An in-Depth Look at Amniotic Fluid Embolism
Published: 03 March 2021
Published: 03 March 2021
Amniotic fluid embolism (AFE) is a rare, potentially fatal, acute and unexpected birth complication that can affect both the mother and fetus. AFE occurs when amniotic fluid enters the maternal circulatory system and causes an allergic-like reaction (AFE Foundation 2018).
Defined as a two-phase response, AFE is characterised initially by rapid respiratory failure that can then progress to cardiac arrest. The second phase is the haemorrhagic phase where the mother experiences profuse bleeding at the wound site (usually the site of placental attachment or caesarean incision). Disseminated intravascular coagulopathy (DIC) (also known as consumptive coagulopathy) then develops, which prevents blood clotting. DIC requires urgent transfusions of blood and blood products (AFE Foundation 2018).
AFE typically presents during labour, or around the time of delivery. Warning signs include a sudden onset of dyspnoea and hypotension, which are often followed by cardiovascular collapse and respiratory arrest. AFE has also been known to occur on rare occasions during first and second-trimester abortions, as late as 48 hours postpartum and following amniocentesis or uterine trauma.
AFE usually develops rapidly with early warning signs that could include:
This may then lead to more serious symptoms including:
(AFE Foundation 2018)
According to Kaur et al. (2016), four specific criteria must be present to make the diagnosis of AFE. These are:
Diagnosis of AFE is usually made in the absence of other causes. In other words, it is a diagnosis of exclusion made only when all other possible clinical explanations for the symptoms have been ruled out(AFE Foundation 2018).
AFE was originally diagnosed only on post-mortem based on the presence of fetal material found in the vasculature of the lungs, but this is no longer considered a valid diagnostic method (AFE Foundation 2018).
Although there is still a great deal of uncertainty about the risk factors related to AFE, international studies suggest that cases may be linked to the induction of labour and maternal age.
Placenta praevia and placental abruption also appear to increase the risk 3 to 10-fold (Payne 2015). Data from the UK also suggests there may be an increased risk of AFE in older women of an ethnic minority. There is also a possible link between postnatal AFE and caesarean delivery.
Kaur et al. (2016) note that AFE is considered both unpredictable and unpreventable with an unknown cause, which makes risk assessment an almost impossible task. It can occur in healthy patients during labour, during caesarean section, after abnormal vaginal delivery or even during the second trimester of pregnancy (Kaur et al. 2016).
Risk factors include:
(Kaur et al. 2016)
Given that AFE cannot be prevented or reversed, treatment of the mother is entirely supportive, focusing on managing individual symptoms as they occur (AFE Foundation 2018).
The initial goal of treatment is to correct hypoxaemia and hypotension so that ischaemic consequences of collapse can be avoided. Multiple blood, plasma and platelet transfusions are usually given, and as a last resort, an emergency hysterectomy may be required to stop the source of the bleeding. In most cases, prompt delivery is indicated to prevent fetal asphyxia and improve neonatal outcome when AFE occurs before birth.
Even though the diagnosis of AFE may be confused with other causes of collapse, effective resuscitation based on the ABCs of adult life support remains the fundamental treatment regardless of the cause (Payne 2015).
Despite the severity of this condition, survival after AFE has improved significantly in recent years due to early recognition of the syndrome along with prompt and early resuscitation.
Previous records suggest that 50% of patients die within the first hour of developing AFE and about two-thirds within five hours of the event, with a high incidence of severe and permanent neurological damage among survivors (Kaur et al. 2016).
Payne (2015) offers slightly more optimistic statistics, suggesting that among those who survive, 25% die within the first hour and most of the remainder within nine hours after presentation. Today, although mortality rates have declined, morbidity remains high with most patients having a poor prognosis.
According to Clark (2010), AFE is 'an enigmatic, but devastating obstetrical condition associated with significant maternal and newborn morbidity and mortality'. Although the true incidence of AFE is unknown due to inaccurate diagnosis and inconsistent reporting of nonfatal cases, it is still considered to be the fifth leading cause of direct maternal mortality in both the UK and Australia (Payne 2015).
Roberts et al. (2010) report on a mortality rate of 0.33 per 100,000 pregnancies and a maternal fatality rate of 35%. Knight et al. (2010) suggest there is a slightly lower incidence in the UK, with an estimated incidence of 2.0 cases per 100,000 deliveries and an estimated fatality rate of 20%.
Either way, maternal mortality due to AFE remains high, and patients who do survive often experience significant morbidity due to cerebral hypoxia (Plymouth NHS Trust 2020).
Although AFE cannot be prevented, early diagnosis and intervention may lead to better outcomes for both the mother and the fetus. Balinger (2015) speaks about an evolving array of novel biomarkers that may help differentiate AFE from other conditions, but none of them currently provide enough early warning to make any real-time impact on diagnosis or treatment.
Even so, as the Amniotic Fluid Embolism Foundation (2018) note, it’s also the case that many labouring women have amniotic fluid or fetal debris enter into their circulatory system and don’t suffer a catastrophic response.
As tragic as this condition is, it remains, for the most part, a mystery that can be neither predicted nor prevented.