DIC in Obstetrics: Etiology

Pregnancy creates a physiological hypercoagulable state through increased fibrinogen (rises to 400-600 mg/dL by term), elevated factors VII, VIII, X, and von Willebrand factor, decreased protein S activity, and increased plasminogen activator inhibitor-1 and -2 (PAI-1, PAI-2). This prothrombotic milieu prepares the hemostatic system for placental separation at delivery but also predisposes to DIC when triggered by obstetric complications. Obstetric DIC triggers include: 1. Placental abruption (most common obstetric cause of DIC): premature separation of the placenta from the uterine wall releases massive amounts of tissue factor from damaged placental tissue and decidua into the maternal circulation. The retroplacental clot consumes clotting factors locally. The severity of DIC correlates with the extent of placental separation — a >50% abruption frequently causes overt DIC. 2. Amniotic fluid embolism (AFE): amniotic fluid containing fetal squamous cells, lanugo, vernix, and tissue factor enters the maternal circulation through disrupted uteroplacental membranes. AFE is an anaphylactoid syndrome causing sudden cardiovascular collapse (hypotension, hypoxia, cardiac arrest), followed rapidly by DIC in >80% of cases. Mortality exceeds 60%. 3. HELLP syndrome (Hemolysis, Elevated Liver enzymes, Low Platelets):...