Dempfle Carl-Erik
Department of Medicine, University Hospital of Mannheim, Mannheim, Germany.
Curr Opin Anaesthesiol. 2004 Apr;17(2):125-9. doi: 10.1097/00001503-200404000-00006.
An update on recent developments in diagnosis and treatment of disseminated intravascular coagulation.
Disseminated intravascular coagulation is defined as a typical disease condition with laboratory findings indicating massive coagulation activation and reduction in procoagulant capacity. Clinical syndromes associated with the condition are consumption coagulopathy, sepsis-induced purpura fulminans, and viral hemorrhagic fevers. Consumption coagulopathy is observed in patients with sepsis, aortic aneurysms, acute promyelocytic leukemia, and other disseminated malignancies. Sepsis-induced purpura fulminans is characterized by microvascular occlusion causing hemorrhagic necrosis of the skin and organ failure. Viral hemorrhagic fevers result in massively increased tissue factor production in monocytes and macrophages, inducing microvascular thrombosis and consumption of platelets and coagulation factors. Current scoring systems do not distinguish between patients with asymptomatic disseminated intravascular coagulation, consumption coagulopathy and thrombotic syndromes. Patients with sepsis may be identified by activated partial thromboplastin time waveform analysis performed as part of routine coagulation testing. Drotrecogin alpha (activated) reduces mortality in patients with severe sepsis with and without disseminated intravascular coagulation and has been used in patients with sepsis-induced purpura fulminans. Tifacogin does not reduce mortality in severe sepsis associated with impaired coagulation. Patients with heterozygous factor V Leiden mutation and severe sepsis showed a lower 28-day mortality than patients without this mutation, supporting the assumption that an enhanced level of coagulation activation may be beneficial in patients with severe sepsis.
Whereas antithrombin and tifacogin failed to improve clinical outcome in severe sepsis, drotrecogin alpha (activated) increased the chances of survival of patients with severe sepsis with and without disseminated intravascular coagulation.
对弥散性血管内凝血诊断和治疗的近期进展进行更新。
弥散性血管内凝血被定义为一种典型的疾病状态,实验室检查结果表明存在大量凝血激活及促凝能力降低。与该病症相关的临床综合征包括消耗性凝血病、脓毒症诱发的暴发性紫癜和病毒性出血热。消耗性凝血病见于脓毒症、主动脉瘤、急性早幼粒细胞白血病及其他播散性恶性肿瘤患者。脓毒症诱发的暴发性紫癜的特征是微血管闭塞导致皮肤出血性坏死和器官衰竭。病毒性出血热导致单核细胞和巨噬细胞中组织因子产生大量增加,引发微血管血栓形成以及血小板和凝血因子的消耗。目前的评分系统无法区分无症状弥散性血管内凝血、消耗性凝血病和血栓形成综合征患者。脓毒症患者可通过作为常规凝血检测一部分进行的活化部分凝血活酶时间波形分析来识别。重组人活化蛋白C降低伴有或不伴有弥散性血管内凝血的严重脓毒症患者的死亡率,已用于脓毒症诱发的暴发性紫癜患者。替法可济不能降低伴有凝血功能障碍的严重脓毒症患者的死亡率。杂合子因子V莱顿突变的严重脓毒症患者28天死亡率低于无此突变的患者,支持这样的假设,即凝血激活水平增强可能对严重脓毒症患者有益。
抗凝血酶和替法可济未能改善严重脓毒症的临床结局,而重组人活化蛋白C增加了伴有或不伴有弥散性血管内凝血的严重脓毒症患者的存活机会。