Sudden Sensorineural Hearing LossMANAGEMENT

ENT AND MAXILLOFACIAL PRESENTATIONS · 12 SECTIONS

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641 items

☷ Legend

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Acute laryngitis Acute pharyngitis Auricular hematoma Bezold's Abscess Cerumen impaction Dry socket Ear foreign body Epistaxis (anterior)Epistaxis (Posterior)Labyrinthitis Ludwig's Angina Malignant Otitis Externa Marcus Gunn Pupil Mastoiditis Meniere's Disease Nasal Bone Fracture Nasal foreign body Nasal Septal Hematoma Otitis externa Otitis Media Post-tonsillectomy hemorrhage Sialolithiasis and sialadenitis Sinusitis Sudden Sensorineural Hearing Loss TMJ dislocation Tympanic membrane perforation Vestibular Neuronitis

Ophthalmologic Presentations19▾

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp44

Immediate priorities

›Otologic emergency recognition

›Definition: >=30 dB hearing loss across >=3 consecutive frequencies within 72 hours

›Unilateral in >95% of cases; bilateral raises concern for stroke or systemic disease

›Treatment window critical — initiate steroids within 3 days for best outcome

›Alarm features requiring immediate escalation

›Bilateral sudden hearing loss — rule out vertebrobasilar ischemia

›Focal neurologic deficits — facial droop, ataxia, diplopia, dysarthria

›Vertical or direction-changing nystagmus — central pathology until proven otherwise

›Severe vertigo with nystagmus suggesting posterior fossa stroke (AICA territory)

›Neurologic emergency exclusion

›Posterior fossa stroke assessment

›Finger-to-nose, gait, Romberg for cerebellar dysfunction

›Nystagmus pattern — direction-changing or down-beating indicates central etiology

›If stroke suspected, activate stroke protocol and obtain MRI DWI

›Cranial nerve survey

›CN VII — facial weakness suggests CPA lesion or brainstem pathology

›CN V — facial numbness

›CN VIII — auditory and vestibular function

›Airway, hemodynamics, and stabilization

›Vital signs including blood pressure and oxygen saturation

›Hypertension as vascular risk factor

›Fever suggesting infectious etiology

›If hemodynamically unstable with neurologic deficits, activate stroke team

›MRI brain with DWI as priority imaging

›Do not delay steroid treatment pending MRI if SSNHL isolated

Monitoring and targets

›Time-sensitive decision points

02History/hx73

Onset and character

›Temporal onset

›Exact time of onset — waking up with loss vs acute onset during activity

›Waking-up onset suggests nocturnal vascular or endolymphatic event

›Activity-associated onset raises barotrauma or perilymph fistula

›Progression pattern — static, fluctuating, or progressive

›Fluctuating low-frequency loss suggests Menière's disease

›Prior episodes of sudden hearing loss

›Recurrence raises concern for autoimmune inner ear disease or Menière's

›Laterality

›Unilateral vs bilateral

›Bilateral — warrants evaluation for vertebrobasilar ischemia, autoimmune disease, ototoxicity

