ENT (Otorhinolaryngology)

THE CONCEPT

Acute suppurative otitis media (ASOM) is an acute suppurative (pus-forming) inflammation of the middle-ear cleft (the middle ear, mastoid air cells and Eustachian tube). It is common in children and usually follows an upper respiratory infection that ascends to the middle ear along the Eustachian tube.

AETIOLOGY

It is caused by bacteria — chiefly Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis — following a viral upper respiratory infection, reaching the middle ear via the Eustachian tube. Children are especially prone because their Eustachian tube is shorter, wider and more horizontal; other risk factors are day-care attendance, bottle-feeding, cleft palate and adenoid hypertrophy.

THE FIVE STAGES

1. Stage of tubal occlusion — Eustachian-tube blockage, a retracted dull drum and mild deafness.
2. Stage of pre-suppuration — hyperaemia and a congested drum (with a 'cartwheel' pattern of vessels), earache and fever.
3. Stage of suppuration — pus in the middle ear, a bulging red drum with loss of landmarks, throbbing pain, high fever and conductive deafness.
4. Stage of resolution — the drum ruptures, giving otorrhoea (discharge), relief of pain and fever, and healing.
5. Stage of complication — if resolution fails (mastoiditis and other complications).

FEATURES & MANAGEMENT

The features are severe throbbing earache, fever, conductive deafness and ear discharge (after perforation); infants show irritability, ear-tugging, fever and vomiting. Management is with antibiotics (amoxicillin first-line for 7–10 days, or amoxicillin–clavulanate), analgesics/antipyretics and nasal decongestants, with myringotomy (a drainage incision in the drum) if the drum is bulging, the pain is severe, or there is no response, and treatment of the underlying cause.

WHY CHILDREN ARE SO PRONE

Understanding why ASOM is overwhelmingly a childhood disease comes down to the anatomy of the Eustachian tube. In a child the tube is shorter, wider and lies more horizontally than in an adult, so nasopharyngeal secretions and organisms during a URI pass more easily up into the middle ear, and the flatter angle drains pus less efficiently. Children also have large, frequently-infected adenoids that obstruct the tube and act as a reservoir of bacteria, and their immature immunity means frequent upper-respiratory infections. As the tube lengthens and becomes more vertical with growth, the incidence falls sharply — which is why recurrent ASOM in a child often improves with age and why treating the adenoids can help.

THE ROLE AND VALUE OF MYRINGOTOMY

Myringotomy deserves emphasis because a well-timed drainage incision can change the course of ASOM. When the drum is tensely bulging with pus, the pressure causes intense pain and threatens an uncontrolled, ragged spontaneous rupture that may heal poorly. A planned myringotomy — a clean radial incision, usually in the antero-inferior quadrant — drains the pus, relieves the pain immediately, and heals neatly, and the pus can be sent for culture to guide antibiotics. It is therefore indicated when the drum is bulging, the pain is severe, the response to antibiotics is poor, or a complication is threatening. Recognising when antibiotics alone are not enough, and adding drainage, is a key clinical judgement in managing ASOM.

• ASOM = acute suppurative inflammation of the middle-ear cleft; children; post-URI via Eustachian tube (S. pneumoniae, H. influenzae, M. catarrhalis).
• 5 stages: tubal occlusion → pre-suppuration (congested drum) → suppuration (bulging red drum, throbbing pain) → resolution (perforation + otorrhoea) → complication.
• Treat: amoxicillin 7–10 days (or amoxicillin–clavulanate) + analgesics/antipyretics + decongestants; myringotomy if bulging drum/severe pain/no response; treat adenoids/URI.

• ASOM = acute suppurative inflammation of the middle-ear cleft; common in children; follows a URI via the Eustachian tube.
• Organisms: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis; children prone (short, wide, horizontal Eustachian tube).
• Five stages: tubal occlusion → pre-suppuration (congested drum) → suppuration (bulging red drum) → resolution (perforation + otorrhoea) → complication.
• Features: throbbing earache, fever, conductive deafness, discharge; infants — irritability, ear-tugging, vomiting.
• Treat: amoxicillin + analgesics + decongestants; myringotomy if the drum bulges, pain is severe, or no response.

THE CONCEPT

Chronic suppurative otitis media (CSOM) is a chronic inflammation of the middle-ear cleft with a permanent perforation of the tympanic membrane and persistent or recurrent ear discharge (for more than 2–3 months). It exists in two types with very different behaviour and danger — the tubotympanic ('safe') and the atticoantral ('unsafe').

