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New Treatments for Intrauterine Growth Retardation

Fetal growth retardation can be caused by multiple factors, which can be classified into three broad categories relating to the substrate: maternal, substrate availability; placental, substrate transfer; and fetal, substrate utilization. Within each category, there are important subgroups. For example, the maternal grouping requires that the critical substrate--glucose--amino acids, and oxygen. Maternal nutrition before and during pregnancy is important in terms of fetal growth. Although most mothers gain about 30 lb in pregnancy, good fetal outcome requires a larger weight gain in a thin woman compared with that in an obese woman.

The placenta group includes those women with pool uterine blood flow or a small placental surface area. If there is maternal vascular disease, such as hypertension with constricted spiral arteries.

A close relation exists between placental surface area and fetal weight.  The mother's failure to recognize and accept fetal antigens could establish an immunologic host defense that would alter placental growth or function and produce an intrauterine growth retardation fetus. The fetal group includes those pregnancies in which even though substrate is in the mother's blood and indeed crosses the placenta, it is not used normally by the fetus. Two general conditions are responsible for this.


The diagnosis of intrauterine growth retardation depends first on a simple, inexpensive clinical screen and then on more expensive laboratory tests to confirm or refute the diagnosis. Several risk-scoring systems have been developed that can select out a population to be concerned about.

Confirmation of the clinical suspicion of intrauterine growth retardation can be done with more sophisticated and expensive tests. The first group are biophysical. The ultrasonographic visualization of the intrauterine cavity has greatly assisted in the diagnosis. The first studies were of fetal head size, but their accuracy was only about 50%. This is not too surprising, since nature allows the brain to continue to grow under the most adverse circumstances as a natural protection for central nervous system (CNS) function. Thus, the brain is the last organ affected in IUGR, giving a brain-sparing effect.

Other studies that can be useful include measurements of placental and fetal biochemical factors that are present in the maternal circulation and related to fetal or placental weight. These include estriol, hPL, and SP1 protein. Amniotic fluid levels of the C peptide fragment of proinsulin and of glucose are also of assistance in the diagnosis. With IUGR, all these biochemical markers tend to be low.


The complications of IUGR are principally those for the infant. Although the mother may have problems that cause the growth retardation, such as hypertension or asthma, the most serious problems are for the infant. By definition, its size will be small for its gestational age. If the condition has been present for a relatively short time, the CNS may continue to grow while other systems, such as the abdomen.


Because of the many serious problems that can occur in the fetus or neonate who is growth-retarded, these pregnancies need to be managed by an experienced perinatal team in a tertiary referral center. The management of these pregnancies depends on the following general principles:

Early detection (e.g., high-risk groups, testing)
Elimination of contributing factors (e.g., diet, smoking, drugs)
Increase uterine blood flow (e.g., bed rest)
Serial fetal surveillance (e.g., weekly nonstress and oxytocin contraction tests and ultrasound)
Early delivery in perinatal center.

To introduce some management program, the cases first need to be detected. Early diagnosis is best because it provides time for intervention before fetal damage occurs. Clinicians must, therefore, be aware of the problem and be testing for it, especially in pregnancies at risk, such as women who are hypertensive, who smoke, who demonstrate poor nutrition or little weight gain, or who have history of intrauterine growth retardation deliveries, because the problem does recur. The use of aspirin as preventive therapy in hypertension is under study and might be useful in the future.

Second, the contributing factors must be eliminated. These include poor dietary intake, smoking, and drug abuse. The diet for a pregnant woman contains about 300 calories per day more than the diet for a woman in the nonpregnant state; therefore, all pregnant women should be instructed to eat a diet of about 2100 to 2300 calories per day. The composition of the diet is less important than the number of calories it contains. Nonetheless, a protein content of 1.3 to 1.5 g/kg/day is recommended. Women on this diet gain differently, depending on their prepregnancy weights. Normal-weight women gain about 30 lb, whereas thin women gain more and obese women gain less.

Uterine blood flow is directly related to maternal blood pressure in a maximally dilated vascular system. For this reason, the third principle of management--to increase uterine blood flow as much as possible--does not mean lowering maternal blood pressure.

Before an intensive fetal surveillance program is begun, a fetal karyotype should be done if there is a serious risk of trisomy in the normally pregnant woman with severe symmetric fetal growth retardation. Either amniotic fluid or umbilical blood can be used. This antepartum surveillance program should be started as soon as something can be done about an abnormal result.