›Affected side clarity

›Hum test — sound lateralizes away from SNHL ear

Aural symptoms

›Associated ear symptoms

›Aural fullness or blockage — most common presenting complaint

›Distinguish from middle ear effusion

›Tinnitus

›Character: ringing, roaring, pulsatile

›Pulsatile tinnitus suggests vascular lesion

›Hyperacusis

›Present in subset of SSNHL cases

›Otalgia or otorrhea

›If present, raises concern for otitis media or external otitis rather than SNHL

Vestibular symptoms

›Vertigo and imbalance

›Vertigo present in approximately 30–40% of SSNHL cases

›Concomitant vestibular syndrome predicts worse hearing recovery

›Dizziness character — true rotatory vertigo vs presyncope vs imbalance

›Rotatory vertigo with severe nausea — labyrinthine or central pathology

›Falls or gait instability

›Suggests significant vestibular involvement

Triggers and exposures

›Precipitating events

›Recent upper respiratory infection

›Viral etiology: HSV-1, EBV, CMV, mumps, COVID-19

›Barotrauma — diving, straining, Valsalva, air travel

›Raises concern for perilymphatic fistula

›Noise exposure — acute acoustic trauma or chronic occupational

›Head or ear trauma

›Ear surgery history

Neurologic review of systems

›Important neurologic symptoms

›Facial weakness or numbness

›Suggests CPA lesion or brainstem pathology

›Visual changes, diplopia

›Suggests vertebrobasilar or posterior fossa involvement

›Headache, ataxia, dysarthria

›Central alarm features — stroke workup warranted

›Limb weakness or numbness

›Suggest posterior circulation stroke

Systemic review of systems

›Constitutional and systemic symptoms

›Fever, weight loss, rash, joint pain

›Autoimmune or infectious systemic etiology

›Oral ulcers, dry eyes or mouth, Raynaud phenomenon

›Systemic autoimmune conditions: SLE, Sjögren, Behçet

›Prior stroke or TIA, cardiovascular disease

›Vascular etiology assessment

›Tick exposure (Lyme disease), sexual history (syphilis, HIV)

›Infectious etiology workup

Risk factors

›Vascular risk factors

›Hypertension, diabetes, hyperlipidemia, smoking, cardiovascular disease

›Retrospective cohorts show elevated stroke risk after SSNHL

›Suggests vascular involvement in subset of cases

›Ototoxic medication exposure

›Aminoglycosides (gentamicin, tobramycin)

›Cochlear and vestibular toxicity

›Cisplatin and carboplatin

›High-frequency hearing loss pattern

›High-dose salicylates

›Usually reversible

›Loop diuretics (furosemide), vancomycin, quinine

›Higher risk with combination use or renal impairment

›Autoimmune and hematologic risk

›Known autoimmune disease: SLE, RA, Behçet, scleroderma, antiphospholipid syndrome

›Hypercoagulable states: sickle cell disease, Waldenström macroglobulinemia

›Family history of autoimmune disease or neurofibromatosis type 2

03Physical Exam/exam47

Otoscopic examination

›External ear canal and tympanic membrane

›Cerumen impaction — must exclude conductive cause before diagnosing SNHL

›Clear canal if significant cerumen present prior to assessment

›Tympanic membrane integrity

›Perforation, effusion, retraction, cholesteatoma

›Middle ear landmarks

›Fluid level or air-fluid interface in middle ear suggests effusion

Tuning fork tests

›Weber and Rinne assessment

›Weber test (512 Hz placed on vertex or forehead)

›Lateralizes away from affected ear in SNHL

›Lateralizes toward affected ear in conductive hearing loss

›Rinne test (512 Hz)

›Air conduction greater than bone conduction bilaterally indicates SNHL

›Bone conduction greater than air conduction on affected side — conductive loss

Cranial nerve examination

›Focused cranial nerve survey

›CN VII — facial symmetry at rest and with movement

›Facial droop suggests CPA mass, Bell's palsy, or brainstem stroke

›CN V — facial sensation

›Numbness along trigeminal distribution — CPA pathology

›CN VIII — gross hearing comparison ear-to-ear

›Finger rub test or phone comparison

›CN IX and X — palate elevation, gag reflex

›Bulbar involvement suggests brainstem pathology

Cerebellar and vestibular examination

›Cerebellar function

04Differential Diagnosis/ddx66

Life-threatening and must-not-miss diagnoses

›Posterior fossa stroke

›AICA (anterior inferior cerebellar artery) territory infarct

›ICD-10: I63.5

›Presents with ipsilateral hearing loss, facial numbness, ipsilateral Horner

›Contralateral limb pain/temperature loss (crossed findings)

›Vertebrobasilar ischemia

›Bilateral hearing loss with brainstem symptoms

›NIHSS and stroke protocol activation

›Vestibular schwannoma (acoustic neuroma)

