The exact mechanisms leading to<unk>  of the umbilical<unk>  in the fetal membranes are unknown, although they are likely to occur in the first trimester. One theory is that<unk>  may arise from the process of placental trophotropism, which is the phenomenon where the placenta migrates towards areas which have better blood flow with advancing gestation. The placenta grows in regions with better blood supply and portions atrophy in regions of poor blood flow. This process of atrophy may result in the exposure of umbilical blood vessels, causing marginal or peripheral placental<unk>  to evolve to<unk><unk>  over time. Placentas with<unk>  have a lower vessel density. As the growth of the fetus is dependent on the organization, mass, and nutrient-transfer capacity of the placenta, fetal development is hence hindered in<unk> . This can lead to fetal malformations and low birth weight. The umbilical vessels may also be longer compared to normal, particularly when the site of<unk>  is in the lower uterine section as the extension of the uterine isthmus as pregnancy advances causes vessel elongation. This results in increased vascular resistance, which impedes nutrient transfer to the fetus. The umbilical vessels experience increased pressure and compression as they are not protected by Wharton's jelly. This can cause decreased or acute cessation of blood flow, decreased cardiac output, and pulmonary complications in the newborn. The elongated, exposed vessels in lower<unk>  cases are more readily compressed by the fetus, hence there is an even greater risk of non-reassuring fetal heart rate pattern and emergency caesarean section. The growth-restricting impacts of placental insufficiency resulting from<unk>  can also augment the effects of increased pressure to the umbilical vessels. Normally in the second half of pregnancy, one-third of fetal cardiac output is directed towards the placenta. This fraction is reduced to around one-fifth in the last few weeks of pregnancy, while the remaining umbilical blood is recirculated in the fetal body, corresponding with decreased fetal reserves of oxygen. In pregnancies with growth restriction, the fraction of fetal cardiac output distributed to the placenta decreases, further lowering fetal reserves. This can result in increased risk of caesarean delivery, fetal hypoxia, and perinatal death in pregnancies with<unk> . Damage to the umbilical<unk>  vessels can occur when the amniotic membranes are ruptured, particularly in the case of vasa previa, potentially leading to fetal exsanguination. If the umbilical vessels are positioned such that their rupture is likely during labor, an elective operative birth at 35–36 weeks gestation may be planned, and corticosteroids may be administered in order to assist with fetal lung maturation. Overall,<unk>  doubles the risk of both preterm birth and acute caesarean section. Risk factors The following have been identified as risk factors for<unk> : *Nulliparity *History of infertility *The use of assisted reproductive technology *Multiple gestation *Maternal smoking *Maternal asthma *Maternal obesity *Chronic hypertension *Type 1 diabetes *Gestational diabetes *Placental anomalies, including low-lying placenta, bilobed placenta, placenta with accessory lobe/s *Previous pregnancy with abnormal<unk><unk>  *Having an umbilical<unk>  with a single umbilical artery *Advanced maternal age
Velamentous cord insertion
Neural clique
Vaginal septum
Uterine septum
Fetal movement
Placental expulsion
Peritomy
Circumvallate placenta