Fetal Alcohol Spectrum Disorders

Interdisciplinary perspectives

Barry Carpenter OBE, Carolyn Blackburn, Jo Egerton, Barry Carpenter OBE, Carolyn Blackburn, Jo Egerton

• Publisher: Routledge
• Year: 2013
• ISBN:
  9781134515509
• Edition: 1
• Topic: Pedagogía
• Subtopic: Educación general

Fetal alcohol spectrum disorders (FASDs) have emerged as a major phenomenon within the education, health, criminal justice and social care systems of many countries, with current prevalence figures suggesting that one in a hundred children and young people have FASDs. In this publication, academics, professionals and families from around the world have shared expertise and insights on FASDs. Their combined interdisciplinary perspective makes an invaluable contribution to how we understand and address the complex social, educational and health needs associated with this growing group of children and young people.

Articulating fundamental knowledge, cutting edge initiatives and emerging trends in FASDs, this book provides an evidence base that will enable services to identify and respond to the need for action on FASDs. It recognises that families – natural, foster or adoptive – are at the heart of this process, and that their rich knowledge base, grounded in their lived experience, is crucial.

Any education, social care, criminal justice or health professional working with children and young people with FASDs and their families will find this book a seminal and authoritative resource.

PART I Introduction

1 A BRIEF INTRODUCTION TO FETAL ALCOHOL SPECTRUM DISORDERS

Barry Carpenter, Carolyn Blackburn and Jo Egerton

DOI: 10.4324/9781315889665-1

Many disabilities have an unknown etiology or cause, but fetal alcohol spectrum disorders (FASDs) are known to be associated with prenatal alcohol exposure, which can cause lifelong, permanent, physical and intellectual disabilities in an unborn child. It is 100 per cent preventable. While FASDs are predominantly associated with maternal alcohol consumption during pregnancy, there are also indications that fathers who are heavy drinkers produce infants with lower birth weight and increased likelihood of heart defects (Cleaver et al. 2011).

The association between alcohol use in pregnant mothers and poor outcomes for children and young people has been recognized for centuries, from Plato (429–347 bc; see University of Chicago 2009) to Bacon (1627) and Sullivan (1899). However, it is only in recent years that researchers and professionals have begun to understand the full impact of a mother’s alcohol use on her developing baby in the womb.

It is well established that alcohol affects the fetus differently depending on the stage of pregnancy and how much the mother drinks (Warren et al. 2011). However, there is risk not only in heavy or binge drinking, but also in moderate to low levels of maternal alcohol use (Gray et al. 2009; Lewis et al. 2012; May et al. 2011; Mukherjee et al. 2005; O’Connor et al. 2006). Other factors, such genetic make-up and maternal age, also influence the outcome for the baby (Jonsson et al. 2009; Mattson and Riley 2011; Morleo et al. 2011). It is therefore impossible to predict how an unborn child will be affected even by a single drink. Only one message gives a 100 per cent guarantee of no alcohol damage for the fetus: ‘Women who are pregnant or trying conceive should avoid alcohol’. Based upon current research, men should also avoid alcohol while trying to conceive (Cleaver et al. 2011).

Public misconceptions and low levels of FASD awareness mean that many birth mothers of children and young people with FASDs who drank alcohol in pregnancy were unaware of the potential harm to their child. MacKinnion (in Mukherjee et al. 2006) found that although 97 per cent of a group of US teenagers realized that alcohol affected an unborn baby, 48 per cent thought this meant that the baby was addicted to alcohol, and over 50 per cent thought any damage could be cured. BBC One’s Inside Out (2009) found similar beliefs among UK teenagers. One way to address this is by training midwives to give accurate information and effective support to mothers who are likely to drink during their pregnancy (Fleisher, Chapter 15, this publication).

Prenatal alcohol exposure and its historic impact

A characteristic pattern of abnormalities in children born to mothers who used alcohol in pregnancy was first documented by Lemoine (Lemoine et al. 1968) and then by Jones and Smith (1973), who coined the term ‘fetal alcohol syndrome’. Jones and Smith were the first to describe in detail a consistent characteristic pattern of impairments associated with prenatal alcohol exposure and to propose diagnostic criteria (Hoyme et al. 2005; see also Elliott, Chapter 2, this publication).

‘Fetal alcohol spectrum disorders’ (FASDs) is an umbrella term, first used by Streissguth and O’Malley (2000), which encompasses the range of possible outcomes of prenatal alcohol exposure, including fetal alcohol syndrome (FAS), partial fetal alcohol syndrome (pFAS), alcohol-related neurodevelopmental disorder (ARND) and alcohol-related birth defects (ARBD) (Bertrand et al. 2005; BMA 2007; Mattson and Riley 2011; see also Mukherjee, Chapter 13, this publication). These effects may include physical, mental, behavioural and/or learning disabilities with lifelong implications (Bertrand et al. 2005).

