Professional Series

Fetal, Neonatal and Early Childhood Effects of Prenatal Methamphetamine Exposure
Mary F Holley MD

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1. Background
Drugs of abuse have a long legacy of causing significant impairment in the development of the human brain. Alcohol abuse during pregnancy results in significant changes that include facial dysmorphisms, neurobehavioral problems such as ADHD, and mental retardation. The full complex of alcohol related dysfunction is known as fetal alcohol spectrum. Methamphetamine exposure has not been identified with a syndrome or an identifiable pattern of malformation or dysfunction, but clusters of symptoms have been associated with neurologic deficits identified on sophisticated brain scanning of children exposed to methamphetamine (Chang 2004). These findings require our attention and reasonable changes in our patterns of practice in the prenatal clinic and the nursery.

There are a number of developmental risk factors that are common to all drugs of abuse and that may overlap with the effects of lower socioeconomic status. These include genetic influences, nutritional status of the mother, poverty and associated stressors, mental illness either as a predisposing factor to addiction, or as a consequence of drug use, infectious diseases and lack of prenatal care. Each of these factors contributes to the environmental stressors impacting the development of the child born into a family affected by drug abuse. We will also consider the risk factors specific to methamphetamine use including placental insufficiency, preterm labor, congenital malformations, and the neurotoxic effects of methamphetamine on the developing brain.

Early identification of drug exposed infants and children is crucial to our efforts to intervene in the lives of these children. Early childhood development is strongly affected by the drug use of parents, particularly mothers. Proactive intervention however demands that we know at the infancy or preschool stage that a child is at risk for drug or alcohol related developmental challenges. In order to effectively intervene in these children’s lives we have to know who they are, and be willing to take action to protect them. The consequences of our failure to do so will be made manifest in the juvenile detention centers of the next decade.

2. Introduction
Methamphetamine use among pregnant US women doubled over the six year span from 1998 to 2004 (Cox 2008) as methamphetamine has gradually replaced cocaine as the drug of choice in many areas of the nation among Americans in general and women of childbearing age in particular. Unlike cocaine, methamphetamine is used by women at rates equal to men (Cohen 2007), primarily for weight loss and increased energy. Methamphetamine is a much more toxic drug than cocaine, causing more rapid and intense addiction (Gonzalez 2000), more symptoms of mental illness (McKetin 2006), and more rapid personal and family disintegration. For all these reasons, methamphetamine has exacted a higher toll on the family, higher even than cocaine, which has already destroyed countless families across this nation.

Both cocaine and methamphetamine produce sexual arousal and promote promiscuous sexual behavior, but methamphetamine produces this effect for far longer than cocaine, and is commonly used by addicts to enhance their sexual experience. As the people using methamphetamine are predominantly of childbearing age, this drug poses greater risks to their unborn children than other comparable drugs of abuse. Increased risk of disease transmission including Sexually Transmitted Diseases, Hepatitis C and HIV, and higher risks of obstetric complications, prematurity and growth restriction are of particular concern as methamphetamine use increases in the mothers of our children (Smith 2006).

Of major concern are the numerous anecdotal reports of significant neurologic dysfunction in children exposed to methamphetamine in utero. Caretakers of these children have reported cases of severe ADHD, conduct disorders, learning disabilities and developmental delays in the children of methamphetamine users. These reports have been of great concern to the family members, adoptive and foster parents who are taking responsibility for these children. Scientifically valid information regarding their prognosis and effective interventions is greatly needed.

Education professionals are concerned about the impact of methamphetamine abuse on the special education demands placed on their schools as large numbers of children with learning disabilities and attention deficits are enrolled in the nation’s public school system. And since children with learning disabilities and academic failure have higher rates of delinquency (Aseltine 2000), methamphetamine exposed children are more likely to grow up to be wards of the juvenile justice system, further straining our criminal justice system. Early identification of the drug affected child would permit intervention and training opportunities before entry into the school system, at a time when such interventions are most likely to be effective. But early identification requires drug testing of neonates at or shortly after birth.

