he incidence of postmaturity syndrome in newborns at 41, 42, or 43 weeks, respectively, has not been conclusively determined. From data, the syndrome complicates 10 to 20 percent of pregnancies at 42 completed weeks (American College of Obstetricians and Gynecologists, 2016d). Associated oligohydramnios substantially raises the likelihood of postmaturity. Trimmer and associates (1990) reported that 88 percent of fetuses were postmature if there was oligohydramnios deined by a sonographic maximal vertical amnionic fluid pocket that measuredr; 1 cm at 42 weeks.
Many believe that postterm pregnancy is an abnormal state. Redman and Staf (2015) posit that limited placental capacity, which is characterized by dysfunctional syncytiotrophoblast, explains the greater risks of the postmaturity syndrome.
Cliford (1954) proposed that the associated skin changes were due to loss of the protective efects of vernix caseosa. He also attributed the postmaturity syndrome to placental senescence, although he did not ind placental degeneration histologically. Still, the concept that postmaturity stems from placental insuiciency has persisted despite an absence of morphological or signiicant quantitative findings (Larsen, 1995; Redman, 2015; Rushton, 1991). here are indings that the
FIGURE 43-3 Mean daily fetal growth during previous week of gestation. (Redrawn from Hendricks CH: Patterns of fetal and placental growth: the second half of pregnancy. Obstet Gynecol 24:357, 1964.) rate of placental apoptosis-programmed cell death-is significantly greater at 41 to 42 completed weeks compared with that at 36 to 39 weeks (Smith, 1999). Several proapoptotic genes such as kisspeptin are upregulated in postterm placental explants compared with the same genes in term placental explants (Torricelli, 2012). The clinical significance of such apoptosis is currently unclear.
Jazayeri and coworkers (1998) investigated cord blood erythropoietin levels in 124 appropriately grown newborns delivered from 37 to 43 weeks. he only known stimulator of erythropoietin is decreased partial oxygen pressure. Thus, they sought to assess whether fetal oxygenation was compromised due to placental aging in postterm pregnancies. All women had an uncomplicated labor and delivery. These investigators found that cord blood erythropoietin levels were significantly higher in pregnancies reaching 41 weeks or more. Although Apgar scores and acid-base studies were normal, these researchers concluded that fetal oxygenation was decreased in some postterm gestations.
Another scenario is that the postterm fetus may continue to gain weight and thus be unusually large at birth. This at least suggests that placental function is not severely compromised. Indeed, continued fetal growth is the norm-albeit at a slower rate beginning at 37 completed weeks (Fig. 43-3). Nahum and colleagues (1995) conirmed that fetal growth continues until at least 42 weeks. However, Link and associates (2007) showed that umbilical blood low did not increase concomitantly.
The principal reasons for increased risks to postterm fetuses were described by Leveno and associates (1984). Both antepartum fetal jeopardy and intrapartum fetal distress were found to be the consequence of cord compression associated with oligohydramnios. In their analysis of 727 postterm pregnancies, intrapartum fetal distress detected with electronic monitoring was not associated with late decelerations characteristic of uteroplacental insuiciency. Instead, one or more prolonged 1008060 -.0 100f80 -0