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1c
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Figure 1:
(1a) T1-weighted sagittal and (1b,1c) T2-weighted sagittal and axial images.
Findings
2a
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Figure 2:
The T1-weighted sagittal image shows irregularity of the endplates at the L2-3 level
(arrowheads)with marked hypointensity in the adjacent endplates (asterisks).
3a
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Figure 3:
The T2-weighted sagittal image confirms endplate irregularity(arrowhead). The disc is markedly
hyperintense.
4a
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Figure 4:
The T2-weighted axial image reveals abnormal hyperintensity in the atrophic left iliopsoas
muscle(asterisk) and a small left paraspinous fluid collection (arrow), suspicious for abscess.
Diagnosis
Introduction
Discitis, infection of the disc and vertebral endplates, has significant morbidity
and mortality. Although early diagnosis and treatment leads to a better
outcome, a delay in diagnosis is common due to nonspecific and inconsistent
clinical signs and symptoms. A variety of imaging modalities may be used to
evaluate suspected discitis with varying degrees of effectiveness.
Epidemiology
Discitis exhibits a bimodal age distribution, with peaks in early childhood and
after age 50. A male predominance is seen. Risk factors for discitis include
diabetes, old age, immunosuppression, IV drug use, alcoholism, and renal
failure. Although rare, there is an increased risk of discitis following invasive
spinal procedures, estimated at 0.5% for anterior cervical discectomy and
0.25% for lumbar discectomy, with an overall rate of 0.1 to 4% of all invasive
spinal procedures. Postoperative discitis accounts for approximately 20-30% of
cases of discitis.1,2
Pathophysiology
Most cases of discitis are secondary to infection elsewhere in the body, with
the most common source being the genitourinary tract; other less common
sources include endocarditis, pneumonia, or the oral cavity.1,3 Contrary to its
name, due to the vascular anatomy of adults, discitis is a primary infection of
the vertebral endplate with secondary extension into the disc. The
metaphyseal arteries of the endplate are the target for septic emboli, which
cause bone infarction and secondary infection. The vascular supply of the disc
ends in the annulus fibrosis; the disc is largely supplied with nutrients via direct
diffusion from the vertebral endplate. Infection thus spreads contiguously to
the disc, spinal canal, and paraspinous soft tissues.1,2 Another postulated
source of blood-borne pathogens is the epidural venous plexus; retrograde
flow from the pelvis may allow the spread of infection from pelvic disease, and
the pelvis is in fact the most common source of infection in discitis. However,
this route of spread is not universally accepted, as pressures required to
generate retrograde flow in animal models are not physiologic.2
5a
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Figure 5:
A 65 year-old male with history of L5 laminotomy several months prior, now with recurrent pain. A
T1-weighted sagittal image demonstrates marked hypointensity of the L4-5 disc(arrowhead) and
adjacent vertebral bodies(asterisks) with irregular, poorly defined endplates and a ventral epidural
soft tissue process (arrows).
6a
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Figure 6:
The corresponding T2-weighted sagittal image reveals a markedly hyperintense intervertebral disc
(arrowhead). Abnormal hyperintensity contiguous with the disc (arrow) extends into the ventral
epidural space.
7a
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7b
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Figure 7:
T1-weighted sagittal (7a) and axial (7b) images after IV gadolinium administration demonstrate
peripheral enhancement of the disc (arrowheads) and marked vertebral enhancement (asterisks). A
moderate amount of uniformly enhancing soft tissue is present in the ventral spinal canal at the
L4-5 level (arrows), suggesting epidural inflammatory changes. The recent left L5 laminotomy
defect is demonstrated (short arrow).
8a
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Figure 8:
A T2-weighted axial image demonstrates loss of normal paraspinous fat planes (arrowheads) and
abnormal signal in the left iliopsoas muscle (asterisk). Diagnosis: Post operative pyogenic discitis
with epidural phlegmon and paraspinous inflammation.
