Download Evaluating Hallucinogenic or Psychedelic Drug Intoxication in an

DRUGS OF ABUSE II
Robert H. Williams, PhD, DABCC, FACB, MT(ASCP)
Timothy Erickson, MD, FACEP, FACMT
Evaluating Hallucinogenic or
Psychedelic Drug Intoxication
in an Emergency Setting
ABSTRACT Under certain conditions or in an overdose
setting, several classes of drugs can induce illusions,
hallucinations, or delusions. However, one of the hallmark
features of hallucinogens or psychedelic agents is their ability
to induce states of altered or distorted perception, thought,
and mood. Many hallucinogens produce classic
sympathomimetic effects; that is, hyperactivity, mydriasis
(dilated pupils), hypertension, tachycardia, and
hyperthermia. However, the effects vary considerably,
depending upon the hallucinogen ingested. Qualitative
confirmation by the laboratory that the patient is suffering
from hallucinogen intoxication such as marijuana use can
be helpful to the clinician. However, the common toxicologic
drug screens used by most clinical laboratories do not detect
many hallucinogenic agents (such as LSD [lysergic acid
diethylamide]). Thus, diagnosis of hallucinogen ingestion
and treatment is often based on history of use and physical
examination.
This is the second article in a 3-part series on clinical toxicology and drugs of abuse.
On completion of this series, the reader will be able to correlate clinical findings from
the poisoned patient with data provided by the clinical laboratory that leads to a
diagnosis and describe the therapeutic interventions used by clinicians for patient
management.
From the Department of Pathology—Division of Clinical Pathology (Dr Williams),
and the Department of Emergency Medicine—Division of Toxicology (Dr
Erickson), University of Illinois at Chicago Medical Center, Chicago.
Reprint requests to Dr Williams, Department of Pathology—Division of Clinical
Pathology (M/C 750), University of Illinois at Chicago Medical Center, 840 S
Wood St, 201G CSB, Chicago, IL 60612; or e-mail: [email protected]
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Case Presentation
History
The patient was a 17-year-old high school student
who was transported to the emergency department
by paramedics after he was found “acting confused
and wandering around the hallways at school.” The
patient was combative and complained of “seeing
lots of bright swirling colors.” In addition to his
aggressive behavior, the patient had dilated pupils
that were equal and reactive, his lungs were clear to
auscultation, and his skin was normal color, but
diaphoretic. His pulse was 100 beats per minute, respiration rate 28 breaths per minute, blood pressure
110/60 mm Hg, and temperature 37.8°C (100.0°F).
The patient’s abdomen was soft and nontender with
normal bowel sounds. An electrocardiogram
revealed a sinus tachycardia with regular rate and
rhythm. Otherwise, he appeared to be a normal
healthy male, and based on discussions with his parents, he had been performing well in school. Suspecting hallucinogen ingestion, the physician
ordered the tests in Table 1 and then gave the patient
benzodiazepines for sedation. After a 6-hour observation period, the patient became more alert and
cooperative. He admitted to doing “LSD (lysergic
acid diethylamide) blotters” at school and “had a bad
trip” for the first time. He also admitted to chronic
use of marijuana for more than 3 months but denied
using it recently or using other drugs of abuse or
ethanol. His positive urine drug screen for cannabinoids supported his history. He was discharged
home with reliable and concerned parents.
