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Substance Abuse Among Children and Adolescents

1997; American Academy of Pediatrics; Volume: 18; Issue: 11 Linguagem: Inglês

10.1542/pir.18.11.394

1529-7233

Marc Fishman, Ann Bruner, Hoover Adger,

Cannabis and Cannabinoid Research

Alcohol and other drug use poses a serious threat to the health of children and adolescents. In addition to the health risks inherent with alcohol and other drug use, substance abuse often is linked with other risk behaviors (early sexual activity, violence, academic failure, truancy/school dropout, delinquency). Pediatricians and other primary care providers are in an ideal position to identify substance abuse and to provide preventive guidance and education to children, adolescents, and their families. In this article, we use the term substance abuse to refer to substance use disorders in general, including abuse and dependence, unless otherwise specified.Following declines in the late 1980s and early 1990s, prevalence rates of alcohol and other drug (AOD) use among adolescents are increasing again. The proportion of eighth graders using an illicit drug in the past year nearly doubled in the period from 1991 to 1995(11% to 21%). Almost 40% of 1995 high school seniors reported use of some type of illicit drug in the past 12 months (up from 30% in 1991). Overall,one of every two adolescents has tried an illicit drug by the time he or she graduates from high school. The most common drug of abuse is alcohol. In 1994, almost 90% of high school seniors reported some experience with alcohol, more than 50% reported use in the last month, and 5% reported daily use. Of the illicit drugs, marijuana is used the most widely. More than 40%of 1995 seniors reported having used marijuana at some point in their lives,35% reported use in the past year, 21% reported some use in the past month,and 5% reported smoking marijuana daily. Use of cocaine increased dramatically during the 1980s; 6% of high school seniors in 1995 reported using cocaine at some time in the past, and 3% reported having ever used“crack.”As disturbing as the increase in the rates of AOD use is the decline in the age of first use. The average age of first use now is 12 to 14 years. Also of concern is the observation that many adolescents are using multiple drugs (an average of 3.4 substances) simultaneously. Clearly,AOD use is a major factor in the deterioration of the health status and morbidity and mortality among adolescents and young adults. The leading causes of death in teenagers are unintended injuries, homicide, and suicide. AOD use is associated with approximately 50% of fatal motor vehicle accidents and homicides and a significant proportion of adolescent suicides.The terminology of AOD use can be very confusing because so many different terms are used—use, abuse, dependence, addiction, drugs,intoxicants, substances—by different clinicians and specialists. Any AOD use that leads to major impairment or distress in life is a problem and should be of concern. Impairment can range from social embarrassment to problems related to discipline, family disruption, relationships, legal consequences of drug-related behaviors, catastrophic medical sequelae, and death. Any use of illicit drugs by adolescents is illegal and, therefore, can be considered as a form of abuse. In most states, alcohol and tobacco products are age-restricted, and both purchase and consumption are prohibited. Acceptance of the concept of “recreational” drug use as a normative part of adolescence is problematic because of the high potential for progression to abuse, dependence, or both. Clearly, not all children and adolescents who use AOD will become problem users. In fact, the majority will not. However, initial casual use quickly progresses to problem use for many adolescents.The criteria used in the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders(DSM-III-R) and now DSM-IV recognize the high variability of patterns in substance use disorders and reflect the application of a more dimensional approach to diagnosis. DSM-IV (Table 1) uses a relatively straightforward definition of substance abuse and dependence that emphasizes the concept of a maladaptive pattern of substance use that leads to clinically significant impairment or distress and lists specific criteria for abuse and dependence. This general approach, independent of social fashions and moral judgments,focuses on the health consequences of AOD use and can be used easily by a broad spectrum of clinicians.Abuse is diagnosed according to the presence of one or more of a distinct and specific set of behaviors occurring within a 12-month period. Another distinct and specific set of behaviors is used to define dependence. Dependence is distinguished from abuse by much more than simply a continuum of severity. Substance dependence refers to drug use that is an integral part of the adolescent’s life and is associated with typical features that distinguish it as an especially