Page 748 - ACCCN's Critical Care Nursing

Pregnancy and Postpartum Considerations 725

more likely cause of pulmonary vasoconstriction, with quickly leading to fetal demise unless the fetus is deliv-
physical obstruction to the pulmonary vasculature ered swiftly. There is variation in the signs and symptoms,
(embolism) not the main mechanism. 112,115 The left ven- and in the timing of their presentation in individual
tricular failure seen in AFE is considered a secondary women. Premonitory symptoms, shortness of breath and
response due to poor left ventricular filling pressures. fetal distress have been reported as the early signs in a UK
116
Concomitantly, substances in the amniotic fluid trigger a study. Overall, haemorrhage and associated coagulopa-
profound consumptive coagulopathy. thy, hypotension and shortness of breath were the most
116
commonly recorded symptoms. Cardiac arrest was
Incidence and Risk Factors documented in 40% of cases and seizure in 15%. Hae-
The incidence of AFE is thought to be in the range of 2–8 morrhage and coagulopathy may not be immediately
women per 100,000 deliveries making it a very rare apparent, some women die before it develops, however
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event. However, the lack of a diagnostic test is a serious these clinical features usually develop in women who
limiting factor for accurate determination of incidence, as survive the initial insult.
clinical diagnoses vary and the accuracy of hospital codes Treatment
that may be used to count the incidence are fraught with
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potential error. There has been geographical variation There is no specific treatment for AFE; all therapy is sup-
in incidence reported, with AFE more common in North portive with the aim to maintain adequate oxygenation
America (1 in 15,200 deliveries) than in Europe (1 in and perfusion, control haemorrhage and correct any
115
53,800 deliveries); this may represent a true difference coagulopathy. Common interventions include: 116
in incidence or reflect differences in clinical diagnosis or l urgent delivery of the fetus
methods of case identification. l emergency hysterectomy to control postpartum
Diagnosis remains one of exclusion and there is a long haemorrhage.
list of differential diagnoses, including air or thrombotic l admission to ICU, with associated support such as
pulmonary emboli, septic shock, cardiomyopathy, acute mechanical ventilation, nitric oxide and extra-
myocardial infarction, anaphylaxis, transfusion reaction, corporeal membrane oxygenation (ECMO)
aspiration, placental abruption, eclampsia, uterine A full range of blood components, including fresh frozen
rupture, local anaesthetic toxicity and primary postpar- plasma, platelets and cryoprecipitate may be required
tum haemorrhage. Older obstetric literature quote to correct the coagulopathy. Adjunct therapies such as
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mortality rates above 80%. More recent larger studies recombinant Factor VIIa have also been used with effect.
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have shown that mortality in developed countries is more Transoesophageal echocardiography may be very helpful
likely to be in the range of 13–30%. 115,116,118 However, AFE to guide fluid and inotrope management to optimise
remains a major contributor to maternal death, account- preload and enhance cardiac output.
ing for 5–15% of all maternal deaths in developed
countries. 52,115 Although it is possible for a woman to experience an AFE
in a subsequent pregnancy, repeat AFE is thought to be
Although controversy exists, the factors that have been unlikely as the trigger for AFE is specific to each fetus the
proposed as contributing to an increased likelihood for woman carries. There have been a number of published
AFE include: 112,113,115,116,118 case reports of women having a successful subsequent
l induction of labour pregnancy and none reporting repeat AFE in the same
l caesarean birth woman.
l multiple pregnancy e.g. twins
l maternal age ≥35 years PERIPARTUM CARDIOMYOPATHY
l forceps delivery Peripartum cardiomyopathy, sometimes referred to as
l placenta praevia, preeclampsia and placental postpartum cardiomyopathy, is new onset heart failure in
abruption. association with pregnancy. Diagnosis is usually depen-
dent on all four of the following criteria: (1) the develop-
Given the rarity of AFE and the commonality of these ment of the disease in the last month of pregnancy or
potential risk factors, astute clinical assessment and early within five months of delivery; (2) absence of any other
clinical suspicion based on the clinical presentation of identifiable cause of heart failure; (3) absence of recogni-
the woman should be the focus for early identification sable heart disease before the last month of pregnancy;
and treatment.
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and (4) left ventricle systolic dysfunction. However,
time of onset outside of the above criteria does occur
Presentation occasionally. Peripartum cardiomyopathy is considered
The symptoms associated with AFE have been well to be a dilated cardiomyopathy, resulting in a dilated left
described and usually comprise premonitory symptoms, atrium and ventricle, and a reduced left ventricular ejec-
120
such as restlessness, agitation and numbness/tingling tion fraction (< 45%). Women commonly present with
121
prior to more severe maternal compromise such as hypo- New York Heart Association Class III or IV heart failure.
tension, dyspnoea, hypoxia, altered mental status and The incidence of peripartum cardiomyopathy varies
115
haemorrhage. Additionally, in pregnant women, col- widely from 1:100 in a small region of sub-Saharan Africa
lapse of the maternal cardiovascular system leads to fetal to 1:4000 in the US, though many studies on peripartum
distress as the placenta is deprived of maternal oxygen, cardiomyopathy were conducted on data that had been