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ERROR: type should be string, got "https://profreg.medscape.com/px/getpracticeprofile.do?method=getProfessionalProfile&urlCache=aHR0cHM6Ly9lbWVkaWNpbmUubWVkc2NhcGUuY29tL2FydGljbGUvMTAxMTYxNS1vdmVydmlldw==\nDrugs & Diseases > Emergency Medicine\nLSD Toxicity\nAuthor: Paul P Rega, MD, FACEP; Chief Editor: Stephen L Thornton, MD more...\nSections LSD Toxicity\nPathophysiology and Etiology\nStudies Related to Complications and Comorbidities\nPrehospital and Emergency Department Care\nAntihypertensives\nLysergic acid diethylamide (LSD), a hallucinogen that is also known as an entactogen (“to touch within” [1] ) is one of the most potent psychoactive compounds known (said to be more than 3000 times more potent than mescaline). Doses as small as 1-1.5 mcg/kg can produce psychoactive effects; an oral dose of 25 µg is capable of producing potential deleterious psychedelic effects. [2, 3]\nThe drug is odorless, colorless, and slightly bitter tasting. It is usually taken by mouth and is rapidly absorbed by the gastrointestinal (GI) tract. The image below depicts LSD in several different pill forms.\nLysergic acid diethylamide (LSD) in assorted pill forms.\nView Media Gallery\nWhile LSD usage reached epidemic proportions in the 1960s, there has been a reduction of abuse owing to constraints on the manufacture and distribution of the drug. It is classified as a Schedule I drug by the US Food and Drug Administration, meaning it is considered a narcotic drug with no known acceptable medical use that has a high potential for abuse, and the possession of any amount of LSD is illegal.\nThere has also been a concerted effort to educate the public that the psychedelic experiences are a health hazard. Nevertheless, LSD continues to be used. Pockets of continued abuse have been documented across the country. [4]\nLSD toxicity can lead to respiratory arrest, coma, emesis, hyperthermia, autonomic instability, and bleeding disorders. In some cases, the patient's altered perceptions can result in behavioral toxicity, in which an individual fails to appreciate dangers in the environment and may be injured.\nPsychomimetic symptoms\nAdverse effects of LSD use can include the following:\nPanic reaction - May be triggered by an unexpected stressful setting\nAmplification of unconscious fears\nSelf aggression\nSuicidal or homicidal ideation\nFear of going insane or of the inability to return to normal\nPerception of rapid aging of self or others\nProfound depression\nSomatic symptoms\nSomatic symptoms of LSD toxicity, which are usually due to sympathomimetic effects, include the following:\nMydriasis\nParesthesias\nHyperactive reflexes\nPiloerection\nMild pyrexia\nSeizures - Rare; typically with doses above 10 mcg/kg\nMassive overdoses can lead to the following [1, 2] :\nRespiratory arrest\nComa - Very rare\nAutonomic instability\nCoagulopathies\nRhabdomyolysis\nLSD 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). [5]\nHPPD and flashbacks\nIn hallucinogen persisting perception disorder (HPPD), patients who are not intoxicated experience symptoms (flashbacks) that initially arose during LSD use. HPPD can last from months to years. According to the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5), all of the following criteria must be met for a diagnosis of HPPD [6] :\nRe-experiencing, after the use of a hallucinogen, of one or more of the perceptual symptoms that were experienced while intoxicated with the hallucinogen\nThe symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning\nThe symptoms are not due to a general medical condition and are not better accounted for by another mental disorder\nPerceptual symptoms include the following [6] :\nGeometric hallucinations\nPerception of movement in peripheral visual fields\nFlashes of color\nIntensified colors\nTrails of images of moving objects\nPostitive afterimages\nHalos around objects\nMacropsia and micropsia\nSee Clinical Presentation for more detail.\nAlthough LSD toxicity is diagnosed primarily by way of history and physical examination, LSD can be detected by radioimmunoassay. levels from 1.5-5.5 ng/mL may be found within 24 hours after the patient has taken a 300-mcg dose of the drug. However, high-performance liquid chromatography or gas chromatography is required for confirmation.\nDiagnostic testing should be directed at identification of complications or exclusion of comorbidities. Coagulation, total creatine phosphokinase, or serum electrolyte studies may be indicated in patients with seizures, coma, or a neuroleptic malignant syndrome–like presentation to identify coagulopathy or rhabdomyolysis or to exclude other diagnoses.