RISK FACTORS AND ETIOLOGIES.................. 849
FETAL-GROWTH RESTRICTION RECOGNITION....... 852
MANAGEMENT................................. 854
FETAL OVERGROWTH......................... 856
RISK FACTORS ................................. 857
MANAGEMENT. ............................... 858
When inants are of large size and abundant, they may mechanicaly throw out of function so great a portion of the placenta as seriousy to inteere with the nutrition of the oetus, and sometimes cause its death. Excessive development of the oetus can usualy be traced to prolongation of pregnancy, large size of one or both parents, advancing age, or multipariy of the mother.
-J. Whitridge Williams (1903) he concept of excessive or impaired fetal growth was not considered in detail by Williams in his irst edition. Abnormally diminished fetal growth was attributed to placental lesions and fetal infections. Conversely, a large fetus was of obvious concern because of associated dystocia. Currently, fetal-growth disorders at both ends of the spectrum are major problems in obstetrics.
Nearly 20 percent of the almost 4 million neonates born in the United States are at the low and high extremes of fetal growth.
In 2015, 8.1 percent of newborns weighed <2500 g at birth, whereas 8.0 percent weighed >4000 g. And, although almost 70 percent of low-birthweight neonates are born preterm, the balance of low-birthweight newborns accounted for approximately 3 percent of term births in 2015 (Martin, 2017). Between 1990 and 2006, the proportion of newborns with birthweights <2500 g grew by more than 20 percent when the rate peaked at 8.3 percent (Martin, 2012). his trend toward smaller babies has slowed since the mid-to late-2000s and might partly be explained by the concurrent movement toward fewer deliveries prior to 39 weeks' gestation (Richards, 2016). In contrast, between 1990 and 2006, the incidence of birth weights >4000 g declined approximately 30 percent to a nadir of 7.6 percent in 2010 (Martin, 2012). This trend away from the upper extreme is diicult to explain because it coincides with the epidemic prevalence of obesity, a known cause of macrosomia (Morisaki, 2013).
Human fetal growth is characterized by sequential patterns of tissue and organ growth, diferentiation, and maturation. However, the "obstetrical dilemma" postulates a conlict between the need to walk upright-requiring a narrow pelvis-and the need to think-requiring a large brain, and thus a large head. Some speculate that evolutionary pressures restrict growth late in pregnancy (Mitteroecker, 2016). Thus, the ability to growth restrict may be adaptive rather than pathological.
Fetal growth has been divided into three phases. The initial phase of hyperplasia occurs in the irst 16 weeks and is characterized by a rapid increase in cell number. The second phase, which extends up to 32 weeks' gestation, includes both cellular hyperplasia and hypertrophy. After 32 weeks, fetal mass accrues by cellular hypertrophy, and it is during this phase that most fetal fat and glycogen are accumulated. The corresponding c 5..,