What is chronic suppurative otitis media?
Chronic suppurative otitis media (CSOM) is a chronic infection and inflammation of the middle ear cleft with persistent or recurrent otorrhoea through a perforated tympanic membrane, usually with conductive hearing loss. StatPearls notes that the duration used in definitions ranges from 2 to 6 weeks, and that the discharge classically lasts more than 6 weeks by the time the patient is seen.
CSOM usually follows an untreated, inadequately treated or recurrent acute otitis media that leaves a permanent perforation. Trauma and iatrogenic causes (grommets, previous ear surgery) can do the same. The middle ear connects to the nasopharynx through the eustachian tube and to the mastoid air cells through the aditus and antrum — which is why infection here can spread to the mastoid, the inner ear, the facial nerve and the brain.
It is a disease of poverty: overcrowding, malnutrition, poor sanitation, passive smoking and limited access to care all raise the risk. Structural risk factors include cleft palate, Down syndrome and other craniofacial anomalies. StatPearls estimates that CSOM affects about 1 in 26 people worldwide and is a leading cause of preventable hearing loss.
How do tubotympanic and atticoantral CSOM differ?
CSOM is divided into two types that behave very differently. The split is clinical and decided at otoscopy: where is the perforation, and is there cholesteatoma?
| Feature | Tubotympanic (mucosal, 'safe') | Atticoantral (squamous, 'unsafe' / danger type) |
|---|---|---|
| Part of middle ear | Anteroinferior middle ear cleft (mucosal disease) | Attic and posterosuperior middle ear, extending to the antrum and mastoid |
| Perforation | Central — a rim of drum remains all round | Marginal (posterosuperior) or attic (pars flaccida) perforation / retraction pocket |
| Discharge | Mucopurulent, often intermittent; worse after water exposure | Persistent, foul-smelling, painless (keratin debris plus infection) |
| Cholesteatoma | Absent | Usually present |
| Bone erosion | Not a feature | Ossicles, scutum, tegmen, lateral canal and facial canal can be eroded |
| Complications | Rare | Intratemporal and intracranial complications |
| Treatment | Medical control, then tympanoplasty | Surgery — mastoidectomy to remove cholesteatoma |

Which organisms cause CSOM and why does it persist?
CSOM is usually polymicrobial. The common isolates are *Pseudomonas aeruginosa* (the most frequent), *Staphylococcus aureus*, Proteus, Klebsiella, diphtheroids and anaerobes, sometimes with fungi. These bacteria form biofilms on the middle-ear mucosa, which protect them from host defences and antibiotics and explain why discharge keeps coming back.
- Eustachian tube dysfunction — negative middle-ear pressure, fluid stasis and mucosal oedema.
- Persistent perforation — bacteria, water and debris enter from the ear canal; patients notice more discharge after bathing or swimming.
- Chronic mucosal inflammation — granulation tissue, mucosal thickening and loss of mucociliary clearance.
- Squamous metaplasia of the middle-ear lining in long-standing disease.
- Ossicular erosion — progressive conductive hearing loss.
What is a cholesteatoma and how does it form?
Cholesteatoma is a misnomer — it contains neither cholesterol nor fat. It is keratinising stratified squamous epithelium growing in the middle ear and mastoid, a sac that keeps filling with keratin debris. Although benign, it destroys bone by pressure-induced resorption and enzymatic (osteoclastic) bone resorption driven by inflammatory cytokines. Inside the cranium the same lesion is called an epidermoid cyst.
| Type | Mechanism / theory | Key point |
|---|---|---|
| Congenital | Epithelial rests from faulty embryogenesis | Behind an intact drum; no history of infection |
| Primary acquired | Retraction pocket (invagination) theory — eustachian tube dysfunction pulls the drum inwards | Pars flaccida is drawn in most often → attic cholesteatoma |
| Secondary acquired | Epithelial migration (immigration) — canal skin grows in through a marginal perforation | Follows a perforation (infection or trauma) |
| Secondary acquired | Squamous metaplasia — chronic irritation turns middle-ear mucosa squamous | Can start before a perforation |
| Secondary acquired | Basal cell hyperplasia (papillary ingrowth) — keratin-filled buds invade Prussak's space | No retraction pocket or perforation needed |
On otoscopy a cholesteatoma looks like a white, pearly or yellow mass in a retraction pocket, typically in the posterosuperior quadrant, often hidden under foul discharge. StatPearls describes the classic presentation as painless, persistent or recurrent otorrhoea; about 85% are unilateral. Vertigo suggests erosion of the labyrinth (a fistula).


How is CSOM diagnosed and which investigations are used?
Diagnosis is clinical — history plus otoscopy. Look for a long history of discharge (often since childhood), hearing loss noticed as poor school performance or speech delay in children, and the type of perforation. Ask about vertigo, facial weakness, headache, fever or vomiting: these suggest a complication.
| Test | Typical finding | When / why |
|---|---|---|
| Otoscopy / otomicroscopy | Central vs marginal/attic perforation, granulations, polyp, keratin | Every patient; suction the discharge first |
| Tuning forks | Rinne negative on the affected side, Weber lateralised to the affected ear | Bedside proof of conductive loss |
| Pure-tone audiometry | Conductive hearing loss (air–bone gap) | Standard in all; before and after surgery |
| Tympanometry | Flat type B tracing | Perforation or effusion |
| Pus culture and sensitivity | Pseudomonas, S. aureus | Refractory, recurrent or complicated disease |
| HRCT temporal bone | Extent of disease, ossicular and scutal erosion, tegmen and lateral canal defects | Preferred imaging for complications and surgical planning |
| MRI with non-echo-planar diffusion-weighted imaging | Cholesteatoma bright on DWI | Suspected intracranial spread; distinguishes cholesteatoma from granulation; follow-up after surgery |
How is active CSOM treated medically?