›ICD-10: D33.3

›Present in approximately 1–3% of SSNHL cases

›Most common intracranial neoplasm presenting as SSNHL

›Unilateral, progressive, or sudden onset

›MRI gadolinium enhancement is gold standard for detection

Inner ear disorders

›Menière's disease

›ICD-10: H81.0

›Fluctuating low-frequency SNHL with episodic vertigo, tinnitus, aural fullness

›Endolymphatic hydrops underlying mechanism

›Recurrent episodes distinguish from single-event SSNHL

›Autoimmune inner ear disease (AIED)

›ICD-10: H83.3

›Bilateral, rapidly progressive, steroid-responsive hearing loss

›Associated with systemic autoimmune conditions in subset

›Perilymphatic fistula

›ICD-10: H83.8

›History of barotrauma, straining, Valsalva, or ear surgery

05Laboratory Tests/lt35

Routine labs

›AAO-HNS guideline on routine labs

›Routine laboratory testing NOT recommended for uncomplicated unilateral SSNHL

›AAO-HNS Clinical Practice Guideline recommendation

›Low yield in isolated unilateral cases

›Glucose and HbA1c as pre-steroid baseline

›Relevant given risk of steroid-induced hyperglycemia

›Baseline HbA1c documents pre-existing diabetes

Directed infectious workup

›Serology for treatable infectious causes

›Syphilis serology — RPR with reflex VDRL/FTA-ABS

›Neurosyphilis a treatable reversible cause

›Relevant in high-prevalence populations or immunocompromised

›Lyme antibody titers (ELISA with reflex Western blot)

›In endemic areas with appropriate exposure history

›HIV testing

›Per local guidelines and risk factors

›Otologic manifestations can occur at any CD4 count

Directed autoimmune workup

›Autoimmune panel for bilateral or recurrent SSNHL

›ANA and anti-dsDNA

›Systemic lupus erythematosus evaluation

›ESR and CRP

›Nonspecific markers of systemic inflammation

›Antiphospholipid antibodies (APLA, anti-cardiolipin, lupus anticoagulant)

›Hypercoagulable state contributing to vascular etiology

›ANCA panel if vasculitis suspected

›Granulomatosis with polyangiitis can affect inner ear

06Diagnostic Tests/dt86

Scoring Systems

›Hearing loss severity classification (WHO/AAO-HNS)

›Normal: pure tone average 0–25 dB HL

›Clinical threshold: >=30 dB loss in >=3 consecutive frequencies for SSNHL diagnosis

›Mild: 26–40 dB HL

›Difficulty with soft speech

›Moderate: 41–60 dB HL

›Difficulty with conversational speech

›Severe: 61–80 dB HL

›Hearing aids required

›Profound: >80 dB HL

›Cochlear implant candidacy range

›Worst prognosis for spontaneous recovery

›Prognostic factors (poor recovery predictors)

›Profound initial hearing loss

›Strongest negative prognostic indicator

›Bilateral involvement

›Suggests systemic etiology with worse prognosis

›Delayed treatment initiation beyond 14 days

›Steroid efficacy diminishes substantially

›Concomitant vestibular symptoms (vertigo)

›Audiology & Neuro-Otology evidence: worse recovery

›Down-sloping audiometric configuration

›High-frequency loss more severe than low-frequency

MRI

›MRI internal auditory canals (IACs) with gadolinium

›Gold standard for retrocochlear pathology exclusion

›Recommended for all patients with confirmed SSNHL (AAO-HNS strong recommendation)

›Rate of pathogenic abnormalities: 4.4–13.75% of SSNHL cases

›Key targets on MRI IAC protocol

›Vestibular schwannoma — enhancing mass in IAC or CPA cistern

›Meningioma — dural-based enhancing lesion

›Labyrinthine enhancement — suggests cochlear inflammation or ischemia

›3D FLAIR sequences pre- and post-gadolinium

›Increases sensitivity for cochlear inflammation

›Detects endolymphatic hydrops in Menière's

›Timing of MRI

›Obtain within 30 days of onset per AAO-HNS

›Do not delay steroid treatment pending MRI if imaging not immediately available

›MRI brain with DWI if stroke suspected

›Diffusion-weighted imaging for acute ischemia

›Posterior fossa sensitivity — DWI may be falsely negative in first 24 hours

›Repeat MRI at 3–5 days if clinical suspicion persists despite negative initial DWI

