imagingofspondylodiscitis · 10 symptomsandsignsofspondylodiscitisare...

European Review for Medical and Pharmacological Sciences

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Abstract. – Background: Spinal infec-tions (pyogenic or non-pyogenic) are increasingin incidence and are a common cause of mor-bidity in high-risk patients (elderly, immunocom-promised patients, diabetic patients, drug ad-dicts, and patients with sickle-cell disease).

Aim: To provide an overview of the radiologi-cal features of spinal infections, focusing onmagnetic resonance (MR) imaging, and to illus-trate the differential diagnosis.

Materials and Methods: We reviewed thespine imaging of 118 patients with spinal infec-tions from our files. All patients underwent radiog-raphy and MR imaging examinations. computedtomography (CT) was performed in 96 patients.

Results: MR imaging has greatly contributedto prompt diagnosis, thus allowing implementa-tion of timely appropriate treatment.

Conclusions: Prompt diagnosis and treatmentare essential to prevent serious bone and jointdestruction, and severe neurologic sequelae.

Key words:

Spine, Spondylodiscitis, Spine Radiography, SpineCT, Spine MR.

Introduction

Infections involving the axial skeleton repre-sent approximately 2-7% of all cases of os-teomyelitis, and are categorized according tothe anatomical location of the pathologicalprocess1. These infections can affect the verte-bral body (spondylitis), the intervertebral disc(discitis), the vertebral body with the interverte-bral disc (spondylodiscitis), the ligaments andparavertebral soft tissues, the epidural space(epidural abscesses), the meninges and sub-arachnoid space, and finally, very rarely, thespinal cord (myelitis, spinal cord abscesses)2.Isolated discitis is more common in infants dueto the anatomy and blood supply to the disc

Imaging of spondylodiscitisA. LEONE, C. DELL’ATTI, N. MAGARELLI, P. COLELLI, A. BALANIKA*,R. CASALE, L. BONOMO

Department of Bioimaging and Radiological Sciences, School of Medicine, Catholic University ofthe Sacred Heart, Rome (Italy)*Department of Radiology, University General Hospital of Athens “Attikon”, Chaidari, Athens (Greece)

Corresponding Author: Antonello Leone, MD; e-mail: [email protected]

whereas in adults, discitis almost always occurssecondary to vertebral body infection, exceptwhen introduced directly through a penetratinginjury, during a surgical procedure or in olderpatients with degenerative disc disease3. Never-theless, the terms spondylitis, spondylodiscitisand discitis are often used interchangeably, asthe diagnosis and management of the three enti-ties are similar in most patients.Spondylodiscitis is a potentially devastating

and rapidly progressing disease which may resultin vertebral collapse, permanent neurologicdeficits, or even death. The diagnosis and differ-entiation from degenerative disease, non-infec-tive inflammatory lesions and spinal neoplasmare often difficult since the clinical features canbe subtle and misleading, and a delayed diagno-sis can increase morbidity and mortality.Age, route of contamination, infective agent,

and any underlying disease define the differentmorphologic appearance and clinical course ofspinal infections2,4.Two major criteria, as presence of characteris-

tic imaging features and isolation of the offend-ing organism from blood or affected site, are es-sential for the correct diagnosis of spinal infec-tions5.Although radiography, scintigraphy and com-

puted tomography (CT) have been used as imag-ing modalities for spinal infections, magneticresonance (MR) imaging is currently the modali-ty of choice for the evaluation of potential spinalinfections because of its high sensitivity andspecificity6. MR imaging is especially effectivefor direct evaluation of the bone marrow, and si-multaneous visualization of the neural structures(i.e., spinal cord, nerve roots) and extradural softtissue.The primary objectives of this article are to re-

view the radiological features of spinal infec-tions, focusing on MR imaging, and to illustratethe differential diagnosis.

2012; 16(Suppl 2): 8-19

Routes of contamination

The routes of spinal infections can be dividedinto the following two main groups: haematoge-neous, and non-haematogeneous5.

