On successfully completing this topic, you will be able to:
appreciate when to consider amniotic fluid embolism (AFE), facilitating early diagnosis
manage the immediate treatment of a suspected AFE
understand the options in treatment following initial assessment and resuscitation.
Introduction
The dramatic nature of AFE and the poor outcome with which it is associated mean that prompt and appropriate management are needed to minimise morbidity and mortality. The evidence upon which this guidance is based comes from retrospective series, including the UK Obstetric Surveillance System (UKOSS)1 and the Confidential Enquiry into Maternal Deaths in the UK.2 All of this evidence is observational and it is improbable that any higher quality evidence will be available. The treatments are largely reported in individual cases and so we can only establish general principles and options to be considered in any individual case.
Incidence
AFE is estimated to occur in between 1/8000 and 1/80 000 pregnancies, but because it is difficult to confirm the diagnosis there is no certainty about these figures. The latest UK figures from UKOSS suggest an incidence of one in 50 000 with a mortality rate of around 20%. The 2009–2012 Confidential enquiry into maternal deaths in the UK MBRRACE report showed a death rate of 0.33/100,000 maternities.
There is wide variation in mortality from AFE worldwide, where it accounts for 13% of direct maternal deaths in France but 30% in Singapore. The percentage of direct maternal deaths caused by AFE in the US and Australia is similar to that of the UK at 7.5–10.0%.
In known AFE cases in the UK, the current mortality rate of 20% is a significant improvement on the previously gloomy outlook for women with AFE (mortality rates from the national registry in the US in 1995 suggested a mortality of 61%) and may be the result of better intensive care. However, recognition of the fact that ‘milder’ cases do occur may also have affected the statistics. Morbidity from this condition is also significant however, and it is particularly noteworthy that the US registry suggests that only 15% of women survived neurologically intact.
Clinical manifestations
Effects of amniotic fluid in the maternal circulation have been studied using animal models and in vitro studies. Details can be found in the further reading suggested at the end of this chapter. In summary, the effects are of:
bronchoconstriction
pulmonary hypertension
left ventricular failure
coagulopathy.
This syndrome of peripartum cardiovascular collapse with coagulopathy is similar to anaphylaxis: the response to the stimulus of fetal material in the maternal circulation is dependent upon the nature and quantity of the material and also the susceptibility of the mother. It is plausible that the effect is sometimes occlusive, sometimes a direct ‘toxic’ effect and sometimes a trigger to a cascade reaction. In some women, events may progress through each element. This suggests that clinical management will be aimed at supportive therapy with an understanding that the patient will pass through different phases of the clinical presentation.
The matter of amniotic fluid in the circulation is important if one is going to consider intraoperative autologous blood transfusion. This has been a concern considered in relation to the use of cell salvage for blood loss at CS; leucocyte depletion filtering seems to reduce particulate contaminants to the level equivalent to maternal venous blood. The safety of intraoperative autologous blood collection has been examined in cohort studies and no demonstrable increase in complications has been found. Cell salvage at CS has been approved by NICE and its use is recommended by RCOG in high-risk patients.
Other clinical manifestations
In order to suspect an AFE, we have to be aware of the features of the condition. The following were described by Clark in the US registry as requirements for the condition and the same features were initially used in the UK register.3,4 To make a diagnosis, there should be:
acute hypotension or cardiac arrest
acute hypoxia (dyspnoea, cyanosis or respiratory arrest)
coagulopathy (laboratory evidence of intravascular coagulation or severe haemorrhage)
onset of all of the above during labour or within 30 minutes of delivery
no other clinical conditions or potential explanations for the symptoms and signs.
However with knowledge of an increasing number of cases, UKOSS has refined the definition to:
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
seizure
shortness of breath.
Excluding: women with maternal haemorrhage as the first presenting feature, in whom there was no evidence of early coagulopathy or cardiorespiratory compromise.
Or
Women in whom the diagnosis was made at postmortem examination, with the finding of fetal squames or hair in the lungs.
It is important to note that the coagulopathy may not develop if there is a rapid deterioration and the woman dies. It will be present, or develop, if the woman survives the initial collapse. It is extremely unlikely that bleeding will be the first presentation.
Symptoms and signs
The initial UK registry paper describes several initial patterns of presentation:
maternal hypotension, shortness of breath, fetal bradycardia then delivery (14%)
maternal loss of consciousness or seizure then delivery (35%)
maternal collapse after delivery of baby at CS (14%)
fetal distress and then maternal collapse (23%)
immediately following delivery loss of consciousness or seizures (14%).
In each case it was followed by coagulation difficulties, and usually also profuse haemorrhage.
The UKOSS data describes the presentations and features shown in Table 10.1.
