Placental vessels

　　The etiology of placental vessels is unknown, and the following are all hypotheses that scholars have not confirmed. In 1900, Franque believed that in normal circumstances, the chorion (the primordium of the umbilical cord) always extends towards the fetus in contact with the most abundant blood supply in the decidua. If, in early pregnancy, the most abundant blood supply is in the covering decidua, the umbilical cord primordium originates from here. However, as pregnancy progresses, the most abundant blood supply area has moved to the basal decidua, where the placenta forms. However, the umbilical cord primordium remains in place, and the villi in this area have atrophied into a smooth chorion, so the vessels in this area are distributed in a sail-like pattern, making the umbilical cord attach to the edge of the placenta. Strausman (1902) proposed that the umbilical cord attached in a sail-like manner initially planted the placenta in the basal decidua, and later, as the placenta extended to a region with better blood perfusion, the umbilical cord, originally attached to the central area, gradually became eccentric and attached to the edge, and the placental lobes around the attachment site regressed into a smooth chorion, finally developing into the sail-like attachment of the umbilical cord. Later, Benirschke and Driscoll (1967) held a similar view.

　　The main complications of this disease are fetal distress, even fetal death. Fetal distress refers to fetal intrauterine hypoxia, which causes fetal acidosis, leading to damage to the nervous system. In severe cases, there may be sequelae, even fetal intrauterine death. It is divided into acute hypoxia and chronic hypoxia, with acute hypoxia most common during labor, and chronic hypoxia common in pregnancy complications and complications affecting placental function.

　　The manifestations of placental vessels are not constant. Some ruptures of placental vessels occur before the rupture of the amniotic membrane and can occur during pregnancy or labor. Sometimes, a blood clot may occur at the site of vessel rupture, which may be due to the rupture of small branches of veins. Due to bleeding, the fetus may develop hypotension, blood flow slows down, and blood clots form, stopping the bleeding, but it can occur again later. If the amount of bleeding is small, the fetal heart rate may not change, but if the amount of bleeding is slightly more, the fetal heart rate often changes, and at this time, one should suspect placental vessel anomaly.

　　Suddenly finding bleeding during artificial amniocentesis should raise the possibility of a placental vessel anomaly. Sometimes, there is no bleeding immediately after artificial amniocentesis, but bleeding occurs later. This is because the initial rupture of the amniotic membrane did not involve the placental vessel anomaly. However, when the rupture of the amniotic membrane mouth expands, it tears the placental vessel and causes bleeding. In a very few cases, the bleeding lasts for several hours, but there are still surviving fetuses, and the fetal heart rate can still show sinusoidal fetal heart rate.

　　Pregnant women should have regular prenatal examinations to detect the condition early. In the later stages of pregnancy, they should reduce their activities to prevent constipation. Do not perform vaginal examinations or rectal examinations. After the fetus matures, selective cesarean section should be performed. If the diagnosis is confirmed during labor and the fetus is still alive, cesarean section should be performed immediately to save the fetus.

　　In addition to clinical manifestations, anterior placental vessels also require laboratory tests. The main methods of examination are laboratory testing and imaging examinations. Imaging examinations mainly include ultrasound, magnetic resonance imaging, and amniocentesis.

　　Patients should pay attention to maintaining a pleasant mood in their daily lives and avoid anger and outbursts. Eat more vegetables and fruits to keep the bowels regular. Do not eat too much, and eat to about 70-80% of fullness. Eat less beef, mutton, pork, and dog meat, and avoid strong alcohol and spicy fried foods, and eat light and nutritious foods instead.

　　If the anterior placental vessels are diagnosed before delivery, pregnancy should be terminated between 37-38 weeks to avoid the risk of the anterior placental vessels being compressed or ruptured during the descent of the fetal head during labor, which could endanger the life of the fetus. The mode of delivery should be cesarean section. In emergencies, cesarean section under local anesthesia can be considered in the delivery room, and the fetal heart should be listened to before the incision is made to confirm that the fetus is still alive. If the anterior placental vessels rupture and the fetus survives, cesarean section should be performed immediately to terminate pregnancy. Newborns generally have severe anemia, pale complexion, and the simplest and most effective method is to squeeze the umbilical cord blood towards the newborn as much as possible before clamping the umbilical cord, or to withdraw 20-30ml of placental umbilical cord blood after clamping the umbilical cord and infuse it into the newborn via the umbilical vein to correct anemia.

　　For pregnant women with vaginal bleeding, continuous fetal heart monitoring with a fetal electronic monitor can detect fetal abnormalities early and timely treatment. Once the rupture of the anterior placental vessels is diagnosed, if the conditions for an immediate vaginal delivery are not yet met, every second should be争取 to perform cesarean section to terminate pregnancy, and neonatologists should be present to participate in neonatal resuscitation. It must be emphasized that after a certain amount of fetal blood loss, the fetal condition deteriorates rapidly, and the fetal heart should be listened to again before surgery to avoid unnecessary cesarean sections.