A coagulation Factor V inhibitor developed in a man 75 yr of age in association with an anaplastic malignancy and drug treatment (including the aminoglycoside antibiotic, gentamicin). The patient did not bleed abnormally, despite both surgical challenge and plasma Factor V activity of <1%. The inhibited plasma had grossly prolonged prothrombin and activated partial thromboplastin times, but a normal thrombin time. Mixing studies indicated progressive coagulation inhibition with normal plasma, but not with Factor V-deficient plasma, and reversal of coagulation inhibition by the addition of bovine Factor V to the patient's plasma. 1 ml of patient plasma inhibited the Factor V activity of 90 ml of normal human plasma. The inhibitor was isolated by sequential affinity chromatography on protein A-Sepharose and Factor V-Sepharose. The IgG isolate markedly inhibits the activity of prothrombinase assembled from purified Factors Xa and Va, calcium ion, and phospholipid vesicles, and partially inhibits prothrombinase assembled from purified Factor Xa, calcium ion, and normal platelets. The Factor V of platelets, however, appears relatively inaccessible to the antibody, inasmuch as platelets isolated from whole blood supplemented for 8 h with the antibody functioned normally with respect to platelet Factor V-mediated prothrombinase function. The absence of obvious hemorrhagic difficulties in the patient, the total inhibition of plasma Factor V by the inhibitor, and the apparent inaccessibility of platelet Factor V to the inhibitor specifically implicate platelet Factor V in the maintenance of hemostasis.
Significant hemostatic abnormalities can occur during orthotopic liver transplantation (OLT). This study addressed three goals: 1)evaluation of the hemostatic mechanism at each stage of the OLT; 2) the relationship of the coagulation process with the thrombelastograph (TEG); and 3) comparison of results in patients requiring retransplantation or who died, with the overall pattern. To evaluate hemostasis during 50 consecutive OLTs, a detailed coagulation and TEG study was done. The surgical procedure was divided into the following stages: Stage I--induction of anesthesia to occlusion of blood flow to the patient’ s diseased liver; Stage II—occlusion of blood flow to the patient’ s diseased liver to reperfusion of the patient’ s new liver; and Stage III—reperfusion of the new liver until skin closure. 28 ml of arterial blood were sampled at the beginning and end of each stage and up to five days posttransplantation for the following: platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, prothrombin, factors V, VII, IX, and X, plasminogen, antiplasmin, antithrombin III (functional and immunologic), fibrinolytic split products, and TEG. The patient’ s core temperature and amount of blood products transfused were obtained intraoperatively during each of the six data times. The ischemia time of the donor liver was recorded. Significant hemostatic abnormalities developed during each of the 50 OLTs, especially during reperfusion of the donor liver. In some instances, this was corrected within one hour, but platelet counts continued to fall, and a number of coagulation factors rebounded only partially. The TEG values correlated with laboratory data and blood loss, but the correlations were not strong. The patient’ s requirement for red cells varied with the operative drop in temperature; however, the donor liver ischemia time and length of Stage II made no significant difference. It is concluded that 1) significant deterioration of coagulation factors occurs during OLT, 2) the TEG is an effective screening test that affords prompt information, 3) aggressive measures should be taken to maintain the patient’ s body temperature at 37°C, 4) patient outcome was not predicted by intraoperative hemostatic evaluation.
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