus
300 to 3,000 Hz
1. Area effect of tympanic membrane ( x 17)
2. Lever action of ossicular chain ( x 1.3)
3. Natural resonance & efficiency of outer & middle ears
4. Phase difference between oval and round window (4 dB)
Tympanic membrane = 55 mm2 (actual area is 80 mm2, but effective area is 55 mm2)
Oval window (Stapes footplate) = 3.2 mm2
55 / 3.2 = 17
17 x 1.3 = 22
Translates to 25 dB
Sound wave travels through the fluid in the cochlea
Outer hair cells adjust basement membranes physical properties so a given frequency
maximally stimulates a specific narrow group of inner hair cells (which carry most of the afferen
responses of the cochlear nerve)
ECOLI:
Eighth nerve
Cochlear nucleus
Olivary nucleus
Lateral lemniscus
Inferior colliculus
Number of fibers in cochlear nerve

Number of fibers in auditory radiation
from thalamus to cortex
Most useful tuning fork
Negative Rinne test means how much
air-bone gap
Bing test
Schwabach test
Gell test
Test battery for audiological evaluation
Octave frequencies
Inter-octave frequencies
Eighth nerve Cochlear nucleus Trapezoid body Contralateral superior olivary nucleus
Lateral lemniscus Inferior colliculus (midbrain) Medical geniculate body (thalamus)
Cortex
25,000
Millions (contrast with only 25,000 in cochlear nerve).
Number of fibers increases as one travels in the auditory pathway.
512 Hz
256 Hz 15 dB
512 Hz 25 dB
1024 Hz 35 dB
Put tuning fork on mastoid and alternately close and open the external auditory canal.
Positive test: sound alternately increases and decreases; implies normal ear
Negative test: sound remains constant; implies conductive loss
Alternately put tuning fork on mastoid of patient and mastoid of doctor.
Normal Schwabach: sound ends at same time for patient and doctor.
Diminished Schwabach:sensorineural loss in patient
Prolonged Schwabach: conductive loss in patient
Put tuning fork on mastoid and apply pressure on tympanic membrane (by pneumatic otoscop
No change in sound: implies conductive loss.
Decrease in sound: implies normal ear.
1. Pure tone audiometry (air conduction, and if air conduction thresholds are > 10 dB, then bon
conduction)
2. Speech audiometry (speech recognition threshold and word recognition score)
3. Impedance / immitance measures (tympanometry and acoustic reflexes)
250, 500, 1000, 2000, 4000, 8000 Hz
Between octave frequencies, e.g. 375, 750, 1500, 3000, 6000 Hz
Done when >25 dB difference between octave frequency thresholds
Baseline audiogram frequencies to

evaluate noise-induced or druginduced (ototoxic) deafness
Inter-aural attenuation
Normal values of inter-aural
attenuation
Why is masking done?
Audiogram symbols
Shapes of audiogram
Speech reception threshold (SRT)
Spondaic word (a.k.a. spondee)
Primary reason to measure speech
reception threshold
Pure Tone Average
When is speech awareness threshold
(SAT, a.k.a. speech detection
threshold SDT) done?
Word recognition score
How is word recognition score
measured
3000 and 6000 Hz.
Reduction in sound energy from one side of skull to the other

Air conduction: 40-65 dB
Insert earphone: 70 dB
Bone conduction: 0-10 dB
Done to counteract crossover
Unmasked Air: X,
Masked Air: ,
Unmasked Bone: >, <
Masked Bone: ], [
Flat, Rising, Sloping, Falling, Notched, Saucer-shaped
Lowest intensity (in dB) at which patient can repeat 50% of spondaic words
Two-syllable word with equal stress on both syllables (e.g. railroad, sidewalk, eardrum)
To confirm pure tone thresholds.
(SRT should be within 10 dB of PTA.)
The average of pure tone thresholds at 500, 1000, and 2000 Hz.
When speech reception threshold (SRT) cannot be done, e.g. small child, physical or mental
disability, language barrier, etc
Reflects how clearly patient can hear speech.

Patient is given word list of 50 phonetically balanced words (or half-list of 25 words) at 30-40 d
SL with respect to SRT and asked to repeat them. His score is the percentage of words correc
understood.
>90%: normal
75-90%: slight difficulty
60-75%: moderate difficulty
40-60%: poor
Immitance
Tests of immitance
Types of tympanometry curves
At what intensity level does acoustic

reflex (stapedial reflex) occur?
When is stapedial reflex absent?
Difference between hearing impaired
and deaf
Classification of hearing loss in adults
<40%: very poor

Common term for Impedance (energy rejected by middle ear) and Admittance (energy accepte
by middle ear).
Tympanometry
Acoustic reflex (a.k.a. stapedial reflex)
1. Normal peak at 0: Normal
2. Low peak at 0:
Otosclerosis
Scarred tympanic membrane
Ossicular fixation
3. High peak at 0:
Flaccid tympanic membrane
Ossicular discontinuity
4. Flat or very low, with rounded peak:
Normal ear canal volume:Fluid in middle ear
High ear canal volume: Perforation or tube in tympanic membrane
Low ear canal volume: Probe is plugged or is against ear canal
5. Negative peak:
Retracted tympanic membrane
Eustachian tube malfunction
Sniffing child
70-100 dB
When there is hearing loss of > 65 dB
Hearing impaired = Any hearing loss
Deaf = Sensorineural hearing loss >90 dB (i.e. profound loss)
0 25 dB = Normal
25 40 dB = Mild
40 55 dB = Moderate
55 70 dB = Moderately severe
70 90 dB = Severe
>90 dB = Profound
How is percentage of hearing loss

measured?
How can we differentiate between
cochlear and retrocochlear hearing
loss on routine testing?
How to differentiate between cochlear
and retrocochlear lesion?
Most effective test to assess integrity

of auditory pathway from cochlear
nerve to cortex
Most sensitive test to detect
retrocochlear lesion
Uses of auditory brain stem response
test
Variables that affect the auditory brain
stem response
Oto-acoustic emissions are generated

from what part of cochlea?
For one ear: [(Average of thresholds at 500, 1000, 2000, and 3000 Hz) 25] x 1.5
For both ears: (5x+y)/6, where x=percentage hearing loss of better ear and y=percentage
hearing loss of worse ear
Speech recognition may be worse than audiogram, i.e. patient will have difficulty in
understanding speech relative to what audiogram suggests.
Alternate binaural loudness balance test
Short increment sensitivity test
Bekesy audiometry
Tone decay test
Performance intensity function
Acoustic reflex decay
Glycerol test (for Menieres disease)
Auditory brain test response
Oto-acoustic emissions
Auditory brain stem response
Auditory brainstem response

1. To assess integrity of auditory system from cochlear nerve to cortex
2. Most sensitive test to detect retrocochlear lesion
3. Neonatal hearing screening
4. Estimating thresholds in patients who cannot undergo pure tone audiometry
Patient variables: Age, Gender, Temperature, Drugs (including alcohol), State of arousal,
Hearing loss
Stimulus variables: Click polarity, Rate, Intensity, Stimulus frequency
Recording parameters: Electrode montage, filter settings
Outer hair cells
Uses of oto-acoustic emissions
Types of oto-acoustic emissions

Absent oto-acoustic emissions does
not necessarily imply cochlear lesion.
Why?
Interpretation of present oto-acoustic
emissions
Absent transient oto-acoustic
emissions
In distortion product oto-acoustic
emissions, the most prominent
distortion product has what frequency?
Ideal stimulus frequencies for
distortion product oto-acoustic
emissions
Practical problem in measuring otoacoustic emissions at birth
How does auditory neuropathy present
on auditory testing?
1. Neonatal hearing screening.

2. Estimate cochlear sensitivity by frequency
3. Differentiate between sensory and neural hearing loss
4. Estimating thresholds in patients who cannot undergo pure tone audiometry
5. Intra-operative monitoring of cochlear function during surgical removal of tumor involving
cochlear nerve (if oto-acoustic emissions are present)
6. Monitoring of cochlear damage by drugs (ototoxicity) or noise. (It is more sensitive than PTA
especially at high frequencies, though PTA is more commonly used for monitoring.)
7. Rule out pseudohypo-acusis: present oto-acoustic emissions imply no conductive loss and
<30-40 dB cochlear loss if any.
1. Spontaneous
2. Evoked: transient, distortion product, sustained-frequency
Acoustic neuroma impinging on cochlear blood supply may cause diminished or absent cochle
emissions, while the true lesion is retro-cochlear.
It means that there is either no sensorineural loss at given frequencies, or loss < 30 40 dB.
It means that there is > 30 40 dB sensorineural loss
2F2-F1, where F1 and F2 are the stimulus frequencies
F2 = 1.2 x F1, where F1 and F2 are the stimulus frequencies
Vernix in outer ear.

Mesenchyme in middle ear.
(May have to wait few days for these to clear out.)
Sensorineural hearing loss on pure tone audiogram (or, if a child, hearing loss on behavioral
testing)
Abnormal auditory brain stem response.
Absent acoustic reflexes (ipsilateral& contralateral).

Poorer word recognition ability than what is suggested by PTA.
Present oto-acoustic emissions.
Behavioral techniques of audiometry in Behavioral observation audiometry
children
Visual reinforcement audiometry
Conditioned play audiometry
Which behavioral technique of
Behavioral observation audiometry.
audiometry in children is the worst,
Because it is neither reliable nor valid.
and why?
In behavioral observation audiometry,
Eye widening.
what kind of responses can be
Eye blink.
observed in the child?
Arousal from sleep.
Cessation of movement.
Cessation of crying.
Change in facial expression.
Movement of limbs.
Turning of head.
Looking toward the sound.
Requirements for binaural hearing
Both ears should be hearing.
Difference of hearing in the two ears should be < 30 dB.
Visual reinforcement audiometry is
6 30 months (0.5 2.5 years)
appropriate for what age range?
Conditioned play audiometry is
30 36 months (2.5 3.0 years)
appropriate for what age range?
Difference between different
Behavioral observation audiometry: The childs response to sound is observed
behavioral techniques of audiometry in Visual reinforcement audiometry: The sound is reinforced by a visual (e.g. lights on a toy), s
children
child is motivated to look toward the sound
Conditioned play audiometry: The child is asked to play a game (e.g. drop a ball) when he
hears the sound
How is speech audiometry done in a
Speech recognition threshold: Child is given spondee picture cards or objects; he points to t
child?
What probe tone is used in children for

tympanometry?
Auditory brain stem response
audiometry is best for what
frequencies?
What are the benefits / issues in
auditory brain stem response testing in
children?
What are the benefits / issues in otoacoustic emission testing in children?
Age at which deaf infant should be
intervened
Risk factors for hearing loss in a child
Under what conditions, screening for

hearing should be definitely done in a
child?
object or to the picture of the word presented.

Word recognition score: Child points to the picture of the word presented. This is the WIPI te
(Word Intelligibility by Picture Identification).
Child > 6 months age: 220-Hz probe tone
Infant < 6 months age: 660-Hz probe tone
1000 4000 Hz
1. Although more objective than behavioral testing, nevertheless behavioral testing is superior
because it tests actual hearing.
2. Easier than behavioral testing in non-compliant children
3. Requires sedation and its requisite life support and recovery services.
1. Requires substantially less time than auditory brain stem testing.
2. Sedation and requisite life support is rarely needed.
3. Cannot be done if child has a middle ear disorder
Before 6 months of age.
1. Illness in neonate requiring > 48 hours admission in NICU

2. Stigmata of syndrome which has hearing loss
3. Family history of childhood deafness
4. Craniofacial anomalies
5. TORCHS infection
6. Parental concern about hearing, speech, language, or developmental delay
7. Infections that can cause deafness, e.g. meningitis
8. Syndromes with progressive hearing loss, e.g. neurofibromatosis, Usher syndrome
9. Neurodegenerative disorders (e.g. Hunter syndrome) or neuropathies (e.g. Friedrichs ataxia
10. Head trauma
11. Recurrent or persistent OME for > 3 months
All risk factors for hearing loss in a child, namely:
1. Illness in neonate requiring > 48 hours admission in NICU
2. Stigmata of syndrome which has hearing loss
Male:Female ratio of pseudohypoacusis in children

Signs of possible pseudohypo-acusis
Tests for suspected pseudohypoacusis
3. Family history of childhood deafness

4. Craniofacial anomalies
5. TORCHS infection
6. Parental concern about hearing, speech, language, or developmental delay
7. Infections that can cause deafness, e.g. meningitis
8. Syndromes with progressive hearing loss, e.g. neurofibromatosis, Usher syndrome
9. Neurodegenerative disorders (e.g. Hunter syndrome) or neuropathies (e.g. Friedrichs ataxia
10. Head trauma
11. Recurrent or persistent OME for > 3 months
M:F = 1:2 (i.e. more common in girls)
1. No difficulty in hearing in normal conversation but hypo-acusis on testing

2. Compensation case
3. Patient can name specific incident causing hearing loss and stands to gain in some way as
result
4. Odd performance on routine tests:
(i) Nakhra behaviors, e.g. leaning head, straining, looking confused, questioning intonation
during testing
(ii) Test-retest reliability worse than 5 dB
(iii) Disparity between pure tone audiometry and speech reception threshold of > 10 dB
(iv) Good word recognition score at speech reception threshold
(v) Acoustic reflexes present despite air-bone gap
(vi) Bone conduction thresholds > 10 dB poorer than air conduction thresholds
(vii) > 65 dB difference of threshold between good and poor ear; cross-over at > 65 dB in air
conduction and > 10 dB in bone conduction
Physiological tests:
1. Acoustic reflex: Present at 5 dB above voluntary auditory threshold

2. Oto-acoustic emissions: Present transient oto-acoustic emissions (implies less than 30-40
dB hearing loss if any)
3. Auditory brainstem response: No hearing loss identified on auditory brainstem response
Behavioral tests:
Stenger effect
Stenger test
Lombard test
1. Stengertest:Positive for pseudohypo-acusis

2. Lombard test: Positive for pseudohypo-acusis
3. Delayed auditory feedback: no longer used
4. Doerfler-Stewart test: no longer used
5. Bekesy audiometry: no longer used
When two tones of the same frequency are presentedsimultaneously to both ears, the patient
will perceive the tone only in the ear in whichthe tone is louder.
Used to test for pseudohypo-acusis. It is based on the Stenger effect.
Present the patient with tone of 5 dB above threshold in good ear and 5 dB below threshold in
poor ear. If he claims to hear the tone, test is negative (i.e. pt. does not have pseudohypoacusis); if he claims to not hear the tone, then test is positive (i.e. pt. has pseudohypo-acusis).
Used to test for pseudohypo-acusis. It is based on the phenomenon that one increases his voi
volume in the presence of noise because noise interferes with self-monitoring.
Patient is asked to read something aloud and then masking noise is introduced through
headphones. If volume of patients voice increases, test is positive for pseudohypo-acusis. If
volume of patients voice does not increase, then patient has true hearing loss and test is
negative for pseudo-hypo-acusis.
Ototoxicity (i.e. drug-induced) affects
High frequencies first (e.g. 10-20,000 Hz), then low frequencies (e.g. speech frequencies, e.g.
which frequencies?
2,000 Hz).
How much hearing loss is defined as
20 dB loss at one frequency, or 10 dB loss at two adjacent frequencies, or any loss at three
ototoxicity?
adjacent frequencies
If there is hearing loss in both ears and The one with hearing loss of 40-70 dB, regardless of whether it is the better or worse ear
you want to fit hearing aid in only one
ear, which ear should it be?
Saturation SPL (a.k.a. SSPL)
Maximum power output of hearing aid
Gain of hearing aid
Gain = Output Input, i.e. it is the amplification or acoustic energy added to the input sound
Signal-to-noise ratio
Components of a hearing aid

Styles of hearing aids
Peak clipping (in hearing aid)
Compression limiting (in hearing aid)
Signal = wanted sound

Noise = unwanted sound
A hearing aid with a high signal-to-noise ratio amplifies the wanted sound more than the
unwanted sound
Essential components: Microphone, Amplifier, Output receiver
Other components: Screwdriver controls, Directional microphones, Telecoil
1. Body aid
2. Behind-the-ear
3. In-the-ear
4. In-the-canal
5. Completely-in-canal
Constant gain until the hearing aids maximum power output is reachedat which point the
amplitude peaks of the excess energy are clipped off.
Advantage: Prevents sound from being too loud.
Disadvantage: Distortion of sound.
Above a certain level, gain is reduced (i.e. compressed).
Two kinds of compression:
(a) input compression at the microphone
(b) output compression at the output receiver.
Dynamic range compression (in

hearing aid)
Advantage: No distortion (unlike peak clipping) as saturation is not reached.

Unlike compression limiting, gain is reduced through much of the range of sound intensity. The
gain decreases as input increases.
Loudness recruitment
Advantage: This is very much like a normal healthy cochlea, as the outer hair cells of the
cochlea compress sound in exactly the same manner and when they are damaged, loudness
recruitment occurs. The idea is to make soft sounds audible and keep loud sounds comfortab
Abnormally rapid loudness growth characteristic of cochlearhearingimpairments.
CROS and t-CROS (in hearing aid)
BiCROS (in hearing aid)

Limit (in dB) of bone conduction
hearing aid
Assistive devices
CROS = contralateral routing of signal

The signal from the un-aidable poor ear is routed to a receiver on the good ear through a wire
radio waves.
t-CROS = transcranial contralateral routing of signal

The signal from the un-aidable poor ear is routed to the good ear directly through the skull bon
BiCROS = bilateral CROS
Both ears are poor; the ear with the hearing aid receives signals from both sides
< 45 dB
Assistive listening devices:
1. Telephone amplifiers
2. FM television listening devices
3. FM systems for large areas
Assistive visual/vibratory devices:
At what frequencies does noiseinduced hearing loss start?

Most common cause of sensorineural
hearing loss after infancy and before
old age
Pattern of noise-induced hearing loss
in shooters
1. Alarm clocks, smoke detectors, security systems, baby-cry detectors, and doorbells with
flashing lights or vibrator.
2. Closed-caption television decoders
3. Text telephones
4. Computers
Typically, noise-induced hearing loss begins in a notch pattern in the 3000- to 6000- Hz region
but with time broadens to the other frequency regions with a less steep slope.
Noise-induced hearing loss
Asymmetrical 4000-Hz notch loss, which is worse in the earopposite the shoulder from which t
gun is fired.
How much protection against noise is

provided by earmuffs or earplugs?
Types of ear protection devices
Active noise reduction

Which components of electrical
response audiometry are used for
threshold estimation?
The benefit of doing electrical
response audiometry (as opposed to
routine audiometry)
The most important waves of auditory
brainstem audiometry
The waves of auditory brainstem
audiometry represent which areas?
How can Menieres disease

(endolymphatichydrops) be diagnosed
on electrocochleography?
An enlarged summating potential on
electrocochleography (i.e. increased
SP:AP ratio, > 0.30) is diagnostic of
what?
20 40 dB of attenuation
Passive (non-electric): Pass moderate sound but reduce high sound level.
Active (electric): Limit output to 85 dB. There is speech distortion because of peak clipping.
Also, active noise reduction, in which the sound phase is inverted by 180 0 to cancel the noise
A method of noise reduction used by certain ear protection devices in which the sound phase i
inverted by 1800 to cancel the noise. It is effective for frequencies of < 1000 Hz.
Short-latency components (as opposed to long-latency components)
Objectivity (as the subject is not required to actively participate in the assessment)
Waves I, III, and V

Wave I: E Eighth nerve (distal part)
Wave II: E Eighth nerve (proximal part)
Wave III: C Cochlear nucleus
Wave IV: O Superior Olivary complex
Wave V: L Lateral lemniscus
Wave VI: I Inferior colliculus
Wave VII: I Inferior colliculus
Enlarged summating potential (i.e. increased SP:AP ratio, > 0.30)
Menieres disease (endolymphatic hydrops)
What are the electric potentials

recorded on electrocochleography?
Recording techniques of
electrocochleography
Uses of electrocochleography
What kind of brain stem response

audiometry (ABR) is used to detect
acoustic neuroma?
When brainstem audiometry is used to
assess hearing thresholds, which
wave is monitored?
What is difference between thresholds
obtained by brainstem audiometry and
behavioral audiometry?
Specific abnormalities in brainstem
audiometry in various kinds of hearing
loss
1. Resting potential
2. Summating potential
3. Compound action potential
4. Cochlear microphonics
Transtympanic:
Transtympanicelectrode, penetrates tympanic membrane at inferior portion and is placed over
the cochlear promontory. Invasive technique, but gives excellent results.
Extratympanic:
TIPtrode (= intrameatal electrode);
Tymptrode electrode (= in direct contact with tympanic membrane)
1. Diagnosis, assessment, and monitoring of Menieres disease(endolymphatichydrops)
increased SP/AP ratio
2. Enhancing wave I of auditory brainstem response audiometry if that wave is absent or difficu
to identify (as it represents cochlea and distal eighth nerve)
3. Monitoring of cochlear function during surgery
4. Objective measurement of audiometric thresholds (though brainstem audiometry is more
commonly used for this)
5. Diagnosis of auditory neuropathy: abnormal brainstem response with normal cochleogram
Neurologic ABR for larger neuromas.
Stacked ABR is best for small acoustic neuromas.
Wave V.
10 20 dB (brainstem thresholds are higher)
Absolute
Wave I
Morphology Interpea
Normal
Conductive
loss
Sensory loss
Neural loss
What is auditory steady-state evoked

potential used for?
Middle latency response potentials (in
electrical audiometry)
Uses of middle latency response
potentials (a type of cortical auditory
evoked potentials)
P300 (in electrical audiometry)
Mismatch negativity response

Types of cortical auditory evoked
responses
Uses of cervical vestibular evoked
myogenic potentials (cVEMP)
latencies
(except wave I)
Normal
Delayed
latency
Normal
Delayed
Normal
Normal
k
intervals
Normal
Normal
Delayed
(Absent or
diminished
wave)
Normal
Poor
Normal
Poor
Delayed
Delayed
Auditory steady-state evoked potential uses a frequency-specific, pure tone stimulus that
activates the cochlea and CNS. It is particularly good at assessing severe/profound hearing los
These are a type of cortical auditory evoked responses
1. Evaluation of the auditory pathway above the brainstem:

(a) Documentation of auditory CNS dysfunction
(b) Localize lesions at the thalamo-cortical and primary auditory cortex
2. Evaluate functional integrity of the auditory pathway
3. Approximate frequency-specific auditory sensitivity upto the cortical level
4. Evaluate effectiveness of electrical stimulation for cochlear implants
A type of cortical auditory evoked response. Assesses auditory temporal processing and
hemispheric asymmetry. Also used to assess higher-level changes in cognition and memory an
age-related decline in central processing.
A type of cortical auditory evoked response. Originates from Heschls gyrus in primary auditory
cortex.
1. Middle latency response potentials
2. P300
3. Mismatch negativity response
Saccule disorder, Conductive hearing loss, Sensorineural hearing loss, Vestibular nerve
disturbance, Tullios phenomenon, Superior canal dehiscence syndrome, Acoustic neuroma,
Vertigo
What is the difference in diagnosis in
rotatory vertigo versus translational or
tilt vertigo?
Differential diagnosis of vertigo
Nystagmus
Types of eye rotations
Direction of nystagums in hypofunction

of labyrinth
Alexanders law
On which side of patient should

examiner stand when conversing with
post-op patient after labyrinthectomy,
vestibular nerve section, or resection
of vestibular schwanomma?
Output from the vestibular nuclei goes
where?
Bilateral vestibular loss, Otosclerosis, Menieres disease, Migraine, Brainstem stroke, Multiple
sclerosis, Spinocerebellar degeneration
Illusion of motion, either of oneself or the world
Rotatory vertigo: Semicircular canal problem
Translational vertigo: Utricle or saccule problem
Vertigo
Lightheadedness
Dysequilibrium
Oscillopsia
Physiologic dizziness
Multi-sensory dizziness
Eye movements driven by gaze-stabilizing reflexes
Yaw rotation: in transverse plane (right, left)
Pitch rotation: in sagittal plane (up, down)
Roll rotation: in coronal plane (clockwise, anticlockwise)
Slow component toward weaker labyrinth.
Fast component toward stronger labyrinth.
When patient looks toward the ear with the stronger labyrinth, speed of nystagmus will increas
(both slow and fast phases).
When patient looks toward the ear with the weaker labyrinth, speed of nystagmus will decreas
(both slow and fast phases).
Examiner should stand on the weaker labyrinths side in order to minimize nystagmus and thu
reduce visual blur and nausea.
1. Oculomotor nuclei
2. Cervical spinal motor neurons
3. Lower spinal motor neurons
Vestibulo-ocular reflex
Vestibulo-collic reflex
Smooth pursuit
Optokinetic nystagmus
Difference between smooth pursuit
and optokinetic nystagmus
Cervico-ocular reflex
What are the gaze-stabilizing reflexes
and how do they work?
Common name for utricle and saccule
Angle of horizontal semicircular canal
(a.ka. lateral semicircular canal) with
horizontal
Difference in sensation of utricle and
saccule
Divisions of vestibular nerve
4. Autonomic centers
5. Cerebellum
6. Cerebral cortex
Output from vestibular nuclei goes to oculomotor nuclei in order to maintain gaze despite chan
in head position
Output from vestibular nuclei goes to cervical spinal motor neurons in order to maintain head-o
body posture
Reflexive eye movements track image on retinal fovea
Reflexive eye movements track image on retina outside fovea
Smooth pursuit = Reflexive eye movements track image on retinal fovea
Optokineticnystagmus = Reflexive eye movements track image on retina outside fovea
Proprioceptors in the neck sense neck movements and send data to the oculomotor nuclei. Th
is the cervico-ocular reflex. It augments the vestibulo-ocular reflex if it is deficient.
Smooth pursuit and optokineticnystagmus (~ 100 ms): For slow, low-frequency head
movements
Vestibulo-ocular reflex (~ 7 ms): For fast, high-frequency head movements
Otolith end organs (a.ka. otoconial end organs or macular end organs)
25o
Utricle senses translational/tilt movement of head in transverse plane.

