Abstract
BackgroundClot strength by Thrombelastography (TEG) is associated with mortality during trauma and has been linked to severity of tissue hypoperfusion. However, the optimal method for monitoring this important relationship remains undefined. We hypothesize that oxygen transport measurements will be associated with clot strength during traumatic shock, and test this hypothesis using a swine model of controlled traumatic shock.MethodsN = 33 swine were subjected to femur fracture and hemorrhagic shock by controlled arterial bleeding to a predetermined level of oxygen debt measured by continuous indirect calorimetry. Hemodynamics, oxygen consumption, systemic central venous oxygenation (ScvO2), base excess, lactate, and clot maximal amplitude by TEG (TEG-MA) as clot strength were measured at baseline and again when oxygen debt = 80 ml/kg during shock. Oxygen transport and metabolic markers of tissue perfusion were then evaluated for significant associations with TEG-MA. Forward stepwise selection was then used to create regression models identifying the strongest associations between oxygen transport and TEG-MA independent of other known determinants of clot strength.ResultsMultiple markers of tissue perfusion, oxygen transport, and TEG-MA were all significantly altered during shock compared to baseline measurements (p < 0.05). However, only ScvO2 demonstrated a strong bivariate association with TEG-MA measured during shock (R = 0.7, p < 0.001). ScvO2 measured during shock was also selected by forward stepwise selection as an important covariate in linear regression models of TEG-MA after adjusting for the covariates fibrinogen, pH, platelet count, and hematocrit (Whole model R2 = 0.99, p ≤ 0.032).ConclusionsAmong multiple measurements of oxygen transport, only ScvO2 was found to retain a significant association with TEG-MA during shock after adjusting for multiple covariates. ScvO2 should be further studied for its utility as a clinical marker of both tissue hypoxia and clot formation during traumatic shock.
Highlights
Clot strength by Thrombelastography (TEG) is associated with mortality during trauma and has been linked to severity of tissue hypoperfusion
We have previously reported that clot strength by TEG is reduced in isolation prior to fluid resuscitation during traumatic shock in an oxygen debt-driven animal model [21]
Paired T-test revealed no significant difference in maximal clot strength (MA) recorded at baseline, during shock, or the change in MA between the two anesthetic regimens (p > 0.2)
Summary
Clot strength by Thrombelastography (TEG) is associated with mortality during trauma and has been linked to severity of tissue hypoperfusion. Blood lactate concentration is currently used to define the severity of hemorrhagic shock in animal models of trauma [4] These metabolic markers of shock severity, while being readily clinical available, are not direct reflections of tissue hypoxia and can be affected by other factors during critical illness including liver/renal dysfunction and ethanol intoxication, limiting their utility [8,9,10]. Viscoelastic clot strength is an aggregate measurement that is dependent on multiple blood components including platelet activity and concentration, fibrinogen concentration, pH, hematocrit, and temperature [18,19,20] It is this presence of multiple confounding influences on both markers of shock severity and viscoelastic clot strength that has made it difficult to precisely define how tissue perfusion is associated with changes in clot strength during trauma
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