True primary prevention would require antenatal identification of the drug using mother in the first trimester of pregnancy, a time when many mothers are amenable to interventions to help their children. Drug testing in the prenatal clinic however is generally not done because of fears such testing would deter women from seeking prenatal care. Lacking reliable prenatal information we are left with secondary prevention, limiting the effects of a disease by controlling its complications – damage control. This we seek to do by neonatal drug testing to detect exposure early and offer remedial assistance to the child and rehabilitation to the mother after prenatal exposure has already occurred.

There is a great deal of controversy over the utility and validity of drug testing of neonates. There are concerns over the accuracy of the tests, false positive results, interactions with prescribed medications, and possible lawsuits by mothers alleging breaches of their privacy rights. There are also concerns over possible legal prosecution against the mothers of these children, actions taken by child protective services workers including termination of parental rights, custody battles, and the lack of rehabilitation facilities accepting mothers with their young children.

An accurate understanding of and response to the epidemic of drug use in this nation is essential to prevent a public health disaster of epic proportions as today’s children become tomorrow’s parents. In view of the significant neurotoxicty of methamphetamine, the anecdotal reports of neurologic dysfunction and learning disability in methamphetamine affected children cannot be dismissed altogether as unreliable. These reports instead must be investigated and fully understood in order to institute preventative measures and offer meaningful intervention to affected children and their families.

3. Non Specific risk factors
Nutrition is a strong variable associated with poor outcomes in drug using pregnancies (Knight 1994). Some drugs of abuse, such as alcohol, replace normal food intake and compete with nutrients for entry into the mother. Other drugs are potent anorectics, among them cocaine and methamphetamine. These drugs can cause profound nutritional deficiencies in chronic users, to the point of starvation. Vitamin deficiencies, anemia and protein calorie malnutrition are significant risks to a pregnancy already complicated by substance abuse.

Poverty is also strongly associated with drug abuse, as addicts are unable to hold down a job or manage their finances appropriately. Some methamphetamine addicts are employed and hold middle income jobs, but all of their resources go to procure drugs and alcohol, and adequate housing and nutrition are not priorities for these people. Uninsured mothers living in poverty are less likely to attend prenatal clinics and more likely to have untreated infections and poor nutrition regardless of their drug abuse status. Chronic stress is often a characteristic of the lifestyle of drug abusing mothers (Derauf 2007). Homelessness is common, and many addicts move from place to place with no permanent address. Addicts sometimes live in cars or abandoned buildings without utilities or a stable food supply, conditions not conducive to a healthy pregnancy. Legal problems are common with multiple arrests, bonds, and fines. Criminal activity and domestic violence are especially common in methamphetamine affected households. Methamphetamine addicts are irritable and impatient, and with the onset of psychotic symptoms sometimes become violent. This violence is often directed at family members.

Mental illness is very common in substance abusers, especially methamphetamine abusers. Addicts sometimes have pre-existing major illnesses such as bipolar or schizophrenia, but more often they develop methamphetamine induced symptoms of mental illness, which may or may not clear after a period of detoxification (Mahoney 2008). Addicts may become paranoid, suspicious and hyper-vigilant. Real and apparent threats are ubiquitous. Addicts feel threatened by other addicts, aggressive dealers, ‘snitches,’ and the authorities and often develop delusions surrounding these and other threats. Their mental problems lead directly to severe distress, and indirectly to occupational failure, economic distress, non-compliance with prenatal care, and poor parental adjustment. Long term methamphetamine use can cause a form of dementia with memory loss and frontal lobe dysfunction leading to severe impairment in some users (McCann 2007).

Infectious disease is common in drug abusing populations regardless of the substance used. Sexually transmitted diseases flourish in the climate of promiscuity, the sex-for-dope economy, and reduced precautions characteristic of methamphetamine abuse. Methamphetamine increases sexual desire and drive much more than other drugs of abuse, and so is associated with extremely high rates of infection with STD’s. Methamphetamine users experience drying of mucous membranes due to the vaso-constrictive effects of the drug further increasing attack rates of STD’s. Methamphetamine addicts engage in higher rates of unprotected sex and larger numbers of anonymous partners. They are less likely to present for medical care and less compliant with treatment for STD’s.