Haematogenous spread, via arterial system, isthe most common source of infection since thevertebral body is richly supplied by an arterialnetwork7. Arteries supplying the vertebrae are de-rived from the vertebral, intercostal, lumbar orsacral arteries, localized at the anterior and an-terolateral surfaces of the vertebral bodies. Eachartery divides into an ascending and descendingbranch, which anastomose with correspondingbranches of the neighbouring vertebrae. Fine arte-rioles from this network ramify within the verte-bral body through central nutrient foramen, beingmost abundant at the end plates7, especially in theanterior subchondral region where the usual pri-mary focus of infective change commences8,9.Haematogenous arterial spread is more fre-

quent than transmission through Batson’s par-avertebral venous system. Batson’ plexus is avalveless venous network so that increased intra-abdominal pressure allows retrogradehaematogenous spread to vertebral column, par-ticularly from the pelvic organs especially in in-stances of sepsis originating in the urinary blad-der, bowel and female pelvic organs4.The distribution of spinal vessels is age relat-

ed. Therefore, the site of infection may be differ-ent according to the different age groups10. Inchildren, until the age of 4 years, end arteriespenetrate beyond the annulus, and the interverte-bral disc is well vascularized10. Therefore, thisgroup of patients will primarily develop discitis.In the elderly disc degeneration may be followedby ingrowth of vascularized granulation tissuecausing secondary vascularization of the discmaterial. This is the reason that primary discitisis possible even in older patients3,10,11.In healthy adults the disc is avascular and nu-

trition is supplied through processes of osmoticdiffusion10. The disease process begins in a focusof cancellous bone, mostly in the anterior part ofthe vertebral body either superiorly or inferiorly,adjacent to the end plate where the blood supplyis particularly evident. The subsequent spread ofinfection to the neighbouring disc and vertebracreates the characteristic lesion of spondylodisci-tis. Uncontrolled infection can breach the boneand track into surrounding soft tissues, causingparavertebral or psoas abscesses, and spread pos-teriorly into the spinal canal, forming an epidural

abscess, subdural abscess and meningitis. Ofnote, pyogenic osteomyelitis of the posterior ele-ments of the vertebrae (pedicles, transverseprocesses, laminae and spinous processes) is veryrarely encountered in haematogenous infectionsdue to their relatively poor blood supply com-pared with the vertebral body12.

Non-haematogenous spread includes threemain routes: 1) post-operative infections; 2) di-rect inoculation, and 3) spread from contiguousinfected tissue.Post-operative infections are increasing in

prevalence due to more frequent and aggressivespinal operations. Surgical treatment such as per-cutaneous discectomy, open discectomy,laminectomy, CT-guided lumbar sympathectomy,and spinal instrumentation can be complicated bydiscitis followed by spondylitis.Direct inoculation is most commonly iatro-

genic following spinal surgery, lumbar punctureor epidural procedures. Depending on the opera-tion procedure different anatomic vertebral struc-tures are primarily involved. For example, duringdiscography and chemonucleolysis, pathogensmay be implanted directly into the disc spacewith primary infective discitis and subsequentvertebral osteomyelitis. Penetrating spinal injuryis an uncommon cause of infective spondylitis.Spread from contiguous infected tissue is a

rare mechanism of infection. It is often difficultto distinguish from direct inoculation and it ismore typical for tuberculous or fungal infec-tions2,4,11. There is, however, almost certainly anassociated haematogenous component.

Clinical aspects

Spinal infection is primarily a disease ofadults, with the majority of patients being morethan 50 years old, but it may appear in all agegroups11,13. Males are affected more frequentlythan females (ratio 2:1). The reason for this malepredominance is not clearly understood14,15. Mosthaematogenous pyogenic spondylodiscitis affectsthe lumbar spine, followed by the thoracic andcervical spine in decreasing frequency (58%,30% and 11% respectively) possibly reflectingthe relative proportions of blood flow16. Tubercu-losis (TB) infections have a predilection for thethoracic spine, and intravenous drug abusers aremore likely to contract an infection of the cervi-cal spine17.

