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Fetal Growth Restriction

  • Author: Michael G Ross, MD, MPH; Chief Editor: Carl V Smith, MD  more...
 
Updated: Nov 10, 2015
 

Overview

Intrauterine growth restriction (IUGR) refers to a condition in which a fetus is unable to achieve its genetically determined potential size. This functional definition seeks to identify a population of fetuses at risk for modifiable but otherwise poor outcomes. This definition intentionally excludes of fetuses that are small for gestational age (SGA) but are not pathologically small. SGA is defined as growth at the 10th or less percentile for weight of all fetuses at that gestational age. Not all fetuses that are SGA are pathologically growth restricted and, in fact, may be constitutionally small. Similarly, not all fetuses that have not met their genetic growth potential are in less than the 10th percentile for estimated fetal weight (EFW).

Of all fetuses at or below the 10th percentile for growth, only approximately 40% are at high risk of potentially preventable perinatal death (see image below). Another 40% of these fetuses are constitutionally small. Because this diagnosis may be made with certainty only in neonates, a significant number of fetuses that are healthy but SGA will be subjected to high-risk protocols and, potentially, iatrogenic prematurity.

Fetal growth restriction. Distribution of small fe Fetal growth restriction. Distribution of small fetuses.

The remaining 20% of fetuses that are SGA are intrinsically small secondary to a chromosomal or environmental etiology. Examples include fetuses with trisomy 18, cytomegalovirus infection, or fetal alcohol syndrome. These fetuses are less likely to benefit from prenatal intervention, and their prognosis is most closely related to the underlying etiology.

The clinician's challenge is to identify IUGR fetuses whose health is endangered in utero because of a hostile intrauterine environment and to monitor and intervene appropriately. This challenge also includes identifying small but healthy fetuses and avoiding iatrogenic harm to them or their mothers.

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Causes of Intrauterine Growth Restriction

Maternal causes of IUGR (adapted from Severi et al, 2000)[1] include the following:

  • Chronic hypertension
  • Cyanotic heart disease
  • Class F or higher diabetes
  • Hemoglobinopathies
  • Autoimmune disease
  • Protein-calorie malnutrition
  • Smoking
  • Substance abuse
  • Uterine malformations
  • Thrombophilias
  • Prolonged high-altitude exposure

Placental or umbilical cord causes of IUGR include the following:

IUGR occurs when gas exchange and nutrient delivery to the fetus are not sufficient to allow it to thrive in utero. This process can occur primarily because of maternal disease causing decreased oxygen-carrying capacity (eg, cyanotic heart disease, smoking, hemoglobinopathy), a dysfunctional oxygen delivery system secondary to maternal vascular disease (eg, diabetes with vascular disease, hypertension, autoimmune disease affecting the vessels leading to the placenta), or placental damage resulting from maternal disease (eg, smoking, thrombophilia, various autoimmune diseases).

Evaluation of causative factors for intrinsic disorders leading to poor growth may include a fetal karyotype, maternal serology for infectious processes, and an environmental exposure history.

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Perinatal Implications

IUGR causes a spectrum of perinatal complications, including fetal morbidity and mortality, iatrogenic prematurity, fetal compromise in labor, need for induction of labor, and cesarean delivery. In a cohort study in Sweden, a 10-fold increase in late fetal deaths was found among very small fetuses. Similarly, Gardosi et al noted in 1998 that nearly 40% of stillborn fetuses that were not malformed were SGA.[2] Fetuses with IUGR who survive the compromised intrauterine environment are at increased risk for neonatal morbidity. Morbidity for neonates with IUGR includes increased rates of necrotizing enterocolitis, thrombocytopenia, temperature instability, and renal failure. These are thought to occur as a result of the alteration of normal fetal physiology in utero.

With limited nutritional reserve, the fetus redistributes blood flow to sustain function and to help in the development of vital organs. This is called the brain-sparing effect and results in increased relative blood flow to the brain, heart, adrenals, and placenta, with diminished relative flow to the bone marrow, muscles, lungs, GI tract, and kidneys. The brain-sparing effect may result in different fetal growth patterns.

In 1977, Campbell and Thoms introduced the idea of symmetric versus asymmetric growth.[3] Symmetrically small fetuses were thought to have some sort of early global insult (eg, aneuploidy, viral infection, fetal alcohol syndrome). Asymmetrically small fetuses were thought to be more likely small secondary to an imposed restriction in nutrient and gas exchange. Investigators since then have disagreed on the importance of this differentiation. Dashe et al examined this issue among 1364 infants who were SGA (20% were asymmetrically grown, 80% symmetrically grown) and 3873 infants who were in the 25-75th percentile (ie, appropriate for gestational age).[4] The Table includes a selected list of statistically significant perinatal outcomes and events among these groups.

Table. Perinatal Events and Outcomes (Open Table in a new window)

Event Asymmetrically SGA Symmetrically SGA Appropriate for Gestational Age
Anomalies 14% 4% 3%
Survivors - No serious morbidity 86% 95% 95%
Labor induction (< 36 wk) 12% 8% 5%
Intrapartum high blood pressure (< 32 wk) 7% 2% 1%
Cesarean delivery for nonreassuring fetal heart rate 15% 8% 3%
Intubated in delivery room 6% 4% 3%
Neonatal ICU admission 18% 9% 7%
Respiratory distress syndrome 9% 4% 3%
Intraventricular hemorrhage (grade III or IV) 2% < 1% < 1%
Neonatal death 2% 1% 1%
Gestational age at delivery 36.6 wk ± 3.5 wk 37.8 wk ± 2.9 wk 37.1 wk ± 3.3 wk
Preterm birth ≤ 32 wk 14% 6% 11%

The symmetrically grown infants who were SGA had outcomes very similar to the infants who were appropriate for gestational age and very different prognoses than the asymmetrically SGA fetuses, thus reinforcing the concept of using growth parameters for diagnostic and outcome counseling.

Several studies have addressed prognostic factors influencing outcome and have consistently reported that the dominant influence on survival is gestational age at birth. Madazli reported experience with IUGR fetuses with absent end-diastolic flow. No fetus less than 28 weeks' and less than 800 g survived. Madazli also noted that all fetuses with absent end-diastolic flow greater than 31 weeks' survived. The variable period for survival occurred between these gestational ages, with antenatal and neonatal survival rates at 28-31 weeks' of approximately 54%.[5]

The stress that results in IUGR has been postulated to also result in advanced maturation of the fetus, resulting in decreased perinatal morbidity compared with age-matched normally grown neonates. Bernstein et al examined this issue by identifying almost 20,000 white or African American neonates from 196 centers who were born at 25-30 weeks' gestation without major anomalies.[6] They categorized infants as IUGR at less than the 10th percentile using race- and sex-specific growth charts. These results do not support the concept of a stress-related protective effect of IUGR.

