Otitis Externa

Otitis externa (OE) encompasses a spectrum of inflammatory conditions affecting the skin of the external ear canal. It can be acute (<3 weeks) or chronic (>3 months). The primary insult is often a breakdown of the ear's protective skin-wax barrier, allowing for bacterial or fungal overgrowth. It is highly prevalent, particularly in humid climates and among swimmers. Common pathogens include Pseudomonas aeruginosa and Staphylococcus aureus. Distinguishing simple OE from Malignant Otitis Externa (MOE) is vital; MOE is a necrotising infection that spreads to the skull base (osteomyelitis) and typically affects immunocompromised or elderly diabetic patients. Chronic OE is often associated with dermatological conditions like eczema or psoriasis and may involve fungal pathogens (Otomycosis), such as Aspergillus niger or Candida albicans. Treatment focuses on aural toilet (cleaning), moisture avoidance, and topical therapy. Systemic antibiotics are rarely indicated unless there is cellulitis spreading to the pinna or the patient is systemically unwell. If the ear canal is too swollen for drops to penetrate, an ear wick must be inserted by an ENT specialist.

The external auditory canal has a unique self-cleaning mechanism and an acidic pH (approx. 3.0–5.0) which inhibits bacterial growth. Cerumen (earwax) provides a hydrophobic protective layer. Pathogenesis begins when this barrier is breached by maceration (excessive swimming/humidity), trauma (cotton buds), or skin disease (dermatitis). Bacterial proliferation follows, leading to inflammation of the thin skin overlying the bony and cartilaginous canal. In Malignant Otitis Externa, the infection penetrates into the deeper tissues through the Fissures of Santorini, leading to skull base osteomyelitis. This process involves the temporal bone and can progress to involve the jugular foramen, causing palsies of CN IX, X, and XI, and eventually the facial nerve (CN VII). The high mortality of MOE is due to its proximity to the sigmoid sinus and meninges.

Presenting symptoms include severe otalgia, often disproportionate to clinical findings, itching (pruritus), and a malodorous discharge. Physical examination reveals an erythematous, oedematous ear canal, often with debris. Pain when moving the pinna or pressing the tragus is a classic diagnostic sign. Fungal OE may show visible spores ('black dots' for Aspergillus). MOE must be suspected in diabetics or elderly patients with 'unremitting' otalgia that is worse at night and non-responsive to topical treatment. Signs of MOE include granulation tissue at the bone-cartilage junction of the canal and cranial nerve palsies. Complications of standard OE include perichondritis or cellulitis of the pinna. Recurrent OE may lead to canal stenosis (thickening of the skin). Hearing loss is usually conductive due to canal occlusion by debris or oedema.

- Bedside: Otoscopy to visualize the canal and TM. Ear swab for culture and sensitivity (MC&S) if first-line treatment fails or infection is severe.
- Bloods: ESR/CRP and HbA1c/Blood glucose if Malignant OE is suspected.
- Imaging: CT temporal bones or MRI for MOE to assess skull base involvement. Technetium-99m bone scan can confirm osteomyelitis, while Gallium-67 scans can monitor resolution.
- Audiology: Only if hearing loss persists after the infection is cleared.

Conservative: Avoidance of water (use earplugs/swimming caps) and no 'poking' with cotton buds. Aural toilet to remove debris periodically. Medical: Topical acetic acid 2% (EarCalm) for mild cases. For moderate/severe: Topical antibiotic + steroid drops/sprays (e.g., Sofradex, Gentisone HC, or Otomize spray) for 7–14 days. If the canal is closed by oedema, refer for ear wick insertion. Fungal OE: Clotrimazole drops or Nystatin. Malignant OE (Emergency): Urgent ENT referral for hospital admission, IV antibiotics (Ciprofloxacin to cover Pseudomonas), and intensive glycaemic control. Chronic OE: Manage underlying eczema with topical steroids and avoid irritants.