Download When Kids Do Drugs: Evaluation And Treatment In The Emergency

October 2006
When Kids Do Drugs:
Evaluation And Treatment In
The Emergency Department
Volume 3, Number 10
Authors
David D Nguyen, MD
Clinical Assistant Professor, Dept. of EM, University of
Texas Medical School at Houston, Assistant Medical
Director, Dept. of EM, Memorial Hermann Southeast
Hospital
It is 8 AM Saturday morning. EMS arrives with a seizing 15-year-old female who
was attending a “rave” and had been there for several hours. Her friends called
911 because she seemed disoriented and then collapsed. No other history is available as the friends were less than forthcoming when questioned about possible drug
use and did not accompany the patient to the hospital. Vital signs are remarkable
for temperature 105°F, heart rate 138, blood pressure 150/90, respiratory rate 20,
and pulse ox 97%. On examination, she is diaphoretic and actively seizing. You
immediately place the patient on 100% nonrebreather mask, establish an IV, place
her on a monitor, give her lorazepam – 2mg IV. She stops seizing within one
minute. You initiate aggressive external cooling. Her bedside blood sugar is 85.
Her mucous membranes are dry, and her teeth are clenched. Her lungs are clear to
auscultation with equal breath sounds. She has fast and thready pulses. At that
moment, two very distraught yet angry parents demand to know what is going on
with their daughter who was supposed to be spending the night at a friend’s house.
I
llicit drug use escalated in the youth population in the mid1960s and it remains a major concern for the nation. Smoking,
drinking, and drug use are leading causes of morbidity and mortality, both during adolescence and later in life. 1 A pervasive difficulty in dealing with this issue is our societal acceptance of drugs and
demand for medications to solve real or perceived health problems.
The influence of the media and medication manufacturers to take
pills fuels this drive for drugs as problem-solving measures. 2 This
article will focus on the most popular drugs of abuse as well as the
newer drugs and their clinical presentations and management.
Editorial Board
Jeffrey R. Avner, MD, FAAP, Professor
of Clinical Pediatrics, Albert
Einstein College of Medicine;
Director, Pediatric Emergency
Service, Children’s Hospital at
Montefiore, Bronx, NY.
Lance Brown, MD, MPH, FACEP,Chief,
Division of Pediatric Emergency
Medicine; Associate Professor of
Emergency Medicine and
Pediatrics; Loma Linda University
Medical Center and Children’s
Hospital, Loma Linda, CA.
T. Kent Denmark, MD, FAAP, FACEP,
Residency Director, Pediatric
Emergency Medicine; Assistant
Professor of Emergency Medicine
and Pediatrics, Loma Linda
University Medical Center and
Children’s Hospital, Loma Linda, CA.
Michael J. Gerardi, MD, FAAP, FACEP,
Assistant Director Emergency
Clinical Assistant Professor,
Services, Lebonheur Children’s
Medicine, University of Medicine
Medical Center, Memphis TN.
and Dentistry of New Jersey;
Director, Pediatric Emergency
Medicine, Children’s Medical
Center, Atlantic Health System;
Department of Emergency
Medicine, Morristown
Memorial Hospital.
Ran D. Goldman, MD, Associate
Professor, Department of
Pediatrics, University of Toronto;
Division of Pediatric Emergency
Medicine and Clinical
Pharmacology and Toxicology, The
Hospital for Sick Children, Toronto.
Martin I. Herman, MD, FAAP, FACEP,
Mark A. Hostetler, MD, MPH,
Lisa Freeman Grossheim, MD, FACEP
Assistant Professor, Dept. of EM, University of Texas
Medical School at Houston
Scott McAninch, MD
Assistant Professor, Dept. of EM, University of Texas
Medical School at Houston
Sally Henin Awad, MD, FACEP
Assistant Professor, Dept. of EM, University of Texas
Medical School at Houston
Peer Reviewers
Stephen D. Docherty, MD, FACEP, FAAEM
Assistant Professor of Clinical EM, Dept. of EM, Keck
School of Medicine, University of Southern California
Sharon Mace, MD
Associate Professor, ED, Ohio State University School
of Medicine, Director of Pediatric Education And Quality
Improvement and Director of Observation Unit,
Cleveland Clinic, Faculty, MetroHealth Medical Center,
EM Residency
CME Objectives
Upon completing this article you should be able to:
1. Recognize the clinical presentations of the most
common drugs of abuse
2. Identify and treat the complications of drugs of
abuse
3. Discuss which patients require admission and
those who may be safely discharged
4. Be familiar with the utility and limitations of
diagnostic testing in drug intoxicated patients
Date of original release: October 6, 2006.
Date of most recent review: September 1, 2006.
See “Physician CME Information” on back page.
Island Region.
Andy Jagoda, MD, FACEP, Vice-Chair
of Academic Affairs, Department of
Emergency Medicine; Residency
Robert Luten, MD, Professor,
Pediatrics and Emergency
Medicine, University of Florida,
Jacksonville, Jacksonville, FL.
Assistant Professor, Department of
Program Director; Director,
Pediatrics; Chief, Section of
International Studies Program,
FACEP, FAAEM, Associate
Emergency Medicine; Medical
Mount Sinai School of Medicine,
Clinical Professor, Children’s
Director, Pediatric Emergency
New York, NY.
Hospital and Health Center/
Department, The University of
Chicago, Pritzker School of
Medicine, Chicago, IL.
Alson S. Inaba, MD, FAAP, PALS-NF,
Pediatric Emergency Medicine
Attending Physician, Kapiolani
Medical Center for Women &
Children; Associate Professor of
Pediatrics, University of Hawaii
John A. Burns School of Medicine,
Professor of Pediatrics,
Honolulu, HI; Pediatric Advanced
Division Critical Care and
Life Support National Faculty
Emergency Services, UT Health
Representative, American Heart
Sciences, School of Medicine;
Association, Hawaii & Pacific
Tommy Y Kim, MD, FAAP, Attending
Physician, Pediatric Emergency
Department; Assistant Professor of
Emergency Medicine and Pediatrics,
Loma Linda Medical Center and
Children’s Hospital, Loma Linda, CA.
Brent R. King, MD, FACEP, FAAP,
FAAEM, Professor of Emergency
Medicine and Pediatrics; Chairman,
Department of Emergency
Medicine, The University of Texas
Houston Medical School,
Houston, TX.
Ghazala Q. Sharieff, MD, FAAP,
University of California, San
Diego; Director of Pediatric
Emergency Medicine, California
Emergency Physicians.
Gary R. Strange, MD, MA, FACEP,
Professor and Head, Department of
Emergency Medicine, University of
Illinois, Chicago, IL.
There are many different classification schemes of
the various illicit drugs. Some agents have characteristics of more than one class, such as the hallucinogenic amphetamines.
Epidemiology
At least sixteen million people in the United States
use drugs. Much of this population consists of
teenagers or adolescents or those who have started
using drugs at that age. Monitoring the Future
Survey (MTF) is an annual survey of drug abuse
among 8th, 10th, and 12th grade students that has
extensively studied drug abuse trends since 1975.
This work, in collaboration with the University of
Michigan’s Institute for Social Research and funded
by the National Institute on Drug Abuse (NIDA), has
included 8th and 10th grade students since 1991. 1
The purpose of the MTF is to demonstrate the 30
day, yearly, and lifetime use of drugs among students in the grade levels described above. Table 2
shows the annual prevalence of drug use by grade
level in 2005. 1 The risk factors for substance abuse in
juveniles are noted in Table 3. 3
The Drug Abuse Warning Network (DAWN) is
an organization that has demonstrated which drugs
are the most common ones seen in the emergency
department (ED) for a patient over 6 years old. 7
DAWN reported that just in the third and fourth
quarters of 2003, there were 627,923 visits to an ED
with a drug related problem. Half of these visits
involved a major substance of abuse with alcohol,
cocaine, and marijuana being the most commonly
abused substances. 7
The Controlled Substances Act regulates the
manufacture, possession, movement, and distribution of drugs in the U.S. It places all drugs in one of
five schedules, as listed in Table 4 on page 4.
Critical Appraisal Of The Literature
Much of the literature on the topic of substance
abuse and overdose consists of review articles and
case reports/case series. This is especially true with
regards to the discussion of the newer drugs and the
effects. Many of the prospective studies are targeted
at epidemiologic data. No thorough practice guidelines were found that addressed evaluation and
management of the suspected drug overdose patient.
Table 1. Classification Of Drugs Of Abuse
Sympathomimetics
Cocaine
Methamphetamine/amphetamine
Hallucinogens
Lysergic acid diethylamide (LSD)
Tryptamines
Entactogens
(hallucinogenic
amphetamines)
3,4 methylenedioxymethamphetamine (MDMA)
Piperazines
Dissociative agents
Phencyclidine (PCP)
Ketamine
Dextromethorphan
Marijuana
Inhalants/Opioids
Nitrous oxide
Fentanyl
Heroin
Sedative/Hypnotics
Rohypnol
Gamma-hydroxybutyrate (GHB)
Raves
Raves are gatherings of hundreds to thousands of
people that revolve around techno music. The rise
and abuse of ecstasy (MDMA), which is described
later in this article, paralleled the growth of the
“rave” culture in Europe in the 1980s. These events
were widely popular with young people and the
rave scene migrated to the United States in the late
1980s. Raves are typically organized and financed
by a local or national enterprise and are widely
advertised. Alcohol use is not as popular at these
events so parents may get a false sense of security
since the event is often advertised as “alcohol-free.”
These events are notorious for the extensive, widespread use of drugs.
Raves feature loud, rapidly pounding music that
is accompanied by psychedelic lights, videos, smoke,
Abbreviations Used In This Article
AMS - Altered Mental Status
BZP - N-Benzylpiperazine
CNS - Central Nervous System
DAWN - Drug Abuse Warning Network
DEA - Drug Enforcement Agency
GC-MS - Gas Chromatography-Mass Spectrometry
GHB - Gamma-Hydroxybutyrate
MDMA - Methylenedioxymethamphetaine
MTF - Monitoring the Future Study
NCPE - Noncardiogenic Pulmonary Edema
NIDA - National Institute on Drug Abuse
NMDA - N-methyl-D-aspartate
SAMHSA - Substance Abuse and Mental Health
Services Association
TFMPP - 1-(3-Trifluoromethyl)piperazine
Pediatric Emergency Medicine Practice©
2
October 2006 • EBMedicine.net
Table 2. Annual Prevalence Of
Drug Use In 2005
Drug Name (by Scholastic
Grade Level)
Any Illicit Drug
8
10
12
Marijuana
8
10
12
Inhalants
8
10
12
Hallucinogens
8
10
12
LSD
8
10
12
PCP
8
10
12
MDMA (Ecstasy)
8
10
12
Cocaine
8
10
12
Crack
8
10
12
Heroin
8
10
12
Amphetamines
8
10
12
Methamphetamines
8
10
12
Rohypnol
8
10
12
GHB
8
10
12
Alcohol
8
10
12
Table 3. Risk Factors For Substance
Abuse In Adolescents 4
Annual
Prevalence
Genetics
Alcoholism among first or second degree relatives
Male gender
Self/individual/personal
Abuse
Antisocial behavior
Parental rejection
Early onset of drug use
Aggressive temperament
Lack of self control
Early sexual activity
Depression
Low self-esteem
Attention-deficit disorders
Poor self-image
Euphoric/mood altering effects of drugs
Body modification (cutting)
Learning disorders
Family
Dysfunctional family dynamics
Permissiveness
Authoritarianism
Parental conflict, divorce, separation
Poor supervision, lack of supervision
Poor parental role modeling
Community/environmental/societal
Easy availability of drugs and alcohol
Cultural and religious sanction
Acceptance of drug use behavior
Unemployment
Poor general quality of life in the neighborhood
Media influence
Low religiosity
Criminal activities in neighborhood
Increased use of drugs and alcohol in certain
ethnic groups
Peer group influence
Drug-using peers
Curiosity
Rebellion
Desire to belong
Rites of passage of puberty
Independence
Risk-taking behavior
Early tobacco use
School/academic
Poor school performance
Poor school environment
Truancy
15.5
29.8
38.4
12.2
26.6
33.6
9.5
6
5
2.4
4
5.5
2
3.5
5
Data unavailable
Data unavailable
1.3
1.7
2.6
3
2.2
3.5
5.1
1.4
1.7
1.9
0.8
0.9
0.8
4.9
7.8
8.6
1.8
2.9
2.5
0.7
0.5
1.2
0.5
0.8
1.1
33.9
56.7
68.6
Reprinted from the Monitoring The Future Survey and the University of
Michigan Institute For Social Research.
EBMedicine.net • October 2006
3
Pediatric Emergency Medicine Practice©
and even fire. A typical rave club layout often consists of a large dance floor with no air conditioning
and a separate “cool down room.” The event often
lasts all night until well into the morning.
Paraphernalia used at raves includes menthol
nasal inhalers, Vicks vapor rub, glow sticks (to
enhance the visual effects of Ecstasy), Skittles,
M&Ms, or similar candies (to hide drugs), lollipops
and pacifiers (to prevent involuntary teeth clenching), and water, juice, and sports drinks (to manage
excessive body heat and dehydration). Ecstasy is
sold openly at these gatherings. 6
Differential Diagnosis
Overdose or intoxication may present with a multitude of signs and symptoms, and should be included
in any differential diagnosis of altered mental status.
In recreational settings, polydrug use is often the
rule, not the exception. It may be difficult to determine which drug is responsible for the clinical symptoms. An admission of ingestion by the patient, or
other persons (EMS, parents, or friends) will be helpful, but is often not available. The patient may not
even know what he or she took. A history of depression, suicide attempts, recreational drug use, empty
bottles, or drug paraphernalia will increase the suspicion of drug ingestion as the cause of altered mental status. For younger children, knowledge of medications or illicit drugs taken by members of the
patient’s household may be helpful, as children may
mistake them for candy. The Poison Control Center
may help with identifying the agent(s) if the substance is found with the patient. The symptomatology will be age dependent, and may be skewed by
the presence of multiple ingestions or exacerbations
of pre-existing medical conditions. If ingestion is
suspected, attempting to identify a toxidrome may
be helpful in making a presumptive diagnosis of an
ingestion; see Table 7 on page 6. Table 6 lists common toxins that can cause altered mental status
(AMS). Also, the patient’s symptoms may be due to
withdrawal rather than intoxication. Such with-
Table 4. Drug Schedules
Schedule I
Drug or substance has high potential for abuse.
Drug or substance has no currently accepted medical
use in treatment in the United States.
There is a lack of accepted safety for use of the drug
or substance under medical supervision.
(Examples: MDMA, GHB, heroin, LSD, marijuana)
Schedule II
Drug or substance has high potential for abuse.
Drug or substance has currently accepted medical use
in treatment in the US or a currently accepted
medical use with severe restrictions.
Abuse of the drug or other substance may lead to
severe physical dependence or addiction.
(Examples: Amphetamine, fentanyl, morphine,
oxycodone)
Schedule III
Drug or substance has a potential for abuse less than
the drugs or other substances in schedules I and II.
Drug or substance has a currently accepted medical
use in treatment in the US.
Abuse of the drug or substance may lead to moderate
or low physical dependence or addiction.
(Examples: Hydrocodone, codeine with
acetaminophen)
Table 5. Common Findings With
Drugs Causing Central Nervous
System (CNS) Depression 15
Anticholinergics
Decreased GI motility, dry
flushed skin, hyperthermia,
mydriasis, tachycardia, urinary
retention, myoclonus
Opioids
Respiratory depression,
miosis, hyporeflexia, hypothermia
Cyclic antidepressants Anticholinergic toxidrome, dysrhythmias, hypotension,
seizures
Sympathomimetics
Diaphoresis, hypertension,
hyperthermia, mydriasis,
seizures, tachycardia
Cholinergics
Miosis, bronchorrhea, salivation, emesis, diarrhea,
diaphoresis, fasciculations,
muscle weakness
Gamma-hydroxybutyrate Minimal respiratory depres(GHB) and related
sion, normal blood pressure,
substances
rapid emergence, nystagmus,
no amnesia
Schedule IV
Drug or substance has a low potential for abuse
relative to the drugs or substances in schedule III.
