fetal alcohol syndrome

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Fetal Alcohol Syndrome



Fetal alcohol syndrome (FAS) is a pattern of birth defects, learning, and behavioral problems affecting individuals whose mothers consumed alcohol during pregnancy.


FAS is the most common preventable cause of mental retardation. This condition was first recognized and reported in the medical literature in 1968 in France and in 1973 in the United States. Alcohol is a teratogen, the term used for any drug, chemical, maternal disease or other environmental exposure that can cause birth defects or functional impairment in a developing fetus. Some features may be present at birth including low birth weight, prematurity, and microcephaly. Characteristic facial features may be present at birth, or may become more obvious over time. Signs of brain damage include delays in development, behavioral abnormalities, and mental retardation, but affected individuals exhibit a wide range of abilities and disabilities. It has only been since 1991 that the long-term outcome of FAS has been known. Learning, behavioral, and emotional problems are common in adolescents and adults with FAS. Fetal Alcohol Effect (FAE), a term no longer favored, is sometimes used to describe individuals with some, but not all, of the features of FAS. In 1996, the Institute of Medicine suggested a five-level system to describe the birth defects, learning and behavioral difficulties in offspring of women who drank alcohol during pregnancy. This system contains criteria including confirmation of maternal alcohol exposure, characteristic facial features, growth problems, learning and behavioral problems, and birth defects known to be associated with prenatal alcohol exposure.
The incidence of FAS varies among different populations studied, and ranges from approximately one in 200 to one in 2000 at birth. However, a study reported in 1997, utilizing the Institute of Medicine criteria, estimated the prevalence in Seattle, Washington from 1975–1981 at nearly one in 100 live births. Avoiding alcohol during pregnancy, including the earliest weeks of the pregnancy, can prevent FAS. There is no amount of alcohol use during pregnancy that has been proven to be completely safe.
There is no racial or ethnic relation to FAS. Individuals from different genetic backgrounds exposed to similar amounts of alcohol during pregnancy may exhibit different signs or symptoms of FAS. Estimates state that 30-45% of women who consume six or more drinks a day throughout pregnancy will give birth to a child with FAS. The risk of FAS appears to increase as a chronic alcoholic woman progresses in her childbearing years and continues to drink. That is, a child with FAS will often be one of the last born to a chronic alcoholic woman, although older siblings may exhibit milder features of FAS. Binge drinking, defined as sporadic use of five or more standard alcoholic drinks per occasion, and "moderate" daily drinking (two to four 12 oz bottles of beer, eight to 16 ounces of wine, two to four ounces of liquor) can also result in offspring with features of FAS. Experts say a few binges early in pregnancy—before a woman may even know she is pregnant—may be enough to be dangerous, even if she stops drinking later.

