SummaryPlasma levels of D-dimer have been found useful as a marker of deep venous thrombosis in those patients in whom thrombosis is suspected, but their usefulness in postoperative screening is less clear. We have investigated the relationship of D-dimer to deep venous thrombosis in 90 patients after total hip and knee arthroplasty. From the first postoperative day the D-dimer levels were found to be highly significantly raised in patients with deep venous thrombosis. A combined result over the first six postoperative days in excess of 1200ng/ml correlated with thrombosis with a specificity of 100%, sensitivity of 45%, positive predictive value of 60%, and negative predictive value of 100%. However, individual estimations were not discriminatory.

Summary The blood of 107 patients undergoing venography for suspected deep vein thrombosis (DVT) was tested for D‐Dimers using enzyme immunoassay (EIA) and two latex agglutination techniques. D‐Dimer levels by EIA were raised in 88% of patients with proven DVT. However, levels detected with the two agglutination tests were much less sensitive, being raised in only 43% patients with DVT. A more sensitive rapid screening test is needed to provide a useful non‐invasive test for the exclusion of DVT.

Difference irn air arnd bone con(duction threshold (dB) Sensitivity and specificity of256 Hz (0) and 512 Hz (0) tuning forks in detecting differences in air and bone conduction of various magnitudes mask the other ear. The figure compares the sensitivity and specificity of a 256 Hz fork with those of a 512 Hz fork in detecting differences in air and bone conduction (air-bone gaps) Chronic urticaria with angio-oedema controlled by warfarin J Berth-Jones, P E Hutchinson, A C B Wicks,We report a case of severe recurrent angio-oedema that responded to warfarin. This was a chance observation and may have implications for the pathogenesis and treatment of chronic urticaria. Case reportThe patient, a 42 year old man, presented in March 1977 with weekly episodes of severe angio-oedema, which were unresponsive to chlorpheniramine and trimeprazine prescribed by his general practitioner. He also had essential hypertension, familial combined hyperlipidaemia, and ischaemic heart disease, having suffered his first myocardial infarction in 1975.Treatment with H1 receptor blocking antihistamines was continued for 18 months, during which time he suffered episodes of urticaria and angio-oedema virtually daily, at times with severe facial swelling necessitating admission to hospital. He was subsequently treated with the H2 antagonist cimetidine combined with HI antagonists, subcutaneous adrenaline, danazol, and systemic steroids. Only the steroids had any effect, and the urticaria eventually became stable when he took prednisolone 12 5 mg on alternate days. Numerous attempts to reduce this dose failed.In February 1981 he had a further myocardial infarction, which was complicated by multiple pulmonary emboli. He was treated with intravenous heparin, prednisolone 40 mg to control his angiooedema, and subsequently oral warfarin. He remained completely free from urticaria throughout this admission and was discharged taking warfarin, prednisolone 12-5 mg on alternate days, cimetidine, and brompheniramine. The dose of steroid was gradually reduced to 2 mg on alternate days, and the antihistamines were withdrawn with no deterioration. In May that year warfarin was stopped and his angio-oedema returned. The warfarin was restarted and his angio-oedema again came under control. He subsequently reported that he had repeated this procedure with the same result. He continued to take warfarin alone for his urticaria until July 1983, when he was admitted to hospital for further investigation and, without being informed or his consent being obtained, was given placebo warfarin tablets. One week later he developed severe generalised angiooedema. Warfarin was restarted, and he subsequently had only occasional mild episodes of urticaria without angio-oedema. These episodes affected small areas of the arms, legs, and trunk; were transient, lasting less than two hours; and were usually associated with a fall in the international normalised ratio to below 2-5 (full anticoagulation (international normalised ratio > 2 5) was required for optimal ben...

A 58 year old man presented with a three year history of impotence, night sweats and ankle swelling. On examination, the patient filfilled the diagnostic criteria for POEMS syndrome, but was unusual in that he also had underlying Waldenstrom's macroglobulinaemia with IgM K paraproteinaemia. The patient was treated with intermittent chlorambucil and made a good recovery. POEMS syndrome has been described in association with osteosclerotic myeloma and Castleman's disease. The paraprotein involved is usually IgG or IgA with k light chains. This case indicates that the presence ofk light chains is not essential for the pathogenesis of POEMS syndrome. It also emphasises the diversity ofplasma celi dyscrasias that can manifest as POEMS syndrome.