Table 1. Laboratory Tests for Patient Suspected of Hallucinogenic (Psychedelic) Drug Ingestion
Tests
Patient Result
Reference Range
Electrolytes
Sodium, mEq/L (mmol/L)
135 (135)
136-145 (136-145)
Potassium, mEq/L (mmol/L)
3.9 (3.9)
3.5-5.0 (3.5-5.0)
Chloride, mEq/L (mmol/L)
108 (108)
99-109 (99-109)
Bicarbonate, mEq/L (mmol/L)
22 (22)
22-28 (22-28)
Serum urea nitrogen, mg/dL (mmol/L)
20 (7.1)
10-20 (3.6-7.1)
Creatinine, mg/dL (mmol/L)
0.8 (71)
0.6-1.2 (53-106)
Glucose, mg/dL (mmol/L)
90 (5.0)
70-105 (3.9-5.8)
4.9 (4.9)
4.7-6.1 (4.7-6.1)
13,500 (13.5)
4,800-10,800 (4.8-10.8)
15 (150)
14-18 (140-180)
45 (0.45)
42-52 (0.42-0.52)
340 (340)
150-400 (150-400)
< 5 (< 1.1)
< 5 (< 1.1)
Amphetamines
None detected
None detected
Cannabinoids
Positive
None detected
Cocaine metabolite
None detected
None detected
Barbiturates
None detected
None detected
Opiates
None detected
None detected
Phencyclidine
None detected
None detected
Complete blood count
RBC count, 3 106/µL (3 1012/L)
WBC count, /µL (3
109/L)
Hemoglobin, g/dL (g/L)
Hematocrit, %
Platelet count, 3
103/µL
Ethanol, mg/dL (mmol/L)
(3
109/L)
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4
rites and for neurologic and psychiatric diseases;
Egyptian papyri document its use in childbirth,
and its medicinal properties were recognized by
the Chinese for 2,700 years. In Eastern Europe
around the 16th century, morning glory seeds
were known to cause hallucinations. Natural ergot
(Claviceps purpurea) has also been associated with
hallucinations and altered mental status.
The synthetic hallucinogen, LSD, was formulated in 1938 by Albert Hofmann, a Swiss chemist
at Sandoz, who several years later developed hallucinations after he accidentally became exposed to
the compound. During the 1950s, psychiatrists
used LSD as an adjunct for analytic psychotherapy4; around this time it also became popular as a
recreational drug. LSD was banned by the federal
government in 19665; it has been classified as an
illicit substance (schedule I agent) with high abuse
potential and no known medical use.
Section
Hallucinogens are a diverse group of drugs that
alter and distort perception, thought, and mood.
Synesthesias (sensory misperceptions such as
hearing colors or seeing sounds) are common.1
Hallucinations are false perceptions that have no
basis in external stimulation. Hallucinogens are
sometimes described as being mind manifesting
(psychedelic), generating a religious experience,
and producing dreams.2
Several cultures have used naturally occurring
hallucinogenic (psychedelic) compounds in ceremonial worship for centuries. The sacramental
substance “soma,” described in the Hindu holy
book, the Rig-Veda, as being godlike and intoxicating is thought to be derived from the juice of the
hallucinogenic mushroom, Amanita muscaria.3
The Assyrians used cannabis during their religious
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Urine drug screen
395
Although hallucinogen use diminished in the
1970s and early 1980s, recent statistics show that
these substances are becoming more popular. In
the United States, marijuana is the most commonly abused illicit psychedelic substance. It is
estimated that more than 20 million people use it,
with increased usage among teenagers.6 The most
frequently abused substance is alcohol, followed
by marijuana, then LSD.7 Approximately 14% of
adolescents have used hallucinogens, with usage
among high school students being about 10%.8
(found in the toad family, genus Bufo); the most
significant phenylethylamines include mescaline
and amphetamine derivatives such as MDMA
(3,4-methylenedioxymethamphetamine); the
major cannabinols are marijuana and hashish
(contain delta-9-tetrahydrocannabinol). Amphetamines and the designer “hallucinogenic”
amphetamines (ie, MDA, MDMA, and MDEA)
are also sympathomimetic drugs, and thus will be
discussed in the final article of this series.
