Bacterial and fungal cultures may guide treatment of nonresponsive cases. Oral antibiotic therapy should be reserved for febrile patients and those with periauricular extension. All patients with OE should be taught to avoid predisposing factors in order to eliminate recurrences. Strategies include ear plugs while swimming or bathing (cotton wool impregnated with Vaseline or commercial ear plugs), occasional, brief use of a hair dryer to remove EAC water, and avoidance of cotton-tipped applicators or other devices to remove cerumen.
Specific treatment of otomycosis consists of antifungal agents such as clotrimazole. Aspergillus is not sensitive to most oral antifungals with the exception of itraconazole.17 With noninfectious OE, removal of the offending agent is the first step in treatment. Topical steroid drops may be used for seborrhea and psoriasis.
Finally, all patients should be instructed to follow up with their primary physician or an otolaryngologist if the condition worsens at any time or does not respond to treatment in 1 week; these patients must be evaluated for the more serious disease of malignant otitis externa.
MALIGNANT OTITIS EXTERNA Definitions Malignant otitis externa (MOE) is a potentially life-threatening infection of the EAC with variable extension to the skull base. It is almost always caused by P. aeruginosa. The term MOE actually refers to a spectrum of disease. When it is limited to the soft tissues and cartilage, it is called necrotizing otitis externa (NOE). When there is involvement of the temporal bone or skull base it is called skull-base osteomyelitis (SBO).
Pathophysiology MOE begins as a simple otitis externa that then spreads to the deeper tissues of the EAC and infects cartilage, periosteum, and bone, with the normal anatomy of the ear serving as the conduit for the spread of infection. The cartilaginous floor of the EAC has clefts, known as the fissures of Santorini, through which the infection may spread to deeper structures. The parotid gland and TMJ are anterior, the mastoid air cells are posterior, and the skull base, carotid artery, jugular bulb, and sigmoid sinus are inferomedial. Infection may spread to any of these structures as well as to the seventh cranial nerve as it exits the stylomastoid foramen and the ninth, tenth, and eleventh cranial nerves at the jugular foramen.
The typical patient with MOE is the elderly diabetic. The impaired immune response of the diabetic, which is further compromised in the elderly, may predispose to the onset of pseudomonal infection. Furthermore, the cerumen of diabetic patients has been found to have a higher pH than that of normal controls; this represents an additional breakdown in local defense mechanisms. Finally, the small blood vessel disease of diabetics may lead to cartilaginous degeneration, further promoting the spread of infection.
Microbiology The most common causative organism of MOE is P. aeruginosa. Aspergillus has been reported to cause SBO, usually in patients who are immunosupressed due to AIDS or other causes. Aspergillus SBO also has a different presentation than typical pseudomonal SBO in that the infection generally begins in the middle ear rather than in the EAC.
Diagnosis Any elderly, diabetic, or immunocompromised patient presenting with OE or any person with persistent OE despite 2 to 3 weeks of topical antimicrobial therapy should be suspected of having MOE. The typical presentation is similar to that of OE: otalgia and edema of the EAC with or without otorrhea. The otalgia may be out of proportion for routine OE. Granulation tissue may be evident on the floor of the EAC near the bone-cartilage junction.
The history and physical examination should also be directed toward determining the extent of progression of the disease by identifying involvement of nearby structures. Parotitis may be present, and trismus indicates involvement of the masseter muscle or TMJ. Cranial nerve involvement is a serious sign; the history and examination should specifically rule out facial palsy and hoarseness or dysphagia. The seventh cranial nerve is usually the first affected, and the presence of dysfunction of the ninth, tenth, or eleventh cranial nerve implies even more extensive disease. Lateral or sigmoid sinus thrombosis and meningitis are also possible complications.
Certain patients may have an atypical clinical presentation and require special mention. MOE in children tends to to be rapidly progressive; thus children may be more ill appearing upon presentation, with fever, leukocytosis, and even bacteremia. Also, the TM, middle ear, and facial nerve are more likely to be involved in children than in adults. AIDS patients with MOE tend to be younger, have etiologic organisms other than Pseudomonas, and tend to have a worse prognosis than patients without AIDS.
Diagnosing MOE depends first on having a high index of suspicion; emergent otolaryngologic consultation is necessary. The next step involves radiographic confirmation and staging of the disease with CT of the head, focusing on the EAC and temporal bone ( T§bJ§...2.31-7.).1,7, taAOcCCAAPtfC SlAGiO
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