Acute pancreatitis in pregnancy, including acute pancreatitis occurring in all stages of pregnancy and the puerperium, has an incidence of 1/4000 to 1/1000; its onset is rapid, progresses rapidly, has many complications, can be misdiagnosed due to atypical clinical manifestations, and may endanger the lives of the mother and child. According to the current literature, it can occur in all stages of pregnancy and postpartum, and is more common in late pregnancy, with the improvement of living standards and changes in dietary structure, the incidence has been on the rise in recent years. The etiology of acute pancreatitis during pregnancy is diverse, and the etiology of pancreatitis in the general population is basically the same, commonly biliary, hyperlipidemic, and other cases such as hyperparathyroidism leading to hypercalcemia induced acute pancreatitis, hypertensive syndrome of pregnancy causing long-term spasm of the pancreatic vessels and ischemic necrosis of the pancreas have also been reported. The identification of the etiology is a guide to the formulation of the treatment plan for acute pancreatitis. Biliary pancreatitis during pregnancy is mostly associated with the metabolic changes in the maternal organism during pregnancy. In the middle and late stages of pregnancy, the cholesterol content of bile secreted by the liver increases while the amount of bile acids and phospholipids decreases, resulting in the formation of cholesterol supersaturated bile; the high level of estrogen in pregnant women reduces the tone of the smooth muscle of the gallbladder, which affects the contraction of the gallbladder and causes the accumulation of bile; the increase in the size of the uterus increases the intra-abdominal pressure and the corresponding ectopic abdominal viscera, which compresses the duodenum and biliary system and affects bile excretion. The above factors make gallstone more frequent during pregnancy, and obstruction of the common channel of the pancreaticobiliary duct in the Vater’s jugular abdomen causes bile reflux, activates pancreatic enzymes, and induces pancreatitis. The secretion of prolactin, estrogen, glucocorticoids and other anti-insulin hormones gradually increases with the gestational weeks and reaches a peak in the late gestational period, the activity of lipoprotein lipase decreases, insulin resistance, and the gradual increase of blood lipid levels in normal pregnant women is a normal physiological response to the strengthening of anabolism during pregnancy. However, in cases such as obesity, rapid growth in body mass, older age, combined gallstone disease, diabetes, preeclampsia and disorders of triacylglycerol metabolism, maternal plasma triacylglycerol, cholesterol, free fatty acids, lipoproteins and other concentrations increase significantly compared to pre-pregnancy, increasing blood viscosity and resistance to blood flow, making it easy to form microthrombi and causing serious obstruction of pancreatic microcirculation, which can also directly induce pancreatitis. Once the complication of necrotizing pancreatitis, the combination of hypertriglyceridemia, fatty acids, cholesterol and the unique hormonal changes during pregnancy will make the condition more dangerous and the consequences more serious. Clinical manifestations of acute pancreatitis in pregnancy Nausea, vomiting and epigastric pain are the three main symptoms of acute pancreatitis in pregnancy, the pain is mostly persistent distension in the upper and middle abdomen or pain radiating to the back in the left upper abdomen, which is not relieved by vomiting, and some patients have a greasy diet before the attack. The possibility of acute pancreatitis should be considered for any epigastric pain during pregnancy, because its abdominal pain can be mild or even atypical, while nausea and vomiting are more severe and frequent in early pregnancy. In late pregnancy, especially at the stage of labor, the sudden onset of epigastric distension and pain from acute pancreatitis is often confused with contraction pain. During pregnancy, the abdominal wall becomes less elastic and relaxed, and the pancreas behind the peritoneum is covered by the nudging gastrointestinal and omental membranes during pregnancy, so the signs of pancreatitis, such as abdominal pressure pain, rebound pain and masses, may not be typical during physical examination, but may only show deep pressure pain in the upper and middle abdomen and soreness in the lower back, and may have fever, diminished bowel sounds and abdominal distension, and biliary pancreatitis can be seen as yellow staining of the skin and