Cranial and Spinal Epidural Abscess

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Epidemiology and Risk Factors. Cranial epidural abscesses develop in the space between the dura and inner table of the skull and are usually caused by the spread of infection from the frontal sinuses, middle ear, mastoid, or orbit. y Epidural abscesses may also develop as a complication of a craniotomy or compound skull fracture. At present, the most common cause of a cranial epidural abscess is craniotomy that has been complicated by an infection of the wound, bone flap, or epidural space.y Epidural abscesses may result from or be associated with an area of osteomyelitis. A spinal epidural abscess develops in the space outside the dura mater but within the spinal canal. The spinal

TABLE 42-2 -- ANTIMICROBIAL THERAPY FOR SUB

DURAL EMPYEMA

Organism

Adult

Dosing Interval

Child

Dosing Interval

Staphylococcus aureus Methicillin-sensitive

Nafcillin 9 to 12 g/d

Every 4 hr

Nafcillin 200 mg/kg/d

Every 4 hr

Staphylococcus aureus Methicillin-resistant

Vancomycin 2 g/d

Every 12 hr

Vancomycin 40 to 60 mg/kg/d

Every 12 hr

Streptococci

Penicillin G 20 to 24 MU/d

Every 4 hr

Penicillin G 250,000 to 400,000 U/kg/d

Every 4 to 6 hr

Gram-negative bacilli

Ceftriaxone 4 to 6 g/d or

Every 12 hr

Ceftriaxone 80 to 100 mg/kg/d or

Every 12 hr

Cefotaxime 8 to 12 g/d or

Every 4 hr

Cefotaxime 200 mg/kg/d or or

Every 6 hr

Ceftazidime 6 g/d

Every 8 hr

Ceftazidime 125 to 150 mg/kg/d

Every 8 hr

Anaerobes

Metronidazole 600 mg/d or

Every 8 hr

Metronidazole 22.5 mg/kg/d or

Every 8 hr

Chloramphenicol 4 g/d

Every 6 hr

Chloramphenicol 100 mg/kg/d

Every 6 hr

Reproduced with permission from Shapiro S: Cranial epidural abscess and cranial subdural empyema. In Roos KL (ed): Central Nervous System Infectious Diseases and Therapy. New York, Marcel Dekker, 1977, pp 499-506.

epidural space is only a true space posterior to the spinal cord and the spinal nerve roots. The anteroposterior width of the epidural space is greatest in the area where the spinal cord is smallest, that is from approximately T4 to T8, and from L3 to S2. d , y The most common location for an epidural abscess is the posterior midthoracic region between the fourth and eighth thoracic vertebrae. y The anterior epidural space is only a potential space because the dura is virtually adherent to the posterior surface of the vertebral bodies along the ventral aspect of the spinal canal from the first cervical to the second sacral vertebrae. Anterior abscesses usually occur at cervical levels. y The most common etiology of a spinal epidural abscess is hematogenous spread of bacteria from a remote site of infection to the epidural space. This includes such sites as the skin, urinary tract, lungs, pelvis, cardiac valves, and pharynx. An epidural abscess may also develop by direct extension from a contiguous infection such as vertebral osteomyelitis. The latter disorder is a particularly common etiology for spinal epidural abscess formation in intravenous drug abusers. Immunosuppression from any cause, but most commonly from AIDS or diabetes mellitus, is a predisposing condition in approximately 50 percent of cases of spinal epidural abscesses. y The formation of a small hematoma owing to mild blunt trauma may also provide a locus minoris resistentiae that may allow for hematogenous seeding of infection resulting in the formation of a spinal epidural abscess.

Pathogenesis and Pathophysiology. Infection in the frontal sinuses, middle ear, mastoid, or orbit is able to reach the epidural space through the retrograde spread of thrombophlebitis in the emissary veins that drain these areas, by way of direct spread of the infection through bone (osteomyelitis), or through direct infection of the epidural space during craniotomy.y As stated earlier, hematogenous spread to the epidural space from a remote site of infection is an extremely rare cause of cranial epidural abscess but an extremely common cause of spinal epidural abscess.

