CHAPTER 19 The Effect of Substance Use Disorders on Children and Adolescents

HOOVER. ADGER, JR. , HAROLYN M.E. BELCHER

Health professionals, including primary care pediatricians and developmental-behavioral pediatricians, encounter large numbers of children, adolescents, pregnant women, and other family members or adult caretakers who have or are affected by alcohol and other drug-related problems. Developmental-behavioral pediatricians and other health professionals are in an ideal position to identify substance use disorders and related problems in the children, adolescents, and families whom they care for and should be able to provide preventive guidance, education, and intervention. Although it is easiest to identify substance use disorders and related problems in children, adolescents, and families who are most severely affected, the bigger challenge is to identify affected individuals early in their involvement and to intervene quickly and effectively. The magnitude of the problem, the nature and effect of substance use disorders on individuals and families, and the role of the health care professional in the prevention, intervention, and treatment of substance use disorders must be appreciated.

INCIDENCE AND PREVALENCE

According to data from the 2004 National Survey of Drug Use and Health,¹ formerly called the National Household Survey, 121 million and 70.3 million U.S. citizens, aged 12 and older, are estimated to be current users of alcohol and tobacco, respectively. In 2004, about 10.8 million underage persons aged 12 to 20 (28.7%) reported drinking alcohol in the previous month. Past-month alcohol use rates ranged from 16.4% among Asians to 19.1% among black persons, 24.3% among Native Americans or Alaska Natives, 26.6% among Hispanic persons, and 32.6% among white persons. Nearly 7.4 million (19.6%) individuals in the age group were binge drinkers, and 2.4 million (6.3%) were heavy drinkers. Among persons aged 12 to 20, binge drinking was reported by 22.8% of white persons, 19.0% of Native Americans or Alaska Natives, 19.3% of Hispanic persons, and 18.0% of persons reporting belonging to two or more races. However, binge drinking was reported by only 9.9% of black persons and 8.0% of Asians. Among youths aged 12 to 17 in 2004, an estimated 3.6 million (14.4%) had used a tobacco product in the previous month, and 3.0 million (11.9%) had used cigarettes. Current cigarette use increased with age up to the mid-20s and then declined. An estimated 2.8% of 12- or 13-year-olds, 10.9% of 14- or 15-year-olds, and 22.2% of 16- or 17-year-olds were current cigarette smokers in 2004.

Another 19.1 million United States citizens (7.9% of the population) aged 12 years or older currently use illicit drugs.¹ Among all youths aged 12 to 17 in 2004, 10.6% were current users of illicit drugs: 7.6% used marijuana, 3.6% used prescription-type drugs for nonmedical reasons, 1.2% used inhalants, 0.8% used hallucinogens, and 0.5% used cocaine.

The highest rate of illicit drug use, 19.4%, was reported among young adults aged 18 to 25 years. It is estimated that 22.5 million U.S. citizens met criteria for alcohol or drug dependence. The percentages of dependence were highest among Native Americans and persons of multiracial heritage: 20.2% and 12.2%, respectively. White and African American individuals had similar rates of dependence: 9.6% and 8.3%, respectively. Asian Americans had the lowest rates of dependence, 4.7%, whereas the rate for Hispanic Americans was 9.8%.²

Among pregnant women aged 15 to 44 years, 3.3%, representing slightly more than 130,000 births per year, reported using illicit drugs the month before interview; this rate was significantly lower than the rate among women who were not pregnant (10.3%).^1,³ Rates of drug use during pregnancy were highest among Native Americans/Alaska Natives (10.1%) and persons reporting a heritage of two or more races (11.4%). In 2002, marijuana was the most widely used illicit drug among pregnant women (2.9%).³ Of all pregnant women in the United States, 1% used illicit drugs other than marijuana, including cocaine (or crack), heroin, hallucinogens, inhalants, or any prescription-type psychotherapeutic for nonmedical use of. Alcohol and tobacco remain significant preventable threats to favorable birth and neurodevelopmental outcomes. Among pregnant women, aged 15 to 25 years, 5% reported alcohol binge drinking (five or more drinks at the same time or within a couple of hours of each other) on at least one day within the month before the survey. Seventeen percent of pregnant women smoked cigarettes within the month before the survey.¹

TOBACCO

Tobacco kills more individuals in the United States each year than do all other substances and firearms combined.⁴ The average smoker starts smoking at age 12 years. Adolescent smokers are more likely to become nicotine dependent through smoking fewer cigarettes a day than are adult smokers.⁵ Worldwide, the Global Youth Tobacco Survey⁶ reports that 24% of youth surveyed began smoking before age 10, and younger women aged 13-15 years are as likely to use tobacco products as are young men. Adolescents see the positive aspects of smoking as helping with boredom, dealing with stress, staying thin, and appearing more mature, and they acknowledge negative aspects such as its making their teeth yellow, interfering with playing sports, being harder to quit, and causing bad breath.

