Imaging in Spondylodiskitis




Infections of the spine may involve different anatomic compartments, including intervertebral disks, vertebral bone, paraspinal soft tissues, epidural space, meninges, and spinal cord. This article focuses on the role of imaging in diagnosis and follow-up of infections of the intervertebral disk and vertebral bone, named respectively diskitis and spondylitis or vertebral osteomyelitis. Often, at the time of diagnosis, the infection already involves both structures; therefore the process is referred as spondylodiskitis. The discussion is extended to infections of paraspinal soft tissues and epidural space, which are commonly associated. Mention is made to the role of imaging in guiding minimally invasive biopsies of the spine in such conditions.


Key points








  • MR imaging is the imaging modality of choice for the diagnosis of spondylodiskitis, from early diagnosis to follow-up.



  • Typical findings of spondylodiskitis are abnormal low signal on T1-weighted images and high signal on fat-suppressed T2-weighted images of the disk and opposing vertebral bodies, with contrast enhancement, associated with erosion and destruction of the vertebral end plates.



  • Soft tissue involvement is a key finding that helps differentiate spondylodiskitis from other common conditions, such as Modic type I degenerative end plate changes and erosive intervertebral osteochondrosis.



  • An image-guided biopsy is recommended in all patients with suspected spondylodiskitis based on clinical, laboratory, and imaging studies, when a microbiologic diagnosis has not been established by blood cultures.






Discussion of problem/clinical presentation


Infectious spondylitis represents 2% to 7% of cases of skeletal infection. Spondylodikcitis (SD) shows a bimodal age distribution, with a peak below 20 years and another peak between 50 and 70 years. A 2:1 to 5:1 male/female ratio has been reported. Risk factors include a remote infection (present in about 25% of cases), spinal interventions, trauma, intravenous drug abuse, advanced age, diabetes mellitus, immunosuppression (long-term systemic administration of steroids, organ transplantation, human immunodeficiency virus), malnutrition, and cancer. The incidence of SD has increased in recent years as a consequence of improved life expectancy, comorbid factors, and higher number of spinal interventions. Postsurgical diskitis represents up to 30% of all cases of pyogenic SD.


SD can occur anywhere in the vertebral column but the most common site is the lumbar spine (58%), followed by the thoracic spine (30%), and the cervical spine (11%), with single level involvement (65%), multiple contiguous levels (20%), and multiple noncontiguous levels (10%).


Since the advent of antibiotics, mortality has dropped to less than 5%. The morbidity of SD is significant and is related to spinal deformity with chronic pain and possible neurologic deficits.


The causative agents are mainly bacteria, less commonly fungi and parasites. The most common cause of pyogenic SD is hematogenous spread of Staphylococcus aureus (60%), followed by Enterobacter species (30%). Other pyogenic agents may be encountered, such as Salmonella , Klebsiella , Pseudomonas , and Streptococcus . Nonpyogenic infections originate from Mycobacterium tuberculosis , Brucella , fungi, and parasites. Human immunodeficiency virus infections have caused an increase in incidence of SD from M tuberculosis (Pott disease) in recent years. Fungal infections ( Cryptococcus neoformans , Candida species, Histoplasma capsulatum , Coccidioides immitis ) are rare and associated with immunodepression.


Persistent back or neck pain, malaise, fever, anorexia, tenderness, and rigidity may be the presenting symptom. A more insidious onset with nonspecific pain and malaise is also possible. The presence of fever is inconstant, reported in 35% to 60% possibly related to common intake of analgesic drugs. Signs of nerve root compression with radiculopathy, meningeal irritation, lower extremity weakness, or paraplegia can be present with epidural involvement. Difficulty in swallowing and torticollis may be present in patients with cervical location. The onset of symptoms may be indolent and there is often a delay of 2 to 12 weeks in diagnosis. In children clinical presentation is even less specific, including failure or refusal to walk, abdominal pain, chronic back pain, irritability, incontinence, and local tenderness. Fever is rare.


Laboratory findings include elevation of erythrocyte sedimentation rate and C-reactive protein (CRP) that are sensitive, although nonspecific, infection markers. CRP normalization is a useful marker to monitor treatment response. The white blood cell count has low sensitivity.




Discussion of problem/clinical presentation


Infectious spondylitis represents 2% to 7% of cases of skeletal infection. Spondylodikcitis (SD) shows a bimodal age distribution, with a peak below 20 years and another peak between 50 and 70 years. A 2:1 to 5:1 male/female ratio has been reported. Risk factors include a remote infection (present in about 25% of cases), spinal interventions, trauma, intravenous drug abuse, advanced age, diabetes mellitus, immunosuppression (long-term systemic administration of steroids, organ transplantation, human immunodeficiency virus), malnutrition, and cancer. The incidence of SD has increased in recent years as a consequence of improved life expectancy, comorbid factors, and higher number of spinal interventions. Postsurgical diskitis represents up to 30% of all cases of pyogenic SD.


