Infection



Fig. 1
35-year-old male patient with right lower back pain for 2 weeks; recent onset of right sciatic pain. Low grade fever. Aspiration-proven Staphylococcus aureus septic sacroiliitis. Coronal STIR image (a) shows fluid signal within the joint (arrowhead) with distension of the joint recesses superiorly and inferiorly (arrows), the latter extending into the sciatic notch. Note surrounding soft tissue edema representing inflammation. Coronal T1-weighted fat suppressed post-contrast image (b) shows rim-enhancing abscesses (arrows) in the gluteus musculature



Tuberculous arthritis (TBa) has a more chronic course compared to pyogenic SA, is common in endemic areas but in developed countries it is seen in immunosuppressed, immigrants, and elderly patients. TBa is considered to occur secondarily to hematogenously induced osteomyelitis, is mostly nonoarticular with the hip being involved up to 15% and if untreated results in joint destruction [18, 19]. Establishment of diagnosis is not possible based on imaging findings alone. The “Phemister’s triad” refers to the presence of periarticular osteopenia, peripheral erosions and gradual joint space narrowing on plain radiographs. Minimal subarticular sclerosis, soft tissue swelling, osteolysis and minimal periosteal reaction may also be seen [18, 19]. Joint space will be narrowed late in the course of the disease. Effusion and synovial hypertophy seen on MRI, are indistinguishable from those seen in other arthritides. Chronic synovitis though, may show minimal on no enhancement at all. Sacroiliac joint involvement may show abscesses, often calcified, and are best appreciated with CT.

In our practice, any patient with joint effusion and clinical suspicion of SA, undergoes image-guided aspiration of the fluid with fluoroscopy, ultrasonography or CT, depending upon the individual joint involvement and the body habitus of the patient.



Cellulitis


Cellulitis is seen as replacement of the normal fat signal in subcutaneous tissues on T1-weighted images, with high signal (though less than fluid) on T2-weighted or STIR images and diffuse enhancement after contrast agent administration. The margins are generally poorly defined. Abscesses appear as a focal collection of signal approximating fluid on T2-weighted or STIR images, with thick rim enhancement on post-contrast T1-weighted images. Sinus tracts are characterized by a thin, discrete line of fluid signal extending through the soft tissues with enhancement of the hyperemic margins. Sinus tracts are visualized as parallel lines of enhancement in a “tram-track” configuration.


Osteomyelitis


Osteomyelitis is characterized by altered bone marrow signal, with low signal (loss of the normal fat signal) on T1-weighted images, edema signal on T2-weighted or STIR images, and enhancement on postgadolinium T1-weighted images (Fig. 2). Other MRI findings in cases of osteomyelitis include cortical disruption and periostitis. Periostitis is seen as a thin, linear pattern of edema and enhancement surrounding the outer cortical margin that will appear thickened if the periostitis is chronic.

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Fig. 2
10-year-old boy with chronic leg pain, fevers. Biopsy-proven osteomyelitis. Axial T2-weighted fat suppressed image (a) of the lower leg demonstrates abnormal signal in the tibia (arrow) representing osteomyelitis. Note surrounding phlegmonous tissue (arrowheads). Sagittal T1-weighted fat suppressed post contrast image (b) and axial T1-weighted fat suppressed pre- and post-contrast images (c) show non-enhancement of the mid tibial shaft (arrow) consistent with devitalization (a sequestrum). A rim of enhancing new bone formation (involucrum, arrowheads) is present

Recognition of abnormal bone marrow signal in the appropriate clinical setting results in high sensitivity for diagnosis of osteomyelitis. Other entities can mimic this alteration in signal, including fracture, tumor, active inflammatory arthritis or neuropathic disease, infarction, or recent postoperative change. However, these other processes usually have different morphology than osteomyelitis and recognition of these patterns often enables differentiation. For example, identification of a fracture line, a discrete lesion, adjacent arthritis or neuropathic disease, or postoperative metal artifact improves specificity. Correlation with radiographs and clinical history is also important. Additionally, over 90% of the time osteomyelitis of the foot and ankle is a result of contiguous spread through the skin1 with the majority of cases demonstrating skin ulceration, cellulitis, soft tissue abscess, or a sinus tract. These findings can be thought of as “secondary signs” of osteomyelitis, recognition of which improves specificity.