Pharmacology

Human and animal studies confirm the addictive effects of nicotine, the primary active ingredient in cigarettes.^7,⁸ It produces a syndrome of dependence and withdrawal. Nicotine is absorbed by multiple sites in the body, including the lungs, skin, gastrointestinal tract, and buccal and nasal mucosa. The average nicotine content of one cigarette is 10 mg, and the average nicotine intake per cigarette ranges from 1.0 to 3 mg. Nicotine, as delivered in cigarette smoke, has a half-life of 10 to 20 minutes, with an elimination half-life of 2 to 3 hours. Nicotine’s effect on the brain takes less than 20 seconds. The action of nicotine is mediated through nicotinic acetylcholine receptors. These receptors are located on noncholinergic presynaptic and postsynaptic sites in the brain. Cotinine is the major metabolite of nicotine via C-oxidation. It has a biological half-life of 19 to 24 hours and can be detected in urine, serum, and saliva.

Clinical Manifestations

Adverse health effects of smoking include chronic cough, increased mucus production, and wheezing. Smoking during pregnancy is associated with an average decrease in fetal weight of 200 g.⁹ Smoking in combination with the use of estrogen-containing oral contraceptives is associated with an increased risk of myocardial infarction.¹⁰ Tobacco smoke induces hepatic smooth endoplasmic reticulum and, as a result, may also influence metabolism of drugs and of endogenously produced hormones. Phenacetin, theophylline, and imipramine are examples of drugs affected in this manner.

Treatment

Consensus panels recommend the use of the “five As” (ask, advise, assess, assist, and arrange) and of nicotine replacement therapy in adults and adolescents, although evidence of efficacy in adolescents is limited. Nicotine patch studies to date in adolescents are suggestive of a positive effect on reducing withdrawal symptoms and that pharmacotherapy should be combined with behavioral therapy to reach higher cessation and lower relapse rates. Medications such as bupropion are not approved for use in anyone younger than 18 years; however, some pilot studies in adolescents report cessation efficacy. Clinical practice guidelines are available for practical office-based counseling strategies.¹¹ Health supervision and supportive counseling are necessary components of smoking cessation management in adolescents and older adults, because relapse is common (Table 19-1).

TABLE 19-1 The Five As: Brief Strategies to Help Adolescents Quit Tobacco Use

Ask	Systematically identify all tobacco users, as well as tobacco experience at every visit. Expand the current documentation of vital signs to include information regarding tobacco use.
Advise	Strongly urge all tobacco users to quit. When providing advice, be sure to offer a clear strong, and personalized message. Clear—“I recommend you stop smoking, as it is harmful to your health.” Strong—“As our doctor, advising you to quit smoking is essential to protecting your health for the short and long term. We will work together in achieving this goal.” Personalized—Tie tobacco use to personal concerns of the patient, such as its impact on health or the high cost of addiction.
Assist	Assist the patient in the development of a quit plan, provide practical counseling, help the patient to identify social support, and recommend appropriate therapy.
	Preparation for a quit plan: Set a quit date. Involve friends, family members, or coworkers to offer support for the plan.
	Provide practical counseling: Identify triggers, events, or events that may lead to relapse. Identify and practice skills to cope. Educate with basic facts. Explain the addictive nature of tobacco-related products.
	Recommend appropriate therapy: Provide information on the use of approved pharmacotherapies.
Arrange	Schedule follow-up and provide encouragement: Establish a follow-up date soon after the quit date. Praise success, and if relapse occurs, have the patient commit to quit again.
Anticipatory guidance	Discuss family and peer use, as well as health risks associated with short and long-term use of tobacco.

From Houston TP, Adger H, Bavishi M: The AFP Guide to Teen Tobacco Use Prevention and Treatment, Illinois Academy of Family Physicians, American Academy of Pediatrics and Illinois Department of Public Health, 2002.

ALCOHOL

By 12th grade, close to three fourths of adolescents in high school report having used alcohol at some point, 25% having had their first drink before age 13 years.¹² The initiation of alcohol use at an early age is associated with an increased risk for alcohol-related problems. Although a legal drug, alcohol contributes to more deaths than do all the other illicit drugs combined. Among studies of adolescent trauma victims, alcohol is reported to be a factor in 32% to 45% of hospital admissions.¹³ Motor vehicle crashes are the most frequent type of event associated with alcohol use; the injuries reported span a wide variety, including self-inflicted wounds. Adolescents with alcohol-positive findings were also more likely to report a history of prior injury.² A study by the Institute of Medicine calls for U.S. society at large to address the underage drinking crisis responsible for costly traffic fatalities, violent crime, and other negative behaviors in youth.¹⁴

Pharmacology and Pathophysiology

Alcohol (ethyl alcohol or ethanol) is rapidly absorbed in the stomach and is transported to the liver and metabolized by two pathways. The primary pathway involves removal of two hydrogen atoms to form acetaldehyde, a reaction catalyzed by alcohol dehydrogenase through reduction of a cofactor nicotinamide-adenine dinucleotide. The removed hydrogen atoms supply energy (7.1 kcal/g of alcohol) and contribute to the excess synthesis of triglycerides, a phenomenon that is responsible for producing a fatty liver, even in persons who are well nourished. Engorgement of hepatocytes with fat causes necrosis, triggering an inflammatory process (alcoholic hepatitis), which is followed by fibrosis, the hallmark of cirrhosis. Early hepatic involvement may result in elevation in glutamyl transpeptidase and serum glutamic-pyruvic transaminase levels.

