Otitis Externa

Otitis externa encompasses a spectrum from mild diffuse infection to life-threatening necrotizing disease. The external auditory canal's defense system relies on cerumen production (acidic pH, lysozymes, antimicrobial peptides), intact stratified squamous epithelium, lateral epithelial migration, and the narrow canal isthmus. Disruption of any component—through moisture, trauma, alkalinization, or immune compromise—initiates the pathological cascade. Pseudomonas aeruginosa is the predominant organism in diffuse OE, capable of forming biofilms on canal skin and producing exotoxins (exotoxin A inhibits protein synthesis, elastase degrades tissue barriers). In necrotizing OE, Pseudomonas invades from the canal through the fissures of Santorini and the tympanomastoid suture into the temporal bone, causing osteomyelitis that can extend to the skull base, petrous apex, and contralateral temporal bone. Cranial nerve involvement occurs as infection spreads along the skull base: CN VII (facial canal), CN IX-XI (jugular foramen), and CN XII (hypoglossal canal). Mortality in necrotizing OE ranges from 10–20% even with treatment. Otomycosis involves fungal colonization (Aspergillus niger, Candida albicans) often as superinfection after antibiotic therapy. The clinician must identify risk factors for necrotizing disease, prescribe targeted therapy, manage complications, and...