Infections of the Spine: A Review of Clinical and Imaging Findings

Vikram K. Sundaram, MD; Amish Doshi, MD

Disclosures

Appl Radiol. 2016;45(8):10-20. 

In This Article

Pyogenic Spondylodiscitis

Pathophysiology

The most common causative bacterial agent in spondylodiscitis in general is overwhelmingly S. aureus, quoted as anywhere between 48–70% in most reviews.[3–6] The remaining cases are somewhat equally distributed amongst other gram positive and gram negative organisms, and may have predilections in select patient populations, including but not limited to: Enterobacteriaceae species such as E. coli (particularly in patients with concurrent urinary tract infections as a source of infection), P. aeruginosa (particularly in patients with a history of IV drug abuse as well as in nosocomial infections), less commonly S. pneumoniae (particularly in patients with diabetes), and more rarely Salmonella species (particularly in those patients with sickle cell disease or asplenia).

Bacterial infections to the vertebral bodies most commonly occur via a hematogenous route, for instance from a secondary source such as endocarditis, and more often via the arterial network than the venous. Based on the typical adult arterial anatomy, hematogenous pyogenic spondylodiscitis often first affects the subchondral region of the vertebral body endplates, and spreads in an anterior to posterior direction. Over time, bacteria with more virulent and proteolytic properties, such as S. aureus, cause cortical destruction and invade beyond the endplates and into the intervertebral discs. They can also spread along the arterial anastomotic networks to multiple, sometimes non-contiguous vertebral bodies, or into the epidural space.

Pyogenic spondylodiscitis can also occur via direct extension, for instance from penetrating trauma, from adjacent infections in the thorax or abdomen, or from surgical interventions and instrumentation. Although pyogenic spondylodiscitis often first affects the anterior region of the vertebral body, bacterial seeding and initial infection of the posterior elements of the spine, including the transverse processes and the pedicles, can be considered in patients with the above clinical histories.

Clinical Findings

Pyogenic spondylodiscitis most often presents in an acute-to-subacute period of time with non-specific back pain, fever, and focal neurological manifestations. In post-surgical patients, where direct inoculation is also a concern for etiology, steadily increasing pain at the surgical site is suggestive of an underlying infection.[7] Relevant laboratory data includes elevated inflammatory markers such as ESR and CRP. Since CRP is very sensitive but not specific in active pyogenic spondylodiscitis, some believe that a normal CRP can be thought to essentially exclude the possibility of an active spinal infection, though rarely inflammatory markers can be within normal limits in cases of chronic or indolent infection, and normal inflammatory marker levels may be present in a non-bacterial source of active infection.[6–9] Leukocytosis and positive blood cultures are often but not always present in spinal infection.[10] Reasons for delayed ordering of imaging studies include non-specific symptoms of pain, lack of or intermittent fevers, lack of focal neurologic symptoms, and culture-negative bacteria. These delays can result in more advanced disease and complications such as abscess formation or involvement of epidural and paraspinal regions. In these cases, surgical drainage is often necessary for proper treatment. Upon diagnosis of pyogenic spondylodiscitis, typical medical management includes 4–6 weeks of IV antibiotics, with repeat imaging typically obtained in cases where symptoms persist and/or laboratory data does not normalize. In cases of surgical implantation, repeat surgery for debridement or possibly removal of hardware is determined by multiple clinical factors, including delays in diagnosis leading to advanced infection compromising hardware, and the presence of bacteria that may produce biofilms (any group of microorganisms in which cells stick to each other on a surface).

Imaging Findings

Plain Radiographs and CT. An osseous lesion from an infectious process typically takes about 10 to 21 days to be evident on plain films.[11] One may also see signs of soft tissue swelling to suggest an underlying infectious process. Associated early chronic degenerative changes that can be seen on plain films include loss of intervertebral disc height and loss of definition at the vertebral endplates with occasional erosions. Later developments include reactive sclerosis, osteophytosis and new bone formation, bony ankylosis, and kyphotic and scoliotic deformities.

CT is limited in fully evaluating potential epidural involvement due to beam-hardening artifacts, and is best used for definition of bony architectural detail and potential paraspinal soft tissue involvement. Findings within the bone can include local osteopenia, cortical bone erosion, lytic fragmentation, and bony sclerosis. There can be hypodensity of affected intervertebral disc spaces, as well as lost of disc space height. Paraspinal soft tissue involvement is seen with loss of fat planes and soft tissue swelling. Contrast may demonstrate enhancement in phlegmanous processes. CT is also useful in percutaneous drainage of focal fluid collections, both for analytic and therapeutic purposes.

Bone Scan. A triple phase bone scan using methylene diphosphonate consists of a flow phase, a blood pool phase ten minutes after injection, and a delayed update phase that is performed three hours after injection. Typically a bone scan will be positive 24–48 hours after the initial infection, and the sensitivity for osteomyelitis ranges from 73–100% when imaging is considered positive on all three phases of the scan.[5,12] One limitation of bone scan imaging is false positive results, such as recent trauma, surgery with or without placement of hardware, and diabetes.[13–15]

Gallium-67 citrate can also be used in the detection of foci of spondylodiscitis. The gallium agent attached to transferrin, where it is deposited at areas of increased inflammation. Images are obtained anywhere from 18–72 hours after injection, and can be performed in conjunction with other radionuclide bone imaging.[5,13] Gallium accumulates in areas of active infection, though it tends to lack fine bony detail and may not distinguish between infection of the vertebral body and that of contiguous tissues such as paraspinal infections.

