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Fetal Alcohol Syndrome And Fetal Alcohol Effects

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Fetal Alcohol Syndrome and Fetal Alcohol Effects Prenatal alcohol exposure is a preventable cause of birth defects, including mental retardation and neurodevelopmental deficits. Since the initial recognition in 1968 of the multiple effects that alcohol can have on the developing fetus [1] and the subsequent delineation in 1973 of fetal alcohol syndrome (FAS), [2] it has become clear that prenatal alcohol exposure can be associated with a wide range of abnormalities. [3] More than 80% of children with FAS demonstrate prenatal and postnatal growth deficiency, mild to moderate mental retardation, microcephaly, infantile irritability, and characteristic facial features. Fifty percent of affected individuals also have poor coordination, hypotonia, attention deficit disorders with hyperactivity, decreased adipose tissue, and other identifiable facial features. Additionally, 20% to 50% of affected children demonstrate a variety of other birth defects, including cardiac anomalies, hemangiomas, and eye and ear anomalies. [2,4,15,16] Even in the absence of growth retardation or congenital abnormalities, children born to womenwho drank alcohol excessively during pregnancy appear to be at increased risk for attention deficitdisorders with hyperactivity, fine-motor impairment, and clumsiness as well as more subtle delays inmotor performance and speech disorders. [4] These findings have been referred to as fetal alcoholeffects (FAE). As recently described, FAS and FAE produce profound cognitive, behavioral, and psychosocial problems that persist to date of follow-up of those affected. In the most comprehensive and far-reaching study to date, Streissguth et al [5] traced the natural history into adulthood and demonstrated the profound, pervasive, and persistent nature of the biopsychosocial manifestations of these disorders. Cognitively those affected maintained subnormal intellectual functioning; demonstrated specific arithmetic deficiency; had extreme difficulty with abstractions such as time and space, cause and effect; and could not generalize from one situation to another. They also demonstrated inattention, poor concentration, memory deficit, impaired judgment, and impaired comprehensive and abstract reasoning. Behavioral problems such as hyperactivity and impulsivity as well as conduct problems such aslying, stealing, stubbornness, and oppositional behavior were manifest. These behavioral problemswere qualitatively and quantitatively different from those found in other forms of mental retardation.[6] None of those in the study [5] were age appropriate in terms of socialization or communicationskills. Maladaptive social function was evidenced by their failure to consider consequences for theiractions, lack of response to appropriate social cues, lack of reciprocal friendships, social withdrawal, sullenness, mood lability, teasing and bullying behavior, and periods of high anxiety and excessive unhappiness. Fetal alcohol syndrome is one of the most common identifiable causes of mental retardation,[3] with a worldwide incidence estimated to be 1.9 per 1000 livebirths. [7] However, when childrenwith less severe manifestations of the syndrome (FAE) are included, the estimated incidence may beas great as 1 in 300 livebirths. [8] Evidence indicates, however, that physicians may not consistentlyinquire about alcohol use during pregnancy [9] or recognize the full spectrum of the effects ofprenatal exposure. [10] There is no established “safe dose” of alcohol for pregnant women. However, mothers ofchildren with fully expressed FAS drink alcohol more and drink earlier in gestation than those withinfants without fully expressed clinical features. Mothers who only drink later in gestation have anincreased frequency of premature deliveries and deliveries of babies small for gestational age. [11] In one study, Mills et al [12] prospectively studied 31604 pregnancies in an attempt todetermine how much drinking in pregnancy is safe. The consumption of at least one to two drinks aday was associated with a substantially increased risk of giving birth to a growth-retarded baby. [12] Alpert and Zuckerman [13] have pointed out confounding risk factors regarding alcohol useduring pregnancy. Problems of historical accuracy in some studies of exposure and other possibleprenatal factors create uncertainty about possible risks to the fetus, particularly when small amountsof alcohol consumption are reported. At present, the evidence for harm to the fetus is much strongerwith large amounts of maternal alcohol consumption than with smaller amounts. Moreover, itappears that all infants prenatally exposed to the same amount of alcohol will not be affected to thesame degree. While there is remaining controversy about the association between maternalconsumption of smaller amounts of alcohol and possible damage to the fetus, current data do notsupport the concept that any amount of alcohol is safe for all pregnant women. It has recently been estimated that the economic cost associated with the growth deficiency,

