Otorrino P2

OTORHINOLARYNGOLOGY
Denisse Alejandra Ochoa Orrico
Universidad Anáhuac Mayab

Agosto-Diciembre 2020
TOPICS
2nd Midterm
1. Audiologic testing 2
a. Pure tone audiogram 2
b. Speech recognition threshold 7
c. Suprathreshold speech recognition scores 7
d. Tympanogram 8
e. Acoustic reflex threshold 10
f. Otoacoustic emissions 13
g. Electrocochleography 14
h. Auditory brainstem response 15
2. Vestibular testing 16
a. Vestibuloocular reflex 18
b. Vestibulospinal reflex 21
c. Caloric test 24
d. VEMP 25
3. Sensorineural hearing loss 26
a. Weber and Rinne test 32
4. Diseases of the external ear 36
a. Congenital anomalies 38
b. Trauma 41
c. Infectious and inflammatory diseases 43
d. Dermatologic diseases 45
e. Obstructive disorders 47
f. Neoplasms 48
5. Otitis media 52
6. Vestibular disorders 59
a. Benign paroxysmal positional vertigo 59
b. Meniere disease 61
c. Vestibular neuronitis 64
d. Superior semicircular canal dehiscence 65
7. Disorders of the facial nerve 67
a. Bell’s palsy 67
b. Herpes zoster oticus 67
c. Other facial nerve disorders 72
8. Benign disorders of the salivary glands 75
a. Infectious inflammatory diseases 76
b. Noninfectious inflammatory diseases 78
c. Noninflammatory diseases 81
d. Benign neoplasms disorders 83
9. Airway management and tracheostomy 85
a. Nonsurgical airway maintenance 87
b. Tracheotomy 90
c. Cricothyroidotomy 92
Things Denisse thinks are important
Things the Dr. asked during class
Things the Dr. said would be on the exam
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Cross-check principle: D
ON’T DO A SINGLE TEST FOR DIAGNOSIS. No auditory test
result should be accepted and used in the diagnosis of hearing loss until it is confirmed or cross
checked by one or more independent measures..
.
BEHAVIORAL AUDIOMETRY-----------------------------------------------
Pure tone audiogram GOLD STANDARD
A pure-tone threshold is the lowest intensity at which the tone is heard 50% of the time.
● Low octave frequencies: 250 Hz-500 Hz

● Mid octave frequencies: 1000 Hz-2000 Hz
● High octave frequencies: 4000 Hz-8000 Hz (only in AC)
Range for human hearing: 16–16,000 Hz or 20–20,000 Hz.
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A.- AIR-CONDUCTION (AC) THRESHOLDS B.- BONE CONDUCTION (BC) THRESHOLDS
How does it work? The sound stimuli enter How does it work? The skull vibration makes
through the ear canal, travel into the cochlea, the sound energy largely to bypass the outer
and get transduced into neural impulses that and middle ears and stimulate the cochlea
continue through the auditory nerve.
How is it performed? Using earphones. How is it performed? With a bone

vibrator/oscillator on the mastoid process.
A hearing loss could be conductive or A hearing loss directly reflects the integrity of
sensorineural. just the sensorineural mechanism.
Air-bone gap (ABG): Difference in dB between the AC threshold and the BC threshold.
BC threshold can’t be poorer to AC thresholds. Otherwise, an instrumentation problem
(calibration) may be present.
HOW TO READ AN AUDIOGRAM

Thresholds are recorded on an audiogram, w
hich should be obtained in a sound-treated
environment such as an audiometric booth or suite.
AC BC SOUND FIELD
W/O Masking With masking W/O Masking With masking S: Sound field unaided
SSS: Filtered speech
“X”: Left ear “⬜”: Left ear “>: Left ear “]”: Left ear A: Sound field aided
“O”: Right ear “ ”: Right ear “<”: Right ear “[”: Right ear
X-axis: Test frequency (Hz)

Y-axis: Intensity (dB)
“↓”: NR. No response at maximum limits or audiometer
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HEARING TYPE CLASSIFICATION

Hearing type AC Thresholds BC Thresholds ABG Affected
classification mechanisms
NORMAL- ≤ 25 dB HL ≤ 15 dB HL* ≤ 10 dB Not applicable

HEARING (nonsignificant)
NORMAL- ≤ 25 dB HL ≤ 15 dB HL* > 10 dB Conductive**

HEARING WITH (significant)
SIGNIFICANT ABG
CONDUCTIVE > 25 dB HL ≤ 15 dB HL* > 10 dB Conductive**

(elevated) (significant)
SENSORINEURAL > 25 dB HL > 15 dB HL ≤ 10 dB Sensorineural***

(elevated) (elevated)* (nonsignificant)
MIXED > 25 dB HL > 15 dB HL > 10 dB Sensorineural***

(elevated) (elevated)* (significant) and conductive**
*Some clinicians use 25 dB HL

**Conductive: Outer and/or middle ear affected.
***Sensorineural: Cochlear and/or auditory nerve affected.
EXAMPLES OF CONDUCTIVE HEARING LOSS DISORDERS:

● Otitis media ● Congenital aural atresia
● Eustachian-tube dysfunction ● Otosclerosis
● Cholesteatoma ● Treacher Collins syndrome
● Ossicular discontinuity
EXAMPLES OF SENSORINEURAL HEARING LOSS DISORDERS:
● Noise-induced hearing loss ● Genetic hearing loss (Connexin 26

● Presbycusis deafness and Usher syndrome).
● Ototoxicity (aminoglycosides and ● Acoustic neuroma (Vestibular
cisplatinum) schwannoma)
● Meniere disease ● Idiopathic sudden hearing loss
HOW DO WE MEASURE THE MAGNITUDE OF HEARING LOSS?

Calculating the pure-tone average (PTA): Average of the AC thresholds at 500, 1000, 2000 and 3000
Hz (these are called the
“speech frequencies”).
Normal < 25 dB Hearing within normal limits
Mild 26-40 dB Has difficulty with soft sounds, background noise, and when at a
distance from the source of the sound
Moderate 41-55 dB Has significant difficulties with normal conversational level

speech and relies on visual cues
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Moderately 56-70 dB Difficulties understanding faint speech, speech at a distance,

severe competitive speech and loud speech.
Severe 71-90 dB Cannot hear conversational speech and misses al speech sounds
Can hear environmental sounds, such as dogs barking and loud
music
Profound >90 dB Hears only loud environmental sounds, such as jackhammers,

airplane engines and firecrackers.
THE BANANA OF THE SPEECH

If I have a threshold out of this area, I may have hearing loss.
AUDIOMETRIC CONFIGURATIONS
A. FLAT CONFIGURATION: (Audiogram B, black line).
Thresholds are similar across the frequency range.
B. SLOPING CONFIGURATION: (Audiogram A). Thresholds

increase with increases in frequency. (Presbycusis)
C. RISING CONFIGURATION: (Audiogram B, white line).

Thresholds are worst at the low frequencies and improve as
the frequency increases. (Early-stage Meniere disease)
D. HIGH-FREQUENCY HEARING LOSS CONFIGURATION:

(Audiogram C, white line). Hearing loss only at the high
frequencies
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E. LOW-FREQUENCY HEARING LOSS CONFIGURATION:

(Audiogram C, black line). Hearing loss only at the low
frequencies
F. NOTCHED AUDIOMETRIC CONFIGURATION: (Audiogram D,

white line). Hearing loss at a single frequency or within a
frequency range (Hearing loss from noise exposure,
otosclerosis (Carhart notch))
G. PEAKED AUDIOMETRIC CONFIGURATION: (Audiogram D,

black line). Normal-hearing thresholds within a narrow
frequency range
H. TROUGH OR SAUCER AUDIOMETRIC CONFIGURATION:

(Audiogram E, white line). Worse thresholds at mid
frequencies and better thresholds at the low and high
frequencies. (Hereditary hearing loss)
I. INVERTED SAUCER OR INVERTED TROUGH

CONFIGURATION: (Audiogram E, black line). Better
thresholds at mid frequencies and poorer thresholds at the
low and high frequencies. (Hereditary hearing loss)
J. FRAGMENTARY OR CORNER AUDIOGRAM: (Audiogram F).

Thresholds near or at the maximum output at the low
frequencies + absence of responses at all higher frequencies. (Hereditary hearing loss)
OTHER CONFIGURATIONS FOR CONDUCTIVE HEARING LOSS
● STIFFNESS EFFECT: H earing loss is greater at the low frequencies. Otosclerosis, middle-ear
effusion
● MASS EFFECT: Hearing loss is greater at the high frequencies. Ossicular discontinuity.
HIGH FREQUENCY AUDIOMETRY

Also called extended-high-frequency or ultra-high-frequency pure-tone audiometry.
Involves obtaining AC pure-tone thresholds at 9000 Hz - 20000 Hz frequencies beyond the
conventional audiometric range (9000 Hz - 20000 Hz).
Utility: To detect early ototoxic effects,early onset of p
resbycusis, early noise-induced hearing loss.
Limitation: Increase in hearing threshold with frequency.
MASKING
Used to obtain hearing thresholds in the test ear (TE), which are not confounded by the
participation of the non-test ear (NTE). Must be presented to the NTE while obtaining the AC
threshold for the TE.
➔ INTERAURAL ATTENUATION: Reduction in intensity of a signal.
◆ 0 dB on BC sounds. You don’t need to obtain unmasked BC for both ears.
◆ 40 dB on AC sounds
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➔ CROSSOVER: The sound goes to the other ear. Determined by the interaural attenuation.
➔ CROSS-HEARING: Occurs when the NTE BC threshold is better than the crossover.
➔ MASKING DILEMMA: If the masking noise delivered to the NTE is heard by the TE
EXAMPLE
1. An AC tone at 500 Hz is delivered to the TE at 65 dB HL
2. It loses 40 dB (interaural attenuation) arriving to the NTE at 25 dB HL (crossover)
3. If NTE BC threshold is at the level of the crossover or better, then cross-hearing occurs.
a. NTE BC threshold = 20 dB HL = Cross-hearing
b. NTE BC threshold = 30 dB HL = No cross-hearing. Masking is not needed.
When do we mask the NTE?
● AC masking:
TE unmasked AC threshold - NTE BC (or AC) threshold > Interaural attenuation of 40-65 dB.
● BC masking: ABG > 10 dB
FACTORS INFLUENCING AUDIOMETRIC INTERPRETATION

1. TACTILE RESPONSES: More likely to occur for BC than for AC testing, at the low frequencies.
a. Symbol “VT” on audiogram.
2. COLLAPSED EAR CANALS: Excessively compliant ear-canal walls narrow due to the pressure
during AC testing. Spurious ABGs that are larger at the high frequencies
HOW DO WE KNOW OUR PATIENT HAS COLLAPSED EAR CANALS? Using 4000 Hz, do the AC
testing with the jaw wide open and with the jaw closed. If the threshold with the open jaw is >5 dB
better than the threshold with the jaw closed, your patient has collapsed ear canals.
And you must
repeat the test with the jaw closed.
3. ACOUSTIC RADIATION: Is the leakage of sound energy from the bone oscillator. Can be
eliminated by occluding the better ear or both ears when testing BC at frequencies >2000 Hz.
Speech audiometry
A.- SPEECH RECOGNITION THRESHOLD B.- SUPRATHRESHOLD SPEECH
(SRT) RECOGNITION SCORES
Based on spondaic bisyllabic words (spondees) Based on monosyllabic words, (sentences, and
continuous discourse may also be used).
Reported in dB HL Reported in %.
UTILITY: Represents the lowest (softest) UTILITY: Reflects the percent of speech stimuli
intensity at which the patient can correctly correctly repeated at 35-40 dB sensation level.
repeat half of the spondees. ➔ Normal >88%.
➔ Confidence limit between both ears:
95%. The width of the limit decreases as
the number of words increases (higher
sensitivity).
PURPOSE: To validate the pure-tone PURPOSE: To evaluate how well a person can
audiogram* understand speech. And if it will obtain
significant benefit from amplification
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*VALIDATION OF PURE-TONE AUDIOGRAM: SRT is ±12 dB than PTA.

If SRT is >12 lower than PTA: Functional (nonorganic) hearing impairment
If SRT is >12 greater than PTA: Misunderstanding of instructions, language factors, central auditory
nervous system disorders
WHEN TO DO MASKING? If:

Speech level in the TE - Interaural attenuation of 40 dB > AC or BC threshold in the NTE.
Behavioral audiologic testing in pediatric population

A.- BEHAVIORAL OBSERVATION AUDIOMETRY (BOA)
● For children <6 months old
● For ruling out moderate or worse hearing impairment in at least 1 ear.
HOW DOES IT WORK?
● Presentation of test stimuli through loudspeakers. No conditioning of responses is done.
● Observe minimum response levels (eye turns, eye widening, sucking behavior, alerting, or
stilling). DOESN’T enable thresholds to be obtained.
B.- VISUAL REINFORCEMENT AUDIOMETRY (VRA)

● For 6 months-2.5 years old children.
● Involves operant conditioning and is based on
localization responses.
HOW DOES IT WORK?
1. Auditory stimuli are delivered via a loudspeaker
2. When a child hears the tone, he/she responds naturally by
head or eye turns toward the source of the sound
3. The child is rewarded by a toy on top of the speaker
LIMITATIONS
1. Represents the hearing sensitivity for only the better ear
C.- PLAY AUDIOMETRY

● For 2.5-4 years old children
HOW DOES IT WORK?
● Child performs a task (throwing a block into a box) whenever a
tone is heard
D.- SRT AND SUPRATHRESHOLD SPEECH RECOGNITION

SCORES FOR CHILDREN
PHYSIOLOGIC MEASURES---------------------------------------------------
Acoustic admittance testing
A.- TYMPANOGRAM
HOW DOES IT WORK?
1. Air pressure (+200 to –300 decapascals [daPa]) into the external ear canal via a probe
2. The admittance (Y) of the middle ear will be graphed. (I'm measuring how much the tympanic
membrane moves with different pressures and sounds)
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3. At the same time, a probe tone at a single frequency (226 Hz) is presented into the ear canal
through a speaker
4. A portion of that energy is admitted and the other is rejected at the tympanic membrane.
5. The rejected energy is detected by a microphone in millimho (mmho) units.
○ 1 mL = 1 mmho
HOW TO READ A TYMPANOGRAM

X-axis: Air pressure (daPa)
Y-axis: Immittance (mmH2O)
TYMPANOMETRIC PEAK PRESSURE (TPP): Occurs when the air pressure introduced = the air
pressure exerted from the middle ear. It is at this point that admittance is maximal. Unit: daPa
● TTP -100 - +100 daPa: Normal
● TTP ≤ -50 daPa: Eustachian-tube dysfunction, with/without middle-ear effusion
● No TTP visible: Stiffening middle-ear pathology
PEAK-COMPENSATED STATIC-ACOUSTIC ADMITTANCE

A - B
A: Total admittance of the ear or admittance at the TPP
B: Admittance at an extreme external ear-canal pressure (+200 or –300 daPa) or ear-canal
admittance (ear-canal volume)
If ear-canal volume >2.5 cm3 (2.0 in children): Tympanic-membrane perforation
. The
tympanogram will be flat.
● 0.35-1.30 mmho: Normal

● <0.35 mmho: Stiffening middle-ear pathology
● >0.75 + significant ABG: Ossicular discontinuity, flaccid tympanic membrane,
otosclerosis. You need to do a high-frequency tympanometry.
HIGH-FREQUENCY TYMPANOMETRY (2 types): obtained for the 678-Hz probe tone
● Conductance (G) tympanogram: Reflects acceptance of sound energy into stiffness
and mass of the ear
● Susceptance (B) tympanogram: Reflects acceptance of sound energy into the
resistive components of the ear.
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TYPES OF TYMPANOGRAMS
TYPE WHAT IT IS OBSERVED? WHAT DOES IT MEAN? PATHOLOGY
TYPE Normal TTP + normal Normal middle ear function None

A (1) peak height Sensorineural problems
TYPE Reduced peak height + Stiffening middle-ear pathology Otosclerosis

AS (2) Normal TPP
TYPE Higher peak height Increased admittance of sound Ossicular discontinuity

AD (3) energy in the middle ear
TYPE Flat tympanogram Stiffening middle-ear pathology or tympanic membrane

B (4) perforation (or a patent tympanostomy tube).
Effusion or something occupying the middle ear (liquid, mucus)
TYPE Significantly negative Eustachian-tube dysfunction

C (5) TPP
B.- ACOUSTIC REFLEX THRESHOLD (ART)

● Is the lowest intensity that yields a just noticeable decrease in acoustic admittance.
● It’s a mechanism of protection of the ear. Elicited by a sufficiently intense sound.
Produces the rejection of sound energy (decreased acoustic admittance).
● Bilateral, even if the sound is presented to one ear only
● It can go ipsilateral (IART) or contralateral (CART). If I have an IART but not a CART, it means I
have a problem (a tumor)
● WHAT IS IT FOR? To detect conductive or retrocochlear pathology.
MUSCLES INVOLVED:
● The stapedius muscle
○ Origin: Pyramidal eminence on the posterior wall of the tympanic cavity
○ Insertion: Neck of the stapes
○ Innervation: Facial nerve
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● Tensor tympani muscle

○ Origin: Anterior wall of the tympanic cavity.
○ Insertion: Neck of the malleus
WHERE IS THE SOUND CONDUCTED THROUGH?

● Afferent (sensory) arc of the ART: Outer and middle ear, cochlea, vestibulocochlear nerve
(CN VIII), cochlear nuclei, and superior olivary complex in the auditory brainstem.
○ The presence of the reflex depends on the dB
● Efferent (motor) arc of the ART: Motor nucleus of the facial nerve (CN VII), facial nerve,
stapedius, and stapes.
○ The presence of the reflex depends on the Hz
DISEASES OF REDUCTION OF ART.