malignant subtype. AOD use continues despite the presence of persistent or recurrent adverse consequences related to use. The use of progressively larger amounts or over longer periods than intended and the development of tolerance (decreased effect from similar amounts of the substance or increased amount needed for similar effect) are characteristic features. Preoccupation with activities necessary to gain access to or to maintain a steady supply of drugs is common. Dependence can (but does not necessarily)include a characteristic physiologic withdrawal syndrome after interruption of use. No single criterion is required to make the diagnosis of dependence,but these features paint a graphic picture of an individual who has lost the ability to control his or her use of AOD and whose use continues despite persistent consequences that are either caused or exacerbated by AOD use. There are important prognostic reasons to distinguish among use, abuse, and dependence. Dependence reliably predicts more severe medical sequelae,poorer treatment outcome, higher relapse rates, and worse overall prognosis.The cause of substance abuse is unknown, and there appears to be general agreement that no single etiology accounts for all types of substance abuse or applies to all types of substance abusers. Substance abuse and dependence reflect a biopsychosocial determination. As with all behavioral disorders, the etiology of substance use disorders is multifactorial; despite all that has been learned about the neurobiology of addictions, it does not appear that a reductionist approach ever will replace a multi-dimensional or multifactorial view.All substances of abuse share a unique property: the capability to produce euphoria and change a person’s perception of reality. Once initiated, addiction carries its own autonomous momentum, which cannot be reduced to any single pathophysiology or “underlying” disorder. For adolescents, AOD use may decrease stress, relieve unhappiness/fear/depression, offer peer acceptance, and provide a cheap and easy “high.” Every chemically dependent adolescent has a thousand reasons why he or she uses and can state a thousand conditions that would keep him or her from using (“if only my parents would stop bugging me”), but there is no simple answer for the primary question of why some develop an addiction and others do not.Various risk factors have been proposed that may contribute to the development of substance abuse and dependence. Not all children and adolescents who use AODs will become problem users, and although risk factors may help to identify those who are most vulnerable, any individual who exhibits them will not inevitably develop problems. It is helpful to examine AOD use and abuse on a continuum. For some, experimental or casual use will progress to heavy use and dependency; for others, even experimental or casual use can lead to tragic outcomes, including death. Hence, it is important to recognize that all adolescents are at risk, but some are at substantially more risk than others.First formulated for alcoholism, the disease model has become increasingly popular over the past 50 years. Its great strengths and contributions have been to destigmatize addiction and encourage treatment, transforming the societal perception of addiction as a moral weakness to addiction as a health problem worthy of medical attention. Weaknesses of the disease model include the potential for patients to deny responsibility for their behavior and an exclusive emphasis on biologic factors.Although beyond the scope of this article, it is clear that each drug of abuse has complex actions within the central nervous system, including differing affinities and actions of the classes of opiate receptors; inhibition of dopamine reuptake by cocaine at the presynaptic terminal; gamma-aminobutyric acid (GABA) modulation by benzodiazepines, barbiturates, and alcohol; and interaction of lysergic acid diethylamide (LSD) and other hallucinogens at serotonin and glutamate receptors. In addition, research on reward pathways that can mediate the reinforcing properties of these drugs has contributed to our understanding of the neuro-biology of addiction. Endogenous opiate reward circuits may serve as a final common pathway for many drugs of abuse. This has had particular clinical relevance for naltrexone, the opiate blocker used in the treatment of alcohol and other drug dependencies.Genetic influences play an important role in determining a person’s predisposition for developing alcoholism and other drug use disorders. A positive family history is important; the presence of first- and second-degree relatives who have AOD dependence is a major risk factor for the development of addiction. Numerous studies document substantially higher rates of alcoholism in relatives of alcoholics than in relatives of nonalcoholics. Children of alcoholics are four to six times more likely to develop alcoholism than are others in the general population. Some research suggests that genetic