In addition to physical findings, laboratory data may be helpful in determining which patient might benefit from imaging of the brain.32,33 White blood cell count, erythrocyte sedimentation rate, and C-reactive protein level can be markedly elevated and may be useful screening tools to decide which patient should be imaged.28 Children with hyperglycemia or diabetes may be at increased risk for sinogenic intracranial empyema.28
Lumbar puncture is contraindicated if there is raised intracranial pressure because of the possibility of cerebral herniation. However, lumbar puncture will be helpful to rule out meningeal infection when increased intracranial pressure has been excluded. Cerebrospinal fluid findings may suggest the presence of infection (Table 4).1,30
Computed tomography (CT) and magnetic resonance imaging (MRI) have been the mainstays of the imaging diagnosis of SDE.5,34
High-resolution, contrast-enhanced CT scanning is the standard technique for quick and noninvasive diagnosis of SDE. If MRI is unavailable, a contrast-enhanced head CT with axial and coronal planes should be obtained. Nonenhanced CT alone lacks sensitivity, and a normal study may be falsely reassuring.28,32,35 On the CT scan, the empyema may be manifested by a hypodense area over the hemisphere or along the falx. The margins are better delineated with the infusion of contrast material (Fig. 1). It will also delineate cerebral involvement. Cranial bone involvement can also be seen with CT scan. Computed tomographic scan is the modality of choice if the patient is comatose or critically ill, and MRI is not possible or is contraindicated.36,37 Computed tomographic scan may miss intracranial SDEs detectable by MRI. Conversely, occasional spinal SDEs may be detected by CT myelography where MRI finding is negative.9
The diagnostic procedure of choice for intracranial and spinal SDE is MRI with gadolinium enhancement.9,28,32,35,38 A fluid collection surrounded by a contrast-enhancing rim is characteristic of SDE. The MRI is superior to CT in demonstrating extraaxial fluid and its rim enhancement.5 Diffusion-weighted imaging has proved to be more sensitive than conventional MRI in detecting the intraaxial involvement.39,40 Magnetic resonance imaging studies demonstrated convexity and interhemispheric collections that have a low signal on T1 weighted images and a relatively high signal on T2 weighted images. Related cerebral edema seems hyperintense on T1 weighted scans.5
Cranial ultrasound has been helpful in differentiating SDE from anechoic reactive subdural effusion in infants with meningitis accompanied by complex features (eg, increased echogenicity in the convexity collections, presence of hyperechoic fibrinous strands or thick hyperechoic inner membrane, and increases in echogenicity of the pia-arachnoid).
Radionuclide brain scanning and angiography have been helpful in diagnosing SDE, but they are not nearly as effective as CT scanning.
Early and accurate diagnosis, timely surgical intervention, and appropriate antibiotic therapy are the keys to a more favorable clinical outcome. Treatment in virtually all cases of intracranial or spinal SDE requires prompt surgical drainage and antibiotic therapy. Pus from the empyema should always be sent for anaerobic, and aerobic, culture.9,14 Treatment of patients with SDE consists of immediate surgical evacuation. Subdural empyema should be treated surgically except in extremely rare circumstances where there are contraindications to surgery or significant mortality risks avoided. Imaging can accurately localize the collection pus that can be evacuated by burr hole placement, but wide craniotomy with irrigation is the procedure of choice because it improves the outcome in SDE by allowing wide exposure, adequate exploration, and better evacuation of subdural purulent material.41,42 Complete evacuation of pus and eradication of the source of infection is the goal of treatment.1,20,36,43 Urgent evacuation of infected material by a neurosurgeon and otolaryngologist team either simultaneously or at the earliest possible opportunity for eradicating the source of infection results in cure and a significant decrease in recollection and reexploration.1,44,45 Occasionally, medical management may suffice.46,47
Because intracranial SDEs may contain multiple organisms, provisional antibiotic therapy for intracranial SDE, where the organism is unknown, should be directed against S. aureus, microaerophilic and anaerobic streptococci, and gram-negative organisms.9,28,48-51 Antibiotics should include the following: (1) nafcillin, oxacillin, or vancomycin; plus (2) a third-generation cephalosporin; plus (3) metronidazole. Provisional antibiotic therapy for spinal SDEs should be directed against S. aureus and streptococci and should include nafcillin, oxacillin, or vancomycin.9
Complications of SDE include seizures; cerebral infarction; cavernous sinus thrombosis from septic thrombosis of adjacent cerebral veins; hydrocephalus from compressed cerebrum resulting in interference with CSF flow; cerebral edema; cranial osteomyelitis, primarily in adjacent cranial bones; and residual neurological deficits (eg,hemiparesis and aphasia).
Delay in surgery leads to clinical worsening and poor results. Of the patients operated within 72 hours, 10% became disabled as against 70% if the surgery took place after 72 hours.52 Patient education should emphasize compliance with medication-both antibiotics and antiepileptic drugs. Intravenous antibiotics for a total period of 3 to 6 weeks can be administered on either an inpatient or outpatient basis. Certain prognostic factors are identified in SDE (Table 5). Outcome is dependent on the preoperative level of consciousness,47,52,53 timing and aggressiveness of treatment,19,31,45 and the rapidity of progress of disease.47
Subdural empyema is associated with the high incidence of morbidity (ie, neurological deficits) because very ill patients who would have died in the past now survive with deficits. Early diagnosis and treatment, more accurate localization with head CT scan, early sinus drainage, and recognition of the prominent role of anaerobes in the disease have reduced the mortality rate in SDE.
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