Articles on adoption, foster care, & pediatrics

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Fetal Alcohol Spectrum Issues

Since prenatal alcohol exposure is a concern that arises so frequently in our preadoption consultations, we've created this page as a resource for families grappling with the alcohol issue. Our experience in this field comes from working at the FAS clinic here at the University of Washington, evaluating and following many alcohol-exposed internationally adopted kids, and volunteering with older orphanage-raised children in Moscow.

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Unfortunately, a study found that 60% of pregnant women in Russia reported drinking during pregnancy, with 8% reporting at least one binge drinking episode during pregnancy. Since these were women that were actually receiving prenatal care, the rates and amounts of prenatal alcohol exposures for children in orphanages are likely to be significantly higher, as those pregnancies do not tend to be supervised. The rate of FAS in Russian orphanages have been estimated at 1-10 per 100, and the rate of alcohol-affected kids is even worse. That’s a lot higher than in this country, where it’s thought to be 1-3 per 1000. Alcohol is also a major concern in other former Soviet Union countries, and is an emerging issue in many other countries.

So … what is fetal alcohol syndrome?

FAS is a permanent birth defect syndrome caused by maternal alcohol consumption during pregnancy. The full FAS diagnosis requires all of the following: growth problems before or after birth, a pattern of minor facial anomalies, evidence of altered brain structure or function, and prenatal alcohol exposure. There is an associated increased risk of eye, hearing, heart, and other associated defects, but those aren’t part of the diagnostic criteria.

What about PFAS, AFAS, FAE, ARBD, ARND, ND-PAE etc etc etc? Partial FAS, atypical FAS, fetal alcohol effect, alcohol-related birth defects, alcohol-related neurodevelopmental disorder, and other names have been used to describe children that seem to be affected by prenatal alcohol exposure but are missing one or more of the four FAS criteria. We use the umbrella term fetal alcohol spectrum disorders (FASD) to describe the range of fetal alcohol diagnoses. FASD includes children with FAS as the “tip of the iceberg”, but also alcohol-affected children with fewer or less severe features of FAS.

We know that alcohol can damage the developing fetus, but the effects of alcohol are quite unpredictable – we’ve seen fraternal twins where, given the same mom and alcohol exposure, one has FAS and the other seems fine. There seem to be unidentified protective and risk factors for mom and babies that make predicting the effects of alcohol exposure very hard to do. No amount of alcohol exposure has been proven to be safe, but heavy and repeated binge drinking is highest risk. We also worry more about older moms and later pregnancies, because they seem to produce kids more affected by alcohol, perhaps because alcoholism is further along in those pregnancies. Involuntary termination of parental rights can also be a clue to social dysfunction and alcohol abuse.

Growth

Let’s look at those 4 FAS criteria, starting with growth. Children affected by prenatal alcohol exposure can be unusually small in weight and/or height, at birth or later. Many show some catch-up in growth by adolescence. Of course, many other adverse influences common to adopted children (maternal stress or illness during pregnancy, prenatal tobacco, malnutrition, neglect, orphanage factors) can impact growth as well. We count growth deficiency towards an FASD diagnosis if the growth is not better explained by other factors, and look at the catch-up growth pattern in the first year home to help us tease out environmental versus prenatal causes. Children who are unusually small compared to others raised in similar environments are at higher risk for developmental and behavioral challenges after adoption.

Facial Features of FAS

What about the facial features? An overly long list of features associated with FAS has piled up over the years, but there are only three features that really count – a thin upper lip, a smooth or absent philtrum (vertical groove between the nose and lip), and small eyes. The face of FAS requires all three of these to be abnormal, and the diagnosis of full-blown FAS requires the face. Unfortunately, since that face gets “created” on only 2-3 days in early pregnancy, there are moms who drink heavily whose kids can be quite alcohol-affected but don’t have the face of FAS. Not having “the face” does not rule out alcohol exposure and effects. But having “the face” dramatically increases your risk for FAS and its associated disabilities.

The other things you’ll hear about - big cupped ears, “clown eyebrows”, wide-spaced eyes, epicanthal folds (“asian” eye appearance), flat nasal bridge, short upturned nose, flat midface, small chin, etc - are not necessarily caused by alcohol exposure. They can be developmental (most babies have short upturned noses), ethnic, or just minor anomalies unrelated to alcohol. We do see them more often in alcohol-affected kids but the thin lip, smooth philtrum, and small eyes combination is more reliable and specific for alcohol damage.

We can often get a decent look at the lip and philtrum from referral photos and videos. That’s two of the three features, and if both are abnormal then we get concerned. If you have a thin lip and smooth philtrum, plus microcephaly (small head), and strong suspicion of alcohol exposure then I’m usually quite worried about damage from alcohol. If we've been relatively happy with the lip and philtrum but have asked to see some trip photos, you might be able to skip the sticker part, but the following photo tips will still be helpful.

FAS Facial Photographic Analysis

In more borderline situations we might need eye measurements. The size of the eyes (measured from the inside to the outside of the visible part of each eye) can only be accurately measured with a specialized photograph, one that you can take on your trip and email to us for computer analysis. Here’s how to take that photo …

The key here is an internal measure of scale – you’ll need a small round sticker 1/2 to 3/4 inches in size, which you can get from an office supply store. Homemade stickers or pieces of tape are not helpful, as they are of variable width. Mark the width in magic marker on the sticker - this is important, as we must know the width of the sticker. Place it on the child’s forehead between the eyebrows … yes, they will look at you funny in the orphanage when you do this, and you want to be sensitive to staff and older children’s feelings. Put some stickers on your own face if you want to goof off, give out extra stickers, and if you can, print/send/bring a nicer smiling photo to the child as a memento. Again, we only need the sticker if the lip or philtrum is worrisome.

Use a digital or 35mm camera – polaroids aren’t good enough. Take a closeup facial portrait photograph so that the head fills the entire frame (but watch the focus). When looking at the face in the viewfinder you should be able to draw an imaginary line from the ear canals through the bony ridge below each eye (lower orbital rim). That makes sure the child isn’t looking up or down. There also should be no left-to-right rotation – make sure both ears are equally visible.

The facial expression is important – smiles or frowns can really distort the features and make a nice thick upper lip and deep philtrum disappear. No smiling! We need a relaxed facial expression with lips gently closed, eyes wide open, and no eyeglasses. For older children, ask them to look at your nose, and breathe through their nose - this often relaxes their expression.

Asking the child to look up with their eyes (“what’s on the ceiling?”) without tilting their head up will help the eyes be wide open; for younger children ask someone to wave something just above your head. It may well be that one photo gives a good look at lip and philtrum, and another one gives us eyes wide open, so keep trying. Please review your photos on the camera screen before packing up, as we get a lot of out-of-focus or otherwise less than useful photos.

