Nadia Hashimi, MD
Robert Karp, MD
SUNY Downstate Medical Center
Department of Pediatrics
____________________________________________________________________
PRE-TEST
Choose the best answer for each question.
Q1. Physicians are able to identify alcoholism in their patients approximately
a. 25% of the time
b. 50% of the time
c. 75% of the time
d. 100% of the time
Q2. Fetal Alcohol Syndrome does not usually include
a. Neurodevelopmental delay
b. Facial dysmorphisms
c. Obesity
d. Growth retardation
Q3. Alcohol’s potential for in-utero damage depends on
a. Quantity of alcohol consumed
b. Pattern of alcohol consumption
c. Overall health and nutritional status of mother
d. All of the above
Q4. Infants born with FAS characteristically have smaller/lower (except for one of the following):
a. head circumference
b. length
c. weight
d. extremities
Q5. FAS is
a. preventable and treatable
b. treatable but not preventable
c. preventable but not treatable
d. neither preventable nor treatable
Q6. T-ACE is more effective than CRAFFT in identifying drinking among adolescents (T/F)
Q7. Advising women about the dangers of drinking during pregnancy has not been shown to have any impact on alcohol consumption. (T/F)
Q8. Children with FAS are at an increased risk for psychiatric comorbidities. (T/F)
Q9. Early on, a poor suck or grasp reflex may be a sign of the effects of in-utero alcohol exposure. (T/F)
Q10. The prevalence of FAS is related to socioeconomic status. (T/F)
OBJECTIVES
On completion of this module, the resident will:
1. Be able to identify the pregnant drinker
2. Appreciate how nutritional status of the mother affects the likelihood of FAS in newborn
3. Identify two ways that alcohol is teratogenic
4. Know the criteria for FAS and identify affected children.
5. Understand long-term implications of FAS on growth and neurodevelopment
6. Be able to address the social and nutritional needs of children living with alcoholic parents
FACILITATOR PREPARATION
Presenters should prepare for presentations by reading:
1. Fetal Alcohol Information. NCBDDD, CDC. Available at http://www.cdc.gov/ncbddd/fas/fasask.htm
2. Material on Maternal factors can be found in Abel E, Hannigan H. Maternal Risk Factors in Fetal Alcohol Syndrome: Provocative and Permissive influences. Neurotoxicology and Teratology. 1995;17:445-462.
3. The historical importance of FAS can be found in Karp RJ, Qazi QH, Moller K, Angelo WA, Davis JM. Fetal alcohol syndrome at the turn of the 20th century: An unexpected explanation of the Kallikak family Arch Ped Adoles Med 1995;149:45-8. [Data showing the connection (not the direction) is in HH Goddard’s book from 1911, Hereditary Feeblemindedness. Macmillan, NY
4. Ann Streissguth’s book from 2003 Fetal Alcohol Synmdrome. Paul Brookes Publishers provides the most comprehensive review of the subject.
5. The first widely circulated recognition of FAS is the classic Jones, Smith, Streissguth and Ulleland paper in Lancet 1973;1(815):999-1001. Shortly afterwards, these authors were informed of a publication by French authors whose observations were ignored in the oenophilist (wine loving) society in which they worked. [We only see what we are prepared to see.] See Lemoine P. et al. Ouest Medical 1967;21:476 and Annales de Pediatrie (Paris), 39:226.
This history is well reviewed by Streissguth.
INTRODUCTION
Fetal Alcohol Syndrome is a problem far more common than health professionals have been willing to admit or consider. There is no known safe level of alcohol consumption during pregnancy, and sadly, drinking during pregnancy is currently on the rise especially among younger women. Alcohol is known to cause dysmorphologies, neurodevelopmental delay and growth retardation. The full extent of alcohol’s impact on nutritional status remains to be clarified, and there is convincing evidence to support a multifactorial etiology for its teratogenicity. The physician’s role should be to promote good nutrition and limit alcohol consumption during pregnancy, identify a child with the stigmata of FAS, and provide early intervention and comprehensive resources for children with FAS.
