Evidence-Based Diagnosis and Management of ENT Emergencies

Michael Winters, MD


February 15, 2007


MOE is a potentially life-threatening ENT infection that involves the external auditory canal, temporal bone, and surrounding structures. Although case reports can be traced to the early 1800s, it was not until the late 1960s that MOE was defined as a clinical disease. Typically, MOE has an aggressive course and is associated with a high mortality rate. Depending on the complications, mortality rates for MOE range from 50% to 80%.[41,42]

MOE almost always occurs in immunocompromised patients. The most common comorbid condition associated with MOE is diabetes mellitus. In one study, up to 90% of patients with MOE were diabetic.[43] There is no difference in predisposition between type 1 and type 2 diabetes mellitus. Recent reports have highlighted the rising incidence of MOE in patients with HIV.[44,45,46] It is important to recognize that HIV patients with MOE tend to be younger than diabetic patients with the disorder. In addition to HIV, lymphoproliferative disorders and medication-induced immunosuppression have been identified as risk factors for MOE.[42]

Pseudomonas aeruginosa is the causative agent in the majority of cases of MOE. This organism is particularly virulent due to its mucoid coating that deters phagocytosis. In addition, some strains release a neurotoxin that is thought to contribute to a number of intracranial complications. Patients with malignancy and HIV are at risk for infection from less common organisms. These include Aspergillus, S aureus, Proteus mirabilis, Klebsiella oxytoca, and Candida species.

Patients with MOE present with severe, unrelenting ear pain. The pain is usually worse at night and aggravated with chewing. It is often associated with temporal headaches and purulent otorrhea. The hallmark physical examination finding is the presence of granulation tissue in the inferior portion of the external auditory canal, at the bone-cartilage junction. As the infection progresses, patients develop cranial nerve abnormalities, most commonly associated with the seventh cranial nerve. The presence of cranial nerve abnormalities other than with cranial nerve 7 should raise suspicion for intracranial complications, namely, abscess and cerebral sinus thromboses. Unfortunately, once cranial nerve abnormalities develop, prognosis is poor. Mortality for patients with MOE and cranial nerve abnormalities approaches 100%.[42]

The diagnosis of MOE is confirmed with imaging studies. Laboratory studies, such as white blood cell counts, are nonspecific and can be normal even in patients with extensive disease. Imaging studies used in the evaluation of MOE include computed tomography (CT), magnetic resonance imaging (MRI), technetium bone scanning, and gallium citrate scintigraphy. CT of the temporal bone is considered by many to be the initial imaging modality of choice. It is important to recognize that anywhere from 30% to 50% of bone must be destroyed before findings are evident on CT. As such, CT can be normal early in the disease process. For patients with a normal CT scan and high suspicion for MOE, obtain either a bone scan or gallium scintigraphy. Although not specific, these studies have high sensitivity for bone erosion. MRI and CT demonstrate equivalent sensitivity and specificity for soft-tissue complications.

Treatment of MOE centers on antimicrobial therapy. Antipseudomonal antibiotics are the drugs of choice and must be initiated early. Fluoroquinolones, primarily ciprofloxacin, are considered by many to be the antibiotic of choice. Cure rates of 90% have been achieved through the use of fluoroquinolones.[47] There are recent reports of MOE from ciprofloxacin-resistant Pseudomonas; however, as of yet, no increase in mortality has been seen in these patients.[48] Initial doses should be given intravenously. There is no role for topical antibiotics in the treatment of MOE. In addition to systemic antibiotics, patients should receive good aural toilet with debridement of granulation tissue. Biopsy of granulation tissue is indicated in most cases to rule out squamous cell malignancy. Recent studies have suggested an adjuvant role for hyperbaric oxygen therapy for MOE.[49,50] To date, there are no randomized controlled trials that demonstrate a benefit to adjunctive hyperbaric oxygen therapy in patients with MOE.[51]


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