\nSee Workup for more detail.\nThe basic tenet of caring for patients who have ingested hallucinogens such as LSD is reassurance in a calm, stress-free environment that is safe for both patient and healthcare professionals. Rarely, patients need to be either sedated or physically restrained. Benzodiazepines can safely be given to treat agitation. [1, 2] Butyrophenones such as haloperidol may be required, although there is a small theoretic risk of lowering the seizure threshold. [1]\nMassive ingestions of LSD should be treated with supportive care, including respiratory support and endotracheal intubation if needed. The following should be treated symptomatically:\nHypotension - Should be treated initially with fluids and subsequently with pressors if required\nSee Treatment and Medication for more detail.\nThe prototype of the hallucinogen class, LSD was first developed in 1938, when the Swiss biochemist Albert Hofmann synthesized it from lysergic acid while researching the medical effects of ergot-derived synthetic molecules. However, the hallucinogenic properties of LSD were not discovered until 1943, when Hofmann unintentionally ingested the substance and experienced an “extremely stimulated experience.\" [7]\nHailed as a wonder drug in the field of psychoanalysis during the 1950s and 1960s, LSD was used in schizophrenia research to produce “experimental psychosis” (through alteration of neurotransmitter systems) and in so-called psycholytic and psychedelic therapies. [8] Multiple reports suggested beneficial effects from the use of LSD in the treatment of depression, obsessive-compulsive disorder, and sexual dysfunction. [9] For over a decade, it was also used to treat children with autism.\nThe 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. Because of the resulting public health concerns, however, restrictions were placed on LSD research and on its use in psychotherapy, and the drug was banned for recreational purposes by federal law in 1966. [10]\nCurrently, 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. (See DDx.)\nPsychoactive effects\nLSD causes changes in thought, mood, and perception, with minimal effects on memory and orientation. The drug primarily produces so-called pseudohallucinations, which are illusions derived from the misinterpretation of actual experiences. These include synesthesias, in which the transposition of certain sensory modes occurs, creating an experience known as sensory crossover . For example, the perception of a sound evoked by a visual image or the impression of hearing colors or feeling sounds would be considered a synesthesia. True hallucinations occur as well; visual hallucinations are the most common.\nExposure 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; however, acute adverse drug effects can include panic reactions, psychoses, and major depression. [11]\nOne case report describes a young man under the influence of LSD and alcohol who amputated his testicles. [12]\nSynthesis and preparation\nLSD 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), a Schedule III substance, is found in the seeds of morning glories and Hawaiian baby woodrose. LSD is produced as a crystalline powder and then mixed with various binding agents.\nAccording to the US Drug Enforcement Administration (DEA), the strength of samples obtained from illicit sources ranges from 20-80 mcg of LSD per dose. Although LSD possesses a wide margin of safety, single doses obtained over recent years were significantly less potent than those available during the 1960s and 1970s, when a dose contained 100-200 mcg or more of LSD.\nUse and availability\nMost LSD manufactured in the United States is intended for illegal use. Primary motivations given for the use of LSD are experimentation, a desire to feel good, and a perceived enhancement of social interactions. It is also inexpensive. Typically, a dose costs less than $15. [2] Although small amounts of the drug are used for research purposes, it has no known medical applications. (See Epidemiology.)\nMost commonly, 20 to 80 µg of this colorless, tasteless, odorless, and water-soluble substance is ingested via a small square of dried \"blotter\" paper that has been saturated with a solution of the compound. With this method, the LDS is sprayed onto the small squares of decorative paper, creating the product known as blotter acid.The blotter paper is often imprinted with fanciful designs or cartoons (ie, trademarks for the manufacturer). Other forms of LSD administration include \"microdots\" (tiny tablets), \"windowpane\" (gelatin sheets), and liquid LSD. [2] See the image below.