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Fetal Alcohol Syndrome - Essay Example

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"Fetal Alcohol Syndrome" paper states that even when the initial stages of pregnancy or even before the pregnancy is detected if alcohol is consumed, it can cause serious damage. Unfortunately, if women wait until a pregnancy is confirmed before they stop drinking it may be too late…
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Fetal Alcohol Syndrome
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Fetal Alcohol Syndrome Introduction When a mother drinks, her unborn child is exposed to alcohol which can have serious consequences. "Fetal alcoholspectrum disorders" (FASD) or Fetal alcohol syndrome is the term describing the range of effects that can occur in a child who was exposed to alcohol while in the womb. The range of effects may include physical, mental, behavioral, and perhaps even learning disabilities with possible lifelong implications (DHHS, 2007). In other words severe effects of alcohol consumption during pregnancy are termed as fetal alcohol syndrome (FAS) and it is one of the important known avoidable causes of mental retardation and birth defects. If a woman drinks alcohol during her pregnancy, there are high chances that her baby can be born with FAS, which is a lifelong condition that causes physical and mental disabilities. In today's world where socializing is considered an important part of life, several times women in their reproductive age expose themselves to alcohol. As a consequence, knowingly or unknowingly alcohol abuse is the leading cause of mental retardation in the western world. The amount and timing of alcohol use by the pregnant women determine the type and extent of resulting birth defects. FAS is characterized by Holoprosencephaly which is a condition that is linked with failure of the brain to divide into two hemispheres. This condition is generally associated with neuro-developmental and facial abnormalities. Additionally, there are also possibilities of associated abnormalities of the corpus callosum, the brainstem and the cerebellum, particularly the anterior portion of the vermis. Children with FAS may also suffer due to absence of olfactory lobes, hypoplasia of the hippocampus and abnormal or absent basal ganglia; usually hypoplastic or absent caudate nuclei. According to the results of the positron emission tomography scans, abnormalities is seen in glucose metabolism, especially in the anterior caudate nucleus and the vermis of the cerebellum, even in the absence of overt structural abnormalities (Canadian PaediatricSociety, 2007). There is lack of proper data on the exact prevalence of FAS/atypical FAS. According to studies conducted by Abel (1995), it is estimated that the overall incidence of FAS at 0.97/1000 (0.097%) live births and 43/1000 (4.3%) among babies of heavy drinkers. Based on three population studies, Sampson et al. (1997) estimated the incidence of FAS to be between 2.8/1000 and 4.8/1000 live births, and the incidence of a combination of FAS and ARND to be at least 9.1/1000 live births. In yet another statistic it is said that though all races are vulnerable to FAS, it is excessively higher among American Indian offspring (Aase, 1981). It is also estimated that each year in the United States, 1 in every 750 infants is born with a pattern of physical, developmental, and functional problems is due to fetal alcohol syndrome (FAS), while another 40,000 are born with fetal alcohol effects (FAE) (KidsHealth, 2007). It is important to note that variation in these rates depends on the population studied and the surveillance methods used which may be different for different research groups. In yet another study conducted by CDC show FAS rates ranging from 0.2 to 1.5 per 1,000 live births in different parts of the United States. Besides, other FASDs are thought to occur roughly three times as often as FAS (Centers for Disease Control and Prevention, 2006). Historical Perspective of Fetal Alcohol Syndrome It is interesting to note that concerns have surrounded the consumption of alcohol during pregnancy since biblical times. However, Dr. William Sullivan, a Liverpool prison physician noted higher rates of stillbirth for 120 alcoholic female prisoners than their sober female relatives in 1899. This is the earliest known observation of possible links between maternal alcohol use and fetal damage. He also pointed out that the causal agent was alcohol use (Sullivan, 1899). A case study was conducted by Henry H. Goddard who belonged to one of the popular families in 1900s the "Kallikak family" (Goddard, 1912). However, a few other studies have suggested that the few members of Kallikak family almost certainly had FAS (Karp, et al. 1994). Earlier