Although phencyclidine (PCP) and ketamine are
considered anesthetics, they are primarily abused
for their hallucinogenic properties. However, this
Common Hallucinogenic or Psychedelic
article is limited to the discussion of cannabinols,
Substances
LSD, and naturally occurring hallucinogenic and
Table 2 lists some of the common hallucinogenic or psychedelic compounds.
psychedelic agents. The major structural classes are
the lysergamides, indolealkyamines, phenylethy- Lysergic Acid Diethylamide
lamines, and cannabinols. The major lysergamides LSD, a potent hallucinogen, is the synthetic diethyinclude LSD and ololihqui (South American morn- lamide derivative of ergot alkaloids. It is water soling glory); the primary indolealkyamines are psilo- uble, colorless, tasteless, and odorless. LSD is
cybin (found in certain mushrooms) and bufotenine commonly sold as liquid-impregnated blotter
paper (Fig 1), microdots (tiny tablets), windowpanes (gelatin squares), liquid, powder, or tablets.7
Table 2. Hallucinogenic or Psychedelic Agents
LSD is readily absorbed by the gastrointestinal
tract, with ingestion being the most common route
LSD (lysergic acid diethylamide)
of exposure. Other routes of administration
Morning glory seeds (Convolvulaceae)
include intranasal, parenteral, sublingual, smokMushrooms
ing, and conjunctival instillation. Typical street
dose ranges from 50 to 300 mg; the minimum
Amanita muscaria
effective dose is 25 mg.9 LSD is about 80% protein
Psilocybin (Psilocybe)
bound and has an elimination half-life of 2.5
Mescaline/peyote
hours. Onset of psychologic effects occurs within
30 to 60 minutes after ingestion, with peak effect at
Phencyclidine (PCP), ketamine
3 to 5 hours. Metabolism by the liver leads to a
Designer amphetamines
pharmacologically inactive compound.
3,4-methylenedioxyamphetamine (MDA, “Love Drug”)
Several naturally occurring plants contain
lysergamides, such as morning glory (Riva
3,4-methylenedioxymethamphetamine (MDMA, “Ecstasy,”
corymbosa) and Hawaiian baby woodrose (Ipo“XTC,” “Adam”)
moea violacea). The lysergamides found in morn3,4-methylenedioxyethamphetamine (MDEA, “Eve”)
ing glory have about one tenth the potency of
Marijuana, hashish
LSD; it takes 200 to 300 pulverized seeds to elicit
a hallucinogenic effect.10
Belladonna alkaloids
Jimson weed (Datura stramonium)
Mandrake (Mandragora officinarum)
Deadly nightshade (Atropa belladonna)
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Indolealkyamines
Psilocybin
Psilocybin is found in 3 major genera of mushrooms: Psilocybe, Panaelous, and Conocybe.11
Mushrooms that contain psilocybin are found in
the southern United States (Fig 2). The mushrooms can be recognized by their blue-green color
after bruising. Psilocybin was first isolated by
Albert Hofmann (of LSD fame). The effects are
similar to LSD, but the duration of action is
shorter (about 4 hours).
Fig 1. LSD blotter papers.
Bufotenine and Related Derivatives
Toads of the genus Bufo have secretions that contain complex mixtures of cardiotoxins and neurotransmitters such as bufotenine, 5-methoxy, -N, N
dimethyltryptamine (5-MeO-DMT), bufotenidine, and dehydrobufotenine. Ingestion of toad
venom from this genus can cause severe reactions
and death.12 The compound 5-MeO-DMT, which
is present only in the toad Bufo alvarius, may be
responsible for the hallucinogenic effect. It
appears that smoking the compound is requisite
to induce the hallucinogenic effect.13
Fig 2. Psilocybin mushrooms, “little brown shrooms.”
N, N-dimethyltryptamine
OH
H 3C
COOH
C5H11
O
THC
OH
CH2OH
H 3C
CH3
O
4
CH3
Phenylethylamines
Peyote/Mescaline
In the dry rocky slopes throughout the southwestern United States and northern Mexico grows the
blue-green Peyote cactus, or Lophophora williamsii. The dried fleshy tips of the cactus are known as
peyote buttons; ingestion of 6 to 12 buttons is necessary to produce a hallucinogenic effect.3 Mescaline is the active hallucinogenic alkaloid found in
the peyote cactus. It is rapidly absorbed in the gastrointestinal tract. Mescaline pills contain either
synthetic mescaline or ground peyote compressed
Scientific Communications
CH3
C5H11
Section
In the Amazon basin grows a plant called the
“yakee” (Virola calophylla). The bark of this plant
contains the compound N, N-dimethyltryptamine
(DMT), which is a potent short-acting hallucinogen. DMT has been used by the shamans as a hallucinogenic snuff.3 DMT is typically smoked,
snorted, or injected, because it is not readily
absorbed by the gastrointestinal tract. Maximum
effect of the compound occurs rapidly (within 5 to
20 minutes); its duration is 30 to 60 minutes.
