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For a fetus to thrive in utero, an adequate number of fetal cells and cells that differentiate properly are both requisite. In addition, nutrients and oxygen must be available via an adequately functioning uteroplacental unit to allow an increase in the number of cells and in cell size. Early in pregnancy, fetal growth occurs primarily through cellularhyperplasia, or cell division, and early-onset IUGR maylead to an irreversible diminution of organ size and, per-haps, function. Early-onset IUGR is also more commonly associated with heritable factors, immunologic abnormal-ities, chronic maternal disease, fetal infection, and multi-ple pregnancies. Later in pregnancy, fetal growth depends increasingly on cellular hypertrophy rather than hyper-plasia alone, so that delayed-onset IUGR may also result in decreased cell size, which may be more amenable to restoration of fetal size with adequate nutrition. The nor-mal fetus grows throughout the pregnancy, but the rate of growth decreases after 37 weeks of gestational age as the fetus depletes fat for cellular growth.
The placenta grows early and rapidly compared with the fetus, reaching a maximum surface area of about 11 m2 and weight of 500 g at approximately 37 weeks of gesta-tional age. Thereafter, there is a slow but steady decline in placental surface area (and, hence, function), primarily because of microinfarctions of its vascular system. Late-onset growth restriction may therefore be primarily related to decreased function and nutrient transport of the utero-placental unit, a condition termed uteroplacental insuf-ficiency. In addition, because there is a close relationshipbetween placental surface area and fetal weight, factors that act to decrease placental size are also associated with decreased (i.e., restricted) growth.
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