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INTRAUTERINE GROWTH RESTRICTION
“Fetal growth restriction” describes infants whose weights are much lower than expected. Population-based norms are used to categorize abnormal growth. A fetus or infantwhose weight is less than the 10th percentile of a specific pop-ulation at a given gestational age is designated as having intrauterine growth restriction [IUGR](Table 18.1).Therefore, careful assignment of gestational age is cru-cial to the diagnosis and management of patients with IUGR.
The term “small for gestational age” (SGA) is used to describe an infant with a birth weight at the lower extreme of the normal birth weight distribution. In the United States, the most commonly used definition of SGA is a birth weight below the 10th percentile for gestational age. The use of the terms “small for gestational age” (SGA) and “intrauterine growth restriction” has been confusing, and the terms often are used interchangeably.
The use of gestational age percentiles remains lim-ited for a number of reasons. First, by definition, the preva-lence of IUGR will be 10%, but not all such neonates are pathologically small. Second, any percentile cut-off fails to take into account an individual’s growth potential. Also, a simple percentile cannot take into account growth rate. The change in percentile over time or change in specific measurements may be more important. Finally, the time when the growth restriction is found may be a factor in morbidity and mortality: growth restriction at earlier gestational ages has greater effects on morbidity and mortality.
The goal of recognizing neonates with growth abnormalities is to identify infants at risk for increased short-term and long-term morbidity or mortality.
In the short-term, the growth restricted fetus potentially lacks adequate reserves to continue intrauterine existence, to undergo the stress of labor, or to fully adapt to neonatal life. These conditions make the infant vulnerable to intra-uterine fetal death, asphyxia, acidemia, and intolerance to labor. Neonatal complications, low Apgar scores, poly-cythemia, hyperbilirubinemia, hypoglycemia, hypothermia, apnea, respiratory distress, seizures, sepsis, meconium aspi-ration, and neonatal death.
Alterations in fetal growth may have lifelong implica-tions. The antenatal response or fetal adaptation to the intrauterine nutritional and metabolic environment may predict or dictate the response to an extrauterine environ-ment. Increasing evidence supports the concept of fetal origins for adult diseases and the association between birth size and long-term health. Associations have been reported between birth weight and adult obesity, cardiovascular dis-ease (coronary heart disease, hypertension, and stroke), insulin resistance, and dyslipidemia. Therefore, intrauter-ine growth may reflect the foundation of many aspects of lifelong physiologic function.
In general, the smaller the fetus with IUGR, the greater its risk for morbidity and mortality. Perinatal morbidity andmortality is significantly increased in the presence of low birth weight for gestational age, especially with weights below the 3rd percentile for gestational age. One study found that 26% of all stillbirths were SGA. Thus, it is important to identify such infants in utero so that management maximizes the quality of their intrauterine environment, permits planning and implementation of delivery using the safest means possible, and provides necessary care in the neonatal period.
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.
IUGR is a descriptive term for a condition that has numerous potential causes. Determining the specific diagnosis is impor-tant for optimal management. Although a number of causes of IUGR have been recognized, a definite etiology of IUGR cannot be identified in approximately 50% of all cases. In addition, because the utilization of a percentile cut-off of 10% alone will result in a high proportion of false-positives, two-thirds or more of such fetuses categorized as IUGR will be simply constitutionally small and otherwise healthy.
Factors that affect fetal growth are extensive and include maternal, fetal, and placental causes; these are listed in Box 18.1.
Maternal factors include viral infections, such as rubella, varicella, and cytomegalovirus, which are associated with high rates of growth restriction, particularly if infection occurs early in pregnancy. Although these infections may manifest only as mild “flu-like” illnesses, injury to the fetus during organogenesis can result in a decreased cell number, resulting in diminished growth with or without multiple congenital anomalies. Five percent or fewer of all cases of IUGR are related to early infection with these or other viral agents. Maternal substance abuse affects fetal growth and almost all infants with fetal alcohol syn-drome will be growth-restricted. Women who smoke during pregnancy deliver babies 200 g smaller on average than do women who do not smoke; moreover, the rate of growth restriction is 3- to 4-fold greater among babies born to women who smoke during pregnancy. Women who use narcotics, heroin, methadone, or cocaine also have rates of growth-restricted babies ranging from as much as 30% to 50%. Medications known to be associ-ated with IUGR include anticonvulsant medications, warfarin, and folic acid antagonists. Altitude may also affect fetal growth.
