Mark,
Thanks for the post on the Bick article. Did you get a reprint from the publisher, or did you get it from Biotime? Neither the University of California library system, nor Medline carry this publication. Can you fax me a copy?
you wrote:
The reports of coagulation problems in patients given generic HES-in-saline must then be due, not to HES, but to the saline solution component of these solutions.
Is this your own conclusion? You think it is the saline that causes coagulopathy beyond hemodilution?! I found it clearly suggested in the papers that the high average weight HES hetastarch causes coagulopathy:
"It is hypothesized that the complex polysaccharide precipitates certain coagulation factors, making them unavailable to the coagulation cascade. HES may form a complex with Factor VIII and fibrinogen, and may also accelerate the action of thrombin in the conversion of fibrinogen to fibrin (the fibrinoplastic effect). This fibrinoplastic effect not only reduces the amount of fibrinogen available for normal coagulation, but also produces a fibrin clot that is lysed more easily. Accordingly, the maximum amplitude of the thromboelastogram was depressed in patients receiving HES, indicating the formation of a clot with decreased strength (2). HES has been suggested to reduce platelet function by coating the platelet surface or inducing platelet damage (1,8,23)."
(from Anesth Analg 1997; 84:206-12)
The same review paper also found 6 studies where no effects of HES on coagulation were found, 8 reporting only laboratory effects, and 4 recording clinically significant effects. In other words, there are a lot of studies out there that suggest there are no non-dilutional coagulopathies associated with hetastarch. Only 4/18 studies found any clinical effects.
Steve
btim.dyn.ml.org |
