Scherer R U, Spangenberg P
Abteilung für Anästhesiologie und Intensivmedizin, Universitätsklinikum Essen, Germany.
Crit Care Med. 1998 Jan;26(1):149-56. doi: 10.1097/00003246-199801000-00031.
To determine the degree of regional and systemic coagulation activation soon after isolated severe head injury.
Prospective, controlled clinical study.
The emergency room and intensive care unit (ICU) of a trauma center in a university hospital serving a population of 5 million people.
Twenty-four trauma victims: 20 patients with isolated severe head injury (head trauma group, Glasgow Coma Score of < or =8) and four patients with isolated bone fracture (control group).
Insertion of central venous, i.e. superior caval vein, jugular bulb, and arterial catheters for blood sampling.
Central venous (i.e., superior caval vein) global coagulation variables (i.e., prothrombin time, activated partial thromboplastin time, fibrinogen concentration, antithrombin III activity, and platelet count) and central venous and jugular bulb activation coagulation and fibrinolysis variables (i.e., prothrombin fragment F1+2, thrombin-antithrombin III complex, soluble fibrin, and D-dimer concentration) were measured soon after trauma (<6 hrs) and 3 hrs later. When compared with the control group patients, upon ICU admission, fibrinogen concentration (p < .005) and platelet count (p < .025) were significantly decreased in the head trauma group. Thrombin-antithrombin III complex (p < .025), prothrombin fragment F1+2 (p < .025), and D-dimer (p < .005) concentrations measured at the time of ICU admission were significantly higher in the head trauma group than in the control group. Only in the head trauma group were soluble fibrin concentrations increased above the normal range; thrombin-antithrombin III complex and the prothrombin fragment F1+2 were found to be significantly higher in cerebrovenous blood than in central venous blood (p < .025). There was no cerebrocentral venous difference in the concentrations of soluble fibrin or D-dimer in either group.
Within 6 hrs after severe isolated head trauma, systemic procoagulant overflow from the traumatized cerebral microvasculature proceeds to the thrombin level and is then inhibited by antithrombin III. Regional and systemic hypercoagulability and increased D-dimer concentrations appear to be common among head trauma patients. Increased procoagulant and consecutive fibrinolytic turnover may, therefore, spark disseminated intravascular coagulation in this patient group.
确定单纯性重度颅脑损伤后不久局部和全身凝血激活的程度。
前瞻性对照临床研究。
一所为500万人口服务的大学医院创伤中心的急诊室和重症监护病房（ICU）。
24名创伤受害者：20例单纯性重度颅脑损伤患者（颅脑创伤组，格拉斯哥昏迷评分≤8分）和4例单纯性骨折患者（对照组）。
插入中心静脉，即上腔静脉、颈静脉球和动脉导管用于采血。
在创伤后不久（<6小时）和3小时后测量中心静脉（即上腔静脉）整体凝血变量（即凝血酶原时间、活化部分凝血活酶时间、纤维蛋白原浓度、抗凝血酶III活性和血小板计数）以及中心静脉和颈静脉球激活凝血和纤溶变量（即凝血酶原片段F1+2、凝血酶-抗凝血酶III复合物、可溶性纤维蛋白和D-二聚体浓度）。与对照组患者相比，在入住ICU时，颅脑创伤组的纤维蛋白原浓度（p<0.005）和血小板计数（p<0.025）显著降低。入住ICU时测量的颅脑创伤组的凝血酶-抗凝血酶III复合物（p<0.025）、凝血酶原片段F1+2（p<0.025）和D-二聚体（p<0.005）浓度显著高于对照组。仅在颅脑创伤组中，可溶性纤维蛋白浓度升高至正常范围以上；发现凝血酶-抗凝血酶III复合物和凝血酶原片段F1+2在脑静脉血中显著高于中心静脉血（p<0.025）。两组中可溶性纤维蛋白或D-二聚体浓度在脑静脉血和中心静脉血之间均无差异。
在单纯性重度颅脑创伤后6小时内，来自受损脑微血管系统的全身性促凝物质溢出至凝血酶水平，随后被抗凝血酶III抑制。局部和全身高凝状态以及D-二聚体浓度升高在颅脑创伤患者中似乎很常见。因此，促凝物质增加和随之而来的纤溶周转增加可能引发该患者群体的弥散性血管内凝血。
