A 38-year-old G₁P₀ woman was admitted at 38⁺⁵ weeks of gestation for an elective cesarean section. Upon admission, the patient exhibited stable vital signs and no labor pains, with the fetus presenting in a cephalic position and in a normal state. On the day of surgery at 08:00 AM, she underwent a lower uterine segment cesarean section. Five minutes after the birth of a vigorous 3700 g infant, the patient experienced a choking cough, followed by an acute drop in oxygen saturation to 86%, accompanied by transient loss of consciousness. Her blood pressure fell transiently to 71/41 mmHg, raising suspicion for AFE. Other potential causes of acute cardiopulmonary instability, including pulmonary thromboembolism, anaphylaxis, air embolism, and anesthetic-related complications, were considered; however, the abrupt onset during delivery combined with early coagulopathy and hypofibrinogenemia supported a diagnosis of amniotic fluid embolism. She was administered intravenous dexamethasone (20 mg push and 40 mg drip), along with norepinephrine infusion and endotracheal intubation to stabilize her blood pressure and oxygen levels. Although the estimated blood loss during the cesarean section was 400 ml, which is within the normal range, bilateral ligation of the uterine arteries was performed, and uterotonics were administered due to signs of a slightly atonic uterus. The patient was subsequently transferred to the intensive care unit (ICU) for further monitoring and management, with blood tests for complete blood count and coagulation function initiated.

Two hours post-surgery (11:00 AM), the patient exhibited increasing vaginal bleeding, with an additional loss of 360 ml without clots. Laboratory tests indicated a mild decrease in hemoglobin from 116 g/L prior to surgery to 101 g/L, prolonged clotting time (international normalized ratio (INR) 1.21), and a significant reduction in fibrinogen level from 4.93 g/L before surgery to 1.34 g/L. D-dimer, indicative of fibrinolytic system activation, increased to 31.20 mg/L, respectively. Rapid fibrinogen decline of <1.5g/L, prolonged INR of >1.2 and increasing vaginal bleeding were considered indicative of early coagulopathy in suspected AFE and served as the trigger for simultaneous bundle transfusion prior to massive hemorrhage. A multidisciplinary team comprising obstetricians, anesthesiologists, hematologists, and ICU staff initiated aggressive supportive care, including a transfusion strategy comprising 1 g of tranexamic acid, 4 g of fibrinogen, 800 IU of human prothrombin complex, 10 units of cryoprecipitate, 800 ml of frozen plasma, and 8 units of packed red blood cells. In addition to uterotonics, digital subtraction angiography followed by uterine artery embolization was employed to manage the postpartum hemorrhage. Although these therapies have no function to treat coagulopathy, they help reduce the speed of bleeding loss, which gives us time to correct coagulation dysfunction, thereby halting the development of DIC.

By 17:00 PM, the fibrinogen level had increased to 2.23 g/L, and the D-dimer level decreased to 9.97 mg/L, with clotting time returning to the normal range (INR 1.02), indicating a successful rescue from coagulopathy. Figure 1Figure 1 summarizes the time course and progression of Case 1. The pregnant woman stayed in the ICU for one day, and extubation was conducted after her consciousness and blood pressure recovered to normal. She was discharged 5 days after birth, without later bleeding or thrombotic events.

A 36-year-old G₂P₁ woman was admitted at 40⁺² weeks of gestation, complaining of irregular uterine contractions without labor progress. She was admitted for induction of labor by COOK cervical dilatation balloon the previous night (18:00 PM), followed by artificial rupture of membranes (7:20 AM) and oxytocin intravenous infusion (9:20 AM) on the following day. At 18:00 PM the contraction interval was 3 minutes, and the fetal heart rate monitoring showed frequent early deceleration; the oxytocin intravenous infusion was stopped. The contraction remained strong, and the fetal head began to decrease. At 20:10 PM, the woman suddenly presented with trembling and a transient increase in heart rate of 170 bpm, but rapidly returned to 110 bpm, and the blood pressure was in the normal range. Considering the unstable state of the woman, intravenous dexamethasone 10mg push was given in case of AFE, and emergent cesarean section was arranged after informed consent. The surgery (21:00-21:50 PM) was smooth, and the blood loss was 300 mL, which was in the normal range. Since the coagulation test before surgery (20:50 PM) showed an increased level of D-dimer to 21.06 mg/L, it was retested at 23:00 PM. At 1:07 AM, we were informed of the dramatic decrease in fibrinogen to 0.96 g/L and prolonged clotting time (INR 1.39). Vaginal bleeding without clot was presented, leading to a total of 545 mL blood loss after surgery. The marked hypofibrinogenemia state of <1g/L, prolonged INR of 1.2, and non-clotting bleeding were considered indicative of coagulopathy and served as the trigger for immediate bundle transfusion. A strategy of simultaneous transfusion, including 1 g of tranexamic acid, 4 g of fibrinogen, 800 IU of human prothrombin complex, 6 U of cryoprecipitate, 400 ml of fresh frozen plasma, and 2 units of packed red blood cells, was conducted to give aggressive support to the patient. Differential diagnoses such as uterine atony–related hemorrhage, placental abruption, sepsis, and thromboembolic events were evaluated, but were considered less likely given the preceding transient cardiopulmonary instability and disproportionate coagulation abnormalities. Uterine massage, oxytocin drip, and prostaglandins were also used to strengthen uterine contractions. At 4:30 AM, the fibrinogen increased to 2.15 g/L, and the clotting time returned to the normal range (INR 1.11), which indicated a relief of AFE. Figure 1Figure 1 presented the time course and progression of Case 2. The woman was discharged 4 days after cesarean section, without other complications including later bleeding or thrombotic events.

Figure 1. The time course and clinical progression of the two cases.