Other maternal factors that affect fetal growth and body composition include demographic factors and med-ical conditions. Extremes in maternal age (age younger than 16 years and older than 35 years) are associated with an increased risk of fetal growth restriction. Medical conditions that alter or affect placental function may also be causative factors.
Although one common pathway has not been clearly identified, many of these disorders occur together. Women with a history of prior obstetric complications have an increased risk of growth abnormalities. Maternal metabo-lism and body composition are two of the strongest regula-tors of fetal growth. Nutritional deficiencies and inadequate weight gain, particularly in teens or in underweight women, may result in IUGR.
The inherent growth potential of the individual is deter-mined genetically. Female fetuses are at greater risk for IUGR than males. In addition, up to 20% of growth-restricted fetuses have a chromosomal abnormality. In addition, single-gene mutations such as the glucokinase gene mutation, or genetic syndromes such as Beckwith-Wiedemann syndrome can also result in abnormalities of growth. Finally, multifetal pregnancies are at increased risk for growth restriction.
The placenta is critical for nutrient regulation and trans-portation from mother to fetus. Abnormalities in placenta-tion or defective trophoblast invasion and remodeling may contribute to fetal growth restriction as well as other dis-orders of pregnancy. In addition, uterine anomalies (uter-ine septum or fibroids) may limit placental implantation and development and, consequently, nutrient transport, result-ing in inadequate nutrition for the developing fetus. Finally, the genetic composition of the placenta is important and abnormalities such as confined placental mosaicism are asso-ciated with growth delay.
Assessment of gestational age is important in early preg-nancy, because dating becomes increasingly imprecise at later gestational ages.Antenatal recognition of IUGR depends upon the recognition of risk factors and the clinical assessment of uterine size, fol-lowed by biometric measurements.
Physical examination is limited in usefulness in recognizing IUGR or in making a specific diagnosis, but it is an impor-tant screening test for abnormal fetal growth. Maternal size and weight gain throughout pregnancy also have limited value, but access to such information is readily available; a low maternal weight or little or no weight gain during pregnancy may suggest IUGR. Serial measurements of fundal height are commonly used as a screening test forIUGR, but have high rates of false-negative and false-positive predictive values. Between 20 and 36 weeks of ges-tation, fundal height should increase approximately 1 cm per week, consistent with gestational age in weeks (Fig. 18.1). A discrepancy may be related to constitutional factors, but a significant discrepancy of more than 2 cm may indicate IUGR and the need for an ultrasound examination. Clinical estimations of fetal weight alone are not helpful in diagnos-ing IUGR, except when fetal size is grossly diminished.
If IUGR is suspected based on risk factors and clinical assessment, ultrasonography should be performed to assess fetal size and growth. Specificfetal biometry measurementsare compared with standardized tables that reflect normal growth at a certain gestational age. The four standard fetal measurements include the (1) biparietal diameter, (2) head circumference (HC), (3) abdominal circumference (AC), and (4) femur length. Conversion of individual morphologic measurements to fetal weight using published equations or ratios of measurements can provide useful estimations of fetal size. An abdominal circumference within the normal range reliably excludes growth restriction, with a false-negative rate of less than 10%. A small abdominal circum-ference or fetal weight estimate below the 10th percentile suggests the possibility of growth restriction, with the likelihood increasing as the percentile rank decreases.
When IUGR is suspected, serial measurements of fetal biometric parameters provide an estimated growth rate. Suchserial measurements are of considerable clinical value in confirming or excluding the diagnosis and assessing the progression and severity of growth restriction. Given the high incidence of genetic and structural defects associated with IUGR, a detailed ultrasound survey for the presence of fetal structural and functional defects may be indicated.
