Section for Transfusion Medicine, Capital Region Blood Bank, Copenhagen, Denmark.
Crit Care Med. 2012 Jun;40(6):1844-50. doi: 10.1097/CCM.0b013e31823e9d15.
High patient age is a strong predictor of poor outcome in trauma patients. The present study investigated the effect of age on mortality and biomarkers of sympathoadrenal activation, tissue, endothelial, and glycocalyx damage, coagulation activation/inhibition, fibrinolysis, and inflammation in trauma patients at admission.
Prospective observational study.
Single level I trauma center.
Eighty adult trauma patients (≥18 yrs) who met criteria for full trauma team activation and had an arterial cannula.
Blood sampling a median of 68 min (interquartile range 48-88) post injury.
Data on demography, biochemistry, Injury Severity Score, and 30-day mortality were recorded and plasma/serum was analyzed for biomarkers reflecting sympathoadrenal activation (adrenaline, noradrenaline), tissue/endothelial cell/glycocalyx damage (histone-complexed DNA fragments, annexin V, thrombomodulin, syndecan-1), platelet activation (soluble CD40 ligand), coagulation activation/inhibition (prothrombin fragment 1.2, thrombin/antithrombin complex, antithrombin, protein C, activated protein C, protein S, soluble endothelial protein C receptor, tissue factor pathway inhibitor, von Willebrand factor, fibrinogen, factor XIII), fibrinolysis (D-dimer, tissue-type plasminogen activator, plasminogen activator inhibitor-1), and inflammation (interleukin-6, terminal complement complex). Patients were stratified according to the median age (46 yrs) of the full cohort.
Older trauma patients had markedly higher noradrenaline (p < .001) but an attenuated increase in adrenaline with increasing Injury Severity Score and lower platelets and leukocytes (both p < .05) compared to the younger patients. Older patients displayed a biomarker profile suggestive of enhanced release, activation, and consumption of the natural anticoagulants (low antithrombin, high activated protein C, protein S, and tissue factor pathway inhibitor) and hyperfibrinolysis (high tissue-type plasminogen activator) (all p < .05 vs. younger patients). Age was an independent predictor of mortality (hazard ratio 1.04 [95% confidence interval 1.01-1.07], p = .005) after adjusting for Injury Severity Score, prehospital Glasgow Coma Scale, and plasma catecholamines.
In trauma patients, the association between age and mortality was confirmed. Older patients had high plasma noradrenaline but attenuated adrenaline release with higher Injury Severity Score, impaired platelet and leukocyte mobilization, enhanced consumption of anticoagulants, and hyperfibrinolysis, which may all contribute to the poor outcome in these patients.
高龄是创伤患者预后不良的一个强有力的预测因素。本研究旨在探讨年龄对创伤患者入院时的死亡率以及去甲肾上腺素能激活、组织、内皮和糖萼损伤、凝血激活/抑制、纤维蛋白溶解和炎症的生物标志物的影响。
前瞻性观察性研究。
一级创伤中心。
80 名成年创伤患者(≥18 岁),符合全面创伤团队激活标准,并进行了动脉插管。
损伤后中位数 68 分钟(四分位距 48-88)采血。
记录人口统计学、生物化学、损伤严重程度评分和 30 天死亡率数据,并分析反映去甲肾上腺素能激活(肾上腺素、去甲肾上腺素)、组织/内皮细胞/糖萼损伤(组蛋白结合 DNA 片段、膜联蛋白 V、血栓调节蛋白、 syndecan-1)、血小板激活(可溶性 CD40 配体)、凝血激活/抑制(凝血酶原片段 1.2、凝血酶/抗凝血酶复合物、抗凝血酶、蛋白 C、活化蛋白 C、蛋白 S、可溶性内皮蛋白 C 受体、组织因子途径抑制剂、血管性血友病因子、纤维蛋白原、因子 XIII)、纤维蛋白溶解(D-二聚体、组织型纤溶酶原激活物、纤溶酶原激活物抑制剂-1)和炎症(白细胞介素-6、终末补体复合物)的生物标志物。根据全队列的中位数年龄(46 岁),将患者分为两组。
与年轻患者相比,高龄创伤患者的去甲肾上腺素(p<0.001)明显升高,但随着损伤严重程度评分的升高,肾上腺素的增加幅度减弱,血小板和白细胞减少(均 p<0.05)。高龄患者表现出生物标志物谱提示天然抗凝剂释放、激活和消耗增加(低抗凝血酶、高活化蛋白 C、蛋白 S 和组织因子途径抑制剂)和纤维蛋白溶解亢进(高组织型纤溶酶原激活物)(均 p<0.05 与年轻患者相比)。在校正损伤严重程度评分、院前格拉斯哥昏迷量表和血浆儿茶酚胺后,年龄是死亡率的独立预测因素(危险比 1.04[95%置信区间 1.01-1.07],p=0.005)。
在创伤患者中,年龄与死亡率之间的关联得到了证实。高龄患者的血浆去甲肾上腺素水平较高,但随着损伤严重程度评分的升高,肾上腺素释放减弱,血小板和白细胞动员受损,抗凝剂消耗增加,纤维蛋白溶解亢进,这些可能都导致了这些患者的不良预后。