During pregnancy, the abdominal pressure has a tendency to increase due to the enlargement of the uterus, pregnancy vomiting and factors such as breath-holding during delivery, coupled with a high-protein, high-fat diet during this period, the load on the liver, bile and pancreas increases significantly and the pressure in the pancreatic duct increases. In addition, the ability of the intestine to absorb fatty acids is greatly enhanced and fat accumulation is higher, and it is believed that the large amount of increased retroperitoneal fat may be an important factor in the susceptibility of pancreatitis to necrosis, secondary infection and abscess formation. It is worth proposing that placental prolactin (HpL) produced by syncytial trophoblasts has a significant lipolytic effect, and triglycerides will release a large amount of free fatty acids, which can cause both acute fat infiltration of pancreatic cells and acute fat embolism of the small arteries and microcirculation of the pancreas, aggravating the condition of acute pancreatitis in pregnancy. Acute pancreatitis in pregnancy is prone to hypovolemic shock, and blood perfusion to the placenta can drop dramatically as a result. At the same time, severe dehydration puts the blood in a hypercoagulable state, and increased fibrin and fibrinogen are deposited in the placental villi, and at this time, because the intima is often combined with inflammation, blood cells tend to collect and form microvascular embolism, which causes narrowing of the vascular lumen, thus further affecting the blood perfusion of the placenta. In addition, in necrotizing pancreatitis, biochemical changes are obviously abnormal, and the accumulation of serum intermediate metabolites will lead to ketoacidosis. In conclusion, the incidence of intrauterine distress of the fetus in acute pancreatitis during pregnancy can be significantly increased as a result. It is also believed that in acute pancreatitis of pregnancy, hepatic blood flow can be reduced by more than 40%, oxidative phosphorylation and other energy metabolism will be impaired, adenosine triphosphate production will be reduced, and the synthesis of coagulation factors will also be decreased, which will increase the occurrence of uterine contraction weakness and postpartum hemorrhage in patients with acute pancreatitis of pregnancy. Acute pancreatitis during pregnancy is not only a local inflammation of the pancreas, but also increases maternal perinatal mortality because it is more likely to be complicated by respiratory failure and cardiac failure and other organ dysfunction.