Complete ENT (Otorhinolaryngology) question bank — ear, nose, throat, larynx, airway & head-neck — in explanation-first exam-topper style, with 72 diagrams.
12chapters144questions77High-Yield
THE CONCEPT
Hearing loss is classified by where in the hearing pathway the lesion lies: a conductive loss impairs the conduction of sound through the outer and middle ear; a sensorineural loss lies in the cochlea (the 'sensory' hair cells) or the auditory nerve/central pathway (the 'neural' part); and a mixed loss combines both. This distinction is fundamental — it determines the likely cause, the tests needed and the treatment.
Where the lesion lies: conductive vs sensorineural
Pinna /ear canal
Tympanicmembrane
Ossicles(middle ear)
Cochlea(hair cells)
VIIInerve
Brain
CONDUCTIVE
SENSORINEURAL
wax, perforation, OME, otosclerosis (treatable)
presbycusis, noise, ototoxicity, Meniere's, neuroma
Locating the lesion: a conductive loss lies in the sound-conducting apparatus of the outer and middle ear (canal, drum, ossicles), whereas a sensorineural loss lies in the cochlea (hair cells) or the eighth nerve and central pathway.
CONDUCTIVE HEARING LOSS (CHL)
Here the cochlea and nerve are normal, but sound cannot reach them. Causes are found along the conducting apparatus: in the external ear (wax, foreign body, otitis externa, canal atresia); the tympanic membrane (perforation, retraction); and the middle ear (ASOM/CSOM, OME/glue ear, ossicular fixation or discontinuity, otosclerosis, tympanosclerosis, cholesteatoma). A conductive loss is usually moderate (a maximum of about 60 dB), the patient often hears better in noisy surroundings (paracusis willisii), and it is frequently treatable/reversible.
SENSORINEURAL HEARING LOSS (SNHL)
Here the fault is in the cochlea (sensory) or the nerve/central pathway (neural). Cochlear causes include presbycusis, noise-induced loss, ototoxicity, Meniere's disease, sudden SNHL and infections (mumps, measles, meningitis, congenital rubella/CMV); retrocochlear causes include acoustic neuroma (vestibular schwannoma) and multiple sclerosis. SNHL can be severe or profound, with poor speech discrimination, recruitment (in cochlear lesions) and tinnitus, and is usually irreversible — so management centres on rehabilitation (hearing aid/implant).
A COMPARISON
Feature
Conductive
Sensorineural
Site
Outer/middle ear
Cochlea/nerve
Rinne
Negative (BC>AC)
Positive (AC>BC)
Weber
To worse ear
To better ear
Severity
≤~60 dB
Up to profound
Discrimination
Good
Often poor
Reversible?
Often
Usually not
💡
CLINICAL PEARL: Deafness is conductive (outer/middle ear — wax, perforation, OME, otosclerosis; treatable, ≤~60 dB, paracusis willisii), sensorineural (cochlea/nerve — presbycusis, noise, ototoxicity, Meniere's, acoustic neuroma; often severe and irreversible → rehabilitation), or mixed. Locate the lesion with tuning-fork tests plus audiometry; the type dictates the cause and the treatment.
WHY THE DISTINCTION MATTERS SO MUCH
The reason the conductive–sensorineural distinction is drilled so hard is that it completely changes the clinical pathway. A conductive loss points to a mechanical, usually treatable problem in the outer or middle ear — wax that can be syringed, an effusion that can be drained, a perforation or ossicular problem that can be repaired, otosclerosis that can be operated on — so identifying it opens the door to a cure. A sensorineural loss points to damage in the cochlea or nerve, which is usually permanent, so the emphasis shifts to finding any treatable cause (a sudden loss to steroid-treat, a drug to stop, a neuroma to image) and otherwise to rehabilitation with aids or implants. Establishing the type at the very first assessment therefore tells the clinician whether to think 'what can I fix?' or 'what caused this and how do I rehabilitate it?' — which is why every hearing assessment begins here.
A NOTE ON MIXED HEARING LOSS
Mixed hearing loss deserves separate mention because it is common and easily under-treated. It arises when a conductive and a sensorineural component coexist in the same ear — for example, chronic suppurative otitis media that has both damaged the ossicles (conductive) and, over years, harmed the cochlea (sensorineural), or otosclerosis that has spread to involve the cochlea (cochlear otosclerosis). On the audiogram it shows as both air and bone thresholds reduced but with an air-bone gap remaining. Its importance is that the conductive part may be surgically correctable even though the sensorineural part is not, so treating the conductive component (or fitting an aid that addresses both) can still meaningfully improve hearing — the loss should not be dismissed as 'just sensorineural and untreatable'.
💊
KEY POINTS / NUMBERS (viva)
Conductive loss (outer/middle ear): wax/foreign body/otitis externa, TM perforation/retraction, ASOM/CSOM/OME, ossicular fixation/discontinuity, otosclerosis, cholesteatoma; ≤~60 dB, paracusis willisii, often treatable.
Sensorineural loss (cochlea/nerve): presbycusis, noise, ototoxicity, Meniere's, sudden SNHL, infections, congenital (TORCH/genetic); retrocochlear — acoustic neuroma, MS; up to profound, poor discrimination, tinnitus, recruitment, usually irreversible.
Mixed = both. Rinne negative + Weber to worse ear = conductive; Rinne positive + Weber to better ear = SNHL.
🔑
KEY POINTS TO REMEMBER
Classify hearing loss by site: conductive (outer/middle ear), sensorineural (cochlea/nerve), or mixed.
Conductive: Rinne negative, Weber to worse ear, air-bone gap; sensorineural: Rinne positive, Weber to better ear, no gap.
Type dictates cause and treatment — confirm with tuning-fork tests + pure-tone audiometry.
