Subdural empyema (SDE) is a life-threatening infection that was first reported in the literature approximately 100 years ago. Subdural empyema is an intracranial focal collection of purulent material located between the dura mater and the arachnoid mater. It has also been referred to as subdural abscess, pachymeningitis interna, and circumscript meningitis.1 Left untreated, SDE is invariably fatal. Since the introduction of antibiotics, the mortality rate for this infection has decreased significantly and now ranges from 14% to 28%.2,3 In the preantibiotic era, the mortality rate approached 100%; this still may be the case in developing countries. However, in the developed world, the mortality rate has improved tremendously, and it is approximately 6% to 35%.4 Rapid recognition and the early institution of appropriate treatment and neurosurgical intervention give the patient a good chance of recovery with little or no neurological deficit.
Subdural empyema is a collection of pus between the dura mater and the arachnoid mater. It is usually unilateral and has a tendency to spread rapidly through the subdural space until limited by specific boundaries (eg, falx cerebri, tentorium cerebelli, base of the brain, and foramen magnum). It accounts for 20% of all cases of intracranial abscesses. The infection is more common in men, who may account for as many as 80% of cases. Approximately two thirds of patients are aged between 10 and 40 years. In infants, SDE is most commonly a complication of purulent meningitis.5,6 In older children, the source of SDE is typically direct extension of sinusitis or otitis media.1,3,5-9 Other causes include spread of infection from distant sites (viz, lungs). Subdural empyema can develop after a cranial surgery or after a trauma, particularly in cases where there is a compound depressed fracture.1,2,4,10 Subdural empyema have been reported after secondary infection of a subdural effusion or hematoma.1,2,5 The infection can spread from mastoid or middle ear infections by eroding the tegmen tympani11 and from the frontal air sinus by erosion of its posterior wall.12 The infection can also spread by retrograde septic thrombophlebitis.8 Subdural empyema, which is associated with venous sinus thrombosis and thrombophlebitis, may cause cerebral abscess or infarction.13,14 Subdural empyema may also occur after surgery; in rare cases, it is associated with septicemia because of the valveless diploic veins.15 As the SDE progresses, it behaves like an expanding mass lesion, which occur after trauma-associated increased intracranial pressure and cerebral intraparenchymal penetration. Cerebral edema and hydrocephalus also may be present secondary to disruption of blood flow or cerebrospinal fluid (CSF) flow caused by the increased intracranial pressure. Thrombosis of the cortical veins or cavernous sinuses or from septic venous thrombosis of contiguous veins in the area of the SDE may lead to cerebral infarction.
The rate of success in culturing bacteria from surgically evacuated pus varies from 54% to 81%.3,12,16 Common causative organisms are anaerobes, aerobic streptococci, staphylococci, Haemophilus influenzae, Streptococcus pneumoniae, and other gram-negative bacilli (Table 1).17 The most common organisms in intracranial SDE secondary to paranasal sinusitis are anaerobic and microaerophilic streptococci, in particular those of the Streptococcus milleri group (S. milleri and Streptococcus anginosus).4,7,9,18,19Staphylococcus aureus is seen in 7% cases of SDE associated with sinusitis and is commonly seen in postoperative/posttraumatic SDE.1,9,20Pseudomonas aeruginosa or Staphylococcus epidermidis may be present in cases related to neurosurgical procedures, and Salmonella species have been detected in patients with advanced acquired immune deficiency syndrome; multiple organisms may be present simultaneously. Spinal SDEs are almost invariably caused by streptococci or by S. aureus.9 In children, SDE is commonly secondary to H. influenzae or S. pneumoniae meningitis.21 Nontyphoidal Salmonella organisms have been reported in SDE in children recently.22-24 However, in adults, nontyphoidal Salmonella organisms have been found in the setting of advanced acquired immune deficiency syndrome infection.25
Stephanov et al26 described SDE "as the most imperative of neurological emergencies," which, if not treated immediately, is associated with high risk of status epilepticus, spreading cortical venous and cortico-venous sinus thrombosis, fulminating cerebritis, brain swelling, cerebral coning, and ultimately leads to death. It is difficult to clinically differentiate between meningitis and SDE. The diagnosis of SDE is based on a strong clinical suspicion (Table 2).1,7,27 The commonest clinical presentation is a triad of fever, sinusitis, and neurological deficits, with a fulminant and rapid downhill course.1,7-9 Other symptoms include headache, nausea/vomiting, first-time seizures, and mental-status changes.8,9,20,28 Headache, initially focal, is a prominent early symptom in as many as 90% of patients. Later, the headache becomes diffuse. As the infection progresses, focal neurological signs may appear. If untreated symptoms may progress over several days to include drowsiness, increasing stupor and eventually, coma. Seizures, either focal or generalized, have been reported in as many as 50% of patients. Examination often reveals a temperature greater than 38°C (100.5°F). Aphasia may occur when the dominant hemisphere is involved. Meningismus is present in 80% to 90% of the patients. Occasionally, palsies of the third and sixth cranial nerves occur. In addition, more than 85% of the patients have contralateral motor deficits. Certain conditions that must be considered in the differential diagnosis of SDE (Table 3) and these conditions can usually be distinguished by clinical findings, lumbar puncture, brain imaging, and appropriate laboratory studies.29-31
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
Magnetic Resonance Imaging
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).
Follow-Up and Prognosis
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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