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PATIENT STORY

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 29-1 and 29-2). The external auditory canal (EAC) was narrowed and contained purulent discharge (Figure 29-3). 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 went home on oral ciprofloxacin 5 days later.

FIGURE 29-1

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

FIGURE 29-2

Another view of the malignant/necrotizing otitis externa. (Reproduced with permission from E.J. Mayeaux, MD.)

FIGURE 29-3

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. (Reproduced with permission from Richard P. Usatine, MD.)

INTRODUCTION

Acute otitis externa (AOE) is among the most common clinical conditions presenting as acute ear pain in the primary care setting. AOE is defined as acute inflammation, often with infection, of the EAC.1

SYNONYMS

Swimmer's ear.

EPIDEMIOLOGY

  • Incidence of AOE is not known precisely; its lifetime incidence was estimated at 10% in one study.2

  • Occurs more in adults than in children.

ETIOLOGY AND PATHOPHYSIOLOGY

  • 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 (<10%) of AOE is caused by fungal pathogens (e.g., Aspergillus and Candida species). Fungal AOE is associated with prior antibiotic use and seen frequently in humid environments (i.e., tropical and subtropical settings).1

  • Pathogenesis of AOE includes the following:

    • Trauma, the usual inciting event, leads to breach 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 ...

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