A “3/4 view” halfway between frontal and side view is also helpful, especially if you have a centrally mounted flash that can wash out the philtrum in frontal photos. A profile view may also help. One last tip is to use your digital camera’s “video clip” function to capture a brief, very upclose view of the face as it moves through different angles – we can pull frames from this video clip that may capture the true lip/philtrum better than a still photo. If you want more information about the photographic analysis, visit our FAS clinic's website. You can also print out instructions for taking screening "sticker" photos for FAS, and view a video animation of proper camera alignment.

Sounds complicated ... but we do this routinely in our clinic, and have a lot of success even with older infants and toddlers. We've found that parents really are able to do this themselves, especially if they practice a bit in the hotel room. Have fun, and good luck!

How Alcohol Affects Brain Structure and Function

Enough about the face … what about the brain? That’s what we really care about, after all. In fact, a lot of young kids with the FAS face are really cute. We can look at the brain structurally by plotting the head circumferences on a growth chart. You should measure the head circumference yourself if there has been any concern – bring a non-stretchable measuring tape, and practice a bit first. Wrap the tape snugly around the widest possible circumference - from the most prominent part of the forehead (often 1-2 fingers above the eyebrow) around to the widest part of the back of the head. Remeasure it 3 times, and take the largest number.

Microcephaly (head circumference less than 3%, or “below the growth chart”) can be evidence of brain damage from alcohol. It’s one of the few things we have to predict later brain function in infants and young toddlers, because meeting early motor milestones does not rule out difficulties later on with learning and behavior. In fact, a lot of the functional disabilities from alcohol damage aren’t apparent before school-age. The lack of concrete predictions about alcohol effects is a constant frustration in this process ... it really is a "time will tell" issue, unfortunately.

“Typical” (in quotes because the outcomes are so variable) functional impacts of prenatal alcohol exposure include problems with inattention and impulsivity (ADHD-like behaviors, sometimes not as responsive to medications), lower IQ scores or mental retardation, math and other specific learning impairments, “executive function” difficulties (the higher-order brain functions that plan and organize how you solve problems), trouble with cause/effect, social and communication challenges, coordination problems, sleep difficulties, and so on. Alcohol commonly affects multiple domains of brain functioning. Teasing this out can require wide-ranging testing by professionals familiar with alcohol effects. Many kids aren’t identified early enough, and are labeled as “difficult”, or “just doesn’t get it”, or other labels that don’t help. Accurate diagnosis as early as possible helps these children.

Raising Children Affected by Alcohol

While these difficulties are usually lifelong, this is not a hopeless diagnosis. Consistent, patient, loving, “industrial-strength” parenting with tons of structure, and appropriate expectations and supports in school can really help kids affected by alcohol reach their full potential. That potential will be limited by alcohol-related brain damage but setting the bar at the right height, and identifying what they CAN’T versus WON’T do can really help them have success in their life, and hopefully prevent some of the “secondary disabilities” of depression, acting out and aggression, victimization, troubles with the law, and especially their own substance abuse potential.

Resources for Caregivers

We have an FASD Resource List with internet and book references that will help give you a better sense of the range of alcohol effects, and what it’s like to parent a child affected by alcohol. A FASD parenting resource is available for free download that has a lot of great ideas on how to manage various behavioral and cognitive challenges. FASD - Strategies Not Solutions is another helpful guide for caregivers.

Resources for Educators

Here are 3 free, downloadable PDF guides for educators (also very useful for parents, who often have a lot of advocacy to do at school):

Teachers can find more practical strategies in the do2learn Teacher Toolbox.

Prenatal Methamphetamine Exposure

Excerpted from our review article for health care providers - Prenatal Alcohol and Drug Exposures in Adoption, originally published in Pediatric Clinics of North America - © 2005 Elsevier Inc. All Rights Reserved.

Overview

Methamphetamine abuse has increased dramatically in the United States in the past decade, especially in the western and midwestern states [105]. In Russia, cheap imported heroin still prevails, but abuse of home-produced ephedrine-based “vint” and other injectable amphetamines is on the rise and already predominates in certain cities, including Vladivostok and Pskov [106]. Methamphetamine abuse is a significant problem in Southeast Asia as well, with 19% of Thai female students using methamphetamine in one school-based study [107]. The UNODC reports large increases in methamphetamine production and abuse in China, Singapore, and Thailand [35]. Because methamphetamine is relatively cheap to manufacture from readily available products, “home labs” are becoming increasingly common in many parts of the world. Unfortunately, the chemicals and byproducts involved are highly toxic and flammable.

Methamphetamine is a CNS stimulant that releases large amounts of dopamine, resulting in a sense of euphoria, alertness, and confidence [108]. It can be injected, smoked, snorted, or ingested orally. Prolonged use at high levels results in dependence and erratic behavior [105]. Evidence on the effects of prenatal methamphetamine use is still emerging, but effects on prenatal growth, behavior, and cognition have been described.

Mechanism

Studies of adult methamphetamine abusers have shown potential neurotoxic effects on subcortical brain structures, namely, decreased dopamine transporters, brain metabolism, and perfusion [108]. Although the impact of methamphetamine use during human pregnancy is currently unknown, animal studies have demonstrated neurotoxic effects of amphetamines and remodeling of synaptic morphology in response to prenatal methamphetamine exposure [109]. One study did describe a smaller putamen, globus pallidus, and hippocampus in methamphetamine-exposed children [108].

Pregnancy

Women using methamphetamine during pregnancy may have an increased rate of premature delivery and placental abruption [110]. Methamphetamine use during pregnancy is linked to fetal growth restriction and, occasionally, withdrawal symptoms requiring pharmacologic intervention at birth [111]. Clefting, cardiac anomalies, and fetal growth reduction have been described in infants exposed to amphetamines during pregnancy. These findings have been reproduced in animal studies [112].

Child Health

Late effects on child health resulting from prenatal methamphetamine use are unknown. Children who live at or visit methamphetamine home labs face acute health and safety hazards from fires, explosions, and toxic chemical exposures, however. The caregiving environments of methamphetamine users are often characterized by chaos, neglect and abuse, and criminal behavior as well as the presence of firearms, contaminated sharps, and other risks [113].

Behavior and Cognition

The scant research describing the outcomes of methamphetamine-exposed children describes possible links with aggressive behavior, peer problems, and hyperactivity [114], [115]. A small recent study found that methamphetamine-exposed children scored lower on measures of visual motor integration, attention, verbal memory, and long-term spatial memory [108]. In rats, even low doses of prenatal methamphetamine exposure can alter learning and memory in adulthood [116].

