eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Toxicology

Toxicity, Hallucinogens - LSD

Stephan Brenner, MD, MPH, Resident Physician, Department of Emergency Medicine, Washington University in St Louis School of Medicine
Bill Dribben, MD, Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine

Updated: Apr 16, 2009

Introduction

Background

Lysergsãurediethylamid (LSD), or lysergic acid diethylamide, is the prototype of the hallucinogen class. It was first synthesized as LSD-25 from lysergic acid in 1938 by the Swiss biochemist Albert Hofmann while researching the medical effects of ergot-derived synthetic molecules. The hallucinogenic properties of LSD were not discovered until 1943, when Hofmann unintentionally ingested the substance and experienced an “extremely stimulated experience." Hailed as a wonder drug in the field of psychoanalysis during the 1950s and 1960s, LSD was used as an experimental drug in schizophrenia research to produce “experimental psychosis” by altering neurotransmitter systems and was used in so-called “psycholytic” or “psychedelic” therapy.¹

The American psychologist, writer, and futurist Timothy Leary popularized LSD and other hallucinogens in the 1960s based on their alleged therapeutic and spiritual benefits; this led to a psychedelic revolution, with large numbers of people using LSD as part of a counterculture movement. As a result of public health concerns, the drug was banned for recreational purposes by federal law in 1966.² Currently, LSD is known for its use as a “club drug” together with gamma-hydroxybutyric acid (GHB); 3,4 methylenedioxymethamphetamine (MDMA), also referred to as ecstasy; and ketamine. Other hallucinogens include mescaline, psilocybin, and ibogaine, which all possess a structural similarity to serotonin.

LSD causes changes in thought, mood, and perception, with minimal effects on memory and orientation. LSD primarily produces so-called pseudohallucinations, which are illusions derived from the misinterpretation of actual experiences. One form of such illusions are synesthesias (the transposition of certain sensory modes), which create an experience known as sensory crossover . Examples include the perception of a sound evoked by a visual image or the impression of hearing colors or feeling sounds. True hallucinations occur as well; visual hallucinations are the most common.

Exposure to LSD causes pleasant and unpleasant emotions, but the overall effects are unpredictable and vary with the ingested amount, the user’s personality and mood, individual expectations, and surroundings. Users are typically aware that visual, auditory, and olfactorial perceptions are distorted and unreal (“good trip”); however, acute adverse drug effects can include panic reactions, psychoses, and major depression (“bad trip”).³

LSD can be synthesized from easily obtainable chemicals or from naturally occurring substances. Ergotamine alkaloids produced from a fungus that grows on rye and other grains contain lysergic acid. Lysergic acid amide (LSA) is found in the seeds of Morning Glories and Hawaiian Baby Woodrose. LSD is one of the most potent psychoactive drugs. It is 3000 times more potent than mescaline, and doses as small as 1-1.5 mcg/kg can produce psychoactive effects; the minimum effective dose is approximately 25 mcg. The drug is odorless, colorless, and slightly bitter tasting. It is usually taken by mouth and rapidly absorbed by the GI tract.

LSD is produced as a crystalline powder and then mixed with various binding agents. It is sold in the streets as tablets (“microdots”), capsules, or in liquid form; often, it is applied to absorbent materials such as blotter paper (“blotter acid”) or gelatin (“window panes”). These are divided into small, decorated squares, with each square representing one dose.

Assorted lysergic acid diethylamide (LSD) blotter paper.

Lysergic acid diethylamide (LSD) in assorted pill forms.

Pathophysiology

Most hallucinogens belong to two structurally distinct classes: indoles and tryptamines (eg, LSD, N,N-dimethyltryptamine [DMT], psilocybin) or phenylethylamines (mescaline, MDMA). The structural similarity to serotonin and the intrinsic potency allow hallucinogens to disrupt the balanced functioning of the serotonin system.