Increased risks of Hepatitis B and C and HIV are well known, particularly in IV drug users and sexually promiscuous users. Methamphetamine appears to act as an adjuvant, increasing the risk of infection when exposed to either Hepatitis C (Ye 2008) or HIV (Nair 2006, Mahajan 2006, Talloczy 2008). These infections are transmitted vertically to the neonate at birth. While measures can be taken to protect the developing fetus from HIV, there are currently no prophylactic treatments available to prevent Hepatitis C from transmitting to the newborn.

Substance abusers are also less likely to present for prenatal care and so are less likely to have been tested and treated for infectious diseases. Methamphetamine abusers often first present to the hospital in advanced labor having no prior relationship with any healthcare provider. Fearing involvement with the legal system, they frequently deny illegal drug exposure. Their drug use can only be detected by drug testing in the presence of high risk behavioral indicators.

4. Methamphetamine specific risk factors
Aside from the general risk factors associated with abuse of any drug, there are also a host of risk factors specific to methamphetamine abuse. These include obstetric complications, poor prenatal growth, increased risk of congenital malformations, and neurologic injury to the neonatal brain related to exposure to a potent neurotoxin. The human fetus and placenta lack enzymes that could metabolize methamphetamine as it crosses the placental barrier (Dixon 1989). Since methamphetamine crosses the placenta very efficiently, blood and tissue levels in the fetus are comparable to maternal blood and tissue levels (Stek 1993, Won 2001). Methamphetamine has a much longer half life than cocaine, particularly in the human fetus. These factors can result in the accumulation of active drug in the fetus, and higher blood levels of the drug have been seen in the developing fetus than seen in the mother under conditions of chronic administration (Stewart 1997).

The immature organ systems of the fetus are therefore exposed to ‘big people’ doses of a potent stimulant drug with all of its vasoconstrictor and cellular toxic properties. The picture is further complicated by the fact that more than 80% of methamphetamine using mothers also use one or more additional drugs of abuse, most commonly alcohol (Brecht 2007). The impact on the developing fetus is thus increased exponentially in its clinical presentation.

Obstetric complications are significantly increased in methamphetamine abusing pregnant mothers. Because of its prolonged half life in humans – twelve to twenty hours – chronic vascular disruption is seen leading to long term complications. Placental insufficiency is often seen leading to intrauterine growth restriction in the fetus (Smith 2006). Some congenital malformations may also be associated with the intense vasoconstriction associated with methamphetamine use (Hoyme 1990). Maternal hypertension associated with methamphetamine is of much longer duration than similar findings in cocaine abusers and can lead to obstetric catastrophe with abruption and fetal distress or fetal demise (Stewart 1997).

Maternal hypertension associated with methamphetamine use is often mistaken for pre-eclampsia or cooccurs with pre-eclampsia (Elliot 1990). Accurate diagnosis is essential since the treatment for hypertension differs for methamphetamine abusers. Treatment with beta blockers such as Labetolol can have untoward results in methamphetamine abusers as these drugs do not block the alpha adrenergic effect of methamphetamine and can lead to rapidly progressive heart failure in methamphetamine abusing gravidas (Samuels 1979 and personal experience). Older anti-hypertensive are preferred such as appressoline or nipride, which block alpha receptors and control the hypertension seen in methamphetamine abuse. These drugs must be dosed carefully and slowly to prevent overshoot hypotension and resulting fetal distress.

Preterm labor, premature rupture of membranes and chorioamnionitis are all increased in methamphetamine affected pregnancies (Eriksson 1981). The result is often a low birth weight newborn with signs of drug withdrawal including tremors, lethargy, poor feeding, excess irritability, and other neurobehavioral abnormalities (Smith 2003). Physical signs of intoxication in the neonate include tachycardia, hypertension, hyper-reflexia, often mixed with symptoms related to the concurrent use of narcotics such as heroin. The Neonatal Abstinence Scoring system is validated for neonates exposed to all drugs of abuse although the findings can be widely different for infants withdrawing from heroin vs. those exposed to stimulants (Oro 1987). Many of these children are exposed to multiple drugs with conflicting effects leading to confusing findings and missed detection of exposed children.