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Imaging of spondylodiscitis

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Symptoms and signs of spondylodiscitis areextremely variable and do not help in diagnosis18.The patient may be afebrile and pain, the mostcommon presenting symptom, is nonspecific. Al-though neurologic compromise may occur laterin the disease process, it is not usually part of theearly manifestation19. Neurologic examinationmay reveal evidence of nerve root compression,leg weakness, paralysis, sensory deficit, andsphincter loss16. Neurologic deficits are morelikely to be associated with epidural abscess, de-layed diagnosis20, cervical lesions21, and TB22.Laboratory results (i.e., white count, erythro-

cyte sedimentation rate, and C-reactive proteinlevel) are often abnormal, but nonspecific. Bloodcultures (aerobic and non-aerobic) with specialcultures for TB are important together with serolo-gy in supporting the imaging features of infection.

Imaging findings

RadiographyAt an early stage of infection, radiographs are

normal because of the very low sensitivity andspecificity of radiography23. The earliest radi-ographic sign of pyogenic spondylodiscitis (be-tween two and eight weeks after the initial symp-toms) is loss of definition of the anterior aspectof vertebral bony end plate, followed by loss ofdisc height, gradual development of osteolysis,and further destruction of the subchondral plate(Figure 1). The progression of infection is char-acterised by further destruction of vertebral body,reactive changes with sclerosis, new bone forma-tion and kyphotic deformity. The vertebral bodyis the most common site for initiation of the pyo-genic infective process; involvement of the pedi-cle, lamina and the spinous process is uncommonand should raise suspicion of TB24.Similar to pyogenic spondylitis, tuberculous

infection usually begins within the anterior sub-chondral part of the vertebral body, but destruc-tive changes are preceded by osteoporosis. Fur-thermore, unlike pyogenic infection, tuberculousinfection does not produce proteolytic enzymes,thus the intervertebral disc and the joint space arepreserved longer than in pyogenic infections25.Characteristically, with untreated tuberculous

spondylitis there is subligamentous spread of in-fection with tendency for distant caudal exten-sion, erosion of the anterior aspect of the verte-bral bodies distant from the primary site of in-volvement and the development of large calcified

soft tissue masses. As in pyogenic spondylodisci-tis, paraspinal abscess formation may be detectedon radiographs as unilateral or bilateral area offusiform soft-tissue swelling around the spine,but soft tissue contrast resolution of radiographyis poor. As the vertebral end plates become in-creasingly involved and the vertebral destructionprogresses, vertebral collapse and anterior wedg-ing occur (Figure 2), leading to characteristicgibbus formation with varying degrees of kypho-sis and scoliosis 26. During the healing phase,ankylosis of the vertebral bodies occurs, withobliteration of the intervening disc space and for-mation of a single vertebral block (Figure 2).

Computed tomographyAdvances in computed tomography (CT) tech-

nology, throughout the last decade, have led to thecurrent generation of multidetector CT scannersthat boast faster acquisition, increased anatomicalcoverage, higher spatial resolution, and isotropicdata acquisition. This has resulted in the improve-

A. Leone, C. Dell’Atti, N. Magarelli, P. Colelli, A. Balanika, R. Casale, L. Bonomo

Figure 1. Lateral radiograph of the lumbar spine in a 56-year-old woman showing infective spondylitis at L2-3 level.Note narrowing of the disc space and the loss of definitionof the opposite end plates (arrow).

ment in diagnostic accuracy and the gain is per-haps best exemplified by the surge in the detailedmultiplanar reformations in spine imaging. Spiral

CT imaging with high quality 2D and 3D refor-matted images allows a clear assessment of verysmall vertebral foci of infection, minimal erosionsof the end plates, bone destruction, and soft tissueinvolvement in the paravertebral and epiduralspaces (Figure 3). Although, it is not as sensitiveas MR imaging, CT remains the preferred imagingmodality for the assessment of sequestra andpathological calcifications. Furthermore, it is par-ticularly helpful in identifying atypical foci of tu-berculosis especially in the posterior neural archallowing differentiation from other destructiveprocesses (i.e. metastases, other infections).Under the guidance of CT, percutaneous diag-

nostic needle biopsy and percutaneous drainageof abscesses with identification of the causativemicro-organism can be done.Large abscesses could be found in the pre- and