Following recognition of altered fetal growth, a search for potential etiology should ensue. Ultrasonography should in-clude a detailed anatomic survey to evaluate for the pres-ence of structural anomalies, given the high incidence of genetic and structural defects with IUGR. Ultrasound eval-uation should also include an assessment of amniotic fluidvolume. The combination of oligohydramnios (dimin-ished amniotic fluid volume) and IUGR is associated with severe disease and increased morbidity. The mechanism of decreased amniotic fluid is thought to be decreased placen-tal perfusion of oxygen and nutrients with a compensatory redistribution of fetal blood favoring the brain, adrenal gland, and heart. The consequent decrease in fetal blood to the kidneys leads to a reduction of urine output, which is the primary source of amniotic fluid in the second half of pregnancy.
Direct invasive studies of the fetus are useful in selected patients with IUGR. Amniocentesis for fetal lung matu-rity may assist delivery planning near term or when there is uncertainty regarding gestational age and concern for growth restriction. Fetal karyotyping and viral cultures and polymerase chain reactions can be performed on fluid obtained by amniocentesis. Rarely, chorionic villus sam-pling (biopsy of placenta) or direct blood sampling (per-cutaneous umbilical blood sampling) may be necessaryfor specific studies.
Doppler velocimetry of fetal vessels provides furtherinsight into the fetal response to altered growth, and has become part of the standard assessment of the fetus once IUGR is diagnosed. Doppler velocimetry has been shown to both reduce interventions and improve fetal outcome in pregnancies at risk for IUGR. Fetal-placental circula-tion is evaluated in the umbilical artery and is measured by a systolic/diastolic (S/D) ratio. The S/D indirectly mea-sures impedance or resistance downstream within the pla-cental vessels. As placental resistance increases, diastolic flow decreases and the S/D ratio rises. A normal S/D ratioat term is 1.8 to 2.0. Fetuses with IUGR with absent or reversed diastolic flow have progressively worse perinatal outcomes (Figure 18.2).
The fetal middle cerebral artery is also evaluated and reflects fetal adaptation. The patho-physiologic response to reduced placental perfusion gen-erally spares the fetal brain, resulting in an increase of diastolic and mean blood flow velocity in the middle cere-bral artery. Ductus venosus may also be evaluated by Doppler ultrasound, and the fetus with abnormal ductus flow is at very high risk of adverse outcome.
The goal of management of a growth-restricted fetus is to deliver the healthiest possible infant at the optimal time. Continued management of pregnancy with IUGR is based on the results of fetal testing.
Serial evaluations of fetal biometry should be performed every 3 or 4 weeks to follow the extent of growth restriction. Fetal monitoring is important, and may include fetal move-ment counting, nonstress testing, biophysical profiles, and Doppler studies. There are no specific therapies that have proven beneficial for pregnancies complicated by IUGR.
The fetus should be delivered if the risk of fetal death exceeds that of neonatal death, although in many cases these risks are difficult to assess.
For example, a fetus with IUGR with normal anatomic sur-vey, normal amniotic fluid volume, normal Doppler studies, and normal fetal testing may not benefit from early delivery. Conversely, the growth-restricted fetus with serial biometry measurements documenting decreasing growth rate and/or mildly abnormal Doppler studies may benefit from deliv-ery, with or without fetal maturity documentation.
Neonatal management of IUGR infants may partially depend on gestational age, but includes preparation for neonatal respiratory compromise, hypoglycemia, hypo-thermia, and hyperviscosity syndrome. Growth-restricted fetuses have less fat deposition in late pregnancy, so newborn euglycemia cannot be maintained by the normal mechanism of mobilization of glucose by fat metabolism. Hyper-viscosity syndrome results from the fetus’s attempt tocompensate for poor placental oxygen transfer by increas-ing the hematocrit to more than 65%. After birth, this marked polycythemia can cause multiorgan thrombosis, heart failure, and hyperbilirubinemia. Overall, growth-restricted infants who survive the neonatal period have a generally good prognosis.
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