Selected References

[105]   Anglin M.D.,  Burke C.,  Perrochet B.,  History of the methamphetamine problem. J Psychoactive Drugs (2000) 32 : pp 137-141.
[106]   Rhodes T.,  Bobrik A.,  Bobkov E.,  HIV transmission and HIV prevention associated with injecting drug use in the Russian Federation. Int J Drug Policy (2004) 15 : pp 1-16.  
[107]   Sattah M.V.,  Supawitkul S.,  Dondero T.J.,  Prevalence of and risk factors for methamphetamine use in northern Thai youth: results of an audio-computer-assisted self-interviewing survey with urine testing. Addiction (2002) 97 : pp 801-808.
[108]   Chang L.,  Smith L.M.,  Lopresti C.,  Smaller subcortical volumes and cognitive deficits in children with prenatal methamphetamine exposure. Psychiatry Res (2004) 132 : pp 95-106.
[109]   Weissman A.D.,  Caldecott-Hazard S.,  Developmental neurotoxicity to methamphetamines. Clin Exp Pharmacol Physiol (1995) 22 : pp 372-374.
[110]   Eriksson M.,  Larsson G.,  Winbladh B.,  The influence of amphetamine addiction on pregnancy and the newborn infant. Acta Paediatrica Scandinavica (1978) 67 : pp 95-99.  
[111]   Smith L.,  Yonekura M.L.,  Wallace T.,  Effects of prenatal methamphetamine exposure on fetal growth and drug withdrawal symptoms in infants born at term. J Dev Behav Pediatr (2003) 24 : pp 17-23.
[112]   Plessinger M.A.,  Prenatal exposure to amphetamines. Risks and adverse outcomes in pregnancy. Obstet Gynecol Clin North Am (1998) 25 : pp 119-138.
[113]   Swetlow K.,  Children at clandestine methamphetamine labs: helping meth's youngest victims 2003. Washington, DC: US Department of Justice, Office of Justice Programs, Office for Victims of Crime.  
[114]   Billing L.,  Eriksson M.,  Jonsson B.,  The influence of environmental factors on behavioural problems in 8-year-old children exposed to amphetamine during fetal life. Child Abuse Negl (1994) 18 : pp 3-9.
[115]   Eriksson M.,  Billing L.,  Steneroth G.,  Health and development of 8-year-old children whose mothers abused amphetamine during pregnancy. Acta Paediatr Scand (1989) 78 : pp 944-949.
[116]   Williams M.T.,  Moran M.S.,  Vorhees C.V.,  Behavioral and growth effects induced by low dose methamphetamine administration during the neonatal period in rats. Int J Dev Neurosci (2004) 22 : pp 273-283.

Prenatal Cocaine Exposure

Excerpted from our review article for health care providers - Prenatal Alcohol and Drug Exposures in Adoption, originally published in Pediatric Clinics of North America - © 2005 Elsevier Inc. All Rights Reserved.

Overview

Cocaine has received much attention since the 1980s, when crack cocaine began to plague urban America. Early alarmist predictions about an epidemic of neurologically damaged “crack babies” gave way to guarded optimism with early reports of neurodevelopmental functioning reporting no differences attributable to cocaine exposure. Follow-up studies with more specific measures, however, suggest effects of prenatal cocaine abuse on aspects of neurobehavior and language, as demonstrated with specific developmental tasks.

The rate of prenatal cocaine exposure in the United States ranges from 0.3% to 31% depending on the population surveyed and method of ascertainment [77], [78] and was 10% in the ongoing Maternal Lifestyle Study [34]. In our clinic's experience, reports of cocaine exposure in the international adoptee population are quite rare. The UNODC estimates the lifetime prevalence of cocaine consumption to be approximately 2% to 5% in a study of Guatemalan teenagers; in Russia, China, Korea, and other frequent countries of international adoption, the prevalence seems to be much less [35].

Mechanism

Cocaine and its metabolites readily cross the placenta, concentrating in amniotic fluid, and may produce direct neurotoxic effects, disturb monoaminergic (eg, dopamine, norepinephrine, serotonin) pathways, and cause vascular-mediated damage [91].

Pregnancy

The use of cocaine in pregnancy has been associated with a number of obstetric complications, such as stillbirth, placental abruption, premature rupture of membranes, fetal distress, and preterm delivery [92]. Growth restriction is often reported but may require higher levels of exposure and does not seem to persist after birth [93]. There may be a dose-response effect of cocaine on newborn head circumference [94]. Other CNS lesions (eg, stroke, cystic changes, possible seizures), cardiac defects, and genitourinary (GU) anomalies have also been reported, but the few available large, controlled, population-based studies on cocaine exposure and malformations have reached contradictory conclusions [95].

Behavior and Cognition

Prenatal cocaine abuse may cause specific neurobehavioral and learning problems, although it is not associated with global cognitive deficits [96], [97]. The largest matched cohort study to date found no significant covariate-controlled associations between cocaine exposure and mental, psychomotor, or behavioral functioning through 3 years of age [98]. Infant neurobehavioral abnormalities like irritability or excitability, sleep difficulties, and state regulation difficulty as well as transient neurologic abnormalities like tremor, hypertonia, and extensor posturing have been reported [99], [100]. Heavy prenatal cocaine use has been linked to poor memory and information processing in infancy [101]. At 3 years of age, increased fussiness, difficult temperament, and behavior problems were described [102]. Language delay has also been described, with foster or adoptive caregiving described as a promising protective factor [103], [104].

Selected References

[91]   Chiriboga C.A.,  Fetal effects. Neurol Clin (1993) 11 : pp 707-728.
[92]   Kain Z.N.,  Mayes L.C.,  Ferris C.A.,  Cocaine-abusing parturients undergoing cesarean section. A cohort study. Anesthesiology (1996) 85 : pp 1028-1035.
[93]   Nordstrom-Klee B.,  Delaney-Black V.,  Covington C.,  Growth from birth onwards of children prenatally exposed to drugs: a literature review. Neurotoxicol Teratol (2002) 24 : pp 481-488.
[94]   Bateman D.A.,  Chiriboga C.A.,  Dose-response effect of cocaine on newborn head circumference. Pediatrics (2000) 106 : pp E33-.
[95]   Vidaeff A.C.,  Mastrobattista J.M.,  In utero cocaine exposure: a thorny mix of science and mythology. Am J Perinatol (2003) 20 : pp 165-172.
[96]   Wasserman G.A.,  Kline J.K.,  Bateman D.A.,  Prenatal cocaine exposure and school-age intelligence. Drug Alcohol Depend (1998) 50 : pp 203-210.
[97]   Singer L.T.,  Minnes S.,  Short E.,  Cognitive outcomes of preschool children with prenatal cocaine exposure. Obstet Gynecol Surv (2005) 60 : pp 23-24.  
[98]   Messinger D.S.,  Bauer C.R.,  Das A.,  The maternal lifestyle study: cognitive, motor, and behavioral outcomes of cocaine-exposed and opiate-exposed infants through three years of age. Pediatrics (2004) 113 : pp 1677-1685.
[99]   Tronick E.Z.,  Frank D.A.,  Cabral H.,  Late dose-response effects of prenatal cocaine exposure on newborn neurobehavioral performance. Pediatrics (1996) 98 : pp 76-83.
[100]   Chiriboga C.A.,  Brust J.C.,  Bateman D.,  Dose-response effect of fetal cocaine exposure on newborn neurologic function. Pediatrics (1999) 103 : pp 79-85.
[101]   Jacobson S.W.,  Jacobson J.L.,  Sokol R.J.,  New evidence for neurobehavioral effects of in utero cocaine exposure. J Pediatr (1996) 129 : pp 581-590.
[102]   Richardson G.A.,  Prenatal cocaine exposure. A longitudinal study of development. Ann NY Acad Sci (1998) 846 : pp 144-152.  
[103]   Delaney-Black V.,  Covington C.,  Templin T.,  Expressive language development of children exposed to cocaine prenatally: literature review and report of a prospective cohort study. J Commun Disord (2000) 33 : pp 463-480.
[104]   Lewis B.A.,  Singer L.T.,  Short E.J.,  Four-year language outcomes of children exposed to cocaine in utero. Neurotoxicol Teratol (2004) 26 : pp 617-627.