● Bell’s palsy. Affects the VII cranial nerve, so there’s going to be a palsy in the half of the face.
so there’s no acoustic reflex on that side.
● Otosclerosis. The stpaedian muscle here is fixed to the footplate and it doesn’t move. so the
muscle doesn’t contract.
● Conductive pathology
● Cochlear hearing loss beyond about 50 dB HL;
● Lesions of the vestibulocochlear nerve, cochlear nuclei, superior olivary complex, motor
nucleus of the facial nerve, or facial nerve
● Lesions of the stapedius
ELECTRICALLY EVOKED STAPEDIUS REFLEX THRESHOLDS (ESRTS)

● Measured during cochlear implant surgery
● Estimates of maximum comfortable levels of stimulation (M-level/C-level) to prevent
overstimulation from the cochlear implant.
● For individuals unable to furnish subjective reports of loudness
● Done with electrical pulses, to identify the lowest level that elicits motion of the stapedius
muscle
● Limitation: It may be absent in low frequencies.
Pathology R CART L CART R IART L IART EXPLANATION
R conductive ↑ or ABS ABS ABS Normal Conductive pathology affects

pathology efferent and afferent reflex arcs.
L conductive ABS ↑ or ABS Normal ABS

pathology
Bilateral ABS ABS ABS ABS The lesion will prevent elicitation of
conductive the reflex
pathology
Cochlear Normal Normal Normal Normal Only aerent arc impacted and
hearing loss degree of cochlear hearing loss is
≤∼50 dB HL not enough to aect the acoustic
reflex
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R cochlear ↑ but < Normal ↑ or Normal Afferent arc affected

hearing loss ≥ 90th ABS
∼ 50 dB HL percentile
L cochlear Normal ↑ but < ↑ or Normal

hearing loss ≥ 90th ABS
∼ 50 dB HL percentile
R 8th ↑ or ABS Normal ↑ or Normal Retrocochlear pathology affects

nerve/low >90th ABS afferent arc
auditory percentile
brainstem
pathology
affecting
afferent arc
(eg, R
vestibular
schwannoma)
L 8th Normal ↑ or ABS Normal ↑ or

nerve/low >90th ABS
auditory percentile
brainstem
pathology
affecting the
afferent arc
(eg, L
vestibular
schwannoma)
Bilateral 8th ↑ or ABS ↑ or ABS ↑ or ↑ or Afferent arc affected in both ears

nerve/low >90th >90th ABS ABS
auditory percentile percentile
brainstem
pathology
affecting the
afferent arc
R 7th nerve Normal ↑ or ABS ↑ or Normal Lesion involves efferent arc so

lesion to the >90th ABS reflex affected is in affected ear
stapedius percentile
L 7th nerve ↑ or ABS Normal Normal ↑ or

lesion to the >90th ABS
stapedius percentile
Bilateral 7th ↑ or ABS ↑ or ABS ↑ or ↑ or Efferent arc affected in both ears

nerve lesion >90th >90th ABS ABS
to the percentile percentile
stapedius
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C.- ACOUSTIC REFLEX ADAPTATION (ARA) OR DECAY TEST

HOW DOES IT WORK? An activating test tone is presented at 10 dB SL re: ART for 10 sec at 500 Hz
and 1000 Hz.
● POSITIVE IF: The adaptation or decay reaches >50% over the 10-second period =
Retrocochlear pathology.
D.- ADMITTANCE ASSESSMENT IN INFANTS

● We don’t use 226-Hz probe tone as in children >3 years and adults. We use 1000-Hz probe
tone (neonates >1 month)
● What happens if we use 226-Hz probe tone in infants?
○ False-positive and false-negative results
○ Irregular or artifactual tympanometric shape
● Infants (1000 Hz probe tone) with Middle-ear effusion if:
○ Flat tympanogram
○ Absent ART
○ Peak-compensated static-acoustic admittance <0.1 or 0.2 mmho.
● Children >3 years old (226-Hz probe tone9 with Middle-ear effusion if:
○ Flat tympanogram.
○ Elevation of the IART >110 dB HL at 1000 Hz + significantly negative TPP
○ Elevation of the IART >110 dB HL at 1000 Hz + peak compensated static-acoustic
admittance < 0.35 mmho
Otoacoustic emissions (OAE’s)

● Cochlear echoes: Produced in response to acoustic stimulation of the ear
● OAEs are low-level sounds that can be recorded using a probe containing a microphone that
is inserted into the external ear canal.
● HOW DOES IT WORK? The sound is a traveling wave that goes along the basilar membrane
in an anterograde direction from the base of the cochlea (high-frequency region) to its apex
(low-frequency region). Then, there’s another wave in retrograde direction
● For newborn screening. We put a probe on the ear and push a button. If it's green the patient
hears and red if not.
● WHAT ARE WE MEASURING? The cochlear status: The sound that the OHC (outer hair cells)
produce. the biomechanical motility of the OHC
○ Lesions affecting the OHCs adversely affect the OAEs.
● Limitation: Middle-ear pathology can reduce or obliterate the OAE
CLASSIFICATION
A. Evoked: Represent an objective, physiologic measure of cochlear (OHC) integrity
a. TEOAEs (Transient otoacoustic emissions). Elicited by transient stimuli such as
clicks or tone bursts
b. DPOAEs (Distortion product otoacoustic emissions). Recorded using 2 tones
simultaneously
B. SOAEs (Spontaneous otoacoustic emissions). Recorded without employing a sound
stimulus.
Not used for clinical audiologic diagnosis.
USEFUL TO DETECT:
A. Sensorineural hearing loss of cochlear etiology
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B. Auditory neuropathy spectrum disorder (ANSD): Normal OAE + Abnormal ABR

C. Ototoxicity monitoring
D. Early detection of OHC damage
ELECTROPHYSIOLOGIC MEASURES----------------------------------
Auditory evoked potentials are electrical potentials (low-amplitude responses) elicited by sound
stimulation.
● More intense stimulus = More amplitude, less latency
CLASSIFICATION
A. Very short/ early latency auditory evoked potentials (1-3 msec)
:
a. Cochlear microphonic (CM):
i. Alternating current (AC) potential
ii. Is the earliest component seen when performing ECochG
iii. Origin: OHC
iv. It mirrors that of the stimulus
b. Summating potential (SP)
i. Direct current (DC) potential
ii. Preceding the AP
iii. Origin: IHC
c. Eighth-nerve action potential (AP)
i. Also known as compound action potential
ii. Reflects the summed activity of the nearly synchronous firing of the individual
afferent fibers of the auditory nerve
iii. 2 negative peaks (N1 and N2)
B. Short/early latency auditory evoked potentials.
C. Middle latency auditory evoked potentials.
D. Long latency auditory evoked potentials.
E. Very long latency auditory evoked potentials.
Electrically evoked action potential (electrical compound action potential) (eCAP)
● Employed during cochlear implantation surgery and postoperatively.
● To assist in mapping the cochlear implant.
Electrocochleography (ECochG)
● For recording the very short/early latency auditory evoked potentials from the cochlea and
distal auditory nerve
● 2 kinds of approaches:
○ TRANSTYMPANIC: To put a needle electrode in the tympanic membrane into the round
window in the promontory.
Yields larger response amplitudes
○ EXTRATYMPANIC: Placement of the active electrode in the ear canal, close to the
tympanic membrane
● GOLD STANDARD for meniere disease/endolymphatic hydrops
○ Enlarged SP and SP/AP ratio
○ Low specificity
■ Improves using tone burst stimuli with transtympanic recordings.
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● Other utilities:
○ ANSD (normal SP and MC, abnormal AP)
○ Identifying wave I of ABRs (using N1 of AP)
EXAMPLE
X-axis: Latency time (msec)
Y-axis: Wave amplitude (nV)
BL: Baseline
SP: Summating potential
AP: Eighth nerve action potential
Auditory brainstem response (ABR or BAEP)

● They represent the short/early auditory evoked potentials
● How to do it and when to do it? In children and newborn
a. I put a sound that is called reverberation
b. The active electrode is placed at the vertex or the forehead and the inverting
electrode at the mastoid or earlobe.
● To differentiate cochlear form retrocochlear pathology. It graphs how the sound travels
through the auditory pathway
● Comprises 5-7 waves: each wave represents a level on the auditory pathway. If there’s no
hearing, there are no waves
1. acoustic nerve (cranial nerve VIII)
a. greater amplitudes for waves I and II than for waves IV and V
b. bifid wave
2. cochlear nuclei
3. Superior olivary complex at the level of the pons
a. bifid wave
4. Lateral lemniscus
a. resting on the upslope of wave V
5. Inferior colliculus
a. resting on the downslope of wave IV
b. Greater amplitude than IV wave
6. Medial geniculate of the thalamus
7. Auditory radiation of the thalamocortical
Waves VI and VII have little clinical utility.
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PATIENT HISTORY------------------------------------------------------------
Symptoms
A.- VERTIGO AND DIZZINESS
PERIPHERAL VERTIGO CENTRAL VERTIGO DIZZINESS
Definition Unreal sense of rotatory movement. It’s an illusion Altered sense of

orientation.
Why does it Impaired tonic Vascular events Central lesions (mostly)

happen? symmetry in the inputs Decompensated status
of the vestibular nuclei. of a peripheral lesion
Vertigo is mostly Vitamin B12 deficiency
caused by peripheral Folic acid deficiency
lesions Hyperlipidemia.
Where’s the lesion? Vestibular nuclei Brainstem -

Cerebellum Cerebellum
Pathways connecting
these structures in the
brainstem
Cortex.
Onset Sudden Gradual
Intensity ++++ +
Duration Seconds (in episodes) Continuous
Nystagmus Fatigable Non-fatigable
Direction of Unidirectional, Multidirectional,

nystagmus horizontal vertical
Associated ✔
neurologic findings
Hearing loss or ✔
tinnitus
Associated nausea Frequent, severe Infrequent

or vomiting
Pathologies BPPV 1 min. Transient ischemic Perilymph fistula.

Perilymph fistula. attack. 2-20 min.
Meniere disease (20
min-24 h)
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Other pathologies Vestibular neuronitis (isolated attack of vertigo w/o hearing loss >24 hours)
Migraine (seconds-days. Bilateral tinnitus w/o hearing loss).
Always ask about precipitating factors:

● Rapid head movement: BPPV (Benign paroxysmal positional vertigo)
● Falling w/o loss of consciousness: Meniere disease
● Noise: Tullio phenomenon
● Valsalva maneuver: Perilymph fistula, Chiari malformation, or dehiscence of the superior
semicircular canal (SCC).
B.- LIGHTHEADEDNESS
Is the sensation of unsteadiness and falling + blurred vision, faded
facial color and syncope.
Causes: Nonvestibular causes: Cardiac causes, anemia, or
vasovagal reflex
C.- IMBALANCE
Inability to maintain the center of gravity. Patients feel unsteady or as
if they’re about to fall.
Causes: Sensory, motor or neurological disease.
D.- OTHERS
● Hearing loss
● Tinnitus
● Facial weakness
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Drug use
● Vestibulotoxic drugs may cause bilateral vestibular damage and oscillopsia:
○ Gentamicin
○ Streptomycin
○ Amikacin
○ Neomycin
○ Cisplatin (also ototoxic)
● GABA analogs and antidepressant drugs (cause dizziness, not vertigo).
Psychological factors
Panic attacks or agoraphobia cause lightheadedness in crowded areas or public places
Hyperventilation may induce symptoms in patients with anxiety and phobic disorders, but it
seldom produces nystagmus.
Family history
History of a balance disorder: Meniere disease, neurofibromatosis, migraine, narrow
endolymphatic duct
EVALUATION AND TESTING-----------------------------------------------

Do this evaluation in order
A.- EVALUATION OF VESTIBULO B. EVALUATION OF VESTIBULOSPINAL

OCULAR REFLEX (VOX) REFLEX (VER) (POSTURAL CONTROL TESTS)
1. Static position of head and eyes 1. Romberg

2. Eye cover test 2. Past-pointing
3. Head thrust 3. Tandem gait
4. Spontaneous nystagmus 4. Fukuda stepping test.
5. Gaze nystagmus
C. CEREBELLAR FUNCTIONS
6. Head shaking nystagmus
7. Gross oculomotor evaluation
D. CRANIAL NERVE EVALUATION
8. Fistula testing
9. Positional tests
10. Visual acuity testing
A.- Vestibuloocular reflex (VOX)

1. STATIC POSITION OF HEAD AND THE EYES
Abnormal findings:
● Skew deviation: Is when 1 eye is misaligned
in the vertical plane relative to the other eye.
○ Caused by peripheral lesions
(otolith-related disease)
○ Is a Low sensitivity (0.30), high
specificity (0.98) finding.
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● Head tilt: Is a sign of peripheral or central vestibular disease.

● Triad of ocular tilt reaction: (sign of central lesion)
1. Skew deviation
2. Head tilt
3. Ocular torsion
2. EYE COVER TEST

https://www.youtube.com/watch?v=Wf8DGL7WE8U
Useful for: Detecting occult skew deviation.
How do I know my patient has skew deviation?
✔If there’s no movement, my patient is healthy and its eyes are aligned.
If there’s any vertical movement on the other eye, there’s occult skew deviation or
strabismus.
3. HEAD THRUST (HEAD IMPULSE TEST [HIT])

https://www.youtube.com/watch?v=fiqAkhYNPRk
Useful for: Testing dynamic nonlinearity in the SCCs
How is it performed? I ask the patient to stare at my nose, and I move its head 15° from the primary
position.
✔If the patient keeps looking at my nose, it’s ok.
If there’s any corrective saccade when the head is rotated toward the lesion side =
inappropriate and compensatory slow-phase eye movement = peripheral lesion.
Patients with a central lesion can do the test successfully with no saccadic movement
4. SPONTANEOUS NYSTAGMUS
https://www.youtube.com/watch?v=rT1iHO964MQ
How is it performed? The patient has to wear Frenzel glasses. If there’s nystagmus, you must note
its direction, frequency and amplitude. Nystagmus has a fast phase and a slow phase.
5. GAZE NYSTAGMUS
Occurs in both peripheral lesions and central lesions.
How is it performed? Holding the index finger at off-center positions.
How to differentiate central lesions from peripheral lesions? 2 acronyms:
● INFARCT
○ Impulse test Normal
○ Fastphase Alternating
○ Refixation on Cover Test
● HINTS
○ Head Impulse test Normal
○ Test of Skew
6. HEAD SHAKING NYSTAGMUS

https://www.youtube.com/watch?v=LuWnB5xjuJc
How is it performed? The patient has to wear Frenzel glasses. We ask the patient to shake its head
horizontally for 20 seconds, and when it stops, we’ll see if there’s nystagmus.
✔If there’s no nystagmus, it’s ok.
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If there’s nystagmus = Asymmetry in bilateral vestibular function. Nystagmus may be

monophasic, biphasic, or triphasic.
7. GROSS OCULOMOTOR EVALUATION

https://www.youtube.com/watch?v=MsBDVW-gdF0
How is it performed? I ask the patient to stare at my finger that is 25 cm away from him. The patient
must keep his eyes on my finger as I move it in different directions.
● Which cranial nerves are we evaluating? III, IV and VI.
● Check if the patient’s eye movements are conjugate or disconjugate.
● Saccadic intrusion: Central lesion,
8. FISTULA TESTING
How do I know if my patient has a fistula?
● Hennebert sign: Applying positive pressure to the outer ear canal with a pneumatic
otoscope will cause nystagmus or the patient will perceive movement of a visual target that
is not actually moving.
○ Perilymph fistula or Meniere disease.
● Tullio phenomenon: A loud noise is applied and it causes nystagmus.
9. DYNAMIC POSITIONAL TESTS

● Dix-Hallpike maneuver:
○ https://www.youtube.com/watch?v=7ePecb9azS4
○ Useful for: Elicit typical nystagmus of BPPV of the vertical SCCs (posterior or anterior).
○ How is it performed?:
● Roll test:
○ Useful for: Diagnosing horizontal variants of BPPV.
○ How is it performed?
■ Patient is placed in the supine position with the head raised 30°
■ Clinician rotates the patient’s head to both sides. If we see:
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● Geotropic nystagmus: It is the side of lesion to which head movement

creates more intense nystagmus.
● Ageotropic nystagmus: It is the side of lesion toward which head
movement causes less intense nystagmus.
10. VISUAL ACUITY TESTING

✔If the patient can read an eye chart while moving the head, it’s ok.
If the patient can’t read while his head is moving = abnormal vestibulo ocular reflex.
B.- Evaluation of vestibulospinal reflex (VER)

☹ These tests have mild sensitivity and speciﬁcity in identifying lesions.
1.- ROMBERG TEST

Useful for: Identifying vestibular impairment
How is it performed? We ask the patient to stand still with eyes closed and feet together and arms
folded against the chest.
✔The patient maintains balance
An increased sway or fall toward either side is considered abnormal.
2. PAST-POINTING TEST
https://www.youtube.com/watch?v=Icoc-WuJxFk
How is it performed?
1. I stand in front of the patient.
2. I ask the patient to extend his arms and touch my fingers
3. Patient has to raise his arms up and bring their index fingers again into contact with mine.
4. The patient has to do the last step 2-3 times with their eyes open
5. Repeat. But now with his eyes closed.
Deviation to 1 side = Problem in the cerebellum
3. TANDEM GAIT
✔Patient can take 10 tandem steps with eyes closed, without deviation.
4. FUKUDA STEPPING TEST

https://www.youtube.com/watch?v=oz1mEtZcJ1g
Patients are asked to march in place with eyes closed. After 50 steps, a rotation
> 30° toward 1 side is considered abnormal
C.- Evaluation of cerebellar functions

3 “D” findings in cerebellar lesions:
1. Dysmetria
2. Dysarthria
3. Dysdiadochokinesia.
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D.- Cranial nerve evaluation

An evaluation of cranial nerve function may reveal hypoesthesia of the outer ear canal and an absent
corneal reflex, as found in acoustic neuromas.
ELECTRONYSTAGMOGRAPHY/VIDEONYSTAGMOGRAPHY
It's the recording and measuring eye movements or eye positions in response to visual or vestibular
stimuli
Is the first test we’ll do when there’s vertigo. Useful for diagnoses of: BPPV, vestibular neuronitis,
Meniere disease, labyrinthitis, ototoxicity, acoustic neuromas.
Abnormal findings in ENG don't necessarily indicate a CNS lesion tho.
Before each test, the system must be calibrated.
A.- Oculomotor tests

They measure the accuracy, latency, and velocity of eye movements for a given stimulus.
How are they performed? The patient is seated upright with the head stabilized. The ENG device has
a LED light array (this will be the stimulus)
1.- SACCADE TEST

Saccades are rapid eye movements that bring objects in the periphery of the visual field onto the
fovea
How is it performed? The LED flashes sequentially in 2 positions: at the center of the array, and then
15° to 20° to the right or left from the center. The patient is asked to follow the LED
What are we evaluating?
1. Latency of the saccades: Is the time difference between the presentation of a target and the
beginning of a saccade.
a. Normal: 192 ± 32 ms
2. Peak eye velocity of the saccades: Is the maximum velocity that eyes reach during a
saccadic movement.
a. Normal: 283-581°/s for 20°
i. It could be lower because of: Sedative drugs, drowsiness, cerebellar
disorders, basal ganglia disorders, and brainstem lesions
ii. It could be faster because of: Calibration errors and eye muscle restrictions.
iii. It could be asymmetric because of: Internuclear ophthalmoplegia, eye
muscle restrictions, ocular muscle palsies, and palsy of cranial nerves III and
VI
3. Accuracy of the saccades.
a. If the saccadic eye movement goes farther than the target position = Hypermetric
saccade (or overshoot dysmetria).
b. If the saccadic movement is shorter than the target position = hypometric saccade
(or undershoot dysmetria). (normal if it’s <10%).
2. SMOOTH PURSUIT TEST

Is the eye movement that is created when the eyes track moving objects. It involves: cortical and
subcortical areas of the brain and the fovea.
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How is it performed? The LED moves back and forth between 2 points on a light bar at a constant
frequency and velocity. The patient is asked to follow this moving target.
What are we evaluating?
1. Gain: Is the ratio of peak eye velocity to the target velocity
a. Normal >0.8
2. Phase: Is the difference in time between eye movement and target movement
a. Normal: 0.
3. Trace morphology.
a. Abnormal: staircase like eye movement
3. OPTOKINETIC NYSTAGMUS (OPK)

Is an involuntary oculomotor response to a moving target that fills >90% of the visual field. OKN aims
to stabilize the visual field onto the retina
Equipment:
360° turning cloth drum with black and white stripes or
An optokinetic projector.
How does it work?
Patients are asked to gaze straight ahead while the target is moved in front of their field of
vision during 1 min.
The normal response to an optokinetic stimulator is a smooth eye movement that follows the
direction of the visual stimulus both clockwise and counterclockwise.
Optokinetic afternystagmus (OKAN) is a form of nystagmus that is produced by the brainstem after
a 10-second, constant-velocity optokinetic stimulus
What are we measuring?
1. Gain. Normal: >0.5.
2. Phase. Applied only for the sinusoidal stimulus of OKN.
3. Initial velocity (OKAN) calculated from the OKAN at the 2nd second.
4. Time constant (OKAN) is the length of time required for the slow-phase velocity to decline to
37% of the initial velocity.
5. Slow-cumulative eye position (OKAN). is a function of both the initial velocity and the time
constant. most useful parameter.
4.- GAZE TEST

