Hess John R, Lawson Jeffrey H
Department of Pathology, University of Maryland Medical Center, Baltimore, 21201, USA.
J Trauma. 2006 Jun;60(6 Suppl):S12-9. doi: 10.1097/01.ta.0000199545.06536.22.
The coagulopathy of trauma is a syndrome of non-surgical bleeding from mucosal lesions, serosal surfaces, and wound and vascular access sites associated with serious injury, hypothermia, acidosis, hemodilution, and occasionally with classic disseminated intravascular coagulation (DIC). It can be largely explained by the effects of cold on platelet function, the effect of pH on coagulation factor activity, and the dilutional effects of resuscitation fluids and conventional blood products. DIC occurs acutely after trauma when brain, fat, amniotic fluid, or other strong thromboplastins enter the circulation. It occurs subacutely when endothelial inflammation or failure reduces clearing of activated coagulation factors allowing microthrombi to cause secondary injury. The coagulopathy of trauma should be anticipated in massive transfusion situations. Early treatment with plasma can delay its onset. The underlying mechanisms should be confirmed with laboratory testing.
创伤性凝血病是一种非手术性出血综合征,表现为黏膜损伤、浆膜表面、伤口及血管穿刺部位出血,与严重损伤、体温过低、酸中毒、血液稀释有关,偶尔还与经典的弥散性血管内凝血(DIC)相关。这在很大程度上可由低温对血小板功能的影响、pH值对凝血因子活性的影响以及复苏液体和传统血液制品的稀释作用来解释。当脑、脂肪、羊水或其他强促凝物质进入循环时,创伤后会急性发生DIC。当内皮炎症或功能障碍导致活化凝血因子清除减少,使微血栓造成继发性损伤时,则会亚急性发生DIC。在大量输血情况下应预见到创伤性凝血病。早期输注血浆可延缓其发生。其潜在机制应通过实验室检查来证实。