Causes and symptoms

FAS is not a genetic or inherited disorder. It is a pattern of birth defects, learning, and behavioral problems that are the result of maternal alcohol use during the pregnancy. The alcohol freely crosses the placenta and causes damage to the developing embryo or fetus. Alcohol use by the father cannot cause FAS. If a woman who has FAS drinks alcohol during pregnancy, then she may also have a child with FAS. Not all individuals from alcohol exposed pregnancies have obvious signs or symptoms of FAS; individuals of different genetic backgrounds may be more or less susceptible to the damage that alcohol can cause. The dose of alcohol, the time during pregnancy that alcohol is used, and the pattern of alcohol use all contribute to the different signs and symptoms that are found.
Classic features of FAS include short stature, low birthweight and poor weight gain, microcephaly, and a characteristic pattern of facial features. These facial features in infants and children may include small eye openings (measured from inner corner to outer corner), epicanthal folds (folds of tissue at the inner corner of the eye), small or short nose, low or flat nasal bridge, smooth or poorly developed philtrum (the area of the upper lip above the colored part of the lip and below the nose), thin upper lip, and small chin. Some of these features are nonspecific, meaning they can occur in other conditions, or be appropriate for age, racial, or family background. Other major and minor birth defects that have been reported include cleft palate, congenital heart defects, strabismus, hearing loss, defects of the spine and joints, alteration of the hand creases, small fingernails, and toenails. Since FAS was first described in infants and children, the diagnosis is sometimes more difficult to recognize in older adolescents and adults. Short stature and microcephaly remain common features, but weight may normalize, and the individual may actually become overweight for his/her height. The chin and nose grow proportionately more than the middle part of the face and dental crowding may become a problem. The small eye openings and the appearance of the upper lip and philtrum may continue to be characteristic. Pubertal changes typically occur at the normal time.
Newborns with FAS may have difficulties with feeding due to a poor suck, have irregular sleep-wake cycles, decreased or increased muscle tone, seizures or tremors. Delays in achieving developmental milestones such as rolling over, crawling, walking and talking may become apparent in infancy. Behavior and learning difficulties typical in the preschool or early school years include poor attention span, hyperactivity, poor motor skills, and slow language development. Attention deficit-hyperactivity disorder is a common associated diagnosis. Learning disabilities or mental retardation may be diagnosed during this time. Arithmetic is often the most difficult subject for a child with FAS. During middle school and high school years the behavioral difficulties and learning difficulties can be significant. Memory problems, poor judgment, difficulties with daily living skills, difficulties with abstract reasoning skills, and poor social skills are often apparent by this time. It is important to note that animal and human studies have shown that neurologic and behavioral abnormalities can be present without characteristic facial features. These individuals may not be identified as having FAS, but may fulfill criteria for alcohol-related diagnoses, as set forth by the Institute of Medicine.
In 1991, Streissguth and others reported some of the first long-term follow-up studies of adolescents and adults with FAS. In the approximate 60 individuals they studied, the average IQ was 68, with 70 being the lower limit of the normal range. However, the range of IQ was quite large, as low as 20 (severely retarded) to as high as 105 (normal). The average achievement levels for reading, spelling, and arithmetic were fourth grade, third grade and second grade, respectively. The Vineland Adaptive Behavior Scale was used to measure adaptive functioning in these individuals. The composite score for this group showed functioning at the level of a seven-year-old. Daily living skills were at a level of nine years, and social skills were at the level of a six-year-old.
In 1996, Streissguth and others published further data regarding the disabilities in children, adolescents and adults with FAS. Secondary disabilities, that is, those disabilities not present at birth and that might be preventable with proper diagnosis, treatment, and intervention, were described. These secondary disabilities include: mental health problems; disrupted school experiences; trouble with the law; incarceration for mental health problems, drug abuse, or a crime; inappropriate sexual behavior; alcohol and drug abuse; problems with employment; dependent living; and difficulties parenting their own children. In that study, only seven out of 90 adults were living and working independently and successfully. In addition to the studies by Streissguth, several other authors in different countries have now reported on long-term outcome of individuals diagnosed with FAS. In general, the neurologic, behavioral and emotional disorders become the most problematic for the individuals. The physical features change over time, sometimes making the correct diagnosis more difficult in older individuals, without old photographs and other historical data to review. Mental health problems including attention deficit, depression, panic attacks, psychosis and suicide threats and attempts, and overall were present in more than 90% of the individuals studied by Streissguth. A 1996 study in Germany reported more than 70% of the adolescents they studied had persistent and severe developmental disabilities and many had psychiatric disorders, the most common of which were emotional disorders, repetitive habits, speech disorders, and hyperactivity disorders.


FAS is a clinical diagnosis, which means that there is no blood, x ray or psychological test that can be performed to confirm the suspected diagnosis. The diagnosis is made based on the history of maternal alcohol use, and detailed physical examination for the characteristic major and minor birth defects and characteristic facial features. It is often helpful to examine siblings and parents of an individual suspected of having FAS, either in person or by photographs, to determine whether findings on the examination might be familial, of if other siblings may also be affected. Sometimes, genetic tests are performed to rule out other conditions that may present with developmental delay or birth defects. Individuals with developmental delay, birth defects or other unusual features are often referred to a clinical geneticist, developmental pediatrician, or neurologist for evaluation and diagnosis of FAS. Psychoeducational testing to determine IQ and/or the presence of learning disabilities may also be part of the evaluation process.