paravertebral region, which may extend into thepsoas muscle, and along the pleura-lined spacesof the thorax. Paraspinal abscess formation maybe better demonstrated on CT or MR images.The thick nodular rim of an abscess on a precon-trast scan represent the hypervascular, hypercel-lular, fibrotic wall of the inflammatory cavity.After contrast administration, there usually isstrong rim enhancement around low attenuationmultiloculated fluid collection27.The identification of a multilocular and par-

tially calcified paraspinal abscess with a rim en-hancement associated to a destructive vertebralbody lesion is highly suggestive for a tuberculousrather than pyogenic infection (Figure 4).

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Figure 2. Lateral radiograph of the thoracic spine in a 51-year-old woman with tuberculous spondylitis. Note verte-bral collapse and anterior wedging of T9 (arrow) and oblit-eration of the disc space at T9-10 level (arrow).

Figure 3. Pyogenic spondylodiscitis at L3-4 level in a 64-year-old man. (a) Axial CT scan at L3 level and (b) sagittal recon-struction CT image show destructive change with fragmentation of the vertebral bodies. Bone fragment is displaced posteriorlyinto the spinal canal (arrow in a). There is prevertebral abscess (black arrow in b) together with a large epidural abscess com-pressing the thecal sac (white arrow in b).

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MR imagingHigh contrast resolution, direct multiplanar

imaging capability, high sensitivity for soft tissueand bone marrow lesions, and absence of ionizingradiation make MR imaging the modality of choicefor the diagnosis of inflammatory disorders andtheir sequelae2,6,28,29. MR imaging should be em-ployed as soon as infection is suspected because ofits high sensitivity and specificity to detect earlyinfection, to evaluate fully the extent of disease af-fecting the spine and to monitor therapeutic re-sponse during the course of spinal infection6,28-30.

A disadvantage of MR imaging is that corticalbone involvement is not as well visualized as by CT.The standard MR imaging protocol should

routinely include fluid-sensitive sequences (i.e.,short-tau inversion recovery [STIR] or fat-satu-rated T2-weighted images) which are highly sen-sitive for early inflammatory oedema and are bet-ter than T2-weighted spin-echo (SE) sequencesfor demonstration of initial infectious focus.With addition of T1-weighted SE pre- and post-contrast fat-suppressed T1-weighted sequences,clear demonstration of all anatomical details anddifferentiation between vascularised and nonvas-cularised, necrotic inflammatory components(abscess, sequestrum) is possible11.The earliest signs of an infective process on

MR imaging are inflammatory oedema and hy-peraemia which manifest by a reduction in signalon T1-weighted SE images with a correspondingincrease in signal on fluid-sensitive images 23,31

(Figure 5). The T1-weighted and fluid-sensitivesequences are more reliable than T2-weightedfast SE sequences because in this early stage thesignal changes on the T2-weighted images maynot be readily apparent, due to the bright signalintensity of marrow fat on fast SE images.Post-contrast fat-suppressed T1-weighted se-

quences can improve contrast between the hyper-emic osseous and soft tissue components andsurrounding normal structures32. Moreover, thesesequences are useful in identifying communica-tions between the bony lesions and the paraspinalmasses33.


Figure 4. Tuberculous spondylodiscitis in a 67-year-oldman. Axial CT through L3 vertebra shows fragmentation ofthe vertebral body with extension of infection into the psoasmuscles (white arrows) and epidural space (black arrow). Rimenhancement of the epidural mass and within the paravertebralsoft tissues denotes abscess formation. Note the minute calcifi-cation within the right psoas abscess (long arrow).

Figure 5. Pyogenic spondylodisci-tis at L5-S1 level in a 47-year-oldman. (a) Sagittal T1-weighted MRimage demonstrating decreased sig-nal within the bodies of L5 and S1and slight loss of sharpness of theadjacent vertebral end plates. (b)Sagittal fat-suppressed T2-weigthedimage and (c) sagittal contrast-en-hanced fat-suppressed image showhyperintensity and enhancement ofL5 and S1 bodies and intervertebraldisc respectively.

