eMedicine Specialties > Radiology > Obstetrics/Gynecology

Intrauterine Growth Retardation

Author: Vikram S Dogra, MD, Professor of Diagnostic Radiology, Urology, and Biomedical Engineering, University of Rochester School of Medicine; Director, Division of Ultrasound, Associate Chair of Education and Research, Department of Imaging Sciences, University of Rochester Medical Center
Coauthor(s): Shweta Bhatt, MBBS, MD, Clinical Fellow, Department of Imaging Sciences, University of Rochester Medical Center, Rochester , NY
Contributor Information and Disclosures

Updated: Nov 17, 2009

Introduction

Background

The term intrauterine growth restriction has largely replaced the term intrauterine growth retardation (IUGR). The definition of IUGR is a problematic one because we do not know the inherent growth potential of the fetus. The most common definition used is fetal weight below the 10th percentile for gestational age.

In most cases of fetal growth restriction, the transcerebellar diameter appears to be spared and can be used as an unbiased measure of gestational age. The transcerebellar diameter in millimeters is equal to gestational age in weeks to 22 weeks of gestation. With this definition, IUGR and "small for gestational age" are synonymous terms.

IUGR has a prevalence of 10% for all pregnancies. However, the figure varies in different patient populations, with rates of 3-5% for healthy mothers and 25% or higher for some high-risk groups, such as hypertensive mothers. Growth-restricted pregnancies are often complicated by a high rate of antepartum and intrapartum fetal distress and the need for cesarean delivery. Infants who are small for their gestational dates are predisposed to low APGAR scores, low cord pH, intraventricular hemorrhage, necrotizing enterocolitis, hypoglycemia, hypocalcemia, and polycythemia.

Recent studies

According to Proctor et al, small placental size and elevated alpha-fetoprotein (AFP) can identify women with low maternal serum pregnancy-associated plasma protein-A (PAPP-A) who are at high risk for IUGR, preterm delivery before 32 weeks' gestation, and stillbirth. The authors noted that screening studies for trisomy 21 have demonstrated that low PAPP-A at 11-13 weeks' gestation is associated with stillbirth, IUGR, and preeclampsia in chromosomally normal fetuses but that the strength of these associations is too weak to justify screening for these placental insufficiency syndromes. They therefore evaluated placental size and uterine artery Doppler imaging as second-stage screening tests for women (90 normal singleton pregnancies) with low PAPP-A and found that the risks of IUGR, preterm delivery before 32 weeks' gestation, and stillbirth were significantly associated with small placental size and elevated AFP but not with abnormal uterine artery Doppler indices.¹

Melchiorre et al found that there is a significant relationship between first-trimester uterine artery Doppler resistance indices (RI) and the subsequent delivery of neonates who are small for gestational age (SGA) or have intrauterine growth restriction (IUGR). They found, however, that the sensitivity of first-trimester uterine artery Doppler is greater for SGA with preeclampsia than it is for IUGR alone and noted that this difference could be the result of different underlying placental abnormalities that are detected variably on first-trimester uterine artery Doppler evaluation. In this study, the first-trimester uterine artery mean RI and prevalence of bilateral notching were significantly higher in women who subsequently delivered neonates with SGA than in women with normal pregnancies. The areas under the receiver-operating characteristics curves for the prediction of SGA without preeclampsia, IUGR, preterm IUGR, and SGA with preeclampsia were 0.602, 0.687, 0.776, and 0.708, respectively.²

Scifres et al evaluated whether maternal demographic and ultrasound parameters predict perinatal mortality (in utero death or neonatal death within the first 28 days of life) in preterm IUGR (delivery gestational age < 35 weeks and birth weight < 10th percentile for gestation). Two hundred thirty singleton pregnancies with preterm IUGR meeting the study inclusion criteria were identified. Oligohydramnios (amniotic fluid index <5) and abnormal umbilical artery Dopplers (absent or reverse end-diastolic flow) were found to have modest predictive value for perinatal mortality.³

In a prospective study (2005-2007) by Bastek et al of 93 women with severe preeclampsia and ultrasound 3 weeks or less before delivery, current ultrasound practice was noted to have moderately good positive and negative predictive values and a high specificity for the diagnosis of IUGR in women with severe preeclampsia. However, according to the authors, the poor sensitivity (56.7%) and low positive likelihood ratio (8.9) indicate that additional modalities are needed to improve the usefulness of ultrasound in detecting IUGR in severe preeclampsia.⁴

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Pathophysiology

Etiology

The causes of intrauterine growth retardation (intrauterine growth restriction; IUGR) can be either fetal or maternal.⁵

Fetal causes of IUGR include aneuploidy, trisomy 13, trisomy 18, triploidy, intrauterine infection, cytomegaloviral infection, and toxoplasmosis.

