///2009 Abstract Details
2009 Abstract Details2019-08-03T15:55:31-06:00

Profound Hemorrhage in a Parturient with Placenta Previa and Percreta Complicated by Amniotic Fluid Embolism and Disseminated Intravascular Coagulation

Abstract Number: 87
Abstract Type: Case Report/Case Series

Scott Harter M.D.1 ; Ed Riley M.D.2


We present a case of severe maternal hemorrhage in a parturient with ultrasound evidence of placenta previa and placenta percreta. The parturient underwent an emergent cesarean section and hysterectomy that was complicated by amniotic fluid embolism (AFE), disseminated intravascular coagulation (DIC), cardiac arrest, and death.


A 38-year-old parturient at 32 weeks gestation with an ultrasound diagnosis of placenta previa and percreta started bleeding at home prior to direct transport to our labor and delivery unit. Initial exam was significant for profuse vaginal bleeding, normal blood pressure, and tachycardia. The institutions massive transfusion protocol (MTP) was initiated and the parturient was taken to the operating room.

Anesthesia was induced with a rapid sequence induction. The airway was secured with an endotracheal tube. Anesthesia was maintained with sevoflurane, oxygen, and nitrous oxide. Two 14-gauge peripheral IVs and a right radial arterial line were placed. Blood products were infused rapidly during the entire surgery in a ratio of 10 units of PRBCs to 6 units of FFP to 1 unit of pooled platelets per the MTP.

Cesarean section was performed and a viable baby was delivered. The obstetricians confirmed placenta percreta and a hysterectomy commenced. Labs showed d-dimers increasing, fibrinogen decreasing, and platelets decreasing. EBL was over 4 liters with the rate of loss increasing. Cryoprecipitate and recombinant factor 7 were administered. A thromboelastogram showed no clot activity. Bleeding began outside the surgical field in the upper abdomen and a large retroperitoneal hematoma was noted. The parturient developed a wide-complex arrhythmia that deteriorated into ventricular tachycardia, ventricular fibrillation, and then asystole. ACLS algorithms were judiciously employed without success.


This catastrophic case of maternal hemorrhage was multifactorial in etiology. Bleeding due to placenta previa and percreta was compounded by the profound coagulopathy related to the AFE that was confirmed by placental pathology post-mortem. The MTP, a strategy designed by trauma researchers for product replacement from severe hemorrhage, was unable to overcome the coagulopathy related to the AFE. The obstetric anesthesiology team administered at total of 66 units PRBCs, 40 units FFP, and 10 units pooled platelets during the resuscitation. Despite holding MAP between 70-80mmHg over the entire surgery, the profound coagulopathy could not be reversed. However, prior to arrest the parturient had a stable blood pressure, the acid-base status was improving, and electrolytes were not wildly out of range. It is unclear whether the parturient died of hypovolemia, metabolic derangement, or a primary cardiac event secondary to the AFE. This case demonstrates that despite attempts to correct the parturients coagulopathy, hypovolemia, and metabolic status, an AFE can still be lethal.

SOAP 2009