Join now to get access to this content and more.
Become a SOAP member and have access to our benefits.
- 2020 SOAP Virtual Meeting Series Videos
- For Review: SOAP Consensus Statement on Neuraxial Procedures in Thrombocytopenic Parturients
- Sample Centers of Excellence Applications
- ASA Corner
- SOAP Policy and Procedure Manual (P&P Manual)
- SOAP Expert Opinions
- SOAP's Learning Modules
- 2019 Annual Meeting Lecture Videos
- December 2018 - SOAP Unofficial Guide to ASA Committees Webinar
- Submit a Position
- View Job Postings
- Previous Meeting Archives
- Previous Meeting Abstract Search
- CMS Guidelines
- Member Benefits
- Newsletter Clinical Articles
- ACOG Documents
- Search our Patient Safety Archive
- Ask SOAP a Question
- Global Health Opportunities
- And more…
Delayed Presentation of Amniotic Fluid Embolism - 2 Days Postpartum
Abstract Number: RF3AC-210
Abstract Type: Case Report Case Series
Amniotic fluid embolism (AFE) is a life-threatening obstetric emergency that is rare but deadly with high mortality rate1. Thought to be due to abnormal proinflammatory response to amniotic debris in maternal circulation, most case reports depict AFEs occurring in laboring and immediate postpartum patients2,3. We present an unusual case of AFE that occurred 46 hours postpartum.
33-year-old G1P0 at 39w1 had spontaneous vaginal birth following induction of labor for severe preeclampsia. Her course was complicated by labial hematoma requiring vaginal packing, but CT scan did not reveal active extravasation. She was hemodynamically stable, afebrile throughout, and packing was removed subsequently. She received Cefoxitin for 24 hours post procedure.
46 hours postpartum, patient reported sudden onset of shaking and shortness of breath while breastfeeding. She was tachycardic, tachypneic, and O2Sat 97% on 2L NC. Within minutes, she became progressively altered, with thready pulse and wheezing requiring urgent intubation. Shortly after, she experienced pulseless electrical activity (PEA) arrest with evidence of disseminated intravascular coagulation (DIC). Despite 85 minutes of ACLS and massive transfusion protocol, patient expired.
Postmortem autopsy did not demonstrate pulmonary emboli, tamponade, coronary occlusions, internal hemorrhage, stroke or anaphylactic edema. Emboli of amniotic fluid squamous cells were not seen. No bacteria in specimen and 16S ribosomal RNA sequencing was also negative. Furthermore, there was no sign of labial purulence or fasciitis, and placenta showed no signs of infection.
The diagnosis of AFE remains clinical and that of exclusion, after eliminating other potential causes of maternal cardiopulmonary and hemostatic derangement4. Typical presentations of AFE include sudden onset cardiorespiratory compromise, DIC, and seizure that can rapidly progress. Amniotic debris is ubiquitously present in all maternal circulation, therefore, AFE occurs in at risk mom-fetal pair5. What is unclear, however, is how long fetal/amniotic tissue remains in maternal circulation. Furthermore, it’s unknown if vaginal manipulation for packing triggered proinflammatory response that then lead to this delayed presentation of AFE 47 hours postpartum.
1. Morau, E. Amniotic fluid embolism. Prat. en Anesth. Reanim. 22, 264–268 (2018).
2. Clark, S. L., et al. Amniotic fluid embolism: Analysis of the national registry. Am. J. Obstet. Gynecol. 172, 1158–1169 (1995).
3. Bonnet, M. P. et al. Maternal Death Due to Amniotic Fluid Embolism: A National Study in France. Anesth. Analg. 126, 175–182 (2018).
4. Kobayashi, H. et al. Comparison of the different definition criteria for the diagnosis of amniotic fluid embolism. J. Clin. Diagnostic Res. 11, (2017).
5. Dildy, G. A., Belfort, M. A. & Clark, S. L. Amniotic Fluid Embolism Historic considerations. (2019).