Definition. In the past, the terms intrauterine growth restriction (IUGR) and small for gestational age (SGA) were used interchangeably. Although related, they are not synonymous. IUGR is the failure to attain optimal intrauterine growth, whereas SGA describes an infant whose weight is lower than population norms or lower than a predetermined cutoff weight. SGA infants are defined as having a birthweight below the 10th percentile for gestational age or >2 standard deviations below the mean for gestational age.
The ponderal index, arrived at by the following formula, can be used to identify infants whose soft tissue mass is below normal for the stage of skeletal development. A ponderal index <10th percentile may be used to identify IUGR infants. Thus all IUGR infants may not be SGA, and all SGA infants may not be small as a result of a growth-restrictive process.
Symmetric IUGR (HC = Ht = Wt, all <10%). The head circumference (HC), length (Ht), and weight (Wt) are all proportionately reduced for gestational age. Symmetric IUGR is due to either decreased growth potential of the fetus (congenital infection or genetic disorder) or extrinsic conditions that are active early in pregnancy.
Asymmetric IUGR (HC = Ht < Wt, all <10%). Fetal weight is reduced out of proportion to length and head circumference. The head circumference and length are closer to the expected percentiles for gestational age than is the weight. In these infants, brain growth is usually spared. The usual causes are uteroplacental insufficiency, maternal malnutrition, or extrinsic conditions appearing late in pregnancy.
Incidence. About 3–10% of all pregnancies are associated with IUGR, and 20% of stillborn infants are growth retarded. The perinatal mortality rate is 5–20 times higher for growth-retarded fetuses, and serious short- or long-term morbidity is noted in half of the affected surviving infants. IUGR is estimated to be the predominant cause for low birthweight in developing countries. It is estimated that a third of infants with birthweights <2500 g are in fact growth retarded and not premature. Term infants with birthweights <3rd percentile have a higher morbidity and a 10 times higher mortality than appropriate for gestational age infants. In the United States, uteroplacental insufficiency is the leading cause of IUGR. An estimated 10% of cases are secondary to congenital infection. Chromosomal and other genetic disorders are reported in 5–15% of IUGR infants. Estimation of IUGR may vary based on neonatal or fetal growth charts used to define IUGR.
Pathophysiology. Fetal growth is influenced by fetal, maternal, and placental factors.
Fetal factors (Table 97–1)
Genetic factors. Approximately 20% of birthweight variability in a given population is determined by fetal genotype. Genetic determinants of fetal growth have their greatest impact in early gestation during the period of rapid cell development. Racial and ethnic backgrounds influence size at birth irrespective of socioeconomic status. Males weigh an average of 150–200 g more than females at birth. This weight increase occurs late in gestation. Birth order affects fetal size; infants born to primiparous women weigh less than subsequent siblings. Genetic disorders such as achondroplasia, Russell-Silver syndrome, and leprechaunism also present with IUGR.
Chromosomal anomalies. Chromosomal deletions or imbalances result in diminished fetal growth. Nearly 20% of fetal growth restriction is due to chromosomal aberrations. Growth retardation is observed as a major feature of uniparental disomy (eg, Silver Russell syndrome), short-arm deletion of chromosome 4, long-arm deletion of chromosome 13, and trisomies 13, 18, and 21. Additional X chromosomes beyond norm are associated with diminished birthweight (eg, XXY, XXXY). The risk for recurrence of fetal aneuploidy is 1%.
Congenital malformations. Anencephaly, gastrointestinal atresia, Potter syndrome, and pancreatic agenesis are examples of congenital anomalies associated with IUGR. Frequency of IUGR increases as the number of congenital defects increases.
Fetal cardiovascular anomalies (with the possible exception of transposition of the great vessels and tetralogy of Fallot). Abnormal hemodynamics are thought to be the basis of IUGR.
Congenital infection. TORCH infections (toxoplasmosis, other, rubella, ...
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