Only FAS can be formally diagnosed using the criteria within the International Classification of Diseases (ICD-10-CM) (WHO 2011), and is the only FASD that can be diagnosed without confirmation of maternal alcohol use during pregnancy. The easiest time to identify FAS is in early childhood when a child is aged between six months and three years and facial and growth differences are most pronounced; for other fetal alcohol exposure conditions, the early school years, when the child is six or seven years old, may be better (Chandrasena et al. 2009; May 2009).

The presence of three key characteristics can lead to a diagnosis of FAS (Gray and Mukherjee 2007; WHO 2011):

• Facial differences – flattening of the mid-line groove between nose and mouth (philtrum), a thin upper lip (vermillion border), and narrowing of the opening between upper and lower eyelids (small palpebral fissures)
• Delayed growth – below average height, weight, or both (< 10th percentile)
• Central nervous system (CNS) abnormalities – structural, neurological, functional or a combination These may include microcephaly, learning disabilities, developmental delay, hyperactivity disorders, seizures and brain structure abnormalities.

Other common non-diagnostic differences include organ and skeletal malformations, sensory impairments, muscle tone and coordination difficulties and otherwise unexplained behavioural and cognitive issues. Although the core diagnostic features may seem unequivocal, non-specialists should not assume a child has FAS based upon these features; they are also found in conditions unrelated to maternal alcohol use (e.g. Williams syndrome, Noonan’s syndrome) (Chudley et al. 2005; Hoyme et al. 2005).

The facial differences associated with FAS form during a specific development window in the first trimester (first three months) of pregnancy (Mattson and Riley 2011; Streissguth and O’Malley 2000). The heart and other organs, including the bones are also at risk at this time. In the early weeks of pregnancy, and during the second trimester, the fetus has an increased risk of spontaneous abortion. In the third trimester, the effects of alcohol on the fetus include impaired height, weight and brain development (Chudley et al. 2005). However, the fetal CNS (including eyes and ears) remains very vulnerable to the effects of alcohol throughout pregnancy (Mattson and Riley 2011; US Department of Health and Human Services et al. 2008).

Although the associated physical differences make FAS easier to diagnose than other FASDs, if there is evidence of the mother’s alcohol intake during pregnancy and detailed historical, biological, neurobehavioural, social and physiological evidence, it is possible to identify children and young people on the wider fetal alcohol spectrum (Gray and Mukherjee 2007; Mukherjee et al. 2005; see also Mukherjee, Chapter 13, this publication).

Differences across the lifespan

The cognitive and behavioural profiles of infants, children and young people with FASDs change over time. One study indicates impaired information processing before birth may have longer term consequences for the ability to learn after birth (see Hepper, Chapter 5, this publication). Riley (2011) notes that newborn babies with FASDs are frequently hyper-reactive to stimulation and have arousal and dysregulation issues. He also mentions ‘high activity levels, disturbed sleep patterns, trouble feeding, and, in extreme cases, a neonatal withdrawal syndrome’. Older babies may have motor problems, developmental delay, language and cognition issues (Riley 2011; see also Nguyen and Riley, Chapter 18, this publication). Learning, behavioural/emotional and social difficulties typically become more evident as the children and young people progress through school. The learning needs of primary and secondary students with FASDs are subtly different from one another. For teenagers, issues around emotions, friendships and sexual behaviour, independence and achievement compound their primary impairments (Connor and Huggins 2005; see also Egerton, Chapter 12, this publication).

Prevalence of FASDs

In the UK, there are currently no reliable prevalence figures for FAS or FASDs as they are not routinely collected or recorded by the British Paediatric Surveillance Unit (BMA 2007). The most quoted prevalence figure is that given by the Institute of Medicine in the USA – about 0.5 to 3 children and young people with FAS per 1,000 of population, and, for those with FASDs, 10 in 1,000. The prevalence of FAS/FASDs is energetically debated, and Gray et al. (2009) point out the need for caution and further research before these figures can be confirmed. However, based on current research among representative populations in Italy, May and his colleagues believe accepted rates for the US and Europe are low. He states:

We believe that the prevalence of FAS is closer to 2 to 7 per 1,000; and rather than FASD existing at 1 per cent, we believe that the rates of FASD … are between 2 per cent and 5 per cent in the general population of developed countries.