Prenatal Marijuana Exposure

Excerpted from our review article for health care providers - Prenatal Alcohol and Drug Exposures in Adoption, originally published in Pediatric Clinics of North America - © 2005 Elsevier Inc. All Rights Reserved.

Overview

Marijuana is a popular recreational drug in many parts of the world. In the United States, 22% of high school students have used marijuana in the past month [76]. Estimates of marijuana use during pregnancy vary between 2% in broad surveys using maternal self-report [77] and 20% to 27% in higher risk populations using urine screens [78], [79]. In the experience of our international adoption clinic, referrals outside North America have not included reports of prenatal marijuana exposure, but the United Nations Office on Drugs and Crime (UNODC) estimates that the annual prevalence of marijuana use is 3.9% in the Russian Federation, 2.4% in Kazakhstan, 0.3% in China, 0.1% in South Korea, and 3.2% in India [35]. In Guatemala, where the rate of drug consumption among young people is on the rise, marijuana consumption by teenagers is at 4% to 6.7% [80].

Mechanism

The principle psychoactive substance in marijuana, delta-9-tetrahydrocannabinol (THC), rapidly crosses the placenta and may remain in the body for 30 days before excretion, thus prolonging potential fetal exposure. THC is also secreted in breast milk. Marijuana smoking produces higher levels of carbon monoxide than tobacco [38], which is hypothesized to be a potential mechanism of action of prenatal marijuana exposure's impact on the developing fetus.

Pregnancy

Marijuana use during pregnancy may have a modest effect on prenatal growth, but the results are inconsistent from study to study and diminish when potential cofounders are controlled [81], [82], [83], [84]. These effects, if any, are not associated with later growth deficiency, although a few studies have suggested an impact on height [81] as well as persistent negative effects on head circumference in the offspring of heavy marijuana users [63]. This review found no consistent link between prenatal marijuana exposure and other adverse pregnancy outcomes or congenital malformations [85].

Behavior and Cognition

Subtle effects of prenatal marijuana exposure on cognition have been observed in two large well-controlled study groups: a predominantly low-risk Ottawa cohort and a higher risk Pittsburgh population. The Ottawa authors argue that although prenatal tobacco exposure is associated with deficits in IQ, impulse control, and other fundamental aspects of performance, prenatal marijuana exposure does not impair IQ or basic visuoperception but influences the application of these skills in problem-solving situations requiring visual integration, analysis, and sustained attention [86]. Marijuana is thus argued to have an impact on higher level executive function and performance in a “top-down” fashion, in contrast to tobacco's “bottom-up” effects [87]. The Pittsburgh study group finds links to inattention and/or impulsivity [88] and subtle deficits in memory and learning [89]. This group also connects prenatal marijuana exposure with academic underachievement, perhaps reflecting less buffering of marijuana's effects by environment in this higher risk population [90].

Selected References

[76]   Grunbaum J.A.,  Kann L.,  Kinchen S.,  Youth risk behavior surveillance—United States, 2003. MMWR Surveill Summ (2004) 53 : pp 1-96.  
[77]   Ebrahim S.H.,  Gfroerer J.,  Pregnancy-related substance use in the United States during 1996–1998. Obstet Gynecol (2003) 101 : pp 374-379.
[78]   Zuckerman B.,  Frank D.A.,  Hingson R.,  Effects of maternal marijuana and cocaine use on fetal growth. N Engl J Med (1989) 320 : pp 762-768.
[79]   MacGregor S.N.,  Sciarra J.C.,  Keith L.,  Prevalence of marijuana use during pregnancy. A pilot study. J Reprod Med (1990) 35 : pp 1147-1149.
[80]   United Nations Office on Drugs and Crime—Guatemala country profile. Available at: http://www.unodc.org/mexico/country_profile_guatemala.html. Accessed June 10, 2005.
[81]   Cornelius M.D.,  Goldschmidt L.,  Day N.L.,  Alcohol, tobacco and marijuana use among pregnant teenagers: 6-year follow-up of offspring growth effects. Neurotoxicol Teratol (2002) 24 : pp 703-710.
[82]   Fried P.A.,  James D.S.,  Watkinson B.,  Growth and pubertal milestones during adolescence in offspring prenatally exposed to cigarettes and marihuana. Neurotoxicol Teratol (2001) 23 : pp 431-436.
[83]   Cornelius M.D.,  Taylor P.M.,  Geva D.,  Prenatal tobacco and marijuana use among adolescents: effects on offspring gestational age, growth, and morphology. Pediatrics (1995) 95 : pp 738-743.
[84]   Day N.L.,  Richardson G.A.,  Geva D.,  Alcohol, marijuana, and tobacco: effects of prenatal exposure on offspring growth and morphology at age six. Alcohol Clin Exp Res (1994) 18 : pp 786-794.
[85]   Shiono P.H.,  Klebanoff M.A.,  Nugent R.P.,  The impact of cocaine and marijuana use on low birth weight and preterm birth: a multicenter study. Am J Obstet Gynecol (1995) 172 : pp 19-27.
[86]   Fried P.A.,  Watkinson B.,  Gray R.,  Differential effects on cognitive functioning in 9- to 12-year olds prenatally exposed to cigarettes and marihuana. Neurotoxicol Teratol (1998) 20 : pp 293-306.
[87]   Fried P.A.,  Adolescents prenatally exposed to marijuana: examination of facets of complex behaviors and comparisons with the influence of in utero cigarettes. J Clin Pharmacol (2002) 42 : pp 97S-102S.
[88]   Goldschmidt L.,  Day N.L.,  Richardson G.A.,  Effects of prenatal marijuana exposure on child behavior problems at age 10. Neurotoxicol Teratol (2000) 22 : pp 325-336.
[89]   Richardson G.A.,  Ryan C.,  Willford J.,  Prenatal alcohol and marijuana exposure: effects on neuropsychological outcomes at 10 years. Neurotoxicol Teratol (2002) 24 : pp 309-320.
[90]   Goldschmidt L.,  Richardson G.A.,  Cornelius M.D.,  Prenatal marijuana and alcohol exposure and academic achievement at age 10. Neurotoxicol Teratol (2004) 26 : pp 521-532.