Saccule senses translational/tilt movement of head in para-sagittal plane.
1. Superior vestibular nerve, formed by fusion of:
(a) Anterior canal ampullary nerve
(b) Lateral canal ampullary nerve
(c) Utricular nerve
2. Inferior vestibular nerve, formed by fusion of:
(a) Posterior canal ampullary nerve
(b) Saccular nerve

Singular nerve
Scarpas ganglion
Different types of hair cells in vestibule
of inner ear
Another name for posterior canal ampullary nerve (branch of the inferior vestibular nerve), call
the singular nerve because it runs alone for ~ 2 mm
Ganglion of vestibular nerve; it is located at fundus of internal auditory canal.
Type of hair cell
Reids plane
Plane of horizontal semicircular canal
(i.e. lateral semicircular canal)
Plane of anterior and posterior
semicircular canals
Rule regarding exciting and inhibiting
of semicircular canals in head rotation
Superior canal dehiscence
Patient says, Loud sound in my left

ear makes the world move down and
twist counterclockwise. What is he
suffering from?
Shape
Type I
Like a flask
Type II
Like a cylinder
Area where
present
In central/striolar
zone
Outside
central/striolar
zone
Type of
synapse
Calyceal
synapse
Bouton synapse
Effect
Stimulatory
Inhibitory
Horizontal plane through the infra-orbital rim and center of external auditory canal
25o above Reids plane (i.e. horizontal plane); thus, if you pitch your nose down by 25 o, your
lateral canals will become truly horizontal
45o from sagittal plane
Each semicircular canal isexcitedbyheadrotationaboutthat semicircular canals axisbringing th

forehead toward the ipsilateral side.
Abnormal absence of bone between the superior semicircular canal (a.k.a. anterior canal) and
middle cranial fossa. Renders the canal sensitive to sound, glottis Valsalva, and nose-pinch
Valsalva.
Left superior canal dehiscence syndrome
The COWS formula for caloric

nystagmus is for slow or fast phase?
Vestibular neuritis affects which
division(s) of the vestibular nerve?
Head thrust test
Which part of vestibule responds to
gravity
Mechanism of action of cVEMP
In what conditions does low-threshold
(i.e. high amplitude) cVEMP occur in?
Why does crisis of Tumarkin occur in
Menieres disease?
What part of cerebellum accounts for
long-term changes in vestibular
function (e.g. vestibular
compensation)?
How does vestibular compensation
take place after unilateral loss of
vestibular function (e.g.
labyrinthectomy, vestibular
neurectomy, labyrinthitis)?
Which is more debilitating, permanent
complete loss or fluctuating incomplete
loss of vestibular function?
What is the philosophy behind ablative
treatment of Menieres disease?
Are vertigo-suppressing drugs helpful
Fast phase
Superior vestibular nerve (hence, lateral & anterior semicircular canals and utricle will be
affected while posterior semicircular canal and saccule will be preserved)
Hold head in both hands and suddenly jerk it toward the direction relevant to the semicircular
canal to be tested; if oscillopsia, then the canal is weak; if no oscillopsia, canal is normal
Saccule (especially lower part)
Saccule gets excited, leading to the cervical vestibular evoked myogenic potential (cVEMP), so
cVEMP tests saccular function. Also used to test superior canal dehiscence syndrome, etc.
1. Superior canal dehiscence syndrome
2. Enlarged vestibular aqueduct syndrome
3. Any problem that abnormally couples saccular mass movement to sound
Possibly due to sudden deformation of utricle or saccule
Flocculonodular lobe
Reweighting of synapse in vestibular nuclei interneurons within 1 to 3 weeks
Fluctuating loss, because permanent loss is compensated within 1 to 3 weeks, but fluctuating
loss cannot be compensated as it is unpredictable
We trade fluctuating loss of vestibular function (which cannot be compensated) for complete,
permanent loss (which can be compensated)
No. They are only helpful for acute relief; when taken for too long, they interfere with the proce
for vestibular compensation in a case

of vestibular hypofunction?
Patient has vertigo on straining. What
could he have?
Patient seems to have vertigo after
starting a certain drug. If it is not true
vertigo, what are the differentials in
this case?
Difference between saccades, smooth
pursuit, and vergence
Tullio phenomenon
Hennebert sign
Fukuda stepping test
Tests of vestibulospinal function
Romberg test
Dix-Hallpike maneuver
Hyperventilation-induced nystagmus
occurs in what conditions?
Head shaking test
Jongkees formula
of compensation
1. Superior canal dehiscence syndrome
3. Perilymphatic fistula
1. Hypotension
2. Sedation
3. Arrhythmia
Saccades: Look at examiners nose first, then look at his finger

Smooth pursuit: Look at examiners finger, which is moving laterally
Vergence: Look at examiners finger, which is moving toward your nose
Vertigo &nystagmus during exposure to loud sound
Vertigo & nystagmus during pneumatic otoscopy or tragal compression
March in place with eyes closed (test of vestibular function)
1. Romberg test
2. Tandem walking
3. Fukuda stepping test
Shake head while eyes are closed, feet are together, and arms are folded across chest; it is te
of vestibular function
Extend neck, turn to side, lie back (test for BPPV)
In demyelinating conditions of vestibular nerve, namely:
1. Vestibular schwanomma
2. Multiple sclerosis
3. Compression of vestibular nerve by blood vessel
Hold head with both hands while chin is angled downward at 25 o (which means lateral
semicircular canals are in horizontal plane); shake head at 2 Hz ~ 30 times. Post-headshake
slow-phase nystagmus will be toward weaker ear and fast-phase nystagmus will be toward
stronger ear. (This test is contra-indicated in patient with cervical spine disease.)
Used to test lateral semicircular canal weakness by caloric method:
Unilateral weakness (UW) = [(RW+RC)] [(LW+LC)]

--------------------------------(RW+RC+LW+LC)
RW means speed of slow-phase of nystagmus when right ear is irrigated with warm water;
similarly, RC is for cold water and so on.
In what situations is rotary chair test

useful to test patient of vertigo?
What is the gold standard test for
measuring vertigo?
What does oVEMP (ocular vestibular
myogenic potentials) test and how is it
carried out?
Most common cause of vertigo
presenting to ENT clinic
What is classic history of BPPV?
BPPV can follow what events?
Latency and duration of vertigo of

BPPV
Treatment of BPPV due to posterior
UW > 25% implies weakness of lateral semicircular canal of one side.

For children, who do not tolerate caloric testing
Quantitative head thrust testing
It tests short-latency excitatory EMG activity in contralateral inferior rectus and inferior oblique.
is recorded with EMG electrodes on skin below eye. Useful for detecting superior canal
dehiscence syndrome
BPPV
Severe vertigo brought on by rolling over in bed (usually toward affected ear) or tilting the head
upward and to the side to look at shelf.
Vertigo reverses direction when patient sits up.
Closed head injury
Roller coaster ride
Ear surgery
Bed rest
Long flight
Vestibular neuritis
Latency = 5 10 seconds
Duration = 10 60 seconds
Conservative:
semicircular canal
1. Epley maneuver
2. Brandt exercise for habituation
3. Sermont liberatory maneuvers
Surgical:
Treatment of BPPV due to lateral

semicircular canal
Epley maneuver
1. Posterior canal occlusion

2. Singular neurectomy
3. Vestibular neurectomy
4. Labyrinthectomy
Log roll toward side of normal ear; if that fails, then log roll in opposite direction (i.e. toward
diseased ear)
Forleft posterior semicircular canal BPPV:
Situp,headturnedtoleft.
Lieback,headhangsoffbed,waitfor30seconds.
Turnheadtoright,waitfor30seconds.
Rollontorightshoulderandpointnosedown,for30seconds.
Situp,waitfor1to2minutes.
Repeat.
Classic history of vestibular neuritis
Patient has vestibular neuritis. What

are his chances of getting BPPV later
on?
Note that Epleys maneuver starts with Dix-Hallpike maneuver.

Sudden onset of severe vertigo that subsides over several days, while dysequilibrium and
unsteadiness last for ~ 3 weeks.
(Note that there is no hearing loss.)
15% (so counsel him regarding that)
Treatment of vestibular neuritis
Definition of Menieres disease
1. Prednisone
2. Sedatives & anti-emetics in short term only. (Long term use compromises on vestibular
compensation)
3. Vestibular rehabilitation
Certain Menieres disease: Definite Menieres plus histopathologic confirmation (only detecte
at autopsy)
Definite Menieres:
1. At least 2 episodes of spontaneous vertigo lasting for > 20 minutes
2. Typically lasting between 20 minutes and 2 hours
3. Sensorineural hearing loss (on PTA, low-frequency)
4. Ear fullness and/or tinnitus
5. All other causes of symptoms have been excluded
Probable Menieres:One episode of Menieres-type vertigo, plus the other criteria
Treatment of Menieres disease
Clinical picture of superior canal

dehiscence syndrome
Possible Menieres:One episode of Menieres-type vertigo, without the other criteria

1. Medical regimen:
(a) Low-salt diet
(b) Diuretic
2. Intra-tympanic injection of dexamethasone
3. Ablative interventions (if non-ablative regimens fail; never ablate if other ear is already
injured):
(a) Intra-tympanic gentamicin
(b) Middle ear exploration and gentamicin treatment
(c) Vestibular nerve transection (saves hearing)
(d) Labyrinthectomy (if hearing is already lost)
(e) Controversial: endolymphatic sac decompression, pressure application devices
1. Vertigo &nystagmus during loud sound (Tullio phenomenon), pressure applied to ear
(Hennebert sign), and straining (nose-pinch or glottis Valsalva)
How would you investigate and treat a

suspected case of superior canal
dehiscence syndrome?
2. Can hear my eyes move.

3. Pulsatile tinnitus; also gaze-evoked tinnitus
4. Autophony
5. Abnormally sensitive bone conduction better than 0 dB threshold
6. May have only vestibular symptoms or only cochlear symptoms
7. May be bilateral (25% cases)
8. Positive fistula sign
Diagnosis:
1. CT scan (high-resolution 0.5 mm slice): shows the dehiscence.
2. cVEMP or oVEMP: will give high amplitudes and low thresholds
Treatment:
Blood supply of inner ear
Infarct of superior branch of internal

auditory artery will damage what
organs?
Infarct of inferior branch of internal
auditory artery will damage what
organs?
Infarct of PICA (posterior inferior
cerebellar artery) will cause what
abnormalities?
1. Surgical plugging of the dehiscence

The inner ear is supplied by the internal auditory artery, which is typically a branch of the AICA
(anterior inferior cerebellar artery).
The internal auditory artery divides into 2 branches: superior and inferior. The superior branch
supplies the lateral and anterior semicircular canals and utricle. The inferior branch supplies th
posterior semicircular canal, saccule and cochlea.
1. Lateral semicircular canal
2. Anterior semicircular canal
3. Utricle
1. Posterior semicircular canal
2. Saccule
3. Cochlea
This condition is called lateral medullary infarction a.k.a. Wallenberg syndrome:
1. Vertigo & nausea
2. Ipsilateral gait and limb ataxia
3. Abnormal saccadic eye movements (overshoot to side of lesion, i.e. lateropulsion)

4. Abnormal smooth pursuit eye movements
5. Ocular tilt reaction (head tilt and eye deviation toward side of lesion)
Wallenberg syndrome
A.k.a. lateral medullary infarction. Caused by infarct of PICA (posterior inferior cerebellar artery
1. Vertigo & nausea
2. Ipsilateral gait and limb ataxia
3. Abnormal saccadic eye movements (overshoot to side of lesion, i.e. lateropulsion)
4. Abnormal smooth pursuit eye movements
5. Ocular tilt reaction (head tilt and eye deviation toward side of lesion)
Infarct of AICA (anterior inferior

cerebellar artery) will cause what
abnormalities?
Infarct of SCA (superior cerebellar

artery) will cause what abnormalities?
How to differentiate migraineassociated vertigo from Menieres

disease?
Treatment of migraine-associated
vertigo
Lateral ponto-medullary infarction:
1. Hearing loss on affected side

2. Ataxia
3. Ipsilateral facial anesthesia
4. Contralateral body anesthesia
Infarct of superior lateral pons, superior cerebellar peduncle, and superior cerebellar vermis an
hemisphere.
Will cause contrapulsion with overshooting of saccades directed contralateral to the side of
lesion.
Patient of migraine-associated vertigo will have:
1. headache
2. variable timing of vertigo episodes (from seconds to hours to days)
3. exacerbation by common triggers (caffeine, chocolate, red wine, etc)
4. hormonal fluctuations
Stop all headache and vertigo medicines. Give 8-week trial of strict avoidance of caffeine and
common trigger foods.
Where are otoliths found?

Number of stereocilia and kinocilia in a
hair cell in the vestibule
Mechanism of working of the hair cells
in the vestibule
Direction of kinocilia of hair cells in the
semicircular canals
How many vestibular nuclei are there
in the brainstem?
Halmagyi maneuver
What is direction of flow of endolymph

in relation to slow and fast phase of
nystagmus?
Types of nystagmus
In the otolithic end organs, namely the utricle and saccule. Otoliths are NOT normally found i
the semicircular canals
Stereocilia = 50 100
Kinocilium = 1
Displacement of the stereocilia (which are embedded in the cupula) of the hair cells toward or
away from the kinocilium alters calcium influx into the cell, leading to release or inhibition of
neurotransmitters.
Lateral canal: the kinocilia are closest to the utricle
Anterior and Posterior canals: the kinocilia are away from the utricle (i.e. toward the crus
commune side of the ampulla)
Four on each side, namely lateral, medial, superior and descending nuclei.
Horizontal high-frequency head thrust maneuver. If after the maneuver, there are refixation
saccades to stabilize eyes on a target, this suggests defect in horizontal vestibulo-ocular
reflex.
Direction of flow of endolymph = Direction of slow phase of nystagmus.
Direction of fast phase of nystagmus is opposite to both of the above.
1. Physiologic: end-point nystagmus noted on lateral gaze > 30 o

2. Spontaneous: present without stimulation
3. Induced: elicited by stimulation
(a) Positional: a form of induced nystagmus; elicited by assuming a specific position
Ewalds laws (in relation to nystagmus) 1. Nystagmus occurs in the plane of the canal being stimulated and in the direction of endolym
flow.
2. Ampullopetal flow causes a greater response than ampullofugal flow in the lateral canal
3. The reverse is true in the anterior and posterior canals.
What are the various methods of
1. Electronystagmography
2. Videonystagmography
testing vestibular function in the
3. Bithermal caloric test
laboratory?
4. Rotational chair testing
5. Scleral search coil
What is the best technique (the gold

standard) for measuring eye
movements (nystagmus, saccades,
etc)
What is the pathway used by the
cervical vestibular evoked myogenic
potential (cVEMP)?
Dynamic posturography
6. Vestibular evoked myogenic potential (cVEMP)

7. Dynamic posturography
Scleral search coil (because there is direct contact with the globe of the eye)
saccule inferior vestibular nerve (lateral) vestibular nucleus (medial) vestibulospinal tr

(ipsilateral) sternocleidomastoid muscle
Determines functional limitations by quantifying and isolating impairments due to the visual,
somatosensory, or vestibular input.
Two tests:
Most commonly involved part of inner

ear in Menieres disease
(endolymphatic hydrops)
Histology and pathophysiology of
Menieres disease
Crisis of Tumarkin
Lermoyez variant of Menieres disease
Cochlear hydrops variant of
Menieres disease
Phases of nystagmus of Menieres
disease
1. Sensory organization test: evaluation of the anterior-posterior body sway under conditions
with eyes opened (eo) or eyes closed (ec)
2. Movement coordination test: assesses patients ability to recover from external provocatio
Pars inferior (i.e. cochlea + saccule)
Bowing and rupture of Reissners membrane leakage of potassium-rich fluid (endolymph) in

perilymph interference with generation of action potential (Na+/K+ intoxication theory)
Sudden unexplained fall without loss of consciousness or associated vertigo; a feature of
Menieres disease
Resolution of deafness and tinnitus with onset of vertigo
Fluctuating hearing loss, aural fullness, and tinnitus without vertigo.
(Contrast with recurrent vestibulopathy.)

1. Irritative phase: Fast phase of nystagmus toward diseased ear
2. Paralytic phase (a.k.a de-afferentative phase): Fast phase of nystagmus toward opposite
What are the findings on pure tone

audiogram in a patient of Menieres
disease?
What investigations would you advise
in case of Menieres disease and what
findings would you expect in them?
Differences between vertigo /
nystagmus of peripheral and central
origin
(i.e. healthy) ear

3. Recovery phase: Again, fast phase of nystagmus toward diseased ear
Low-frequency sensorineural loss which fluctuates over time
Pure tone audiogram: Low-frequency sensorineural loss which fluctuates over time
Electrocochleography: Increased summating potential : action potential ratio ( > 0.30)
Electronystagmography: unilateral weakness
Vertigo
CNS symptoms
Slow phase
Smooth pursuit
Saccades
Fixation /
Suppression
Caloric tests
Common causes of inner ear

dysfunction
Delayed endolymphatic hydrops

Secondary endolymphatic hydrops
Peripheral loss
Severe
Absent
Constant
Normal
Normal
Yes
Central
Not so severe
Present
Constant or increasing
or decreasing
Saccadic
Dysmetric
No
Loss
Intact or reversed
1. BPPV
2. Menieres disease
3. Recurrent vestibulopathy
4. Vestibular neuropathy
5. Acoustic neuroma
Meniere-type attacks of vertigo in patient with past history of profound hearing loss
Due to syphilis.
Early syphilis: Vertigo of variable intensity and duration, with vegetative features lasting days
Late syphilis: May present after years or decades. Meniere-like symptoms (vertigo and
sensorineural hearing loss) plus interstitial keratitis.
Cogan syndrome
Diagnosed by VDRL or RPR and FTA-ABS (confirmatory).

Treatment: Long course of penicillin plus short course of steroid.
Auto-immune disease
1. Interstitial keratitis (non-suppurative)
2. Audio-vestibular dysfunction (rapidly progressive bilateral e.g. hearing loss, ataxia,
oscillopsia)
3. Vasculitis (multi-system involvement)
Recurrent vestibulopathy
Difference between cochlear hydrops

and recurrent vestibulopathy
Treatment is with steroid, immunosuppressants.

Recurrent Meniere-like attacks of vertigo, but without hearing loss.
Treatment is symptomatic.
(Contrast with cochlear hydrops.)
Both are variants of Menieres disease.
In cochlear hydrops, there are cochlear symptoms fluctuating sensorineural hearing loss, au
fullness, tinnitus but no vertigo.
What is perilymphatic fistula

Causes of perilymphatic fistula
In recurrent vestibulopathy, there are vestibular symptoms severe episodic Meniere-like verti
but no hearing loss.
Abnormal communication between perilymph and endolymph, or between perilymph and midd
ear
Basic pathology is trauma, caused by:
1. Baro-trauma
2. Penetrating trauma
Clinical picture of perilymphatic fistula
3. Stapedectomy
4. Cholesteatoma
5. Physical exertion
Vertigo mild to moderate to severe
Hennebert phenomenon
Tullio phenomenon
Positive fistula sign: nystagmus on tragal compression with fast phase toward diseased ear
often false negative).
Treatment of perilymphatic fistula
Cervicogenic vertigo
CNS causes of dizziness
Most common congenital sensory

deficit
Is congenital deafness more of
environmental or more of genetic
cause?
Is congenital deafness more
syndromic or more non-syndromic?
Increased SP:AP ratio (>0.3) with straining on electrocochleogram.

Bed rest, elevate head, laxatives.
Monitor hearing and vestibular function.
Surgery if hearing loss worsens or vestibular symptoms persist.
Abnormalities in the cervico-ocular reflex following trauma causes episodic vertigo
1. Vertebrobasilar insufficiency
2. Wallenberg syndrome (lateral medullary syndrome)
3. Head trauma
4. Vestibulocerebellar degeneration
5. Brainstem encephalitis
6. Multiple sclerosis
7. Chiari malformation
8. Pseudotumor cerebri
9. Normal pressure hydrocephalus
Deafness
Environmental 50%
Genetic 50%
Non-syndromic 70% (usually mutation in single gene)
Syndromic 30%
Is genetic deafness more autosomal

recessive or more autosomal
dominant?
Rubella syndrome
How does kernicterus cause

deafness?
Why is Hennebert sign positive in
congenital syphilis?
Congenital syphilis affects what sites

in the body?
Hutchison teeth
Autosomal recessive 80%

Autosomal dominant 20%
X-linked 1%
Chromosomal 1%
A.k.a. Gregg syndrome
Deafness
Cataract
Microphthalmia
Retinitis
Blueberry muffin skin lesions
Cardiovascular anomalies
Mental retardation
Damages cochlear nuclei and inferior colliculus. There is high-frequency hearing loss.
Two theories:
1. Fibrous bands between footplate of stapes and membranous labyrinth
2. Excessively mobile footplate of stapes
Ears: Deafness
Nose: Nasal cartilages and/or bones
Teeth: Hutchison teeth
Eyes: Interstitial keratitis (cloudy cornea)
Bones:
(a) Peri-osteitis of cranial bones (bossing)
(b) Peri-osteitis of tibia (saber shin)
(c) Epiphyseal cartilages (short stature)
Gummas (tertiary syphilis): in auricle, mastoid, middle ear, and petrous apex. May cause
conductive deafness
Feature of congenital syphilis
Tullio phenomenon occurs in what

conditions?
Features of congenital hypothyroidism

(a.k.a. cretinism)
Histopathology of syphilitic ear
Common disorders of congenital

deafness due to environmental factors
Most common mutation in nonsyndromic congenital deafness

How are the gene loci labeled in nonsyndromic congenital deafness?
1. Semicircular canal fistula

2. Semicircular canal dehiscence
3. Congenital syphilis
4. Post-fenestration patient (if footplate of stapes is mobile and fenestrum is patent)
5. Fistula in patient of CSOM
(Tullio phenomenon will occur only if middle ear function is intact.)
1. Congenital deafness (mixed hearing loss)
2. Growth retardation
3. Mental retardation
Inner ear (sensorinerual deafness):
Temporal bone osteitis
Mononuclear leukocytosis
Obliterative end-arteritis
Endolymphatic hydrops
Micro-gummata
Degeneration of organ of Corti
Cochlear neuron loss
Middle ear (conductive deafness):
Ossicular involvement (osteitis and gummas)
CMV infection
Rubella syndrome
Kernicterus
Syphilis
Hypothyroidism
Mutation in connexin-26 molecule
Autosomal dominant DFNA
Autosomal recessive DFNB
Branchio-oto-renal syndrome
X-linked DFN
Deafness (sensorineural, conductive, or mixed)
Branchial anomalies (ear pit, ear tag, or cervical fistula)
Renal anomalies
The syndrome is autosomal dominant.
Compare and contrast the types of

neurofibromatosis
Type 1
Caf-au-lait spots, cutaneous
neurofibromas, plexiform neuromas,
pseudo-arthrosis, Lisch nodules of
iris, optic gliomas
Unilateral acoustic neuromas, and
only in 5% of patients
NF1 gene on chromosome 17q
Autosomal dominant
Deafness only if neurofibroma
encroaches upon middle or inner
ear
Osteogenesis imperfecta
Cause of otosclerosis
Type 2
Caf-au-lait spots, subcapsular
cataracts
Bilateral acoustic neuromas, and in

95% of patients
NF2 gene on chromosome 22q
Autosomal dominant
The bilateral acoustic neuromas are
asymptomatic at birth and become
symptomatic in early adulthood
Deafness (sensorineural, conductive, or mixed)

Fragile bones
Blue sclera
Hyper-elasticity of joints and ligaments
Subtype: van der Hoeve syndrome
Not known. Possibly measles virus, hormonal influence, or COLIA1 gene.
Stickler syndrome
Treacher Collins syndrome
Most common form of autosomal

dominant syndromic congenital
deafness
Waardenberg syndrome
Deafness (sensorineural or mixed)

Cleft palate
Micrognathia
Myopia
Retinal detachment
Cataract
Marfanoid habitus
Deafness (conductive or sensorineural or mixed)
Malar hypoplasia
Downward slanting palpebral fissure
Coloboma of lower eyelids
Hypoplastic mandible
Malformations of external ear or ear canal
Dental malocclusion
Cleft palate
Bilateral and symmetrical facial features
Type 1: Congenital sensorineural deafness, heterochromia irides, white forelock, patchy

hypopigmentation, dystopia canthorum
Type 2: Type 1 minus dystopic canthorum
Type 3: Type 1 plus microcephaly, skeletal abnormalities, mental retardation
Type 4: Type 2 plus Hirschsprungs disease (= Waardenberg-Shah syndrome; it is autosomal
recessive)
Common autosomal dominant

syndromes having congenital
deafness
Common autosomal recessive

syndromes having congenital
deafness
Jervell & Lange-Nielson syndrome
Pendred syndrome
Most common form of autosomal

recessive syndromic congenital
deafness
Usher syndrome
Branchio-oto-renal syndrome
Neurofibromatosis
Osteogenesis imperfecta
Otosclerosis
Stickler syndrome
Treacher Collins syndrome
Jervell & Lange-Nielson syndrome
Pendred syndrome
Usher syndrome
Deafness (sensorineural)
Cardiac arrhythmias (ECG shows large T waves and prolonged QT interval) child presents w
syncopal episodes
The syndrome is autosomal recessive
Euthyroid goiter
Diagnosis is by perchlorate discharge test.
The syndrome is autosomal recessive.
Usher syndrome
Variable loss of vestibular function
Retinitis pigmentosa
Type 1: Profound deafness + absent vestibular function + retinitis pigmentosa
Type 2: Moderate deafness + normal vestibular function + retinitis pigmentosa
Type 3: Progressive deafness + variable vestibular function + retinitis pigmentosa
Alport syndrome
The syndrome is autosomal recessive.