factors account for about 30% of the variance in familial transmission of alcoholism; the extension of these results to other addictive disorders is supported by some studies.The significant genetic component is supported by studies of twins that show increased concordance of alcoholism and other drug abuse among monozygotic twins compared with dizygotic twins. Further support comes from adoption studies showing that children(especially sons) of alcoholic parents (especially fathers) reared by nonalcoholic parents have significantly higher rates of alcoholism than the background population or the adopted-away children of nonalcoholic parents who are raised by either alcoholics or nonalcoholics.Some work has suggested that a genetic marker, the A1 allele of the D2 dopamine receptor on chromosome 11, may be associated with some types of alcoholism. Other promising avenues of research on the heritability of and vulnerability to alcoholism have emphasized that tolerance may play a role. Sons of alcoholic fathers have been shown to have increased alcohol tolerance regardless of their personal alcohol histories and even at first exposure. The putative mechanism is that the lack of early aversive effects (eg, hangover,dysphoria, nausea) in genetically tolerant individuals may contribute to greater salience of reinforcing effects, earlier escalation of dose, and increased early exposure.Clearly, the development of alcohol and other drug use disorders represents an extraordinarily complex process involving factors of varying degrees of specificity and effect. Although it is well-established that vulnerability to alcoholism, in particular, is influenced genetically, much remains to be learned about the interplay among specific genes, nonspecific genetic influences, and the modification of these factors by the environment and experience. A better understanding of both biologic and environmental factors may lead to a better understanding of these disorders.Household drug use,especially parental use, is a major risk factor for initiation and progression of adolescent substance abuse. Exposure to and modeling of substance use/abuse behaviors, as well as exposure to the substances themselves, are likely major mechanisms. Although transient familial disruption such as divorce is not predictive of adolescent substance abuse,ongoing disruption of families (persistent chaos in living situations or relationships) is a major risk factor. The importance of parental attitudes toward drug use often is underestimated; parental tolerance of drugs,independent of parental use, correlates positively with adolescent AOD use. This is true particularly for “gateway” drugs (tobacco, alcohol,marijuana) for which parents initially might think, “It’s not that big of a deal…”. Poor parental monitoring and supervision as well as antisocial behaviors are independent risk factors for adolescent substance abuse. Childhood physical or sexual abuse has not been shown to be an independent risk factor for adolescent AOD use, although parental substance abuse is related very strongly to child abuse and neglect, and familial AOD use is a strong risk factor for adolescent substance abuse. Conversely,there are protective factors: clear, parent-defined conduct norms; close emotional ties between adolescents and their parents; siblings intolerant of AOD use; maintenance of consistency surrounding important family activities or “rituals,” such as vacations, meal times, holidays; and the consistent presence of significant others in the life of the child or adolescent.One of the strongest risk factors for adolescent substance abuse is AOD use in the peer group. Some authors metaphorically describe the peer group as the “vector” for transmission, similar to infectious disease models. Conversely, a nondrug-using peer group is a known protective factor. Discontinuity of a peer group, such as when moving or changing schools, increases vulnerability transiently. The power of the peer group reflects both its influence in shaping attitudes, values, and behaviors and the selection of a peer group based on shared values and behaviors.Research findings clearly have demonstrated that age of first exposure and age of first intoxication both are highly correlated with development and progression of substance abuse. The earlier a young person begins to drink alcohol or use other drugs, the greater the likelihood of later developing AOD problems.The concept of an “addictive personality” has not been supported, but certain personality traits do increase vulnerability to addiction. Excitement-seeking, mood lability, easy boredom, extroversion, decreased attention span, “difficult”temperament, aggressiveness, and insecurity all have been implicated as vulnerability factors. Conversely, obsessiveness or carefulness seem to be protective.Many types of psychopathology and behavioral difficulties during childhood and adolescence are associated with higher subsequent rates of addictive disorders. Antisocial, delinquent, and