\nAssorted lysergic acid diethylamide (LSD) blotter papers.\nMost illegal laboratories making LSD are found on the West Coast. The drug is sold under more than 80 street names, including \"A\", acid, Adams, back breaker, battery acid, beast, blotter, blue chairs, blue cheers, blue mist, brown dot, buttons, California triple dip, cube, dose, dot, Elvis, flat blues, gelatin, green wedge, hawk, looney toons, Lucy in the sky with diamonds, M and Ms, mellow yellow, mescal, microdot, mighty Quinn, mind detergent, Owsley acid, Owsley blue dot, pane, pearly gates, pink wedge, pink Owsley, purple Owsley, Sandoz's, strawberries, sugar cube, sunshine, Superman, uncle, vacation, wedding bells, window pane, and Zen.\nMost hallucinogens belong to 1 of the following 2 structurally distinct classes:\nIndoles and tryptamines - Eg, LSD, psilocybin, and N,N-dimethyltryptamine (DMT)\nPhenylethylamines - Mescaline and MDMA\nThe most common route of exposure to LSD is oral; the drug is absorbed rapidly from the GI tract. Dermal absorption has not been well documented. LSD can be aerosolized and is absorbed by the lungs if the particle diameter is 5 micrometers or less.\nDisruption of the serotonin system\nBecause of their structural similarity to serotonin and their intrinsic potency, hallucinogens disrupt the balanced functioning of the serotonin system. [3, 7]\nHallucinogens have a high affinity for serotonin (5-HT) receptors, at which LSD exhibits agonist and antagonist properties. [13]\nThe 5-HT2A 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 are responsible for the sympathomimetic effects of the drug (hypertension, tachycardia, dizziness, loss of appetite, dry mouth, sweating, nausea, numbness, tremor).\nAffinities to other serotonin receptors differ between the 2 hallucinogen classes, which makes attributing specific effects to a single 5-HT receptor subtype impossible. LSD also stimulates dopamine D2 receptors. [14] This leads to a biphasic pharmacologic 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. [15, 16]\nAfter oral administration, the early drug effects of LSD appear after 30-60 minutes. More profound psychoactive effects peak at 2-4 hours and some effects may last as long as 12 hours. [2] 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. The LSD metabolites N-demethyl-LSD (nor-LSD), lysergic acid ethylamide (LAE), iso-LAE, mono-oxylated LSD, and hydroxylated LSD are excreted in the urine. The elimination half-life of LSD is 3-5 hours.\nAlthough 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-HT2A receptors. Long-term effects of chronic use can result in persistent psychosis and hallucinogen persisting perception disorder (HPPD), so called “flashbacks.\" LSD remains one of the most potent mood-altering and perception-altering drugs. [11]\nIn 2017, the American Association of Poison Control Centers' (AAPCC) National Poison Data System (NPDS) reported 594 single exposures to LSD and no deaths. [17]\nThe overall prevalence of LSD use among adolescents and young adults ages 15 to 34 years in Europe is estimated to be under 1.0%, although higher prevalence has been reported in Finland (1.3%) and the Czech Republic (1.4%). [18]\nWhile LSD is included in national drug trending reports, the accuracy of these for actual LSD use is complicated by novel non-lysergamide hallucinogenic compounds being marketed as LSD. For example, a new class of designer research chemicals includes highly potent hallucinogenic serotonin agonists. Of these, 25I-NBOMe and 25C-NBOMe are the most common type called \"Bomb\" or \"N-Bomb\" and are sold on blotter paper. The drug is taken via the buccal or sublingual route, just like LSD. NBOMes are commonly misrepresented as LSD because of their similar routes of administration and effects. [19]\nA survey of 682 adults (aged 18–25 years) in 2015 entering electronic dance music (EDM) events at nightclubs and festivals in New York City found 2.9% of respondents reported lifetime use of LSD. In addition, LSD use significantly increased the risk of novel psychoactive substance (NPS) use (adjusted odds ratio = 4.64, p = 0.004). [19] Another study of self-reported NPS use in a US nationally representative sample found that 73.7% of NPS users reported lifetime LSD use. [20]\nIn the United States, LSD is used predominantly by whites. [21] While use by blacks and Hispanics is less common, it has been reported in surveys of urban populations, being especially used in clubs and raves. [19]\nMales use LSD more frequently than do females. The typical LSD user is a risk-taking, white male in high school or college. However, a survey of women attending university-based ambulatory reproductive health clinics revealed that 13% had used LSD in the past. [22] There was also an association between LSD and high-risk sexual behavior.