MRI. Early pyogenic infection within bone marrow typically results in inflammatory exudate, replacement of fat by stimulation of bone marrow to produce white blood cells in response to the infection, some vascular proliferation, and some degree of minor ischemia. Thus, on MRI one expects to see low T1 signal intensity abnormalities, indicating the presence of fluid within the vertebral body, as well as heterogeneous contrast enhancement, indicating the presence of acute or subacute inflammation. Contrast can also help distinguish between the presences of phlegmon, an inhomogeneous blush of enhancement that is treated with conservative medical management, and a peripherally enhancing abscess that requires drainage for disease resolution.

High T2 signal intensity abnormalities are also expected, and can be made more conspicuous using fat-suppressed T2/STIR sequences (Figure 2). Over time, T2 sequences demonstrate erosions and cortical disruptions at the vertebral body endplates, as well as potential extension toward the longitudinal ligaments (Figure 3). Signal alteration of an infected intervertebral disc can be indicated by the loss of a low T2 signal equatorial band known as the intranuclear cleft, and eventually by the presence of granulation tissue (Figures 2, 4). Extension into the epidural space and/or paraspinal regions is also possible, though primary infections from these locations can also extend into the vertebral bodies (Figure 5). In chronic cases, one expects frank bony and disc destruction.

Figure 2.

T1 precontrast (A), T1 postcontrast (B), and T2 FSE (C) sagittal sequences of the lumbar spine of a 55-year-old man with pyogenic spondylodiscitis at L4-L5. T1 precontrast images demonstrate low signal indicating edema, and T1 postcontrast images demonstrate enhancement at and adjacent to the disc (A and B, arrows). T2 FSE demonstrates disc involvement (C, arrow).

Figure 3.

T1 precontrast (A), T1 postcontrast (B), DWI (C), and T2 FSE (D and E) sagittal sequences of the lumbar spine of a 27-yr-old woman with pyogenic spondylodiscitis at L2-L3. Findings include depressed superior endplate at L3 (A, B, and D, solid arrows), peripheral enhancement at L2-L3 with surrounding patchy enhancement, and paravertebral collection without spinal canal stenosis. Off-midline sagittal imaging better demonstrates subligamentous extension (E, dotted arrow).

Figure 4.

Axial T1, FS postcontrast (A), axial T2 (B), sagittal T1 (C), and sagittal T2 (D) sequences of the lumbar spine of a 57-yr-old man with pyogenic spondylodiscitis at L3-L4. Axial images demonstrate a right psoas muscle abscess (A and B, arrow). There is paravertebral and anterior prevertebral extension (C and D, arrows) along with severe disc space loss.

Figure 5.

Sagittal CT (A) as well as T1 precontrast (B), T1 postcontrast (C), and T2 (D) sagittal sequences of the cervical spine of a 74-yr-old woman with pyogenic spondylodiscitis at C5-C6. CT demonstrates loss of intervertebral disc height, sclerosis and fragmentation at C5-C6. MR sequences demonstrate T1 hypointensity, contrast enhancement, and T2 hyperintensity at C5-C6, along with prevertebral phlegmon (C, arrows) and epidural inflammation.

Diffusion-weighted MR imaging not only helps to highlight the extent of pyogenic spondylodiscitis, but can also help distinguish it from other potential pathology. Foci of bacterial infection typically have high signal intensity on DW-MRI, and with ADC mapping one sees relatively low signal indicating diffusion restriction. It is thought that the high cellularity and presence of pus contributes to the diffusion restriction in infectious processes. Sterile effusions and normal CSF typically do not demonstrate such low diffusion restriction values as in pyogenic spondylodiscitis.[16] Modic type 1 degenerative changes can be distinguished from infection on DW-MRI by the "claw sign," described as a well-marginated, linear region of high signal within the adjacent vertebral bodies at the interface of normal and abnormal marrow.[17] In patients with Modic type 1 signal changes of the intervertebral disc space on MRI and a positive claw sign, there is a high likelihood of degenerative changes as the etiology of patient symptoms compared to pyogenic spondylodiscitis (Figure 6).

Figure 6.

T1 precontrast (A), T2 (B), T1 postcontrast (C), and DWI (D and E) sequences of the lumbar spine demonstrates Modic type I changes at L4-L5. DWI images demonstrate the "claw sign" (D, arrows) of granulation tissue and edema separated from normal bone marrow by a linear section of high signal. A drawing (F) depicts the different tissue layers in Modic type I changes (images courtesy of L. Tanenbaum, Icahn School of Medicine at Mount Sinai, NY).

As the infection resolves, reactive bony changes, such as new bone formation, osteophytosis, sclerosis, and spondylolisthesis, can indicate bone healing in a resolving infection. Normalization of T1 signal intensity within a previously infected vertebral body can indicate reconstitution of fatty marrow, while a decrease in T2 signal intensity suggests sclerosis or fibrosis in the healing bone. Contrast enhancement should lessen as the inflammatory reaction subsides. The low T2 signal of the intranuclear cleft should reappear as the infection resolves.

Follow-up Imaging

If repeat imaging is obtained, it may be necessary to not only scan the infected vertebral bodies, but potentially the entire spine if there are concerns for spread of infection or for lesions that were missed on prior imaging. For instance, a patient with lumbar pain found to have a lumbar pyogenic spondylodiscitis might also have thoracic lesions that are not imaged since the patient did not have focal symptoms at the region of the thoracic spine.[3] Importantly, missed lesions can increase morbidity if patients are not treated for an adequate amount of time or if they do not receive the proper interventions such as drainage or surgery. Typical imaging modality in follow-up cases would include CT, MRI, and bone scan, often depending on what exams would provide the best comparison to pre-treatment imaging.

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