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
Tuning-fork tests are simple bedside tests that differentiate conductive from sensorineural hearing loss by comparing air conduction (AC) with bone conduction (BC). A 512 Hz fork is used (a 256 Hz fork gives too much tactile vibration, and a 1024 Hz fork decays too quickly).
Rinne (AC vs BC)
BC (mastoid)
AC (ear)
Normal/SNHL: AC>BC (Rinne +)
Conductive: BC>AC (Rinne −)
Weber (midline)
Conductive → lateralises to WORSE ear
SNHL → lateralises to BETTER ear
Use a 512 Hz fork · mask in severe unilateral SNHL (false-negative Rinne)
The tuning-fork tests. Rinne compares air conduction (fork at the ear) with bone conduction (fork on the mastoid) in the same ear: air normally beats bone (Rinne positive); bone beating air (Rinne negative) means a conductive loss. Weber (fork on the midline) lateralises to the worse ear in conductive loss and to the better ear in sensorineural loss.
RINNE TEST
The Rinne compares AC (fork held near the ear canal) with BC (fork on the mastoid) in the same ear:
Rinne positive (AC > BC) — normal hearing OR a sensorineural loss.
Rinne negative (BC > AC) — a conductive loss in that ear (indicating an air-bone gap).
False-negative Rinne — in a severe unilateral SNHL, the sound crosses to the opposite (better) cochlea by bone, so BC seems greater than AC; the other ear must be masked.
WEBER TEST
The fork is placed on the vertex or forehead in the midline and the patient says where the sound is heard (lateralisation):
Central (no lateralisation) — normal, or a symmetrical loss.
Lateralises to the WORSE ear — a conductive loss (that ear, shielded from ambient noise, hears bone-conducted sound better).
Lateralises to the BETTER ear — a sensorineural loss (the good cochlea hears it).
OTHER TESTS
The Absolute Bone Conduction (ABC) test compares the patient's BC with the examiner's (normal) BC — reduced in SNHL. The Schwabach test compares the duration of BC — shortened in SNHL and lengthened in conductive loss.
💡
CLINICAL PEARL: Tuning-fork tests (a 512 Hz fork) separate conductive from sensorineural loss. Rinne: AC > BC (positive) = normal/SNHL; BC > AC (negative) = conductive. Weber: lateralises to the worse ear = conductive; to the better ear = SNHL. ABC/Schwabach are reduced/shortened in SNHL. Beware a false-negative Rinne in severe unilateral SNHL — mask the other ear.
WHY A 512 Hz FORK, AND HOW TO INTERPRET TOGETHER
It is worth understanding both the choice of fork and how the tests combine. A 512 Hz fork is the standard because lower-frequency forks (256 Hz) produce a strong tactile vibration the patient may feel rather than hear (giving false results), while higher-frequency forks (1024 Hz) decay too quickly to compare air and bone reliably — 512 Hz is the practical compromise of adequate duration with minimal tactile artefact. The real power comes from reading Rinne and Weber together: a negative Rinne in one ear with the Weber lateralising to that same ear confirms a conductive loss there, whereas a positive Rinne bilaterally with the Weber lateralising away from the affected ear indicates a sensorineural loss. Combining the two tests cross-checks the result and guards against the traps (like the false-negative Rinne) that either test alone can fall into.
THE IMPORTANCE OF THE FALSE-NEGATIVE RINNE
The false-negative Rinne is a classic pitfall worth emphasising because it can completely mislead. In a patient with a severe or 'dead' sensorineural loss in one ear, when the fork is placed on that ear's mastoid the sound is conducted through the skull and picked up by the opposite, healthy cochlea — so the patient reports hearing bone conduction 'better than' air conduction in the bad ear, giving a Rinne that looks negative (suggesting a conductive loss) when the ear is in fact profoundly sensorineural. The give-away is that the Weber lateralises to the good ear, the opposite of a true conductive loss. The way to expose it is to mask the non-test (good) ear with noise, after which the true (positive/absent) response emerges. Recognising this trap prevents a profoundly deaf ear being mislabelled as a correctable conductive one.
💊
KEY POINTS / NUMBERS (viva)
Use a 512 Hz fork (256 Hz — too much vibration; 1024 Hz — decays fast).
Rinne (AC vs BC, same ear): positive AC>BC = normal/SNHL; negative BC>AC = conductive loss; false-negative in severe unilateral SNHL (mask other ear).
Weber (midline): lateralises to WORSE ear = conductive; to BETTER ear = SNHL; central = normal/symmetrical. ABC reduced in SNHL; Schwabach shortened in SNHL, lengthened in conductive.
🔑
KEY POINTS TO REMEMBER
Tuning-fork tests (512 Hz) differentiate conductive from sensorineural loss by comparing air (AC) and bone (BC) conduction.
Weber (midline): lateralises to the WORSE ear = conductive; to the BETTER ear = sensorineural.
ABC (vs examiner's BC) reduced in SNHL; Schwabach shortened in SNHL, lengthened in conductive loss.
False-negative Rinne in severe unilateral SNHL (sound crosses to the better cochlea) — mask the non-test ear.
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Pure-tone audiometry (PTA) is the standard test that quantifies hearing thresholds across frequencies for both air and bone conduction, plotting the results on an audiogram. It measures the type and degree of hearing loss. (It is subjective — it needs the patient's response — but standardised.)
Conductive020406080100air-bone GAP (bone normal)Sensorineural020406080100air = bone, NO gapred ○ = air conduction · grey = bone conduction · y-axis dB HL (0 = top)x-axis 250–8000 HzAudiogram patterns. In a conductive loss the bone line stays near normal while the air line drops, leaving an air–bone gap. In a sensorineural loss the air and bone lines fall together with no gap.