\nThe 2017 AAPCC-NPDS reported that 58% of reported exposures to LSD were in adolescents aged 13-19 years. [17]\nSince 2000, there has been a considerable falloff in reported availability among middle- and high-school students, which is reflected in the significant decline in use among younger adolescents. [23]\nThe long-term prognosis for persons who use LSD is good provided that they stop using it, and most users voluntarily decrease or stop the use of the drug 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.\nFor those who use LSD chronically, there is the enhanced risk for schizophreniform psychosis and derangements in memory function, problem solving, and abstract thinking. Long-term complications from LSD use may include prolonged psychotic reactions, severe depression, or an exacerbation/unmasking of a preexisting psychiatric illness. LSD potentially may exacerbate comorbid conditions in elderly patients.\nIn 2017, AAPCC reported only 1 death related to LSD exposure. [17] Because of its large index of toxicity, patients must have access to unusually concentrated forms of LSD if they are to overdose. The lethal dose of LSD has been estimated to be 14,000 mcg. However, only a few cases of massive ingestions have been reported. For example, eight individuals who believed they had cocaine accidentally insufflated an extremely high dose of LSD. Their plasma LSD levels were reported as between 1000 and 7000 μg/100 ml. These individuals all became comatose, with hyperthermia, vomiting, light gastric bleeding, and respiratory problems. With hospital treatment, however, all were reported to have survived without apparent residual effects. [24]\nThe 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. Users may believe that they are invincible or possess superpowers and may do things they would not normally consider, such as believing they can fly, jumping from buildings, or incurring severe ocular damage by prolonged staring at the sun. [24] Extreme agitation brought on by disturbing hallucinations has been known to lead to suicide or to unintentional death, as users have tried to flee from these drug-induced illusions.\nDespite early reports of LSD-related fetal malformations, inadequate evidence exists to establish causality.\nHallucinogen persisting perception disorder (HPPD) has an estimated prevalence of 4.2%. With HPPD, individuals who are not intoxicated experience symptoms (flashbacks) that initially arose during the use of LSD. Flashbacks tend to occur during times of psychological stress and can last for minutes to hours. HPPD may last several months; however, some patients report these experiences for as long as 5 years, with many of these individuals having an underlying psychiatric illness. [25]\nCounsel patients on the potential dangers of LSD use, including driving automobiles while intoxicated or combining LSD ingestion with ethanol, marijuana, or other illicit drugs. Because the metabolism of LSD is not fully understood, HIV-positive patients on highly active antiretroviral therapy should be counseled to not use LSD, due to the possibility of adverse drug-drug interactions.\"Mind Over Matter,\" an educational tool, is designed to encourage young people in grades 5-9 to learn about the effects of drug abuse on the body and brain (see National Institute on Drug Abuse, Mind Over Matter).\nFor patient education information, see Substance Abuse.\nWu L. Lysergic Acid Diethylamide (LSD) and Other Hallucinogens. Olson KR, ed. Poisoning & Drug Overdose. 6th ed. New York, NY: McGraw-Hill; 2012. Chapter 95.\nPrybys KM, Hansen KN. Hallucinogens. Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York, NY: McGraw-Hill; 2011. Chapter 182.\nO'Brien CP. Drug Addiction. Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 12th ed. New York, NY: McGraw-Hill; 2011. Chapter 24.\nMello NK, Mendelson JH. Cocaine and Other Commonly Abused Drugs. Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, eds. Harrison's Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. Chapter 394.\nMartin TG. Serotonin syndrome. Ann Emerg Med. 1996 Nov. 28(5):520-6. [Medline].\nAmerican Psychiatric Association. Substance Related Disorders. Diagnostic and Statistical Manual of Mental Disorders (DSM-5). 5th Edition. Washington, DC: American Psychiatric Association; 2013. 531-532.