Packed red cells in acute blood loss: Dilutional coagulopathy as a cause of surgical bleeding

D. J. Murray, B. J. Pennell, S. L. Weinstein, J. D. Olson

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174 Scopus citations


The purpose of this study was: 1) to define coagulation abnormalities in patients who receive red cell concentrates rather than whole blood for large volume blood loss (greater than 0.5 blood volume); and 2) to determine when coagulation abnormalities lead to increased bleeding in the massively transfused surgical patient. We studied 32 ASA physical status I or II patients (mean age 15.6 ± 2.3 yr) who lost more than 50% of their blood volume during elective posterior spinal stabilization. Crystalloid solutions and packed red cell concentrates were used to replace blood and fluid losses. Invasive hemodynamic measures, urinary output, and serial hematocrit determinations were used to help maintain a constant intravascular volume and confirm the estimates of blood loss. The quality of hemostasis was assessed during operation. In 15 of the 32 patients, surgical hemostasis remained effective throughout posterior spinal fusion. A coagulation profile (prothrombin time [PT] and activated partial thromboplastin time [aPTT], platelet count, and fibrinogen) was measured at the conclusion of operation in these patients. In 17 patients, increased surgical bleeding as a result of decreased clot formation and increased bleeding from the wound was present. In these 17 patients at the time increased bleeding was diagnosed, hemostatic tests (PT, aPTT, fibrinogen, platelet count, and coagulation factor assays V, VIII, and IX) were obtained. Prior to the return of the test results, fresh frozen plasma (FFP) was administered (10 mL/kg) to replace approximately 15%- 20% of normal coagulation factor levels. After FFP infusion, hemostasis was reassessed and repeat PT and aPTT were obtained. Patients with increased clinical bleeding (n = 17) sustained greater blood loss and blood volume loss (3.6 ± 1.2 L and 1.14 ± 0.28 blood volumes) than patients (2.6 ± 1.3 L and 0.87 ± 0.22 blood volumes) who did not experience increased bleeding. The PT (15.4 ± 1.4 s) and aPTT (74 ± 40 s) increased more in patients with clinical bleeding than in patients who had effective hemostasis (PT = 14.2 ± 1.2 s and aPTT = 45 ± 12.7 s). Platelet counts (178 ± 62 abnormal hemostasis vs 202 ± 47 x 103/mm3) and fibrinogen levels (128 ± 47 abnormal hemostasis vs 145 ± 38 mg/dL) declined similarly in both groups. Factors V and IX decreased with increasing blood volume loss. FFP was judged effective i n correcting abnormal hemostasis in 14 of the 17 patients. The PT and aPTT after FFP were similar to that in patients who had no evidence of increased clinical bleeding. Increased PT and aPTT were frequent hemostatic test abnormalities in patients who received packed red cells and crystalloid solutions to replace more than 50% of their blood volumes (30 of 32 patients). Patients who had increased surgical bleeding, had greater increases in PT and aPTT (> 1.5 times mean control) than patients without evidence of increased bleeding. In contrast to emergency surgical patients who developed thrombocytopenia as a cause of bleeding, elective surgical patients who receive packed red cells experience a coagulation factor deficit as the initial abnormality in clinical hemostasis.

Original languageBritish English
Pages (from-to)336-342
Number of pages7
JournalAnesthesia and Analgesia
Issue number2
StatePublished - 1995


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