METHOD
In a soundproof room, pure tones at different frequencies (250–8000 Hz) are presented at varying intensities and the threshold (softest level heard) is found for each frequency. Air conduction (via headphones) tests the whole pathway (outer, middle and inner ear), while bone conduction (via a vibrator on the mastoid) bypasses the outer/middle ear to test the cochlea and nerve directly. The non-test ear is masked when necessary.
INTERPRETING THE AUDIOGRAM
The audiogram plots frequency on the x-axis and hearing level in dB on the y-axis (0 at the top, increasing downward). The key concept is the air-bone gap (the difference between the air and bone thresholds):
Conductive loss — bone conduction is normal but air conduction is reduced, so there is an air-bone gap.
Sensorineural loss — air and bone are both reduced together, with no gap.
Mixed loss — both are reduced and there is a gap.
DEGREE OF LOSS & USES
The degree (in dB HL) is graded: normal ≤25, mild 26–40, moderate 41–55, moderately severe 56–70, severe 71–90 and profound >90. PTA is used to define the type and degree of loss, monitor progression, assess candidacy for hearing aids/implants, and for medicolegal purposes (e.g. noise-induced loss).
💡
CLINICAL PEARL: PTA measures hearing thresholds for air (whole pathway) and bone (cochlea/nerve) conduction across 250–8000 Hz, plotting an audiogram (dB HL, 0 at top). Conductive = bone normal, air reduced → air-bone gap; sensorineural = air and bone both reduced, no gap; mixed = both reduced + a gap. Degrees: mild 26–40, moderate 41–55, severe 71–90, profound >90 dB.
WHY BONE CONDUCTION IS THE KEY MEASUREMENT
The single most informative element of the audiogram is the bone-conduction threshold, and understanding why makes interpretation straightforward. Because the bone vibrator drives the cochlea directly, bypassing the outer and middle ear entirely, the bone-conduction threshold reflects the pure state of the cochlea and nerve — the 'sensorineural reserve'. The air-conduction threshold, by contrast, measures the whole pathway. So the gap between them (the air-bone gap) isolates exactly how much of the loss is due to the conducting mechanism: if bone is normal but air is depressed, the entire loss is conductive; if bone is depressed and air matches it, the loss is entirely sensorineural; if bone is depressed and air is worse still, the loss is mixed. Reading the bone line first, then measuring the gap, is the disciplined way to interpret any audiogram.
THE ROLE OF MASKING
A technical but important point is the need for masking, without which an audiogram can be badly misleading. Because a loud enough sound presented to one ear can cross the skull and be heard by the opposite cochlea (especially via bone conduction), testing a poorer ear may record a threshold that actually belongs to the better ear — a 'shadow' curve. To prevent this, a masking noise is delivered to the non-test ear to keep it 'busy' while the test ear is measured, so that the threshold obtained genuinely reflects the ear under test. Proper masking is essential whenever the two ears differ substantially, and its omission is a common cause of erroneous audiograms — which is why it is a routine part of good audiometric technique.
💊
KEY POINTS / NUMBERS (viva)
PTA: pure tones 250–8000 Hz in a soundproof room; threshold = softest level heard. Air conduction (headphones) = whole pathway; bone conduction (mastoid vibrator) = cochlea/nerve; mask the non-test ear.
Air-bone gap: conductive = bone normal + air down (gap); sensorineural = air = bone (no gap); mixed = both down + gap.
Degree (dB HL): normal ≤25, mild 26–40, moderate 41–55, moderately severe 56–70, severe 71–90, profound >90.
🔑
KEY POINTS TO REMEMBER
PTA quantifies air- and bone-conduction thresholds across 250–8000 Hz, plotted on an audiogram (dB HL, 0 at top).
Air conduction (headphones) tests the whole pathway; bone conduction (mastoid vibrator) tests the cochlea/nerve directly; mask the non-test ear.
Conductive: bone normal, air reduced → air-bone gap; sensorineural: air = bone, no gap; mixed: both reduced + gap.
Degree: normal ≤25, mild 26–40, moderate 41–55, moderately severe 56–70, severe 71–90, profound >90 dB.
Uses: type/degree of loss, monitoring, hearing-aid/implant candidacy, medicolegal (noise-induced loss).
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Sensorineural hearing loss (SNHL) results from damage to the cochlear hair cells (sensory) or the auditory nerve/pathway (neural). It is usually irreversible, so management centres on identifying any treatable cause and on rehabilitation.
Presbycusis020406080100high-frequency down-slopeNoise-induced0204060801004 kHz notch (recovers at 8 kHz)both are sensorineural, bilateral & symmetrical (dB HL vs 250–8000 Hz)Two classic sensorineural patterns: presbycusis gives a bilateral high-frequency down-sloping loss, while noise-induced loss produces a characteristic notch at 4 kHz that recovers at 8 kHz.
CAUSES
Congenital causes include genetic disorders (syndromic and non-syndromic), congenital infections (TORCH — rubella, CMV), birth hypoxia, kernicterus and prematurity. Acquired causes include:
Presbycusis — age-related, the commonest (bilateral, symmetrical, high-frequency).
Infections — mumps, measles, meningitis, syphilis; Meniere's disease (low-frequency fluctuating loss with vertigo); sudden SNHL (an emergency).
Acoustic neuroma — a unilateral, progressive loss with tinnitus and poor discrimination (retrocochlear).
FEATURES & INVESTIGATION
Features are hearing loss (which may be profound), poor speech discrimination (especially in retrocochlear/central lesions), tinnitus, recruitment (an abnormal growth of loudness in cochlear lesions) and no air-bone gap. Investigation includes PTA, speech audiometry, tympanometry, BERA/OAE, and MRI for any unilateral/asymmetric loss (to exclude an acoustic neuroma).