The nutritional status of the mother has a hitherto unrecognized role to play in the severity of the alcohol effects on the fetus mediated through multiple factors including the mother’s age, parity, nutritional status, hepatic function, other toxic ingestions, and current diet. These are all reviewed below.
Fetal Alcohol Syndrome (FAS) is a constellation of effects seen in children with a history of prenatal ethanol exposure. FAS is a permanent condition characterized by facial deformities, growth retardation, and neurodevelopmental delay. Children who have only some of the characteristics of FAS have either Alcohol Related Neurodevelopmental Disorder (ARND) or Alcohol Related Birth Defects (ARBD). The Center for Disease Control (CDC) has reported that FAS rates range from 0.2 to 1.5 per 1,000 live births in different communities of people in the United States. Additionally, the CDC believes that other alcohol-related conditions, such as ARND and ARBD occur approximately three times as often as FAS. The term “Fetal Alcohol Effects” (FAE) is used to describe a milder variant of the syndrome.
The high prevalence and preventability of FAS makes it imperative that health care professionals focus on identifying a) communities at risk for ARBDs and b) women who drink during pregnancy. Of note, one in thirty women who acknowledge being pregnant admit to “risk drinking”, defined as 7 or more drinks per week or 5 or more drinks on any one occasion (Fetal Alcohol). The question remains – if we are aware that alcohol has such deleterious effects on a developing fetus, why are we not identifying pregnant women who drink?
The reasons are as diverse as plentiful. By some reports, clinicians fail to diagnose alcoholism in at least three of four alcohol-abusing patients. On the part of the patients, many alcoholics can complicate arriving at a diagnosis by concealing their drinking or by an inability to relate their physical symptoms (insomnia, heartburn, irritability) or social disruptions (family disintegration, job difficulties) to their alcohol abuse.
Women in particular are reluctant to seek treatment or volunteer information about their drinking because of the stigma attached to alcohol use in pregnancy. Furthermore, physicians are hesitant to investigate because of bias regarding their own abuse, inadequate training for the task, poor awareness of the problem and its consequences and time restrictions. Many physicians are also fearful of offending the patient or believe that patients will simply deny alcohol use (Estes 320).
Case study of a mother prior to birth of child:
Matilda F, a 28-year-old pregnant woman, is seen by her OB for a prenatal check up. She is in her 2nd trimester and started seeing her OB one month ago. In taking the history, the obstetrician found that this is an unplanned pregnancy and that the woman only recently thought to take a home pregnancy test for her missed periods. Review of systems reveals complaints of heartburn and difficulty sleeping. She denies any medical problems, previous hospitalizations or surgeries. She admits that she used to smoke but now smokes less since she discovered she was pregnant. She also states that she knows she should avoid taking any medications but is unsure if she has taken any in the last few weeks.
She lives with her boyfriend in an apartment and is currently working as a secretary in a law firm, a job she has had for the last six months.
Q1. Why and how do you identify a pregnant drinker?
A1. Several convincing arguments exist for actively screening patients for alcohol abuse. First of all, screening is effective. The popular T-ACE questionnaire (a variation of the CAGE screen that is more specific for pregnant women) accurately identifies 69% of risk drinkers. While a negative screen may miss alcoholics, a positive screen is reliably accurate.
The “T-ACE” is one effective method.
• Tolerance - How many drinks does it take for you to feel high?
• Are you Annoyed by people complaining about your drinking?
• Have you ever tried to Cut down on your drinking?
• Do you start your morning with an Eye-opener?
For the first question, one point is given for one drink and two points are given for any number greater than one. All other affirmative responses each receive one point. A total score of two or more on the T-ACE qualifies as a positive screen. Because no safe amount of alcohol consumption in pregnancy has been identified, a useful screening test need only identify the presence of alcohol use, not just high quantity drinkers. Trials have shown that brief interventions by clinicians, such as education regarding the harmful effects of alcohol to a fetus, make a significant impact in decreasing alcohol consumption (Chang).