Maternal causes of IUGR include use of drugs (including recreational drugs such as marijuana), alcohol consumption, placental insufficiency, diabetes, late conception (possible cause), and a history of having a baby small for his or her age.

Asymmetrical vs symmetrical IUGR

In most cases of IUGR, especially those due to primary placental insufficiency, the fetal abdomen is small, but the head and extremities are normal or near normal. This finding is known as the head-sparing effect. In cases of severe, early-onset IUGR (those due to chromosomal anomalies), the fetus tends to be more symmetrically small. This condition leads to the existence of 2 distinct subgroups; however, these subgroups significantly overlap.

Fetal villus circulation

The placenta is the lifeline to the fetus, and when challenged, it has a remarkable ability to adapt. Developmental problems can occur from the maternal side, the fetal side, or both. To understand these problems, knowledge of the development and the physiology of the villus circulation is needed.

In the first trimester, the endometrium is invaded by the mesenchymal villi, which are made up of trophoblast, stroma, and a core of vessels. Early in pregnancy, the mesenchymal villi transform into immature intermediate stem villi, which then differentiate into stem villi. The primary-, secondary-, and tertiary-stem villi form the scaffolding from which subsequent villi develop. The histologic structure of the terminal villi optimizes maternal-fetal transfer of nutrients and oxygen. Vascularization of the villi occurs in the first and second trimesters by the process of branching angiogenesis.

Three basic theories regarding the mechanics of the placental circulation are described. As reported in one color Doppler investigation, the theory that best suits these findings is the Ramsey theory. In this mechanism, blood enters the intervillous spaces via the spiral arteries. While moving within the intervillous space, the maternal blood bathes the individual units, which are composed of a fetal arterial, venous, and capillary network. The maternal blood then leaves the intervillous space by the draining basal veins.

The transfer of oxygen and nutrients occurs at the interface between the terminal and intermediate mature villi and the intervillous space. Oxygen and nutrients enter the fetal villous venous circulation and are transferred to the fetus via the umbilical cord.

Kingdom et al demonstrated that maldevelopment of the villus tree in pregnancies complicated by fetal growth restriction is associated with abnormal uterine artery waveforms, which are Doppler findings indicating abnormal uteroplacental blood flow.⁶ In pregnancies also complicated by absent end-diastolic umbilical flow, the placental villi are elongated, and the capillary loops are uncoiled and sparse. These findings are correlated with an increase in fetal-placental vascular impedance and impair gas and nutrient exchange. An enhanced branching angiogenesis represents an adaptive response to impaired uteroplacental blood flow.

Frequency

United States

By definition, the prevalence of intrauterine growth retardation (intrauterine growth restriction; IUGR) is 10%; fetuses with an estimated weight of less than 10% for gestational age are defined as being growth restricted.

Mortality/Morbidity

The perinatal mortality for infants with intrauterine growth retardation (intrauterine growth restriction; IUGR) is 6-10 times greater than that of a normal-growth population. IUGR is a major cause of intrapartum fetal distress, intrapartum asphyxia, hypoglycemia, hypocalcemia, meconium aspiration, and intrauterine demise.

Sex

Intrauterine growth retardation (intrauterine growth restriction; IUGR) affects only pregnant women.

Age

The incidence of intrauterine growth retardation (intrauterine growth restriction; IUGR) increases with increasing maternal age.

Presentation

Intrauterine growth retardation (intrauterine growth restriction; IUGR) is usually related to preeclampsia.

Preferred Examination

The preferred method for evaluating intrauterine growth retardation (intrauterine growth restriction; IUGR) is ultrasonographic examination.⁷

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