The incidence of congenital malformations has been studied in chart review studies (Forester 2007a and b), or retrospective studies of affected children (Torfs 1994), but these studies did not include a routine neonatal drug testing protocol and instead relied on patient report and sporadic drug testing in response to risk factors over the course of normal obstetric care. Both methods of detection are fraught with difficulty as only 25% of drug abusing mothers admit to drug use when questioned (Ostrea 1992), and drug testing is often done based on stereotype, missing many drug using mothers who do not fit the profile of the ‘drug addict.’ As a result we do not know the true incidence of congenital malformations in the infants of methamphetamine abusing mothers. Anecdotal reports have linked methamphetamine abuse with gastroschisis, eye and ear malformations, cardiac defects, renal anomalies, and limb reduction defects, all of which are exceedingly rare (Bays1990).

Effects of methamphetamine exposure on the developing brain have been extensively studied particularly in light of the overwhelming evidence that methamphetamine is a neurotoxin in the adult brain (for a review Yamamoto 2005). Most of these studies have been done on rodent species. Very few human studies have been done to assess human brain development in methamphetamine exposed children, but those that have been done suggest a significant effect. And a long lasting effect, with behavioral changes and increased social problems extending into adolescence.

5. Methamphetamine effect on brain development
Theoretically, methamphetamine should have a significant impact on brain development. It is a potent vasoconstrictor, reducing blood supply to the placenta and thus delivery of oxygen and nutrients to the developing fetus. It is also a potent neurotoxin, releasing free radical compounds that cause neural cell death (Yamamoto 2005). And indeed stimulants do impact embryogenesis of the developing central nervous system. Cell proliferation and migration are impacted and synaptogenesis is impaired (Weissman 1995). There is reduction in neural growth factor and a marked increase in reactive oxygen species and free radicals (Jeng 2005, Wells 2005). These toxic chemicals are known neurotoxins and have been implicated in the progression of cellular damage to the brain in adult methamphetamine users (Açikgöz 2000).

Animal models, rats, mice and gerbils, have been used to study the fetal effects of many drugs including methamphetamine. Rodents metabolize methamphetamine differently from humans; the half life of methamphetamine in rodents is only around one hour, compared with twelve hours in humans (Cho 2001). Rodents also mature their central nervous system in the first month post-natally while humans do so in the third trimester of pregnancy (Gomez- DeSilva 1998). This explains the significant differences in dosing of animals compared to typical human use patterns. Rodents are born at an earlier gestational maturity than humans, and so are usually dosed ten – twenty days after birth to simulate third trimester human exposure. Neonatal rodents have been found to be relatively resistant to the effects of methamphetamine compared to adults. These differences often cloud interpretation of animal data by clinicians who accuse animal researchers of vastly overdosing the animals. Because of the markedly reduced half life of methamphetamine in rodents, these studies more likely underestimate the impact of fetal methamphetamine exposure, rather than overestimating it. Overall, methamphetamine appears to be a much more neurotoxic drug than cocaine, as might be expected based on its metabolic profile.

A summary of the most recent research in the field of methamphetamine’s effect on brain development reveals some disturbing trends. Acevedo (2006) studying mice found significant disruption of hippocampus dependent cognitive function in adult animals exposed to methamphetamine in the neonatal stage. Cognitive functions affected included spatial learning, memory and object recognition. Vorhese (2007) looked at rats and also found spatial learning and memory deficits that persisted into adulthood, suggesting a permanent structural change in brain development. In an older but well done study, Hildebrandte (1997) localized the site of methamphetamine induced injury to the dentate gyrus of the hippocampus, specifically to impaired granule cell proliferation (a 34% deficit). Even low dose methamphetamine exposure caused significant spatial learning deficits in rats suggesting that there is no safe level of exposure during pregnancy (Williams 2004a).