- Aural toilet — mechanical removal of discharge and debris (suction and microinstruments under the otomicroscope). It lets topical drops reach the middle ear and is the foundation of treatment.
- Topical fluoroquinolone drops (ciprofloxacin, ofloxacin) — first line. They cover Pseudomonas and S. aureus and are not ototoxic even with a perforation.
- Avoid ototoxic drops — aminoglycoside drops (neomycin, gentamicin) are cheap and effective but can cause sensorineural loss and vestibular damage when the drum is perforated.
- Granulation tissue control — topical steroid–antibiotic drops or chemical cautery with silver nitrate.
- Systemic antibiotics — only for systemic infection, complications, or failure of topical therapy; guided by culture.
- Dry-ear precautions — keep water out of the ear.
- Topical antiseptics — an alternative where antibiotic drops are not available (WHO guidance for low-resource settings).
When is surgery needed and which operations are done?
StatPearls lists the indications for surgery as otorrhoea persisting 4–6 weeks despite medical treatment, a perforation that does not heal, cholesteatoma, conductive hearing loss and coalescent mastoiditis. Possible contraindications include operating on the only hearing ear, poor general health or high anaesthetic risk, or severe complications such as brain abscess that need treating first.
| Operation | What it does | Used for |
|---|---|---|
| Tympanoplasty / myringoplasty | Repairs the perforation (graft: temporalis fascia, cartilage) ± ossicular reconstruction | Safe (tubotympanic) disease once the ear is dry |
| Mastoidectomy | Clears disease from the mastoid air cells | Chronic mastoid disease, cholesteatoma, persistent infection |
| Canal wall-up tympanomastoidectomy | Keeps the posterior canal wall | Better cosmesis and hearing, no cavity care — but higher residual/recurrent cholesteatoma, so second look or DWI-MRI follow-up |
| Canal wall-down tympanomastoidectomy | Removes the posterior canal wall to make an open mastoid bowl | Extensive cholesteatoma, sinus tympani disease, labyrinthine fistula, preoperative facial weakness; lower recurrence but lifelong cavity cleaning and water precautions |
| Ossiculoplasty | Rebuilds the sound-conducting chain (reshaped incus or prosthesis) | Eroded ossicles |
The goal of cholesteatoma surgery is a safe, dry ear first, and hearing second. Recurrence is common — in one study quoted in StatPearls, the 5-year recurrence after primary surgery was 38% in children vs 14% in adults. Many surgeons plan a second-look operation at 6–12 months or follow up with diffusion-weighted MRI.
What are the complications of CSOM?
Complications arise mainly from atticoantral disease with cholesteatoma. Infection spreads by bone erosion, through thrombophlebitis of small veins, and along pre-formed pathways. They are classically split into intratemporal (extracranial) and intracranial.
| Group | Complication | Exam clue |
|---|---|---|
| Intratemporal | Mastoiditis / subperiosteal abscess | Mastoid tenderness and swelling, postauricular erythema; abscess at the periphery of the skull over the mastoid |
| Intratemporal | Facial nerve palsy | Seen in about 1–3.4% of cholesteatomas; LMN facial weakness on the same side |
| Intratemporal | Labyrinthitis / labyrinthine fistula | Vertigo; fistula in 4–15% of cholesteatomas, lateral (horizontal) semicircular canal most common; positive fistula test |
| Intratemporal | Petrositis (Gradenigo syndrome) | Otorrhoea + retro-orbital pain + abducens (VI) palsy |
| Extratemporal | Bezold abscess | Pus in the sheath of the sternocleidomastoid |
| Intracranial | Meningitis | Most frequent intracranial complication |
| Intracranial | Brain abscess | Second most common; temporal lobe (about 54%) or cerebellum (about 44%) |
| Intracranial | Lateral (sigmoid) sinus thrombosis | Pain in the mastoid region, spiking fever, anaemia; Griesinger sign |
| Intracranial | Extradural / subdural abscess | Headache, fever, focal signs |
Otogenic abscess reaches the temporal lobe through erosion of the tegmen tympani, and the cerebellum through Trautmann's triangle or by thrombophlebitis of the sigmoid sinus. In one series reported in PMC, about 95% of otogenic brain abscesses occurred with chronic otitis media and cholesteatoma. Meningitis and brain abscess remain the main causes of death from otitis media.
How is CSOM asked in NEET PG and INI-CET?
- Otoscopy image — central perforation (safe) vs attic/marginal perforation with white keratin (unsafe).
- Most common organism — Pseudomonas aeruginosa.
- Theories of cholesteatoma — retraction pocket, epithelial migration, squamous metaplasia, basal cell hyperplasia (Prussak's space).
- Commonest site of labyrinthine fistula — lateral semicircular canal.
- Griesinger sign and Gradenigo syndrome — match the sign to the complication.
- Most common intracranial complication — meningitis; brain abscess sites — temporal lobe and cerebellum.
- Investigation of choice — HRCT temporal bone for bone; DWI-MRI for cholesteatoma and intracranial spread.
- Topical treatment — quinolone drops; aminoglycoside drops are ototoxic through a perforation.