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Vertebral osteomyelitis (VO) and spinal epidural abscess (SEA) have the potential to cause significant long-term disability and even death if not properly diagnosed and treated. To obtain the best patient outcomes, these spinal infections require prompt diagnosis and appropriate treatment. They may develop acutely or subacutely or become chronic; it is therefore important to understand the diagnosis and treatment options for VO and SEA thoroughly, as prompt and appropriate intervention can potentially prevent devastating long-term consequences, especially with the increasing incidence of these conditions in recent years. This chapter reviews the latest updates on VO and SEA epidemiology, pathophysiology, risk factors, microbiology, clinical presentation, radiographic imaging, treatment options, and expected outcomes.
Spinal infections account for 2% to 7% of all musculoskeletal infections. Their overall incidence continues to rise, in part due to an increase in susceptible patient populations and improvements in diagnostic accuracy. , Historically, VO and SEA were thought to be infrequent infections of the vertebral column. The estimated annual incidence of VO was as low as 0.06 to 1 episode per 100,000 persons ; however, more recent studies have demonstrated a significant increase, with incidences ranging from 5.4 to 7.4 per 100,000 persons in developed countries. , Similarly, SEA traditionally accounted for only 0.2 to 1.2 cases per 10,000 hospital admissions, whereas more recent studies document the incidence at approximately 2 to 5 cases per 10,000 hospital admissions, a more than fivefold increase. ,
VO and SEA tend to affect males (51% to 69%) more than females, with a peak incidence in the sixth and seventh decades of life. , Newer studies have demonstrated a rising incidence of these infections in adult patients with impaired immune systems, frequent bacteremia, or both. In particular, patients with AIDS and intravenous drug users have been shown to have exceedingly high relative rates of VO or SEA. , Patients with diabetes, abusive alcohol consumption, liver cirrhosis, renal disease on dialysis, and those on chronic immunosuppression have demonstrated a proclivity to develop spinal infections as well. ,
The widespread use of magnetic resonance imaging (MRI) technology coupled with the greater concentration of these patients at tertiary care centers may account for at least a portion of the increased relative incidence of spinal infections in recent years. It is unlikely that the increased incidence of VO and SEA will reverse in the near future, as improved life expectancy, the continued presence of comorbid factors, utilization of spinal instrumentation, increased awareness and improved diagnostic techniques are all contributors to the increasing documentation of spinal infections. , ,
The primary pathogenesis of VO varies by patient age. In children, the intervertebral disc receives a direct blood supply through collateral vessels associated with the vertebral end plates. Thus, systemic bacteria are able to penetrate the vertebral body. By the third decade of life, the collateral vessels present in childhood often involute, such that there is no direct vascular connection between the systemic circulation and the vertebral body.
The adult vertebral body’s blood supply is equivalent to the metaphyseal blood supply of the long bones, which are areas of slow blood flow susceptible to hematogenous bacterial seeding and arteriolar occlusion. Hematogenous seeding accounts for approximately 50% of pyogenic VO, whereby transient bacteremia seeds relatively avascular regions adjacent to subchondral bone. Direct inoculation is the second most common cause of VO and can occur after routine procedures such lumbar puncture, epidural block, laminectomy, discectomy, radiofrequency and stabilization procedures, or other spinal surgeries. The lumbar spine is the most commonly affected region and subsequent destruction of the osseous anatomy or intervertebral disk can result in instability, pathologic fracture, and possible neurologic compromise.
The pathogenesis of SEA typically occurs through direct extension from a VO primary site, by hematologic seeding, or from direct contamination, as through surgical intervention or trauma. Most cases of SEA develop in the posterior epidural space; however, some studies indicate that SEA may generally be confined to the anterior portion of the spinal canal. Once a SEA has developed, it is typically limited to three or four vertebral segments and most commonly occurs in the thoracic spine. Expansion of the SEA can result in neurologic deficit through either direct compression, vascular occlusion of the adjacent spinal cord, or cauda equina.
Several systemic risk factors have been associated with osteomyelitis and SEAs; many of these are associated with an immunocompromised state, predisposing such patients to develop spinal infections. Diabetes impairs the immune response and is associated with the development of both VO and SEA. Studies have shown diabetes to be associated with VO in 10% to 37% of cases , , and SEA in 22% to 36% of cases. , Intravenous drug abuse is also a common risk factor for spinal infection; such abuse has been found in 6% to 11% of patients with VO , and 25% to 39% of those with a SEA. , , Additional identified risk factors for spinal infection include chronic kidney disease, liver disease, endocarditis, obesity, corticosteroid use, malignancy, and human immunodeficiency virus. , , , , ,
Since one of the major causes of VO and SEA includes hematogenous dissemination of an infection from a remote source, infections and bacteria originating from other parts of the body serve as risk factors for spinal infections. Therefore spinal infections have been associated with bacterial endocarditis, which can be present in up to one-third of patients with a spinal infection. Other sources of infection resulting in hematogenous spread to the spine include urinary tract infections, dental infections, pneumonia, and skin infections. Skin and soft tissue may be the most frequent source of bacteremia and can be responsible for up to 25% of SEA. , , , The most common source of infection for VO seems to be the urinary tract.
Spinal infections may also develop from direct seeding of bacteria via an invasive procedure such as prior spinal surgery, recent spine trauma, lumbar punctures, epidural injections, or catheter placement. Prior spinal surgery has been reported as a risk factor in 17% to 39% of patients who develop VO or SEA. , , , Postprocedural spinal infections may be increased by prolonged operative time during the index procedure as well as by the instrumentation, extensive soft tissue devitalization, or the creation of significant dead space. Interestingly, the rate of infection associated with less invasive procedures seems to be greater than that due to open spinal surgeries. This may be attributed to the less strict sterilization criteria applied during these procedures. In addition, many minimally invasive procedures are currently performed by nonsurgical specialists. Recent studies have found the risk of developing a SEA after epidural catheterization to range from 0.04% to 0.07%. Moreover, leaving catheters and drains in place at the time of surgery may increase the risk of acquiring a spinal infection. , Trauma to the spine, resulting in disruption of anatomic barriers, has also been associated with the development of SEA and VO.
Bacterial pathogens remain the primary infectious agents responsible for most cases of VO and SEA. Fungal agents occasionally cause disease, particularly in immunosuppressed patients, and some parasitic agents have been associated with VO and SEA in endemic regions. Among bacterial pathogens, Staphylococcal infections, including Staphylococcus aureus and Staphylococcus epidermidis , most often drawn from a primary skin or soft tissue infection, are by far the most common pathogens responsible for VO and SEA. Specifically, S. aureus is identified in 32% to 67% of VO infections, , , and this incidence continues to rise on an annual basis. In SEA, S. aureus is isolated in approximately 70% of patients. , Less common pyogenic causes of VO and SEA include gram-negative bacteria such as Escherichia coli , Pseudomonas aeruginosa, Haemophilus influenzae , and Klebsiella pneumoniae . Approximately 9% of cases may be polymicrobial, and up to 50% of VO and 40% of SEA may be culture negative. ,
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