There is no treatment for FAS that will reverse or change the physical features or brain damage associated with maternal alcohol use during the pregnancy. Most of the birth defects associated with prenatal alcohol exposure are correctable with surgery. Children should have psychoeducational evaluation to help plan appropriate educational interventions. Common associated diagnoses such as attention deficit-hyperactivity disorder, depression, or anxiety should be recognized and treated appropriately. The disabilities that present during childhood persist into adult life. However, some of the secondary disabilities mentioned above may be avoided or lessened by early and correct diagnosis, better understanding of the life-long complications of FAS, and intervention. Streissguth has describe a model in which an individual affected by FAS has one or more advocates to help provide guidance, structure and support as the individual seeks to become independent, successful in school or employment, and develop satisfying social relationships.


The prognosis for FAS depends on the severity of birth defects and the brain damage present at birth. Miscarriage, stillbirth or death in the first few weeks of life may be outcomes in very severe cases. Major birth defects associated with FAS are usually treatable with surgery. Some of the factors that have been found to reduce the risk of secondary disabilities in FAS individuals include diagnosis before the age of six years, stable and nurturing home environments, never having experienced personal violence, and referral and eligibility for disability services. The long-term data helps in understanding the difficulties that individuals with FAS encounter throughout their lifetime and can help families, caregivers and professionals provide the care, supervision, education and treatment geared toward their special needs.
Prevention of FAS is the key. Prevention efforts must include public education efforts aimed at the entire population, not just women of child bearing age, appropriate treatment for women with high-risk drinking habits, and increased recognition and knowledge about FAS by professionals, parents, and caregivers.

Key terms

Cleft palate — A congenital malformation in which there is an abnormal opening in the roof of the mouth that allows the nasal passages and the mouth to be improperly connected.
Congenital — Refers to a disorder that is present at birth.
IQ — Abbreviation for Intelligence Quotient. Compares an individual's mental age to his/her true or chronological age and multiplies that ratio by 100.
Microcephaly — An abnormally small head.
Miscarriage — Spontaneous pregnancy loss.
Placenta — The organ responsible for oxygen and nutrition exchange between a pregnant mother and her developing baby.
Strabismus — An improper muscle balance of the ocular musles resulting in crossed or divergent eyes.
Teratogen — Any drug, chemical, maternal disease, or exposure that can cause physical or functional defects in an exposed embryo or fetus.



Committee of Substance Abuse and Committee on Children with Disabilities. "Fetal Alcohol Syndrome and Alcohol-Related Neurodevelopmental Disorders." Pediatrics 106 (August 2000): 358-361.
Cramer, C., and F. Davidhizar. "FAS/FAE: Impact on Children." Journal of Child Health Care 3 (Autumn 1999): 31-34.
"Fetal Alcohol Syndrome Is Still a Threat, Says Publication." Science Letter September 28, 2004: 448.
Hannigan, J. H., and D. R. Armant. "Alcohol in Pregnancy and Neonatal Outcome." Seminars in Neonatology 5 (August 2000): 243-54.
"Prenatal Exposure to Alcohol." Alcohol Research and Health 24 (2000): 32-41.


Fetal Alcohol Syndrome Family Resource Institute. PO Box 2525, Lynnwood, WA 98036. (253) 531-2878 or (800) 999-3429. http://www.fetalalcoholsyndrome.org.
Institute of Medicine. National Academy Press, Washington, DC. http://www.come-over.to/FAS/IOMsummary.htm.
March of Dimes Birth Defects Foundation. 1275 Mamaroneck Ave., White Plains, NY 10605. (888) 663-4637. resourcecenter@modimes.org. http://www.modimes.org.
Nofas. 216 G St. NE, Washington, DC 20002. (202) 785-4585. http://www.nofas.org.
Gale Encyclopedia of Medicine. Copyright 2008 The Gale Group, Inc. All rights reserved.