MANAGEMENT
Management is to treat any reversible cause (steroids for sudden SNHL; stop ototoxic drugs), avoid noise, and rehabilitate — with hearing aids (moderate–severe loss), a cochlear implant (severe–profound loss) and auditory training, supported by newborn/genetic screening.
💡
CLINICAL PEARL: SNHL = damage to the cochlear hair cells (sensory) or auditory nerve (neural); usually irreversible. Causes: presbycusis (commonest), noise (4 kHz notch), ototoxicity, congenital (TORCH/genetic), Meniere's, sudden SNHL, acoustic neuroma (unilateral → MRI). It gives poor discrimination, tinnitus, recruitment and no air-bone gap. Manage by treating reversible causes (sudden SNHL = steroids) and rehabilitation (hearing aid/cochlear implant).
WHY DISCRIMINATION AND RECRUITMENT MATTER
Two features of sensorineural loss — poor speech discrimination and recruitment — deserve emphasis because they explain the patient's real-world difficulty and help localise the lesion. Recruitment is an abnormally rapid growth of loudness found in cochlear (hair-cell) lesions: soft sounds are inaudible, yet once sounds become audible they quickly seem uncomfortably loud, which is why simply turning up the volume (or a hearing aid) can be unpleasant. Speech discrimination — the ability to understand words even when they are loud enough — is disproportionately poor in retrocochlear (nerve) lesions such as an acoustic neuroma, where the patient may hear that speech is present but cannot make out the words. So a loss with recruitment suggests a cochlear problem, whereas a loss with strikingly poor discrimination out of proportion to the pure-tone loss suggests a nerve lesion and prompts MRI.
THE UNILATERAL LOSS THAT MUST BE IMAGED
A rule worth stressing is that an asymmetric or unilateral sensorineural loss must be investigated with MRI to exclude an acoustic neuroma (vestibular schwannoma). Most sensorineural loss (presbycusis, noise, ototoxicity) is bilateral and symmetrical, so a loss that is clearly worse in one ear — particularly with unilateral tinnitus and disproportionately poor speech discrimination — is a red flag for a retrocochlear tumour on that side. Although benign and slow-growing, an acoustic neuroma can enlarge to threaten the facial nerve, brainstem and life, and is far easier to manage when small. This is why the finding of an unexplained one-sided sensorineural loss is not simply rehabilitated with a hearing aid but is first imaged — a key safety principle in audiology.
A NOTE ON WHAT IS ACTUALLY TREATABLE
Although sensorineural loss is 'usually irreversible', it is a mistake to regard it as always untreatable, and picking out the reversible or specifically-treatable causes is the most important immediate task. A sudden sensorineural loss may recover with prompt corticosteroids; an ototoxic drug can be stopped before more damage accrues; Meniere's disease has its own medical management; and a retrocochlear tumour needs identification and treatment in its own right. Only after these have been considered does the loss become a matter for rehabilitation. This is why the assessment of every sensorineural loss actively asks 'is any part of this treatable or reversible?' — checking the speed of onset, drug history, symmetry and associated symptoms — before settling on hearing aids or an implant, so that a recoverable ear is not simply written off.
💊
KEY POINTS / NUMBERS (viva)
SNHL = cochlear hair-cell (sensory) or nerve (neural) damage; usually irreversible; no air-bone gap; recruitment (cochlear), poor discrimination (retrocochlear).
SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
For hearing loss that cannot be cured — especially sensorineural loss — rehabilitation restores useful hearing, either by amplifying sound (hearing aids) or, for severe–profound loss, by directly stimulating the cochlear nerve (a cochlear implant), together with auditory-verbal training.
HEARING AIDS
A hearing aid amplifies sound: its microphone picks up sound, an amplifier boosts it, and a receiver (speaker) delivers it to the ear. Types include behind-the-ear (BTE), in-the-ear (ITE), in-the-canal (ITC/CIC) and body-worn aids, and bone-conduction/bone-anchored aids (BAHA) for conductive/mixed loss or single-sided deafness. They are indicated for mild-to-severe loss with residual hearing (especially SNHL where medical/surgical cure is not possible, and for conductive loss when surgery is declined).
Cochlear implant
processor
coil
receiver
electrode → cochlea
Sound → processor → coil → receiver → electrode stimulates the cochlear nerve (bypasses hair cells)
A cochlear implant bypasses the damaged cochlear hair cells: an external microphone and speech processor send the signal across the skin via a coil to an implanted receiver, whose electrode array in the cochlea directly stimulates the cochlear nerve.
COCHLEAR IMPLANTS
A cochlear implant is for severe-to-profound SNHL that does not benefit from hearing aids. It bypasses the damaged hair cells and directly stimulates the cochlear nerve fibres via an electrode array in the cochlea. It has an external part (microphone, speech processor and transmitter coil) and an internal part (a receiver-stimulator and the electrode array). The best results come from pre-lingually deaf children implanted early (before the critical language period, ideally under 2–3 years) and post-lingually deafened adults, always with auditory-verbal rehabilitation.
OTHER MEASURES
Additional options are the bone-anchored hearing aid (BAHA), auditory brainstem implant (when the nerve is absent), and non-device measures — auditory training, lip-reading, sign language and special education.
💡
CLINICAL PEARL: Rehabilitation of irreversible deafness = hearing aids (amplify sound; BTE/ITE/canal; for residual hearing) or a cochlear implant (severe–profound SNHL not helped by aids — it bypasses the hair cells, its electrode stimulating the cochlear nerve; external processor + internal receiver/electrode). Implant deaf children early (under 2–3 years) for language, with auditory-verbal training. Use a BAHA for conductive/single-sided loss.
