Amniotic fluid embolism

This term refers to a rare and potentially devastating syndrome of the peripartum period, in which acute hypoxia, haemodynamic changes and coagulopathy coexist.There is an increase in the number of maternal deaths associated with the condition (May 1999).Amniotic fluid embolism (AFE) is a clinical diagnosis, and there is no specific or consistent confirmatory test. It has been described in association with normal labour (or immediately postpartum), Caesarean section, therapeutic abortion, amniocentesis, and artificial rupture of the membranes.The exact aetiology is unknown, but it appears to be associated with exposure of maternal blood vessels to fetal tissue.Whilst amniotic fluid, which contains electrolytes, nitrogenous compounds, lipids, prostaglandins and fetal elements such as squames, hairs, vernix and meconium, has been found in the lungs, it is probably not an embolus according to the strict definition of the term.The syndrome has been said to resemble both anaphylaxis and septic shock, and Clark et al (1995) believe that a more appropriate term would be 'anaphylactoid syndrome of pregnancy'.

Earlier papers suggested that pulmonary hypertension was the principal haemodynamic feature of the condition, and that treatment should be with pulmonary vasodilators. More recently, invasive haemodynamic monitoring has been undertaken in several patients in the acute stage of the disease.An initial period of pulmonary hypertension, hypoxia and increased right heart pressures is succeeded by left ventricular failure secondary to impaired left ventricular function (Clark et al 1988, Clark 1991,Vanmaele et al 1991).The haemodynamic findings would therefore vary, according to the stage at which monitoring was first undertaken. This would account for the high incidence (70%) of pulmonary oedema seen on the CXR of survivors, and the variety of features described in the few patients in whom invasive monitoring has been undertaken.These features include pulmonary hypertension (Shah et al 1986), left heart failure (Girard et al 1986,Vanmaele et al 1990, Choi & Duffy 1995), and left and right heart failure (Moore et al 1982).

There is increasing evidence that the pathophysiology involves a two-stage response to

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