of or pertaining to a fetus or to the period of its development.
fetal acoustic stimulation test a test used to assess fetal health in compromised pregnancies; a vibroacoustic stimulus such as an electronic artificial larynx is applied either externally or directly to the fetus and resultant fetal movements, cardioacceleration, and alterations in respiration are compared to those of normal fetuses.
fetal alcohol syndrome a group of symptoms characterized by mental and physical abnormalities of the infant and linked to the maternal intake of alcohol during pregnancy. Clinical manifestations, which can be present in varying degrees, include prenatal and postnatal growth deficiency, mental retardation, irritability in infancy, hyperactivity in childhood, microcephaly, short palpebral fissures, smooth philtrum, thin vermilion border of upper lip, small distal phalanges, and ventricular septal defects. Although the exact amount of alcohol consumption that will produce fetal damage is unknown, the risk and extent of abnormalities are most likely to be increased when the daily intake of pure alcohol exceeds 2 ounces. The periods of gestation during which the alcohol is most likely to result in fetal damage are three to four and a half months after conception and during the last trimester. Abstinence from alcohol during pregnancy is recommended.
fetal assessment determination of the well-being of the fetus; techniques and procedures include: (1) medical and nursing histories and physical examination of the mother, (2) assays of amniotic fluid obtained by amniocentesis, (3) ultrasonography, (4) chemical assessment of placental function, (5) electronic and ultrasonic fetal heart rate monitoring, and (6) chorionic villus sampling. Extensive and thorough assessment of the health status of the fetus is indicated when maternal characteristics, obstetrical complications, and familial and genetic factors place the fetus at risk.

Amniotic fluid assay is most often done to establish the diagnosis of a genetic disorder, to monitor the fetus sensitized against the mother's rh factor, or to determine fetal lung maturity. Cells floating in the amniotic fluid sample can be examined to detect genetic disorders caused by chromosomal abnormalities and to detect certain metabolic aberrations. neural tube defects such as spina bifida and anencephaly are detected by analyzing the amniotic fluid for alpha-fetoprotein (AFP). When an open neural tube defect is present, the amount of alpha-fetoprotein can be increased as much as eight times the normal value.

The amniotic fluid also can be assayed for bilirubin, an indicator of the severity of Rh incompatibility between maternal and fetal blood. Fetal lung maturity can be assessed by evaluating the presence of pulmonary surfactant, a phospholipid protein, in the amniotic fluid. In normal fetal development the production of surfactant, a substance essential to lung expansion and adequate ventilation after birth, begins at about the 22nd week of gestation; however, surfactant is not present in sufficient quantities until 35 to 36 weeks. Two of its principal constituents, lecithin and sphingomyelin, can be evaluated by measuring the lecithin-sphingomyelin ratio (L/S ratio) in a sample of amniotic fluid. In general, a ratio greater than 2:1 indicates that the fetal lungs are mature and the newborn infant is not likely to develop respiratory distress syndrome of the newborn.

Ultrasonography is a noninvasive technique helpful in diagnosing unusual fetal presentations, placenta previa, multiple pregnancy, and fetal abnormalities such as hydrocephalus and hydronephrosis. It also can be used to trace fetal growth by periodic measurement of the biparietal diameter of the head of the fetus, femur length, or head:abdominal circumference ratio.

Chorionic villus sampling is a technique by which a small sample is obtained from the fetal portion of the placenta by aspiration through the cervical canal. It can be used for diagnosis of genetic abnormalities as early as the first trimester.

Chemical assessment of the nutritive and respiratory functions of the placenta can be accomplished by determining the amount of the hormone estriol in the maternal blood or urine. Throughout gestation a normally functioning placenta produces increasing amounts of estriol, the precursors for the production of which are provided by the fetal adrenal glands. Thus, a normal estriol value in maternal blood or urine indicates that both the placenta and the fetus are healthy.

