Osteomyelitis

Infection of the vertebral column in infants and children is much less common than osteomyelitis of the pelvis or long bones. Only about 2% of pediatric osteomyelitis cases involve the vertebrae. In children, the 10 to 15 year age group is most commonly affected. The vertebral infection typically occurs by way of hematogenous inoculation (arterial or venous). Other potential mechanisms include penetrating trauma, iatrogenic introduction of organisms (e.g., lumbar puncture or spinal surgery), and spread from a paravertebral abscess. Spread of infection from the vertebral column can lead to paravertebral cellulitis, meningitis, spinal epidural abscess, or psoas abscess. In decreasing order of frequency, the locations of vertebral osteomyelitis are lumbar, thoracic, and cervical.^1,2

Most instances of vertebral osteomyelitis likely involve an arterial septic microembolus that lodges in a metaphyseal artery of the subchondral portion of the vertebral body. The subchondral portions of the vertebral bodies are metaphyseal equivalents. The microembolus deposits organisms at the site and causes a small septic infarct of the bone, which is apparently an important component of the pathophysiology of vertebral osteomyelitis. The extensive subchondral intraosseous anastomoses that are present in the vertebral bodies of infants and young children are relatively protective against infarction. This is an important factor in the lower frequency of vertebral osteomyelitis in young children as compared to adolescents and adults.

The most commonly isolated organism in children with vertebral osteomyelitis is Staphylococcus aureus. Other bacteria that can infect the spine include Streptococcus species, Kingella kingae, E. coli, Pseudomonas (common with intravenous drug abusers), Salmonella, and Klebsiella. The spine is a relatively common skeletal site for tuberculosis. Vertebral osteomyelitis and epidural abscess can occur in children with cat scratch disease. The clinical manifestations of vertebral osteomyelitis partly relate to the virulence of the organism and the host response. The clinical spectrum ranges from an acute febrile presentation to an indolent course with nonspecific back pain. Blood cultures are positive in some patients; image guided percutaneous aspiration is useful for others.^3–5

Radiographs are often normal early in the course of vertebral osteomyelitis, when the infection is confined to the subchondral zone of the vertebral body. The initial radiographic finding often consists of intervertebral disc space narrowing, apparently due to the release of proteolytic enzymes that destroy the disc. The margins of the vertebral endplates are usually indistinct at this point. Frank destruction of subchondral bone typically becomes evident within 1 to 2 weeks after the onset of infection. These osseous changes tend to be most prominent in the anterior two-thirds of the vertebral body.

With progression of the infection, radiographic findings of vertebral body infection include bony endplate destruction, cortical permeation, and blurring of the disc space margins. There may be loss of height of the involved vertebral body. Prominence of the paravertebral soft tissues is often visible, particularly with a thoracic or cervical infection. In the later stages of infection and during the healing process, sclerosis occurs. In some patients, there is at least partial reconstitution of the vertebral body. In others, osseous fusion of adjacent previously infected vertebrae may occur. An indolent infection sometimes leads to sclerosis with only minimal preceding radiographic evidence of bone destruction. Sclerosis of a pedicle by this mechanism may lead to radiographic findings that overlap those of osteoid osteoma or a stress injury.⁶

In comparison to standard radiographs, CT more accurately depicts the osseous and soft tissue manifestations of vertebral infection. Contrast-enhanced images are useful for documenting a secondary abscess in the epidural space or paravertebral region (Figure 23-1). MR is exquisitely sensitive for the marrow edema that is the earliest manifestation of vertebral infection. MR is of equal or greater sensitivity as skeletal scintigraphy for the detection of vertebral osteomyelitis. Fat-suppressed T2-weighted sequences (e.g., short tau inversion recovery [STIR]) are essential for evaluation of these patients. Marrow edema produces relatively low signal intensity on T1-weighted images and high signal intensity on T2-weighted images (Figure 23-2). Secondary involvement of an adjacent intervertebral disc appears as signal alteration and loss of height. Edema in the extraosseous soft tissues leads to soft tissue thickening and hyperintensity (Figure 23-3). The inflamed soft tissues enhance prominently with contrast. An abscess appears as a nonenhancing focus surrounded by a hyperemic rim.⁷

As with bone infections elsewhere, skeletal scintigraphy becomes positive early in the course of vertebral osteomyelitis (Figure 23-4). Increased radiopharmaceutical uptake may occur in a single vertebra or 2 adjacent vertebrae. Spread of infection into the paravertebral region causes prominent blood-pool activity on early images. A large paravertebral abscess may produce a photopenic area with surrounding hyperemia.

Discitis

Discitis (diskitis) is an inflammatory or infectious abnormality of the intervertebral disc. In a minority of patients with discitis, there is laboratory or histological confirmation of an infectious process. More often, however, this localized inflammatory condition is idiopathic. The peak age range of discitis is 6 months to 5 years, although this condition occurs throughout the pediatric age group. Any portion of the spine can be involved. The L4-L5 interspace accounts for approximately 40% of cases; the L5-S1 inter-space is the next most frequent site.