How is it performed? recording eye movements while patients fix their vision on the center of a
target
5.- FIXATION SUPPRESSION TESTING

Is ratio of the slow-phase velocity with fixation to the slow-phase velocity without fixation when doing
“Spontaneous nystagmus” test.
Normal: <50%
B.- Positional test

Purpose: To determine the effect of different stationary head positions (not head movements) on eye
movements.
Positions we’ll try on our patient (during 20 sec).
1. Head turned right and then left while sitting
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2. Head turned right and then left in the supine position,

3. Head turned right and then left in a decubitus position
4. Head hanging straight down.
Positional nystagmus caused by a peripheral lesion is suppressed by fixation
The direction-changing nystagmus may be indicative of a CNS lesion.
C.- Caloric test

Is about comparing magnitude of the induced horizontal nystagmus on the right and left sides.
DON’T DO IT on patients with tympanic membrane perforation.
How is it performed?
● Patients should be in the supine position, with their head tilted 30° upward
● We have to apply a stimulus and observe if there’s nystagmus. The stimulus could be
water or air.
● A cold stimulus (7° below normal temperature: 30°C): The cupula will move away from
the utricle, creating a nystagmus toward the opposite side.
● A warm stimulus (7° over normal temperature: 44°C): : Endolymph will rise, resulting in
a fast phase nystagmus toward the stimulus side.
COWS
Cold = Opposite side
Warm = Same side
● The water stimulators could be:
1. Open loop. Delivers water directly into the outer ear canal.
2. Closed loop. The water circulates in an expandable rubber medium to
preserve its temperature. Less reliable and reproducible results
● We apply 250 mL of water to the outer ear canal over 30-40 seconds.
○ Or 2 air stimuli (24°C and 50°C) with a flow rate of 8 L/min for 60 seconds
● Four caloric stimuli are given with an interval of 5 minutes (IN ORDER):
○ Right warm
○ Left warm
○ Right cold
○ Left cold
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● The nystagmus begins just before the end of the caloric stimulus and reaches a peak at 60
seconds of stimulation; it then slowly decays over the next minute. This is normal, because
I’m stimulating the horizontal SCC.
● When it reaches its peak, patients are asked to fixate their eyes on a central point to check
the fixation suppression index.
Testing parameters
The most reliable and consistent parameter is the peak slow-phase velocity of the induced
nystagmus.
Premature caloric reversal is a finding that can be observed in patients with Friedreich ataxia and
brainstem lesions
VESTIBULAR EVOKED MYOGENIC POTENTIALS (VEMP)-

An intact middle ear is required for the response quality of VEMP.
Two kinds of VEMP:
A.- cVEMP (CERVICAL) B.- oVEMP (OCULAR)
Recorded from the SCM muscle Recorded from the rectus inferior muscle.
Origin: Ipsilateral saccule Origin: Contralateral utricle
Provides diagnostic information about: Provides diagnostic information about:

Saccular nerve and inferior vestibular nerve Contralateral utricle and superior vestibular
nerve.
Where do we put the electrodes? Where do we put the electrodes?

1. A noninverting surface electrode is 1. Active electrodes are placed just inferior
placed at the middle third of the SCM to each eye
muscle. 2. Reference electrodes are placed 1 cm
2. An inverting electrode is located at the below.
sternoclavicular junction.
3. A ground electrode is placed on the
forehead.
HOW IS IT PERFORMED?
We place the electrodes, and with a probe in the ear we’ll give a loud sound and the muscle will
contract. This is positive. We measure this in both ears, and calculate the asymmetry ratio (AR) of the
waves produced in both ears. The waves will form a positive peak (P13) and a negative peak (N23). If
AR it’s:
● >36% (Augmented VEMP): Saccular hydrops
● Absent: Meniere disease, apical hydrops, vestibular neuronitis, otosclerosis
● Elevated or absent: Vestibular schwannoma
● Prolonged P13 latency: Retrolabyrinthine lesions (large vestibular schwannoma and
multiple sclerosis)
● Low VEMP: Superior canal dehiscence syndrome
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Sensorineural hearing loss occurs when:

● Sensorial hearing loss: The function of the cochlear hair cells is lost.
● Neural hearing loss: The cochlear nerve is affected
● Central hearing loss: Damage to the brain stem or auditory cortices.
EPIDEMIOLOGY---------------------------------------------------------------
● All ages.
○ Infants: 1-3/1000 are completely deaf
○ Children: 3 million
○ Adults: 10%
○ Elderly: 30-35% (Presbycusis)
ETIOLOGY------------------------------------------------------------------------
Sensorineural hearing loss means that there are Problems in the middle ear, inner ear or central
auditory pathways.
Hearing loss often results from a combination of insults rather than a single isolated etiology
ETIOLOGY EXAMPLE
Developmental and
hereditary
Syndromic Alport syndrome, Usher syndrome
Nonsyndromic Large vestibular aqueduct syndrome
Infectious Otitis media, CMV, syphilis, labyrinthitis
Pharmacologic toxicity Aminoglycosides, loop diuretics, antimalarials, salicylates
Trauma Head injury, noise-induced, barotraumas, irradiation
Neurologic disorders Multiple sclerosis
Vascular and Migraine, cryoglobulinemia, sickle cell, blood dyscrasia

hematologic disorders
Immune disorders Polyarteritis nodosa, HIV
PATHOGENESIS----------------------------------------------------------------
Hearing is produced by air conduction and bone conduction.
Bone conduction
1. The sound source, in contact with the head, vibrates the bones of the skull
2. This vibration produces a traveling wave in the basilar membrane of the cochlea
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Air conduction
1. When a sound is presented, the movement of the tympanic membrane in turn moves the
ossicles (malleus, incus, stapes)…
2. ...which give an impedance matching mechanism...
3. ….which pushes the oval window.
4. The oval window moves the fluid in the inner ear…
5. ...stimulating the hair cells...
6. ...which will stimulate the Corti organ...
7. ...to give a signal to the auditory cortex, so we can hear.
The cochlea contains (at birth):

● 3500 inner hair cells
○ For transduction of fluid movement to electricity
● 12000 outer hair cells
○ For sound stimulation
INTENSITY OF SOUND:
● Amount of neural activity in individual neurons
● Number of neurons that are active
● Specific neurons that are activated
TYPES OF SENSORINEURAL HEARING LOSS-------------------

A.- Congenital hearing loss
● More than half of childhood hearing impairment will be hereditary
● It will be classified as
A. Nonsyndromic hearing loss
B. Syndromic hearing loss
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NONSYNDROMIC HEARING LOSS (66%) SYNDROMIC HEARING LOSS (33%)

Hearing loss is the only clinical abnormality Hearing loss is associated with anomalies in
other organ systems
70-80% autosomal-recessive: Onset in Usher syndrome: (most common) Retinitis

adolescence or adulthood and varies in severity pigmentosa + hearing loss
15-20% autosomal-dominant: Congenital and
profound Waardenburg syndrome: Pigmentary
abnormality + hearing loss
<5% X-linked
Pendred syndrome: Thyroid organification
defect + hearing loss
Alport syndrome: Renal disease + hearing loss

GJB2 encoding for connexin 26: most common
non syndromic cause of deafness Jervell and Lange-Nielsen syndrome:
Prolonged QT interval + hearing loss
B.- Infectious
Viral infections are a common cause of sudden hearing loss
● Otitis media ● TORCH Infections (congenital hearing
● Maternal rubella infection loss)
● Bacterial meningitis ○ Toxoplasmosis
● Intrauterine teratogenic exposure ○ Other [syphilis, varicella-zoster]
● Labyrinthitis (viral: herpes and ○ Rubella
varicella-zoster) ○ Cytomegalovirus
● HIV ○ Herpes
C.- Pharmacologic ototoxicity

● Aminoglycosides ● Antimalarial drugs: Quinine
● Cisplatinum and carboplatinum ● Salicylates
● Loop diuretics ● Vancomycin
● Macrolides: Erythromycin ● Opiates.
D.- Presbycusis
● Hearing loss associated with age >65.
● Most common cause of hearing loss in adults.
● High frequency (>2000 Hz) hearing loss first.
● Is characterized by a loss of discrimination for phonemes, recruitment (abnormal growth
of loudness), and particular difficulty in understanding speech in noisy environments.
● The basal turn of the cochlea is generally affected first
● Exposure to loud sounds can contribute to presbycusis (>80 dB).
● Genetic presbycusis: GRM7 gene.
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E.- Noise-induced hearing loss

>33% of all cases of hearing loss are related to noise exposure.
When exposed to noise, cochlear hair cells and supporting cells become damaged, resulting in
the degeneration of auditory nerve fibers. The effects of noise exposure may be:
a. Temporary: Recovers in 24 to 48 hours.
b. Permanent
The causes are:
Workers at highest risk for noise-induced hearing loss:
● Mining ● General manufacturing
● Wood product manufacturing ● Agriculture
● Construction ● Utilities
● Real estate/rental leasing occupations ● Transportation
● Military ● Musicians
Recreational noise exposures:

● Headphones
F.- Trauma
● Fractures
○ Transverse fractures through the otic capsule
○ Profound and irreversible hearing loss
○ Vestibular symptoms
● Labyrinthine concussion
○ Caused by traumatic forces (particularly blast or acceleration/deceleration)
○ Injury to the cochlear membranes or hair cell epithelium
G.- Neoplasms
Due mainly to cerebellopontine angle tumors:
● Vestibular schwannoma (acoustic ● Hemangiomas
neuroma) (most common, 80%) ● Vascular tumors
● Meningiomas ● Petrous apex lesions
● Paragangliomas ● Brainstem tumors
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Sensorineural hearing loss that results from neoplasms is most commonly asymmetric and slowly
progressive. Therefore, any patient with asymmetric sensorineural hearing loss must undergo
an appropriate workup to rule out neoplasm.
Neural hearing loss may also be due to demyelinating (multiple sclerosis), vascular, infectious,
degenerative or trauma etiologies.
H.- Idiopathic sudden sensorineural hearing loss

● Is a decrease in hearing of ≥ 30 decibels affecting at least 3 contiguous frequencies
● Most cases are attributed to viral etiology. Others:
○ Vascular
○ Autoimmune
● Requires evaluation for retrocochlear pathology MRI
● Treatment: Corticosteroids (oral or intratympanic injection)
I.- Meniere disease

● Fluctuating episodes of hearing loss, vertigo (hours), tinnitus, and aural fullness.
● Pathophysiology: Increase in fluid pressure within the endolymphatic compartment that
results in periodic tears in the delicate cochlear membranes.
● Treatment:
○ Low-salt diet
○ Diuretic therapy.
○ Steroid therapy for acute exacerbations
○ Others:
■ Meniett device
■ Endolymphatic sac decompression
■ Vestibular ablation with intratympanic gentamicin injection
■ Vestibular nerve section
■ Labyrinthectomy surgery.
J.- Hidden hearing loss

Subjective hearing loss in the setting of a normal audiogram
● Pathophysiology: Central auditory processing disorder that results in difficulty with speech
clarity in the presence of background noise.
○ Loss of cochlear nerve synapses
○ Irreversible hair cell loss
K.- Mixed hearing loss

Conductive + Sensorineural hearing loss
● Otosclerosis (involves the ossicles and cochlea) (most common)
● Head trauma
● Chronic otitis media (damage to the nerve also).
● Cholesteatoma.
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DIAGNOSIS----------------------------------------------------------------------
Evaluation goals:
● Conductive or sensorineural?
● Mild, moderate, severe or profound?
● Anatomy of the impairment? Where's the damage?
● Etiology?
A.-History
1. ONSET AND DURATION OF THE DEAFNESS.
a. Sudden:
■ Unilateral without tinnitus may represent an inner ear viral infection or
vascular accident
b. Gradual:
■ Otosclerosis
■ Noise-Induced hearing loss
■ Meniere disease: Episodic vertigo, tinnitus, and aural fullness
■ Vestibular schwannomas: Asymmetric, tinnitus and imbalance (rarely vertigo)
2. UNILATERAL OR BILATERAL
3. ASSOCIATED SYMPTOMS: Tinnitus, vertigo, imbalance, aural fullness, hyperacusis,
otorrhea, headache, facial nerve dysfunction, head or neck paresthesia.
4. HISTORY OF: Head trauma, ototoxic exposure, noise exposure, otologic surgery
5. FAMILY HISTORY: HHI, sensitivity to aminoglycosides, presbycusis.
B.- Physical examination

1. EXAMINATION OF THE EAR
● Evaluate the auricle, external ear canal, and
tympanic membrane.
● Evaluate the Pars tensa (the lower two-thirds of
the eardrum) and pars flaccida (superior to the
short process of the malleus)
Retraction pockets that may be evidence of chronic eustachian
tube dysfunction or cholesteatoma (See image).
● Insufflate the ear canal to assess tympanic
membrane mobility and compliance.
● Binocular microscopy is often helpful for a
precise examination.
2. EXAMINATION OF OTHER STRUCTURES

● Evaluate: Nose, nasopharynx, and upper respiratory tract
● Cranial nerves: V and VII.
○ These nerves are associated with tumors involving a cerebellopontine angle.
● Vestibular testing if necessary.
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3. EVALUATION WITH A TUNING FORK

It can be a useful clinical screening tool to differentiate between conductive and sensorineural
hearing loss. We need a 256-Hz or 512-Hz fork
RINNE TUNING FORK TEST WEBER TUNING FORK TEST
Hearing loss Conduction Localization
Compares the ability to hear by air A 5-dB difference in hearing

conduction with the ability to hear between the 2 ears is required for
by bone conduction. lateralization
How does it work? The patient is asked to indicate The patient is asked whether the
whether the tone is louder by air tone is heard in both ears or in 1 ear
conduction or bone conduction better than in the other.
RESULTS
None Air > bone Midline
Sensorineural Air > bone Normal ear
Conductive (>30 dB) Bone > Air Affected ear
EXAMPLES:
Hearing loss Rinne Weber
Left sensorineural Positive bilaterally Lateralized to the right
Right conductive Negative on the right Lateralized to the right
Bilateral Positive bilaterally No lateralization

sensorineural
Symmetric Negative bilaterally No lateralization

conductive
C.- Audiologic assessment

This helps to determine if the hearing loss is sensory (cochlear) or neural (retrocochlear).
● Pure-tone AC and BC thresholds ● Tympanometry
● Speech reception threshold ● Acoustic reflex
● Discrimination score ● Acoustic reflex decay
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D.- Imaging studies

AXIAL AND CORONAL CT SCAN OF THE TEMPORAL BONE
Mainly for patients with conductive hearing loss
For determining:
● The caliber of the external auditory canal
● The integrity of the ossicular chain
Useful to identify:
● Middle ear or mastoid disease
● Inner ear malformations
● Cochlear height
● Lateral semicircular canal bony island width
● Vestibular aqueducts.
● Bone erosion (chronic otitis media and cholesteatoma)
● Superior semicircular canal dehiscence (with Poschl and Stenver reconstructions)
MRI OF THE HEAD WITH GADOLINIUM

Mainly for patients with sensorineural hearing loss
For imaging retrocochlear pathology (vestibular schwannomas, meningiomas, demyelinating
lesions of the CNS, brain tumors, and other lesions of the cerebellopontine angle)
TREATMENT-------------------------------------------------------------------
A.- Reversibility
CAN HEARING LOSS BE REVERSIBLE? Not in most cases. But some of them can be reversible using
steroid therapy.
WHAT KINDS OF HEARING LOSS CAN BE REVERSIBLE?
● Idiopathic sudden sensorineural hearing loss
● Acute hearing drops in Meniere disease
● Some instances of acoustic trauma
B.- Creating a Favorable Environment for Hearing

● Eliminate or reduce unnecessary noise (eg, radio or television)
● Optimizing a listener’s location within a room to minimize background noise from all fronts
(eg corner table at a restaurant)
● Lip reading: Sit in front of the patient when you’re talking so he can read your lips. Also, you
must speak slowly.
C.- Amplification
● Rehabilitation with hearing aids: Mild, moderate, and severe sensorineural hearing loss (eg,
“Lyrichearing aid”)
● Hearing aids for unilateral deafness: Bone anchored hearing aid (BAHA) or Contralateral
routing of signal (CROS) hearing aid
● Assistive devices include infrared and FM transmission: For situations like lectures and the
theater
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● Implantable hearing aids:

○ For moderate to severe hearing loss with preserved speech discrimination.
○ Make use of piezoelectric or electromagnetic technology
○ May be partially implantable or fully implantable
■ Partially implantable: A magnet or driver is surgically implanted onto the
ossicles and require an external processor
■ Fully implantable: All components are implanted. Settings can be controlled
by remote control
D.- Cochlear implants

● For in case that a hearing aid provides inadequate rehabilitation
● In profound hearing impairment, the auditory hair cells are lost, but the spiral ganglion cells
of the VIII nerve are preserved.
● How does it work? Is an electrode that converts mechanical sound energy into electrical
signals that are delivered to the neurons of the cochlear nerve.
○ A microphone is used to pick up acoustic information that is sent to an external
speech processor (on the body or at ear level).
○ This processor converts the mechanical acoustic wave into an electric signal
○ The signal is transmitted via the surgically implanted electrode array in the cochlea to
the auditory nerve.
○ Within 3 months of implantation, patients can understand speech without visual cues.
● Which patients may need it?
○ Severe to profound hearing loss
○ Score <60% hearing in noise test
○ >1 year old children with congenital and acquired profound hearing impairment who
have failed a hearing-aid trial
● It’s too expensive and we don’t have it Mexico
E.- Brainstem Auditory Implant

● Which patients may need it?
○ Both VIII nerves destroyed:
■ Trauma
■ Bilateral vestibular schwannomas
■ Neurofibromatosis II
○ Severely malformed ears
○ Congenital absence of the VIII nerve
● Placed near the cochlear nucleus
● Similar to the cochlear implant (but the signal travels to the brainstem now)
G.- Molecular therapy

● Human hair cells lose their regenerative capacity after development
● To avoid this we could use gene therapy and stem cell technology (Atoh1 gene).
● Still under investigation. Not available yet.
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H. Therapy for tinnitus

● Can’t be cured, but do can be minimized. How?:
● Masking it with background sounds
● Hearing aids: Tinnitus maskers
● Antidepressants
PREVENTION--------------------------------------------------------------------
VACCINATION
● Haemophilus influenzae type B meningitis
● Measles
● Mumps
● Rubella.
NOISE AVOIDANCE
● Regular use of earplugs or fluid-filled muffs
● Education: Hearing conservation, over an 8 hour period averages 85 dB.
● Workers: Pre Employment and annual audiologic assessment. And mandatory use of hearing
protectors.
PROGNOSIS----------------------------------------------------------------------
TEMPORARY HEARING LOSS
● It recovers within 24-48 h
● If the noise is of high enough intensity or is repeated often enough, permanent hearing loss
results
IRREVERSIBLE HEARING LOSS
● Sensorineural hearing loss generally is irreversible
● Presbycusis: Progressive (1–2 dB/year) and irreversible
● Acoustic trauma: Permanent (not temporary) hearing loss
Given the poor prognosis the primary goals in management are the prevention of further losses
and functional improvement with amplification and auditory rehabilitation.
35
ANATOMY AND PHYSIOLOGY---------------------------------------------

