Cranial EDA is a collection of pus that forms in the potential space between the dura and calvar-ium. Cranial EDA is relatively uncommon, accounting for only 5% of all localized intracranial infections [16,17]. Most cranial EDAs result from trauma with implantation of foreign material, following craniotomy or in association with infection of the para-nasal sinuses, although occasional cases are related to orbital cellulitis, sinus thrombophlebitis or congenital dermal sinuses. Rarely is cranial EDA related to invasive carcinoma of the head and neck that has eroded through the skull. Other conditions occasionally associated with cranial EDA include rhinocere-bral mucormycosis, fetal monitoring and insertion of skull tongs for skeletal traction [16,17].
The bacteriology of cranial EDA correlates with the underlying cause of infection. Cases associated with para-nasal sinusitis, otitis and mastoiditis reflect the organisms of the underlying infection, most often hemolytic or microaerophilic streptococci and anerobes. Post-traumatic and or post-operative cases are most often caused by staphylococci.
As opposed to sub-dural empyema (SDE) (discussed later), the majority of patients with cranial EDA present with a relatively "benign" clinical course. A recent history of craniofacial trauma, sinusitis, ENT or neurosurgical procedure may provide an initial clue to the diagnosis. The typical patient reports a dull headache, which may be localized or diffuse. Periorbital swelling may occur, especially in cases related to frontal sinusitis. Signs of mild systemic illness such as fever are common and, while the patient may appear ill, signs of toxicity are usually conspicuously absent. Not infrequently, symptoms may be present for weeks to months, while the abscess slowly enlarges. Focal neurological signs are occasionally noted, usually due to mass effect from the epidural collection. Occasionally, an EDA located at the petrous apex can produce ipsilateral facial pain associated with sixth nerve palsy (Gradenigo's syndrome). However, the presence of progressive focal neurological deficit, seizures or a deteriorating sensorium should raise the suspicion of a concomitant SDE which is present in approximately 10% of patients.
Laboratory findings in EDA are non-specific and include elevation of the sedimentation rate (ESR), with or without an elevated blood leukocyte count. Lumbar puncture is potentially dangerous and adds little information. Plain skull radiographs may demonstrate bone destruction if there is an associated osteomyelitis, but the study of choice is either CT or MRI. EDA frequently involves a relatively large volume of fluid that usually appears as a lenticular-shaped extra-axial mass on both CT and MRI. The collection usually appears hypodense on CT with peripheral contrast enhancement. On MRI, EDA appears as a hyperintense signal abnormality on both T1WI and T2WI; the latter may be more sensitive than CT in detecting small collections early in the course of the disease.
The management of cranial EDA entails antibiotic therapy and surgical evacuation of the abscess. Not uncommonly, there will be a fluctuant sub-galeal component associated with the EDA that may be aspirated to obtain culture so that antibiotic therapy can be initiated. However, the notion that simple aspiration of the purulent material through the scalp, followed by antibiotics, might be adequate therapy should be condemned. Similarly, while burr-hole drainage may be attempted, it is usually inadequate. The optimum surgical management of EDA should consist of craniotomy or craniectomy, drainage of all purulent material, debridement of necrotic devitalized tissue and copious irrigation . If there is an underlying frontal sinusitis, this can also be addressed with cranialization and exenteration of the sinus. Friable granulation tissue is usually encountered adherent to the dura and prudence must be exercised in attempting to remove this material. If it is not particularly adherent and can be easily removed, it should be done; however, this tissue is often quite vascular and adherent and the risk of creating a dural tear with contamination of the sub-dural space far outweighs the benefits of complete removal. Indeed, in the absence of compelling clinical and/or radiographic evidence to suggest the presence of an associated SDE, the sub-dural space should not be routinely explored . Proper management of the bone flap following drainage of an EDA is debatable. If the bone appears "healthy" and radiographic signs of osteomyelitis are lacking, the bone flap can be soaked in an antiseptic solution and replaced . It such instances, a
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