Amniotic fluid embolism (AFE) has traditionally been estimated to occur in 1 in 8000 to 1 in 80,000 deliveries, the wide range reflecting the difficulty in its accurate diagnosis. More recent evidence suggests an incidence in the UK of ~2 in 100,000 births. Despite its rarity, AFE has been implicated in 10-12% of direct maternal deaths in the UK, making it one of the major causes of mortality; it is ranked as the fifth leading cause of direct maternal death in the 2018 report of the Confidential Enquiries into Maternal Deaths.
The traditional explanation of AFE is that amniotic fluid enters the maternal circulation following forceful contractions, causing embolic obstruction similar to thromboembolism. However, the mechanism now proposed is systemic release of inflammatory mediators causing cardiovascular collapse, although the trigger for mediator release is still disputed (amniotic fluid, meconium, fetal cells or other substances all having been suggested). The role of amniotic fluid itself is uncertain, since infusion of amniotic fluid may be well tolerated experimentally. The UK Obstetric Surveillance System (UKOSS) has reported that AFE is associated with increased maternal age, induction of labour and multiparity, and is seen more in women from ethnic minorities. Although AFE is most common during labour, it may also occur during caesarean section or even after delivery.
Problems and special considerations
Features of AFE include cardiovascular collapse with left ventricular failure, respiratory failure secondary to pulmonary hypertension and ventilation-perfusion mismatch, and disseminated intravascular coagulation (DIC). Thus symptoms may include dyspnoea, cyanosis and haemodynamic collapse or non-specific complaints including sweating, shivering, convulsions and unexplained fetal compromise (in 20% of cases). Collapse is typically profound, rapid and resistant to treatment; thus the initial problem of AFE is its immediate management.
In addition, there are many causes of sudden collapse (see Chapter 80, Collapse on the labour ward), and it may be difficult to diagnose the underlying condition. Although the diagnosis of AFE is often based on the demonstration of fetal squames in the maternal circulation or lung, this has been shown to be neither a sensitive nor a specific test, since normal mothers may demonstrate circulating fetal squames while ‘classic’ cases of AFE may not. For reporting purposes to UKOSS, the diagnostic criteria include:
• The absence of an alternative clear cause, and either
- Acute maternal collapse with one or more of the following features: acute fetal compromise; cardiac arrest; cardiac rhythm problems; coagulopathy; hypotension; maternal haemorrhage; premonitory symptoms, e.g. restlessness, numbness, agitation, tingling; seizures; shortness of breath, or
- The finding of fetal squames or hair in the lungs of women at post-mortem.
Women with maternal haemorrhage as the first presenting feature in whom there was no evidence of early coagulopathy or cardiorespiratory compromise are excluded.
A final problem - and one that hinders development of effective methods of prevention and treatment - is the debate over the nature of AFE itself, even whether it represents a separate entity at all (the term ‘sudden obstetric collapse syndrome’ has been suggested as being more appropriate). Since the mechanism is so poorly understood, the condition remains an enigma.
AFE is a theoretical risk of intraoperative cell salvage. However, leucocyte depletion filters have been shown to reduce amniotic fluid contamination significantly, and no cases of AFE associated with cell salvage use in obstetrics have been reported as yet.
Management options
Management is supportive, with basic resuscitative manoeuvres (remembering uterine displacement), management of bleeding and correction of DIC. If cardiac arrest occurs, perimortem caesarean section should occur within 5 minutes. Concurrent triggering of the major obstetric haemorrhage protocol is advised (see Chapter 78, Major obstetric haemorrhage). There have been limited case reports of novel techniques being used successfully in the treatment of AFE, including intravenous steroids, prostacyclin, plasma exchange, inhaled nitric oxide, cardiopulmonary bypass and extracorporeal membrane oxygenation. A mortality rate of 60-80% was traditionally reported, but the lower mortality rate in more recent reports (~20%) suggests that recognition and management of the syndrome has improved.
Key points
• Amniotic fluid embolism is probably a misnomer, but represents a catastrophic event on the labour ward.
• Features include convulsions, respiratory and cardiovascular collapse, disseminated intravascular coagulation and fetal compromise.
• There is no specific treatment, but with prompt recognition and supportive therapy the prognosis is improved.
Further reading
Knight, M, Berg C, Brocklehurst P, et al. Amniotic fluid embolism incidence, risk factors and outcomes: a review and recommendations. BMC Pregnancy Childbirth 2012; 12: 7.
Knight M, Nair M, Tuffnell D, et al.; MBRRACE-UK. Saving Lives, Improving Mothers’ Care: Lessons learned to inform maternity care from the UK and Ireland Confidential Enquiries into Maternal Deaths and Morbidity 2013-15. Oxford: National Perinatal Epidemiology Unit, University of Oxford, 2017.
McDonnell NJ, Percival V, Paech MJ. Amniotic fluid embolism: a leading cause of maternal death yet still a medical conundrum. Int J Obstet Anesth 2013; 22: 329-36.
Pacheco LD, Saade G, Hankins GD, Clark SL; Society for Maternal-Fetal Medicine. Amniotic fluid embolism: diagnosis and management. Am J Obstet Gynecol 2016; 215: B16-24.