Anemia-induced increase in the bleeding time: implications for treatment of nonsurgical blood loss

BACKGROUND: Preoperative bleeding time (BT) does not correlate with postope rative bleeding in patients subjected to surgical procedures. A significant positive correlation has been reported between the BT 2 hours after cardio pulmonary bypass surgery and the nonsurgical blood loss during the first 4 hours after bypass surgery. This study was done to investigate the effect o f Hct and platelet count on the BT measurement in normal, healthy men and w omen. STUDY DESIGN AND METHODS: To assess the relative effect of RBCs and platele ts on the BT, 22 healthy male and 7 healthy female volunteers were subjecte d to the removal of 2 units of RBCs (360 mL), followed by the return of the platelet-rich plasma (PRP) from both units and the infusion of 1000 mL of 0.9-percent NaCl. Four of the men and all seven women received their RBCs 1 hour after their removal. Shed blood levels of thromboxane B-2 (TXB2), 6-k eto prostaglandin F-1 alpha, and peripheral venous Hot were measured. BTs w ere measured in 15 men and 13 women before and after a plateletpheresis pro cedure to collect 3.6 x 10(11) platelets per unit. RESULTS: The 2-unit RBC apheresis procedure produced a 60-percent increase in the BT associated with a 15-percent reduction in the peripheral venous H ct and a 9-percent reduction in the platelet count. The plateletpheresis pr ocedure produced a 32-percent decrease in the platelet count, no change in peripheral venous Hct, and no change in the BT. After the removal of 2 unit s of RBCs, the shed blood TXB2 level decreased significantly. Reinfusion of 2 units of RBCs restored the BT and restored the TXB2 level to the baselin e levels. CONCLUSION: The acute reduction in Hct produced a reversible platelet dysfu nction manifested by an increase in BT and a decrease in the shed blood TXB 2 level at the template BT site. Return of the RBCs restored both the BT an d the shed blood TXB2 level to normal. The platelet dysfunction observed wi th the reduction in Hot was due in part to a reduction in shed blood TXB2 a nd other, unknown mechanisms.