Fetal alcohol syndrome

Fetal alcohol syndrome

Fetal alcohol syndrome (FAS) is a disorder that can occur to the embryo when a pregnant woman ingests alcohol during pregnancy. An ingestion of alcohol does not always result in FAS. The current recommendation of both the US Surgeon General and the UK Department of Health is not to drink alcohol at all during pregnancy.[1][2]

Alcohol crosses the placental barrier and can stunt fetal growth or weight, create distinctive facial stigmata, damage neurons and brain structures, and cause other physical, mental, or behavioral problems.[3][4][5] Surveys found that in the United States, 10-15% of pregnant women admit to having recently used alcohol, and up to 30% use alcohol at some point during pregnancy.[6][7][8] The main effect of FAS is permanent central nervous system damage, especially to the brain. Developing brain cells and structures are underdeveloped or malformed by prenatal alcohol exposure, often creating an array of primary cognitive and functional disabilities (including poor memory, attention deficits, impulsive behavior, and poor cause-effect reasoning) as well as secondary disabilities (for example, mental health problems, and drug addiction).[5][9] The risk of brain damage exists during each trimester, since the fetal brain develops throughout the entire pregnancy.[10]

Fetal alcohol exposure is the leading known cause of mental retardation in the Western world.[11][dubious – discuss] In the United States the FAS prevalence rate is estimated to be between 0.2 and 2.0 cases per 1,000 live births, comparable to or higher than other developmental disabilities such as Down syndrome or spina bifida.[12][dubious – discuss] The lifetime medical and social costs of each child with FAS are estimated to be as high as US$800,000.[13]

Fetal alcohol syndrome Signs and symptoms

Growth deficiency: Growth deficiency is defined as significantly below average height, weight or both due to prenatal alcohol exposure, and can be assessed at any point in the lifespan. Growth measurements must be adjusted for parental height, gestational age (for a premature infant), and other postnatal insults (e.g., poor nutrition), although birth height and weight are the preferred measurements.[14] Deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the patient's population.[15]

The CDC and Canadian guidelines use the 10th percentile as a cut-off to determine growth deficiency.[12][16] The "4-Digit Diagnostic Code" allows for mid-range gradations in growth deficiency (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile.[14] Growth deficiency (at severe, moderate, or mild levels) contributes to diagnoses of FAS and PFAS (Partial Fetal Alcohol Syndrome), but not ARND (Alcohol-Related Neurodevelopmental Disorder) or static encephalopathy.

Growth deficiency is ranked as follows by the "4-Digit Diagnostic Code:"[14]

Severe — Height and weight at or below the 3rd percentile.
Moderate — Either height or weight at or below the 3rd percentile, but not both.
Mild — Both height and weight between the 3rd and 10th percentiles.
None — Height and weight both above the 10th percentile.

Facial features: Several characteristic craniofacial abnormalities are often visible in individuals with FAS.[17] The presence of FAS facial features indicates brain damage, though brain damage may also exist in their absence. FAS facial features (and most other visible, but non-diagnostic, deformities) are believed to be caused mainly during the 10th and 20th week of gestation.[18]

Refinements in diagnostic criteria since 1975 have yielded three distinctive and diagnostically significant facial features known to result from prenatal alcohol exposure and distinguishes FAS from other disorders with partially overlapping characteristics.[19][20] The three FAS facial features are:

A smooth philtrum — The divot or groove between the nose and upper lip flattens with increased prenatal alcohol exposure.
Thin vermilion — The upper lip thins with increased prenatal alcohol exposure.
Small palpebral fissures — Eye width decreases with increased prenatal alcohol exposure.