OH
THCCOOH
H3 C
CH3
C5H11
O
11-OH-THC
Fig 3. Major metabolic route for THC [delta-9-tetrahydrocannabinol], including
the primary active metabolite, 11-OH-THC, and the primary inactive metabolite,
THCCOOH. SOURCE: Huestis MA. Marijuana. In: Levine BA, ed. Principles of
Forensic Toxicology. Washington, DC: AACC Press; 1999:247. Used with
permission.
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into a tablet. Use of mescaline often produces side Depending on the dose inhaled, the psychoactive
effects, such as nausea, vomiting, and diaphoresis, effects of marijuana may last from 1 to 4 hours.22
before the user experiences a psychedelic effect.
High doses can result in image distortion, a loss of
personal identity, and fantasies and hallucinaCannabinols
tions. Marijuana smoking can cause a 5-fold
Marijuana, along with hashish, joint, pot, reefer, increase in the carboxyhemoglobin level comand Colombian ganga are common names given pared with tobacco.23 Also, in pregnant female
to the psychoactive substance, delta-9-tetrahydro- smokers, studies have shown that a number of
cannabinol (THC), obtained from the Indian neonatal neurobehavioral disturbances correlate
hemp plant or Cannabis sativa. The primary active with marijuana usage. These problems appear to
metabolite of THC is 11-hydroxy THC; the pri- disappear during infancy and reappear later in
mary inactive metabolite is THC carboxylic acid early childhood.24
(Fig 3). Although the plant contains about 60
other resins called cannabinoids, these substances Diagnosis of
have very little if any psychoactivity compared Hallucinogenic Toxic Effects
with THC. In addition to the cannabinoids, the The differential diagnosis of hallucinogenic (psyplant also contains more than 200 chemical com- chedelic) drug use can be overwhelming, because
pounds that may contribute to medical problems every drug class can induce hallucinations in difoften seen with marijuana use.10 Hashish and ferent patient populations. The diagnosis of halluhashish oil (hashish plus tobacco) are also derived cinogen use is often made on the basis of history
from Cannabis sativa; they are smoked in pipes and physical examination. Drug-induced condiand contain higher concentrations of THC than tions associated with perceptual changes are generfound in marijuana.
ally accompanied by physiologic abnormalities.
With the hallucinogens, sympathomimetic effects
Pharmacologic Actions of
are common, occur shortly after ingestion, and
LSD and Marijuana (THC)
usually precede the hallucinogenic effects. DelirThe mechanism of action of most hallucinogenic ium or psychosis, however, is also observed with
(psychedelic) drugs is poorly understood; how- other drugs that exhibit similar effects, such as
ever, it is thought to involve neurotransmitters in PCP, amphetamines, cocaine, and anticholinerthe central nervous system.14 For example, LSD gics.10 Patients with amphetamine intoxication
appears to alter thought and perception by its typically present with elaborate and paranoid deluactions on the serotonergic neurons.15,16 Sero- sion, as well as visual disturbances.10 Uncontroltonin (5-hydroxytryptamine or 5-HT) regulates
platelet function and smooth muscle in the gasTable 3. Clinical Findings Associated
trointestinal tract and cardiovascular system and
With Hallucinogenic (Psychedelic)
occurs as a neurotransmitter in the brain.17
Drug Intoxication
Because LSD is structurally related to serotonin, it
Visual hallucinations
can serve as an agonist for several types of sero18
tonin receptors, such as 5-HT1 and 5-HT2. All
Dilated pupils (mydriasis)
the major classes of the hallucinogens appear to
Tachycardia
show a strong relationship between their interacHypertension
tion with the 5-HT2 receptor and the production
19
of a hallucinogenic effect. Antagonists of this
Tachypnea
receptor appear to block many of the effects of
Diaphoresis
hallucinogenic drugs.20
Vomiting and diarrhea
The effects of marijuana depend upon the
route of administration and the concentration of
Hyperthermia
THC in the product. Although smoking usually
Hyperactivity
leads to immediate effects, the effects with oral
Mental status changes
ingestion are slow and often unpredictable owing
21
to the effects of acid pH of the stomach on THC.