\nSanders-Bush E, Hazelwood L. 5-Hydroxytryptamine (Serotonin) and Dopamine. Brunton LL, Chabner BA, Knollmann BC, eds. Goodman & Gilman's The Pharmacological Basis of Therapeutics. 12th ed. New York, NY: McGraw-Hill; 2011. Chapter 13.\nPassie 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].\nVollenweider FX, Kometer M. The neurobiology of psychedelic drugs: implications for the treatment of mood disorders. Nat Rev Neurosci. 2010 Sep. 11(9):642-51. [Medline].\nFusar-Poli P, Borgwardt S. Albert Hofmann, the father of LSD (1906-2008). Neuropsychobiology. Epub 2008 Sep 18. 58(1):53-4.:[Medline].\nNational Institute on Drug Abuse. NIDA Research Report Series- Hallucinogens and Dissociative Drugs. Drugabuse.gov. Available at https://www.drugabuse.gov/publications/research-reports/hallucinogens-dissociative-drugs/director. February 2015; Accessed: June 11, 2018.\nBlacha C, Schmid MM, Gahr M, et al. Self-inflicted testicular amputation in first lysergic acid diethylamide use. J Addict Med. 2013 Jan-Feb. 7(1):83-4. [Medline].\nHalberstadt AL, Geyer MA. Multiple receptors contribute to the behavioral effects of indoleamine hallucinogens. Neuropharmacology. 2011 Sep. 61(3):364-81. [Medline]. [Full Text].\nMarona-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). 2005 Jul. 180(3):427-35. [Medline].\nHolohean AM, White FJ, Appel JB. Dopaminergic and serotonergic mediation of the discriminable effects of ergot alkaloids. Eur J Pharmacol. 1982 Jul 30. 81(4):595-602. [Medline].\nNichols DE. Hallucinogens. Pharmacol Ther. 2004 Feb. 101(2):131-81. [Medline].\nGummin DD, Mowry JB, Spyker DA, Brooks DE, Osterthaler KM, Banner W. 2017 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 35th Annual Report. Clin Toxicol (Phila). 2018 Dec. 56 (12):1213-1415. [Medline]. [Full Text].\nEuropean Monitoring Centre for Drugs and Drug Addiction (EMCDDA). European Drug Report 2018: Trends and Developments. Luxembourg: Publications Office of the European Union; 2018. [Full Text].\nPalamar JJ, Acosta P, Sherman S, Ompad DC, Cleland CM. Self-reported use of novel psychoactive substances among attendees of electronic dance music venues. Am J Drug Alcohol Abuse. 2016 Nov. 42 (6):624-632. [Medline]. [Full Text].\nPalamar JJ, Martins SS, Su MK, Ompad DC. Self-reported use of novel psychoactive substances in a US nationally representative survey: Prevalence, correlates, and a call for new survey methods to prevent underreporting. Drug Alcohol Depend. 2015 Nov 1. 156:112-119. [Medline]. [Full Text].\nSubstance Abuse and Mental Health Services Administration. Key substance use and mental health indicators in the United States: Results from the 2017 National Survey on Drug Use and Health. (HHS Publication No. SMA 18-5068, NSDUH Series H-53). Rockville, MD: Center for Behavioral Health Statistics and Quality, Substance Abuse and Mental Health Services Administration; 2018. [Full Text].\nRickert VI, Siqueira LM, Dale T, Wiemann CM. Prevalence and risk factors for LSD use among young women. J Pediatr Adolesc Gynecol. 2003 Apr. 16(2):67-75. [Medline].\nJohnston, LD, Miech RA, O'Malley PM, et al. Monitoring the Future national survey results on drug use: 1975-2017: Overview, key findings on adolescent drug use. Available at http://www.monitoringthefuture.org//pubs/monographs/mtf-overview2017.pdf. January 2018; Accessed: June 11, 2018.\nNichols DE. Psychedelics. Pharmacol Rev. 2016 Apr. 68 (2):264-355. [Medline]. [Full Text].\nAbraham HD. Visual phenomenology of the LSD flashback. Arch Gen Psychiatry. 1983 Aug. 40(8):884-9. [Medline].\nRopper AH, Samuels MA. Disorders of the Nervous System Caused by Drugs, Toxins, and Other Chemical Agents. Ropper AH, Samuels MA, eds. Adams and Victor's Principles of Neurology. 9th ed. New York, NY: McGraw-Hill; 2009. Chapter 43.\nAbert B, Ilsen PF. Palinopsia. Optometry. 2010 Aug. 81(8):394-404. [Medline].\nKlock 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].\nHalpern JH, Pope HG Jr. Hallucinogen persisting perception disorder: what do we know after 50 years?. Drug Alcohol Depend. 2003 Mar 1. 69(2):109-19. [Medline].\nRaval 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. 2008 Aug. 19(8):1227-30. [Medline].\nBerrens Z, Lammers J, White C. Rhabdomyolysis After LSD Ingestion. Psychosomatics. 2010 Jul. 51(4):356-356.e3. [Medline].\nDolder PC, Liechti ME, Rentsch KM. Development and validation of a rapid turboflow LC-MS/MS method for the quantification of LSD and 2-oxo-3-hydroxy LSD in serum and urine samples of emergency toxicological cases. Anal Bioanal Chem. 2015 Feb. 407 (6):1577-84. [Medline].