The Effects of Hydroxyethyl Starches of Varying Molecular Weights on Platelet Function

Franz, Alexander; Bräunlich, P.; Gamsjäger, Thomas; Felfernig, Michael; Gustorff, Burkhard; Kozek‐Langenecker, Sibylle A.

doi:10.1097/00000539-200106000-00008

Cited by 210 publications

(154 citation statements)

References 24 publications

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“…The lower MW TS has an average MW of 130 kD and a range from 110 to 150 kD,25 and has a clearance that is 26‐ to 31‐fold faster than HS,17 with a terminal half‐life after a single bolus of about 12 hours. The persistence of the prolonged CT for up to 24 hours might also have been seen because the larger HES molecules are more likely to impair platelet function 20. This property might have also resulted in the relatively slower rate of aggregation of platelets seen in the HS group with optical aggregometry.…”

Section: Discussionmentioning

confidence: 99%

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Cardiovascular, Colloid Osmotic Pressure, and Hemostatic Effects of 2 Formulations of Hydroxyethyl Starch in Healthy Horses

Epstein

Bergren

Giguère

et al. 2013

Veterinary Internal Medicne

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BackgroundLower molecular weight and molar substitution formulations of hydroxyethyl starch (HES) solutions might maximize cardiovascular function and colloid osmotic pressure (COP) and minimize adverse effects on coagulation.Hypothesis/ObjectivesTo compare effects of 1 low and 1 high molecular weight and molar substitution HES solution on cardiovascular variables, COP, and hemostasis in normal horses.AnimalsEight healthy adult horses.MethodsRandomized, crossover designed study: 10 mL/kg bolus of 6% HES (600/0.75) (hetastarch) (HS), 6% HES (130/0.4) tetrastarch (TS), and 0.9% NaCl (NS). Variables recorded included central venous pressure (CVP), noninvasive arterial blood pressure, packed cell volume (PCV), COP, and automated platelet analysis (CT).ResultsCentral venous pressure was increased for 8 hours after all treatment (baseline = 8.4 ± 3.8; 8 hours = 10.3 ± 3.5 cm H2O; P < .001). HS and TS produced an increase in systolic arterial pressure (HS = 109.1 ± 11.9; TS = 109.5 ± 10.9 mmHg) and mean arterial pressure (HS = 80.4 ± 13.0; TS = 82.3 ± 10.1 mmHg) compared to NS (SAP = 103.2 ± 13.2 [P = .023]; MAP = 74.2 ± 11.4 mmHg [P = .048]). PCV decreased transiently with HS (baseline = 37.1 ± 4.4%; 1.5 hours = 31.6 ± 3.9%) and TS (baseline = 38.4 ± 3.9%; 1.5 hours = 32.2 ± 3.3%), but not NS (P = .007). COP was greater with HS (1 hour; 24.0 ± 2.1 mmHg) and TS (8 hours; 25.9 ± 2.1 mmHg) than NS (1 hour = 20.8 ± 2.6; 8 hours = 22.9 ± 3.1 mmHg; P < .001). CT was greater at 8 (HS = 178.6 ± 36.9; TS = 121.9 ± 33.3; NS = 108.3 ± 23.6 seconds) and 24 hours (HS = 174.2 ± 41.7; TS = 100.8 ± 26.0; NS = 118.7 ± 38.7 seconds; P < .001) in horses receiving HS than TS or NS.Conclusion and Clinical ImportanceBoth TS and HS resulted in more effective volume expansion and arterial pressure support than NS. TS produced a more sustained effect on COP with shorter duration of adverse effects on platelet function than HS.

