How do I distinguish sensorineural hearing loss from wax or a fluid problem?

Otoscopy and two bedside tuning-fork tests reliably separate them. A 512 Hz Weber test (fork on vertex or mid-forehead) lateralises to the better ear in sensorineural loss, and to the worse ear in conductive loss. A Rinne test (mastoid then 1 cm from ear canal) is positive (air conduction greater than bone conduction) in sensorineural loss — the same as normal — and negative (bone greater than or equal to air) in conductive loss above 25 dB. A normal tympanic membrane on otoscopy with sudden unilateral hearing loss, Weber lateralising to the better ear, and positive Rinne: treat as sudden sensorineural hearing loss until audiometry confirms.

Does timing really matter — can I watch and wait for a few days?

Yes, timing matters substantially. The treatment window for oral corticosteroids is approximately 14 days from symptom onset, with better outcomes when treatment begins under 7 days. After 4 weeks, outcomes are largely fixed and intervention rarely changes the result. The biological rationale: outer hair cells become irreversibly apoptotic as cochlear inflammation progresses, and the steroid response depends on interrupting that process early. Each day of delay is a day of the treatment window that cannot be recovered. Do not adopt a 'wait and see' approach for sudden unilateral hearing loss — act on the day of presentation.

What is the treatment and how does it work?

First-line treatment is oral prednisolone 1 mg/kg/day (maximum 60 mg/day) for 10–14 days, then tapered over 5–7 days. The rationale: outer hair cells in the cochlea are steroid-responsive; high-dose glucocorticoids reduce cochlear inflammation, limit hair-cell apoptosis, and may address an autoimmune component in idiopathic cases. Co-prescribe a PPI if there are gastric risk factors. Warn patients about mood changes, insomnia, fluid retention, and glycaemic excursion in people with diabetes. Steroids are started by the GP and continued through the ENT review — they should not be deferred while waiting for specialist appointment.

Is the MRI scan really necessary if hearing has come back on its own?

Yes. The AAO-HNS 2019 clinical practice guideline gives MRI of the brain and internal auditory canals a strong recommendation regardless of recovery. The reason: approximately 5–10% of patients with unilateral sudden hearing loss harbour a vestibular schwannoma on imaging despite a completely normal neurological examination. A schwannoma missed because hearing recovered spontaneously is a vestibular schwannoma that continues to grow undetected. MRI with gadolinium is the only reliable method to exclude it. CT scanning does not identify schwannoma and should not be substituted.

What happens after the steroid course if hearing has not fully returned?

Intratympanic (IT) steroid injection is the standard salvage treatment. The ENT specialist injects dexamethasone or methylprednisolone through the tympanic membrane at 2–6 weeks after incomplete oral response — the HARLOR trial (Rauch JAMA 2011) and subsequent salvage RCTs demonstrate approximately 25% benefit in non-responders. If significant hearing loss persists at 4–6 weeks, repeat audiometry establishes the prognosis. Referral for a hearing-aid trial via the Hearing Services Program, or cochlear implant assessment for severe-profound or single-sided deafness causing significant disability, is the rehabilitation pathway.

Which other treatments are sometimes suggested for sudden hearing loss?

Hyperbaric oxygen therapy (HBOT) is a conditional option in the AAO-HNS 2019 guidelines when used within 3 months, with limited Australian access (RPA Sydney, Alfred Melbourne, Wesley Brisbane, Fiona Stanley Perth). It is not a replacement for the steroid pathway. Antivirals (aciclovir, valaciclovir) do not benefit idiopathic sudden sensorineural hearing loss — multiple RCTs are negative; AAO-HNS 2019 recommends against their use. The exception is Ramsay Hunt syndrome (VZV reactivation with ear vesicles and facial palsy), which is a separate entity and does require antivirals plus prednisolone. Vasodilators, vitamins, ginkgo biloba, and pentoxifylline are not recommended — evidence does not support them.

Sudden sensorineural hearing loss

Sudden hearing loss: treat early — the AU general practice approach

By Dr HB Lo, FACRRM Reviewed 20 September 2026 10 min read

Sudden sensorineural hearing loss — ≥30 dB across ≥3 frequencies within 72 hours — is an ENT emergency. Treatment window is roughly 14 days from onset.

Start oral prednisolone 1 mg/kg/day (maximum 60 mg) for 10–14 days, arrange same-day audiometry, and refer urgently to ENT. About one third recover fully, one third partially, and one third do not recover significant hearing.

MRI of internal auditory canals is mandatory even after recovery — 5–10% harbour a vestibular schwannoma undetectable on clinical examination.

