DOI: 10.1097/RHU.0b013e318181b47d
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PMID: 18766131
Issn Print: 1076-1608
Publication Date: 2008/08/01
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Excerpt
The medical history was unremarkable except for vitamin B12 deficiency-induced anemia, treated with weekly intramuscular hydroxycobalamin injections and rib contusions 2 years before.
At the first visit, the knee pain had resolved completely, but right shoulder pain had evolved. Physical examination showed painful and impaired abduction and elevation consistent with capsular impairment. X-rays of the right shoulder revealed cranial subluxation of the humerus, touching the undersurface of the acromion. The humeral head was deformed. Subchondral sclerosis and soft tissue calcifications were noted (Fig. 1A). The x-ray of the left shoulder was characterized by cranial position of the humerus in combination with subacromial bony spurs (Fig. 1B). The right knee showed destruction of the lateral tibial plateau, effusion, and valgus deformation (Fig. 1C). The diagnosis Milwaukee shoulder/knee syndrome was made and the patient was offered regular intraarticular injections in combination with analgesic and antiinflammatory medication.
Two months later a huge effusion of the left shoulder had developed with a hematoma emerging below the deltoid muscle. She was unable to move the left arm. Gross neurologic examination was normal including temperature and pain sensation, thus, precluding neuropathic Charcot arthropathy as can be seen in case of a cervical syrinx.1 Repeated x-ray of the left shoulder showed complete destruction of the humeral head and soft tissue swelling with calcifications due to bony debris or crystal depositions (Fig. 1D). Laboratory investigation revealed the following: erythrocyte sedimentation rate 42 mm/h, normal serum calcium, phosphate, albumin, and uric acid concentrations. No serum and urine M-proteins were found. IgM rheumatoid factor was 3.0 IU/L, antinuclear antibodies were absent. Microscopic examination of the synovial fluid showed 0.3 × 103 leukocytes/mm3, many red blood cells, and clumps of fibrils with shiny irregular, nonbirefringent chunks suggestive of apatite, staining strongly positive with alizarin red S. Auramine staining and culture of the synovial fluid were negative. MRI scanning revealed total rupture of the cuff. Furthermore, firm attachment of a prosthesis in the humerus could not be guaranteed because of demineralization, and therefore orthopedic intervention was not deemed feasible. She is currently being treated symptomatically with analgesics and repeated steroid injections.
The term Milwaukee shoulder syndrome was proposed by McCarty in 1981.2 Eighty percent of patients are elderly women with an average age of 72.5 years.3 Bilateral shoulder involvement occurs in 60% of cases; the knees are affected in 50%. Precipitating factors include trauma or overuse, concurrent Calcium PyroPhosphate Deposition disease, neuro- (Charcot) arthropathy, dialysis, and hyperparathyroidism.4,5 The disease course was originally described as relatively benign; in some patients the symptoms had been present for over 10 years.4 Recent reports emphasized a more rapid and unfavorable disease course6,7; and involvement of other joints in a similar process.8 Synovial fluid typically contains an abundant number of erythrocytes, a low leukocyte count and in the majority of cases apatite also called basic calcium phosphate (BCP) depositions. Admixture with calcium pyrophosphate crystals can occur.