Relative risks associated with IUGR using morbidity and mortality parameters, from the study by Bernstein et al, are as follows:

  • Relative risk of death, 2.77; 95% confidence interval (CI), 2.31-3.33
  • Relative risk of respiratory distress syndrome, 1.19; 95% CI, 1.03-1.29
  • Relative risk of intraventricular hemorrhage, 1.13; 95% CI, 0.99-1.29
  • Relative risk of severe intravascular hemorrhage, 1.27; 95% CI, 0.98-1.59
  • Relative risk of necrotizing enterocolitis, 1.27; 95% CI, 1.05-1.53

Increasingly, data support the idea that long-term consequences of IUGR last well into adulthood. Several authors have noted that these individuals have a greater predisposition to develop a metabolic syndrome later in life, manifesting as obesity, hypertension, hypercholesterolemia, cardiovascular disease, and type 2 diabetes. Several hypotheses have been proposed to explain this relationship. Hales and Barker proposed the so-called thrifty phenotype in 1992. This idea suggests that intrauterine malnutrition results in insulin resistance, loss of pancreatic beta-cell mass, and an adult predisposition to type 2 diabetes.

Other authors found that prepubertal individuals who had IUGR at birth show a greater insulin response than prepubertal individuals who had healthy growth as infants. This suggests that the increased risk of type 2 diabetes in adults who had restriction as infants stems, instead, from increased peripheral insulin resistance allowing the brain-sparing physiology to occur but with a permanent reduction in skeletal-muscle glucose transport. This ultimately results in beta-cell burnout. Although the causative pathophysiology is uncertain, the risk of a metabolic syndrome in adulthood is clearly increased among individuals who had IUGR at birth.

Organ system specific morbidity, as a result of growth restriction, is now being evaluated using different animal species and models. Human studies have clearly show organ specific sequelae of IUGR. Kaijser et al, using a large cohort, were able to demonstrate an association between low birth weight and adult risk of ischemic heart disease.[7] Hallan et al demonstrated that adult kidney function is adversely affected by restricted intrauterine growth.[8]

In addition to an increased risk for physical sequelae, mental health problems have been found more commonly in children with growth restriction. In a study performed in Western Australia, Zubrick et al showed that children born below the second percentile for weight were at significant risk for mental health morbidity (odds ratio, 2.9; 95% CI, 1.18-7.12), academic impairment (odds ratio, 6; 95% Cl, 2.25-16.06), and poorer general health (odds ratio, 5.1; 95% Cl, 1.69-15.52).[9] Specifically, Tideman et al have shown that impaired fetal circulation, as demonstrated by Doppler studies, in association with IUGR, results in worsened cognitive function in adulthood.[10]

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Diagnosis and Surveillance

Criteria for diagnosis of IUGR

For most purposes, an EFW at or below the 10th percentile is used to identify fetuses at risk. Importantly, however, understand that this is not a definitive cutoff for uteroplacental insufficiency. A certain number of fetuses at or below the 10th percentile may be constitutionally small. In these cases, short maternal or paternal height, the neonate's ability to maintain growth along a standardized curve, and a lack of other signs of uteroplacental insufficiency (eg, oligohydramnios, abnormal Doppler findings) can be reassuring to the clinician and parents. Customized growth curves for ethnicity, parental size, and gender are in development so as to improve sensitivity and specificity of diagnosing IUGR.[11, 12]

Importantly, review the dating criteria before offering intervention to treat growth restriction in a fetus. If dates are uncertain or unknown, obtaining a second growth assessment over a 2- to 4-week interval may be of value unless strong supportive data or risk factors warrant an immediate change in management plans.

Screening the fetus for growth restriction

Although no single biometric or Doppler measurement is completely accurate for helping make or exclude the diagnosis of growth restriction, screening for IUGR is important to identify at-risk fetuses. Dependent upon the maternal condition associated with IUGR (see Maternal causes of IUGR) patients may undergo serial sonography during their pregnancies. An initial scan may be obtained in the middle of the second trimester (at 18-20 wk) to confirm dates, evaluate for anomalies, and identify multiple gestations. A repeat scan may be scheduled at 28-32 weeks' gestation to assess fetal growth, evidence of asymmetry, and stigmata of brain-sparing physiology (eg, oligohydramnios, abnormal Doppler findings).

Screening for IUGR in the general population relies on symphysis–fundal height measurements. This is a routine portion of prenatal care from 20 weeks' until term. Although recent studies have questioned the accuracy of fundal height measurements, particularly in obese patients, a discrepancy of greater than 3 cm between observed and expected measurements may prompt a growth evaluation using ultrasound.[13] The clinician should be aware that the sensitivity of fundal height measurement is limited, and he or she should maintain a heightened awareness for potential growth-restricted fetuses. In an unselected hospital population, only 26% of fetuses that were SGA were suggested to be SGA based on clinical examination findings.

One study using fundal height curves that customized for maternal weight, height, and ethnicity was able to increase the detection rate from 29.2% in the control group to 47.9% in the study population. As Yoshida et al indicated, these inaccuracies occur (1) because of the limited accuracy of predicting birth weight within 10% using ultrasonography in the third trimester, (2) because not all fetuses that are SGA have IUGR, (3) because individual and unpredictable changes in growth potential occur, and (4) because growth distribution is a continuum.[14]

Biometry and amniotic fluid volumes

Most ultrasonographic machines report aggregate gestational age measurements and individual parameters. Assessing individual values is important to identify a fetus that is growing asymmetrically. In the presence of normal head and femur measurements, abdominal circumference (AC) measurements of less than 2 standard deviations below the mean appear to be a reasonable cutoff to consider a fetus asymmetric. Baschat and Weiner showed that a low AC percentile had the highest sensitivity (98.1%) for diagnosing IUGR (birth weight < 10th percentile). The sensitivity of EFW (birth weight below the 10th percentile) is 85.7%; however, an AC below the 2.5 percentile had the lowest positive predictive value (36.3%), while a low EFW had a 50% positive predictive value.[15]