Prenatal Tobacco Exposure

Excerpted from our review article for health care providers - Prenatal Alcohol and Drug Exposures in Adoption, originally published in Pediatric Clinics of North America - © 2005 Elsevier Inc. All Rights Reserved.

Overview

Tobacco smoking during pregnancy is one of the most ubiquitous prenatal exposures. The prevalence of smoking during pregnancy in the United States is estimated by maternal self-report at 11% and is higher in teens (18%) and women with less than 12 years of formal education (27%) [44]. Fortunately, these rates are declining [45]. In Russia, the prevalence was 16% of pregnant women in one study and seems to be increasing [46]. In Kazakhstan, it is estimated that one third of the adult population smokes [47]. In China, the prevalence of tobacco use among pregnant women has been estimated at 2% but is increasing [48], and 60% of nonsmoking pregnant women in Guangzhou had husbands who smoked [49]. The World Health Organization reports that in South Korea, 7% of women smoke tobacco; in Guatemala, 17% of women smoke [47]. True exposure rates are likely to be significantly higher, because parental self-report routinely underestimates actual exposure. Unfortunately, adoptee tobacco exposure status is often unknown.

Prenatal tobacco exposure has consistently been associated with poor fetal growth and is the single most important cause of LBW in developed countries [50]. Even environmental smoke exposure has been implicated in LBW, fetal death, and preterm delivery [51]. Myriad perinatal complications and child health problems are linked to fetal and childhood smoke exposure. Finally, a growing body of evidence is implicating smoking during pregnancy in a range of adverse behavioral and cognitive outcomes.

Mechanism

Cigarette smoke contains tar, nicotine, and carbon monoxide. Tar contains numerous substances (lead, cyanide, cadmium, and more) known to be harmful to the fetus [52]. Nicotine readily crosses the placenta and distributes freely to the CNS, having direct and indirect effects on neural development [38]. Intrauterine hypoxia, mediated by carbon monoxide and reduced uterine blood flow, is a major mechanism of the growth impairment linked to prenatal tobacco exposure.

Pregnancy

Tobacco smoking during pregnancy has been associated with placenta previa, placental abruption, premature rupture of membranes, preterm birth, intrauterine growth restriction, and sudden infant death syndrome (SIDS) [53]. A dose-dependent association with cleft lip anomalies has also been noted [54].

Tobacco's impact on fetal growth is perhaps the most consistent and concerning, given the range of potential impacts on health and developmental outcomes. Maternal smoking has an impact on fetal growth symmetrically in a dose-related fashion [55] and causes an estimated 5% reduction in relative weight for every pack of cigarettes smoked per day [56]. Because pregnant women who smoke deliver babies weighing 150 to 250 g less than babies of nonsmokers, tobacco smoking essentially doubles the chance of having a LBW baby [57]. Unfortunately, maternal smoking is also associated with a smaller head circumference at birth [58].

Child Health

It is difficult to differentiate the impact of prenatal smoking and environmental tobacco smoke on childhood health problems, such as respiratory and ear infections, pulmonary function, asthma, and SIDS. Postnatal smoke exposure increases the incidence of middle ear disease, asthma, wheeze, cough, phlegm production, bronchitis, bronchiolitis, pneumonia, and impaired pulmonary function, and it has also been associated with snoring, adenoidal hypertrophy, tonsillitis, and sore throat [59]. Smoking during pregnancy does cause poor lung growth, affecting pulmonary function in infancy and childhood [60], [61], and seems to confer additional risk to postnatal smoke exposures [62].

With respect to tobacco-associated growth impairment, children generally demonstrate “catch-up” with their weight and height percentiles during their first few years of life, with less catch-up noted in head circumference [63], [64]. In fact, a trend toward obesity is noted [65].

Behavior and Cognition

Dose-effect impacts of prenatal tobacco exposure on behavioral and cognitive outcomes of children have been reported, even after controlling for confounders like socioeconomic status, parental education and mental health, prenatal growth, other prenatal exposures (eg, alcohol), and postnatal disadvantages [66].

Infants born to mothers who smoke tobacco display higher rates of impaired neurobehavior, with reduced habituation, lower arousal, hypertonicity and tremors, sucking difficulties, worse autonomic regulation, and altered cries [67]. Nursery evaluations suggest a withdrawal effect as well [68]. The international adoptee population seems less likely to have these dysregulations repaired by consistent and regulating caregiving while residing in a hospital or orphanage.

There is a consistent association described between prenatal exposure to tobacco and attention deficit hyperactivity disorder (ADHD)–like symptoms [67] and externalizing behavior problems [69], [70]. Antisocial traits like disruptive behavior, conduct disorder, and later delinquency have been linked to prenatal tobacco exposure as well [71]. Although these associations are clear, proving the causal relation is challenging, because not all these studies control for confounders, such as prenatal alcohol exposure.
There is a stronger link between prenatal smoking and behavioral outcomes than that described with impaired cognition. Smoking during pregnancy was associated with decreased IQ scores for children by an average of 4 points [72], however, which was prevented by smoking cessation [73]. Other studies are inconsistent but have suggested persistent deficits in auditory-related tasks like verbal memory, language, and auditory processing [74].

It is unclear if these outcomes can be attenuated by nurturing and regulating home environments and to what extent the effects of tobacco interact with other biologic, prenatal, and postnatal risk factors. For internationally adopted children, the potential interaction of these developmental modifiers seems particularly complex, with tobacco-associated risks (eg, LBW and microcephaly, infant neurobehavior, toddler negativity [75], childhood attention and/or impulse control deficits, antisocial behavior) occurring within a trajectory of caregiving moving from early institutional neglect to later nurturing and stimulating family environments.