Drug or substance has a currently accepted medical
use in treatment in the US.
Abuse of the drug or substance may lead to limited
physical dependence or addiction relative to the
drugs or other substances in Schedule III.
(Example: Benzodiazepines)
Schedule V
Drug or substance has a low potential for abuse
relative to the drugs or substances in schedule IV.
Drug or substance has a currently accepted medical
use in treatment in the US.
Abuse of the drug or substance may lead to limited
physical dependence or addiction relative to the
drugs or other substances in Schedule IV.
(Example: cough syrups containing codeine)
Pediatric Emergency Medicine Practice©
4
October 2006 • EBMedicine.net
drawal can occur in the neonate, who inadvertently
shared their mother’s cocaine or other substances
during pregnancy. Although substance abuse is a
common cause of AMS in a young person, especially
during or after a social gathering, it is important to
consider head trauma, infection, and hypoglycemia
as a potential etiology.
on patients with respiratory failure, impending respiratory failure, or altered mental status. Low blood
pressure should be treated with intravenous fluid
boluses. Oxygen supplementation, intravenous
access, and electrocardiographic and pulse oximetry
monitoring are indicated in any patient with altered
mental status. Perform a glucose check on all
patients with altered mental status and correct if low.
Seizures may be treated with benzodiazepines.
Certain overdose patients may benefit from more
extensive pre-hospital interventions.
Opioid intoxication is suggested by pinpoint
pupils, hypoventilation, and altered mentation.
Naloxone is a mixed opioid agonist-antagonist,
whose antagonistic effects may reverse opioid effects.
Naloxone can be given intravenously, intramuscularly, subcutaneously, via the endotracheal tube, or
intranasally. Intranasal naloxone reduces the risk of
Pre-Hospital Care
The most important role of the emergency medical
services (EMS) is to support a patent airway, ensure
adequate breathing, and monitor/support circulation.
Airway compromise may occur due to foreign bodies
including aspiration of vomitus, drugs, or drug paraphernalia. Breathing difficulties may require supplemental oxygen, as well as non-invasive airway
maneuvers. Tracheal intubation should be performed
Table 6. Classes Of Drugs/Toxins That Cause Central Nervous System Depression 15
Class
Anticholinergic Agents
Group
Examples
Antihistamines
Belladonna alkaloids
Anticonvulsants
Antidepressants
Cyclic antidepressants
Selective serotonin reuptake inhibitors
Nonselective serotonin reuptake inhibitors
Miscellaneous
Neuroleptic Agents
Butyrophenones
Phenothiazines
Dibenzodiazepines
Opioids
Sedatives/Hypnotics
Alcohols
Barbiturates
Benzodiazepines
Miscellaneous
Sympathomimetics
EBMedicine.net • October 2006
5
Diphenhydramine, chlorpheniramine
Hyoscyamine, scopolamine
Carbamazepine
Phenobarbital
Phenytoin
Valproate
Amitriptyline
Imipramine
Fluoxetine
Sertraline
Venlafaxine
Gamma-hydroxybutyrate (GHB) and
related compounds
Ibuprofen (rare, in large overdoses)
Isoniazid
Lead
Lithium
Phencyclidine (PCP)
Haloperidol
Chlorpromazine
Mesoridazine
Thioridazine
Clozapine
Olanzapine
Meperidine, fentanyl, heroin, methadone,
morphine
Ethanol, ethylene glycol, methanol
isopropanol
Secobarbital, Phenobarbital
Diazepam, lorazepam
Ethchlorvinyl meprobamate
Amphetamines, cocaine
Pediatric Emergency Medicine Practice©
blood exposure and is a safe and effective means of
managing opioid intoxication. 8-10 Precautions for
patients “awakening” with agitation from opioid
intoxication should be readied before naloxone
administration.
appropriate, maintain proper spinal precautions during the evaluation or if there is a suspicion of trauma. Place the patient on cardiac and pulse oximetry
monitors, provide supplemental oxygen, and obtain
adequate intravenous access.
Check a serum glucose level if EMS has not
already done so. If glucose was given by EMS, ask if
any clinical improvement occurred as a result and
recheck the level in the ED. Thiamine has classically
been recommended prior to administration of dextrose to prevent Wernicke-Korsakoff syndrome, particularly in malnourished or alcoholic patients.
However, there is increasing data that dextrose
Emergency Department Evaluation
Initial Stabilization
ED treatment for all patients with altered mental status begins with the basics of the ABCs – airway,
breathing, and circulation. Ensure a patent airway
with chin lift or jaw thrust and examine the mouth
and pharynx for vomitus and foreign material. If
Table 7. Clinical Toxidromes 63
Pediatric Emergency Medicine Practice©
6
October 2006 • EBMedicine.net
should not be withheld for administration of thiamine as the consequences of prolonged hypoglycemia can be devastating. 16 In addition, consider
a trial of naloxone if there are any clinical clues of
opiate overdose. The dose of naloxone varies per
patient and ranges from 0.4 to 2.0 mg IV per dose for
a child or adult and 0.01 to 0.03 mg/kg IV per dose
for a neonate.
as concomitant diseases such as diabetic ketoacidosis
may be present. Undress the patient fully to look for
needle markings, weapons, signs of body packing
(internal or external), traumatic injuries, or any other
signs of pathology.
If there is an ingestion of a single agent, the
physical exam may follow a classic toxidrome.
These findings of the toxidromes are summarized in
Table 8.
History
The history of a patient that has used a drug can be
elusive at best, and unreliable and unavailable at
worst. An even more complex and mixed picture
may result with the presence of multiple substances
in the body. The patient may choose not to or may
be unable to surrender all of the information about
what substances that s/he has used other than
“some pill someone gave me.” The patient should
also be asked about “body packing” which can
involve swallowing bags filled with drugs or placing
drugs in the rectum or vagina for transport. Ask if
there are any drugs present in the home or environment where the patient was last seen. This is particularly important for younger children who may have
accidentally ingested a rock of crack cocaine or
unknown pills they found lying around. Contacting
a Poison Control Center can also help elucidate substances ingested and significantly help with patient
management. A Poison Control Center can be immediately reached by calling 1-800-222-1222. Table 8
lists some indications of drug abuse.
Date Rape Drugs
Date rape drugs are typically colorless, odorless, and
tasteless drugs given often unknowingly to the victim that allows a sexual assault to occur and renders
the victim amnestic to the event and perpertrator(s).
These drugs typically reduce sexual inhibitions and
exert potent sedation. Typical date rape drugs are
listed in Table 9. 3
Table 9. Date Rape Drugs
• Gamma-hydroxybutyrate (GHB)
• Rohypnol (Flunitrazepam)
• Methamphetamine
• Methylenedioxymethamphetamine (Ecstasy, MDMA)
• Ketamine
• LSD (lysergic acid diethylamide)
Individual Substances
Pharmacology, Toxicology, And Clinical
Presentation
Table 8. Physical Indicators
Of Substance Abuse 2
• Unexplained weight loss
• Hemoptysis
• Hypertension
• Chest pain
• Red eyes
• Wheezing
• Nasal irritation
• Frequent unexplained
• Frequent "colds" or "allergies"
• Hoarseness
Sympathomimetics – Cocaine,
Methamphetamine/Amphetamine
Cocaine is a pervasive, highly addictive central nervous system stimulant derived from the leaves of
Erythroxylon coca. It is used by 3% of teenagers
between the ages 12 to 17, including 1% who have
reported daily use. 18 It has many different routes of
use such as intravenous injection, snorting, smoking,
or oral ingestion. Cocaine’s speed of onset and duration of action depends on the patient’s tolerance,
dose, and route with which the drug is delivered.
Injected and smoked cocaine can produce symptoms
as quickly as two minutes. Nasally snorted cocaine
effects are noticed within 10 minutes, and oral ingestion has been reported to produce effects from 10 to
30 minutes. The half-life of injected and smoked
cocaine is between 20 to 30 minutes, while the halflife of snorted or ingested cocaine is 60 to 90 minutes. 19, 23
injuries
• Needle tracks
• Chronic cough
Physical Examination
The physical exam may be useful in helping determine what type of toxic substances the patient has
ingested. In addition to vital signs, emphasis should
be placed on mental status, pupil size and ocular
reaction, lung and bowel sounds, muscle tone, and
skin appearance. 16, 17 Any odors should also be noted
EBMedicine.net • October 2006
7
Pediatric Emergency Medicine Practice©
The formation and production of cocaine goes
through an intricate process. Once it is derived from
the leaves of the coca plant, it is added to hydrochloric acid to form a cocaine hydrochloride salt. This
mixture is water soluble and can be injected or snorted. The cocaine hydrochloride salt can also be dissolved in water and mixed with baking soda and
heated. This process produces a hard piece of crack
cocaine, as its name is derived from the popping
noise made by the crystallized cocaine as it is heated
and smoked. 20 Snorting is the most popular route of
cocaine abuse, followed by smoking cocaine as crack.
Sympathomimetics such as cocaine and amphetamines bind to presynaptic neuronal receptors ultimately preventing the reuptake of dopamine, norepinephrine, and serotonin. 21,22 With the relative
increase in dopamine remaining in the synaptic cleft,
the postsynaptic neuron is stimulated and causes the
euphoric feeling that many abusers seek. 19
The systemic effects of cocaine can be devastating to the body. Many of the reported symptoms of
cocaine abuse range from less severe symptoms to
those that are life threatening. Anxiety, agitation,
psychosis, hyperthermia, vasculitis, vasospasm,
seizures, alveolar hemorrhage, pulmonary hypertension, angina, dilated cardiomyopathy, dysrhythmias,
hypertension, rhabdomyolysis, myocardial infarction, intracranial hemorrhage, and sudden death
have been reported with cocaine use. 23-28 There have
also been reported cases of spontaneous intestinal
perforation and ischemic bowel in crack abusers, and
this has been hypothesized to be due to mesenteric
vasoconstriction from norepinephrine. 29
Chest pain is the most common complaint associated with cocaine use. 110 Approximately 40% of
patients that use cocaine presenting to the hospital
have chest pain as their complaint. 30 In one study of
cocaine-associated chest pain patients, 57% were hospitalized; this has reflected an average cost of $83
million annually. 31, 32 There has also been a reported
6% incidence in myocardial infarction in two studies
of patients with cocaine-associated chest pain. 31, 33
Cocaine use is associated with myocardial infarction
in as many as 25% of patients aged 18 to 45 years
who otherwise have no risk factors for coronary
artery disease. 34, 110
Aortic dissection is another life threatening event
that also must be considered in cocaine-induced
chest pain. In one study of 38 reported cases of aortic dissection at San Francisco General Hospital
between 1981 to 2001, 14 37% were associated with the
Pediatric Emergency Medicine Practice©
use of cocaine. The average time between use of
cocaine and the occurrence of chest pain was 12
hours in this group, but the duration ranged
between 0 to 24 hours. All 14 of the patients reported having used cocaine within the past 24 hours. 35
Additional causes of chest pain in patients who
have insufflated or inhaled cocaine includes pneumothorax, pneumomediastinum, or pneumopericardium. Agitation, anxiety, and hallucinations are
common. Amphetamine or cocaine use can cause an
acute toxic psychosis in healthy persons and can
cause a psychotic episode in those with psychiatric
illness. Seizures may also occur. Intracranial hemorrhage, non-hemorrhagic stroke, vasospasm, cerebral
edema, and cerebral vasculitis can also be caused by
amphetamines or cocaine.
Methamphetamine, also known as “meth,”
“speed,” “crank,” or “ice,” is a powerful, addictive
stimulant that affects the central nervous system. It
is closely related to amphetamine, but has longer
lasting and more toxic effects on the central nervous
system. It is the N-methyl homolog of amphetamine
and has increased penetration of the blood-brain barrier. This leads to higher CNS stimulant activity and
less peripheral nervous system and less cardiovascular stimulation than amphetamine. It has a high
potential for abuse and addiction. Users rapidly
develop tolerance and seek higher doses.
Methamphetamine is a synthetic drug produced and
sold as pills, capsules, or powder that can be
smoked, snorted, injected, or swallowed. Most adolescents snort or smoke the drug. 36 Epidemic abuse
has been described in some groups of adolescents
citing availability, low cost, and a longer duration of
action than cocaine as reasons for their drug preference. 37 Methamphetamine is relatively easy to synthesize but may be contaminated by impurities such
as lead or strychnine. Methamphetamine may be
mixed with many drugs, including cocaine. 38
Peak effects of methamphetamine are observed
approximately 30 minutes after being injected or
smoked and two to three hours after oral ingestion.
The effects produced by methamphetamine, cocaine,
and various designer amphetamines are similar and
may be difficult to clinically differentiate, although
methamphetamine has a longer pharmacokinetic
half-life. The rapid onset of intense euphoria can
result in an acute psychotic episode characterized by
violent behavior, severe paranoia, and hallucinations.
This “hyperviolence syndrome” may result in severe
injury or death of family or friends of users. 39
8
October 2006 • EBMedicine.net
Snorting the drug or taking it orally leads to a more
pleasant euphoria of longer duration. 24 The adverse
effects of methamphetamine are those common to all
sympathomimetics. These include tachycardia,
hypertension, tachypnea, hyperthermia, agitation,
and tremors.
dosage ingested. Patients ingesting LSD may present
to the ED with tachycardia, palpitations, fever, hypertension, headache, blurred vision secondary to mydriasis, or generalized weakness. They may also present
with psychotic symptoms which can be difficult to
distinguish from adverse effects of the drug if the
patient has had a history of a psychotic disorder. 1, 2
The ingestion of LSD with other substances such
as marijuana or antihistamines can often increase the
chance of having a flashback. 3 These are essentially
recurrences of the symptoms of LSD ingestion without actually taking the drug. Patients experiencing
these symptoms may inadvertently be diagnosed
with a psychiatric disorder because of the similarity
of the symptoms without a recent ingestion of the
substance. Ingestion of large amounts of LSD have
been associated with seizures, hyperthermia, coagulopathies, and rhabdomyolysis.
Hallucinogens
Pharmacology, Toxicology, Clinical Presentation
LSD
D-lysergic acid diethylamide (LSD) is one of the classic hallucinogens, and it has been in use for at least
the past five decades. It was discovered in 1938 by
Albert Hofmann, a Swiss scientist, during his
research on the medical utility of the Ergot fungus. 40
In 1943, Hofmann was exposed to a small amount of
LSD on his finger during one of his experiments. He
later described it as an “inebriated condition without
leaving a hangover.” In 2006, Hofmann celebrated
his 100th birthday, and is still a proponent for the use
of LSD for medical, particularly psychiatric, research.
LSD has multiple known street names such as
“L,” “dots,” “cubes,” “blotters,” “Big D,” “sugar,”
and “acid.” 2 Its use had declined in the 1970s which
was attributed to multiple concerns such as “bad
trips,” flashbacks, or uncontrolled behavior while
using the drug. Unfortunately, a general resurgence
in this drug has occurred since 1991, and this is
believed to be secondary to a decrease in the perceived deleterious effects of LSD.
LSD’s action on serotonin and dopamine receptors is responsible for its clinical effects. LSD is a
chemical without color or odor, but often has a slight
bitter taste. It can be packaged in many forms including tablets, pills, or liquids, or it can be mixed with
other substances such as sugar cubes. 2 The main form
of distribution for LSD is on sectioned absorbent blotter paper. Each section, or “square,” is equivalent to
one dose of LSD. Today, one LSD square ranges from
20 to 80 micrograms per dose. This is lower than
doses used in the 1960s and 1970s which had 100 to
200 micrograms or higher per dose. 1, 17
LSD is usually ingested orally and the user feels
multiple effects within 30 to 90 minutes of use. 19
Although the desired endpoint for use is a euphoric
sensation, many users experience hallucinations and
an activation of the sympathetic nervous system. The
effects of the drug are usually dose-dependent, but
they cannot always be predicted based upon the
EBMedicine.net • October 2006
Tryptamines
Tryptamines are synthetic hallucinogenic indolealkylamines similar to hallucinogenic compounds found
in mushrooms such as psilocybin and psilocyn.