Supporting evidence of a hostile intrauterine environment can be obtained by specifically looking at amniotic fluid volumes (AFVs). Chauhan et al found that in a group of normal pregnancies greater than 24 weeks', the rate of IUGR was 19% with an amniotic fluid index (AFI) of less than 5 and 9% with an AFI higher than 5 (odds ratio, 2.13; 95% CI, 1.10-4.16).[16] Banks and Miller also noted a significantly increased risk of IUGR in a group of fetuses with borderline amniotic fluid (AFI of 5-10) relative to a group of normal fetuses (AFI >10) (13% vs 3.6%; rate ratio, 3.9; 95% CI, 1.2-16.2).[17] These results confirm much earlier work by Chamberlain et al.[18]

These authors showed an increased rate of IUGR among fetuses with decreasing maximum vertical pocket (MVP) values. An MVP measurement of larger than 2 cm was associated with an IUGR rate of 5%, an MVP value smaller than 2 cm was associated with an IUGR rate of 20%, and an MVP measurement of smaller than 1 cm was associated with an IUGR rate of 39%. Chamberlain et al concluded that decreased AFI may be an early marker of declining placental function.[18]

Uterine artery Doppler measurement

Both arterial Doppler and venous Doppler have been used in recent literature to support expectant management or delivery of IUGR fetuses and to identify fetuses at risk. Doppler velocimetry has been shown to contribute to the identification of fetuses at risk of IUGR. To follow is an overview of the various Doppler techniques and their clinical applications.

Flow patterns of maternal uterine arteries have been shown to reflect the impact of placentation on maternal circulation. Albaiges et al suggest that a one-stage uterine artery screening at 23 weeks' gestation is effective in identifying pregnancies that will have poor perinatal outcomes prior to 34 weeks' gestation related to uteroplacental insufficiency. In their study of 1751 women who were seen at 23 weeks' gestation for any reason, an abnormal uterine artery study result included bilateral uterine artery notches or a mean pulsatility index (PI) of greater than 1.45 in both arteries.[19]

These criteria were observed in approximately 7% of the population. Within this 7% were 90% of the women who later developed preeclampsia and required delivery before 34 weeks' gestation, 70% of women with a fetus below the 10th percentile who required delivery before 34 weeks' gestation, 50% of placental abruptions, and 80% of fetal deaths. Importantly, the negative predictive value for these adverse events prior to 34 weeks' gestation was higher than 99%.

Chien and colleagues conducted an overview of published studies on the efficacy of uterine artery Doppler findings as a predictor of preeclampsia, IUGR, and perinatal death.[20] In reports of studies performed on low-risk women, an abnormal uterine artery Doppler result yielded a likelihood ratio (LR) of developing IUGR of 3.6 (95% CI, 3.2-4), while a normal test result reduced the risk to below background, with an LR of 0.8 (95% CI, 0.08-0.09). For women at high risk, an abnormal test result indicated an LR of 2.7 (95% CI, 2.1-3.4), while a normal result reduced the risks by 30% (LR of 0.7; 95% CI, 0.6-0.9).

Although these measurements appear promising, the sensitivity and specificity of uterine artery Doppler measurements is relatively low, and, because no proven interventions are available to prevent IUGR, uterine artery blood flow measurements are not included in routine surveillance protocols.

Umbilical artery Doppler measurement

In normal pregnancies, umbilical artery (UA) resistance shows a continuous decline; however, this may not occur in fetuses with uteroplacental insufficiency. The most commonly used measure of gestational age–specific UA resistance is the systolic-to-diastolic ratio of flow, which changes from a baseline value to an elevated value with worsening disease. As the insufficiency progresses, end-diastolic velocity is lost and, finally, reversed. The clinical significance of this progression has been well documented by Mandruzzato et al, who reported a significant difference in mean birth weight and perinatal mortality for absent end-diastolic velocity (20%) versus reversed end-diastolic velocity (68%).[21]

The status of UA blood flow corroborates the diagnosis of IUGR and provides early evidence of circulatory abnormalities in the fetus, enabling clinicians to identify the high-risk status of these fetuses and to initiate surveillance (see Management and Delivery Planning).

UA Doppler measurements may help the clinician decide whether a small fetus is truly growth restricted.

Baschat and Weiner looked at UA resistance to determine if it can help improve the accuracy of diagnosing IUGR and help identify a small fetus at risk of chronic hypoxemia. These investigators identified 308 babies greater than 23 weeks' at the time of delivery who had an AC of less than the 2.5 percentile, an EFW of less than the 10th percentile, or both criteria. UA measurements were obtained on all of these fetuses. The positive predictive values of AC alone and EFW alone for the diagnosis of IUGR were 36.6% and 50%, respectively. An elevated UA systolic-to-diastolic ratio yielded a positive predictive value of 53.3% for postnatally confirmed IUGR.

Among all 138 identified fetuses with an elevated UA systolic-to-diastolic ratio, a 10-fold increase occurred in the rate of admission to and the duration of stay in neonatal ICUs and in the frequency and severity of respiratory distress syndrome. Equally importantly, no fetus with normal Doppler measurements was delivered with documented metabolic acidemia.[15]

Middle cerebral artery Doppler

Fong and colleagues identified 297 singleton pregnancies in which EFW was below the 10th percentile in anatomically normal fetuses. These investigators studied middle cerebral artery (MCA), renal artery, and UA Doppler findings. They addressed outcomes, including cesarean delivery for fetal distress, cord pH less than or equal to 7.10, and Apgar score less than or equal to 7 at 5 minutes. They concluded that a normal MCA Doppler finding may be useful to help identify small fetuses that are not likely to have a major adverse outcome with a reported negative predictive value of 86%.[22]

Hershkovitz et al also looked at MCA Doppler finds in small fetuses. They found that those fetuses with abnormal MCA study results had earlier deliveries, lower birth weights, fewer vaginal deliveries, and increased admissions to neonatal ICUs. Importantly, only 7 of 16 fetuses with Doppler evidence of brain-sparing physiology had elevated UA Doppler findings. This emphasized the possible presence of a gradient in the degree of fetal redistribution and that when performing Doppler studies, evaluating only the UAs may not be sufficient.[23]

Specific MCA Doppler changes were evaluated by Mari et al. They specifically evaluated MCA peak systolic velocity (PSV) and pulsatility index (PI) in growth-restricted fetuses that were longitudinally evaluated. They found that while an abnormal PI preceded an abnormal PSV, the PI demonstrated an inconsistent pattern. MCA-PSV, however, consistently showed an increase in blood velocity and immediately prior to demise, a decrease. They concluded that MCA-PSV is a better predictor of IUGR-associated perinatal mortality than any other single measurement.[24]

Venous Doppler waveforms

Venous Doppler has been measured at the ductus venosus (DV), umbilical vein (UV), inferior vena cava (IVC), and 7 other sites. This provides information about fetal cardiovascular and respiratory responses to its intrauterine environment. These measurements have been reported to become consistently abnormal when a fetus is severely compromised, thus providing evidence in support of an expedited delivery. Bilardo et al completed a prospective study of the cardiotocography, UA, and DV values of 70 IUGR fetuses and their outcomes.[25] They reported that only the DV measurements consistently predicted adverse perinatal outcomes from 0-7 days prior to delivery. While the optimal vessel for use for venous Doppler evaluations has not been identified, the knowledge gained from these measurements may provide additional information for the timing of delivery, especially in extremely premature (< 32 wk) gestations.