Hallucinogens have a high affinity for serotonin (5-HT) receptors where LSD exhibits both agonist and antagonist properties. The 5-HT_2A receptor plays a major role in the modulation of sensory signals and is predominantly found in pyramidal neurons of the prefrontal cerebral cortex where hallucinogens have effects on cognition, mood, perception, and emotions ranging from fear to euphoria. These receptors are also thought to be responsible for the pathology and therapy of schizophrenia. Serotonin receptors found in the locus coeruleus are important for sensory modulation and responsible for the sympathomimetic effects of the drug (hypertension, tachycardia, dizziness, loss of appetite, dry mouth, sweating, nausea, numbness, tremor).
 
Affinities to other serotonin receptors differ between the two hallucinogen classes, which makes attributing specific effects to a single 5-HT receptor subtype impossible. LSD also stimulates dopamine D2 receptors.⁵ This leads to a biphasic pharmacological pattern of early serotoninlike effects (15-30 min after administration) and late mediated dopaminelike effects (60-90 min after administration). The relationship between the dopaminergic and serotonergic systems is not fully understood.^6,7

LSD is absorbed rapidly after oral administration, and early drug effects appear after 30-60 minutes. More profound psychoactive effects peak at 2-4 hours and some effects may last as long as 12 hours. A typical dose to obtain the desired effects ranges from 50-200 mcg. LSD is rapidly metabolized in the liver by N-demethylation, N-deethylation, and aromatic hydroxylation after oral ingestion. Its metabolites N-demethyl-LSD (nor-LSD), lysergic acid ethylamide (LAE), iso-LAE, monooxylated LSD, and hydroxylated LSD are excreted in the urine. The elimination half-life of LSD is 3-5 hours.

Although LSD does not cause physical or psychological addiction, users quickly develop a high degree of short-lived tolerance (tachyphylaxis), which is due to down-regulation of 5-HT_2A receptors. Long-term effects of chronic use can result in persistent psychosis and hallucinogenic persisting perception disorder (HPPD), so called “flashbacks." LSD remains one of the most potent mood-altering and perception-altering drugs.³

Frequency

United States

Emergency department (ED) visits from patients with adverse reactions to hallucinogens are relatively uncommon. In 2006, the Drug Abuse Warning Network (DAWN) estimated 4,002 LSD related ED visits out of a total of 958,164 ED visits involving illicit drugs (approximately 1.3 ED visits per 100,000 population).⁸ However, this is a 2-fold increase in LSD-related ED visits compared with 2005. Given its popularity as a club drug, LSD-related ED visits often involve multidrug use, including MDMA and others. According to DAWN data, LSD users in the United States tend to be white males aged 12-24 years and of lower socioeconomic backgrounds.

Mortality/Morbidity

Deaths caused by primary LSD effects have not been well documented. The lethal dose of LSD has been estimated to be 14,000 mcg. Few cases of massive ingestions have been reported; because of its large index of toxicity, patients must have access to unusually concentrated forms of LSD if they are to overdose. Massive overdoses can lead to respiratory arrest, coma, emesis, hyperthermia, autonomic instability, and bleeding disorders. No suicide attempts using LSD intoxication have been reported.

Age

In general, adolescents and young adults are now the most frequent LSD users after it regained popularity since the 1990s. Low cost (prices ranging from $2-5 per single dose or hit, with prices of $1 or less at wholesale lots), easy availability, alleged mind-expanding properties, and attractive paper designs make LSD especially intriguing to junior-high and high-school students.⁹

In 2002, 13% of young American aged 16-23 years used LSD according to a report on age-related drug use based on the National Survey on Drug Use and Health (NSDUH).¹⁰ LSD was the second most frequent used drug after MDMA in this age group.