Measurement of FAS facial features uses criteria developed by the University of Washington. The lip and philtrum are measured by a trained physician with the Lip-Philtrum Guide,[21] a 5-point Likert Scale with representative photographs of lip and philtrum combinations ranging from normal (ranked 1) to severe (ranked 5). Palpebral fissure length (PFL) is measured in millimeters with either calipers or a clear ruler and then compared to a PFL growth chart, also developed by the University of Washington.[22]

Ranking FAS facial features is complicated because the three separate facial features can be affected independently by prenatal alcohol. A summary of the criteria follows:[14][23]

Severe — All three facial features ranked independently as severe (lip ranked at 4 or 5, philtrum ranked at 4 or 5, and PFL two or more standard deviations below average).
Moderate — Two facial features ranked as severe and one feature ranked as moderate (lip or philtrum ranked at 3, or PFL between one and two standard deviations below average).
Mild — A mild ranking of FAS facial features covers a broad range of facial feature combinations:

Two facial features ranked severe and one ranked within normal limits,
One facial feature ranked severe and two ranked moderate, or
One facial feature ranked severe, one ranked moderate and one ranked within normal limits.

None — All three facial features ranked within normal limits.

These distinctive facial features in a patient do strongly correlate to brain damage. Sterling Clarren of the University of Washington's Fetal Alcohol and Drug Unit told a conference in 2002:

I have never seen anybody with this whole face who doesn't have some brain damage. In fact in studies, as the face is more FAS-like, the brain is more likely to be abnormal. The only face that you would want to counsel people or predict the future about is the full FAS face. But the risk of brain damage increases as the eyes get smaller, as the philtrum gets flatter, and the lip gets thinner. The risk goes up but not the diagnosis.

At one-month gestation, the top end of your body is a brain, and at the very front end of that early brain, there is tissue that has been brain tissue. It stops being brain and gets ready to be your face ... Your eyeball is also brain tissue. It's an extension of the second part of the brain. It started as brain and "popped out." So if you are going to look at parts of the brain from alcohol damage, or any kind of damage during pregnancy, eye malformations and midline facial malformations are going to be very actively related to the brain across syndromes ... and they certainly are with FAS.[24]

Central nervous system damage

Central nervous system (CNS) damage is the primary feature of any FASD diagnosis. Prenatal alcohol exposure, a teratogen, can damage the brain across a continuum of gross to subtle impairments, depending on the amount, timing, and frequency of the exposure as well as genetic predispositions of the fetus and mother.[25][26] While functional abnormalities are the behavioral and cognitive expressions of the FAS disability, CNS damage can be assessed in three areas: structural, neurological, and functional impairments.

All four diagnostic systems allow for assessment of CNS damage in these areas, but criteria vary. The IOM system requires structural or neurological impairment for a diagnosis of FAS.[25] The "4-Digit Diagnostic Code" and CDC guidelines state that functional anomalies must measure at two standard deviations or worse in three or more functional domains for a diagnoses of FAS.[12][14] The "4-Digit Diagnostic Code" further elaborates the degree of CNS damage according to four ranks:

Definite — Structural impairments or neurological impairments for FAS or static encephalopathy.
Probable — Significant dysfunction of two standard deviations or worse in three or more functional domains.
Possible — Mild to moderate dysfunction of two standard deviations or worse in one or two functional domains or by judgment of the clinical evaluation team that CNS damage cannot be dismissed.
Unlikely — No evidence of CNS damage.

Related signs

Other conditions may commonly co-occur with FAS, stemming from prenatal alcohol exposure. However, these conditions are considered Alcohol-Related Birth Defects[25] and not diagnostic criteria for FAS.

Cardiac — A heart murmur that frequently disappears by one year of age. Ventricular septal defect most commonly seen, followed by an atrial septal defect.
Skeletal — Joint anomalies including abnormal position and function, altered palmar crease patterns, small distal phalanges, and small fifth fingernails.
Renal — Horseshoe, aplastic, dysplastic, or hypoplastic kidneys.
Ocular — Strabismus, optic nerve hypoplasia[32] (which may cause light sensitivity, decreased visual acuity, or involuntary eye movements).
Occasional abnormalities — Ptosis of the eyelid, microophthalmia, cleft lip with or without a cleft palate, webbed neck, short neck, Tetralogy of Fallot, coarctation of the aorta, Spina bifida, and hydrocephalus.