SD can occur anywhere in the vertebral column but the most common site is the lumbar spine (58%), followed by the thoracic spine (30%), and the cervical spine (11%), with single level involvement (65%), multiple contiguous levels (20%), and multiple noncontiguous levels (10%).


Since the advent of antibiotics, mortality has dropped to less than 5%. The morbidity of SD is significant and is related to spinal deformity with chronic pain and possible neurologic deficits.


The causative agents are mainly bacteria, less commonly fungi and parasites. The most common cause of pyogenic SD is hematogenous spread of Staphylococcus aureus (60%), followed by Enterobacter species (30%). Other pyogenic agents may be encountered, such as Salmonella , Klebsiella , Pseudomonas , and Streptococcus . Nonpyogenic infections originate from Mycobacterium tuberculosis , Brucella , fungi, and parasites. Human immunodeficiency virus infections have caused an increase in incidence of SD from M tuberculosis (Pott disease) in recent years. Fungal infections ( Cryptococcus neoformans , Candida species, Histoplasma capsulatum , Coccidioides immitis ) are rare and associated with immunodepression.


Persistent back or neck pain, malaise, fever, anorexia, tenderness, and rigidity may be the presenting symptom. A more insidious onset with nonspecific pain and malaise is also possible. The presence of fever is inconstant, reported in 35% to 60% possibly related to common intake of analgesic drugs. Signs of nerve root compression with radiculopathy, meningeal irritation, lower extremity weakness, or paraplegia can be present with epidural involvement. Difficulty in swallowing and torticollis may be present in patients with cervical location. The onset of symptoms may be indolent and there is often a delay of 2 to 12 weeks in diagnosis. In children clinical presentation is even less specific, including failure or refusal to walk, abdominal pain, chronic back pain, irritability, incontinence, and local tenderness. Fever is rare.


Laboratory findings include elevation of erythrocyte sedimentation rate and C-reactive protein (CRP) that are sensitive, although nonspecific, infection markers. CRP normalization is a useful marker to monitor treatment response. The white blood cell count has low sensitivity.




Pathology and relevant anatomy


Hematogenous Arterial Spread


Hematogenous arterial spread is the most recognized route of infection. The disk space is rather avascular in adults, whereas it is penetrated by anastomotic vessels in children. End plates provide nutrients to the disk of adults through simple diffusion. The disk end plates are highly vascular, whereas posterior vertebral elements have lower vascularity. The richest arteriolar network is located in the subchondral regions of the vertebral body, which is the equivalent of the metaphysis of a long bone. Hematogenous spread occurs at the end arterioles adjacent to the end plates posterior to the anterior longitudinal ligament. Septic emboli induce bone infarcts and infection in the end plate, whereas the disk space is usually secondarily involved by the enzymatic damage activity of pathogens. However, because of lack of immediate blood defense mechanisms in the disk, infection rapidly establishes. Spreading to the posterior vertebral structures is rare because of their minor vascular supply, and occurs more frequently in fungal and tubercular SD. In children, because of vascularity of disk spaces, the infection may be located first within the disk. In tubercular SD there is typical involvement of the anterior part of the inferior end plate, spread beneath the anterior longitudinal ligament to the superior end plate of the adjacent vertebra, and possible formation of subligamentous and intraosseous abscess. The disk is spared until late phases. Hematogenous venous spread throughout the venous plexus of Batson is also a possible but less recognized route of infection.


Contiguous Tissues Spread


A contiguous tissue spread is rare and may occur in the context of adjacent infection, including esophageal ruptures, retropharyngeal abscesses, or infections of aortic implants.


Direct Inoculation


Direct inoculation is frequently iatrogenic: postsurgical, more rarely after lumbar puncture, epidural, or intradiskal injections. Other sources are penetrating trauma, direct exposure related to skin breakdown, or open wounds.




Imaging modalities and protocols


Radiography


Plain radiographs have low sensitivity and specificity, especially in the early phases.


Computed Tomography


Nonenhanced computed tomography (CT) provides excellent evaluation of bone changes, detects gas and calcifications, and contrast-enhanced CT allows evaluation of associated paraspinal and to a lesser extent of epidural soft tissue involvement. CT is inaccurate in evaluating disk spaces, intradural compartment, and neural elements. CT is also routinely used for guidance in percutaneous needle biopsy.