Three-dimensional ultrasonography

With the introduction and use of obstetrical 3-dimensional ultrasonography, many new applications for this technology are constantly explored. The use of these techniques in the evaluation of the growth-restricted fetus has been evaluated as well. As fetal femur dysplasia is associated with IUGR, Chang et al used 3-dimensional ultrasonography to measure fetal femur volume as a predictor of IUGR. They found a 10th percentile femur volume threshold, which differentiates growth-restricted fetuses from normal fetuses. Using this technique, they obtained a sensitivity of 71.4%, specificity of 94.1%, positive predictive value of 62.5%, negative predictive value of 96.0%, and accuracy of 91.3% in prediction of growth restriction. As a single biometric measurement, fetal femur volume is better in prediction of growth restriction than fetal AC and biparietal diameter.[26] Chang et al also evaluated 3-dimensional ultrasonographic measurement of fetal humerus volume in evaluationofIUGR.Again,a10th percentile humerus volume threshold was found to differentiate growth-restricted fetuses from normal fetuses.[27]

Therapeutic options

Although multiple therapeutic strategies have been tested to promote intrauterine growth and decrease perinatal morbidity and mortality, limited, if any, success has been achieved in this area. Gülmezoglu et al reported results of meta-analyses of studies, the goals of which were to treat impaired growth. In this review, 3 interventions were shown to be helpful. First, behavioral strategies to quit smoking result in a lower rate of low birth weight in babies at term among mothers who smoke. Second, balanced nutritional supplements in undernourished women and magnesium and folate supplementation (in some studies) decrease the rate of SGA newborns. Third, if malaria is the etiologic agent, maternal treatment of malaria can increase fetal growth.[28]

Pollack et al additionally examined in-hospital bed rest as a way to promote fetal growth and found no improvement.[29] Newnham et al studied women receiving 100 mg of aspirin versus placebo after a diagnosis of IUGR based on abnormal UA Doppler findings, and they did not find a clinically significant difference.[30]

Other options have been considered with a goal of decreasing perinatal morbidity and mortality. In 2003, Say et al reviewed maternal estrogen administration, maternal hyperoxygenation, and maternal nutrient supplementation as therapies for suspected impaired fetal growth.[31, 32, 33] They concluded that evidence to evaluate the risks and benefits of these therapies was lacking. However, they did suggest that further trials of maternal hyperoxygenation seem warranted.

Additional therapies that have been proposed and may warrant further study are maternal hemodilution and intermittent abdominal negative pressure. These are also poorly studied, carry potential maternal and fetal harm, and should be considered experimental.

The only intervention that has been shown to decrease neonatal morbidity and mortality is the administration of steroids to premature fetuses when delivery is anticipated. Bernstein et al described the effect of maternal prenatal glucocorticoid administration in growth-restricted fetuses and found the benefits to be similar to those found in gestational age–matched, normally grown fetuses.

Odds ratio reduction with steroids, from Bernstein et al, is as follows:

  • Relative risk of death, 0.54; 95% CI, 0.48-0.62
  • Relative risk of respiratory distress syndrome, 0.51; 95% CI, 0.44-0.58
  • Relative risk of intraventricular hemorrhage, 0.67; 95% CI, 0.61-0.73
  • Relative risk of severe intravascular hemorrhage, 0.5; 95% CI, 0.43-0.57
  • Relative risk of necrotizing enterocolitis, no difference noted

Recently, several studies have questioned the metabolic and cardiovascular response of IUGR fetuses to maternal glucocorticoid administration. Simchen et al performed a prospective longitudinal study of chromosomally normal IUGR fetuses at 24-34 weeks' with absent or reversed end-diastolic flow. They found a divergent response between the 2 groups of fetuses as measured by UA Doppler. Almost 45% of these fetuses had transient improvement in their Doppler waveforms, and these fetuses had significantly better outcomes than their counterparts who had no improvement of their waveforms, even transiently. These authors suggest that daily Doppler-based monitoring after the administration of steroids can help delineate a group of fetuses at extremely high risk of acidosis and mortality. They also suggest that further work is needed to elucidate the efficacy of steroids versus immediate delivery in this very high-risk subset of IUGR fetuses.[34]

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Management and Delivery Planning

Once IUGR has been detected, the management of the pregnancy should depend on a surveillance plan that maximizes gestational age while minimizing the risks of neonatal morbidity and mortality. This should include steroid administration when at all feasible, based on the monitoring and delivery strategies discussed below (see image below and Harman and Baschat's integrated fetal testing for IUGR). Fetal lung maturity studies by amniocentesis, in fetuses greater than 34 weeks', may additionally influence delivery timing.

The goal in the management of IUGR, because no effective treatments are known, is to deliver the most mature fetus in the best physiological condition possible while minimizing the risk to the mother. Such a goal requires the use of antenatal testing with the hope of identifying the fetus with IUGR before it becomes acidotic. Developing a testing scheme, following it, and having a high index of suspicion in this population when results of testing are abnormal is important. The positive predictive value of an abnormal antenatal test result in fetuses with IUGR is relatively high because the prevalence of acidemia and chronic hypoxemia is relatively high.

Although numerous protocols have been suggested for antenatal monitoring of IUGR fetuses, the mainstay includes a weekly nonstress test (NST). Additional modalities may include amniotic fluid volume determination, biophysical profiles, and/or Doppler assessments. Other more complex protocols have been proposed. The protocol for antenatal testing suggested by Kramer and Weiner (see image below) is one example. It relies heavily on the use of UA Doppler testing because severely abnormal Doppler findings (absent or reversed end-diastolic flow) can precede an abnormal fetal heart rate by several weeks. Harman and Baschat suggested a different proposed antenatal testing strategy. This protocol integrates multiple venous and arterial Doppler measurements and the biophysical profile score (BPS); this strategy may be used at institutions where these measurements are routinely obtained by qualified technicians.[35]

Fetal growth restriction. Sample protocol for ante Fetal growth restriction. Sample protocol for antenatal testing for intrauterine growth restriction at 32 weeks' gestation or after. IUGR is intrauterine growth restriction, BPP is biophysical profile, and EDF is end-diastolic flow.