›MR angiography of posterior circulation if vertebrobasilar disease suspected

›Vertebral artery dissection or stenosis

›CT temporal bone

›Indications for temporal bone CT

›MRI contraindicated (pacemaker, cochlear implant, severe claustrophobia)

›Conductive or mixed hearing loss on audiometry suggesting ossicular or bony pathology

›Suspected cholesteatoma or chronic otitis media with complications

›Findings on CT temporal bone

›Ossicular chain disruption

›Cochlear or semicircular canal anomalies (congenital SNHL)

›Tegmen or dehiscence abnormalities

›CT head (non-contrast)

›NOT recommended routinely for isolated SSNHL

›AAO-HNS Clinical Practice Guideline: insufficient evidence to support routine CT

›MRI superior for posterior fossa and IAC pathology

›Indicated if MRI unavailable and stroke is suspected

›To exclude hemorrhage before thrombolytics considered

Ultrasound

›Carotid and vertebral Doppler ultrasound

›Indications for vascular ultrasound

›Pulsatile tinnitus suggesting vascular lesion

›Significant cardiovascular risk factors with bilateral SSNHL

›Suspected vertebral artery dissection

›Findings

›Internal carotid artery stenosis or occlusion

›Vertebral artery flow abnormality

›Tympanometry (acoustic immittance)

›Type A tympanogram — normal middle ear compliance in SNHL

›Distinguishes SNHL from conductive hearing loss

›Type B tympanogram — flat curve suggests middle ear effusion

›Rules in conductive cause if present

›Type C tympanogram — negative middle ear pressure

›Eustachian tube dysfunction

›Pure tone audiometry (primary confirmatory test)

›Diagnostic criterion: >=30 dB loss in >=3 consecutive frequencies

›Ideally obtained within 14 days of symptom onset

›Air and bone conduction thresholds bilaterally

›Speech audiometry

›Word recognition score — poor score suggests retrocochlear pathology

›Rollover phenomenon associated with vestibular schwannoma

›Auditory brainstem response (ABR)

›Alternative if MRI contraindicated

›Detects retrocochlear pathology: prolonged I–V interwave latency

›Less sensitive than MRI for small vestibular schwannomas

›Useful for retrocochlear screening in cooperative patients

›Wave V absent or prolonged in retrocochlear lesions

07Disposition/dispo33

Discharge criteria

›Outpatient management criteria

›Unilateral SSNHL without neurologic deficits

›Hemodynamically stable, no alarm features

›No focal neurologic signs on examination

›Steroid prescription initiated in ED

›Oral prednisone 60 mg/day or 1 mg/kg/day

›Counseling on side effect monitoring

›Urgent ENT referral arranged within 1–3 days

›Intratympanic steroid consideration

›Audiology arranged for confirmatory testing

Admission indications

›Inpatient or observation admission criteria

›Bilateral sudden hearing loss

›Stroke protocol activation

›Systemic disease evaluation

›Focal neurologic deficits suggesting posterior fossa pathology

›Neurology consult

›MRI DWI priority imaging

›Inability to tolerate oral steroids (diabetes, active infection, psychiatric history)

›IV steroids or intratympanic steroids under ENT supervision

›Suspected meningitis or systemic infectious etiology

›Infectious disease consultation

›Severe systemic comorbidities requiring monitoring during steroid therapy

Follow-up requirements

›Outpatient follow-up planning

›ENT follow-up within 1–3 days for all SSNHL patients

›Intratympanic steroid evaluation

08Treatment/t69

Primary steroid therapy

›Oral systemic corticosteroids

›Prednisone oral 60 mg/day or 1 mg/kg/day (maximum 60 mg)

