Department of Surgery, The University of Texas Health Science Center, Houston, Texas 77030, USA.
J Trauma Acute Care Surg. 2012 Aug;73(2):365-70; discussion 370. doi: 10.1097/TA.0b013e31825c1234.
Hyperfibrinolysis (HF) has been reported to occur in a range of 2% to 34% of trauma patients. Using rapid thromboelastography (r-TEG), we hypothesized that HF is (1) rarely present at admission on patients with severe injury and (2) associated with crystalloid hemodilution. To further strengthen this hypothesis, we created an in vitro hemodilution model to improve our mechanistic understanding of the early HF.
The trauma registry was queried for patients who were our highest-level trauma activations and admitted directly from the scene (October 2009-October 2010). HF was defined as more than 7.5% amplitude reduction 30 minutes after maximal amplitude (LY30). Using r-TEG, we then created an in vitro hemodilution model (0.9% NS) with and without tissue injury (addition of tissue factor and tissue plasminogen activator) to identify crystalloid volumes and injury needed to achieve specific LY30 values.
Admission r-TEG values were captured on 1996 consecutive admissions. Only 41 patients (2%) had HF at admission r-TEG. The groups were similar in demographics. Compared with patients without HF, the HF group had more prehospital crystalloid (1.5 vs. 0.5 L), higher median Injury Severity Score (25 vs. 16), greater admission base deficit (20 vs. 2), and higher mortality (76% vs. 10%); all p < 0.001. Controlling for Injury Severity Score and base deficit on arrival, prehospital fluid was associated with a significant increase in likelihood of HF. In fact, each additional liter of crystalloid was associated with a 15% increased odds of HF. The in vitro model found that hemodilution to 15% of baseline and tissue factor + tissue plasminogen activator was required to achieve an LY30 of 50%.
Although uncommon immediately after injury, HF is associated with prehospital crystalloid administration and shock at admission and is highly lethal. Our in vitro model confirms that tissue injury and significant crystalloid hemodilution result in severe and immediate HF.
据报道，在 2%至 34%的创伤患者中存在高纤维蛋白溶解（HF）。使用快速血栓弹性描记术（r-TEG），我们假设（1）在严重创伤患者入院时很少出现 HF，（2）与晶体液稀释相关。为了进一步加强这一假设，我们创建了一个体外血液稀释模型，以提高我们对早期 HF 的机制理解。
从 2009 年 10 月至 2010 年 10 月期间的最高级别创伤激活和直接从现场入院的患者中查询创伤登记处。HF 的定义为最大幅度后 30 分钟振幅减少超过 7.5%（LY30）。然后，我们使用 r-TEG 在有和没有组织损伤（添加组织因子和组织纤溶酶原激活物）的情况下创建了一个体外血液稀释模型（0.9% NS），以确定达到特定 LY30 值所需的晶体液量和损伤。
在 1996 例连续入院患者中采集了入院 r-TEG 值。只有 41 例（2%）患者在入院 r-TEG 时出现 HF。两组在人口统计学方面相似。与无 HF 组相比，HF 组院前晶体液量更多（1.5 比 0.5 L），中位数损伤严重程度评分更高（25 比 16），入院时基础缺陷更大（20 比 2），死亡率更高（76%比 10%）；所有 p 值均 < 0.001。在校正入院时的损伤严重程度评分和基础缺陷后，院前液体与 HF 发生的可能性显著增加相关。实际上，每增加 1 升晶体液，HF 的可能性就会增加 15%。体外模型发现，需要稀释至基线的 15%并添加组织因子+组织纤溶酶原激活物才能达到 LY30 为 50%。
尽管在受伤后立即不常见，但 HF 与院前晶体液的使用和入院时的休克相关，并且具有高度致命性。我们的体外模型证实，组织损伤和显著的晶体液稀释会导致严重且立即的 HF。