Sudden hearing loss — acting inside the window

Sudden sensorineural hearing loss (SSNHL) is one of the more common otological emergencies encountered in Australian general practice. The condition has a time-sensitive treatment window. The first clinical encounter — typically with a GP or emergency department — is rate-limiting: prompt recognition, same-day audiometry, early steroids, and urgent ENT referral determine whether the patient has any chance of recovering useful hearing.

The working definition from AAO-HNS 2019 guidelines and Therapeutic Guidelines (eTG) is sensorineural hearing loss of ≥30 dB across ≥3 contiguous audiometric frequencies developing within 72 hours. Most cases (~95%) affect one ear. About 90% are idiopathic. Incidence is approximately 5–20 per 100,000 Australians per year — approximately 2,000–4,000 new cases annually — with a peak age of 50–60 years and no clear sex predominance.

The treatment window is approximately 14 days from symptom onset, ideally under 7 days. After 4 weeks, outcomes are largely fixed. About one third of patients recover fully, one third partially, and one third do not recover significant hearing. Acting early is the GP’s primary contribution to outcome.

A. Core clinical — the AU general-practice framework

Distinguishing sensorineural from conductive at the bedside

This single step determines the urgency of the response. Conductive hearing loss — from cerumen, acute otitis media, middle ear effusion, or tympanic membrane perforation — has a different clinical pathway. Sensorineural hearing loss with sudden onset demands immediate action.

At the bedside with a 512 Hz tuning fork:

Weber test — fork struck and placed on the vertex or mid-forehead. In sensorineural hearing loss, sound lateralises to the better (unaffected) ear. In conductive hearing loss, it lateralises to the worse (affected) ear. A central or unlateralised result indicates normal hearing or equal bilateral loss.
Rinne test — fork struck and placed first on the mastoid (bone conduction), then 1 cm in front of the ear canal (air conduction). In sensorineural hearing loss, air conduction is greater than bone conduction (positive Rinne) — the same result as normal hearing. In conductive hearing loss of more than 25 dB, bone conduction is greater than or equal to air conduction (negative Rinne).

Weber to the better ear, positive Rinne on the affected side, and a normal tympanic membrane on otoscopy = SSNHL until audiometry confirms. A normal TM with sudden unilateral hearing loss is SSNHL until proven otherwise.

History to take

Time course — exact onset (date and time), step-change vs gradual, fluctuation (fluctuating low-frequency loss with vertigo and aural fullness raises Ménière’s disease)
Associated features — tinnitus (~80% of SSNHL), vertigo or imbalance (~30%, predicts worse prognosis), aural fullness, otalgia, otorrhoea
Triggers — barotrauma (diving, air travel, Valsalva straining), head trauma, loud-noise exposure, recent upper respiratory tract infection
Systemic clues — fever, skin rash, joint pain (autoimmune inner-ear disease), neurological symptoms (cerebellar or brainstem features suggest vascular cause), recent herpes zoster (Ramsay Hunt), sexual history (syphilis/neurosyphilis), tick exposure or overseas travel (Lyme)
Medications — aminoglycosides, cisplatin, loop diuretics, high-dose NSAIDs or salicylates (all potentially ototoxic)
Past medical history — diabetes, hypertension, hyperlipidaemia, atrial fibrillation (vascular risk); autoimmune disease; prior ear surgery; occupational noise exposure

Examination

Otoscopy bilateral — exclude cerumen impaction, acute otitis media, middle ear effusion, tympanic membrane perforation, cholesteatoma, or vesicles in the external auditory canal (Ramsay Hunt syndrome)
Tuning fork tests (512 Hz) — Weber and Rinne as above
Cranial nerves — V (facial sensation; large schwannomas compress), VII (facial movement — Ramsay Hunt vesicles, schwannoma compression), VIII, cerebellar signs (dysmetria, gait — AICA territory infarct)
Vestibular — head impulse test, spontaneous or gaze-evoked nystagmus, Romberg, Dix-Hallpike if positional component
General — blood pressure, pulse rhythm (atrial fibrillation), skin (zoster, autoimmune rash)

Investigations

Audiogram — same day or next day (within 24–48 hours). Pure-tone audiometry, tympanometry, and speech audiometry confirm the diagnosis, quantify severity, and establish the baseline for monitoring treatment response. AAO-HNS 2019 and ASOHNS are explicit: audiometry cannot be deferred. Most metropolitan Australian audiology clinics will accommodate urgent SSNHL appointments within 24–48 hours when contacted by phone with a GP referral.

