Lysergic acid diethylamide toxicity
(Redirected from LSD)
Background
- Also known as d-lysergic acid diethylamide and LSD
Mechanism
- Similar to chemical properties of serotonin
- 5-HT2 agonists, mediating excitatory neurotransmitter release.[1]
- LSD also binds to dopaminergic receptors, contributing to its psychogenic affects.[2]
Pharmacology
- Known as one of the most potent psychoactive drug, doses of minimum of 25μg. Doses of 1 to 1.5 μg/kg produce psychedelic effects, with the “optimum” dosage for a typical fully unfolded LSD reaction is estimated to be in the range of 100–200 μg.
- Route of administration can be PO (most common), IM, or IV.[3]
- PO: Usual Dose 100-250μg, Onset 30-45mins, Peak effect 1-2.5hrs, Total duration 9-12hrs
- IM: Usual Dose 100-250μg, Onset 15-20mins, Peak effect 1hr, Total duration 9-10hrs
- IV: Usual Dose 40-180μg, Onset 3-5mins, Peak effect 1hr, Total duration 9-10hrs
- Tolerance to LSD-25 builds up over consistent use and cross-tolerance has been demonstrated between LSD, mescaline and psilocybin.[4]
Clinical Features
- Effects begin around 20-40 minutes after injection
- Euphoria
- Dizziness
- Visual and auditory hallucinations
- Synesthesia ("seeing sounds" and "hearing colors")
- Paranoia
- Acute panic reactions / agitation
- Effects taper off after about 6-8 hours, depending on dose
Differential Diagnosis
Hallucinations
Serotonin-Like Agents
- Lysergic acid diethylamide (LSD)
- Psilocybin ("magic mushrooms")
- N,N-Dimethyltryptamine (DMT)
- 5-methoxy- dimethyltryptamine (5-MeO-DMT)
- 25C-NBOMe
Enactogens
- Designer amphetamines
- Bath salts
- Ecstasy (MDMA)
- Mescaline (peyote)
- Synthetic cannabinoids
Dissociative Agents
- Phencyclidine (PCP)
- Ketamine
- Dextromethorphan
- Nitrous oxide
Plant-based Hallucinogenics
- Marijuana
- Salvia
- Absinthe
- Isoxazole Mushrooms
- Hawaiian baby woodrose (Argyreia nervosa)
- Hawaiian woodrose (Merremia tuberosa)
- Morning glory (Ipomoea violacea)
- Olili- uqui (Rivea corymbosa)
Organic causes
- Delirium
- Intracranial mass to occipital or temporal lobes
- Encephalitis, limbic encephalitis, anti-NMDA receptor encephalitis
- Migraine
- Seizure
- Hypocalcemia/Hypercalcemia
- Rift valley fever
- Rabies
- Syphilis
- Vitamin B7 deficiency
- Pellagra
- Dementia
Other Toxicologic Causes
- Alcohol withdrawal
- Anticholinergic Toxicity
- Tricyclic (TCA) Toxicity
- Synthetic cannabinoids
- Inhalant abuse
- Nitrogen narcosis
- GHB withdrawal
- Hydrocarbon toxicity
- Heavy metal toxicity
- Multiple medications: montelukast, doxapram, hyoscyamine, tizanidine, peramivir, amantadine, rimantadine, bromocriptine, methylergonovine, benztropine, doxepin, voriconazole, acyclovir, valacyclovir, ganciclovir, cimetidine, penicillin G Procaine, clarithromycin, metoclopramide
- Inhalant abuse
Psychiatric Causes [5]
- Schizophrenia, schizoaffective disorder, schizophreniform disorder
- Depression with psychotic features
- Bipolar disorder
- Charles Bonnet Syndrome (in the visually impaired)
Evaluation
- Usually clinical, based on history and presentation
Most blood and urine tests are restricted to research and unavailable for clinical usage
Research Tests
- Found in blood specimens (6–12 hours) and urine (2–4 days) after usage
- Metabolite (2-oxo-3-hydroxy-LSD) present in urine for a longer time than LSD itself.[6]
Management
- Principally supportive
- Assess for signs of trauma or exposure
- Assure patient and staff safety
- Agitation:
- Ativan 1-2mg IV, titrate to effect
- Haloperidol 5-10mg IV, titrate to effect (use as 2nd line agent as may lower seizure threshold)
Consider co-ingestions, hypoglycemia, and risk for rhabdomyolysis[7]
Disposition
- Simple LSD ingestion can be safely discharged after a period of observation, once patient has returned to sober baseline and has a safe disposition plan (~4-6 hours)
- Symptoms lasting longer than 8-12hrs can be managed in an observation unit or admitted
- Further work-up and admission is indicated for persistent psychosis or altered mental status,
See Also
External Links
References
- ↑ Ly, B. "Hallucinogens", Rosen's Emergency Medicine: Concepts and Clinical Practice. 7th Ed. Pgs 2010-2012
- ↑ Marona-Lewicka D, Thisted RA, Nichols DE (2005). "Distinct temporal phases in the behavioral pharmacology of LSD: Dopamine D2 receptor-mediated effects in the rat and implications for psychosis". Psychopharmacology 180 (3): 427–435.
- ↑ Passie, T. "The Pharmacology of Lysergic Acid Diethylamide: A Review". CNS Neuroscience & Therapeutics, Volume 14, Issue 4, pages 295–314, Winter 2008
- ↑ Passie, T. "The Pharmacology of Lysergic Acid Diethylamide: A Review". CNS Neuroscience & Therapeutics, Volume 14, Issue 4, pages 295–314, Winter 2008
- ↑ Visual Hallucinations: Differential Diagnosis and Treatment. PMID PMC2660156
- ↑ Passie, T. "The Pharmacology of Lysergic Acid Diethylamide: A Review". CNS Neuroscience & Therapeutics, Volume 14, Issue 4, pages 295–314, Winter 2008
- ↑ Glaspy, J. "Drugs of Abuse". Emergency Medicine Manual, 6th Ed. Chapt 103, Pgs 502-504.