Fetal monitoring using either ultrasound or direct electronic monitoring equipment to measure fetal heart rate and uterine contractions and the nonstress test to evaluate fetal heart rate changes in response to uterine contractions and fetal movements are discussed under fetal monitoring.
fetal circulation the circulation of blood from the placenta to and through the fetus and back to the placenta. Fetal circulation can be traced as follows: The oxygenated blood is carried from the placenta to the fetus via the umbilical vein. About half of this blood passes through the hepatic capillaries and the rest flows through the ductus venosus into the inferior vena cava. Blood from the vena cava is mostly deflected through the foramen ovale into the left atrium, then to the left ventricle, into the ascending aorta and on to the head and upper body. The arterial oxygenation of this blood is approximately 25 to 28 mm Hg; thus the fetal coronary circulation and brain receive the blood with the highest level of oxygenation.

Deoxygenated blood from the superior vena cava flows into the right atrium, right ventricle, and then into the pulmonary artery. Because of high pulmonary vascular resistance, only about 5 to 10 per cent of the blood in the pulmonary artery flows to the lungs, the majority of it being shunted through the patent ductus arteriosus and then down the descending aorta. The PaO2 of the blood in the descending aorta is about 22 mm Hg.
Postnatal Changes. After birth the changes in circulation involve closure of three fetal channels, the ductus venosus, the foramen ovale, and the ductus arteriosus. The ductus venosus closes with the clamping of the umbilical cord and inhibition of blood flow through the umbilical vein. The foramen ovale functionally closes after the first few breaths as pressure within the left atrium rises above that in the right atrium. The ductus arteriosus constricts partly in response to higher arterial oxygen levels that occur after the first few breaths. Other postnatal changes include a decrease in pulmonary vascular resistance and a decrease in pulmonary artery pressure. These changes result in the transport of 100 per cent of the cardiac output from the right heart to the lungs for oxygenation and then to the left heart and thence to the aorta.
A simplified scheme of the fetal circulation. From Betz et al., 1994.
fetal monitoring continuous intrapartal monitoring of the fetal heart rate and uterine contractions for the purpose of reducing preventable fetal and neonatal death by more accurate diagnosis and correction of problems related to fetal distress during labor, such as compression of the umbilical cord or placental insufficiency.
Noninvasive (Indirect) Monitoring. The fetal heart rate is measured using the techniques of ultrasonography or phonocardiography. Evaluations of this kind provide good data on the fetal heart rate and, unlike direct fetal monitoring, can be used while the amniotic membranes are still intact and the cervix has not yet dilated. These techniques are easier to use than invasive techniques but do not provide information as accurate and precise as that obtained by direct monitoring.

The duration and relative strength of uterine contractions and the length of intervals between them can be measured externally by placing a tokodynamometer on the mother's abdomen at the site of greatest uterine activity. The force of contractions is displayed on a screen. Layers of fat in obese patients and restlessness of the mother interfere with precise external monitoring of uterine contractions. Therefore high-risk patients can be more effectively monitored by internal techniques.
Invasive (Direct) Monitoring. Invasive techniques of fetal and maternal monitoring require direct access to the fetus and amniotic sac via the vagina and dilated cervix. Direct electrocardiography of the fetal heart is accomplished by attaching an electrode to the fetal presenting part. Proper placement of the electrode makes the risk to the mother and fetus negligible, and the data obtained are extremely accurate. Direct monitoring of uterine contractions uses an intrauterine amniotic fluid catheter to measure intrauterine pressure changes.

Simultaneous monitoring of the fetal heart rate and uterine contractions is essential to accurate interpretation of events taking place within the uterus during labor. Patterns of a slowing heart rate (deceleration) or increase in rate (acceleration) are examined in the context of the phase of the contraction in which the change in rate occurs. For example, decelerations that take place early during uterine contractions may indicate compression of the fetal head, a normal and expected event. However, a deceleration occurring late in the contraction may indicate placental pathology and uteroplacental insufficiency, a very serious and life-threatening condition. However, maternal hypotension and uterine hypotonus, both of which can be alleviated or corrected, may also cause late deceleration.
Contraction Stress Tests:Oxytocin Challenge Test. The purpose of this test, which is usually not done before the 28th week of gestation, is to assess the respiratory function of the placenta; that is, to determine whether the placenta and fetus will be able to withstand the stress of repetitive contractions during labor, and if they cannot, when and how delivery of the infant should be carried out. It is indicated for high-risk mothers, such as those with diabetes, hypertensive disease of pregnancy, history of a previous stillbirth, or anything else affecting the health status of the fetus. The oxytocin challenge test should not be attempted if placenta previa is present or if the mother has had a previous delivery by midline-incision cesarean section.

