Amniotic fluid embolism (AFE) triggers disseminated intravascular coagulation (DIC) through a two-phase pathological cascade. In Phase 1, amniotic fluid containing fetal squamous cells, lanugo hair, vernix caseosa, mucin, and tissue factor enters the maternal circulation via disrupted endocervical veins, placental implantation site, or uterine lacerations. This material activates the extrinsic coagulation pathway: fetal tissue factor binds Factor VII, forming the TF-VIIa complex that activates Factor X, generating massive thrombin (Factor IIa). Simultaneously, amniotic fluid activates complement (C3a, C5a) and triggers an anaphylactoid immune response with mast cell degranulation, histamine release, and leukotriene production, causing acute pulmonary vasospasm, right ventricular failure, and cardiovascular collapse. In Phase 2, the consumptive coagulopathy develops: widespread microvascular thrombi consume circulating fibrinogen, platelets, and clotting factors (V, VIII, XIII) faster than the liver can replace them. Secondary fibrinolysis activates as plasmin breaks down the deposited fibrin, generating elevated D-dimer and fibrin degradation products (FDPs) that further inhibit fibrin polymerization and platelet aggregation, creating a vicious cycle of coagulation failure. The resulting DIC produces simultaneous thrombosis (organ ischemia) and hemorrhage (coagulation factor depletion). Thromboelastography (TEG) or rotational...