Fetal growth restriction: Evaluation and management Author Robert Resnik, MD Section Editor Charles J Lockwood, MD Deputy Editor

Vanessa A Barss, MD

Last literature review version 19.1: January 2011 | This topic last updated: January 25, 2011 (More) INTRODUCTION Fetal growth restriction (FGR) presents a complex management problem. Growth aberrations that result from intrinsic fetal factors such as aneuploidy, congenital malformations, and fetal infection carry a guarded prognosis that often cannot be improved by any intervention. By comparison, FGR related to inadequate substrates for fetal metabolism and decreased oxygen availability has a better prognosis. The obstetrical provider's tasks are to identify when inadequate growth occurs, determine its cause and severity, counsel the parents, consult with neonatal colleagues, carefully monitor fetal growth and well-being, and select the appropriate time and mode of delivery. INITIAL DIAGNOSTIC EVALUATION Diagnosis of FGR is based upon sonographic findings, which are discussed in detail separately. (See "Diagnosis of fetal growth restriction".) A complete history and physical examination is performed to look for maternal, placental, or fetal disorders associated with impaired fetal growth (eg, alcohol or tobacco use, maternal vascular disease). Additional imaging and laboratory evaluations are also directed toward determining an etiology. (See "Overview of causes of and risk factors for fetal growth restriction".) A detailed fetal anatomic survey is recommended in all cases since major congenital anomalies are frequently associated with failure to maintain normal fetal growth. Among malformed infants, the frequency of FGR ranges from 20 to 60 percent, with the highest risk in infants with multiple anomalies [1]; approximately 10 percent of FGR is accompanied by congenital anomalies [2]. Anomalies associated with FGR include omphalocele, diaphragmatic hernia, skeletal dysplasia, and congenital heart defects; thus, examination of the fetal heart (fetal echocardiogram) and skeleton are particularly important. Microcephaly, although rare, is associated with several syndromes manifesting growth restriction. Polyhydramnios is associated with trisomy 18 and several congenital anomalies. (See "Prenatal sonographic diagnosis of fetal cardiac anomalies" and "Polyhydramnios".)Fetal karyotyping is suggested if FGR is early (<32 weeks), severe (<3rd percentile), or accompanied by polyhydramnios (suggestive of trisomy 18) or structural anomalies [3]. From 10 to 40 percent of structurally abnormal growth restricted fetuses will have an abnormal karyotype [3,4], the highest risk is in those with multiple anomalies or certain types of anomaly. By comparison, only 2 percent of structurally normal growth restricted fetuses have a chromosomal abnormality [4]. Early onset FGR is commonly observed with trisomy 18, trisomy 13,

and triploidy (table 1). Ultrasound markers suggestive of aneuploidy include echogenic bowel, nuchal thickening, and abnormal hand positioning. (See "Sonographic findings associated with fetal aneuploidy".)When there is a clinical suspicion of viral infection (eg, maternal or fetal signs/symptoms of cytomegalovirus, rubella, varicella), maternal serum should be examined for evidence of seroconversion. Specific amniotic fluid viral DNA testing can also be performed, when indicated. Sonographic markers for viral infection are often nonspecific but include echogenicity and calcification of the brain and liver, and hydrops. (See individual topic reviews on viral infections during pregnancy).Assessment for congenital and acquired thrombophilic disorders may be considered, but the evidence for an association between the inherited thrombophilias and FGR is weak and based on case-control or cohort studies [5-8]. (See "Inherited thrombophilias in pregnancy".) If the fetus is small, but anatomically normal with an appropriate amniotic fluid volume and growth rate, the outcome will usually be a normal, constitutionally small neonate. In this regard, it is important to recognize ethnic and geographic differences in growth potential. As an example, if one compares fetal growth curves derived from US national data to those from Japan and China, it is clear that the slopes of the curves are similar, but there are disparate weight cut-offs at the 10th percentile [9-11]. This had led to the development of "customized" growth curves, which take into account fetal growth potential based upon the mother's height, prepregnant weight, parity, and