lunedì 2 aprile 2007
Malignant otitis externa
Figure 1: Initial CT of the skull base on bone widows shows subtotal opacification of the mastoid air cells without bony destruction.
Figure 2: CT of the skull base on soft tissue windows shows an inflammatory soft tissue mass filling the external auditory canal extending into the surrounding soft tissues without involvement of the middle ear.
Figure 3: On subsequent CT of the skull base with soft tissue windows, the inflammatory soft tissue mass remains with partial destruction of the auricular cartilage. It now crosses the tympanic membrane and opacifies the middle ear with osteolysis of the anterior, bony portion of the external auditory canal.
Figure 4: Axial bone windows reveal destruction of the anterior wall of the mastoid air cells.
Figure 5: Sagittal reconstruction with bone windows reveals coalescing mastoiditis with destruction of the bony septae and resultant enlargement of the air cells. The inflammatory mass displaces the mandibular condyle anteriorly out of the articular fossa.
Figure 6: Coronal reconstruction with bone windows reveals soft tissue opacifying the middle ear with partial destruction of the tympanic portion of the temporal bone.
Diagnosis: Malignant otitis externa
Malignant otitis externa (MOE) also referred to as necrotizing otitis externa or skull base osteomyelitis can be defined as otitis externa with progression to skull base osteomyelitis. The causative organism is almost universally Pseudomonas, which invades via the fissures of Santorini, located in the cartilaginous, lateral 1/3 of the external auditory canal (EAC). Affected patients are typically immunocompromised, often diabetic and present with symptoms of otitis externa unresponsive to topical antibiotics. Examination demonstrates purulent otorrhea with granulation tissue in the EAC. Cranial nerve involvement in the setting of otitis externa is an ominous sign and suggests progression to malignant otitis externa. Leukocytosis and signs of systemic infection are not typically present.
When diagnosing MOE, imaging is mandatory. CT is the exam of choice, demonstrating osteolysis in association with mastoid opacification and marked soft tissue inflammation centering on the external auditory canal. CT is relatively insensitive for early disease; osteolysis is not seen until at least 30% of the bone has been destroyed. Nuclear scans are generally sensitive but not specific, and may play an adjunctive role. Due to the lack of marrow in the affected bones, MR is of limited use, but may be complimentary to demonstrate soft tissue involvement.
Imaging can only suggest the diagnosis of MOE, and biopsy is necessary for confirmation.
The anatomy of the temporal bone means that the disease may disrupt the TMJ or the middle ear. Involvement of the facial nerve may occur. Intracranial spread is more ominous still, leading to venous sinus thrombosis, meningitis and abscess formation.
The historical mortality for MOE was 77%; however with current treatment the mortality is closer to 10%. Systemic antibiotics are the mainstay of therapy however surgical debridement may be necessary.