›Duration: 10–14 days with taper

›Taper over 5–7 days after full-dose course

›Initiate immediately when SSNHL suspected, before audiometry or MRI

›Evidence base for systemic steroids

›Current standard of care per AAO-HNS Clinical Practice Guideline

›Limited high-quality placebo-controlled RCT data

›Initiating within 3 days: OR 0.42 for incomplete recovery vs later treatment

›Steroid screening before initiation

›Glucose and HbA1c — diabetic patients at risk for hyperglycemia

›Blood pressure — uncontrolled hypertension may worsen

›Active infection — defer systemic steroids; consider intratympanic route

›Psychiatric history — steroid psychosis risk

›GI ulcer history — proton pump inhibitor co-prescription

Intratympanic steroid therapy

›Intratympanic corticosteroids

›Primary intratympanic therapy indications

›Systemic steroids contraindicated (uncontrolled diabetes, active infection, psychiatric illness)

›Patient preference for targeted therapy

›Dexamethasone intratympanic injection

›Concentration: 4–24 mg/mL; typically 10–24 mg/mL used

›Volume: 0.4–0.8 mL per injection

›Schedule: 3–4 injections over 7–14 days

›Methylprednisolone intratympanic injection

›Concentration: >=30 mg/mL as alternative

›Similar efficacy to dexamethasone in small trials

›Combined oral and intratympanic steroids

›May increase proportion achieving hearing improvement

›Evidence is low certainty (Cochrane review)

›Reasonable option particularly for severe or profound loss

Salvage therapy

›Intratympanic steroids for incomplete recovery

›Recommended by AAO-HNS for incomplete recovery at 2–6 weeks

›Dexamethasone 10–24 mg/mL intratympanic injection

›3–4 injections over 7–14 day course

›Timing of salvage therapy

›Efficacy diminishes if initiated beyond 18 days from onset

›Still reasonable to offer up to 2–3 months in selected patients

›Hyperbaric oxygen therapy (HBOT)

›Indications per AAO-HNS guideline

›Combined with steroids within 2 weeks as primary therapy (optional recommendation)

›Combined with salvage steroids within 1 month (optional recommendation)

›Mechanism

›Increases perilymph oxygen tension

›Theoretical benefit for cochlear ischemia etiology

›Logistics

›Typically 10–20 sessions at 2.0–2.4 atmospheres absolute

›Limited availability in most centers

Therapies not recommended

›Contraindicated or not recommended interventions

›Antiviral agents (e.g., acyclovir, valacyclovir)

›Not recommended by AAO-HNS — no proven benefit

›Do not add to steroid regimen routinely

›Thrombolytics

›Not recommended for idiopathic SSNHL

›Risk-benefit unfavorable without proven vascular cause

›Vasodilators and vasoactive substances

›Carbogen, papaverine, pentoxifylline — not recommended

›No evidence of benefit in controlled trials

›Anticoagulation

›Not routinely indicated for idiopathic SSNHL

›Consider if underlying hypercoagulable state identified

Audiologic rehabilitation

›Management of residual hearing loss

›Hearing aid evaluation for incomplete recovery

›Standard hearing aid for mild-to-moderate residual loss

›CROS (Contralateral Routing of Signal) device for unilateral profound loss

›Bone-anchored hearing aid (BAHA)

›Option for unilateral profound SNHL with normal contralateral ear

›Cochlear implant candidacy evaluation

›Profound unilateral or bilateral SNHL with poor word recognition

›Referral to cochlear implant center for evaluation

09Special Populations/sp49

Pregnancy

›Pregnancy-specific considerations

›SSNHL incidence in pregnancy

›Rare; exact incidence unknown in pregnancy

›Preeclampsia and hypercoagulable states may contribute to vascular etiology

›Steroid use in pregnancy

›Prednisone and prednisolone considered relatively safe in pregnancy

›Category C; benefit typically outweighs risk for acute SSNHL

›Intratympanic dexamethasone preferred if systemic steroids contraindicated

›Imaging in pregnancy

›MRI without gadolinium preferred in first trimester

›Gadolinium crosses placenta — avoid unless essential; use in second/third trimester if benefit outweighs risk

