Lustenberger Thomas, Talving Peep, Kobayashi Leslie, Barmparas Galinos, Inaba Kenji, Lam Lydia, Branco Bernardino Castelo, Demetriades Demetrios
Division of Acute Care Surgery (Trauma, Emergency Surgery, and Surgical Critical Care) at the Los Angeles County + University of Southern California Medical Center, Los Angeles, California, USA.
J Trauma. 2010 Dec;69(6):1410-4. doi: 10.1097/TA.0b013e3181cdae81.
The purpose of this study was to examine the incidence of tissue hypoperfusion in victims of severe traumatic brain injury (sTBI) and to determine the associations between hypoperfusion and TBI coagulopathy.
This is a retrospective analysis of a prospectively collected cohort admitted to the surgical intensive care unit from June 2005 to December 2007 sustaining isolated sTBI, defined as sTBI [head Abbreviated Injury Scale (AIS) ≥ 3] with chest, abdomen, and extremity AIS < 3. Criteria for TBI-associated early coagulopathy included isolated sTBI in conjunction with thrombocytopenia (platelet count < 100,000 per mm³) or elevated international normalized ratio > 1.2 or prolonged activated partial thromboplastin time > 36 seconds at admission. Hypoperfusion was defined by the presence of an arterial base deficit (BD) > 6 mmol/L. Univariate and multivariate analysis was performed to identify associations among hypoperfusion, coagulopathy, and mortality.
A total of 132 patients met the study criteria. TBI-associated early coagulopathy occurred in 48 patients (36.4%). With increasing head injury severity, the incidence of coagulopathy increased in a stepwise fashion. Mean BD values and mean lactate values were significantly higher among patients with coagulopathy compared with their noncoagulopathic counterparts at hospital admission. The coagulopathic cohort presented more frequently with a BD > 6 mmol/L at admission (39.6% vs. 20.2%, p = 0.016). In the stepwise logistic regression analysis, head AIS = 5 and an admission BD > 6 mmol/L were independently associated with early coagulopathy. Coagulopathy was associated with increased mortality in patients after blunt head trauma, adjusted odds ratio (95% confidence interval): 3.79 (1.06-13.51); adjusted p = 0.04.
Hypoperfusion is an independent risk factor for the development of early coagulopathy in patients with isolated sTBI. Nevertheless, early coagulopathy after sTBI does not occur exclusively in patients experiencing tissue hypoperfusion.
本研究旨在调查重度创伤性脑损伤（sTBI）患者组织灌注不足的发生率，并确定灌注不足与TBI凝血病之间的关联。
这是一项对2005年6月至2007年12月入住外科重症监护病房的前瞻性收集队列的回顾性分析，该队列患者患有孤立性sTBI，定义为sTBI（头部简明损伤量表[AIS]≥3）且胸部、腹部和四肢AIS<3。TBI相关早期凝血病的标准包括孤立性sTBI合并血小板减少症（血小板计数<100,000/mm³）或入院时国际标准化比值升高>1.2或活化部分凝血活酶时间延长>36秒。灌注不足定义为动脉碱缺失（BD）>6 mmol/L。进行单因素和多因素分析以确定灌注不足、凝血病和死亡率之间的关联。
共有132例患者符合研究标准。48例患者（36.4%）发生了TBI相关早期凝血病。随着头部损伤严重程度的增加，凝血病的发生率呈逐步上升趋势。与入院时无凝血病的患者相比，凝血病患者的平均BD值和平均乳酸值显著更高。凝血病队列入院时BD>6 mmol/L的情况更频繁出现（39.6%对20.2%，p = 0.016）。在逐步逻辑回归分析中，头部AIS = 5和入院时BD>6 mmol/L与早期凝血病独立相关。凝血病与钝性头部创伤患者死亡率增加相关，调整后的优势比（95%置信区间）：3.79（1.06 - 13.51）；调整后p = 0.04。
灌注不足是孤立性sTBI患者发生早期凝血病的独立危险因素。然而，sTBI后的早期凝血病并非仅发生在经历组织灌注不足的患者中。