MRI brain with internal auditory canals (gadolinium-enhanced) — mandatory. AAO-HNS 2019 gives this a strong recommendation: MRI is required even if hearing recovers fully, because approximately 5–10% of patients with unilateral sudden hearing loss harbour a vestibular schwannoma on imaging despite a normal neurological examination. MRI cannot be substituted by ABR or CT in current practice.

Targeted blood tests. Syphilis serology (RPR) is recommended routinely — inexpensive and the condition is treatable. Beyond that: FBC, ESR/CRP (autoimmune/infective), fasting glucose/HbA1c (vascular risk), and ANA/ANCA if features suggest autoimmune inner-ear disease. AAO-HNS 2019 explicitly recommends against routine broad blood-panel ordering in idiopathic SSNHL.

Management

The management sequence follows eTG, AAO-HNS 2019, ASOHNS, and RACGP:

Step 1 — Confirm sensorineural loss. Otoscopy (exclude conductive cause), tuning forks, same-day or next-day audiogram.

Step 2 — Start oral corticosteroids within the 14-day window. Do not defer steroids while awaiting the audiogram or ENT appointment:

Prednisolone 1 mg/kg/day (maximum 60 mg/day) orally for 10–14 days, then taper over 5–7 days (e.g. 60 → 40 → 20 → 10 mg → stop)
Co-prescribe gastroprotection (PPI) if risk factors are present
Counsel regarding common side effects: mood disturbance, fluid retention, insomnia, glycaemic excursion in people with diabetes

When systemic steroids are relatively contraindicated (poorly controlled diabetes, active peptic ulcer, glaucoma, severe psychiatric illness, untreated tuberculosis), intratympanic steroid administered by the ENT specialist is the first-line alternative — not withholding treatment.

Step 3 — Urgent ENT referral. Same day where possible; within 72 hours at most. Phone referral with a brief clinical summary and audiogram result is appropriate given the urgency. Steroids started by the GP proceed in parallel with — not waiting for — the ENT review.

Step 4 — Organise MRI (internal auditory canals with gadolinium). Most ENT specialists will request this at first review; a GP can also initiate an urgent radiology referral with appropriate indication.

B. Treatment evidence — steroids, intratympanic, and what does not work

Oral steroids — standard of care on conditional evidence. The primary RCT, Wilson Arch Otolaryngol 1980, was small. The Wei Cochrane 2013 review concluded that evidence remains unclear. The AAO-HNS 2019 recommendation is a conditional option, not a strong one. Despite this, oral steroids within the treatment window represent the clinical standard: a blinded placebo-controlled trial withholding treatment from a patient with reversible hearing loss is no longer ethically feasible, the biological rationale (outer hair cell steroid-responsiveness, cochlear anti-inflammatory effect) is sound, and the risk-benefit calculation strongly favours a 10–14 day course.

Intratympanic (IT) steroid. Dexamethasone 24 mg/mL or methylprednisolone 40 mg/mL injected through the tympanic membrane by the ENT specialist is equivalent to oral steroids as primary therapy — demonstrated in the landmark HARLOR trial (Rauch JAMA 2011), which showed non-inferiority of IT vs oral steroid for idiopathic SSNHL. As salvage at 2–6 weeks after incomplete oral response, IT steroid demonstrates approximately 25% benefit in non-responders across multiple RCTs, and is now an AAO-HNS 2019 recommendation rather than an optional adjunct.

Antivirals — not recommended for idiopathic SSNHL. Multiple RCTs have shown no benefit from aciclovir or valaciclovir in idiopathic SSNHL. AAO-HNS 2019 recommends against their use. Important exception: Ramsay Hunt syndrome (VZV reactivation with auricular vesicles, facial palsy, and hearing loss or vertigo) is a distinct entity — treat with valaciclovir plus prednisolone. Any patient with ear vesicles or concurrent facial palsy needs Ramsay Hunt workup rather than the idiopathic SSNHL pathway alone.

What to avoid. Vasodilators, pentoxifylline, vitamins, ginkgo biloba, and antioxidants as primary treatments are not recommended — the evidence does not support them (Reisser 2001; AAO-HNS 2019). Routine CT scanning does not identify schwannoma, delays MRI, and is explicitly not recommended by AAO-HNS 2019.

Hyperbaric oxygen therapy (HBOT). A conditional option in AAO-HNS 2019 guidelines when used within 3 months of onset, with limited evidence per the Bennett Cochrane 2012 review. Australian access is limited to a small number of metropolitan hyperbaric centres. HBOT should never replace the steroid pathway and is never sole therapy.