The pinna
● Funnel-shaped cartilaginous structures
● FUNCTION: To focus and localize sound.
External auditory canal (EAC)

● During early childhood, the canal is straight, but takes on
an S shape by the age of 9 years.
● 24 mm length
● Vol. 1-2 ml. If it’s bigger, there could be a perforation
● Lateral ⅓ = Fibrocartilage
● Medial ⅔ = bone
● Narrowest point: Fibrocartilaginous junction
● The temporomandibular joint (TMJ) is anterior to the EAC. So in a disease in this joint, there
will be otalgia, but it doesn’t mean that the problem is in the ear.
Skin
● Stratified squamous epithelium
● Subcutaneous layer 1 mm
○ Hair follicles
○ Sebaceous and ceruminous glands. Surrounded
by myoepithelial cells and are organized into
apopilosebaceous units
● Skin of the osseous canal 0.2 mm. Directly adherent to
periosteum
● Cerumen
○ Hydrophobic
○ Acid pH
○ Antibacterial function. Prevents canal maceration
36
Innervation
● Great auricular nerve (cervical
plexus): (pink). The pinna laterally,
inferiorly, and posteriorly
● Arnold’s nerve (a branch of the vagus
nerve): (purple). The inferior bony
canal, the posterosuperior
cartilaginous canal, and corresponding
segments of the tympanic membrane
and the cymba concha.
● Branches of the facial VII nerve: The
posterosuperior bony EAC
● Auriculotemporal branch of V3 of the
trigeminal V nerve: (green) The pinna
anteriorly.
● Glossopharyngeal nerve: Internal
surface of tympanic membrane
Lymphatic drainage
● Preauricular lymph nodes: The anterior and superior wall of the EAC and tragus
● Infra-auricular lymph nodes: The helix and the inferior wall of the EAC
● Mastoid lymph nodes: The concha and antihelix
Vascular supply
● Posterior auricular artery and superficial temporal artery (both from the external carotid
artery): The auricle and lateral EAC.
● Deep auricular branch of the maxillary artery: Medial EAC and the external surface of the
tympanic membrane.
● Posterior auricular and superficial temporal veins: The external ear.
Physiologic functions of the external ear

● Serves as a functional resonator for the speech frequencies: Aids in the efficient
transmission of sound to the tympanic membrane
● Protection for the tympanic membrane and middle ear by the hairs in the lateral canal, the
depth and tortuosity of the EAC, and the self-cleaning nature of the EAC.
Embryology
Development is completed by the 28th week.
● External ear: 1st & 2nd branchial arches. Includes ectodermal and mesodermal components
● Pinna: Differentiation of the 6 auricular hillocks (6th week), derived from the 1st and 2nd
branchial arches
● EAC: From a solid epithelial plate of ectodermal cells, and the meatal plug
● Tympanic membrane: Meatal plug
37
CONGENITAL ANOMALIES-----------------------------------------------
● The causes of these disorders may be genetic or environmental in etiology
● Associated syndromes in 20-60% of the patients:
○ Oculoauriculovertebral (OAV) spectrum (Goldenhar/hemifacial debridement)
○ Branchio-oto-renal Sx.
○ Treacher Collins Sx.
○ Townes-Brocks Sx.
○ Robinow Sx.
A.- Microtia
GRADE I GRADE II GRADE III GRADE IV
Mild deformity Atypical microtia Classic microtia or Anotia

Dysmorphic helix and Some of the auricular “peanut ear”
antihelix. framework is present, Few or no
Low-set ears Tissue deficiency recognizable
Lop ears Significant deformity landmarks of the
Cupped ears Mini-ear, conchal auricle.
Mildly constricted bowl, and cup ear Ear lobule anteriorly
ears. All major deformities. positioned.
structures of the
external ear are
present to some
degree.
TREATMENT
● Observation
● equire daily maintenance and may compromise the vascularity
Bone-anchored prosthesis R
● Single-stage reconstruction with implant
● Staged autologous costochondral reconstruction. We wait until the patient is 6 years
old, and we take rib cartilage from him to reconstruct the ear.
○ BRENT TECHNIQUE (4 stages)
■ Stage I: Cartilage Implantation from the synchondrosis of ribs 6, 7, and
free-floating rib 8
■ Stage II: Lobule Transfer 2-3 months after stage I
■ Stage III: Postauricular Skin Grafting 3 months after stage II, a postauricular
sulcus is created from the groin, lower abdomen, buttocks, contralateral
postauricular sulcus, or back.
38
■Stage IV: Tragal Reconstruction and Soft-Tissue Debulking reconstructs the

tragus with grafts from the contralateral auricle and deepens the concha
○ NAGATA TECHNIQUE (2 stages)
■ Stage I: cartilage implantation and lobule transposition. From the 6th-9th
costal cartilages
■ Stage II: elevation of the ear and creation of the postauricular sulcus. 6
months after stage I. Uses skin grafts and a temporoparietal fascial flap.
Complications of Auricular Reconstruction
● Infection
● Hematoma formation
● Skin-flap necrosis
● Scar contracture
● Poor contouring.
B.- Atresia and stenosis

DIAGNOSIS
● 90% have microtia (grade III)
● Audiologic testing
○ Audiogram: Hearing loss (50-70 dB)
○ ABR: Because is a children and we
can’t put a probe inside for screening.
● Axial and coronal CT scan
○ To assess for ossicular, facial nerve,
and otic capsule abnormalities
○ To assess for the degree of temporal
bone pneumatization
○ To identify a cholesteatoma (accumulation of keratin inside the ear)
TREATMENT
● Surgery: canalplasty. The disadvantage is scar stenosis, so it requires multiple re-interventions.
● Bone-anchored hearing aids.
C.- Protruding ears (Prominauris)

Is most frequently bilateral and affects nearly 5% of the population.
PATHOGENESIS
● An increase in the distance from the helical rim to the mastoid due to a
lack of the antihelical fold and prominence of the conchal bowl.
● Aurículocephalic angle: 20-25º
● Auricolomastoid distance 15-20 mm
TREATMENT
● Otoplasty. GOLD STANDARD Do it on patients >8 years old.
● Ear splinting and molding
● Mustardé technique: To recreate the antihelical fold utilizing 2 to 4
horizontal mattress sutures through the cartilage and anterior
perichondrium.
● Converse cartilage-cutting technique: For stiffer cartilage.
39
● Combination of suturing and cartilage-cutting techniques: For conchal excess

● Cartilage-sparing technique: Developed by Furnas
COMPLICATIONS OF TREATMENT
● Hematoma (3%) most common
● “Telephone ear” deformity: Because of excessive overcorrection of the middle third of the
ear
D.- First branchial cleft anomalies

Branchial cleft anomalies (BCA) may represent >33% of congenital neck masses
1st BCA represent 10% of all BCA
PATHOGENESIS
● Anomalous fusion of the 1st and 2nd branchial arches, with incomplete obliteration of the
1st branchial cleft
● Entrapment of elements of the cervical sinus of His or epithelial rests associated with
Waldeyer’s ring. All are associated with an epithelial-lined cyst.
CLINICAL FINDINGS
● Infection, pain, swelling in the preauricular and cervical regions along the anterior border of
the sternocleidomastoid
● Drainage from the ear
● A membranous band between the medial aspect of the floor of the ear canal and the
tympanic membrane at the manubrium of the malleus
WORK CLASSIFICATION
TYPE 1 TYPE 2 more common
Duplicates the membranous EAC only Duplicates both the membranous and
cartilaginous EAC
Preauricular mass or sinus that parallels the EAC Mass or draining tract along the anterior border
of the sternocleidomastoid muscle.
Terminates in the EAC or middle ear. Terminates in the concha or at the

bony-cartilaginous junction of the EAC
Lateral to the facial nerve Variable relationship to the facial nerve.
40
TREATMENT
● Complete excision. We dye the lesion with Methylene blue
⚠The tract may be intimately involved with the facial nerve, which is at risk during
excision. You can do a parotidectomy to identificate the nerve before the excision.
Incomplete excision, or incision and drainage alone, predisposes the patient to recurrence and
re-infection
TRAUMA---------------------------------------------------------------------------
A.- Auricular hematoma
Accumulation of blood in the subperichondrial space, usually secondary to blunt trauma.
PATHOGENESIS
1. Cartilage lacks blood supply: It relies on the vascularity of the perichondrium via diffusion.
2. Blunt trauma creates a barrier for diffusion between the cartilage and the perichondrial
vascular supply. This leads to...
3. Necrosis predisposes to infection. This results in…
4. A permanent disfigurement known as cauliflower ear.
CLINICAL FINDINGS
● Edematous, fluctuant, and ecchymotic pinna
● Loss of the normal cartilaginous landmarks
TREATMENT
● Drainage. Incision parallel with the natural auricular skin folds. The pocket is then irrigated
with sterile saline.
● Splints after drainage. To prevent reaccumulation of hematomas.
○ Cotton bolsters, plaster molds, silicon putty, water-resistant thermoplastic splints and
whiptype absorbable mattress sutures
● Quinolone antibiotics. Are cartilage-penetrating
B.- Auricular laceration or avulsion

Caused by penetrating or severe blunt trauma
TREATMENT
Expeditious repair and Prevention of infection are important.
● Clean and debride the lesion first
● Simple lacerations can be closed primarily. But more severe
cases may require…
○ Undermining
○ Flap reconstruction
○ Tissue grafts
● Direct reattachment when diameter <15 mm. If diameter is greater:
○ Microvascular replantation best option
○ Skin puncture or leech therapy. For venous congestion
○ Baudet technique: Removes the skin from the posterior aspect of the amputated
auricle, creating windows into the cartilage to allow vascular access to the wound
bed, and replanting the ear into the bed.
41
● Pressure dressings to prevent edema and hematoma formation

● Quinolone antibiotics
● Second reconstruction if resultant defects are not satisfactory
PROGNOSIS
● Excellent cosmetic results can be achieved with surgery
● If the ear is still attached to the helical root or with a 6-mm skin pedicle, it can often be
successfully reattached due to its excellent vascular supply.
C.- Auricular frostbite

Rare injury resulting from cold exposure (<10°C), that leads to vasoconstriction, cold-mediated
dehydration, endothelial injury, thrombosis, and ischemia of auricular tissue.
CLINICAL FINDINGS
● Initially pale and then cyanotic ear
● Pain, erythema, and subcutaneous bullae
TREATMENT
● Rewarming of the ear to 40-42°C.
● Debridement of nonhemorrhagic blisters
● Pain medicine and antibiotics
○ Aloe vera (anti thromboxane properties) + ibuprofen for re-establishing circulation
● Hyperbaric oxygen and vasodilators
PROGNOSIS
● In the early stage, it may be reversible, but over time, it leads to tissue n
ecrosis.
● A late complication is auricular ossification.
D.- Auricular burns

Extension Clinical findings Treatment
1st degree Superficial layer Erythema, moderate pain, Moisturizing creams or s ilver
(Superficial) of epidermis do not scar sulfadiazine
Silver-based dressings,
2nd degree Epidermis and Blisters that blanch on silicon-coated nylon, and
(Partial extension to direct pressure and are very biosynthetic dressings*
thickness) dermis painful.
May heal without scarring Debridement of blisters
Antibiotic ointment
3rd degree Full thickness of Less pain Topical and systemic

(Full dermis cartilage-penetrating antibiotics
thickness) Gray/black eschars. Heals Mafenide acetate: Penetrates
with scarring. May be eschar and reduces chondritis
4th degree Subcutaneous complicated by Early debridement and closure
(Subdermal) tissue, fat, muscle, suppurative chondritis with skin grafts or vascularized
tendon, cartilage, tissue: If there’s exposed
bone Painless. cartilage
Secondary reconstruction: 1
year after injury
42
*May work better than silver sulfadiazine
INFECTIOUS AND INFLAMMATORY DISEASES-------------------

A.- Otitis externa
ETIOLOGY
● Pseudomona aeruginosa and S. aureus
● Less commonly: Proteus species, S. epidermidis, diphtheroids, and E. coli.
● Fungal: 10%
PATHOGENESIS
● Predisposing Factors: Heat, humidity, maceration, absence of cerumen, alkaline pH
○ It causes edema of the stratum corneum and occlusion of the apopilosebaceous
units.
● Inflammatory stage: bacterial overgrowth, progressive edema and intensified pain.
● Chronic inflammatory stage: Incomplete resolution or persistent inflammation>3 months
CLINICAL FINDINGS
● Otalgia ● Hearing loss ● Occlusion
● Otorrhea ● Pain (tragus ● Lymphadenopathy (periauricular
● Aural fullness sign) anterior cervical lymph nodes)
● Tenderness to ● Erythema ● Cellulitis
palpation ● Edema ● Thickened skin (chronic)
● Pruritus ● Crusting ● Scant, clear discharge (chronic)
TREATMENT
● Debridement of EAC with binocular microscopy.
● Analgesia (NSAIDs, opioids, topical steroids (to reduce edema and otalgia))
● Culture: For refractory cases only
● Antiseptic, acidifying, or antibiotic Otic drops best option
○ Antiseptic: Acetic and boric acid, ichthammol, phenol, aluminum acetate, gentian
violet, thymol, thimerosal (Merthiolate), Cresylate, alcohol
○ Antibiotic: Ofloxacin, ciprofloxacin, colistin, polymyxin B, neomycin, tobramycin,
chloramphenicol, gentamicin.
Polymyxin B and neomycin are often used for S aureus and P aeruginosa infections.
Ofloxacin and ciprofloxacinhave an excellent spectrum of coverage and are the less ototoxic
drugs
● Systemic antibiotics: For infections that spread beyond the EAC.
● Canalplasty: Chronic otitis externa.
● Avoid water exposure and EAC manipulation
B.- Otomycosis
Represent 10% of the diagnosis of otitis externa
ETIOLOGY
● Aspergillus (80%)
● Candida
● Phycomycetes, Rhizopus, Actinomyces, and Penicillium
43
PREDISPOSING FACTORS
● DM, immunocompromised state, mastoid bowl after a canal wall-down procedure
CLINICAL FINDINGS
● Pruritus ● Pain
● Itchy ears ● Otalgia
● Aural fullness ● Hearing loss
● Otorrhea ● Otoscopy: Mycelia and white, gray or black fungal debris
DIAGNOSIS
● Positive potassium hydroxide (KOH) preparation
● Fungal culture.
TREATMENT
● Debridement of EAC
● Acidifying EAC (vinegar)
● Antifungal agents
○ Nonspecific: Gentian violet, thimerosal (Merthiolate)
○ Specific: Clotrimazole, nystatin (otic drops or powder), ketoconazole
○ CSF powder (chloramphenicol, sulfamethoxazole or sulfanilamide, and
fungizone/amphotericin B)
○ Topical ketoconazole, cresylate otic drops, and aluminum acetate otic drops
● Avoid water exposure
C.- Skull base osteomyelitis

Is a bacterial infection of the EAC and skull base. Also known as
Malignant otitis externa (MOE) or Necrotizing otitis externa (NOE).
It begins as an external otitis that progresses to involve the temporal
bone.
ETIOLOGY
● Pseudomona aeruginosa (90%)
● Others: S aureus, S epidermidis, Proteus, and Klebsiella
● Aspergillus in HIV patients
RISK FACTORS
● Elderly, DM, Immunocompromised
PATHOGENESIS
● Begins in the soft tissues of the EAC and progresses to
cellulitis, chondritis, osteitis, and, ultimately, osteomyelitis
Difference with otitis media: Otitis media spreads through the pneumatized portion of the
temporal bone. NOE disseminates through Haversian canals, fissures of Santorini, foramina, and
vascularized spaces of the skull base.
● Cranial neuropathies:
○ Facial nerve (stylomastoid foramen) most frequently
○ Hypoglossal nerve (hypoglossal canal)
○ Abducens and trigeminal nerves (petrous apex)
○ Glossopharyngeal, vagus, and spinal accessory nerves (jugular foramen)
44
CLINICAL FINDINGS
● Long standing otalgia (worse at ● Facial palsy
night) ● Edema
● Otorrhea ● Periauricular lymphadenopathy
● Aural fullness ● Trismus
● Pruritus ● Otoscopy: Granulation tissue at the
● Hearing loss osseocartilaginous junction (pathognomonic)
DIAGNOSIS
● Elevated inflammatory markers:
○ ESR (erythrocyte sedimentation rate)
○ CRP (C-reactive protein)
● Culture
● CT (bony sequestra)
● MRI (soft tissue changes, intracranial abnormalities)
● Technetium-based bone scans (TC-99 SCAN)
● Gallium Scan (to track the resolution: Leukocytes and areas of inflammatory cell activity)
DIFFERENTIAL DIAGNOSIS
● Carcinoma ● Fibrous dysplasia
● Chronic granulomatous disease ● Nasopharyngeal carcinoma
● Paget disease
TREATMENT
● Long-term parenteral antibiotics (6 weeks) 1st line treatment
○ Aminoglycosides (tobramycin)
○ Antipseudomonal (B-lactam: piperacillin-tazobactam (PIP, TZN), cefepime, or
ceftazidime
○ Fluoroquinolones (Ciprofloxacin, ofloxacin). For early presentations
● Control of hyperglycemia and immunosuppression
● Surgical debridement try to preserve hearing and facial nerve function introducing
vascularized tissue into the surgical defect
● Hyperbaric oxygen for cases refractory to antibiotics.
PROGNOSIS
● If unrecognized or untreated: Sigmoid sinus thrombosis, meningitis, sepsis, and death
DERMATOLOGIC DISEASES--------------------------------------------
A.- Atopic dermatitis
Is a chronic relapsing and remitting dermatitis of immune-mediated
origin.
RISK FACTORS
● Family atopy history
PATHOPHYSIOLOGY
Th2 T-lymphocytes, which produce inflammatory mediators.
1. Skin barrier breakdown and allergic inflammation. This leads to…
2. Intense pruritus, inflammation, and scratching. This leads to…
45
3. More skin barrier breakdown.

