A CATASTROPHIC COMPLICATION OF PREGNANCY. You can also think of this condition as anaphylactoid syndrome of pregnancy (ASP) - this is the preferred term. This is a rare (1 in 40k deliveries) but sometimes fatal condition where varying material from the fetal compartment enter maternal circulation. The disruption of the fetal/maternal interface can be a normal phenomenon, but some mothers have a systemic inflammatory response. This is not isolated to just amniotic fluid either, it could also be related to any kind of fetal debris - think hair (lanugo), and/or meconium entering her bloodstream - which then kicks off a series of detrimental cascades. Of note, this condition has been documented in both vaginal and c-section deliveries. What scares me the most is that it is unpreventable and unpredictable. 40% of AFE patients will NOT survive. That certainly gets my attention.
The typical presentation of amniotic fluid embolism is very dramatic, and many times the mother will feel a sense of doom and have an altered mental status, additionally, AFE includes a triad of sudden hypoxia and hypotension, followed in many cases by coagulopathy, all occurring in relation to labor and delivery. The diagnosis of amniotic fluid embolism is clinical, based on the presence of these elements and the exclusion of other likely causes. Amniotic fluid embolism should be considered in the differential diagnosis in any pregnant or immediately postpartum woman who suffers sudden cardiovascular collapse or cardiac arrest, seizures, severe respiratory difficulty, or hypoxia, particularly if such events are followed by a coagulopathy that cannot be otherwise explained.
The respiratory failures can lead to acute RV failure first and ultimately complete cardiovascular collapse with LV involvement and pulmonary edema which complicates matters even more. The coagulopathy I mentioned before manifests itself into systemic fibrin clot formation and DIC which leads to tissue hypoxia, bleeding and in the worst cases irreversible end organ damage and failure. As you can imagine mortality and morbidity for mom is extremely high.
When ASP occurs after birth, effects on the neonate are minimized; however, ASP can also occur during labor. Fetal distress during labor can be a presenting sign of ASP, seen as changes in the fetal monitoring strips showing late decelerations and bradycardia. Early recognition is the key to positive outcomes for both patients. While I realize our diagnostic tools around fetal monitoring may be limited in the field -- our detailed physical assessment of the mother can tell us a lot.
Some quick things you can be on the look for regarding diagnostic criteria include:
Sudden onset of cardiopulmonary arrest or both hypotension and respiratory compromise
Documentation of overt disseminated intravascular coagulation after appearance of initial signs and symptoms
Clinical onset during labor or within 30 minutes of passing of placenta
No fever during labor
In addition, the above don't forget to include things like as part of your differential diagnosis -- don't get tunnel vision.
Hemorrhagic shock - postpartum hemorrhage is very real and much more common than AFE
Sepsis
PE - remember moms have produced more clotting factors as a protective mechanism around delivery related blood loss. They are in a hypercoagulable state - this is normal
Eclampsia
Placental abruption or uterine rupture
Myocardial infarction
Actual anaphylaxis - treat as you normally would with IM Epi
Our goals in the back of the ambulance are mainly supportive in nature. Maintain mom's oxygenation status and if her condition worsening into full cardiac arrest - utilize your ACLS skill set. In the hospital a large group of moms may even be put on ECMO at some time during their clinical course... yes, they are that sick. Some research from a few years ago suggest that at the onset of symptoms, the initiation of the therapeutic regimen of atropine, ondansetron, and ketorolac has been shown to cause reversal of symptoms. It has been suggested that the atropine and ondansetron inhibit serotonin and vagal stimulation, thus improving cardiovascular function and systemic vascular tone, improving cardiac output and hypotension. Ketorolac is used to inhibit thromboxane and block the cause of the coagulopathy. Atropine, Ondansetron, and Ketorolac A-OK for short! I realize you may not have established protocols on this condition and the above regimen is strictly for educational and informative purposes. Nothing here will supersede or trump your own local patient care guidelines. Your medical director approved protocols are what you should be following in your daily practice of pre-hospital medicine.
If you'd like to find out more on this topic, I encourage you to visit: AFE Research and Education for Clinicians - Amniotic Fluid Embolism Foundation
January 27, 2025
Author: Joshua Ishmael, MBA, MLS(ASCP)CM, NRP
Pass with PASS, LLC
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