The second metabolic pathway, which is used at high serum alcohol levels, involves the microsomal system of the liver, in which the cofactor is reduced nicotinamide-adenine dinucleotide phosphate. The net effect of activation of this pathway is to decrease metabolism of drugs that share this system and to allow for their accumulation, enhanced effect, and possible toxicity (e.g., drinking alcohol and ingesting tranquilizers results in the potentiation of each).

Clinical Manifestations

Alcohol acts primarily as a central nervous system (CNS) depressant. It produces euphoria, grogginess, and talkativeness; impairs short-term memory; and increases the pain threshold. Alcohol’s ability to produce vasodilation and hypothermia is also centrally mediated. At very high serum levels, respiratory depression occurs. Alcohol’s inhibitory effect on pituitary antidiuretic hormone release is responsible for its diuretic effect. The gastrointestinal complications of alcohol use can occur as a result of a single large ingestion. The most common is acute erosive gastritis, which is manifested by epigastric pain, anorexia, vomiting, and guaiac-positive stools. Less commonly, vomiting and midabdominal pain may be caused by acute alcoholic pancreatitis; diagnosis is confirmed by the finding of elevated serum amylase and lipase activities.

In addition to the general risk factors noted for substance use, a positive family history of alcohol abuse is significant. The genetic influences for the predisposition to alcoholism are supported by family, twin, and adoption studies.¹⁵^–¹⁸ Children of alcoholic parents demonstrate a threefold to ninefold increased risk for alcoholism.

The alcohol overdose syndrome should be suspected in any teenager who appears disoriented, lethargic, or comatose. Although the distinctive aroma of alcohol may assist in diagnosis, confirmation by analysis of blood is recommended. There is a high correlation between results obtained by serum and breath analyses; therefore, the latter method may be reliable. At serum levels greater than 200 mg/dL, the adolescent is at risk of respiratory depression, and levels greater than 500 mg/dL (median lethal dose) are usually associated with a fatal outcome. When the level of depression appears excessive for the reported blood level, head trauma or ingestion of other drugs should be considered as possible confounding factors.

Treatment of Acute Alcohol Overdose Syndrome

The usual mechanism of death from the alcohol overdose syndrome is respiratory depression, and artificial ventilatory support must be provided until the liver can eliminate sufficient amounts of alcohol from the body. In a naive drinker, it generally takes about 20 hours to reduce the blood level of alcohol from 400 mg/dL to zero. Dialysis should be considered when the blood level is higher than 400 mg/dL. As a follow-up to acute management, patients can benefit from further assessment and referral for treatment of an identified alcohol use disorder. In emergency room settings, even brief interventions have shown some success in decreasing alcohol use and alcohol-related problems in adolescents.

INHALANTS

Young adolescents are attracted to these substances because of their rapid action, easy availability, and low cost. The inhalants most popular among adolescents are glue, gasoline, and volatile nitrites. “Huffing”—directly inhaling, or inhaling deeply from a paper bag containing a chemical-soaked cloth—is the common method used by teenagers.

Clinical Manifestations

The major effects of inhalants are psychoactive. Toluene, the main ingredient in airplane glue and some rubber cements, causes relaxation and hallucinations for up to 2 hours. Tolerance and physical dependence may occur. Gasoline, a substance popular among some adolescents, contains a complex mixture of organic solvents. Euphoria is followed by violent excitement, and coma may result from prolonged or rapid inhalation. Volatile nitrites, such as amyl nitrite, butyl nitrite, and related compounds marketed as room deodorizers, are used as euphoriants, enhancers of musical appreciation, and aphrodisiacs among older adolescents and young adults. Their use may result in headaches, syncope, and lightheadedness; profound hypotension and cutaneous flushing, followed by vasoconstriction and tachycardia; transiently inverted T waves and depressed ST segments on electrocardiography; methemoglobinemia; increased bronchial irritation; and increased intraocular pressure.

Complications

Toluene-based products such as airplane glue have been responsible for a wide range of complications related to chemical toxicity, to the method of administration (e.g., in plastic bags, with resultant suffocation), and to the often dangerous setting in which the inhalation occurs (e.g., inner-city roof tops). Gasoline toxicity is acute and chronic. Death in the acute phase may result from cerebral or pulmonary edema or myocardial involvement. Chronic use may cause pulmonary hypertension, restrictive lung defects or reduced diffusion capacity, peripheral neuropathy, acute rhabdomyolysis, hematuria, tubular acidosis, and possibly cerebral and cerebellar atrophy. Other behavioral disturbances such as inattentiveness, lack of coordination, and general disorientation have been linked to chronic solvent abuse.