CLINICAL FINDINGS
● Pruritic erythematous patches or weeping plaques
● Lesions persist >1 month
● Secondary infections with S aureus, herpes simplex virus, vaccinia, and m. contagiosum
TREATMENT
● Emollients after Soaking baths 1st line nonprescription therapy
● Topical corticosteroids 1st line prescription therapy
● In advantage stages
○ Calcineurin inhibitors (tacrolimus, sirolimus)
○ UV-B phototherapy
○ Systemic immunomodulators
● Antihistamines
● Antibiotics for secondary infections
B.- Psoriasis
Chronic inflammatory disorder that affects 2% of the population (USA)
● 18% affects the external ear (on the concha and meatus of the EAC)
PATHOGENESIS
● Genetic component
● Triggered by: NSAIDs, beta blockers lithium carbonate, antimalarial, infection, trauma, stress
● Th1 and Th17 cells drive a cytokine-mediated immune response
CLINICAL FINDINGS
● Erythematous papules
● Salmon-pink plaques with silvery white scales on
elbows, knees, scalp, and buttocks
● Auspitz sign: Lesions bleed in pinpoint areas when
scratched
● “Oil spots” of the nails, and subungual hyperkeratosis
● Koebner phenomenon: Lesions over areas of trauma
● Psoriatic arthritis (5-10%)
TREATMENT
● Avoid excessive drying of the skin
● Topical non fluorinated corticosteroids (low dose)
○ Alclometasone, mometasone, desonide, clocortolone, hydrocortisone valerate,
butyrate creams, and calcipotriene
● Warm water soaks
● 1-5% Coal tar
● Urea-based therapy
● Anthralin C
● Oral psoralens + UVA phototherapy
● Others: Methotrexate, retinoids, calcineurin inhibitors, a PDE4 inhibitor, biologic agents
targeting TNFα, IL-12/23, and IL-17
46
C.- Contact Dermatitis

Caused by contact with an allergen or irritant (nickel jewelry, earplugs, hearing aids and cosmetic
products)
PATHOGENESIS
● Type IV hypersensitivity.
CLINICAL FINDINGS
● Allergic contact dermatitis: Indurated, erythematous,
pruritic, and poorly demarcated process.
● Irritant dermatitis: Well-defined areas of exposure.
TREATMENT
● Skin testing to identify contact allergens
● Avoidance of irritants and allergens
● High dose topical glucocorticoids
D.- Relapsing polychondritis

Is a severe, waxing and waning, progressive inflammatory disease involving cartilaginous
structures in the ears, nose, and laryngo tracheobronchial tree. May also affect the heart, large
arteries, skin, and eyes.
OBSTRUCTIVE DISORDERS---------------------------------------------
A.- Foreign bodies
They could be beads, pills, batteries, and insects.
CLINICAL FINDINGS
● Pain ● Infection
● Pruritus ● Granulation tissue
● Hearing loss ● Liquefactive or pressure necrosis and
● Bleeding low-voltage injury (batteries)
TREATMENT
Atraumatic manner removal.
● Operating microscope
● Proper instrumentation (eg, right-angle pick, curet, forceps, and suction)
● General Anesthesia (2% lidocaine) (also useful to euthanize the insect)
B.- Keratosis obturans and EAC Cholesteatoma

KERATOSIS OBTURANS EAC CHOLESTEATOMA
DEFINITION Accumulation of desquamated Invasion of surrounding bone by

debris in the EAC. squamous epithelium.
PATHOPHYSIOLOGY Secondary to a defect in epithelial migration
47
PATIENTS’ AGE More common in young patients More common in elderly patients
CLINICAL FINDINGS Acute pain Dull pain
Hearing loss May not have hearing loss
May not have otorrhea Otorrhea
Otitis externa
Chronic bronchitis and sinusitis
IMAGING STUDIES Circumferential bony widening. Localized bony erosion
PATHOLOGY Layered epithelium within the Random layering of squamous

STUDIES obstructing lesion tissue.
TREATMENT Removing the epithelial plug Suctioning, debridement, and

Lifelong surveillance and cleaning of topical antibiotics
the EAC Local removal of necrotic bone
Canalplasty Tympanomastoidectomy or canal
wall-down mastoidectomy
NEOPLASMS--------------------------------------------------------------------
A.- Basal cell carcinoma
Most common malignant neoplasm (45%)
5 clinical subtypes nodular-ulcerative, cystic, superficial multicentric,
micronodular, and morpheaform.
PATHOGENESIS
● Risk factors: Sun exposure UVB
○ Fair skin, outdoor occupations, history of skin
carcinoma.
● Arises de novo: p53 mutation and Hedgehog signaling
pathway
CLINICAL FINDINGS
● Nodular ulcerated lesion
● Bleeding
● In the helix or the preauricular area
NONSURGICAL TREATMENT
● Photodynamic therapy with aminolevulinic acid
● Topical 5-fluorouracil
● Imiquimod
● Radiation therapy. May increase the risk of subsequent cutaneous malignancy development
3-fold.
● Targeted therapies (vismodegib) Targets the Hedgehog pathway, for advanced or metastatic
BCC.
48
SURGICAL TREATMENT
● Curettage Electrodesiccation More effective in smaller lesions
● Cryosurgery with liquid nitrogen
● Wide local excision <2 cm lesions
● MOHS micrographic surgery GOLD STANDARD
● Good prognosis
B.- Squamous cell carcinoma

● 20% of all cutaneous malignant neoplasms
● More common in elderly males
● Greater risk of metastasis than BCC
PATHOGENESIS
● Risk factors: UV radiation, immunosuppression,
advanced age, a nonhealing ulcer, and exposure to
chemicals (arsenic, soot, coal, tar, paraffin, and
petroleum oil)
● Precursor lesions (actinic keratoses, Bowen disease)
● Mutations: p53, Wnt, Ras, and p16.
CLINICAL FINDINGS
● Plaques, nodules and ulcerations
● Bleeding
● In the helix or preauricular region
TREATMENT
● 5-fluorouracil
● Photodynamic therapy (for actinic keratoses only, not for SCC)
● Laser ablation and chemical peels
● Radiation therapy
● Targeted therapies, epidermal growth factor antagonists, and tyrosine kinase inhibitors
for advanced or metastatic stages.
● Curettage with Electrodesiccation
● Wide local excision or MOHS micrographic surgery GOLD STANDARD
● Good prognosis
C.- Melanoma
● 1-2% of all melanomas. 10% of all auricular malignancies.
● Survival 10 years 70%
CLINICAL FINDINGS
● Helix
● Lesions may ulcerate and bleed
DIAGNOSIS
● Chest X-ray (lung metastases)
● Lactate dehydrogenase levels
● Radionuclide bone scans (bony metastases)
49
D.- Osteomas and Exostoses

OSTEOMAS EXOSTOSES
True neoplastic benign outgrowths near the Firm, bony, broad-based lesions composed of a
bony-cartilaginous junction. lamellar bone
Unknown etiology Due to reactive bone formation and cold-water

exposure (refrigerative osteitis, surfer ear)
Pedunculated lesions Multiple lesions
Arise from the bony portion of the EAC
Mostly asymptomatic. But there could be cerumen impaction, otitis externa, and hearing loss
CT scan for diagnosis
Most cases require no intervention

Transcanal or postauricular approach if needed
GLANDULAR TUMORS------------------------------------------------------
4 types are included.
1.- PLEOMORPHIC ADENOMA

● Subepithelial proliferation of glandular structures
● Nests of myoepithelial components
● In a chondromyxoid stroma
2.- CERUMINOUS ADENOMA
● Arise from the ceruminous apocrine glands of the EAC.
● Reddish, polypoid, painless masses
● Hearing loss, otitis externa
● Epithelium may show apical “snouts” of apocrine secretion
3.- CERUMINOUS ADENOCARCINOMA
● Arise from the ceruminous apocrine glands of the EAC
● Higher rates of mitosis and cellular atypia.
● Moderately aggressive
50
4.- ADENOID CYSTIC CARCINOMA

● Found in salivary gland tissue.
● Arise from eccrine sweat glands or ectopic salivary glands.
● Perineural, perivascular, and fatty infiltration
● Lung metastasis
● Parotidectomy should be considered
CLINICAL FINDINGS
● Nodular mass, otorrhea, aural fullness, otalgia, and hearing loss.
TREATMENT
● Benign tumors: Wide local excision.
● Malignant tumors: Pittsburgh classification + Temporal bone resection
51
“Inflammatory process localized in the middle ear cleft”.

The middle ear cleft comprises 3 contiguous components:
1. Eustachian tube
2. Tympanic cavity (middle ear)
3. Mastoid air cells.
EPIDEMIOLOGY------------------------
● More common in children (peak at 2 years old)
○ 19-62% at 1 year old
○ 50-84% at 2 years old
● Trisomy 21 or cleft palate=higher incidence
● 3-15% in adults
● 10% of acute otitis media (AOM) patients develop
chronic otitis media with effusion (OME)
CLASSIFICATION---------------------------------------------------------------
ACUTE OTITIS MEDIA (AOM) OTITIS MEDIA WITH EFFUSION (OME)
Rapid onset. Develops after unsolved episodes of AOM

Pyrexia and otalgia. No effusion Effusion. Asymptomatic
Also known as Acute suppurative or purulent Also known as Secretory, nonsuppurative, and
OM serous OM
Recurrent AOM Chronic OME

● ≥ 3 episodes in 6-months or... ● Effusion for ≥ 3 months.
● ≥ 4 episodes in 12-months Occurs in ~25% of OME patients
Complete resolution between episodes.
RISK FACTORS-----------------------------------------------------------------
● Eustachian tube dysfunction (most important) ● Genetic predisposition
● Age (children) ● Infectious factors*
● Allergic tendency ● Environmental factors.
While most episodes of OM are precipitated by viral infections, most of AOM have a bacterial
component:
1. S pneumoniae
2. H influenzae
3. M catarrhalis.
52
Risk factors for AOM and subsequent OME

● Family history of AOM ● Absence of breastfeeding
● Day care attendance ● Craniofacial anomalies
● Immunodeficiency ● Adenoid hypertrophy
● Parental smoking ● Allergic rhinitis
PATHOGENESIS---------------------------------------------------------------
Obstruction of the eustachian tube results in the development of OM. Obstruction could be:
● Functional (failure of contraction of tensor veli palatini during swallowing)
● Anatomic (Adenoid hypertrophy, cleft palate)
The eustachian tube is connected to the nasopharynx by the torus tubarius. Physiologically, it is
closed, and it is opened by the tensor veli palatini and the levator veli palatini muscles when we do
a Valsalva maneuver.
The infant eustachian tube is shorter, wider, and more horizontal than the adult tube, which is
attained by age 7 years.
Functions of the eustachian tube

1. Aerates the middle ear space, providing pressure equivalent to atmospheric pressure. main
function
When we’re on a plane, the pressure outside our body creates a great negative pressure, so the
tympanic membrane retracts, creating aural fullness.
When we yawn or chew a gum, tensor veli palatini muscle contracts and opens the eustachian
tube, and the pressure will be regulated.
2. Mucociliary clearance of the middle ear space
The effusion is the production of liquid of the mucosa of the middle ear. The liquid is sterile.
53
3. Protects the middle ear from entrance of nasopharyngeal contents because of the positive
pressure. If there was a negative pressure, nasopharyngeal contents could enter the middle ear.
DIAGNOSIS--------------------------------------------------------------------------
Otoscopy: COMPLETES
*Other conditions: If there are bullae, we should do the differential diagnosis with meningitis
bullosa (vesicles of liquid all over the tympanic membrane)
**Position: Bulging:
Audiologic testing
Do it if OME ≥ 3 months or for at-risk children (speech/language delay, developmental disability,
trisomy 21, or craniofacial abnormalities).
● Audiogram. Reevaluate in 3-6 intervals ● Speech awareness testing

until effusion and hearing loss resolved. ● Behavioral observation
● Speech-reception threshold (SRT) ● ABR
Clinical picture: Clinical picture:

● Otalgia ● Asymptomatic
● Pyrexia (fever) ● Effusion
● Decreased appetite ● Persistent hearing loss (more common
● Upper respiratory infection than in AOM)
● Fatigue
● Otorrhea (if there’s perforation)
● Hearing loss
54
● Children:
○ Fussiness
○ Insomnia
○ Generalized irritability.
Tympanic membrane (Otoscopy): Tympanic membrane (Otoscopy):

● Thickened ● Dull gray or yellow
● Opache ● Immobile
● Immobile ● Bubbles or air fluid levels
● Hyperemic and bulging
Tympanogram: Is not usually performed, Tympanogram:

because the diagnosis is clinical. ● Type B (flat)
.
TREATMENT---------------------------------------------------------------------
MEDICAL MANAGEMENT
Resolves spontaneously mostly -
Antibiotic therapy Antibiotic therapy

● ≥ 6 months with unilateral AOM and Is not that useful in this case.
severe symptoms May increase the risk of diarrhea, vomiting, and
● < 24 months with bilateral AOM rash.
Amoxicillin (high-dose) 1st line
β-lactamase if patient has received amoxicillin
in the past 30 days or if also has purulent
conjunctivitis
Observation for Nonsevere AOM.You can give Observation. You better do this only by now,
antibiotics if patient fails to improve or worsens ok?
in 48-72 h
Adjunctive therapy: Decongestants, Adjunctive therapy: Not recommended

vasoconstrictors
SURGICAL MANAGEMENT
In refractory cases only: Purpose:

Provide ventilation of the middle ear
55
● Tympanocentesis. Perforate the and prevent sequelae,

tympanic membrane and drain the Recommended for:
liquid. May also help for the selection of ● Chronic OME and hearing loss
appropriate antibiotic therapy ● Recurrent AOM+evidence of OME
● At-risk patients (trisomy 21 or
craniofacial abnormalities)+type B
tympanogram
Tympanostomy tubes. GOLD STANDARD for

OME and chronic OME
● Placement of tympanostomy tubes In
case of complications Adenoidectomy:
Not recommended for patients < 4 years old
unless there was chronic adenoiditis or nasal
obstruction
Could be done alone or in combination with
tympanostomy tubes if patient >4 years old.
Others (but not that useful): Myringotomy and

tonsillectomy
.
COMPLICATIONS----------------------------------------------------------------
1. Perforation. 1. Conductive hearing loss

2. Mastoiditis. 2. Speech delay
a. Coalescent 3. Atelectasis
b. Masked 4. Cholesteatoma
c. Chronic
3. Petrous apicitis
4. Facial nerve paresis
5. Labyrinthitis
6. Intracranial complications
a. Meningitis
b. Otitic hydrocephalus
c. Abscess
i. Epidural
ii. Subdural
iii. Brain
d. Sigmoid sinus thrombophlebitis
.
AOM
1.- PERFORATION
● Due to accumulating inflammation and ischemia of the tympanic membrane
● Heal spontaneously within 2-3 weeks.
● If not, it could give us hearing loss, chronic otorrhea, or migratory cholesteatoma.
56
2.- MASTOIDITIS
● Most common intratemporal complication
● Patient has fevers, postauricular erythema tenderness, and ear proptosis.
● CT scan demonstrates loss of mastoid air cell trabeculations, bone destruction, and soft
tissue within the mastoid cavity and middle ear cleft
● Bony erosion is an indication for cortical mastoidectomy and tympanostomy tube placement.
● Bezold abscesses:
○ Occur when the infection extends through the mastoid tip and tracks inferiorly along
the sternocleidomastoid muscle (SCM)
○ Occur in older children with fully pneumatized mastoid tips and in adults with
mastoiditis or cholesteatoma.
● Citelli abscesses
○ Occur when infection extends from the mastoid and penetrates the posterior belly of
the digastric muscle.
● Chronic mastoiditis: History of multiple AOM episodes, and present purulent otorrhea, dull
otalgia, TM perforation, or cholesteatoma.
3.- PETROUS APICITIS

● Occurs when infection spreads within the temporal bone into the petrous apex.
● Gradenigo syndrome:
1. Retro-orbital pain
2. AOM
3. Ipsilateral abducens nerve paresis
● Radiographic findings: Bony destruction of the petrous apex.
4.- FACIAL NERVE PARESIS

● 2 different mechanisms
○ Release of locally produced bacteria-mediated toxins
○ Direct effect of inflammatory tissue adjacent to the facial nerve
● Tests for facial nerve function
○ Maximum nerve excitability
○ Electromyography
○ Electroneurography
○ MRI with gadolinium
● In adults, it occurs in the setting of cholesteatoma. In children, in the setting of AOM.
● Sudden onset of facial nerve paresis in AOM is an indication for placement of tympanostomy
tubes.
5.- LABYRINTHITIS
● Sudden sensorineural hearing loss, severe vertigo, nystagmus, nausea and vomiting.
● Subsequent development of meningitis.
6.- INTRACRANIAL COMPLICATIONS

● Meningitis:
○ Fever, headache, photophobia, fluctuating mental status, and neck rigidity.
○ Treat it with myringotomy.
○ Mondini dysplasia: Congenital defect in which the cochlea has only 1.5 coils (and not
2.5) and allows for communication between the CSF and the middle ear space.
● Otitic hydrocephalus
○ Increased intracranial pressure
○ Headaches, lethargy, and papilledema
● Abscesses
○ streptococci, S aureus, S pneumoniae, H influenzae, P aeruginosa, B fragilis, and
57
Proteus.
○ Brain and subdural abscesses tx: Require urgent neurosurgical drainage
○ Extradural abscesses tx: Mastoidectomy
● Sigmoid sinus thrombophlebitis
○ Occurs if virulent AOM or mastoiditis penetrates the sigmoid sinus
○ Diurnal or “picket fence” fever curves, septicemia, and torticollis
○ MRI with gadolinium for diagnosis
OME
1.- CONDUCTIVE HEARING LOSS AND SPEECH/LANGUAGE DELAY
● OME-associated hearing loss is often temporary
● Alterations in language: Articulation, receptive vocabulary, and phonological awareness,
2. ATELECTASIS
● Is a grossly retracted or collapsed TM.
● Leads to an altered migration pattern of squamous epithelium, accumulation of squamous
debris, and cholesteatoma formation.
● May lead to ossicular erosion and conductive hearing loss
3. CHOLESTEATOMA
● 2 categories: primary or secondary.
○ Primary
■ Consequence of an atelectatic TM
■ Arise in the epitympanum adjacent to the pars flaccida.
○ Secondary
■ Consequence of squamous migration through a TM perforation into the
middle ear.
● Expands locally destroying nearby structures: scutum, ossicles, mastoid cavity, tegmen, or
otic capsule.
● May lead to facial paralysis, labyrinthitis, meningitis, and hearing loss.
58
GENERAL SIGNS AND SYMPTOMS

● Dizziness: chief complaint
● Vertigo: Illusion of movement
● and hearing loss
○ Duration?
○ Periodicity?
○ Associated symptoms?
○ Peripheral or central lesion?
● Neurologic abnormalities = Central
vertigo
⚠Remember Vestibular testing. (See image)

You must also include audiologic testing and
image studies for diagnosis.
GENERAL PATHOPHYSIOLOGY
The central compensation for vestibular
injury occurs via the cerebellum, which
provides a “clamping” response to the injured
vestibular system to modulate the effects of
the lesion
VESTIBULAR REHABILITATION
1. Habituation exercises extinguish
pathologic responses to head motion
2. Postural control exercises
3. General conditioning exercises.
---BENIGN PAROXYSMAL--
---POSITIONAL VERTIGO---
Epidemiology
● 5th decade (No gender bias)
● 20% of all vertigo patients
● 10-15% familiar history of vestibular neuronitis
● 20% history of head trauma
Pathogenesis
Result of debris in the posterior (may also be horizontal or superior) semicircular canal.
1. Debris in the semicircular canal
a. Attached to the cupula (cupulolithiasis) or...
b. Free floating in the endolymph that will occlude the canal (canalolithiasis)
2. Movement of debris in response to gravity
3. Deflection of the cupula
4. Vertigo
59
Clinical findings
A.- SYMPTOMS AND SIGNS
● Peripheral Vertigo
○ Sudden
○ 10-20 seconds
○ Triggering positions:
■ Rolling over in bed into a lateral position
■ Getting out of bed
■ Looking up and back (top-shelf vertigo)
■ Bending over
● Nausea
● NO hearing loss
● NO spontaneous nystagmus
● NORMAL neurologic evaluation
B.- IMAGE STUDIES: MRI WITH GADOLINIUM CONTRAST

Reserved for when:
● No characteristic nystagmus ● No response to treatment
● Neurological findings ● Recurrent symptoms.
Useful for evaluating:
● Brainstem ● Internal carotid artery (ICA)
● Cerebellopontine angle (CPA) ● Posterior fossa tumors.
C.- SPECIAL TESTS