WHY EARLY IMPLANTATION MATTERS IN CHILDREN
A point worth emphasising in rehabilitation is the critical importance of timing in a deaf child. The developing brain has a critical period for acquiring spoken language, during which the auditory pathways must receive sound to develop normally; if a profoundly deaf child is not given access to sound within the first few years, the capacity to develop speech and language through hearing is progressively and permanently lost. This is why a cochlear implant gives its best results when placed early — ideally under the age of two to three — in a pre-lingually deaf child, and why universal newborn hearing screening exists: to identify these children in time to intervene. In post-lingually deafened adults, who already have language, implantation can be very successful at any age, but in children the window is time-limited — making early diagnosis and early implantation, backed by intensive auditory-verbal therapy, one of the highest priorities in paediatric otology.
A NOTE ON CHOOSING AID VERSUS IMPLANT
A practical principle in rehabilitation is that the choice between a hearing aid and a cochlear implant depends on how much usable hearing remains. A hearing aid simply amplifies sound, so it works only when there are enough surviving cochlear hair cells to respond to that amplified sound — it is the right choice across mild, moderate and many severe losses. When the loss becomes severe-to-profound and even powerful amplification no longer yields useful speech understanding, amplification has nothing left to work with, and the patient crosses the threshold to needing a cochlear implant, which bypasses the failed hair cells altogether and stimulates the nerve directly. Deciding between them therefore rests on a careful assessment of aided performance (especially speech discrimination), not on the pure-tone loss alone — an aid is tried and its benefit measured, and an implant is offered when the aid can no longer deliver useful hearing.
💊
KEY POINTS / NUMBERS (viva)
Hearing aid = amplifies (microphone → amplifier → receiver); types BTE/ITE/ITC-CIC/body-worn; BAHA (bone-anchored) for conductive/mixed/single-sided; for mild–severe loss with residual hearing.
Cochlear implant = for severe–profound SNHL not helped by aids; bypasses hair cells, electrode stimulates cochlear nerve; external (mic + processor + coil) + internal (receiver-stimulator + electrode array).
Best results: pre-lingual children implanted EARLY (<2–3 y, before critical language period) + post-lingual adults; needs auditory-verbal rehabilitation. Also BAHA, auditory brainstem implant, lip-reading/sign language/special education.
🔑
KEY POINTS TO REMEMBER
Rehabilitation restores useful hearing when a cure isn't possible (especially SNHL): hearing aids or cochlear implants + auditory training.
Hearing aids amplify sound (mic → amplifier → receiver); BTE/ITE/ITC-CIC/body-worn; BAHA for conductive/mixed/single-sided; for residual hearing.
Cochlear implant: for severe–profound SNHL not helped by aids; bypasses hair cells, electrode stimulates the cochlear nerve.
Implant children early (<2–3 y, before the critical language period); add auditory-verbal rehabilitation; consider BAHA/brainstem implant/sign language.
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat; Scott-Brown's Otorhinolaryngology.
THE CONCEPT
Impedance audiometry is an objective test of middle-ear function that measures how the tympanic membrane and middle ear reflect sound (their compliance/admittance) as the ear-canal pressure is varied. It has two parts — tympanometry (a compliance-versus-pressure curve) and the acoustic reflex — and needs no voluntary response from the patient.
Tympanometry curves
0−400+200 daPa
compliance
A (normal, peak at 0)
B (flat → OME/fluid)
C(neg.)
A normal · B flat (middle-ear fluid/perforation) · C negative peak (Eustachian dysfunction)
Tympanometry curves: type A (a normal peak at zero pressure), type B (flat — middle-ear fluid or a perforation), and type C (the peak shifted to negative pressure — Eustachian-tube dysfunction/retraction).
TYMPANOGRAM TYPES (Jerger)
Type A — a normal peak at 0 daPa (normal middle ear); variants As (shallow — otosclerosis/fixation) and Ad (deep — ossicular discontinuity/flaccid drum).
Type B — a flat curve with no peak (middle-ear fluid/OME, or a perforation — with a high canal volume).
Type C — the peak shifted to negative pressure (Eustachian-tube dysfunction/retraction).
ACOUSTIC REFLEX & USES
The acoustic (stapedial) reflex is absent in ossicular fixation, severe SNHL and facial-nerve lesions, and helps localise the problem. Impedance audiometry is used to diagnose OME (type B) — especially in children — Eustachian-tube dysfunction (type C) and ossicular problems; it is objective, quick and needs no patient response.
A NOTE ON ITS VALUE IN CHILDREN
Impedance audiometry is especially valuable in young children, in whom it is often difficult to obtain reliable behavioural responses. Because it is objective, quick and painless and needs no cooperation, a flat type-B tympanogram provides strong, reproducible evidence of a middle-ear effusion (glue ear) — the commonest cause of childhood hearing loss — and a type-C curve documents the Eustachian-tube dysfunction that so often precedes it. This makes tympanometry a mainstay in the assessment and monitoring of paediatric ear disease, both to confirm the diagnosis and to decide when watchful waiting has failed and intervention (such as grommets) is warranted.
THE BOTTOM LINE
Impedance audiometry objectively assesses the middle ear — a flat type-B tympanogram indicates fluid (glue ear), a type-C curve indicates Eustachian-tube dysfunction — making it invaluable, especially in children.
A further practical point is that impedance audiometry complements the pure-tone audiogram rather than replacing it: the audiogram tells you how much hearing is lost and of what type, while tympanometry tells you the state of the middle ear that may be causing a conductive component — so together they build a complete picture, for example confirming that a conductive loss on the audiogram is due to a type-B effusion rather than an ossicular problem.
🔑
KEY POINTS TO REMEMBER
Impedance audiometry = objective test of middle-ear function (compliance vs ear-canal pressure) + acoustic reflex; no voluntary response needed.
