Five cases of accidental intra‐arterial injection of sodium tetradecyl sulphate during the treatment of varicose veins are presented and compared with 3 previously reported cases. Severe ischaemic damage with gangrene may occur. Immediate treatment with heparin and low molecular weight dextran may be of value in the management of this situation.

SummaryEighty-two consecutive women with varicose ulcers werc treated by compression sclerotherapy; 73 (8900) of them were reviewed 46 to 69 months after treatment. The cure rate at follow-up for the whole group was 8200. In obese patients the cure rate was 76",,, while in non-obese patients it was 89",,. These results compare favourably with those of surgery.

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CorrespondenceTuberculosis complicated by ARDS Dear Editor, The incidence of tuberculosis (TB) is increasing. Due to the increase in immigration and the spread of high risk groups such as HIV-infected patients and atypical forms, uncommon complications are more frequent A 49-year-old woman was referred from another host pital with fever and pancytopenia (white cell count [WCC] 2,800; platelet count 80,000; erythrocyte sedimentation rate [ESR] 25) and on amoxycillin. On examination, her temperature was 38.5'C, pulse 80 bpm, blood pressure 100/40mmHg and respiratory rate 46. She was pallor and jaundiced but had no lymphadenopathy. Coarse crepitations were heard over the right lung base. A bone marrow aspirate revealed hypocellularity with dysplasic traits in leukocytes, platelets and red cells. Radiographs of the chest revealed alveolar opacities in the right upper lobe. Oxygen saturation was 84.3% on ambient air. Abdominal ultrasound showed a 15cm splenomegaly. Specimens of urine and blood were obtained for culture, antigen and antibody tests for agents such as cytomegalovirus (Ig1VI) and hepatitis A and B virus. Serologic testing for HIV was refused. A tuberculin skin test was negative. Serum test for antinuclear antibodies, antineutrophilic cytoplasmic antibodies, antibodies against glomerular basement membrane and rheumatoid factor were negative. C3-C4 levels were normal. Ceftazidime, amikacin and erythromycin were commenced. On the fourth hospital day, the temperature rose to 40°C. CT scan of the thorax (see Figure 1 ) revealed pneumonia in right lung field, patchy opacities in left lung field and a rightsided pleural effusion. Respiratory failure with refractory hypotension developed. Haemodynamic measurements via pulmonary catheter were consistent with RDS. The pulmonary artery wedge pressure was 8mmHg and the systemic vascular resistance was 30dynes/cm.seg. Mechanical ventilation and intravenous isoniazid and rifampin were started but failed.Autopsy revealed granulomas with central necrosis and caseation involving the lungs. Several tissues, such as heart, liver and kidney showed acid fast bacilli that were consistent with Mycobacterium tuberculosis and disseminated tuberculosis. The cultures from lungs, liver and kidneys were positives to M. tuberculosis with no resistance to antituberculosis drugs.Tuberculosis, as a primary cause of respiratory failure requiring mechanical ventilation, is relatively uncommon. Respiratory decompensation often coincides with the development of adult respiratory disease syndrome (ARDS), which can be difficult to differentiate from a confluent pulmonary tuberculosis infection with septic shock. The pathogenesis of ARDS resulting from M. Tuberculosis infection and Gram-negative sepsis is alike. Lipopolysaccharide (LPS) is thought to play a key role in the triggering of acute lung injury in sepsis and lipoarabinomannan (a tuberculosis cell wall component), acts similarly to LPS in that it activates macrophages to release cytok.ines.' Alveolar macrophages secrete cytokines such ...

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