Selected References

[44]   National Center for Health Statistics Health. United States, 2004, with chartbook on trends in the health of Americans 2004. Hyattsville, MD: National Center for Health Statistics.  
[45]   Hamilton B.E.,  Martin J.A.,  Sutton P.D.,  Births: preliminary data for 2003. Natl Vital Stat Rep (2004) 53 : pp 1-17.
[46]   Grjibovski A.,  Bygren L.O.,  Svartbo B.,  Housing conditions, perceived stress, smoking, and alcohol: determinants of fetal growth in Northwest Russia. Acta Obstet Gynecol Scand (2004) 83 : pp 1159-1166.
[47]   World Health Organization Tobacco or health. A global status report. Available at: http://www.cdc.gov/tobacco/who/. Accessed June 10, 2005.
[48]   Lam S.K.,  To W.K.,  Duthie S.J.,  The effect of smoking during pregnancy on the incidence of low birth weight among Chinese parturients. Aust NZ J Obstet Gynaecol (1992) 32 : pp 125-128.  
[49]   Loke A.Y.,  Lam T.H.,  Pan S.C.,  Exposure to and actions against passive smoking in non-smoking pregnant women in Guangzhou, China. Acta Obstet Gynecol Scand (2000) 79 : pp 947-952.
[50]   Kramer M.S.,  Intrauterine growth and gestational duration determinants. Pediatrics (1987) 80 : pp 502-511.
[51]   Kharrazi M.,  DeLorenze G.N.,  Kaufman F.L.,  Environmental tobacco smoke and pregnancy outcome. Epidemiology (2004) 15 : pp 660-670.
[52]   Lee M.J.,  Marihuana and tobacco use in pregnancy. Obstet Gynecol Clin North Am (1998) 25 : pp 65-83.
[53]   Andres R.L.,  Day M.C.,  Perinatal complications associated with maternal tobacco use. Semin Neonatol (2000) 5 : pp 231-241.
[54]   Chung K.C.,  Kowalski C.P.,  Kim H.M.,  Maternal cigarette smoking during pregnancy and the risk of having a child with cleft lip/palate. Plast Reconstr Surg (2000) 105 : pp 485-491.
[55]   Macmahon B.,  Alpert M.,  Salber E.J.,  Infant weight and parental smoking habits. Am J Epidemiol (1965) 82 : pp 247-261.
[56]   Kramer M.S.,  Olivier M.,  McLean F.H.,  Determinants of fetal growth and body proportionality. Pediatrics (1990) 86 : pp 18-26.
[57]   Samet J.M.,  The 1990 report of the Surgeon General: the health benefits of smoking cessation. Am Rev Respir Dis (1990) 142 : pp 993-994.
[58]   Kallen K.,  Maternal smoking during pregnancy and infant head circumference at birth. Early Hum Dev (2000) 58 : pp 197-204.
[59]   DiFranza J.R.,  Aligne C.A.,  Weitzman M.,  Prenatal and postnatal environmental tobacco smoke exposure and children's health. Pediatrics (2004) 113 : pp 1007-1015.
[60]   Stick S.M.,  Burton P.R.,  Gurrin L.,  Effects of maternal smoking during pregnancy and a family history of asthma on respiratory function in newborn infants. Lancet (1996) 348 : pp 1060-1064.
[61]   Gilliland F.D.,  Berhane K.,  McConnell R.,  Maternal smoking during pregnancy, environmental tobacco smoke exposure and childhood lung function. Thorax (2000) 55 : pp 271-276.
[62]   Jedrychowski W.,  Flak E.,  Maternal smoking during pregnancy and postnatal exposure to environmental tobacco smoke as predisposition factors to acute respiratory infections. Environ Health Perspect (1997) 105 : pp 302-306.
[63]   Fried P.A.,  Watkinson B.,  Gray R.,  Growth from birth to early adolescence in offspring prenatally exposed to cigarettes and marijuana. Neurotoxicol Teratol (1999) 21 : pp 513-525.
[64]   Vik T.,  Jacobsen G.,  Vatten L.,  Pre- and post-natal growth in children of women who smoked in pregnancy. Early Hum Dev (1996) 45 : pp 245-255.
[65]   Wideroe M.,  Vik T.,  Jacobsen G.,  Does maternal smoking during pregnancy cause childhood overweight?. Paediatr Perinat Epidemiol (2003) 17 : pp 171-179.
[66]   Weitzman M.,  Byrd R.S.,  Aligne C.A.,  The effects of tobacco exposure on children's behavioral and cognitive functioning: implications for clinical and public health policy and future research. Neurotoxicol Teratol (2002) 24 : pp 397-406.
[67]   Olds D.,  Tobacco exposure and impaired development: a review of the evidence. MRDD Research Reviews (1997) 3 : pp 257-269.  
[68]   Law K.L.,  Stroud L.R.,  LaGasse L.L.,  Smoking during pregnancy and newborn neurobehavior. Pediatrics (2003) 111 : pp 1318-1323.
[69]   Williams G.M.,  O'Callaghan M.,  Najman J.M.,  Maternal cigarette smoking and child psychiatric morbidity: a longitudinal study. Pediatrics (1998) 102 : pp e11-.
[70]   Fergusson D.M.,  Horwood L.J.,  Lynskey M.T.,  Maternal smoking before and after pregnancy: effects on behavioral outcomes in middle childhood. Pediatrics (1993) 92 : pp 815-822.
[71]   Wakschlag L.S.,  Pickett K.E.,  Cook E., Jr,  Maternal smoking during pregnancy and severe antisocial behavior in offspring: a review. Am J Public Health (2002) 92 : pp 966-974.
[72]   Olds D.L.,  Henderson C.R., Jr,  Tatelbaum R.,  Intellectual impairment in children of women who smoke cigarettes during pregnancy. Pediatrics (1994) 93 : pp 221-227.
[73]   Olds D.L.,  Henderson C.R., Jr,  Tatelbaum R.,  Prevention of intellectual impairment in children of women who smoke cigarettes during pregnancy. Pediatrics (1994) 93 : pp 228-233.
[74]   Fried P.A.,  O'Connell C.M.,  Watkinson B.,  60- and 72-month follow-up of children prenatally exposed to marijuana, cigarettes, and alcohol: cognitive and language assessment. J Dev Behav Pediatr (1992) 13 : pp 383-391.
[75]   Brook J.S.,  Brook D.W.,  Whiteman M.,  The influence of maternal smoking during pregnancy on the toddler's negativity. Arch Pediatr Adolesc Med (2000) 154 : pp 381-385.

Prenatal Opiate Exposure

Excerpted from our review article for health care providers - Prenatal Alcohol and Drug Exposures in Adoption, originally published in Pediatric Clinics of North America - © 2005 Elsevier Inc. All Rights Reserved.