Many of these compounds can be produced synthetically. Their effects are thought to be due to modulation of serotonin neurotransmission. 46 Street names
include “Dimitri,” “The Substance,” and the
“Businessman’s Special.”
The most common tryptamine, dimethyl tryptamine (DMT) is found in plants in South America and
North America, as well as the glands of some tropical toads (Bufo alvarius). It can also be produced synthetically. It has been used in South America at least
since the 8th century for religious ceremonies in a
drink known as ayahuasca. The prevalence of tryptamine use is unknown but seems to be increasing in
popularity. This is likely due to the fact that many
tryptamines are not scheduled by the Drug
Enforcement Administration (DEA) and may be purchased over the internet. Tryptamine itself lacks significant stimulant and hallucinogenic properties but
derivatives of tryptamine contain indole ring structures and ethylamine substitutions that result in its
Table 10. Common Tryptamines
DMT
Dimethyl tryptamine
5-MeO-DIPT
5-Methoxy-alpha-methyltryptamine ("Foxy methoxy")
9
AMT
Alpha-methyltryptamine
DPT
Diphenyl tryptamine
Pediatric Emergency Medicine Practice©
pharmacologic activity. 46, 137
Various routes of administration are available for
the hallucinogenic tryptamines. Some are active
when ingested while others must be smoked or
insufflated. Most are available in capsule, tablet,
powder, or liquid form. The liquid may be impregnated on sugar cubes or blotter paper.
DMT can be orally ingested, used in snuff
(yopo), smoked, injected, and snorted. Oral ingestion is popular in the form of the drink called
ayahuasca. Ayahuasca is a combination of the plant
roots containing DMT (Psychotria viridis) and those
containing MAO inhibitors, such as Harmala alkaloids (Banisteriopsis caapi). The oral form is commonly used for religious purposes. Smoking DMT is the
most common route used for non-religious purposes.
Smoking DMT results in onset within 10 to 60 seconds and users experience intense hallucinations
within 5 to 20 minutes. The “tryp” lasts the duration
of a noon-time meal, hence its nickname the
“Businessman’s Special.” A “tryp sitter” is often
present to catch the pipe after the quick onset of the
high. When injected or snorted, DMT lasts slightly
longer than when smoked. The agents have variable
onset and duration times. Effects may last as long as
12 to 24 hours.
Symptoms of tryptamine intoxication include
visual or auditory hallucinations and euphoria.
Symptoms consistent with serotonin syndrome can
occur and include tachypnea, hyperthermia,
diaphoresis, mydriasis, hypersalivation, vomiting and
diarrhea, agitation, tachycardia, hypertension,
diaphoresis, dystonia, mydriasis, tremors, seizures,
auditory and visual hallucinations, and confusion. 47-51
The smoke is harsh and may result in oropharyngeal
irritation and bronchospasm.
that becomes red or brown when impurities are
added. 3 It is typically taken as a tablet or capsule.
MDMA is a selective serotonergic neurotoxin
that causes massive release of serotonin. It is
thought that MDMA damages serotoninergic neurons in the CNS and leads to memory dysfunction,
cognitive disabilities, and behavioral problems with
long-term use. 52-53
MDMA causes many of the same adverse effects
as the sympathomimetic drugs. Acutely, patients
may have tachycardia, hypertension, muscle tension,
bruxism (teeth grinding), jaw clenching, nausea,
blurred vision, diaphoresis, anxiety, and chills or
sweating. Within one hour, these sympathomimetic
effects are replaced by feelings of relaxation, euphoria, and increased empathy. Drowsiness, dizziness,
confusion and hypotension may occur as well. 43, 97
Psychological effects such as confusion, depression, sleep problems, drug craving, and severe anxiety can occur acutely or even weeks after taking
MDMA. Serotonin syndrome can result from MDMA
use. This is a condition in which central serotonin
receptor hyperstimulation results in hyperthermia,
mental status changes, autonomic instability, and
altered muscle tone or rigidity. Hyponatremia is a
well-documented consequence of ecstasy use. 45, 58
The occurrence of hyponatremia after MDMA use is
thought to be multifactorial caused by polydipsia,
excessive sweating with physical exertion, and the
release of vasopressin leading to the syndrome of
inappropriate anti-diuretic hormone secretion
(SIADH). 45 Most cases of hyponatremia will resolve
with fluid restriction and judicious administration of
normal saline in severe cases. 98
Piperazines
Piperazines have recently emerged as drugs of abuse
due to their ability to mimic the effects of MDMA.
These agents were initially used as anti-helminthic
drugs in the 1950s and were later investigated as
Entactogens – Hallucinogenic Amphetamines
Pharmacology, Toxicology, Clinical Presentation
Table 11. Piperazines
MDMA
MDMA (3, 4 methylenedioxymethamphetamine) is a
synthetic drug chemically similar to methamphetamine and the hallucinogen mescaline. Street names
for MDMA include “Ecstasy,” “Love Drug,” “E,”
“Adam,” and “XTC.” MDMA has both stimulant
and psychedelic effects. MDMA has a widespread
reputation as being a safe drug that produces intense
euphoria of long duration, ranging from 3 hours to
several days. In its pure form, it is a white powder
Pediatric Emergency Medicine Practice©
Benzylpiperazines
N-benzylpiperazine (BZP)
1-(3,4-methylenedioxybenzyl)piperazine (MDBP)
Phenylpiperazines
1-(3-chlorophenyl)piperazine
(mCPP)
1-(4-methoxyphenyl)piperazine (MeOPP)
1-(3-trifluoromethylphenyl)
piperazine (TFMPP)
10
October 2006 • EBMedicine.net
potential anti-depressants. 46 However, due to their
reported stimulant-like side effects, further clinical
research for these agents was not recommended. 47
The derivatives of the piperazines are divided
into two major classes: the benzylpiperazines and the
phenylpiperazines; 46 see Table 11. N-benzylpiperazine (BZP) and 1-(3-trifluoromethylphenyl)piperazine (TFMPP) are the most popular piperazines;
they are also known as “A2” or “Molly,” respectively,
or collectively as “Legal X” or “Legal E.” 46
Piperazines are structurally related to amphetamines and therefore may share similar biochemical
properties. When ingested, piperazines, like
MDMA, have been reported to cause serotonin and
dopamine release from neurons. 46, 51 As a result, hallucinogenic and stimulant effects as well as euphoria
are seen. 52, 53 The hallucinogenic properties reflect
that of MDMA, while its stimulant effects mirror that
of amphetamines. 54 The effects of piperazines can
last between six to eight hours. Many of the piperazines sold have been marketed as MDMA, or as an
MDMA substitute. 51, 57 The combination of BZP and
TFMPP produces a synergistic effect similar to
MDMA. Two deaths have been reported with BZP
use, although the users also ingested MDMA with
the BZP. 55, 56
while inhalation and oral ingestion result in the
slowest onset.
PCP works by inhibiting catecholamine reuptake
in the central nervous system. In general, PCP use
has serum dose-dependent effects lasting between
four to six hours, but chronic symptoms have been
reported to last for many days to weeks. This is
believed to be secondary to PCP’s lipophilic molecular structure, and hence its ability to be deposited in
bodily fat. Serum PCP levels of 20 to 30 ng/mL
have been associated with irritability, increased
activity, and mood stimulation. Levels between 30 to
100 ng/mL can result in psychosis, paranoia, ataxia,
and hostile behavior. When levels are greater than
100 ng/mL, more serious conditions such as hypertension, seizures, stupor or coma, and even death
may occur. However, these value ranges are generalizations as the severity of the symptoms and concomitant findings often do not correlate well with
the urine drug levels. 23, 59
McCarron et al reviewed 1,000 patients presenting to the ED with acute PCP intoxication. They
noticed that 35% of the patients were violent, 34%
were agitated, and 29% exhibited bizarre behavior.
46% of the patients were alert and oriented, while
others presented with alterations in mental status
that included the characteristic blank stare, lethargy,
coma, and seizures. 59 Nystagmus (either vertical,
horizontal, or rotatory) and hypertension occurred in
57% of patients, while other physical exam findings
such as diaphoresis, bronchospasm, hypersalivation,
and urinary retention occurred in less than 5% of
cases. The characteristic pattern of nystagmus is
not seen in any other drug intoxication. 23, 59
Twenty-eight patients in the entire group were
noted to be apneic, and three were in cardiac
arrest upon presentation. Patients may also
present with severe symptoms of delirium or in an
acutely psychotic state.
Serious complications can result with ingestion
of PCP. Physiologic complications such as alterations in vital signs, hyperthermia, rhabdomyolysis
with and without kidney failure, and hypertensive
emergencies have been reported. 60-62 Approximately
2% of patients that abuse PCP develop rhabdomyolysis. Patel et al reported eight cases of renal failure
associated with PCP over a 36 month period, and
three of these patients subsequently required dialysis. 64 In addition, there are case reports in the literature of intracranial and subarachnoid hemorrhage
associated with PCP use. 23, 65, 66
Dissociative Agents
Pharmacology, Toxicology, Clinical Presentation
PCP
Phencyclidine (PCP) is another drug that was initially intended for medical use. It was developed as a
general anesthetic in the 1950s, but was discontinued
due to post-operative problems such as severe agitation, delirium, and psychosis. 1, 17 PCP is now produced and distributed illegally in the United States
and sold under various names such as “angel dust,”
“sheets,” “ozone,” “hog,” “wack,” “peace pill,” or
“rocket fuel.” 3
PCP is usually distributed in a powder form,
although liquid, tablet, and combinations with
other illicit drugs have been seen. “Fry,” “hydro,”
“illy,” or “killer joints” are some of the common
names referred to as the combination of marijuana
with PCP, while “space base” or “tragic magic”
refers to its use with cocaine.1 There are multiple
ways the drug can be used. It can be smoked, snorted, ingested, or used intravenously. Onset of symptoms usually occurs fastest by the intravenous route,
EBMedicine.net • October 2006
11
Pediatric Emergency Medicine Practice©
names include “robo,” “red devil,” “dex,” and
“DXM.” Popular preparations than contain dextromethorphan include Robitussin (Whitehall-Robins
Healthcare, Madison, NJ) which users call “robotripping” or “robocop” and Coricidin HBP Cough and
Cold (Shering-Plough, Kenthworth, NJ), which users
call “CCC.” 44 Abuse of dextromethorphan by adolescents ages 13 to 19 years has increased more than
300% over a three year period. 72 Coricidin is the
most popular form of detromethorphan that is
abused. Adolescent abusers often choose dextromethorphan because they think it is a “smart
choice” without the stigma associated with street
drugs. It is easily available over-the-counter and is
inexpensive. Each pill contains 30 mg of dextromethorphan. The pills are easy to carry and conceal and don’t cause the nausea and vomiting associated with the ingestion of large amounts of syrup.
Toxicity may also arise from coingestants.
Chlorpheniramine is a histamine antagonist with
anticholinergic properties that is often combined
with dextromethorphan in cough and cold preparations. Acetaminophen is an important coingestant as
well as pseudoephedrine. 73
The metabolite of dextromethorphan reaches
peak plasma concentrations about 1 ½ hours after
ingestion and clinical effects can be seen for two to
six hours. The effects seen depend on the dose
ingested. The first sign of toxicity may be movement
abnormalities such as an episode of unresponsiveness, staring, dystonia, nystagmus, and ataxia. 74
The recommended dose for cough suppression is 15
to 30 mg every six to eight hours. One 12 ounce bottle of Robitussin contains 710 mg of dextromethorphan. 44
Mild intoxication (doses 100 to 200 mg) produces
tachycardia, hypertension, vomiting, diaphoresis,
nystagmus, mydriasis, euphoria, and loss of motor
control. 75 Moderate intoxication can also cause hallucinations and an ataxic gait. In severe intoxications
(1500 mg), the patient may become markedly agitated with resultant dehydration, rhabdomyolysis, and
hyperthermia. Respiratory depression may occur
but is rare. Severe dextromethorphan intoxication
can mimic PCP intoxication. 77
Ketamine
Ketamine was derived from PCP in the 1960s as a
dissociative anesthetic. It was introduced as a general anesthetic to replace PCP which had a reputation
for unpleasant post-anesthetic emergence reactions.
It is also commonly used in veterinary medicine.
Ketamine is one of the drugs with the most rapidly
increasing instances of abuse in some parts of the
United States, especially near the Mexican border as
it can be obtained inexpensively from veterinary
pharmacies in Mexico. Its street names include
“Special K,” “Vitamin K,” “cat valium,” “kit-kat,”
“super acid,” and “jet.” 24 Ketamine is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist that blocks the actions of the excitatory amino
acids glutamate and aspartate. Abusers often use it
to temper the “crash” associated with the end of a
cocaine or amphetamine binge. 67 It causes anesthesia
without respiratory depression by inhibiting neuronal uptake of dopamine, serotonin, and glutamate
activation in the NMDA receptor channel. 68
Ketamine is difficult to manufacture, so it is usually
obtained from human and veterinary anesthesia
products. It is dried to a powder and smoked in a
mixture of marijuana or tobacco or taken intranasally. The nasal inhaler is called a “bullet” or a
“bumper” and inhalation is called a “bump.”
Ketamine is often found in “trail mixes” of methamphetamine, cocaine, sildenafil citrate (Viagra) or
heroin. 69 Other common routes of administration
include subcutaneous or intramuscular injection or
rectal infusion. The effects have a rapid onset of
action and last up to an hour. Clinical effects include
sensations of floating outside the body, visual hallucinations, confusion, anterograde amnesia, and delirium. It also produces nystagmus, tachycardia, palpitations, hypertension, respiratory depression, and
apnea. 70, 71 Other dangerous toxic effects include
severe agitation and paranoid psychoses.
Dextromethorphan
Dextromethorphan (d-3-methoxy-N-methylmorphine) is a dissociative agent. Originally created in
the 1960s as an antitussive agent, it is a codeine analog that binds to the phencyclidine site of the NMDA
receptor. It also increases the release and blocks the
reuptake of serotonin, thus accounting for its serotonergic properties. 44 Clinically, it decreases the sensitivity of cough receptors and interrupts the transmission of cough impulses in the medulla. Its street
Pediatric Emergency Medicine Practice©
Marijuana
Marijuana is a derivative of the Cannabis sativa plant
that has been used for thousands of years. One of
the first documented utilities of marijuana was in
2700 BC by the Chinese for medicinal uses, and the
12
October 2006 • EBMedicine.net
Cannabis plant was the first nonfood-bearing plant
cultivated by mankind. 79 Currently, marijuana is the
most widely used illegal drug worldwide. 19
The main component of Cannabis that is responsible for its psychoactive properties is tetrahydrocannabinol (THC). Marijuana is the dried leaf component of Cannabis and contains between 2 to 4% THC,
while hashish is the dried resin containing 10 to 15%
THC. Each marijuana cigarette, also known as a
“joint,” contains approximately 20 mg of THC. 2, 19
Marijuana, also known as “weed,” can be smoked or
ingested orally. If smoked, its effects are often
noticed immediately by abusers and can last
between one to three hours. Oral ingestion with food
items such as brownies can take between 30 minutes
to an hour for effects to occur, and symptoms may be
experienced up to four hours later. The elimination
half life of marijuana is seven days, but this can take
up to one month to be completely removed and
excreted in the urine. 19
THC decreases gamma-aminobutyric acid
(GABA) release in the brain, which ultimately
increases dopamine release. Patients experience feelings of relaxation or euphoria. However, adverse
effects are not uncommon and may include lethargy,
amotivational syndrome, tremors or seizures, cognitive dysfunction, hallucinations, coma, and even
cerebellar infarctions. 2, 80
Chronic use of marijuana may result in tolerance,
psychological cravings or dependence, and withdrawal symptoms. 3, 24 Signs and symptoms include
conjunctival injection anxiety, weight loss, insomnia,
and irritability. 81
The street names “fry,” “dank,” or “AMP” refer
to marijuana soaked in formaldehyde for the purpose of enhancing its effects. Users of this form of
marijuana may experience excessive salivation,
diaphoresis, and tremor. Similar effects as PCP
intoxication may be seen as well. 111
hallucinogenic properties and the fact that they are
cheap, legal, and easily obtainable. 82, 83 The substances most commonly inhaled include gasoline
(57%), freons (40%), butane (38%), glue (30%), and
(23%). 84
Inhalants are inhaled through the nose or mouth
in a variety of ways. Sniffing involves inhaling
fumes from an open container and offers the lowest
concentration of inhalant. Huffing describes using
rags that are soaked in a chemical substance and
then held to the face or stuffed in the mouth. This
allows for a higher concentration of inhalant than
sniffing. Bagging occurs when fumes are inhaled
from substances sprayed or deposited inside a paper
or plastic bag. Bagging offers the highest concentration of inhalant. Other methods include spraying
aerosols directly into the nose or mouth or pouring
inhalants onto the user’s collar, sleeves, or cuffs and
sniffing them over a period of time (such as during a
class in school).1 Fire breathing entails forcefully
exhaling liquids, such as butane, into a flame held in
front of the mouth to create a more profound flame.