In 2006, the National Institutes of Health (NIH) reported that 9.5% of Americans aged 12 years and older have used LSD at least once in their lifetime, and 0.3% had used it in the year prior to the survey.¹¹

Clinical

History

• Although hallucinogen use, such as lysergic acid diethylamide (LSD) use, rarely results in presentation to health care facilities, patients that present to the emergency department (ED) typically do so after acute panic reactions, massive ingestions, or unintentional ingestions (children or adults who have unknowingly ingested the drug). Altered perception can lead to behavioral toxicity, in which judgment is impaired and prevents an appreciation of the dangers in the environment, resulting in situations in which injury can occur.
• Patients who present after recent hallucinogen abuse are often oriented and capable of providing a history of drug ingestion. The subjective effects of LSD use, or "trip," widely vary with the user's preconceived beliefs and expectations about the drug and the environment in which the ingestion occurred. In general, hallucinogens can intensify the current mood when the drug is taken; pleasant feelings can be augmented to euphoric feelings with the achievement of new insights or an expanded consciousness. Negative feelings, personal flaws, or depressive symptoms can be amplified to a dysphoric experience. Changes produced in consciousness lead to loss of boundaries between the user and the environment. Users often report intensification or alterations of colors and sound (synesthesia) and the perception that common objects appear novel, fascinating, or awe-inspiring.

Physical

• Patients generally present with a combination of somatic and psychomimetic symptoms:¹²
  • Somatic symptoms are usually due to sympathomimetic effects, including mydriasis, hypertension, tachycardia, flushing, sweating, loss of appetite, nausea, dry mouth, drowsiness, sleeplessness, weakness, paresthesias, tremors, and hyperthermia.
  • Psychomimetic symptoms can include alterations in mood (euphoria/dysphoria), distorted sense of time, difficulties expressing thoughts and/or focusing on objects, depersonalization, dreamlike feelings, sharpened sense of hearing, synesthesias, and visual hallucinations.
• Patients can be agitated or withdrawn, and adverse reactions are usually seen in inexperienced users or in patients who have unknowingly taken the drug. An unexpected stressful setting can cause an acute panic reaction, even in experienced users. Children can appear agitated, withdrawn, or catatonic. In pediatric cases of known LSD intoxication, parental abuse or neglect must be assumed and investigated.
• Drug-induced persistent psychosis manifests as distorted and disorganized thoughts, dramatic mood swings, mania, depression, vivid visual disturbances, and hallucinations that persist even after the drug effects have ended. Although rare, these symptoms may last for years.
• LSD has been found to be responsible for triggering serotonin syndrome in patients already using precipitating drug combinations (serotonin precursors or agonists, serotonin-release stimulators, selective serotonin reuptake inhibitors [SSRIs], nonselective serotonin-reuptake inhibitors, nonspecific inhibitors of 5-HT metabolism).¹³
• Hallucinogen persisting perception disorder (HPPD) describes spontaneous, repeated or continuous recurrences of sensory distortions including hallucinations, visual disturbances, seeing false motion in the peripheral vision field, bright colored flashes, halos, or trails attached to moving objects. These perceptual symptoms remain unchanged for long periods and often last for years after initial drug use. Such patients often present after previous negative work-up for brain damage or psychiatric disorders.^14,3
• Ergotism related to LSD ingestion is an extremely rare but reported complication. It is thought to be caused by ergot-derived LSA containing ergotlike precursors. Eponymously termed “Saint Anthony’s fire,” ergotism refers to ergot-induced vasoconstriction that leads to burning pain from limb ischemia, dry gangrene of fingers and toes, tissue desquamation, peripheral pulselessness, sensation loss, and edema. Ergotism can also present with convulsive symptoms leading to headache, paresthesias, seizures, and other CNS effects, which are often preceded by GI symptoms like nausea, vomiting, and diarrhea. LSD-induced ergotism often presents as vasoconstrictive effects in combination with hallucinations, mania, or psychosis.¹⁵
• In rare cases, increased morbidity or even mortality have been associated with complications of hyperthermia such as rhabdomyolysis, myoglobinuric renal failure, hepatic necrosis, and disseminated intravascular coagulopathy.
• Generally, LSD-related deaths result from behavioral toxicity. One reported case involved a user that was killed after attempting to stop a train barehanded. The extreme agitation of a “bad trip” can lead to suicide or unintentional death as a result of fleeing from negative hallucinations.