›CT head avoided due to ionizing radiation unless neurologic emergency

›Multidisciplinary approach

›Obstetrics and ENT co-management

›Preeclampsia and hypercoagulable workup if indicated

Geriatric

›Older adult-specific considerations

›Baseline presbycusis complication

›Pre-existing age-related high-frequency hearing loss may confound SSNHL diagnosis

›Prior audiogram helpful if available for comparison

›Vascular risk burden

›Higher prevalence of hypertension, diabetes, cardiovascular disease

›Vascular etiology more likely; stroke must be excluded vigilantly

›Steroid risks in older adults

›Increased risk of steroid-induced hyperglycemia

›Osteoporosis — consider calcium and vitamin D supplementation with steroid course

›Fluid retention and blood pressure exacerbation

10Background/b74

Epidemiology

›Incidence and prevalence

›Incidence: 5–20 per 100,000 per year

›Approximately 4,000 new cases annually in the United States

›Likely underestimated due to spontaneous recovery before diagnosis

›Age distribution

›Most common in adults aged 40–60 years (NEJM data)

›Can occur at any age including children and elderly

›Sex distribution

›Roughly equal male and female distribution

›Laterality

›Unilateral in approximately 95% of cases

›Bilateral SSNHL in approximately 2–4% — associated with worse prognosis

›Prognosis and recovery

›Spontaneous recovery rate

›One-third to two-thirds of patients achieve spontaneous recovery

›Most recovery occurs within first 2 weeks without treatment

›Identified cause found in only approximately 10% of cases

›Remainder classified as idiopathic SSNHL

›Treatment response

›Early steroid treatment (within 3 days): OR 0.42 for incomplete recovery vs delayed

›Treatment beyond 14 days shows substantially diminished efficacy

Pathophysiology

›Proposed mechanisms

›Viral etiology

›Presumed most common underlying cause in idiopathic SSNHL

›Direct viral invasion: HSV-1, EBV, CMV, mumps, COVID-19

›Viral-induced cochlear inflammation and hair cell injury

›Vascular etiology

›Cochlear blood supply: end-artery from labyrinthine artery (branch of AICA)

›Cochlea has no collateral circulation — highly vulnerable to ischemia

›Microvascular thrombosis, vasospasm, or thromboembolism

›Elevated stroke risk observed in retrospective cohorts after SSNHL

›Autoimmune etiology

›Autoimmune-mediated cochlear inflammation and inner ear damage

›Molecular mimicry following viral infection proposed

›Explains steroid responsiveness in subset of patients

›Endolymphatic hydrops

›Increased endolymph pressure within membranous labyrinth

›Overlaps with Menière's disease spectrum

›Anatomy relevant to pathophysiology

›Cochlear hair cells

›Outer hair cells most vulnerable to ischemia and ototoxic injury

›High metabolic demand and poor regenerative capacity in mammals

›Stria vascularis

›Maintains endocochlear potential — highly oxygen-sensitive

›Primary site of injury in ischemic and toxic SNHL

Therapeutic Considerations

›Steroid mechanism of action

›Anti-inflammatory effects

›Suppression of cochlear inflammation and edema

›Inhibition of pro-inflammatory cytokines (TNF-alpha, IL-1, IL-6)

