Etiology

The majority of spinal infections are pyogenic infections (i.e., caused by bacteria). Other causes included tuberculosis, fungi (granulomatous infection), and parasites (rare). The most common bacterial organisms are Staphylococcus aureus and streptococcus ( Fig. 122-1 ). Approximately 2% to 15% of S. aureus are reported to be methicillin-resistant S. aureus , often catheter-related or nosocomial. Gram-negative bacilli are commonly found in intravenous drug users. Mycobacterium tuberculosis , Pseudomonas , gram-negative bacteria, and fungal infections are more often found in immunocompromised patients. Salmonella may also be found in immunocompromised patients and patients with a history of sickle cell anemia. Patients with penetrating trauma can present with anaerobic spinal infections ( Table 122-2 ). Unfortunately, in a third of the patients, the infective organism cannot be identified.

Sagittal CT ( A ) and T2 MRI ( B ) showing L4-L5 discitis with associated vertebral osteomyelitis.

Infectious processes can spread to the spinal elements from (1) hematogenous dissemination from a distant location, usually the skin, respiratory, gastrointestinal, or genitourinary tract, or (2) direct extension from an infected contiguous source or directly from an external source, including iatrogenic. Hematogenous spread can be via venous or arterial circulations. The vertebral venous plexus, known as the Batson plexus, is a potential route for the spread of infection. It is part of the cerebrospinal venous system and allows flow from the pelvic venous plexus to the perivertebral plexus. Due to the vascular supply of the spine, hematogenous spread is most common to the lumbar spine (55% to 60%), followed by the thoracic spine (30% to 35%), and less commonly to the cervical spine (10% to 15%). The urinary tract is a frequent source of infection. Tuberculosis, with the respiratory system as the local source, mainly affects the thoracic spine and usually extends beyond one level ( Fig. 122-2 ).

Sagittal ( A and B ) and axial ( C and D ) T2 MRI and CT ( E ) showing tuberculosis with four-level disease and extensive bony destruction. Postoperative anteroposterior ( F ) and lateral ( G ) radiographs demonstrate debridement of the vertebral bodies with anterior mesh cage and posterior instrumentation and fusion.

In pediatric patients, an extensive arterial anastomotic network is present in the spine and into the intervertebral discs, resulting in discitis by direct hematogenous spread. However, the arterial network also allows the body to combat these infections, resulting in only a small portion of bony destruction. As patients age, the intervertebral discs become avascular and the anastomotic network becomes end arteries in the vertebrae, usually by age 15. Septic emboli travel to and become trapped in these end arteries and result in a larger area of potential bony necrosis and spread to the intervertebral disc from adjacent metaphyseal regions. This can cause vascular bone infarcts, rupture of end plates, osteolysis, and compression fractures leading to spinal instability with possible compression of the spinal cord or nerve roots. Contiguous spread of infection to the spine is from adjacent structures, included esophageal perforation, retropharyngeal abscess, or aortic implants. Often the etiology is iatrogenic, and the infection may result following epidural procedures.

Clinical Presentation

When diagnosing spinal infections, a high index of suspicion is required. Notably, delayed diagnosis in immunocompromised patients is common due to a decreased immune response and minimal clinical complaints. Signs and symptoms of spinal infections in all patients are vague and nonspecific, have a low specificity, and often present similar to degenerative disease, noninfectious inflammatory disorders, and spinal neoplasms. This therefore results in a delay in diagnosis, often 2 to 6 months after the onset of symptoms.

The most common complaints of patients presenting with spinal infections include nonspecific neck and back pain not relieved by rest. Often, the patients note constant pain that is worse at night. Constitutional symptoms, including fevers and night sweats, are less common, often occurring in only 50% of patients with pyogenic infections and 17% of patients with tuberculosis. Loss of weight and poor appetite are usually later symptoms. Other signs may include localized spinal tenderness, muscle spasm, and significantly decreased range of motion. Cervical spinal infections most often present with neck stiffness. They may also form a retropharyngeal abscess and can cause dysphagia and dysphonia as well as torticollis. In the pediatric population, symptoms are even more nonspecific. They include irritability; refusal to crawl, sit, or walk; and incontinence. Lumbar lordosis can also be seen. However, fever and neurologic deficits are rare in children.

Later in the course of the infection, neurologic deficits and sepsis are the most worrisome complications. Neurologic deficits are likely primarily from mechanical compression and secondarily from vascular compromise, most notably with epidural abscesses. These neurologic symptoms may include leg weakness, numbness, and incontinence. In addition, spinal infections can spread to the adjacent spinal column, resulting in progressive bony destruction and a structural kyphosis or gibbus deformity, or they can spread to the surrounding muscles and cause a psoas abscess.