studies on alcoholism in the mid-1900s were typically based on a heredity argument (Haggard and Jellinek, 1942). A few studies had noted differences between the children of mothers who used alcohol during pregnancy or breast-feeding and those who did not, but identified alcohol use as a possible contributing factor rather than heredity (Streissguth, 1997). Though FAS was only named in the year 1973, there are several studies that showed that consumption of alcohol during pregnancy could lead to deformities in the child. For instance, Dr. Paul Lemoine had published a study in a French medical journal in the year 1968 about children with distinctive features whose mothers were alcoholics (Lemoine, et al. 1968), and Christy Ulleland and colleagues at the University of Washington Medical School in the U.S. (Ulleland, 1972), had carried out an 18-month study during 1968-1969 documenting the risk of maternal alcohol consumption among the offspring of 11 alcoholic mothers. Drs. Kenneth Lyons Jones and David W. Smith of the University Of Washington Medical School in Seattle are the two dysmorphologists who named Fetal Alcohol Syndrome in 1973. They were responsible for identifying a pattern of "craniofacial, limb, and cardiovascular defects associated with prenatal onset growth deficiency and developmental delay" in eight unrelated children belonging to three ethnic groups, and all born to mothers who consumed alcohol (Jones, et al. 1973). Though this was a fact, many still argued that it had a hereditary link. Researchers in United States France, and Sweden were all surprised to note the similar looking children, though they were not belonging to same family or were not related to each others, they behaved in the same unfocused and hyperactive manner (Olegard, et al. 1979). After the 1973 studies, animal studies, including non-human primate studies were carried out at the University Of Washington Primate Center by Dr. Sterling Clarren, had confirmed that alcohol was a teratogen. By the year 1978, 245 cases of FAS had been reported by medical researchers. Dr. Smith named FAS after the causal agent of the symptoms because he believed that by doing so would encourage prevention. He thought that if people especially the pregnant women knew that maternal alcohol consumption caused the syndrome, then they would abstain during pregnancy (Clarren, 2005). Later on subsequent research and clinical experience suggested that a range of effects including physical, behavioral, and cognitive could arise from alcohol consumption during pregnancy and the term Fetal Alcohol Spectrum Disorder (FASD) was developed to include FAS as well as other conditions resulting from prenatal alcohol exposure. At present, FAS is the only expression of prenatal alcohol exposure defined by the International Statistical Classification of Diseases and Related Health Problems and assigned ICD-9 and ICD-10 diagnoses (Clarren and Smith, 1978). Signs and Symptoms of Fetal Alcohol Syndrome The following are some of the common signs and symptoms of FAS: low birth weight developmental delay small head circumference organ dysfunction facial abnormalities, which includes smaller eye openings, flattened cheekbones, and indistinct or smoother philtrum epilepsy behavioral problems, which includes hyperactivity, inability to concentrate, social withdrawal, stubbornness, impulsiveness, and anxiety learning difficulties, which includes poor memory, inability to understand concepts such as time and money, poor language comprehension, poor problem-solving skills poor coordination/fine motor skills poor socialization skills, which includes difficulty building and maintaining friendships and relating to groups lack of imagination (KidsHealth, 2007). Diagnosis As of today, there is no objective laboratory test for diagnosing FAS. In other words, it is difficult to diagnose if a child will have FAS. However, if it is known that the mother is alcoholic, then the diagnosis of FAS relies on a pattern of abnormalities that make up the syndrome and reports of alcohol use/misuse by the mother during pregnancy and especially around the time of conception. The importance is on the occurrence of a set of criteria as each of the individual abnormalities are often restrained, difficult to detect, and may also occur in situations where alcohol is not a factor (Aase, 1994). Over the years a number of paradigms have been described for diagnosing FAS, but each has retained the following key features which occur in a majority of cases: growth retardation, characteristic facial features and central nervous system anomalies. A number of associated anomalies that occur more frequently with FAS have been documented, but none have been reported to occur in the majority of cases (Clarren and Smith, 1978). Abnormalities