Kidney disease (glomerulonephritis)
Pathophysiology: The collagen of basement membranes of kidneys and inner ear is affected. I
the inner ear, the basilar membrane, spiral ligament, and stria vascularis are affected. In the
kidney, there is glomerulonephritis.
Norrie syndrome
Oto-palato-digital syndrome
Wildervaank syndrome
Mohr-Tranebjaerg syndrome
The syndrome is X-linked.

Eye symptoms (variable)
Mental disturbance
Deafness (conductive, because of ossicular malformations)
Hypertelorism
Craniofacial deformities: supra-orbital area, flat midface, small nose, cleft palate
Short stature
Broad fingers
Varying length of toes; excessively wide space between first and second toe
Deafness (sensorineural or mixed)
Klippel-Feil sign (fused cervical vertebrae)
6th cranial nerve paralysis (lateral rectus palsy)
Deafness (postlingual, sensorineural)
Progressive dystonia, spasticity, dysphagia, and optic atrophy (Similar to Freidrichs ataxia,
except that there is no cardiomyopathy)
X-linked Charcot-Marie-Tooth
syndrome
Goldenhar syndrome
Turners syndrome
Common X-linked syndromes having

congenital deafness
Common mitochondrial syndromes

Peripheral neuropathy
Foot problems
Champagne bottle calves
Deafness
Hemifacial microtia
Otomandibular dysostosis
Epibulbar lipodermoids
Coloboma of upper lid
Vertebral anomalies
The syndrome is a.k.a. oculo-auriculo-vertebral dysplasia.
Multiple genes are involved in this syndrome.
Deafness (sensorineural or conductive or mixed)
Gonadal dysgenesis
Short stature
Webbed neck
Shield chest
The syndrome is a.k.a. trisomy 13.
Alport syndrome
Norrie syndrome
Oto-palato-digital syndrome
Wildervaank syndrome
Mohr-Tranebjaerg syndrome
X-linked Charcot-Marie-Tooth syndrome
Kearns-Syre syndrome
having congenital deafness
Patient was given normal dose of

aminoglycoside (e.g. gentamicin). He
developed sensorineural deafness.
Why?
Michel aplasia
Mondini aplasia
MELAS (mitochondrial encephalopathy, lactic acidosis, and stroke)

MERRF (myoclonic epilepsy with ragged red fibers)
Leber hereditary optic neuropathy
Many mitochondrial mutations cause enhanced sensitivity to ototoxic effects of aminoglycoside

Patient may have one of many mitochondrial mutations which cause increased sensitivity to
ototoxic effects of aminoglycosides.
Complete agenesis of petrous bone. There is no inner ear. Presents with complete sensorineu
deafness. Hearing aid or cochlear implant is useless.
Developmentally deformed cochlea in which only the basal coil can be identified clearly. The
upper coils assume a cloacal form and the interscalar septum is absent. The endolymphatic
duct is also enlarged.
There is abnormal communication between endolymphatic and perilymphatic spaces of inne

ear and subarachnoid space. Thus, there is higher risk of perilymphatic fistula.
Scheibe aplasia
Mondini aplasia occurs in several syndromes, e.g. Pendred, Waardenberg, Treachers Collins,
Wilderwaank, CMV infection, and CHARGE syndrome.
Aplasia of scala media of inner ear, with poorly differentiated organ of Corti, deformed tectoria
membrane, and collapsed Reissners membrane.
Scheibe aplasia occurs in several forms of non-syndromic and syndromic deafness, e.g. Jerve
& Lange-Nielson, Refsum, Usher, Waardenberg, and Rubella syndrome.
Most common form of inner ear

aplasia
Scheibe aplasia is a.k.a. cochlear-saccular dysplasia or pars inferior dysplasia. It is the

most common form of inner ear aplasia.
Scheibe aplasia (a.k.a. cochlear-saccular dysplasia or pars inferior dysplasia)
Alexander aplasia
Proportion of bilateral and unilateral
deafness in congenital deafness.
Enlarged vestibular aqueduct
syndrome
Most common congenital semicircular

canal malformation
What are the various inner ear
structural malformations that cause
congenital deafness?
Limited differentiation of cochlear duct at level of basal coil of cochlea, causing malfunction o
organ of Corti and cells of spiral ganglion.
Bilateral: 65%
Unilateral: 35%
Definition: Vestibular aqueduct >1.5 mm as measured midway between operculum and commo
crus on CT scan.
Presents as fluctuating sensorineural deafness due to hydrodynamic changes in inner ear.
Lateral semicircular canal deformity
1. Michel aplasia
2. Mondini aplasia
3. Scheibe aplasia
4. Alexander aplasia
6. Semicircular canal malformations
Classification of external / middle ear

deformities
Class I
Class II
Class III
Abnormal
ossicles
Atretic canal &

microtia
Poorly aerated
middle ear &
mastoid
Difference between congenitally fixed

footplate of stapes and otosclerosis
Congenitally fixed footplate of
stapes
Onset during childhood
Otosclerosis
Late onset
Constant
Negative family history
Flat 50-60 dB conductive deafness (
no notch)
No Schwartze sign
Progressive
Positive family history
Carhart notch
Schwartze sign
A couples firstborn is congenitally deaf 10-15%

with unexplained cause. What is the
chance of the second child being
congenitally deaf too?
Components of a hearing aid
Microphone
Amplifier (= signal processor)
Receiver (= loudspeaker)
Power source
Properties of a hearing aid
Frequency response usually upto 3000 4000 Hz
Gain ratio of output power and input power
OSPL-90 a.k.a. SSPL-90, i.e. saturated sound pressure level; it is the maximum output
The two most important factors which
Word recognition score (should be high, e.g. > 50%)
predict success of a hearing aid
Dynamic range (should be wide)
Dynamic range of a hearing aid
Difference between the uncomfortable loudness level and speech reception threshold:
Most comfortable level of a hearing aid

Occlusion effect of a hearing aid
Large venting of a hearing aid
Advantages and disadvantages of the
various styles of hearing aid
(Uncomfortable loudness level) (Speech reception threshold)

It is usually midway between the uncomfortable loudness level and the speech reception
threshold
Reverberation of low frequencies in a closed ear canal
Leaves ear canal open so low frequencies can escape from the occlusion effect. Unfortunate
this cannot be done if patient has low-frequency hearing loss.
Behind-The-Ear, In-The-Ear, In-The-Canal, Completely-in-the-Canal
Which style of hearing aid is best for

children?
Advantages and disadvantages of
implantable hearing aid over
conventional hearing aid
The more one enters the canal, the better the cosmesis, but the worse the venting. Thus,
Behind-The-Ear achieves best venting but worst cosmesis, while Completely-in-the-Canal
achieves worst venting but best cosmesis.
Behind-the-Ear
Advantages of implantable aid:
1. Better sound fidelity
2. No occlusion effect
3. Few feedback problems
Disadvantages of implantable aid:
Types of implantable hearing aids

BAHA (Bone Anchored Hearing Aid)
Uses of BAHA (Bone Anchored
Hearing Aid)
DACS hearing aid (Direct Acoustic

Cochlear Stimulation)
1. High cost
2. Need for surgical battery replacement
3. MRI incompatibility
4. Iatrogenic ossicular discontinuity to reduce feedback (in some devices)
1. Electromagnetic
2. Piezoelectric
Device is surgically implanted in temporal bone behind ear. It picks up sound from the air and
transfers it to the cochlea via the temporal bone.
1. Conductive loss
2. Mixed loss with significant conductive element
3. Mastoid cavity which is draining
4. Conductive loss not otherwise correctable (e.g. congenital atresia with ossicular
malformations)
Electromagnetic partially implantable device for sensorineural deafness with some cochlear
reserve. It drives the stapes or stapes footplate directly.
Benefit of DACS over BAHA is that only one cochlea is stimulated (while BAHA stimulates both
cochleas).
Properties of ideal middle ear

prosthesis
Common materials used in ossicular

prosthesis
How would you surgically correct an

ossicular defect?
Lightweight
Made of bio-compatible material
Easy to trim, handle, and adjust
Stable in the middle ear
MRI compatible
Plastipore
Hydroxyapatite
HAPEX (hydroxyapatite with polyethylene)
Titanium
For malleus-incus defect: PORP (Partial Ossicular Reconstruction Prosthesis). Spans the
distance between the stapes supra-structure and the tympanic membrane.
For malleus-incus-stapes defect: TORP (Total Ossicular Reconstruction Prosthesis). Replac

the entire ossicular chain. Spans the distance between the stapes footplate and the tympanic
membrane. (A footplate shoe may be used to stabilize the prosthesis on the stapes footplate.)
In both PORP and TORP, a thin layer of cartilage may be placed between the prosthesis head
and the tympanic membrane to reduce the chance of extrusion.
Difference between stapedectomy and

stapedotomy
If both ears are deaf, on which ear

should stapedectomy be done?
What kind of patient who requires
stapedectomy should rather be offered
For incus defect (e.g. discontinuity at incudo-stapedial joint): Synthetic prosthesis or nativ
incus interposition. In native incus interposition, the incus is removed, sculpted, and
repositioned.
Stapedectomy: Removal of stapes suprastructure and all (or most) of the stapes footplate.
Stapedotomy: Removal of stapes suprastructure and fenestration of the stapes footplate (to
accommodate the prosthesis).
The worse-hearing ear.
1. Patient with osteogenesis imperfecta: patient has brittle bones and surgeon may damage
the tympanic ring
a hearing aid instead of

stapedectomy?
Complications of stapedectomy /
stapedotomy
2. Patient with Menieres disease: surgeon may damage the saccule (as patient has
endolymphatic hydrops) and cause dead ear
3. Patient is blind: patient may not be able to compensate for even minor vestibular
complications
4. Patient with contralateral peripheral vestibulopathy: as above, patient may not be able t
compensate for even minor vestibular complications
5. Patient with mixed hearing loss: patient should be advised that he may need hearing aid
after surgery
Intra-operative complications:
1. Tympanic membrane perforation
2. Floating footplate
3. Facial nerve paralysis (due to dehiscent tympanic segment)
4. Hemorrhage from persistent stapedial artery
Delayed complications:
Styles of stapes prostheses used in

stapedectomy
Cochlear implant bypasses what part
of the cochlea?
Components of a cochlear implant
Disorders in which cochlear implant is

contra-indicated
1. Persistent conductive hearing loss

2. Vertigo
3. Sensorineural hearing loss
1. Piston style
2. Bucket handle
Cochlear implant bypasses the hair cells and directly stimulates the ganglion cells and cochle
nerve.
Microphone
Processor
Transmission link
Electrode array
1. Michel deformity (because of absent cochlea)
2. Narrow internal auditory canal syndrome (because of absent cochlear nerve)
3. Neurofibromatosis type 2 (because of bilateral vestibular schwannomas)
Is intra-cochlear ossification
(secondary to labyrinthitis ossificans) a
contra-indication to cochlear implant
Child with cochlear implant has
developed middle ear effusion. What
should you do?
How is a patient selected for cochlear
implant?
No, it is not. (But intra-cochlear ossification can limit the type and insertion depth of the electro
array that can be introduced into the cochlea.)
Nothing. Treat only if effusion becomes infected.
Age: Minimum age of 12 months is currently recommended.

History (otologic) and physical examination. Determine cause of deafness if possible.
Rule out absolute contra-indications: Michel deformity, narrow internal auditory canal
syndrome, neurofibromatosis type 2
High-resolution CT or T2-weighted MRI: To identify cochlear malformations, labyrinthitis

ossificans (best picked on CT), sclerosing labyrinthitis (best picked on MRI), anamolous facial
nerve, and status of cochlear nerve. None of these conditions is a contra-indication to cochlea
implantation.
Status of ear: Ear should be stable. Tympanic membrane should be intact. There should be n
middle ear effusion and no chronic otitis media. If any of these condtions is present, treat them
before placing the implant.
Audiological criteria: Severe to profound hearing loss and poor word recognition scores.
Psychological assessment: To rule out organic brain dysfunction, mental retardation,
undetected psychosis, or unrealistic expectations. Also to assess family dynamics that may
impact on implant acceptance and performance.
Vaccination: Patient should be vaccinated with Pneumococcal vaccine >2 weeks before
implantation
Definition of post-lingual deaf

Boundaries of facial recess
Complications of cochlear implant
What additional help can a patient with

cochlear implant get?
Narrowest part of fallopian canal
Relations of facial nerve on medial
wall of middle ear
Most commonly injured part of intratemporal facial nerve
Where does communication between
vagus nerve and facial nerve take
place?
Special cases:
Previously operated ear with mastoid cavity: can be implanted, but cavity will need to be
obliterated.
Adolescent with little experience with speech: may find the sound disturbing. Counseling may
help in this case.
Onset of deafness at 5 years of age
Facial recess is a triangular area bound by:
1. Fossa incudis superiorly

2. Chorda tympani nerve laterally and anteriorly
3. Facial nerve medially and posteriorly
1. Post-auricular flap breakdown
2. Facial nerve injury
3. CSF leak
4. Infection
5. Intra-cochlear ossification
Cochlear implant in one ear and hearing aid in same ear.
Cochlear implant in one ear and hearing aid in other ear.
Cochlear implant in one ear and cochlear implant in other ear (i.e. implant in both ears).
Start of labyrinthine segment of facial nerve, namely the meatal canal. It is also the narrowe
part of the facial nerve.
Medial to cochleariform process
Superior to oval window
Inferior to lateral semicircular canal
Post-geniculate ganglion, namely tympanic and mastoid parts
Mastoid segment of facial nerve receives communication from auricular branch of vagus nerve
Pes anserinus
The five terminal branches of the facial
nerve
Landmarks for identification of extratemporal facial nerve
Landmarks for identification of intratemporal facial nerve

Lengths of various parts of intratemporal facial nerve
Most common part of facial nerve

injured by:
1. mastoid surgery
2. middle ear surgery
3. temporal bone fracture
4. CSOM
Extensive network of anastomosis between various limbs of facial nerve within the substance o
the parotid gland
Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical
1. Tragal pointer: nerve is 1 cm infero-medial to it
2. Tympano-mastoid suture: nerve is 7 mm below the inferior drop off of the suture
3. Insertion of posterior belly of digastric on mastoid process: nerve is just anterior to it
(stylomastoid foramen the point of exit)
4. Parotid gland: follow the nerve branches proximally to find the main trunk
1. Cochleariform process: nerve is medial to it (tympanic segment)
2. Lateral semicircular canal: nerve is inferior to it (second genu)
3. Digastric ridge: nerve is anterior to it (stylomastoid foramen the point of exit)
Intra-cranial: 24 mm
Meatal: 8 mm
Labyrinthine: 4 mm
Tympanic: 8 mm
Mastoid: 12 mm
Extra-temporal (before branching): 16 mm
1. Mastoid surgery: Pyramidal turn (postero-lateral to the lateral semicircular canal). This
in the tympanic part of the nerve.
2. Middle ear surgery: Part of the nerve superior to oval window. This is in the tympanic
part of the nerve. (Understandably, it is also most common site of dehiscence of the
nerve.)
3. Temporal bone fracture: Labyrinthine segment, especially geniculate ganglion
4. CSOM: Tympanic and mastoid segments.
Most common site of dehiscence of

facial nerve in the fallopian canal
What features of facial nerve paralysis
are suggestive of neoplastic etiology?
Ramsay Hunt syndrome
House-Brackmann grading of facial

nerve paralysis
Features of central cause of facial

paralysis (as opposed to peripheral
cause)
Part of the nerve superior to oval window. (This is part of the tympanic segment of the nerve
Suggestive if slow course:
Progression of >3 weeks, or
No improvement after >4 months
Highly suggestive if slow course + one of the following:
Facial twitching
Additional cranial nerve involvement
Sensorineural deafness or vestibular symptoms
Ipsilateral recurrence of facial nerve paralysis
Parotid mass
History of cancer
Facial nerve paralysis
Vesicular eruptions on face/ear
Severe otalgia
Vertigo
Tinnitus
Grade 1: Normal
Grade 2: Mild
Grade 3: Moderate
Grade 4: Moderately severe
Grade 5: Severe
Grade 6: Total
Only lower face involved contralateral side.
Also, no loss of emotional facial expression, lacrimation, taste, and salivation. However, Bells
phenomenon is lost.
What are the relative merits and

demerits of doing CT scan and MRI for
investigation of facial nerve paralysis?
Compare and contrast neurapraxia,
axonotmesis, and neurotmesis
Synkinesis
Bogorad syndrome
(In peripheral cause, there is involvement of both upper and lower part of face ipsilateral side
There is loss of emotional facial expression, and there may be loss of lacrimation, taste, or
salivation.)
CT scan for intra-temporal course, as it is good study for bone (temporal bone).
MRI for extra-temporal course, as it is good study for soft tissue (parotid gland).
Axonal
integrity
Endoneural
sheath
Prognosis
Preserved
Preserved
Wallerian
degeneratio
n
No
Yes
Neurapraxia
Axonotmesi
s
Preserved
Disrupted
Neurotmesi
s
Disrupted
Disrupted
Yes
Poor
Excellent
Excellent
Electrophys
iological
tests
Normal
Rapid and
complete
degeneratio
n
Rapid and
complete
degeneratio
n
Note: Neurapraxia is due to local compression and resolves completely when the compression
is relieved. In axonotmesis, although there is Wallerian degeneration distal to the lesion, there
complete recovery because the endoneural sheath of the nerve is preserved.
Loss of discrete facial movements after facial nerve paralysis.
Occurs due to axons innervating numerous and separated muscles.
Occurs after facial nerve paralysis when regenerating nerve fibers destined for the
submandibular gland innervate the lacrimal gland. Patient cries while eating. Hence, the
syndrome is a.k.a. crocodile tear syndrome.
Crocodile tear syndrome
What are the various electrophysiologic tests of facial nerve

function?
Occurs after facial nerve paralysis when regenerating nerve fibers destined for the
submandibular gland innervate the lacrimal gland. Patient cries while eating.
A.k.a. Bogorad syndrome.

Nerve excitability test: Minimal stimulus causing muscle twitch is given to both paralyzed and
non-paralyzed side. Difference in stimulus (in milli-amperes) is calculated; 3.5 mA suggests
degeneration.
Maximum stimulation test: Maximal stimulus causing muscle contraction is given to both
paralyzed and non-paralyzed side. Difference in muscle contraction is estimated.
Electro-neurography: Supra-threshold stimulus causing muscle contraction is given to both

paralyzed and non-paralyzed side. Difference in muscle contraction is calculated by measuring
the CMAP (compound muscle action potential).
Which of the electro-physiologic tests

of facial nerve function is superior?
Schirmers test
Electro-myography: A needle electrode is inserted into the muscle on both paralyzed and non
paralyzed side. Difference in muscle contraction is calculated by measuring the action potentia
of individual motor units (at rest and on voluntary contraction).
Electro-myography is valuable on any Day after onset of facial nerve paralysis.
Electro-neurography is valuable from Day 3 to Day 14 of onset of facial nerve paralysis.
Maximum stimulation test should be done only if electro-neurography or electro-myography are

not available.
Nerve excitability test is obsolete.
Test to evaluate paralysis of greater superficial petrosal nerve (branch of facial nerve). Paper
strips are placed in the conjunctival fornix of both eyes. After five minutes, the length of paper
moistened is compared. Decreased lacrimation to < 25 mm after five minutes is significant.
The test is not as important as a topo-diagnostic tool as it is to evaluate the protective
Most common cause of acute facial

nerve paralysis
Chance of recurrent paralysis after
one episode of Bells palsy
Cause of Bells palsy
How is Bells palsy diagnosed?
Treatment of Bells palsy
mechanism of the eye in patient of facial nerve paralysis.

Bells palsy
~ 10%, more likely on contralateral side
Unknown (idiopathic). Likely cause is type 1 herpes virus (HSV-1).
The diagnosis is clinical:
Acute onset
Paralysis (or paresis) of all muscle groups (both upper and lower) of one side of face
Absence of signs of CNS disease, ear disease, or cerebellopontine angle disease (diagnosis o
exclusion)
ADULTS:
Steroid
Surgical decompression if complete facial nerve paralysis with extensive nerve
degeneration (>90% degeneration in first 2 weeks after onset of paralysis as measured by
electro-neurography and absence of action potentials on voluntary electro-myography). This
should be done to avoid permanent damage and synkinesis.
CHILDREN:
Second most common cause of facial

nerve paralysis
Management of post-op facial nerve
paralysis
Steroid not given.

Eye protection is important.
Trauma? Herpes zoster?
Make sure that the paresis/paralysis is not due to effect of local anesthetic or pack in middle ea
or mastoid pressing on dehiscent nerve. Management depends upon what surgeon feels abou
the extent of injury:

Surgeon feels that paresis is due to minor trauma and edema:
This is the most common cause. Surgeon should give systemic steroid. He should follow the
paralysis with electro-physiologic tests. (If and when electro-myography shows no action
potentials, surgeon should explore the nerve and decompress or repair it.)
Most common cause of post-op facial

nerve paralysis
Differences between longitudinal and
transverse fractures of temporal bone
Surgeon feels that nerve may be seriously injured:

Surgeon should explore the nerve and decompress or repair ASAP.
Minor trauma and edema. (In such case, it should be treated conservatively.)
Longitudinal
Per cent of temporal bone
fractures
Chance of facial nerve
paralysis
Mechanism of facial nerve
paralysis
Fracture is caused by
trauma to:
Part of ear involved
Clinical presentation
Transverse
80%
20%
25%
50%
Compression and ischemia
Severance
Temporo-parietal area
Occiput
Middle ear
1. Bleeding from middle ear
or external ear
2. Laceration of tympanic
membrane
3. Conductive deafness
4. Facial nerve paralysis
Inner ear
1. Hemo-tympanum
2. Vestibular symptoms
3. Severe sensorineural or
mixed deafness
4. Facial nerve paralysis
Patient got facial nerve paralysis after

sustaining gunshot injury to head.
What is the mechanism of injury to the
nerve?
Management of traumatic facial nerve
paralysis
Thermal and compression injury. (NOT severance.)
TRAUMA TO INTRA-TEMPORAL NERVE:

Get CT scan and audiometry done.
Incomplete paralysis:
Conservative (steroid)
Delayed onset paralysis:
Conservative (steroid)
Complete paralysis:
Surgery: if electro-neurography shows >90% degeneration within 2 weeks of injury. Can
compromise on 2 weeks window period if CT scan shows obvious bone fragment impinging on
nerve.
If nerve is intact and there is no injury, then decompress.
If nerve is intact and there is significant injury, then resect and re-anastomose or graft.
If nerve is severed, then re-anastomose or graft.
Grafting is done when there is tension in the nerve. Graft should be taken from great auricula
nerve (if small segment is required) or sural nerve (if long segment is required).
TRAUMA TO EXTRA-TEMPORAL NERVE:
Assess:
1. Site of injury (electro-physiologic testing may be helpful for this); proximal injury is extremely
debilitating, while distal injury has less morbidity
2. Soft tissue injury including eyeball, parotid duct, and mouth
3. Amount of contamination
Repair the nerve ASAP.
Exceptions:
If injury is distal to lateral canthus and oral facial crease, then manage conservatively.
What surgical approach should be

used to decompress an injured facial
nerve?
Treatment of Ramsay Hunt syndrome
Compare prognosis of Bells palsy and
Ramsay Hunt Syndrome
Management of facial nerve paralysis
caused by ASOM
If there is significant soft tissue loss or extensive gross contamination, then explore
immediately, debride the wound and tag nerve branches and repair the nerve later on within 3
days.
If hearing is good: Use middle fossa approach. Can combine trans-mastoid approach if
decompression of distal tympanic and mastoid segments.
If hearing is poor: Use trans-labyrinthine approach.