Because of its brief effect, inhalant use is unlikely to be diagnosed unless there is a complication or death from use. Complete blood cell counts, coagulation studies, and hepatic and renal function studies may reveal the complications. In extreme intoxication, a user may manifest symptoms of restlessness, general muscle weakness, dysarthria, nystagmus, disruptive behavior, and occasionally hallucinations; thus, inhalant use is part of the differential diagnosis for acute intoxication of an adolescent. Toluene is excreted rapidly in the urine as hippuric acid, and the residual is detectable in the serum by gas chromatography.

Treatment of Acute Intoxication/Overdose

Treatment is generally supportive and directed toward control of arrhythmia and stabilization of respirations and circulation.

COCAINE

Cocaine, an alkaloid extracted from the leaves of the South American Erythroxylon coca, is supplied as the hydrochloride salt in crystalline form. It is rapidly absorbed from the nasal mucosa, detoxified by the liver, and excreted in the urine as benzoyl ecgonine. Its half-life is slightly more than 1 hour. The perceived effect of “snorting” cocaine may be influenced by some of the many diluents now being added to or actually substituted for the drug (heroin, amphetamines, phencyclidine, or fillers such as mannitol or quinine). Smoking the cocaine alkaloid (“freebasing”) in pipes or cigarettes, mixed with tobacco, marijuana, or parsley, or as a paste, has become a popular method of use.

Accidental burns are potential complications of this practice. With crack cocaine, the smoker feels “high” almost immediately. The risk of addiction with this drug is higher, and the addiction more rapidly progressive, than from snorting cocaine. Tolerance develops, and the user must increase the dose or change the route of administration, or both, to achieve the same effect.

Clinical Manifestations

Cocaine produces euphoria, increased motor activity, decreased fatigability, and, occasionally, paranoid ideation. Its sympathomimetic properties are responsible for pupillary dilatation, tachycardia, hypertension, and hyperthermia. Binge patterns of use are common. Neurological effects such as dizziness, paresthesia, and seizures can occur. Use in group settings has been associated with sexual promiscuity and increased risks of acquiring sexually transmitted infections. Lethal effects are possible, especially when cocaine is used in combination with other drugs, such as heroin, in an injectable form known as a “speedball.” Pregnant women who use cocaine place their fetus at risk for premature delivery, complications of low birth weight, and possibly congenital malformations and developmental disorders.

AMPHETAMINES

Stimulants, particularly amphetamines, are among the most frequently reported illicit drugs other than marijuana used by high school students. Methamphetamine, commonly known as “ice,” accounts for more than 25% of stimulant use. Methamphetamine is particularly popular among adolescents and young adults because of its potency and ease of absorption. It can be ingested by snorting, by smoking, orally, or by absorption across mucous membranes, such as vaginal mucosa. Its use is especially common in the western and southwestern regions of the United States. Amphetamines have multiple CNS effects, among them the release of neurotransmitters and an indirect catecholamine agonist effect. In high doses, they may also affect serotonergic receptors.

Clinical Manifestations

The effects of amphetamines can be dose related. High doses produce slowing of cardiac conduction in the face of ventricular irritability. Hypertensive and hyperpyrexic episodes can occur, as can seizures. Binge effects result in the development of psychotic ideation with the potential for sudden violence. Cerebrovascular damage and psychosis can result from chronic use. There is a withdrawal syndrome associated with amphetamine use, with early, intermediate, and late phases. The early phase is characterized as a “crash” phase with depression, agitation, anergia, and desire for more of the drug. Loss of physical and mental energy, limited interest in the environment, and anhedonia characterize the intermediate phase. In the final phase, drug craving returns, often triggered by particular situations or objects.

Treatment of Acute Intoxication

Agitation and delusional behaviors can be treated with haloperidol or droperidol. Phenothiazines are contraindicated; they may cause a rapid drop in blood pressure or seizure activity. Other supportive treatment consists of a cooling blanket for hyperthermia and treatment of the hypertension and arrhythmias, which may respond to sedation with lorazepam (Ativan) or diazepam (Valium).

OPIATES

Heroin is hydrolyzed to morphine, which undergoes hepatic conjugation with glucuronic acid before excretion, usually within 24 hours of administration. The route of administration influences the timing of the onset of action. When the drug is inhaled (“snorted”), almost 30 minutes are required before the desired effect is achieved. Ingestion through the subcutaneous route (“skin-popping”), produces the effect within minutes; when the drug is injected intravenously, the effect is immediate. Tolerance develops with regard to the euphoric effect and only rarely to the inhibitory effect on smooth muscle, which causes both constipation and miosis.

Clinical Manifestations

The clinical manifestations are determined by the pharmacological effects of heroin or its adulterants, combined with the conditions and the route of administration. The cerebral effects include euphoria, diminution in pain sensation, and pinpoint pupils. An effect on the hypothalamus is suggested by the lowering of body temperature. Vasodilation is a major cardiovascular manifestation related to the method of administration of the drug. Respiratory depression is mediated centrally and is characterized by alveolar hypoventilation.