Overview

In the United States, 2.3% of pregnancies in the Maternal Lifestyle Study involved heroin or methadone exposure [34]. In international adoption, the most commonly reported prenatal opiate exposure is heroin. Heroin use has made a resurgence in recent years, particularly in Eastern Europe and the former Soviet Union. The United Nations Office for Drug Control and Crime Prevention reported that the number of known heroin addicts rose by 30% in Russia in 1999 and had quadrupled since 1995, with a current prevalence of heroin abuse at 2.1% [11], [35]. In Kazakhstan, the prevalence of heroin abuse is estimated at 1.3% [35]. Opiate use is also prevalent in the countries of Southeast Asia and parts of China, particularly near areas where opium is grown and in more urban areas. Although there are no official reports from China, unofficial estimates say that there could be up to 12 million total heroin users [36]. Pregnant women who enter drug treatment programs for addiction receive another opiate, methadone, as a substitute for heroin or opium. Because drug treatment programs are on the rise in Russia and China, prenatal exposure to methadone may also occur [36], [37].

Mechanism

Despite the detrimental effects of opiates on the user, including the risk of addiction and exposure to the hazards of intravenous drug use (hepatitis B and C and HIV), opiate exposure to the developing fetus is not considered teratogenic. There is no known congenital malformation associated with prenatal opiate exposure. There have been harmful fetal effects described with heroin and methadone use, however, and infants born to addicted women can suffer withdrawal in the newborn period. Any child referred for international adoption with a maternal history of intravenous drug use should be considered at increased risk for HIV and hepatitis B and C.

Pregnancy

LBW and symmetric intrauterine grown retardation have been reported in the offspring of heroin abusers [38]. Pregnant heroin addicts also have a statistically significant increased risk of preterm delivery. Methadone use seems to have less effect on fetal growth and has not been shown to increase the risk of premature birth. For children born after a pregnancy complicated by opiate use, prenatal growth may be affected by maternal malnutrition and comorbid infections as well as by opiate exposure.

Neonatal Abstinence Syndrome

Neonatal abstinence syndrome (NAS) has been well described in infants born to opiate-dependent mothers. The symptoms of NAS include CNS symptoms (eg, hyperirritability, tremors, convulsions), gastrointestinal distress, respiratory distress, and autonomic disturbances [39]. It has been reported that the infants of methadone-addicted mothers experience more severe symptoms for a longer time, partly because of the longer half-life of this opiate. Treatment of symptomatic infants generally consists of providing children with a tapering schedule of tincture of opium, morphine, or phenobarbital while monitoring clinical symptoms. During the withdrawal period, infants may dramatically influence normal caretaker interactions because they are often resistant to cuddling or soothing and have a decreased ability to respond normally to auditory or visual stimuli. The long-term impact of these early alterations in socialization may be detrimental, particularly in an orphanage setting, where nurturing caretaking may already be less frequent.

The onset of withdrawal symptoms is usually between 48 and 72 hours after birth. It is highly unlikely that a child born overseas is going to be available for adoption at this point; thus, most families adopting internationally do not directly encounter NAS. Clues to NAS may be present in the preadoption record, however, and should alert families and professionals to the possibility of prenatal opiate exposure and other risks associated with injection drug use in birth mothers (HIV and hepatitis B and C).

Behavior and Cognition

In some early studies, concerns about prenatal opiate exposure and poor developmental outcome were described. Reported neurodevelopmental problems included a short attention span, hyperactivity, and sleep disturbances in prenatally exposed children assessed at the age of 12 to 34 months [40]. More recent studies also suggest mild memory and perceptual difficulties in older children, but overall test scores are still within the normal range [41]. In general, it is difficult to differentiate the impact of a poor postnatal environment and prenatal heroin exposure on children's long-term outcome. One study suggests that opiate-exposed children have increased susceptibility to adverse environmental influences compared with nonexposed children [42]. Conversely, a study from Canada suggests that drug-exposed infants adopted out at birth were equivalent to Canadian matched controls in terms of educational achievement and IQ. The adopted children did, however, have increased rates of early adult depression [43].

Selected References

[34]   Lester B.M.,  El Sohly M.,  Wright L.L.,  The Maternal Lifestyle Study: drug use by meconium toxicology and maternal self-report. Pediatrics (2001) 107 : pp 309-317.  
[35]   UNODC Research and Analysis Section United Nations Office on Drugs and Crime—World Drug Report 2004. Available at: http://www.unodc.org/unodc/world_drug_report.html. Accessed June 10, 2005.
[36]   Kulsudjarit K.,  Drug problem in southeast and southwest Asia. Ann NY Acad Sci (2004) 1025 : pp 446-457.  
[37]   Somlai A.M.,  Kelly J.A.,  Benotsch E.,  Characteristics and predictors of HIV risk behaviors among injection-drug-using men and women in St. Petersburg, Russia. AIDS Educ Prev (2002) 14 : pp 295-305.  
[38]   Chiriboga C.A.,  Fetal alcohol and drug effects. Neurologist (2003) 9 : pp 267-279.  
[39]   Finnegan L.P.,  Effects of maternal opiate abuse on the newborn. Fed Proc (1985) 44 : pp 2314-2317.  
[40]   Rosen T.S.,  Johnson H.L.,  Long-term effects of prenatal methadone maintenance. NIDA Res Monogr (1985) 59 : pp 73-83.  
[41]   Lifschitz M.H.,  Wilson G.S.,  Patterns of growth and development in narcotic-exposed children. NIDA Res Monogr (1991) 114 : pp 323-339.  
[42]   Marcus J.,  Hans S.L.,  Jeremy R.J.,  A longitudinal study of offspring born to methadone-maintained women. III. Effects of multiple risk factors on development at 4, 8, and 12 months. Am J Drug Alcohol Abuse (1984) 10 : pp 195-207.  
[43]   Lipman E.L.,  Offord D.R.,  Boyle M.H.,  Follow-up of psychiatric and educational morbidity among adopted children. J Am Acad Child Adolesc Psychiatry (1993) 32 : pp 1007-1012.  

How to Take FAS Photos

Excerpted from our Fetal Alcohol Spectrum Issues topic ...

Facial Features of FAS

What about the facial features? An overly long list of features associated with FAS has piled up over the years, but there are only three features that really count – a thin upper lip, a smooth or absent philtrum (vertical groove between the nose and lip), and small eyes. The face of FAS requires all three of these to be abnormal, and the diagnosis of full-blown FAS requires the face. Unfortunately, since that face gets “created” on only 2-3 days in early pregnancy, there are moms who drink heavily whose kids can be quite alcohol-affected but don’t have the face of FAS. Not having “the face” does not rule out alcohol exposure and effects. But having “the face” dramatically increases your risk for FAS and its associated disabilities.

The other things you’ll hear about - big cupped ears, “clown eyebrows”, wide-spaced eyes, epicanthal folds (“asian” eye appearance), flat nasal bridge, short upturned nose, flat midface, small chin, etc - are not necessarily caused by alcohol exposure. They can be developmental (most babies have short upturned noses), ethnic, or just minor anomalies unrelated to alcohol. We do see them more often in alcohol-affected kids but the thin lip, smooth philtrum, and small eyes combination is much more reliable and specific for alcohol damage.