The clinical presentation of discitis in children differs from that of adults and is
characterized by fever, sudden onset of back pain, refusal to flex the lumbar
spine, irritability, and refusal to walk.1,2
Imaging of discitis
Discitis is most commonly seen in the lumbar spine, followed by the cervical
spine, and least commonly involves the thoracic spine (except for in atypical
cases, such as those caused by tuberculous involvement).2 Several imaging
modalities may be used in the assessment of discitis.
Plain films
Findings on plain radiographs usually require 10-14 days to develop and lag
behind clinical symptoms. As a result, a negative plain film does not exclude
early discitis. Eventual changes include loss of definition of the end plates and
decrease in disc space height, followed by lucency of the vertebral body, loss
of trabeculations, and finally frank bone destruction. Progressive kyphosis or
scoliosis can develop in cases of chronic infection. Sclerosis is seen after
2,3
healing with a high incidence of fusion of the disc space.2,3
Gallium scans and technetium-99M scans are highly sensitive for the detection
of discitis, with positive scans seen in 90% of patients that have been
symptomatic for longer than 2 days. The increased uptake in the affected
endplates and decrease in disc space height produces a characteristic
“sandwich” appearance. However, because of the poor anatomic resolution of
nuclear medicine studies and the advent of more sensitive and specific
imaging modalities, these studies are usually utilized in cases of fever of
unknown origin or, in the case of gallium scan, as part of treatment follow-up.
Technetium-99m scans remain positive long after healing has occurred, and
are thus not useful in assessing treatment efficacy.3
Computed tomography
The T2-weighted sagittal image shows hyperintensity of the disc and vertebral bodies (asterisks)
and confirms endplate destruction (arrowheads). The anterior soft tissue process demonstrates
increased T2 signal (arrows).
11a
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Figure 11:
The T2-weighted axial image demonstrates a large, irregular fluid collection along the left pelvic
sidewall (arrowheads) extending into the left sacroiliac joint (arrow), with abnormal hyperintensity
of the left iliac bone and left sacral ala (asterisks). Diagnosis: L4-5 discitis with secondary infection
of the left sacroiliac joint and associated pelvic sidewall abscess.
In acute discitis, hypointensity of the disc and destruction of the endplate are
often seen on T1-weighted imaging, due to inflammation and necrosis
replacing the normal fatty marrow. However, these findings are not consistent.
A phenomenon known as “pseudosparing” of the endplate has been described
in up to 71% of patients, caused by loss of the normal chemical shift
phenomenon seen with fatty marrow that typically causes the superior
endplate to appear thin and the inferior endplate to appear thick. When the
normal marrow is lost in discitis, the decrease in the chemical shift artifact in
the inferior endplate allows visualization of the actual endplate thickness,
masking endplate thinning and erosion.5
The “nuclear cleft sign” is another traditionally described MRI finding in discitis.
However, Ledermann et al. found that loss of the nuclear cleft was not
consistently seen in affected discs and was not a reliable indicator of the
presence or absence of discitis; in fact, in many patients, the nuclear cleft
could not be identified in unaffected discs.6 Loss of disc space height is
another common finding in discitis that is nonspecific and found in many other
conditions.
The most reliable MRI findings in discitis are hyperintensity of the disc on T2-
weighted imaging (sensitivity 93%); the presence of paraspinous or epidural
inflammation/abscess, (sensitivity 98%); and contrast enhancement of the disc
and adjacent bone marrow (sensitivity 95%). Vacuum disc phenomenon is
rarely seen in discitis and is a negative predictor, usually indicating a
degenerative etiology.6
14a
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14b
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Figure 14:
(14a) T2-weighted and (14b) post-gadolinium T1-weighted axial images show a peripherally
enhancing fluid collection in the ventral epidural space at L5-S1 (arrows) displacing the let S1 nerve
root. Diagnosis: Post operative discitis with epidural abscess.
Tuberculous discitis
Differential diagnosis
Several other conditions can mimic the appearance of discitis on various
imaging modalities.
Degenerative disc disease in the early, inflammatory stage can mimic discitis.
