sudden deafness final

8/3/2019 Sudden Deafness Final

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Sudden Deafness


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Definition

30 decibel (dB) loss over threecontiguous frequencies occurringwithin 3 days

Abrupt and rapidly progressivelosses

Awakening with it in the morningor developing a progressive lossover 12 hours or less


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Epidemiology

Incidence: 5 to 20

cases /100.000

Male = Female

More on left ear???

Bilateral loss: 1%

- 2% Age at

presentation: 40-

54 years


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Etiology

Defined Cause

Idiopathic: >>>


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Defined Cause of SSNHL


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Idiopathic SSNHL

Viral infection

Vascular compromise

Intracochlear membrane rupture Immune inner ear disease


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Viral infection

History of recent viral infection

28% report a viral-like upperrespiratory infection within 1

month Recent viral seroconversion

Increased viral titers

Pathologic changes: Loss of hair cells, supporting cells,

atrophy of the tectorial membrane,atrophy of the stria vascularis, and

neuronal loss


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Viral infection can be implicated

as a cause of ISSHL, but it cannot

as yet be proved

Mumps, Arenavirus, Measles,

Rubella, Herpes Zoster oticus,

Mononucleosis


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Vascular Compromise

AICA

No collateralvasculature

Cochlearfunction:sensitive tochanges in blood

supply Thrombosis,

Embolus,Reduced blood

flow, Vasospasm


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Intracochlear Membrane

Rupture

Rupture of intracochlear

membranes would allow mixing of

perilymph and endolymph,

effectively altering theendocochlear potential


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Immune inner ear disease

Progressive hearing loss

Cogan's syndrome, SLE, Temporal

arteritis, Polyarteritis nodosa


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Diagnosis

History

Onset, time course, associated

symptoms

Risk factor, past medical history

Medication

PE

Complete H & N examination

Pneumaotoscopy: find for fistula

sign


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Diagnosis 2

Ancillary Procedure

Audiometric testing (PTA, Speech

Audiometry, OAE, ABR,

Tympanometry)

VNG (if vestibular symptoms and/or

signs are present)

Lab Imaging study

MRI with contrast (Acoustic Neuroma)

CT Scan (Mondini, LVA)


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Diagnosis 3

Imaging study

MRI with contrast

(Acoustic

Neuroma)

CT Scan (Mondini,

LVA)


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Lab Test


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Treatment

90% of cases will be Idiopathic

Treat known causes by

addressing the underlying

condition


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Treatment

Therapy for ISSNHL is

controversial

Difficult to study

High spontaneous recovery rate

Low incidence

Makes validation of empiric

treatment modalities difficult


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Treatment

Vasodilators

Rheologic agents

Antiinflammatory agents Antiviral agents

Diuretics

Triiodobenzoic acid derivatives Surgery


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Vasodilators

Improve blood supply to cochlea

Reversing hypoxia

Histamine, Nicotinic acid,Papaverine, Procaine, Niacin

Carbogen inhalation(5% carbon

dioxide and 95% oxygen)


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Rheologic Agents

Altering blood viscosity to

improve blood flow and oxygen

delivery

LMW Dextrans, Pentoxifylline

Heparin, Warfarin

Dextrans

hyper-volemic hemodilution and

affect Factor VIII


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Antiinflammatory Agents

Corticosteroids

The mechanism of action of

corticosteroids is unknown

Reduction of cochlea and auditory

nerve inflammation is the

presumed pathway


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Antiviral Agents

Acyclovir, Amantadine,

Famciclovir, Valacyclovir

Viral etiology


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Diuretics

Cochlear endolymphatic hydrops

The mechanism of action is not

understood.


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Triiodobenzoic Acid

Derivatives

Diatrizoate meglumine

(angiographic contrast agent)

Affect the stria vascularis and

assist in maintaining the

endocochlear potential


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Surgery

Repair of oval and round window

perilymph fistulae


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Results

Recovery rates: 47% - 63% Mattox & Simmons

complete recovery: PTA < 10 dB orequaling the uninvolved ear

good recovery: PTA < 40 dB or > 50 dBimprovement from the initial audiogram

Wilson complete recovery: Recovery to within 10

dB of the prehearing loss speech receptionthreshold (SRT) or PTA

Partial recovery was defined as recovery towithin 50% of the prehearing loss SRT orPTA


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Evidence Based 1

Vasodilator:

Several studies using vasodilator

therapy as a component of treatment

failed to show significant differencesfrom placebo

Based on controlled studies, littledata support vasodilator therapy


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Evidence Based 2

Rheologic agents

LMW dextrans or Pentoxifylline did

not demonstrate recovery rates

better than placebo


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Evidence Based 3

Steroid

61% (oral steroids) vs 32% (placebo)

Transtympanic steroid: high delivery

concentration to the inner ear andlow systemic concentrations

Differences in delivery technique,

corticosteroid, dose, and dosing

schedule, direct comparisons are

difficult

large, randomizied, prospective, blinded

study is warranted for this treatment


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Evidence Based 4

Antiviral

Multicenter, randomized, prospective,

double-blind trial comparing prednisolone

against prednisolone and acyclovir did not

show a significant beneficial effect ofacyclovir - Stokroos 98

No significant benefit from the addition of

valacyclovir to concurrent oral prednisonetherapy in a larger multicenter,

randomized, prospective trial - Tucci 2002


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Evidence Based 5

Triiodobenzoic acid derivatives

No significant difference in recovery

using diatrizoate in a multidrug

regimen, compared withspontaneous recovery rates

Wilkins 87


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Evidence Based 5

Repair of perilymphatic fistulae

A universal standard for positive

identification of a fistula has not

been achieved Without uniform standards, outcomes

of surgical repair are difficult to

compare


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Prognostic factor

Wilson (1980)

Vertigo not statistically significant

Age less than 40 years favorable for

recovery Type of audiogram

Midfrequency loss with best recovery

Profound loss less likely to have recovery

Loss between 40 dB 85 dB more likely torespond to steroid therapy


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Wilson (1980)


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Cinamon (2001)

Low frequency loss improved more

High frequency loss improved less

Patients without vertigo have better

outcome


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Four prognostic variables

Time since onset

Audiogram type

Vertigo

Age

sudden deafness final

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