Inhalants are rapidly absorbed through the alveoli and quickly enter the central nervous system and
other lipid rich tissues. 82 The exact mechanism of
action to neuronal cells is unclear. However, it is
known that the onset of action in the brain is within
Table 12. Clinical Presentation
of Inhalant Intoxication 82
Neurologic
Intoxication
Ataxia
Headache
Seizures
Coma
Sensorimotor dysfunction
Cardiovascular
Dysrhythmias
Sudden death
Gastrointestinal
Nausea/vomiting
Abdominal pain
Endocrine
Hypokalemia
Hypocalcemia
Renal
Hematuria
Proteinuria
Muscular
Weakness
Inhalants/Solvents
Pharmacology, Toxicology, Clinical Presentation
Inhalants are a very popular “gateway” drug for
adolescents that may start them on a potentially progressive and devastating journey of drug abuse. 85
Inhalants are cheap, easily obtainable, and provide a
quick “high.” Despite the ban of sale of aerosols to
minors, the overall use of inhalants remains significant. The typical inhalant abuser is a teenage male
who is attracted to solvents for their euphoric and
EBMedicine.net • October 2006
13
Hallucinations
Nystagmus
Lethargy
Respiratory depression
Agitation
Cognitive dysfunction
Hypotension
Hematemesis
Metabolic acidosis
Hypophosphatemia
Pyuria
Rhabdomyolysis
Pediatric Emergency Medicine Practice©
Pediatric Emergency Medicine Practice©
14
October 2006 • EBMedicine.net
EBMedicine.net • October 2006
15
Pediatric Emergency Medicine Practice©
seconds to minutes, and inhalants accumulate in the
brain. Inhalants also affect the heart, lungs, and liver
as described below.
The signs and symptoms of inhalant abuse are
variable and affect many different systems; see Table
12 on page 13. Individuals seek the intoxicating high
that lasts from minutes to hours. Death may result
from asphyxia due to a high fume concentration
after inhaling the chemicals in an enclosed space. 2
Any adolescent who presents with unexplained mental status changes, cerebellar findings, cardiac
rhythm disturbances, syncope, hypokalemia, methemoglobinemia, carbon monoxide toxicity, or cardiac
arrest should be suspected of inhalant abuse. 82 Any
event causing a surge of catecholamines may induce
a malignant dysrhythmia, leading to heart failure
and death while a user is inhaling or shortly thereafter. For example, being discovered during the act
of using inhalants may induce a malignant heart
rhythm, leading to death, even in the first-time user.
Often a high degree of suspicion is needed to make
the diagnosis of inhalant abuse.
Acute intoxication produces immediate feelings
of stimulation, lightheadedness, euphoria, and
decreased inhibition leading to potentially dangerous actions. The patient often appears intoxicated
and hyperactive initially. Trauma may be incurred as
a result of this disinhibition. As symptoms progress,
CNS depression worsens with lethargy, confusion,
and auditory or visual hallucinations. Severe intoxication can result in seizures or coma. 82, 85
The cardiovascular effects of acute inhalant
intoxication can be fatal. Ventricular and supraventricular dysrhythmias as well as heart block can
occur. Bass postulated that inhalants sensitize the
myocardium to the effects of endogenous catecholamines, predisposing to dysrhythmias. 86 This
has been supported by subsequent research. 87-89
Asphyxia may occur if the plastic bag surrounds the
face and the patient becomes unconscious. Airway
obstruction may occur from oropharyngeal burns.
Respiratory compromise may also occur due to bronchospasm, chemical pneumonitis, central respiratory
depression, and muscle weakness. Abdominal pain,
nausea, vomiting, and hematemesis are common
gastrointestinal complaints. 82
Chronic consequences of inhalant abuse primarily affect the central nervous system. Depression, agitation, weight loss, memory loss, dysarthria, ataxia,
nystagmus, tremor, and non-specific motor weakness
may occur. Computed tomography (CT) scans of the
brain often reveal diffuse atrophy, ventricular
enlargement, and frontal or temporal sulci widening.
Electroencephalograms may show diffuse slowing.
Chronic inhalant use may result in specific sequelae
in various organ systems, as listed; see Table 13. For
example, toluene is a principal ingredient in airplane
glue and some rubber cements. Chronic toluene
abuse impairs the distal renal tubule and results in
type I distal renal tubular acidosis with a normal
anion gap. 90 This can present with life-threatening
hypokalemia. Methylene chloride is found in some
solvents and paint stripping products. It is metabolized to carbon monoxide and carbon dioxide. This
may produce significant elevations in carbon monoxide. CO levels may increase up to nine hours after
exposure due to this metabolism and the carboxyhemoglobin half-life is longer than that seen after direct
CO exposure. The role of hyperbaric oxygen as
treatment in methylene chloride is unclear.
Nitrous Oxide
Nitrous oxide is an inhalational anesthetic agent that
has become a common inhalational drug of abuse.
Nitrous oxide is abused by 23% of those who abuse
inhalants. 92 A cartridge of nitrous oxide is called a
Table 13. Sequelae Of Inhalent Abuse74
System
Inhalant
Effect
CNS*
Toluene
Encephalopathy
CVS*
Hydrocarbons
Cardiac dysrhythmias
Pulmonary
Hydrocarbons
Chemical pneumonitis, hypoxia, asphyxiation
Renal
Toluene
Renal tubular acidosis, kidney stone
Liver
Chlorinated hydrocarbons
Hepatitis, liver failure
Blood
Nitrites, benzenes
Methemoglobinemia, malignancies, lymphoma
*CNS, central nervous system; CVS, cardiovascular system.
Pediatric Emergency Medicine Practice©
16
October 2006 • EBMedicine.net
“whippit.” Whippits are small compressed bulbs of
nitrous oxide that are intended for use as a propellant for whipped cream. Abusers attach a whippit to
an inflatable object and inhale. Nitrous oxide can
also be inhaled using a tank with a regulator and a
mask. Injuries such as facial burns from direct discharge of the compressed gas and death from misuse
of nitrous oxide tanks has been reported. 93, 94 Nitrous
oxide inactivates vitamin B12 which is an important
cofactor in hematopoesis and myelin formation. This
leads to anemia and neuropathy. The neuropathy
presents as a progressive sensory loss with paresthesias and pain, often beginning in the hands. 12
Inhalant abusers may develop acute withdrawal
approximately two to five days after cessation of
inhalants. Symptoms include agitation, insomnia,
tremors, and nonspecific abdominal pain. 93, 94
one minute of the injection and lasts from one to a
few minutes. This is followed by a period of sedation
lasting about an hour. The euphoria associated with
heroin use is extremely addictive. The majority of
heroin overdoses occur in experienced users, as they
use escalating doses to overcome their tolerance and
achieve the euphoria they seek. 102 Heroin is highly
lipid soluble and rapidly penetrates the brain. The
half-life of heroin is 15 to 30 minutes.
Heroin is commonly contaminated or diluted
with substances having clinical and toxic effects of
their own. These include alkaloids, cocaine, amphetamines, quinine, phenobarbital, lidocaine, caffeine,
methaqualone, fentanyl, and other opiates. Street
heroin often has substances commonly used to
increase the bulk of a street sample including talc,
dextrose, flour, and mannitol. Heroin acts on multiple central and peripheral receptors. Stimulation of
these receptors results in analgesia, euphoria, respiratory depression, delayed gastrointestinal motility,
miosis, and ultimately the development of physical
dependence. 103
Depressed mental status, respiratory depression,
and miosis are the clinical hallmarks of opioid overdose. The presence of co-ingestions, adulterants, and
preexisting or concomitant medical or psychiatric
conditions can confound the clinical presentation
and physical findings.
Patients may present with CNS symptoms such
as analgesia, drowsiness, difficulty in mentation, and
even profound coma; in some cases, patients may
present with agitated delirium and convulsions if
they have concomitant coingestants, hypoxia, hypoglycemia, or CNS injury.
Respiratory symptoms are usually the result of
CNS depression. The brain’s response to changes in
carbon dioxide is blunted with heroin. With high
doses, the brain’s response to hypoxia is blunted as
well. This results in severe respiratory depression
progressing to apnea. Patients with heroin overdose
may also present with tachypnea. This may result
from pulmonary edema, concomitant coingestants,
hypoxia, hypoglycemia, or CNS injury.
Noncardiogenic pulmonary edema (NCPE) is a
notable but infrequent complication of heroin overdose. The clinical symptoms of NCPE are clinically
apparent either immediately or within four hours of
the overdose. Mechanical ventilation is necessary in
only about one-third of patients. 103 In one retrospective review, 10% of overdose patients presented with
NCPE. All of the patients in this study were inexpe-
Opioids
Pharmacology, Toxicology, Clinical Presentation
Heroin
Heroin, also known as “Black tar,” “China white,”
“dust,” “H,” “horse,” “J junk,” “Mexican mud,”
“scag,” or “smack,” is an opiate derived from the
dried sap of the opium poppy (Papaver somniferum).100
DAWN lists heroin and morphine among the four
most frequently mentioned drugs reported in drugrelated death cases in 2002. Nationwide, heroin
emergency department mentions were statistically
unchanged from 2001 to 2002, but have increased 35
percent since 1995. 1
Heroin is typically produced as a fine, white
powder while black tar heroin is produced in Mexico
using less refined morphine. The opium from which
heroin is produced is a brown-to-black, gummy latex
containing about 10% morphine. The effects of black
tar heroin are identical to powder heroin with one
caveat. Black tar heroin destroys the user’s veins
much more rapidly than powder heroin, forcing
many users to inject subcutaneously. 101
Heroin can be smoked, sniffed, or injected.
Intravenous abuse is most popular and is responsible
for the most complications. 104 Heroin can be combined with amphetamine (known as “bombita”),
with cocaine (known as “dyna-mite,” “speedball,” or
“whizbang”), or with marijuana (known as “atom
bomb” or “A-bomb”).
When injected intravenously, users experience a
sensation of intense pleasure, which begins within
EBMedicine.net • October 2006
17
Pediatric Emergency Medicine Practice©
rienced users. All cases of NCPE resolved within 24
hours without sequelae. 104 The incidence of NCPE
related to heroin overdose has decreased substantially in the last few decades. 110
Hypoxia-induced lung damage is likely to play a
major role in the development of NCPE but its exact
mechanism is unknown. On auscultation, the lungs
are initially clear. Tachypnea, tachycardia, and the
development of bilateral rales herald the onset of
pulmonary edema. Wheezing may also indicate
bronchospasm secondary to histamine release. The
presence of localized rales and wheezing should
raise suspicion of aspiration pneumonia.
The presence of miosis in the setting of overdose
is highly suggestive of opioid toxicity. However,
mydriasis may develop in heroin overdose when
severe hypotension, acidosis, and anoxia have
occurred. It can also occur in patients with mixed
overdoses. The blood pressure in heroin overdose is
usually well maintained unless the body is stressed
by hypoxia, hypovolemia, or acidosis. Patients with
heroin overdose may present with bradycardia and
mild hypotension. Hypotension due to opioid overdose is generally attributable to histamine release.
Heroin decreases gastric motility, thereby prolonging
gastric emptying time by as much as 12 hours.
Heroin overdose patients may have flushing due to
vasodilatation of the cutaneous blood vessels and
may also have pruritus. Patients may also have track
marks, fresh puncture wounds, and “skin-popping”
marks.
the manufacturer-recommended 72 hours still has
2800 mcg of fentanyl remaining in a 10 mg patch. 46
The patches can be ground up, the contents extracted, and then smoked, ingested, or injected. The dosing in this form of abuse is unpredictable and several
fatalities have been reported. 95, 96
Fentanyl has been combined with heroin resulting in fatal respiratory depression. Fentanyl is deliberately added to the heroin as an enhancement
intended to improve the product. Several hundred
overdoses and about 130 deaths have been reported
in the Chicago and Philadelphia areas since February
2006 from this highly potent combination. 107
Sedatives/Hypnotics
Pharmacology, Toxicology, Clinical Presentation
GHB
Gamma-hydroxybutyrate (GHB) is a designer drug
made from simple ingredients with multiple recipes
easily found on the internet. 71, 109, 110 It was first synthetically created in France in 1960 for anesthetic
purposes, but ultimately gained popularity as a
recreational drug and supplement for bodybuilders.
GHB has gone through many classification and regulation schemes since its creation. In 1990, nonprescription sales were stopped in the United States
because of severe uncontrolled movements as well as
respiratory and nervous system depression. In 2000,
GHB was moved into the schedule I controlled substances class due to concerns of overdose as well as
its use in cases of date rape. In 2002, a schedule III
formulation of GHB known as sodium oxybate was
created and is used in the treatment of narcolepsy.
Sodium oxybate has also been studied in alcohol
withdrawal syndromes. 71
The incidence of GHB use has steadily declined
according to a sample population in California from
1999 to 2003. This sample from the California Poison
Control System (CPCS) was compared to corresponding data from the American Association of Poison
Control Centers and DAWN. In this study,
Anderson et al found a 76% overall decrease in the
total number of cases reported to the CPCS.
However, they cautioned that the lack of lab tests to
confirm GHB ingestion, the retrospective design of
the study, and the lack of reporting by the physician
and the patient may have influenced their results. 112
Despite this perceived general decline of its use,
GHB is still a very important component of drug use
Fentanyl
Fentanyl is a high-potency synthetic opioid that is
widely used intravenously in the hospital setting for
analgesia and anesthesia. It is a schedule II drug
that is also available in oral (lollipop) and transdermal formulations. Fentanyl is often obtained for
illicit use by theft from pharmacies and nursing
homes and fraudulent prescriptions. Over 12 different forms of fentanyl analogues have been produced
illegally for distribution. 105 Outpatient use of fentanyl has increased dramatically. The DEA reported
an increase from 500,000 prescriptions written in
1994 to 5.7 million prescriptions in 2003. 113 The biological effects of fentanyl are indistinguishable from
heroin, with the exception that fentanyl is hundreds
of times more potent. Fentanyl is most commonly
used intravenously but may be snorted or smoked. 106
Fentanyl patches (Duragesic) are often sold and
abused. A discarded patch that has been worn for
Pediatric Emergency Medicine Practice©
18
October 2006 • EBMedicine.net
and ED presentation.
GHB is found in different formats such as pills,
tablets, or clear liquids, but is most commonly available in a dissolvable white powder form. GHB is a
potent CNS depressant that is tasteless, colorless,
and odorless. As a result, it can be unknowingly dissolved in drinks to cause amnestic and sedative
properties. 3 The effects of GHB are generally dosedependent, and its sedative effects begin within 10 to
20 minutes of ingestion and last approximately four
to six hours. 2, 23 GHB is rapidly cleared from the
body with a half-life of 20 minutes and, as a result, it
is difficult to detect this drug with standard laboratory tests. 2 However, specialized urine, blood, and
even hair detection tests are being studied and developed; this is primarily to help verify GHB intoxication after a sexual assault. 114-116
In low doses, GHB causes euphoria, drowsiness,
dizziness, nausea, and visual changes. It may be
taken voluntarily for this reason, often in conjunction
with other drugs such as alcohol, heroin, or LSD.