ethnicity, all strong contributors to ultimate fetal weight [12,13]. This approach more reliably distinguishes those fetuses who are truly growth restricted and at increased risk of morbidity and mortality from those who are small but normal [14-16]. It is imperative to distinguish between the constitutionally small fetus and the fetus with pathologic growth restriction so that unnecessary interventions can be avoided. (See "Diagnosis of fetal growth restriction".) SUBSEQUENT OBSTETRICAL MANAGEMENT The optimal method(s) of monitoring the fetus with suspected FGR has not been established. Periodic assessment, once or twice weekly from the age of viability, using the biophysical profile (BPP) and Doppler velocimetry is acceptable. The purpose of antenatal monitoring is to try to identify those fetuses who are at highest risk of in utero demise and neonatal morbidity, and thus may benefit from intervention by preterm delivery. Ultrasound evaluation of fetal growth, fetal behavior, amniotic fluid volume, and impedance to blood flow in fetal arterial and venous vessels form the cornerstone of evaluation of the fetal condition and decision making. Serial examinations should be performed with the frequency based upon the severity of findings and whether the examinations are being done to monitor fetal well-being (one to seven times per week) or fetal growth (every three to four weeks). Serial fetal weight assessment Fetal weight estimates are calculated using various published equations and formulae. The computed weight is then plotted on a standard growth curve, which allows the clinician to determine when the estimated weight is below the 10th percentile (table 2) and to follow growth velocity. Serial sonograms are typically obtained at three- to four-week intervals [3]; persistent growth deficiency in multiple examinations over many weeks strengthens the likelihood of FGR. Conversely,

normal growth velocity in the otherwise small fetus is reassuring. (See "Prenatal sonographic assessment of fetal weight" and "Diagnosis of fetal growth restriction".) Biophysical profile The biophysical profile (BPP) is a useful method for monitoring the fetus because it provides an evaluation of multiple acute and chronic fetal physiologic parameters (amniotic fluid volume, nonstress test, fetal movement/tone/breathing), is relatively easy to perform, and is a reliable test of fetal well-being (fetal death within one week of a normal test score is rare) [17]. However, application of the BPP to the growth restricted fetus remote from term may be less reliable since the preterm fetus may not have achieved maturity of the biophysiologic processes measured by this test. Furthermore, although many large observational studies have demonstrated the usefulness of the BPP in antepartum fetal assessment, there is a paucity of evidence derived from randomized trials [18]. (See "The fetal biophysical profile".) The BPP is typically obtained once or twice per week; however, more frequent testing, as often as daily, is indicated for fetuses at highest risk, including but not limited to, severe FGR (less than the fifth percentile), severe oligohydramnios, absent or reversed umbilical artery flow on Doppler velocimetry, or equivocal BPP score (ie, 6/10). Very preterm, severely growth restricted fetuses can deteriorate rapidly; they should be monitored closely using multiple modalities if delivery is to be delayed [19,20]. Amniotic fluid volume Observational studies have shown that FGR pregnancies complicated by oligohydramnios, defined as a single vertical pocket less than 2 x 1 cm or an amniotic fluid index less than 6 cm, have a sharply increased risk of perinatal mortality. Conversely, normal amniotic fluid volume is less frequently associated with either FGR or fetal demise, unless the cause is a congenital malformation or aneuploidy. Therefore, amniotic fluid volume should be assessed serially as part of the BPP or modified BPP (nonstress test and assessment of amniotic fluid volume). Some evidence suggests that use of the single deepest vertical pocket rather than the amniotic fluid index results in a lower cesarean delivery rate for fetal distress and fewer unnecessary interventions [21]. (See "Oligohydramnios".) Doppler velocimetry Doppler velocimetry is recommended as the primary surveillance tool for monitoring pregnancies in which FGR is suspected [22]. It has been well established by numerous randomized trials that the use of Doppler velocimetry can significantly reduce perinatal death as