Etiology
Several risk factors or comorbidities are associated with the development of a spinal epidural abscess (SEA). The most common is intravenous drug use (IVDU), which has been reported to be associated with up to 53% of cases. Comorbidities associated with SEA include diabetes mellitus (21% to 42% of cases); immunosuppression, such as that related to HIV infection (up to 22%) or malignancy; chronic kidney or liver disease; alcohol misuse; and spinal trauma. Spinal surgery and other invasive procedures (e.g., epidural anesthesia or long-term spinal catheter) are also associated with SEAs. A patient with SEA may have one or more of these predisposing factors, but up to 20% to 50% of patients have none of them.[2][9]
Spread of infection causing SEA is hematogenous in up to 50% of cases (e.g., from the skin, mouth, urinary system, respiratory system, or infectious endocarditis). Up to 30% of SEAs result from direct extension of local infection, such as vertebral osteomyelitis, psoas abscess, or contiguous soft-tissue infection. The remainder are attributable to direct inoculation due to surgery or other invasive procedures.[9][17][18][19]
The most common pathogen in patients with SEA is Staphylococcus aureus, associated with around two-thirds of cases. MRSA is increasingly reported, particularly for patients with spinal surgery or implanted devices. Other causative organisms include Pseudomonas species (primarily in patients who inject drugs); other gram-negative bacteria (primarily in patients who inject drugs and in older men, with the urinary tract as a common source of infection); Mycobacterium tuberculosis (especially in developing countries); and Streptococcus species. Fungal and parasitic pathogens less commonly cause SEAs. However, no causative organism is identified in up to 25% of cases.[9][20][21]
Pathophysiology
The spinal epidural space lies between the dura and the adjacent spinal column. The epidural space is greater posteriorly throughout the spinal cord; anteriorly, the dura adheres closely to the vertebral body. The space is filled with fatty tissue, blood and lymphatic vessels, and spinal roots. The epidural venous plexus is a series of thin-walled veins running from the foramen magnum to the sacrum. These valveless veins and the lymphatics offer a ready pathway for local spread of an infection. Posterior compressive lesions are more often seen in hematogenous infections, whereas the anterior space is often the site of direct extension of contiguous infection (e.g., from a vertebral body).
With abscess development, neurologic impairment occurs both as a consequence of vascular compromise of the spinal cord or roots and by direct pressure on this tissue. Regional pain is the result of activated pain fibers in the spinal segment (annulus, endplate, ligaments, and dorsal roots) and may also be associated with paraspinal muscle spasm. Further neurologic impairment can then occur, such as radicular pain and paresthesias; motor weakness; sensory loss; sphincter dysfunction; and ultimately paralysis.
Classification
Anatomic level
Spinal epidural abscess (SEA) may be classified on the basis of the spinal level:
Lumbar
Thoracic
Cervical.
However, infection can involve multiple different anatomic levels. Some patients will have noncontiguous SEAs.[3]
Clinical staging
Four clinical stages that document progressive neurologic deficit have been described:
Localized muscle and bone pain
Radicular pain and paresthesias
Muscular weakness, sensory loss, and sphincter dysfunction
Paralysis.
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