Hypercoagulability in response to elevated body temperature and central hypovolemia

Abstract

BackgroundCoagulation abnormalities contribute to poor outcomes in critically ill patients. In trauma patients exposed to a hot environment, a systemic inflammatory response syndrome, elevated body temperature, and reduced central blood volume occur in parallel with changes in hemostasis and endothelial damage. The objective of this study was to evaluate whether experimentally elevated body temperature and reduced central blood volume (CBV) per se affects hemostasis and endothelial activation. MethodsEleven healthy volunteers were subjected to heat stress, sufficient to elevate core temperature, and progressive reductions in CBV by lower body negative pressure (LBNP). Changes in hemostasis were evaluated by whole blood haemostatic assays, standard hematologic tests and by plasma biomarkers of coagulation and endothelial activation/disruption. ResultsElevated body temperature and decreased CBV resulted in coagulation activation evidenced by shortened activated partial tromboplastin time (−9% [IQR −7; −4]), thrombelastography: reduced reaction time (−15% [−24; −4]) and increased maximum amplitude (+4% (2; 6)), all P < 0.05. Increased fibrinolysis was documented by elevation of D-dimer (+53% (12; 59), P = 0.016). Plasma adrenaline and noradrenaline increased 198% (83; 346) and 234% (174; 363) respectively (P = 0.006 and P = 0.003). ConclusionsThis experiment revealed emerging hypercoagulability in response to elevated body temperature and decreased CBV, whereas no effect on the endothelium was observed. We hypothesize that elevated body temperature and reduced CBV contributes to hypercoagulability, possibly due to moderate sympathetic activation, in critically ill patients and speculate that normalization of body temperature and CBV may attenuate this hypercoagulable response.