MR Imaging


MR imaging is the imaging of choice in all phases of the disease because of high sensitivity, specificity, and accuracy (96%, 92%, and 94%, respectively). With multiplanar T1-weighted, fat-suppressed T2-weighted, and fat-suppressed contrast-enhanced T1-weighted sequences, as routinely performed, on high field (1.5–3.0 T) magnets, MR imaging offers excellent depiction of bone edema, disk inflammation, paraspinal and epidural soft tissue involvement, compression of neural structures, and intradural compartment spread. It is important that T2-weighted and enhanced T1-weighted images are acquired with fat-suppression, otherwise even extensive inflammatory lesions might result as invisible. Diffusion-weighted spinal imaging (DWI) might help differentiate acute SD from degenerative Modic type I changes but its clinical use is still debated.


Nuclear Medicine


Three-phase technetium-99m scintigraphy is sensitive (90%) but nonspecific (78%) in SD. Specificity may be increased by combining technetium-99m scintigraphy with gallium-67 or performing a scan with indium-111 labeled white blood cells that accumulate in areas of inflammation. The spatial resolution is low and the detection of epidural abscess is inferior compared with MR imaging. These techniques are therefore reserved for patients with contraindication to MR imaging or when MR imaging is inconclusive. PET scanning with 18 F-fluorodeoxyglucose has a diagnostic accuracy similar to that of MR imaging. However, this technique is not widely available and offers less anatomic information; PET-CT can be used as a problem-solving technique in selected cases.




Imaging findings


Imaging in the Acute Phase (<3 Weeks)


Radiography


Radiographs are typically negative for 2 to 3 weeks after the onset of infection ( Fig. 1 ). The earliest radiographic sign is loss of definition, irregularity, and hazy porotic changes of the vertebral end plate related to depletion of the bony matrix, usually starting anterosuperiorly.




Fig. 1


Very early MR imaging signs of spondylodiskitis are nonspecific and can be overlooked. This patient presented with low back pain for 3 weeks and mildly elevated inflammatory markers. The first plain films ( A ) were unremarkable; MR imaging ( B , D ) showed high T2 signal ( B ) and focal contrast enhancement ( C , D ) in the anulus fibrosis and end plate at L3-L4. Untreated, the back pain worsened; follow-up plain films 3 weeks later ( E ) showed disk space narrowing and loss of definition of the end plates’ cortex ( arrow ). MR imaging ( F H ) showed typical findings of spondylodiskitis, with edema and enhancement of the opposed vertebral bodies and of the adjacent perivertebral soft tissue, also visible on axial fat-suppressed enhanced T1-weighted image ( H ).


Computed tomography


CT scans may appear normal in the early phases of disease. Subtle areas of erosion or osseous destruction may be visible.


MR imaging


MR imaging is the most sensitive imaging method, showing osseous edema, caused by inflammation, as low signal on T1-weighted and high signal on fat-suppressed T2-weighted images, with common contrast-enhancement of the disk and adjacent vertebral bodies visible on fat-suppressed postcontrast T1-weighted images (see Fig. 1 ). The disk, after an initial and rarely seen increase of height, shows height reduction and typically shows loss or distortion of the internuclear cleft, a normal anatomic structure that seems to be a constant feature in subjects 30 years of age or older. In children, infection usually involves the disk primarily and the infected disk shows decreased T2-signal intensity.


Imaging in the Subacute Phase (3 Weeks–3 Months)


Radiography


Typical signs are progressive erosive osteolysis and osteopenia of end plates, and disk space narrowing (see Fig. 1 ). The presence of a paraspinal mass is visible as thickened retropharyngeal space in cervical SD, displacement of the parietal pleura in thoracic SD, and indistinct margins of the psoas muscle in lumbar SD.


Computed tomography


Typical findings are loss of disk height with disk hypodensity, erosion of end plates cortex, subperiosteal defects, and osteopenia ( Fig. 2 ). Marked osseous erosion and destruction of the end plates might actually give the appearance of a widened intervertebral space ( Fig. 3 ). The vertebral body erosions are caused by inflammation and by necrosis from obstruction of the vascular supply to the bone. Soft tissue involvement might be visible as obliteration of fat planes and swelling. Gas component may be visible within the disk, the vertebral body, and the paraspinal soft tissues, but has low specificity because it is commonly observed also in degenerative noninfectious conditions ( Fig. 4 ). Epidural extension of the disease can be depicted. Soft tissue calcification may be visible in tubercular SD.




Fig. 2


A patient with history of intravenous drug abuse presented with 6 weeks history of thoracic back rigidity and tenderness. Unenhanced CT ( A ) showed wedge deformity of a midthoracic vertebral body, with adjacent disk space narrowing and cortical irregularity and fraying of the superior end plate. MR imaging showed edema on T1-weighted ( B ) and short tau inversion recovery (STIR) ( C ) images, with contrast enhancement of adjacent vertebral bodies and perivertebral soft tissue on fat-suppressed enhanced T1-weighted images ( D , E ). There is thickening and enhancement, with no fluid necrotic components, in the ventral epidural space, likely combination of early phlegmon and epidural venous congestion, concurring to initial spinal cord compression.



