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    Lysergic Acid Diethylamide Toxicity

    Metabolic / Endocrine, Psychiatric and Behaviour, Toxicology

    Last Updated Jun 08, 2022
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    By Julian Marsden, William Howling


    • Lysergic Acid Diethylamide, LSD, or ‘acid’ among others.
    • A psychoactive drug belonging to a subset of hallucinogenic drugs called psychedelics, which cause altered perception due to their serotonergic properties.
    • The subjective experience of LSD is dose dependent and corresponds to the time course of plasma concentrations with no evidence of acute tolerance.
    • LSD follows first-order elimination kinetics with peak plasma concentration approximately 1.4-1.5h after administration and a half-life of approximately 2.6h with a mean duration of subjective effects of 8-11h.
    • Toxicity in humans has been demonstrated to be very low with no documented deaths due to LSD at recreational doses.
    • Currently there is significant renewed interest in psychedelic drugs generally, primarily for treatment of mental health disorders (although not LSD specifically).

    Diagnostic Process

    Typically, use of LSD results in:

    • A sense of euphoria.
    • Perceptual changes such as a loss of boundaries between the user and environment, the sensation that colors and sounds are distorted and intensified, and the perception that usual objects appear novel, fascinating, or awe-inspiring.
    • Orientation to person, place, and time is usually preserved.

    Less typically:

    • Occasionally users report intense dysphoric experiences accompanied by suffering (eg, that of dying or being born)
      • Also known as a ‘bad trip’.
    • Behaviour may be agitated or withdrawn.
    • Severe intoxication may cause delirium, disorientation, and altered levels of consciousness.
    • Associated sympathomimetic effects include dilated pupils and moderate increases in blood pressure, heart rate, and rarely temperature.
    • Lack of awareness of dangers in the environment, resulting in injury.
    • Psychosis after LSD trips has been reported, and schizophrenia (overt or borderline) may worsen.
    • Flashbacks, or hallucinogen persisting perceptual disorder (HPPD), are transient episodes of altered consciousness that occur months or years after an LSD trip.
    • Hyperactivity may also be seen, with marked auditory and visual hallucinations.
    • Massive ingestion (rare) may result in coma and decreased responsiveness to painful stimuli. Fixed and dilated pupils, diaphoresis, vomiting, hyperthermia, rhabdomyolysis, coagulopathy, and seizures may result.

    The diagnosis of LSD intoxication is clinical.

    • Physical exam:
      • Vitals: temperature, which may be normal; blood pressure, can be increased; heart rate, often high; respiratory rate, can be elevated; oxygen saturation, normal in most cases.
      • General: alertness and orientation may be off from baseline; patients can be diaphoretic and appear disheveled in appearance; loss of appetite.
      • HEENT: mydriasis, xerostomia, nystagmus.
      • Respiratory: increased respiratory rate.
      • Cardiovascular: increased heart rate and blood pressure.
      • Skin: hyperhidrosis.
      • Neurologic: impaired coordination.
      • Psychiatric: auditory and visual hallucinations, panic, psychosis, paranoia, synesthesia, time perturbations, emotional lability, aggression, depersonalization, suicidal ideation, religiosity, depression.

    Diagnostic testing:

    • A basic metabolic profile along with serum ethanol and glucose levels may be helpful in patients with unclear ingestions, co-ingestants, or underlying disorders.
    • Laboratory testing to identify LSD and LSD metabolites is not routinely used in clinical settings.

    Differential diagnosis:

    • Other drugs
      • Other hallucinogenic/psychedelic drugs (e.g. psilocybin, MDMA)
      • Stimulants
      • Sympathomimetics
      • Ethanol
    • Acute psychosis
    • Schizophrenia
    • Hallucinogen persisting perception disorder (HPPD)
    • CNS infections or tumors
    • Electrolyte disturbance


    • Since taking Psilocybin (mushrooms) or LSD produces similar effects (wide individual variation) beware of toxic mushrooms if history of ingestion unclear – mushrooms are more of a whole-body experience, whereas an LSD largely cerebral.
      • Muscarinic mushroom poisoning – cholinergic toxidrome = exhaustion, irritability, muscular cramps, salivation, frothing from mouth, sweating, lacrimation, blurring of vision, miosis, ptosis, bronchorrhea, cough, wheeze, tachypnea, rhonchi, bradycardia, hypotension, abdominal cramps, vomiting, and diarrhea.
      • Death Cap – Amanita Phalloides – causes liver and kidney dysfunction – initially present with stomach pain, N, V, D; then remission; then over 2-3 days develop jaundice renal failure, hypoglycemia, seizures.
    • Serotonin syndrome
      • St. John’s wort, SSRIs, MAOIs, or other antidepressants, ingesting LSD or mushrooms can result in high levels of serotonin potentially resulting in serotonin syndrome:
        • Confusion, disorientation, irritability, anxiety
        • Muscle spasms, rigidity
        • Tremors, shivering
        • Hyperreflexia
        • Mydriasis

    Recommended Treatment

    • Reassurance and supportive care are the cornerstones of management.
      • Empathetic reassurance in a calm, quiet environment with decreased external stimuli is an effective therapeutic modality. The drug effects last for hours but, when it wears off, the patient feels normal again.
      • Patients with anxiety or panic reactions are often easily talked down, with little clinical intervention.
    • There is no specific antagonist to the effects of serotonergic agents.
    • Because most hallucinogens are rapidly absorbed and most patients with adverse events do not present until several hours after ingestion, gastric decontamination is rarely indicated.
    • If patient is severely agitated, sedation with benzodiazepines may be indicated.
      • Diazepam, lorazepam, and midazolam have all been successfully used in this setting.
        • When sedation is achieved ensure respiratory status is stable.
      • For patients with IV access:
        • Diazepam: 5-10mg IV every 5 minutes until sedation achieved.
          • Rapid onset, easily titratable, sustained effect due to active metabolites.
        • Lorazepam: 1-2mg IV every 5 minutes also acceptable.
      • For patients without IV access (due to agitation):
        • Midazolam: 10mg IM to facilitate subsequent interventions.
          • Lorazepam can also be administered IM but requires 15 minutes to reach peak sedation and repeated doses given at more frequent intervals may accumulate, causing oversedation and respiratory depression.
    • If patient is experiencing drug-induced psychosis or agitation states from other drugs (including cocaine, amphetamines, and phencyclidine), butyrophenone antipsychotic agents such as haloperidol is rapidly effective and generally safe.
      • Haloperidol: 5-10mg IV or IM, may be repeated every 20-30 minutes as needed for clinical sedation.
    • Agitated patients who require sedation and do not have complications can be discharged after the acute toxicity stage resolves following a 4- to 6-hour observation period.
    • Behavior should be observed until their mental status returns to baseline.
    • Patients with altered mental status that does not normalize after 8 to 12 hours of observation in the ED, or who present after a massive ingestion with medical complications, require admission to a monitored setting for serial reassessments.

    Quality Of Evidence?


    Information about LSD pharmacokinetics in humans remains limited and for this reason the genuine toxicity of the drug is not yet clearly understood.


    Related Information


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