Steroid
Anti-viral
In Ramsay Hunt Syndrome, the facial nerve paralysis is more progressive and more severe an
has worse prognosis.
IV antibiotics
Myringotomy
If coalescent mastoiditis or intra-cranial extension of infection (seen on CT scan), then cortical
mastoidectomy
No need for surgical decompression
How can ASOM and CSOM cause

facial nerve paralysis?

caused by CSOM
What infections of the ear can cause
facial nerve paralysis?

caused by malignant otitis externa
Most common neurologic sign of Lyme
disease
Presentation and management of
Lyme disease
Causes of bilateral facial nerve

paralysis
Heerfordt disease
Uncommon but important causes of
facial nerve paralysis
ASOM: Exposure of dehiscent nerve to infection or inflammatory mediators
CSOM: Cholesteatoma or chronic inflammatory tissue involving the nerve (tympanic or mastoi
segment)
IV antibiotics
Tympano-mastoidectomy (remove the cholesteatoma or inflammatory tissue)
Steroid
ASOM
CSOM
Mastoiditis
Malignant otitis externa
IV antibiotics
Surgical debridement only if there is obvious necrotic bone
Flu-like symptoms
Skin rash: erythema chronicum migrans (rash starts as flat, reddened area and extends with
central clearing)
Facial paralysis: only 10% chance, but may be bilateral
Deafness: sensorineural, extremely rare chance
Rx: Doxycycline x 4 weeks; prognosis is excellent

Guillain Barre syndrome (most common cause)
Lyme disease
Sarcoidosis (Heerfordt disease, a.k.a. uveo-parotid fever)
Mobius syndrome
Uveo-parotid fever, i.e. fever with uveitis and parotitis and cranial nerve paralysis (e.g. bilatera
facial nerve paralysis). It is a form of sarcoidosis.
Guillain Barre syndrome
Infectious mononucleosis
Electro-physiologic hallmarks of
neoplastic etiology of facial nerve
paralysis
Most common benign tumors of facial
nerve
Tumors that cause facial nerve
paralysis
What per cent of malignant parotid

tumors cause facial nerve paralysis?
Incidence of facial nerve paralysis in
newborn
Most common cause of facial nerve
paralysis in newborn
Causes of facial nerve paralysis in
newborn
Clinical features of facial nerve
paralysis in newborn due to birth
trauma
Sarcoidosis
HIV infection
Electro-neurography: reduced amplitude of CMAP (compound muscle action potential)
Electro-myography: fibrillation and polyphasic re-innervation potentials
Facial neuroma, Hemangioma of facial nerve
They present with facial nerve paralysis
Intra-cranial:
Facial neuroma
Hemangioma of facial nerve
Acoustic neuroma
Meningioma
Congenital cholesteatoma
Adenoid cystic carcinoma
Arachnoid cyst
Extra-cranial:
Parotid tumor (benign & malignant)
~ 15%
1 in 2,000
Birth trauma
Birth trauma
Congenital, e.g. Mobius syndrome, CULLP
Unilateral facial nerve paralysis
Prolonged or complicated delivery
Echhymosis of face or temporal region
Hemotympanum
Mobius syndrome
Hypoplasia / aplasia of depressor

anguli oris

in newborn
Congenital bilateral facial nerve paralysis

6th nerve (abducens nerve lateral rectus) paralysis unilateral or bilateral
Other cranial nerve paralysis (III, IV, IX, X, XII)
Limb anomalies (e.g. absent pect. major muscle Poland syndrome)
A.k.a. CULLP (congenital unilateral lower lip paralysis)
Infant presents with facial asymmetry when crying. Infant may have other anomalies of head &
neck and cardiovascular system.
Complete physical examination (partial vs. complete paralysis, otoscopy, other anomalies, e
Electro-physiologic testing:
Traumatic case: Electro-neurography is normal at birth and declines afterwards. Electromyography is normal at birth and shows fibrillation potentials afterwards.
Congenital case: Electro-neurography shows reduced responses at birth and remains constan
afterwards. Electro-myography also shows reduced responses at birth and remains constant
afterwards.
Most common complication of facial

nerve paralysis
What are the factors that cause
corneal dessication and exposure
keratitis in patient of facial nerve
paralysis?
Eye care of patient of facial nerve
paralysis
Treatment:
Conservative. Traumatic cases improve spontaneously and completely. Congenital cases have
residual dysfunction. If surgery is planned, it is deferred until adolescence.
Corneal dessication and exposure keratitis.
Lagophthalmos (i.e. incomplete closure of eyelids)
Lower lid ectropion (i.e. outwardly turned lower eyelid)
Diminised lacrimation
Altered corneal reflex
Absent normal Bells phenomenon
Eye lubrication
Protective moisture chamber at night
Protective eyewear during day
Common complications of facial nerve

paralysis
Methods of facial re-animation in
patient of facial nerve paralysis
Surgery: Gold weight, palpebral spring, tarsorrhaphy. Procedure of choice is gold weight.
Corneal dessication and exposure keratitis
Hemifacial spasm
Hyperkinetic blepharospasm
Direct nerve repair: with or without grafting (neurorrhaphy)
Synergistic nerve crossover anastomosis: contralateral buccal nerve is anastomosed with
paralyzed nerve via sural nerve graft
Nerve substitution: done when the proximal nerve is not available. Hypoglossal-facial
anastomosis is successful. However, the resultant hemi-tongue paralysis result in severe
problems in speech, mastication, and swallowing. A hypoglossal-facial interpositional jump gra
can reduce these problems.
Neuromuscular pedicle transfer, muscle transposition, and facial slings: done when ther
is irreversible atrophy of facial muscles. Cosmetic results are not good, but provide important
protection to the eye and mouth.
Eyelid procedures: browlifting, upper eyelid implant, canthoplasty, tarsorrhaphy
Blood supply of facial nerve

Bells phenomenon
Most common cause of bilateral facial
nerve paralysis
Why does epiphora (tearing) occur in
Botox: Clostridium botulinum A toxin, used to treat hemifacial spasm and hyperkinetic
blepharospasm
External carotid artery Posterior auricular artery Stylomastoid artery
External carotid artery Middle meningeal artery Greater superficial petrosal artery
The eyeball turns up and out (supero-lateral) during an attempt to close the eyes. It is a norma
protective mechanism.
Guillain Barre syndrome
Epiphora will occur in only those cases where lacrimation is preserved, i.e. the greater superfic
some cases of facial nerve paralysis?
petrosal nerve is functional and the lesion is post-geniculate ganglion. In other cases, there wil
be decreased lacrimation and dry eye.
Epiphora occurs because of:
Hitselberger sign
Bells palsy is associated with which
disease?
Most common area of facial nerve that
is compressed in Bells palsy
Melkersson-Rosenthal syndrome
Speed of regeneration of facial nerve

Derivatives of branchial arches (nerve
supply)
What is common to all the branchial

arch cysts?
Where do the branchial arch cysts
open?
Meckels cartilage
Reicherts cartilage
1. paralysis of Horner muscle, which dilates the orifice of the nasolacrimal duct
2. ectropion that produces malposition of the puncta
3. absence of blinking (i.e.lack of the pumping action)
Decreased sensitivity in concha (supplied by facial nerve); it suggests space-occupying lesion
the internal auditory canal
Diabetes mellitus
Labyrinthine segment. (It is also the narrowest part of the nerve and the fallopian canal.)
Recurrent unilateral or bilateral facial nerve paralysis of unknown etiology.
Facial edema
Tongue fissuring
3 mm per day
1st arch: Trigeminal (V3)
2nd arch: Facial (VII)
3rd arch: Glossopharyngeal (IX)
4th arch: Superior laryngeal (X)
5th arch: Recurrent laryngeal (X)
They all lie anterior to the sternomastoid muscle.
2nd arch cyst: tonsillar fossa
3rd arch cyst: pyriform fossa
4th arch cyst: lower part of pyriform fossa or larynx
Cartilage of 1st branchial arch
Cartilage of 2nd branchial arch
Arteries of the branchial arches
Embryological development of the

tongue
Embryological development of tonsils
and adenoids
Embryological development of salivary
glands
How does choanal atresia develop?
Embryological development of
nasolacrimal duct
Which paranasal sinus pneumatizes at
birth?
When does the hyoid bone ossify?
When do the laryngeal cartilages
ossify?
Level of larynx in infant and adult
Primary palate and Secondary palate
How does cleft palate develop?
1st arch: Degenerates

2nd arch: Degenerates (OR persistent stapedial artery)
3rd arch: Common & Internal carotid arteries
4th arch: Aorta (L) and Subclavian (R) artery
5th arch: Pulmonary arteries
Anterior 2/3rd: Lateral lingual swellings (from 1st arches) and central tuberculum impar (from
between 1st and 2nd arches)
Posterior 1/3rd: Central cupula (between 2nd and 3rd arches)
Palatine tonsil: 2nd pouch
Lingual tonsil: 2nd and 3rd arch
Adenoids: sub-epithelial infiltration of lymphocytes
All the major salivary glands (parotid, submandibular, sublingual) are derived from the 1st pouc
and are of ectodermal origin.
Usually, the bucconasal membrane ruptures to form the choana. Failure of the membrane to
rupture results in choanal atresia.
Fusion of maxillary process with lateral nasal process creates a groove called the nasolacrima
groove. The epithelium of the groove becomes buried and is resorbed, forming a canal called t
nasolacrimal duct.
Maxillary sinus. (The others pneumatize during childhood.)
The hyoid bone is cartilaginous at birth. Ossification starts at birth and is completed at 2
years of age.
Ossification of the laryngeal cartilages starts after 20 years of age.
Infant: C2-C3
Adult: C5-C6
Primary palate: Alveolar ridge + Hard palate anterior to incisive foramen
Secondary palate: Hard palate posterior to incisive foramen + Soft palate
Cleft of primary palate: Lack of fusion between maxillary prominence and medial nasal
prominence
Pierre Robin Syndrome
Most common facial congenital

anomaly
Rule of 2/3rd with regard to facial
clefting
Incidence of facial clefting (cleft lip

and/or palate)
Degrees of facial clefting
Cleft of secondary palate: Lack of fusion between maxillary prominences of both sides
Micrognathia
Glossoptosis
Cleft palate (U-shaped)
Facial clefting (cleft lip and/or palate)
2/3rd of cleft lips are males.
2/3rd of cleft palates are females.
Also:
2/3rd of cleft lips are left-sided.
~ 1 in 1000
CLEFT LIP:
Microform cleft: Dehiscence of orbicularis oris only
Incomplete cleft: Dehiscence of orbicularis oris and skin only
Complete cleft: Dehiscence of orbicularis oris and skin and nasal floor
CLEFT PALATE:
Management of cleft lip and/or palate
Bifid uvula: Self-explanatory

Submucous cleft: Dehiscence of palatal muscles only
Incomplete cleft: Dehiscence of palatal muscles and part of secondary palate
Complete cleft: Dehiscence of palatal muscles and whole of secondary palate
Feeding: Modified nipple; need to be burped more frequently
Airway: If part of Pierre Robin syndrome, may require airway help
Genetics: Genetic counseling
Surgical repair: Various techniques of palatoplasty

Ear problems: Tympanostomy tubes for COME
Clinical features of velopharyngeal

insufficiency
Most common cause of bacterial

infection of pinna
Causes of bacterial infection of pinna
Differential diagnosis of bacterial

infection of pinna
Velopharyngeal insufficiency: Speech therapy for > 6 months. If speech therapy fails, then
surgery (Orticochea sphincteroplasty for poor lateral wall closure and posterior pharyngeal flap
for anterior-posterior wall motion). If surgery is not possible, then dental obturator.
History:
Hypernasal speech
Nasopharyngeal regurgitation with feeding & drinking
Physical examination:
Hypernasal speech
Mirror placed under nose will fog during speech
Pinch nostrils closed to hear effect of blocked nasal escape of air
Nasopharyngoscopy will show the defect
Trauma (Blunt trauma or Ear piercing)
Trauma (Most common)
Burn
Extension of otitis externa
Extension of sub-periosteal abscess
Post-op complication of ear surgery
Relapsing perichondritis
Cutaneous lymphoma
Gouty typhus
Fungal infection of pinna
Clinical features of bacterial infection

of pinna
Treatment of bacterial infection of
pinna
Tzanck smear
Clinical features and treatment of

fungal infection of pinna
Terminology of acute otitis externa
Risk factors for acute otitis externa

(bacterial or fungal)
Rarely:
Cutaneous leishmaniasis
Scabies
Leprosy
Cutaneous tuberculosis
Pain, erythema, induration/edema, fluctuation (if abscess), cartilage deformity (if advanced)
Mild infection: Oral antibiotics

Severe infection or immunocompromised patient: IV antibiotics (coverage of Pseudomona
important)
Perichondritis or chondritis: IV antibiotics (coverage of Pseudomonas important) + drainage
abscess if present
Look for multi-nucleated giant cell at base of ruptured vesicle.
Used for diagnosis of herpes zoster. Also positive in herpes simplex, CMV, and pemphigus
vulgaris.
Similar to picture of bacterial infection, except that it is unresponsive to oral or IV antibiotics.
Patient may have signs of systemic fungal disease. Patient may be immunocompromised.
Treatment is with topical anti-fungals for mild disease and IV anti-fungals for severe or
disseminated disease.
Furuncle: Localized abscess of apo-pilo-sebaceous unit
Carbuncle: Confluence of multiple furuncles
Acute otitis externa: Diffuse cellulitis; may be result of ruptured furuncle
Warm, humid climate
Swimmer
Trauma to EAC (e.g. cotton bud)
Chronic skin disease: Eczema, Psoriasis, Seborrheic dermatitis
Immunocompromised
Long, narrow canal with poor self-cleaning capability
Obstructive exostosis
Clinical features of acute otitis externa
Patient has acute onset of otalgia and

otorrhea. How will you definitively
distinguish between acute suppurative
otitis media (ASOM) and acute otitis
externa (AOE)?
Treatment of acute otitis externa
Clinical features of acute myringitis
Treatment of acute myringitis
Clinical features of chronic myringitis
Lack of cerumen
Fungal overgrowth in patient with post-surgical mastoid cavity
Pain, pruritis, edema, erythema, otorrhea, and normal tympanic membrane mobility. No fever
(unless infection extends to peri-auricular tissue).
Note: Presentation of bacterial and fungal acute otitis externa is similar, except that in fungal
otitis externa, the fungal hyphae may be visible.
Tympanic membrane mobility.
It will be reduced in ASOM (due to perforation).
It will be normal in AOE.
1. Painkiller
2. Debridement of EAC
3. Otowick if obstructive edema (should be replaced regularly to avoid toxic shock syndrome)
4. Keep ear dry
5. Topical antibiotic or anti-fungal clotrimazole as per etiology
6. If severe peri-auricular cellulitis or immunocompromised patient, then oral antibiotic or IV an
fungal as per etiology
7. Incision and drainage of furuncle / carbuncle
Acute myringitis is an uncommon sequel of ASOM. It presents with severe pain in the ear.
Acute bullous myringitis: Blisters on lateral surface of tympanic membrane.
Acute hemorrhagic myringitis: Blood on lateral surface of tympanic membrane.
1. Topical antibiotic
2. Lance the bullae (for pain control)
3. Treat the ASOM
4. Keep ear dry
Chronic disease with relapsing and recurring symptoms.
Painless otorrhea, pruritis.
Tympanic membrane: beefy, weeping granulation tissue; perforation or healed perforation.
Treatment of chronic myringitis
Clinical features of chronic otitis

externa
Etiology of chronic otitis externa

How would you investigate a case of
chronic otitis externa?
Treatment of chronic otitis externa
Clinical features of malignant otitis

externa

malignant otitis externa?
Conductive deafness (due to TM thickening) and/or canal stenosis in long-standing cases.

No middle ear pathology.
1. Topical antibiotic
2. Keep ear dry
3. Cautery: chemical (silver nitrate) or laser (CO 2)
4. Surgery: tympanoplasty with canaloplasty for severe disease with canal obliteration
Thickened skin of EAC, Keratosis, and Lichenification
Pruritis
No otalgia
Late disease: obliteration
Chronic skin conditions, e.g. seborrheic dermatitis, atopic dermatitis
Characteristic clinical features
Biopsy (especially if granulation is present)
Frequent debridement
Treat the underlying skin disorder
Topical antibiotic
Topical steroid
If obliteration: canaloplasty with split thickness skin graft
Diabetic or immunocompromised patient
Deep-seated otalgia which is out of proportion to examination findings
Otorrhea
Granulation tissue along the tympano-mastoid suture line
Edema
Cranial nerve paralysis: facial nerve is most commonly affected, but 3rd, 4th, 6th, 9th, 10th, 11th, an
12th may be affected
Thrombosis of cavernous, sigmoid, or transverse sinuses, and/or internal jugular vein
Intra-cranial abscess and/or meningitis leading to death
Biopsy of granulation tissue to rule out cancer
Technetium (Tc99) scintigraphy (bone scan) to confirm diagnosis (remains positive foreve
Gallium 67 every 4 weeks to follow treatment response
Treatment of malignant otitis externa
What is otomycosis?
Most common cause for visit to
pediatrician
Risk factors for ASOM in children
Clinical features of ASOM

What pathologic feature of the
tympanic membrane is the best
indicator of ASOM?
Treatment of ASOM
CT scan to evaluate extent of bony destruction; contrast for associated abscess or cellulitis
MRI if intra-cranial extension is suspected
1. Aggressive diabetic control
2. Correct immunodeficiency (if possible)
3. Debridement of EAC (gently)
4. Antibiotic 1st line: oral fluoroquinolone; 2nd line: IV amino-penicillin
5. IV anti-fungal (amphotericin B) if cause is fungal
6. Surgery drainage of abscess and debridement of bony sequestrum
Another name for fungal acute otitis externa
Acute suppurative otitis media (ASOM)
Ethnicity
Premature birth
Cleft palate
Down syndrome
Lack of breastfeeding in first 6 months of life
Supine bottle feeding
Lower socio-economic status
Presence of siblings
Attendance at day care facility
Second hand smoke exposure
Otalgia, irritability, fever, otorrhea
Tympanic membrane: bulged, perforated, not moving, with air-fluid level behind
Bulging of the tympanic membrane
Pain control:
Panadol
Brufen
Topical anesthetic drops
Myringotomy
If <2 years age, then treat immediately.
If >2 years age, then observe; if symptoms do not abate in 48 72 hours, then treat.
Antibiotic:
Mild to moderate disease: Amoxicillin 90 mg/kg/d divided tid for 10 days (If child is >5 years,
can give for 7 days only)
Severe disease (fever >390C or severe otalgia): Augmentin with same dose of amoxicillin
If patient is allergic to penicillin: macrolide (azithromycin / clarithromycin / erythromycin)
If treatment failure (i.e. symptoms do not improve within 48 72 hours): Amoxicillin Augmen
IV ceftriaxone Tympanocentesis with culture / sensitivity
Definition of Recurrent ASOM
If patient has cochlear implant: If <2 months since implantation, then IV antibiotic (ceftriaxone)
>2 months since implantation, then oral antibiotic (amoxicillin / Augmentin), but monitor closely
as there is risk of meningitis or biofilm infection of the electrode
3 episodes of ASOM in 6 months OR 4 episodes of ASOM in 12 months.
Treatment of recurrent ASOM
Must be asymptomatic between episodes.

Tympanostomy tube (Causes less chance of ASOM, and even if it occurs, there will be only
painless otorrhea which can be managed with topical antibiotics)
Biofilm
Prophylactic antibiotics are not recommended.

As opposed to free-floating bacteria (planktonic bacteria), the bacteria in a biofilm are encased
a matrix cortaining oligopolysaccharides and bacterial toxins. The matrix elicits host response
but prevents the bacteria from the immune system and from antibiotics
Which area of the tympanic membrane Pars flaccid (upper part between anterior and posterior malleal folds at the notch of Rivinus)
is most susceptible to retraction?
Compare and contrast the
In all cases, URTI causes inflammation of Gerlachs tonsil of the Eustachian tube, leading to
pathophysiology of ASOM, CSOM,
Eustachian tube dysfunction and stasis of middle ear secretions. Moreover, bacteria harbore
and COME
in the adenoids reflux into the middle ear (nasopharyngeal reflux), thus causing infection in t
middle ear secretions.
There are additional factors in CSOM:
Clinical features of CSOM

CSOM?
Treatment of CSOM
Biofilm
Tympanostomy tube or perforation in tympanic membrane
Chronic or intermittent otorrhea
Aural fullness
Deafness (conductive confirmed by tuning forks)
Tympanic membrane retraction and/or keratin debris
Tympanic membrane perforation
Middle ear mucosa inflamed
Granulation tissue and/or aural polyp
Clinical features are diagnostic.
Audiometry
CT temporal bone if cholesteatoma or complications are suspected or if treatment failure
MRI with contrast if intra-cranial complications are suspected
Biopsy of persistent granulation tissue that does not respond to topical antibiotic therapy (t
rule out cancer, TB, Wegeners granulomatosis, etc.)
Goal is to get a dry, safe ear
Debridement
Topical antibiotic for 4 6 weeks (fluoroquinolone)
Tympanoplasty if cause of CSOM is recurrent water exposure
Tympano-mastoidectomy if cholesteatoma or refractory to topical treatment. (Goal of tympan
A 30-year-old man comes to you with

right-sided middle ear effusion. What
is the most important thing you should
do?
Clinical features of COME
Definition of COME
COME?
Treatment of COME
Complications of COME
Specific population of children who

have high risk of developing COME
Compare and contrast the clinical

features of CSOM and tuberculous
otitis media
mastoidectomy is to remove cholesteatoma and granulation tissue and to restore continuity

between middle ear cleft and mastoid cavity.)
Examine his nasopharynx to rule out nasopharyngeal mass or cancer.
(While middle ear effusions are common in children, a unilateral middle ear effusion in an adul
should raise suspicion of nasopharyngeal mass.)
Aural fullness
Deafness (conductive confirmed by tuning forks)
Intact tympanic membrane
Visible middle ear effusion
Frequently asymptomatic, especially in children
Inflammation within the middle ear space resulting in a collection of fluid behind an intact
tympanic membrane. There is no otalgia and no systemic symptoms such as fever and malais
Clinical features
Pneumatic otoscopy is key.
Tympanometry if clinical evaluation is equivocal.
Nasopharyngoscopy if unilateral effusion (to rule out nasopharyngeal mass or cancer)
Watchful waiting most cases will resolve spontaneously
If complication deafness, speech delay, developmental disability, or tympanic membrane
atelectasis then surgery (tympanostomy tube)
Ossicular damage (conductive deafness)
Tympanic membrane atelectasis (conductive deafness)
Cholesteatoma
Cleft palate
Down syndrome
In both cases, the etiology is Eustachian tube dysfunction

Both are chronic conditions and the clinical features are similar, except that in tuberculous otiti
media:

tuberculous otitis media?
Treatment of tuberculous otitis media

Complications of otitis media
the otorrhea is thin and cloudy

the perforations in the tympanic membrane are multiple, which later join to form one large
perforation
the tympanic membrane is thickened
the disease is unresponsive to standard antibiotic and surgical treatment
there is higher risk for facial nerve paralysis
Biopsy for AFB
Chest X-ray
Skin testing with PPD
CT temporal bone will show chronic otitis media
As for pulmonary TB (PESTRI pyrazinamide, ethambutol, streptomycin, rifampicin, isoniazid)
INTRA-TEMPORAL:
Hearing loss (conductive, sensorineural)
Vestibular dysfunction
Tympanic membrane perforation
Mastoiditis (complication of ASOM)
Cholesteatoma (acquired)
Labyrinthine fistula
Petrous apicitis
EXTRA-TEMPORAL:
Extra-cranial:
Sub-periosteal abscess
Citelli abscess
Bezold abscess
Lucs abscess
Zygomatic root abscess
Most common ossicular chain

complication of CSOM
What per cent of cases of ASOM and
CSOM develop tympanic membrane
perforation?
Clinical features of acute mastoiditis

acute mastoiditis?
Coalescent mastoiditis
Intra-cranial:
Meningitis
Lateral sinus thrombosis
Subdural empyema
Epidural abscess
Intra-parenchymal abscess
Otic hydrocephalus
Fibrous union of incudo-stapedial joint
ASOM: Only 5%. Resolves spontaneously.
CSOM: 100%. Does not resolve spontaneously.
History of recent ASOM
Mastoid pain and tenderness
Auricular protrusion
Post-auricular skin changes
Fullness of skin of postero-superior EAC
Fever
Clinical features
CBC: Increased white cell count (leukocytosis)
Acute mastoiditis plus the following additional features evident on CT scan:
Pus in the mastoid
Erosion of bone and bony destruction of mastoid air cells
Treatment of acute mastoiditis
There is high risk for infection to spread to adjacent tissues. Coalescent mastoiditis is an
indication for urgent surgery.
Infection limited to mastoid:
IV antibiotic (3rd generation cephalosporin) (No response) Tympanostomy tube (No

response) Mastoidectomy
Coalescent mastoiditis:
IV antibiotic + Mastoidectomy
Treatment of labyrinthine fistula

caused by cholesteatoma in CSOM
Infection beyond mastoid:

IV antibiotic + Mastoidectomy + Incision & Drainage of any abscess
Remove matrix (of cholesteatoma) completely and repair the fistula or obliterate with bone wax
or pate. Leave canal wall up.
OR
Petrous apicitis
Leave part of matrix over fistula. Do canal wall down.

