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A 40-year-old woman with type 2 diabetes presents to her family physician with a 2-day history of bilateral otalgia, otorrhea, and hearing loss. Symptoms started in the right ear and then rapidly spread to the left ear. She had a low-grade fever and was systemically ill. The external ear was swollen with honey-crusts (Figures 27-1 and 27-2). The external auditory canal (EAC) was narrowed and contained purulent discharge (Figure 27-3). Ear, nose, and throat (ENT) was consulted and she was admitted to the hospital for the presumptive diagnosis of malignant otitis externa. The MRI showed some destruction of the temporal bone. She was started on IV ciprofloxacin and the ear culture grew out Pseudomonas aeruginosa sensitive to ciprofloxacin. The patient responded well to treatment and was able to go home on oral ciprofloxacin 5 days later.

Figure 27-1

Malignant/necrotizing otitis externa in a 40-year-old woman with diabetes. Note the swelling and honey-crusts of the pinna. The EAC and temporal bone were involved. (Courtesy of E.J. Mayeaux, MD.)

Figure 27-2

Another view of the malignant/necrotizing otitis externa. (Courtesy of E.J. Mayeaux, MD.)

Figure 27-3

Chronic suppurative otitis media with purulent discharge chronically draining from the ear of this 25-year-old man. This image could be seen in acute otitis media with perforation of the tympanic membrane or in a purulent otitis externa. (Courtesy of Richard P. Usatine, MD.)

Otitis externa (OE) is common in all parts of the world. OE is defined as inflammation, often with infection, of the EAC.1

  • Incidence of OE is not known precisely; its lifetime incidence was estimated at 10% in one study.2
  • Occurs more in adults than in children.

  • Common pathogens, which are part of normal EAC flora, include aerobic organisms predominantly (P. aeruginosa and Staphylococcus aureus) and, to a lesser extent, anaerobes (Bacteroides and Peptostreptococcus). Up to a third of infections are polymicrobial. A small proportion (2% to 10%) of OE is caused by fungal overgrowth (e.g., Aspergillus niger usually occurs with prolonged antibiotic use).1
  • Pathogenesis of OE includes the following:
    • Trauma, the usual inciting event, leads to breech in the integrity of EAC skin.
    • Skin inflammation and edema ensue, which, in turn, leads to pruritus and obstruction of adnexal structures (e.g., cerumen glands, sebaceous glands, and hair follicles).
    • Pruritus leads to scratching, which results in further skin injury.
    • Consequently, the milieu of the EAC is altered (i.e., change in quality and quantity of cerumen, increase in pH of EAC, and dysfunctional epithelial migration).
    • Finally, the EAC becomes a warm, alkaline, and moist environment—ideal for growth of different pathogens.

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