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New Treatments for Fetal Growth Restriction and Intrauterine Growth Restriction

Fetal growth restriction used to be known in the non-politically correct world as intrauterine fetal growth retardation. Every time you say 'retardation' to a patient, it had a very different connotation than what you really intended. It is a subset of neonates whose birth weights fall below an arbitrarily defined lower limit. The limit is derived from the weight to age distribution curves and the most common limit is birth weight below the tenth percentile. This was not really designed by someone looking at neonates in a prospective fashion and determining where we need to make the cutoff; it was done by convention many years ago. It has actually held up to be quite accurate as a cutoff, I believe. It occurs in about five to ten percent of pregnancies. The discrepancy between the frequency of fetal growth restriction and that tenth percentile cutoff is fetal growth restriction and intrauterine growth restriction.

Fetal growth restriction is a risk factor for perinatal morbidity and mortality and fetal growth restriction is observed in twenty-five percent of all stillbirths. Risk factors for fetal growth restriction include aneuploidy, genetic disorders, congenital anomalies and infection. Maternal risk factors include hypertension, pre-eclampsia, cyanotic heart disease, diabetes with vasculopathy, systemic lupus - particularly in the presence of antiphospholipid antibodies or renal disease, smoking, drugs and alcohol. The placental risk factors that we list include infarction.

If we look at some of the earliest data that looked at birth weight percentiles with fetal death rates, we find a study published in 1966 by Scott and Usher. They found that the fetal death rate increased approximately eight times between the eighth and third percentile. If you look at those fetuses born who weighed below the third percentile, the fetal death rate was actually 20 times.

We basically have the types of patterns of fetal growth restriction. One is symmetric fetal growth restriction. That accounts for about twenty-five to thirty-five percent of all fetal growth restriction. People also call this type I. These are cases in which you see small babies; it is based upon small head size and small abdominal size. The injury in this case is usually early, in the first phase of growth, in the phase of cellular hyperplasia.

The next type of growth is asymmetric growth restriction, or what we call type II growth restriction. These are cases where there is usually head sparing. In other words, the head continues to be larger than the abdomen. These are cases that are usually due to extrinsic factors; something that leads to decreased supply of nutrients and oxygen to the baby.

The last group is an intermediate or mixed type. These are cases where there seems to be an insult probably more like at the end of the second trimester or beginning of the third trimester, where it affects the time where there is both cellular hyperplasia and cellular hypertrophy. We see not only a change as far as the number of cells, but the size of the cells.

When we have different patterns of growth, we end up seeing different things in babies. If you look at overall fetal growth restriction, about seventy to eighty percent of all fetuses with growth restriction are actually going to be normally small babies. They are not abnormal at all; they are symmetric and they continue to grow normally. A small group are going to be abnormally small babies. These are usually babies who don't continue to grow normally; they fall off on growth.

In the dysmature fetus with fetal growth restriction, there is fetal adaptation and compensation that occurs. The hypoxic reflex redistribution of cardiac output leads to reduced perfusion of the kidneys and lungs; babies don't need these. It sustains cerebral blood flow.

There are some additional adaptations; endocrine responses include increased arginine vasopressin. This contributes to further decreasing renal blood flow. Increased catecholamines actually may also lead to increased vasospasm of placental vessels and may lead to decreased blood flow. It can almost be a downward spiral once these changes start to occur.

The goal of diagnosis and management of fetal growth restriction is really to differentiate between the normal small, abnormal small and dysmature fetus and the attempt to reduce the perinatal morbidity and mortality in the dysmature fetus.

For suspected fetal growth restriction, clinically twenty-five percent of cases when you use menstrual history is utilized and only five percent when ultrasound dating is utilized. An argument like this may actually be one in which you could say that you can save money by doing a routine.

Stuart Campbell, who is distinguished in the arena of ultrasound, presented to what used to be the Society of Perinatal Obstetricians about a decade ago, when Doppler first came out, the premise that Doppler would replace everything that we use for both diagnosis and screening in cases of placental dysfunction. That was the initial promise.

What is the management for fetal growth restriction? The first thing you try to do is to reduce risk factors. If somebody smokes, you eliminate the smoking or reduce the smoking. If somebody has hypertension, you try to control their hypertension; however, controlling the hypertension will not eliminate fetal growth restriction. You pay attention to the risk factors and try to minimize those. We recommend serial growth assessment.