Background: 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.
Methods: 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.
Results: 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%.
Conclusion: 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.