in each of the three main categories exclude most other birth defect syndromes (Rosett, 1980, Sokol and Clarren, 1989), while confirmation of diagnosis requires a history of maternal alcohol use during pregnancy (Aase, 1994). Diagnosis of FAS is usually made on infants and young children, as the features of FAS often undergo change as the age increases (Streissguth, 1994, Larkby and Day, 1997). Besides, studies show that central nervous system dysfunction and the facial morphology may be difficult to evaluate before two years of age (Rosett, 1980, Larkby and Day, 1997). Other longitudinal studies suggest that with adolescence the FAS facial morphology becomes less distinct and the weight approaches the mean. The other manifestations of FAS, such as the behavioral problems, poor IQ or intellectual problems, and poor skills continue to be persistent throughout adulthood (Streissguth, 1994). According to a study in Germany, the developmental changes occurring in adolescents diagnosed with FAS were investigated in forty-four FAS patients (Spohr et al., 1994) found that their findings may help with diagnosing FAS during late childhood and adolescence. The typical FAS facial features are known to change with puberty, but a number of symptoms persist including microcephaly, mild micrognathia, smoother philtrum, a thin upper lip and short palpebral fissures. Nasal features also undergo change with the development of a large nose and a distinctive nasal bridge. Besides, this study also showed that physical height and head circumference both remained below the norm with 60% and 42% (respectively) remaining 2 SD below the population mean. There was a variation in weight between males and females with 54% of males 2 SD below the population mean, while only 19% of females fell within this category. The intelligence level of seventy-five percent of these adolescents remained in the borderline categories with poor or low intelligence. The authors also identified the presence of a number of psychiatric disorders in the adolescents (Leary, 2002). Treatments and Interventions As we all know that prevention is better than cure. FAS are totally preventable-if a woman does not drink alcohol while she is pregnant or trying for pregnancy. If a woman is drinking during pregnancy, it is never too late for her to stop. Since researcher still now have not been able to pinpoint the time of the dose of alcohol which causes FAS, the sooner a woman stops drinking, the better it will be for both herself and her baby. As of today there is no cure for FAS, because the CNS damage creates a permanent disability, but treatment is possible. Each of these individuals has specific needs. For instance, CNS damage and secondary disabilities needs vary broadly by individual, there is no single treatment type that works for everyone. Instead, comprehensive, multi-model approaches based on the needs of the patient must be used. Researchers have identified several treatment models, but irrespective of the predominant approach, most in the studies recommend a combination of multiple types of interventions to ameliorate the negative effects. Intervention should be based on need, and should not be delayed in accessing definitive diagnostic services. The consequences of delaying treatment can be serious especially for children with FAS. Traditional medical interventions (i.e., psychoactive drugs) are frequently tried on those with FAS because many FAS symptoms are mistaken for or overlap with other disorders, particularly ADHD (Buxton, 2005). For example, an FAS patient who does not concentrate, does not complete schoolwork, and cannot stay seated has characteristics that overlap with symptoms of ADHD, particularly if the patient is not yet diagnosed with FAS. In such cases improper treatments could lead to problems. Since the learning system of children with FAS is damaged, behavioral interventions are not always successful, or not successful in the long run, especially because overlapping disorders frequently stem from or are exacerbated by FAS. Studies conducted by Kohn (1999) suggest that a rewards-punishment system in general may work in the short-term but is unsuccessful in the long-term. Additionally, Kohn's minority challenge to behavioral interventions does demonstrate the significance of factors beyond learning theory when trying to support improved outcomes for FAS, and recommends a more multi-model approach that can be found in varying degrees within the advocacy model and neurobehavioral approach. We all know that alcohol is a teratogen, and the only certain way to prevent FAS is to avoid drinking alcohol during pregnancy. To decrease prenatal alcohol exposure, prevention efforts should target not only pregnant women who are presently drinking, but also to those women who