Another questionnaire, the “CRAFFT,” was designed specifically to identify alcohol abuse in the adolescent population. An affirmative answer to two or more of the questions indicates a significant substance abuse problem (Knight).
The CRAFFT
• C – Have you ever ridden in a Car driven by someone (including yourself) who was “high” or had been using alcohol or drugs?
• R – Do you ever use alcohol or drugs to Relax, feel better about yourself or fit in?
• A – Do you ever use alcohol or drugs while you are by yourself, Alone?
• F – Do your family or Friends ever tell you that you should cut down on your drinking or drug use?
• F – Do you ever Forget things you did while using alcohol or drugs?
• T – Have you ever gotten into Trouble while you were using alcohol or drugs?
The case study continues
Matilda has significant positive response to both the TACE (3 points) and the CRAFFT (2 points). She is a “steady state” drinker who does not get high or drunk, but is very tolerant of alcohol, is jittery in the morning, and drinks alone to relax. She has wine for breakfast and lunch, beer with dinner and a shot of hard liquor prior to bedtime.
Q2. What is the relationship between FAS and nutritional status?
A2. Chronic alcoholism has always been closely connected to poor nutrition and the case of the pregnant drinker is no different. Six mechanisms have been described:
TABLE 1. Specific alcohol/nutrition interactions likely to increase in-utero effects
TEACHING CAPTION: The nature and severity of the birth injury will be affected by the duration and pattern of drinking as well as, for binge drinkers, when in pregnancy the drinking occurred. Older women are more likely to have an affected infant because of deterioration in their nutritional status. (see Abel and Harrington)
Many studies have sought to investigate the role of the maternal nutritional status in the development of FAS. The first question in determining causality is whether alcoholism creates an increased micronutrient need or if it is simply associated with decreased micronutrient intake. Further complicating the picture, alcohol abuse has a high rate of association with smoking and abuse of other drugs, with overlap in resulting effects. Over time, many alcoholics experience a decrease in their oral intake and alterations in their gastrointestinal and hepatic function.
The hepatic dysfunction associated with chronic alcoholism alters the detoxification process for other drugs of abuse as well as for environmental pollutants allowing toxic metabolites to reach the fetus. A contemporary view from Charles Lieber is that "at cellular, biochemical and molecular levels, the nutritional and toxic effects of alcohol converge." Thus, polydrug abuse concomitant to aging of mothers creates a nutrient deprived in-utero environment that increases the risk for teratogenic consequences of drug exposure on the growing fetus. A model for teratogen [x] malnutrition effects, derived by Karp from the work of Lieber, (3) is shown as Figure 4.
Q3. In what ways is alcohol teratogenic?
A3. Here are possible explanations for FAS:
Teratogenic substances can affect the fetus in any or all of the following ways
TABLE 2. Three mechanisms for teratogenesis to occur:
TEACHING CAPTION: Alcohol is known to have the second and third effects. High dose alcohol (binging) will affect specific organ systems increasing the likelihood of congenital cardiac, renal, or bony defects. The metabolic effects include a mineraliuria (Zn++, and Mg++) that lasts into the postnatal period. What is not known is whether these effects occur beyond a threshold quantity (meaning some alcohol is safe) or not (no alcohol consumption is safe). Derived from Chestin Berlin in Pediatrics in Review 1991; 12: 232-37.
Investigations have explored five major pathways by which ethanol abuse can negatively impact the developing fetus.
1. Alcohol use compromises the absorption of several vitamins and minerals and increases the body’s overall metabolic demands. There is an impact on B vitamins, and at least one study found that ethanol use resulted in decreased zinc levels in maternal plasma and cord blood. Ethanol induces metallothionine in the maternal liver, which subsequently increases hepatic zinc stores and decreases plasma levels. This translates to diminished zinc supply to the developing fetus. There is also an increased rate of iron depletion in women consuming alcohol and chronic ethanol abuse is also known to mobilize vitamin A stores from the maternal liver, possibly leading to vitamin A toxicity in the fetus (Cogswell 1729).
