Amniotic fluid embolism is a series of pathophysiologic changes caused by the entry of amniotic fluid into the mother’s circulation, resulting in pulmonary hypertension, hypoxia, and multi-organ failure. The onset of amniotic fluid embolism is rapid, the condition is aggressive, the onset is unpredictable, and the morbidity and mortality rate is high. The etiology of amniotic fluid embolism is still unclear, and there are several theories about its pathogenesis: 1. Excessive pressure in the amniotic cavity: the fetus is wrapped in the amniotic membrane in the mother’s body. After labor, especially in the second stage of labor, when the uterus contracts, the pressure in the amniotic cavity rises. When the pressure in the amniotic cavity is higher than the venous blood pressure, amniotic fluid is squeezed into the mother’s blood circulation. 2. Opening of blood sinus: After rupture of blood sinus due to injury of cervix or uterine body, amniotic fluid can enter into maternal blood circulation through broken blood vessel or blood sinus behind placenta. 3. Rupture of fetal membranes: Current research suggests that most amniotic fluid embolisms occur after rupture of the fetal membranes, and that amniotic fluid can enter the circulation through small, broken blood vessels. Amniotic fluid embolism is more likely to occur in women of advanced maternal age, PMS women, women with excess amniotic fluid, multiple pregnancies, strong uterine contractions, and women who give birth in an emergency. Once it occurs, aggressive resuscitation is needed.