Fetal alcohol syndrome Diagnosis

Several diagnostic systems have been developed in North America:
The Institute of Medicine's guidelines for FAS, the first system to standardize diagnoses of individuals with prenatal alcohol exposure,[25]
The University of Washington's "The 4-Digit Diagnostic Code," which ranks the four key features of FASD on a Likert scale of one to four and yields 256 descriptive codes that can be categorized into 22 distinct clinical categories, ranging from FAS to no findings.[14]
The Centers for Disease Control's "Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis," which established general consensus on the diagnosis FAS in the U.S. but deferred addressing other FASD conditions,[12] and
Canadian guidelines for FASD diagnosis, which established criteria for diagnosing FASD in Canada and harmonized most differences between the IOM and University of Washington's systems.[16]

Fetal alcohol syndrome is the only expression of FASD that has garnered consensus among experts to become an official ICD-9 and ICD-10 diagnosis. To make this diagnosis (or determine any FASD condition), a multi-disciplinary evaluation is necessary to assess each of the four key features for assessment. Generally, a trained physician will determine growth deficiency and FAS facial features. While a qualified physician may also assess central nervous system structural abnormalities and/or neurological problems, usually central nervous system damage is determined through psychological, assessment. A pediatric neuropsychologist may assess all areas of functioning, including intellectual, language processing, and sensorimotor. Prenatal alcohol exposure risk may be assessed by a qualified physician or psychologist.

The following criteria must be fully met for an FAS diagnosis:[12][25][14][16]

Growth deficiency — Prenatal or postnatal height or weight (or both) at or below the 10th percentile[15]
FAS facial features — All three FAS facial features present[22]
Central nervous system damage — Clinically significant structural, neurological, or functional impairment
Prenatal alcohol exposure — Confirmed or Unknown prenatal alcohol exposure

Differential diagnosis

The CDC reviewed nine syndromes that have overlapping features with FAS; however, none of these syndromes include all three FAS facial features, and none are the result of prenatal alcohol exposure:[12]

Aarskog syndrome
Williams syndrome
Noonan's syndrome
Dubowitz syndrome
Brachman-DeLange syndrome
Toluene syndrome
Fetal hydantoin syndrome
Fetal valproate syndrome
Maternal PKU fetal effects

Fetal alcohol syndrome Prevention

The only certain way to prevent FAS is to simply avoid drinking alcohol during pregnancy.[5] A number of studies have shown that light to moderate drinking during pregnancy might not pose a risk to the fetus, although no amount of alcohol during pregnancy can be guaranteed to be absolutely safe.[33][34][35] The Royal College of Obstetricians and Gynaecologists conducted a study of over 400,000 women, all of whom had consumed alcohol during pregnancy. No case of fetal alcohol syndrome occurred and no adverse effects on children were found when consumption was under 8.5 drinks per week.[36] A review of research studies found that fetal alcohol syndrome only occurred among alcoholics; no apparent risk to the child occurred when the pregnant women consumed no more than one drink per day. [37] A study of moderate drinking during pregnancy found no negative effects and the researchers concluded that one drink per day provides a significant margin of safety, although they did not encourage drinking during pregnancy.[38] A study of pregnancies in eight European countries found that consuming no more than one drink per day did not appear to have any effect on fetal growth. A follow-up of children at 18 months of age found that those from women who drank during pregnancy, even two drinks per day, scored higher in several areas of development.[39] An analysis of seven medical research studies involving over 130,000 pregnancies found that consuming two to 14 drinks per week did not increase the risk of giving birth to a child with either malformations or fetal alcohol syndrome.[40]

In the United States, the Surgeon General recommended in 1981, and again in 2005, that women abstain from alcohol use while pregnant or while planning a pregnancy, the latter to avoid damage in the earliest stages of a pregnancy, as the woman may not be aware that she has conceived.[1] In the United States, federal legislation has required that warning labels be placed on all alcoholic beverage containers since 1988 under the Alcoholic Beverage Labeling Act.

