Key result
Etomidate induction significantly inhibited platelet function, prolonged operation time, and increased transfusion volume compared to thiopental in patients undergoing vascular surgery.
Why the study?
Does etomidate compared to thiopental inhibit platelet function in patients undergoing vascular surgery?
Cohort (n=46)
Does etomidate compared to thiopental inhibit platelet function in patients undergoing vascular surgery?
Etomidate and, to a lesser extent, thiopental exhibit significant platelet inhibitory properties that may lead to higher transfusion rates and prolonged operation times during vascular surgery.
May warrant caution with etomidate induction in vascular surgery; hypothesis-generating and requires RCT confirmation before practice change.
BACKGROUND: Postoperative platelet hyperaggregability following general anesthesia has been reported in patients undergoing major vascular surgery. In contrast, since anesthetic agents inhibited platelet function both in vitro and in vivo, an increased risk for postoperative bleedings due to prolonged platelet dysfunction has been discussed. Nevertheless, data describing platelet-affecting properties of induction agents such as etomidate and thiopental in patients undergoing major vascular surgery are lacking. METHODS: Platelet function was determined at 0, 2, 20, and 200 microg/ml thiopental and at 0, 0.2, 2, 20 microg/ml etomidate in vitro in blood samples drawn from 16 patients suffering from severe occlusive arterial disease. In addition, 30 patients undergoing vascular surgery were investigated before (PRE) and after anesthesia induction (T0) either with etomidate (ETO group, n=16) or thiopental (THIO group, n=14), and 2 h after the beginning of surgery (T2). Platelet function was determined according to platelet aggregation, in vitro bleeding time, and flow cytometric measurements. RESULTS: In vitro, P-selectin expression was inhibited by etomidate at 2 and 20 microg/ml (-28% and -38%, respectively) and also by thiopental at 200 microg/ml (-27%). In patients undergoing vascular surgery, anesthesia induction in the ETO group resulted in a 31% prolongation of the in vitro bleeding time and an inhibition of ADP- and collagen-induced platelet aggregation (-30% and -17%, respectively) and of P-selectin expression (-25%) at T0. In the THIO group, only ADP-induced platelet aggregation was affected (-16%). At T2, all parameters had reached PRE level again in both groups. Furthermore, in comparison with the THIO group, operation time was significantly prolonged and transfusion volume was significantly increased in the ETO group. In addition, platelet count and hematocrit significantly decreased at T2, whereas levels of tPA, PAI-1, fibrinogen and antithrombin III and partial thromboplastin time remained unchanged in both groups during the study period. CONCLUSIONS: In the present study, etomidate and, to a minor extent, thiopental offered significant platelet inhibitory properties. Anesthetic-induced platelet inhibition may lead to higher transfusion rates and prolonged operation times. Therefore, anesthetic-related platelet inhibitory properties should be considered when searching for the anesthetic agent of choice, especially in patients with compromised hemostasis and co-existing bleeding disorders.
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Gries et al. (2001) conducted a cohort in Severe occlusive arterial disease requiring infrainguinal vascular surgery (n=46). Etomidate vs. Thiopental was evaluated on Platelet function (platelet aggregation, in vitro bleeding time, and P-selectin expression). Etomidate induction significantly inhibited platelet function, prolonged operation time, and increased transfusion volume compared to thiopental in patients undergoing vascular surgery.
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