Coma
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Laboratory Evaluation
of Hallucinogen Toxic Effects
4
Common tests requested by clinicians for patients
suspected of hallucinogen overdose include electrolytes, glucose, renal function tests, and toxicology tests that help to confirm the presence of
hallucinogens or compounds that may give rise to
Scientific Communications
Patient Management
The basic approach for any patient with altered
mental status who is suspected of taking a hallucinogenic drug should include consideration of
administration of dextrose, thiamine, and naloxone as indicated (ie, patients who have hypoglycemia, Wernicke encephalopathy, or concurrent
use of opiates, respectively) and a vigorous search
for other etiologies.10 Table 4 lists the overall
approach to managing a patient suspected of hallucinogen intoxication. The most common
adverse effect is acute panic reactions, which present as frightening illusions, tremendous anxiety,
apprehension, and terrifying loss of control.10
Thus, placing the patient in a quiet area may help
to reduce his or her anxiety. The psychedelic
agents rarely produce life-threatening problems.
Sedation with benzodiazepines is usually sufficient to treat hypertension and tachycardia.10
Patients with hyperthermia, however, must be Test Your
aggressively treated with hydration, active external Knowledge!
coolants, and muscle relaxants ranging from ben- Look for the CE
zodiazepines to paralytic agents, depending on the Update exam on
Drugs of Abuse (005)
degree of hyperthermia. Complications of hyper- in the September
thermia, which include rhabdomyolysis, myoglo- issue of Laboratory
binuric renal failure, hepatic necrosis, and Medicine. Participants
disseminated intravascular coagulation, con- will earn 3 CMLE
tribute to the morbidity and mortality found in credit hours.
hallucinogenic drug intake.
Table 4. Treatment of Patient With Hallucinogenic or Psychedelic
Drug Intoxication
Patient should be placed in a quiet room with close observation.
Most patients generally require only supportive care.
Support airway and administer oxygen, if comatose.
Administer naloxone if concurrent opiate use suspected.
If agitated, combative, or hyperactive, administer
benzodiazepines—diazepam (Valium) or lorazepam (Ativan).
If benzodiazepines ineffective, may give haloperidol (Haldol).
Cool, if hyperthermic, and watch for rhabdomyolysis.
Substance abuse/detoxification referral and counseling.
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Section
lable behavior or extreme agitation along with
marked hyperthermia should suggest possible
exposure to drugs such as cocaine or PCP.
Table 3 lists the common clinical findings
associated with hallucinogen ingestion. Other
clinical findings observed include muscle weakness, ataxia, and hippus (spasmodic rhythmic
pupillary dilation and constriction).25 The psychologic effects of LSD are dose related and effect
changes in arousal, emotion, perception, thought
processes, and self-image. The response to the
drug is related to the person’s mindset, emotions,
or expectations at the time and can be altered by
the group or setting.26 Altered perceptions are
common with synesthesias and loss of body
image and alteration in visual perceptions, that
is, distortion of people’s faces and bodies and
undulation of objects. These effects usually last 6
to 12 hours.10
Hallucinogen persisting perception disorder,
also called “flashbacks” (often induced by prolonged stress, illness, or exercise), can occur up to
18 months after ingestion.10 Special attention
should be given to patients who ingest LSD and
receive therapeutic doses of lithium or a selective
serotonin-reuptake inhibitor, because they are at
greater risk for seizures and flashbacks.27,28
The usual effects of marijuana use are fairly
predictable and also include alterations in sensation, perception, cognition, and psychomotor
functions. Physiologic effects are usually dose
related; however, psychologic effects usually do
not correlate with the amount taken. Increase in
heart rate, urinary retention, mydriasis, and
hypothermia are common clinical findings. Other
effects with acute marijuana usage include
decreased intraocular pressure and increased
appetite (thus, its recommended use in the treatment of glaucoma and AIDS patients, respectively). Currently there is 1 prescription product
called dronabinol (Marinol, Roxane Laboratories,
Columbus, OH), that contains synthetic THC. In
an attempt to promote the clinical usefulness of
marijuana use, 5 states (CA, AZ, NH, MI, and
MO) as of 1997 have passed nonbinding resolutions urging the federal government to make
marijuana medically available.
