[Disseminated intravascular coagulations].

Cahiers d'anesthesiologie Pub Date : 1996-01-01
P Amstutz, J S Moyo
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Abstract

Disseminated intravascular coagulation (DIC) syndromes can be defined as the formation of fibrin deposits within the microcirculation, occurring in definite clinical situations. Their biological counterpart is a consumption coagulopathy. The clinical profiles of DIC have been well known for decades, are multiform and range from latency to overwhelming haemorrhagic diatheses, including also characteristic but rare situations, such as purpura fulminans, acral cyanosis and pictures resembling thrombotic thrombocytopenic purpura or haemolytic-uraemic syndrome. Biological tests of DIC show a consumption coagulopathy, displayed on the standard haemostasis sheet; along with signs of paracoagulation and/or of secondary fibrinolysis (FDP). New tests have recently been introduced: D-dimers are specific and sensible; Antithrombin-III, protein C and alpha 2-antiplasmin also can sometimes be useful. The knowledge of the pathophysiology of DIC has made advances with passing years. Fibrin deposits may be non-occlusive, and indeed they are swiftly removed by a secondary fibrinolysis. Except in very rare situations, such as those leading to a cortical renal necrosis, and perhaps in some ARDS, there is little evidence relating DIC to organ failure syndromes. Moreover, there is no clear relationship between the severity of the consumption coagulopathy and the prognosis. For instance, the mortality is much lower in abruptio placentae, where the coagulopathy is very severe, than in septic shock, where it is usually moderate. In septic shock, the disorders of haemostasis were related initially to a platelet activation, then to an activation of the contact system (releasing kinins and triggering complement cascade), and nowadays to the activation of the extrinsic coagulation system. The treatment of DIC is mainly the treatment of its cause. Indications for heparin therapy should be strictly limited to a few exceptional circumstances. When haemorrhagic diathesis threatens, FPC and/or platelet transfusion may be indicated. Aprotinin can be useful in rare cases of overwhelming secondary fibrinolysis. Trials with antithrombin-III or C1-esterase inhibitors are in progress.

弥散性血管内凝血。
弥散性血管内凝血(DIC)综合征可以定义为纤维蛋白沉积在微循环内的形成,在特定的临床情况下发生。它们的生物对应物是消费性凝血病。DIC的临床表现几十年来众所周知,是多种形式的,从潜伏期到压倒性的出血性疾病,也包括特征性但罕见的情况,如暴发性紫癜、肢端紫绀和类似血栓性血小板减少性紫癜或溶血性尿毒综合征的症状。DIC的生物学试验显示消耗性凝血功能障碍,显示在标准止血片上;伴有凝准和/或继发性纤维蛋白溶解(FDP)的迹象。最近引入了新的检测方法:d -二聚体具有特异性和敏感性;抗凝血素- iii、蛋白C和α 2-抗纤溶蛋白有时也很有用。随着时间的推移,DIC的病理生理学知识已经取得了进展。纤维蛋白沉积可能是不闭塞的,确实它们被继发性纤维蛋白溶解迅速清除。除了非常罕见的情况,如导致肾皮质坏死的情况,可能在一些ARDS中,几乎没有证据表明DIC与器官衰竭综合征有关。此外,消耗性凝血病的严重程度与预后之间没有明确的关系。例如,胎盘早剥的死亡率要低得多,其中凝血功能非常严重,而感染性休克通常是中度的。在感染性休克中,止血障碍最初与血小板激活有关,然后与接触系统的激活有关(释放激肽并触发补体级联),现在与外源性凝血系统的激活有关。DIC的治疗主要是对其病因的治疗。肝素治疗的适应症应严格限制在少数特殊情况下。当有出血性威胁时,可能需要FPC和/或血小板输注。抑酶蛋白可用于罕见的压倒性继发性纤维蛋白溶解病例。抗凝血酶- iii或c1 -酯酶抑制剂的试验正在进行中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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