The cause of postmaturity is generally unknown, but previous postterm delivery increases the risk 2- to 3-fold. Postmaturity may be caused by abnormalities that affect the fetal pituitary-adrenal axis (eg, anencephaly, adrenal gland hypoplasia, congenital adrenal hyperplasia) and by x-linked ichthyosis associated with placental sulfatase deficiency.
In most cases, fetal growth continues until delivery. However, in some cases, the placenta involutes as pregnancy progresses and multiple infarcts and villous degeneration develop, causing placental insufficiency. In these cases, the fetus receives inadequate nutrients and oxygen from the mother, resulting in a thin (due to soft-tissue wasting), undernourished infant with depleted glycogen stores and decreased amniotic fluid volume. Such infants are dysmature and, depending on when placental insufficiency develops and the severity of the condition, they may be small-for-gestational-age. Although placental insufficiency with dysmaturity can occur at any gestational age, it is most common in pregnancies that progress beyond 41 to 42 weeks.
Postmature infants have higher morbidity and mortality than term infants due in large part to
Perinatal asphyxia may result from placental insufficiency as well as cord compression secondary to oligohydramnios.
Meconium aspiration syndrome may be unusually severe because amniotic fluid volume is decreased and thus the aspirated meconium is less dilute. Persistent pulmonary hypertension often occurs after meconium aspiration.
Neonatal hypoglycemia is a complication caused by insufficient glycogen stores at birth. Because anaerobic metabolism rapidly uses the remaining glycogen stores, hypoglycemia is exaggerated if perinatal asphyxia has occurred.
Postmature infants are alert and appear mature. They have a decreased amount of soft-tissue mass, particularly subcutaneous fat. The skin may hang loosely on the extremities and is often dry and peeling. The fingernails and toenails are long. The nails and umbilical cord may be stained with meconium passed in utero.
Improved obstetric care over the past two decades has markedly decreased the number of infants delivered past 41 weeks gestation, which has also decreased the incidence of meconium aspiration syndrome.
Postmature and dysmature infants are at risk of hypoglycemia and should be monitored and managed accordingly.
For infants with perinatal asphyxia, management depends on the severity of the disease process. Therapeutic hypothermia may help infants with moderate or severe encephalopathy who had severe acidosis at birth, a low Apgar score at ≥ 5 minutes, and/or a need for prolonged resuscitation.
Neither the incidence nor the severity of meconium aspiration syndrome is reduced by endotracheal suction at the time of delivery, regardless of the apparent viscosity of the fluid or the infant's level of activity, so endotracheal intubation should be reserved for infants who need ventilatory assistance. Infants with meconium aspiration syndrome may require assisted ventilation; high-frequency ventilation is sometimes helpful. Sedation is often necessary.
Surfactant treatment does not decrease overall mortality but does reduce the likelihood of the need for treatment with extracorporeal membrane oxygenation (ECMO), so surfactant is frequently used in infants with significant respiratory distress. ECMO is available in a relatively few neonatal centers and is reserved for infants with hypoxic respiratory failure refractory to conventional medical treatment.
Persistent pulmonary hypertension is treated with supportive therapies and inhaled nitric oxide or other pulmonary vasodilators.