Differential Diagnoses

Other Problems to Be Considered

Encephalitis
Meningitis, aseptic

Workup

Laboratory Studies

Most routine drug screens do not detect lysergic acid diethylamide (LSD). It is primarily excreted in the urine as 2-oxy-lysergic acid diethylamide, which is pharmacologically inactive. Only small amounts of LSD are excreted unchanged in the urine.

The drug can be detected by radioimmunoassay; however, high-performance liquid chromatography or gas chromatography is required for confirmation. Radioimmunoassay may detect levels from 1.5-5.5 ng/mL within 24 hours after having taken a 300-mcg dose of LSD. Urine test results may be positive for LSD for as long as 120 hours after ingestion of the drug. Because of the complexity of detecting LSD, testing for the agent is not clinically useful and is most often done in forensics.¹⁶

Treatment

Medical Care

The basic tenet of caring for patients who have ingested hallucinogens such as lysergic acid diethylamide (LSD) is reassurance in a calm, stress-free environment. Toxic co-ingestions should be treated with appropriate measures. Rarely, patients need to be either sedated or physically restrained. Excessive physical restraint should be avoided because of the potential complication such as hyperthermia and/or rhabdomyolysis.

Benzodiazepines can safely be given to treat agitation. Neuroleptic medications such as Haldol may have adverse psychomimetic effects and thus are not indicated in patients with LSD intoxication. Patients with a history of psychedelic ingestion may have co-ingested other substances, so the care provider must be aware of other toxidromes.

Because LSD is rapidly absorbed through the GI tract, activated charcoal and gastric emptying are of little clinical value by the time a patient presents to the emergency department (ED). These procedures may even cause the patient to become more frightened and agitated and increase the risk of vomiting with aspiration. Guidelines for detoxification and substance abuse treatment have been established by the Substance Abuse and Mental Health Services Administration.¹⁷

Massive ingestions should be treated with supportive care, including respiratory support and endotracheal intubation if needed. Hypertension, tachycardia, and hyperthermia should be treated symptomatically. Hypotension should be treated initially with fluids and subsequently with pressors if required.

Ergotism is treated with discontinuation of any inciting drugs and supportive care. Intravenous administration of anticoagulants, vasodilators, and sympatholytics may be useful. The use of balloon percutaneous transluminal angioplasty in severe cases has been reported.¹⁵

Consultations

Management of simple hallucinogen intoxications can usually be accomplished without consultation. Patients with a history of substance abuse should be referred for drug treatment. Patients who require admission should have consultation with a medical toxicologist or regional poison control center.

Medication

If placing a patient who has used lysergic acid diethylamide (LSD) in a quiet environment with minimal stimuli is not effective, a benzodiazepine (lorazepam or diazepam) is the medication of choice, especially in patients with dysphoric reactions. Benzodiazepines decrease both central and peripheral sympathomimetic drug effects.

Benzodiazepines

These agents may be indicated for extremely agitated patients.

Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.
Although seizures may be promptly brought under control, a significant proportion of patients experience a return to seizure activity, presumably because of the short-lived effect of diazepam after IV administration.