With larger doses of GHB, the CNS depression worsens and eventually the patient may develop vomiting, aspiration, seizures, bradycardia, hypothermia,
respiratory acidosis, coma, and even death. 3, 6, 23 In
combination with other sedatives or depressants,
GHB can become an even more deadly agent as it
can severely depress the nervous system and result
in deeper sedation. Patients presenting with GHB
intoxication with severe apnea, decreased respiratory
rate, or significant nervous system depression may
require intubation. Emesis has also been reported,
and this can result in aspiration if not properly controlled. 117, 118
GHB has a reputation among drug addicts as
being a safe drug, due possibly to the fact that it is
FDA-approved to treat narcolepsy and it is used by
body-builders for unproven claims of muscle development enhancement. 3
With prolonged use of GHB, tolerance and even-
Table 14. Clinical Diagnostic Aids63
Clinical Sign
Hypothermia
Hyperpyrexia
Bradypnea
Tachypnea (secondary to toxininduced metabolic acidosis, noncardiogenic pulmonary edema, or
direct pulmonary insult)
Bradycardia
Tachycardia
Hypotension
Hypertension
Alternating depression and excitation of nervous system
Ataxia
Coma
Delirium, psychosis
Miosis
Mydriasis
Nystagmus
Seizures
Cardiovascular
Wide QRS complex on 12-lead
ECG
Dysrhythmia
EBMedicine.net • October 2006
Intoxicant
Alcohols, barbiturates, ethanol, narcotics, sedatives/hypnotics
Amphetamines, anticholinergics, antihistamines, cocaine, phencyclidine, sympathomimetics
Alcohol, narcotics, sedative/hypnotics
Amphetamines, hydrocarbons
Alcohols, narcotics, sedative/hypnotics
Alcohol, amphetamines, anticholinergics, cocaine, phencyclidine, sympathomimetics
Narcotics, opiates, sedative/hypnotics
Amphetamines, anticholinergics, antihistamines, cocaine, phencyclidine, sympathomimetics
Phencyclidine
Alcohol, hydrocarbons, sedative/hypnotics
Alcohols, anticholinergics, GHB, hydrocarbons, inhalants, narcotics
sedatives/hypnotics
Alcohol, anticholinergics (including cold remedies), cocaine, heroin, LSD, marijuana, phencyclidine, sympathomimetics
Ethanol, narcotics, phencyclidine
Amphetamines, cocaine, LSD, marijuana, phencyclidine
Ethanol, phencyclidine (both vertical and horizontal), sedatives/hypnotics
Alcohols, amphetamines, anticholinergics, GHB, hydrocarbons, opioids, phencyclidine, physostigmine
Tricyclic antidepressants
Sympathomimetics
19
Pediatric Emergency Medicine Practice©
tually dependence occur. 121 Some symptoms that
have been described with GHB withdrawal include
agitation, hallucinations, hypertension, and tachycardia. 122 If GHB withdrawal is suspected, large doses
of benzodiazepines, phenobarbital, or propofol may
be required. 2 Craig et al reported one case of severe
GHB withdrawal requiring 120 mg of diazepam and
507 mg of lorazepam over the course of 3.75 days,
while Chin reported a withdrawal case requiring
1,138 mg of lorazepam over a span of 4 days. 123, 124
companies that employ commercial class drivers to
have a drug testing system in place. This testing
program must test for five specific categories of
drugs collectively known as “NIDA 5.” Because of
this requirement, most drug testing companies offer
a basic urine test that screens for drugs in these categories; see Table 15.
The Substance Abuse and Mental Health
Services Association (SAMHSA) has guidelines for
what qualifies as a positive test, based on cutoff levels. If the immunoassay is positive, a second gas
chromatography must be done to confirm this.
The length of time that drugs can be detected
in the urine is variable. The ranges depend on
factors such as the amount and frequency of use,
metabolic rate, body mass, age, and drug tolerance; 132
see Table 16.
Rohypnol
Flunitrazepam (rohypnol) is a potent benzodiazepine
with rapid onset of action, usually within 30 minutes. It is legally available in more than 60 countries
for preoperative anesthesia, sedation, and treatment
of insomnia. It became an active recreational sedative
in the 1990s and gained popularity as a date rape
drug due to its rapidity of onset and amnestic properties. 71 It is also taken to alter the effects of other
drugs such as heroin and cocaine. 125
Rohypnol is supplied as a 1 or 2 mg tablet that is
olive green in color. The pills used to be white
which facilitated the ability to dissolve in the drink
of an unsuspecting person. The manufacturer,
Roche, added the dye to make improper use of the
drug more difficult. 6 The half-life of rohypnol is 16
to 35 hours and may cause loss of consciousness for
up to 48 hours. 126 Adverse effects include hypotension, lethargy, dizziness, confusion, and visual disturbances. All effects of the drug are more pronounced with the concomitant ingestion of other
sedating drugs such as alcohol.
False Positive Drug Screens
There are many anecdotal reports of various substances causing false positive results on urine drug
screens. The literature is contradictory on the ability
of different drugs to cause a false positive result for
an opiate. Dextromethorphan is one such drug. A
prospective study was performed in which 20
patients were given dextromethorphan, codeine,
and placebo in both the standard and the double
dose. An Enzyme-Multiplied Immunoassay
Technique (EMIT) screen performed six hours after
ingestion was negative for all patients. 135 A false positive result for PCP is possible, but the GC-MS will be
negative. 74, 131, 134
The fluoroquinolones, especially levofloxacin
and ofloxacin, can give a false positive opiate result
for at least 24 hours after the last dose. 131 Rifampin
can also cause a false positive opiate result. 95 Poppy
seeds contain codeine and morphine and can cause a
positive result on the initial assay. All potential false
positive results can be confirmed or contradicted by
GC-MS.
Emergency Department Management
Diagnostic Evaluation
Urine Immunoassays For Drugs Of Abuse
Urine collection is simple, noninvasive, and generally contains high concentrations of drugs and their
metabolites. 131 Immunoassays are the most commonly used method to screen urine samples for drugs of
abuse. Immunoassays are specific only for a class of
drugs and not an individual substance. Positive test
results are confirmed with either gas chromatography (GC) or GC in combination with mass spectrometry (GC-MS), which is considered to be the gold
standard. These confirmatory tests are expensive
and time consuming. 131
Federal government guidelines, including the
National Institute on Drug Abuse (NIDA), require
Pediatric Emergency Medicine Practice©
Table 15.
Drugs Detected in Basic Urine Drug Screen (NIDA 5)
Cannabinoids
Opiates
Cocaine
Phencyclidine
Amphetamines
Drugs Detected by Expanded Screens
Barbiturates
Methadone
Hydrocodone
Propoxyphene
Methaqualone
MDMA (Ecstasy)
Benzodiazepines
20
October 2006 • EBMedicine.net
Treatment
Secure the ABCs. Intubation is necessary for severe
respiratory distress, respiratory failure, airway
obstruction, or altered mental status that does not
rapidly clear. Agitation from most overdoses will
respond to adequate doses of benzodiazepines.
However, it is crucial to exclude trauma, hypoxia,
hypercarbia, and hypoglycemia as a cause of agitation prior to sedation and further evaluation. The
central nervous system plays a key role in sympathomimetic toxicity. Benzodiazepines will decrease
agitation and attenuate the rise in blood pressure
and heart rate secondary to cocaine and amphetamines. 110 Hyperthermia is often seen with agitation
and can be profound. It can be treated with appropriate passive and/or active cooling measures,
depending on the severity. The hyperthermia,
hypertension, and tachycardia will often resolve once
the agitation is controlled. Severe hypertension
refractory to benzodiazepines may be treated with
nitroglycerin, nitroprusside, or phentolamine.
Traditionally, beta blockers have been avoided in the
setting of sympathomimetic-induced hypertension
and tachycardia, based on the rationale that beta
blockade would lead to the unopposed alpha adrenergic stimulation caused by the drug, leading to
increased heart rate and blood pressure. Labetalol
has been used in this setting with success. Labetalol
is a mixed beta and alpha antagonist, with the beta
effects predominating. No clinical ED studies were
found that prospectively investigated the use of
labetalol in sympathomimetic toxicity. However,
several authors argue for the safety and efficacy of
selective beta blockers in treating the cardiotoxic
effects of cocaine. 110, 111, 113
Those that have orally ingested cocaine or
amphetamines should receive activated charcoal, and
whole-bowl irrigation may be necessary in body
packers who consume large quantities or drugs. 23
Surgical consultation is often necessary in body
packers that develop bowel obstruction or a ruptured packet, and endoscopic removal is contraindicated in these packers due to risking increased packet perforation. 23
Stimulant-induced cardiac ischemia should be
treated with benzodiazepines and nitrates, as needed.
The role for aspirin and thrombolytics is less clear.
Rhabdomyolysis can occur with many drugs, especially in the setting of agitation. It is treated with
aggressive hydration and alkalinization of the urine.
Seizures will also respond to benzodiazepines
Management Of Drug Intoxication
The management of the adverse effects of illicit
drugs is largely symptomatic and not specific to any
particular drug class. Treatment of illicit drug overdose is limited to supportive care and search for
complications in most cases. However, there are a
few caveats for certain drugs that will be discussed.
Diagnostic Testing
Useful tests to obtain in a patient with known or suspected substance abuse include electrolytes, blood
urea nitrogen, creatinine, urinalysis, liver enzymes,
complete blood count (CBC), and a pregnancy test,
when appropriate. Unexpected abnormalities of electrolytes may suggest the diagnosis in a patient not
previously suspected of inhalant abuse. 82 A chest
radiograph is necessary to exclude pneumothorax,
pneumomediastinum, chemical pneumonitis, aspiration, and pulmonary edema. An electrocardiogram
may detect dysrhythmias or conduction delays or
raise suspicion for unsuspected coingestants such as
tricyclic antidepressants. Ischemic changes may be
seen with stimulant toxicity. A CBC may identify
aplastic anemia in benzene intoxication but has little
utility as a routine screening test. An elevated white
blood cell count may raise suspicion of infection as
the cause of altered mental status, but a normal WBC
count does not exclude infection. Methylene chloride intoxication should prompt evaluation of carboxyhemoglobin levels. Elevated liver enzymes may
identify toxic hepatitis from carbon tetrachloride
intoxication which may be amenable to treatment
with N-acetylcysteine (NAC). Animal studies have
shown promise for the use of NAC and deferoxamine in the treatment of hepatic necrosis due to carbon
tetrachloride toxicity. 96 A creatinine kinase level is
indicated to exclude rhabdomyolysis. Any patient
with unexplained altered mental status needs a CT
scan of the brain. Qualitative or quantitative tests to
detect solvents are not readily available at most hospitals and thus are not indicated in the emergency
department setting. Concomitant acetaminophen or
aspirin toxicity should be sought as these overdoses
require specific treatment. Alcohol is a common coingestant and may explain some of the symptoms.
An alcohol level is a reasonable test as this will help
predict how long it will take the patient’s mental status to clear if alcohol is the sole intoxicant.
EBMedicine.net • October 2006
21
Pediatric Emergency Medicine Practice©
Ten Pitfalls To Avoid
was using PCP. Who knew that the dextromethorphan he was given for his cough
would cause a false positive drug screen?”
1. “The urine drug screen was negative so I didn’t
think he had done any drugs.”
A basic urine drug screen is designed to detect
the major drug classes. There are many substances of abuse that are not detected on basic
screens. A negative screen does not rule out an
intoxicant as the source of symptoms.
Use caution when interpreting the results of a
basic urine drug screen, as many things can
cause a false positive result.
7. “I didn’t think about accidental cocaine ingestion as a cause of the child’s seizure and hypertension. The mother did not say that there was
any cocaine in the house.”
2. “He woke up after receiving naloxone and wanted to go home so I let him. How should I have
known he would stop breathing at home?”
The presence of illegal drugs in a home is not
something people will readily disclose. An
unsupervised child will often put anything in
their mouth that they find, including drugs.
Inquiry about the presence of drugs is indicated
in any clinical situation that raises suspicion. A
urine drug screen may be helpful in situations
where the possibility of accidental drug ingestion exists.
The duration of action of naloxone is shorter
than the duration of action of many narcotics.
Therefore the naloxone may wear off before the
effects of the narcotic(s) do. There is a risk of
recurrence of respiratory depression and the
patient may not be safe for discharge.
3. “I thought her agitation was due to Ecstasy. She
said she took some. She didn’t tell me she had
been assaulted. I never thought she would
have a subdural hematoma.”
8. “He took a handful of pills three hours ago on a
dare. Now he has nausea and mild tachycardia.
He needs a gastric lavage, right?”
Even with a history of drug ingestion, use caution in attributing symptoms solely to the drug
without excluding other causes of altered mental
status.
Gastric lavage is no longer recommended in
most overdose patients. It is usually reserved for
potentially lethal ingestions that present early,
often within an hour of ingestion.
4. “She told me she only took some MDMA. I
didn’t think to check for acetaminophen or
aspirin toxicity.”
9. “Her oxygen saturation is 98%. She seemed to
be breathing fine. Why did she have a respiratory arrest?”
Aspirin and acetaminophen are common coingestants in intentional overdoses, but may also
be present in a patient who has taken unknown
pills that were given to them by someone else.
Toxicity with these agents can be fatal but is
treatable if detected in time. Consider checking
these levels on any patient that has taken pills.
Patients with altered mental status and hypoventilation may have a normal or near normal oxygen saturation. However, inadequate ventilation
will lead to respiratory acidosis and an increasing pCO2. The acidosis may progress to such
severity that respiratory arrest occurs. An arterial blood gas (ABG) is useful in this setting to
exclude hypercarbia, although the ABG should
not be the sole determining factor in a patient
clinically requiring intubation.
5. “He says he had been huffing solvents and now
has wheezing and shortness of breath. Why
did the albuterol make him develop ventricular
tachycardia?”
Volatile substance abuse can sensitize the
myocardium to catecholamines. The use of a
beta-agonist in this setting can be helpful, but its
use is also dangerously unpredictable as cardiac
dysrhythmias may develop.
10. “I thought Flumazenil was the treatment for
benzodiazepine overdose. Why is he seizing?”
Flumazenil is useful in an acute overdose of a
benzodiazepine in a patient who does not use
these drugs chronically. It can precipitate
intractable seizures in someone who uses benzodiazepines chronically and should be used with
caution.
6. “After I got off the phone with patient relations,
I realized that it was probably not a good idea
to tell the parents of a 16-year-old boy that he
Pediatric Emergency Medicine Practice©
22
October 2006 • EBMedicine.net
and will rarely require antiepileptic medications.
Antipsychotic agents are best avoided as they may
precipitate seizures in association with certain overdoses, such as PCP.
There are no specific antidotes for inhalant toxicity in most cases. The patient should be removed
from the source of exposure and given supplemental
oxygen and intravenous access should be obtained.
Decontaminate the patient’s skin, eyes, and mucous
membranes with irrigation. 82 Bronchospasm can be
treated with inhaled beta-agonists, but extreme caution must be applied in providing beta-agonist bronchodilating agents to an inhalant-sensitized
myocardium. There is no absolute way to determine
whether or not the patient’s myocardium has
become sensitized. Vasopressors should be used cautiously as well for this reason. Corticosteroids and
prophylactic antibiotics are not recommended. 82 The
priority of a patient presenting with a narcotic overdose is an assessment of their respiratory status. If
they do not require any respiratory support, observation alone should be sufficient. An arterial blood gas
is useful to assess oxygenation and ventilation.
Naloxone is an important adjunct in the treatment of narcotic overdose. Naloxone is a pure opioid antagonist that has been in use since the 1970s.