well as unnecessary induction of labor in the preterm growth restricted fetus. A Cochrane intervention review of 11 studies comparing the use of Doppler to no Doppler in high risk pregnancies showed a trend in reduction of perinatal deaths by 29 percent (OR 0.71, 95% CI 0.5-1.01), and significantly fewer labor inductions and hospital admissions [23]. There were no differences between groups in the diagnosis of fetal distress in labor or cesarean delivery. Absence or reversal of end-diastolic flow in the umbilical artery is suggestive of poor fetal condition, whereas normal or decreased umbilical Doppler flow is rarely associated with significant morbidity and provides strong evidence of fetal well-being when delivery is delayed to achieve further fetal maturity [24]. In general, when the Doppler systolic/diastolic ratio remains within normal limits or is not progressively rising, the pregnancy can be followed with weekly Doppler evaluation. The biophysical

profile should be used either as an interval test between Doppler examinations or twice weekly, with one test at the time of the Doppler examination. One trial reported that growth restricted fetuses with normal umbilical artery Doppler impedance could be safely evaluated (and with fewer interventions) with fortnightly, rather than twice weekly, surveillance [25]. This approach would be cost effective without compromising clinical efficacy, but requires further corroboration. The growth restricted fetus seems to be at highest risk of imminent demise when Doppler abnormalities are observed in the venous circulation (ductus venosus and umbilical vein) [26]. The temporal sequence of abnormal Doppler changes in the peripheral and central circulatory systems of the growth restricted fetus have been described: early abnormal Doppler findings in the umbilical and middle cerebral arteries are followed by reversal of flow in the ductus venosus or pulsatile umbilical venous flow in the week before delivery is necessitated (figure 1) [19,27-29]. However, the cardiovascular (Doppler) and behavioral (BPP) manifestations of fetal deterioration in FGR fetuses can occur largely independent of each other resulting in discordant Doppler and BPP findings [30]. The best approach when this occurs is not clear, and the physician must analyze each case individually taking into account such factors as the obstetrical situation, gestational age, degree of abnormality, and results from other tests of fetal well-being. Antenatal glucocorticoids The efficacy of antenatal glucocorticoids in the management of the preterm growth restricted fetus remains controversial, with two large studies showing conflicting results [31,32]. Until more information is available, it is appropriate to administer a course of antenatal glucocorticoids to the preterm growth restricted fetus to decrease neonatal pulmonary and central nervous system morbidity if preterm delivery occurs. Multiple series have found that both spontaneous and indicated preterm delivery are more common in growth restricted fetuses [33-35]. (See "Antenatal use of glucocorticoids in women at risk for preterm delivery".) Three studies observed that growth restricted fetuses with absent end-diastolic flow often show transient improvement in blood flow after glucocorticoid administration [3638]. Moreover, fetuses that did not show increased end-diastolic flow appeared to have poorer neonatal outcomes. The reason sicker fetuses are unable to mount a vascular response to glucocorticoid administration is unclear. One action of glucocorticoids is to enhance the tropic effect of catecholamines on heart muscle. It is hypothesized that inotropy does not improve in sicker fetuses because they have impaired cardiac wall compliance. Fetal blood sampling Antepartum fetal hypoxemia and acidemia are not associated with neonatal cerebral dysfunction if fetal cardiovascular compensation with increased cerebral blood flow occurs [39]. However, if asphyxia persists, brain damage and death may occur. In the past, fetal blood sampling (FBS) was used in the assessment of fetal acid base status in severely growth restricted fetuses to assist in the identification of the optimal timing for delivery. However, FBS carries a nine to 14 percent rate of procedure related loss among growth restricted fetuses, thus its value for longitudinal assessment of fetal well-being is mitigated by the high risk of fetal death. Since FGR can be managed adequately without invasive techniques, FBS is not recommended to follow fetal status.