● Audiogram: Normal ● Tympanogram: Normal
D.- SPECIAL EXAMINATIONS

● Dix-Hallpike test: Nystagmus https://www.youtube.com/watch?v=wgWOmuB1VFY
○ Latency of 1-2 seconds before onset of vertigo and nystagmus
○ Mixed: Torsional + vertical
○ Geotropic (downbeating & rotatory)
○ Fatigable
○ Vertigo and nystagmus increase and decrease within 20 seconds
Treatment
A.- NONSURGICAL MEASURES
● Epley maneuver (particle or canalith repositioning procedure)
○ https://www.youtube.com/watch?v=9SLm76jQg3g
○ Repeat if the patient is still symptomatic.
● Semont maneuver (liberatory maneuver)
B.- SURGICAL MEASURES
For patients that have failed repositioning maneuvers and have no intracranial pathology
● Posterior semicircular canal occlusion.
○ A mastoidectomy is performed and the posterior semicircular canal is fenestrated.
○ May cause a temporary mixed hearing loss
60
Prognosis
● Remission over a few months.
● >30% of patients may have symptoms for >1 year.
● Most patients improve with a repositioning maneuver.
● Rate of recurrence: 10-15% per year
○ Retreat with repositioning maneuvers.
● Balance rehabilitation therapy for patients with other balance disorders
MENIERE DISEASE-----------------------------------------------------------
● Also known as endolymphatic hydrops
● Idiopathic
● 5th decade of life (no gender bias)
● Between age 20-70
Pathogenesis
https://www.youtube.com/watch?v=qrk7OyAB_ss
Increased endolymphatic fluid owing to impaired
reabsorption of endolymphatic fluid in the endolymphatic
duct and sac.
● Attributed to anatomic, infectious, immunologic, and
allergic (inhalant or food) factors.
● Genetic: Mutation in the COCH gene or implication of
AQPs and ion channels
● Histopathology: Blockage in the longitudinal flow of
endolymph in…
○ Endolymphatic duct, Endolymphatic sinuses,
Utricular ducts, Saccular ducts, Ductus
reuniens.
Normal endolymphatic sacs:

● Role in metabolic homeostasis: Secretes glycoprotein conjugates in response to osmotic
challenges
● Process antigens and mount a local antibody response. May be vulnerable to immunologic
injury because of the hyperosmolarity of its contents and the fenestrations in its vasculature
Endolymphatic sacs in Meniere disease:
● Smaller
● Less absorptive tubular epithelium
● Increased perisaccular fibrosis
● Immune complex (IgM and C1q) deposition and injury.
● Low IgA levels
● Autoantibodies to an inner ear antigen (Western blot) (30%)
● Increased rate of expression of HLA antigens (eg, A3, Cw7, B7, and DR2)
Endolymphatic ducts in Meniere disease:

● Smaller
● Decrease in type II vestibular hair cells
61
Clinical findings
1. Hearing loss
a. Unilateral, fluctuating
b. Low frequencies
2. Peripheral Vertigo
a. Episodic. Minutes to hours
3. Tinnitus
a. Constant or intermittent
b. Increasing before or during the vertiginous attack
4. Aural fullness.
B.- LABORATORY
● Fluorescent treponemal antibody absorption (FTA-ABS) to rule out syphilis.
● Autoimmune serologic tests t o rule out Autoimmune ear disease
C.- IMAGE STUDIES: MRI WITH GADOLINIUM CONTRAST

To exclude retrocochlear pathology (vestibular neuroma)
D.- SPECIAL TESTS

● Audiogram: Sensorineural hearing loss
○ Low frequencies or Low + High frequencies
○ Flat as it progresses
○ Glycerol dehydration test: Measuring serial pure-tone thresholds and discrimination
scores during diuresis. H
earing must improve after this test in Meniere disease.
■ Positive in only 50%
● Electrocochleography (ECOG)
○ Measures the sound-evoked electrical potentials from the inner ear.
○ 3 phenomena measured from the external canal:
■ Cochlear microphonic
■ Summating potential (SP): Will be greater, so there’ll be a greater SP/AP ratio
■ Action potential.
● Electronystagmography (ENG) + caloric testing
○ Shows peripheral vestibular dysfunction
○ The caloric response decreases during the 1st decade of the disease and usually
stabilizes at 50% of normal function.
● Vestibular-evoked myogenic potential (VEMP) testing
○ Diminished or absent
Differential diagnosis
● Poor vision, decreased proprioception ● Syphilis
(diabetes mellitus) ● Autoimmune ear disease: more
● Cardiovascular insufficiency aggressive course and early bilateral
● Cerebellar or brainstem strokes involvement
62
● Neurological conditions (eg, migraines, ● Retrocochlear pathology (Vestibular

multiple sclerosis) neuroma)
● Metabolic disorders ● Side effects of medications
Treatment
1. DIETARY MODIFICATIONS AND VESTIBULAR SUPPRESSANTS
● Sodium-restricted diet (≤ 2000 mg/d)
● Restrictions on caffeine, nicotine, alcohol, and theophylline (chocolate).
● Diuretics (diazide).
● Vestibular suppressants (meclizine and diazepam [Valium]) for acute attacks
● Antiemetic medications (prochlorperazine [Compazine] suppository).
2. AMINOGLYCOSIDE THERAPY
● Intratympanic gentamicin
● Stop the treatment if there’s persistent hearing loss.
⚠The risk of hearing loss increases as the dose and frequency of injections are increased
3. STEROID THERAPY
● Intratympanic
4.- SURGERY
● Endolymphatic sac surgery
○ Involves a mastoidectomy and locating the endolymphatic sac on the posterior fossa
dura
● Vestibular nerve section
○ Definitive treatment of unilateral Meniere disease in patients with serviceable hearing
○ May be approached via the rectosigmoid (less risk to facial nerve) or middle fossa
○ Acutely vertigo and nystagmus (fast phase away from the operated ear) for a few
days until central compensation takes effect.
● Transmastoid Labyrinthectomy + fenestration of the bony semicircular canals and
vestibule + removal of the membranous neuroepithelium
○ Control of vertigo in nearly all patients with unilateral Meniere disease and poor
hearing.
○ Rate of control may decline in 10 years because aging, poorer vision, and Meniere
disease in the contralateral ear.
63
VESTIBULAR NEURONITIS-------------------------------------------------
● Middle age people
● Antecedent or concurrent viral illness
Pathogenesis
Reactivation of a latent herpes simplex virus type 1 (HSV-1) infection causes injury in the superior
vestibular nerve:
● Degenerative changes in the vestibular nerve, Scarpa ganglion, and vestibular
neuroepithelium
● Other Proposed etiologies: Viral infection, vascular occlusion, and immunologic mechanisms
Clinical findings
● Vertigo
○ Sudden (acute)
● Nausea and vomiting
● Postural instability toward the injured ear. Still able to walk without falling
● Spontaneous nystagmus
○ Horizontal + torsional
○ Suppressed by visual fixation
○ Slow phase is toward the injured ear
○ Fast phase is away from the injured ear.
○ Alexander’s law: Intensified by looking toward the fast phase and decreased by
looking toward the injured ear.
● NO hearing loss
● NO other neurologic signs or symptoms
B.- IMAGE STUDIES

● MRI: Look infarction and hemorrhage in the brainstem and cerebellum in patients with:
○ Risk factors for stroke
○ Additional neurological abnormalities
○ No improvement within 48 hours.
● CT scan: To evaluate the brainstem, cerebellum, and fourth ventricle
C.- SPECIAL TESTS

● Caloric response: Complete or reduced in the injured ear
● VEMP: Attenuated or absent.
Differential diagnosis
● Brainstem or cerebellar stroke
○ Diplopia
○ Dysmetria, Dysarthria, Abnormal reflexes
○ Motor and sensory deficits
○ Inability to walk without falling
64
○ Central nystagmus: not affected by visual fixation and may change directions with
changes in gaze.
○ Purely vertical or purely torsional nystagmus = Central lesion
● Vestibular neuronitis
Treatment
● Symptomatic and supportive care during the acute phase of the illness.
● Vestibular suppressants and antiemetics to control the vertigo, nausea, and vomiting.
⚠Withdrawn as soon as possible to avoid interfering with the central vestibular
compensation.
Prognosis
● Complete or partial recovery within a few weeks to months.
● Most patients recover with no sequelae
● 15% have significant vestibular symptoms even after 1 year.
● May later develop BPPV.
● Vestibular rehabilitation for patients with residual symptoms.
SUPERIOR SEMICIRCULAR CANAL DEHISCENCE------------

● Could be congenital or developmental
● Usually bilateral
● Obesity may be a risk factor
Pathogenesis
Due to exposure to external pressure along the dehiscent superior canal that is transmitted to the
inner ear.
● Thinning (≤ 0.1 mm) of the temporal bone
● Bilateral dehiscence of the superior canal in the floor of the middle cranial fossa
Clinical findings
● Vertigo when...
○ Tullio phenomenon: Vertigo when exposed to loud noises
○ Valsalva maneuvers
○ Pressure changes in the ear (Hennebert sign)
○ Factors that raise intracranial pressures (jogging, jugular venous compression)
● Oscillopsia
● Chronic disequilibrium.
● Increased sensitivity to bone-conducted sounds
● Hearing their pulse sound
● Hearing their eye movements
● Autophony
65
B.- IMAGE STUDIES

● High-resolution CT of the temporal bone.
● Pöschl view with 0.5-mm collimated helical CT scans
C.- AUDIOLOGIC TESTING

● Audiogram: Low-frequency conductive hearing loss: Mimics otosclerosis
● Acoustic reflex: present
D.- SPECIAL EXAMINATIONS

● Eye movements align with the affected superior canal and follow Ewald law.
● The nystagmus is in the plane of the canal, and the fast phase is toward the stimulated canal.
● Cervical and ocular VEMP testing: lower-than-normal thresholds
Treatment
● Avoidance of loud noises, jogging, or singing
● Surgery:
○ Tympanostomy tube: For symptoms are associated with pressure in the ear canal
○ Repair of the dehiscence of the superior canal (middle cranial fossa or
transmastoid approach) If there are debilitating symptoms
■ Canal plugging or resurfacing procedures
■ Post-operative hearing loss
SUMMARY--------------------------------------------------------------------------
66
FACIAL NERVE’S MOTOR FUNCTIONS:

● Eye protection
● Speech articulation
● Chewing
● Swallowing
● Emotional expression
Unilateral palsy is more common than bilateral
Bilateral involvement = systemic disorder.
BELL’S PALSY-------------------------------------------------------------------
● Peripheral nerve dysfunction. Associated dysfunction
of cranial nerves V, VIII, IX and X.
● EPIDEMIOLOGY:
○ 60-70% of cases of acute facial palsy
○ Recurrent facial palsy 7-12%
● History of Bell’s palsy
● Diabetes mellitus
● Immunodeficiency
● ETIOLOGY: No identifiable cause. Is the inflammatory
facial-motor component of a wider cranial
polyneuropathy that is induced by viral agents
● CLINICAL PICTURE:
○ Unilateral
○ Rapid onset and evolution (<48 h)
○ Pain or numbness affecting the ear, mid-face, and tongue
○ Hearing loss and dizziness may be present
HERPES ZOSTER OTICUS------------------------------------------------

● Also known as Ramsay Hunt Syndrome
● Acute peripheral facial palsy associated with otalgia and varicella-like cutaneous lesions
● May involve cranial nerves: V, VIII, IX and X.
● EPIDEMIOLOGY:
○ 10-15% of acute facial palsy cases
○ Higher incidence of cochleo saccular
dysfunction.
● CLINICAL PICTURE
○ Varicelliform rash in:
■ External meatal skin
■ Preauricular skin
■ Skin of the EC
■ Soft palate
○ Hearing loss, dysacusis, and vertigo
67
EPIDEMIOLOGY-----------------------------------------------------------------
● Incidence: 15-40/100’000 persons
○ Increases with age
● Infrequent in patients <10 years old
● More common in females in their teens and twenties
ETIOLOGY--------------------------------------------------------------------------
A.- VIRAL NEURITIS
● Poliomyelitis, mumps, geniculate ganglionitis, Epstein-Barr virus and rubella infections. They
cause progressive neural dysfunction with subtotal regeneration
● Herpes simplex virus:
○ Predilection for sensory neurons
○ They are in a Latent phase in sensory cell bodies of the ganglion
B.- ISCHEMIC INSULT

● Small-vessel ischemia
● The pathological process is thought to involve the intrinsic system of vessels. Facial nerve’s
blood supply:
1. Labyrinthine artery (proximally)
2. Middle meningeal artery (centrally),
3. Stylomastoid artery (distally)
● Pressure elevations within the intraneural compartments produce:
○ Venous stasis
○ Stagnation of capillary flow
○ Cycle of additional edema
○ Elevation in intraneural pressure
● Tissue damage through acidosis and anoxia is produced.
C.- IMMUNOLOGIC INJURY

● Is a potential cofactor in Bell’s palsy
● Neuropathological findings of segmental demyelination accompanied by lymphocytic
infiltration of the perineurium
● Humoral and cellular autoimmunity
● Immune complexes found in the chorda tympani nerve fibers = viral–antibody (type III)
immunologic reaction
RISK FACTORS-------------------------------------------------------------------
● Diabetes
● Pregnancy (3rd trimester)
● Preeclampsia
● Immunodeficiency and HIV infections
PATHOGENESIS----------------------------------------------------------------
Impaired facial nerve conduction within the temporal bone: Physiological bottleneck
1. The facial nerve is admitted to the temporal bone via the meatal foramen
68
2. The meatal foramen is constricted

(“physiological bottleneck”) in the presence of
neural edema.
3. Intraneural vascular congestion
4. Inflammation and ischemia of the nerve
5. Leukocytic infiltration and demyelination of the
somatic portion of the facial nerve
CLINICAL FINDINGS----------------
A.- PATIENT EVALUATION
● Severity of the palsy
○ Ability to close the eyelid
● Vesicles within the auricle or external
auditory canal (EAC) = of herpes zoster
oticus
● Pain or numbness affecting the ear, midface,
and tongue
● Taste disturbances
B.- LABORATORY FINDINGS
● Blood and cerebrospinal fluid studies not that useful
● Atypical cases: Look for Lyme disease or paraneoplastic syndrome
C.- IMAGE STUDIES
⚠Routine radiological evaluation is not recommended. When do we use image studies?
➔ Incomplete recovery over 3 months’ time
➔ Recurrent palsy
➔ Associated cranial nerve deficits development
● MRI
● High-resolution CT scan to define the bony detail in the course of the facial nerve within the
fallopian (facial) canal.
HOUSE-BRACKMANN FACIAL NERVE GRADING SCALE---
69
I. Normal
II. Mild dysfunction
III. Moderate dysfunction
IV. Moderately severe dysfunction
V. Severe dysfunction
VI. Total paralysis
TREATMENT----------------------------------------------------------------------
Both pharmacological and surgical treatments are designed to reduce the likelihood of residual facial
dysfunction
Steroid therapy
➔ Methylprednisolone IV: Ramsay Hunt syndrome
➔ Prednisolone VO: Bell’s palsy
◆ Start with 60 mg/5 days. And for the next 5 days, reduce the dose gradually
Why shouldn't we stop treatment from a day to another? Abrupt withdrawal may be followed by
a rebound of disease activity.
✔Effects:
● Reducing the risk of denervation if initiated early (<72 h after palsy onset)
● Preventing or lessening synkinesis
● Preventing progression of incomplete to complete paralysis
● Hastening recovery
● Preventing autonomic synkinesis (crocodile tearing).
Side effects:
● Hyperglycemia ● Increased intraocular pressure
● Emotional instability ● Avascular necrosis
● Acute psychosis ● Gastrointestinal irritation.
● Fluid and electrolyte disturbances ● Category C for pregnant patients
● Acne ● More susceptibility to infection.
70
Antiviral therapy
Antiviral monotherapy is NOT recommended. You better use it in combination with steroids.
➔ Aciclovir IV
◆ Indicated in all cases of herpes zoster oticus. Limited efficacy on Bell’s palsy, but it
may also be used orally.
◆ (<72 h after palsy onset)
◆ Dosing:
● 10 mg/kg/8 h /7 days IV for Bell’s palsy
● 400-800 mg/5 times/7-10 days VO for Bell’s palsy
● 4000 mg/day VO for herpes zoster oticus.
● IV dosing for immunocompromised individuals with severe infection
➔ Other Oral antivirals:
◆ Are better absorbed after administration
◆ valacyclovir, famciclovir, and penciclovir
Side effects:
● Nausea ● Mild renal insufficiency.
● Malaise ● Category B for pregnant patients
● Injection site reactions
Physical therapy
TRANSCUTANEOUS ELECTRICAL (GALVANIC) STIMULATION OF FACIAL MUSCLES
● To maintain membrane conductivity and reduce muscle atrophy.
● To limit residuals such as persistent paresis
● To improve function in chronic facial palsy.
● For Patients with partial deficits
● Electromyographic and mirror feedback has been used to facilitate muscle reeducation to
assist in the recovery of symmetric facial tone and expression.
EYE CARE
● Corneal protection (moistening): The cornea is vulnerable to drying and foreign-body
irritation due to orbicularis oculi dysfunction. Not needed in mild facial palsy, but in
dysfunction of cranial nerve V, and moderate-severe palsies.
○ Artificial tears during the daytime, and ocular ointments at night
○ Sunglasses
○ Lateral canthopexy or tarsorrhaphy for longer standing palsies.
● Examination of the cornea by slit-lamp biomicroscopy and fluorescein or rose bengal
staining
Surgical measures
NERVE DECOMPRESSION
● May reduce axonal ischemia
● PREOPERATIVE CONSIDERATIONS
1. 3-14 days after onset palsy, do a electroneuronography (ENoG) to help stratify the
patient
71
2. If patient has < 10% function relative to the contralateral side = Undergo
electromyography (EMG)
3. If EMG, too, confirms poor responses relative to the contralateral side
● Transmastoid approach more useful for Ramsay Hunt Syndrome
● Middle cranial fossa approach
○ Complications: Permanent ipsilateral auditory and vestibular loss, meningitis, and
subarachnoid hemorrhage
NERVE GRAFTING
● Using a section of normal peripheral nerve over a damaged area
● May be augmented by muscle transfer procedures
● Aberrant regeneration may be treated with Botulinum toxin.
PROGNOSIS------------------------------------------------------------------------
● Nerve decompression:
○ 91% recovered completely or with slight residual deficits
○ Only 42% suggesting a benefit of this surgical approach
● Electroneuronography (ENoG) and electromyography (EMG) are the primary tests used to
prognosticate facial nerve outcomes.
○ Not recommended in patients with incomplete paralysis as they’re not candidates for
surgical therapy
OTHER FACIAL NERVE DISORDERS---------------------------------

Next to Bell palsy, the most common causes of acute, peripheral facial paralysis are trauma, herpes
zoster oticus, bacterial infection, perinatal factors, and neoplastic involvement of the nerve.
1.- Facial nerve neoplasms