Harman and Baschat's integrated fetal testing for IUGR, in increasing order of severity from 1 (least severe) to 5 (most severe), is as follows:[35]

Situation 1

See the list below:

  • Test results – AC less than fifth percentile, low AC growth rate, high ratio of head circumference to AC; BPS greater than or equal to 8 and AFV normal; abnormal UV and/or cerebroplacental ratio; normal MCA
  • Interpretation – IUGR diagnosed, asphyxia extremely rare, increased risk for intrapartum distress
  • Recommended management – Intervention for obstetric or maternal factors only, weekly BPS, multivessel Doppler every 2 weeks

Situation 2

See the list below:

  • Test results – IUGR criteria met, BPS greater than or equal to 8, AFV normal, UA with absent or reversed end-diastolic velocities, decreased MCA
  • Interpretation – IUGR with brain sparing, hypoxemia possible and asphyxia rare, at risk for intrapartum distress
  • Recommended management – Intervention for obstetric or maternal factors only; BPS 3 times a week; weekly UA, MCA, and venous Doppler

Situation 3

See the list below:

  • Test results – IUGR with low MCA PI; oligohydramnios; BPS greater than or equal to 6; normal IVC, DV, and UV flow
  • Interpretation – IUGR with significant brain sparing, onset of fetal compromise, hypoxemia common, acidemia/asphyxia possible
  • Recommended management – If at more than 34 weeks' gestation, deliver (route determined by obstetric factors). If at less than 34 weeks' gestation, administer steroids to achieve lung maturity and repeat all testing in 24 hours.

Situation 4

See the list below:

  • Test results – IUGR with brain sparing, oligohydramnios, BPS greater than or equal to 6, increased IVC and DV indices, UV flow normal
  • Interpretation – IUGR with brain sparing, proven fetal compromise, hypoxemia common, acidemia/asphyxia likely
  • Recommended management – If at more than 34 weeks' gestation, deliver (route determined by obstetric factors and oxytocin challenge test [OCT] results). If at less than 34 weeks' gestation, individualize treatment with admission, continuous cardiotocography, steroids, maternal oxygen, and/or amnioinfusion and then repeat all testing up to 3 times a day depending on status.

Situation 5

See the list below:

  • Test results – IUGR with accelerating compromise, BPS less than or equal to 6, abnormal IVC and DV indices, pulsatile UV flow
  • Interpretation – IUGR with decompensation, cardiovascular instability, hypoxemia certain, acidemia/asphyxia common, high perinatal mortality, death imminent
  • Recommended management – If fetus is considered viable by size, deliver as soon as possible at tertiary center. Route determined by obstetric factors and OCT results. Fetus requires highest level of natal ICU care.

The diagnosis of severe IUGR before 32 weeks' gestation is associated with a poor prognosis, and therapy must be highly individualized. Once a decision has been made to effect delivery, the mode of delivery is governed by evidence of acidemia, gestational age, and Bishop score. Cesarean delivery without a trial of labor may be appropriate (1) in the presence of evidence of fetal distress by nonstress testing or reversed diastolic flow or (2) for traditional obstetrical indications for cesarean delivery (ie, malpresentation, prior cesarean delivery).

Li et al investigated the success rate of induction of labor in IUGR fetuses with and without UA blood flow changes and the neonatal outcomes of induced fetuses with a negative result after an OCT. They found that fetuses with abnormal (but not absent or reversed) UA blood flow who had a normal OCT result had similar success in induction of labor, without indications of detrimental fetal hypoxia or distress.[36] This suggests that in fetuses with altered UA blood flow, an OCT may be appropriate to select fetuses that will tolerate labor induction.

When a trial of labor is undertaken, continuous heart rate monitoring should optimize the success of the induction.

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Future Directions and Prevention

Prevention of IUGR is highly desirable, and several studies have addressed this potential. Investigators have looked at altering the thromboxane-to-prostacyclin ratio by administering aspirin with or without dipyridamole to mothers of fetuses with IUGR. The studies examining these agents for prevention of IUGR are difficult to compare. Different doses of aspirin, different times of administration in pregnancy, and different indications for use make comparisons difficult; however, the following is a summary of the studies:

  • Wallenburg et al studied a population of women at high risk for IUGR in a nonrandomized trial using historic controls. They noted a decline in the rate of IUGR from 61.5% in the historic controls to 13.3% in those treated with aspirin and dipyridamole. [37]
  • Sibai et al studied low-risk nulliparous women in a double-blinded, placebo-controlled, randomized trial. Patients were treated from weeks 13-26 with either placebo or 60 mg/d of aspirin. This study showed a small decrease in the rate of preeclampsia but not IUGR (4.6% vs 5.8% in controls), at the risk of increased chance of abruption. [38]
  • In the Essai Preeclampsia Dipyridamole Aspirine (EPREDA) randomized controlled trial, high-risk patients received placebo, aspirin only, or aspirin plus dipyridamole. No difference in the rate of IUGR was found between those receiving aspirin alone and those receiving aspirin plus dipyridamole. The control rate of IUGR was 26%; in the 2 groups receiving aspirin with or without dipyridamole, the rate was 13%. [39]
  • In an Italian study, women considered to be at moderate risk of IUGR or pregnancy-induced hypertension at 16-32 weeks' gestation were randomly assigned to receive either 50 mg aspirin or no treatment. No difference in any outcome studied was found between the 2 groups. [40]
  • Harrington et al identified patients with abnormal uterine artery Doppler findings at 20 weeks' gestation. Participants were started on aspirin, and therapy was discontinued at 24 weeks' if repeat Doppler results normalized. No difference in the rate of fetuses that were SGA below the 10th or third percentile was found between the treated and control groups. [41]
  • Trudinger et al performed a double-blinded, randomized clinical trial using 150 mg of aspirin in pregnant women with abnormal UA Doppler findings. The result was an increase in birth weight of 516 g and an increase in placental weight. [42]
  • The Collaborative Low-Dose Aspirin Study in Pregnancy trial, which investigated both prevention and treatment of IUGR, showed no change in the rate of IUGR in treated and control patients with the administration of 60 mg of aspirin. [43]
  • Leitich et al performed a meta-analysis of 13 trials in which women were enrolled for prophylactic aspirin therapy. In women treated, the odds ratio for IUGR was 0.82 (95% Cl, 0.66-1.08). Among those trials in which women were hypertensive or had other risk factors, the risk of IUGR was clearly decreased. Leitich et al found that beginning 100-150 mg/d of aspirin at less than 17 weeks' gestation decreased the rate of IUGR by approximately 65% and the rate of perinatal mortality by approximately 60%. [44]
  • The Disproportionate Intrauterine Growth Intervention Trial At Term (DIGITAT) suggests that women who have had a previous singleton pregnancy beyond 36 weeks’ gestation can safely choose expectant management with intensive maternal and fetal monitoring if induction is not wanted. [45] Choosing induction to prevent neonatal morbidity or stillbirth is reasonable.