2. Ethanol has a disruptive effect on the epiblast layer, as well as its subsequent mesodermal structures in the developing embryo. Ethanol also causes dystrophic and destructive changes in several cell types, including neuronal cells and myocytes. The induction of apoptotic pathways has been implicated as one mechanism of ethanol’s detrimental effects on dividing cells (Chaudhuri 1038).
3. Alcohol consumption leads to the generation of destructive free oxygen radicals in the fetus both directly and via its metabolite, acetaldehyde. These free radicals are particularly harmful to the developing fetus whose tissues are lacking in free radical scavengers such as superoxide dismutase, peroxidase, catalase and alpha-tocopherol (Chaudhuri 1035).
4. Alcohol also causes a reduction of free retinoic acid levels in the fetus. Retinioic acid is a recognized signal in embryonic development and is synthesized in part by the enzyme alcohol dehydrogenase. Ethanol interferes with the synthesis of retinoic acid and thereby influences the normal sequence of cell signaling (Chaudhuri 1738).
5. Lastly, alcohol decreases fetal levels of growth factors such as insulin-like growth factor (IGF-1, IGF-2) and epidermal growth factor (Chaudhuri 1740).
Q4. At what level is alcohol consumption during pregnancy dangerous? Is there a “safe level” of drinking for the mother?
A4. As noted above, we do not know at what level deleterious effects can be found. If it were certain that alcohol operated as a teratogen with a threshold for effects, this amount might be determined. We do not know this. In the absence of a known threshold, the question is not “At what level are there effects?” Rather, the better question is “At what level of consumption can we determine the affect of alcohol in-utero?”
The example of lead poisoning should always be kept in mind. Until quite recently, lead levels of up to 40 ugm/dl (from the 1960s to 1981) then 25 ugm/dl (up to 1991) and now 10ugm/dl were considered toxic. The CDC is about to lower that acceptable limit to 5 ugm/dl. Similarly, what was acceptable alcohol consumption is no longer considered safe. At lowest levels of intake, the risk for defects related to alcohol may be lower than the risk associated with spontaneous mutation. There are, however, risks to fetal development associated with alcohol use prior to pregnancy --“mutageneic” rather than “teratogenic” effects. Reduced consumption of or unmet increased need for B vitamins in alcohol consuming mothers could affect fetal development.
Thus, we can be assured that the only safe level of alcohol consumption during pregnancy is “none.” Beyond that, knowledge is uncertain with danger being determined by panoply of nutritional, genetic and consumption factors affecting impact of alcohol on the fetus.
Brent and colleagues suggest that mutagens (Berlin’s first category of teratogenesis) are not likely to have a threshold for effect. That is, damage begins with minimal dosages. Those substances causing toxic metabolic effects (Berlin’s third category), however, are not likely to cause damage at doses below a threshold. One can not say, however, what impact low dosages of alcohol have on organ formation (category 2) leaving us with a conservative formulation “The only known safe level of alcohol consumption in pregnancy is none.”
See figure 1 in Brent RL, Tanski S, Weitzman M. A pediatric perspective on the unique vulnerability and resilience of the embryo and child to environmental toxins. Pediatrics 2004;113:S933-44.
See also Figure 2 in Samet JM.. Risk Assessment and child health. Pediatrics 2004;113:S95-56.
Case study continues
The child is a boy. He is premature and small for dates with a decreased head circumference but better-preserved length as predicted by the data shown above. An examination for dysmorphic features shows that he has small, wide set eyes and mid-face hypoplasia suggesting the Fetal Alcohol Syndrome. The mother decides that she cannot keep a child at home and places him for adoption.
Q5. How is FAS identified?