Gomez-DeSilva (2004) demonstrated increased catecholamines in neonatal rat brains exposed to methamphetamine, particularly in the substantia nigra, caudate putamen, and nucleus accumbens. Williams (2004b) demonstrated injury to the hippocampus, nucleus accumbens and parietal lobes in rats exposed to methamphetamine. These findings have been replicated repeatedly by numerous researchers demonstrating a significant neurotoxic effect of methamphetamine in brain development with functional loss of memory and coordination.

The mechanism of this damage was elucidated by Jeng (2005) who investigated the metabolic pathways by which methamphetamine damages developing neural tissue. He found that methamphetamine causes oxidative cell injury in the brains of mice exposed to neonatal methamphetamine. Oxygen free radicals are produced by the metabolism of both methamphetamine and the mono-amine neurotransmitters released in response to methamphetamine. These free radicals are potent neurotoxins. The fetal brain lacks key enzymes needed to metabolize mono-amines and methamphetamine, leading to the build up of high levels of oxygen free radicals and consequent long term impairment of brain development (Wells 2005).

These neurotoxic changes persist into adulthood and sensitize the adult brain to the effects of adult exposure to methamphetamine, particularly in males. Neurotoxicity to the dopaminergic projections in response to methamphetamine challenge in adulthood was significantly increased in animals that had been exposed to methamphetamine prenatally, suggesting a persistent sensitivity (Heller 2001). This finding has significant implications for meth exposed children growing up in meth abusing homes who learn early in life how to solve their problems with a pipe.

6. Human studies of methamphetamine impact
Clearly methamphetamine should not be given to neonatal rats, mice or gerbils. It damages their little brains. But what about humans? Do the animal studies apply to the human infant? Most human methamphetamine users are poly-drug users and have multiple other risk factors in addition to their drug use including poverty, stress, nutritional deficiencies and infections to name a few. For these reasons the rodent studies more likely underestimate the impact of the total prenatal environment on the human fetus and its development.

The earliest studies on human response to fetal methamphetamine exposure were grim indeed. Tests of visual recognition in human infants exposed to methamphetamine showed significant decreases (Hansen 1993) and corresponding differences in attention, distractibility and activity level (Struthers 1992). Changes in visual recognition in the infant are strongly associated with cognitive function later in life. Dixon and Bejar at UCSD (1989) found that 35% of neonates exposed to cocaine and /or methamphetamine in utero had abnormalities in brain structure at birth, including intraventricular hemorrhage, necrotic echodensities, and cavitary lesions. These lesions were thought to be due to the severe vaso-constrictive effects of stimulant drugs of abuse. A significant number of stimulant exposed infants (10%) had ventricular dilation reflecting diffuse atrophy of cortical tissue.

But the human brain is not quite the same as a rodent brain. Cortical areas are much more richly developed in humans, and the human cortex continues postnatal development over the first 21 years of life, especially in the first three years of life. The developmental window that extends from birth to age three is a time of explosive growth in cognitive, emotional, verbal and social development. Given adequate interaction, stimulation and nutrition, the human cortex increases in size significantly, though subcortical structures do so to a much lesser degree. If the meth exposed child is sent home with responsible parents, much (though perhaps not all) of the brain injury sustained before birth could be compensated for and its impact diminished. Early intervention in methamphetamine exposed children could be extremely important to the long term prognosis for human cognitive and social development.

And indeed that is what the studies demonstrate. When methamphetamine exposed children are studied at age eight to ten, the cavitary lesions and ventricular dilation are no longer seen (Smith 2001) . All of the children in this study had been exposed to methamphetamine with very low levels of exposure to other drugs of abuse, including alcohol. Children with diagnosed developmental delay, impaired growth, seizure disorders, or ADHD were excluded. Only those children who looked perfectly normal were studied. Although these children did have signs of metabolic changes in the basal ganglia, no cavitary lesions were found.