TUBOTYMPANIC ('SAFE'/MUCOSAL) CSOM

• A central perforation of the pars tensa (the margin of the drum is intact).
• Disease of the mucosa; the discharge is profuse, mucoid/mucopurulent, non-foul-smelling and intermittent (worse with a URI).
• Causes conductive hearing loss, has no cholesteatoma, and carries a low risk of complications ('safe').
• Management: aural toilet, topical antibiotic–steroid drops and treatment of infection/allergy; then myringoplasty/tympanoplasty to repair the drum once the ear is dry.

ATTICOANTRAL ('UNSAFE'/SQUAMOSAL) CSOM

WHY 'SAFE' AND 'UNSAFE' IS THE KEY DISTINCTION

The most important idea in CSOM is the division into 'safe' and 'unsafe' disease, because it dictates the entire approach. The safe (tubotympanic) type is a disease of the mucosa — there is a central perforation but no cholesteatoma and no bone erosion — so it discharges profuse, non-foul mucus, threatens little beyond hearing, and can be managed medically and later repaired. The unsafe (atticoantral) type carries cholesteatoma, which erodes bone, so even though it discharges only scanty, foul pus it can silently destroy the ossicles, the labyrinth and the bony plates separating the ear from the facial nerve and brain, causing life-threatening complications. This is why the clinician's first task in any chronically discharging ear is to decide whether it is safe or unsafe — the safe ear can be watched and repaired, whereas the unsafe ear must be operated to remove the cholesteatoma.

READING THE PERFORATION & THE DISCHARGE

Two clinical clues reliably separate the two types at the bedside, and it is worth knowing how to read them. The site of the perforation is the most telling: a central perforation, with a rim of drum all around it, indicates safe disease, whereas an attic or marginal (postero-superior) perforation, reaching the bony annulus, indicates unsafe disease with likely cholesteatoma. The nature of the discharge supports this: safe disease gives profuse, mucoid, odourless discharge (from inflamed mucosa), while unsafe disease gives scanty but persistently foul-smelling discharge — the foul smell coming from bone erosion by the cholesteatoma. A foul-smelling ear with an attic perforation must therefore never be dismissed as a trivial 'chronic ear', because it signals dangerous, surgically-treatable disease.

A NOTE ON MANAGING THE SAFE EAR

For the safe (tubotympanic) ear, it is worth understanding the logic of treatment, which proceeds in two phases. First, the ear is made dry and inactive by regular aural toilet (removing discharge so that drops can reach the mucosa), topical antibiotic–steroid ear drops, and treatment of the sources of infection — the nose, sinuses, adenoids and any allergy — that keep re-seeding the middle ear. Only once the ear has been dry for a period is the second phase, surgical repair of the perforation (myringoplasty/tympanoplasty), undertaken, because grafting a wet, infected ear fails. This staged approach — settle the disease, then reconstruct — gives the perforation the best chance of healing and the hearing the best chance of recovery.

A COMPARISON

• CSOM = chronic middle-ear inflammation + permanent perforation + persistent/recurrent discharge (>2–3 months).
• Tubotympanic (safe/mucosal): central pars-tensa perforation, profuse mucoid NON-foul discharge, conductive loss, NO cholesteatoma, low risk → aural toilet + topical antibiotic-steroid + myringoplasty.
• Atticoantral (unsafe/squamosal): attic/marginal perforation + CHOLESTEATOMA + bone erosion, scanty FOUL discharge, dangerous complications → mastoidectomy.

• CSOM = chronic middle-ear inflammation with a permanent tympanic-membrane perforation and persistent/recurrent discharge.
• Tubotympanic ('safe'): central perforation (pars tensa), mucosal disease, profuse mucoid non-foul discharge, no cholesteatoma, low complication risk.
• Atticoantral ('unsafe'): attic/marginal perforation with cholesteatoma and bone erosion, scanty foul-smelling discharge, high risk of complications.
• Safe type: aural toilet + topical antibiotic-steroid drops, then myringoplasty/tympanoplasty once dry.
• Unsafe type: needs mastoidectomy to remove the cholesteatoma/disease — it cannot be managed medically alone.

THE CONCEPT

A cholesteatoma is a sac of keratinising stratified squamous epithelium ('skin') in the middle ear and mastoid, which accumulates keratin debris and erodes the surrounding bone. Despite its name it is neither a tumour nor made of cholesterol — it is best thought of as 'skin in the wrong place'. It is the hallmark of unsafe (atticoantral) CSOM and is dangerous because of its bone erosion.

