Otitis Externa and Necrotizing Otitis Externa

Epidemiology and Clinical Manifestations

Otitis externa is an infection of the skin of the hairy and glabrous parts of the ear canal. Acute otitis externa (i.e., swimmer’s ear) is usually unilateral and is often associated with head immersion in water. Any source of prolonged ear canal moisture can cause otitis externa, including hearing aid use and drainage from otitis media with a perforated tympanic membrane. Other predisposing factors include radiation exposure and immunocompromised states. Prolonged exposure to ear buds also has been reported in children with otitis externa.

In temperate climates, the disease incidence peaks in the summer. When the skin of the ear canal is wet for prolonged periods, local defense mechanisms are impaired. Cerumen, which has antimicrobial properties, is washed away; the thickness of the keratin layer is reduced; the pH of the canal increases; the skin may become macerated; and microscopic fissures develop. This can cause itching of the ear canal that may predispose to further trauma from cotton-tipped swabs. Gram-negative bacteria, most commonly Pseudomonas spp., flourish in the moist environment and invade superficial layers of skin.

The ensuing inflammatory dermatitis progresses through three stages. ^, Each is associated with pain and tenderness exaggerated by movement of the tragus or pinna. Fever is uncommon. In mild otitis externa , pain is ameliorated by simple analgesics. The skin of the hairy part of the ear canal is erythematous but not edematous. In moderate otitis externa , there is increasing pain. The patient resists the insertion of anything into the ear canal. The skin of the hairy part of the ear canal is intensely red under the macerated pieces of desquamated skin. Edema of the canal skin increases, and the canal lumen is narrowed to less than 50% of its normal diameter, obscuring the tympanic membrane. Severe otitis externa is characterized by intense pain, often requiring narcotics; inflammatory edema, which narrows the external auditory meatus to barely admit a nasopharyngeal swab; and desquamated debris that precludes visualization of the tympanic membrane. Granulation tissue also may be seen in the ear canal. The patient may or may not have otorrhea, and the auricle can be swollen and painful. In advanced cases, tender preauricular or postauricular lymphadenopathy, protrusion of the auricle, and contiguous cellulitis of the skin overlying the mastoid area can be seen. Unlike acute mastoiditis, the entire auricle not only protrudes but also is edematous, and the posterior auricular sulcus is preserved. Suctioning of the ear canal is difficult to perform without adequate analgesia.

Advanced cases of otitis externa are difficult to differentiate from necrotizing otitis externa, which is a perichondritis of the cartilaginous outer third of the ear canal. It also can be difficult to distinguish from noninfectious disorders involving the ear canal, including malignancies (e.g., rhabdomyosarcoma), Langerhans cell histiocytosis, and Wegener granulomatosis.

Etiologic Agents

In healthy individuals, the ear canal microflora includes coagulase-negative staphylococci , corynebacteria , and micrococci. With prolonged exposure to water, gram-negative bacteria predominate. Pseudomonas aeruginosa is responsible for most cases of otitis externa associated with swimming or due to persistent otorrhea from a patent tympanostomy tube, although Staphylococcus aureus is also a common cause. S. aureus and Streptococcus pyogenes are the usual causes of acute otitis externa that occurs as an extension of a focal infection.

Fungi are uncommon causes of otitis externa, in most series comprising less than 5% of cases. However, in some studies, fungi constitute a higher proportion of isolates. Aspergillus spp. account for about two-thirds, and Candida spp. account for the remainder. Prolonged use of topical antibacterial agents appears to be a risk factor for otomycosis. ^,

Viruses rarely cause otitis externa. Reactivation of latent varicella-zoster virus in the seventh cranial nerve results in herpes zoster oticus, which is characterized by unilateral otalgia, auricular vesicles, and hearing and vestibular symptoms. When these findings are associated with peripheral facial paralysis, the complex is known as Ramsay Hunt syndrome.