oto adult hearing loss Flashcards
Where is the site of damage in chronic noise-
induced SNHL?
Outer hair cells are damaged with chronic exposure to loud
noise. With brief exposure to extremely loud sound (e.g.,
explosions), the impulse can lead to trauma of the cochlear
membranes.
Describe the characteristic audiogram findings
with noise-induced hearing loss.
4-kHZ notch. Hearing loss is almost always bilateral and is
greater in the high frequencies compared with lower
frequencies.
Describe the Occupational Safety and Health
Administration (OSHA) sound level requirements.
If workplace noise levels are > 85 dB averaged over an 8-
hour period, a hearing-conservation program is required
with regular testing.
Permissible noise exposure levels are based on duration:
8 hours at 90 dB; 6 hours at 92 dB; 4 hours at 95 dB; 3 hours
at 97 dB; 2 hours at 100 dB; 1.5 hours at 102 dB; 1 hour at
105 dB; 0.5 hours at 110 dB; 0.25 hours at 115 dB
What is the definition of sudden sensorineural
hearing loss?
Greater than 30 dB loss over three contiguous pure-tone
frequencies occurring within a 3-day period
What percentage of patients with sudden SNHL can expect to experience some degree of spontaneous recovery?
Approximately two-thirds of patients
Describe the evaluation of sudden SNHL.
Patients should be evaluated for retrocochlear pathology
(MRI with gadolinium), but routine laboratory testing should
not be pursued unless there is clinical suspicion for an
underlying cause based on history or physical examination.
Review the treatment of idiopathic sudden SNHL.
Options include early oral corticosteroid treatment and
hyperbaric oxygen therapy within 3 months of diagnosis.
Intratympanic steroid perfusion is offered to patients with
incomplete recovery after initial therapy. Routine use of antivirals, thrombolytics, vasodilators, vasoactive substances, or antioxidants should be avoided.
What is the role of CT in evaluating patients with
sudden SNHL?
Generally, MRI is preferred over CT. Relative exceptions
include patients with focal neurologic findings, recent head
trauma, severe claustrophobia, or devices that preclude MRI
scanning (e.g., certain pacemakers).
What clinical variables are associated with a more
favorable prognosis after sudden SNHL?
Young age, less severe hearing loss, absence of dizziness,
low-frequency pattern of hearing loss, early treatment
Describe the diagnostic criteria for primary auto-
immune inner ear disease.
Characterized by progressive (over weeks to months)
bilateral SNHL loss that responds to immunosuppressive
treatment (steroids). Other causes of progressive SNHL
must be ruled out.
What is the first line of treatment for suspected
autoimmune inner ear disease?
High-dose corticosteroids with a prolonged taper
What is the 68-kD inner ear antigen?
About 20 to 80% of patients with autoimmune inner ear
disease will have a positive anti-68 kDa antibody test.
Describe the clinical manifestations of Susac syndrome.
An autoimmune small vessel disease characterized by the
triad of encephalopathy, branch retinal artery occlusions
and SNHL
Describe the clinical manifestations of Cogan syndrome.
A syndrome of nonsyphilitic interstitial keratitis and audio-
vestibular symptoms. Most patients have bilateral sudden progressive SNHL. Dizziness is typically episodic. Although
bilateral interstitial keratitis occurs, vision loss is rare. Systemic
manifestations commonly include headache and fever.
What are the potential routes of communication
that permit inner ear involvement in patients with
meningitis?
Cochlear aqueduct and modiolus