similar symptoms. Laboratory tests that can detect
LSD exposure include immunoassays (radioimmunoassay, enzyme-multiplied immunoassy technique; enzyme-linked immunosorbent assay) and
gas chromatography–mass spectrometry for the
detection of LSD and its urinary metabolite, 2-oxyLSD.29,30 However, these assays are not routinely
performed in most clinical laboratories. Also, some
compounds, such as ergotamine, tricyclic antidepressants, verapamil, sertraline, and fentanyl can
cross-react with LSD immunoassays.31 Although
most laboratories do not analyze for the presence
of LSD, most are capable of rapid immunoassay
screening for other drugs that produce similar
symptoms, that is, cocaine (as its metabolite, benzoylecgonine), amphetamines, PCP, and cannabinoids or marijuana (as its metabolite, THC).
Nevertheless, it still is important to recognize that
most standard screens for drugs of abuse do not
include hallucinogens such as LSD.32 Testing for
esoteric hallucinogens such as mescaline, psilocybin, and bufotenine, is generally performed by reference laboratories that specialize in toxicology.
THC in marijuana is hydrophobic; thus, it
accumulates in the lipid tissue; it also is highly
protein bound and undergoes enterohepatic
cycling. These combined properties of THC result
in its slow elimination from the body. Immunoassays used to screen for THC contain antibodies
directed toward delta-9-tetrahydrocannabinolcarboxylic acid (THCCOOH), the primary “inactive” metabolite, because little or no parent THC
or 11-OH-THC “active” metabolite (Fig 3) is present in urine.33 However, the antibodies can crossreact with any of the metabolites (most of which
lack psychoactivity), and their cross-reactivity varies
considerably, depending upon the immunoassay
method. They can also cross-react with other compounds such as ketoprofen, tolmetin, naproxen,
ibuprofen, and acetylsalicylic acid, although such
reactions do not appear to be a problem at the lowest level of sensitivity with immunoassays that are
currently available.31 THC can be detected with
immunoassays at a variety of sensitivity levels: 20,
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50, and 100 ng/mL. Clinically it may be more
important to use the lowest level. For federal
workplace testing, the Substance Abuse Mental
Health Services Administration of the Department of Health and Human Services, has established a screening cutoff of 50 ng/mL for
cannabinoids.34 Unlike most clinical applications,
federal workplace testing also requires confirmation of THCCOOH by gas chromatography–mass
spectrometry at a cutoff of 15 ng/mL.35 It should
be noted that passive exposure to marijuana
smoke could give false-positive screening results,
depending on the room concentration even after a
single exposure.36 Studies have shown that THC
can be detected for 1 to 3 days with single acute
use and up to 4 weeks with daily (chronic) use.37
The detection of marijuana use depends on several factors, such as the lipid stores of the patient
for THC, its frequency of use, and the sensitivity
level used for its detection. The test result can be
positive for more than 2 months.10
Although detection of marijuana in the urine
can be rapidly determined using immunoassay
methods, its presence rarely dictates the physician’s
approach to patient management. There are no
known cases of death associated with sole use of
marijuana. The benefit of its detection, however,
may be to rule out other potential hallucinogenic
or psychoactive substances with similar signs and
symptoms or to counsel a pregnant female on its
possible side effects with fetal development. It is
noteworthy that marijuana is often used in conjunction with other drugs such as opium, alcohol,
cocaine, heroin, phencyclidine, and ketamine and,
on rare occasions, with formaldehyde.38
Conclusion
Patients who come to the emergency department
with hallucinogen intoxication often have myriad
signs and symptoms seen with other sympathomimetic drugs. The clinician often relies on history and physical examination, because most
clinical laboratories cannot routinely rule in hallucinogen ingestions such as LSD and mescaline.