(See "Fetal blood sampling: Indications and invasive fetal therapy", section on 'Intrauterine growth restriction'.) Medical interventions There is a paucity of evidence from randomized trials that any specific antenatal treatment for the growth restricted fetus is beneficial. Numerous approaches have been used, including nutritional supplementation, plasma volume expansion [40], low-dose aspirin, heparin, bed rest, maternal oxygen therapy, and betamimetics/calcium channel blockers to improve blood flow to the placenta [41-43]. None have consistently been shown to be of value. In smokers, an intensive smoking cessation program might be of value, and has other pregnancy and health benefits [44,45]. (See "Smoking and pregnancy".) Short-term, maternal hyperoxia may improve fetal acid base status at the time of delivery. Although its long-term use has been reported to lower perinatal mortality compared to controls, the differences may be due to more advanced gestational age in the oxygen-treated group [46]. Antihypertensive therapy of hypertensive gravidas does not improve fetal growth [47-49]. TIMING OF DELIVERY Overview There is little consensus about the optimal timing of delivery of the high risk preterm growth restricted fetus [50]. The decision is determined by both gestational age and fetal condition. The body of information applicable to management and evaluation of these fetuses is complex and in evolution. Nevertheless, a few reasonable conclusions regarding practical clinical management may be drawn. The growth restricted fetus should be delivered if the risk of fetal death, as determined by antepartum monitoring tests, exceeds the risk of neonatal death. The difficulty in making this assessment was illustrated by the Growth Restriction Intervention Trial (GRIT), which randomly assigned pregnant women between 24 and 36 weeks to immediate (n = 296) or delayed (n = 291) delivery if their obstetrician was uncertain about when to intervene [50]. Ninety percent of the pregnancies were complicated by clinical evidence of growth restriction and 40 percent had absent or reversed end diastolic umbilical artery flow. In the delayed delivery group, delivery occurred when the obstetrician was no longer uncertain about intervening (median delay 4.9 days). Deaths prior to hospital discharge were similar in both groups (29 deaths with immediate delivery and 27 deaths with delayed delivery). The immediate delivery group had fewer stillbirths (2 versus 9), but more neonatal and infant deaths (27 versus 18). Follow-up data at two years of age showed that the proportion of children with death or severe disability was similar for both groups (19 percent of immediate and 16 percent of delayed births) [51]. The small excess risk of mortality/severe disability in the immediate delivery group was primarily related to children randomized before 31 weeks of gestation. For this reason, the authors recommended delayed delivery in very preterm gestations if there was uncertainty about the need for intervention. Follow-up data at age 6 to 13 years showed no differences between groups in cognition, language, motor, or parent-assessed behavior scores on standardized tests; follow-up

was achieved in approximately 70 percent of survivors [52]. Cognition scores were close to the standardized normal range. The overall proportion of children dead or with severe disability was also similar for both groups (14 percent of immediate and 17 percent of delayed births). Taken together, these data suggest that delaying delivery of the preterm growth restricted fetus in the setting of uncertainty results in some stillbirths, but immediate delivery produces an almost equal number of neonatal deaths, and neither approach results in better long-term neurodevelopmental outcome. A prospective multicenter study came to similar conclusions. Over 600 singleton fetuses at less than 33 weeks of gestation with normal anatomy and karyotype, FGR, intact membranes, and elevated umbilical artery resistance were followed with serial examinations [53]. At very preterm gestations, gestational age was the most important factor predicting outcome: neonatal survival was less than 50 percent before 26 weeks of gestation; intact survival was less than 50 percent before 28 weeks of gestation. After 26 to 28 weeks, fetal assessment tests (ductus venous Doppler, biophysical profile) were useful in deciding whether to continue expectant management to allow further growth and maturation versus intervention to prevent in utero demise. A birth weight over 600 g was also an important predictor of survival. The table summarizes our evaluation and management of FGR (table 3). Remote from term In growth restricted fetuses remote from term, evidence of normal umbilical artery flow by Doppler velocimetry is reassuring with regard to immediate fetal outcome; prolongation of pregnancy to gain further fetal maturity is reasonable in these cases. However, absence