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Substance use and abuse in adolescence
is a major public health problem. Identification of adolescents
at risk or those currently abusing substances in the health care
setting is often missed, or the substance abuse undertreated. Although
the prevalence for substance use over the past decade has decreased
from higher rates in the late 1970s, the 2007 lifetime prevalence
rates of alcohol use and cigarette smoking among adolescents remain
high at 72.2% and 46.2% respectively.1,2 Lifelong substance
use habits are formed during adolescence and young adulthood and
are associated with short-term and long-term health consequences.
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Substance use begins in adolescence or earlier. Among 8th-grade
students, the peak years for smoking initiation are between 11 and
13 years of age.1 The average age of first use
of alcohol is 14 years,3 and first marijuana use
is 16.1 years.4 The most common drugs of use and
abuse include alcohol, nicotine, and marijuana. Other substances
are drugs used as part of the nightclub/bar and trance
scenes, such as ecstasy, rohypnol, γ-hydroxybutyrate,
and ketamine. Substances also include over-the-counter drugs, such
as sleeping aids, cough and cold medicines and inhalants; and prescription
medications, such as pain relievers, amphetamines, and stimulants.
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There is no pathognomonic clinical presentation of drug abuse.
Signs of drug abuse in an adolescent may manifest in an increasing
degree of emotional and physical isolation from the rest of the
family, absent or hostile communication, deteriorating school attendance/performance,
decrease in athletic performance, a change in peer group, crime
involvement, and unplanned/unsafe sexual practices. Known risk
factors for the development of substance abuse and dependence are
multifold and include male gender, household member drug abuse (eg,
by parents), use by peers, earlier age of onset, cognitive disability,
and psychiatric comorbidities such as attention deficit hyperactivity
disorder and depression.
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Common Substances of
Abuse
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Table 71-1 provides a summary of common substances;
examples of commercial and street drug names; route of administration;
onset of action and duration; and common intoxication effects, withdrawal
symptoms and potential consequences.
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++
Alcohol is fermented from fruits or grains (wine, beer), and
fortification (port, sherry), distillation (brandy, whiskey, gin,
vodka), vaporization, or condensation can increase its potency.
Ethanol content in brewed beverages is measured as “percent” (weight
to volume) and in distilled beverages as “proof” units.
In the United States, 1 proof means 0.5% alcohol, or twice
the percent (eg, 80 proof is 40% alcohol). Ethanol content
is highly variable (beer, 3–6%; wine, 12–14%;
distilled spirits, 40–60%).
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Clinical Pharmacology
and Toxicology
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Ethanol acts as a central nervous system depressant with local
and general anesthetic properties and competes with antidiuretic
hormone. During acute intoxication, its actions can result in considerable
fluid loss. Ethanol is rapidly absorbed from the stomach (20%)
and small intestine (80%). Metabolism occurs almost exclusively
in the liver by alcohol dehydrogenase with the remainder excreted
in the urine. Blood ethanol level decreases at a fixed rate of about
1 ounce (30 cc) per hour, or 28 mg/dL/hr, or 6
mmol/L/hr.
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Alcohol use can result in addiction and physical dependence (Table 71-1). Laboratory findings may include
elevated osmolar gap, hypokalemia, and metabolic (lactic) acidosis.
Hypoglycemia may present as coma or convulsions more than 3 hours
postingestion and can occur with blood ethanol levels as low as
50 mg/dL.
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In the acutely intoxicated patient, management depends on severity.
Mild intoxication (< 350 mg/kg of ethanol) can be managed
with close observation, hydration, and analgesics. Moderate to severe
intoxication (> 350 mg/kg of ethanol, or blood alcohol
level [BAL] > 300 mg/dL) requires provision
of appropriate airway management and supportive care. Normal doses
of activated charcoal do not effectively adsorb ethanol. Hemodialysis should
be considered in patients with BAL greater than 500 mg/dL
or clinical deterioration despite conservative support.
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Treatment for withdrawal depends on the degree of symptoms. In
mild withdrawal, rest and hydration are sufficient. For severe symptoms,
use of benzodiazepines may be helpful. For seizures, treat with
diazepam or phenytoin. For hallucinosis or delirium, treat with
haloperidol.
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Early intervention in the outpatient setting depends on the degree
of the alcohol problem; options range from brief office-based interventions
to residential treatment programs. Pharmacologic interventions are
limited with regard to adolescent alcohol use disorders.5
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Tobacco remains the leading cause of preventable deaths6 in
the United States and is one of the most heavily used addictive
drugs. Because a majority of chronically addicted adult smokers
begin before the age of 18, tobacco dependence should be viewed
as a pediatric disease. There is increasing evidence that habituation
to tobacco occurs at relatively low levels of use and that the pharmacokinetics
of tobacco metabolism may be different in adolescence than in adults.7
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Clinical Pharmacology
and Toxicology
++
Derived from the tobacco plant, nicotine is a natural alkaloid
and acts as a central nervous system stimulant. Metabolism occurs
in the liver and excretion by the kidneys. A single cigarette contains
8 to 9 mg of nicotine, and about 1 mg is delivered to the user while smoking.
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Nicotine is highly addictive and toxic, and dependence can develop quickly
(Table 71-1). In addition to nicotine, tars
and other carcinogens in tobacco products are known to be associated
with malignancies, and carbon monoxide in smoke is known to increase
the risk of cardiovascular disease. Secondhand smoke has also been
shown to cause lung cancer in adults and greatly increase the risk
of respiratory illnesses in children and of sudden infant death.
