Usually presents with respiratory distress, hypotension, hypoxia. May lead to an anaphylactoid reaction that produces pulmonary hypertension and right heart failure (which can eventually progress to biventricular failure and cardiac arrest). Mortality rate is 60% [Clark SL et al. Am J Obstet Gynecol 172: 1158, 1995], and 70% of these deaths will be due to cardiopulmonary collapse.
Clark’s original article on the pathophysiology of AFE found left ventricular failure as the only unifying event in available human case reports [Clark SL et al. Am J Obstet Gynecol 151: 617, 1985]. He later described a bi-phasic model of acute pulmonary hypertension and vasospasm, followed by left ventricular failure due to hypoxia, mechanical considerations (left shift of the interventricular septum), and myocardial depression secondary to the fluid itself.
A case report of AFE in a 26 year old woman who received an echo probe describe the TEE as follows – “It showed acute right ventricular failure, suprasystemic right-sided pressures, bulging of the interatrial and interventricular septum from right to the left, severe tricuspid regurgitation, and a small pericardial effusion (Figures 1 and 2). Pulmonary artery systolic pressure (from tricuspid regurgitation jet) was 45 mm Hg, while at the same time no arterial pulse was palpable. The left ventricle was small and compressed. Its lateral wall had normal contraction and thickening. The bulging interventricular septum was thickening, but had abnormal contraction” [Shechtman et al.].
Although originally thought to be an embolic phenomena, because of the similarities with anaphylaxis, some authors believe that AFE is an immunologic phenomena, and go so far as to suggest that the name “amniotic fluid embolism” is a misnomer [Clark SL et al. Am J Obstet Gynecol 172: 1158, 1995]
Treatment is with ABCs – intubation and ionotropic support. AFE are extremely rare (somewhere between 1:8000 – 1:120,000 pregnancies), thus always maintain a reasonable list of differential diagnoses (VTE, VAE, aspiration). Establish rapid, large bore IV access in anticipation of massive transfusion (blood and products) and central access should be attempted to facilitate administration of vasoactive agents. Coagulopathies are almost always imminent. Factor VIIa has been used with some success although it significantly increases the risk of thrombus. Novel treatments include inhaled nitric oxide, cardiopulmonary bypass, IABP, and ECMO [Gist et al.].