Does Intraoperative Hetastarch Administration Increase Blood Loss and Transfusion Requirements After Cardiac Surgery?

Mayo School of Health-Related Sciences, Mayo Graduate School of Medicine, Rochester, Minnesota 55905, USA.
Anesthesia & Analgesia (Impact Factor: 3.47). 04/2000; 90(4):801-7. DOI: 10.1097/00000539-200004000-00006
Source: PubMed


Hetastarch is used for intravascular volume expansion in cardiac surgery. Studies show conflicting effects of intraoperative hetastarch administration on postoperative bleeding. Hetastarch was routinely used for volume expansion during cardiovascular surgeries at our institution until its use was discontinued intraoperatively. We performed a retrospective chart review on patients undergoing primary coronary artery bypass grafting, valve repair or replacement requiring cardiopulmonary bypass (n = 444), 234 of which received intraoperative hetastarch and 210 did not. There was no difference in demographics, cardiac surgery, or cardiopulmonary bypass duration between the two groups. Blood loss for 0-4 h postoperatively was 377 +/- 244 mL in the group not receiving hetastarch compared with 515 +/- 336 mL in the group that received hetastarch (P < 0.001). For 0-24 h postoperatively, blood loss was 923 +/- 473 mL versus 1,283 +/- 686 mL in the absence and presence of hetastarch, respectively (P < 0.001). Allogeneic transfusion requirements (cryoprecipitate, fresh frozen plasma, and platelets) were larger in the hetastarch group (all P < 0.001). Nearly all (99%) patients in the hetastarch group received less than the manufacturer's recommended dose (20 mL/kg) of hetastarch. IMPLICATIONS: Our large retrospective study suggests that intraoperative use of hetastarch in primary cardiac surgery with cardiopulmonary bypass may increase bleeding and transfusion requirements. A large prospective study is needed to determine if intraoperative administration of hetastarch should be avoided during cardiovascular surgery.

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    • "There have also have been small studies associating the use of HES with intracranial bleeding and coagulopathy in the setting of subarachnoid hemorrhage (Damon et al. 1987; Knutson et al. 2000). The mechanisms causing this acquired coagulopathy include qualitative platelet dysfunction , decreases in Factor VIII/von Willebrand's factor complexes (sometimes referred to as " Acquired von "
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