MR imaging criteria with good to excellentsensitivity include evidence of either paraspinalor epidural inflammatory tissue, contrast en-hancement of the disc, hyperintensity or fluid-equivalent signal intensity on STIR or T2-weighted fat-suppressed images, and erosion ordestruction of the vertebral endplates on T1-weighted images30.Pathophysiologically, the earliest response to

infection in a vertebral body is the accumulationof extracellular fluid within the marrow. MRimaging demonstrates this accumulation of oede-ma within the marrow before the destructive bonechanges take place. The infective process usuallyis adjacent to vertebral end plates and on sagittalT1-weighted SE noncontrast images, the endplates are ill defined, the intervertebral disc andadjacent vertebral bodies are of low signal inten-sity, while the STIR or fat-saturated T2-weightedimages show high signal intensity within the bonemarrow and the affected intervertebral disc (Fig-ure 5). Non-visualization of the nuclear cleft inthe infected disc on T2-weighted MR images wasreported to be indicative of spinal infection23,34.However, this sign is only rarely applicable sincethe nuclear cleft is rarely visible in the cervicaland thoracic spine on T2-weighted images and itsclinical use is, therefore, limited30,34.Following the intravenous administration of

gadolinium compounds disc enhancement pat-terns such as homogeneous enhancement of mostof the disc, patchy nonconfluent areas of en-hancement, and thick or thin areas of peripheralenhancement may be seen. Infected bone marrowalso enhances diffusely after contrast material isadministered32 (Figure 5).If the infective process is left untreated, signal

change progresses across the disc to involve theadjacent vertebral body giving the classical ap-pearance of involvement of two vertebrae on ei-ther side of an involved disc with destruction ofthe vertebral end plates. An early extension of in-flammatory oedema beyond the limits of the ver-tebral bodies and the annulus fibrosus into theparavertebral fat will cause low signal intensityon T1-weighted SE non-contrast images, hyperin-tensity on STIR or fat-saturated T2-weighted im-ages, and enhancement on post-contrast fat-sup-pressed T1-weighted sequences. The infectiveprocess can extend posteriorly into the epiduralspace, and posterolaterally into the intervertebralforamina, which is well demonstrated onparasagittal and axial images, with obliteration ofthe perineural fat. Abnormal soft tissue within the

epidural space is due to an epidural inflammatoryphlegmon (a mass of granulation tissue) or anepidural abscess. Most epidural phleg-mon/abscess is anteriorly located, usually close tothe primary infectious site. More rarely, distantepidural involvement or isolated epidural abscessmay occur4. Differentiation between a phlegmonand an abscess is extremely important since thetreatment differs between the conditions, surgerybeing often indicated for an abscess, whereasthere is more conservative approach with antibiot-ic therapy for a phlegmon. This differentiation ispossible only after the intravenous administrationof gadolinium compounds35. Diffuse homoge-neous contrast enhancement is consistent with aphlegmon, while rim enhancement around a non-enhancing liquefied centre indicates the presenceof an abscess (Figures 6, 7).Postinflammatory phase is histologically char-

acterised by the presence of vascularised fibroustissue, fat bone marrow transformation, subchon-dral fibrosis and osteosclerosis, changes which areclearly demonstrated by MR imaging. Therefore,MR imaging allows assessment of the response toconservative treatment6,11. This manifests by a re-duction in paravertebral soft tissue swelling, reso-lution of canal compromise, reduced enhancementof tissues and quiescence of signal changes withinthe intervertebral disc and adjacent marrow (Fig-ure 7). The disc space remains narrowed, but thehigh STIR or fat-satured T2-weighted signalchanges regress. The STIR or fat-saturated T2-weighted sequences, so sensitive at demonstratinghigh signal activity, are also good at demonstratingresolution of changes. Their high sensitivity, how-ever, may result in high signal persisting for sometime after the patient has improved clinically. Withhealing of bone, a progressive increase in signalintensity on T1-weighted images within previous-ly affected vertebrae suggests fatty marrow re-placement and indicates healing and has beenfound to correlate well with resolving clinicalsigns and symptoms32.Continuing destructive bone changes suggest

inappropriate diagnosis or treatment.Although MR imaging cannot diagnose the

specific causative pathogen, there are some fea-tures which suggest certain infections. Spinal TBwhich most commonly involves the thoraco-lum-bar junction, is characterised by meningeal in-volvement, subligamentous spread of infectionand paravertebral and intraosseous abscesseswhich can be well demonstrated on post-contrastfat-suppressed T1-weighted images6,28.

