eMedicine Specialties > Psychiatry > Addiction

Hallucinogens: Treatment & Medication

Author: Brooke S Parish, MD, Assistant Professor, Department of Psychiatry, University of New Mexico School of Medicine
Coauthor(s): Michael E Richards, MD, MPA, FACEP, Associate Professor, Department of Emergency Medicine, University of New Mexico School of Medicine; Scott Cameron, MD, Consulting Staff, Department of Emergency Medicine, Regions Hospital
Contributor Information and Disclosures

Updated: Oct 30, 2009

Treatment

Medical Care

  • As with any toxic ingestion, proper attention first should be directed to the assessment and stabilization of the patient's airway, breathing, and circulation.
  • For any person presenting with hallucinations or psychosis, even if a hallucinogen is strongly suggested as the inciting agent, the basic approach to a patient with altered mental status should be followed. This includes administration of dextrose (or demonstration of a normal blood glucose level), thiamine, and naloxone. Other etiologies for the patient's symptoms should not be discounted.
  • Prehospital care providers should attempt to ascertain the type and amount of hallucinogen ingested and the presence of any other co-ingested drugs or psychoactive substances.
  • A basic principle in the care of persons who have ingested hallucinogens is calm reassurance. Patients presenting with an acute panic reaction should be placed in a quiet nonthreatening environment with minimal stimuli. Reassure patients that their anxiety is caused by the drug and that the effect will wear off in several hours. However, patients that are medically stable but 1) remain anxious or agitated, 2) have continued hallucinations 3) remain a danger to themselves or others, or 4) would not be able to care for themselves after several hours of observation, should be admitted to a psychiatric hospital.
  • Patients should be physically or chemically restrained if they are a danger to themselves or others. However, avoid prolonged or excessive physical restraint because this can contribute to hyperthermia, rhabdomyolysis, and acidosis, and it can exacerbate the patient's paranoia. Aggressive cooling measures (fans and mist) should be undertaken if significant hyperthermia is noted. In severe cases, paralyzation and endotracheal intubation should be undertaken. Rhabdomyolysis, if diagnosed, should be treated with fluid repletion and alkalinization of the urine.
  • Benzodiazepines are the cornerstone of treatment for anxious or agitated patients. They reduce anxiety and the sympathomimetic effects of hallucinogens.
    • Phenothiazines should be avoided. They may reduce the seizure threshold, and their anticholinergic effects only serve to worsen the patient's hyperthermia and tachycardia.
    • The role of butyrophenones, particularly droperidol and haloperidol, is less clear. Condemned by some as epileptogenic, they remain in wide use to chemically restrain violent and psychotic patients.
  • The hypertension and tachycardia associated with hallucinogens rarely require any treatment beyond a benzodiazepine. In the rare case of severe hypertension or tachycardia, treatment with nifedipine or nitroprusside may be indicated. Avoid beta-blockers because many of these drugs have both alpha- and beta-adrenergic effects. Isolated beta-blockade leads to unopposed alpha-adrenergic activity, worsening the hypertension and increasing mortality.

Consultations

  • Strongly consider consulting a toxicologist or the local poison control center in the following situations:
    • Co-ingestion of potentially deadly substances
    • Any ingestion causing severe and/or potentially life-threatening adverse effects
    • Ingestion of a drug or plant not readily familiar to the treating physician (An unknown mushroom ingestion should prompt a call to not only the poison control center but also perhaps to a trained mycologist.)
  • A consultation or transfer to a mental health professional should be considered in the following circumstances:
    • Any ingestion in the circumstance of a suicide attempt
    • Any individual demonstrating psychotic symptoms after organic causes have been eliminated or after the psychoactive effects of the hallucinogen should have worn off
  • All individuals demonstrating signs and symptoms of substance abuse should be referred to the appropriate rehabilitation facility. Substance abuse professionals now have evidence that abusers become dependent.

Medication

The goals of pharmacotherapy are to neutralize the effects of the toxic agent, to reduce morbidity, and to prevent complications.

Benzodiazepines

Lorazepam and diazepam, in particular, are the DOCs for hallucinogen ingestion. Anxiolytic and sedating properties calm agitated patients and help blunt coexisting hypertension and tachycardia.


Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life. Increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation. When patients need to be sedated for longer than a 24-h period, this medication is excellent.