A.k.a. Gradenigo syndrome:
Otorrhea
Retro-orbital pain
Diplopia (caused by 6th nerve paralysis)
It is a complication of CSOM with cholesteatoma

Treatment of petrous apicitis
IV antibiotics
Followed by surgical management of cholestetoma
Gradenigo syndrome
Another name for petrous apicitis. Triad of otorrhea, retro-orbital pain, and diplopia.
Treatment of sub-periosteal abscess of It is typically an extension of mastoiditis.
mastoid
Small children: IV antibiotic + Needle aspiration
Older children & adults: IV antibiotic + Incision & drainage + Cortical mastoidectomy
Citelli abscess
Abscess in occipital bone. It is a complication of CSOM
Bezold abscess
Abscess inside sternomastoid muscle with erosion of tip of mastoid. It is a complication of
Lucs abscess
Zygomatic root abscess
Most common intra-cranial
complication of ASOM and CSOM
Clinical features of meningitis
(complication of ASOM and CSOM)

meningitis (complication of ASOM and
CSOM)?
Treatment of meningitis (complication
of ASOM and CSOM)?
Clinical features of lateral sinus

thrombosis (complication of CSOM)?
Griesinger sign
lateral sinus thrombosis (complication
CSOM.
Sub-periosteal abscess in squamous part of temporal bone (temporal area). It is a complicatio
of CSOM.
Abscess in root of zygoma. It is a complication of CSOM.
Meningitis
History of ASOM or CSOM
Severe headache
Fever
Meningismus
Photophobia or Phonophobia
Positive Brudzinski and Kernig signs
CT temporal bone
CT brain (to rule out mass effect)
Lumbar puncture (for diagnosis and CSF culture / sensitivity)
IV antibiotic with good CSF penetration
IV steroid (decreases chance of neurologic sequelae)
Monitor hearing: Audiogram and CT temporal bone to evaluate for ossification of cochlea. (If
ossification, then urgent cochlear implantation.)
History of otorrhea
Severe headache
Picket-fence fever
Swelling and tenderness of mastoid (Griesinger sign)
Papilledema
Septic emboli to lungs
Jugular vein thrombosis
Palsy of 9th, 10th, 11th cranial nerves
Swelling (edema) and tenderness of mastoid. It is a feature of lateral sinus thrombosis.
CT brain with contrast: (Delta sign: Rim enhancement of lateral sinus with central
hypodensity)
of CSOM)?
Delta sign
Treatment of lateral sinus thrombosis
(complication of CSOM)
Clinical features of subdural empyema

subdural empyema (complication of
CSOM)?
Treatment of subdural empyema
Patient of CSOM develops an epidural

abscess. What parts of the cranium
are likely to harbor the abscess?
Clinical features of epidural abscess
epidural abscess (complication of
CSOM)
Treatment of epidural abscess
MRV (magnetic resonance venography): Flow void in lateral sinus

Intra-operative needle aspiration of lateral sinus: If blood returns, no intervention; if no bloo
returns, then ligate sinus and evacuate clot
CT brain with contrast shows rim enhancement of lateral sinus with central area of hypodensity
It indicates lateral sinus thrombosis.
IV antibiotic
Mastoidectomy with possible ligation of sinus and evacuation of clot
Anti-coagulation
History of otorrhea
Altered mental status
Focal neurologic deficits
Increased intra-cranial pressure
MRI with contrast: shows enhancing fluid collection in subdural space
Lumbar puncture: do only if intra-cranial pressure is normal
IV antibiotic
Drain the abscess (call Neurosurgery)
Prognosis is not good: high mortality rate and risk of neurologic sequelae
Middle and Posterior fossa (as these are adjacent to the middle ear).
Similar to coalescent mastoiditis

CT temporal bone with contrast: shows enhancing fluid collection in epidural space
IV antibiotic
Patient of CSOM develops an intraparenchymal brain abscess. What

parts of the brain are likely to harbor
the abscess?
Clinical features of intra-parenchymal
brain abscess (complication of CSOM)
Prognosis is good.
Cerebellum and temporal lobe (as these are adjacent to the middle ear)
History of otorrhea.
Three stages of brain abscess:

1. Encephalitis: Headache, mental status change, fever, seizures, and increased intra-cranial
pressure
2. Coalescence: May be relatively asymptomatic at this stage
3. Rupture: Increasing headache, meningeal signs, and systemic collapse
Treatment of intra-parenchymal brain

abscess (complication of CSOM)
Clinical features of otitic

hydrocephalus (complication of ASOM
or CSOM)
otitic hydrocephalus (complication of
ASOM or CSOM)?
Treatment of otitic hydrocephalus
Focal deficits in many patients:

1. Cerebellum: ataxia, dysmetria, nystagmus, nausea, or vomiting
2. Temporal lobe: aphasia, visual defects, or headache (if dominant hemisphere)
IV antibiotic (broad-spectrum, including coverage for anaerobes)
When patient becomes stable, surgical management of otologic disease
Prognosis is poor if abscess ruptures into ventricle.
Headache
Photophobia or phonophobia
Increased intra-cranial pressure
Fundoscopic examination: Papilledema
Do not do lumbar puncture (because of risk of tonsillar brain herniation with elevated intra-cran
pressure)
Mannitol
(complication of ASOM or CSOM)
Compare and contrast the

pathophysiology of serous labyrinthitis
and suppurative labyrinthitis
Compare and contrast the clinical

features of serous labyrinthitis and
suppurative labyrinthitis
Diuretics
Serial ophthalmological examination: if increased papilledema and visual compromise, then op
nerve decompression
Surgical management of otologic disease
Serous labyrinthitis: In ASOM or CSOM, bacterial toxins or inflammatory mediators ente
the inner ear through the round window or labyrinthine fistula. They cause dysfunction by
changing ionic potentials. The dysfunction is reversible once the infection is cleared.
Suppurative labyrinthitis: In ASOM or CSOM, the bacteria themselves enter the inner ear
through labyrinthine fistula or congenital abnormality. In meningitis, infection is transmitted via
CSF through internal auditory canal to the cochlear modiolus or cochlear aqueduct
Patient of suppurative labyrinthitis is more sick than patient of serous labyrinthitis.
Serous labyrinthitis
Sensorineural deafness mild or moderate
or severe; unilateral
Vestibular symptoms sometimes
No fever
Absent meningeal signs
Absent cranial nerve palsies
Symptoms resolve gradually with time

serous labyrinthitis (complication of
ASOM or CSOM)?
Audiogram
Vestibular testing
Suppurative labyrinthitis
History of ASOM or CSOM or meningitis (in
meningitic suppurative labyrinthitis)
Sensorineural deafness profound; bilatera
in meningitic suppurative labyrinthitis
Vestibular symptoms severe
Fever
Meningeal signs (if meningitis)
Cranial nerve palsies (indicates disease has
spread outside otic capsule)
Symptoms do not resolve without treatment
Treatment of serous labyrinthitis

(complication of ASOM or CSOM)
Oral antibiotic
Myringotomy if ear is not draining
Tympano-mastoidectomy if cholesteatoma is the source
Audigram
suppurative labyrinthitis (complication
Vestibular testing
of ASOM or CSOM or meningitis)?
Culture via myringotomy (ASOM or CSOM) or lumbar puncture (meningitis)
CT to evaluate cholesteatoma, congenital inner ear abnormality, or intra-cranial complication
If cause is meningitis, serial audiogram and CT to evaluate for labyrinthitis ossificans.
Most common bacteria associated with Streptococcus pneumoniae
deafness
Treatment of suppurative labyrinthitis
IV antibiotic
(complication of ASOM or CSOM or
Tympanostomy tube (if cause is ASOM)
meningitis)
Tympano-mastoidectomy is cholesteatoma is the source
IV steroid (if cause is meningitis)
Serial audiogram and CT for monitoring of labyrinthitis ossificans
What per cent of patients with syphilis Congenital syphilis: 30%
become deaf?
Acquired syphilis: 80% of patients with neuro-syphilis
Clinical features of syphilitic ear
Deafness may be sudden onset, fluctuating, or slowly progressive
Endolymphatic hydrops
Positive Tullio phenomenon
Positive Hennebert sign
VDRL or RPR: for screening
syphilitic ear?
FTA-ABS: for confirmation
Slit lamp examination: to evaluate for interstitial keratitis
Lumbar puncture: test for VDRL (indicates active infection)
CT temporal bone: leutic osteitis of otic capsule
Treatment of syphilitic ear
IV penicillin G x qid x 3 weeks
Steroid x 2 weeks
Patient with tuberculous meningitis
Patients deafness is due to spread of the mycobacterial infection into the inner ear. Treatment
develops sensorineural deafness. How as for tuberculous meningitis.
will you manage him?

Most common cause of non-syndromic
congenital sensorineural deafness
Patient has deafness due to CMV
infection. What would be the clinical
picture?
Patient has deafness due to mumps.

What would be the clinical picture?
Patient has deafness due to measles

(rubeola virus). What would be the
clinical picture?
Gregg syndrome
What are the viruses that commonly
cause infection of inner ear (and
sensorineural deafness)?
Most common bacteria causing

various ear infections
CMV infection
Deafness
Hepato-splenomegaly
Jaundice
Microcephaly
Intra-cerebral calcifications
Deafness
Salivary adenitis
Orchio-epididymitis
Meningitis
Deafness
Koplik spots (grain of rice on red base in oral mucosa)
3 Cs: cough, coryza, conjunctivitis
Rash macules & papules
High-grade fever
Encephalitis
Subacute sclerosing pan-encephalitis (rare)
Congenital rubella. Features include deafness, cataract, microphthalmia, retinitis, blueberry
muffin skin lesions, cardiovascular anomalies, and mental retardation.
CMV
Mumps
Rubeola (measles)
Herpes simplex virus 1
Herpes zoster
Rubella (German measles)
ASOM, Recurrent ASOM, Acute mastoiditis, Acute myringitis, Serous labyrinthitis, Suppurative
labyrinthitis: Streptococcus pneumonia
Acute otitis externa (of pinna or EAC), Malignant otitis externa: Pseudomonas
CSOM: Haemophilus influenza

Chronic otitis externa: Proteus mirabilis
Chronic myringitis: Pseudomonas
Tuberculous otitis media: Mycobacterium tuberculosis
Intra-parenchymal brain abscess (complication of ASOM or CSOM): Staphylococcus aureus
Most common site of bite on pinna
Lobule
Patient has erythema, pruritis,
Likely cause is contact dermatitis.
blisters, and crusting on pinna where Differential diagnosis includes cellulitis and herpes zoster.
she wears jewellery. What is the likely
cause? What is the differential
diagnosis?
Most common cancer of the ear
Basal cell carcinoma
Difference in physical appearance of
Basal cell carcinoma: Erythematous lesion with raised margins and silvery scales
basal cell carcinoma and squamous
Squamous cell carcinoma: Painful polyp with granular appearance with bloody discharge
cell carcinoma of pinna
Most common skin condition of EAC
Eczema
Keratosis obturans
Rapid accumulation of keratin debris in EAC, which gets plugged. Can be a cause of otitis
externa. Treatment is with topical steroid.
Osteoma in EAC
Pedunculated bone mass developing along suture lines tympano-mastoid and tympanosquamous. Occluding osteoma may require surgical removal.
Exostosis in EAC
Lamellar thickening of bone of EAC due to exposure to cold water. Causes EAC stenosis,
cerumen impaction, and difficulty in viewing tympanic membrane. Is a risk factor for otitis
externa.
What kind of hemangioma involutes in Capillary hemangioma involutes in childhood.
childhood, and what kind does not?
Cavernous hemangioma does not involute in childhood.
Cholesterol granuloma
Blue-domed cyst with motor oil color. Contains hemosiderin, cholesterol crystals, and chronic
inflammation.
May present in EAC, mastoid, posterior fossa, or petrous apex.
Patient has traumatic perforation of

tympanic membrane. When would you
like to do a tympanoplasty?
How does Wegener granulomatosis
present to an ENT?
How does polyarteritis nodosa present

in the ear?
How does sarcoidosis present to an
ENT?
Male:Female ratio of otosclerosis

Carhart notch
Clinical features of otosclerosis
Schwartzes sign
Parcusis willis
Treatment of otosclerosis
Ossicular fixation (malleus or incus)
Treatment is surgical removal, except if in EAC, when aspiration can be easily done.
I will do a tympanoplasty if the perforation has not healed in 4 months and there is >20 dB
hearing loss.
There is chronic inflammation and granulation tissue formation. C-ANCA, anti-myeloperoxidas

and anti-proteinase 3 antibodies are positive.
Ear: COME (Chronic otitis media with effusion)
Nose: Nasal crusting, epistaxis, rhinorrhea, and secondary rhino-sinusitis
Larynx: Cough, hoarseness, stridor, subglottic stenosis
Sensorineural deafness
Non-caseating granulomas. Serum ACE levels may be elevated.
Ear: Cochlear-vestibular neuropathy, Facial nerve paralysis

Nose: Nasal obstruction, postnasal discharge, and recurrent sinusitis
Larynx: Granulomas (pale, submucous masses) on epiglottis
1:2 (Otosclerosis is twice as common in females.)
Notch in audiogram. Occurs in otosclerosis.
Progressive conductive or mixed deafness. Also, tinnitus, vertigo, and paracusis willis.
Schwartzes sign may be positive.
Hyperemia of promontory, visible on otoscopy. The sign is sometimes positive in otoscleros
Hearing better in noise. It is a feature of otosclerosis.
Sodium fluoride, calcium, vitamin D
Surgery
After age 50: Ossification of anterior malleolar ligament (malleus)
Congenital: Incomplete absorption of Reicherts or Meckels cartilage
Treatment:
Malleus: Anterior atticotomy with division of anterior malleolar ligament and mobilization of
Facial nerve prolapse

Congenital cholesteatoma
Causes of sudden sensorinueral

deafness
Drugs causing ototoxicity
Rollover
Most common form of fungal sinus
disease
How is allergic fungal rhino-sinusitis
diagnosed?
malleus
Incus: Incus interposition or partial ossicular prosthesis
Dehiscent nerve impinging on stapes supra-structure. Causes flat conductive deafness of ~ 20
dB.
Cholesteatoma with no history of otitis media and intact tympanic membrane.
Often found in the middle ear, but may present in the mastoid, petrous apex, geniculate
ganglion, and posterior fossa.
May present at any age (2 60 years age) with deafness, vertigo, facial paralysis, or vision
changes.
Infection (viral, bacterial)
Vascular
Auto-immune ear disease
Trauma (Fracture, Barotrauma, Surgery)
Tumors
Ototoxic medications
Aminoglycosides
Macrolides
Diuretics
Salicylates
Cisplatin
(Radiation)
Loss of word recognition with increased intensity of speech. Suggestive of retro-cochlear
disorder.
Allergic fungal rhino-sinusitis
Clinical features:
Unilateral (mostly) rhino-sinusitis with nasal polyp and dramatic bony expansion of paranasal
sinuses.
Classic criteria for diagnosis:
Charcot-Leyden crystals
Allergic fungal rhino-sinusitis is
associated with which disease?
Samter triad
What class of inflammatory responses,
cells, and mediators are involved in
the pathogenesis of chronic rhinosinusitis?
Causes of CSF leak
Management of spontaneous CSF

leak
CSF leak?
Keisselbachs plexus
1. Type 1 hypersensitivity
2. Nasal polyposis
3. Characteristic CT appearance (hyper-dense material in sinus cavity)
4. Positive fungal stain or culture
5. Thick, eosinophilic mucin (Charcot-Leyden crystals)
Thick, eosinophilic mucin. Diagnostic of allergic fungal rhino-sinusitis
Asthma
1. Nasal polyp
2. Asthma
3. Aspirin sensitivity
Inflammatory response: Th-2 type
Inflammatory cells: Eosinophils
Inflammatory mediators: Leukotrienes
Trauma (accidental, iatrogenic)

Tumor
Spontaneous
Congenital
Surgical repair followed by lumbar CSF drainage, or long-term therapy to lower CSF pressure
(e.g.acetazolamide), or ventriculo-peritoneal shunt. These procedures are done because of hig
risk of repeated leak secondary to raised CSF pressure.
Beta-2 transferrin test
Nasal endoscopy with intra-thecal fluorescin
CT to identify dehiscence in skull base
MRI to identify brain parenchyma and CSF that have herniated into sinus
A.k.a. Littles area
Anastomosis in anterior part of nose of following arteries:
1. Sphenopalatine artery
Littles area
2. Anterior ethmoid artery

3. Greater palatine artery
4. Superior labial artery
A.k.a. Keisselbachs plexus
Anastomosis in anterior part of nose of following arteries:
Woodruffs plexus
2. Anterior ethmoid artery
3. Greater palatine artery
4. Superior labial artery
A.k.a. naso-nasopharyngeal plexus
Anastomosis in postero-inferior part of lateral wall of nose, inferior to the inferior turbinate, of
following arteries:
Naso-nasopharyngeal plexus
1. Posterior nasal arteries

2. Posterior ethmoid artery
4. Ascending pharyngeal artery
A.k.a Woodruffs plexus
Anastomosis in postero-inferior part of lateral wall of nose, inferior to the inferior turbinate, of
following arteries:
Lymphatic drainage of nose
1. Posterior nasal arteries

2. Posterior ethmoid artery
4. Ascending pharyngeal artery
Submandibular nodes
Upper deep cervical nodes
Histology of respiratory epithelium of

nose
Mucous blanket of the nose
Functions of nose
Narrowest area of nose and its

borders
Male:Female ratio of choanal atresia

Choanal atresia is more common on
which side, right or left?
Clinical features of choanal atresisa
Choanal atresia is associated with
what syndromes?
Treatment of choanal atresia
Retropharyngeal nodes
Pseudo-stratified columnar epithelium with ciliated (and non-ciliated) columnar cells, mucinsecreting goblet cells (1 goblet cell for every 5 columnar cells), and basal cells
Gel phase: superficial, produced by goblet cells and submucous glands, to trap particulate
matter
Sol phase: deep, produced by microvilli, to facilitate movement of cilia
Airway
Filtration
Humidification
Heating
Nasal reflex
Chemo-sensation
Olfaction
Nasal valve, a.k.a. internal nasal valve.
Borders: Lower edge of upper lateral cartilage, anterior end of inferior turbinate, and nasal
septum
1:2 (Twice as common in females)
Right side
Bilateral: Presents at birth as paradoxical cyanosis (i.e. cyanosis relieved by crying)

Unilateral: Presents at 6 24 months age with unilateral obstruction and nasal discharge
CHARGE
Apert syndrome
Crouzon disease
Treacher-Collins syndrome
Bilateral: Stabilize airway with oral airway, or McGovern nipple, or intubation; then Surgery
Unilateral: Surgery
Surgery: Trans-palatal approach, Trans-nasal approach, Endoscopic approach
Congenital midline masses of the nose
Dermoid
Glioma
Most common location of skull base

defect causing encephalocele
Encephalocele
Furstenberg test
Teratoma
Most common teratoma in head &
neck region
Rathkes pouch cyst
Dermoid
Glioma
Encephalocele
Teratoma
Cysts (Rathkes pouch cyst, Thornwaldts cyst, Intra-adenoidal cyst, Branchial cleft cyst)
Congenital midline mass of nose
May be intra-nasal, intra-cranial, or extra-nasal (on dorsum)
Remnant of dura which has not regressed back into cranial cavity
Tendency for repeated infection, so must be surgically excised.
May be intra-nasal or extra-nasal (on dorsum).
Remnant of glial tissue due to abnormal closure of fonticulus frontalis.
Need to rule out intra-cranial connection before surgical excision.
Occipital

Congenital herniation of CNS tissue through skull base defect
May be intra-nasal, naso-pharyngeal, or extra-nasal (on nose, glabella, or forehead)
Pulsatile mass, expands with crying or straining
Tendency for CSF leak, meningitis, or herniation, so must be surgically excised and repaired.
Midline nasal mass expands with compression of internal jugular veins. Implies it is
encephalocele.
Plain x-ray shows calcification
Cervical teratoma.
(Second most common is naso-pharyngeal teratoma.)
Congenital midline cyst of nose
Rathkes pouch cyst is a remnant of Rathkes pouch, which is an invagination of the
nasopharyngeal epithelium in the posterior midline. Is usually asymptomatic but may pres
on pituitary or optic chiasma.
Craniopharyngioma
Thornwaldts cyst
Intra-adenoidal cyst
Branchial cleft cyst
Difference in clinical features of
allergic and non-allergic rhinitis
Types of non-allergic rhinitis
What drugs are known to cause druginduced rhinitis?
Treatment of rhinitis medicamentosa

What is atrophic rhinitis a.k.a.?
Tumor of Rathkes pouch is craniopharyngioma.

Tumor of Rathkes pouch
Develops from remnant of notochord. May be asymptomatic, or present with otitis media with
effusion. Treatment is marsupialization through endoscopic approach.
Retention cyst in adenoid caused by occlusion of adenoid crypt
Position may be lateral. Formed by 1st or 2nd branchial arch. Treatment is surgical excision.
In non-allergic rhinitis, there is consistent presence of symptoms and lack of nasal or ocul
pruritis.
In allergic rhinitis, the symptoms are episodic and there is nasal or ocular pruritis.
Infectious rhinitis
Vasomotor rhinitis
Hormonal rhinitis
Occupational rhinitis
Drug-induced rhinitis
Rhinitis medicamentosa
Gustatory rhinitis
NARES (non-allergic rhinitis of eosinophilia syndrome)
ACE-inhibitors
Beta blockers
NSAIDs
Oral contraceptives
Stop decongestant
Give steroid nasal spray
Rhinitis sicca
Ozena
Causative organism of atrophic rhinitis

Clinical features of atrophic rhinitis
Types of atrophic rhinitis
Empty nose syndrome
Causative organism of rhinoscleroma
Clinical features of rhinoscleroma
rhinoscleroma?
Mikulicz cells
Russell bodies
Causative organism of rhinosporidiosis
Clinical features of rhinosporidiosis
Histopathology of rhinosporidiosis
Definition of rhino-sinusitis
Klebsiella ozenae
Foul smell with yellow / green nasal crusting. There may be history of trauma or nasal surgery.
Primary atrophic rhinitis: unknown cause
Secondary atrophic rhinitis: secondary to trauma or nasal surgery.
Nasal surgery causes roomy nose (empty nose) leading to atrophic rhinitis
Klebsiella rhinoscleromatis
Rhinitis Granulomas Sclerosis (and narrowing of nasal passage)
Mikulicz cells: large macrophages with clear cytoplasm containing bacilli
Russell bodies: in plasma cells
Large macrophages with clear cytoplasm containing bacilli.
Diagnostic of rhinoscleroma.
Present in plasma cells
Diagnostic of rhinoscleroma
Rhinosporidium seeberi
Friable red nasal polyp, nasal obstruction, and epistaxis
Pseudo-epitheliomatous hyperplasia.
Presence of Rhinosporidium seeberi.
Both 1 and 2 should be present:
1. Nasal obstruction (or blockage or congestion) or Nasal discharge (anterior nasal drip or
posterior nasal drip)
2. Facial pain/pressure or hyposmia/anosmia
Classification of rhino-sinusitis
In chronic rhino-sinusitis, there should be in addition, endoscopic or radiologic evidence of

mucosal inflammation or polyp in nasal cavity or middle meatus.
Acute rhino-sinusitis: <4 weeks with complete resolution
Subacute rhino-sinusitis: 4 12 weeks with complete resolution
Chronic rhino-sinusitis: >12 weeks without complete resolution
Recurrent rhino-sinusitis: 4 episodes per year, each lasting 7 10 days, with complete
resolution between episodes
Acute exacerbation of chronic rhino-sinusitis: sudden worsening of baseline chronic rhinosinusitis with return to baseline after treatment
Most common viruses causing acute
Rhinovirus
viral rhino-sinusitis
Influenza
Common bacteria causing acute rhino- Haemophilus influenzae
sinusitis
Streptococcus pneumoniae
Moraxella catarrhalis
What factors are associated with
Anatomic abnormalities
chronic rhino-sinusitis?
Osteo-meatal compromise
Mucociliary impairment
Asthma
Bacterial infection
Fungal infection
Allergy
Staphylococcal superantigen
Osteitis
Biofilms
Samters triad
Granulomatous vasculitis
Most common fungus found in fungal
Aspergillus fumigates
ball
Most common sinus involved in fungal Maxillary sinus
ball
Types of fungal rhino-sinusitis
Fungal ball
Allergic fungal rhino-sinusitis
Acute invasive fungal rhino-sinusitis
Chronic invasive fungal rhino-sinusitis
Chronic granulomatous fungal rhino-sinusitis
Most common fungus causing chronic Aspergillus flavus
granulomatous fungal rhino-sinusitis
Complications of rhino-sinusitis
Blood:
Thrombophlebitis (retrograde, through valveless veins veins of Breschet)
Direct:
Osteomyelitis (through lamina papyracea)
Mucocele ( Mucopyocele)
Eye:
Preseptal cellulitis Orbital cellulitis Sub-periosteal abscess Orbital abscess
Cavernous sinus thrombosis
Neurologic:
Meningitis
Epidural abscess
Subdural abscess
Brain abscess
Superior orbital fissure syndrome

Orbital apex syndrome
Potts puffy tumor
What per cent of viral URTIs are
complicated by bacterial sinusitis in
children?
What factors predispose to chronic
rhinosinusitis in children?
Bone:
Osteomyelitis (spread through diploic veins)
Potts puffy tumor
Involvement of cranial nerves 3, 4, 6 and V1 due to orbital abscess
Involvement of cranial nerves 2, 3, 4, 6, and V1 due to orbital abscess
Sub-periosteal abscess of frontal bone secondary to frontal sinusitis
~ 10%
Viral URTIs
Day care attendance
Allergic rhinitis
Anatomic abnormalities
Treatment of acute rhino-sinusitis
GERD
Immune deficiency
Second hand smoke
Ciliary dysfunction
Tonsillitis
Otitis media
Mild disease (mild pain and fever <38o C): Defer antibiotic for 5 days. If no improvement or
symptoms worsen, start antibiotic.
Moderate to severe disease (moderate to severe pain and fever > 38 oC): Start antibiotic.
1. Antibiotic: Amoxicillin or Augmentin for 7 14 days; if no improvement in 72 hours, then

high-dose Augmentin or respiratory quinolone (levofloxacin, moxifloxacin)
2. Analgesic
3. Decongestant
4. Mucolytic
5. Nasal steroid
6. Oral antihistamine if history of allergic rhinitis
Treatment of chronic rhino-sinusitis
Surgery only if complication occurs