Fetal alcohol syndrome Treatment

There is no cure for FAS, because the CNS damage creates a permanent disability, but treatment is possible. Because CNS damage, symptoms, secondary disabilities, and needs vary widely by individual though, there is no one treatment type that works for everyone. Instead, comprehensive, multi-model approaches based on the needs of the patient must be used. Several treatment models have been identified, but regardless of the predominant approach, most in the current literature recommend multiple types of interventions to ameliorate the negative effects.

Medical interventions

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, most notably ADHD.[41] For instance, an FAS patient who is inattentive, does not complete schoolwork, and cannot stay seated has characteristics that an untrained person could easily mistake as ADHD, especially if the patient is not yet diagnosed with FAS. A common course of action would be a medication referral to a pediatrician, who might recommend a trial of Ritalin for the symptoms.

Medications are often important in treating FAS, but should be used in conjunction with other intervention approaches to address the multiple disabilities that arise from FAS.

Behavioral interventions

Traditional behavioral interventions are predicated on learning theory, which is the basis for many parenting and professional strategies and interventions.[42] Along with ordinary parenting styles, such strategies are frequently used by default for treating those with FAS, as the diagnoses Oppositional Defiance Disorder (ODD), Conduct Disorder, Reactive Attachment Disorder (RAD), etc. often overlap with FAS (along with ADHD), and these are sometimes thought to benefit from behavioral interventions. Frequently, a patient's poor academic achievement results in special education services, which also utilizes principles of learning theory, behavior modification, and outcome-based education.

Because the "learning system" of a patient with FAS is damaged, however, 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.[42] Kohn (1999) suggests that a rewards-punishment system in general may work somewhat in the short-term but is unsuccessful in the long-term because that approach fails to consider content (i.e., things "worth" learning), community (i.e., safe, cooperative learning environments), and choice (i.e., making choices versus following directions).[43] While these elements are important to consider when working with FAS and have some usefulness in treatment, they are not alone sufficient to promote better outcomes.[42] Kohn's minority challenge to behavioral interventions does illustrate the importance of factors beyond learning theory when trying to promote improved outcomes for FAS, and supports a more multi-model approach that can be found in varying degrees within the advocacy model and neurobehavioral approach.

