Epidural and Subdural Infections
Subdural empyema is a focal purulent infection between the dura mater and arachnoid mater. More than 95% of cases of subdural empyema occur in the intracranial space rather than the spinal neuraxis.1 Subdural empyemas make up 15 to 22% of focal intracranial infections. The historically high mortality rate of more than 80% before the widespread availability of antibiotics was reduced to 15.6 to 41% after the advent of antimicrobial therapy.1 Once an empyema is established within the subdural space, there are few anatomic barriers to the spread of infection. From 70 to 80% of these cases occur over the cerebral convexities, although they can also have a parafalcine, tentorial, or infratentorial location. Concomitant intracerebral abscess is present in up to 6 to 22% of cases, whereas epidural abscess is found in 9 to 17% of cases.2–4
Epidural abscess develops between the skull and the dura mater. The adherence of the dura mater to the calvaria can limit the expansion of an intracranial epidural abscess. Autopsy studies reveal evidence of the spread of epidural infection into the subdural space in 80% of cases.5
Epidemiology and Pathophysiology
A majority of cases of subdural empyema develop by the direct local extension of infection rather than by hematogenous spread. In infants, most cases of subdural empyema result from the infection of subdural effusions associated with meningitis.4 Local spread of infection most commonly occurs from frontal, ethmoid, or sphenoid sinusitis; osteomyelitis; and retrograde thrombophlebitis of the valveless diploic veins.
Rarely do mastoid infections lead to epidural abscess or subdural empyema. The vascularity of the diploic system is at its most prominent in men in their second and third decades of life. The frontal sinus also continues to develop during this period. Most cases of complicated sinusitis occur in otherwise healthy men in this age group. There is a predisposition for subdural empyema to develop in males, with a male-to-female ratio of 3:1.2,4,6–8
Direct extension of infection into the subdural space occurs in chronic otitis media and rarely as a consequence of mastoiditis. Infection can be introduced after the application of cranial pins and traction devices, neurosurgical or otolaryngologic procedures, and penetrating head trauma. Infection can also occur as a complication of preexisting subdural collections and with rare pulmonary and hematogenous diseases. Tuberculous subdural empyema has been reported.1,4,5,8–11
Like subdural empyema, epidural abscesses occur most frequently in males during the second and third decades of life, corresponding to the population with the highest likelihood of developing complicated sinusitis. Intracranial epidural abscesses arise from direct extension in association with sinusitis, osteomyelitis, cranial pin and traction device placement, penetrating head trauma, or postoperative infection.4,5,8,10
The focus of this chapter is limited to intracranial epidural abscess and subdural empyema. However, it is important to note that the spine, in contrast to the intracranial compartment, provides a relatively large space that can allow significant extension of a spinal epidural abscess. The spread can be hematogenous by direct extension of a contiguous local infection, and the pathophysiology of spinal epidural abscess is different from that of intracranial epidural abscess. Epidural abscess is estimated to occur nine times more frequently in the spine than intracranially.5
Clinical Features
In cases of subdural empyema, the most common presenting features are fever and headache. Clinical symptoms of sinusitis or a history of sinusitis may or may not be present. Altered mental status is frequent. Other presenting features of subdural empyema include meningismus, hemiparesis, nausea, vomiting, sinus tenderness, local swelling/inflammation, speech difficulty, homonymous hemianopsia, decreased visual acuity, photophobia, cranial nerve palsies, and papilledema. Seizures occur in 8 to 20%. Neurologic symptoms are typically due to inflammation of the cerebrum and meninges, mass effect, and thrombophlebitis of the cerebral venous drainage. Focal deficits and seizures develop as disease progression increases the mass effect or causes cerebritis.1,12
Patients with intracranial epidural abscess generally present with signs and symptoms of infection and an expanding extra-axial intracranial mass. These may include fever, headache, altered mental status, malaise, nausea, vomiting, focal neurologic deficits, seizures, sinus tenderness, or local inflammation. In cases of postoperative infection after craniotomy, over 90% of patients with epidural abscess have evidence of a wound infection.5,12 Compared with that of subdural empyema, the clinical presentation of intracranial epidural abscess is generally described as more indolent, although cases may vary.12
