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MS WordPerinatologist Corner - C.E.U/C.M.E. Modules
Fetal Growth Restriction
Sponsored by The Indian Health Service Clinical Support Center
3. Read the background material
Background
Definition
By definition, ten percent of infants in any population will have birth weights at or below the 10th percentile. This is the usual definition of fetal growth restriction as made by ultrasonographic determination of fetal weight. Perinatal morbidity and mortality, however, do not usually begin to rise until birth weights are below the 3rd-5th percentile for gestational age. For practical clinical purposes, in order to avoid the sequelae of severe F.G.R., it is therefore prudent to address the problem when presented with an estimated fetal weight below the 10th percentile.
By convention, the term "small for gestational age" (S.G.A.) should be used to refer to the infant after birth, and the term "intrauterine growth restriction" (I.U.G.R.), or better, "fetal growth restriction" (F.G.R.), should be used to refer to the fetus before birth. The latter really refers to a fetus that fails to achieve its inherent growth potential as a consequence of either intrinsic genetic factors or extrinsic environmental influences. It is best to avoid the term "growth retardation" as many parents will wrongly infer that you are referring to their child's future intellectual performance.
Fetal growth is also somewhat population- and ethnicity-dependent, as not all ethnic groups will conform to "California sea-level" standards. Notably, many North American Native American and Mexican-American groups will have larger babies and many Central American and Southeast Asian women will have constitutionally smaller offspring. Accurate pregnancy dating is also of paramount importance in making the diagnosis and is perhaps the most common confounder in clinical practice.
Significance
As noted above, growth-restricted fetuses are at risk for increased perinatal mortality and morbidity. They are at significantly increased risk of intrauterine fetal demise (I.U.F.D.), especially if post term, and they may have up to a 30% incidence of fetal intolerance of labor as a result of placental insufficiency, and may develop hypoxemia and acidemia when stressed by uterine contractions. S.G.A. newborns may have problems with low Apgar scores, hypoglycemia, hypothermia, hypocalcemia, polycythemia, apneic episodes, seizures, and feeding difficulties.
The combination of prematurity and growth restriction is especially pejorative for the neonate. The birthplace of such infants should be a facility equipped to manage their special requirements. Long-term effects have been more difficult to quantify, but there is a definite increase in neurological sequelae, prominent among which are learning and behavioral disorders. SGA infants may also be more prone to adult-onset hypertension and ischemic heart disease.
Etiology
Risk factors for F.G.R. include those due to maternal, placental, or fetal antecedents. Maternal medical disorders may contribute to poor fetal growth, especially maternal vascular disorders such as chronic hypertension, renal disease, diabetes with microvascular pathology, and systemic lupus erythematosus. Likewise, maternal disorders characterized by under-oxygenation such as severe asthma or cyanotic congenital heart disease are associated with low birth weight.
Maternal smoking is associated with a 3.5-fold increase in S.G.A. infants, is clearly dose related, and may even be affected by passive smoke exposure. Likewise, maternal cocaine or methamphetamine users, as well as narcotic-addicted women, may have a 30-50 % incidence of FGR. A combination of vascular and nutritional effects may be involved in such women. There is a clear association between heavy maternal alcohol use and impaired fetal growth.
The role of maternal malnutrition is a significant worldwide problem. When maternal caloric intake is restricted to below 1500 kcal/day, as is common in many developing nations, a measurable effect on birth weight will become evident, as a result of both preterm birth and fetal growth restriction. Coagulation disorders, such as those that occur in women with a thrombophilic coagulopathy or the antiphospholipid antibody syndrome, may result in placental microvascular thrombi and result in impaired fetal perfusion and oxygenation and subsequent growth impairment or death.
Viral or protozoal infections such as cytomegalovirus, varicella, toxoplasmosis, malaria, and Chagas' disease, as well as syphilis, may all cause a severe placental villitis and result in severe F.G.R. or I.U.F.D. as a result. Fetal aneuploidy, as well as confined placental mosaicism, are also well recognized causes of S.G.A. infants. Multiple gestation, especially when associated with monochorionicity, may be associated with a placental reserve that is inadequate to support the growth of both fetuses, or unequal sharing of that reserve.