A5. For the most part, physicians encounter FAS once it has already begun to manifest itself in a child. It is important for the clinician to be able to recognize the features of FAS in the hopes that appropriate management will improve the long-term outcome of the child. FAS often goes undiagnosed until a child is noticed to be a slow learner in school. Sadly, this precludes the possibility of early intervention. Early identification requires awareness of characteristics seen in FAS.
TABLE 3. Fetal Alcohol Syndrome is identified as follows:
“In the context of excess or inappropriate maternal alcohol consumption there is/are
TEACHING CAPTION: One must always have reliable information on alcohol consumption of the mother. Not all of the subsequent consequences are seen consistently. This phenomenon is called “Fetal Alcohol Effects” or FAE with developmental problems and “Alcohol Related Birth Defects” or ARBD for alcohol associated congenital anomalies.
Alcohol causes both prenatal and postnatal growth retardation with little potential for postnatal growth catch up. This seems to be a result of irreversible changes in body structure. There is a distinct decrease in body parameters such as weight, height and head circumference and, indeed, many children with FAS are in the 5th percentile for height.
Table 4. Three measures of growth for three forms of Intra-Uterine Growth Retardation (IUGR) and prematurity
TEACHING CAPTION: Categories 1 and 2 are Intra-uterine Growth Retardation (IUGR). Category 3 is characteristic of Fetal Alcohol Syndrome while the low birth weight found with prematurity and normal growth is category 4. Be suspicious of in-utero toxicity, possibly from alcohol, where head circumference is not protected.
The vertebral system demonstrates abnormal bony fusion and delays in mean bone age. As shown above, the facial dysmorphisms of FAS include microcephaly, frontal bossing, long and narrow forehead, hypoteleorism, maxillary and mandibular hypoplasia, narrow palpebral fissures, thin elongated philtrum and vermilion of the upper lip, dental malocclusion and saddle nose. The severity of some of these deformities diminishes as the child ages, in contrast to the permanent effects on growth.. A photo of an older child is shown in the next part of the case study.
Q6. How does this affect the child?
A6. Alcohol’s effects on the central nervous system are undoubtedly the most tragic and debilitating. FAS is considered the most common cause of mental retardation in children. Early on, caretakers may note sleep and sucking disturbances in the infant. Commonly seen are learning disabilities, developmental disabilities such as speech and language delays, and mental retardation or low IQ. Many children reach an intellectual plateau in high school. As the child ages, coordination deficits, problems with daily living, poor reasoning and judgment skills may become more apparent and problematic. A variety of behavioral disorders have been recognized in children with FAS including hyperactivity, attention deficit disorders and autistic behaviors (Prenatal Exposure). More in-depth investigations have revealed that alcohol’s effects on mental capacities are more specific than global and target learning, short-term memory, visual-spatial functions and the performance of more complex tasks (Fantus e19). Of note, the identification of alcohol effects in utero was delayed by researchers convinced that mental retardation (“Hereditary feeble-mindedness”) caused alcoholism rather than maternal alcoholism causing mental retardation (Karp 45).
CAPTION: This young woman, Pauline “Kallikak,” illustrates the full fetal alcohol syndrome.
Aside from the above-described primary manifestations of alcohol exposure, there are also secondary conditions that are not inherently present at birth but may be acquired as a result of FAS. These conditions include a risk for psychiatric problems, criminal behavior, inability to conform to accepted social norms of behavior and conduct, unemployment, and incomplete education (Grisham 315). Once a child has been diagnosed with FAS, the goal of management and early intervention should be to help the child achieve independence and avoid the secondary conditions listed.
Case study continues at early school age
Bill F is an 8-year-old adopted child. His mother’s drinking habits are described above. He is brought to his pediatrician for a regular annual visit. His adoptive mother reports recent “cold” symptoms but nothing out of the ordinary. He is currently in 1st grade and doing below average. Teachers have recommended extra help in reading and have indicated that the child has trouble keeping up with classmates when instructions are given for a project.