A spinal epidural abscess may develop as a result of the hematogenous spread of infection from a distant focus of infection to the epidural space. There may also be hematogenous spread of infection to a vertebral body or disc that results in discitis and/or osteomyelitis that subsequently extends into the spinal epidural space. Infection of the epidural space may also occur from direct extension of infection from decubitus ulcers, infected abdominal wounds, or psoas abscesses. y The pathophysiology of spinal cord dysfunction from spinal epidural abscess has been investigated in a rabbit model. y , y The gross appearance of the spinal cord at the level of the epidural abscess is usually normal. Microscopically, scattered areas of softening, vacuolization of the cord, areas of necrosis with the disappearance of cells, loss of myelin, and axonal swelling are frequently seen. Myelomalacia occurring in the spinal cord beneath an epidural abscess results from the direct compression of neural tissue and inflammatory thrombosis in the intraspinal vessels with subsequent infarction.

Clinical Features. The clinical presentation of an intracranial epidural abscess is an unrelenting hemicranial headache or persistent fever that develops during or after treatment for frontal sinusitis, mastoiditis, or otitis media. Focal neurological deficits, seizures, and signs of increased ICP do not develop until the infection extends into the subdural space. y Approximately 10 percent of epidural abscesses are associated with a subdural empyema. y An epidural abscess that develops near the petrous bone and involves the fifth and sixth cranial nerves presents with ipsilateral facial pain and lateral rectus weakness (Gradenigo's syndrome). A spinal epidural abscess presents as fever and pain at the affected spinal level. Heusner y described a characteristic clinical pattern of symptom progression. Back pain is the initial symptom, which is followed by radicular pain in the extremities or pain in an intercostal thoracic dermatomal pattern within 2 to 3 days. As the disease progresses, paresis of appendicular muscles is associated with loss of sensation below the level of the lesion and the loss of bowel and bladder control. Finally, there is complete paralysis of appendicular muscles and a loss of all sensory modalities below the level of the lesion.

Evaluation. The MRI is the diagnostic procedure of choice to demonstrate a cranial epidural abscess because it is free from bony artifacts adjacent to the inner table of the skull, and is easily able to demonstrate extracerebral fluid collections. The epidural fluid will be of higher signal intensity on both MRI T1- and T2-weighted images than the ventricular CSF. Following the administration of gadolinium,

a significant enhancement of the dura on MRI T1- weighted images is seen. y On the noncontrasted CT scan, an epidural abscess has the appearance of a poorly defined lentiform area of low density adjacent to the inner table of the skull. After the administration of contrast, the convex inner side of the low-density lesion enhances. This represents the inflamed dural membrane.y

MRI is also the procedure of choice to demonstrate a spinal epidural abscess. A spinal epidural abscess extends three spinal segments on average and may extend for as long as 13 segments.y MRI is able to visualize the entire extent of the epidural abscess in all directions and the degree of spinal cord compression. An epidural abscess is isointense to CSF on MRI T1-weighted images and hyperintense as compared with CSF on MRI T2-weighted images. Following the administration of gadolinium, enhancement of the lesion occurs. Because spinal epidural abscess is usually a result of the hematogenous seeding of the epidural space, there may be evidence of systemic illness with a peripheral leukocytosis or an elevation in the erythrocyte sedimentation rate. The examination of the CSF may be useful to determine the infecting organism. A lumbar puncture should not be performed, however, when the possibility of a lumbar abscess exists because of the risk for spread of the infection from the epidural space to the subarachnoid space.

Management. The primary treatment of a cranial epidural abscess is surgical debridement, Gram's stain and culture of the purulent material, and intravenous antibiotic therapy. Recommendations for the choice of empiric antibiotic therapy are the same as that described for empiric therapy of subdural empyema and should cover aerobic and anaerobic streptococci, staphylococci, gram-negative bacilli, and anaerobes.

An acute spinal epidural abscess must be managed with an immediate laminectomy and decompression and drainage of the epidural space, followed by 4 to 6 weeks of intravenous antibiotic therapy and then 2 to 3 months of oral antibiotic therapy. y Empiric antibiotic therapy should include coverage for S. aureus because this organism is the etiological agent in the majority of spinal epidural abscesses. There is an increasing incidence, however, of spinal epidural abscess due to gram-negative aerobic bacilli, aerobic streptococci, anaerobes, and Mycobacterium tuberculosis. Empiric therapy should also include antituberculous chemotherapy, including isoniazid, rifampin, ethambutol, pyrazinamide and either streptomycin, rifabutin, or clofazimine. A tuberculous spinal epidural abscess is usually associated with vertebral osteomyelitis.

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