In a follow-up study by the same group, Chang in 2004 investigated further the changes seen in the basal ganglia of methamphetamine exposed children. Using some of the same subjects, again excluding children with obvious developmental delays or ADHD, significant subcortical changes were seen. Methamphetamine exposed children had significantly smaller hippocampus, globus palidus, putamen and caudate (17-26% smaller), the same areas that are impaired in animal models according to multiple studies.

A corresponding decrement in neuropsychological testing was also observed in these methamphetamine exposed children. They scored lower on measures of visual-motor integration, attention, verbal memory and long term spatial memory, all essential functions in efficient learning. Again, these were children who had not been identified as having a developmental delay or ADHD by teachers or caregivers. These children looked perfectly normal and were in performing normally in school, but they were challenged by the effects of their prenatal methamphetamine exposure.

Long term follow-up of methamphetamine exposed children over a period of up to fifteen years shows the impact of these challenges. Billings (1994) demonstrated increased aggressive behavior and poor adjustment in children eight to ten years old exposed to methamphetamine prenatally. The same children followed up to fifteen years of age (Cernerud 1996 and Eriksson 2000) showed higher rates of academic failure and poor social adjustment. These methamphetamine exposed children were three times more likely to be behind in school (15% were one year or more behind) and had lower grades than non-exposed peers.

These long term studies did not attempt to control for alcohol exposure. Indeed 81% of these children were also exposed to alcohol prenatally. Fetal Alcohol Syndrome has clearly been linked to significant neurobehavioral abnormalities including ADHD, learning disability, verbal memory deficits, and mental retardation (Pie 2008). Most of these children (80%) were also exposed to nicotine, which has been linked to abnormalities of the auditory association area (Dwyer 2008) and dysregulation of emotion and attention (Shea 2008). The majority (78%) of these children did not live with their birth mothers throughout childhood. Many were wards of the state and had moved from foster home to foster home, a condition that is strongly linked academic failure and delinquency (National Center on Addiction and Substance Abuse at Columbia University 2004).

We do not know the true incidence or severity of psychomotor or neurocognitive disability in children exposed to methamphetamine because routine drug testing is not being done, and so the majority of affected children are not identified at birth or assessed as they mature. Human studies will always be complicated by concurrent alcohol and other drug abuse since most meth addicts use other drugs as well. We do not yet have the necessary data to assess the true incidence and risk of methamphetamine exposure to the development of the human brain.

7 Early Detection and Intervention
Primary prevention of drug related disability in the infant requires that the drug abusing mother be identified and counseled early in the prenatal course so that disease and impairment is prevented. Screening of obstetric patients for drug and alcohol abuse is required by the laws of most states, yet is inconsistently done by most providers and even more seldom reported or acted upon during the pregnancy. This is in spite of the fact that a poor obstetric outcome is likely in the event of drug abuse during pregnancy, and that the poor outcome is likely to be attributed to substandard obstetric care if the existence of drug abuse has not been documented.

Prenatal screening is fraught with difficulty because of the fear that the drug abusing gravida will simply avoid prenatal care if serious attention is directed to her drug or alcohol abuse, especially in the form of drug testing. Screening is thus limited to verbal questioning with its attendant under-estimation of the extent of the problem at hand.

For verbal screening to be effective, questioning should be incorporated into the routine intake interview so that a rapport is established with the health care provider and suspicion as to the intentions of the provider is minimized. Questioning should begin with an inquiry into family history of substance abuse, ideally in the context of a general family history review. This line of questions is less threatening to the patient and less likely to raise resistance than a direct assault on her fitness to be a mother. If the family addiction is then recorded as an illness, not a moral failure, the patient may be more likely to admit to her ‘addictive illness,’ than she would be to admit to her ‘illegal drug use’ with its criminal intonations.

Early prenatal identification of a drug or alcohol problem permits primary prevention of the neonatal complications – the ideal situation – rather than just damage containment obtainable with neonatal drug testing. Prenatal identification requires an informed, concerned and honest patient, who has been apprised of the risks drug abuse poses to her and her baby’s health, a non-judgmental attitude on the part of the medical provider, and the availability of appropriate inpatient or outpatient treatment facilities.