Oxytocin is given to stimulate enough uterine contractions to provide a sample of fetal response and determine whether there is adequate placental respiratory reserve to maintain the fetus for the remainder of the pregnancy and through labor. Data from the recorded fetal heart rate patterns during contractions are used to assess the status of the fetus and to make decisions about either allowing the pregnancy to continue until the fetus is more mature, or intervening promptly to avoid severe and perhaps fatal stress on the fetus.

Prior to the administration of the oxytocin, the fetal heart rate is monitored for 30 minutes or more to determine baseline variability and fetal movement. Spontaneous movement of the fetus without oxytocin may mean it is not necessary. However, if there is no spontaneous movement, oxytocin is given in quantities sufficient to trigger three or four contractions.
Nipple Stimulation. This involves the application of warm, moist washcloths to the breasts, followed by 10 minutes of massaging and rolling of the nipples. If it is successful in inducing uterine contractions, it obviates the need for an oxytocin challenge test.
Nonstress Test. This test relies on spontaneous fetal activity rather than on oxytocin-induced fetal movement to assess fetal response to uterine contractions. If there is no spontaneous fetal activity, it may be elicited by external rubbing or gentle pressure on the mother's abdomen. Fetal heart rate is monitored externally and correlated with fetal activity. Acceleration of the heart rate can also be induced by vibroacoustic stimulation using an external source of sound such as an artificial larynx applied to the maternal abdomen over the fetal head. Increased confidence in the validity and accuracy of the nonstress test has led to its widespread use and, in many cases, its preference over the more time-consuming and often contraindicated oxytocin challenge test.
Accelerations and Decelerations. Periodic heart rate changes are evaluated in reference to a fetal “baseline” that is determined when there is no stress present. Deviations from the baseline occur in response to uterine contractions and fetal activity that affect fetal oxygenation and transfer of carbon dioxide.

Accelerations are transient increases of the fetal heart rate, occurring at the same time as uterine contractions and coming at anytime during labor. They may be the earliest indicators of fetal distress; however, without other abnormalities of fetal heart rate pattern, they are thought to be reassuring when in response to manipulation, stimulation, or fetal movement.

Decelerations are decreases in the fetal heart rate. The three types are early, late, and variable. Early deceleration is believed to be caused by fetal head compression. The fetal heart rate returns to the baseline at or before the end of the uterine contraction and is not associated with an abnormality. Late deceleration occurs after the uterus has begun to contract and may not cease with the contraction. It is an ominous sign of fetal distress, is believed to be caused by uteroplacental insufficiency, and is frequently associated with high-risk pregnancy and with maternal hypotension or uterine hyperactivity. Variable deceleration occurs at various times in relation to uterine contractions. It could be associated with umbilical cord compression and may be relieved by changing the mother's position.

Early signs that suggest fetal distress include irregularity and mild variable decelerations. Early signs of fetal compromise that are more ominous include further decreased variability, heart rate increased over baseline, and variable or late decelerations. Late signs of fetal distress include no variability, severe variable or late decelerations with minimal variability, bradycardia in relation to baseline heart rate, and a sinusoid pattern to the fetal heart rate.
External fetal monitoring. The heart rate of the fetus is evaluated, particularly in response to uterine activity or contractions. From Malarkey and McMorrow, 2000.
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

fe·tal al·co·hol syn·drome

a pattern of malformation with growth deficiency, craniofacial anomalies, and functional deficits including mental retardation that can result when a woman drinks alcohol during pregnancy.
Farlex Partner Medical Dictionary © Farlex 2012

fetal alcohol syndrome

n. Abbr. FAS
A group of abnormalities occurring in an infant as a result of excessive alcohol consumption by a woman during pregnancy, including growth retardation, cranial, facial, or neural abnormalities, and developmental disabilities.
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.