Type A: normal peak at 0 (As shallow — otosclerosis; Ad deep — ossicular discontinuity).
Type B: flat — middle-ear fluid (OME) or perforation (high volume); Type C: negative-pressure peak — Eustachian-tube dysfunction/retraction.
Acoustic reflex absent in ossicular fixation, severe SNHL, facial-nerve lesions; used to diagnose OME (esp children), ET dysfunction, ossicular problems.
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Presbycusis is age-related sensorineural hearing loss — the commonest cause of hearing loss in the elderly — arising from degeneration of the cochlea (and the central auditory pathway) with ageing.
FEATURES
It is bilateral, symmetrical and gradual, affecting the high frequencies first (a down-sloping audiogram). There is difficulty hearing in noisy places and understanding speech (especially consonants) — the classic 'I hear but I don't understand' — often with tinnitus and recruitment.
TYPES & MANAGEMENT
Schuknecht described types by the site of degeneration: sensory (hair-cell loss), neural (spiral-ganglion-cell loss), strial/metabolic (stria vascularis) and cochlear conductive (basilar-membrane stiffening). There is no cure (it is irreversible); management is hearing aids (the mainstay), auditory rehabilitation and communication strategies, with a cochlear implant if the loss is severe and aids are inadequate.
A NOTE ON THE COMMUNICATION DIFFICULTY
The most disabling feature of presbycusis is not the loss of volume but the disproportionate difficulty understanding speech, especially in background noise. Because the high frequencies carry the consonant sounds that distinguish words, their early loss means the patient hears that someone is speaking but cannot make out what is said — the classic complaint of 'I can hear but I can't understand', worst in noisy places like restaurants and family gatherings. Appreciating this explains why simply speaking louder does not help, why the condition causes such social withdrawal and isolation in the elderly, and why rehabilitation focuses as much on communication strategies and well-fitted, noise-managing hearing aids as on amplification alone.
THE BOTTOM LINE
Presbycusis is the common, irreversible, high-frequency sensorineural loss of ageing whose main handicap is poor speech understanding in noise, managed with hearing aids and communication strategies.
It is also worth noting that presbycusis is frequently compounded by other age-related factors — impacted wax, coexisting noise damage, ototoxic medication and cognitive decline — so a full assessment looks for these treatable contributors, since removing wax or optimising a hearing aid can make a real difference even when the underlying age-related loss cannot be reversed.
In practical terms, presbycusis is usually managed in primary and community ENT settings by well-fitted hearing aids and simple communication advice — facing the person, reducing background noise, speaking clearly rather than loudly — and the earlier a patient accepts amplification, the better they adapt, which is why unaddressed age-related hearing loss (with its link to isolation and cognitive decline) is increasingly treated as something to correct proactively rather than tolerate.
🔑
KEY POINTS TO REMEMBER
Presbycusis = age-related SNHL; commonest cause of hearing loss in the elderly (cochlear + central degeneration).
Bilateral, symmetrical, gradual, high-frequency first (down-sloping audiogram); poor speech understanding in noise ('hear but don't understand'), tinnitus, recruitment.
Irreversible; manage with hearing aids (mainstay) + rehabilitation/communication strategies; cochlear implant if severe and aids inadequate.
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Noise-induced hearing loss (NIHL) is sensorineural hearing loss from prolonged exposure to loud noise (occupational — industry — or recreational), which damages the cochlear outer hair cells, especially at the basal turn.
FEATURES
It is bilateral, symmetrical and gradual, with a classic notch at 4000 Hz on the audiogram (a dip at 4 kHz with recovery at 8 kHz) that later spreads. A temporary threshold shift (which recovers) progresses to a permanent threshold shift, and tinnitus is common.
PREVENTION & MANAGEMENT
A NOTE ON WHY PREVENTION IS EVERYTHING
Because noise-induced hearing loss is entirely preventable yet completely irreversible once established, the whole clinical emphasis falls on prevention. Once the outer hair cells are destroyed they do not regenerate, so no treatment restores the lost hearing — which makes protecting the ear before damage occurs the only effective strategy. In practice this means identifying hazardous noise, engineering it down at source, limiting exposure time, enforcing hearing protection, and screening exposed workers with regular audiometry to catch an early 4 kHz notch before it spreads into the speech frequencies. Its predictable, dose-related nature is also why it carries such medicolegal weight, with occupational-health programmes and compensation schemes built around these preventive measures.
THE BOTTOM LINE
Noise-induced hearing loss is a preventable but irreversible sensorineural loss with a classic 4 kHz notch, making protection and audiometric monitoring of exposed workers the central strategy.
A further point is that the 4 kHz notch is so characteristic that it is used both diagnostically and medicolegally: because it reflects the frequency at which the cochlea is most vulnerable to noise, its presence in an exposed worker's audiogram, sparing the very highest frequencies, is strong evidence that the loss is noise-induced rather than age-related, which typically slopes down continuously without recovery at 8 kHz.
In practice, the diagnosis rests on the combination of a history of significant noise exposure and the characteristic audiogram, and management is overwhelmingly about halting further loss — removing or reducing the exposure, ensuring consistent use of protection, and monitoring — since the hearing already lost cannot be recovered and will otherwise continue to deteriorate with ongoing exposure.
⚠️
DANGER / REMEMBER: NIHL is preventable but irreversible, so prevention is paramount: engineering noise controls, limiting exposure (the permissible limit is about 85 dB over 8 hours), hearing protection (ear plugs/muffs), audiometric monitoring of workers and education. It has medicolegal importance (compensation). There is no cure — hearing aids and prevention of further exposure.
Bilateral, symmetrical, gradual; classic 4000 Hz notch (recovers at 8 kHz), later spreads; tinnitus common.
