Otology
The ear looks like the most memorisation-heavy part of ENT, with dozens of conditions and a vocabulary of its own.
Two questions collapse most of it.
For hearing loss, where is the block? Sound reaches the cochlea through the outer and middle ear, and is then transduced and carried centrally. A failure before the cochlea is conductive; a failure at or beyond it is sensorineural. Tuning forks answer this at the bedside, before any audiogram.
For vertigo, how long does an attack last? Duration is a far more reliable diagnostic instrument than any description of the spinning. Seconds, hours and days each point to a different disease, and patients describe the sensation itself so variably that it is nearly useless.
A third principle runs underneath both: the ear sits in a bone that also contains the facial nerve, the labyrinth and a thin plate separating it from the brain, which is why chronic middle ear disease is dangerous out of all proportion to its symptoms.
1. Locating the Block
Tuning forks
Rinne compares air conduction with bone conduction in the same ear. Air conduction better than bone conduction is normal and is called Rinne positive. Bone conduction better than air conduction indicates a conductive loss.
Weber places the fork on the midline and asks where the sound is heard. It lateralises toward a conductive loss and away from a sensorineural loss.
The lateralisation toward a conductive loss is counterintuitive and reliably examined. A conductively deaf ear is shielded from ambient noise, so bone-conducted sound in it is not masked and seems louder.
The false negative Rinne is the trap. In a severe unilateral sensorineural loss, the fork placed on the mastoid is heard by the opposite cochlea through the skull, so bone conduction appears better than air conduction and mimics a conductive loss. Weber, which lateralises to the good ear, exposes the error.
The audiogram
An air-bone gap means conductive loss. Air and bone thresholds both depressed and running together means sensorineural loss. Both features together means a mixed loss.
Two patterns are worth recognising instantly. A notch at 4 kHz indicates noise-induced loss. A notch in bone conduction at 2 kHz, the Carhart notch, suggests otosclerosis and disappears after successful surgery.
2. The External Ear
Otitis externa is usually bacterial, commonly Pseudomonas aeruginosa, and is treated with aural toilet and topical drops rather than systemic antibiotics.
Necrotising otitis externa is the one that kills. It occurs in elderly diabetics and the immunocompromised, is almost always pseudomonal, and is not really an otitis at all but a skull base osteomyelitis.
The clues are severe pain out of proportion to the appearance, granulation tissue at the bony-cartilaginous junction of the canal, and failure to settle with ordinary treatment. Facial nerve palsy indicates spread and is a poor prognostic sign.
It requires prolonged systemic antipseudomonal therapy, glycaemic control and imaging, and is monitored with nuclear medicine scanning rather than resolution of symptoms alone.
3. Otitis Media
Acute otitis media
Common in children because the Eustachian tube is shorter, wider and more horizontal. The usual organisms are Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis.
The drum is red and bulging with loss of the light reflex. Perforation relieves pain abruptly, which is why sudden relief with discharge is a sign rather than a recovery.
Amoxicillin is first-line where antibiotics are used, and watchful waiting is reasonable in older children with mild unilateral disease.
Otitis media with effusion
Glue ear is the commonest cause of childhood hearing loss. The drum is dull and retracted with fluid behind it and a flat type B tympanogram.
The evidence for grommets is more modest than practice suggests. Cochrane review finds only short-term hearing benefit in otherwise healthy children, which is why watchful waiting for around three months is standard before intervention. Adjuvant adenoidectomy reduces persistence and recurrence.
In an adult, a unilateral effusion is a nasopharyngeal carcinoma until the nasopharynx has been examined. The paediatric explanation does not apply once the adenoid has involuted.
Chronic otitis media
The essential division is between mucosal and squamosal disease, and it determines everything that follows.
| Feature | Mucosal (safe) | Squamosal (unsafe) |
|---|---|---|
| Defect | Central perforation | Attic or marginal perforation, or retraction pocket |
| Discharge | Profuse, mucoid, odourless | Scanty, foul-smelling |
| Cholesteatoma | Absent | Present or developing |
| Complications | Uncommon | Characteristic |
| Treatment | Medical, then repair | Surgical |
The terms safe and unsafe are old but capture the point exactly: mucosal disease is a wet ear, squamosal disease is a destructive one.