fetal alcohol syndrome

Alcohol embryopathy A condition due to in utero exposure to alcohol, resulting in a menagerie of birth defects; alcohol-related birth defects–ARBDs; when multiple ARBDs are present, the term fetal alcohol syndrome is used Clinical Prenatal and postnatal growth retardation, facial dysmorphia–short palpebral fissure, epicanthal folds, short up-turned nose, thin upper lip, long smooth or poorly-developed philtrum, short nose, micrognathia, maxillary hypoplasia, prematurity, perinatal asphyxia, mild to profound developmental delays, mental dysfunction, microcephaly, cranial defects, atrial septal defect, muscular hypotonia, bone anomalies–vertebral malformation and spina bifida with joint contraction. See Alcoholism, Embryopathy.
McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.

fe·tal al·co·hol syn·drome

(FAS) (fē'tăl al'kŏ-hol sin'drōm)
Malformation or alteration present in varying degrees that includes growth deficiency, hyperactivity, craniofacial anomalies, and limb defects, found among children of mothers with long-term alcoholism during pregnancy; mental retardation is often demonstrated later.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012

fetal alcohol syndrome

The group of damaging effects caused to the growing fetus by sustained high levels of alcohol in the mother's blood during pregnancy. They include low birth weight, a small head (microcephaly) with protruding jaws and receding upper teeth, congenital heart disease, mental retardation and a high fetal death rate.
Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005

fe·tal al·co·hol syn·drome

(fē'tăl al'kŏ-hol sin'drōm)
Pattern of malformation with growth deficiency, craniofacial anomalies, and functional deficits including mental retardation that can result when a woman drinks alcohol during pregnancy.
Medical Dictionary for the Dental Professions © Farlex 2012
References in periodicals archive ?
Bell on treating patients with fetal alcohol exposure, visit MDedge.com/ Psychiatry and click on the MDedge Psychcast.
Putting fetal alcohol spectrum disorder (FASD) on the map in New Zealand: A review of health, social, political, justice and cultural developments.
However, until I read that suicide was responsible for 15% of deaths with external causes among patients with fetal alcohol syndrome--patients whose life expectancy averages only 34 years--it did not occur to me that affect dysregulation also was likely to lead to suicide attempts among patients with ND-PAE.
Identification is less problematic on the severe end of the spectrum--where fetal alcohol syndrome (FAS) lies--because it is characterized by obvious growth retardation, central nervous system (CNS) dysfunction, and a specific pattern of craniofacial anomalies (see figure 1A).
Interestingly, the risk of developing fetal alcohol syndrome is also increased if the father consumes alcohol in the long term.
Despite the older age cohort and focus on a period prevalence, the prevalence estimates obtained from the Fetal Alcohol Syndrome Surveillance Network II are similar to previously reported birth prevalence estimates using records-based methodology and much lower than those estimated by in-person, expert assessment of children (3).
Fetal alcohol spectrum disorders can cause small head size and facial deformities, short stature, hyperactivity, poor coordination, poor memory, learning disabilities, speech and language delays, low IQ, and vision, hearing, heart, kidney and bone problems.
of Hamburg, Germany), Blackburn, and Egerton bring together 24 chapters that take an interdisciplinary perspective on fetal alcohol spectrum disorders.
Scientists have identified a molecular signaling pathway that plays an important role in the development of fetal alcohol spectrum disorders (FASD).A0x20The new research in cells and mice, supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health, points to candidate genes for FASD susceptibility and may open new avenues for developing drugs to prevent alcohol damage to the fetal brain.A0x20A report of the study is now online in the journal Proceedings of the National Academy of Sciences.
Fetal Alcohol Spectrum Disorders or FASD is an umbrella term used to describe adverse health effects that can occur in an individual whose mother drank alcohol during pregnancy.

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