Modic Type 1 changes in the endplates due to disruption of the endplate and
vascularized fibrous tissue in the adjacent marrow cause hyperintensity in the
endplate on T2-weighted images and enhancement after the administration of
gadolinium. However, lack of disc hyperintensity on T2-weighted images and
the absence of paraspinous inflammation indicate a degenerative etiology.3,10
In addition, while endplate irregularities are common in degenerative disease,
actual loss of endplate definition or endplate destruction are not
characteristics of Modic Type 1 changes.
15a
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Figure 15:
A 62 year-old male with back pain radiating to both legs. A T1-weighted sagittal image shows loss
of disc space height at T12-L1 (arrow) with marked hypointensity of the endplates. Mild endplate
irregularity is present and a Schmorl's node is seen within the superior endplate of L1 (arrowhead).
16a
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16b
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Figure 16:
Corresponding (16a) T2-weighted and (16b) STIR sagittal images redemonstrate the Schmorl's
node at the superior endplate of L1 (arrowheads), hypointensity of the disc (arrows) and edema in
the adjacent endplates (asterisks).
17a
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Figure 17:
The T1 weighted axial image shows well-defined paraspinous fat planes at the level of T12-L1
(asterisks). Diagnosis: Modic Type 1 degenerative endplate changes. The lack of hyperintensity of
the disc on T2 weighted images, the clearly defined endplates, and the lack of paraspinous
inflammation make infection highly unlikely.
18a
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18b
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Figure 18:
A 56 year-old female with chronic back pain radiating into right hip; the patient is on dialysis for
renal failure. T1- (18a) and T2- (18b) weighted sagittal images show endplate destruction at the L4-
5 and L5-S1 levels (arrowheads). Of note, the discs remain relatively isointense to the unaffected
discs on T2 weighted images. Marrow signal intensity is markedly decreased in all vertebral bodies,
consistent with the history of renal failure.
19a
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Figure 19:
T1-weighted off-midline sagittal images show erosion and inflammation of the right facet joint at
L4-5 (arrow) with surrounding soft tissue inflammatory changes (asterisk). Involvement of the
facets by discitis is uncommon.
20a
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Figure 20:
The T2-weighted axial image at the L4-5 level shows involvement of the facet joints and absence
of paraspinous inflammation. Diagnosis: Dialysis-related spondyloarthropathy.
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21b
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21c
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Figure 21:
A 67 year-old male with lower back pain radiating into the right leg. (21a) T1- and (21b) T2-
weighted sagittal images and a (21c) fat saturated T2-weighted sagittal image reveal
heterogeneous, abnormal signal in the T11 vertebral body (asterisk) with loss of vertebral body
height and posterior epidural extension (arrowheads). The vertebral body is predominantly
hypointense to CSF on T2 weighed images. The endplates are intact, and the adjacent discs are
spared. Diagnosis: Metastatic disease involving the T11 vertebrae with pathologic fracture.
Although MRI is frequently used to follow patients during treatment, it has not
been shown to be an effective modality for assessing response to treatment.
Although paraspinous inflammation and epidural enhancement improves in
most patients, other findings such as disc space enhancement, marrow
edema, and vertebral body enhancement can persist and actually worsen
despite a favorable clinical response. In addition, post-gadolinium
enhancement can persist for longer than 4 months; this may be due to
development of hypervascular fibrous scar tissue during the healing phase. For
these reasons, the use of MRI in routine follow-up of patients with discitis is
not recommended.1,16
The overall mortality rate of discitis is between 2 and 11%. The presence of an
epidural abscess increases mortality to 10% or greater. Up to 16% of patients
with spontaneous discitis experience a recurrence, usually within 6 months of
cessation of antibiotic treatment. Recurrence in cases of discitis complicating
spine surgery is less common, ranging from 0 to 4%; this may be in part due to
increased vigilance in the postoperative period leading to earlier diagnosis of
infection.1,2,17
Discitis commonly presents with nonspecific signs and symptoms and has
significant morbidity and mortality, but prognosis is improved by early
diagnosis. MRI is the imaging study of choice in evaluating possible discitis due
to its high sensitivity and ability to define associated complications, such as
epidural and paraspinous abscess, and should be performed if discitis is
suspected even if plain films and CT are non-diagnostic. MRI can also
distinguish between discitis and other conditions with similar presentations,
allowing the clinician to make informed treatment decisions. However,
because MRI findings do not correlate well with treatment response, follow up
with serial plain films and monitoring of laboratory studies is recommended.