Naloxone has a rapid onset of action (1 min) and a
short half-life (20 min). Naloxone is preferably given
intravenously. It can also be given intramuscularly
and subcutaneously or through the endotracheal
tube if intravenous access is not available. Its duration of action is 20 to 60 minutes, and patients may
redevelop respiratory depression after naloxone
wears off because of the longer half life of heroin and
other opiates such as methadone and propoxyphene.
Naloxone reverses the respiratory depression and the
analgesia, coma, and miosis that occur with heroin
overdose and may prevent the need for mechanical
ventilation. It may also reverse the cardiovascular
effects of an overdose. Naloxone use may precipitate
withdrawal syndrome in patients who are dependent
on narcotics. In patients with concomitant drug overdose, naloxone may unmask the effects of other
drugs. For example, high doses of naloxone that
completely blocks the effects of heroin may lead to
unopposed alpha receptor stimulation in mixed overdoses that involve cocaine or amphetamines and lead
to seizures, dysrhythmias, or combativeness. 103, 104
The dose of naloxone in a child less than 20 kg is
0.1 mg/kg IV/IM every two to three minutes as
needed based on response. For children greater than
20 kg, the dose of naloxone is the same as in adults.
The naloxone adult dose is 0.2 to 2 mg IV/IM every
two to three minutes until desired effect or total of 10
mg is reached. Naloxone infusions are often
required to counteract the longer-acting narcotics.
The infusion usually consists of two-thirds of the
dose required to reverse the narcotic given as an
hourly infusion. 138 Nalmefene, an opioid antagonist
with a half-life of 8 to 11 hours, is currently being
further studied in children but has been shown to be
safe in treating the reversal of opiate procedural
sedation in this patient population. 139, 140
Use of atropine has also been recommended in
cases of symptomatic bradycardia associated with
GHB intoxication. 118 There have also been reports of
improvement with physostigmine. Yates and Viera
reported using 2 mg of IV physostigmine in two separate patients intoxicated with GHB. They noted
that both patients awoke within five minutes of
physostigmine administration. 42 However, Traub et
al indicated that there is inadequate evidence to fully
support the use of physostigmine in treating GHB
intoxication in the ED. 119 In addition, this medication
Table 16. Detection Periods and Detection Cutoffs for Positive Results
Drug
Detection period in urine
Immunoassay
GC-MS
1 to 4 days
1000 ng/ml
500 ng/ml
Opiates
8 hours to 4 days
300 ng/ml
300 ng/ml
Cocaine
4 to 5 days
300 ng/ml
150 ng/ml
Cannabis
2 days to 12 weeks
50 g/ml
15 ng/ml
3 to 7 days
25 ng/ml
25 ng/ml
Amphetamine
PCP
EBMedicine.net • October 2006
23
Pediatric Emergency Medicine Practice©
tions, confusion, and seizures along with peripheral
symptoms such as tachycardia, hyperpyrexia, and
mydriasis. Dramatic reversal of the anticholinergic
symptoms can be seen after the administration of
physostigmine. The duration of action is 45 to 60
minutes. The reversal of delirium after administration of physostigmine might confirm an anticholinergic cause and potentially prevent the need for further
diagnostic testing such as CT. A retrospective review
examined 39 patients who were given physostigmine
in the ED. Nineteen patients had a purely anticholinergic cause of their delirium and all had full
reversal of their delirium with physostigmine.
However, 90% had a relapse of symptoms while in
the ED. One patient had a brief seizure after the
medication was administered, but he had had a
seizure before the drug was administered as well.
Asystole or ventricular tachycardia are the most significant complications of physostigmine use, but fortunately, are rare. 128, 129, 136
Physotigmine has also been proposed as a treatment for GHB toxicity. This recommendation was
based on a relatively small case series. It was noted
to be effective but many confounding factors were
present. Due to the limited experiences in the use of
physostigmine with GHB and the lack of experience
with its use under the conditions prevalent in the
ED, there is insufficient evidence to recommend its
routine use in the treatment of GHB toxicity. 5, 41, 119, 91, 97
The dose is 0.5 mg to 2 mg IV slow, IV push, or
IM. The pediatric dose is 0.02 mg/kg IV or IM.
Dosage may be repeated at five to ten minute intervals to a maximum of 2 mg. Most anticholinergic
agents have a longer half-life than physostigmine, so
multiple boluses or an infusion are required. A toxicologist should be consulted before physostigmine is
used in the ED. 136
may be particularly dangerous in patients that have
also ingested other substances such as tricyclic antidepressants, where asystole can occur. 120
Most patients with drug overdose can be discharged with a responsible adult friend or family
member after symptoms abate after approximately
six hours of ED observation. Admission is indicated
for severe symptoms or presence of a complication
such as rhabdomyolysis, pulmonary edema, or status
epilepticus.
Controversies
The purpose of this section is to discuss the areas
where the dogma has changed in recent years, such
as with GI decontamination or where a test may not
provide the information the clinician seeks, such as a
urine drug screen.
Gastrointestinal Decontamination
GI decontamination for known or potentially toxic
ingestions remains an area of controversy. A full discussion of this topic is outside the scope of this article. Some issues involving GI decontamination are
unresolved, but the majority of the literature supports the following conclusions: 127
1. Activated charcoal adsorbs almost all commonly
ingested drugs and should be given as quickly as
possible to most patients who have ingested a
potentially toxic substance. It is not useful in
ingestions of iron, lithium, ethanol, potassium,
caustics, petroleum distillates, methanol, or ethylene glycol.
2. Gastric lavage is of unproven benefit for routine
use. It is best reserved for patients who have
recently ingested a toxic amount of a poison with
life-threatening potential.
3. Cathartics are of unproven benefit.
4. There is theoretical but unproven benefit of
whole bowel irrigation in ingestions such as sustained-release preparations or illicit drug packet
ingestions.
5. Activated charcoal is typically given as a waterbased slurry via mouth or NG tube. The dose is
50 g for adults and 1 g/kg for children.
Flumazenil
Flumazenil is a benzodiazepine antagonist that binds
at the benzodiazepine receptor and reverses the
GABA effects in the CNS. Flumazenil reverses benzodiazepine-induced sedation in one to two minutes. It
also reverses other effects of benzodiazepines, such as
the anticonvulsant effects. Respiratory depression
may be incompletely reversed. Seizures have been
reported after flumazenil administration. In one
study that reviewed the use of flumazenil in 750
patients, five patients experienced seizures after
receiving large boluses of flumazenil. Three of the
five patients had taken large overdoses of tricyclic
Physostigmine
Physostigmine is a reversible acetylcholinesterase
inhibitor that can temporarily reverse the effects of
anticholinergic agents. The anticholinergic syndrome can present with delirium, anxiety, hallucina-
Pediatric Emergency Medicine Practice©
24
October 2006 • EBMedicine.net
medications. In another study of 497 patients given
flumazenil, six patients experienced seizures. All of
the patients had either taken cyclic antidepressants,
had a history of seizure disorder, or had jerking movements prior to the administration of flumazenil. 98
The use of flumazenil should not replace appropriate supportive care of the patient with altered
mental status. It is contraindicated in the presence of
hypoxia, hypotension, and dysrhythmias or in
patients who have ingested proconvulsant agents.
Despite the potential utility in patients with altered
mental status (AMS) of unclear etiology or the desire
to prove benzodiazepine ingestion as the cause of
AMS, avoid the temptation to use flumazenil in
undifferentiated AMS. The risk of seizures outweighs the benefits in most patients. Its use should
be reserved for iatrogenic benzodiazepine overdose
or in children with known isolated benzodiazepine
ingestion with absence of the known contraindications. 130
Flumazenil for benzodiazepine reversal is generally not recommended in acute patients in the ED as
its use can cause seizures in patients who have been
using benzodiazepines for prolonged periods.
However, a benzodiazepine overdose is not usually
life-threatening if adequate ventilation is assured, so
the administration of an agent that may cause
intractable seizures is not often indicated.11, 13, 14
action than naloxone. It is not recommended in
patients who are dependent on opiates as it may precipitate withdrawal symptoms for an extended period of time.
Disposition
Most drug intoxication patients can be discharged
with a responsible adult after their symptoms have
resolved and their diagnostic studies are normal.
Most authors agree that six hours is a reasonable
amount of observation time in the ED or an observation unit. Indications for admission are noted in
Table 17.
References
Evidence-based medicine requires a critical appraisal
of the literature based upon study methodology and
number of subjects. Not all references are equally
robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight
than a case report.
To help the reader judge the strength of each reference, pertinent information about the study, such
as the type of study and the number of patients in
the study, will be included in bold type following the
reference, where available.
1.
Johnston LD, O’Malley PM, Bachman JG, et al. Teen
drug use down but progress halts among youngest
teens. University of Michigan news and information
services: Ann Arbor, MI. [On-line]. Available at:
http://www.monitoringthefuture.org/data/05data/pr
05t1.pdf and http://www.monitoringthefuture.org/
data/05data.html#2005data-drugs. Accessed: April,
2006.
2. Greydanus DE, Patel DR. The adolescent and substance abuse: current concepts. Dis Mon 2005;51(7):392431. (Review)
3. Greydanus DE. Patel DR. MD Substance abuse in adolescents: a complex conundrum for the clinician Pediar
Clin North Am 2003;50(5):1179-1223. (Review)
4. Patel DR, Greydanus DE. Substance abuse: a pediatric
concern. Indian J Pediatrics 1999;66:557–567. (Review)
5. Ries NL, Dart RC. New developments in antedotes.
Med Clin North Am 2005;89:1379-1397. (Review)
6. U.S. Drug Enforcement Administration. August, 2006.
Available at: www.dea.gov. Accessed: April, 2006.
7. Drug Abuse Warning Network: Trends from drug
abuse warning network, Final Estimates 1995-2002,
DAWN series: D-24, 2003, Rockville, MD: Office of
Applied Studies, SAMHSA, Drug Abuse Warning
Nalmefene
Nalmefene (Revex) is a narcotic antagonist that may
be effective in reversing the respiratory and CNS
depression associated with opioid overdose.
Nalmefene has a considerably longer duration of
Table 17. Indications For Admission In
Intoxicated Patients
Persistent severe hypertension or tachycardia
Cardiac ischemia
Prolonged or recurrent hypoxia/hypoventilation
Rhabdomyolysis
Renal insufficiency
Metabolic acidosis
Methemoglobinemia
Dysrhythmias
Unable to tolerate oral intake
Severe agitation
Unreliable/unstable home situation
Acetaminophen or aspirin toxicity
Persistent severe hypotension or bradycardia
EBMedicine.net • October 2006
25
Pediatric Emergency Medicine Practice©
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
21.
22.
Network; 2003. Available at http://www.dawninfo.
samhsa.gov. Accessed: March 15, 2006.
Ashton H, Hassan Z. Best evidence topic report.
Intranasal naloxone in suspected opioid overdose.
Emerg Med J 2006;23(3):221-223. (Review)
Barton ED, Colwell CB, Wolfe T, et al. Efficacy of
intranasal naloxone as a needleless alternative for
treatment of opioid overdose in the prehospital setting.
J Emerg Med 2005;29(3):265-271. (Prospective, 95
Patients)
Kelly AM, Kerr D, Dietze P,et al. Randomised trial of
intranasal versus intramuscular naloxone in prehospital treatment for suspected opioid overdose. Med J
Aust 2005;182(1):24-27. (Prospective, 155 Patients)
Seger DL. Flumazenil—treatment or toxin. J Toxicol
Clin Toxicol 2004;42(2):209-211. (Review)
Miller MA, Martinez V, McCarthy R, et al. Nitrous
oxide “whippit” abuse presenting as clinical B12 deficiency and ataxia. Am J Emerg Med 2004;22(2):124.
(Case Report)
Haverkos, GP, DiSalvo RP, Imhoff TE. Fatal seizures
after flumazenil administration in a patient with mixed
overdose. Ann Pharmacother 1994;28(12):1347-1349
(Case Report)
Mordel A, Winkler E, Almog S, et al. Seizures after
flumazenil administration in a case of combined benzodiazepine and tricyclic antidepressant overdose.
Crit Care Med 1992;20(12):1733-1734. (Case Report)
Delaney KA, Kolecki P. CNS Depression. In: Ford MD,
Delaney KA, Ling LJ, eds. Clinical Toxicology. 1st ed.
Philadelphia, PA: W B Saunders; 2001: 137-145.
(Textbook)
Mokhlesi B, Leiken JB, Murray P, et al. Adult Toxins in
Critical Care Part I: General approach to the intoxicated patient. Chest 2003:123(2):577-592. (Review)
Del Rios M, Lanigan M, Zayas V. Drugs of abuse: providing the best in evidence-based care to “self-medicated” patients. Emergency Medicine Practice 2005;7:5
(Review)
Boghdadi MS, Henning RJ. Cocaine: pathophysiology
and clinical toxicology. Heart Lung 1997;26(6):466-481.
(Review)
Reynolds EW, Bada HS. Pharmacology of drugs of
abuse. Obstr and Gyn Clin 2003;30(3):501-522. (Review)
Shanti CM, Lucas CE. Cocaine and the critical care
challenge. Crit Care Med 2003;31(6):1851-1859. (Review)
Ritz MC, Lamb RJ, Goldberg SR, et al. Cocaine receptors on dopamine transporters are related to selfadministration of cocaine. Science 1987;237:1219-1223.
(Basic Science)
Reith ME, Meisler BE, Sershen H, et al. Structural
requirements for cocaine congeners to interact with
dopamine and serotonin uptake sites in mouse brain
Pediatric Emergency Medicine Practice©
23.
24.
25.
26.
27.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
26
and to induce stereotyped behavior. Biochem Pharmacol
1986;35:1123-1129. (Basic Science)
Mokhlesi B, Leiken JB, Murray P, et al. Adult Toxins in
Critical Care Part II: Specific poisonings. Chest
2003:123(3):897-922. (Review)
Rimsza ME, Moses KS. Substance abuse on the college
campus. Pediatr Clin North Am 2005;52(1):307-319.
(Review)
Wolff AJ, O’Donnell AE. Pulmonary effects of illicit
drug use. Clin Chest Med 2004;25(1)203-216. (Review)
Friedman MJ, Sharieff GQ. Seizures in children. Pediatr
Clin North Am 2006;53(2):257-277. (Review)
Velasquez EM, Anand RC, Newman WP 3rd, et al.
Cardiovascular complications associated with cocaine
use. J La State Med Soc 2004;156(6):302-310. (Review)
O’Connor AD, Rusyniak DE, Bruno A. Cerebrovascular
and cardiovascular complications of alcohol and sympathomimetic drug abuse. Med Clin North Am
2005;89(6):1343-1358. (Review)
Muniz AE, Evans T. Acute gastrointestinal manifestations associated with use of crack. Am J Emerg Med
2001;19(1):61-63. (Case Series)
Brody SL, Slovis CM, Wrenn KD. Cocaine-related medical problems: consecutive series of 233 patients. Am J
Med 1990;888(4):325-331. (Retrospective, 233 Patients)
Hollander JE, Hoffman RS, Gennis P, et al. Prospective
multicenter evaluation of cocaine-associated chest
pain. Cocaine Associated Chest Pain (COCHPA) Study
Group. Acad Emerg Med 1994;1(4):330-339. (Prospective
Observational, 246 Patients)
Hollander JE, Henry TD. Evaluation and management
of the patient who has cocaine-associated chest pain.
Cardiol Clin 2006;24(1):103-114. (Review)
Weber JE, Chudnofsky CR, Boczar M, et al. Cocaineassociated chest pain: how common is myocardial
infarction? Acad Emerg Med 2000;7(8):873-877.
(Retrospective, 250 Patients)
Pletcher MJ, Kiefe CI, Sidney S, et al. Cocaine and
coronary calcification in young adults: The Coronary
Artery Risk Development in Young Adults (CARDIA)
Study. Am Heart J 2005;150:921-926. (Prospective, 3038
Patients)
Hsue PY, Salinas CL, Bolger AF, et al. Acute aortic dissection related to crack cocaine. Circulation
2002;105(13):1592-1595. (Retrospective, 38 Patients)
NIDA. NIDA InfoFacts: Methamphetamine. Available
at: http://www.drugabuse.gov/infofacts/methamphetamine.html. Accessed: March 12, 2006.