You ask about the family and birth history knowing that Bill is adopted, but the mother reports that it was all done privately and she has almost no information except that the mother seemed to be a very sensible person. Thus, you have no information about the child’s earliest life experiences or his biologic family, but you do know that the immunizations are up to date and that there have been no surgeries or hospitalizations since at least one year of age.
On exam, Bill is thin, measuring in just under the 25th percentile for both height and weight. He is grinning, friendly and cooperative with your examination. Billy has a “cocktail party” personality. There is some nasal congestion but the chest sounds clear and you find no other significant physical findings. You look closely at Bill and see small wide-set eyes, an absent philtrum, and midface hypoplasia. Looking from the side, you see a thin upper lip. With permission you take a full frontal and lateral photograph.
CAPTION: These illustrations show the ratio of palpebral fissures to width of bridge of nose is <1:1. The upper lip is quite thin. As shown by Astley and Clarren, this is highly suggestive of FAS. The figure is derived from Figure 6 of Astley and Clarren. It was altered to show the dysmorphic features of FAS.
Q7. The natural next question is “what can the physician do for the child with FAS?”
A7. From a nutritional standpoint, no specific supplements have been identified as useful for the condition. What is more important in improving overall outcome is addressing the needs of these children with a special focus on the social context. Irrespective of the presence of FAS, children living under the care of an alcoholic may be forced prematurely into adulthood and can suffer from inadequate fulfillment of parental roles. Additionally, they may be emotionally neglected, at high risk for abusive treatment and have poor models of healthy adult behavior. These children are vulnerable to future alcohol abuse themselves, creating a cycle of FAS and alcoholism that has been demonstrated in family pedigrees studied for this reason (Grisham 311).
Interventions by family or children’s advocacy agencies should address a range of services including prevention, comprehensive treatment, and aftercare services tailored to the individual and his/her family’s needs while promoting parental responsibility, child safety and permanency. Parents should be made to understand how their substance abuse impacts their child’s well being and must be willing to work towards recovery and appropriate parenting. Neighborhood-based services help to remove barriers to accessibility. The substance abuse should be addressed in the context of other issues affecting the child and family such as domestic violence, health, mental health, criminal justice involvement, nutrition, housing, education and employment. Whenever possible, health care workers should coordinate with the child welfare system to remove barriers and create integrated systems of care with improved accessibility for the families (Substance Abuse).
Q8. How do we approach intervention?
A8. Physicians should strive to obtain multidisciplinary early intervention programs with speech therapy, physical therapy, and occupational therapy and focused educators for children with FAS. Whenever possible, training for basic life skills, vocational training and structured living situations should be provided for those children transitioning to independent lifestyles. Parental guidance should be provided to prevent frustration and optimize their developing experience. A set of guidelines from the Fetal Alcohol Consultation and Training Services recommends the use of concrete terminology, consistency in all respects, repetition of information, routines to decrease anxiety, simplicity, structure and supervision for educators and parents interacting with children with FAS (Evensen).
Q9. How does this case study conclude?
A9. It is worthwhile to stop and consider the possible outcome for Bill. What do you think might happen?
Directions to Presenter:
Some concluding thoughts for the physician concerned about FAS and its consequences: (from Karp RJ and Qazi Q,1993)
FAS is a preventable but untreatable disease whose occurrence depends, in part, on inherited characteristics that cannot be predicted.
• The growth and neurological disabilities associated with alcohol consumption in pregnancy (both FAS and FAE) persist even when the child grows up in a good home. (See The Broken Cord, an account by Michael Dorris of his experience raising a son with FAS).
• Poverty alone does not predict alcoholism, but poor women are at high risk for undernutrition, which increases vulnerability of the fetus to the effects of alcohol. These effects (FAE) provide additional impediments to learning in situations in which resources for recognition and rehabilitation are limited.
• The provider should keep in mind that past drinking and dietary behavior may be kept hidden.