● Incidence of sudden facial palsy in neoplasms: 27%
● Most common: Facial neuroma (9%)
○ History of surgery for recurrent facial palsy
○ It extends into the labyrinth and cranial fossae.
● Facial nerve hemangiomas
○ Recurrent and progressively more severe episodes of unilateral facial palsy
○ Treatment: Surgical excision + propranolol
CLINICAL FEATURES
● Progression of a facial palsy over 3 weeks or longer
● No return of facial function within 3–6 months
● Failure to resolve an incomplete paresis within 2 months
● Facial hyperkinesia, particularly hemifacial spasm, antecedent to the palsy
● Associated dysfunction of regional cranial nerves
● Prolonged otalgia or facial pain
● Mass in the middle ear, external ear canal, digastric region, or parotid gland
● Recurrent ipsilateral palsy
72
2. Melkersson-Rosenthal Syndrome
● Unilateral facial palsy, episodic or progressive facial edema,
and lingua plicata (scrotal tongue)
● Usually sporadic (familial occurrence has been described
too).
PATHOPHYSIOLOGY
● Noncaseating granulomatous changes
● Autonomic dysfunction and vasomotor instability.
● Associated with migraine headaches and megacolon
● SLC27A1 gene
TREATMENT
● Anti-inflammatory (steroid) therapy
● Nerve decompression (meatal and labyrinthine segments)
● TNF-α inhibitor (adalimumab)
3. Lyme disease
● Multisystem infection induced by Borrelia burgdorferi spirochete.
● Unilateral palsy is more common than bilateral
● More common in summer
SYMPTOMS AND SIGNS
● Erythema migrans (classic target-shaped rash)
○ The interval between the onset of the rash and facial palsy is <2 months
○ 1-4 week incubation period
● Other neurological deficits produced by meningoencephalitis and radiculoneuritis.
● Flu Like symptoms
● Arthritic symptoms
LABORATORY TREATMENT
● Serological testing with ELISA ● Tetracycline (for adults) 3 weeks
○ IgG and IgM antibodies ● Penicillin (for children) 3 weeks
● Alternative choice: Erythromycin
4. Acute Otitis Media and Mastoiditis

● May be the result of toxic neuritis
● Concomitant hearing loss, otorrhea, and vestibular symptoms.
● Typically seen in children who appear toxic and manifest otoscopic findings of middle ear
empyema.
● Radiographic evaluation of the temporal bone may rarely disclose coalescence of infection in
the mastoid.
TREATMENT
● Myringotomy and systemic antibiotics
● Cortical mastoidectomy if the above fail.
73
5. Chronic Otitis Media

● Mucosal inflammation or cholesteatoma
● Reflects a toxic neuritis, external compression, or intraneural compression from edema or
abscess.
● Surgical removal of irreversible disease in the middle ear and mastoid as soon as possible.
6. Necrotizing (Malignant) Otitis Externa

● Pseudomonas aeruginosa
● In patients with diabetes mellitus or immunocompromised
CLINICAL FINDINGS
● Ótorrhea + progressive, disabling otalgia
● The pathognomonic signs are otoscopic evidence of ear canal inflammation or a breach
(filled with granulation tissue) of the external canal skin at the bony-cartilaginous junction.
DIAGNOSIS
● Radioisotope gallium and technetium scanning that demonstrates osteomyelitis of the
temporal bone.
TREATMENT
● Antipseudomonal antibiotics 8-12 weeks
● Aggressive debridement of granulation tissue within the ear canal to promote the
replacement of necrotic bone with viable tissue.
7. Perinatal Facial Palsy

● Bell’s palsy is the most common etiology for childhood facial palsies
● Also known as “asymmetric crying facies”
TRAUMATIC PERINATAL FACIAL PALSY
● Consequence of compression from the maternal sacrum. Prolonged labor and forceps
delivery may trigger facial nerve trauma.
● The extratemporal facial nerve is at risk because the absence of an overlying mastoid tip
places the vertical segment of the nerve at risk for injury
● Causes: Hemotympanum, periauricular ecchymosis, progressive decline of facial nerve
responsiveness to an applied stimulus.
● Recovered function within 24 days.
CONGENITAL PERINATAL FACIAL PALSY
● CLINICAL FINDINGS
○ Craniofacial malformations (involving 1st and 2nd branchial arch derivatives)
■ Microtia and facial clefts
○ Cardiac conductive and anatomic anomalies
● Otologic, electrodiagnostic, and radiological evaluations
● MÖBIUS SYNDROME:
○ Bilateral absence of facial and abducens nerve function
○ Abnormal ABR
○ HOX domain genes implicated in the pathogenesis.
● The prognosis for effective facial animation with congenital facial palsies is poor.
● Facial motor rehabilitative procedures and reconstructive procedures to affect better
symmetry may be indicated later in life.
74
ANATOMY-----------------------------------------------------------------------------
The salivary glands consist of multiple secretory units:
● Distal end: Ductal unit:
○ Intercalated duct
○ Striated duct
○ Excretory duct.
● Proximal end: Acinus
○ Surrounded by myoepithelial cells that
extend to the intercalated duct to enable
secretion.
Functions of the serous and/or mucous secretions of salivary glands:
● Provide digestive enzymes
● Bacteriostatic functions
● Lubrication
● Hygienic activities
SALIVA:
● Produced by the clustered acinar cells
○ 500 to 1500 mL daily
● Contains electrolytes, enzymes (eg, ptyalin and maltase), carbohydrates, proteins, inorganic
salts, and even some antimicrobial factors
● Alkaline pH
PAROTID GLANDS SUBMANDIBULAR SUBLINGUAL MINOR SALIVARY

GLANDS GLANDS GLANDS
Serous saliva secretion Predominantly mucous Predominantly mucous Predominantly mucous

stimulated by the secretions stimulated secretions secretions
autonomic nervous by the autonomic
system nervous system
Largest: 25 g 2nd largest: 10-15 g - -
Lateral to the Occupies the In the submucosa, In the hard and soft
masseter muscle submandibular superficial to the palates, oral cavity,
anteriorly triangle. mylohyoid muscle. lips, tongue, and
Posteriorly over the oropharynx
sternocleidomastoid
muscle
75
Divided by the cranial Divided by the - When identified by

nerve VII: posterior edge of the groups: Blandin-Nuhn
● Superficial lobe mylohyoid muscle:
● Deep lobe ● Superficial lobe
● Deep lobe
The Stensen duct The Wharton duct, Ducts of Rivinus open -

courses anteriorly courses anteriorly directly into the oral
from the parotid gland above the mylohyoid cavity
over the masseter muscle and ends in Some of these ducts
muscle and pierces the anterior floor of unite to form the major
the buccinator muscle the mouth. ducts of Bartholin.
to enter through the Is inelastic: Causes
buccal mucosa pain when obstructed.
2 layers of draining - - -
lymph nodes (beneath
the capsule and within
the parotid
parenchyma)
INFECTIOUS INFLAMMATORY DISEASES------------------------

Mumps (Acute viral)
● Paramyxovirus
● Most common viral disorder causing parotitis
● Peak incidence: 4-6 years
● Incubation period: 14-21 days. It's contagious.
CLINICAL FINDINGS DIAGNOSIS

● Bilateral swelling ● Serologic testing: Antibodies for the mumps S, mumps V,
● Pain and hemagglutination antigens
● Erythema
● Tenderness COMPLICATIONS
● Malaise ● Meningitis, encephalitis, hearing loss, orchitis, pancreatitis,
● Fever and nephritis.
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● Trismus TREATMENT
(occasionally) ● Symptomatic (it’s self-limiting)
● 4 days isolation
VACCINE ● NSAIDs, abundant fluids
● SRP
● 12 months, 6 years
Acute suppurative sialadenitis

● Parotid glands
● Postoperative (30-40%), elderly, chemotherapy and radiation patients
ETIOLOGY SYMPTOMS AND SIGNS

● S. aureus ● Acute parotid swelling
● S. pneumoniae ● Erythema
● E. coli ● Pain
● H. influenzae. ● Tenderness
● Others from chronic ill: Klebsiella, ● Trismus
Enterobacter, Pseudomonas, and Candida. ● Purulent ductal discharge
● Induration
RISK FACTORS ● Fevers
● Dehydration
● Immunosuppression COMPLICATIONS
● Trauma ● Abscess
● Debilitation. ● Induration
● Doughlike consistency of the gland.
PATHOGENESIS ● Suspect 48 h without improvement
1. Stasis of salivary flow
2. Antimicrobial activity decreases TREATMENT
3. Stricture, or obstruction, of the ducts ● Rehydration
4. Hematogenously spreading ● IV penicillinase-resistant
gram-positive coverage antibiotics
DIAGNOSIS ● Warm compresses
● Saliva culture ● Massage
● Sialogogues
PROGNOSIS ● Oral hygiene
● Most patients respond to medical therapy. ● Parotidectomy or ultrasound guided
● If failure of improvement in submandibular fine-needle aspiration if there's an
sialadenitis, consider: duct obstruction, abscess
abscess, salivary stones, or tumors.
● Submandibular abscesses can mimic
Ludwig angina that can lead to airway
obstruction.
HIV infection of the parotid glands: Lymphoepithelial cysts

● Parotid glands and submandibular glands (unusual)
● This is because parotid glands have intraglandular lymph nodes.
77
SYMPTOMS AND SIGNS TREATMENT

● Bilateral symmetric multicystic parotid swelling ● Observation or serial drainage
● Painless of cysts
● Xerostomia ● Sclerotherapy
● Cervical lymphadenopathy ● Gland excision if there’s
submandibular glands
DIAGNOSIS involvement
● CT scan or US to see the cystic masses
● Fine-needle aspiration of cysts Amylase in the PROGNOSIS
fluid ● There is little malignant
● Serologic testing for HIV antibodies confirms the transformation.
diagnosis
Chronic granulomatous sialadenitis

SYMPTOMS AND SIGNS DIAGNOSIS
● Acute salivary gland swelling ● Consider tuberculosis if there are risk
● Chronic unilateral glandular swelling. factors for exposure
● Minimal pain ● Fine-needle aspiration
DIFFERENTIAL DIAGNOSIS
A. Cat-Scratch Disease B. Sarcoidosis
● Bartonella henselae ● Noninfectious
● Affects the periparotid and intraparotid ● Parotid glands
lymph nodes. ● Noncaseating granulomas
● Acute submandibular mass without ● May occur as part of a syndrome known
causing ductal obstruction as uveoparotid fever or Heerfordt
● Warthin–Starry silver stain and syndrome.
increased IgG for diagnosis ● Parotid enlargement, facial palsy, and
● Self-limiting uveitis.
● Leads to xerostomia and xerophthalmia
C. Actinomycosis ● Spontaneous resolution
● Sulfur granules.
● Painless parotid swelling + history of D. Granulomatosis with Polyangiitis
recent dental infection or trauma. (Wegener granulomatosis)
Trismus ● Painful unilateral mass in the gland
● Tx: Penicillin ● Necrotizing inflammation and vasculitis
● Cytoplasmic antineutrophil cytoplasmic
antibody (c-ANCA) for diagnosis
● Tx: Steroids + immunosuppressants
NONINFECTIOUS INFLAMMATORY DISEASES-----------------

Sialolithiasis
● Submandibular gland (80-90%) Parotid glands (10-20%).
● Any age. Predilection in men.
78
RISK FACTORS IMAGE STUDIES

● Long illnesses with dehydration ● X-rays: intraoral, lateral and colossal
● Gout views
● Diabetes ● Digital subtraction sialography: most
● Hypertension. precise + CT or MRI
● US
PATHOGENESIS ● Sialoendoscopy
● Normal saliva contains abundant
hydroxyapatite COMPLICATIONS
● Mineralized debris in the duct form a ● Salivary stasis
nidus, promoting ● Recurrent infection
○ Calculi formation ● Abscess formation
○ Salivary stasis
○ Obstruction. TREATMENT
● Submandibular glands has: ● Intraoral extraction: If the stone is
○ Longer course of its duct palpated or visualized in the anterior
○ Higher salivary mucin and portion of the submandibular duct
alkaline content ● Surgical excision: When the stone is too
○ Higher concentrations of big
calcium and phosphate. ● Endoscopic techniques: Sialendoscopy
open sialolithectomy
SYMPTOMS AND SIGNS ● Others: wire basket extraction under
● Recurrent swelling and pain radiologic guidance, pulsed dye laser
exacerbated when eating lithotripsy, and extracorporeal shock
● Erythema wave lithotripsy.
● History of xerostomia
● History of sand-like foreign bodies PROGNOSIS
● Stone in the floor of the mouth ● Recurrence 20%
● Induration
Chronic Sialadenitis
● Decreased production of saliva or alterations in the salivary flow leading to salivary stasis.
● There may or may not be associated obstruction
● In adults
● Slow, progressive, inflammatory process
RISK FACTORS SYMPTOMS AND SIGNS

● Conditions: Repeated acute infections, ● Chronic, intermittent, painful, bilateral
trauma, radiation, immunocompromised swelling, exacerbated when eating
conditions. ● Calculi may be present
● Permanent histologic changes for
radiation IMAGE STUDIES
● Smoking ● CT and MRI: To exclude malignant
tumors
PATHOGENESIS ● Sialography: Obstruction, acinar atrophy,
irregular duct dilation.
79
1. Retrograde infection from normal oral TREATMENT

flora and chronic inflammation from ● Conservative and superficial
repeated acute infections parotidectomy
2. Changes in the ductal epithelium ● Oral hygiene, hydration, massage,
3. Increased mucin in secretions, sialogogues
decreased flow, and formation of ● Antibiotics for acute exacerbations
mucous plugs.
4. Mucous cell, squamous, or oncocytic COMPLICATIONS
metaplasia ● Fibrous mass or pseudotumors
5. Ductal dilatation and atrophy of the ● Pain
acinar cells. ● Acinar unit and ductal epithelium
6. Fibrosis and infiltration with permanent damage.
lymphocytes.
Sjögren syndrome
● Autoimmune disorder characterized by
○ Parotid enlargement
○ Xerostomia
○ Keratoconjunctivitis sicca.
● Associated with a connective tissue disease (rheumatoid arthritis or systemic lupus
erythematosus)
● 6th decade of life females
SYMPTOMS AND SIGNS COMPLICATIONS

● Bilateral nontender salivary gland ● Difficulty with speaking, swallowing,
enlargement (Intermittent or constant) masticating
● Dry eyes and mouth ● Dental decay
● Dry skin ● Oral mucosa disconfort
● Altered taste ● Lymphoma
● Myalgia
● Vaginal dryness TREATMENT
● Vasculitis ● Symptomatic
● Arthritis ● Steroids and topical steroid eyedrops
for severe symptoms
DIAGNOSIS ● Parotidectomy: For severe recurrent
● SS-A or SS-B autoantibodies infections
● Rheumatoid factor
● Antinuclear antibodies PROGNOSIS
● Microscopic examination of biopsy: ● Increased incidence in malignant
Confirms diagnosis lymphoma or lymphoepithelial
○ Focus score: >1 Focus/4 mm2 carcinoma
● Histopathologic findings: Lymphocytic
infiltrate in acinar units and
epimyoepithelial islands surrounded by
lymphoid stroma
80
Benign lymphoepithelial lesions

● Also known as Godwin tumor, Mikulicz syndrome, or punctate parotitis.
● 5-6th decade of life females
● Associated with multicystic disease in HIV patients
PATHOGENESIS TREATMENT
1. Lymphocytic infiltration around salivary ● Mostly symptomatic
gland ducts and parenchyma ● Aspiration drainage, sclerotherapy,
2. Progressive acinar atrophy low-dose radiation, and antiretroviral
3. Replacement of the acini medications
4. The ductal epithelia proliferate ● Complete submandibular excision
5. Ductal obstruction.
COMPLICATIONS
● Lymphoepithelial carcinoma, low-grade
CLINICAL FINDINGS
B-cell lymphoma of MALT
● Unilateral firm or cystic swelling of the
pseudolymphoma, and non-Hodgkin
parotid gland
lymphoma
● With or without pain (painless in the
● Association with Kaposi sarcoma in
submandibular gland)
HIV-infected patients.
● Lymphadenopathy
DIAGNOSIS
● Fine-needle aspiration
● Sialography when a stone is suspected.
NONINFLAMMATORY DISEASES-----------------------------------------
Sialadenosis/Sialosis
● Bilateral, diffuse, and painless enlargement of the parotid glands and submandibular
glands.
● Age 20-60
● Persists >20 years
PATHOGENESIS DIAGNOSIS
1. Peripheral autonomic neuropathy of the ● Fine-needle aspiration
salivary glands ● CT scan
2. Degenerative changes to the autonomic ● Histopathologic findings: Acinar
innervation of the glands enlargement.
RISK FACTORS TREATMENT

● Obesity, diabetes ● Directed at the underlying conditions
● Alcoholic, Cirrhosis (except neuropathy)
● Hyperlipidemia ● Parotidectomy if the parotid enlargement
● Hypothyroidism is cosmetically unacceptable .
● Anemia ● Surgical resection
● Pregnancy, menopause
● Malnutrition
● Medications (eg, clozapine).
81
Parotid cysts
● Fluctuant swelling of the salivary glands
● HIV as differential diagnosis
CONGENITAL ACQUIRED
● Branchial cleft anomalies ● Tumors

○ Type 1 ● Trauma
■ Duplication anomaly of ● Sialolithiasis
the ectodermal external ● Chronic sialadenitis
auditory canal ● Ductal stricture
■ Anteroinferior to the ear ● Benign lymphoepithelial lesions.
lobule ● Radiation injury
○ Type 2
■ Ectodermal and
mesodermal elements
■ Anteriorly to
sternocleidomastoid
muscle or external
auditory canal
○ Both may have sinus tracts
○ Tx: Excision: Parotidectomy for
both
● Dermoid cysts:
○ Results from trapped embryonic
epidermis
○ Rounded mass
○ Contains keratinizing squamous
epithelium and sweat glands
○ Tx: Excision
Mucoceles/mucous retention cysts

● Dilatations of the minor salivary gland and sublingual glands
○ Because of the continuous mucous secretions in these glands.
● In the lip (60%–70%), buccal mucosa, floor of the mouth (then it is called
ranula),and palate
CLINICAL FINDINGS PATHOGENESIS

● Pale, smooth, bluish-hued submucosal ● Trauma or rupture of minor salivary
cysts. gland ducts
● Painless ● Accumulated mucous secretions
● Ranulas: Unilateral, round, fluctuant ● Mucous extravasations into connective
masses in the mouth floor. tissue
○ Simple ranula:
■ Is a true cyst with an DIFFERENTIAL DIAGNOSIS
epithelial lining ● Cystic hygroma, lymphangioma,
■ Intraoral thyroglossal duct cyst, dermoid cyst,
■ Elevation of the mouth mucoepidermoid carcinoma.
floor.
82
○ Plunging ranula TREATMENT

■ Extends below the ● Complete surgical intraoral excision
mylohyoid muscle, ● Simple ranula:
beyond the sublingual ○ Simple excision of the cyst +
space removal of the gland
■ Painless submandibular ○ Marsupialization of the cyst wall
or cervical neck mass. (more recurrences)
■ NO epithelial lining (is a ● Plunging ranulas:
pseudocyst) ○ Intraoral excision
○ Excision + cervical incision +
extirpation of the gland
BENIGN NEOPLASMS DISORDERS------------------------------------

● 6-7th decade of life
● 64-80% parotid gland
○ 75-85% are benign
○ Most of them are epithelial tumors
● 7-15% submandibular gland
○ 50-60% are benign
● 1% sublingual glands
○ 35% are benign
○ Most common: Pleomorphic adenoma and basal cell adenoma.
SYMPTOMS AND SIGNS
● Slow-growing, painless enlarging, solitary masses often in the tail of the gland.
● Deep parotid lobe tumors may present as a painless, asymmetric swelling of the soft palate.
DIAGNOSIS
● Fine-needle aspiration (85% accuracy)
● Diffusion-weighted MRI: may help identify deep lobe tumors
● Immunohistochemical markers and fluorescence in situ hybridization.
TREATMENT
● Complete surgical excision with uninvolved margins
Pleomorphic adenomas/Benign mixed tumors

