To estimate the frequency of disseminated intravascular coagulation (DIC); elucidate the genesis of hemostatic dysfunction; and characterize associated hemolysis in women with acute fatty liver of pregnancy.
Hemostatic function was measured in 51 women. Disseminated intravascular coagulation was assessed using the International Society of Thrombosis and Haemostasis DIC score. Hepatic and hemostatic function was quantified with measurement of fibrinogen, fibrin–fibrinogen split products, cholesterol, and coagulation testing. As a comparison of fibrinogen synthesis, these women were compared with 25 women with placental abruption. Hemolysis was assessed indirectly by quantification of reticulocytosis and nucleated red blood cells with determination of erythrocyte morphotypes.
Eighty-percent of women were classified as having unequivocal DIC (mean score 5.9±1.8) at delivery, which persisted 4–5 days postpartum. Fibrinogen regeneration with placental abruption was rapid, whereas it remained depressed for 4–5 days with acute fatty liver of pregnancy; fibrin–fibrinogen split products were also cleared more rapidly after abruption than women with acute fatty liver (P<.001 for interaction for both using random effects modeling). Kaplan-Meier survival analysis of fibrinogen recovery to a set point of 280 mg/dL after delivery was also different between the two cohorts (median 1.7 compared with 4.2 days, P=.046). Continuing hepatic dysfunction with acute fatty liver of pregnancy was exemplified by diminished procoagulant production. Reticulocytosis, nucleated red blood cells, and elevated serum bilirubin levels reflected ongoing hemolysis.
Hemostatic dysfunction with acute fatty liver of pregnancy persists 4–5 days postpartum and results from substantive ongoing DIC in concert with reduced procoagulant synthesis and clinically significant hemolysis.
Hemostatic dysfunction related to acute fatty liver of pregnancy results from substantive ongoing consumptive coagulopathy accompanied by reduced procoagulant synthesis and hemolysis.
University of Texas Southwestern Medical Center at Dallas, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, Dallas, Texas.
Corresponding author: David B. Nelson, MD, Division of Maternal-Fetal Medicine, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75390-9032; e-mail: DavidB.Nelson@UTSouthwestern.edu.
Financial Disclosure The authors did not report any potential conflicts of interest.