Pulmonary edema is common in death from the overdose syndrome, but it may also be an incidental radiological finding in an otherwise asymptomatic heroin abuser. The most common dermatological lesions are the “tracks,” the hypertrophic linear scars that follow the course of large veins. Smaller, discrete peripheral scars, resembling healed insect bites, may be easily overlooked. Injection of heroin subcutaneously may lead to fat necrosis, lipodystrophy, and atrophy over portions of the extremities.

Attempts at concealment of these stigmata may include amateur tattoos in unusual sites. Abscesses secondary to unsterile techniques of drug administration are commonly found. A heroin user may resort to prostitution to support his or her habit, thus increasing the risk of acquiring sexually transmitted diseases (including human immunodeficiency virus infection), pregnancy, and other hazards.

Constipation results from decreased smooth muscle propulsive contractions and increased anal sphincter tone. Hepatic enzyme levels are frequently elevated in heroin users, and there may be serological evidence of viral infection with hepatitis B and/or C. The absence of sterile technique in injection may lead to cerebral microabscesses or endocarditis, usually caused by Staphylococcus aureus. Abnormal serological reactions, including false-positive Venereal Disease Research Laboratory and latex fixation test results, are also common.

Withdrawal Syndrome

After a period of 8 hours or more without heroin, the addicted individual undergoes, during a period of 24 to 36 hours, a series of physiological disturbances referred to collectively as withdrawal or the abstinence syndrome. The earliest sign is excessive yawning, followed by lacrimation, mydriasis, insomnia, “goose flesh,” cramping of the voluntary musculature, hyperactive bowel sounds and diarrhea, tachycardia, and systolic hypertension. The administration of buprenorphine, an opiate agonist/antagonist is the most common method of detoxification. Another commonly used agent is methadone. This synthetic opiate is effective by the oral route and is pharmacologically similar to heroin, except for its lack of euphoric effect.

Overdose Syndrome

The overdose syndrome is an acute reaction after the administration of an opiate. It is the leading cause of death among drug users. The clinical signs include stupor or coma, seizures, miotic pupils (unless severe anoxia has occurred), respiratory depression, cyanosis, and pulmonary edema. The differential diagnosis includes CNS trauma, diabetic coma, and hepatic (and other) encephalopathy, as well as overdose of alcohol, barbiturates, phencyclidine, or methadone. Diagnosis of opiate toxicity is facilitated by intravenous administration of the opiate antagonist naloxone, 0.01 mg/kg (2 mg is a common initial dose for an adolescent or adult), which causes dilation of pupils constricted by the opiate. Diagnosis is confirmed by the finding of morphine in the serum. The treatment of acute overdose consists of maintaining adequate oxygenation and, when necessary, continued administration of naloxone every 5 minutes to improve and maintain adequate ventilation. Naloxone may have to be continued for 24 hours if methadone, rather than shorter-acting heroin, has been taken.

CLUB DRUGS

Flunitrazepam (Rohypnol), 3,4-methylenedioxymethamphetamine (MDMA), γ-hydroxybutyrate (GHB), and ketamine are among a group of drugs used by adolescents and young adults who are part of a nightclub, bar, rave, or trance scene; the drugs are often referred to as club drugs. Raves and trance events are generally night-long dances, often held in warehouses. Although many people who attend raves and trances do not use drugs, those who do may be attracted to their generally low cost and to the intoxicating highs that are said to deepen the rave or trance experience. Studies have shown changes to critical parts of the brain from use of these drugs.

MDMA

MDMA is a synthetic, psychoactive drug chemically similar to the stimulant methamphetamine and the hallucinogen mescaline. Street names for MDMA include “ecstasy,” “XTC,” and “hug drug.” In high doses, MDMA can interfere with the body’s ability to regulate temperature. This can lead to a sharp increase in body temperature (hyperthermia), resulting in liver, kidney, and cardiovascular system failure. Research in humans suggests that chronic MDMA use can lead to changes in brain function, affecting cognitive tasks and memory. MDMA can also lead to symptoms of depression several days after its use. These symptoms may occur because of MDMA’s effects on serotonergic neurons. The serotonin system plays an important role in regulating mood, aggression, sexual activity, sleep, and sensitivity to pain. A study in nonhuman primates showed that exposure to MDMA for only 4 days caused damage of serotonin nerve terminals that was evident 6 to 7 years later.

γ-Hydroxybutyrate

Since about 1990, GHB has been abused in the United States for its euphoric, sedative, and anabolic (body building) effects. GHB is colorless, tasteless, and odorless and has been involved in poisonings, overdoses, date rapes, and deaths. It can be added to beverages and unknowingly ingested. It is a CNS depressant that was widely available over the counter in health food stores during the 1980s and until 1992. It was purchased largely by body builders to aid in fat reduction and muscle building. Street names include “liquid ecstasy,” “soap,” “easy lay,” “vita-G,” and “Georgia home boy.” Coma and seizures can occur after abuse of GHB. Combining use with other drugs such as alcohol can result in nausea and breathing difficulties. GHB may also produce withdrawal effects, including insomnia, anxiety, tremors, and sweating.