C. The Australian access pathway — audiology, ENT, and rehabilitation

Getting the audiogram. Phone audiology clinics directly, explaining the presentation and specifying suspected SSNHL — most clinics will prioritise this given the time window. In rural and remote areas, urgent audiometry may require referral to the nearest regional hospital audiology service or public ENT clinic.

ENT referral. Phone referral with a verbal summary is appropriate given urgency. Most Australian public hospital ENT departments maintain access pathways for urgent SSNHL. Most private ENT specialists will accommodate an appointment within the week when SSNHL is the indication.

MRI. Gadolinium-enhanced MRI of the brain and internal auditory canals is arranged with radiology, citing AAO-HNS 2019 strong recommendation as the indication. The medico-legal standing of this recommendation supports urgent scheduling.

Post-treatment audiology. Repeat audiogram at 10–14 days assesses treatment response. If significant hearing loss persists at 4–6 weeks, referral for hearing-aid trial or cochlear implant assessment is appropriate.

Hearing Services Program. Eligible adults (Australian citizen or permanent resident with a pension card, DVA Gold or White card, Centrelink Sickness Allowance, ADF membership, NDIS participation, or ATSI aged 50+) can access subsidised hearing aids and audiological rehabilitation via Hearing Australia and licensed providers under the Hearing Services Program.

D. Australian operations

MBS items. GP consults: 23 / 36 / 44. Complex / extended consults: 132 / 133. Audiometry: 11324 (post-2023 audiology restructure). Tympanometry: 11332. MRI brain and internal auditory canals (specialist-requested, ENT/neurology indication): 63007. Syphilis serology (RPR): 69384. ENT specialist consultation: 104 / 105. Chronic-disease management for persistent hearing loss with comorbidity: GPMP 965 / 967. Mental Health Care Plan for tinnitus distress or adjustment disorder: 2715 / 2717.

PBS items. Prednisolone tablets (25 mg, 5 mg, 1 mg) are on the PBS General Schedule (unrestricted). Intratympanic dexamethasone is typically prepared by hospital or compounding pharmacy and is not on the PBS as an intratympanic preparation — cost is usually bundled with the ENT procedural charge. Valaciclovir and aciclovir are PBS-listed, relevant only for confirmed Ramsay Hunt syndrome.

Medico-legal context. Missed SSNHL within the treatment window is the dominant medico-legal risk in this area. A “wait and see — probably wax” disposition for a patient with same-day onset unilateral hearing loss, normal otoscopy, and Weber lateralising to the better ear is indefensible. Document at every step: time of symptom onset, audiogram timing, date treatment commenced, MRI referral date, and ENT referral pathway.

E. Special populations

Elderly and frail. Steroid side effects (fluid retention, hyperglycaemia, delirium in cognitively impaired patients, osteoporosis acceleration) carry greater weight. Intratympanic steroid avoids systemic exposure and is an appropriate first-line choice for frail or multimorbid patients — arrange urgent ENT review specifically for this purpose.

ATSI patients. Standard access pathway with additional support for audiology access in rural and remote settings. ATSI patients aged 50+ are eligible for the Hearing Services Program. Indigenous-specific hearing loss from otitis media with effusion in childhood is a distinct entity — ensure clear distinction from acute SSNHL before initiating the emergency pathway.

Bilateral simultaneous SSNHL. Rare. Prompt workup for autoimmune inner-ear disease (ANA, ANCA, complement, immunology referral), ototoxic cause, paraneoplastic syndrome, haematological cause, and syphilis. Treat as urgent ENT referral with same-day steroid commencement.

Ramsay Hunt syndrome. VZV reactivation presenting as auricular vesicles, facial palsy, and hearing loss or vertigo. Treatment is valaciclovir (or aciclovir) plus prednisolone — not the idiopathic SSNHL protocol. Any patient with ear vesicles or concurrent facial palsy needs assessment for Ramsay Hunt before initiating the SSNHL pathway.

Children. Rare in paediatric practice but warrants the same urgency of audiogram and ENT referral. Congenital causes, genetic syndromes, and infectious causes should be considered alongside idiopathic SSNHL.

When to escalate

Urgent ENT referral (same day) — confirmed or strongly suspected SSNHL for intratympanic steroid if systemic steroid is contraindicated, and to coordinate MRI and audiogram follow-up
Emergency department — SSNHL with concurrent neurological signs (cerebellar ataxia, brainstem features, sudden severe headache, new facial palsy without preceding vesicles, inability to stand or walk) — posterior fossa stroke or AICA territory infarct must be excluded urgently
Cochlear implant centre — bilateral severe-profound persistent hearing loss, or unilateral severe-profound loss with significant functional disability
Mental health / MHCP — adjustment disorder, depression, anxiety, or tinnitus distress post-loss (see MHCP items 2715/2717)

What this article is and is not

This is general health information drawn from current Australian and international ENT guidelines — Therapeutic Guidelines, RACGP, ASOHNS, AAO-HNS 2019, and Cochrane evidence — for educational purposes. It is not personal medical advice and does not create a doctor–patient relationship. Individual management decisions — including steroid dosing, referral urgency, and audiological rehabilitation — are made with your own GP, ENT specialist, and treating team.