Acute mastoiditis
The mastoid air cells communicate directly with the middle ear, so acute otitis media that does not drain can progress to a mastoid empyema.
The signs are a tender, boggy swelling behind the ear with loss of the postauricular sulcus and a pinna pushed forward and downward. That displaced pinna is the finding that separates mastoiditis from simple otitis externa with periauricular oedema.
It is a surgical emergency in the sense that it may need cortical mastoidectomy alongside intravenous antibiotics, and it can progress to the same intracranial complications as cholesteatoma.
4. Cholesteatoma
Cholesteatoma is keratinising squamous epithelium where it does not belong, in the middle ear or mastoid.
It is not a tumour and not made of cholesterol. It behaves badly for a mechanical and enzymatic reason: it accumulates keratin, expands, and resorbs surrounding bone through osteoclast activation and enzymatic action.
Bone resorption is what makes it dangerous, because everything adjacent to the middle ear is important.
| Structure eroded | Consequence |
|---|---|
| Ossicles | Conductive hearing loss |
| Lateral semicircular canal | Labyrinthine fistula, vertigo on pressure |
| Facial canal | Facial nerve palsy |
| Tegmen tympani | Meningitis, extradural or brain abscess |
| Sigmoid plate | Lateral sinus thrombosis |
The fistula sign, vertigo and nystagmus provoked by pressure on the tragus or by a pneumatic otoscope, indicates erosion into the labyrinth.
Treatment is surgical, because no medical therapy removes squamous epithelium from the middle ear. Modern reporting uses the ChOLE system, which records cholesteatoma extension, ossicular chain status and life-threatening complications together.
Any patient with chronic ear discharge who develops headache, fever, vertigo, facial weakness or altered consciousness has a complication until proved otherwise.
5. Otosclerosis
Otosclerosis is abnormal bone remodelling in the otic capsule, characteristically at the fissula ante fenestram, which fixes the stapes footplate.
It is inherited in an autosomal dominant pattern with incomplete penetrance, presents in young adults, is commoner in women, and characteristically worsens during pregnancy.
The signature findings are worth listing precisely.
Progressive conductive hearing loss with an intact, normal-looking drum. Paracusis Willisii, hearing better in noisy surroundings, because background noise makes others raise their voices. Carhart notch at 2 kHz on bone conduction, which resolves after successful surgery. Schwartze sign, a flamingo-pink blush through the drum from vascular active disease.
Treatment is a hearing aid or stapedotomy with prosthesis insertion, and the choice is genuinely the patient's, since a hearing aid carries no surgical risk to an ear that hears.
6. Sensorineural Hearing Loss
| Pattern | Cause |
|---|---|
| Symmetrical, high frequency, gradual | Presbycusis |
| Notch at 4 kHz | Noise-induced |
| Bilateral, drug-related | Aminoglycosides, cisplatin, loop diuretics |
| Unilateral, progressive, with tinnitus | Vestibular schwannoma until excluded |
Sudden sensorineural hearing loss is an otological emergency. It is defined as a loss of 30 dB or more across three contiguous frequencies developing within 72 hours.
Corticosteroids are offered as initial therapy, and the window matters: treatment is recommended within two weeks of onset, with intratympanic steroid used as salvage where systemic therapy fails or is contraindicated.
MRI is required to exclude vestibular schwannoma, because a proportion of these patients have a retrocochlear lesion.
Screening and implantation
Newborn hearing screening uses otoacoustic emissions followed by auditory brainstem response in those who refer. India's National Programme for Prevention and Control of Deafness provides the framework, and cochlear implantation for children from lower-income families is supported under the ADIP scheme of the Ministry of Social Justice and Empowerment.
The rationale for early identification is developmental rather than audiological. The auditory cortex requires input during a critical period, so a child implanted early acquires speech in a way that a child implanted late does not.