Despite the theoretical benefit of aspirin in many studies, the role of aspirin, if any, in the prevention of IUGR is still unclear. A large randomized controlled trial using a standardized high-risk population with a standardized treatment regimen could serve to better answer this question.

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Conclusion

IUGR remains a challenging problem for clinicians. Most cases of IUGR occur in pregnancies in which no risk factors are present; therefore, the clinician must be alert to the possibility of a growth disturbance in all pregnancies. No single measurement helps secure the diagnosis; thus, a complex strategy for diagnosis and assessment is necessary. The ability to diagnose the disorder and understand its pathophysiology still outpaces the ability to prevent or treat its complications. The current therapeutic goals are to optimize the timing of delivery to minimize hypoxemia and maximize gestational age and maternal outcome. Further study may elucidate preventive or treatment strategies to assist the growth-restricted fetus.

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Contributor Information and Disclosures
Author

Michael G Ross, MD, MPH Professor of Obstetrics and Gynecology, University of California, Los Angeles, David Geffen School of Medicine; Professor, Department of Community Health Sciences, Fielding School of Public Health at University of California at Los Angeles

Michael G Ross, MD, MPH is a member of the following medical societies: American Association for the Advancement of Science, American College of Obstetricians and Gynecologists, Phi Beta Kappa, Society for Reproductive Investigation, Society for Maternal-Fetal Medicine, Society for Neuroscience, American Federation for Clinical Research, Perinatal Research Society, American Gynecological and Obstetrical Society, American Physiological Society, American Public Health Association, Association of Professors of Gynecology and Obstetrics

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Lumara Health; Cervilenz Inc<br/>Received income in an amount equal to or greater than $250 from: Lumara Health; Cervilenz Inc.

Coauthor(s)

Roy Zion Mansano, MD Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center

Roy Zion Mansano, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, Society for Maternal-Fetal Medicine, AAGL

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Carl V Smith, MD The Distinguished Chris J and Marie A Olson Chair of Obstetrics and Gynecology, Professor, Department of Obstetrics and Gynecology, Senior Associate Dean for Clinical Affairs, University of Nebraska Medical Center

Carl V Smith, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Institute of Ultrasound in Medicine, Association of Professors of Gynecology and Obstetrics, Central Association of Obstetricians and Gynecologists, Society for Maternal-Fetal Medicine, Council of University Chairs of Obstetrics and Gynecology, Nebraska Medical Association

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors Teresa (Terry) C Harper, MD; Garrett Lam, MD; and Nancy C Chescheir, MD to the development and writing of this article.

References
  1. Severi FM, Rizzo G, Bocchi C, et al. Intrauterine growth retardation and fetal cardiac function. Fetal Diagn Ther. 2000 Jan-Feb. 15(1):8-19. [Medline].

  2. Gardosi J, Mul T, Mongelli M, Fagan D. Analysis of birthweight and gestational age in antepartum stillbirths. Br J Obstet Gynaecol. 1998 May. 105(5):524-30. [Medline].

  3. Campbell S, Thoms A. Ultrasound measurement of the fetal head to abdomen circumference ratio in the assessment of growth retardation. Br J Obstet Gynaecol. 1977 Mar. 84(3):165-74. [Medline].

  4. Dashe JS, McIntire DD, Lucas MJ, Leveno KJ. Effects of symmetric and asymmetric fetal growth on pregnancy outcomes. Obstet Gynecol. 2000 Sep. 96(3):321-7. [Medline].

  5. Madazli R. Prognostic factors for survival of growth-restricted fetuses with absent end-diastolic velocity in the umbilical artery. J Perinatol. 2002 Jun. 22(4):286-90. [Medline].

  6. Bernstein IM, Horbar JD, Badger GJ, et al. Morbidity and mortality among very-low-birth-weight neonates with intrauterine growth restriction. The Vermont Oxford Network. Am J Obstet Gynecol. 2000 Jan. 182(1 Pt 1):198-206. [Medline].

  7. Kaijser M, Bonamy AK, Akre O, et al. Perinatal risk factors for ischemic heart disease: disentangling the roles of birth weight and preterm birth. Circulation. 2008 Jan 22. 117(3):405-10. [Medline].

  8. Hallan S, Euser AM, Irgens LM, Finken MJ, Holmen J, Dekker FW. Effect of intrauterine growth restriction on kidney function at young adult age: the Nord Trøndelag Health (HUNT 2) Study. Am J Kidney Dis. 2008 Jan. 51(1):10-20. [Medline].

  9. Zubrick SR, Kurinczuk JJ, McDermott BM, et al. Fetal growth and subsequent mental health problems in children aged 4 to 13 years. Dev Med Child Neurol. 2000 Jan. 42(1):14-20. [Medline].

  10. Tideman E, Marsal K, Ley D. Cognitive function in young adults following intrauterine growth restriction with abnormal fetal aortic blood flow. Ultrasound Obstet Gynecol. 2007 Jun. 29(6):614-8. [Medline].

  11. Gardosi J. New definition of small for gestational age based on fetal growth potential. Horm Res. 2006. 65 Suppl 3:15-8. [Medline].

  12. Groom KM, Poppe KK, North RA, McCowan LM. Small-for-gestational-age infants classified by customized or population birthweight centiles: impact of gestational age at delivery. Am J Obstet Gynecol. 2007 Sep. 197(3):239.e1-5. [Medline].

  13. Jelks A, Cifuentes R, Ross MG. Clinician bias in fundal height measurement. Obstet Gynecol. 2007 Oct. 110(4):892-9. [Medline].

  14. Yoshida S, Unno N, Kagawa H, et al. Prenatal detection of a high-risk group for intrauterine growth restriction based on sonographic fetal biometry. Int J Gynaecol Obstet. 2000 Mar. 68(3):225-32. [Medline].

  15. Baschat AA, Weiner CP. Umbilical artery Doppler screening for detection of the small fetus in need of antepartum surveillance. Am J Obstet Gynecol. 2000 Jan. 182(1 Pt 1):154-8. [Medline].