The clinical laboratory, however, can be helpful in
ruling out other drugs of abuse that may precipitate similar signs and symptoms. Most patients
can be readily treated with sedation and by placing
them in a quiet area for observation.l
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21. Ohlsson A, Lingren JE, Wahlen A, et al. Plasma delta-9tetrahydrocannabinol concentrations and clinical effects after
oral and intravenous administration and smoking. Clin Pharmacol Ther. 1980;28:409-416.
22. Chait LD, Burke KA. Preference for high- versus lowpotency marijuana. Pharmacol Biochem Behav. 1994;49:643-647.
23. Wu TC, Tashkin DP, Djahed B, et al. Pulmonary hazards
of smoking marijuana as compared with tobacco. N Engl J
Med. 1988;318:347-351.
24. Richardson GA, Day NL, McGauhey PJ. The impact of
prenatal marijuana and cocaine use on the infant and child.
Clin Obstet Gynecol. 1993;36:302-318.
25. Leikin JB, Krantz AJ, Zell-Kanter M, et al. Clinical features
and management of intoxication due to hallucinogenic drugs.
Med Toxicol Adverse Drug Exp. 1989;4:324-350.
26. Bowers MB, Freedman DX. Psychedelic experiences in
acute psychoses. Arch Gen Psychiatry. 1966;15:240-248.
27. Jackson TW, Hornfeldt CS. Seizures activity followed
recreational LSD use in patients treated with lithium and fluoxetine [abstract]. Vet Hum Toxicol. 1991;33:387.
28. Markel H, Lee A, Holmes RD, et al. LSD flashback syndrome exacerbated by selective serotonin reuptake inhibitor
antidepressants in adolescents. J Pediatr. 1994;125:817-819.
29. Jenkins AJ. Hallucinogens. In: Levine BA, ed. Principles
of Forensic Toxicology. Washington, DC: AACC Press;
1999:286-308.
30. Fenton J. Lysergic acid diethylamide (LSD). In: Fenton J,
ed. The Laboratory and the Poisoned Patient. A Guidebook for
Interpreting Laboratory Data. Washington, DC: AACC Press;
1998;225-228.
31. Smith ML. Immunoassay. In: Levine BA, ed. Principles of
Forensic Toxicology. Washington, DC: AACC Press; 1999:130-152.
32. Gold MS, Dackis CA. Role of the laboratory in the evaluation of suspected drug overdose. J Clin Psychiatry.
1986;47(suppl):17-23.
33. Huestis MA. Marijuana. In: Levine BA, ed. Principles of
Forensic Toxicology. Washington, DC: AACC Press; 1999:246-263.
34. Department of Health and Human Services. Substance
Abuse Mental Health Services Administration. Mandatory
Guidelines for Federal Workplace Drug Testing Program
Notice. Washington, DC. 59 Federal Register 29921 (1994).
35. Department of Health and Human Services, Substance
Abuse Mental Health Services Administration: Mandatory
Guidelines for Federal Workplace Drug Testing Program
Notice. Washington, DC. 59 Federal Register 29922 (1994).
36. Cone EJ, Johnson RE, Darwin WD, et al. Passive inhalation of marijuana smoke: urinalysis and room air levels of
delta-9-tetrahydrocannabinol. J Anal Toxicol. 1987;11:89-96.
37. Ellis GM, Mann MA, Judson BA, et al. Excretion patterns
of cannabinoid metabolites after last use in a group of chronic
users. Clin Pharmacol Ther. 1985;38:572-578.
38. Hawks RL. The constituents of cannabis and the disposition and metabolism of cannabinoids. In: Hawks RL, ed.
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