References
1
Cottle L, Riordan T. Infectious Spondylodiscitis. J Infect, Jun 2008; 56(6):401-
12.
2
Jallo GI, Keenan MA. Diskitis. Medline, Feb 2011.
3Varma R, Lander P, Assaf A. Imaging of Pyogenic Infectious Spondylodiskitis.
Radiol Clin of N Amer, March 2001; 39(2):203-213.
4 Viola RW, King HA, Adler SM, et al. Delayed Infection After Elective Spinal
Instrumentation and Fusion: A Retrospective Analysis of Eight Cases. Spine,
1997; 22:2444-2450 (tel:2444-2450).
5Wolansky LJ, Heary RF, Patterson T, Friedenberg JS, Tholany J, et al.
Pseudosparing of the Endplate: A Potential Pitfall in Using MR Imaging to
Diagnose Infectious Spondylitis. AJR, 1999; 172:777-780.
6 Ledermann HP, Schweitzer ME, Morrison WB, Carrino JA. MR Imaging
Findings in Spinal Infections: Rules or Myths? Radiology, 2003; 228:506-514.
7 Eguchi Y, Ohtori S, Yamashita M, Yamaguchi K, Suzuki M, Orita S, et al.
Diffusion Magnetic Resonance Imaging to Differentiate Degenerative from
Infectious Endplate Abnormalities in the Lumbar Spine. Spine, Feb 2011;
36(3):E198-202.
8Kiss E, Keutch G, Zanetti M, Jung T, Schwartz A, Schocke M, Jaschke W,
Czermak BV. Dialysis-Related Amyloid Revisited. AJR, 2005; 185:1460-1467.
9
9Taylor DJ, Brown GC, Moore RJ, Walters R, Chapple DC, Goss DL, Fraser RJ.
Early Detection of Lumbar Discitis by MRI. Proc Intl Soc Mag Reson Med, 2001;
9:249.
10Modic MT, Ross JS. Lumbar Degenerative Disc Disease. Radiology, October
2007; 245(1):43-57.
11Hovi I, Lamminen A, Salomen O, et al. MR Imaging of the Lower Spine. Acta
Radiol, 1994;35:532-540.
12Park YH, Taylor JA, Szollar SM, et al. Imaging Findings in Spinal
Neuroarthropathy. Spine, 1994; 19:1499-1504.
13Nachtigal A, Cardinal E, Bureau NJ, et al. Vertebral Involvement in SAPHO
Syndrome: MRI Findings. Skeletal Radiol, 1999; 28:163-168.
14Toussirot E, Dupond JL, Wendling D. Spondylodiscitis in SAPHO Syndrome:
A Series of Eight Cases. Ann Rheum Dis, 1997; 56:52-58.
15Karadimas EJ, Bunger C, Lindblad BE, Hansen ES, Hoy K, et al.
Spondylodiscitis: A Retrospective Study of 163 Patients. Acta Orthop, Oct
2008; 79(5):650-659.
16
Kowalski, TJ, Layton, KF, Berbari, EF, Steckelberg, JM, Huddleston PM, et al.
Follow-up MRI Imaging in Patients with Pyogenic Spine Infections: Lack of
Correlation with Clinical Features. Am J Neuroradiol, Apr 2007; 28:693-699.
17Jimenez-Mejias ME, de Dios Colmenero J, Sanchez-Lora FJ, Palomino-
Nicas J, et al. Postoperative Spondylodiskitis: Etiology, Clinical Findings,
Prognosis, and Comparison with Non-Operative Pyogenic Spondylodiskitis.
Clin Inf Dis, 1999; 29:339-345.
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