1. Pathogenesis: The etiology of feto-maternal transfusion is not well understood and may be due to the formation of a pressure difference between the fetal umbilical artery and the chorionic villous space, causing fetal blood to enter directly into the chorionic villous space and to seep retrogradely into the maternal circulation [1]. This rarely occurs under normal circumstances and may only occur in cases of chorionic villus injury. Therefore, the occurrence of feto-maternal transfusion syndrome is often associated with prenatal hemorrhage, abdominal trauma, placental vascular malformation, placental abruption, amniotic cavity or umbilical cord puncture, placental tumor, cesarean section, and hypertension, and other maternal abnormalities, whereas the cause of most feto-maternal transfusions is unknown. 2. Clinical manifestations: The clinical manifestations of FMH depend on the rate and amount of blood loss from the fetus. The clinical manifestations of FMH depend on the speed and amount of fetal blood loss, which can cause severe fetal anemia, intrauterine hypoxia, and even stillbirth. If there is chronic and recurrent hemorrhage during pregnancy, the fetus has been able to adapt and is born with only pallor and unexplained anemia. In case of acute transmission, shock may be present in severe cases. In the case of chronic massive blood transmission, the fetus presents with generalized edema and ascites. In case of ABO blood group incompatibility between the fetus and the mother, the mother may also have a transfusion reaction. 3. Laboratory diagnosis: FMH has a relatively insidious clinical presentation, and the diagnosis often depends on laboratory tests. When the newborn is obviously anemic and there is no postpartum hemorrhage and hemolytic anemia is excluded, the following tests should be performed to clarify the diagnosis. (1) Fetal erythrocytes in maternal blood circulation (erythrocyte acid elution test KB method); (2) Fetal hemoglobin quantification in maternal blood, which should be <3% in normal adult blood, but increases to 5.7% during pregnancy; (3) Methemoglobin quantification in maternal blood, which is related to the integrity of the placental barrier, and the probability of fetal-mother transfusion syndrome increases with elevated methemoglobin levels; (4) Fetal hemoglobin quantification in maternal blood, which is related to the integrity of the placental barrier. (4) determination of placental alkaline phosphatase level. (4) Placental alkaline phosphatase level measurement: Immature infants with high bleeding after clear diagnosis should be closely monitored, treated with small doses of umbilical cord or fetal intraperitoneal transfusion, and prolonged gestational weeks. After delivery, the newborn should be treated according to the degree of anemia. In case of severe anemia in the newborn, transfusion should be administered promptly. In case of maternal-fetal RH blood group incompatibility, it is estimated that the fetal blood loss exceeds 30 ml and the mother should be given RH immunoglobulin transfusion to counteract RH-positive red blood cells and reduce antibody production to avoid adverse effects on further pregnancies. Because of the lack of specificity and low incidence of prenatal manifestations of FHM, clinicians are not aware of this disease, so it is difficult to make prenatal diagnosis, but it is more dangerous to the mother and child. It has been reported that 5% of fetal deaths in utero are caused by FMH. Therefore, regular maternal checkups and timely fetal heart monitoring during pregnancy can effectively reduce neonatal mortality by detecting abnormalities and making early diagnosis.