Amniotic Fluid Embolism:

Latest Concepts and Current Research

This site is intended to provide background on Amniotic Fluid Embolism and give readers information about on-going research about this leading cause of maternal mortality in developed countries.

Frequently Asked Questions


1.         What is the fatality rate of Amniotic Fluid Embolism?

            The answer depends on the study but varies from a low of roughly 20% to a high of 90%.  Although the literature is fairly consistent on the clinical definition of amniotic fluid embolism, the disease is uncommon so that the nuances of diagnosis are often unknown to obstetricians.  Although estimates of mortality have steadily declined over the past 80 years, there remains a widespread perception that if a patient survives, whatever she had is not truly amniotic fluid embolism.  In a recent paper from Japan, 70 patients out of 135 succumbed (just over half).[1]

            At least as important, is the rate of permanent injury/disability for both mother and baby.  Unfortunately, there is much less information on these issues, particularly as long-term follow-up outside of the hospital would be required.  It is clear that among survivors, full recovery is not always the case and some women have permanent sequalae.


2.         Is Amniotic Fluid Embolism preventable or predictable?

            In short, the answer is no.  As would be expected without a molecular mechanism, it is not possible to predict or prevent the disease.  Even so, there is a fairly robust literature on “risk factors.”  These studies are very problematic  for two types of reasons.  First, these studies are inevitable retrospective examinations of clinical associations with the disease.  Commonly, cesarean section is seen as a risk factor, which makes a certain amount of sense, since the procedure involves opening the uterine wall which could allow greater entrance of fetal material into the maternal circulation.  Unfortunately an association in time and place does not prove a cause and effect relationship.  It is quite possible that Cesareans are associated with AFE because Cesarean delivery is actually a treatment for fetal bradycardia, uterine atony, and cardiac arrest—all possible consequences of the disease in the first place. 

            The second problem with studies that look for risk factors in AFE is the inconsistent nature of the diagnosis.  Again, although the literature is consistent in describing the clinical diagnosis, this consistency and understanding is not necessarily uniform among obstetricians.  As a result, investigators have to rely on diagnoses made by a large group of individual doctors—which introduces another, and difficult to quantify variable.  Perhaps this is best demonstrated in two studies with a common author that looked at the diagnosis of AFE in two separate populations of 3,000,000 North American Women.[2],[3]  One study found a relationship between the administration of oxytocin to induce/augment labor, while the other did not.  Two studies of millions of pregnancies on the same continent, with the same methodology:  opposite conclusions.

            The problem inherent in confusing association in time and place with cause and effect, together with the inconsistency of applying the diagnosis among obstetricians make all assertions about “risk factors” scientifically suspect.  It is in part for this reason that the emphasis in the research described on this web-site is hypothesis driven, rather than focused on looking at clinical associations to gain insight on causation.


3.         Is there specific treatment for AFE?

            No.  Treatment is directed at addressing the clinical manifestation—respiratory arrest, hemorrhage, etc.  Again the lack of a molecular basis for disease is quite limiting.


4.         What about future pregnancies in those who survive AFE?

            The answer is not what might be expected.  There are several case reports of women who have survived AFE and have had unaffected subsequent pregnancies.   In contrast, there are no reports of subsequent AFE in survivors.  Although the best evidence points to an immunologic cause, the little data that is available do not support increased risk for survivors.  It is important to note that with small numbers of reported pregnancies, and probable incomplete reporting of all pregnancy outcomes in survivors, substantial increased risk has not be excluded.  At the very least, it is probably safe to conclude that a reoccurrence in future pregnancies is not inevitable.


5.         Are there specific laboratory tests that specifically confirm the diagnosis of AFE?

            With the exception of finding fetal material in the maternal pulmonary vasculature at autopsy, the answer is no.  There is not yet enough evidence to support using Complement either as confirmation or refutation of the diagnosis.

[1] Oi H, Naruse K, Noguchi T, et. al.  Fatal Factors of Clinical Manifestations and Laboratory Testing in Patients with Amniotic Fluid Embolism.  Gynecol Obstet Invest.  2010;  70:  138-44.

[2] Kramer MS, Rouleau J, Baskett TF, Joseph KS; Maternal Health Study Group of the Canadian Perinatal Surveillance System. Amniotic fluid embolism and medical induction of labour:  a retrospective, population-based cohort study. Lancet 2006; 368:1444-8.

[3] Abenhaim HA, Azoulay L, Kramer MS, Leduc L. Incidence and risk factors of amniotic fluid embolisms: a population-based study on 3 million births in the United States. Am J Obstet Gynecol 2008; 199: 49.e1-8.