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肝素诱导的血小板减少症。

Heparin-induced thrombocytopenia.

作者信息

Krzych Łukasz J, Nowacka Elżbieta, Knapik Piotr

机构信息

Department of Cardiac Anaesthesia and Intensive Therapy, Medical University of Silesia, Silesian Centre for Heart Diseases, Zabrze, Poland.

出版信息

Anaesthesiol Intensive Ther. 2015;47(1):63-76. doi: 10.5603/AIT.2015.0006.

Abstract

Heparin-induced thrombocytopenia (HIT) is a clinical immune-mediated syndrome; symptoms of HIT result from the development of arterial and venous thrombosis and are correlated with the severity of the thrombocytopenia. In all patients receiving heparin preparations in intensive care units, platelet counts should be monitored every 2-3 days throughout therapy, particularly during days 4-14 when HIT is most likely to develop. The major screening tests should always involve a clinical assessment of HIT probability (4Ts or HEP scoring systems) and enzymatic immunoassays (IgG antibodies) for patients with a moderate to high risk of HIT. The full possibilities of such advanced diagnostic procedures are limited in Poland because functional tests are still not widely available. If the diagnosis is questionable, all heparin preparations should be withdrawn and an alternative method of anticoagulation instituted until HIT has been conclusively excluded. The use of new-generation anticoagulants (direct thrombin or Xa factor inhibitors) is currently considered the treatment of choice. Old-generation anticoagulants should not be administered (vitamin K antagonists) as they can aggravate thrombosis. If administered, their action should be reversed by vitamin K once HIT is confirmed. Antithrombotic therapy with "new" anticoagulants should be carried out at least until platelet counts return to the baseline values; the recommended duration of therapy is 4 weeks in patients with isolated thrombocytopenia or 4 months in those with thrombotic complications. Vitamin K antagonists should not be applied until the normal platelet count is restored (usually > 150 G L⁻¹). When the therapy with vitamin K antagonists is reintroduced, "old" antagonists should be administered simultaneously with a "new" anticoagulant for at least 5 days due to an initial decrease in protein C concentration concentration, provided that the therapeutic value of INR is maintained (> 2) for at least 2 days.

摘要

肝素诱导的血小板减少症(HIT)是一种临床免疫介导综合征;HIT的症状源于动静脉血栓形成,且与血小板减少症的严重程度相关。在重症监护病房接受肝素制剂治疗的所有患者中,整个治疗过程应每2 - 3天监测一次血小板计数,尤其是在第4 - 14天,此时最易发生HIT。主要的筛查检测应始终包括对HIT可能性的临床评估(4Ts或HEP评分系统)以及针对HIT中度至高度风险患者的酶免疫测定(IgG抗体)。由于功能检测在波兰仍未广泛应用,此类先进诊断程序的全部可能性受到限制。如果诊断存疑,应停用所有肝素制剂,并采用替代抗凝方法,直至最终排除HIT。目前认为新一代抗凝剂(直接凝血酶或Xa因子抑制剂)是首选治疗方法。不应使用旧一代抗凝剂(维生素K拮抗剂),因为它们会加重血栓形成。一旦确诊HIT,若已使用旧一代抗凝剂,应通过维生素K逆转其作用。使用“新型”抗凝剂进行抗血栓治疗应至少持续至血小板计数恢复到基线值;对于单纯血小板减少症患者,推荐的治疗持续时间为4周,对于有血栓并发症的患者为4个月。在血小板计数恢复正常(通常>150 G L⁻¹)之前,不应应用维生素K拮抗剂。当重新引入维生素K拮抗剂治疗时,由于蛋白C浓度最初会降低,“旧”拮抗剂应与“新型”抗凝剂同时使用至少5天,前提是国际标准化比值(INR)的治疗值至少维持在>2水平至少2天。

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