›Vasoactive effects

›Improved cochlear microvascular perfusion

›Immunosuppressive effects

›Suppression of autoimmune-mediated cochlear injury

›Treatment timing evidence

›Otology & Neurotology evidence: steroid initiation within 3 days

›OR 0.42 for incomplete recovery vs later treatment

›Efficacy diminishes substantially beyond 14 days

›Intratympanic route advantages

›Achieves higher perilymph concentrations than systemic steroids

›Avoids systemic side effects

›Effective salvage option when systemic steroids contraindicated or failed

›Audiologic recovery trajectory

›Most spontaneous recovery occurs within 2 weeks

›Plateau of hearing threshold by 4–6 weeks

›Residual tinnitus common even with hearing recovery

›Management: sound therapy, cognitive behavioral therapy

›Vestibular dysfunction may persist

›Vestibular rehabilitation exercises

›Hyperbaric oxygen evidence

›AAO-HNS optional recommendation for combined HBOT plus steroids

›Within 2 weeks as primary therapy

›Within 1 month as salvage therapy

›Mechanism: raises perilymph oxygen partial pressure

›Theoretical benefit for ischemic etiology

11Patient Discharge Instructions/pdi34

copy discharge instructions

›Diagnosis explanation

›Sudden sensorineural hearing loss — sudden decrease in hearing in one or both ears

›Cause often not identified; treatment started to improve recovery chances

›One-third to two-thirds of people recover, often within 2 weeks

›Medication instructions

›Take prednisone exactly as prescribed — do not stop suddenly

›Take with food to reduce stomach upset

›Report blood sugar symptoms if diabetic: increased thirst, frequent urination

›Antacid or stomach acid medication may be prescribed with steroids

›Take as directed to protect stomach lining

›Follow-up appointments

›See ENT/ear specialist within 1–3 days — this is urgent

›Further ear injections with steroid medication may be recommended

›Hearing test (audiometry) should be completed within 2 weeks

›Repeat hearing test in 6 weeks to assess recovery

›If MRI not done in the emergency department, it will be arranged through specialist

›Activity and precautions

›Avoid loud noise exposure during recovery period

›Use hearing protection if noise exposure unavoidable

›Avoid diving, heavy straining, or Valsalva maneuvers

›Could worsen inner ear if perilymph fistula present

›Do not drive if experiencing significant dizziness or vertigo

›Notify employer if occupation requires binaural hearing

›Return to emergency department immediately if

›Facial drooping or weakness on either side

›Could indicate stroke

›New or worsening dizziness, loss of balance, or inability to walk

12References/r31

Guidelines and key sources

›AAO-HNS Clinical Practice Guideline: Sudden Hearing Loss

›American Academy of Otolaryngology — Head and Neck Surgery

›Strong recommendation: systemic steroids as primary treatment

›Strong recommendation: MRI IAC with gadolinium for all SSNHL

›Against routine antiviral, thrombolytic, or vasodilator use

›Optional recommendation: intratympanic steroids as primary or salvage

›NEJM review: Sudden Sensorineural Hearing Loss

›Definition: >=30 dB across >=3 consecutive frequencies within 72 hours

›Incidence 5–20 per 100,000/year; approximately 4,000 US cases annually

›Age peak 40–60 years

›Otology & Neurotology evidence on treatment timing

›Steroid initiation within 3 days: OR 0.42 for incomplete recovery

›Efficacy substantially diminished beyond 14 days from onset

›Cochrane review: steroids for sudden sensorineural hearing loss

›Combined oral and intratympanic may improve outcomes

›Low certainty evidence

›Audiology & Neuro-Otology: vestibular symptoms and prognosis

›Concomitant vestibular syndrome predicts worse hearing recovery

›Important counseling point for patients with vertigo at presentation

Landmark trials and guidelines

›Lancet: epidemiology, autoimmune and vascular etiologies

›Autoimmune inner ear disease — bilateral, steroid-responsive

›Associated systemic autoimmune conditions in subset

›Vascular risk factors associated with elevated stroke risk post-SSNHL

›Neurology: posterior fossa stroke and SSNHL overlap

›AICA territory infarct presenting as isolated sudden hearing loss

›High vigilance required for crossed neurologic findings

Learn More: Sudden Sensorineural Hearing Loss→

Comprehensive Clinical Review

Structured, evidence-informed, long-form analysis for deeper understanding.

Evidence & Review

Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

SymptomDx is an educational tool for medical professionals. It does not replace clinical judgment. Verify all clinical data and drug dosages with authoritative sources.