criminal behaviors often are predictive of and coincident with problem drug use in adolescents. For many adolescents, substance abuse is part of a broader pattern of deviant problem behaviors in numerous spheres. Cognitive disability, attention deficit hyperactivity disorder, mood disorders,anxiety disorders, and problems of impulse control and aggression all have been linked with substance abuse. Poor academic performance, truancy, and dropping out of school are other risk factors.In 1994, the American Medical Association published GAPS: Guidelines for Adolescent Health Prevention, which recommends annual risk behavior screening for every adolescent. One useful psychosocial screen is the HEADS examination (Table 2). Interviewing style is extremely important. There is no single best approach, but one effective method is to begin with open-ended general health questions, establishing rapport and confidence by pursuing less controversial and less threatening subjects, then gradually inquiring more specifically about risk behaviors. Probing questions can include such topics as peer group attitudes and behaviors, drug knowledge, social activities,and parental attitudes. The CAGE mnemonic (Table 3) offers useful screening questions for substance abuse. Use of the CAGE or other questions for gathering information about alcohol, tobacco, and other drug use should be a routine part of history-taking. If positive, this initial screening sets the stage for further inquiry.A longer, more exhaustive assessment should be performed whenever drug use is suspected or problems associated with drug use are part of the differential diagnosis. Assessment is a structured process de-signed to determine the extent of AOD involvement and associated problems, to explore coexisting medical and psychiatric conditions, and to assist in treatment planning. A comprehensive assessment requires information about the medical, psychological, behavioral, and social aspects of the patient’s life. Because of the broad scope of a comprehensive assessment, some clinicians may prefer to make a referral to a substance abuse specialist. Denial, defensiveness, minimization, and misrepresentation often are core features of abuse and dependence and can make data gathering a challenge. Hence, the clinician must anticipate that the truth may be revealed only gradually over time and after many encounters with the adolescent and his or her family. Some sample probing questions for adolescents and family members relevant to AOD use are given in Table 4. Finally, no assessment is complete without explicit, directed questioning about individual drugs. General questions about drinking are not sufficient;specific questions about how much beer, wine, or liquor and how often the adolescent drinks alcohol need to be asked. Specific questions about method of use (smoked, inhaled, injected, swallowed), circumstance of use(clubs/parties, school, home, alone, with friends), subjective effects of use(what do you like about AOD), and consequences of use (hangover, trouble with parents, school, law) are important. Questions may need to be asked repeatedly using different phrasing to obtain the complete history.Adolescents, in particular, may not feel initially that their AOD use is a problem, suggesting instead that adults are overreacting, unfairly criticizing them, and not understanding them. The substance-abusing adolescent frequently seeks crisis relief only to get out of trouble due to some consequence of drug use. One of the primary goals of assessment is to set the stage for treatment by establishing a meaningful relationship with the adolescent, collecting appropriate information that can be used to help the adolescent understand that he or she has a problem with the way AOD use affects his or her life, and serving as a conduit to initiation of treatment.Occasionally, an adolescent spontaneously volunteers information about AOD use. At other times, adolescents who have AOD problems will be identified by clinicians using risk behavior screening questions during health encounters. However, the majority of adolescents are referred for substance use evaluation by family members or other concerned parties(teachers or representatives of the juvenile services, social services, or justice system) who suspect use based on behavioral changes or other indicators.This raises important and difficult questions regarding consent, confidentiality, and the doctor-patient relationship. AOD use should be included in the differential diagnosis of all adolescents who exhibit behavioral, educational, and psycho-social problems. Signs and symptoms of AOD use can be subtle (eg, mood and sleep disturbance, decline in school performance, truancy, change in peer group) or dramatic (eg,weight loss, school suspension, suicide, delinquency). Generally, the degree of involvement parallels the degree of impairment or dysfunction;adolescents who are experimenting with AOD often exhibit few behavioral changes. Irrespective of the adolescent’s