could become pregnant, are drinking at high-risk levels, and are having unprotected sex. In conclusion, it can be said that several studies suggest that drinking alcohol is dangerous to the fetus. It is not only important to create awareness through proper education to the pregnant women or women in her reproductive age, it is also important that the entire family become aware of the problems of FAS. The fetus is most susceptible to different types of injuries depending on the stage of development in which alcohol is encountered. Besides, research is yet to find a safe amount of drinking during pregnancy, and all major authorities agree that women should not drink at all during pregnancy. Even when the initial stages of pregnancy or even before the pregnancy is detected, if alcohol is consumed, it can cause serious damage. Unfortunately, if women wait until a pregnancy is confirmed before they stop drinking it may be too late. By then, the embryo/fetus has gone through several weeks of critical development. Having a child with FAS is a real pain and difficult situation for both mother and child. Hence it is always better to avoid alcohol completely during pregnancy. References Abel E.L. (1995) An update on Incidence of FAS: FAS is not an equal opportunity birth defect. Neurotoxicol Teratol; Vol. 17:437-443. Aase J.M. (1981) The fetal alcohol syndrome in American Indians: A high risk group. Neurobehav Toxicol Teratol; Vol. 3:153-156. Aase, J. M. (1994) Clinical recognition of FAS: difficulties of detection and diagnosis, Alcohol Health & Research World, Vol. 18, 5-10. Buxton, B. (2005). Damaged Angels: An Adoptive Mother Discovers the Tragic Toll of Alcohol in Pregnancy. New York: Carroll & Graf. ISBN 0-7867-1550-2. Canadian PaediatricSociety (2007) Fetal alcohol syndrome, Paediatrics & Child Health 2002; Vol. 7(3): 161-174. Centers for Disease Control and Prevention, (2006) Fetal Alcohol Spectrum Disorders, National Center on Birth Defects and Developmental Disabilities Retrieved on 13 July 2007 from http://www.cdc.gov/ncbddd/fas/fasask.htm#how Clarren, S.K., & Smith, D.W. (1978). Fetal alcohol syndrome. New England Journal of Medicine, 298, 1063-1067. Goddard, H.H. (1912). The Kallikak Family: A Study in the Heredity of Feeble-Mindedness. New York: Macmillan. Haggard, H.W., and Jellinek, E.M. (1942). Alcohol Explored. New York: Doubleday. Karp, R.J., Qazi, Q.H., Moller, K.A., Angelo, W.A., and Davis, J.M. (1995). Fetal alcohol syndrome at the turn of the century: An unexpected explanation of the Kallikak family. Archives of Pediatrics and Adolescent Medicine, Vol. 149(1), 45-48. KidsHealth, (2007) Fetal alcohol syndrome, The Nemours Foundation, Retrieved on 13 July 2007 from http://www.kidshealth.org/parent/medical/brain/fas.html Kohn, A. (1999). Punished by Rewards: The Trouble with Gold Stars, Incentive Plans, A's, Praise, and Other Bribes. Boston: Houghton Mifflin. ISBN 0-618-00181-6. Larkby, C. and Day, N. (1997) The effects of prenatal alcohol exposure, Alcohol Health & Research World, Vol. 21, 192-197. Leary, C.O. (2002) Fetal Alcohol Syndrome: A Literature Review, Commonwealth of Australia, ISBN 0 642 82118 6 Olegard, R., Sabel, K.G., Aronsson, M. Sandin, B., Johannsson, P.R., Carlsson, C., Kyllerman, M., Iversen, K. & Hrbek, A. (1979). Effects on the child of alcohol abuse during pregnancy. Acta Paediatrica Scandinavica, Vol. 275, 112-121. Rosett, H. L. (1980) A clinical perspective of the fetal alcohol syndrome, Alcoholism: Clinical and Experimental Research, Vol. 4, 119-122. Sampson PD, Streissguth AP, Bookstein FL, et al. (1997) Incidence of fetal alcohol syndrome and prevalence of alcohol-related neurodevelopmental disorder. Teratology; Vol. 56:317-326. Sokol, R. J. and Clarren, S. K. (1989) Guidelines for use of terminology describing the impact of prenatal alcohol on the offspring, Alcoholism: Clinical and Experimental Research, Vol. 13, 597-598. Spohr, H. L., Willms, J. and Steinhausen, H. C. (1994) The fetal alcohol syndrome in adolescence, Acta Paediatr, Vol. 404, 19-26. Streissguth, A. (1997). Fetal Alcohol Syndrome: A Guide for Families and Communities. Baltimore: Brookes Publishing. Streissguth, A. P. (1994) A long-term perspective of FAS, Alcohol Health & Research World, Vol. 18, 74-82. Sullivan, W.C. (1899). A note on the influence of maternal inebriety on the offspring. Journal of Mental Science, Vol. 45, 489-503. U.S. Department of Health and Human Services (DHHS) (2007) How Fetal Alcohol Spectrum Disorders Co-Occur With Mental Illness. Retrieved on 13 July 2007 from http://www.fascenter.samhsa.gov/documents/WYNK_CoOccurMentalIllnes.pdf Ulleland, C.N. (1972). The offspring of alcoholic mothers. Annals New York Academy of Sciences, Vol. 197, 167-169. Read More
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