7. Vertigo: Duration Names the Disease
Ask how long a single attack lasts, not what it feels like.
| Duration | Diagnosis | Confirming feature |
|---|---|---|
| Seconds, on head movement | Benign paroxysmal positional vertigo | Dix-Hallpike, treated by Epley |
| 20 minutes to 12 hours | Meniere disease | Fluctuating low-frequency loss, tinnitus, aural fullness |
| Days, then slowly settling | Vestibular neuritis | No hearing loss; labyrinthitis if hearing is affected |
| Minutes to days, with headache | Vestibular migraine | Photophobia, migraine history |
| Progressive, with unilateral loss | Vestibular schwannoma | Asymmetric SNHL and tinnitus, MRI |
Meniere disease is the one with all three of vertigo, hearing loss and tinnitus in the same attack, and the hearing loss is characteristically low-frequency and fluctuating early on.
The examination that matters most
In a patient with continuous vertigo of acute onset, the question is whether this is a peripheral vestibular neuritis or a posterior circulation stroke, and imaging is unreliable early.
The HINTS examination answers it, and its logic is inverted in a way that catches people out.
A normal head impulse test suggests a central lesion. A patient with vestibular neuritis has a damaged peripheral vestibular apparatus, so the head impulse test is abnormal with a corrective saccade. If the peripheral apparatus is intact and the patient is still vertiginous, the problem is central.
Direction-changing nystagmus and skew deviation likewise point centrally. A reassuring rule is that in this specific setting HINTS performed by a trained examiner is more sensitive for stroke than early MRI.
8. Tinnitus and the Ear That Will Not Be Quiet
Tinnitus is a symptom rather than a disease, and the useful first division is between subjective and objective.
Subjective tinnitus is heard only by the patient and usually accompanies sensorineural hearing loss, most often presbycusis or noise damage. It is best understood as central compensation: deprived of input at particular frequencies, the auditory cortex increases its gain and generates perceived sound.
That model explains why the most effective treatment is not silence but sound. Hearing aids, which restore the missing input, frequently reduce tinnitus, and sound enrichment plus cognitive behavioural therapy outperform any drug.
Objective tinnitus can be heard by the examiner and always has a physical source. Pulsatile tinnitus synchronous with the pulse suggests a vascular cause, including glomus tumour, arteriovenous malformation, carotid stenosis or raised intracranial pressure, and requires imaging.
Two features make tinnitus a red flag rather than a nuisance. Unilateral tinnitus with asymmetric hearing loss requires MRI to exclude vestibular schwannoma, and pulsatile tinnitus requires vascular assessment. Symmetrical bilateral tinnitus with symmetrical hearing loss rarely does.
9. The Facial Nerve
The facial nerve runs a long course through the temporal bone, which is why ear disease and ear surgery threaten it.
Distinguish upper from lower motor neurone weakness first. The forehead has bilateral cortical representation, so it is spared in an upper motor neurone lesion and involved in a lower motor neurone one. A stroke does not paralyse the forehead.
Bell palsy is an idiopathic lower motor neurone palsy of acute onset. Corticosteroids started within 72 hours improve outcome, and antivirals add little except in severe cases.
Ramsay Hunt syndrome is varicella zoster reactivation in the geniculate ganglion, with vesicles in the ear canal or on the pinna, more pain and a worse prognosis than Bell palsy. It is treated with steroids and antivirals together.
Eye care is not optional in either. An eye that cannot close develops exposure keratitis, and the cornea is lost while everyone watches the face.
10. Worked Examples
Example 1. A patient has Rinne showing bone conduction better than air conduction in the right ear, and Weber lateralising to the left. What is going on?
This combination is internally inconsistent for a right conductive loss, because a right conductive loss would lateralise Weber to the right.
It is a false negative Rinne. The right ear has a severe sensorineural loss, so the tuning fork placed on the right mastoid is being heard by the left cochlea through skull conduction, giving an apparent bone conduction better than air conduction on the right. Weber lateralising to the left, the better ear, is the finding that exposes the error and confirms a right sensorineural loss.
Example 2. A 9-year-old has had a foul-smelling scanty right ear discharge for a year, with an attic perforation. He now has a headache, fever and neck stiffness. What has happened?
Cholesteatoma with an intracranial complication, most likely meningitis. Squamosal chronic otitis media is characterised by attic or marginal defects, scanty foul discharge and progressive bone erosion. Erosion through the tegmen tympani gives access to the middle cranial fossa, producing meningitis, extradural abscess or brain abscess.