Dosing

Adult

Moderate anxiety: 2-5 mg IV/IM, may repeat q3-4h
Severe anxiety: 5-10 mg IV/IM, may repeat q3-4h
Status epilepticus: 5-10 mg IV, repeat at 10-min to 15-min intervals, not to exceed 30 mg IV cumulative dose

Pediatric

Neonates <30 days: Not established
Infants and children 30 days to 5 years: 0.05-0.3 mg/kg/dose IV slowly q2-5min, not to exceed 5 mg IV cumulative dose
Children >5 years: 0.05-0.3 mg/kg/dose IV q15-30min for 2-3 doses, not to exceed 10 mg IV cumulative dose

Interactions

Increased CNS toxicity with coadministration of other CNS depressants (eg, phenothiazines, barbiturates, alcohols, MAOIs); cimetidine may decrease clearance

Contraindications

Documented hypersensitivity; acute narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Observe the usual precautions in treating patients with impaired hepatic function; metabolites of diazepam are excreted by the kidneys, avoid their excess accumulation by exercising caution; may produce hypotension or muscular weakness, particularly when used with narcotics, barbiturates, or alcohol; prolonged CNS depression observed in neonates, apparently because of inability to biotransform diazepam into inactive metabolites

Lorazepam (Ativan)

May depress all levels of CNS (eg, limbic and reticular formation) by increasing activity of GABA, which is a major inhibitory neurotransmitter in the brain. Preferred due to longer duration of action.

Dosing

Adult

Sedation: 0.05 mg/kg IM, not to exceed 4 mg IM; 0.044 mg/kg IV initially, 2 mg IV total
Status epilepticus: 4 mg IV over 2-5 min, may repeat second dose in 10-15 min, not to exceed 8 mg IV cumulative dose

Pediatric

Status epilepticus:
Neonates: 0.05 mg/kg IV over 2-5 min, may repeat once in 10-15 min prn
Infants and children: 0.1 mg/kg IV over 2-5 min, second dose of 0.05 mg/kg IV at 10-15 min prn
Adolescents: Administer as in adults

Interactions

Produces additive CNS depression when administered with other CNS depressants (eg, ethyl alcohol, phenothiazines, barbiturates, MAOIs, other antidepressants); coadministration with scopolamine may increase sedation, hallucinations, and irrational behavior; rare reports exist of significant respiratory depression, stupor, and/or hypotension with concomitant use of loxapine; marked sedation, excessive salivation, ataxia, and, rarely, death have been reported with concomitant clozapine use; apnea, coma, bradycardia, arrhythmia, heart arrest, and death have been reported with concomitant haloperidol use; risk in combination with scopolamine, loxapine, clozapine, haloperidol, or other CNS-depressant drugs has not been evaluated systematically; therefore, caution is advised if concomitant administration of these drugs is required
Valproate may decrease total clearance and the formation of metabolites; oral contraceptive steroids associated with a 55% decrease in half-life and a 50% increase in volume of distribution, thereby resulting in an almost 3.7-fold increase in total clearance; probenecid may prolong half-life by 130% and decrease total clearance by 45%

Contraindications

Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Use extreme caution when administering lorazepam injection in elderly age, severe illness, or limited pulmonary reserve because of the possibility that hypoventilation and/or hypoxic cardiac arrest may occur; reports of possible propylene glycol toxicity (eg, lactic acidosis, hyperosmolality, hypotension) and possible polyethylene glycol toxicity (eg, acute tubular necrosis) during administration of lorazepam injection at higher than recommended doses; symptoms may be more likely to develop in renal impairment; contains benzyl alcohol, which may be toxic to infants in high doses

Follow-up

Further Inpatient Care

• Patients who have used lysergic acid diethylamide (LSD) and have only minor agitation can usually be treated safely in the emergency department (ED) with observation and supportive care until symptoms have resolved.
• Patients with persistent or unexplained psychotic symptoms should have a psychiatric evaluation.
• Admission should be considered if the etiology for the patient's abnormal behavior is unclear or if toxic co-ingestions are suspected.

