In AFE, amniotic fluid enters maternal circulation via ruptured membranes or ruptured uterine or cervical vessels down a pressure gradient from the uterus to veins. Although the site of placental implantation is one portal of entry, small tears in the lower uterine segment and endocervix are thought to be the most common site of entry.
The pathophysiology of AFE syndrome is unclear. In the past, it was thought to be due to fetal tissue/amniotic fluid forcibly entering maternal circulation causing transient pulmonary vasospasm, cardiac failure, hypoxaemia, and death. However, in 1995, Clark suggested that the syndrome arose from an immune rather than embolic process. According to Clark, AFE is caused by fetal antigens in the amniotic fluid stimulating a cascade of endogenous immune-mediators, producing a reaction similar to anaphylaxis. Amniotic fluid contains various components that contribute to the pathophysiology of AFE in different ways (Table 1). Biochemical mediators found in the solution are thought to trigger the main features of anaphylactoid reaction with multi-system involvement. The products found in suspension are responsible only for the minor effects caused by actual mechanical obstruction. Clark suggested that ‘the syndrome of acute peripartum hypoxia, haemodynamic collapse and coagulopathy should be described as anaphylactoid syndrome of pregnancy ’and not AFE. There are also striking similarities between clinical and haemodynamic findings in AFE and septic shock, which suggests a common pathophysiological mechanism.