Adult

0.01-0.05 mg/kg IV (1-4 mg)

Pediatric

0.05 mg/kg IV

Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

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

Caution in patients with renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease


Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Adult

0.5-4 mg IV/IM

Pediatric

0.05-0.1 mg/kg IV/IM; not to exceed 4 mg

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohol, and MAOIs

Documented hypersensitivity; narrow-angle glaucoma, respiratory depression, and hypotension

Pregnancy

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

Precautions

Caution in patients taking other CNS depressants, with low albumin levels, or hepatic disease (may increase toxicity)

Neuroleptics

For severe agitation and/or psychosis. May decrease seizure threshold.


Haloperidol (Haldol)

Butyrophenone noted for high potency and low potential for causing orthostasis. Downside is high potential for EPS/dystonia.

Adult

0.5-5 mg IV/IM

Pediatric

0.025 mg/kg IV/IM

May increase TCA serum concentrations and hypotensive action of antihypertensive agents; phenobarbital or carbamazepine may decrease effects; coadministration with anticholinergics may increase intraocular pressure; encephalopathylike syndrome associated with concurrent administration of lithium

Documented hypersensitivity; narrow-angle glaucoma, bone marrow suppression, severe cardiac or liver disease, severe hypotension, or subcortical brain damage

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Severe neurotoxicity manifesting as rigidity or inability to walk or talk may occur in patients with thyrotoxicosis also receiving antipsychotics; caution in patients with Parkinson disease; if IV/IM, watch for hypotension; caution in patients diagnosed with CNS depression or cardiac disease; if history of seizures, benefits must outweigh risks; significant increase in body temperature may indicate intolerance to antipsychotics (discontinue if occurs)

Antidotes

Basic approach to treat patients with altered mental status includes administration of dextrose (or demonstration of normal blood glucose level), thiamine, and naloxone.


Dextrose (D-glucose)

Monosaccharide absorbed from the intestine and then distributed, stored, and used by the tissues.

Adult

10-20 g PO; repeat in 10 min if necessary

Pediatric

<2 years: Not recommended
>2 years: Administer as in adults

Caution when administering parenteral fluids to patients receiving corticosteroids or corticotropin, especially if the solution contains sodium ions

Do not administer to a patient in diabetic coma if blood sugar levels are extremely high; avoid in severely dehydrated patients; do not administer concentrated solution if intraspinal or intracranial hemorrhage is present; avoid in dehydrated patients diagnosed with delirium tremens, hepatic coma, or glucose-galactose malabsorption syndrome

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause nausea, which also may occur with hypoglycemia; IV dextrose solutions may result in dilution of serum electrolyte concentrations or overhydration in the presence of fluid overload; caution in patients in congested states or those with pulmonary edema
Hypertonic dextrose given peripherally may cause thrombosis (instead, administer through central venous catheter); caution in patients with subclinical diabetes mellitus or carbohydrate intolerance; increased risk of inducing significant hyperglycemia or hyperosmolar syndrome if solution is administered rapidly, especially in patients with chronic uremia or carbohydrate intolerance
Concentrated solutions should not be administered SC/IM; rates of dextrose infusion faster than 0.5 g/kg/h may produce glycosuria; at infusion rates of 0.8 g/kg/h, the incidence of glycosuria is 5%; closely monitor fluid balance, electrolyte concentrations, and acid-base balance; dextrose administration may produce vitamin B complex deficiency


Thiamine (Thiamilate)

To correct thiamine deficiency.

Adult

100 mg IV initially, followed by 50-100 mg/d IV/IM

Pediatric

50 mg IV initially, followed by 10-25 mg/d IV/IM

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Sensitivity reactions can occur (intradermal test dose recommended in patients with possible sensitivity); deaths have resulted from IV use; sudden onset or worsening of Wernicke encephalopathy may occur following glucose administration in patients with a thiamine deficiency; administer before or together with dextrose-containing fluids in patients with a possible thiamine deficiency


Naloxone (Narcan)

Prevents or reverses opioid effects (hypotension, respiratory depression, sedation), possibly by displacing opiates from their receptors.

Adult

0.4-2 mg IV/IM/SC q2-3min prn; use increments of 0.1-0.2 mg in patients who are opioid dependent

Pediatric

0.1 mg/kg IV/IM/SC repeat q2-3min prn

Decreases analgesic effects of narcotics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with cardiovascular disease; may precipitate withdrawal symptoms in patients dependent on opiates

More on Hallucinogens

Overview: Hallucinogens
Differential Diagnoses & Workup: Hallucinogens
Treatment & Medication: Hallucinogens
Follow-up: Hallucinogens
Multimedia: Hallucinogens
References

References

  1. de la Torre R, Farre M. Neurotoxicity of MDMA (ecstasy): the limitations of scaling from animals to humans. Trends Pharmacol Sci. Oct 2004;25(10):505-8. [Medline].

