Department of Surgery, University of California, San Francisco, CA, USA.
J Trauma Acute Care Surg. 2012 Jul;73(1):13-9. doi: 10.1097/TA.0b013e318256deab.
The increased morbidity and mortality associated with coagulopathy and thrombocytopenia after trauma are well described. However, few studies have assessed platelet function after injury.
Blood samples were prospectively collected from 101 patients with critical injury and trauma on arrival to the emergency department and serially after admission to a Level I urban trauma intensive care unit from November 2010 to October 2011 and functionally assayed for responsiveness to adenosine diphosphate, thrombin receptor-activating peptide, arachidonic acid (AA), and collagen using multiple electrode impedance aggregometry.
Of the 101 enrolled patients, 46 (45.5%) had below-normal platelet response to at least one agonist ("platelet hypofunction") at admission, and 92 patients (91.1%) had platelet hypofunction some time during their intensive care unit stay. Admission platelet hypofunction was associated with low Glasgow Coma Scale score and a nearly 10-fold higher early mortality. Logistic regression identified admission Glasgow Coma Scale (odds ratio, 0.819; p = 0.008) and base deficit (odds ratio, 0.872; p = 0.033) as independent predictors of platelet hypofunction. Admission AA and collagen responsiveness were significantly lower for patients who died (p < 0.01), whereas admission platelet counts were similar (p = 0.278); Cox regression confirmed thrombin receptor-activating peptide, AA, and collagen responsiveness as independent predictors of in-hospital mortality (p < 0.05). Receiver operating characteristic analysis identified admission AA and collagen responsiveness as negative predictors of both 24-hour (AA area under the curve [AUC], 0.874; collagen AUC, 0.904) and in-hospital mortality (AA AUC, 0.769; collagen AUC, 0.717).
In this prognostic study, we identify clinically significant platelet dysfunction after trauma in the presence of an otherwise reassuring platelet count and standard clotting studies, with profound implications for mortality. Multiple electrode impedance aggregometry reliably identifies this dysfunction in injured patients, and admission AA and collagen responsiveness are sensitive and specific independent predictors of both early and late mortality.
创伤后凝血功能障碍和血小板减少症相关的发病率和死亡率增加已得到充分描述。然而,很少有研究评估损伤后的血小板功能。
从 2010 年 11 月至 2011 年 10 月,前瞻性地采集了 101 例严重创伤和创伤患者的血液样本,在到达急诊科后以及在一级城市创伤重症监护病房入院后连续采集,并使用多电极阻抗聚集法对血小板对二磷酸腺苷、血栓素受体激活肽、花生四烯酸(AA)和胶原的反应性进行功能测定。
在纳入的 101 例患者中,46 例(45.5%)在入院时至少有一种激动剂的血小板反应异常(“血小板功能低下”),92 例(91.1%)在重症监护病房期间的某个时间血小板功能低下。入院时血小板功能低下与格拉斯哥昏迷量表评分低和早期死亡率高近 10 倍有关。逻辑回归确定入院时格拉斯哥昏迷量表(优势比,0.819;p=0.008)和基础不足(优势比,0.872;p=0.033)是血小板功能低下的独立预测因子。死亡患者的入院 AA 和胶原反应性显著降低(p<0.01),而入院血小板计数相似(p=0.278);Cox 回归证实血栓素受体激活肽、AA 和胶原反应性是住院死亡率的独立预测因子(p<0.05)。受试者工作特征分析确定入院 AA 和胶原反应性是 24 小时(AA 曲线下面积[AUC],0.874;胶原 AUC,0.904)和住院死亡率(AA AUC,0.769;胶原 AUC,0.717)的阴性预测因子。
在这项预后研究中,我们在血小板计数和标准凝血研究令人安心的情况下发现了创伤后临床上显著的血小板功能障碍,对死亡率有深远影响。多电极阻抗聚集法可靠地识别出受伤患者的这种功能障碍,入院时 AA 和胶原反应性是早期和晚期死亡率的敏感和特异的独立预测因子。