OTOLOGY SEMINAR
Anesthesia and Hearing Impairment
R3 蘇鉉釗
2003-9-3
Introduction
 Subclinical, unnoticed uless audiometry is performed
 Conductive or sensorineural, unilateral or bilateral, transient or permanent
Anesthesia and Hearing loss
Hearing loss and spinal anesthesia (SA)
Background and clinical presentations
 1914 Terrien: 1st case of hearing loss associated with SA reported in 1914
 1956 Vandam and Dripps: 0.4%, total 9,277 patients of SA had auditory
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complaints (hearing loss, tinnitus)
1990 Michel et al. : described 9 cases of hearing loss following myelography,
lumbar puncture, and SA, lower frequencies (125~1000 Hz), 6/9 full recovery in
one month without treatment
1990 Dreyer et al. : 16/100 after SA had audiometrically documented hearing
loss, 125~2000 Hz, detected on the 2nd day after SA, all resolved in 3 days
Incidence
 10~50% patients receiving SA had audimetrically measured low-frequency
SNHL
 Less than one forth of these patients have subjective hearing loss
Symptoms and Signs
 HL, tinnitus, usually masked by other unpleasant complications of dural puncture:
headache, nausea, vomiting
 Vertigo is less reported
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PTA: one or both ears, HL of 10~40 dB over low frequency, common below
1000 Hz
Factors associated HL
 Fog et al.: 22-gauge used SA had more significant HL of lower frequency than
26-gauge
 Oncel et al.: compared epidural anesthesia, SA (22G), SA (25G)  no HL in
epidural group, significant HL on 22G vs. 25G
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Sundberg et al.: compared the effect of 22G cutting-tip (Quincke) to pencil-point
(Whitacre)  24% in Quincke group vs 9% in Whitacre group (HL of 10dB
below 1000 Hz)
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Gultekin et al.: compare <30 y/o and >60 y/o, younger group had significant
lower frequency HL, 52% vs 16%
Mechanism
Intracochlear hydrodynamics: perilymph and endolymph
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1.
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Perilymph hydrostatic fluid pressure in guinea pig: 200 Pa (2cm H2O), slow
(<5Hz) respiratory and pulsatory oscillations, physiological variation: -100 to
+700 Pa
20% of contralateral HL after acoustic neuroma surgery  CSF leak may cause
HL
CSF pressure-mediated stretch or pressure injury to CN VIII ?
1991 Walsted : SA  CSF laek  decrease in CSF pressure  prompt
transmitted through a patient cochlear aqueduct  pressure change in perilymph
 pressure gradient of endolymph to perilymph  distortion of Reissner’s
membrane and basilar membrane
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The animals model of CSF loss showed a small increase in threshold and latency
of compound action potention
Lower frequency: basilar membrane over apex is more compliant, more sensitive
to pressure change  lower frequency loss (endolymphatic hydrop)
Vestibular is less sensitive to perilymph-endolymph pressure imbalance
Unilateral hearing loss: 7% anatomically obstructed aqueduct, 30% functionally
obstructed
Loss of perilymph induces compensatory expansion of the endolymphatic space:
perilymphatic fistula (spontaneous or traumatic) and intracranial hypotension
with a patent cochlear aqueduct
Treatment and Prognosis
 More than 95% fully recover of HL
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Position change form sitting to supine
Epidural blood patches, 10~20 ml patient’s own blood
Epidural dextran 40 infusion
Hearing loss and general anesthesia (GA)
 Rare for noncardiopulmonary bypass surgery
 35 reported case through 2001
 Nitrous oxide (N2O) used is the most documented etiology
Middle ear pressure and Nitrous oxide
 N2O was found to cause oscillation of middle ear pressure in 1960s  tympanic
perforation
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N2 O enters the air cavities faster than nitrogen can leave, 34-fold difference
between the blood/gas coefficients of the two gases (0.013 for nitrogen versus
0.46 for N2 O)
Middle ear pressure can reach 375 mm H2 O within 30 minutes of the start of
N2 O and negative ear pressure of -285 mm H2 O can occur within 75 minutes of
discontinuation of N2 O
Uptake or elimination phase of N2O  outward or inward displace of tympanic
membrane graft  failure of tympanoplasty
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Patency of E-tube play a role in potential injury
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Complication prevention: concentration < 50%, discontinue administration 15
minutes before closure of the middle ear
Excessive or sudden changes in middle ear pressure  disrupt tympanic
membrane, round window (perilymph fistula) and ossicular chain dislocated
Idiopathic SNHL happened in GA?
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Hearing loss and cardiopulmonary bypass (CPB)
 More frequently in CPB than other surgery in GA
 Arenberg et al. presented the 1st case in 1971
 Incidence of permanent HL: less than 0.1%, a review of 5975 cases of open hear
surgery  0.18% of sudden unilateral HL
Mechanism
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Emboli generated during CPB  inner ear is supplied by end aritery, no
collateral circulation
 Number of arterial microemboli is significant increased during
extracorporeal perfusion
 Emboli: air, fat, particulate matter from aortic plaque or calicified valve
Hypoperfusion and infraction of cochlea due to decrease perfusion pressure in
CPB and atherosclerosis of basilar artery system
N2O cause implosive force
Treatment and prognosis
 Poor prognosis, 26 patients had partial recovery, no complete recovery
 Multiple etiologies for HL after GA  no single treatment is applicable to every
case
Conclusion
Referrence:
Sprung J. et al. Perioperative Hearing Impairment, Anesthesiology, 98, 2003, p241-57
Broome I.J. Hearing loss and dural puncture, The Lancet, 341, 1993, 667-8
Bohmer A. Hydrostatic pressure in the inner ear fluid compartments and its effect on
inner ear function, Acta Otolaryngol Supp,. 507, 1993, 3~24
Evan K.E. et al Sudden sensorineural hearing loss after general anesthesia for
nonotologic surgery, Laryngoscope, 107, 1997, 747-52
Portier F et al. Spontaneous intracranial hypotension: a rare cause of labyrinthine
hydrops, Ann Otol Rhinol Laryngol 111, 2002, 817-20
Walsted A et al. Cerebrospinal fluid loss and threshold changes.
Electrocochleographic changes of the compound action potential after CSF aspiration:
an experimental study, Audiol Neurooto 5, 1996, 256-64
Miller: Anesthesia, 5th ed., 2000 Churchill Livingstone, Anesthesia for ear sugery,
p2193-4