TEACING CAPTION: The three features marked (*) when found in context of maternal drinking, are required to make the diagnosis of FAS
RESIDENT EXERCISE
1. What challenges might you face in managing the many needs of a child with FAS?
2. What aspect of this case is most concerning to you as a pediatrician?
3. What concerns do you have in approaching a pregnant drinker about her alcohol consumption?
4. How would your approach differ if the pregnant woman were a teenager?
REFERENCES
Abel E & Hannigan. Maternal Risk Factors in Fetal Alcohol Syndrome: Provocative and Permissive Influences. Neurotoxicology and Teratology. 1995; 17: 445-462.
Berlin CM. Pediatrics in Review. 1991; 12: 232-37.
Brent RL, Tanski S, Weitzman M. A pediatric perspective on the unique vulnerability and resilience of the embryo and child to environmental toxins. Pediatrics. 2004;113:S933-44.
Chang G. Substance Use in Pregnancy. Up-to-date online. www.uptodate.com
Chaudhuri, J. Alcohol and the developing fetus – a review. Med Sci Monit. 2000; 6(5): 1031-1041.
Cogswell M, Weisberg P, Spong C. Cigarette Smoking, Alcohol Use and Adverse Pregnancy Outcomes: Implications for Micronutrient Supplementation. J Nutrition. 2003; 133: 1722S-1731S.
Estes N and Heinemann ME. Issues in identification of alcoholism. Alcoholism: Development, Consequences and Interventions. 3rd ed, Mosby, 1986: 317-333.
Evensen D, Lutke J. 8 Magical Keys: Developing Successful Interventions for Students with FAS. Fetal Alcohol Consultation and Training Services. 1997: www.fasalaska.com
Fantus E. Prenatal Alcohol Exposure and Neurocognitive Impairment in Adolescence. Critical Review. J FAS Int. 2003; 1:e19.
Fetal Alcohol Information. NCBDDD, CDC. http://www.cdc.gov/ncbddd/fas/fasask.html
Grisham K and Estes N. Dynamics of alcoholic families. Alcoholism: Development, Consequences and Interventions. 3rd ed, Mosby, 1986: 303-316.
Karp RJ, Qazi QH, Moller KA, Angelo WA, Davis JM. Fetal Alcohol Syndrome at the Turn of the 20th Century: An Unexpected Explanation of the Kallikak Family. Arch Pediatric Adolescent Medicine. 1995;149:45-48.
Knight, John. Youth Screening for Alcohol/Substance Abuse – CRAFFT questionnaire. Children’s Hospital Boston.
Nelson’s Textbook of Pediatrics. Ed. Behrman RE, Kleigman RM, Jenson HB: 16th Edition. Philadelphia. WB Saunders 2000; 531.
Prenatal Exposure to Alcohol. 10th Special Report to the US Congress on Alcohol and Health. DHHS, PHS, NIH, NIAAA. June 2000.
Samet JM.. Risk Assessment and child health. Pediatrics. 2004;113:S95-56.
Substance Abuse Principles. NYC Administration for Children’s Services. http://www.ci.nyc.ny.us/html/acs/html/whatwedo/principles_substance_abuse.html
ANNOTATED ANSWERS
A1. Answer - Physicians only rarely identify affected teenages. Much work is to be done. See sytems for identification. And the CRAFFT is for teens
A2. C - FAS children are no more likely to be obese than unaffected children.
A3. D - All of the elements listed affect the likelihood of FAS
A4. D - Extremity length is fine.
A5. C - It is possible to prevent FAS, but treatment is for the comorbidities and not for the disease itself.
A6. FALSE. The T-ACE and CAGE are for adults. The CRAFFT focuses on events likely in a teen-ager’s life.
A7. FALSE. Recognition of the drinking mother will often reduce alcohol intake, increase nutritional value of diet and reduce likelihood of FAS
A8. TRUE. The FAS child has both neurodevelopmental and social consequences from the alcohol in-utero. Remaining in the home of the alcoholic parent increases risk
A9. TRUE. There are ongoing affects of alcohol in-utero
A10. TRUE. SES affects nutritional status of the mother