(May 2009: 21)

Many researchers and clinicians also report that children with FASDs are often misdiagnosed with conditions such as attention deficit hyperactivity disorder, reactive attachment disorder and oppositional defiant disorder, among others (Coles 2011; Dubovsky 2009; FASCETS 2010; Mukherjee et al. 2006; O’Malley 2007).

Prevalences of FASDs among populations with traditionally high alcohol use are much greater. Golden (2005) reports one in 170 live births among aboriginal populations in New Zealand, Australia and the United States (see also Elliott, Chapter 23, this publication, for a discussion of most recent Australian findings), while in certain very high-risk South African communities, the prevalence has been estimated at 68.0–89.2 per 1,000 (see also Viljoen, Chapter 22, this publication). Elevated prevalence is also seen in moderate alcohol-using communities – 3.7–7.4 per 1,000 children and young people, and 20.3–40.5 per 1,000 for FASDs in some Italian populations (May et al. 2006). Gray (see Chapter 3, this publication) describes how alcohol in three populations has given rise to increased risk of FASDs and a cycle of deprivation and disadvantage.

Responding to FASDs

Early childhood intervention (ECI) is now well documented as providing both developmental and economic benefits for vulnerable children (see also: Blackburn, Chapter 10, this publication; Frances, Chapter 9, this publication). Moreover, children’s rights to ECI are embodied within the Convention on the Rights of the Child and the Convention of the Rights of Persons with Disabilities for State Parties, and it is quite simply ‘the right thing to do’ (Brown and Guralnick 2012: 283).

Early diagnosis and intervention for children and young people with FASDs are crucial so that an effective network of professional and social support can be put in place from an early age to support both the children and their families (Benz et al. 2009; Mattson and Riley 2011; May 2009). However, the current situation is far from ideal. Families describe the unrelenting battle for services and the hardships, alongside the joys, of parenting children with FASDs (see also: Brown and Brown, Chapter 6, this publication; Muir-Timmins and Timmins, Chapter 7, this publication; McCormick, Chapter 17, this publication). These interventions will require an ongoing interdisciplinary approach to assessment, diagnosis and support, as FASDs are not only complex and multi-factoral, but change and evolve as children mature into adults (see also O’Malley, Chapter 19, this publication). Without diagnosis and support, unrealistic expectations from themselves and others may lead to children and young people developing serious defensive behavioural, cognitive and psychological secondary disabilities leading to mental health problems, disrupted school experience, trouble with the law, inappropriate sexual behaviour, addiction, problems with independent living and attempted suicide (Baer et al. 2003; Kelly 2009; O’Connor et al. 2002; Riley 2003; Streissguth and O’Malley 2000; Streissguth et al. 1996).

Some people oppose diagnosing children and young people with FASDs because they believe it stigmatizes them and their families, but as Substance Abuse and Mental Health Services Administration (SAMHSA 2010) points out:

inaccurate diagnosis can be harmful. Persons with an undiagnosed FASD may be mislabeled as noncompliant, uncooperative, or unmotivated. In addition, treatments are selected on the basis of the diagnosis. If the diagnosis is not correct, the treatment will not be correct. For example, medications for ADHD may not help a person whose attention deficits stem from prenatal alcohol exposure.

Morgan Fawcett, a young man with an FASD, also emphasizes the importance of diagnosis:

I had no clue [that] I was struggling because parts of my brain didn’t develop … so I simply felt stupid. But the more I read [about FAS], the more I … understood why I did or didn’t think in certain ways, why I did or didn’t understand certain subjects, and that was huge. It was like 1,000 lbs was lifted off my shoulders.

I can’t tell you how many times people have said to me, ‘Well, I don’t want to label my child’ … Well, denial doesn’t help. But acceptance and knowing that you have a disability … not only brings relief, but it also gives you a base of where you can need help. Knowing and understanding where your deficits lie helps you build upon your strengths

(NOFAS 2012)

So what do we need?

Today, there are major societal issues surrounding excessive consumption of alcohol (see Plant, Chapter 4, this publication), and the increase in the identification of FASDs in children is widely reported (BMA 2007). Regularly, the popular press reports growing concerns regarding the fast-growing ‘binge-drinking culture’. In developed countries, this phenomenon is causing political and social concern (see Black, Chapter 21, this publication, for a discussion of the European response to FASDs). In alcohol awareness education in schools, we educate young people to ‘know your limits’, and to take ‘personal responsibility’ for identifying their own safe levels of alcohol consumption. Public Health campaigns reflect a similar message, with television and media campaigns giving a focus to issues such as drink-driving at peak times such as Chr...