Ketamine

Ketamine is an anesthetic that has been approved for both human and animal use in medical settings since 1970; about 90% of the ketamine legally sold is intended for veterinary use. It can be injected or snorted. Ketamine is also known as “special K” or “vitamin K.” Certain doses of ketamine can cause dreamlike states and hallucinations. In high doses, ketamine can cause delirium, amnesia, impairment of motor function, high blood pressure, depression, and potentially fatal respiratory problems.

Flunitrazepam (Rohypnol)

Flunitrazepam belongs to the benzodiazepine class of drugs. It can produce “anterograde amnesia,” and may be lethal when mixed with alcohol and/or other depressants. It is not approved for use in the United States, and its importation is banned. Illicit use of flunitrazepam started appearing in the United States in the early 1990s, where it became known as “rophies,” “roofies,” “roach,” and “rope.”

Hallucinogens

Lysergic acid (LSD; also known as “acid,” “big[d,]” and “blotters”) is one of the constituents found in rye fungus. Morning glory seeds contain lysergic acid derivatives, although the commercially packaged varieties have often been treated with toxic chemicals such as insecticides and fungicides. Although the specific mechanisms of action of LSD are still under study, it is proposed to alter neurotransmitters mediated by serotonin. LSD is a very potent hallucinogen; doses as low as 20 mg cause effects in some individuals. Its high potency allows effective doses to be applied to objects as small as postage stamps and paper blotters. It is rapidly absorbed from the gastrointestinal tract. The onset of action can occur in between 30 and 60 minutes, and its action peaks between 2 and 4 hours. By 10 to 12 hours, the user returns to the predrug state.

CLINICAL MANIFESTATIONS

The effects of LSD can be divided into three categories: somatic (physical effects), perceptual (altered changes in vision and hearing), and psychic effects (changes in sensorium). The common somatic symptoms are dizziness, dilated pupils, nausea, flushing, elevated temperature, and tachycardia. The sensation of synesthesia, such as “seeing” smells and “hearing” colors, has been reported with LSD use. Delusional ideation, body distortion, and suspiciousness to the point of toxic psychosis are the more serious of the psychic symptoms.

TREATMENT

An individual is considered to have a “bad trip” when the setting causes the user to become terrified or panicked. These episodes should be treated by removing the individual from the aggravating situation or setting and attempting to reestablish contact with reality through calm verbal interaction. Any physical complications such as hyperthermia, seizure, or hypertension should be treated supportively. “Flashbacks”—LSD-induced states that occur after the drug has worn off—and tolerance to the effects of the drug are additional complications of its use.

Phencyclidine

Phencyclidine (also known as “PCP,” “angel dust,” “hog,” “peace pill,” and “sheets”) is an arylcyclohexalamine whose popularity is related, in part, to its ease of synthesis in home laboratories. One of the by-products of home synthesis causes cramps, diarrhea, and hematemesis. The drug is thought to potentiate adrenergic effects by inhibiting neuronal reuptake of catecholamines. Phencyclidine is available as a tablet, liquid, or powder, which may be used alone or sprinkled on cigarettes (“joints”). The powders and tablets generally contain 2 to 6 mg of phencyclidine, whereas joints contain an average of 1 mg for every 150 mg of tobacco leaves, or approximately 30 to 50 mg per joint.

CLINICAL MANIFESTATIONS

The clinical manifestations are dose related. Euphoria, nystagmus, ataxia, and emotional lability occur within 2 to 3 minutes after smoking 1 to 5 mg and last for hours. Hallucination may involve bizarre distortions of body image that often precipitate panic reactions. With doses of 5 to 15 mg, a toxic psychosis may occur, with disorientation, hypersalivation, and abusive language, lasting for more than 1 hour. Hypotension, generalized seizures, and cardiac arrhythmias commonly occur with plasma concentrations from 40 to 200 mg/dL. Death from hypertension, hypotension, hypothermia, seizures, and trauma has been reported during psychotic delirium. The coma caused by phencyclidine may be distinguished from that caused by the opiates by the absence of respiratory depression; the presence of muscle rigidity, hyperreflexia, and nystagmus; and lack of response to naloxone. Phencyclidine psychosis may be difficult to distinguish from schizophrenia. In the absence of history of use, analysis of urine must be depended on for diagnosis.

TREATMENT OF ACUTE INTOXICATION

Management of the phencyclidine-intoxicated patient includes placement in a darkened, quiet room on a floor pad, to provide safety from injury. Gastric absorption is poor; thus, for recent oral ingestion, induction of emesis or gastric lavage is useful. Diazepam, in a dose of 5 to 10 mg orally or 2 to 5 mg intravenously, may be helpful if the patient is agitated and not comatose. Rapid excretion of the drug is promoted by acidification of the urine. Supportive therapy for the comatose patient is indicated, with particular attention to hydration, which may be compromised by phencyclidine-induced diuresis.

