BACKGROUND: Hypothermia and acidosis were reported to influence coagulopathy in different clinical settings. We evaluated whole blood coagulation to determine the effects of hypothermia and/or acidosis on hemostasis. METHODS: Whole blood samples (3.000 microL) from 10 healthy volunteers (2 female, 8 male) were acidified by adding 40 microL of hydrochloric acid of increasing molarity to achieve a blood pH (alpha-stat) between 7.0 and 7.37, and coagulation was analyzed by rotational thromboelastometry after an incubation period of 30 min using both intrinsically (InTEM) and extrinsically (ExTEM) activated assays. To assess temperature-dependent effects, all tests were performed at blood/thromboelastometer temperatures of 30, 33, 36, and 39 degrees C, respectively. An additional extrinsically activated test with addition of cytochalasin D was performed to examine clot formation without platelet contribution. RESULTS: Hypothermia at a normal pH produced an increased coagulation time [ExTEM: 65 s +/- 3.6 (36 degrees C) vs 85 +/- 4 (30 degrees C), P < 0.001; coagulation time, InTEM: 181 s +/- 10 (36 degrees C) vs 226 +/- 9, P < 0.001] and clot formation time [ExTEM: 105 s +/- 5 (36 degrees C) vs 187 +/- 6 (30 degrees C), P < 0.001]; clot formation time [InTEM: 101 s +/- 5 (36 degrees C) vs 175 +/- 7, P < 0.001], as well as decreased alpha angle [ExTEM: 65.6 +/- 1.8 (36 degrees C) vs 58 +/- 1.1, P < 0.01, P < 0.01; InTEM: 70.5 +/- 1.8 (36 degrees C) vs 60.2 +/- 1.5, P < 0.001]. Maximum clot firmness was significantly impaired only in InTEM assays [56.9 mm +/- 0.9 (36 degrees C) vs 52.7 +/- 0.9, P < 0.05]. In contrast, acidosis per se had no significant effects during normothermia. Acidosis amplified the effects of hypothermia, and synergistically impaired clotting times, alpha angle, and decreased maximum clot firmness, again in both extrinsically and intrinsically activated assays. Formation of a fibrin clot tested after abolition of platelet function by cytochalasin D was not impaired. Clot lysis decreased under hypothermic and/or acidotic conditions, but increased with hyperthermia. CONCLUSIONS: In this in vitro study, hypothermia produced coagulation changes that were worsened by acidosis whereas acidosis without hypothermia has no significant effect on coagulation, as studied by thromboelastometry. This effect was mediated by the inhibition of coagulation factors and platelet function. Thus, thromboelastometry performed at 37 degrees C overestimated integrity of coagulation during hypothermia in particular in combination with acidosis.
BACKGROUND:Hypothermia and acidosis were reported to influence coagulopathy in different clinical settings. We evaluated whole blood coagulation to determine the effects of hypothermia and/or acidosis on hemostasis. METHODS: Whole blood samples (3.000 microL) from 10 healthy volunteers (2 female, 8 male) were acidified by adding 40 microL of hydrochloric acid of increasing molarity to achieve a blood pH (alpha-stat) between 7.0 and 7.37, and coagulation was analyzed by rotational thromboelastometry after an incubation period of 30 min using both intrinsically (InTEM) and extrinsically (ExTEM) activated assays. To assess temperature-dependent effects, all tests were performed at blood/thromboelastometer temperatures of 30, 33, 36, and 39 degrees C, respectively. An additional extrinsically activated test with addition of cytochalasin D was performed to examine clot formation without platelet contribution. RESULTS:Hypothermia at a normal pH produced an increased coagulation time [ExTEM: 65 s +/- 3.6 (36 degrees C) vs 85 +/- 4 (30 degrees C), P < 0.001; coagulation time, InTEM: 181 s +/- 10 (36 degrees C) vs 226 +/- 9, P < 0.001] and clot formation time [ExTEM: 105 s +/- 5 (36 degrees C) vs 187 +/- 6 (30 degrees C), P < 0.001]; clot formation time [InTEM: 101 s +/- 5 (36 degrees C) vs 175 +/- 7, P < 0.001], as well as decreased alpha angle [ExTEM: 65.6 +/- 1.8 (36 degrees C) vs 58 +/- 1.1, P < 0.01, P < 0.01; InTEM: 70.5 +/- 1.8 (36 degrees C) vs 60.2 +/- 1.5, P < 0.001]. Maximum clot firmness was significantly impaired only in InTEM assays [56.9 mm +/- 0.9 (36 degrees C) vs 52.7 +/- 0.9, P < 0.05]. In contrast, acidosis per se had no significant effects during normothermia. Acidosis amplified the effects of hypothermia, and synergistically impaired clotting times, alpha angle, and decreased maximum clot firmness, again in both extrinsically and intrinsically activated assays. Formation of a fibrin clot tested after abolition of platelet function by cytochalasin D was not impaired. Clot lysis decreased under hypothermic and/or acidotic conditions, but increased with hyperthermia. CONCLUSIONS: In this in vitro study, hypothermia produced coagulation changes that were worsened by acidosis whereas acidosis without hypothermia has no significant effect on coagulation, as studied by thromboelastometry. This effect was mediated by the inhibition of coagulation factors and platelet function. Thus, thromboelastometry performed at 37 degrees C overestimated integrity of coagulation during hypothermia in particular in combination with acidosis.
Authors: Aleksander Trąbka-Zawicki; Marek Tomala; Aleksander Zeliaś; Elżbieta Paszek; Wojciech Zajdel; Ewa Stępień; Krzysztof Żmudka Journal: Cardiol J Date: 2017-07-11 Impact factor: 2.737
Authors: Gareth R Davies; Suresh Pillai; Matthew Lawrence; Gavin M Mills; Robert Aubrey; Lindsay D'Silva; Ceri Battle; Rhodri Williams; Rowan Brown; Dafydd Thomas; Keith Morris; Phillip Adrian Evans Journal: Intensive Care Med Date: 2016-09-03 Impact factor: 17.440
Authors: Francisco Vaz-Guimaraes; Shirley Y Su; Juan C Fernandez-Miranda; Eric W Wang; Carl H Snyderman; Paul A Gardner Journal: J Neurol Surg B Skull Base Date: 2015-04-27