Since primary prevention often is not accomplished, we are left with damage containment measures that focus on identification of the affected newborns and rehabilitation of their mothers after delivery. But even post delivery ‘damage control’ interventions are often not carried out because of poor detection of drug and alcohol abuse in the neonatal stage. The period of hospitalization presents our best opportunity to detect and intervene in the addiction process because of the prolonged period of intense observation by skilled professionals in the labor and delivery suite. Professionals trained in recognition of the signs of addiction can identify mothers and infants with risk factors for addiction and in most states can order a neonatal drug test at the slightest hint of a problem. The most seriously affected children are likely to be identified in this way, however not all drug addicts look, act, and smell like drug addicts. Not all labor and delivery professionals are alert to the signs and symptoms of addiction, and not all doctors and hospitals permit drug testing on their favored (insured) patients. Some doctors and hospitals, wishing to avoid all the hassle associated with drug testing, do testing on only the most egregious cases, missing many affected children. The extremely short hospitalizations for delivery that are now common also limit the ability of trained professionals to observe mothers over an extended time and recognize abnormal patterns of behavior and failures in bonding.

Most children exposed to drugs of abuse are not identified at birth, and most of them go home with their drug abusing parents without any intervention. These children, who have already been exposed to a potent neurotoxin, are then exposed to poor nutrition, domestic violence and child abuse, infectious diseases, and a host of environmental problems associated with poverty and addiction. They are at significant risk for academic and social failure if their problems are not addressed in a proactive manner. Proactive intervention however demands that we know at the infancy or preschool stage that a child is at risk for drug or alcohol related developmental challenges. Early identification offers us the opportunity to intervene in the development of a child and reduce the likelihood of a poor outcome.

Despite a long history of neonatal testing for medical problems and inborn errors of metabolism in our newborns (e.g. PKU and hypothyroid) the United States has no systematic program for testing all neonates for exposure to neurotoxic drugs of abuse. This is in spite of the large numbers of children thought to suffer from these exposures and the ease of testing by meconium or hair analysis. (Garcia - Bournissen F 2007). Testing is instead based on stereotypes and behavioral indications that may unfairly stigmatize some segments of the population and at the same time fail to detect the majority of cases. Basic public health science tells us that this is a totally inadequate system of detection of a major public health risk.

Large numbers of affected children are missed when testing is based solely on risk factors. In a large study of universal meconium drug testing, 44% of all neonates in an inner city hospital tested positive for illicit drug exposure. The majority of children with prenatal exposure to illegal drugs appeared normal at birth, and so would not have been tested under most protocols. Only one in four drug abusing mothers admitted to their drug use on questioning in the perinatal setting (Ostrea 1992). Of those who admitted to drug use at any time during pregnancy, around 90% of their infants had a positive meconium drug screen at birth.

Current neonatal indications for drug testing include obvious withdrawal symptoms, low birth weight, neurobehavioral abnormalities, seizures, stroke, cardiac problems and NEC in a term baby. Only severely affected infants will display symptoms this severe – around 4% of methamphetamine positive neonates (Smith 2003). Most methamphetamine affected children (>50%) do not have any significant withdrawal symptoms, but are still at risk for developmental delay or learning disability. Identification of these children is essential for effective intervention to prevent social and academic failure.

Current maternal indications for neonatal drug testing include a known history of drug abuse, lack of prenatal care, home delivery or precipitous delivery, preterm labor, poor weight gain in pregnancy, hypertension without proteinuria, abruption, fetal distress, sexually transmitted disease, and obvious intoxication. Poor, single, or homeless mothers are much more likely to be tested for drug abuse than mothers who are employed and have stable family relationships.

The currently practiced methods for drug testing of neonates rely heavily on stereotypes of how drug abusing mothers typically behave. This approach is dangerous and misleading for two reasons. First, women from disadvantaged backgrounds may fit the ‘profile’ of the drug abusing mother and may be selected for testing at a higher rate. This risk factor based testing leads to a stigmatized feeling of reproach, being held under suspicion merely for being poor or unmarried or homeless.