  16. Chauhan SP, Scardo JA, Hendrix NW, et al. Accuracy of sonographically estimated fetal weight with and without oligohydramnios. A case-control study. J Reprod Med. 1999 Nov. 44(11):969-73. [Medline].

  17. Banks EH, Miller DA. Perinatal risks associated with borderline amniotic fluid index. Am J Obstet Gynecol. 1999 Jun. 180(6 Pt 1):1461-3. [Medline].

  18. Chamberlain PF, Manning FA, Morrison I, et al. Ultrasound evaluation of amniotic fluid volume. I. The relationship of marginal and decreased amniotic fluid volumes to perinatal outcome. Am J Obstet Gynecol. 1984 Oct 1. 150(3):245-9. [Medline].

  19. Albaiges G, Missfelder-Lobos H, Lees C, Parra M, Nicolaides KH. One-stage screening for pregnancy complications by color Doppler assessment of the uterine arteries at 23 weeks' gestation. Obstet Gynecol. 2000 Oct. 96(4):559-64. [Medline].

  20. Chien PF, Arnott N, Gordon A, et al. How useful is uterine artery Doppler flow velocimetry in the prediction of pre-eclampsia, intrauterine growth retardation and perinatal death? An overview. BJOG. 2000 Feb. 107(2):196-208. [Medline].

  21. Mandruzzato GP, Bogatti P, Fischer L, Gigli C. The clinical significance of absent or reverse end-diastolic flow in the fetal aorta and umbilical artery. Ultrasound Obstet Gynecol. 1991 May 1. 1(3):192-6. [Medline].

  22. Fong KW, Ohlsson A, Hannah ME, et al. Prediction of perinatal outcome in fetuses suspected to have intrauterine growth restriction: Doppler US study of fetal cerebral, renal, and umbilical arteries. Radiology. 1999 Dec. 213(3):681-9. [Medline].

  23. Hershkovitz R, Kingdom JC, Geary M, Rodeck CH. Fetal cerebral blood flow redistribution in late gestation: identification of compromise in small fetuses with normal umbilical artery Doppler. Ultrasound Obstet Gynecol. 2000 Mar. 15(3):209-12. [Medline].

  24. Mari G, Hanif F, Kruger M, Cosmi E, Santolaya-Forgas J, Treadwell MC. Middle cerebral artery peak systolic velocity: a new Doppler parameter in the assessment of growth-restricted fetuses. Ultrasound Obstet Gynecol. 2007 Mar. 29(3):310-6. [Medline].

  25. Bilardo CM, Wolf H, Stigter RH, et al. Relationship between monitoring parameters and perinatal outcome in severe, early intrauterine growth restriction. Ultrasound Obstet Gynecol. 2004 Feb. 23(2):119-25. [Medline].

  26. Chang CH, Tsai PY, Yu CH, Ko HC, Chang FM. Prenatal detection of fetal growth restriction by fetal femur volume: efficacy assessment using three-dimensional ultrasound. Ultrasound Med Biol. 2007 Mar. 33(3):335-41. [Medline].

  27. Chang CH, Yu CH, Ko HC, Chen CL, Chang FM. Fetal upper arm volume in predicting intrauterine growth restriction: a three-dimensional ultrasound study. Ultrasound Med Biol. 2005 Nov. 31(11):1435-9. [Medline].

  28. Gulmezoglu M, de Onis M, Villar J. Effectiveness of interventions to prevent or treat impaired fetal growth. Obstet Gynecol Surv. 1997 Feb. 52(2):139-49. [Medline].

  29. Pollack RN, Yaffe H, Divon MY. Therapy for intrauterine growth restriction: current options and future directions. Clin Obstet Gynecol. 1997 Dec. 40(4):824-42. [Medline].

  30. Newnham JP, Godfrey M, Walters BJ, et al. Low dose aspirin for the treatment of fetal growth restriction: a randomized controlled trial. Aust N Z J Obstet Gynaecol. 1995 Nov. 35(4):370-4. [Medline].

  31. Say L, Gulmezoglu AM, Hofmeyr GJ. Hormones for suspected impaired fetal growth. Cochrane Database Syst Rev. 2003. CD000109. [Medline].

  32. Say L, Gulmezoglu AM, Hofmeyr GJ. Maternal nutrient supplementation for suspected impaired fetal growth. Cochrane Database Syst Rev. 2003. CD000148. [Medline].

  33. Say L, Gulmezoglu AM, Hofmeyr GJ. Maternal oxygen administration for suspected impaired fetal growth. Cochrane Database Syst Rev. 2003. CD000137. [Medline].

  34. Simchen MJ, Alkazaleh F, Adamson SL, et al. The fetal cardiovascular response to antenatal steroids in severe early-onset intrauterine growth restriction. Am J Obstet Gynecol. 2004 Feb. 190(2):296-304. [Medline].

  35. Harman CR, Baschat AA. Arterial and venous Dopplers in IUGR. Clin Obstet Gynecol. 2003 Dec. 46(4):931-46. [Medline].

  36. Li H, Gudmundsson S, Olofsson P. Prospect for vaginal delivery of growth restricted fetuses with abnormal umbilical artery blood flow. Acta Obstet Gynecol Scand. 2003 Sep. 82(9):828-33. [Medline].

  37. Wallenburg HC, Dekker GA, Makovitz JW, Rotmans P. Low-dose aspirin prevents pregnancy-induced hypertension and pre-eclampsia in angiotensin-sensitive primigravidae. Lancet. 1986 Jan 4. 1(8471):1-3. [Medline].

  38. Sibai BM, Caritis SN, Thom E, et al. Prevention of preeclampsia with low-dose aspirin in healthy, nulliparous pregnant women. The National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units. N Engl J Med. 1993 Oct 21. 329(17):1213-8. [Medline].

  39. Uzan S, Beaufils M, Breart G, et al. Prevention of fetal growth retardation with low-dose aspirin: findings of the EPREDA trial. Lancet. 1991 Jun 15. 337(8755):1427-31. [Medline].

  40. Italian Study of Aspirin In Pregnancy. Low-dose aspirin in prevention and treatment of intrauterine growth retardation and pregnancy-induced hypertension. Italian study of aspirin in pregnancy. Lancet. 1993 Feb 13. 341(8842):396-400. [Medline].

  41. Harrington K, Kurdi W, Aquilina J, et al. A prospective management study of slow-release aspirin in the palliation of uteroplacental insufficiency predicted by uterine artery Doppler at 20 weeks. Ultrasound Obstet Gynecol. 2000 Jan. 15(1):13-8. [Medline].

