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A postmature infant is an infant born after 42 wk gestation.
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 (see Inherited ichthyoses) associated with placental sulfatase deficiency.
In most cases, continued fetal growth between 39 and 43 wk gestation results in a macrosomic infant. However, sometimes the placenta involutes, and multiple infarcts and villous degeneration cause placental insufficiency syndrome. In this syndrome, the fetus receives inadequate nutrients and O 2 from the mother, resulting in a thin (due to soft-tissue wasting), small-for-gestational-age (see Small-for-Gestational-Age (SGA) Infant), undernourished infant with depleted glycogen stores. Post term, the amniotic fluid volume eventually decreases (oligohydramnios—see Oligohydramnios).
Postmature infants have higher morbidity and mortality than term infants. During labor, postmature infants are prone to develop
Asphyxia may result from 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. Neonatal hypoglycemia is 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 but 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.
Diagnosis is by clinical appearance (see Figure: Assessment of gestational age—new Ballard score.) and estimated date of delivery.
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