Derlet RW, Heischober B: Methamphetamine-Stimulant
of the 1990s? West J Med 1990;153:625-628. (Review)
Allcott JV III, Barnhart RA, Mooney LA. Acute lead
poisoning in two users of illicit methamphetamine.
JAMA 1987;258:510-511 (Case Series)
October 2006 • EBMedicine.net
39. Mackenzie RG, Heischober B. Methamphetamine.
Pediatr Rev 1997;18:305-309. (Review)
40. Albert Hoffman: LSD My Problem Child: How LSD
Originated. Available at: http://www.flashback.se/
archive/my_problem_child/chapter1.html Accessed:
October, 2006
41. Henderson RS, Holmes CM. Reversal of the anesthetic
action of sodium gamma-hydroxybutyrate. Anaesth
Intensive Care 1976;4:351-354. (Prospective, 25
Patients)
42. Yates SW, Viera AJ. Physostigmine in the treatment of
gamma-hydroxybutyric acid overdose. Mayo Clin Proc
2000;75(4):401-402. (Case Series)
43. Baylen CA, Rosenberg H. A review of the acute subjective effects of MDMA/ecstasy. Addiction
2006;101(7):933-947. (Review)
44. Haroz R, Greenberg M. Emerging Drugs of Abuse.
Med Clin of North America 2005;89(6):1259-1276.
(Review)
45. Brvar M, Kozelj G, Osredkar J, et al. Polydipsia as
another mechanism of hyponatremia after ‘ectasy”
ingestion. Eur J Emerg Med 2004;11:302-304. (Case
Report)
46. Haroz R, Greenberg MI. New drugs of abuse in North
America. Clin Lab Med 2006;26:147-164. (Review)
47. Bye C, Munro-Faure AD, Peck AW, et al. Comparison
of the effects of 1-benzylpiperazine and dexamphetamine on human performance tests. Eur J Clin Pharmacol
1973;6(3):163-169. (Basic Science)
48. Drug Enforcement Agency. Drug Intelligence Brief.
Trippin’ on tryptamines. Oct 2003. (Review)
49. Smolinske SC, Rastogi R, Schenkel S. Foxy methoxy: a
new drug of abuse. Int J Med Toxicol 2004;7(1):3. (Case
Report)
50. Long H, Nelson LS, Hoffman RS. Alpha-methyltryptamine revisited via easy Internet access. Vet Human
Toxicol 2003;45(3):149. (Review)
51. Baumann MH, Clark RD, Budzynsk AG, et al. N-substituted piperazines abused by humans mimic the
molecular mechanism of 3,4-methylenedioxymethamphetamine (MDMA, or ‘Ecstasy’).
Neuropsychopharmacology 2005;30(3):550-560. (Basic
Science)
52. Tancer ME, Johanson CE. The subjective effects of
MDMA and mCPP in moderate MDMA users. Drug
Alcohol Depend 2001;65(1):97-101. (Basic Science)
53. NIDA. NIDA InfoFacts: MDMA (Ecstasy). Available at:
http://www.nida.nih.gov/Infofacts/ecstasy.html.
Accessed May 10, 2006.
54. Maurer HH, Kraemer T, Springer D, et al. Chemistry,
pharmacology, toxicology, and hepatic metabolism of
designer drugs of the amphetamine (ecstasy), piperazine, and pyrrolidinophenone types: a synopsis. Ther
EBMedicine.net • October 2006
55.
56.
57.
58.
59.
60.
61.
62.
63.
64.
65.
66.
67.
68.
69.
70.
27
Drug Monit 2004;26(2):127-131. (Review)
Wikstrom M, Holmgren P, Ahlner J. A2 (N-benzylpiperazine) a new drug of abuse in Sweden. J Anal
Toxicol 2004;28(1):67-70. (Review)
Anonymous. The Vaults of EROWID. Piperazine
Basics. Available at: http://www.erowid.org/
chemicals/piperazines/piperazines_basics.shtml.
Accessed: April 2006.
de Boer D, Bosman IJ, Hidvegi E, et al. Piperazine-like
compounds: a new group of designer drugs-of-abuse
on the European market. Forensic Sci Int 2001;121(12):47-56. (Review)
Ajaelo I, Koenig K, Snoey E. Severe hyponatremia and
inappropriate antidiuretic hormone secretion following
ecstasy use. Acad Emerg Med 1998;5:839-840. (Case
Report)
McCarron MM, Schulze BW, Thompson GA, et al.
Acute phencyclidine intoxication: incidence of clinical
findings in 1,000 cases. Ann Emerg Med 1981;10:237242. (Retrospective, 1000 Patients)
Akmal M, Valdin JR, McCarron MM, et al.
Rhabdomyolysis with and without acute renal failure
in patients with phencyclidine intoxication. Am J
Nephrol 1981;1:91-96. (Retrospective, 1000 Patients)
Eastman JW, Cohen SN. Hypertensive crisis and death
associated with phencyclidine poisoning. JAMA
1975;231:1270-1271. (Case Series)
Baldridge EB, Bessen HA. Phencyclidine. Emerg Med
Clin North Am 1990;8(3):541-550. (Review)
Johns Hopkins: The Harriet Lane Handbook: A Manual for
Pediatric House Officers. 17th ed. Mosby 2005.
Patel R, Das M, Palazzolo M, et al. Myoglobinuric
acute renal failure in phencyclidine overdose: report of
observations in eight cases. Ann Emerg Med
1980;9(11):549-553. (Case Series)
Bessen HA. Intracranial hemorrhage associated with
phencyclidine abuse. JAMA 1982;248(5):585-586. (Case
Report)
Boyko OB, Burger PC, Heinz ER. Pathological and
radiological correlation of subarachnoid hemorrhage in
phencyclidine abuse: case report. J Neurosurg
1987;67:446-448. (Case Report)
Clark RF, Williams SR. Hallucinogens. In: Marx JA,
Hockberger RS, Wall RM, et al, eds. Rosen’s Emergency
Medicine: Concepts and Clinical Practice. 5th ed. St.
Louis: Mosby; 2002:2149. (Textbook)
Krystal JH, Karper LP, Seibyl JP, et al. Subanesthetic
effects of the noncompetitive NMDA receptor antagonist, ketamine, in humans. Arch Gen Psychiatriy
1994;51:199-214. (Basic Science)
Tellier PP. Club drugs: is it all ecstasy? Pediatr Ann
2002;31:550-556. (Review)
Jansen KL. Non-medical use of ketamine. BMJ
Pediatric Emergency Medicine Practice©
71.
72.
73.
74.
75.
76.
77.
78.
79.
80.
81.
82.
83.
84.
85.
86.
87.
1993;306:601-602. (Review)
Gahlinger PM. Club drugs: MDMA, gamma-hydroxybutyrate (GHB), rohypnol, and ketamine. Amer Fam
Phys 2004;69(11):2619-2626. (Review)
Watson W. Toxic exposure surveillance system dextromethorphan data. 2003; Washington, DC: American
Association of Poison Control Centers.
Miller SC. Letter to the editor. Coricidin HBP cough
and cold addiction. J Amer Acad Child Adolesc Psychiatry
2005;44(6). (Letter)
Green JP, Ahrendt D, Stafford EM. Adolescent abuse of
other drugs. Adolesc Med Clin 2006;17(2):283-318.
(Review)
White W. The dextromethorphan experience FAQ.
Available at: www.erowid.org. Accessed May, 2005.
Kurtzman TL, Otsuka KN, Wahl RA. Inhalant abuse by
adolescents. J Adolesc Health 2001;28:170–180. (Review)
Wolfe T, Caravati E. Massive dextromethorphan ingestion and abuse. Am J Emerg Med 1995;13:174-176. (Case
Report)
Schier J, Diaz JE. Letter to the editor. Avoid unfavorable consequences: dextromethorphan can bring about
a false positive PCP urine drug screen. J Emerg Med
2000;18(3):379-383. (Letter)
Childers SR, Breivogel CS. Cannabis and endogenous
cannabinoid systems. Drug Alcohol Depend 1998;51(12):173-187. (Review)
Bonkowsky JL, Sarco D, Pomeroy SL. Ataxia and shaking in a 2-year old girl: acute marijuana intoxication
presenting as a seizure. Pediatr Emerg Care
2005;21(8):527-528. (Case Report)
Copersino ML, Boyd SJ, Tashkin DP, et al. Cannabis
withdrawal among non-treatment-seeking adult
cannabis users. Am J Addict 2006;15(1):8-14.
(Retrospective, 104 Patients)
Gussow LM. Inhalants of abuse. In: Ford MD, Delaney
KA, Ling LJ, eds. Clinical Toxicology 1st ed.
Philadelphia, PA: W B Saunders; 2001:651-655.
(Textbook)
Massengale ON, Glaser HH, LeLievre RE, et al.
Physical and psychologic factors in glue sniffing.
NEJM 1963;269:1340. (Review)
Grunbaum, Jo Anne, et al. Youth Risk Behavior
Surveillance—United States, 2003 Morbidity & Mortality
Weekly Report 2004;53(SS-2):1–29. (Government Report)
Sakai JT - Adolescent inhalant use among male
patients in treatment for substance and behavior problems: two-year outcome. Am J Drug Alcohol Abuse
2006;32(1):29-40. (Prospective, 80 Patients)
Bass M. Sudden sniffing death. JAMA
1970;212(12):2075-2079. (Case Report)
Cruz SL, Orta-Salazar G, Gauthereau MY, Millan-Perez
Pena L, Salinas-Stefanon EM. Inhibition of cardiac
Pediatric Emergency Medicine Practice©
sodium currents by toluene exposure. Br J Pharmacol
2003;140(4):653-60. (Basic Science)
88. El-Menyar AA, El-Tawil M, Al Suwaidi J. A teenager
with angiographically normal epicardial coronary
arteries and acute myocardial infarction after butane
inhalation. Eur J Emerg Med 2005;12(3):137-141. (Case
Report)
89. Pfeiffer H, Al Khaddam M, Brinkmann B, Kohler H,
Beike J. Sudden death after isobutane sniffing: a report
of two forensic cases. Int J Legal Med 2005;1-6. (Case
Series)
90. Streicher HZ, Gabow PA, Moss AH, et al. Syndromes
of toluene sniffing in adults. Ann Intern Med
1981;10:262. (Observational)
91. Yates SW, Viera AJ. Physostigmine in the treatment of
gamma-hydroxybutyrate toxicity: a review. J Toxicol
Clin Toxicol 2002;40:781-787. (Review)
92. McGarvery EL, Clavet GJ, Mason W. Adolescent
inhalant abuse: environments of use. Am J Drug Alcohol
Abuse 1999;25(4):731-741. (Prospective, 285 Patients)
93. Winek CL, Wahba WW, Rozin L. Death by nitrous
oxide inhalation. Forensic Sci Int 1995;73:139-141. (Case
Report)
94. Litovitz TL. 2000 Annual report of American
Association of Poison Control Centers Toxic Exposure
Surveillance System. Am J Emerg Med 2000;19:337-395.
95. Purucker M, Swann W. Potential for duragesic patch
abuse. Ann Emerg Med 2000;35(3):314. (Review)
96. Tharp AM, Winecker RE, Winston DC, et al. Fatal
intravenous fentanyl abuse. Am J Forensic Med Pathol
2004;25(2):178-181. (Case Series)
97. Allen L. Best evidence topic report: gammahydroxybutyrate overdose and physotigmine. Emerg Med J
2006;23:301-302. (Review)
98. Geller E, Crome P, Schaller MD, et al. Risks and benefits of therapy with flumazenil in mixed drug intoxications. Eur Neurol 1991;31:241-250. (Review)
99. Erowid. Types of inhalants. Available at:
http://www.erowid.org/chemicals/inhalants/inhalan
ts_info3.shtml. Accessed: May 10, 2006.
100. NIDA. NIDA InfoFacts: Heroin. Available at:
http://www.nida.nih.gov/infofacts/heroin.html.
Accessed: May 10, 2006.
101. http://www.tnccdaar.org/index.asp?view=
news_story_2&articleID=17069|CDC: Accessed: May
10, 2006.
102. Gossop M, Griffiths P, Powis B, et al. Frequency of
non-fatal heroin overdose: survey of heroin users
recruited in non-clinical settings. BMJ 1996;313-402.
(Prospective)
103. Sporer, KA. Acute heroin overdose. Ann Intern Med.
1999;130(7):584-590. (Review)
104. Sterrett C, Brownfield J, Korn CS, et al. Patterns of
28
October 2006 • EBMedicine.net
presentation in heroin overdose resulting in pulmonary edema. Am J Emerg Med 2003;21(1):32-34.
(Retrospective, 125 Patients)
105. U.S.Drug Enforcement Administration. Fentanyl.
Available at: http://www.usdoj.gov/dea/
concern/fentanyl.html Accessed: June 14, 2006.
106. U.S.Drug Enforcement Administration. Fentanyl.
Available at: http://www.usdoj.gov/dea/
concern/fentanyl.html Accessed: June 14, 2006.
107. http://www.usdoj.gov/dea/programs/
forensics/microgram/mg0506/mg0506.html
Accessed: May 1, 2006.
108. http://www.chron.com/cs/CDA/
printstory.mpl/nation/3970767 Accessed: Feb 15, 2006.
109. Neonjoint. How to make GHB. Available at:
http://www.neonjoint.com/drug_recipes/chapter4.ht
ml Accessed: Feb 15, 2006.
110. Sporer KA, Dorn E. Heroin-related non-cardiogenic
pulmonary edema: a case series. Chest
2001;120(5):1628-1632. (Case Series)
111. Spector I. AMP: a new form of marijuana. J Clin
Psychiatry 1985;46:498-499. (Review)
112. Anderson IB, Kim SY, Dyer JE, et al. Trends in gammahydroxybutyrate (GHB) and related drug intoxication:
1999 to 2003. Ann Emerg Med 2006;47(2):177-183.
(Review)
113. Drug Enforcement Administration. Fentanyl. Drugs
and chemicals of concern. DEA Diversion Program.
October 2004. (Government Report)
114. Elian AA. A novel method for GHB detection in urine
and its application in drug-facilitated sexual assaults.
Forensic Sci Int 2000;109(3):183-187. (Basic Science)
115. Saudan C, Augsburger M, Kintz P, et al. Detection of
exogenous GHB in blood by gas chromatography-combustion-isotope ratio mass spectrometry: implications
in postmortem toxicology. J Anal Toxicol 2005;29(8):777781. (Basic Science)
116. Goulle JP, Cheze M, Pepin G. Determination of
endogenous levels of GHB in human hair. Are there
possibilities for the identification of GHB administration through hair analysis in cases of drug-facilitated
sexual assault? J Anal Toxicol 2003;27(8):574-580. (Basic
Science)
117. Chin RL. A case of severe withdrawal from gammahydroxybutyrate [letter]. Ann Emerg Med 2001;37:551552.
118. Li J, Stokes SA, Woeckener A. A tale of novel intoxication: a review of the effects of gamma-hydroxybutyric
aid with recommendations for management. Ann
Emerg Med 1999;33(4):475-476. (Review)
119. Traub SJ, Nelson LS, Hoffman RS. Physostigmine as a
treatment for gamma-hydroxybutyrate toxicity: a
review. J Toxicol Clin Toxicol 2002;40(6):781-787.
EBMedicine.net • October 2006
(Review)
120. Mullins ME, Dribben W. Physostigmine treatment of
gamma-hydroxybutyric acid overdose: appropriate or
inappropriate use of a reversal agent? Mayo Clin Proc
2000;75:872-873. (Letter)
121. Gonzalez A, Nutt DJ. Gamma hydroxybutyrate abuse
and dependency. J Psychopharmacol 2005;19(2):195-204.
