Helling H, Stephan B, Pindur G
University Hospital of North Norway, Tromsoe, Norway.
Saarland University Hospital, Homburg, Germany.
Clin Hemorheol Microcirc. 2015;61(2):185-93. doi: 10.3233/CH-151993.
Activation of coagulation and inflammatory response including the complement system play a major role in the pathogenesis of critical illness. However, only limited data are available addressing the relationship of both pathways and its assessment of a predictive value for the clinical outcome in intense care medicine. Therefore, parameters of the coagulation and complement system were studied in patients with septicaemia and multiple trauma regarded as being exemplary for critical illness. 34 patients (mean age: 51.38 years (±16.57), 15 females, 19 males) were investigated at day 1 of admittance to the intensive care unit (ICU). Leukocytes, complement factors C3a and C5a were significantly (p < 0.0500) higher in sepsis than in trauma, whereas platelet count and plasma fibrinogen were significantly lower in multiple trauma. Activation markers of coagulation were elevated in both groups, however, thrombin-antithrombin-complex was significantly higher in multiple trauma. DIC scores of 5 were not exceeded in any of the two groups. Analysing the influences on mortality (11/34; 32.35% ), which was not different in both groups, non-survivors were significantly older, had significantly higher multiple organ failure (MOF) scores, lactate, abnormal prothrombin times and lower C1-inhibitor activities, even more pronounced in early deaths, than survivors. In septic non-survivors protein C was significantly lower than in trauma. We conclude from these data that activation of the complement system as part of the inflammatory response is a significant mechanism in septicaemia, whereas loss and consumption of blood components including parts of the coagulation and complement system is more characteristic for multiple trauma. Protein C in case of severe reduction might be of special concern for surviving in sepsis. Activation of haemostasis was occurring in both diseases, however, overt DIC was not confirmed in this study to be a leading mechanism in critically ill patients. MOF score, lactate, C1-inhibitor and prothrombin time have been the only statistically significant predictors for lethal outcome suggesting that organ function, microcirculation, haemostasis and inflammatory response are essential elements of the pathomechanism and clinical course of diseases among critically ill patients.
凝血激活以及包括补体系统在内的炎症反应在危重病发病机制中起主要作用。然而,关于这两条途径之间的关系及其对重症医学临床结局预测价值的评估,现有数据有限。因此,我们以败血症和多发伤患者作为危重病的典型病例,研究了凝血和补体系统的参数。34例患者(平均年龄:51.38岁(±16.57),女性15例,男性19例)在入住重症监护病房(ICU)的第1天接受了调查。败血症患者的白细胞、补体因子C3a和C5a显著高于多发伤患者(p<0.0500),而多发伤患者的血小板计数和血浆纤维蛋白原显著低于败血症患者。两组的凝血激活标志物均升高,但多发伤患者的凝血酶 - 抗凝血酶复合物显著更高。两组患者的弥散性血管内凝血(DIC)评分均未超过5分。分析对死亡率(11/34;32.35%)的影响,两组死亡率无差异,与幸存者相比,非幸存者年龄显著更大,多器官功能衰竭(MOF)评分、乳酸水平、凝血酶原时间异常且C1抑制物活性更低,在早期死亡患者中更为明显。败血症非幸存者的蛋白C显著低于多发伤患者。从这些数据我们得出结论,作为炎症反应一部分的补体系统激活是败血症的重要机制,而包括凝血和补体系统部分成分在内的血液成分的丢失和消耗在多发伤中更为典型。严重降低时的蛋白C可能是败血症患者存活的特别关注点。两种疾病均发生了止血激活,然而,本研究未证实明显的DIC是危重病患者的主要机制。MOF评分、乳酸水平、C1抑制物和凝血酶原时间是仅有的对致命结局有统计学意义的预测指标,表明器官功能、微循环、止血和炎症反应是危重病患者发病机制和临床病程的基本要素。