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Figure 6. Spondylodiscitis in a 57-year-old woman. (a) Sagittal T1-weighted image shows reduction of disc height at the T5-6level with destruction of the vertebral end plates (white arrow). There is decreased signal within the vertebral bodies of T5 andT6, a soft tissue mass posterior to the T5 and T6 bodies and a posteriorly located epidural mass (black arrow) causing compres-sion of the cord. (b) Sagittal contrast-enhanced fat-suppressed image shows almost uniform enhancement of the epidural collec-tion indicative of a phlegmon (black arrows). The T5-6 disc and the adjacent vertebral bodies are also enhanced. Note also dis-placement of the anterior longitudinal ligament (white arrow). (c) Sagittal fat-suppressed T2-weigthed image and (d) sagittalcontrast-enhanced fat-suppressed image obtained after decompressive laminectomy show disappearance of the epidural phleg-mon, rim enhancement of a large intraosseous abscess (white arrow in c and d), and remnants of T5 body impinging the cord(black arrow in c). The T5-T6 bodies are hyperintense on fat-suppressed T2-weigthed image and enhanced on contrast-enhancedfat-suppressed image. Culture of surgical specimens was negative. Surgery and chemotherapy allowed full recovery.

Figure 7. Tuberculous spondylitis in a 52-year-old man. (a) Sagittal T1-weighted image shows decreased signal within thevertebral bodies of C5 and C6 (white arrows) and a soft tissue mass posterior to the C5 and C6 bodies (black arrow). (b) Cor-responding contrast-enhanced T1-weighted image shows uniform enhancement of the epidural collection indicative of a phleg-mon (arrow) and infective involvement at C5-6 level with enhancement of the affected vertebral bodies and intervertebral disc.(c) Sagittal T1-weighted image obtained after 2 months of chemotherapy. As compared to the previous T1-weighted image theepidural mass is smaller (black arrow) and there is an increased signal in the affected vertebral bodies (white arrows), the ex-pression of medullary fat replacement indicative for healing.

The classical appearance of spinal TB is twoadjacent vertebrae collapsed anteriorly with sub-sequent destruction of the intervening disc. Ex-tension of TB from the vertebra and disc to ad-joining ligaments and soft tissues is seen fre-quently and usually occurs antero-laterally. Fur-thermore, because of subligamentous spread (be-neath the anterior longitudinal or below the pos-terior longitudinal ligaments), multiple vertebrallevels may be involved in a non-contiguous fash-ion, manifested as skip lesions of vertebral bodyor posterior neural arch destruction6,11,28,36.Epidural inflammatory tissue, which may causeneural compromise, is demonstrated by thecalsac displacement and spinal cord distortion. Post-contrast-enhanced, fat suppressed T1-weightedsequences invariably delineate the degree ofcompression of the thecal sac (Figure 8) as wellas the meningeal involvement35.The associated paraspinal abscesses may vary

from small, single, rounded soft tissue swelling,

often poorly delineated, to extensive and often bi-lateral paraspinal masses (Figure 8). In the lum-bar spine, the sheath of the psoas muscles maybecome visibly distended, while the abscesses as-sociated with cervical lesions are evident asretropharyngeal swellings37. A well-definedparaspinal region with abnormal signal intensity;a smooth abscess wall; subligamentous spread tothree or more vertebral levels; and multiple verte-bral or entire-body involvement are findings moresuggestive of tuberculous spondylodiscitis than ofpyogenic spondylodiscitis. These lesions subse-quently may undergo contraction and sometimescalcification as activity of the infection subsides.Calcification within a large paraspinal abscess isvirtually diagnostic for tuberculosis, but MRimaging is less sensitive than radiography or CTfor identifying paraspinal calcifications32.Differential diagnosis between tuberculous and

pyogenic spondylodiscitis is of clinical impor-tance, but may be difficult on the basis of radio-