Complications

• In massive overdoses, respiratory arrest, coma, emesis, hyperthermia, autonomic dysregulation, and bleeding disorders can occur.
• The patient's altered perceptions can lead to behavioral toxicity, in which the patient does not appreciate the dangers in the environment and may be injured. The extreme agitation of a bad trip has been known to lead to suicide or to unintentional deaths as users have tried to flee from their hallucinations.
• Long-term complications may include prolonged psychotic reactions, severe depression, or an exacerbation/unmasking of a preexisting psychiatric illness. Hallucinogen persisting perception disorder (HPPD) is a Diagnostic and Statistical Manual IV (DSM-IV) diagnosis, in which patients who are not intoxicated experience symptoms (flashbacks) that occurred during the use of LSD. Patients can have both perceptual and visual disturbances during these brief episodes. HPPD may last several months; however, some patients report these experiences for as long as 5 years and often have an underlying psychiatric illness.

Prognosis

• Most users of LSD voluntarily decrease or stop its use over time.
• LSD is not considered an addictive drug because it does not produce compulsive drug-seeking behavior; however, LSD does produce a physiologic tolerance, requiring subsequent increased doses to achieve the same effect.

Patient Education

• For excellent patient education resources, visit eMedicine's Substance Abuse Center. Also, see eMedicine's patient education article Substance Abuse.

Multimedia

Media file 1: Assorted lysergic acid diethylamide (LSD) blotter paper.

Media file 2: Lysergic acid diethylamide (LSD) in assorted pill forms.

References

1. Passie T, Halpern JH, Stichtenoth DO, Emrich HM, Hintzen A. The pharmacology of lysergic acid diethylamide: a review. CNS Neurosci Ther. 2008;14(4):295-314. [Medline].

2. Fusar-Poli P, Borgwardt S. Albert Hofmann, the father of LSD (1906-2008). Neuropsychobiology. Epub 2008 Sep 18.;58(1):53-4.:[Medline].

3. NIDA Research Report - Hallucinogens and Dissociative Drugs: NIH Publication No. 01-4209, Printed March 2001. Available at http://www.nida.nih.gov/PDF/RRHalluc.pdf.

4. DEA Office of Diversion Control, d-Lysergic Acid Diethylamide. Available at http://www.usdoj.gov/dea/concern/lsd.html.

5. Marona-Lewicka D, Thisted RA, Nichols DE. Distinct temporal phases in the behavioral pharmacology of LSD: dopamine D2 receptor-mediated effects in the rat and implications for psychosis. Psychopharmacology (Berl). Jul 2005;180(3):427-35. [Medline].

6. Holohean AM, White FJ, Appel JB. Dopaminergic and serotonergic mediation of the discriminable effects of ergot alkaloids. Eur J Pharmacol. Jul 30 1982;81(4):595-602. [Medline].

7. Nichols DE. Hallucinogens. Pharmacol Ther. Feb 2004;101(2):131-81. [Medline].

8. US Department of Health and Human Services Department Visits Substance Abuse and Mental Health Services Administration. National Estimates of Drug-Related Emergency. Drug Abuse Warning Network. Available at http://dawninfo.samhsa.gov/files/ED2006/DAWN2k6ED.pdf. Accessed 2006.

9. Gold MS, Schuchard K, Gleaton T. LSD use among US high school students. JAMA. Feb 9 1994;271(6):426-7. [Medline].

10. Wu LT, Schlenger WE, Galvin DM. Concurrent use of methamphetamine, MDMA, LSD, ketamine, GHB, and flunitrazepam among American youths. Drug Alcohol Depend. Sep 1 2006;84(1):102-13. [Medline].

11. National Institutes of Health, US Department of Health and Human Services. Monitoring the Future: National Results on Adolescent Drug Use. Overview of Key Findings, 2007. Available at http://www.monitoringthefuture.org/pubs/monographs/overview2007.pdf.

12. Klock JC, Boerner U, Becker CE. Coma, hyperthermia, and bleeding associated with massive LSD overdose, a report of eight cases. Clin Toxicol. 1975;8(2):191-203. [Medline].