TYPES & PATHOGENESIS

• Congenital — behind an intact drum, from an embryonic epithelial rest.
• Acquired — primary (invagination of a retraction pocket of the pars flaccida/attic) or secondary (squamous epithelium migrating in through a marginal/attic perforation).

Once squamous epithelium is trapped in the middle ear it keeps producing keratin, which accumulates and expands the sac; the matrix releases enzymes (collagenase) that erode bone — the ossicles, the scutum, the semicircular canal, the facial canal and the tegmen.

WHY IT IS DANGEROUS

WHY CHOLESTEATOMA IS SO DESTRUCTIVE

The danger of cholesteatoma lies not in any malignant potential — it is benign tissue — but in its relentless, enzyme-driven erosion of bone in a confined, vital space. As the trapped squamous epithelium sheds keratin into an enclosed sac, the sac expands and its matrix releases osteolytic enzymes (collagenase) that dissolve whatever bone it touches. Because the middle ear and attic are surrounded by critical structures — the ossicles, the bony labyrinth, the facial-nerve canal, and the thin tegmen plate separating the ear from the brain — this slow erosion translates directly into deafness, vertigo, facial palsy and intracranial infection. It is this combination of continuous growth, bone destruction and a perilous location that makes an otherwise harmless piece of misplaced skin a genuinely life-threatening condition, and explains why it must be removed surgically rather than merely suppressed.

WHY SURGERY, NOT MEDICINE, IS THE ANSWER

A defining principle is that cholesteatoma cannot be cured medically — it must be removed surgically. Ear drops and antibiotics can temporarily settle the infection and reduce the discharge, but they do nothing to remove the keratin-producing sac itself, which continues to grow and erode bone. Leaving it in place, or treating it only with medicine, allows the silent progression toward complications. The definitive treatment is therefore mastoidectomy to eradicate the cholesteatoma completely (canal-wall-up or canal-wall-down, depending on the extent), often followed by reconstruction of the drum and ossicular chain to restore hearing. Understanding that medicine only temporises — while surgery removes the disease — is central to the correct management of every cholesteatoma.

CLINICAL FEATURES, INVESTIGATION & MANAGEMENT

It presents with scanty, foul-smelling ear discharge, hearing loss and an attic/marginal perforation containing whitish flakes or a pearly mass (often with a polyp or granulations). Investigation is with otoscopy/microscopy, an HRCT of the temporal bone (to map the extent and bone erosion) and audiometry. Treatment is surgical — mastoidectomy to remove the cholesteatoma completely (canal-wall-down or canal-wall-up), with reconstruction (tympanoplasty/ossiculoplasty); it cannot be cured medically.

• Cholesteatoma = sac of keratinising squamous epithelium in the middle ear/mastoid; not a tumour, not cholesterol ('skin in the wrong place').
• Congenital (intact drum) vs acquired — primary (attic/pars flaccida retraction pocket) or secondary (through marginal/attic perforation); keratin accumulates + collagenase erodes bone.
• Erodes ossicles (deafness), labyrinth (vertigo/fistula), facial canal (palsy), tegmen (intracranial — meningitis/abscess/lateral sinus thrombosis). HRCT temporal bone; treatment = surgical (mastoidectomy), never medical alone.

• Cholesteatoma = keratinising squamous epithelium ('skin') in the middle ear that accumulates keratin and erodes bone; not a tumour/not cholesterol.
• Congenital (behind intact drum) vs acquired — primary (retraction pocket) or secondary (through a marginal/attic perforation).
• Erodes ossicles (hearing loss), labyrinth (vertigo/fistula), facial canal (palsy), tegmen → intracranial spread (meningitis, abscess, lateral sinus thrombosis).
• Presents with scanty foul discharge, hearing loss, attic/marginal perforation with pearly debris; HRCT temporal bone maps it.
• Treatment is surgical — mastoidectomy to remove it completely (canal-wall-up/down) + reconstruction; cannot be cured medically.

THE CONCEPT

Otitis media with effusion (OME, serous otitis media, 'glue ear') is a collection of non-purulent fluid (serous or mucoid) in the middle ear behind an INTACT tympanic membrane, without the signs of acute infection. It is the commonest cause of hearing loss in children and results from Eustachian-tube dysfunction.

AETIOLOGY & PATHOGENESIS

Eustachian-tube dysfunction creates a negative middle-ear pressure that draws out a transudate of fluid. The common causes are adenoid hypertrophy (the commonest in children), recurrent URIs/ASOM, allergy and cleft palate.