● Most common neoplasms of the salivary glands
● 60% to 70% of all parotid tumors and 90% of submandibular benign tumors.
● 3-6th decade of life
● Arise from distal portions of salivary ducts
SYMPTOMS AND SIGNS COMPLICATIONS

● Isolated swelling or mass in the ● Carcinoma ex pleomorphic adenoma
submandibular gland + little pain. TREATMENT
● Deep parotid lobe = parapharyngeal ● Complete surgical excision with
space tumor with soft palate swelling. uninvolved margins
DIAGNOSIS ● Superficial parotidectomy with clear
● Immunohistochemical stains margins (in superficial lobes)
83
● Histopathologic findings: epithelial,

myoepithelial, and stromal elements
Warthin tumor/Papillary cystadenoma lymphomatosum

● Parotid gland exclusively DIAGNOSIS
● Arises from the ectopic ductal ● CT scan: Well-defined mass in the
epithelium posteroinferior segment of the
● 5-7th decade of life in males superficial lobe of the parotid.
● Bilateral and multicentric ● Radio Sialography: Increased activity of
RISK FACTORS oncocytes and increased mitochondrial
● Smoking content.
TREATMENT ● Histopathology: Double layers of
● Complete excision of the affected granular eosinophilic cells or oncocytes,
portion of the gland with uninvolved cystic changes, and mature lymphocytic
margins. infiltration
..
84
INITIAL EVALUATION-----------------------------------------------------------
Ask about:
● Age of the patient
● Timing of last meal
● Acute or chronic obstruction?
● Mechanism and type of injury
○ Laryngeal trauma: Perilous endotracheal intubation and worsening airway
compromise. Tracheotomy is a better option.
○ Maxillofacial trauma: May preclude normal translaryngeal intubation. You better do a
flexible fiber optic intubation or a tracheotomy
● PATIENT FACTORS:
➔ Obesity ➔ History of head and neck cancer
➔ Obstructive sleep apnea ➔ History of difficult intubation
➔ Prior surgery or radiation to the head ➔ GERD
and neck ➔ Opioid use
Physical examination
Key element in diagnostic upper airway obstruction
ASSESSMENT OF THE GENERAL STATE OF THE PATIENT
● Quality of respiration
○ Stridor, or noisy respiration
■ Inspiratory stridor = Laryngeal obstruction or above
■ Expiratory stridor = Distal obstruction (trachea).
■ Biphasic stridor = Subglottic obstruction.
● Quality of Voice
○ Muffled voice = Supraglottic obstruction (epiglottitis, peritonsillar abscess, or
Ludwig angina).
○ Hoarse voice = Laryngeal involvement (vocal fold papilloma)
○ Breathy or weak voice or cry = Vocal cord paralysis
● Examination of the head and neck
○ Trismus ○ High Mallampati or Friedman grades (see image
○ Limited interincisal gap (< 30 mm) below)
○ Short thyromental distance (< 3 ○ Limited range of neck motion
fingerbreadths) ○ Short neck length
○ Limited chin protrusion ○ Large neck circumference (> 50 cm)
85
● Other signs:
○ Suprasternal or substernal retractions, tachypnea, and cyanosis.
○ Inability of a patient to handle his own secretions (drooling or spitting)
○ Signs/symptoms of aspiration (wet, garbled voice and coughing)
FLEXIBLE FIBER OPTIC LARYNGOSCOPY

● To rapidly assess the airway. Information obtained forms the basis of our airway strategy.
● Performed transnasally
1. Patient is seated upright, breathing spontaneously.

2. Decongestion of the nose with an alpha agonist nasal spray (oxymetazoline)
3. Give topic lidocaine
4. Lubrication of the scope.
5. Explore the base of tongue and lingual tonsils, position of the epiglottis, mobility of the vocal
folds, and the patency of the glottic airway
6. Concerning findings:
● Obstructive pharyngeal or laryngeal mass
● Edema of the supraglottic or glottic airway.
Setting and Acuity

The physical location of a patient is an important consideration to know what tools and support will
be available. For example, if the patient is at:
● Intensive care unit (ICU): Senior intensivists around to assist and a crash cart or airway cart
stocked with laryngoscopes, bougies, or suction catheters may be available
● Inpatient floor: These tools and support may not be available. ☹
○ Then, what am I supposed to do? Bring a flexible fiber optic scope for evaluation and
call early for additional assistance
Also, you should consider if securing the airway will be more optimal in the location of initial
consultation or if the patient should be moved to an operating room (OR).
Anticipation and Preparation

Reliance on any single technique is dangerous: You'd better make sure you have multiple devices
available
86
Also, the anesthesiology team must have immediate access to necessary medications; for
example, they should be prepared if endotracheal intubation fails and the patient must be woken
from general anesthesia.
Communication and Coordination

All team members must be knowledgeable about the airway plan, location of necessary tools, role
definitions, and order of operations.
● 3 failed attempts at securing an airway = A more experienced team member must take the
lead for future attempts.
● When called to assist the anesthesiologist, he must ask:
○ Which steps have already been taken?
○ How long attempts have been underway?
○ Is the patient ventilatable via bag-mask technique?
Execution: Airway Strategy

Before starting, Discuss the plan, the plan B, and the equipment that will be needed.
● You must always have a Plan B if the initial attempt at airway control fails,
If there’s not time for discussing the above: The consultant should ask:
● Is this emergent or urgent?
● What techniques to secure the airway have already been attempted?
● What is the location of the patient and what airway equipment is at the bedside?
Also, an extubation plan is critical, and teams should be prepared for regaining an airway if
extubation (or decannulation) fails.
● For patients with tracheotomies, a tracheotomy tube of the same size and of 1 size smaller
should always be kept at bedside.
NONSURGICAL MEASURES SURGICAL MEASURES
● Oxygen administration ● Cricothyroidotomy

● Topical decongestants and steroids ● Tracheotomy
● Oropharyngeal and nasopharyngeal ● Percutaneous tracheotomy
airways
● Translaryngeal intubation
● Jackson sliding laryngoscope
● Guided endotracheal intubation
● Laryngeal mask airway
Definition of difficult airway: Situation in which a conventionally trained anesthesiologist

experiences difficulty with mask ventilation, endotracheal intubation, or both.
NONSURGICAL AIRWAY MAINTENANCE-----------------------------

Oxygen administration
● 1st and most important task: RELIEVE HIPOXIA
87
● Helium-oxygen mixture
○ 80% helium
○ 20% oxygen
Topical decongestant and steroids

Decrease upper airway obstruction if there’s a component of soft edema
● Racemic epinephrine and epinephrine aerosols
○ Topical decongestants: decrease edema
○ Short effect, and rebound effect of used repeatedly
● Methylprednisolone sodium succinate
○ 125 mg IV (1st dose)
○ Dexamethason 8 mg IV/8 h
Oropharyngeal and nasopharyngeal airways

● Definitive nonsurgical control
● Prevent obstruction caused by a relaxed and prolapsed tongue
● Indications: Patients emerging from anesthesia or suffering from an altered mental state
● Contraindications: Laryngeal trauma, obstructing tumor
BAG-MASK VENTILATION
● Objective: Increase the patient’s chest rise, breath sounds on chest auscultation,
condensation on the mas, and end-tidal CO2 on capnography.
● A seal is created over the mouth and nose with a face mask.
● The ventilator bag is used to support a patient’s ventilation and respiration.
● If there’s Difficult bag-mask ventilation:
○ Lift the chin of the patient
○ Place an oropharyngeal or nasopharyngeal airway.
Translaryngeal intubation
● Definitive nonsurgical control
● Contraindications: Laryngeal trauma, obstructing tumor
Jackson sliding laryngoscope

● Makes it easier to manipulate past obstruction lesions or edematous soft tissue
● Once the glottis is identified, and endotracheal tube is passed into the trachea and the
laryngoscope floor can be slid out to facilitate removal of the laryngoscope
Guided endotracheal intubation

● Using a flexible fiberscope
● Useful for an intubation in an awake, spontaneously breathing patient with a known or
suspected difficult airway
● Can be performed either via nasal or an oral route
88
Laryngeal mask airway

● Routine elective cases and many emergency situations involving difficult airways
● It can easily be inserted into the hypopharynx; insertion is complete when resistance is felt
● No neck movement or laryngoscopy is required
● Less potential for laryngeal injuries
● Risks: Pulmonary aspiration or regurgitated stomach contents.
Other nonsurgical measures

● Esophageal combitube
○ Patients requiring rapid airway control
● Light wand
● Bullard laringoscope
○ Can provide lifesaving emergency ventilation and oxygenation until a surgical airway
can be established
○ Contraindications: Children and very small adult patients.
SURGICAL MEASURES---------------------------------------------------------
INDICATIONS FOR SURGICAL AIRWAY: “cannot intubate, cannot ventilate.”
1. Severe maxillofacial trauma in which injuries make the airway inaccessible for
translaryngeal intubation
2. Significant laryngeal trauma in which intubation may potentially cause more damage
3. Excessive hemorrhage or emesis obscuring landmarks required for successful intubation
4. Cervical spine injury with vocal cords that are difficult to visualize
5. Failed translaryngeal intubation
6. Nonsurgical measures are not possible or have failed.
CRICOTHYROIDOTOMY TRACHEOTOMY
Fast and simple to perform. Requires very few Technically more difficult, bloody, and
instruments. dangerous
When should we prefer a tracheotomy over a cricothyroidotomy?

● True subglottic obstruction (carcinoma or large thyroid tumors)
● Children <10 years old
89
Tracheotomy
Tracheotomy or tracheostomy?
● Tracheotomy: Procedure that involves opening the trachea.
● Tracheostomy: Procedure that exteriorizes the trachea to the cervical skin, resulting in a
more permanent tracheal cutaneous fistula.
INDICATIONS
● Bypassing an upper airway obstruction
● Providing a means for assisting mechanical ventilation (ie, chronic ventilator dependence),
● Enabling pulmonary hygiene
● Temporarily securing an airway in patients undergoing major head and neck surgery
● Relieving obstructive sleep apnea
● Eliminating pulmonary “dead space.”
PROCEDURE
Most easily performed if the patient is already intubated and general anesthesia has been
administered
1. The patient is placed in the supine position with a shoulder roll to extend the neck.
a. If the patient is awake, he should be placed in a semi upright position
2. Landmarks are marked (the thyroid notch, the cricoid, the sternal notch, and planned incisions).
3. The neck and upper chest are then prepped and draped in a standard sterile fashion.
4. Before doing the incision, palpate the wound inferiorly to ensure that a high-riding
innominate artery is not present
5. A transverse skin incision approximately 2 fingerbreadths above the sternal notch or 1 cm
below the cricoid cartilage is made with a 15 blade.
6. The incision is infiltrated with local anesthesia containing epinephrine, to help decrease
bleeding.
90
EMERGENT TRACHEOTOMY
● It is best performed through a vertical incision, beginning at the level of the cricoid cartilage
and extending approximately 1.0-1.5 in
● The incision is made through skin, platysma, and subcutaneous tissues in one swift motion
● To incise the trachea where the 2nd and 3rd tracheal ring is estimated to be
● Once the airway is entered, the endotracheal tube is inserted into the trachea.
● A cricoid hook placed in the cricoid or first tracheal ring is used to retract the cricoid
superiorly and pull the trachea forward. This technique is particularly helpful in the patient
with an obese neck
● During the procedure, significant bleeding ignored until the airway is established
PEDIATRIC TRACHEOTOMY
● A simple vertical incision in the trachea is used
● Should be performed with a bronchoscope or endotracheal tube in place to secure the
airway
● Use nonabsorbable monofilament guide or stay sutures
● Emergent tracheotomy should be avoided (A Björk flap or the excision of tracheal rings)
PERCUTANEOUS TRACHEOTOMY
● Critically ill patient population
● Include transcutaneous entry with a needle into the trachea, guide wire passage into the
lumen and serial dilation
● A tracheotomy tube is then passed into the lumen: Blind entry
○ Use flexible bronchoscopic guidance to confirm entry into the trachea
● Advantages: Easy to perform, has a shorter operative time, ability to perform at bedside,
lower expense, lack of need to transport the patient to the OR
● Patients with obese necks also pose difficult candidates
AWAKE TRACHEOTOMY
● When can we do it?
○ In a stable patient with an obstructive supraglottic mass
○ The airway cannot be identified on flexible fiber optic laryngoscopy
● Indications:
○ Previously failed airway management
○ Maxillofacial trauma
○ Airway obstruction (oropharyngeal carcinoma, inflammation, or deep neck infection)
POSTOPERATIVE CARE
● Humidifying inspired air is necessary to prevent crusting and tracheitis
● Suctioning the tube and trachea: Clear secretions and prevent plugging
● Stay sutures and Björk flap sutures can be removed in approximately 3-5 days
○ Changing the tracheotomy tube
DECANNULATION
● The disease process that resulted in the need for a tracheotomy must be resolved
● Good airway patency allows for successful decannulation
● Patency can be evaluated
91
○ Mirror exam of the larynx

○ Direct fiberoptic endoscopy
● Practical approach is to change the tube to a smaller uncuffed tube.
COMPLICATIONS
EARLY DELAYED
● Infection ● Tracheal innominate artery fistula

● Hemorrhage ● Tracheal stenosis
● Subcutaneous emphysema ● Delayed tracheoesophageal fistula
● Pneumomediastinum ● Tracheocutaneous fistula
● Pneumothorax
● Tracheoesophageal fistula
● Recurrent laryngeal nerve injury
● Tube displacement
Cricothyroidotomy
Is the most emergent surgical airway. Performed more quickly and with less bleeding
PROCEDURE
1. The cricothyroid membrane is palpated between the laryngeal prominence and cricoid.
2. A transverse incision is made with a number 15 scalpel
3. Use a bougie to enter the trachea.
4. An endotracheal tube is advanced over the bougie
5. Tube placement is confirmed through positive ventilation and oxygenation markers.
COMPLICATIONS
● Stenosis
92

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OTORHINOLARYNGOLOGY

Denisse Alejandra Ochoa Orrico

Universidad Anáhuac Mayab

● Low octave frequencies: ​250 Hz-500 Hz

A.- AIR-CONDUCTION (AC) THRESHOLDS B.- BONE CONDUCTION (BC) THRESHOLDS

How is it performed? ​Using earphones. How is it performed? ​With a bone

HOW TO READ AN AUDIOGRAM

X-axis:​ Test frequency (Hz)

HEARING TYPE CLASSIFICATION

NORMAL- ≤ 25 dB HL ≤ 15 dB HL* ≤ 10 dB Not applicable

NORMAL- ≤ 25 dB HL ≤ 15 dB HL* > 10 dB Conductive**

CONDUCTIVE > 25 dB HL ≤ 15 dB HL* > 10 dB Conductive**

SENSORINEURAL > 25 dB HL > 15 dB HL ≤ 10 dB Sensorineural***

MIXED > 25 dB HL > 15 dB HL > 10 dB Sensorineural***

*Some clinicians use 25 dB HL

EXAMPLES OF ​CONDUCTIVE​ HEARING LOSS DISORDERS:

EXAMPLES OF ​SENSORINEURAL​ HEARING LOSS DISORDERS:

● Noise-induced hearing loss ● Genetic hearing loss (Connexin 26

HOW DO WE MEASURE THE MAGNITUDE OF HEARING LOSS?

Normal < 25 dB Hearing within normal limits

Moderate 41-55 dB Has significant difficulties with normal conversational level

Moderately 56-70 dB Difficulties understanding faint speech, speech at a distance,

Profound >90 dB Hears only loud environmental sounds, such as jackhammers,

THE BANANA OF THE SPEECH

B. SLOPING CONFIGURATION: ​(Audiogram A). ​Thresholds

C. RISING CONFIGURATION: ​(Audiogram B, white line).

D. HIGH-FREQUENCY HEARING LOSS CONFIGURATION:

E. LOW-FREQUENCY HEARING LOSS CONFIGURATION:

F. NOTCHED AUDIOMETRIC CONFIGURATION: ​(Audiogram D,

G. PEAKED AUDIOMETRIC CONFIGURATION: ​(Audiogram D,

H. TROUGH OR SAUCER AUDIOMETRIC CONFIGURATION:

I. INVERTED SAUCER OR INVERTED TROUGH

J. FRAGMENTARY OR CORNER AUDIOGRAM: ​(Audiogram F).

HIGH FREQUENCY AUDIOMETRY

FACTORS INFLUENCING AUDIOMETRIC INTERPRETATION

Reported in​ ​dB HL Reported in​ ​%.

*VALIDATION OF PURE-TONE AUDIOGRAM: ​SRT is ±12 dB than PTA.

WHEN TO DO MASKING?​ If:

Behavioral audiologic testing in pediatric population

B.- VISUAL REINFORCEMENT AUDIOMETRY (VRA)

C.- PLAY AUDIOMETRY

D.- SRT AND SUPRATHRESHOLD SPEECH RECOGNITION

HOW TO READ A TYMPANOGRAM

PEAK-COMPENSATED STATIC-ACOUSTIC ADMITTANCE

● 0.35-1.30 mmho:​ ​Normal

TYPE WHAT IT IS OBSERVED? WHAT DOES IT MEAN? PATHOLOGY

TYPE Normal TTP + normal Normal middle ear function None

TYPE Reduced peak height + Stiffening middle-ear pathology Otosclerosis

TYPE Higher peak height Increased admittance of sound Ossicular discontinuity

TYPE Flat tympanogram Stiffening middle-ear pathology or tympanic membrane

TYPE Significantly negative Eustachian-tube dysfunction

B.- ACOUSTIC REFLEX THRESHOLD (ART)

● Tensor tympani muscle

WHERE IS THE SOUND CONDUCTED THROUGH?

DISEASES OF REDUCTION OF ART.

ELECTRICALLY EVOKED STAPEDIUS REFLEX THRESHOLDS (ESRTS)

Pathology R​ ​CART L CART R IART L IART EXPLANATION

R conductive ↑ or ABS ABS ABS Normal Conductive pathology affects

L conductive ABS ↑ or ABS Normal ABS

● Low octave frequencies: 250 Hz-500 Hz

How is it performed? Using earphones. How is it performed? With a bone

X-axis: Test frequency (Hz)

EXAMPLES OF CONDUCTIVE HEARING LOSS DISORDERS:

EXAMPLES OF SENSORINEURAL HEARING LOSS DISORDERS:

B. SLOPING CONFIGURATION: (Audiogram A). Thresholds

C. RISING CONFIGURATION: (Audiogram B, white line).

F. NOTCHED AUDIOMETRIC CONFIGURATION: (Audiogram D,

G. PEAKED AUDIOMETRIC CONFIGURATION: (Audiogram D,

J. FRAGMENTARY OR CORNER AUDIOGRAM: (Audiogram F).

Reported in dB HL Reported in %.

*VALIDATION OF PURE-TONE AUDIOGRAM: SRT is ±12 dB than PTA.

WHEN TO DO MASKING? If:

● 0.35-1.30 mmho: Normal

Pathology R CART L CART R IART L IART EXPLANATION

B. Auditory neuropathy spectrum disorder (ANSD): Normal OAE + Abnormal ABR

Pathologies BPPV 1 min. Transient ischemic Perilymph fistula.

Always ask about precipitating factors:

● Head tilt: Is a sign of peripheral or central vestibular disease.

● Geotropic nystagmus: It is the side of lesion to which head movement

Origin: Ipsilateral saccule Origin: Contralateral utricle

Sensorineural hearing loss occurs when:

The cochlea contains (at birth):

70-80% autosomal-recessive: Onset in Usher syndrome: (most common) Retinitis

Alport syndrome: Renal disease + hearing loss