Fig. 3


In the subacute phase CT exquisitely shows osseous changes of spondylodiskitis. In the first case ( A , B ) there were mixed phenomena of cortical irregularities, bony resorption, and subchondral sclerosis along the L4-L5 end plates. In the second case ( C , D ) the CT showed to much better extent the degree of osseous destruction of the cortical and spongious subchondral bone on the opposed sides of the L4-L5 disk space.



Fig. 4


A patient who underwent surgical hardware fixation of a sacral and pelvic fracture had a postoperative CT ( A ) and MR imaging ( B , C ) showing multilevel degenerative disk pathology with disk space narrowing and gas vacuum. Four weeks later because of worsening low back pain a follow-up CT was obtained, showing interval erosion of the anteroinferior corner of the L5 vertebral body ( arrow on D ); subsequent MR imaging showed to much better extent the edematous changes across L5-S1 disk space ( arrows on E and F ), on T1-weighted ( E ) and STIR ( F ) images, strongly suggesting spondylodiskitis. As in this case, presence of gas can be seen in spondylodiskitis, but has no specificity.


MR imaging


The typical findings in SD are high T2 signal and contrast enhancement of the disk and adjacent bone marrow, with almost invariable involvement of paraspinal and epidural soft tissues (see Figs. 1–3 ). The infection extending to the epidural space and to the paraspinal soft tissues causes phlegmon or abscesses (see later). Infection may cause engorgement of epidural basivertebral veins by direct extension of the inflammatory process, by mechanical obstruction to venous drainage, or by both (see Fig. 2 ). However, prominence and contrast enhancement of the epidural venous plexus should not be confused with epidural infection. Disk height loss is visible when present.


Imaging in the Chronic Phase (>3 Months) and Sequelae of Spondylodiskitis


Radiography


After approximately 10 weeks, plain radiographs may show reactive sclerosis, new bone formation with osteophytosis, kyphotic deformity, scoliosis, spondylolisthesis, and bony ankylosis.


Computed tomography


Osseous changes described previously related to SD are better depicted with CT ( Fig. 5 ).




Fig. 5


In the late healing phase, MR imaging findings slowly regress, but some degree of edema and enhancement along end plates and opposed vertebral bodies ( A , B ) can persist beyond clinical resolution and normalization of inflammatory markers. CT shows the final result of the stabilized osseous abnormalities, such as destruction, sclerosis, osteophytes, ankylosis, deformity, and pseudoarthrosis ( C , D ).


MR imaging


Signs of edema and contrast enhancement gradually resolve, leaving behind sclerotic changes, with low T1 and T2 signal, sometimes with minimal residual contrast enhancement. Vertebral body height changes, kyphosis, scoliosis, spondylolisthesis, and ankylosis can all be seen during the late/healing stage of the infectious process (see Fig. 5 ). In infants, SD may present as progressive dissolution of involved vertebral bodies without loss of disk height. Years later, the kyphotic deformity from this infection may mimic congenital kyphosis.


Epidural Spread


Infections in the epidural space is a threatening condition because of the risk of spinal cord injury, either from direct compression, or because of thrombosis or thrombophlebitis of epidural veins and consequent spinal cord infarction. Severe back pain associated with progressive neurologic deficit and fever are the most common symptoms. Laboratory studies show elevated erythrocyte sedimentation rate and CRP; leukocytosis may be present. MR imaging is the modality of choice to investigate epidural infections. A phlegmon must be distinguished from an abscess. Phlegmons appear as ill-defined soft tissues changes, hypointense on T1-weighted and hyperintense on T2-weighted images, in the perivertebral and epidural spaces, with little mass effect, and homogeneous contrast enhancement ( Fig. 6 ). Abscesses are characterized by a necrotic center, hyperintense on T2-weighted images, isointense to hypointense on T1-weighted images, with linear thin or thick enhancing peripheral rim, and usually exert mass effect if in the epidural space. DWI can show restricted diffusion (visible as brilliant hyperintense signal on b500–800, and low signal on ADC maps) in the pyogenic abscess cavity. A phlegmon reflects hyperhemia and inflammation, is not drainable, and can be treated pharmacologically, whereas an abscess might require urgent percutaneous or surgical drainage, especially when in the epidural space ( Fig. 7 ).


Sep 18, 2017 | Posted by in MAGNETIC RESONANCE IMAGING | Comments Off on Imaging in Spondylodiskitis

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