WHY GLUE EAR MATTERS IN A CHILD

Although OME is painless and often overlooked, it is important precisely because it strikes at a critical time for a child's development. The persistent conductive hearing loss it causes can go unnoticed for months — the child simply seems inattentive, turns up the television, or falls behind at school — yet during these years the child is acquiring speech, language and social skills that depend on hearing. Untreated persistent glue ear can therefore cause speech and language delay and educational and behavioural problems. This is why a child with suspected hearing loss must be tested rather than reassured, and why persistent OME with significant hearing loss is actively treated — to restore the hearing the child needs for normal development — rather than simply left because it does not hurt.

THE ADULT WITH UNILATERAL GLUE EAR

A rule that must never be forgotten is that a unilateral OME in an adult is a red flag for nasopharyngeal carcinoma until proven otherwise. Whereas glue ear in children is common and usually due to adenoids, an adult who develops persistent fluid in one ear may have a tumour in the nasopharynx obstructing the opening of the Eustachian tube on that side. Because nasopharyngeal carcinoma is otherwise silent early on, this ear finding may be its first presentation. The essential clinical response is therefore to examine the nasopharynx (with endoscopy) and biopsy any suspicious lesion in any adult with unexplained unilateral OME, rather than simply inserting a grommet and treating the effusion — a classic and important teaching point.

CLINICAL FEATURES & OTOSCOPY

The child has an insidious conductive hearing loss (inattentiveness, poor school performance, turning up the television), a sensation of a blocked/full ear, and it is painless with no fever; speech and language may be delayed. Otoscopy shows a retracted, dull, amber or grey drum with loss of the light reflex, an air–fluid level or air bubbles behind it, and reduced mobility.

INVESTIGATION & MANAGEMENT

The key test is tympanometry (a flat, 'type B' curve), with pure-tone audiometry showing a conductive loss, and examination of the nose/adenoids in a child (or the nasopharynx in an adult). Management is watchful waiting (many resolve within 3 months), treating allergy/URI and autoinflation; and, if it persists beyond 3 months with hearing loss, myringotomy with grommet (ventilation-tube) insertion, often with adenoidectomy.

• OME (glue ear) = non-purulent serous/mucoid fluid behind an INTACT drum, no acute infection; commonest cause of childhood hearing loss.
• Eustachian-tube dysfunction → negative pressure → effusion; causes — adenoids (commonest), recurrent URI/ASOM, allergy, cleft palate. ADULT unilateral OME → exclude nasopharyngeal carcinoma.
• Painless conductive deafness, dull retracted drum, fluid level/bubbles; tympanometry type B (flat), audiometry conductive loss. Manage: watchful waiting (3 months) → myringotomy + grommet ± adenoidectomy if persistent.

• OME (glue ear) = non-purulent serous/mucoid fluid behind an intact tympanic membrane, without acute infection; commonest cause of childhood hearing loss.
• Eustachian-tube dysfunction → negative middle-ear pressure → effusion; commonest cause in children is adenoid hypertrophy (also allergy, URI, cleft palate).
• Painless, insidious conductive hearing loss; dull retracted drum, amber/grey, fluid level or bubbles, reduced mobility.
• Tympanometry flat (type B) is diagnostic; audiometry shows conductive loss; adult unilateral OME → exclude nasopharyngeal carcinoma.
• Manage: watchful waiting (~3 months) + treat allergy/URI + autoinflation; persistent → myringotomy + grommet ± adenoidectomy.

THE CONCEPT

Complications arise when infection spreads beyond the middle-ear cleft, most often in unsafe (atticoantral) CSOM with cholesteatoma (through bone erosion) or in severe/neglected ASOM. They are divided into extracranial (within the temporal bone) and intracranial, and several are life-threatening emergencies.

EXTRACRANIAL COMPLICATIONS

• Acute mastoiditis — the commonest.
• Facial-nerve palsy — from erosion of the facial canal.
• Labyrinthitis / labyrinthine fistula — causing vertigo and sensorineural deafness.
• Petrositis (Gradenigo's syndrome — otorrhoea + retro-orbital pain + sixth-nerve palsy/diplopia).
• Subperiosteal abscess — postauricular, a Bezold's abscess (into the neck along sternomastoid) or Luc's abscess.

INTRACRANIAL COMPLICATIONS

• Meningitis — the commonest intracranial complication.
• Brain abscess — temporal lobe or cerebellar.
• Extradural abscess.
• Lateral (sigmoid) sinus thrombophlebitis — with 'picket-fence' fever and Griesinger's sign.
• Otitic hydrocephalus.