Oral antibiotic (macrolide) for >12 weeks
Nasal steroid
Nasal saline irrigation
If nasal polyp: Systemic steroid at 1 mg/kg initial dose and taper over 10 days
Surgery if:
Fails medical treatment
Underlying anatomical abnormality
Massive polyposis
Mucocele formation
Suspected fungal rhino-sinusitis
Categories of obstructive sleep apnea
Definition of obstructive sleep apnea

syndrome
From mildest to severest:
Snoring Upper airway resistance syndrome Obstructive sleep apnea syndrome Obesi
hypoventilation syndrome
15 respiratory events per hour of sleep
OR
5 respiratory events per hour of sleep, plus daytime symptoms (i.e. excessive daytime
sleepiness, unrefreshing sleep, fatigue, insomnia, or witnessed periods of apnea)
Complications of obstructive sleep

apnea syndrome
Differential diagnosis of obstructive

sleep apnea syndrome
Epworth sleepiness scale
Clinical features of obstructive sleep
apnea syndrome
Note: The term respiratory event means hypopnea or apnea of 10 second duration or
respiratory effort- related arousal.
Hypertension
Cardiovascular disease
Arrhythmias
Myocardial infarction
Cerebro-vascular accident
Congestive heart failure
Insomnia
Circadian rhythm sleep disorder
Insufficient sleep syndrome
Questionnaire to objectively assess degree of daytime sleepiness
History:
Snoring, Restless sleeping, Gasping, Choking, Waking up during night, Early morning fatigue,
Daytime sleepiness, Waking up with headaches
Height, Weight, Body mass index, Neck circumference
Upper airway:
Grades of tonsillar hypertrophy
What are the common areas of

pharyngeal collapse in obstructive
sleep apnea syndrome?
Mallampati classification
Mueller maneuver

obstructive sleep apnea syndrome
Nose: congestion, infection, DNS, turbinate hypertrophy, polyp, mass, nasal valve collapse
Nasopharynx: hypertrophied adenoid, polyp, mass
Oral cavity: dental occlusion, size or position of tongue, scalloping of lateral edges of tongue,
retrognathia, prognathia, hypoplastic mandible, mandibular or palatal tori
Oropharynx: tonsils, soft palate and uvula (Mallampati classification), webbing of tonsillar
pillars, hypertrophied or prominent lateral pharyngeal walls
Hypopharynx: size and position of base of tongue, lingual tonsillar hypertrophy, mass
Larynx: mobility of vocal cords, mass, polyp
Grade 0 No tonsils
Grade 1 Tonsils hidden in fossa
Grade 2 Tonsils extend upto the pillars
Grade 3 Tonsils extend beyond pillars
Grade 4 Tonsils meeting in midline
Retro-palatal area of oropharynx
Retro-lingual area of hypopharynx
Patient opens his mouth wide and protrudes his tongue
Class I: Uvula completely visible
Class II: Most of uvula visible
Class III: Only base of uvula visible
Class IV: Uvula not visible at all
With nasopharyngoscope in place, patients nose is pinched and he is instructed to attempt
inhalation with closed nose and mouth. Pharyngeal collapse is observed with the
nasopharyngoscope. The procedure is done with the patient sitting up and then lying down.
Clinical features
Nasopharyngoscopy
Drug-induced sleep endoscopy
Cephalometry
Polysomnography
What are the parameters that are

measured in polysomnography?
EEG
ECG
EOG
EMG
Nasal and oral airflow
Blood oxygen concentration
Thoracic and abdominal movements
Body position
Snoring
Treatment options for obstructive sleep Medical:
apnea syndrome
Behavioral modifications (no alcohol or sedative at bedtime, weight reduction, positional
therapy)
Continuous positive airway pressure (CPAP)
Oral appliances (e.g. mandibular repositiong device)
Expiratory positive airway pressure
What is the gold standard treatment
Surgery (if medical options fail):

Nasal surgery (nasal valve surgery, septoplasty, turbinate reduction, polypectomy,
adenoidectomy)
Oropharyngeal surgery (tonsillectomy)
Palatopharyngeal surgery (uvulo-palato-pharyngoplasty, trans-palatal advancement
pharyngoplasty, expansion sphincteroplasty, uvulopalatal flap, laser-assisted uvulo-palatoplast
cautery-assisted palatal stiffening, radio-frequency ablation of soft palate, palatal implants,
injection snoreplasty)
Hypopharyngeal surgery (radio-frequency ablation of base of tongue, genioglossus
advancement, hyoid suspension, tongue suspension, trans-oral midline glossectomy, mandibu
advancement, maxillo-mandibular advancement)
Tracheotomy
Continuous positive airway pressure (CPAP)
for obstructive sleep apnea syndrome?

Most effective surgical procedure for
Maxillo-mandibular advancement
obstructive sleep apnea syndrome
M cells
Specialized epithelial cells in tonsils and adenoids that actively transport macro-molecules from
surface into germinal centers through pinocytosis
What is the major immune function of
1. Generation of antigen-specific B cells in the tonsillar follicles
2. Production of secretory IgA
tonsils and adenoids?
Clinical features of allergy in ENT
Eyes:
Allergic shiners
Long, silky eyelashes
Peri-orbital edema and puffiness
Dennies lines
Injection of bulbar conjunctiva
Nose:
Itching
Supra-tip horizontal crease
Facial grimacing
Allergic salute
Nasal obstruction (due to mucosal edema, turbinate hypertrophy, or increased mucus secretio
Sneezing
Rhinorrhea
Mouth:
Chronic mouth breathing (because of nasal obstruction)
Palatal itching
Nocturnal bruxism
Pharynx:
Dry, inflamed mucosa (because of mouth breathing and direct allergen exposure)
Repeated throat clearing
Cobblestoning of posterior pharyngeal wall
Larynx:
Intermittent dysphonia
Throat clearing
Cough
Allergic shiners
Dennies lines
Supra-tip horizontal crease
Allergic salute
Tachyphylaxis
Compare and contrast the side-effects
of 1st generation antihistamines and
2nd generation antihistamines
What is benefit of topical antihistamine

over systemic antihistamine?
Side effects of topical and systemic
Lungs:
Cough
Wheezing
Dyspnea
Darkening under eyes due to chronic deposition of hemosiderin in tissues. Feature of allergy.
Fine horizontal lines in the lower eyelids. They occur through spasms of Mueller muscles in the
lids. Feature of allergy.
Develops through chronic rubbing of nose. Feature of allergy.
Characteristic rubbing of the nose with the heel of the hand. Feature of allergy.
Efficacy of medicine decreases with increased use
First generation antihistamines (diphenhydramine, chlorpheniramine, etc.):
Sedation
Anti-cholinergic effects (dry mouth, blurred vision, constipation, urinary retention)
Tachyphylaxis
Second generation antihistamines (loratadine, cetrizine, fexofenadine, etc.) have little, if any, o
these side effects.
Topical antihistamine reduces nasal congestion while systemic antihistamine does not redu
nasal congestion. Also, topical antihistamine has more rapid onset of action.
Systemic decongestants: Increased blood pressure in hypertensive patients, increased
decongestants
Treatment options for allergic rhinitis
Stensons duct
Whartons duct
Difference between lymph nodes of
parotid and submandibular glands
Rivinus duct
Bartholin duct
Number of minor salivary glands
Physiology of saliva formation in
salivary glands
Which salivary gland produces
predominantly stimulated secretion?
appetite, increased cardiac symptoms (tachycardia, arrhythmia)
Topical decongestants: Tachyphylaxis, rhinitis medicamentosa

Antihistamines (Systemic and Topical)
Decongestants (Systemic and Topical)
Steroids (Systemic and Topical)
Cromolyn sodium (Topical only for prophylaxis)
Leukotriene receptor antagonists (Systemic monteleukast)
Duct of parotid gland
Duct of submandibular gland
Submandibular gland: Peri-glandular nodes
Parotid: Peri-glandular and intra-glandular nodes
Duct of sublingual gland that opens directly into floor of mouth.
(If it opens into Whartons duct, it is called Bartholin duct.)
Duct of sublingual gland when it opens into Whartons duct.
(If it opens directly into floor of mouth, it is called Rivinus duct.)
600 1000
Acinar cell secretes Na+, Cl-, and HCO3 into the acinar lumen. Water enters the lumen through
osmosis. In the ductal lumen, the ductal cells (which are water impermeable) reabsorb NaCl an
secrete KHCO3. Thus, saliva is less isotonic and more alkaline.
Stimulated secretion: Parotid gland
Unstimulated secretion: Submandibular gland
Which produces predominantly

unstimulated secretion?
Difference between saliva produced by
parotid and submandibular glands
Which protein is the most abundant
protein in saliva?
Functions of saliva
Submandibular gland secretion has more Ca2+, more mucin, more calculi, more antimicrob
activity, higher basal flow rate, and is predominantly unstimulated.
Alpha amylase
Starts digestion of starch (amylase)
Pathophysiology of saliva formation in

cystic fibrosis
Most common cause of xerostomia
(dry mouth)
Common causes of xerostomia (dry
mouth)
Ductal system of salivary gland
Ebner glands
Adenomatoid hyperplasia
Sialadenosis
Oncocytic metaplasia
Sebaceous metaplasia
Fordyce granules
Necrotizing sialometaplasia
Most common location of accessory
salivary gland tissue
Most common location of heterotopic
salivary gland tissue
Difference between accessory and
heterotopic salivary gland tissue
Congo red stain
Lubricates food bolus and thus helps in mastication, swallowing, taste, and speech
Buffers with bicarbonate
Antimicrobial proteins
Dental protective function (prevents plaque and promotes remineralization)
Excretes viruses and inorganic elements (e.g. lead)
Promotes oral wound healing (oral epidermal growth factor)
NaCl is not re-absorbed in ductal cells, resulting in more viscous saliva. There is decrease in
flow rate and sludging of saliva.
Prescription drugs, namely anti-cholinergic drus, i.e. antihistamines and antidepressants.
Prescription drugs (antihistamines and antidepressants)

Dehydration
Aging (loss of acinar cells leading to decreased salivary flow)
Acinar duct Intercalated duct Striated duct Excretory duct
Serous minor salivary glands on posterior aspect of tongue
Asmptomatic nodule on hard palate; biopsy reveals minor salivary glands. Cause is unknown.
Painless enlargement of salivary glands
The mitochondria of the cells in a salivary gland become larger and more numerous. Cause
is unknown. Most commonly occurs in parotid gland.
Sebaceous cells replace cells of the intercalated or striated ducts. Cause is unknown. Most
commonly occurs in parotid gland.
Yellow-colored sebaceous cells in oral mucosa. It is a benign developmental anomaly.
Squamous metaplasia in minor salivary glands with considerable inflammation. May look like
cancer but is benign condition.
Along buccal branch of facial nerve. Drains into the main parotid duct.
Cervical lymph nodes
Accessory tissue: has a duct
Heterotopic tissue: acini without duct system
Positive in amyloidosis (e.g. of salivary gland)
Lipomatosis of salivary gland

Cheilitis glandularis
Typical presentation of acute
suppurative sialadenitis of parotid
gland
Most common bacteria involved in
acute supurative sialadenitis
Treatment of acute suppurative
sialadenitis
Kuttners tumor
Difference in etiology of acute and
chronic sialadenitis
Treatment of chronic sialadenitis
Specific presentations of salivary

gland pathology in HIV positive patient
Actinomycosis of salivary gland
Warthin-Starry stain reaction
Forms of Sjogren syndrome
Clinical features of Sjogren syndrome
Accumulation of fat in salivary gland.

Associated with diabetes, aging, alcoholism, and malnutrition.
Nodular swollen lower lip in an adult male. Can express saliva.
Elderly, debilitated, or postsurgical patient with unilateral painful swelling of parotid gland and
pus in Stensons duct
Staphylococcus aureus. (Others include streptococcus viridans and anaerobes.)
Antibiotic (beta-lactamase and anaerobic sensitive)
Hydration
Sialagogue
Heavy lymphoid infiltrate in submandibular gland secondary to chronic sialadenitis
Acute: Salivary stasis
Chronic: Sialolithiasis
Similar to that for acute suppurative sialadenitis:
Antibiotic
Hydration
Sialagogue
Lympho-epithelial cyst only happens in parotid as it contains lymph nodes inside it
Diffuse infiltrative lymphocytosis syndrome (DILS) a sicca syndrome similar to Sjogren
syndrome
Sulfur granules. Sinus tracts. Multiloculated abscesses. May be due to poor oral hygiene. Trea
with penicillin G.
Used to diagnose Bartonella henselae (cat scratch disease)
Primary: Dry eyes (xerophthalmia), Dry mouth (xerostomia)
Secondary: Dry eyes (xerophthalmia), Dry mouth (xerostomia) plus collagen vascular diseas
(rheumatoid arthritis)
Parotid enlargement (bilateral) with dry eyes and dry mouth. May be associated collagen
vascular disease (rheumatoid arthritis). Higher risk of non-Hodgkin lymphoma.

Sjogren syndrome?
Difference between stones of
submandibular and parotid gland
What kind of stones can be removed
by sialendoscopy?
Treatment options for sialolithiasis
Anti-Ro (SS-A) and Anti-La (SS-B).

Minor salivary gland biopsy shows increased lymphocyte infiltration.
Submandibular gland: stone often in duct
Parotid: stone often in parenchyma
Those whose size is <5 mm
Intra-oral sialolithotomy
Sialendoscopy
Lithotripsy
Recurrent parotitis of childhood
Weekly or monthly recurring parotitis in a child of 3 10 years age. There is no pus from the
duct. Cause is often Staph. aureus. Treat with antibiotic and dilation of Stensons duct.
What are the congenital cysts of
Parotid dermoid
salivary glands?
Dermoid floor of mouth (in midline, unlike ranula)
Branchial cyst
Polycystic parotid gland
What are the acquired cysts of salivary Ranula retention cyst
glands?
Mucocele pseudocyst
Most common location of mucocele of Lower lip
salivary gland
Most common salivary tumor in
Vascular tumor (hemangioma, lymphangioma)
children
Most common solid tumor of salivary
Benign mixed tumor
glands in children
Most common cancer of salivary
Muco-epidermoid carcinoma
glands in children
Child with sialorrhea. What could be
Causes: Cognitive disability, metal poisoning
the cause? What is the treatment?
Treatment:
Medical: Anti-cholinergics (glycopyrrolate, scopolamine, Botox)
Surgical: Bilateral parotid duct ligation and submandibular gland excision
Boundaries of oral cavity

Boundaries of oropharynx
Boundaries of hypopharynx
Boundaries of esophagus
Papillae of the tongue
Linea terminalis
Blood supply of palatine tonsil
Gerlachs tonsil
Lateral pharyngeal bands
Dehiscences in area of cricopharynx
Phases of swallowing
Vermillion border to junction of soft and hard palate plus circumvallate papillae (linea terminalis
Junction of soft and hard palate plus circumvallate papillae (linea terminalis) to valleculae &
phayngo-epiglottic folds (plane of hyoid bone)
Level of hyoid bone (valleculae & pharyngo-epiglottic folds) to level of inferior border of cricoid
cartilage
From inferior border of cricoid cartilage to cardia of stomach
Filiform: no taste function
Fungiform: all over surface
Foliate: on lateral surface
Circumvallate: In V shape at junction of anterior 2/3rd and posterior 1/3rd (linea terminalis)
A.k.a. sulcus terminalis
V-shaped line, separates anterior 2/3rd of tongue from posterior 1/3rd
Just behind this line lie the circumvallate papillae
Facial tonsil (main branch to tonsil)
Facial Ascending palatine tonsil
Ascending pharyngeal tonsil
Lingual Dorsal lingual tonsil
Maxillary Lesser palatine tonsil
Lymphoid tissue in lip of fossa of Rosenmuller; involves Eustachian tube
Rests of lymphoid tissue just behind posterior pillars
Killians dehiscence: Between inferior constrictor and cricopharyngeus; allows Zenkers
diverticulum to pass through
Laimer Haeckerman space: Between cricopharyngeus and esophagus posteriorly
Killian Jamieson space: Between cricopharyngeus and esophagus laterally (allows branches
of inferior thyroid artery to pass)
1. Oral phase: voluntary
2. Pharyngeal phase: ~ 1 sec
(a) Nasopharyngeal closure
(b) Cessation of respiration
(c) Glottic closure
(d) Bolus propulsion
Meissners and Auerbachs plexus

Types of peristalsis
Angle of His
Lower esophageal sphincter
Dilaceration
Complications of alveolar abscess of
tooth
Papillon-Lefevre syndrome
Peri-odontosis
Vincents angina
(e) Laryngeal elevation and pharyngeal shortening

(f) Epiglottic rotation
(g) Relaxation of cricopharyngeus
3. Esophageal phase: ~ 3 6 sec
Meissners plexus: in submucosa of esophagus
Auerbachs plexus: in muscle layers of esophagus; a.k.a. myenteric plexus
Primary normal peristalsis (physiologic)
Seondary reverse peristalsis (pathologic)
Tertiary segmental constriction without propulsion (pathologic)
Oblique angle between esophagus and stomach at their meeting point. It prevents reflux. The
angle of His is absent in infants, hence their high rate of reflex
Prevents reflux through following mechanisms:
1. Increased tone in esophageal muscle 1 2 cm above and below the diaphragm
2. Oblique angle of His (not present in infants, hence high rate of reflux)
3. Diaphragmatic crurae create a sling (not present in hiatus hernia, hence high rate of reflux)
Angular malformation of tooth root during childhood. Occurs in rickets and cretinism.
Sinusitis
Ludwigs angina
Osteomyelitis
Bacteremia
Peri-odontosis (i.e. chronic degeneration of peri-odontal tissue)
Hyperkeratosis (of soles of feet and palms of hands)
Calcification of dura
Chronic degeneration of peri-odontal tissue
A.k.a. acute necrotizing ulcerative gingivitis
A.k.a. trench mouth
Due to Borrelia vincentii and other anaerobes
Clinical features: Bad breath, excessive salivation, and bleeding gums
Most common viral infection of mouth

Herpangina
Noma
Causes of oral thrush
Sutton disease
Erythema multiforme
Lichen planus
Behcets disease
Osler-Weber-Rendu disease
Sturge-Weber syndrome
Menopausal gingivostomatitis
Clinical features of vitamin deficiency
in ENT
Kaposi sarcoma
Melanosis
Amalgam tattoo
Peutz-Jeghers syndrome
Strawberry tongue
Treatment: Oral hygiene, Penicillin

Herpes labialis
Vesicles on soft palate, with fever and coryza.
Due to coxsackie A virus
Similar to Vincents angina, it is an acute necrotizing gingivitis due to Borrelia and other
anaerobes. It rapidly spreads into adjacent soft tissue.
Immunocompromised
Dry mouth (xerostomia)
Taking inhaled steroid
Recurrent large and deep aphthous ulcers that cause scarring in oral cavity
Iris-like lesions on oral cavity, conjunctiva, and skin
Reticular branching pattern of leukoplakia on oral cavity mucosa. It is pre-malignant
Oral ulceration
Iritis
Conjunctivitis
Urethritis
A.k.a. hereditary hemorrhagic telengiectasia
Spider-like blood vessels on oral mucosa, tongue, nasal mucosa, and gut mucosa. May presen
with epistaxis.
Port wine stain on face, oral cavity, or tongue
Vascular malformations of meninges and brain
Dry, erythematous, and shiny oral mucosa with burning sensation
Deficiency of Riboflavin, Pyridoxine, Nicotinic acid, Vitamin C
Atrophic glossitis, angular cheilosis, gingivitis
Violaceous macules on oral mucosa. It is an AIDS-defining condition.
Dark patches in oral mucosa. It is physiological pigmentation.
Mucosal laceration causes dental amalgam to tattoo the gingiva.
Peri-oral melanotic macules
Feature of Kawasaki disease and scarlet fever
Most common site of leukoplakia

Leukoplakia
Erythroplakia
Which has more chance of cancer,
leukoplakia or erythroplakia?
Nodular leukoplakia
Median rhomboid glossitis
Most common cyst of oral cavity
Dentigerous cyst
Hairy tongue
Epulis
Ranula
Torus palatini
Why is there Eustachian tube disorder
in cleft palate?
Quinckes disease
Causes of uvular swelling
Angio-neurotic edema
Differential diagnosis of tonsillar mass

(enlarged tonsil)
Lip (Vermillion border)

White, hyperkeratotic lesion in oral cavity. It is pre-malignant. (10% chance of cancer.)
Granular erythematous lesion in oral cavity. It is pre-malignant (50% chance of cancer.)
Erythroplakia = 50% chance
Leukoplakia = 10% chance
Nodular leukoplakia = Leukoplakia + Erythroplakia.
Has high risk of cancer.
Smooth reddish area in midline of tongue devoid of papillae. It is a developmental anomaly.
Radicular cyst
Developmental abnormality. Associated with un-erupted tooth crown.
Is due to hyperplasia of filiform papillae
Nonspecific term for tumor or tumor-like mass of gingiva. Often a pyogenic granuloma.
Mucocele of sublingual gland. Simple ranula presents in floor of mouth. Plunging ranula presen
as a soft submental neck mass.
Exostosis in midline of hard palate. It is a benign condition, though it may continue to grow
beyond puberty.
Tensor palati fails to open the Eustachian tube on swallowing.
Swelling of uvula + Acute bacterial tonsillitis
1. Trauma
(a) Heroic snoring
(b) Burn from hot food or hot drink
2. Quinckes disease
Three forms:
1. Familial (C1 esterase deficiency)
2. Allergic
3. Due to ACE inhibitor
1. Acute tonsillitis
2. Tonsillolith
3. Peritonsillar abscess
4. Infectious mononucleosis

acute tonsillitis
Complications of peritonsillar abscess
5. Parapharyngeal space mass

6. Lymphoma
7. Squamous cell cancer
Group A Beta hemolytic streptococcus
1. Parapharyngeal abscess
2. Venous thrombophlebitis, bactermia, and endocarditis
3. Arterial thrombosis, hemorrgae, and pseudo-aneurysm
4. Mediastinitis
5. Brain abscess
6. Airway obstruction
7. Aspiration pneumonia
8. Nephritis
9. Peritonitis
10. Dehydration
Indications of tonsillectomy
1. Recurrent tonsillitis (3 per year for 3 years, or 5 per year for 2 years, or 7 per year for 1 year
or >2 weeks of school or work missed in 1 year)
2. Tonsillar enlargement causing upper airway obstruction (sleep apnea)
3. Peritonsillar abscess
4. Possibility of cancer (either unilaterally enlarge, or search for unknown primary)
5. Tonsillar enlargement causing dysphagia
6. Recurrent tonsillitis causing febrile seizures
7. Diphtheria carrier
Morbidity and mortality of tonsillectomy Morbidity = ~ 3% (hemorrhage)
Mortality = 1:25,000
Cobblestoning of posterior pharyngeal Due to inflammation of lymphoid rests on the wall.
wall
Eagle syndrome
Pain in wall of oropharynx due to elongated styloid process
Mendelson maneuver
Patient has dysphagia due to failure of laryngeal elevation. Cause is often neurological.
Patient is instructed to hold larynx as high as possible and for as long as possible with
each swallow.
Specific neuromuscular causes of

dysphagia
Barrett esophagitis
Barrett ulcer
Esophageal diverticuli
1. Tongue base weakness

2. Oral dysfunction
3. Pharyngeal sensory loss
4. Vocal cord paralysis
5. Vocal cord weakness
6. Failure of laryngeal elevation
7. Generalized pharyngeal weakness
8. Failure of opening of upper esophageal sphincter
9. Disorders of peristalsis
Metaplasia of squamous lower esophageal epithelium to columnar epithelium
Deep peptic ulcer in an area of Barrett esophagitis
Zenkers diverticulum:
Occurs in Killians dehiscence between inferior constrictor and cricopharyngeus. Presents with
regurgitation of undigested food and dysphagia. Treatment is cricopharyngeal myotomy, wit
or without excision / suspension / inversion of sac, or endoscopic diverticulotomy with laser
stapler.
Traction diverticulum:
Mid-esophageal, on left side, due to traction from an adjacent inflammatory process (usually T
Most common form of hiatus hernia

Sandifer syndrome
Saints triad
Epiphrenic diverticulum:
Just superior to gastro-esophageal junction on right side
Sliding hernia
(The other less common form is para-esophageal hernia.)
Abnormal contortion of neck
Hiatus hernia
The syndrome occurs in children and the hernia is often unrecognized.
Hiatus hernia
Gallbladder disease
Colonic diverticular disease
Motility disorders causing dysphagia
Polymyositis: involves striated muscle of upper part of esophagus. Upper esophageal

sphincter is involved. Presents with proximal muscle weakness of hips and shoulders. In
dermatomyositis, there is also a skin rash. Lower part of esophagus is normal.
Scleroderma: involves smooth muscle of lower part of esophagus. Lower esophageal
sphincter is involved. Patient may have reflux esophagitis and secondary stricture. Upper part
esophagus is normal.
Schatzkis ring
Most common location of esophageal

web in wall of esophagus
Plummer-Vinson syndrome

Plummer-Vinson syndrome
Achalaisa: Aperistalsis, esophageal dilatation, and failure of lower esophageal sphincter

relaxation, which shows as air-fluid level on upright Barium swallow. Primary achalasia is due
idiopathic degeneration of ganglion cells of Auerbach plexus. Secondary achalasia has various
causes.
Concentric ring of mucosa in lower esophagus at the gastro-esophageal junction. Often
asymptomatic. May present with intermittent dysphagia.
Difference between peptic stricture and Schatzkis ring is that peptic stricture involves both
mucosa and muscle while Schatzkis ring involves only mucosa.
Anterior wall. (Unlike rings and strictures, webs are asymmetric.)
Iron-deficiency anemia
Upper esophageal web (causes dysphagia, but dysphagia may be present without web)
Hypothyroidism
Glossitis
Cheilitis
Gastritis
Increased risk of postcricoid cancer
CBC
Serum iron
Serum ferritin
Treatment of Plummer Vinson

syndrome
Boerhaave syndrome
Barium swallow
Iron replacement
Web dilatation
A liner tear 1 4 cm in length through all three layers of esophagus due to sudden increase in
esophageal pressure, usually due to vomiting. Most occur in males, and most are on left side
Mallory-Weiss syndrome
Presents with severe knife-like epigastric pain radiating to left shoulder after bout of vomiting.
Patient develops respiratory difficulty, subcutaneous emphysema, and shock. Chest x-ray first
shows widened mediastinum, then left pleural effusion or hydropneumothorax.
Tear of gastric cardia due to forceful vomiting. Typical case is middle-aged alcoholic man wh
presents with massive hematemesis.
After procedure, patient develops sore throat, neck pain, chest pain, fever, tachycardia
(which is out of proportion to the fever), and subcutaneous emphysema.
Clincial features and management of

iatrogenic esophageal perforation
Chest x-ray and CT to confirm diagnosis.