surgical repair of structural defects, treatment of perceptual and cognitive problems, and mentalretardation associated with FAS in the United States is at least $321 million per year. [7] The mentalretardation related to FAS has by itself been estimated to account for as much as 11% of the annualcost for all mentally retarded institutionalized residents in the United States and may account for upto 5% of all congenital anomalies. [7,14] Nonfiscal costs to families and affected children in terms of emotional and social impact are enormous.Since there is no known safe amount of alcohol consumption during pregnancy, the American Academy of Pediatrics recommends abstinence from alcohol for women who are pregnant or who are planning a pregnancy. Special efforts should be directed toward educating women, prior to and during the childbearing years, regarding the harmful effects of alcohol on the developing fetus. Major efforts at all levels of society should be made to develop quality educational programs regarding the deleterious consequences of alcohol on the unborn child. These programs should be integrated into mandatory curriculum for all elementary, junior high, and high school students. They should be a part of the educational curriculum in all postsecondary and adult centers of learning. Pediatricians and other health professionals caring for women and their newborns should increase their own awareness and that of their patients about FAS and FAE and their prevention. Pediatricians should increase their awareness of maternal alcohol exposures during pregnancy to help identify the possible cause of birth defects and to help identify other adverse fetal outcomes in future pregnancies. Those infants and children who are thought to have FAS or FAE should be evaluated by a pediatrician who is knowledgeable, skilled, and competent in the evaluation of neurodevelopmental and psychosocial problems. Otherwise, the necessity for a skilled evaluation requires early referral to a specialist in this area. If such problems are identified or if the child is considered to be at risk for the later identification of developmental problems, referral should be made for early educational services available under the provisions of the Education for All Handicapped Children Act (PL 94-142 and PL 99-457). The American Academy of Pediactrics supports federal legislation that would require the inclusion of health-and-safety messages in all print and broadcast alcohol advertisements, based on the US Surgeon General’s warning: “Drinking during pregnancy may cause mental retardation and other birth defects. Avoid alcohol during pregnancy.” The Academy supports the development of state legislation that makes information about FAS and FAE available at marriage-licensing bureaus and other appropriate public places, including points of alcohol sale.REFERENCES 1. Lemoine P, Harrousseau H, Borteyro JP, et al. Les enfants de parents alcoholiques. OuestMed. 1968;21:476-4922. Jones KL, Smith DW, Ulleland CW, et al. Pattern of malformation in offspring of chronicalcoholic mothers. Lancet. 1973;1:1267-12713. Gorlin RJ, Cohen MM, Levin LS. Teratogenic agents. In: Syndromes of the Head and Neck.3rd ed. New York, NY: Oxford University Press Inc;1990:16-194. Streissguth AP. The behavioral teratology of alcohol: performance, behavioral, andintellectual deficits in prenatally exposed children. In: West JR, ed. Alcohol and BrainDevelopment. New York, NY: Oxford University Press Inc; 1986:3-445. Streissguth AP, Aase JM, Clarren SK, et al. Fetal alcohol syndrome in adolescents andadults. JAMA. 1991;265:1961-19676. Harris JC. Psychological adaptation and psychiatric disorders in adolescents and youngadults with Down syndrome. In: Pueschel SM, ed. The Young Person With Down Syndrome:Transition From Adolescence to Adulthood. Baltimore, MD: PH Brookes; 1988:35-517. Abel EL, Sokol RJ. Incidence of fetal alcohol syndrome and economic impact ofFAS-related anomalies. Drug Alcohol Depend. 1987;19:51-708. Olegard R, Sabel KG, Aronsson M, et al. Effects on the child of alcohol abuse duringpregnancy. Acta Paediatr Scand Suppl. 1979; (No. 275):112-1219. Donovan CL. Factors predisposing, enabling, and reinforcing routine screening of patientsfor preventing fetal alcohol syndrome: a survey of New Jersey physicians. J Drug Educ.1991;21:35-4210. Little BB, Snell LM, Rosenfeld CR, et al. Failure to recognize fetal alcohol syndrome innewborn infants. AJDC. 1990;144:1142-114611. Jones KL, Smith DW, Streissguth AP, Myrianthopoulos NC. Outcome in offspring ofchronic alcoholic women. Lancet. 1974;1:1076-107812. Mills JL, Graubard BI, Harley EE, Rhoads GG, Berends HW. Maternal alcoholconsumption and birth weight: how much drinking in pregnancy is safe? JAMA.1984;252:1875-187913. Alpert JJ, Zuckerman B. Alcohol use during pregnancy: what is the risk? Pediatr Rev.1991;12:375-37914. Charness ME, Simon RP, Greenberg DA. Ethanol and the nervous system. N Engl J Med.1989;321:442-45415. Clarren SK, Smith DW. The fetal alcohol syndrome. N Engl J Med. 1978;298:1063-106716. Jones KL. Fetal alcohol syndrome. Pediatr Rev. 1986;8:122-126