Mild hypothermia increases blood loss and transfusion requirements during total hip arthroplasty.

Background There is no therapy known to reduce the risk of complications or death after coronary bypass surgery Because platelet activation constitutes a pivotal mechanism for injury in patients with atherosclerosis, we assessed whether early treatment with aspirin could improve survival after coronary bypass surgery Methods At 70 centers in 17 countries, we prospectively studied 5065 patients undergoing coronary bypass surgery, of whom 5022 survived the first 48 hours after surgery We gathered data on 7500 variables per patient and adjudicated outcomes centrally The primary focus was to discern the relation between early aspirin use and fatal and nonfatal outcomes Results During hospitalization, 164 patients died (32 percent), and 812 others (160 percent) had nonfatal cardiac, cerebral, renal, or gastrointestinal ischemic complications Among patients who received aspirin (up to 650 mg) within 48 hours after revascularization, subsequent mortality was 13 percent (40 of 2999 patients), as compared

Aspirin and mortality from coronary bypass surgery.

THE combination of anesthetic-induced impairment of thermoregulatory control and exposure to a cool operating room environment makes most surgical patients hypothermic. Several prospective, randomized trials have demonstrated various hypothermia-induced complications. There is no widely accepted definition for the term mild hypothermia. Furthermore, the term is not even used consistently in the literature. For the purpose of this review, mild hypothermia refers to core temperatures between 34 and 36°C.

/pdf/complications-and-treatment-of-mild-hypothermia-4pddmqzdlm.pdf

Complications and treatment of mild hypothermia

A hypothermia-induced hemorrhagic diathesis is associated with cardiopulmonary bypass, major surgery, and multiple trauma, but its pathophysiological basis is not well understood. We examined the hypothesis that hypothermia reversibly inhibits human platelet activation in vitro and in vivo. Platelet activation was studied in normal volunteers by whole blood flow cytometric analysis of modulation of platelet surface GMP-140 and the glycoprotein (GP) Ib-IX complex in: a) shed blood emerging from a standardized in vivo bleeding time wound; b) peripheral blood activated in vitro with either thrombin (in the presence of gly-pro-arg-pro, an inhibitor of fibrin polymerization) or the stable thromboxane (TX) A2 analogue U46619. Platelets in peripheral whole blood were activated at temperatures between 22 degrees C and 37 degrees C. the forearm skin temperature was maintained at temperatures between 22 degrees C and 37 degrees C prior to and during the bleeding time incision. Platelet aggregation was studied in shed blood by flow cytometry and in peripheral blood by aggregometry. Generation of TXB2 (the stable metabolite of TXA2) was determined by radioimmunoassay. In vitro, hypothermia inhibited both thrombin- and U46619-induced upregulation of GMP-140, downregulation of the GPIb-IX complex, platelet aggregation, and TXB2 generation. These inhibitory effects of hypothermia were all completely reversed by rewarming the blood to 37 degrees C. In vivo, platelet activation was inhibited by hypothermia as shown by 5 independent assays of shed blood: upregulation of GMP-140, downregulation of the GPIb-IX complex, platelet aggregate formation, TXB2 generation, and the bleeding time.(ABSTRACT TRUNCATED AT 250 WORDS)

Reversible inhibition of human platelet activation by hypothermia in vivo and in vitro.

Cardiopulmonary bypass duration is an independent predictor of morbidity and mortality after cardiac surgery.

Hematologic changes during and after cardiopulmonary bypass and their relationship to the bleeding time and nonsurgical blood loss.

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Hematologic changes during and after cardiopulmonary bypass and their relationship to the bleeding time and nonsurgical blood loss.