Patients with discitis most often present with back pain, sometimes accompanied by a limp or refusal to walk. Vague pain in the buttocks, thigh, or knee is the only manifestation in some patients. Physical examination may reveal point tenderness over the affected portion of the spine. Limitation of lower back flexion and loss of lumbar lordosis are common. Herniation of an infected disc can cause neurologic symptoms. Mild leukocytosis and elevation of the erythrocyte sedimentation rate are common. Cultures from blood or needle aspiration are positive in less than one-third of patients. The most commonly isolated organism is Staphylococcus aureus; Salmonella and anaerobic bacteria are occasional isolates. Kingella kingae accounts for some culture-negative disease. The presentation and clinical course of discitis are much milder than are typical of vertebral osteomyelitis. Fever occurs in only about one-quarter of patients.^8,9

The optimal treatment approach for discitis is controversial. Most patients are treated empirically with antibiotics, even if cultures are negative. A rapid clinical response occurs in many patients. However, many children with discitis fully recover without antibiotic therapy. Percutaneous needle aspiration of the disc space is an option for selected patients with a clinically severe form of discitis. Immobilization with a brace or cast is sometimes useful to improve patient comfort or treat malalignment.^10,11

The earliest radiographic manifestation of discitis is subtle narrowing of the involved disc space (Figure 23-5). This finding may occur as early as 10 days after the clinical onset. The subsequent findings vary greatly between patients. With mild disease and prompt initiation of therapy, there may be only mild subsequent progression in disc space narrowing. Most often, however, there is at least moderate progression in disc narrowing over the next several weeks. There are usually irregular erosions in the adjacent vertebral endplates (Figure 23-6). Paravertebral soft tissue thickening is common (Figure 23-7). The end-plates eventually become sclerotic. In approximately 20% of patients, partial or complete vertebral body fusion occurs; this may eventually lead to clinically evident spinal deformity (e.g., kyphosis). In most others, there is at least partial disc reconstitution, sometimes resulting in nearly normal disc height by the second or third year after the acute phase.^7,12

Bone scintigraphy becomes positive as early as 48 hours after the onset of symptoms of discitis, and should be abnormal in nearly all patients with symptomatic discitis of more than 7 days duration. The typical scintigraphic appearance is that of symmetrically increased radiopharmaceutical accumulation in the vertebral endplates adjacent to the inflamed disc (Figure 23-8). Single-photon emission computed tomography (SPECT) increases the sensitivity and specificity of the examination.

In comparison to skeletal scintigraphy, MR provides equal or greater sensitivity for the early diagnosis of discitis. Both T1-weighted and T2-weighted images demonstrate signal abnormality within the involved disc (Figure 23-9). The inflamed disc enhances prominently with gadolinium. T2-weighted images may show hyperintense edema within the adjacent vertebral bodies, although this is not a prominent finding early in the course of the disease. Paraspinal soft tissue thickening is usually mild. Some children with discitis have neurologic manifestations such as decreased muscle strength and/or hyporeflexia in the lower extremities. MR sometimes shows intraspinal inflammatory changes in these patients. Nerve root compression can occur due to protrusion of the infected disc (Figure 23-10). Findings of bone destruction can be present with aggressive forms of discitis. In the late phase of discitis, vertebral body sclerosis leads to diminished signal intensity within the endplates.^13,14

There is considerable overlap in the clinical and imaging features of discitis and vertebral osteomyelitis, and it is sometimes not possible to differentiate these 2 entities. Inflammatory edema in the adjacent vertebral bodies occurs in most patients with discitis. Secondary disc involvement is common with vertebral osteomyelitis, sometimes including extension across the disc into the adjacent vertebra (Figure 23-11). A key differentiating feature between these entities, particularly early in the process, is the predominant location of the inflammation. With discitis, there is usually symmetric involvement of the adjacent vertebra. With osteomyelitis, the inflammation is limited to, or predominates in, a single vertebra. Bone destruction and paraspinal soft tissue involvement tend to be more pronounced with osteomyelitis than with discitis. Fever is more common in patients with osteomyelitis. Discitis tends to occur in younger children than does vertebral osteomyelitis.⁷

Tuberculosis

Tuberculous spondylitis is a common cause of infectious spondylitis in endemic regions of the world. The term “spondylitis” refers to infection or inflammation that involves any of the components of the spinal column, including the vertebra, intervertebral discs, paraspinal soft tissues, and epidural space. The spine accounts for about half of musculoskeletal tuberculous infections. There is an increased risk for tuberculous spondylitis in patients who are immunocompromised. The potential for permanent spinal deformities and neurological deficits in patients with tuberculous spondylitis mandates prompt diagnosis and treatment.

Spinal tuberculosis occurs by way of deposition of Mycobacterium via the end arterioles in the vertebral body adjacent to the anterior aspect of the vertebral endplate. As the infection progresses, the cortex becomes disrupted and infection may spread to the subligamentous region, the paraspinal soft tissues, the epidural space, or the adjacent intervertebral disc. Subligamentous spread from a single focus can cause infection at multiple levels of the spine. Intervertebral disc involvement usually does not occur until late in the process. An abscess or inflammatory mass in the epidural space can produce symptomatic spinal cord compression. Paraspinal spread from cervical spine tuberculosis can involve the retropharyngeal region. Soft tissue extension from a thoracic or lumbar spine focus can sometimes lead to a cutaneous sinus tract at a remote site, such as the buttock or chest.

The typical radiographic appearance of tuberculous osteomyelitis of the spine is that of slowly progressive localized bone destruction. Multiple adjacent vertebrae may be involved. In comparison to bacterial osteomyelitis, the rapidity and severity of bone destruction are usually less pronounced in patients with tuberculous spondylitis. The degree of reactive sclerosis varies between patients. Soft tissue changes due to edema, cellulitis, lymphadenopathy, or abscess formation are common (Figure 23-12). Calcified paraspinal granulation tissue and lymph nodes may be present. Skeletal scintigraphy shows nonspecific increased uptake in the involved portion of the spinal column.⁶