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Figure 8. Tuberculous spondylitis at L1-2 level in a 32-year-old man. (a) Axial contrast-enhanced fat-suppressed imagethrough L2 vertebra demonstrating enhancement of the vertebral body and paravertebral soft tissues (black arrows). Uniform en-hancement of the epidural mass (white arrow) causing slight compression of the thecal sac is indicative of an epidural phlegmon.(b) Coronal contrast-enhanced fat-suppressed image shows tuberculous involvement of vertebral bodies and intervertebral disc atL1-2 level (white arrows), as well as the large peripherally enhancing abscesses in the psoas muscles (black arrows).

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logical findings alone. However, some character-istic but not pathognomonic signs may supportthe specific diagnosis. Pyogenic spondylitis mostcommonly involves the lumbar spine and onespinal motion segment. The presence of a smalland no calcified paraspinal mass and paraverte-bral new bone formation in the early healingphase are strongly suggestive of a pyogenic le-sion. The classical appearances of spinal TB arethoracic site, multiple levels of infection, pres-ence of skip lesions, relative preservation of theintervertebral disc and subligamentous spread ofinfection, a large paraspinal mass containing cal-cifications, and the absence of reactive sclerosis.Specific diagnosis is more of a problem when

a less typical pattern of TB is found. For exam-ple, erosions and destruction of pedicles or trans-verse processes may resemble metastatic carcino-ma38. Tuberculous involvement of a single verte-bral body or of posterior elements, although oc-curring less frequently, has been well document-ed39. Moreover, in children the vertebra plana ap-pearance characteristic of eosinophilic granulo-ma can be produced by tuberculous infection.

Differential diagnosis

MR imaging is the first-line diagnostic modal-ity for spinal infections. In most cases, a firm di-agnosis can be made distinguishing infectionsfrom other destructive conditions. However, thereare a number of diseases which can mimic infec-tions including malignancy, degenerative and in-flammatory diseases.In the differential diagnosis of infection from

malignancy, the appearance of the disc space andvertebral end plates may be diagnostic. A processcentered around the intervertebral disc, with lossof definition or erosion of the vertebral endplates, is strongly suggestive of infection, where-as, malignancy is more likely to primary involvevertebral body and posterior elements41.Degenerative disc disease is not infrequently

associated with loss of disc height, but vertebralend-plate are well defined. On MR imaging,there may be reduction of disc hydration, and de-generative discogenic vertebral changes can benoted on endplates bordering the intervertebraldiscs (Modic types 1-3)42.Modic type-1, representing bone marrow

oedema (decreased signal on T1-weighted, in-creased signal on T2-weighted images, and post-

contrast enhancement) may give rise to confu-sion. However, bone marrow oedema is limitedto the subchondral region, the vertebral end plateremains well defined and the degenerated disc isof low signal intensity rather than of increasedsignal as not infrequently seen with spinal infec-tion on T2-weighted images (Figure 9).Erosive intervertebral osteochondrosis, which

represents disc degeneration with widespreaderosions of the end plates, may clinically and ra-diologically mimic infectious spondylodiscitis.On MR imaging, however, vacuum phenomenonand T2-hypointensity within the disc, bandlikesubchondral oedema, and lack of epidural orparaspinal inflammatory changes suggest inter-vertebral osteochondrosis11,43.Intraosseous disc herniation (Schmorl’s nodes)

represents another condition which may mimic in-fectious spondylodiscitis. There may be MR signalchange of an inflammatory pattern in the adjacentmarrow, and post-contrast enhancement of discmaterial which can lead to confusion. However, inthis condition signal within the disc is usually nor-mal or reduced, the remainder of the vertebral endplate remains defined and T1-weighted imageswell recognize the intraosseous disc herniation.Seronegative inflammatory spondyloathropathies