Temporary threshold shift → permanent threshold shift; preventable but irreversible.
Prevention (key): noise controls, limit exposure (~85 dB/8 h), ear plugs/muffs, audiometric monitoring, education; medicolegal importance; treat with hearing aids + avoid further exposure.
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Sudden sensorineural hearing loss (SSNHL) is a sensorineural loss of ≥30 dB over at least three contiguous frequencies developing within 72 hours — an otologic emergency, usually unilateral.
CAUSES & FEATURES
It is often idiopathic (with viral, vascular, autoimmune or membrane-rupture theories), but may reflect an acoustic neuroma, Meniere's disease or trauma. It presents with sudden hearing loss (often noticed on waking), tinnitus, aural fullness and sometimes vertigo; on testing, the Weber lateralises to the good ear and the Rinne is positive (confirming SNHL).
INVESTIGATION & MANAGEMENT
A NOTE ON WHY IT IS AN EMERGENCY
Sudden sensorineural hearing loss is emphasised as an emergency because the chance of recovery falls with every day of delay. There is a narrow therapeutic window in which corticosteroids can rescue hearing, so a patient who presents promptly and is treated early has a substantially better chance of recovery than one treated weeks later, by which time the loss may be fixed. This is why sudden one-sided hearing loss should never be dismissed as 'wax' or a blocked ear without testing: a quick tuning-fork check that shows a sensorineural pattern (Weber to the good ear) should trigger urgent referral for audiometry and steroid treatment, plus an MRI to exclude a neuroma. Treating it as urgent — rather than routine — is what preserves hearing.
THE BOTTOM LINE
Sudden sensorineural hearing loss is an otologic emergency in which early corticosteroids offer the best chance of recovery, and an MRI is needed to exclude an acoustic neuroma.
For completeness, the diagnosis is defined audiometrically (a drop of at least 30 dB across three contiguous frequencies within three days), which distinguishes true sudden sensorineural loss from the far commoner sudden conductive causes such as wax or a middle-ear effusion — hence the value of a quick tuning-fork test, which points to a sensorineural pattern and prompts the urgent pathway.
In practice, the message for both clinicians and patients is simple: sudden one-sided hearing loss is an emergency to be seen the same day, not a wax problem to be reviewed the following week, because the window in which steroids can rescue the hearing is measured in days, and imaging is still needed afterwards to be sure a neuroma is not the cause.
⚠️
DANGER / REMEMBER: Investigation is with PTA (to confirm), MRI (to exclude an acoustic neuroma) and blood tests. Management is urgent — systemic (and/or intratympanic) corticosteroids started as early as possible (ideally within days) give the best chance of recovery, with treatment of any identified cause. The prognosis is better with early treatment, a less severe loss and no vertigo. It is a 'do-not-miss' diagnosis — refer urgently.
🔑
KEY POINTS TO REMEMBER
SSNHL = SNHL ≥30 dB over ≥3 contiguous frequencies within 72 hours; otologic emergency; usually unilateral.
Often idiopathic (viral/vascular/autoimmune); exclude acoustic neuroma, Meniere's, trauma.
Sudden loss (often on waking), tinnitus, fullness, ± vertigo; Weber to the good ear, Rinne positive (SNHL).
PTA (confirm) + MRI (exclude neuroma); urgent systemic ± intratympanic steroids (start early); better prognosis if early, less severe, no vertigo.
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Ototoxicity is damage to the cochlea (hearing) and/or the vestibular system (balance) by drugs or chemicals. Recognising the responsible agents is important because some damage is preventable and some reversible.
COMMON OTOTOXIC DRUGS
Aminoglycosides (gentamicin, streptomycin) — cochlear and vestibular (streptomycin/gentamicin are more vestibulotoxic).
Cisplatin — cochlear; loop diuretics (furosemide) — usually reversible.
Quinine/chloroquine, salicylates/aspirin (reversible tinnitus and loss), vancomycin and erythromycin.
EFFECTS, RISK FACTORS & PREVENTION
Effects are SNHL (bilateral, high-frequency first), tinnitus and vertigo/imbalance (with vestibulotoxic agents). Risk factors include high dose, prolonged use, renal impairment, old age, concurrent ototoxics and genetic susceptibility (the mitochondrial A1555G mutation to aminoglycosides). Prevention is by monitoring (audiometry, drug levels, renal function), avoiding combinations and using the lowest effective dose. Aspirin and loop-diuretic effects are often reversible, whereas aminoglycoside and cisplatin damage is often permanent.
A NOTE ON MONITORING HIGH-RISK PATIENTS
The practical key to ototoxicity is anticipating and monitoring it in high-risk patients rather than discovering it too late. Patients receiving aminoglycosides or cisplatin, especially with renal impairment, old age or prolonged courses, should have baseline and serial audiometry (including the high frequencies, which are affected first), careful attention to drug levels and renal function, and avoidance of combining ototoxic agents. Because the earliest damage is in the high frequencies — outside the speech range — it can be detected before the patient notices any handicap, allowing the drug to be modified or stopped in time. Being alert to the mitochondrial susceptibility (A1555G), which can cause severe deafness even after a single dose, is an important additional safeguard in at-risk families.
THE BOTTOM LINE
Ototoxicity is preventable drug-induced cochleovestibular damage — chiefly from aminoglycosides and cisplatin — that is anticipated and caught early by monitoring high-risk patients.
It is also worth appreciating the distinction between cochleotoxic and vestibulotoxic effects: some agents (such as streptomycin and gentamicin) preferentially damage the vestibular system, producing imbalance and oscillopsia rather than deafness, so monitoring high-risk patients means asking about dizziness and unsteadiness as well as testing hearing, since the earliest toxicity may be to balance rather than to hearing.
