Service de Rhumatologie, Médecine Physique et Réhabilitation, Centre Hospitalier Universitaire Vaudois, CHUV 1011 Lausanne, Switzerland
SIR, Iliopsoas abscess and pyomyositis are rare clinical entities. Except for a few cases of carcinoma or focal myositis mimicking abscesses [1, 2], they are infectious. The concurrence of spondylodiscitis and bilateral psoas abscesses is virtually pathognomonic of an infectious process, Staphylococcus, Brucella and Mycobacterium tuberculosis being the most likely organisms. We report a case of calcium pyrophosphate crystal deposition (CPPD) disease presenting with erosive spondylodiscitis associated with an aseptic inflammatory reaction of both psoas muscles which mimicked such an infectious process.
A 76-yr-old woman was admitted for exacerbation of chronic low back pain with leg weakness and repetitive falls. There was a history of diabetes with discrete polyneuropathy, chronic venous insufficiency, hypertension and mild chronic renal insufficiency. She had CPPD disease with radiological chondrocalcinosis at the wrists, knees and lumbar spine. Two years previously, a L2L3 erosive discitis associated with a herniated disc had been treated conservatively.
On admission, she complained of some morning stiffness and occasional night sweats and fever, but denied any weight loss, recent surgical procedures and urogenital or gastrointestinal problems. Examination demonstrated severe limitation of lumbar spine mobility with muscle spasms and tenderness of the paralumbar region. There was no sign of sacroiliac joint involvement. Light touch sensation was diminished over the anterior thigh, and both knee and ankle jerks were absent. There was no fever, cutaneous lesions, abdominal tenderness, signs of cardiac involvement or any other signs of an infectious process. The psoas sign was absent on both sides. The white cell count was 12 000/mm3 and the erythrocyte sedimentation rate 75 mm/h. There was mild inflammatory anaemia and routine laboratory tests were normal except for a moderate increase in creatinaemia. Spine radiographs demonstrated multiple discopathies from D9 to L4 and a previously known increased density of the body of L2.
After 3 weeks of standard conservative therapy consisting of analgesia, rest and non-steroidal anti-inflammatory drugs (NSAIDs), she presented an exacerbation of the weakness of the quadriceps muscle. A magnetic resonance imaging (MRI) study demonstrated spondylodiscitis of the L2L3 space infiltrating the vertebral bodies from L1 to L3. An image compatible with an abscess or intradural sequester as well as cellulitis and myositis of both psoas muscles with enhanced gadolinium uptake evoking abscesses were further demonstrated (Fig. 1).
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Clinical diagnosis of chondrocalcinosis can be very difficult, as signs and symptoms are not specific and can mimic simple osteoarthritis and also rheumatoid arthritis. Most cases involve the pelvis and the extremities, but spine involvement is well recognized [710]. In most cases, chondrocalcinosis of the spine will be asymptomatic, with observation of silent radiographic disc degeneration. Rarely, acute and chronic chondrocalcinosis may be symptomatic and produce destructive lesions of the vertebral bodies very similar to those observed with infections or ankylosing spondylitis. Erosions may then proceed to secondary instability and pseudospondylolisthesis. Such spondylitis complicates CPPD disease in about 57.5% of cases [8, 11]. Myelopathy, with medullar compression secondary to nodular deposition of CPPD crystals in the ligamentum flavum, has also been reported [12]. Finally, involvement of the nucleus pulposus with calcification has been demonstrated at autopsy as well as at surgery. It can produce an intraspinal mass with acute radiculopathy, as seen in our case [7].
Radiographically, asymptomatic calcification of the intervertebral disc is observed in up to 30% of patients with systemic chondrocalcinosis, frequently at the L2L3 level [10]. MRI studies of CPPD involvement of the spine have not been performed to our knowledge, but there should be a low signal intensity on all sequences, a finding consistent with calcification, as opposed to infectious spondylodiscitis, which has a low signal on T1-weighted images but a hypersignal on T2-weighted images [13]. Definitive diagnosis is usually made by demonstration of the crystals, but they can be absent in destructive or erosive lesions [14]. Rest and NSAIDs are the mainstay of treatment, but decompression surgery has been necessary in selected cases with neurological deficit [15].
Thus, while crystal-related diseases are known to be a cause of erosive discitis, and had actually been recognized 2 yr previously in our patient, the association of myositis and fasciitis of both psoas muscles with erosive discitis was regarded as pathognomonic of an infectious process. All cultures, even from surgical biopsies, and serologies were negative, arguing against such an infectious process. Biopsies demonstrated an inflammatory infiltrate with giant cells but without granulomas. No calcium pyrophosphate crystals were demonstrated, but this description is compatible with previous observations in peripheral destructive CPPD arthropathy [14]. The aseptic causation is further supported by the favourable evolution without antibiotic treatment.
To our knowledge, this is the first observation of pseudo-psoas abscesses associated with erosive discitis in a case of CPPD disease. Now that imaging techniques such as CT and MRI are becoming increasingly prevalent, we believe it to be important to recognize that CPPD spine disease can be accompanied by a severe inflammatory reaction of the psoas muscles which can mimic abscess images. This should avoid unnecessary, costly and aggressive investigations to exclude an infectious process.
We would like to thank Dr Guillou, Department of Pathology, for the histological photography and Dr Landry, Department of Radiology, for the MRI examination.
Notes
Correspondence to: J. Dudler, Service de Rhumatologie, CHUV 1011 Lausanne, Switzerland.
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