Devitalization


Changes related to ischemia should be taken into account when interpreting MRI of the diabetic foot. Documentation of the presence and extent of ischemic and devitalized areas facilitate surgical planning for débridement and limited, foot-sparing amputations. Pre- and postcontrast MR images can detect ischemia and devitalization of the foot as focal or regional lack of soft tissue contrast enhancement. Devitalization, or foot “infarction,” is seen as a focal area of nonenhancement with a sharp cutoff with increased enhancement in the surrounding reactive, hypervascular tissue. Only contrast-enhanced images allow reliable recognition of gangrenous tissue because T2- and T1-weighted images reveal uncharacteristic signal alterations.

Underlying infection, including osteomyelitis, cellulitis, and abscess would not be expected to enhance within necrotic areas (Fig. 2). In this setting, signal characteristics on T1- and T2-weighted images should be primarily relied on for diagnosis of soft tissue and osseous infection. If intravenous contrast is provided, the radiologist should be familiar with the appearance of devitalized tissue to reduce false-negative readings for infection.


Evaluation of Extent of Involvement


Extent of infection in soft tissue and bone is fairly well delineated on postcontrast MR images. However, infection does not tend to remain confined by fascial planes and spreads centripetally from the inoculation site across fascial compartments, into and across joints, and through tendons. Soft tissue involvement is often more extensive than the osseous disease, requiring careful examination of the soft tissues proximal to the source of infection. Without proper débridement the patient may fail the foot-sparing procedure and require more extensive amputation.



Spinal Infection


Infectious spondylodiscitis is an inflammatory disorder which involves the osseous structures, vertebral bodies (osteomyelitis) and the discs (discitis). Posterior elements, isolated facet joint infection and paravertebral soft tissue abscesses may also occur. The earlier the diagnosis is made, the better the prognosis is. Since clinical symptoms, physical examination findings and laboratory data are often non specific, imaging has a crucial role in early diagnosis and treatment planning. Spinal infection represents around 3–5% of all cases of osseous infection and is increasing in prevalence due to increased number of mobile population, diabetes mellitus, intravenous drug abuse, immunocompromised patients of any cause, increased number of surgical and diagnostic image guided procedures and higher awareness. Diabetic men in the 5th and 6th decades of life and elderly of both sexes are more commonly afflicted. In about 25% of patients, the organisms cannot be identified. Early diagnosis is associated with good outcome whereas delay in diagnosis may be life threatening. Spinal infection may be caused by bacteria, fungi and parasites.

The routes of infection include arterial spread from distal septic foci, venous spread through the Batson’s plexus from pelvic infections, and direct extension from adjacent soft tissue or implantation, either iatrogenically or rarely by penetrating injury [20]. The lumbar spine is more commonly involved (50%) followed by thoracic spine (35%) [21]. Septic emboli location depends upon the age group. In children under age 4, end arteries enter the intervertebral disc and thus discitis may be the initial and perhaps the only demonstration due to the rich intraosseous network of arterial anastomoses. In adolescents and adults, the richest arterial network lies beneath the anterior endplate which is the equivalent to long bone metaphysis. Thus, infection appears first in the anterior vertebral body and then spreads through the endplates into the disc and the contiguous vertebral body. Pre/paravertebral and epidural extension may occur via sub-ligamentous route. Epidural abscess formation is an emergency situation and the role of radiologist in prompt diagnosis is crucial [22].