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Section: Discussionmentioning

confidence: 99%

“…While this property decreases the risk for tissue accumulation, it also shortens the duration of effect 17. Formulations with increased molecular weight and higher molar substitution ratios are more likely to interfere with coagulation 4, 18, 19, 20…”

mentioning

confidence: 99%

Cardiovascular, Colloid Osmotic Pressure, and Hemostatic Effects of 2 Formulations of Hydroxyethyl Starch in Healthy Horses

Epstein

Bergren

Giguère

et al. 2013

Veterinary Internal Medicne

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“…In the present study, neither modern HES nor gelatin altered platelet MCF, even after CPB, which is a very important property of colloid solution administered after cardiac surgery. The minimal effect of HES 130/0.38-0.45 on platelets has also been demonstrated (Franz et al 2001). …”

Section: Mechanisms Of Colloid-induced Coagulopathymentioning

confidence: 91%

Post‐operative volume therapy in cardiac surgery: effects on hemostatic and circulatory variables

Schramko¹

2011

Acta Anaesthesiol Scand

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“…53,54,64 Several mechanisms have been proposed: some studies have shown that colloids may reduce levels of von Willebrand factor (vWF) and factor VIII, 65,66 whereas other studies have reported on masked expression of glycoprotein IIb/IIIa on activated platelets. 67,68 More recently, an acquired deficiency of fibrinogen with abnormal fibrin polymerization have been proposed as the main determinant of dilutional coagulopathy. 69,70 The dilutional coagulopathy observed after administration of moderate amounts of hydroxyethyl starch solutions could be completely corrected by administration of fibrinogen concentrate.…”

Section: Dilutionmentioning

confidence: 99%

New insights into acute coagulopathy in trauma patients

Ganter

Pittet

2010

Best Practice & Research Clinical Anaesthesiology

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Abnormal coagulation parameters can be found in 25% of trauma patients with major injuries. Furthermore, trauma patients presenting with coagulopathy on admission have worse clinical outcome. Tissue trauma and systemic hypoperfusion appear to be the primary factors responsible for the development of acute traumatic coagulopathy immediately after injury. As a result of overt activation of the protein C pathway, the acute traumatic coagulopathy is characterised by coagulopathy in conjunction with hyperfibrinolysis. This coagulopathy can then be exacerbated by subsequent physiologic and physical derangements such as consumption of coagulation factors, haemodilution, hypothermia, acidemia and inflammation, all factors being associated with ongoing haemorrhage and inadequate resuscitation or transfusion therapies. Knowledge of the different mechanisms involved in the pathogenesis of acute traumatic coagulopathy is essential for successful management of bleeding trauma patients. Therefore, early evidence suggests that treatment directed at aggressive and targeted haemostatic resuscitation can lead to reductions in mortality of severely injured patients. ABSTRACTAbnormal coagulation parameters can be found in 25% of trauma patients with major injuries. Furthermore, trauma patients presenting with coagulopathy on admission have worse clinical outcome. Tissue trauma and systemic hypoperfusion appear to be the primary factors responsible for the development of acute traumatic coagulopathy immediately after injury. As a result of overt activation of the protein C pathway, the acute traumatic coagulopathy is characterized by coagulopathy in conjunction with hyperfibrinolysis. This coagulopathy can then be exacerbated by subsequent physiologic and physical derangements like consumption of coagulation factors, hemodilution, hypothermia, acidemia, and inflammation; all factors being associated with ongoing hemorrhage and inadequate resuscitation or transfusion therapies. Knowledge of the different mechanisms involved in the pathogenesis of acute traumatic coagulopathy is essential for successful management of bleeding trauma patients. Therefore, early evidence suggests that treatment directed at aggressive and targeted hemostatic resuscitation can lead to reductions in mortality of severely injured patients.

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The Effects of Hydroxyethyl Starches of Varying Molecular Weights on Platelet Function

Cited by 210 publications

References 24 publications

Cardiovascular, Colloid Osmotic Pressure, and Hemostatic Effects of 2 Formulations of Hydroxyethyl Starch in Healthy Horses

Cardiovascular, Colloid Osmotic Pressure, and Hemostatic Effects of 2 Formulations of Hydroxyethyl Starch in Healthy Horses

Post‐operative volume therapy in cardiac surgery: effects on hemostatic and circulatory variables

New insights into acute coagulopathy in trauma patients

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