level of involvement with AOD, the clinician’s initial task is to complete a thorough assessment, provide the adolescent and family with accurate and specific information supporting his or her concerns about AOD use and its negative impact on the adolescent’s life, and assist the patient and family in selecting an appropriate treatment alternative, if necessary.Urine drug testing has an important but often misunderstood role in the assessment of substance abuse. Drug screening tests are not a litmus test for addiction, but rather a spot test for the presence of certain drugs and metabolites. They are subject to the limitations of laboratory technical specifications as well as the usual but variable persistence of drugs and metabolites in the body after use. Another limitation of urine screening is that a variety of techniques can be used to “beat” the tests, such as substituting someone else’s urine (“clean” urine is a marketable commodity) and masking the urine with additive agents. Although precautions can be taken(direct observation, chain-of-custody procedures, temperature monitors),rarely is there substantial additional yield from use of such cumbersome techniques in the primary care setting. Results of urine drug screening without a complete history are not very valuable; these tests must be interpreted within the appropriate clinical context. The sensitivity of commonly available urine drug tests often is overestimated, and false-negative results are common. Just because drugs are not detected in the urine does not mean that a teenager who has a suggestive history does not have a drug problem, and an adolescent who has a positive urine screening result is not necessarily chemically dependent. It is vital to obtain a thorough history and view urine drug screening as an adjunctive assessment tool that has real limitations.Cocaine is one of the most addictive substances known. In animal self-administration models, it is the most reinforcing of all the drugs. Animals will work harder for cocaine rewards than for food, water, or sex and will endure electric shocks to get cocaine. Unlimited access to cocaine in laboratory primates is associated with essentially 100% mortality;the animals will continue to self-administer cocaine to the point of exhaustion, starvation, seizures, hyperthermia, and death. Similarly,cocaine-dependent patients report that cocaine, unlike other drugs, does not produce satiety; they report never feeling that they have had “enough.” Rather, they report an unsatisfiable craving.Cocaine is sniffed or snorted nasally in the powdered hydrochloride form, smoked in chunks or“rocks” in pipes as the alkaloid or “freebase” form(crack), or injected intravenously. In addition to its stimulant and euphoric properties, cocaine can create an overenergized, aggressive, suspicious state and can cause psychosis with transient hallucinations and paranoid delusions. Acute medical sequelae of cocaine use can include hypertensive crisis, coronary vasospasm with ischemia, cardiac arrhythmia, cerebral ischemia, and rhabdomyolysis. These sequelae, especially arrhythmia, are not necessarily dose-related.Previously, heroin was used primarily by the intravenous route. However, the introduction of purer forms of heroin has made nasal sniffing an increasingly popular and efficient method of use. Nasal heroin use is becoming more prevalent among younger and less experienced users. Like other opiates, heroin typically causes sedation, and while intoxicated, heroin users often intermittently “nod” off to sleep. One of the most notable signs of acute opiate intoxication is pupillary meiosis. Heroin users describe the sought-after feeling that they get from the drug as soothing or numbing.Opiates are direct respiratory depressants, and the most dangerous acute medical sequela is apnea/respiratory arrest, which is dose-related but unpredictable because of variations in drug purity. Chronic medical sequelae include generalized pruritus, constipation, and bronchospasm. Cessation of chronic heroin use provokes a characteristic physiologic withdrawal syndrome lasting 3 to 5 days; withdrawal is rarely dangerous (except in very debilitated patients and infants), but is extremely uncomfortable. Symptoms of withdrawal include sweats and chills, diarrhea, nausea, insomnia, myalgias, and irritability. Milder subacute withdrawal symptoms can persist for 2 to 3 weeks.Marijuana is one of the primary gateway drugs. Although it is relatively less toxic than other illicit drugs, it is not benign with heavy use. Marijuana is a depressant that has mild hallucinogenic properties;users often describe feeling relaxed or “mellow.” Chronic users sometimes are characterized by apathy, decreased motivation, and flattened emotions (“burned out”). Less well characterized is a global cognitive impairment that seems to affect particularly cognitive speed,problem-solving, and memory. It has been described as a reversible,subcortical dementia. Other medical sequelae include mild