or reversal of flow is an ominous finding, and prompt delivery is often indicated because of a high risk of fetal demise. (See "Doppler ultrasound of the umbilical artery for fetal surveillance".) Changes in the venous circulation, including evidence of flow reversals in the ductus venosus or pulsatile umbilical venous flow, generally occur later than those observed in the arterial circulation; they appear to be more predictive of impending adverse outcome, and warrant immediate delivery regardless of gestational age [22,54]. The use of venous Doppler interrogation in the growth restricted fetus remains largely investigational. However, a growing number of perinatologists are using the information gained from such studies in fetuses with absent end-diastolic arterial flow very remote from term in an effort to avoid very preterm deliveries. In these pregnancies, the absence of abnormal flow patterns in the ductus venosus might be used to support the decision to extend such a pregnancy. (See "Venous Doppler for fetal assessment".) Term or late preterm Delivery of the term or late preterm (>34 weeks) growth restricted fetus is recommended if there is maternal hypertension, arrest of growth over a three- to fourweek interval, the BPP score is low, and/or umbilical arterial Doppler velocimetry reveals absence or reversal of flow. However, the specific clinical situation in each case must be considered and management individualized.When FGR is mild and uncomplicated (no fetal abnormalities or contributing maternal disorders), end diastolic

flow is present, and antepartum fetal testing results are reassuring, delivery can be delayed until at least 37 weeks when pulmonary maturity is likely [55,56].In general, pregnancies complicated by FGR should not extend beyond 40 weeks of gestation. INTRAPARTUM MANAGEMENT Growth restricted fetuses may exist in a state of mild-to-moderate chronic oxygen and substrate deprivation, which may result in antepartum or intrapartum/neonatal hypoxia and neonatal ischemic encephalopathy, fetal heart rate abnormalities, meconium aspiration, polycythemia, hypoglycemia, and other metabolic abnormalities [57]. Consequently, it is imperative to optimize the timing of delivery as discussed above, perform continuous intrapartum fetal monitoring to detect nonreassuring fetal heart rate patterns suggestive of progressive hypoxia during labor, and provide immediate skilled neonatal care [58]. Umbilical cord blood analysis should be considered. (See "Umbilical cord blood acid-base analysis".) The risk of fetal heart rate abnormalities related to hypoxia is highest among fetuses with abnormal Doppler velocimetry. In one series of 323 FGR fetuses, those with a systolic/diastolic ratio >90th percentile for gestational age had significantly lower umbilical artery and vein pH values at birth (artery, 7.23 +/- 0.08 versus 7.25 +/- 0.1; vein, 7.31 +/- 0.01 versus 7.34 +/- 0.09) and an increased likelihood of nonreassuring fetal heart rate patterns (26 versus 9 percent) [59]. No fetus with normal Doppler velocimetry was delivered with a metabolic acidemia associated with chronic hypoxemia Labor with careful intrapartum monitoring and vaginal delivery is a reasonable approach in the presence of normal antenatal testing [60]. The clinician should be prepared for rapid intervention if there is any evidence of fetal intolerance to labor. OUTCOME If the fetus is small, but anatomically normal with an appropriate amniotic fluid volume and growth rate, the outcome will usually be a normal, constitutionally small neonate. By comparison, truly impaired fetal growth is associated with increased perinatal mortality and morbidity, and can have long-term effects on growth, development, and cardiovascular health. Mortality Fetal, neonatal, and perinatal mortality are increased in small for gestational age (SGA) compared to appropriate for gestational age (AGA) infants [16,61-64]. Mortality increases as growth restriction becomes more severe, rising abruptly when birth weight is less than or equal to the fifth percentile (figure 2) [65]. Both the severity of growth restriction and degree of prematurity contribute to the increased risk of neonatal death in these fetuses. Although neonatal mortality is higher in SGA than in AGA infants at every gestational age, neonatal mortality is similar for SGA and AGA infants at any given birth weight [50]. Congenital malformations, perinatal asphyxia, and transitional cardiorespiratory disorders contribute to the high mortality rate in term SGA infants. Complications of prematurity play a greater role as gestational age decreases [64]. (See "Small for gestational age infant".) Morbidity SGA infants have a higher risk of neonatal morbidity, particularly among those born very preterm [66-69]. Both spontaneous and induced preterm birth are more common in pregnancies complicated by FGR. (See "Risk factors for preterm labor and delivery", section on 'Fetal factors'.)