and particularly ankylosing spondylitis may also re-semble infectious spondylodiscitis. Early ankylosingspondylitis can present with disc hyperintensity onT2-weighted sequences, subchondral bone marrowoedema, and discovertebral erosions. However,these erosions are usually bordered by a scleroticmargin and there is absence of epidural andparaspinal inflammation11. In advanced disease, pa-tients with ankylosing spondylitis may develop apseudoarthrosis following fracture which may mim-ic chronic spondylodiscitis. Extension of fractureline into the posterior elements may be demonstrat-ed, and the pseudoarthrosis is typically hypointenseon all pulse sequences43.Destructive spondyloarthropathy (DSA) in

long-term haemodialysis is thought to be closelyrelated to a hemodialysis-related systemic amy-loidosis, in which β2-microglobulin has beenidentified as the major component of the deposit-ed amyloid fibrils44,45. It is essential to differenti-ate changes secondary to renal osteodystrophyfrom spondylodiscitis, because of clinical man-agement consequences. This differentiation maybe difficult in some instances, because DSA mayclosely resemble spondylodiscitis in all the imag-ing procedures. Even the MR imaging features ofDSA, which may be associated with prominent


prevertebral soft tissue, are not pathognomonic45.An increased signal intensity on long TR/longTE images and homogeneous enhancement aftergadolinium injection from the affected discs andadjacent end plates may be found. The high sig-nal intensity on the T2-weighted images, andthe contrast enhancement may be due to the cy-tokine-mediated reactive inflammation aroundβ2-microglobulin amyloid deposition46. Howev-er, the lower segment of the cervical spine is thearea most frequently involved in DSA, contraryto early spinal infection, the endplate erosionsare surrounded by pronounced sclerosis, and iflow signal in T2-weighted images is present, aninfection can be excluded.Several investigations47-49 have focused on the

MR imaging spinal involvement in patients withSynovitis, Acne, Pustulosis, Hyperostosis, Os-teitis (SAPHO) syndrome, which often seamssimilar to infective spondylitis. Anterior vertebralcorner erosion, absence of an abscess or ofepidural involvement, multiple foci, and earlierproductive changes seen in this condition helpdifferentiate SAPHO syndrome from infection.

Other diseases may also resemble the imagingfeatures of infectious spondylodiscitis, includingthose found on neuropathic spinal disease andrheumatoid arthritis4.

Conclusions

Spinal infection is a potentially devastatingand rapidly progressing disease which, unrecog-nised, may result in neurological compromise, oreven death. The role of imaging is a prompt diag-nosis, evaluation of extent of infection with spe-cial regard to potential neural compromise, dif-ferential diagnosis, guidance of diagnostic biopsyand/or drainage procedures, planning of treat-ment (medical vs surgical), and assessment of re-sponse to therapy. Prompt diagnosis, the corner-stone of treatment, relies heavily on characteris-tic MR imaging findings. Image-guided biopsy,will then be required for histological confirma-tion and subsequent culture and sensitivity to an-tibiotics. MR imaging is the modality of choicefor an early diagnosis and follow-up of vertebral

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Figure 9. Modic type 1 degenerative marrow signal intensity changes parallel those of osteomyelitis. (a) Sagittal T1-weight-ed image shows confluent decreased signal intensity of the vertebral bodies bone marrow (arrows) and intervertebral disc atT7-8 level caused by degenerative disc disease. However, at the same level, (b) a T2-weighted image shows increased signalintensity of the vertebral bodies bone marrow (arrow). (c) Corresponding contrast-enhanced, sagittal T1-weighted imageshows enhancement in the same areas (arrow). The lack of increased signal intensity of the intervertebral disc on T2-weightedimage and the clinical setting differentiate degenerative disc disease from spondylitis.

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infection because it is the only method whichcombines high sensitivity with satisfactory speci-ficity. It is extremely sensitive in detecting anddelineating infective lesions irrespective of theirspinal location. The specificity of MR imagingdepends on the signal characteristics and anatom-ic distribution of the infection.Although many aetiologically different spinal

diseases may simulate a spinal infection, in mostcases, using MR imaging patterns may help dif-ferentiate spinal infection from other conditions.

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