Work-Up and Diagnosis
Laboratory Studies
Laboratory studies apply to both subdural empyema and epidural abscess. They include complete blood counts, which reveal a leukocytosis with a predominance of polymorphonuclear neutrophils. Abnormalities of the erythrocyte sedimentation rate and C-reactive protein level are nonspecific findings, with an ESR that is elevated but generally less than 100 mm/h.4,12–14 Blood, urine, and sputum should be cultured to identify potential organisms and sources of infection. A metabolic panel should be obtained to allow correction of any electrolyte abnormalities, such as hyponatremia, and to screen for underlying metabolic dysfunction in light of medical and antibiotic treatment.1,14,15 Lumbar puncture is typically not recommended for subdural empyema or intracranial epidural abscess because of the risk for brain herniation due to increased intracranial pressure. Cerebrospinal fluid (CSF) studies are often nonspecific and show a moderate pleocytosis with predominantly polymorphonuclear neutrophils, moderately elevated protein, and normal to low glucose levels. Gram stain and CSF studies are negative in over 75% cases of both epidural abscess and subdural empyema. Normal or sterile CSF samples do not exclude the diagnosis of intracranial epidural abscess or subdural empyema.4,12 Causative organisms vary with the etiology of the primary infection ( Tables 10.1 and 10.2 ). Sterile intraoperative cultures are reported in up to 50% of cases of epidural abscess and subdural empyema, presumably as a result of the preoperative administration of antibiotics. For this reason, empiric administration of antibiotics before the collection of a specimen for culture should be avoided.4,12–14
Imaging
Although magnetic resonance (MR) imaging is recognized to be more sensitive for showing morphological detail, detecting intraparenchymal abnormalities, and delineating the extent of infection, computed tomography (CT) is still the imaging modality most widely available and accessible in a timely manner. CT is most helpful when obtained with and without intravenous contrast, allowing differentiation between chronic subdural or epidural hematoma, postoperative changes, and infectious processes. CT findings for subdural empyema typically demonstrate a hypodense subdural lesion with enhancement, particularly along the medial border of the lesion at the pial surface, inward displacement of the gray–white junction, and effacement of the ventricles, cortical sulci, and basal cisterns ( Fig. 10.1 ). Mass effect is often caused more by edema than by the empyema collection itself. Vasogenic edema is prominent in cases of subdural empyema that are complicated by cerebritis, sinusitis, skull osteomyelitis, compound skull fracture, or craniotomy defect.6,8,13,16 On MR imaging, subdural empyemas generally appear hypointense or variable on T1-weighted images and hyperintense on T2-weighted images; they have high signal on diffusion-weighted images, indicating restricted diffusion. Rim enhancement is seen following gadolinium administration. Intracranial epidural abscesses exhibit hyperintensity on T2-weighted images, variable intensity on T1-weighted images, and restricted diffusion, and they most often demonstrate contrast enhancement at the periphery1,4,13,17 ( Fig. 10.2 ).
Associated Source | Organisms |
Paranasal sinusitis (frontal, ethmoid, sphenoid) | α-Hemolytic streptococci |
Staphylococci | |
Anaerobic/microaerophilic streptococci | |
Aerobic gram-negative bacilli | |
Bacteroides species | |
Otitis media/mastoiditis | Aerobic and anaerobic streptococci |
Pseudomonas aeruginosa | |
Bacteroides species | |
Enterobacter species | |
Staphylococci | |
Postoperative infection | Staphylococci |
Enterobacter species | |
P. aeruginosa | |
Propionibacterium species | |
Penetrating head trauma | Staphylococci |
Aerobic gram-negative bacilli | |
Clostridium species | |
Meningitis (neonate) | Group B streptococci |
Enterobacter species | |
Listeria monocytogenes | |
Meningitis (child) | Streptococcus pneumoniae |
Haemophilus influenzae | |
Neisseria meningitidis | |
Escherichia coli |
Associated Source | Organisms |
Paranasal sinusitis (frontal, ethmoid, sphenoid) | α-Hemolytic streptococci |
Staphylococci | |
Anaerobic/microaerophilic streptococci | |
Aerobic gram-negative bacilli | |
Bacteroides species | |
Otitis media/mastoiditis | Aerobic and anaerobic streptococci |
Pseudomonas aeruginosa | |
Bacteroides species | |
Enterobacter species | |
Staphylococci | |
Postoperative infection | Staphylococci |
Enterobacter species | |
P. aeruginosa | |
Propionibacterium species | |
Penetrating head trauma | Staphylococci |
Aerobic gram-negative bacilli | |
Clostridium species |
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