He needs urgent imaging, neurosurgical and ENT involvement, intravenous antibiotics and surgical clearance of the disease. The point to hold is that the volume of discharge is inversely related to the danger: profuse mucoid discharge is mucosal and safe, while scanty foul discharge is squamosal and destructive.
Example 3. A 28-year-old woman has progressive bilateral hearing loss that worsened during pregnancy. Her drums look normal. Audiometry shows a conductive loss with a dip in bone conduction at 2 kHz. What is the diagnosis?
Otosclerosis. A progressive conductive loss with a normal-looking drum in a young adult woman is the classic presentation, and worsening during pregnancy is characteristic. The dip at 2 kHz is the Carhart notch, an artefact of stapes fixation affecting bone conduction rather than true cochlear loss, and it resolves after successful stapedotomy. She may also report hearing better in noisy environments, which is paracusis Willisii. Management options are a hearing aid or stapedotomy, and the choice is genuinely hers.
Example 4. A 55-year-old man wakes with severe continuous vertigo, vomiting and unsteadiness. There is no hearing loss. He has hypertension and diabetes. How do you distinguish vestibular neuritis from a stroke?
By the HINTS examination, which in trained hands outperforms early MRI for posterior circulation stroke. The logic is inverted: an abnormal head impulse test with a corrective saccade indicates a damaged peripheral vestibular apparatus and therefore favours vestibular neuritis, while a normal head impulse test in a patient who is still vertiginous means the periphery is intact and the lesion must be central.
Direction-changing nystagmus and skew deviation also point centrally. His vascular risk factors raise the prior probability of stroke, so a reassuring peripheral pattern must be convincing before he is discharged.
Example 5. A 40-year-old notices sudden hearing loss in one ear on waking three days ago, with tinnitus. Otoscopy is normal. What is the diagnosis, and what must be done now and later?
Sudden sensorineural hearing loss, defined as at least 30 dB across three contiguous frequencies within 72 hours. It is an otological emergency.
Confirm with audiometry, and start corticosteroids without delay, since treatment is recommended within two weeks of onset and earlier is better. Intratympanic steroid is used as salvage if systemic treatment fails or is contraindicated, for instance in poorly controlled diabetes. Later, MRI of the internal auditory meati is required to exclude a vestibular schwannoma, because a meaningful proportion of these patients have a retrocochlear lesion that the audiogram cannot distinguish.
Summary
For hearing loss ask where the block is; for vertigo ask how long an attack lasts.
Rinne compares air with bone conduction; Weber lateralises to a conductive loss and away from a sensorineural one.
A false negative Rinne occurs in severe unilateral sensorineural loss, and Weber exposes it.
An air-bone gap is conductive; a 4 kHz notch is noise; a 2 kHz bone conduction notch is Carhart.
Necrotising otitis externa is a pseudomonal skull base osteomyelitis in elderly diabetics.
Glue ear is the commonest cause of childhood hearing loss, and grommets give only short-term benefit.
An adult with a unilateral effusion needs the nasopharynx examined.
Mucosal chronic otitis media is profuse and safe; squamosal is scanty, foul and destructive.
Cholesteatoma erodes bone, threatening ossicles, labyrinth, facial nerve, tegmen and sigmoid sinus.
A positive fistula sign means erosion into the lateral semicircular canal.
Otosclerosis: young woman, normal drum, conductive loss, Carhart notch, paracusis, Schwartze sign.
Sudden sensorineural hearing loss is 30 dB across three frequencies in 72 hours and needs steroids within two weeks.
MRI is required after sudden loss to exclude vestibular schwannoma.
Seconds of vertigo is BPPV; 20 minutes to 12 hours is Meniere; days is vestibular neuritis.
Meniere has vertigo, fluctuating low-frequency hearing loss and tinnitus together.
A normal head impulse test in an actively vertiginous patient suggests a central lesion.
The forehead is spared in upper motor neurone facial weakness and involved in lower motor neurone weakness.
Bell palsy gets steroids within 72 hours; Ramsay Hunt gets steroids and antivirals and does worse.
Eye protection is mandatory in any facial palsy that prevents closure.