Developmental and Behavioral Implications of Long Term Use of Drugs of Abuse

Although each of the drugs of abuse may have individual variation, they are similar in that they have a common pathway of biochemical interactions that are channeled through the reward system in the brain, and they all work by causing changes in brain chemistry. It is these changes in brain chemistry that lead to the experience of euphoria and secondarily to changes in behavior, and the changes in behavior are what often bring individuals to medical attention. Therefore, including drug use in the list of possible causes of unexplained behavior change, particularly in adolescents, is important. Moreover, early identification and intervention can play an important role in preventing many of the consequences that are associated with repeated and chronic use.

FAMILY EFFECTS OF ALCOHOL AND OTHER DRUG USE

Children of Parents Affected by Substance Use Disorders

The familial effects of substance use disorders, particularly for alcoholism, are well documented. Approximately one fourth of all children in the United States younger than 18 years are exposed to familial alcohol abuse or alcohol dependence.¹⁹ Furthermore, it has been shown that children of an alcoholic parent are overrepresented in the mental health and general medical systems. They have higher rates of injury, poisoning, admissions for mental disorders and substance abuse, and general hospital admissions; longer lengths of stay; and higher total health care costs. Children of an alcoholic parent are at higher risk for learning disabilities. The effects of prenatal exposure to alcohol and the fetal alcohol syndrome (FAS)—the term generally applied to children who have been exposed and display a certain constellation of symptoms, such as growth retardation, CNS involvement to include behavioral and/or intellectual impairment, and characteristic facies (short palpebral fissures, thin upper lip, and elongated, flattened midface and philtrum)—are well known.

Some studies have demonstrated that parental alcoholism is associated with increased risk for attention-deficit/hyperactivity disorder (ADHD) in offspring, conduct disorder, or anxiety disorders. These offspring have been shown to have more diagnosable psychiatric disorders (i.e., depression, ADHD, conduct disorder) and lower reading and math achievement scores.

Children of substance-abusing parents are at risk for neglect. These children appear to have more behavior disorders, anxiety disorders, poorer competency scores, and higher scores on both internalizing and externalizing subscales of the Child Behavior Checklist than do control groups of children.^20,²¹ Other investigators have questioned whether the increased psychiatric problems seen in these children are caused by the parental substance abuse or by the comorbid psychiatric disorders in these parents.²² For example, there may be a link between both substance abuse and antisocial personality disorder (a frequent comorbid psychiatric disorder) in parents and conduct disorder in offspring or a link between both substance abuse and major depression in parents and conduct disorder in offspring.^23,²⁴ Finally, the children of substance-abusing parents are at extreme risk to abuse substances themselves. This increased risk arises from two phenomena: First, there is a genetic predisposition for the development of substance use disorders; second, these children often receive inadequate parental supervision, which itself is a risk factor for the initiation of substance abuse.^25,²⁶

Core Competencies for Addressing Children and Adolescents in Families Affected by Substance Use Disorders

National leaders from pediatrics, family medicine, nursing, social work, and adolescent health have previously collaborated in the development of a set of core competencies (Core Competencies for Involvement of Health Care Providers in the Care of Children and Adolescents in Families Affected by Substance Abuse) that outline the core knowledge, attitudes, and skills that are essential for meeting the needs of children and youth affected by substance use disorders in the family.²⁷ These core competencies outline a model of practice and delineate the desired knowledge and skills of health professionals in this area. The model is an attempt to recognize and account for individual differences among health providers. Furthermore, it represents a recognition that although primary health and behavioral professionals may be responsible for identifying the problem, they should not be expected to manage it by themselves. Accordingly, three distinct levels of care are articulated that allow for flexibility of individuals to choose their role and degree or level of involvement (Table 19-2). A baseline or minimal level (level I) of competence is established, and all primary health care professionals should strive to achieve it. However, most developmental-behavioral pediatricians want and are expected to do more than is indicated in the level I competencies. For health professionals who desire competence at a higher level (levels II and III), a different and more advanced set of knowledge and skills is required.

TABLE 19-2 Core Competencies for Involvement of Health Care Providers in the Care of Children and Adolescents in Families Affected by Substance Abuse

Level I

For all health professionals with clinical responsibility for the care of children and adolescents:

1. Be aware of the medical, psychiatric, and behavioral syndromes and symptoms with which children and adolescents in families with substance abuse present.

2. Be aware of the potential benefit to both the child and the family as a result of of timely and early intervention.

3. Be familiar with community resources available for children and adolescents in families with substance abuse.

4. As part of the general health assessment of children and adolescents, include appropriate screening for family history or current use of alcohol and other drugs.

5. On the basis of screening results, determine family resource needs and services currently being provided, so that an appropriate level of care and follow-up can be recommended.

6. Be able to communicate an appropriate level of concern, and offer information, support, and follow-up.

Level II

In addition to level I competencies, health care providers accepting responsibility for prevention, assessment, intervention, and coordination of care of children and adolescents in families with substance abuse should

1. Apprise the child and family of the nature of alcohol and other drug abuse and dependence and its effect on all family members and strategies for achieving optimal health and recovery.

2. Recognize and treat, or refer, all associated health problems.

3. Evaluate resources—physical health, economic, interpersonal, and social—to the degree necessary to formulate an initial management plan.