Treatment is with antibiotics, fluids, and early surgical exploration and repair.
Clinical features of GERD

GERD?
Complications of GERD
(Iatrogenic esophageal perforation most commonly occurs at sites of narrowing.)

Typical (Gastro-esophageal reflux): Substernal chest pain, water brash
Atypical (Laryngo-pharyngeal reflux): Hoarseness, voice change, sore throat, globus, cough
Diagnosis is clinical. May be confirmed by 24-hr pH metry OR esophageal biopsy OR
response to empiric therapy. Barium swallow is NOT used for diagnosis though it may be do
to investigate esophagitis or stricture, etc.
Esophageal:
Ulceration
Stricture
Barrett esophagitis
Cancer
Laryngeal:
Chronic laryngitis
Vocal process granulomata
Ulceration
Subglottic edema
Treatment of gastro-esophageal reflux

or laryngo-pharyngeal reflux
Most common type of tracheoesophageal fistula

Bayford syndrome
Pulmonary:
Asthma
Elevate head of bed
Dietary changes
Avoid caffeine and nicotine
Medicines: H2 blocker, proton pump inhibitor
Distal tracheo-esophageal fistula with proximal esophageal atresia (85% of cases)
A.k.a. dysphagia lusoria
Symptomatic compression of esophagus by anomalous right subclavian artery. The anomalou

artery is originating directly from descending aorta and passing behind the esophagus. The rig
recurrent laryngeal nerve is not recurrent. There may be aneurysms of aorta and the aberrant
right subclavian artery.
Management of esophageal burn
Barium swallow shows posterior compression. CT confirms the diagnosis. Treatment is ligation
and division with anastomosis of right subclavian to carotid.
History: alkali or acid? (Alkali is more harmful.)
Physical examination: Oral burn may or may not be found.
Esophagoscopy (within 24 hours) No burn found Barium swallow after 2 weeks

Esophagoscopy (within 24 hours) Burn found Do not advance beyond burn Treat with
antibiotic and steroid
Petiole
Sesamoid cartilages of the larynx
Cartilage of Santorini
Cartilage of Wrisberg
Movements of vocal process of
arytenoids cartilage
Which membrane is pierced for
emergency tracheotomy
Broyles ligament
Macula flava
Vestibule of larynx
Ventricle of Morgagni
Posterior commissure
Nerve of Galen
Lymphatic drainage of larynx
What changes occur in the larynx

during adolescence?
Functions of larynx
Patient will have scar and stricture formation at 6 weeks.

Point of attachment of epiglottis to thyroid cartilage
Corniculate, Cuneiform, and Triticeous cartilage
Corniculate cartilage
Cuneiform
Medially and inferiorly
Laterally and superiorly
Crico-thyroid membrane (Crico-thyrotomy)
Insertion point of anterior commissure (both vocal ligaments) to thyroid cartilage is called
Broyles ligament. It is a source of spread of glottis cancer anteriorly beyond the larynx to the
neck.
Anterior macula flava and Posterior macula flava are condensations of the vocal ligament at its
anterior and posterior ends respectively.
Area from laryngeal inlet to false vocal cords
The ventricle of the larynx (deep recess between the true and false vocal cords)
The inter-arytenoid area, which contains the inter-arytenoid muscle covered by mucosa
Communicating nerve between superior laryngeal and recurrent laryngeal nerve.
Supraglottis: Upper deep cervical nodes (bilateral)
Glottis: Sparse drainage (ipsilateral)
Subglottis: Lower deep cervical and pre-tracheal (bilateral)
In males, it doubles in anterior-posterior diameter, and undergoes further descent. The result is
deeper voice than females.
In both males and females, the sub-epithelial connective tissue of the vocal cord (namely, the
lamina propria) undergoes differentiation into three layers (superficial, middle, and deep).
1. Prevents aspiration during swallowing
2. Cough
3. Variation of glottic resistance according to respiratory demand
4. Valsalva (for muscular actions, defecation, vomiting, and childbirth)
Bernoulli effect
What are the causes of acute

laryngitis?
What is the pathophysiology of acute
and chronic laryngitis?
Air passing between the vocal cords is rapid; hence the pressure falls in the glottis and the voc
cords are pulled together.
(Pressure from beneath the vocal cords pushes them apart again and the cycle repeats.)
URTI (Laryngitis is due to cough rather than direct infection)
Vocal abuse
Gastro-esophageal reflux
Coughing, vocal abuse, or gastro-esophageal reflux cause inter-arytenoid edema by irritating
the posterior glottis. The inter-arytenoid edema limits glottis closure, thus causing hoarseness.
If left untreated, acute laryngitis turns into chronic laryngitis because:
linical features of acute laryngitis
Treatment of acute laryngitis
Clinical features of vocal cord nodules
1. More force is used to close the glottis; this exacerbates the edema.
2. The edema creates a globus sensation, so patient makes frequent attempts to clear his thro
which ironically further exacerbates the edema.
History: Sudden onset of hoarseness. History of URTI or vocal abuse or gastro-esophageal
reflux.
Physical examination: May reveal signs of URTI. Vocal cords are normal (moving normally a
no lesion on vocal cords) and there may be inter-arytenoid edema.
1. Treat the cause:
(a) URTI cough suppressant, mucolytic, decongestant
(b) Vocal abuse vocal hygiene
(c) GERD H2 blocker or proton pump inhibitor
2. Hydration
History: More commonly in females and children, and particularly in singers and teachers.
Presents with chronically raspy voice with frequent bouts of laryngitis. If singer, may repo
reduced vocal range or require longer warm-up before singing.
Physical examination: Examination reveals symmetric swelling on each vocal cord opposing
Treatment of vocal cord nodules
Clinical features of vocal cord polyp
Treatment of vocal cord polyp

Most common location of laryngeal
ulcer or granuloma
Clinical features of laryngeal ulcer or
granuloma
Treatment of laryngeal ulcer or

granuloma
Write a short note on vocal cord cyst
Write a short note on vocal cord sulci
each other, at junction of anterior 1/3rd and posterior 2/3rd.

Voice rest
Voice therapy
Surgery if voice therapy fails (because nodules may be too large or too firm to regress)
History: Chronic hoarseness with frequent bouts of laryngitis. Large polyp may cause dyspnea
Physical examination: Polyp on vocal cord
Sugery: Excision via micro-laryngoscopy
Voice therapy: Voice may improve, though polyp will not regress
Vocal process of arytenoid cartilage
History: Similar to chronic laryngitis. History of intubation or voice abuse or GERD
Physical examination: Granuloma or ulcer visible on vocal process of arytenoids with mirror o
flexible laryngoscope
Vocal hygiene
Voice therapy: if history of vocal abuse
Treatment of GERD: if history of GERD
Surgery: if medical therapy fails or if suspicion of tumor
Vocal cord cysts may be congenital or may form by voice abuse. They may be mucus retention
cysts or epidermoid cysts. In addition, pseudocysts are submucosal collections of scar or
connective tissue. Cysts present with chronic hoarseness and are diagnosed on laryngoscopy.
small, they may be visible only on stroboscopy or direct laryngoscopy. Treatment is excision vi
micro-laryngoscopy.
Vocal cord sulci may be congenital or may form by voice abuse. Sulci are depressions in the
mucosa of the vocal cord edge. They may be epithelial lined pockets (due to ruptured cyst?) o
area of deficient lamina propria (a.k.a. sulcus vergeture). Sulci present with chronic hoarsenes
and are diagnosed on laryngoscopy. If small, they may be visible only on stroboscopy or direct
laryngoscopy. Treatment is surgery; various techniques include excision, collagen injection,
steroid injection, mucosal slicing, and mucosal elevation with submucosal grafting.
What are the pre-malignant lesions of

laryngeal mucosa?
Treatment of keratosis / leukoplakia of
laryngeal mucosa
What is laryngocele?
Difference between internal and
external laryngocele
What people are more prone to
develop laryngocele?
Clinical features of laryngocele

laryngocele?
Treatment of laryngocele
Write a short note on laryngeal
papilloma
Most common site of laryngeal

chondroma
What are the benign tumors of the
larynx?
Clinical features of vocal cord
paralysis
Keratosis
Leukoplakia
Treat the cause: e.g. stop smoking, give anti-reflux therapy, voice therapy
Surgery (if suspicion of cancer): Excisional biopsy
Dilation of the appendix of the laryngeal ventricle
Internal laryngocele remains within the thyroid framework while external laryngocele extends
through the thyrohyoid membrane to present as a mass in the neck
Glass blowers and wind instrument players (due to increased intra-pharyngeal pressure)
Internal laryngocele: Presents with hoarseness. Examination shows enlarged false vocal cor
or enlarged supraglottis.
External laryngocele: Presents with hoarseness or mass in neck which increases in size on
doing puffing maneuver.
CT or MRI is definitive diagnosis
Internal laryngocele: Endoscopic marsupialization

External or recurrent laryngocele: External approach
It is transmitted from mothers with genital warts. Presents with hoarseness stridor
dyspnea. Findings on indirect or flexible laryngoscopy are suggestive, but definitive diagnosis
through biopsy. Treatment is direct laryngoscopy and excision with micro-debrider or CO
laser. Other approaches include cryotherapy, photodynamic therapy, and injection of antiviral
agents (cidofovir). Obstructive lesion may require airway management, including tracheotomy
Posterior plate of cricoid cartilage
Papilloma
Chondroma
Rare: neurofibroma, granular cell myoblastoma, adenoma, lipoma
Adult: asymptomatic (unilateral), hoarseness, aspiration, stridor (bilateral)
Causes of vocal cord paralysis
Neonate: weak cry, inspiratory stridor, feeding difficulties

ADULT:
Cancer: lung, thyroid, esophagus, etc
Surgery: thyroidectomy, cervical spine
Cardiovascular: aortic aneurysm, cardiac hypertrophy
Inflammatory: sarcoidosis, syphilis
CNS lesion: multiple sclerosis, stroke
Idiopathic: (~ 20%)
NEONATE:
Most common cause of bilateral vocal

cord paralysis
Pathophysiology of vocal cord
paralysis
How would you differentiate vocal cord

paralysis from mechanically fixed
vocal cords?
vocal cord paralysis?
Idiopathic
Birth trauma
Cardiomegaly
Arnold-Chiari malformation
Ligation of persistent ductus arteriosus
Thyroidectomy
Vocal cords are in cadaveric position immediately after injury. If denervation is complete, the
remain in that position. If injury is incomplete, regeneration occurs, but regeneration is only of
nerve fibers supplying the adductors, while the abductors (posterior crico-arytenoids) remain
paralyzed. Thus, the vocal cords shift to a paramedian position over a few months.
Electromyography is helpful, but definitive diagnosis is with direct laryngoscopy and
palpation of the vocal cord.
ADULT:
1. Differentiate neurological paralysis from mechanical fixation. Electromyography is helpful, b
definitive diagnosis is through direct laryngoscopy with palpation of the vocal cord.
2. Do a thorough search for the cause.
Treatment of vocal cord paralysis
NEONATE:
1. Flexible laryngoscopy
2. Imaging to rule out cardiac and neurologic causes
3. Barium swallow to detect aspiration
UNILATERAL VOCAL CORD PARALYSIS IN ADULT:
Voice therapy
Injection laryngoplasty: Teflon no longer used due to granuloma formation; Gelfoam
effective for 8 to 10 weeks; autologous fat unpredictable survival; commercial substances
hydroxyapatite, collagen, etc persist for long time.
Type II thyroplasty: Vocal cord is medialized by permanent implant placed in paraglottic spac
via a window in thyroid cartilage.
Arytenoid adduction: Muscular process of arytenoid is exposed by transecting the attachmen
of the inferior constrictor muscle to the thyroid ala, and reflecting the pyriform fossa mucosa.
Suture through muscular process is passed through anterior thyroid cartilage, and traction
applied to rotate arytenoids internally.
Laryngeal re-innervation: Branch of ansa cervicalis is anastomosed to the distal recurrent
laryngeal nerve. Restores tone and bulk to the muscles but does not restore functional motion.
BILATERAL VOCAL CORD PARALYSIS IN ADULT:
Tracheotomy
Arytenoidectomy
Endoscopic cordotomy, cordectomy, or suture lateralization
Arytenoid abduction
Re-innervation
VOCAL CORD PARALYSIS IN NEONATE:
Passy-Muir valve
Clinical features of spasmodic
dysphonia
Treatment of spasmodic dysphonia
Treatment of severe aspiration

candidiasis
Observation for mild stridor

Tracheotomy for severe stridor (usually bilateral paralysis)
Definitive laryngeal surgery after recovery and growth
Laryngeal re-innervation at 5 years of age
Valve in tracheotomy tube for speech
History:
Adductor form (90% cases): Strained and strangled voice with frequent voice breaks. Breaks
commonly occur at onset of words beginning with vowels (e.g. eggs)
Abductor form (10% cases): Whispering or breathy voice. Voice breaks between plosive
consonants and vowels (e.g. puppyy)
Examination:
Normal vocal cords
1. Botulinum injection of thyro-arytenoid muscle
2. Surgery:
(a) Berke procedure: transection of adductor branches of recurrent laryngeal nerves an
re-innervation with branches of ansa cervicalis
(b) Lateralization thyroplasty: for adductor spasmodic dysphonia
(c) Medialization thyroplasty: for abductor spasmodic dysphonia
Tracheotomy (with cuffed tube)
Laryngo-tracheal separation
Epiglottic flap to arytenoids
Lindemans tracheo-esophageal diversion procedure: proximal trachea to esophagus
anastomosis and creation of distant permanent tracheostomy
Suturing vocal cords together
Total laryngectomy
History: Presents with progressive hoarseness, cough, and/or globus sensation. There may b
history of use of inhaled steroids, use of antibiotics, GERD, or immune compromise.
Physical examination: White patches on bright red mucosa which may look like leukoplakia.

epiglottitis
Clinical features of acute epiglottitis

acute epiglottitis?
Treatment of acute epiglottitis
Clinical features of croup (a.k.a acute

laryngo-tracheo-bronchitis)
Treatment: Systemic anti-fungal (NOT local anti-fungal). Patient should stop using inhaled
steroids.
Haemophilus influenza
History:
Sore throat, dysphagia, drooling, fever, stridor, dyspnea (relieved somewhat by leaning forward
hot potato voice
Be careful. Be gentle. Do not stimulate gag. Do not use tongue blade.
Point tenderness at hyoid level in midline.
Investigation should not delay treatment if there is high index of suspicion.
X-ray soft tissue neck lateral view: shows the swollen epiglottis (thumb sign)
CT: may show abscess in epiglottis (rare occurrence)
Airway: Tracheotomy or intubation (Can be bypassed if mild disease, but close monitoring i
essential)
IV antibiotic
Steroid
History:
Little child presenting with barking cough and hoarseness, progressing to stridor
Signs of respiratory obstruction may be evident:
Suprasternal retractions
Use of accessory muscles of inspiration
Agitation

croup (a.ka. acute laryngo-tracheobronchitis)?
Treatment of croup (a.k.a. acute
laryngo-tracheo-bronchitis)
Clinical features of bacterial tracheitis

How would you investigate and treat a
case of bacterial tracheitis?
Increased pulse
Circumoral pallor
Cyanosis
X-ray chest (AP view): shows steeple sign (subglottic narrowing due to edema)
Cool mist inhalation

Steroid
Humidified oxygen
Intermittent racemic epinephrine
Antibiotic: if fever and/or positive culture
Airway intervention: if obstruction is severe
Operative endoscopy: for recurrent croup to investigate possible anomaly such as subglottic
stenosis, cyst, or hemangioma
Bacterial tracheitis is often a complication of bronchitis or croup. Symptoms are of severe crou
with high fever and stridor.
Bronchoscopy: reveals obstruction due to pus, edema, sloughed necrotic mucosa, and mucu
casts. The debris must be removed.
IV antibiotic: based on results of culture
Most common site of laryngeal TB

diphtheria
There is high incidence of progression to pneumonia.

Posterior larynx
(Second most common site is laryngeal surface of epiglottis.)
Etiology: Caused by Corynebacterium diphtheria.
History: Insidious onset of hoarseness and croupy cough.
Physical examination: Grayish-white membrane in the throat and wet mouse smell. Attemp
to remove the membrane cause bleeding.
Less common laryngeal infections
How does rheumatoid arthritis affect

the larynx and how is it treated?
What are the systemic diseases that

affect the larynx?
Clinical features of laryngeal

amyloidosis
amyloidosis?
Clinical features of laryngeal trauma
Treatment: Secure airway. Give antitoxin and penicillin.

Syphilis
Scleroma
Glanders
Leprosy
Mycotic infections (Blastomycosis, Histoplasmosis)
Inflammatory fixation of the crico-arytenoid joint: Treat the rheumatoid arthritis (steroids,
other anti-inflammatories). Tracheotomy to relieve airway obstruction.
Inflammatory nodules on the vocal cords: Excise with micro-surgery.

Sarcoidosis
Rheumatoid arthritis
SLE
Wegener granulomatosis
Relapsing polychondritis
Pemphigus & pemphigoid
Amyloidosis
History: Hoarseness, stridor, globus, dysphagia
Physical examination: Waxy gray / orange lesions on epiglottis
Congo red stain is positive
When viewed under polarized light, shows apple green birefringence
History:
Airway obstruction: Dyspnea and stridor. Half of patients asphyxiate at site of accident. Others
may develop airway obstruction after a fairly asymptomatic interval, and can be suddenly fatal.
Dysphonia / Aphonia
Cough / Hemoptysis
Dysphagia / Odynophagia
How would you manage a case of

laryngeal trauma?
Lack of neck contour due to flattening of thyroid cartilage
Neck hematoma
Subcutaneous emphysema
Crepitus overy laryngeal framework
Acute airway distress: Tracheotomy under L/A Direct laryngoscopy under G/A to assess
injury
Stable airway: Flexible laryngoscopy

(a) Flexible laryngoscopy is normal Manage conservatively with observation,
humidification, and steroid
(b) Flexible laryngoscopy shows hematoma, swelling, decreased motion, or other distortion
do CT
(i) CT is normal Manage conservatively with observation, humidifcation, and steroid
(ii) CT shows displaced fracture Repair surgically
(c) Flexible laryngoscopy shows lacerations or exposed cartilage Tracheotomy under L/A
Direct laryngoscopy under G/A to assess injury
Causes of laryngeal and tracheal

stenosis
Surgery:
Midline thyrotomy to expose laryngeal mucosa.
Carefully suture all lacerations.
Close defects with local flaps or free mucosal flaps.
Remove any arytenoid cartilage that is completely avulsed and displaced.
Reduce and immobilize laryngeal cartilage fracture with plates.
May add laryngeal stent, though it can stimulate granulation tissue.
Intubation trauma
External injury
Systemic disease
GERD
Treatment of laryngeal and tracheal

stenosis
Idiopathic
Supraglottic stenosis:
Endoscopic excision of scar
External excision
Glottic stenosis (Vocal folds usually fixed due to posterior scarring):
Arytenoidotomy
Cordotomy
Tracheotomy
Subglottic stenosis:
Endoscopic excision (if scar is thin and not circumferential)
Laryngo-tracheoplasty
Cricotracheal resection
Tracheotomy
Tracheal stenosis:
Resection and end-to-end anastomosis
Most common cause of neonatal

stridor
Clinical features of laryngomalacia
laryngomalacia?
Treatment of laryngomalacia
Second most common cause of
Multiple sites:
T-tube, to stent the airway
Laryngomalacia
Stridor noted soon after birth. Breathing is better in prone position.
Flexible laryngoscopy: Omega-shaped epiglottis which falls back during inspiration
Observation and assurance that it will resolve by 12 to 16 months
Endoscopic epiglottoplasty for severe stridor or failure to thrive
Tracheotomy may be required.
Laryngeal paralysis
neonatal stridor
Clinical features and investigation of
laryngeal hemangioma in neonate
(Most common cause is laryngomalacia)

History:
Progressive inspiratory stridor with onset soon after birth
Normal voice
Skin hemangioma in 50% of cases
Most common site of laryngeal

hemangioma in neonate
Treatment of laryngeal hemangioma in
neonate
Write a short note on laryngeal atresia
Write a short note on laryngeal web
Most common site of laryngeal web

Cri du Chat syndrome
Investigation:
Direct laryngoscopy and/or bronchoscopy shows the hemangioma. Most often, it is in the
anterior subglottis. Extent can be assessed by CT / MRI.
Anterior subglottis
Observation: Will expand for several months and then involute

Systemic steroid and racemic epinephrine: for acute stridor
Systemic propranolol
CO2 laser excision, or external excision, or tracheotomy: If no response to propranolol
Laryngeal atresia presents with complete obstruction at birth, unless a distal tracheoesophageal fistula provides some connection from trachea to outer air. Other anomalies are
usually present and mortality is quite high. Death may follow if not promptly recognized and
treated.
Laryngeal web usually involves anterior part of the larynx. Small web may be asymptomatic,
but larger web will present with weak or hoarse cry in the neonate. Flexible endoscopy will sho
the pathology. Tracheotomy may be required for relief of airway obstruction. The web is best
corrected when child is larger and anatomy is more distinct.
Anterior part of larynx
Laryngomalacia with poor approximation of posterior vocal cords and stridor
Mental retardation
Microcephaly
Hypertelorism
Midline oral clefts
Most common cause of accidental

death in infants
Clinical features of foreign body
aspiration

foreign body aspiration?
(Cri du Chat syndrome is caused by a B group chromosome with a short arm.)

