The main link in the pathogenesis of post-term pregnancy is changes in the placenta (placental insufficiency). They cause intrauterine oxygen deficiency in the fetus. Such a deviation leads to pronounced changes and a violation of the child's condition. At the same time, placental dysfunction, an imbalance in the fetal endocrine system, and the presence of risk factors for overbearing do not allow childbirth to begin on time, exacerbating existing disorders.
During pregnancy, placental dysfunction is manifested by impaired blood flow in the uterine arteries and / or umbilical cord arteries. In the morphological study of the placenta, signs of reduced blood circulation, the formation of small blood clots, sclerosis of the villi and blood vessels, and a decrease in the number of capillaries are diagnosed. Calcifications can also be found in it - local accumulations of calcium in the focus of impaired blood flow.
For the survival of the fetus with a deficiency of oxygen supplied to it, the body starts the process of centralization of blood circulation. At the same time, in the vital organs of the baby, such as the brain, heart and liver, the blood flow is maintained, and in the muscles, intestines, kidneys and other organs it decreases.
Due to a decrease in blood flow in the kidneys of the fetus, urine output is significantly reduced, oligohydramnios develops. The nature of the amniotic fluid also changes: they lose their transparency, become cloudy, acquire a yellowish or greenish tint due to the admixture of meconium - the first feces of the child.
Due to changes in the composition of amniotic fluid, the production of surfactant is disrupted - a substance that prevents the alveoli from sticking together during exhalation. This causes pathology of the lung tissue and respiratory failure after birth. The protective function of the lungs also decreases: the number of bacteria in the water increases, which increases the risk of infection of the lung tissue.
Against the background of placental insufficiency, the umbilical cord becomes thin. Because of this, the risk of compression of the umbilical cord, the occurrence of hypoxia or asphyxia during childbirth increases. The reduced supply of oxygen to the baby's body leads to the accumulation of metabolic products - acidification of the internal environment of the fetus (metabolic acidosis) develops, against which there is oxygen deficiency in the tissues.
Tissue hypoxia increases the permeability of the vascular walls in the fetus, which leads to fluid retention in the tissues. If fluid accumulates in the brain, cerebral edema may develop. This condition is an unfavorable factor during childbirth: it increases the sensitivity of the brain to the effects of oxygen deficiency and increases the risk of complications with a possible birth injury.
A consequence of intrauterine hypoxia is also a violation of myocardial contraction in the fetus. It affects the metabolism, which ultimately makes it difficult for the newborn to adapt to new extrauterine life conditions.