Secondly, stereotype based drug testing misses many infants whose mothers do not fit the ‘profile’ but who are abusing illegal drugs, especially methamphetamine. Methamphetamine differs from other major drugs of abuse in that many low dose users do not consider themselves ‘drug users.’ Methamphetamine abusers are often well educated highly functioning individuals, working two jobs, highly driven and successful. They use methamphetamine to work harder and longer, get more focus and enhance attention, or to lose weight and/or preventweight gain. They consider methamphetamine a ‘medication’ not a ‘drug’ and so will deny ‘drug use.’ Methamphetamine users frequently do not fit the stereotype of the ‘addict.’ Drug testing based on stereotypes misses this sizable population of mothers, and so their methamphetamine exposed newborns are not detected.

Universal drug testing offers a major improvement to our current protocols based on perceived risk factors. State laws to provide for testing of all newborns for exposure to drugs of abuse, just as we currently test all neonates for PKU and thyroid dysfunction, would permit detection of the vast majority of drug affected newborns. The basis for testing for PKU and thyroid dysfunction is that early intervention is life saving and prevents severe disability in affected children. This rationale also applies to the drug exposed newborn. Identified mothers could be offered treatment and counseling, and a major cause of child abuse would be prevented. Children could be screened for learning disabilities and receive the special attention they need to develop normally.

We currently screen children for learning disabilities in early elementary school, long after the best window of opportunity for intervention- birth to age three- has passed. Universal neonatal testing for drug exposure would permit earlier intervention in the child’s cognitive and social development, and would also permit earlier intervention for the mothers of drug exposed children allowing more of them to obtain the treatment they need to preserve the family. None of these interventions can happen if we do not know a newborn has been exposed to substance abuse.

If all newborns were tested, no mother would feel singled out or stigmatized, and no affected children would be missed. Counseling and follow-up could be offered to mothers and their children and early detection of learning difficulties could be facilitated. Early detection could lead to better outcomes for children and their families as addictions are identified in earlier stages when treatment outcomes are more favorable. Earlier detection of the subtle learning disabilities associated with methamphetamine exposure permits educational intervention to mitigate the long term impact of these challenges.

The major limitation of universal neonatal drug testing is that it would only detect late second and third trimester use, and would miss those children whose mothers didn’t like the hyperemesis treatment offered by their obstetrician, and elected to use their college friend’s hangover treatment instead. These women are extremely unlikely to admit to drug use, and if their children exhibit learning difficulties or neurologic injury, they will find someone else to blame.

Another limitation is the incidence of false positive results even with the use of gas chromatography or mass spectrometry confirmation testing. Meconium screens are not reliable for PCP exposure – the use of dextromethorphine (Robitussin) cough medicine is enough to make the PCP screen positive. The meconium screen would also be positive for amphetamines in the case of prescription use of stimulants such as Adderall and Desoxyn. These drugs are not recommended for use in pregnancy (Category C) as alternative treatments are readily available for their indications.

But the most common reason for failure to obtain a drug test is denial, usually based on stereotyping of the mother and fear of offending the favored (insured) patient. Patients are in denial, their families are in denial, and often healthcare workers join them in the assurance that everything must be just fine. A good mother like her couldn’t possibly be using illegal drugs. Denial is generally discouraged in the medical field since lives are at risk if a serious diagnosis is missed.

8. Denial Doesn’t Work
Denial on a societal scale is just as dangerous as denial on an individual level. Our reluctance to ‘label’ drug affected children results in a complete inability to assist them since we do not know who they are. Universal drug testing of neonates would break down barriers to treatment and intervention for children and their families. Family drug courts could assure compliance with treatment on the part of parents and assemble the wide range of services and programs that could prevent the disintegration of these fragile families.

When affected children are missed, opportunities for intervention are missed. We lose opportunities to impact the child and family with drug treatment options, prevent child abuse and neglect, improve cognitive performance and prevent academic failure. We miss the opportunity to prevent second generation drug abuse in these children as they grow up with poor self esteem and fall into delinquency. Universal drug testing offers us an inroad to identify and assist families and children at risk. We would be remiss if we fail to take action.