Fetal alcohol syndrome
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The current recommendation of both the US Surgeon General and the UK Department of Health is not to drink alcohol at all during pregnancy.[1][2] Alcohol crosses the placental barrier and can stunt fetal growth or weight, create distinctive facial stigmata, damage neurons and brain structures, and cause other physical, mental, or behavioral problems.[3][4][5] Surveys found that in the United States, 10-15% of pregnant women admit to having recently used alcohol, and up to 30% use alcohol at some point during pregnancy.[6][7][8] The main effect of FAS is permanent central nervous system damage, especially to the brain. Developing brain cells and structures are underdeveloped or malformed by prenatal alcohol exposure, often creating an array of primary cognitive and functional disabilities (including poor memory, attention deficits, impulsive behavior, and poor cause-effect reasoning) as well as secondary disabilities (for example, mental health problems, and drug addiction).[5][9] The risk of brain damage exists during each trimester, since the fetal brain develops throughout the entire pregnancy.[10] Fetal alcohol exposure is the leading known cause of mental retardation in the Western world.[11][dubious – discuss] In the United States the FAS prevalence rate is estimated to be between 0.2 and 2.0 cases per 1,000 live births, comparable to or higher than other developmental disabilities such as Down syndrome or spina bifida.[12][dubious – discuss] The lifetime medical and social costs of each child with FAS are estimated to be as high as US$800,000.[13] Fetal alcohol syndrome Signs and symptoms Growth deficiency: Growth deficiency is defined as significantly below average height, weight or both due to prenatal alcohol exposure, and can be assessed at any point in the lifespan. Growth measurements must be adjusted for parental height, gestational age (for a premature infant), and other postnatal insults (e.g., poor nutrition), although birth height and weight are the preferred measurements.[14] Deficiencies are documented when height or weight falls at or below the 10th percentile of standardized growth charts appropriate to the patient's population.[15] The CDC and Canadian guidelines use the 10th percentile as a cut-off to determine growth deficiency.[12][16] The "4-Digit Diagnostic Code" allows for mid-range gradations in growth deficiency (between the 3rd and 10th percentiles) and severe growth deficiency at or below the 3rd percentile.[14] Growth deficiency (at severe, moderate, or mild levels) contributes to diagnoses of FAS and PFAS (Partial Fetal Alcohol Syndrome), but not ARND (Alcohol-Related Neurodevelopmental Disorder) or static encephalopathy. Growth deficiency is ranked as follows by the "4-Digit Diagnostic Code:"[14] Severe — Height and weight at or below the 3rd percentile. Moderate — Either height or weight at or below the 3rd percentile, but not both. Mild — Both height and weight between the 3rd and 10th percentiles. None — Height and weight both above the 10th percentile. Facial features: Several characteristic craniofacial abnormalities are often visible in individuals with FAS.[17] The presence of FAS facial features indicates brain damage, though brain damage may also exist in their absence. FAS facial features (and most other visible, but non-diagnostic, deformities) are believed to be caused mainly during the 10th and 20th week of gestation.[18] Refinements in diagnostic criteria since 1975 have yielded three distinctive and diagnostically significant facial features known to result from prenatal alcohol exposure and distinguishes FAS from other disorders with partially overlapping characteristics.[19][20] The three FAS facial features are: A smooth philtrum — The divot or groove between the nose and upper lip flattens with increased prenatal alcohol exposure. Thin vermilion — The upper lip thins with increased prenatal alcohol exposure. Small palpebral fissures — Eye width decreases with increased prenatal alcohol exposure. Measurement of FAS facial features uses criteria developed by the University of Washington. The lip and philtrum are measured by a trained physician with the Lip-Philtrum Guide,[21] a 5-point Likert Scale with representative photographs of lip and philtrum combinations ranging from normal (ranked 1) to severe (ranked 5). Palpebral fissure length (PFL) is measured in millimeters with either calipers or a clear ruler and then compared to a PFL growth chart, also developed by the University of Washington.[22] Ranking FAS facial features is complicated because the three separate facial features can be affected independently by prenatal alcohol. A summary of the criteria follows:[14][23] Severe — All three facial features ranked independently as severe (lip ranked at 4 or 5, philtrum ranked at 4 or 5, and PFL two or more standard deviations below average). Moderate — Two facial features ranked as severe and one feature ranked as moderate (lip or philtrum ranked at 3, or PFL between one and two standard deviations below average). Mild — A mild ranking of FAS facial features covers a broad range of facial feature combinations: Two facial features ranked severe and one ranked within normal limits, One facial feature ranked severe and two ranked moderate, or One facial feature ranked severe, one ranked moderate and one ranked within normal limits. None — All three facial features ranked within normal limits. These distinctive facial features in a patient do strongly correlate to brain