Asphyxia from foreign body aspiration
History:
Choking event (may be observed or not observed) Asymptomatic interval Wheezing or
chronic cough Recurrent pneumonia
Biphasic stridor, with audible slap or palpable thud (implies tracheal foreign body)
OR
Expiratory wheeze, with decreased breath sounds on one side (implies bronchial foreign body
side of decreased sounds)
Chest x-ray: Shows the foreign body if radio-opaque; obstructive emphysema and
consolidation may be seen
Fluoroscopy: inspiration shows atelectasis, and expiration shows hyper-inflation on the sid
of the foreign body
Treatment of foreign body aspiration

Complications of foreign body
aspiration
Bronchoscopy: indicated whenever diagnosis is suspected, even if all symptoms and signs a
not present
Removal by rigid ventilation bronchoscope
Steroid to reduce edema
Respiratory obstruction
Edema
Bronchitis
Pneumonia
Ulceration
Granulation tissue
Pneumothorax
Pneumomediastinum
Difference between tracheotomy and
tracheostomy
Indications of tracheotomy
Post-op care of tracheotomy
Complications of tracheotomy
Tracheotomy: Temporary opening in trachea

Tracheostomy: Permanent opening in trachea; the trachea is brought to the skin and sewn in
place
1. Airway obstruction at or above level of larynx
2. Inability to clear secretions
3. Need for prolonged mechanical ventilation
4. To reduce upper airway resistance and dead space in certain lung conditions
5. Severe obstructive sleep apnea
1. Secure tube tightly to prevent accidental dislodgement
2. Chest x-ray, AP and lateral, to confirm position of tube and to rule out pneumomediastinum
pneumothorax
3. Do not change tube for 3 4 days to prevent entry into false passage
4. Frequent suctioning and removal and cleaning of inner cannula
Immediate:
Bleeding
Pneumothorax
Pneumomediastinum
Subcutaneous emphysema
Dislodged or obstructed tube
False passage with tube outside trachea
Post-obstructive pulmonary edema
Apnea due to loss of hypoxic drive
Tube too short or inappropriate shape (especially in morbidly obese patients)
Delayed:
Space of Burns
Danger space
Lincoln highway of neck
Contents of parapharyngeal space
Infection of which teeth spread into
Granulation tissue
Stomal infection
Subglottic or tracheal stenosis
Tracheomalacia
Tracheo-esophageal fistula
Displacement of tube
Tracheo-innomiante fistula
Persisting tracheo-cutaneous fistula after decannulation
Properly known as the suprasternal space of Burns.
It is the space in the suprasternal area formed by the splitting of the superficial layer of deep
cervical fascia.
The space between the alar and prevertebral layers of prevertebral fascia
Another name for the carotid sheath. So named because it is a potential avenue for rapid
spread of infection.
Prestyloid compartment:
Fat
Lymph nodes
Internal maxillary artery
Inferior alveolar, lingual, and auriculotemporal nerves
Medial & lateral pterygoid muscles
Deep lobe of parotid gland
Poststyloid compartment:
Internal carotid artery
Internal jugular vein
Cranial nerves 9, 10, 11, & 12
Sympathetic chain
Sublingual space: 1st molar and anterior to it
sublingual space? Infection of which

teeth spread into submandibular (or
submaxillary) space?
Most common cause of neck space
infection in adults
Most common cause of neck space
infection in children
Potts abscess
Clinical features of neck space
infection
Submandibular space: 2nd and 3rd molars
Dental infection
(In children, it is acute pharyngitis.)
Acute pharyngitis (involvement of Waldeyers ring)
(In adults, it is dental infection.)
Abscess of cervical vertebral body caused by Mycobacterium tuberculosis. Spreads into
prevertebral space
History:
1. Inflammatory symptoms: Pain, fever, swelling, redness
2. Localizing symptoms:
(a) Retropharyngeal abscess: dysphagia / odynophagia / drooling
(b) Peritonsillar abscess: hot potato voice
(c) Hoarseness, dyyspnea, ear pain, neck swelling
3. History of recent infection: dental, sinusitis, otitis
4. History of recent trauma: including IV drug abuse
5. History of recent surgery: dental, intubation, endoscopy
1. Palpation: Localizing tenderness, crepitus
2. Ear & Nose: Otitis, rhinosinusitis, foreign body
3. Oral cavity & Pharynx:
(a) Poor dentition (teeth infection)
(b) Trismus (parapharyngeal, pterygomandibular, masticator spaces)
(c) Edema of floor of mouth or tongue swelling (sublingual, submandibular spaces)
(d) Purulent discharge from Whartons or Stensons duct (parotid, sublingual,

neck space infection?
Treatment of neck space infection
submandibular space)
(e) Unilateral tonsillar swelling with deviation of uvula (peritonsillar space)
4. Flexible nasopharyngoscopy identifies need for intubation: mandatory if hoarseness,
dyspnea, stridor, dysphagia, odynophagia without obvious cause
1. CBC (leukocytosis)
2. BSR
3. RFTs
4. Plain x-ray:
(a) Jaw x-ray lucency at dental root (odontogenic abscess)
(b) Lateral neck x-ray air-fluid level (retropharyngeal abscess) also, >5 mm thickening
in child or >7 mm thickening in adult is suggestive; epoglottic thickening, i.e. thumb sign
(supraglottitis)
(c) Chest x-ray widened mediastinum (mediastinitis); lower lobe infiltrate (pneumonia)
5. CT with contrast: best investigation for overall visualization; determines need for
drainage
6. Ultrasound: helpful for accessible abscesses
1. Airway management:
(a) First-line therapy: Oxygen, humidity, IV steroid, epinephrine nebulizer, ICU
(b) Intubation or tracheotomy if worsening stridor or dyspnea or >50% obstruction
(c) Flexible nasopharyngoscopy confirms need for intubation or tracheotomy
(d) Elective tracheotomy if prolonged airway edema (>48 hours) expected
2. Fluids: if dehydrated, 1 -2 L of normal saline
3. IV antibiotic: empiric broad-spectrum before culture result
4. Surgery:
(a) done if air-fluid level or gas-forming organism or abscess or threatened airway
compromise or failure to respond to IV antibiotic in 48 72 hours
(b) goal of surgery: drain abscess, sample fluid, irrigate neck space, and put drain
(c) Options: needle aspiration, transoral I & D, tonsillectomy, trans-cervical I & D
(d) Needle aspiration for lymph node containing small abscess, congenital cyst, or
peritonsillar abscess
(e) Transoral I & D for peritonsillar abscess, buccal space, masticator space, and
pterygomandibular space
What is the main cause of mortality in

neck space infection?
Clinical features of cavernous sinus
thrombosis
Lemierre syndrome
Lemierre syndrome
Tobey-Ayer test
Infection of which neck spaces can

lead to carotid artery pseudoaneurysm or rupture?
Infection of which neck spaces can
lead to mediastinitis?
What are the life-threatening
complications of neck space infection?
(f) Tonsillectomy for peritonsillar abscess

(g) Trans-cervical I & D: 3 approaches:
(i) Modified Blair incision
(ii) Horizontal lateral neck incision (2 cm below body of mandible)
(iii) Horizontal lateral neck incision mid-neck (level 3 at cricoid cartilage)
Loss of airway
History:
Fever
Lethargy
Orbital pain
Proptosis
Reduced extra-ocular mobility
Dilated pupil
Reduced pupillary light reflex
Thrombophlebitis of internal jugular vein
Fusobacterium necrophorum
Test for internal jugular vein thrombophlebitis.

Compress the vein while doing lumbar puncture. If CSF pressure increases, then vein is norma
If CSF pressure does not increase, it implies thrombophlebitis.
Retropharyngeal space
Parapharyngeal space
Retropharyngeal space (most common)
Danger space
Cavernous sinus thrombosis
Lemierre syndrome
Size of thyroid gland
Pyramidal lobe of thyroid gland is

present in how many people?
Embryological origin of parafollicular C
cells of thyroid gland
Embryological origin of pyramidal lobe
of thyroid gland
Most common location of thyroglossal
duct cyst
Delphian lymph node
Lymphatic drainage of thyroid gland
Difference between true thyroid

capsule and perithyroid sheath
Ligament of Berry (and its surgical

significance)
What areas do the superior laryngeal
Carotid artery pseudo-aneurysm or rupture

Mediastinitis
Necrotizing fasciitis
Height: 4 cm
Width: 1.5 cm
Depth: 2 cm
In 40% of people
Neural crest cells of 4th pharyngeal pouch
Pyramidal lobe is remnant of inferior part of thyroglossal duct
Midline of neck, close to hyoid bone
Prominent pre-laryngeal midline lymph node

Isthmus + Medial thyroid Delphian + Pretracheal + Superior mediastinal lymph nodes
Lateral thyroid Internal jugular chain
Inferior pole Paratracheal nodes (close to recurrent laryngeal nerve)
True thyroid capsule: is tightly adherent to the thyroid parenchyma and is continuous with the
fibrous septa within the thyroid which divide the gland into lobules.
Perithyroid sheath: is loose areolar tissue around the thyroid gland which is easily dissected
away during thyroidectomy.
Ligament of Berry is the posterior suspensory ligament of the thyroid gland. It is actually a
condensation of the true capsule of the thyroid. Both anterior and posterior suspensory
ligaments serve to attach the thyroid with the trachea.
In some people, the recurrent laryngeal nerve passes through the ligament of Berry and can g
injured during surgery.
Superior laryngeal nerve, internal branch:
and recurrent laryngeal nerves

supply?
General sensation to supraglottis

General sensation to part of hypopharynx and base of tongue
Taste sensation to epiglottic taste buds
Superior laryngeal nerve, external branch:
Motor to cricothyroid muscle
Motor to inferior constrictor muscle
Which recurrent laryngeal nerve is

more lateral at the level of thoracic
inlet the right or the left one?
At what point does the superior
laryngeal nerve divide into internal and
external branches?
Which nerve is closely associated with
the upper pole of the thyroid gland?
Which nerve lies on the inferior
constrictor muscle?
Which nerve is at risk of injury during
thyroidectomy when the vascular
pedicle of the upper lobe of thyroid
gland is ligated?
Arterial supply of thyroid gland
Recurrent laryngeal nerve:

Motor to intrinsic muscles of larynx (except cricothyroid)
Motor to inferior constrictor
General sensation to glottis and subglottis
General sensation to upper esophagus and trachea
Parasympathetic motor to larynx, upper esophagus, trachea, and hypopharynx
The right recurrent laryngeal is more lateral.
~ 2 3 cm above the upper pole of the thyroid gland
External branch of superior laryngeal nerve

External branch of superior laryngeal nerve. (In some people, the nerve runs within the fascia
the muscle and is difficult to visualize during surgery.)
External branch of superior laryngeal nerve
Superior thyroid artery (branch of external carotid artery)

Inferior thyroid artery (branch of thyrocervical trunk from subclavian artery)
Venous drainage of thyroid gland
What is liothyronine?
Thyroid ima artery (branch of innominate or carotid or aortic arch present in 5% of people)
Superior thyroid vein (drains into internal jugular vein)
Middle thyroid vein (drains into internal jugular vein)
Inferior thyroid vein (drains into internal jugular vein or brachiocephalic vein)
Note: The superior thyroid vein travels with the artery of the same name, but the middle and
inferior thyroid veins do not accompany any artery.
It is exogenous form of T3 hormone.
Liothyronine is a.k.a. levo-tri-iodothyronine.
Note: Endogenous T3 is called tri-iodo-thyronine.
Differences between T3 and T4

hormone
T3
Endogenous T3 is a.k.a. tri-iodo-thyronine
Exogenous T3 is a.k.a. levo-tri-iodothyronine
and a.k.a lio-thyronine
10% of thyroid hormone production
Much more potent than T4
Half-life is 1 day, so re-assessment of thyroid
function tests after dose change of exogenous
T3 is done at 1 2 weeks
Effects of thyroid hormones (T3 and T4)

on the body
What is the effect of thyroid stimulating

hormone on the thyroid gland?
What single test can be used to
Stimulate calorigenesis
Potentiate epinephrine
Lower cholesterol level
Have roles in normal growth and development
It increases gland size and vascularity
TSH
T4
Endogenous T4 is a.k.a thyroxine
Exogenous T4 is a.k.a. levo-thyroxine
90% of thyroid hormone production
Much less potent than T3
Half-life is 6 7 days, so re-assessment of
thyroid function tests after dose change of
exogenous T4 is done at 5 6 weeks
diagnose hyper- or hypo-thyroidism?

What is subclinical hypothyroidism? In
what condition is it typically found?
What is subclinical hyperthyroidism? In
what condition is it typically found?
What is myxedema?
Write a short note on Graves disease
Subclinical hypothyroidism = High TSH and normal T4

Subclinical hypothyroidism is typically found in early Hashimotos thyroiditis.
Subclinical hyperthyroidism = Low TSH and normal T4
Subclinical hyperthyroidism is typically found in multinodular goiter.
Myxedema is nonpitting edema caused by increased glycosaminoglycans in tissue. Myxedem
occurs in severe hypothyroidism.
Etiology:
Auto-immune; antibodies against TSH receptor activate the receptor, causing hyperthyroidism.
History:
Typically, young female presents with anodular diffusely enlarged thyroid.
Thyroid bruit
Eye: Exophthalmos
Skin: Myxedema (e.g. pre-tibial), Acropachy (i.e. edema of hands & feet + digital clubbing)
Investigation:
I123 scanning shows diffusely increased uptake.
Jod-Basedow phenomenon
Similarities and differences between

Graves disease and toxic multinodular
goiter
Treatment:
First, anti-thyroid medication to make patient euthyroid. Then, either radio-iodine (I 131) ablation
surgery.
When patient with subclinical hyperthyroidism and multinodular goiter is given exogenous iodin
(e.g. iodine CT contrast), he may develop overt hyperthyroidism. This phenomenon is called Jo
Basedow phenomenon.
Similarities:
1. Both are more common among females.
2. Both cause thyroid enlargement.
3. Both cause hyperthyroidism.
Differences:
1. There are eye and skin changes in Graves. No such changes in toxic MNG.
2. There is diffusely enlarged anodular goiter in Graves. There is multinodular thyroid in toxic
MNG.
3. Graves starts off with overt hyperthyroidism. Toxic MNG starts off with subclinical
hyperthyroidism (i.e. clinically euthyroid but chemically hyperthyroid), which progresses to
overt hyperthyroidism and autonomy.
123
4. I scan shows diffuse uptake in Graves. I123 scan shows focal hot zones with absence of
adjacent gland in toxic MNG.
Treatment of Graves disease and toxic First, anti-thyroid medication to make patient euthyroid. Then, either radio-iodine (I 131) ablation
multinodular goiter
surgery.
What are the issues with radio-iodine
Contra-indicated in pregnancy and lactation.
131
(I ) ablation for Graves disease or
Conception must be delayed for 6 months.
toxic multinodular goiter?
Patient has high chance of becoming hypothyroid.
There is a certain low risk of getting cancer.
Compare and contrast propyl-thiouracil Both propyl-thiouracil and methimazole are drugs are used to treat hyperthyroidism.
and methimazole
They are given over 6 8 weeks before patient becomes euthyroid.
Dose of propyl-thiouracil is one tablet every 3 days.
Dose of methimazole is one tablet every day.
Both drugs are contra-indicated in pregnancy and lactation.
Both drugs can cause rash, fever, lupus-like reaction, and bone marrow suppression.
Lugols solution
However, propyl-thiouracil can cause liver failure in children. For this reason, methimazole is
the drug of choice.
A.k.a. potassium iodide.
Used in treatment of hyperthyroidism.
What is role of Lugols solution

(potassium iodide) in treatment of
hyperthyroidism?
Wolff-Chaikoff effect
What is role of beta blockers in the
treatment of hyperthyroidism?
What are the contra-indications to use
of beta blockers in a patient of
hyperthyroidism
When is surgery better than radioablation to treat hyperthyroidism?

What are the best surgical options for
treatment of Graves disease and toxic
multinodular goiter?
Most common form of thyroiditis
Most common thyroid disease
Compare and contrast Graves disease
and Hashimotos thyroiditis
Potassium iodide is given pre-operatively to decrease vascularity of thyroid gland.
Potassium iodide cannot be used to treat hyperthyroidism on long-term basis because its antithyroid effect is lost after 2 weeks.
Potassium iodide given to hyperthyroid patient loses its anti-thyroid effect after 2 weeks. This is
called the Wolff-Chaikoff effect.
Beta blockers block the peripheral effects of thyroid hormone and have no effect on the
production of thyroid hormone. Thus, they are used only for symptomatic control or in short-live
forms of hyperthyroidism (namely, thyroiditis).
Asthma
COPD
Cardiac failure
IDDM
Brady-arrhythmia
Patient taking MAO inhibitor
1. Need for rapid return to euthyroid status. (Radio-iodine ablation takes 6 8 weeks to make
patient euthyroid.)
2. Massive goiter
3. Wish to avoid radio-active iodine
Graves disease: Total thyroidectomy
Toxic multinodular goiter: Resection of involved portion of gland
Hashimotos thyroiditis
Hashimotos thyroiditis
Similarities:
1. Both diseases are more common in females.
2. Both are auto-immune diseases.
3. Both have lymphocyte infiltration (found on histology).
4. Both cause painless, diffuse, symmetric, anodular goiter.
Differences:
Write a short note on Hashimotos

thyroiditis
1. The antibodies in Graves increase thyroid function, causing hyperthyroidism, while the
antibodies in Hashimotos decrease thyroid function, causing hypothyroidism.
123
2. I scanning is investigation of choice in Graves. I123 scanning is useless in Hashimotos.
3. Graves does not develop into cancer, but Hashimotos can develop into thyroid lymphoma.
4. Graves is treated by anti-thyroid medication, while Hashimotos is treated by exogenous
thyroid hormone.
5. Surgery is an excellent option for Graves, but not usually done for Hashimotos.
Etiology:
Auto-immune; antibodies against thyroid gland cause hypothyroidism.
History:
Typically, young female presents with anodular diffusely enlarged thyroid.
Anodular diffusely enlarged thyroid
Investigation:
Thyroid peroxisome antibodies are positive.
I123 scanning is not needed.
Write a short note on de Quervains

thyroiditis
Most common cause of painful thyroid

Write a short note on lymphocytic
Treatment:
Exogenous thyroid hormone. Surgery only if medication fails or goiter is large or symptomatic.
de Quervains thyroiditis is a.k.a. subacute granulomatous thyroiditis. Patient with recent
history of URTI presents with fever, malaise and an enlarged, painful thyroid. Pain radiates up
angle of jaw and ear. Cause is viral. Patient may become hyperthyroid or hypothyroid. If
hypethyroid, I123 scanning will show very little uptake and so easily differentiate from Graves or
toxic MNG. The disease is self-limiting and resolves in a few weeks. Treatment is symptomatic
with NSAIDs.
de Quervains thyroiditis
Postpartum female presents with painless diffuse thyroid enlargement. Patient may become
thyroiditis
Write a short note on acute
suppurative thyroiditis
Write a short note on Reidels struma
Causes of goiter
Write a short note on management of

euthyroid goiter
hyperthyroid. Disease is auto-immune and self-limitng. No treatment needed.

Patient with recent history of URTI develops bacterial thyroid infection with abscess formation.
Treatment is with I & D and IV antibiotic. After treatment, look for left pyriform sinus fistula if
patient is child.
Reidels struma occurs due to idiopathic extensive fibrosis within the thyroid gland which
extends to surrounding structures too. Patient presents with large, painless, nontender goite
with woody consistency and fixed to surrounding structures. Patient has pressure
symptoms, namely progressive dysphagia, dyspnea, and recurrent laryngeal nerve
paralysis. Treatment is isthmectomy, which relieves the pressure symptoms.
Sporadic
Iodine deficiency
Inherited metabolic defect
Exposure to goitrogenic agents
History:
Patient with euthyroid goiter may have diffuse or multinodular goiter which has remained
constant in size over the years or has been growing slowly. Patient may give history of a nodul
in MNG undergoing rapid painful enlargement due to hemorrhage.
Patient may be asymptomatic or may present with chronic cough, nocturnal dyspnea,
choking, and difficulty breathing in different neck positions or in recumbency. Patient m
also present with acute airway distress.
Assessment of vocal cord mobility and evaluation of respiratory status, tracheal deviation
and substernal extension should be done.
Investigation:
TSH test should be done to rule out subclinical hyperthyroidism.
For MNG, ultrasound and I123 scan should be done. Any nodule with micro-calcification or intr
nodular hypervascularity on ultrasound is suspicious. Any isofunctioning or hypofunctioning
nodule on I123 scan is also suspicious. All suspicious nodules should be aspirated.
Axial CT should be done if there is concern about airway (tracheal deviation, tracheal
compression, or substernal extension).
Treatment:
Thyroxine may be given to reduce goiter size. However, results are unpredictable and goiter
recurs after cessation of treatment.
Pembertons sign
Management of thyroid nodule
Goiter should be treated surgically in the following situations:

(a) Symptomatic goiter
(b) Goiter with radiographic evidence of airway obstruction (even if asymptomatic)
(c) Substernal goiter
(d) Cosmetic issues
Venous engorgement or dyspnea when arms are extended over the head in patient of goiter. It
suggests obstruction of thoracic inlet.
Most thyroid nodules are colloid nodules, adenomas, thyroid cysts, focal thyroiditis, or cancer.
History:
Increased risk of cancer if:
(a) age is <20 or >60
(b) history of exposure to ionizing radiation
(c) large nodule
(d) firm nodule

(e) lymphadenopathy
(f) vocal cord paralysis
(g) family history of medullary cancer
Investigation:
TSH: to assess thyroid status euthyroid, hypothyroid, or hyperthyroid.
Thyroid peroxidase antibodies: to rule out Hashimitos thyroiditis (if suspected).
Ultrasound: gives baseline status of nodule.
FNA: investigation of choice
Treatment:
If FNA is benign, then follow patient or give suppressive therapy.
If FNA is cystic, then drain the cyst. If cyst recurs, then surgery.
If FNA is follicular, then surgery (as follicular carcinoma cannot be ruled out)
If FNA is Hurthle-cell-predominant, then surgery (as Hurthle cell carcinoma cannot be ruled
out)
Hurthle cell
Elastography
Note:
Follicular FNA implies follicular cell adenoma or follicular cell carcinoma, but differentiation
cannot be done, so surgery is best option.
Hurthle-cell-predominant FNA implies Hurthle cell adenoma or Hurthle cell carcinoma or other
disorder, but differentiation cannot be done, so surgery is best option.
Large polygonal follicular cell with granular cytoplasm in the thyroid gland
Newly developed test to differentiate benign from malignant nodules, especially in those cases
Complications of thyroid surgery
where FNA is indeterminate. It is based on the observation that malignant lesions tend to be
hard and benign lesions tend to be soft. The test evaluates the degree of distortion of an
ultrasound beam when an external force is applied to the nodule. It gives an estimate of the
elasticity of the nodule.
Paralysis of recurrent laryngeal nerve paralysis: unilateral (hoarseness, no stridor) or
bilateral (stridor, no hoarseness)
Paralysis of external branch of superior laryngeal nerve: Loss of high pitch; the affected
vocal cord is lowered and bowed.
Difference between parathyroid

adenoma and parathyroid hyperplasia
Write a short note on

hyperparathyroidism
Hypoparathyroidism: Peri-oral and digital paresthesias. Also, spontaneous carpopedal spasm

abdominal cramps, laryngeal stridor, mental status changes, QT prolongation on ECG, and
tetanic contractions. Chvostek sign may be positive.
Adenoma: Benign enlargement of a single parathyroid gland while the other glands remain
normal.
Hyperplasia: Benign enlargement of all parathyroid glands.

Primary hyperparathyroidism: can be spontaneous, familial, or associated with MEN
syndromes. It may be a single gland adenoma or four-gland hyperplasia or (rarely) parathyroid
carcinoma.
Secondary hyperparathyroidism: is a hyperplastic response to systemic issue (typically rena

failure).
Tertiary hyperparathyroidism: is continuation of secondary hyperparathyroidism even after
calcium levels have returned to normal.
Benign familial hypo-calci-uric hypercalcemia: is an autosomal dominant inherited disease

High level of parathyroid hormone causes excess calcium reabsorption from kidneys, so serum
calcium is high and urinary calcium is low.

You want to surgically remove a
Sestamibi scanning (Technetium 99m methoxy-isobutyl isonitrile = Tc99MIBI) is the investigat
parathyroid adenoma in a patient. How of choice. In addition, SPECT or hybrid SPECT/CT increases the sensitivity.
would you localize the pathology preoperatively?
MRI, CT, and ultrasound are not good at localizing parathyroid adenoma.
You have just surgically removed a
Two options:
parathyroid adenoma. How can you be
certain that you removed the correct
1. Intra-operative parathyroid hormone level: If it drops significantly, it means we have
gland?
removed the correct gland.
2. Frozen section of resected tissue: confirms the parathyroid adenoma
Gliding sign
In surgery of parathyroid glands, the parathyroid glands can be identified as gliding discrete
bodies within the surrounding fat when the fat is gently manipulated.
Reconstructive ladder
1. Healing by secondary intention
2. Primary closure
3. Grafting:
(a) Skin: split thickness, full thickness
(b) Cartilage: septal, auricular, costal
(c) Bone: cortical, cancellous
(d) Nerve: great auricular, medial antebrachial cutaneous, radial, sural
(e) Composite: conchal bowl (skin + cartilage)
4. Local flap: advancement, rotation, transposition, bilobed transposition, rhombic
interposition, tubed skin flap
5. Regional flap:
(a) Fascial, fascio-cutaneous, & mucosal flaps: paramedian forehead flap, temporal
fasica flap, delto-pectoral flap, palatal island flap
(b) Muscular & myocutaneous flaps: temporalis flap, pectoralis major flap, trapezius flap
latissimus dorsi flap, sternomastoid flap, etc.
6. Prosthetic reconstruction
7. Micro-neurovascular free tissue transfer:
(a) Fascial & fascio-cutaneous flaps: temporo-parietal fascia free flap, radial forearm fre
flap, lateral arm free flap, antero-lateral thigh free flap, lateral thigh free flap
(b) Muscular & myocutaneous free flaps: latissimus dorsi free flap, rectus abdominus fre
Angiosome
Choke artery
flap, gracilis free flap

(c) Bone containing free flaps: radial forearm free flap, fibular free flap, iliac crest free
flap, scapular free flap
(d) Visceral free flaps: jejunal free flap, omental free flap
Tissue volume supplied by a single artery and vein
A connecting artery between angiosomes is called a choke artery.
A.k.a. oscillating artery.

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Question

Decibel levels of common sounds

Pinna is more helpful for what kind of

Bekesys traveling wave theory

Number of fibers in cochlear nerve

Test battery for audiological evaluation

Baseline audiogram frequencies to

3000 and 6000 Hz.

Reduction in sound energy from one side of skull to the other

Reflects how clearly patient can hear speech.

At what intensity level does acoustic

<40%: very poor

How is percentage of hearing loss

Most effective test to assess integrity

Oto-acoustic emissions are generated

Auditory brainstem response

Uses of oto-acoustic emissions

Types of oto-acoustic emissions

1. Neonatal hearing screening.

F2 = 1.2 x F1, where F1 and F2 are the stimulus frequencies

Vernix in outer ear.

Absent acoustic reflexes (ipsilateral& contralateral).

What probe tone is used in children for

Under what conditions, screening for

object or to the picture of the word presented.

1. Illness in neonate requiring > 48 hours admission in NICU

Male:Female ratio of pseudohypoacusis in children

Tests for suspected pseudohypoacusis

3. Family history of childhood deafness

1. No difficulty in hearing in normal conversation but hypo-acusis on testing

1. Acoustic reflex: Present at 5 dB above voluntary auditory threshold

1. Stengertest:Positive for pseudohypo-acusis

Components of a hearing aid

Peak clipping (in hearing aid)

Compression limiting (in hearing aid)

Signal = wanted sound

Dynamic range compression (in

Advantage: No distortion (unlike peak clipping) as saturation is not reached.

CROS and t-CROS (in hearing aid)

BiCROS (in hearing aid)

CROS = contralateral routing of signal

t-CROS = transcranial contralateral routing of signal

At what frequencies does noiseinduced hearing loss start?

How much protection against noise is

Active noise reduction

How can Menieres disease

Waves I, III, and V

Menieres disease (endolymphatic hydrops)

What are the electric potentials

What kind of brain stem response

10 20 dB (brainstem thresholds are higher)

What is auditory steady-state evoked

P300 (in electrical audiometry)

Mismatch negativity response

1. Evaluation of the auditory pathway above the brainstem:

Direction of nystagums in hypofunction

On which side of patient should

Utricle senses translational/tilt movement of head in transverse plane.

(b) Saccular nerve