In practice, ototoxicity is best prevented by prescribing these drugs only when necessary, at the lowest effective dose and shortest duration, with dose adjustment for renal function, therapeutic drug monitoring where relevant, and a low threshold for baseline and follow-up audiometry in anyone receiving a prolonged or high-dose course.
🔑
KEY POINTS TO REMEMBER
Ototoxicity = drug/chemical damage to the cochlea (hearing) and/or vestibular system (balance).
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Objective tests of hearing assess hearing without needing the patient's voluntary response, which is essential in infants, uncooperative patients and suspected malingerers. The two key tests are otoacoustic emissions (OAE) and brainstem evoked response audiometry (BERA/ABR).
OTOACOUSTIC EMISSIONS (OAE)
OAEs are sounds generated by the healthy cochlear outer hair cells in response to a stimulus, recorded in the ear canal. Their presence indicates normal cochlear (outer-hair-cell) function, and because the test is quick and non-invasive it is used for newborn hearing screening.
BERA / ABR
BERA records electrical potentials (waves I–V) from the auditory nerve and brainstem via scalp electrodes in response to clicks. It is used to estimate the hearing threshold objectively, to detect retrocochlear pathology (an acoustic neuroma delays the waves), and to confirm hearing loss in infants (as the confirmatory step after OAE screening). The usual newborn pathway is OAE screening followed by BERA to confirm.
A NOTE ON UNIVERSAL NEWBORN SCREENING
The greatest impact of these objective tests is in universal newborn hearing screening, which allows congenital hearing loss to be identified in the first weeks of life rather than years later. Because OAE and BERA need no response from the baby, every newborn can be screened — typically with a quick OAE test, and BERA to confirm any that fail — so that deaf infants are picked up during the critical period for language development and can be fitted with aids or referred for implantation early. This shift from late, chance detection (when a toddler fails to speak) to systematic screening at birth is one of the most important advances in paediatric audiology, and it depends entirely on the objectivity of these two tests.
THE BOTTOM LINE
OAE and BERA assess hearing objectively without patient response, underpinning universal newborn hearing screening and the detection of retrocochlear disease.
A useful additional point is that OAE and BERA test different parts of the pathway and so are complementary: OAE checks that the cochlear outer hair cells are working, while BERA checks the integrity of the nerve and brainstem pathway up to the level of the brainstem — which is why a baby can 'pass' an OAE yet have auditory neuropathy detectable only on BERA, and why confirmatory BERA follows OAE screening.
In practice, these objective tests have transformed paediatric audiology by allowing hearing to be measured reliably at an age when a child cannot cooperate, so that diagnosis no longer waits until a toddler's speech is obviously delayed but is made in the newborn period, when intervention is far more effective.
🔑
KEY POINTS TO REMEMBER
Objective tests assess hearing without voluntary response — for infants, uncooperative patients, malingerers.
OAE = sounds from healthy cochlear outer hair cells recorded in the canal; present = normal cochlear function; used for newborn screening (quick, non-invasive).
Newborn pathway: OAE screen → BERA to confirm; also used for medicolegal and difficult-to-test cases.
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.
THE CONCEPT
Early detection of hearing loss in children is critical, because hearing is essential for speech and language development during a critical period — the guiding principle is 'detect early, intervene early'.
CAUSES & RED FLAGS
Prelingual causes include genetic disorders (the commonest, around half), congenital infections (TORCH — rubella, CMV), perinatal problems (hypoxia, prematurity, kernicterus, low birth weight), meningitis and ototoxicity; the commonest acquired conductive cause is OME (glue ear). Red flags are no startle to sound, absent babble, delayed speech, not responding to the name and poor school performance.
ASSESSMENT & MANAGEMENT
Assessment uses universal newborn hearing screening (OAE/BERA), age-appropriate behavioural tests (behavioural observation audiometry, visual reinforcement audiometry, play audiometry, then PTA when older), tympanometry, and a high-risk register. Management is early diagnosis and intervention — treating conductive loss (grommets), fitting hearing aids or a cochlear implant early, auditory-verbal therapy and special education — before the critical language period closes.
A NOTE ON THE COST OF LATE DIAGNOSIS
The urgency behind evaluating a deaf child comes from the heavy, lifelong cost of a missed or late diagnosis. A child who cannot hear during the years in which the brain is wired for language will suffer delayed or absent speech, impaired language, educational underachievement and social and emotional difficulties that become progressively harder to remedy as the critical period passes. By contrast, a child identified and rehabilitated early — with grommets for glue ear, or hearing aids/a cochlear implant and therapy for sensorineural loss — can often develop near-normal speech and language. This stark difference in outcome, hinging on the timing of detection, is exactly why newborn screening, prompt investigation of any parental concern, and early intervention are so strongly emphasised.
THE BOTTOM LINE
Evaluating a deaf child hinges on early detection through newborn screening and prompt intervention, because the cost of late diagnosis — lost speech and language — is lifelong.
Finally, it is worth remembering that a parent's concern about a child's hearing should never be dismissed, as parents are often the first to notice a problem; any such concern, or any speech/language delay or failure to respond to sound, warrants formal testing rather than reassurance, because early confirmation and intervention are what protect the child's development.
In practice, a structured approach — newborn screening for every baby, a high-risk register for those with risk factors, and prompt, age-appropriate testing whenever hearing is questioned — ensures that no deaf child is missed, and that each is brought into treatment while the developing brain can still make the most of restored hearing.
🔑
KEY POINTS TO REMEMBER
Early detection of childhood deafness is critical for speech/language development ('detect early, intervene early').
Manage early: treat conductive loss (grommets), hearing aids/cochlear implant, auditory-verbal therapy, special education — before the critical period closes.
📚
SOURCES: Dhingra — Diseases of Ear, Nose and Throat.