Consumer resources: HealthDirect — Hearing loss · Hearing Australia · ASOHNS — Patient information · Tinnitus Australia.

Sources cited

Frequently asked questions

How do I distinguish sensorineural hearing loss from wax or a fluid problem?

Otoscopy and two bedside tuning-fork tests reliably separate them. A 512 Hz Weber test (fork on vertex or mid-forehead) lateralises to the better ear in sensorineural loss, and to the worse ear in conductive loss. A Rinne test (mastoid then 1 cm from ear canal) is positive (air conduction greater than bone conduction) in sensorineural loss — the same as normal — and negative (bone greater than or equal to air) in conductive loss above 25 dB. A normal tympanic membrane on otoscopy with sudden unilateral hearing loss, Weber lateralising to the better ear, and positive Rinne: treat as sudden sensorineural hearing loss until audiometry confirms.
Does timing really matter — can I watch and wait for a few days?

Yes, timing matters substantially. The treatment window for oral corticosteroids is approximately 14 days from symptom onset, with better outcomes when treatment begins under 7 days. After 4 weeks, outcomes are largely fixed and intervention rarely changes the result. The biological rationale: outer hair cells become irreversibly apoptotic as cochlear inflammation progresses, and the steroid response depends on interrupting that process early. Each day of delay is a day of the treatment window that cannot be recovered. Do not adopt a 'wait and see' approach for sudden unilateral hearing loss — act on the day of presentation.
What is the treatment and how does it work?

First-line treatment is oral prednisolone 1 mg/kg/day (maximum 60 mg/day) for 10–14 days, then tapered over 5–7 days. The rationale: outer hair cells in the cochlea are steroid-responsive; high-dose glucocorticoids reduce cochlear inflammation, limit hair-cell apoptosis, and may address an autoimmune component in idiopathic cases. Co-prescribe a PPI if there are gastric risk factors. Warn patients about mood changes, insomnia, fluid retention, and glycaemic excursion in people with diabetes. Steroids are started by the GP and continued through the ENT review — they should not be deferred while waiting for specialist appointment.
Is the MRI scan really necessary if hearing has come back on its own?

Yes. The AAO-HNS 2019 clinical practice guideline gives MRI of the brain and internal auditory canals a strong recommendation regardless of recovery. The reason: approximately 5–10% of patients with unilateral sudden hearing loss harbour a vestibular schwannoma on imaging despite a completely normal neurological examination. A schwannoma missed because hearing recovered spontaneously is a vestibular schwannoma that continues to grow undetected. MRI with gadolinium is the only reliable method to exclude it. CT scanning does not identify schwannoma and should not be substituted.
What happens after the steroid course if hearing has not fully returned?

Intratympanic (IT) steroid injection is the standard salvage treatment. The ENT specialist injects dexamethasone or methylprednisolone through the tympanic membrane at 2–6 weeks after incomplete oral response — the HARLOR trial (Rauch JAMA 2011) and subsequent salvage RCTs demonstrate approximately 25% benefit in non-responders. If significant hearing loss persists at 4–6 weeks, repeat audiometry establishes the prognosis. Referral for a hearing-aid trial via the Hearing Services Program, or cochlear implant assessment for severe-profound or single-sided deafness causing significant disability, is the rehabilitation pathway.
Which other treatments are sometimes suggested for sudden hearing loss?

Hyperbaric oxygen therapy (HBOT) is a conditional option in the AAO-HNS 2019 guidelines when used within 3 months, with limited Australian access (RPA Sydney, Alfred Melbourne, Wesley Brisbane, Fiona Stanley Perth). It is not a replacement for the steroid pathway. Antivirals (aciclovir, valaciclovir) do not benefit idiopathic sudden sensorineural hearing loss — multiple RCTs are negative; AAO-HNS 2019 recommends against their use. The exception is Ramsay Hunt syndrome (VZV reactivation with ear vesicles and facial palsy), which is a separate entity and does require antivirals plus prednisolone. Vasodilators, vitamins, ginkgo biloba, and pentoxifylline are not recommended — evidence does not support them.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.