Infections of the Thoracic Spine

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47 Infections of the Thoracic Spine

KEY POINTS

Introduction

The last several decades have witnessed a rise in reported spinal infections. This increase has largely been attributed to factors associated with a growing elderly population. Improvements in medical care have directly resulted in prolonged life expectancy with more individuals living longer with chronic diseases. As a result, various medical conditions associated with advanced age, such as diabetes or illnesses that lead to immunocompromise, predispose patients to developing spinal infections. Additionally, as individuals are living longer, more elderly patients are seeking to undergo spinal procedures for degenerative conditions that otherwise, left untreated, result in debilitating pain. Both minor procedures such as discography and epidural injections and extensive spinal fusion surgeries pose the risk of direct bacterial inoculation of the spine.

Infections of the spine are characterized either by their microbiology or by the location of pathology. From a microbiology standpoint, spinal infections are differentiated by pyogenic or granulomatous etiologies. Pyogenic infections are generally of bacterial origin. Granulomatous spinal infections encompass fungal etiologies, but include some bacterial sources, and refer primarily to the histologic course of the infection. Spinal tuberculosis is by far the most common of the granulomatous spinal infections worldwide.

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.

Spinal osteomyelitis is estimated to occur in 1 in 100,000 to 250,000, and accounts for 2% to 7% of all cases of osteomyelitis. Spinal osteomyelitis occurs more commonly among older individuals, with approximately one half of all patients being over 50 years of age. Similarly, epidural abscesses occur in adults and are estimated to occur in 0.2 to 1.2 per 10,000 hospital admissions annually. When bacterial spinal infections occur in younger individuals, they are more commonly seen in intravenous drug users. Both osteomyelitis and epidural abscesses generally occur in the thoracic and lumbar spine, with thoracic infections representing over a third to half of all cases, and lumbar infections accounting for a majority of the remainder. Cervical spine infections are estimated to account for only 5% to 14% of all cases.

Outside the United States, spinal tuberculosis still represents a considerable health care problem. Tuberculosis is relatively common in underdeveloped countries where malnutrition and overcrowding are present. It is estimated that 2 billion people have tuberculosis worldwide, with 9 million new cases each year. Approximately 5% of these patients have spinal involvement. Spinal tuberculosis is a major source of morbidity, representing the most common cause of nontraumatic paraplegia in underdeveloped countries.

While the incidence of spinal infections is increasing, management of these conditions is also dramatically evolving. Earlier detection, better screening and surveillance, and advanced imaging modalities have improved diagnosis of spinal infections and identification of pathogenic organisms. More effective antimicrobial pharmacotherapy has led to better medical treatment with clearance of infection and less recurrence. Surgical treatment options have incorporated advances in surgical technique, instrumentation, and biomedical technology to increase eradication of infection, preservation of neurological function, restoration of spinal alignment, and prevention of deformity and chronic pain.

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

Hematogenous seeding of the spine may occur via either arterial or venous pathways. The venous plexi that drain from within the spinal canal communicate with plexi that form a venous ring around each vertebral body. This venous system communicates with the venous drainage of the pelvis. Batson demonstrated that this venous pathway is a valveless system in which microorganisms may circulate and lodge in the low-flow end-organ vasculature surrounding the vertebral body. Alternatively, direct bacterial seeding of the vertebral body may occur from ascending and descending arterial branches that send penetrating vessels to the vertebral body.

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.

Clinical Presentation

The clinical presentation of bacterial spinal infections often depends on the virulence of the organism, the duration of infection, and the overall integrity of the patient’s immune system. Improved diagnostic modalities have led to earlier detection of disease, with initiation of appropriate medical therapy often before patients develop systemic illness or potentially irreversible neurological compromise. Over 90% of patients with pyogenic osteomyelitis present with axial neck or back pain as the primary complaint. The pain is generally characterized as insidious and nonmechanical in nature, and unrelieved by recumbency. Patients frequently note local spine tenderness with limited range of motion. Constitutional symptoms associated with infection such as fevers, chills, and malaise may also be present: however, an elevated temperature is only found in 52% of patients at time of presentation.

Neurological findings are less common with pyogenic osteomyelitis. A review of the literature reveals that only 17% of patients with bacterial osteomyelitis have neurological signs or symptoms on initial presentation. Alternatively, neurological complaints are frequently associated with acute bacterial epidural abscess, with 56% of patients presenting with motor deficits, and 36% with radicular pain. The clinical triad of localized spine pain, fever, and progressive neurological deficit is seen, however, in only 36% of patients with epidural abscess.

Spinal tuberculosis has a similar presentation to bacterial osteomyelitis, with most presenting with spine pain and localized tenderness. Unlike bacterial osteomyelitis, however, patients with tuberculosis present with a more insidious course. A mean duration of symptoms prior to diagnosis is 6.1 months. neurological deficits at the time of presentation are also more prevalent with tuberculosis, with 44.9% of patients having neurological findings. Motor function abnormalities are present in 34.6% of patients with spinal tuberculosis, with 6.4% being paraplegic at time of presentation.

