The amount of amniotic fluid increases with the week of gestation and is currently considered to be about 1000 ml (800-1200 ml) at full term of normal pregnancy. The medical definition of amniotic fluid in China is that the amount of amniotic fluid in any period of pregnancy exceeds 2000ml, which is called hyperhydramnios. Because the amount of amniotic fluid is difficult to measure accurately, the incidence of excessive amniotic fluid is difficult to quantify. The cause of excessive amniotic fluid is very complex, as the production and absorption of amniotic fluid is in a dynamic balance, with the fetus constantly exchanging with the mother through swallowing, breathing, urination, pre-keratosis skin and the umbilical cord, etc. Once the regulatory mechanism of amniotic fluid is out of balance or transport is impaired, abnormal amniotic fluid volume will occur. The exact cause of excessive amniotic fluid is not well understood. Fetal abnormalities, maternal abnormalities and placental abnormalities can all lead to excessive amniotic fluid. Fetal anomalies About 12-30% of cases of hyperhydramnios are combined with fetal anomalies, with neural tube anomalies and gastrointestinal anomalies being the most common. (1) The neural tube anomalies account for about 50% of the cases, and anencephaly, spina bifida, and cerebral dilatation are the most common. The cerebrospinal tissue is exposed, the choroidal tissue proliferates, and the exudate increases, resulting in excessive amniotic fluid. In anencephalic children and children with severe hydrocephalus, there is a lack of central swallowing function, no swallowing reflex, and a lack of antidiuretic hormone leading to an increase in urine volume, resulting in excessive amniotic fluid. (2) Gastrointestinal anomalies account for about 25% of cases, and are commonly caused by atresia of the digestive tract, such as esophageal atresia, duodenal atresia, duodenal stenosis, and congenital pancreatic torsional dysplasia. For fetal GI atresia, there is almost always excess amniotic fluid and fetal swallowing is inhibited. (3) Some renal anomalies, such as congenital polycystic kidney and congenital hydronephrosis, can also be combined with hyperhydramnios. (4) Abdominal wall defects, such as umbilical bulge and ventral fissure, can cause excessive amniotic fluid due to irritation of the exposed blood vessels as the peritoneum abuts the amniotic membrane. (5) Heartless malformations, the vast majority of which occur in twin fetuses, cause excessive amniotic fluid in heartless fetuses due to abnormal blood perfusion. (6) Fetal chromosomal abnormalities, etc. The majority of twin pregnancies are associated with single chorionic villus and double amniotic sac, and most of them are associated with twin fetus transfusion syndrome. The number of fetuses with amniotic fluid in the fetus is about 20%, such as maternal diabetes mellitus, maternal and child blood type incompatibility (especially Rh blood type incompatibility), and intrauterine fetal infection. In diabetes mellitus, the cause of excessive amniotic fluid may be increased fetal blood glucose, and the fetus urinates a lot and drains into the amniotic fluid. In the case of maternal and child blood group incompatibility, placental edema increases, and chorionic edema affects fluid exchange, resulting in excessive amniotic fluid. B19 destroys fetal red blood cells, causing severe fetal anemia and further excessive amniotic fluid. Placental lesions such as placental chorionic villous hemangioma can also be combined with excessive amniotic fluid. Idiopathic hyperhydramnios About 40% (or more) of cases are unexplained hyperhydramnios without fetal malformations or maternal comorbidities. However, some studies have concluded that although indicators during pregnancy fail to suggest the cause of excessive amniotic fluid, in about 10% of cases the abnormality is only clear after delivery. Hypohydramnios is the lack of amniotic fluid, which is below normal levels. The amniotic fluid content is more stable in the early and middle stages of pregnancy, and varies greatly among individuals in the late stages of pregnancy, with less than 300 ml of amniotic fluid at full term. In early and mid-term pregnancies, low amniotic fluid often ends in miscarriage, while clinically, low amniotic fluid is found after 28 weeks of gestation, which is a complication of pregnancy, and is mostly associated with high-risk pregnancy, high-risk children and fetal urinary tract anomalies. 1. Fetal malformations Many congenital malformations, especially urinary tract malformations, are associated with low amniotic fluid, such as congenital renal agenesis, renal dysplasia, polycystic kidney and urethral stricture or atresia. The above malformations lead to a decrease or inability to generate urine, the generated urine cannot be excreted or the excretion is reduced, there is no urine or little urine, which leads to a decrease in amniotic fluid generation and normal amniotic fluid absorption, and finally, there is too little amniotic fluid. 2, placental insufficiency The placenta is an organ for material exchange between the fetus and the mother, and a decrease in placental function can lead to a decrease in fetal blood volume and a decrease in fetal kidney blood supply finally leading to a decrease in fetal urine production. Placental function is determined by placental blood supply, maternal-paternal barrier of the placenta and effective working area of the placenta. Decreased placental function usually includes decreased placental blood supply, decreased placental maternal-paternal barrier permeability and decreased effective area of the placenta. Decreased placental blood supply theoretically includes a variety of causes such as decreased maternal blood volume decreased maternal blood pressure and abnormalities in the supply vessels of the placenta, but it is mostly believed that decreased maternal blood volume is the main cause of decreased placental blood supply. The basic structure of the placenta for material exchange between mother and child is the maternal-paternal barrier of the placenta. The maternal-paternal barrier of the placenta can be dysfunctional due to edema, thrombosis, fibrosis, calcification and other pathological mechanisms, and the material exchange between the fetus and the mother decreases, which finally leads to a decrease in amniotic fluid production. In term pregnant women, the total placental volume remains the same, but due to the above mentioned changes in the placental-maternal barrier, the total effective placental area of material exchange decreases and finally low amniotic fluid production occurs. In clinical work, it is often seen that the placenta is small in size and thin in thickness and may be combined with calcified fibrosis on the maternal surface of the placenta, the basic placental maternal barrier may be normal or decreased, but the total effective placental area is decreased and the placenta is severely incompetent, this placenta is usually combined with low amniotic fluid and intrauterine growth retardation. 3, the role of drugs Many drugs can cause amniotic fluid, the common non-steroidal antipyretic analgesics and angiotensin converting enzyme inhibitors two types, non-steroidal antipyretic analgesics in the most studied is indomethacin. Indomethacin can cause decreased uterine and placental circulation, decreased fetal blood volume and renal blood volume, and decreased urine production.