  2. Wilcox JA, Wilcox AH. Movement disorders and MDMA abuse. J Psychoactive Drugs. Jun 2009;41(2):203-4. [Medline].

  3. SAMHSA. 2003 National Survey on Drug Use and Health. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Office of Applied Studies. Available at http://www.oas.samhsa.gov/nhsda/2k3nsduh/2k3Results.htm. Accessed October 30, 2009.

  4. Lin DL, Liu HC, Liu RH. Methylenedioxymethamphetamine-related deaths in Taiwan: 2001-2008. J Anal Toxicol. Sep 2009;33(7):366-71. [Medline].

  5. Erowid. The Vaults of Erowid: Documenting the Complex Relationship Between Humans and Psychoactives [Web site]. [Full Text].

  6. Greene SL, Kerr F, Braitberg G. Review article: amphetamines and related drugs of abuse. Emerg Med Australas. Oct 2008;20(5):391-402. [Medline].

  7. Halpern JH, Sewell RA. Hallucinogenic botanicals of America: a growing need for focused drug education and research. Life Sci. Dec 22 2005;78(5):519-26. [Medline].

  8. Ompad DC, Galea S, Fuller CM, et al. Club drug use among minority substance users in New York City. J Psychoactive Drugs. Sep 2004;36(3):397-9. [Medline].

  9. 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].

  10. Prisinzano TE. Psychopharmacology of the hallucinogenic sage Salvia divinorum. Life Sci. Dec 22 2005;78(5):527-31. [Medline].

  11. SAMSHA. Ecstasy, Other Club Drugs, & Other Hallucinogens. Available at http://www.oas.samhsa.gov/ecstasy.htm.

  12. Tucker JR, Ferm RP. Lysergic acid diethylamide and other hallucinogens. In: Goldfrank LR, Flomenbaum NE, Lewin NA, Weisman RS, Howland MA, Hoffman RS, eds. Goldfrank's Toxicological Emergencies. 6th ed. Stamford, Conn: Appleton & Lange; 1998:1111-9.

  13. Williams LC, Keyes C. Psychoactive drugs. In: Ford MD, Delaney KA, Ling LJ, Erickson T, eds. Clinical Toxicology. Philadelphia, Pa: WB Saunders; 2001:640-9.

Further Reading

Keywords

psychedelics, LSD, acid, phencyclidine, PCP, psilocybin, psilocin, MDMA, ecstasy, ketamine, peyote, mescaline, MDEA, Eve, enactogens, cannabinols, THC, DMT, bufotenine, 5-MeO-DMT, foxy, Amanita muscaria, psychoactives, Colorado River toad, ibotenic acid, hallucinogenic drugs, drug abuse, illicit drugs, illegal drugs, drugs of abuse, lysergic acid diethylamide, Delysid, lysergamide, phenylethylamine, piperidine, indolealkylamine, cannabinol, morning glory, Hawaiian baby woodrose, bufotenin, dimethyltryptamine, methamphetamine, ketamine, special K, tetrahydrocannabinol, marijuana, Mary Jane, pot, herb, weed, ganja, dope, dip dope, indica, grass, hashish, hash, microdot, window pane, acid, cid, synesthesia, flashbacks, hallucinogen persisting perception disorder, HPPD, ecstasy, Sernylan, peace pill, angel dust, magic mushrooms, shrooms

Contributor Information and Disclosures

Author

Brooke S Parish, MD, Assistant Professor, Department of Psychiatry, University of New Mexico School of Medicine
Brooke S Parish, MD is a member of the following medical societies: American College of Physicians and American Psychiatric Association
Disclosure: Nothing to disclose.

Coauthor(s)

Michael E Richards, MD, MPA, FACEP, Associate Professor, Department of Emergency Medicine, University of New Mexico School of Medicine
Michael E Richards, MD, MPA, FACEP is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Scott Cameron, MD, Consulting Staff, Department of Emergency Medicine, Regions Hospital
Scott Cameron, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Ronald C Albucher, MD, Chief Medical Officer, Westside Community Services; Consulting Staff, California Pacific Medical Center
Ronald C Albucher, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Eduardo Dunayevich, MD, Adjunct Assistant Professor, Department of Psychiatry, University of Cincinnati; Clinical Research Physician, Neuroscience, Lilly Research Laboratories
Eduardo Dunayevich, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: Nothing to disclose.

CME Editor

Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer  Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research

Chief Editor

Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.