Diagnostic Workup

Initially, laboratory workup for spinal infections includes an assessment of white blood cell count (WBC count), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). An elevated WBC is seen in only two-thirds of patients. An elevated ESR is more sensitive, and an elevated CRP is seen in 90% of patients with spondylodiscitis. Both can also be used to monitor a therapeutic response. CRP is more sensitive and returns to baseline sooner, although a 25% reduction in ESR at 1 month is also an excellent indicator of a favorable therapeutic response. Blood cultures should also be obtained prior to administration of antibiotics. Almost two-thirds of blood cultures are positive and can be used to tailor antibiotic treatment.

Plain radiographs should be performed at the initial evaluation. The earliest sign of spinal infection that can be seen on plain radiographs is the loss of definition and irregularity of vertebral end plates. This usually occurs 2 to 8 weeks after the onset of symptoms. This leads to fragmentation of the end plates and a decreased intervertebral disc height. Radiographs are also valuable in the evaluation of global malalignment that may have been caused by the infection and bony destruction (coronal or sagittal).

Computed tomography (CT) is the most sensitive modality to assess bony changes. The most common changes are seen in the peridiscal area, adjacent to the vertebral end plate, as the infection spreads to the motion segment. Early changes in vertebral end plates can be picked up sooner with CT, as well evidence of bony necrosis and tuberculous pathologic calcifications. Ventral spinal column involvement is usually characterized by scalloping of the vertebral body. Infections can spread to adjacent vertebrae under the anterior longitudinal ligament. Central involvement can often be mistaken for a tumor. Posterior spine involvement, including the pedicles, lamina, and spinous processes, are rare due to the decreased vascularity of the area. Infections in this area are usually due to tuberculosis. CT myelography is able to provide additional detail of the spinal canal and is an important adjunct if magnetic resonance imaging (MRI) is contraindicated.

MRI has the highest sensitivity and specificity for imaging of spinal infections. It has a sensitivity of 96% and specificity of 94%. In addition, it provides greater epidural and soft-tissue detail. Spinal infections demonstrate a hypointense signal of the disc and vertebral body on T1 and a hyperintense signal on T2 due to edema. Gadolinium-enhanced MRI helps differentiate infection from degenerative and tumor pathology and significantly increases the accuracy of MRI. Degenerative disease demonstrates a hypointense signal on T2 imaging due to end plate changes without the resultant edema. Tumor lesions demonstrate a relative T1 hypointense signal to the normal bone marrow. However, no single differentiating imaging finding is able to clearly distinguish neoplasm from an infection. MRI findings of tuberculosis spondylitis include extensive bony destruction with sparing of the intervertebral disc, with heterogenous enhancement of the vertebral body and the presence of a paravertebral abscess ( Table 122-3 ). MRI findings, however, may worsen even following treatment and clinical improvement. Loss of gadolinium uptake and restoration of bone are MRI findings of a resolving infection; however, they tend to appear much later than clinical improvement and therefore should not be used as an early determination of infection resolution. Repeat MRI is not indicated if clinical and laboratory improvement is seen.

Bone scans do not provide the same level of detail as an MRI, but they do provide improved specificity. A three-phase bone scan is 87% to 98% sensitive and 91% to 100% specific. Gallium-67 citrate scan is less sensitive to bone remodeling and is helpful for follow-up. For improved specificity, there has been interest in [18F]fluoro-2-deoxy-D-glucose (FDG) positron emission tomography (PET) scan. FDG uptake is highest in areas of inflammation composed of neutrophils and macrophages, allowing for high-resolution imaging with acute and chronic infections and no FDG uptake in degenerative disease and fractures.

Obtaining a tissue diagnosis is the cornerstone in guiding antibiotic treatment in adults. In pediatric patients, a biopsy is indicated only if the patient failed empirical treatment or if there is a concern for fungal or mycobacterial infection. In adults, a biopsy should be performed prior to any antibiotic therapy unless it is an emergency situation requiring patient stabilization. Antibiotics prior to biopsy can lead to a negative result, as can insufficient tissue obtained for analysis. Percutaneous CT-guided biopsy is preferred for spinal lesions with an accuracy of 70%, depending on the facility and its capabilities. A core sample biopsy is preferred to fine-needle aspiration unless an abscess cavity can be easily accessed.

If a closed biopsy fails to identify the organism, if the infection is inaccessible, or if the patient presents with surgical indications including neurologic deficits and painful progressive spinal deformity, then an open biopsy is indicated.

Biopsy specimens should be sent for Gram stain and aerobic, anaerobic, fungal, and tuberculosis cultures. Mycobacterium tuberculosis can take 6 to 8 weeks to grow and therefore should be kept for a prolonged period of time. If a high-index of suspicion for tuberculosis is present, an interferon-gamma release assay (IGRA) from whole blood plasma and an acid-fast bacilli (AFB) smear and culture can be used with a sensitivity of up to 88%. If any concern for tumor or fungal disease is present, biopsy specimens should also be sent for histopathologic analysis.