Jeffrey R. Wohlgethan

Long-term follow-up of corticosteroid injection for traumatic olecranon bursitis.

Forty-seven patients with traumatic olecranon bursitis were evaluated after a mean follow-up of 31 months (range 6 to 62 months). Twenty-two patients treated with bursal aspiration had delayed recovery and no complications of therapy. Twenty-five patients treated with intrabursal injection of 20 mg of triamcinolone hexacetonide had rapid recovery, usually within one week, but suffered complications such as infection (3 cases), skin atrophy (5 cases), and chronic local pain (7 cases). Since spontaneous resolution can be expected, a conservative approach is suggested in the treatment of traumatic olecranon bursitis.

The clinical and biochemical spectrum of hereditary amyloidosis

Familial amyloidosis, once described as a puzzling and highly unusual form of polyneuropathy, is now recognized to be a collection of familial diseases with usually autosomal-dominant inheritance and widespread ethnic distribution. Familial amyloidosis occurs throughout the world and encompasses an extremely broad spectrum of clinical manifestations. In some families, progressive peripheral neuropathy dominates the illness, while in others, renal failure, ocular amyloid deposits, cardiac decompensation, or intracranial hemorrhage is the most significant clinical feature. The Portuguese (type I) and the Iowa (type III) neuropathies characteristically begin with lower limb involvement, while in the Indiana (type II) form, upper limb neuropathy is seen first; in the Japanese families with familial amyloid polyneuropathy, symptoms first become evident around age 40, whereas in the Texas family, onset is in the seventh decade. The prognosis for the different families is highly variable. Current classification of the familial amyloid polyneuropathy syndromes is based on their characteristic clinical presentations, but ongoing biochemical identification of the protein composition of amyloid substance in each form will make a more rational nosology feasible in the near future. To date, no therapy has been shown to arrest or reverse the progressive accumulation of amyloid deposits in most forms of familial amyloidosis. Familial Mediterranean fever is a major exception, and the incidence of amyloidosis associated with this disease has been dramatically reduced by the widespread prophylactic use of colchicine. Technology currently available permits the reliable identification of asymptomatic relatives at risk for developing amyloid neuropathy as well as the prenatal identification of carriers of the mutant transthyretin gene. These strategies can be used in genetic counseling aimed at reducing the continued propagation of the mutant gene.

Foucher's sign of the Baker's cyst.

We investigated the mechanism of Fouchers sign, the change in pressure in the Bakers cyst with extension and flexion of the knee, by echography, arthrography, and computed tomography. With extension the gastrocnemius and the semimembranosus muscles approximate each other and the joint capsule compressing the cyst against the deep fascia. Opposite effects in flexion allow the cyst to relax.

Recurrent Cerebral Infarction and Antibodies to Cardiolipin: A Case Report

Recurrent Cerebral Infarction and Antibodies to Cardiolipin: A Case Report To the Editor: The association between elevated anticardiolipin antibody (ACA) titers and stroke has only rarely been reported. We studied a patient with ACAs in whom recurrent cerebral ischemic events were the sole thrombotic manifestations of this hypercoagulable state during 23 years of follow-up. In May 1963, this previously healthy 39-year-old man presented with fever, malaise, weight loss, arthralgias, and Raynauds phenomenon of 4 months duration. Blood pressure was 160/120 mm Hg. General and neurologic examinations were normal. Prothrombin time (PT) was 17.1 seconds with a control of 13.6 seconds. Erythrocyte sedimentation rate (ESR) was 25 mm; serum latex fixation test was positive. He was treated with aspirin. In August 1963, he had a generalized seizure followed by stupor, motor aphasia, and right hemiparesis predominating in his arm and face. Cardiovascular examination and routine laboratory tests were unremarkable. Bilateral carotid angiography showed mass effect in the left parietal area without arterial stenosis or evidence of vasculitis. The diagnosis of embolic stroke was made. He was discharged on diphenylhydantoin, phenobarbital, and hydrochlorthiazide but had to be readmitted 2 months later with transient binocular visual disturbance. A falsepositive VDRL and normal blood pressure were documented in 1966, and, at a routine follow-up visit in 1979, the partial thromboplastin time (PTT) was 42.3 seconds with a control of 31.0 seconds, but PT was normal. He presented in January 1985 with headache, lethargy, and a transient visual disturbance. He was slightly euphoric and unconcerned about his condition. New facial and arm weakness with sensory and visual neglect were noted on the left side in addition to the old mild aphasia and right hemiparesis. Blood pressure, PT, PTT, and echocardiogram were normal. Brain computed tomography (CT scan) was consistent with new right temporo-parietal and old left frontal and parietal infarcts. Cerebral angiogram showed moderate stenosis of the petrous segment of the right internal carotid artery, with nonfilling of the ipsilateral middle cerebral arterys inferior division branches. Warfarin was started. Follow-up ACA, ANA, anti-RNP, and anti-Sra antibodies were all positive. A diagnosis of systemic lupus erythematosus was made. Reevaluation in December 1986 confirmed the elevated ACA titers (Table 1). He was maintained on warfarin.

Aspiration of the retrocalcaneal bursa.

We aspirated the retrocalcaneal bursa in cadavers to determine the characteristics of bursal fluid. A small amount of clear, viscous fluid was constantly present in the bursa. Leucocyte count was low, and the mucin clot test was good. With the same technique we aspirated the retrocalcaneal bursae of 4 patients. Three had Reiters syndrome; the bursal fluid was inflammatory, and symptoms promptly resolved after local corticosteroid injection. The fourth patient presented with heel pain; intracellular, positively birefringent crystals were present in the aspirate, consistent with the diagnosis of pseudogout.

Acute non-infectious arthritis of the hip in rheumatoid arthritis: synovial membrane findings.

A case of acute hip pain in rheumatoid arthritis is presented, with synovial membrane findings. A patient with classical rheumatoid arthritis suffered three unusual bouts of sudden, severe but transient hip pain. The hips were clinically normal between these episodes. The clinical picture on two of these occasions strongly suggested septic arthritis. Although the synovial fluid was highly inflammatory, cultures were negative. The synovial membrane showed mild lining cell hyperplasia, vascular congestion, and scattered inflammatory cells, predominantly lymphocytes. These findings were not compatible with either pyogenic infection or longstanding rheumatoid arthritis. The clinical and pathological features of acute non-infectious arthritis of the hip appear to delineate a distinct syndrome.