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Withdrawal symptoms are less severe in those who quit gradually.
Relapse is frequent, especially in the first few weeks, but diminishes
considerably after 3 months. Brief, office-based counseling has
been shown to be effective in helping patients consider quitting. Pharmacological
combined with psychological treatment results in the highest long-term
abstinence rates. Nicotine replacement therapy comes in many forms,
such as chewing gum, transdermal patches, nasal sprays, and inhalers.
Only nicotine chewing gum and transdermal patches are FDA approved
for use in adolescents. Bupropion plus brief counseling has short-term
efficacy in helping adolescents quit smoking.8 Bupropion
helps to control nicotine craving or thoughts about cigarette use.
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Cannabis is a collective term for the various preparations
of the hemp plant Cannabis sativa. Its potency
in street samples has increased over the past 2 decades. It
is the most common illicit drug used by children and adolescents
in the United States, and its use may precede the use of other more
dangerous drugs, is not innocuous, and can have significant social,
academic, developmental, and legal ramifications.9
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Clinical Pharmacology
and Toxicology
++
The active ingredient in cannabis is Δ-9-tetrahydrocannibol
(THC), which is known to bind specific central nervous system receptors.
The exact mechanism by which THC produces clinical effects is unknown.
The liver metabolizes THC, but 20% is excreted unchanged
in the urine and feces. Approximately 20% of an inhaled
dose is absorbed, compared to less than 10% after ingestion.
THC is highly lipid soluble, and almost 100% is bound to
plasma proteins. Regardless of THC content, the amount of tar inhaled
and level of carbon monoxide absorbed are 3 to 5 times greater than
among tobacco smokers.
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Animal studies suggest physical dependence can develop, and some people
report withdrawal symptoms (Table 71-1).
Reproductive effects include gynecomastia (reversible), decreased
sperm count and motility (reversible), decreased testosterone levels,
and pubertal arrest. Use of cannabis potentiates
sedation when used with alcohol and other sedatives.
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Therapeutic treatment programs may be indicated for chronic users.
For acute intoxication, anxiety and panic attacks can be treated
with benzodiazepines and a calm environment. Gastric emptying and
activated charcoal may be considered for accidental ingestion. No
treatment is necessary for withdrawal symptoms.
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Screening and Counseling
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The American Academy of Pediatrics recommends annual screening
of adolescents for tobacco, alcohol, and illicit drug use, including other
abusable drugs (eg, over-the-counter products, sports supplements,
and prescription drugs).10 Beyond the annual visit,
it also emphasizes that pediatricians incorporate discussions about
substance abuse in all routine health care visit to identify at-risk
individuals.11
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When obtaining a substance use history, the provider should create
an environment of mutual respect and trust and utilize an empathetic approach
to engage the adolescent patient. The adolescent patient should
be interviewed privately and assessed regarding the types of substances
used, route of administration, reason for use, pattern of use (eg,
frequency, quantity, binging behaviors), settings in which drug
use occurs, and consequences of use including health and legal problems.
Also assess for family history of substance abuse and psychiatric
illness.
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Optimal prevention counseling on substance use and abuse should
be initiated in the preadolescent years, and techniques of using refusal
skills should be incorporated as a tool. For alcohol users, counseling
should include the consequences of intoxication, particularly drinking
and driving. For tobacco and marijuana users, counseling should
include advice to quit.
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Physician diagnosis and recommendations should be unequivocal
and nonjudgmental. Identify the patient’s
state of readiness for change using a framework such as Prochaska’s theoretical
model for change (or stages of change) to identify whether the patient
is in a precontemplative, contemplative, determination, action,
or maintenance stage for change.12 Depending on
the patient’s stage, the clinician can tailor counseling
accordingly. Patient relapse is common, should be anticipated, and should
not be considered as failure. It is also common for patients to
cycle through stages of change multiple times.
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The treatment process must also address the adolescent’s
experience, including his or her developmental stage, age, gender,
cultural background, disability status, and readiness to change.
Coercive pressure to seek treatment is generally not conducive to
behavior change. Treatment or placement should depend on where the
adolescent falls on the substance use continuum, should involve
the family, and, whenever possible, should be adolescent-specific.
Programs can include but are not limited to brief office-based interventions,
residential treatment programs, cognitive behavioral therapy, motivational
interviewing, therapeutic communities, and family therapy (Table 71-2).
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The vast majority of abused substances can be detected in the
blood or urine for days to weeks after use (see Table
71-3). Certain drugs, such as γ-hydroxybutyrate,
may not be analyzed on standard drug screens. Thus, being familiar
with an institution’s drug screens and/or making
special requests if testing is indicated may be necessary. In general,
testing should be performed on a voluntary basis with the patient’s
consent unless the patient lacks decision-making capacity or there
are strong medical indications or legal requirements to do so. The
American Academy of Pediatrics opposes involuntary testing of adolescents for drugs of abuse and
states that laboratory testing for drugs under any circumstances
is improper unless the patient and clinician can be assured that
the test procedure is valid and reliable and that patient confidentiality
is ensured.11 Home and school-based testing is
not routinely recommended. Any information obtained from drug screening
should be used for therapeutic rather than punitive purposes.
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