feminization(gynecomastia, testicular atrophy), galactorrhea, menstrual irregularities,and decreased sperm count.LSD and phencyclidine (PCP) are two of the hallucinogens used most commonly. Acutely, an LSD “trip”causes somatic (dizziness, paresthesias, weakness), perceptual (altered visual/auditory sense, including hallucinations), and psychic (altered mood and sense of time, dream-like feelings) changes. Prolonged use of LSD can cause sustained perceptual derangements (flashbacks) that can occur long after the period of acute intoxication. Flashbacks consist of perceptual distortions of actual auditory and visual stimuli; examples include motion artifacts such as trails or halos, false registration of motion (walls that move rhythmically or “breathe”), difficulties with depth perception (elongation of corridors, shifting prominence of various features of geometric designs, causing the illusion of motion), distortion of ambient sounds, and mistaken and fanciful interpretations of peripheral movements. Flashbacks also can feature vivid recollections of previous periods of intoxication, either as perceptual scenes or as fantasy-like scenarios. Also known as hallucinogen-induced perceptual disorder, flashbacks can persist for weeks to months. They gradually decrease in frequency and intensity,usually resolving within 6 months of last LSD use. Frank hallucinations,although common during acute intoxication, are rare in flashbacks.PCP shares many of the features of LSD, although it has several other particular dangers. Acute PCP intoxication can induce aggressive, enraged, assaultive states often compounded by a false sense of confidence or power as well as a peculiar indifference to pain. Therefore, individuals who have acute PCP intoxication are especially dangerous and often prone to violence. PCP also can produce a variety of persistent psychotic states that usually remit within weeks, but can last much longer. Both of these hallucinogens can cause severe cognitive processing difficulties, including prominent impairment of expressive and receptive language.Alcohol is the most widely used and abused of the drugs of abuse (excluding cigarettes). Acute intoxication can be severe enough to lead to respiratory depression and death. Another serious consequence of acute alcohol intoxication, which can occur with other drugs as well, is the experience of an amnestic episode-loss of retrograde memory for a period of intoxication during which the patient does not know subjectively at the time that he or she is in such a state and later cannot recall the events of the episode. When the amnesia is complete, these episodes are called “blackouts”; partial amnesia is sometimes called a “brownout.” Although often trivialized and minimized by problem drinkers, blackouts are quite rare in the general population and are considered by many to be clear evidence of alcoholism.Cessation of heavy, daily drinking provokes a characteristic physiologic withdrawal syndrome. In its most severe forms, alcohol withdrawal can include delirium tremens (DTs), hallucinosis, seizures, and autonomic instability that can be life-threatening. DTs rarely are seen in adolescent patients, who have not had time to amass a sufficient alcohol history simply as a function of age. Adolescents usually experience less severe forms of alcohol withdrawal that may include sweats and chills,tremor, tremulousness, mild hypertension, tachycardia, nausea, insomnia, and irritability. Symptoms peak about 24 hours after the last alcohol intake. The more severe medical sequelae of alcohol toxicity, such as cirrhosis,peripheral neuropathy, cerebellar atrophy, and ataxia, result from years of alcohol exposure and are rare in adolescents. Acute symptoms such as alcohol-related gastritis, however, are common findings in adolescents who ingest a significant amount of alcohol. Hence, a thorough alcohol history should be obtained from all adolescents who present with gastritis, peptic ulcer disease, or recurrent, undiagnosed abdominal pain.A variety of organic solvents, fuels, and other compounds (toluene, paint thinner,glue, spray paint, gasoline, freon, propane) are grouped in the category of inhalants. Delivery usually is by direct inhalation from a container(leading to a pathognomonic perioral frost or pigmentation) or by a technique called “huffing” in which a cloth soaked in the substance is placed in a paper bag from which fumes are inhaled repeatedly. Inhalants typically are abused by younger adolescents because of their widespread availability and low cost. Inhalants cause a dream-like delirious state,often accompanied by hallucinations. Heavy or prolonged use can lead to unconsciousness either from hypoxia or direct central nervous system depression. Seizures occur in some users. The most common cause of death due to accidental overdose is arrhythmia. These agents are potent nervous system toxins, and acute and chronic/permanent sequelae include tremor, ataxia, and peripheral neuropathies. Cognitive and behavi