4. Determine the need for involving family members and significant other persons in the initial management plan.

5. Develop a long-term management plan in consideration of these standards and with the child’s or adolescent’s participation.

Level III

In addition to level I and level II competencies, the health care provider with additional training who accepts responsibility for long-term treatment of children and adolescents in families with substance abuse should

1. Acquire knowledge, by training and experience, in the medical and behavioral treatment of children in families affected by substance abuse.

2. Continually monitor the child’s or adolescent’s health needs.

3. Be knowledgeable about the proper use of consultations.

4. Throughout the course of health care treatment, continually monitor and treat, or refer for care, any psychiatric or behavioral disturbances.

5. Be available to the child or adolescent and the family, as needed, for ongoing care and support.

EARLY IDENTIFICATION OF SUBSTANCE USE DISORDERS

In one study, 38% of Americans stated they had a family member with alcoholism.²⁸ Because of its high prevalence and lack of socioeconomic boundaries, developmental-behavioral pediatricians should expect to encounter families with alcoholism and other drug use disorders routinely. Several studies suggest strongly that children of women who are problem drinkers have an increased risk of experiencing serious, unintentional injuries and that children exposed to two parents with alcohol problems are at even greater risk.²⁹ Studies of the link between parental substance abuse and child maltreatment suggest that substance abuse is present in at least half of families known to the public child welfare system.³⁰

If these families and children are identified early, some of the associated morbidity might be avoided. Developmental-behavioral pediatricians and other child and adolescent health care providers can have a tremendous influence on families of substance-abusing parents because of their understanding of family dynamics and their close long-standing relationship with the family. Information about family alcohol and other drug use should be obtained as part of routine history taking and when there are indications of family dysfunction, child behavioral or emotional problems, school difficulties, and recurring episodes of apparent accidental trauma and in the setting of recurrent or multiple vague somatic complaints by the child or adolescent. In many instances, family problems with alcohol or drug use are not blatant; rather, their identification requires a deliberate and skilled screening effort.

Another study indicated that fewer than half of pediatricians ask about problems with alcohol when taking a family history.³² In contrast, Graham and colleagues³³ found that patients wanted their physicians to ask about family alcohol problems and believed that the physician could help them and/or the abusing family member deal with their problems. A family history of alcohol and other drug abuse is more likely than many other aspects of history to affect a child’s immediate and future health. A thorough understanding of family members’ use of alcohol or other drugs is as important as a history for hypertension, cancer, or diabetes mellitus. In addition, family problems with alcohol or other drugs can jeopardize a parent’s ability to carry out necessary therapeutic regimens for their child.

The primary task of initial screening is to identify families with alcohol or other drug use problems that put their children and youths at risk for associated physical or mental health complications. Screening questions help identify individuals most likely to have a problem related to alcohol or other drug use. Information gathered should help the clinician decide whether there is a need for additional assessment by either the primary provider or a consultant. Screening is an important and time-efficient first step to identifying the probable existence of a problem, but it differs from assessment and establishing a final diagnosis. Assessment is a more lengthy and structured process designed to determine the extent of the problem, explore comorbid conditions, and assist in treatment planning for the entire family.

Screening can occur at three different levels. The first is screening the child or adolescent for physical or mental health problems that may be associated with alcohol- or drug use-related problems among other family members. As the child grows older, it becomes increasingly important to establish diagnostic concerns and related treatment plans that can be implemented with the child or adolescent directly. Many older children and adolescents can be assessed fully without need for referral.

A second screening concern relates to identifying family members at high risk for substance use problems. Family members who appear to be at high risk for substance use disorders probably need referral for more detailed assessment by substance abuse professionals. Screening for and intervening with other family members affected by the family situation are necessary endeavors to maximize the health of the child.

Third, as adolescents grows older, it is increasingly important to identify their own alcohol and other drug use problems, because children from homes or who have parents with substance use disorders are at higher risk for developing their own problems with alcohol and other drugs.

Although the ability to perform an in-depth assessment and make an actual diagnosis may be beyond the time limitations and skills of many practitioners, all developmental-behavioral pediatricians are responsible for screening and initial management or referral. The difficulty encountered sometimes in obtaining accurate social and psychological histories and behavioral self-reports related to alcohol or other drug use by family members should not deter the clinician from including such histories and interviews as part of routine office procedures.

INTERVIEWING CHILDREN, YOUTH, AND FAMILIES

Since the 1980s, there has been an increasing level of interest in, and appreciation for, the complexity of communication skills needed to establish effective physician-patient/family relationships. In efforts to organize concepts and knowledge about medical interviewing, investigators have established useful models for the medical interview.³⁴ In one particularly useful model for child and adolescent health care, the medical interview is viewed as having three central functions: (1) to collect information regarding a potential problem; (2) to respond to the patient and family’s emotions; and (3) to educate the family and influence behavior.³⁵ These functions are highly germane to the identification and intervention of children living with substance-abusing parents, because all three functions may need to occur simultaneously and are necessary to promote the well-being of these children adequately.