Pyogenic


Pyogenic spondylodiscitis (PS) is the most commonly encountered spine infection. Common causative bacteria are Staphylococcus aureus (up to 60%) followed by Enterobacter (up to 30%), Streptococcus, Pseudomonas, Klebsiella and Salmonella. The course may be acute or chronic and the symptoms are non specific. Elevated ESR, PRC and WBC, are not constant laboratory findings. The primary radiologic finding is destruction of two contiguous vertebral bodies and the intervertebral disc. Plain radiographs are not sensitive in the early stages and become positive 2–4 weeks after onset of symptoms. Progressive osteolysis beneath the anterior endplate and loss of endplate definition, are signs highly suggesting PS (20). A rapid loss of the intervertebral space matched with loss of definition in the opposing endplate and associated osteolysis beneath it, suggest spread to the contiguous vertebral body. As a rule, the presence of gas (“vacuum” in the disc and “cleft” beneath the endplate), rules out infection. CT is more sensitive to earlier changes showing in addition to plain films effacement of paravertebral fat planes and contrast enhancement of paravertebral soft tissue changes. It may be useful when MRI findings are equivocal, by showing the presence of disc “vacuum” sign and the lack of endplate destruction which help to rule out infection. It offers in addition a guidance of the route for diagnostic aspiration. MRI is the method of choice for early detection and accurate diagnosis of PS. Low on T1-weighted and high on fluid sensitive sequences bone marrow edema initially, followed by loss of the “black” outline of the endplate cortex, are the acute phase imaging findings [20, 21]. Bone marrow edema is located underneath the disrupted endplate cortex. Later, high signal on fluid sensitive sequences is seen within the involved disc. Fat suppressed images following contrast medium administration, show enhancement of the bone marrow and the disc, excluding the necrotic areas [20, 21]. Occasionally, depending on the duration of symptoms, a paraspinal or intra-canalicular phlegmon may be seen. A peripheral rim enhancement corresponds to abscess formation, often in thoracic spine. Εpidural abscesses result in high morbidity and mortality and may be the initial feature of the disease from a remote underlying infection in cases of extension from facets and retroperitoneum or from hematogenous spread directly to this anatomic location. Subdural abscess is a rare and urgent disorder, suggested on MRI when the shape of the sac and the epidural fat are preserved. Major differential diagnosis of PS should include Modic type I endplate degenerative changes [2022]. In favor of infection are the high signal of the disc and lack of the normal intranuclear cleft on T2-weighted images as well as presence of disc enhancement. Dialysis-associated destructive spondyloarthropathy, showing sharply demarcated endplate erosions and low T2 signal in the paraspinal lesions, should also be included in the differential diagnosis [20]. Paraspinal edema and enhancement may be seen in axial spondyloarthritis-related enthesopathy. Acute Schmorl’s node and aseptic spondylodiscitis, previously known as Andersson’s lesion in the context of axial spondylarthropathy, may simulate early infection. A useful sign of PS healing on MRI is the focal return of bone marrow fatty signal on T1-weighted images. However, MRI is not recommended for follow-up as it lags 4–8 weeks behind clinical and serologic improvement in successful treatment [20, 23]. Thus, persistent or worse MRI findings in patients with clinical improvement, do not suggest a failed treatment. Newer techniques, such as diffusion-weighted imaging may show increased diffusivity and drop in the ACD values in PS, often indistinguishable from malignancy [24] but helpful in differentiating infectious from degenerative changes in the endplates, the latter showing lower ADC values [25]. Radionuclide imaging is not currently used routinely as it is limited by false negative results, inability to detect soft tissue involvement and the fact that it remains abnormal during the normal healing phase after resolution of infection [26]. Indeed, it is reserved for cases that MRI findings are inconclusive, for depicting multiple foci and for patients with contraindication for MRI. FDG-PET/CT may be more accurate than MRI in low-grade spondylodiscitis and useful particularly when severe degenerative changes coexist [26].

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Jun 25, 2017 | Posted by in MUSCULOSKELETAL MEDICINE | Comments Off on Infection

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