sclera. In the middle and late stages of pregnancy, the pressure in the abdominal cavity rises due to the enlargement of the uterus and the elevation of the diaphragm, while the blood volume of pregnant women increases by 40% to 45% and the cardiac output increases, and the heart rate and respiration increase during the onset of the disease, so it is necessary to strengthen monitoring and prevent shock. The diagnosis and evaluation of acute pancreatitis in pregnancy includes the following four questions: (1) how to confirm the diagnosis of acute pancreatitis (how to diagnose and exclude other diseases); (2) how serious is acute pancreatitis; (3) what is the cause; (4) at which stage of pregnancy the patient is. The diagnosis of acute pancreatitis requires a combination of past medical history, clinical manifestations, laboratory and imaging studies. In patients with a history of biliary disease, pancreatitis, diabetes mellitus, or familial hyperlipidemia prior to pregnancy, the possibility of an acute pancreatitis attack should be considered once there is an acute onset of abdominal pain during pregnancy. As mentioned earlier, the presence of three major symptoms of nausea, vomiting and epigastric pain strongly suggests acute pancreatitis during pregnancy, but because the symptoms and signs of abdominal pain during an attack are not typical, they need to be differentiated from acute pneumonia, penetrating duodenal ulcer, splenic rupture, acute appendicitis, ectopic pregnancy rupture, severe pregnancy vomiting and pre-eclampsia. Among the laboratory tests, the commonly used indicator is blood and urine amylase. Serum amylase usually exceeds 3 times the upper limit of normal value within 24 h of onset of disease and peaks after 48 h, while urinary amylase increases. The elevation of blood lipase is later than serum amylase, usually starts 24-72h after onset and lasts 7-10d. It is valuable for patients who present late after onset, and is less interfered by pregnancy and has high specificity. A transient increase in blood amylase followed by a rapid decrease can also be caused by massive necrosis of pancreatic tissue and must be judged in the context of the patient’s changing condition. Abnormal liver enzymes and elevated bilirubin suggest the possibility of biliary pancreatitis. Some patients with hyperlipidemia may have celiac-like changes in plasma specimens, and timely measurement of lipid levels can clarify the cause as early as possible. Acute pancreatitis is likely to occur when triacylglycerol is >11.3 mmol/L, and needs to be reduced to below 5.6 mmol/L within a short period of time. Severe hypercalcemia suggests hyperparathyroidism, while persistent elevated blood glucose and hypocalcemia suggest a serious condition. Reliable imaging data are important for diagnosis. Ultrasound examination of the abdomen is preferred during pregnancy. It can show swelling of the pancreas and accumulation of peripancreatic fluid exudation, as well as gallbladder stones and bile duct dilatation, but is easily disturbed by gastrointestinal gas, especially for those who are obese. Pregnant women also need ultrasound to assess the fetal gestational age and growth level for early detection of obstetric abnormalities such as intrauterine distress and intrauterine fetal death. Currently, the most accurate imaging test to assess the condition of pancreatitis is enhanced CT, and the use of CT during pregnancy is limited by the effects of radiation on the fetus. The International Society for Radiological Protection believes that the teratogenic risk of radiation below 0.05 Gy is negligible compared to other risk factors during pregnancy. The radiation dose to the fetus can be less than 0.01Gy for CT of the upper abdomen and less than 0.03Gy for CT of the lower abdomen and pelvis (layer spacing 7.5mm). For late pregnancy with severe symptoms, CT results are needed to assess the condition of the pancreas in the abdominal cavity and to decide whether to terminate the pregnancy. On balance, CT of the abdomen is still an option for grading the severity of acute pancreatitis with organ dysfunction, or the presence of The severity of acute pancreatitis is graded as acute severe pancreatitis with local complications such as necrosis, abscess or pseudocyst, or both, with an APACHE II score of 8 or more; fulminant acute pancreatitis is classified as fulminant acute pancreatitis even after adequate fluid resuscitation within 72h of onset of disease. Severe pancreatitis and fulminant pancreatitis treatment has its own specificity, early diagnosis is conducive to timely intervention in surgical treatment.