tailieunhanh - Blood and Blood Transfusion - part 5

Thromboembolus tĩnh mạch dự phòng thường xuyên trong các đơn vị chăm sóc đặc biệt là một vấn đề khác có liên quan. Bệnh nhân trong ICU có một số vấn đề có thể ngăn cản heparin dự phòng. Họ có thể chảy máu công khai, họ có thể có thrombopenia hoặc một loạt các sự kiện sau phẫu thuật | CRITICAL CARE FOCUS BLOOD AND BLOOD TRANSFUSION Venous thromboembolus prophylaxis Routine venous thromboembolus prophylaxis in the intensive care unit is another relevant issue. Patients in ICU have several problems that may preclude prophylactic heparin. They may be bleeding overtly they may have thrombopenia or a variety of post surgical events leg ulcer wounds peripheral arterial disease. There is no optimal prophylactic consensus. In a study by Hirsch and co-workers in 1995 19 deep venous thrombosis DVT as detected by ultrasonography with colour Doppler imaging was detected in 33 of 100 medical ICU patients. This unexpectedly high rate of DVT occurred despite prophylaxis in 61 and traditionally recognised risk factors failed to identify patients who developed DVT. Two large studies in 1996 showed that subcutaneous low molecular weight heparin is as effective as unfractionated heparin for prophylaxis of thromboembolism in bedridden hospitalised medical 21 It therefore appears that low molecular weight heparin is the prophylactic of choice for venous thromboembolism. Vascular access thrombosis One area that may cause problems in ICU is vascular access thrombosis in patients with indwelling lines. The possible causes are given in Box . Hypercoagulability related to the underlying pathology is especially relevant. Increased thrombotic tendency with platelet activation and coagulation factor abnormalities that predispose to thrombosis can be mediated through a variety of mechanisms given in Box . Haemofiltration Continuous haemofiltration may be affected by premature closure or thrombosis of the filter and there are various factors that potentially contribute to this increased thrombotic tendency. The situation is compounded by loss of endothelial integrity and neutralisation of haemostatic activation. It is usually caused by aggressive activation of the contact system Factor XIIa increases and most important of all there is increased monocyte .

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