13. Martin TG. Serotonin syndrome. Ann Emerg Med. Nov 1996;28(5):520-6. [Medline].

14. Halpern JH, Pope HG Jr. Hallucinogen persisting perception disorder: what do we know after 50 years?. Drug Alcohol Depend. Mar 1 2003;69(2):109-19. [Medline].

15. Raval MV, Gaba RC, Brown K, Sato KT, Eskandari MK. Percutaneous transluminal angioplasty in the treatment of extensive LSD-induced lower extremity vasospasm refractory to pharmacologic therapy. J Vasc Interv Radiol. Aug 2008;19(8):1227-30. [Medline].

16. Taunton-Rigby A, Sher SE, Kelley PR. Lysergic acid diethylamide: radioimmunoassay. Science. Jul 13 1973;181(95):165-6. [Medline].

17. Center for Substance Abuse Treatment (CSAT). Physical detoxification services for withdrawal from specific substances. Rockville, MD: Substance Abuse and Mental Health Services Administration; Jan 18, 2006. 41-115.

Keywords

LSD, lysergic acid diethylamide, hallucinogens, psychedelics, lysergide, "A", acid, Adams, buttons, the beast, blotter, blue chairs, blue cheers, blue mist, brown dot, California triple dip, cube, dot, flat blues, gelatin, green wedge, hawk, Lucy in the sky with diamonds, M and Ms, mescal, microdot, mighty Quinn, mind detergent, Owsley acid, Owsley blue dot, pearly gates, pink wedge, pink Owsley, purple Owsley, Sandoz's, strawberries, sugar cube, sunshine, uncle, vacation, wedding bells, window panes, LSD overdose, LSD poisoning, LSD toxicity, treatment, schizophrenia, synesthesias, good trip, bad trip, hallucinate, hallucinogenic persisting perception disorder, HPPD, flashbacks, respiratory arrest, coma, emesis, hyperthermia, autonomic instability, bleeding disorders, depression, serotonin syndrome, ergotism, Saint Anthony's fire, rhabdomyolysis, hepatic necrosis, myoglobinuric renal failure, disseminated intravascular coagulopathy, DIC

Contributor Information and Disclosures

Author

Stephan Brenner, MD, MPH, Resident Physician, Department of Emergency Medicine, Washington University in St Louis School of Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Bill Dribben, MD, Assistant Professor, Department of Emergency Medicine, Washington University School of Medicine
Bill Dribben, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Halim Hennes, MD, MS, Pediatric Emergency Medicine Research Director, Professor, Departments of Pediatrics and Emergency Medicine, Medical College of Wisconsin
Halim Hennes, MD is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Jeffrey R Tucker, MD, Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut and Connecticut Children's Medical Center
Jeffrey R Tucker, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Pediatrics, and Massachusetts Medical Society
Disclosure: Merck Salary Employment

CME Editor

Paul D Petry, DO, FACOP, FAAP, Consulting Staff, Freeman Pediatric Care, Freeman Health System
Paul D Petry, DO, FACOP, FAAP is a member of the following medical societies: American Academy of Osteopathy, American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Chief Editor

Timothy E Corden, MD, Associate Professor of Pediatrics, Co-Director, Policy Core, Injury Research Center, Medical College of Wisconsin; Associate Director, PICU, Children's Hospital of Wisconsin
Timothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, and Wisconsin Medical Society
Disclosure: Nothing to disclose.

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author Amanda Wood, MD, to the original writing and development of this article.

• Brunton L L, Lazo JS, Parker KL. Goodman and Gillman's The Pharmacological Basis of Therapeutics. 11th ed. New York, NY: McGraw-Hill Professional; 2006.
• Goldfrank L, Flomenbaum N, Lewin N, Howland MA, et al. Goldfrank's Toxicologic Emergencies. 7th ed. New York, NY: McGraw-Hill Professional; 2002.

© 1994- by Medscape.
All Rights Reserved
(http://www.medscape.com/public/copyright)