(Review)
122. Mason PE, Kerns WP 2nd. Gamma hydroxybutyric
acid (GHB) intoxication. Acad Emerg Med 2002;9(7):730739. (Review)
123. Craig K, Gomez HF, McManus JL, et al. Severe
gamma-hydroxybutyrate withdrawal: a case report
and literature review. J Emerg Med 2001;20(4):418-420.
(Case Report)
124. Chin RL, Sporer KA, Cullison B, et al. Clinical course
of gamma-hydroxybutyrate overdose. Ann Emerg Med
1998;31(6):716-722. (Review)
125. Waltzman ML. Flunitrazepam: a review of “roofies”.
Pediatr Emerg Care 1999;15:59-60. (Review)
126. Gussow L, Carlson A. Ch. 159 Inhalants of abuse. In:
Marx JA, Hockberger RS, Wall RM, et al, eds. Rosen’s
Emergency Medicine: Concepts and Clinical Practice.
5th ed. St. Louis: Mosby; 2002:2212. (Textbook)
127. American College of Emergency Physicians: Clinical
policy for the initial approach to patients presenting
with acute toxic ingestion or inhalation exposure. Ann
Emerg Med 1999;33:735-761. (Practice Parameter)
128. Tong TG, Benowitz NL, Becker CE, et al. Tricyclic
antipdepressant overdose. Drug Int Clin Pharm
1976;10:711-713. (Review)
129. Shannon M. Toxicoloy reviews: physostigmine. Pediatr
Emerg Care 1998;14:224-225. (Review)
130. Ford MD, Delaney KA, Ling LJ, eds. Clinical
Toxicology. 1st ed. Philadelphia, PA: W B Saunders;
2001;580. (Textbook)
131. Zacher JL, Givone DM. False-positive urine opiate
screening associated with flouroquinolone use. Ann
Pharmacology 2004;38:1525-1528. (Review)
132. Eskridge KD, Guthrie SD. Clinical issues associated
with urine testing of substances of abuse.
Pharmacotherapy 1997;17:497-510. (Review)
133. Ritter C, Reinke A, Andrades M, et al. Protective effect
of N-acetylcysteine and deferoxamine on carbon tetrachloride-induced acute hepatic failure in rats. Crit Care
Med 2004;32(10):2079-2084. (Basic Science)
134. Karp HN, Kaufman ND, Anand SK. Brief clinical and
laboratory observation: phencyclidine poisoning in
young children. J Pediatr 1980;97:1006-1009. (Review)
135. Storrow AB, Magoon MR, Norton J. The dextromethorphan defense: dextromethorphan and the
opioid screen. Acad Emerg Med 1995;2(9):791-794.
(Review)
29
Pediatric Emergency Medicine Practice©
seizures.
c. Most of cocaine’s adverse effects require only
treatment with benzodiazepine sedation.
d. Cocaine use is associated with acute myocardial infarction in 25% of patients aged 18 to
45 years who otherwise have no coronary
artery disease risk factors.
e. All of the above statements are true.
136. Schneir AB, Offerman SR, Ly BT, et al. Complications
of diagnostic physostigmine administration to emergency department patients. Ann Emerg Med
2003;42(1):14-19. (Retrospective, 39 Patients)
137. Drug Enforcement Agency. Drug Intelligence Brief.
Trippin’ on tryptamines. October 2003. (Government
Report)
138. Henry K, Harris CR. Deadly Ingestions. Pediatr Clin
North Am 2006;53(2):293-315. (Review)
139. Hantsch CE, Gummin DD. Opiods. In: Marx JA,
Hockberger RS, Wall RM, et al, eds. Rosen’s Emergency
Medicine: Concepts and Clinical Practice. 5th ed. St.
Louis: Mosby; 2002:2185. (Textbook)
140. Chumpa A, Kaplan RL, Burns MM, et al. Nalmefene
for elective reversal of procedural sedation in children.
Am J Emerg Med 2001;19(7):545-548. (Open-Label
Clinical Trial, 15 Patients)
52. Methamphetamine:
a. Has a shorter duration of action than
amphetamines.
b. Has less CNS stimulant and more cardiovascular stimulant effects than amphetamines.
c. Produces similar adverse effects to those
seen with cocaine toxicity.
d. Has not been associated with violent behavior or paranoia.
53. Which statement is true regarding LSD toxicity?
a. The doses commonly found in LSD preparations are higher now than in the 1960s and
1970s.
b. The main form of distribution of LSD is in
cigarettes.
c. LSD is generally a safe drug and has not
been associated with seizures, hyperthermia,
or rhabdomyolysis.
d. Most LSD toxicity can be managed with provision of a quiet environment or sedation in
more severe cases.
e. Excessive use of LSD does not cause stimulation of the sympathetic nervous system.
CME Questions
47. Which of the following is considered a hallucinogen?
a. Rohypnol
b. Tryptamines
c. Cocaine
d. Fentanyl
e. Nitrous oxide
48. Which drug is the most common drug of abuse
worldwide?
a. Cocaine
b. Methamphetamine
c. Heroin
d. Marijuana
e. LSD
54. Which statement regarding tryptamines is false?
a. Tryptamines are synthetic hallucinogenic
compounds similar to those found in certain
mushrooms.
b. DMT is the most commonly used tryptamine.
c. All tryptamines are scheduled by the DEA.
d. Toxicity can mimic serotonin syndrome.
e. Tryptamines have variable duration of
effects from less than one hour to 24 hours.
49. Which is an example of a schedule III drug?
a. Ativan
b. Hydrocodone
c. Marijuana
d. Cough syrup with codeine
e. GHB
50. Which route of cocaine use produces the most
rapid effects?
a. Injected or smoked
b. Nasally snorted
c. Oral ingestion
d. All have equal rapidity of onset
55. Which of the following agents has a specific
antidote?
a. Acetaminophen
b. Cocaine
c. Marijuana
d. PCP
e. Ketamine
51. Which statement regarding cocaine is TRUE?
a. Chest pain is the most common complaint
associated with cocaine use.
b. Cocaine abuse can present with agitation,
hyperthermia, delirium, hypertension, and
Pediatric Emergency Medicine Practice©
56. Which statement is incorrect regarding MDMA?
a. MDMA is a hallucinogenic amphetamine
know as Ecstasy.
30
October 2006 • EBMedicine.net
depression, and mydriasis.
b. Noncardiogenc pulmonary edema (NCPE) is
a frequent complication.
c. It can be treated with naloxone which has
rapid onset of action and a long half-life
(two to four hours).
d. It is a highly lipid soluble and rapidly penetrates the brain.
b. It is typically taken as a ytablet or capsule.
c. It is well known to cause hypernatremia.
d. It may cause many of the same symptoms as
the sympathomimetic drugs.
e. Piperazines are often used to mimic the
effects of MDMA.
57. A 20-year-old male is brought to the ED by the
police after assaulting his girlfriend. He is
very agitated, and has ataxia, nystagmus, and
tachycardia. He has to be restrained by several
police officers and ED staff. Which drug has
he most likely ingested?
a. Marijuana
b. LSD
c. DMP
d. PCP
e. Ketamine
62. A 15-year-old female is brought in by EMS after
being found unconscious on the street. She is
initially somnolent but as she regains consciousness, she states the last thing she remembers is being given a drink by some guy she
met at the club she was at using her older sister’s fake ID. On examination, it appears that
she has been sexually assaulted. You are concerned that she may have ingested a “date
rape” drug. Which statement is false regarding
these drugs?
a. GHB is most commonly available as a dissolvable white powder.
b. GHB and Rohypnol are readily detected on
routine urine drug screens.
c. GHB intoxication manifests as marked sedation and hypoventilation.
d. Rohypnol is a benzodiazepine
e. Rophypnol is legally available in many
countries outside the United States.
58. Which statement is false regarding the abuse of
ketamine?
a. Ketamine cannot be smoked.
b. Ketamine blocks the actions of glutamate
and aspartate.
c. It can cause hallucinations, respiratory
depression, nystagmus, and tachycardia.
d. It is often used to temper the crash associated with the end of a cocaine or amphetamine
binge.
e. The effects last about one hour.
59. Which statement is false regarding dextromethorphan (DXM) abuse?
a. Coricidin is the most popular form of DXM
that is abused.
b. Respiratory depression is common with
DXM overdose.
c. Severe DXM intoxication can mimic PCP
intoxication.
d. DXM ingestion can cause a false positive for
PCP on a urine drug screen.
e. Clinical effects can last up to six hours
depending in the dose ingested.
Jump Ahead of the Class!
Emergency Medicine Practice's 2007 Lifelong
Learning and Self-Assessment is designed exclusively to save you time and money while preparing for next years ABEM exam. Pre-order yours
today to lock in the low rate of $149---a $50 savings off the regular price of $199! Your study
guide includes reprints of the original articles,
summaries and in-depth discussions of each article, sample questions with answers and explanations, and 35 CME credits at no extra charge! Your
study guide is backed by a 100% money-back
guarantee; if you are unsatisfied for any reason,
simply call us to receive an immediate refund of
the full purchase price.
60. Sudden death during inhalant abuse is most
likely due to:
a. Hyperkalemia
b. Pulmonary embolism
c. Intracranial hemorrhage
d. Ventricular dysrhythmia
e. Hypocalcemia
Call 1-800-249-5770 to order yours today!
Expected ship date: January 2007.
61. Which of the following is true regarding heroin
overdose?
a. Clinical hallmarks include coma, respiratory
EBMedicine.net • October 2006
31
Pediatric Emergency Medicine Practice©
Physician CME Information
Binders
Accreditation: This activity has been planned and implemented in accordance with
the Essentials and Standards of the Accreditation Council for Continuing Medical
Education (ACCME) through the joint sponsorship of Mount Sinai School of
Medicine and Pediatric Emergency Medicine Practice. The Mount Sinai School of
Medicine is accredited by the ACCME to provide continuing medical education for
physicians.
Pediatric Emergency Medicine Practice has sturdy
binders that are great for storing all your issues.
To order your binder for just $20, please email
[email protected], call 1-800-249-5770, or go
to www.empractice.com, scroll down, and click
"Binders" on the left side of the page.
Credit Designation: The Mount Sinai School of Medicine designates this educational activity for a maximum of 48 AMA PRA Category 1 Credit(s)TM per year.
Physicians should only claim credit commensurate with the extent of their participation in the activity.
Credit may be obtained by reading each issue and completing the printed post-tests
administered in December and June or online single-issue post-tests administered
at EBMedicine.net.
If you have any questions or comments, please
call or email us. Thank you!
Target Audience: This enduring material is designed for emergency medicine physicians.
Needs Assessment: The need for this educational activity was determined by a
survey of medical staff, including the editorial board of this publication; review of
morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for emergency physicians.
Date of Original Release: This issue of Pediatric Emergency Medicine Practice was
published October 6, 2006. This activity is eligible for CME credit through October
6, 2009. The latest review of this material was September 1, 2006.
Coming in Future Issues:
Discussion of Investigational Information: As part of the newsletter, faculty may
be presenting investigational information about pharmaceutical products that is
outside Food and Drug Administration approved labeling. Information presented
as part of this activity is intended solely as continuing medical education and is
not intended to promote off-label use of any pharmaceutical product. Disclosure of
Off-Label Usage: This issue of Pediatric Emergency Medicine Practice discusses
no off-label use of any pharmaceutical product.
Eye Injuries
Rashes
Domestic Violence Screening
Class Of Evidence Definitions
Faculty Disclosure: It is the policy of Mount Sinai School of Medicine to ensure
objectivity, balance, independence, transparency, and scientific rigor in all CMEsponsored educational activities. All faculty participating in the planning or implementation of a sponsored activity are expected to disclose to the audience any
relevant financial relationships and to assist in resolving any conflict of interest
that may arise from the relationship. Presenters must also make a meaningful disclosure to the audience of their discussions of unlabeled or unapproved drugs or
devices.
Each action in the clinical pathways section of Pediatric Emergency
Medicine Practice receives a score based on the following definitions.
Class I
• Always acceptable, safe
• Definitely useful
• Proven in both efficacy and
effectiveness
Level of Evidence:
• One or more large prospective
studies are present (with rare
exceptions)
• High-quality meta-analyses
• Study results consistently positive
and compelling
Class II
• Safe, acceptable
• Probably useful
Level of Evidence:
• Generally higher levels of evidence
• Non-randomized or retrospective
studies: historic, cohort, or casecontrol studies
• Less robust RCTs
• Results consistently positive
Class III
• May be acceptable
• Possibly useful
• Considered optional or alternative
treatments
Level of Evidence:
• Generally lower or intermediate
levels of evidence
• Case series, animal studies, consensus panels
• Occasionally positive results
In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for
this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Nguyen, Dr. Grossheim, Dr. McAninch, Dr. Awad,
Dr. Mace, and Dr. Docherty report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation.
Indeterminate
• Continuing area of research
• No recommendations until further
research
For further information, please see The Mount Sinai School of Medicine website at
www.mssm.edu/cme.
Level of Evidence:
• Evidence not available
• Higher studies in progress
• Results inconsistent, contradictory
• Results not compelling
ACEP Accreditation: Pediatric Emergency Medicine Practice is also approved by
the American College of Emergency Physicians for 48 hours of ACEP Category 1
credit per annual subscription.
AAP Accreditation: This continuing medical education activity has been reviewed
by the American Academy of Pediatrics and is acceptable for up to 48 AAP credits. These credits can be applied toward the AAP CME/CPD Award available to
Fellows and Candidate Fellows of the American Academy of Pediatrics.
Significantly modified from: The
Emergency Cardiovascular Care
Committees of the American Heart
Association and representatives
from the resuscitation councils of
ILCOR: How to Develop EvidenceBased Guidelines for Emergency
Cardiac Care: Quality of Evidence
and Classes of Recommendations;
also: Anonymous. Guidelines for
cardiopulmonary resuscitation and
emergency cardiac care. Emergency
Cardiac Care Committee and
Subcommittees, American Heart
Association. Part IX. Ensuring effectiveness of community-wide emergency cardiac care. JAMA
1992;268(16):2289-2295.
Earning Credit: Two Convenient Methods
• Print Subscription Semester Program: Paid subscribers with current and valid
licenses in the United States who read all CME articles during each Pediatric
Emergency Medicine Practice six-month testing period, complete the post-test
and the CME Evaluation Form distributed with the December and June issues,
and return it according to the published instructions are eligible for up to 4 hours
of CME credit for each issue. You must complete both the post test and CME
Evaluation Form to receive credit. Results will be kept confidential. CME certificates will be delivered to each participant scoring higher than 70%.
• Online Single-Issue Program: Current, paid subscribers with current and valid
licenses in the United States who read this Pediatric Emergency Medicine
Practice CME article and complete the online post-test and CME Evaluation Form
at EBMedicine.net are eligible for up to 4 hours of Category 1 credit toward the
AMA Physician’s Recognition Award (PRA). You must complete both the post-test
and CME Evaluation Form to receive credit. Results will be kept confidential. CME
certificates may be printed directly from the Web site to each participant scoring
Pediatric Emergency Medicine Practice is not affiliated with any pharmaceutical firm or medical device manufacturer.
CEO: Robert Williford President and Publisher: Stephanie Williford
Direct all editorial or subscription-related questions to EB Medicine: 1-800-249-5770 • Fax: 1-770-500-1316 • Non-U.S. subscribers, call: 1-678-366-7933
EB Practice, LLC • 305 Windlake Court • Alpharetta, GA 30022
E-mail: [email protected] • Web Site: EBMedicine.net
Pediatric Emergency Medicine Practice (ISSN Print: 1549-9650, ISSN Online: 1549-9669) is published monthly (12 times per year) by EB Practice, LLC, 305 Windlake Court, Alpharetta, GA 30022.
Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is intended to
supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained
herein are not intended to establish policy, procedure, or standard of care. Pediatric Emergency Medicine Practice is a trademark of EB Practice, LLC. Copyright © 2006 EB Practice, LLC. All rights
reserved. No part of this publication may be reproduced in any format without written consent of EB Practice, LLC. Subscription price: $299, U.S. funds. (Call for international shipping prices.)
Pediatric Emergency Medicine Practice©
32
October 2006 • EBMedicine.net