Discitis-Osteomyelitis

Introduction

Infections of the spine are not uncommon in clinical practice. There are many terms used to describe essentially the same pathologic entity at different stages of evolution. In adults, pyogenic infections typically spread hematogenously to the vertebral endplate (vertebral osteomyelitis), continue through the intervertebral disc to involve the adjacent vertebral body (discitis-osteomyelitis), and may develop abscesses in paraspinal and epidural spaces (psoas or epidural abscesses) ( Fig. 26.1 ).

Less common routes of transmission include direct inoculation from spinal procedures, direct extension from nearby infection, and hematogenous spread to the facet joints (facet septic arthritis). In the pediatric population, the disc may be the initial site of infection due to its residual vascularization.

A distinction should be drawn between pyogenic and non-pyogenic infections. Tuberculous spondylitis, a form of non-pyogenic infection, has similar consequences, although different imaging evolution and distinct clinical management, which will be discussed separately.

The clinical diagnosis of a spinal infection can be challenging. The typical presentation is insidious and nonspecific focal back pain, with fever present in only half of patients. Laboratory findings of leukocytosis and elevated erythrocyte sedimentation rate (ESR)/C-reactive protein (CRP) are also nonspecific, but may help exclude infectious etiologies if normal. Blood cultures are useful when positive and can also be used to identify the most effective antibiotic therapy. The causative bacteria are often Staphylococcus aureus ; however, other organisms may be encountered, particularly with immunocompromised patients or intravenous (IV) drug users. As a result of these clinical factors, there is typically a delay in presentation, diagnosis, and definitive therapy of spinal infections. If left untreated, infections of the spine can have devastating consequences related to spinal instability, which threatens the integrity of the spinal canal and its contents.

Imaging Evolution: Overview

Magnetic resonance imaging (MRI) has become critical to the early diagnosis of spinal infections. Early pathologic findings of bone marrow edema, T2 hyperintense disc signal, and abnormal disc enhancement are only identifiable by MRI. As such, MRI with and without contrast is the imaging study of choice for the early diagnosis of suspected spinal infections. Ultimately, the utility of computed tomography (CT) and radiographs for the initial diagnosis of infectious spondylitis is limited by the fact that a normal examination does not exclude the diagnosis of an early evolving spinal infection. Also, MRI is most valuable to differentiate an infectious process from the more commonly encountered degenerative processes of the spine that may present in a similar fashion.

Late imaging manifestations of endplate erosion and disc height loss may be identified by radiographs or CT, although complications of advanced disease, such as paraspinal abscess and spinal canal stenosis, are best seen by MRI. As such, CT should not be relied upon to assess the complete extent of infection unless MRI is contraindicated. Of note, CT and radiographs can be useful in preoperative evaluation prior to treatment of spinal instability in the setting of known spinal infection. Gallium-67 SPECT and F-18 FDG PET studies may also provide useful information when the diagnosis is in doubt or when MRI is contraindicated.

Imaging Evolution: in Greater Depth

Early Disease (1 to 3 Weeks)

Plain films and CT are often normal in the early phase of spinal infection or will show changes that are similar to degenerative disc disease. However, MRI can demonstrate bone marrow edema (T1 hypointense, T2 hyperintense signal) on both sides of an abnormal T2 hyperintense disc, which is often the earliest imaging abnormality encountered ( Fig. 26.2 ). Fat-saturated T2 or short tau inversion recovery (STIR) images should be routinely used to improve conspicuity of this pattern of osseous edema. Importantly, active degenerative disc disease with endplate edema (Modic type I changes) may have a similar pattern of bone marrow edema, although the intervening disc typically demonstrates T2 hypointense signal, which is more consistent with disc desiccation, as opposed to discitis.

While the most well recognized early imaging pattern of bone marrow edema involves two contiguous vertebrae and the intervening intervertebral disc, other atypical patterns of disc/vertebral involvement may be encountered including only one vertebral body, one vertebral body and one disc, or two vertebral bodies with a normal appearing intervening disc ( Fig. 26.3 ). These “variants” likely reflect early states of infection that begin at a single vertebral level and have yet to clearly involve or cross the disc space. These patterns may be reported more frequently as the availability of MRI increases.

Gadolinium enhancement may help differentiate infection from other pathologies. The presence of abnormal enhancement of the disc or adjacent soft tissues is more suggestive of an infectious etiology rather than degenerative disease. Notably, diffuse bone marrow enhancement or focal endplate enhancement within the area of bone marrow edema can be seen in both infectious and degenerative disc disease (see Mimics and Differential Diagnosis discussion later). Therefore the benefit of postcontrast imaging is to better evaluate the surrounding soft tissues and intervening disc.

When the diagnosis is in doubt, follow-up imaging may be obtained, which can show more specific imaging findings of infection in as little as 8 to 22 days (see Fig. 26.3 ). Often a multidisciplinary team approach is required to make a diagnosis of vertebral osteomyelitis in the acute stage.

Late Disease (Weeks to Months)

The most classical and specific imaging findings of infectious spondylodiscitis are typically seen in the late stages of infection. As the infection progresses, bony erosions occur along the vertebral endplates and there may be progressive loss of disc space height with persistent or progressive abnormal T2 hyperintense disc signal. Enhancing phlegmon may develop in the adjacent epidural and paraspinal spaces, including the psoas muscles. These phlegmonous changes can evolve further to abscesses, which classically demonstrate fluid-like signal centrally (T2 hyperintense) with peripheral enhancement. Diffusion-weighted imaging (DWI) may be useful in confirming adjacent soft tissue abscess formation, which should demonstrate central restricted diffusion.

Diffusion sequences have limited utility in confirming or identifying the extent of infection in osseous structures. However, one study has described the MR appearance of sagittal diffusion imaging of the spine in patients with Modic type I degenerative changes of the vertebral bodies as a concentric pattern of bony reaction with diffusion restriction at the outer margin of bone marrow edema, as opposed to diffuse confluent diffusion signal abnormality, which may be seen in discitis-osteomyelitis. This peripheral pattern of diffusion signal abnormality that is suggestive of active bony degenerative change has been termed the “claw sign” (see Fig. 26.7 , mimics section).

Progressive vertebral body height loss and collapse may be seen later in the disease course and surgical consultation is often warranted to determine if decompression or stabilization is required.

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