A ‘pilot’ study on air‐travel and venous thromboembolism

treatment, the creatinine clearance improved (43Æ4 ml/min) and the lepirudin dose was increased to 0Æ009 mg/kg/h. Antifactor IIa levels observed during this period ranged from 0Æ2 to 0Æ65 lg/ml, with a median value of 0Æ4 lg/ml. Throughout the lepirudin treatment, two to six dose adjustments per day were necessary to maintain anti-factor IIa values around 0Æ5lg/ml. An oral anticoagulant (acenocoumarol) was introduced after 12 d of lepirudin therapy. The treatment overlap was monitored on the basis of anti-factor IIa, INR and factor X values. Lepirudin was stopped on the fifth day of coumadin treatment. No thrombotic or haemorrhagic complication occurred. Danaparoid has been shown to be a safe and effective antithrombotic drug in critically ill patients presenting HIT (Magnani, 1997), even in those at risk of haemorrhage (TardyPoncet et al, 1999). We preferred to use lepirudin in this context because of its shorter plasma elimination half-life, even though this is prolonged in the context of renal dysfunction like that of danaparoid. Furthermore, moderate to severe renal impairment has been found to be an important risk factor for major bleeding (odds ratio: 13Æ2, IC 95%: 3Æ53–49Æ10) (Tardy et al, 2006). To limit the haemorrhagic risk in this patient, we greatly reduced the lepirudin doses and no haemorrhagic complication or extension of the thrombosis was observed. With close monitoring of these low doses of lepirudin, this treatment of HIT was safe and effective. However, it would be easier to manage such a patient with an antithrombotic drug eliminated via the liver, such as argatroban, which has been widely used to treat HIT (Lewis et al, 2001) but is not yet available in France.