damage. Sterling Clarren of the University of Washington's Fetal Alcohol and Drug Unit told a conference in 2002: I have never seen anybody with this whole face who doesn't have some brain damage. In fact in studies, as the face is more FAS-like, the brain is more likely to be abnormal. The only face that you would want to counsel people or predict the future about is the full FAS face. But the risk of brain damage increases as the eyes get smaller, as the philtrum gets flatter, and the lip gets thinner. The risk goes up but not the diagnosis. At one-month gestation, the top end of your body is a brain, and at the very front end of that early brain, there is tissue that has been brain tissue. It stops being brain and gets ready to be your face ... Your eyeball is also brain tissue. It's an extension of the second part of the brain. It started as brain and "popped out." So if you are going to look at parts of the brain from alcohol damage, or any kind of damage during pregnancy, eye malformations and midline facial malformations are going to be very actively related to the brain across syndromes ... and they certainly are with FAS.[24] Central nervous system damage Central nervous system (CNS) damage is the primary feature of any FASD diagnosis. Prenatal alcohol exposure, a teratogen, can damage the brain across a continuum of gross to subtle impairments, depending on the amount, timing, and frequency of the exposure as well as genetic predispositions of the fetus and mother.[25][26] While functional abnormalities are the behavioral and cognitive expressions of the FAS disability, CNS damage can be assessed in three areas: structural, neurological, and functional impairments. All four diagnostic systems allow for assessment of CNS damage in these areas, but criteria vary. The IOM system requires structural or neurological impairment for a diagnosis of FAS.[25] The "4-Digit Diagnostic Code" and CDC guidelines state that functional anomalies must measure at two standard deviations or worse in three or more functional domains for a diagnoses of FAS.[12][14] The "4-Digit Diagnostic Code" further elaborates the degree of CNS damage according to four ranks: Definite — Structural impairments or neurological impairments for FAS or static encephalopathy. Probable — Significant dysfunction of two standard deviations or worse in three or more functional domains. Possible — Mild to moderate dysfunction of two standard deviations or worse in one or two functional domains or by judgment of the clinical evaluation team that CNS damage cannot be dismissed. Unlikely — No evidence of CNS damage. Related signs Other conditions may commonly co-occur with FAS, stemming from prenatal alcohol exposure. However, these conditions are considered Alcohol-Related Birth Defects[25] and not diagnostic criteria for FAS. Cardiac — A heart murmur that frequently disappears by one year of age. Ventricular septal defect most commonly seen, followed by an atrial septal defect. Skeletal — Joint anomalies including abnormal position and function, altered palmar crease patterns, small distal phalanges, and small fifth fingernails. Renal — Horseshoe, aplastic, dysplastic, or hypoplastic kidneys. Ocular — Strabismus, optic nerve hypoplasia[32] (which may cause light sensitivity, decreased visual acuity, or involuntary eye movements). Occasional abnormalities — Ptosis of the eyelid, microophthalmia, cleft lip with or without a cleft palate, webbed neck, short neck, Tetralogy of Fallot, coarctation of the aorta, Spina bifida, and hydrocephalus. Fetal alcohol syndrome Diagnosis Several diagnostic systems have been developed in North America: The Institute of Medicine's guidelines for FAS, the first system to standardize diagnoses of individuals with prenatal alcohol exposure,[25] The University of Washington's "The 4-Digit Diagnostic Code," which ranks the four key features of FASD on a Likert scale of one to four and yields 256 descriptive codes that can be categorized into 22 distinct clinical categories, ranging from FAS to no findings.[14] The Centers for Disease Control's "Fetal Alcohol Syndrome: Guidelines for Referral and Diagnosis," which established general consensus on the diagnosis FAS in the U.S. but deferred addressing other FASD conditions,[12] and Canadian guidelines for FASD diagnosis, which established criteria for diagnosing FASD in Canada and harmonized most differences between the IOM and University of Washington's systems.[16] Fetal alcohol syndrome is the only expression of FASD that has garnered consensus among experts to become an official ICD-9 and ICD-10 diagnosis. To make this diagnosis (or determine any FASD condition), a multi-disciplinary evaluation is necessary to assess each of the four key features for assessment. Generally, a trained physician will determine growth deficiency and FAS facial features. While a qualified physician may also assess central nervous system structural abnormalities and/or neurological problems, usually central nervous system damage is determined through psychological, assessment. A pediatric neuropsychologist may assess all areas of functioning, including intellectual, language processing, and sensorimotor. Prenatal alcohol exposure risk may be assessed by a qualified physician or psychologist. The following criteria must be fully met for an FAS diagnosis:[12][25][14][16] Growth deficiency — Prenatal or postnatal height or weight (or both) at or below the 10th percentile[15] FAS facial features — All three FAS facial features present[22] Central nervous system damage — Clinically significant structural, neurological, or functional impairment Prenatal alcohol exposure — Confirmed or Unknown prenatal alcohol exposure Differential diagnosis The CDC reviewed nine syndromes that have overlapping features with FAS; however, none of these syndromes include all three FAS facial features, and none are the result of prenatal alcohol exposure:[12] Aarskog syndrome Williams syndrome Noonan's syndrome Dubowitz syndrome Brachman-DeLange syndrome Toluene syndrome Fetal hydantoin syndrome Fetal valproate syndrome Maternal PKU fetal effects Fetal alcohol syndrome Prevention The only certain way to prevent FAS is to simply avoid drinking alcohol during pregnancy.