Diagnostic Evaluation

The initial evaluation of a patient suspected of spinal infection includes standard serologic markers for infection or inflammation. A basic panel includes peripheral white blood cell count (WBC), erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). WBC is elevated at time of presentation, however, in only 42% of cases, and often normalizes in patients with chronic infection. ESR and CRP are markers of inflammation and demonstrate high sensitivity for spinal infection. CRP, an acute phase protein, increases within 4 to 6 hours of infection. ESR begins to increase only several days after the onset of infection and peaks at 7 to 8 days. ESR is elevated in over 90% of patients with spinal infection; however, ESR and CRP lack specificity, and may be increased in patients either with infection or with other inflammatory disorders. Individuals suspected of tuberculosis are assessed with a PPD and subsequently sputum staining for acid-fast bacilli.

Definitive diagnosis of spinal infection is made upon identifying the causative organism from positive culture. Prompt blood and urine cultures are obtained immediately on presentation, as infection commonly spreads to the spine either from the genitourinary tract or hematogenously. Positive blood cultures identify the inciting organism in 25% to 59% of cases. Ideally, cultures are obtained prior to initiating antimicrobial therapy to obviate the potential of a sterile nondiagnostic culture.

Biopsy of an abnormal spinal lesion can confirm the diagnosis of infection as well as isolate the inciting organism. Percutaneous closed biopsy is performed using computed tomography (CT) or fluoroscopic guidance. Closed biopsy demonstrates a reported accuracy of 70% to 100% in identifying the causative organism. Open surgical biopsy is indicated in the setting of a nondiagnostic closed biopsy in a patient with persistent clinical infection or deterioration despite broad-spectrum medical therapy, or for lesions inaccessible percutaneously. Open biopsy is diagnostic in over 80% of patients, likely due to a larger bony sample. A high concordance rate is observed in patients with both positive blood and biopsy specimens, reinforcing the importance of early blood culture sampling prior to initiating antimicrobial pharmacotherapy.

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.

Radionuclide studies are capable of detecting and localizing infection before abnormal findings are observed on plain radiographs. Gallium scanning demonstrates 89% sensitivity, 85% specificity, and 86% accuracy for diagnosing disc space infections. Technetium scanning is 90% sensitive, 78% specific, and 94% accurate. Combined gallium and technetium scanning is reported to have 94% accuracy. SPECT is a sensitive bone scintigraphic modality for early detection of osteomyelitis and is often performed in conjunction with technetium and gallium scanning.

CT imaging is beneficial for evaluating the extent of bony destruction. Axial CT imaging demonstrates the presence of retropulsed fragments and the degree of canal compromise in the setting of pathologic fracture. Sagittal reconstructed CT imaging may reveal endplate osteopenia as an early finding of infection. Superb detailing of bony anatomy may be useful for preoperative planning in cases necessitating surgical intervention. Also, CT imaging can delineate adjacent soft tissue abscess or granulation tissue that may require operative debridement.

Magnetic resonance imaging (MRI) is the gold standard for radiologic evaluation of spinal infection. MRI demonstrates high sensitivity (96%), specificity (92%), and accuracy (94%). Intravenous gadolinium further delineates areas of abnormal enhancement and facilitates localization of infection to the vertebral body, intervertebral disc, or epidural space. Optimal visualization of the neural elements allows for evaluation of canal compromise or spinal cord compression. MRI is readily capable of delineating paravertebral abscesses. Multiplanar imaging allows for full evaluation of the complete spinal column in sagittal and axial planes to assess for the extent of involvement.

Management

Management of spinal infections has dramatically evolved over the last several decades. Advances in imaging allow for prompt diagnosis with initiation of appropriate antimicrobial pharmacotherapy, often early in the clinical course. Improved surgical technique combined with developments in spinal instrumentation has resulted in decreased surgical morbidity and better long-term clinical outcomes. The general principles of treatment for spinal infections, regardless of medical or surgical intervention, are fundamentally the same. The primary objectives are to eradicate infection, preserve neurological function, maintain spinal alignment, and prevent pain.

Medical Therapy

Medical therapy for spinal infection consists primarily of antimicrobial pharmacotherapy. Most patients with vertebral osteomyelitis respond successfully to nonsurgical treatment. The main tenet of medical therapy is identification of the inciting organism with either a positive blood or biopsy specimen, and initiation of an appropriate antimicrobial agent. The selection of either a single or multi-drug regimen is dictated by the virulence and resistance of the causative organism. Therefore, optimal treatment is entirely dependent on isolating an organism. As a result, antimicrobial treatment is withheld in patients that are neurologicalally and clinical stable until definitive cultures are obtained. Patients presenting with sepsis or progressive deterioration may necessitate empirical broad-spectrum coverage until an organism is identified.

Antimicrobial therapy is generally delivered parenterally for a minimum of 6 weeks. A 25% failure rate is observed in patients treated with antibiotics for less than 4 weeks. Serial serologic evaluation of ESR is an effective measure of therapeutic response. After 6 weeks of intravenous antibiotics, some advocate continuing oral therapy until the ESR has diminished by a minimum of one half the pretreatment level to prevent relapse. A two-thirds reduction in ESR from pretreatment levels is an indication of complete eradication of infection. In addition to antimicrobial pharmacotherapy, immobilization with an external orthosis is recommended for patients with severe pain, greater than 50% vertebral height loss, or involvement of the thoracolumbar junction.

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