Hypothermic anticoagulation

Abstract

Selective incircuit blood cooling could be an effective anticoagulation strategy during hemodialysis. However, it is currently unknown what blood temperature would ensure sufficient anticoagulation. Similarly, no information exists about potential interindividual variability in response to graded hypothermia. Therefore, the aim of this study was to analyze effects of profound hypothermia on human coagulation. Furthermore, a mathematical relationship between blood temperatures and coagulation was sought to predict individual responses to blood cooling. It was designed as a laboratory study. Thromboelastography (TEG) measurements were taken at a temperature range of 38-12°C. To enable measurements below 20°C, the TEG device was placed into an air conditioned chamber allowing for setting of the temperatures over a wide range. The data were analyzed by regression analysis for pooled and individual measurements. Decreasing temperatures always led to a progressive reduction in blood coagulation by delaying the initiation of thrombus formation, as well as by decreasing the speed of its creation and growth. However, the response to cooling was not uniform and the interindividual variability exists. The relationship between blood temperature and coagulation is not linear but exponential (parameters R and K) and sigmoid (parameter α-angle). The lower the blood temperature, the more significant effect on blood coagulation decline. To predict an individual response of the coagulation system over a wide range of temperatures, a mathematical modeling can be used.

Therapeutic Hypothermia and the Risk of Hemorrhage

“…The effects of hypothermia on coagulation have been studied mostly in vitro. 19 – 26 Mild hypothermia (down to 35 °C) has no effect on platelet counts or function or the coagulation cascade. 19 – 26 Temperatures cooler than 35 °C might have induced mild platelet dysfunction and sometimes a slight decrease in platelet count.…”

“… 18 Impaired platelet function, thrombocytopenia, and derangement of the coagulation cascade have been reported. 19 – 26 Therefore, patients with bleeding diathesis have often been excluded from enrolment in TH clinical trials 11 , 12 and from treatment with TH in real practice because of concern over the increased risk of hemorrhage.…”

Platelet aggregation and clot formation in comatose survivors of cardiac arrest treated with induced hypothermia and dual platelet inhibition with aspirin and ticagrelor; a prospective observational study

“…This observational study did not include a normothermic control group, thus the cause for the increased platelet aggregability and viscoelastic clot formation between stable hypothermia (T1) and stable normothermia (T2) is not known but two possible explanations will be discussed. Hypothermia has been shown to decrease haemostasis measured with viscoelastic methods [ 11 , 18 , 19 , 28 ] and with platelet function testing [ 16 , 17 , 21 ]. Thus, the lower temperature at T1 could be responsible for the decreased values as compared to T2.…”

Thrombin generation and fibrin clot formation under hypothermic conditions: An in vitro evaluation of tissue factor initiated whole blood coagulation

“…(20-24) Thromboelastrographic profiling has the advantages of providing a comprehensive assessment of blood coagulation and fibrinolysis while utilizing whole blood samples at defined temperatures and controllable environments. Thus, TEG profiling allows for a thorough evaluation of coagulopathy and is developing into a useful clinical tool (25). Specifically, TEG has been shown to provide a more accurate measure of hypothermic and hemodilution effects on traumatic coagulopathy.…”

“…Specifically, TEG has been shown to provide a more accurate measure of hypothermic and hemodilution effects on traumatic coagulopathy. (20, 25)…”