[5] A number of studies have shown that light to moderate drinking during pregnancy might not pose a risk to the fetus, although no amount of alcohol during pregnancy can be guaranteed to be absolutely safe.[33][34][35] The Royal College of Obstetricians and Gynaecologists conducted a study of over 400,000 women, all of whom had consumed alcohol during pregnancy. No case of fetal alcohol syndrome occurred and no adverse effects on children were found when consumption was under 8.5 drinks per week.[36] A review of research studies found that fetal alcohol syndrome only occurred among alcoholics; no apparent risk to the child occurred when the pregnant women consumed no more than one drink per day. [37] A study of moderate drinking during pregnancy found no negative effects and the researchers concluded that one drink per day provides a significant margin of safety, although they did not encourage drinking during pregnancy.[38] A study of pregnancies in eight European countries found that consuming no more than one drink per day did not appear to have any effect on fetal growth. A follow-up of children at 18 months of age found that those from women who drank during pregnancy, even two drinks per day, scored higher in several areas of development.[39] An analysis of seven medical research studies involving over 130,000 pregnancies found that consuming two to 14 drinks per week did not increase the risk of giving birth to a child with either malformations or fetal alcohol syndrome.[40] In the United States, the Surgeon General recommended in 1981, and again in 2005, that women abstain from alcohol use while pregnant or while planning a pregnancy, the latter to avoid damage in the earliest stages of a pregnancy, as the woman may not be aware that she has conceived.[1] In the United States, federal legislation has required that warning labels be placed on all alcoholic beverage containers since 1988 under the Alcoholic Beverage Labeling Act. Fetal alcohol syndrome Treatment There is no cure for FAS, because the CNS damage creates a permanent disability, but treatment is possible. Because CNS damage, symptoms, secondary disabilities, and needs vary widely by individual though, there is no one treatment type that works for everyone. Instead, comprehensive, multi-model approaches based on the needs of the patient must be used. Several treatment models have been identified, but regardless of the predominant approach, most in the current literature recommend multiple types of interventions to ameliorate the negative effects. Medical interventions 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, most notably ADHD.[41] For instance, an FAS patient who is inattentive, does not complete schoolwork, and cannot stay seated has characteristics that an untrained person could easily mistake as ADHD, especially if the patient is not yet diagnosed with FAS. A common course of action would be a medication referral to a pediatrician, who might recommend a trial of Ritalin for the symptoms. Medications are often important in treating FAS, but should be used in conjunction with other intervention approaches to address the multiple disabilities that arise from FAS. Behavioral interventions Traditional behavioral interventions are predicated on learning theory, which is the basis for many parenting and professional strategies and interventions.[42] Along with ordinary parenting styles, such strategies are frequently used by default for treating those with FAS, as the diagnoses Oppositional Defiance Disorder (ODD), Conduct Disorder, Reactive Attachment Disorder (RAD), etc. often overlap with FAS (along with ADHD), and these are sometimes thought to benefit from behavioral interventions. Frequently, a patient's poor academic achievement results in special education services, which also utilizes principles of learning theory, behavior modification, and outcome-based education. Because the "learning system" of a patient with FAS is damaged, however, 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.[42] Kohn (1999) suggests that a rewards-punishment system in general may work somewhat in the short-term but is unsuccessful in the long-term because that approach fails to consider content (i.e., things "worth" learning), community (i.e., safe, cooperative learning environments), and choice (i.e., making choices versus following directions).[43] While these elements are important to consider when working with FAS and have some usefulness in treatment, they are not alone sufficient to promote better outcomes.[42] Kohn's minority challenge to behavioral interventions does illustrate the importance of factors beyond learning theory when trying to promote improved outcomes for FAS, and supports a more multi-model approach that can be found in varying degrees within the advocacy model and neurobehavioral approach.
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