Short-term morbidities of SGA infants include impaired thermoregulation, hypoglycemia, polycythemia/hyperviscosity, and impaired immune function. Increased risks of acidemia, respiratory distress, intraventricular hemorrhage, and necrotizing enterocolitis have also been described for mildly preterm SGA infants [66]. Studies have shown a broad range of long-term outcomes, including normal to small decreases in IQ (which are statistically, but not clinically, significant) [70], a reduction in scores for executive cognitive functions (reflectiveness, visual memory and visual motor coordination, planning and sequential processing) [71], and a sharply increased risk of cerebral palsy [72,73]. One report suggested that FGR has a negative impact on intellectual outcome even in the presence of catch-up growth [74]. As might be anticipated, the worst outcomes have been observed in the more severely growthrestricted infants who are preterm, and who exhibit the most overt evidence of impaired umbilical flow [75,76]. Subsequent studies have confirmed the increased risk of intellectual disabilities and lower school achievement among infants who are born growth restricted [77-79]. The prognosis for intact neurologic function is presumably more favorable in the growth restricted fetus when the cause is related to substrate deprivation, the timing of delivery is carefully selected, the fetus remains well oxygenated intrapartum, and the infant receives skilled neonatal care. There may also be deleterious effects on adult health. The Barker hypothesis proposed that the endocrine-metabolic reprogramming that enabled the growth restricted fetus to compensate for the hostile intrauterine environment might lead to a metabolic syndrome in later life with development of hypertension, hypercholesterolemia, impaired glucose tolerance, and ischemic heart disease [80,81]. A systematic review of 80 studies found that blood pressure fell 2 mmHg with each kilogram of increasing birth weight and small head circumference was most consistently associated with high blood pressure [82]. Other studies have reported that FGR is associated with an increased risk of adult ischemic heart disease [81], low-normal renal function [83], and type 2 diabetes in later life [84]. (See "Possible role of low birth weight in the pathogenesis of essential hypertension" and "Overview of the risk factors for cardiovascular disease".) RECURRENCE RISK There is a tendency to repeat SGA or low birth weight deliveries in successive pregnancies [85,86]. Data derived from over 30,000 Norwegian births to women who delivered their first three children within a 10 year period showed that the risks of an SGA birth in a second pregnancy in women whose first delivery was 'not SGA' or 'SGA' were 9 and 29 percent, respectively [85]. After two consecutive SGA births, the risk of a third was 44 percent. Furthermore, uteroplacental insufficiency may manifest in different ways in different pregnancies. As an example, growth restriction, preterm delivery, preeclampsia, abruption, and stillbirth can all be sequelae of impaired placental function. The association between the birth of a SGA infant in a first pregnancy and stillbirth in a subsequent pregnancy was illustrated by analysis of data from the Swedish Birth Register (table 4) [87]; a subsequent US study reported similar findings [88]. The highest risk was in women who delivered a SGA infant prior to 32 weeks of gestation. Another series suggested a sibling delivered after the birth of a SGA infant (even if

mildly SGA) was at increased risk of sudden infant death syndrome [89]. (See "Sudden infant death syndrome".) Prevention In subsequent pregnancies, we address any potentially treatable causes of FGR (eg, encourage cessation of smoking and alcohol intake, give antimalarial prophylaxis in areas where malaria is prevalent, provide balanced energy/protein supplementation in women with significant nutritional deficiencies) [90]. Avoiding a short interpregnancy interval may also be beneficial. (See "Interpregnancy interval and pregnancy outcome".) Although some randomized trials reported low-dose aspirin prophylaxis during pregnancy reduced the risk of recurrent FGR in women at high-risk (eg, fetal growth restriction in a previous pregnancy) [91,92] larger randomized trials did not confirm significant risk reduction [93]. Aspirin may be effective when FGR is related to preeclampsia. In a systematic review of 36 randomized trials including 23,638 women at high risk of developing preeclampsia, use of antiplatelet agents compared to placebo was associated with a 17 percent reduction in the risk of preeclampsia and a 10 percent reduction in the risk of SGA births (RR 0.90, 95% CI 0.83-0.98) [94]. Further study is needed. Antihypertensive therapy of hypertensive women, long-chain polyunsaturated fatty acid supplements, beta-mimetics, and bedrest do not prevent FGR [43,47-49,95,96]. Management of subsequent pregnancies Accurate dating by early ultrasonography is important to establish gestational age and intermittent ultrasound examinations are used to monitor fetal growth. Otherwise, management is routine. SUMMARY AND RECOMMENDATIONS Initial approach A detailed fetal anatomic survey is recommended in all cases of fetal growth restriction since major congenital anomalies are frequently associated with failure to maintain normal fetal growth.Fetal karyotyping is suggested if there are structural anomalies, early (<32 weeks) or severe (<3rd percentile) growth restriction, or polyhydramnios (suggestive of trisomy 18) since each of these findings is associated with an increased frequency of karyotypic abnormality.Maternal serum should be examined for evidence of seroconversion if there are maternal or fetal signs suggestive of viral infection. (See 'Initial diagnostic evaluation' above.) Antepartum management Serial ultrasound evaluation of fetal growth, fetal behavior, amniotic fluid volume, and impedance to blood flow in fetal arterial and venous vessels form the cornerstone of evaluation of the fetal condition and decision making. The frequency is based upon the severity of findings and whether the examinations are being done to monitor fetal wellbeing (one to seven times per week) or fetal growth (every two to four weeks). (See 'Subsequent obstetrical management' above.)Doppler velocimetry is recommended for monitoring pregnancies in which growth restriction is suspected because delivery prompted by abnormal Doppler ultrasonography reduces the frequency of perinatal

death. Normal Doppler findings are reassuring and thus potentially allow prolongation of pregnancy and reduction in the number of unnecessary preterm inductions. (See 'Doppler velocimetry' above.)A course of antenatal glucocorticoids is recommended for preterm gestations. Delivery Timing of delivery is determined by both gestational age and fetal condition: Remote from term, evidence of normal umbilical artery flow by Doppler velocimetry is reassuring with regard to immediate fetal outcome so continued fetal monitoring is reasonable to achieve further fetal maturity. However, absence or reversal of flow is an ominous finding; in these cases prompt delivery is often indicated because of a high risk of fetal demise. (See 'Timing of delivery' above.)The term or late preterm growth restricted fetus is delivered if there is evidence of maternal hypertension, failure of apparent growth over a two to four week interval, the biophysical profile score is low (less than 6), and/or umbilical arterial Doppler velocimetry reveals absence or reversal of flow. However, the specific clinical situation in each case must be considered and management individualized.When growth restriction is mild and uncomplicated (no fetal abnormalities or contributing maternal disorders), end diastolic flow is present, and antepartum fetal testing results are reassuring, delivery can be delayed until at least 37 weeks when pulmonary maturity is likely. (See 'Term or late preterm' above.) Labor and vaginal delivery is a reasonable approach in the presence of normal antenatal testing. During labor, continuous intrapartum fetal monitoring is recommended to look for nonreassuring fetal heart rate patterns suggestive of progressive hypoxia during labor. The clinician should be prepared for rapid intervention if there is any evidence of fetal intolerance to labor. Recurrence There is a tendency to repeat SGA or low birth weight deliveries in successive pregnancies. Growth restriction, preterm delivery, preeclampsia, abruption, and stillbirth can all be sequelae of impaired placental function that may manifest in different ways in different pregnancies. (See 'Recurrence risk' above.)