///2017 Abstract Details
2017 Abstract Details2019-08-02T15:54:53-05:00

Can Amniotic Fluid Embolism (AFE) Occur without Hypoxia? A Case of Atypical AFE Presentation.

Abstract Number: SUN-57
Abstract Type: Case Report/Case Series

Corrie A Burke MD1 ; Heather C Nixon MD2

Amniotic fluid embolism (AFE) is a rare but life-threatening complication of childbirth. As such, AFE is a leading cause of maternal death and is typically characterized by a two-phase response; the first phase is defined by acute respiratory failure (83-93%) and cardiac collapse(100%), and the second phase is characterized by coagulopathy and uncontrolled bleeding (83-100%). AFE presenting with severe coagulopathy and uterine atony without concomitant or limited respiratory compromise is rare. Such atypical presentation has been referred to as disseminated intravascular coagulopathy-type AFE, and may be difficult to diagnose.

An otherwise healthy 39 yo G1P0 at 38+1 weeks gestational age, was admitted in spontaneous labor and received a CSE for labor analgesia. Despite successful neuraxial placement and adequate sensory level, the patient continued to have lower abdominal pain. Due to nonreassuring fetal heart tones, the decision was made to proceed with an urgent primary cesarean delivery. Lidocaine with epinephrine was epidurally administered for surgical anesthesia, however, the block was inadequate. Fetal deceleration necessitated general anesthesia; rapid sequence induction and intubation were performed uneventfully. Following fetal delivery, the patient became extremely hypotensive and phenylephrine and epinephrine boluses were given. The surgical field did not reveal bleeding and uterine tone was deemed sufficient. Following skin closure, examination revealed additional vaginal bleeding (1.6L); uterotonic agents were administered. Bleeding continued (3L) despite good uterine tone and a Bakri Balloon was placed as the abdomen was noted to be enlarging. The patient continued to require fluid and pressor support. Laboratory values were consistent with consumptive coagulopathy. PT 20.4 sec, PTT 42 sec, INR 1.8, FBG 108 mg/dl, and platelet count 95,000/mm3. ABG was consistent with anion gap metabolic acidosis; p02 was 158 mmHg on 100% O2 administration. Following aggressive fluid and blood resuscitation, an emergency laparotomy was performed to evacuate a diffuse abdominal hematoma. The patient received a total of 17U pRBCs, 14U FFP, 6U cryoprecipitate, and 2U platelets, with a total EBL of 14.7L. She was stabilized and taken to ICU. On POD#2, uterine artery embolization was performed. Her labs normalized and she was discharged on POD#6.

While the etiology of AFE is unknown, it is speculated to be caused by a localized anaphylactoid reaction that usually leads to pulmonary vasospasm with platelet and complement system activation. Initial signs of hypoxemia and bronchospasm that usually accompany AFE may be masked in an intubated patient receiving supplemental O2 and early administration of epinephrine for hypotension. This case highlights the challenges of diagnosing AFE in a patient receiving general anesthesia for cesarean delivery.

J Obstet Gynaecol Res. 2016 Dec;42(12):1881-1885.


SOAP 2017