  42. Trudinger BJ, Cook CM, Thompson RS, et al. Low-dose aspirin therapy improves fetal weight in umbilical placental insufficiency. Am J Obstet Gynecol. 1988 Sep. 159(3):681-5. [Medline].

  43. Collaborative Low-dose Aspirin Study in Pregnancy Collaborative Group. CLASP: a randomised trial of low-dose aspirin for the prevention and treatment of pre-eclampsia among 9364 pregnant women. CLASP (Collaborative Low-dose Aspirin Study in Pregnancy) Collaborative Group. Lancet. 1994 Mar 12. 343(8898):619-29. [Medline].

  44. Leitich H, Egarter C, Husslein P, et al. A meta-analysis of low dose aspirin for the prevention of intrauterine growth retardation. Br J Obstet Gynaecol. 1997 Apr. 104(4):450-9. [Medline].

  45. Boers KE, Vijgen SM, Bijlenga D, et al. Induction versus expectant monitoring for intrauterine growth restriction at term: randomised equivalence trial (DIGITAT). BMJ. 2010 Dec 21. 341:c7087. [Medline]. [Full Text].

  46. Baschat AA, Gembruch U, Reiss I, et al. Absent umbilical artery end-diastolic velocity in growth-restricted fetuses: a risk factor for neonatal thrombocytopenia. Obstet Gynecol. 2000 Aug. 96(2):162-6. [Medline].

  47. Baschat AA, Hecher K. Fetal growth restriction due to placental disease. Semin Perinatol. 2004 Feb. 28(1):67-80. [Medline].

  48. Battaglia C, Artini PG, D'Ambrogio G, et al. Maternal hyperoxygenation in the treatment of intrauterine growth retardation. Am J Obstet Gynecol. 1992 Aug. 167(2):430-5. [Medline].

  49. Burke G, Stuart B, Crowley P, et al. Is intrauterine growth retardation with normal umbilical artery blood flow a benign condition?. BMJ. 1990 Apr 21. 300(6731):1044-5. [Medline]. [Full Text].

  50. Cnattingius S, Haglund B, Kramer MS. Differences in late fetal death rates in association with determinants of small for gestational age fetuses: population based cohort study. BMJ. 1998 May 16. 316(7143):1483-7. [Medline].

  51. Gardosi J, Francis A. Controlled trial of fundal height measurement plotted on customised antenatal growth charts. Br J Obstet Gynaecol. 1999 Apr. 106(4):309-17. [Medline].

  52. Hales CN, Barker DJ. Type 2 (non-insulin-dependent) diabetes mellitus: the thrifty phenotype hypothesis. Diabetologia. 1992 Jul. 35(7):595-601. [Medline].

  53. Hepburn M, Rosenberg K. An audit of the detection and management of small-for-gestational age babies. Br J Obstet Gynaecol. 1986 Mar. 93(3):212-6. [Medline].

  54. Heyl W, Boabang P, Faridi A, Rath W. Evaluation of the success of hemodilution therapy for fetal growth retardation by Doppler sonography. Clin Hemorheol Microcirc. 1997 May-Jun. 17(3):225-30. [Medline].

  55. Kanaka-Gantenbein C, Mastorakos G, Chrousos GP. Endocrine-related causes and consequences of intrauterine growth retardation. Ann N Y Acad Sci. 2003 Nov. 997:150-7. [Medline].

  56. Kramer WB, Weiner CP. Management of intrauterine growth restriction. Clin Obstet Gynecol. 1997 Dec. 40(4):814-23. [Medline].

  57. Maisonet M, Correa A, Misra D, Jaakkola JJ. A review of the literature on the effects of ambient air pollution on fetal growth. Environ Res. 2004 May. 95(1):106-15. [Medline].

  58. Nicolaides KH, Campbell S, Bradley RJ, et al. Maternal oxygen therapy for intrauterine growth retardation. Lancet. 1987 Apr 25. 1(8539):942-5. [Medline].

  59. Seeds JW, Peng T. Impaired growth and risk of fetal death: is the tenth percentile the appropriate standard?. Am J Obstet Gynecol. 1998 Apr. 178(4):658-69. [Medline].

  60. Shimonovitz S, Yagel S, Zacut D, et al. Intermittent abdominal decompression: an option for prevention of intrauterine growth retardation. Br J Obstet Gynaecol. 1992 Aug. 99(8):693-5. [Medline].

  61. Siristatidis C, Salamalekis E, Vitoratos N, et al. Intrapartum surveillance of IUGR fetuses with cardiotocography and fetal pulse oximetry. Biol Neonate. 2003. 83(3):162-5. [Medline].

  62. Charoenratana C, Leelapat P, Traisrisilp K, Tongsong T. Maternal iodine insufficiency and adverse pregnancy outcomes. Matern Child Nutr. 2015 Sep 1. [Medline].

  63. Milnerowicz-Nabzdyk E, Bizon A. How does tobacco smoke influence the morphometry of the fetus and the umbilical cord?-Research on pregnant women with intrauterine growth restriction exposed to tobacco smoke. Reprod Toxicol. 2015 Aug 24. 58:79-84. [Medline].

  64. Clemente DB, Casas M, Vilahur N, et al. Prenatal ambient air pollution, placental mitochondrial DNA content, and birth weight in the INMA (Spain) and ENVIRONAGE (Belgium) birth cohorts. Environ Health Perspect. 2015 Aug 25. [Medline].

 
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Fetal growth restriction. Distribution of small fetuses.
Fetal growth restriction. Sample protocol for antenatal testing for intrauterine growth restriction at 32 weeks' gestation or after. IUGR is intrauterine growth restriction, BPP is biophysical profile, and EDF is end-diastolic flow.
Table. Perinatal Events and Outcomes
Event Asymmetrically SGA Symmetrically SGA Appropriate for Gestational Age
Anomalies 14% 4% 3%
Survivors - No serious morbidity 86% 95% 95%
Labor induction (< 36 wk) 12% 8% 5%
Intrapartum high blood pressure (< 32 wk) 7% 2% 1%
Cesarean delivery for nonreassuring fetal heart rate 15% 8% 3%
Intubated in delivery room 6% 4% 3%
Neonatal ICU admission 18% 9% 7%
Respiratory distress syndrome 9% 4% 3%
Intraventricular hemorrhage (grade III or IV) 2% < 1% < 1%
Neonatal death 2% 1% 1%
Gestational age at delivery 36.6 wk ± 3.5 wk 37.8 wk ± 2.9 wk 37.1 wk ± 3.3 wk
Preterm birth ≤ 32 wk 14% 6% 11%
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