We can often get a decent look at the lip and philtrum from referral photos and videos. That’s two of the three features, and if both are abnormal then we get concerned. If you have a thin lip and smooth philtrum, plus microcephaly (small head), and strong suspicion of alcohol exposure then I’m usually quite worried about damage from alcohol. If we've been relatively happy with the lip and philtrum but have asked to see some trip photos, you might be able to skip the sticker part, but the following photo tips will still be helpful.

FAS Facial Photographic Analysis

In more borderline situations we might need eye measurements. The size of the eyes (measured from the inside to the outside of the visible part of each eye) can only be accurately measured with a specialized photograph, one that you can take on your trip and email to us for computer analysis. Here’s how to take that photo …

The key here is an internal measure of scale – you’ll need a small round sticker 1/2 to 3/4 inches in size, which you can get from an office supply store. Homemade stickers or pieces of tape are not helpful, as they are of variable width. Mark the width in magic marker on the sticker - this is important, as we must know the width of the sticker. Place it on the child’s forehead between the eyebrows … yes, they will look at you funny in the orphanage when you do this, and you want to be sensitive to staff and older children’s feelings. Put some stickers on your own face if you want to goof off, give out extra stickers, and if you can, print/send/bring a nicer smiling photo to the child as a memento. Again, we only need the sticker if the lip or philtrum is worrisome.

Use a digital or 35mm camera – polaroids aren’t good enough. Take a closeup facial portrait photograph so that the head fills the entire frame (but watch the focus). When looking at the face in the viewfinder you should be able to draw an imaginary line from the ear canals through the bony ridge below each eye (lower orbital rim). That makes sure the child isn’t looking up or down. There also should be no left-to-right rotation – make sure both ears are equally visible.

The facial expression is important – smiles or frowns can really distort the features and make a nice thick upper lip and deep philtrum disappear. No smiling! We need a relaxed facial expression with lips gently closed, eyes wide open, and no eyeglasses. For older children, ask them to look at your nose, and breathe through their nose - this often relaxes their expression.

Asking the child to look up with their eyes (“what’s on the ceiling?”) without tilting their head up will help the eyes be wide open; for younger children ask someone to wave something just above your head. It may well be that one photo gives a good look at lip and philtrum, and another one gives us eyes wide open, so keep trying. Please review your photos on the camera screen before packing up, as we get a lot of out-of-focus or otherwise less than useful photos.

A “3/4 view” halfway between frontal and side view is also helpful, especially if you have a centrally mounted flash that can wash out the philtrum in frontal photos. A profile view may also help. One last tip is to use your digital camera’s “video clip” function to capture a brief, very upclose view of the face as it moves through different angles – we can pull frames from this video clip that may capture the true lip/philtrum better than a still photo. If you want more information about the photographic analysis, visit our FAS clinic's website. You can also print out instructions for taking screening "sticker" photos for FAS, and view a video animation of proper camera alignment.

Sounds complicated ... but we do this routinely in our clinic, and have a lot of success even with older infants and toddlers. We've found that parents really are able to do this themselves, especially if they practice a bit in the hotel room. Have fun, and good luck! 

Prenatal Alcohol and Drug Exposures

We just had a review article published in Pediatric Clinics of North America, in an issue dedicated to international adoption that's chock full of articles on pre- and post-adoption medical and developmental issues. The abstract of our article is as follows:

Prenatal alcohol and drug exposures are a significant concern in many domestic and international adoptions. This article addresses the following substance exposures for children: alcohol, opiates, tobacco, marijuana, cocaine, and methamphetamines. For each substance, we review the teratogenicity of the exposure and identify the spectrum of neurodevelopmental issues that can present in children exposed to this substance. Diagnosis of the spectrum of fetal alcohol outcomes is also discussed. When possible, we provide country-specific statistics on exposure risks for adopted children.

It's a lengthy, in-depth review that was written for other health care providers, but should also be accessible to parents, caregivers, and other adoption workers. We hope you find it helpful ...

Country Profiles in Alcohol Consumption

The World Health Organization has published the WHO Global Status Report on Alcohol 2004, an exhaustive review of drinking patterns and trends around the world. There's unfortunately very little evidence on rates of fetal alcohol spectrum disorders, but it can be helpful to read the country profiles to learn about recent trends in total alcohol consumption, binge drinking, youth drinking, traditional alcoholic beverages, and unrecorded alcohol consumption.

 

Prenatal Drug Exposures

Enough with the Alcohol Already… Other Prenatal Drug Exposures:


Prenatal Drug Research in General

•    Impossible to fully control for genetic (cognitive, mental health), other prenatal exposures, LBW/prematurity, and environmental factors
•    Alcohol may be cofounder in many studies
•    Prenatal drug exposure may make kids more vulnerable to other biomedical and environmental risks

Tobacco

•    BIG association with low birth weight
•    Higher rates of spontaneous abortion, late fetal deaths, prematurity, cleft lip
•    SIDS, ear infections, asthma, etc …
•    Impaired infant state regulation
•    Assoc with lower mental scores/babbling @1yo – cognitive effects minimal by 2yo
•    More externalizing behaviors and inattention/hyperactivity

Marijuana

•    Modest effect on fetal growth (hypoxia)
•    Some subtle infant neurobehavior effects
•    No cognitive /language effects at 1-2yo
•    Memory and verbal outcomes at 4yo possibly impacted by heavy prenatal exposure
•    Some impact on motor development as well

Opiates (heroin, methadone)

•    Low Birthweight (more with heroin)
•    Newborn withdrawal syndrome: jitters/tremor, hypertonia, irritability, high-pitched cry, convulsions, stuffiness, fever, mottling, sweating, loose stools/vomiting, poor feeding
•    Treated with slow opiate taper
•    “Subacute withdrawal” – 3-6mo with irritability, poor state control
•    Subtle late differences in visual-motor and perceptual tasks

Cocaine and Crack

•    Spont abortion, abruption, stillbirths, prematurity, distress (vasoconstriction)
•    Neonatal stokes, focal seizures
•    Urogenital and other malformations
•    Microcephaly
•    Early excitability/irritability in infancy
•    Preschool impulse control issues
•    No cognitive differences on broad scales ...
•    Subtle differences in specific functions (state regulation, lang, attn/impulsivity, visual memory, temperament, aggression)

Speed and Meth

•    Sharp rise in the 90s, especially rural
•    Meth labs – bigtime fire and chemical risks
•    Preterm delivery, abruption
•    LBW, cardiac and cleft defects, smaller subcortical brain volumes
•    Not much data on developmental effects
•    Visual memory, verbal memory, executive function, attention/impulsivity, and long-term spatial memory may be affected

Want more detailed information and some country-specific statistics?  Click the headings above ...