Effect of in vitro hemodilution with hydroxyethyl starch and dextran on the activity of plasma clotting factors

Abstract

Both NaCl and Ringer solution cause measurable effects on coagulation factors at 10:4 hemodilution that can be explained by hemodilution alone. The effects on clotting factors of 10:4 hemodilution with HAES and Oncovertin were not significant. Even at 10:10 hemodilution with HAES or Oncovertin, the reduction in factor activities, although significantly (p <.04) different from baseline, was less than what was expected by dilution alone.

Dilutional Coagulopathy, an Underestimated Problem?

“…Measuring with activated thrombeleastography and markedly shortened measuring time was, however, not able to confirm this phenomenon [37,38]. Moreover, Petroianu et al [39] concluded that hemodilution with crystalloids and colloids caused a decrease in the activity of various clotting factors in vitro. Thus, why hemodilution should activate coagulation while activated coagulation markers remain unchanged and the activity of various coagulation factors and the thrombocyte count decrease, is not known.…”

Effects of Hextend Hemodilution on Plasma Coagulation Kinetics in the Rabbit: Role of Factor XIII-Mediated Fibrin Polymer Crosslinking

“…The hemostatic consequences of hydroxyethyl starch (HES) administration have been intensely investigated in vitro [1][2][3][4][5][6][7][8][9] and in vivo [4, 10 -15]. In particular, administration of high molecular weight HES has been associated with increased post-operative hemorrhage after cardiopulmonary bypass [16,17].…”

“…In particular, administration of high molecular weight HES has been associated with increased post-operative hemorrhage after cardiopulmonary bypass [16,17]. A universal finding has been that dilution in vitro or administration in vivo with high molecular weight HES with a large degree of substitution (DS) of hydroxyethyl groups per glucose unit is associated with a decrease in ex vivo measures of coagulation such as activated partial thromboplastin time [9,10,14], prothrombin time [5,9,10,13,14], or via thrombelastographic parameters [1-8, 10 -12, 14, 15]. With regard to thrombelastographic variables, the diagnosis of hypocoagulability can be made based on an increase in the time to clot initiation (prolonged reaction time, R), a decrease in the speed of clot propagation (decreased angle, ␣), or a decrease in clot strength (smaller amplitude, A; or shear elastic modulus, G).…”

“…With regard to thrombelastographic variables, the diagnosis of hypocoagulability can be made based on an increase in the time to clot initiation (prolonged reaction time, R), a decrease in the speed of clot propagation (decreased angle, ␣), or a decrease in clot strength (smaller amplitude, A; or shear elastic modulus, G). As for the mechanisms responsible for HES-associated hypocoagulability, a decrease in factor VIII complex (VIII:C) activity after in vivo administration of HES has been reported [11,13,14]; however, no direct effect on VIII:C activity in vitro has been noted [9,18]. Further, in vivo administration of a medium molecular weight (200 kDa) HES has been associated with decreased platelet function and expression of glycoprotein IIb/IIIa compared to PBS controls [19].…”

“…Further, in vivo administration of a medium molecular weight (200 kDa) HES has been associated with decreased platelet function and expression of glycoprotein IIb/IIIa compared to PBS controls [19]. Thus, both coagulation protein activity or release and platelet activity are affected by HES of all tested molecular weights (70 -450 kDa) and in various carrier fluids [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20].…”