SPREAD, WARNING SIGNS & MANAGEMENT

Infection spreads by bone erosion (cholesteatoma), through the oval/round window (labyrinth), by venous thrombophlebitis, or along preformed pathways. Warning signs in a patient with ear disease are persistent headache, fever, vertigo, facial weakness, neck stiffness or altered consciousness. Management is an emergency: intravenous antibiotics, urgent surgery (mastoidectomy to remove the source, with drainage of any abscess), neurosurgical involvement and imaging (CT/MRI).

HOW COMPLICATIONS ARE STILL RELEVANT TODAY

Although antibiotics have made them less common, the complications of otitis media remain important and still occur, particularly in unsafe CSOM with cholesteatoma, in neglected or inadequately-treated disease, and in resource-poor settings. Their importance is out of proportion to their frequency because they are potentially fatal and are often heralded by subtle signs in a patient with 'just a chronic ear'. The clinician's task is therefore to maintain a high index of suspicion: to recognise that a patient with chronic ear disease who develops a persistent headache, fever, vertigo, facial weakness or drowsiness may be developing an intracranial or intratemporal complication, and to investigate and treat urgently. Knowing the complications and their warning signs allows them to be caught before they become irreversible.

THE PRINCIPLE OF SOURCE CONTROL

A unifying principle in managing every complication is source control — removing the underlying focus of infection, not just treating the complication itself. Because these complications arise from an ongoing middle-ear/mastoid infection (usually cholesteatoma), antibiotics and drainage of an abscess alone are not enough: the disease will keep seeding the complication until the focus is eradicated. This is why the definitive treatment nearly always combines intravenous antibiotics with urgent mastoid surgery (mastoidectomy) to remove the cholesteatoma and diseased tissue and to expose and address the complication (for example, exposing the sinus in lateral sinus thrombosis or the dura in an extradural abscess), alongside neurosurgical drainage of an intracranial abscess where needed. Treating the complication without removing its source is a recipe for recurrence.

A NOTE ON EXTRA- VERSUS INTRACRANIAL

It helps to hold the complications in two clear groups defined by where the infection has reached. The extracranial (intratemporal) complications stay within the temporal bone — mastoiditis, facial palsy, labyrinthitis, petrositis and subperiosteal abscess — and tend to present with local signs (swelling, facial weakness, vertigo, deep pain). The intracranial complications have breached into the cranial cavity — meningitis, extradural and brain abscess, lateral sinus thrombosis and otitic hydrocephalus — and present with neurological and systemic signs (headache, fever, altered consciousness, seizures, focal deficits, raised intracranial pressure). Thinking in these two groups helps the clinician anticipate which features to look for, decide how urgently imaging and neurosurgical help are needed, and appreciate that an extracranial complication left untreated is often the stepping-stone to an intracranial one.

THE BOTTOM LINE

The complications of otitis media are uncommon but potentially fatal spreads of infection beyond the middle ear — extracranial (led by mastoiditis) and intracranial (led by meningitis) — that demand a high index of suspicion and emergency treatment combining intravenous antibiotics, imaging and mastoid surgery to remove the source.

• Complications spread beyond the middle-ear cleft — esp unsafe CSOM/cholesteatoma (bone erosion); extracranial vs intracranial; life-threatening.
• Extracranial: acute mastoiditis (commonest), facial-nerve palsy, labyrinthitis/fistula, petrositis (Gradenigo's — otorrhoea + retro-orbital pain + VI palsy), subperiosteal/Bezold's abscess.
• Intracranial: meningitis (commonest), brain abscess (temporal/cerebellar), extradural abscess, lateral sinus thrombophlebitis (picket-fence fever, Griesinger's sign), otitic hydrocephalus. Emergency: IV antibiotics + mastoidectomy + drainage + imaging.

• Complications occur when otitis media spreads beyond the middle-ear cleft — usually unsafe CSOM/cholesteatoma (bone erosion) or severe ASOM.
• Extracranial: acute mastoiditis (commonest), facial-nerve palsy, labyrinthitis/fistula, petrositis (Gradenigo's), subperiosteal/Bezold's abscess.
• Intracranial: meningitis (commonest), brain abscess, extradural abscess, lateral (sigmoid) sinus thrombophlebitis, otitic hydrocephalus.
• Warning signs: persistent headache, fever, vertigo, facial palsy, neck stiffness, altered consciousness in a patient with ear disease.
• Emergency management: IV antibiotics + urgent mastoidectomy (remove source) + drainage of abscess + neurosurgery + CT/MRI.