Historically, research on fetal tissue or amniotic fluid entering the maternal circulation has been scarce, and clinical cases of suspected amniotic fluid embolism have been rare. Consequently, conducting a large-scale prospective study has been virtually impossible.Due to the lack of reliable research data, it was previously thought that amniotic fluid embolism primarily resulted from fetal amniotic fluid entering the mother's blood vessels or body, subsequently obstructing vascular or pulmonary gas exchange functions, leading to asphyxia and shock.
Following amniotic fluid embolism, maternal mortality rates reached 61%, with most deaths occurring within 30 minutes to two months after onset. Survivors often suffered permanent neurological damage.The fetal mortality rate following amniotic fluid embolism is 21%, largely due to earlier intervention and rapid delivery of the fetus. Unfortunately, only half of the surviving infants experience no neurological impairment in later life. These data indicate that when amniotic fluid embolism occurs, most mothers and fetuses inevitably face significant loss of life.
Recent molecular biology research, however, suggests that the condition is less about amniotic fluid clogging maternal blood vessels or lungs, and more about a severe allergic shock triggered by an immune response to amniotic fluid or fetal tissue entering the mother's body.Therefore, clinically, the symptoms of amniotic fluid embolism are nearly identical to those of anaphylactic shock, including hypotension, pulmonary edema, adult respiratory distress syndrome, cardiopulmonary failure, cyanosis, coagulation abnormalities, convulsions, and bronchoconstriction.When a mother exhibits these symptoms, fetal distress occurs in nearly 100% of cases. Thus, amniotic fluid embolism not only threatens the mother's life but also severely jeopardizes the fetus's prognosis.