47 Infections of the Thoracic Spine
KEY POINTS
Introduction
Spinal infections are also classified by the primary location of pathogenesis. Sole involvement of the disc space is referred to as discitis. Osteomyelitis is an infection of the bony spine (Figure 47-1). Osteodiscitis or spondylodiscitis is combined involvement of the intervertebral disc and the vertebra. Abscess or granulation formation can occur in a subdural, epidural, or paravertebral location (Figure 47-2). Frequently, spinal infections invade all compartments of the spinal column, including the soft tissues, bony spine, and within the spinal canal.
Pathophysiology
The pathophysiology of spinal infection ultimately begins with the individual’s underlying predisposing risk factors. Advanced age, diabetes, and multiple medical comorbidities are associated with increased risk for spinal infection. Additionally, spinal surgery, intravenous drug use, and immunocompromise contribute to further risk. Infection generally metastasizes hematogenously to the spine from extraspinal sources such as the urinary tract, respiratory system, skin or soft tissue infections, or cardiac vegetations. Direct inoculation from surgery, percutaneous procedures, or penetrating trauma is an additional modality for bacterial seeding. Local invasion to the spine also occurs from infected adjacent or contiguous sources such as the retroperitoneal, abdominopelvic, pleural, or retropharyngeal spaces. Spread of infection can also occur within the spinal column by direct extension from the bony or soft tissue elements to the epidural space.
Bacterial Pathogenesis
Pathologic sequelae of spinal infection include loss of spinal alignment with progressive deformity, and risk of neurological compromise. Bacterial involvement of the spinal column with subsequent inflammatory infiltration causes bony destruction and eventually erodes the subchondral plate to involve the relatively avascular disc space (Figure 47-3). Advanced bone loss, particularly across multiple adjacent segments, combined with disc space narrowing, leads to progressive kyphotic deformity. neurological compromise may result from severe bony destruction, resulting in pathologic fracture with retropulsed bony fragments into the canal. Epidural abscess formation or extension of inflammatory granulation tissue into the canal can cause direct compression of the spinal cord or nerve roots. Additionally, septic thrombosis of veins within the epidural space or the arteriolar supply can cause ischemic injury. Particularly, in a spinal cord already compromised by mechanical compression from either an abscess or fracture, hypoperfusion from thrombosed feeding arteries or draining veins may lead to rapid neurological deterioration.
Gram-positive cocci are the most prevalent inciting organism, representing 50% to 67% of all causative organisms. Staphylococcus aureus is the most prevalent bacteria identified, accounting for 80% of all gram-positive infections, and 55% of all spinal infections. In a meta-analysis of 915 patients with epidural abscess, S. aureus was identified as the causative organism in 73.2% of cases. Gram-negative bacteria, particularly Escherichia coli and Proteus, are more frequently identified in patients with preexisting urinary tract infections. Pseudomonas aeruginosa is most common among immunocompromised patients or intravenous drug users. Indolent infections are more likely to occur with low-virulence organisms such as Streptococcus viridans or Staphylococcus epidermisdis.
Pathogenesis of Tuberculosis
Tuberculosis of the spine results from hematogenous spread of Mycobacterium tuberculosis from well-established extraspinal foci, primarily originating from the respiratory or genitourinary tract. Unlike pyogenic osteomyelitis, spinal tuberculosis may begin in the paradiscal area and spread under the anterior longitudinal ligament to involve adjacent vertebral bodies, while relatively preserving the disc space. Additionally, spinal tuberculosis frequently involves the posterior spinal arch, whereas pyogenic osteomyelitis is primarily a disease of only the anterior spinal column. Because spinal tuberculosis often causes widespread destruction of a spinal segment, vertebral collapse with pathologic subluxation, kyphosis, and retropulsion occur in severe cases and present greater risk for acute neurological compromise than bacterial osteomyelitis (Figure 47-4). Delayed chronic paresis also occurs with progressive deformity or in the setting of epidural granulomas that result from longstanding tuberculous infection.
Diagnostic Evaluation
Imaging
Plain spine x-rays may demonstrate characteristic findings associated with osteomyelitis or osteodiscitis, and often serve as a rapid method for surveying the full spinal axis for potential infection. Disc space narrowing is the earliest and most consistent radiographic finding, occurring in 74% of cases, generally after approximately 2 to 4 weeks. Enlargement of the paravertebral shadow may indirectly suggest a thoracic paravertebral abscess. After 3 to 6 weeks, leukocyte infiltration into the subchondral bone and vertebral body leads to bony destructive changes, appearing as a lytic area in the anterior aspect of the vertebral body adjacent to the disc, or blurring of the endplates. With advanced bone loss, the vertebral body collapses. Thirty-six inch standing x-rays are essential for assessing progression of sagittal and coronal plane deformity in severe cases. With chronic disease (after 8 to 12 weeks), reactive bone formation and endplate sclerosis occurs. Ultimately, the reparative process results in new bone formation and hypertrophic changes. Eventually, 50% of cases lead to spontaneous fusion; however, it may require several years for this to take place. The remaining cases likely form a fibrous ankylosis which may similarly effectively immobilize the involved segment.