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Toxicity, Hallucinogens - LSD: Treatment & Medication
Updated: Apr 16, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
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.
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
Increased CNS toxicity with coadministration of other CNS depressants (eg, phenothiazines, barbiturates, alcohols, MAOIs); cimetidine may decrease clearance
Documented hypersensitivity; acute narrow-angle glaucoma
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.
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
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%
Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma
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
More on Toxicity, Hallucinogens - LSD |
| Overview: Toxicity, Hallucinogens - LSD |
| Differential Diagnoses & Workup: Toxicity, Hallucinogens - LSD |
 Treatment & Medication: Toxicity, Hallucinogens - LSD |
| Follow-up: Toxicity, Hallucinogens - LSD |
| Multimedia: Toxicity, Hallucinogens - LSD |
| References |
| Further Reading |
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References
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].
Fusar-Poli P, Borgwardt S. Albert Hofmann, the father of LSD (1906-2008). Neuropsychobiology. Epub 2008 Sep 18.;58(1):53-4.:[Medline].
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.
DEA Office of Diversion Control, d-Lysergic Acid Diethylamide. Available at http://www.usdoj.gov/dea/concern/lsd.html.
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].
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].
Nichols DE. Hallucinogens. Pharmacol Ther. Feb 2004;101(2):131-81. [Medline].
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.
Gold MS, Schuchard K, Gleaton T. LSD use among US high school students. JAMA. Feb 9 1994;271(6):426-7. [Medline].
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].
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.
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].
Martin TG. Serotonin syndrome. Ann Emerg Med. Nov 1996;28(5):520-6. [Medline].
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].
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].
Taunton-Rigby A, Sher SE, Kelley PR. Lysergic acid diethylamide: radioimmunoassay. Science. Jul 13 1973;181(95):165-6. [Medline].
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.
Further Reading
- 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.
Keywords
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