Most clinical studies support theview that diminished amnionic fluid determined by various sonographic methods identifies a postterm fetus with increased risks. Indeed, decreased amnionic luid in any pregnancy signiies increased fetal risk (Chap. 11r, p. 231). Unfortunately, lack of an exact method to define "decreased amnionic luid" has limited investigators, and many diferent criteria for sonographic diagnosis have been proposed. Fischer and colleagues (1993) attempted to determine which criteria were most predictive of normal versus abnormal outcomes in postterm pregnancies. As shown in Figure 43-5, the smaller the amnionic luid pocket, the greater the likelihood that there was clinically signiicant oligohydramnios. Importantly, normal amnionic luid volume did not preclude abnormal outcomes. lfirevic and coworkers (1997) randomly assigned 500 women with postterm pregnancies to assessment using either the amnionic luid index (AFI) or the deepest vertical pocket described in Chapter 11 (p. 226). They concluded that the AFI overestimated the number of abnormal outcomes in postterm pregnancies.
Regardless of the criteria used to diagnose oligohydramnios in postterm pregnancies, most investigators have found a higher incidence of some measure of "fetal distress" during labor. Thus, oligohydramnios by most definitions is a clinically meaningful finding. Conversely, reassurance of continued fetal well-being in the presence of "normal" amnionic luid volume is tenuous. This may be related to how quickly pathological oligohydramnios develops. Although such cases are unusual, Clement and coworkers (1987) described six postterm pregnancies in which amnionic luid volume diminished abruptly over 24 hours, and in one of these, the fetus died.
: 80 00 20 : 6.7em< 5em< 2em< 1 em
FIGURE 43-5 Comparison of the prognostic value of various pregnancies. Abnormal outcomes include cesarean or operative vaginal delivery for fetal jeopardy, 5-minute Apgar score �6, umbili cal arterial blood pH <7.1, or admission to the neonatal intensive care unit. (Redrawn from Fischer RL, McDonnell M, Bianculli KW, et al: Amniotic fluid volume estimation in the postdate pregnancy: a comparison oftechniques. Obstet Gynecol 81 :698, 1993.) he velocity of fetal weight gain peaks at approximately 37 weeks (see Fig. 43-3). Although growth velocity slows at that time, most fetuses continue to gain weight. For example, the percentage of fetuses born in 2009 whose birthweight exceeded 4000 g was 8.2 percent at 37 to 41 weeks and increased to 11.0 percent at 42 weeks or more (Martin, 2011). According to Duryea and associates (2014), the 95th percentile at 42 weeks is 4475 g. Even so, in some studies, brachial plexus injurywas not related to postterm gestation (Walsh, 2011). Intuitively, it seems that both maternal and fetal morbidity associated with macrosomia would be mitigated with timely induction to preempt urther growth. This, however, does not appear to be the case. The American College ofObstetricians and Gynecologists (2016c) has concluded that current evidence does not support such a practice in women at term with suspected fetal macrosomia. Moreover, the College concluded that in the absence of diabetes, vaginal delivery is not contraindicated for women with an estimated fetal weight up to 5000 g (Chap. 27, p. 520). Obvious problems with all such recommendations are substantive variations in fetal weight estimation.