\nBerg T, Jørgenrud B, Strand DH. Determination of buprenorphine, fentanyl and LSD in whole blood by UPLC-MS-MS. J Anal Toxicol. 2013 Apr. 37(3):159-65. [Medline].\nPedersen AJ, Dalsgaard PW, Rode AJ, Rasmussen BS, Müller IB, Johansen SS, et al. Screening for illicit and medicinal drugs in whole blood using fully automated SPE and ultra-high-performance liquid chromatography with TOF-MS with data-independent acquisition. J Sep Sci. 2013 Jul. 36(13):2081-9. [Medline].\nTaunton-Rigby A, Sher SE, Kelley PR. Lysergic acid diethylamide: radioimmunoassay. Science. 1973 Jul 13. 181(95):165-6. [Medline].\nRega PP. Psychosis. Chanmugam A, Triplett P, Kelen G, eds. Emergency Psychiatry. Cambridge, UK: Cambridge University Press; 2013. Chapter 5.\nBrown EJ, Whelan L. Psychiatric Emergencies. Humphries RL, Stone C, eds. CURRENT Diagnosis & Treatment Emergency Medicine. 7th ed. New York, NY: McGraw-Hill; 2011. Chapter 49.\nCenter for Substance Abuse Treatment (CSAT). Physical detoxification services for withdrawal from specific substances. Substance Abuse and Mental Health Services Administration. Jan 18, 2006.\nPaul P Rega, MD, FACEP Assistant Professor, Department of Public Health and Preventive Medicine, Assistant Professor, Emergency Medicine Residency Program, Department of Emergency Medicine, The University of Toledo College of Medicine; Director of Emergency Medicine Education and Disaster Management, OMNI Health Services\nPaul P Rega, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians\nStephen L Thornton, MD Associate Clinical Professor, Department of Emergency Medicine (Medical Toxicology), University of Kansas Hospital; Medical Director, University of Kansas Hospital Poison Control Center; Staff Medical Toxicologist, Children’s Mercy Hospital\nStephen L Thornton, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology\nTimothy 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\nTimothy E Corden, MD is a member of the following medical societies: American Academy of Pediatrics, Phi Beta Kappa, Society of Critical Care Medicine, Wisconsin Medical Society\nStephan Brenner, MD, MPH Resident Physician, Department of Emergency Medicine, Washington University in St Louis School of Medicine\nRobert G Darling, MD, FACEP Adjunct Clinical Assistant Professor of Military and Emergency Medicine, Uniformed Services University of the Health Sciences, F Edward Hebert School of Medicine; Associate Director, Center for Disaster and Humanitarian Assistance Medicine\nRobert G Darling, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Telemedicine Association, and Association of Military Surgeons of the US\nWilliam H Dribben, MD Assistant Professor, Division of Emergency Medicine, Washington University in St Louis School of Medicine\nWilliam H Dribben, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine\nAlan H Hall, MD, FACEP Assistant Professor of Emergency Medicine, Division of Toxicology, Texas Tech University Health Sciences Center at El Paso; President, Chief Medical Toxicologist, Toxicology Consulting and Medical Translating Services, Inc\nHalim Hennes, MD, MS Division Director, Pediatric Emergency Medicine, University of Texas Southwestern Medical Center at Dallas, Southwestern Medical School; Director of Emergency Services, Children's Medical Center\nHalim Hennes, MD, MS is a member of the following medical societies: American Academy of Pediatrics\nC Crawford Mechem, MD, MS, FACEP Professor, Department of Emergency Medicine, University of Pennsylvania School of Medicine; Emergency Medical Services Medical Director, Philadelphia Fire Department\nC Crawford Mechem, MD, MS, 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\nDisclosure: Medscape Salary Employment\nJeffrey R Tucker, MD Assistant Professor, Department of Pediatrics, Division of Emergency Medicine, University of Connecticut School of Medicine, Connecticut Children's Medical Center\nDisclosure: Merck Salary Employment\nSuzanne White, MD Medical Director, Regional Poison Control Center at Children's Hospital, Program Director of Medical Toxicology, Associate Professor, Departments of Emergency Medicine and Pediatrics, Wayne State University School of Medicine\nSuzanne White, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Clinical Toxicology, American College of Epidemiology, American College of Medical Toxicology, American Medical Association, and Michigan State Medical Society\nAmanda Wood, MD Resident Physician, Emergency Medicine Resident, Division of Emergency Medicine, Barnes Jewish and St Louis Children's Hospitals\nencoded search term (LSD Toxicity) and LSD Toxicity\nAdjuncts to the Forensic Autopsy\nForensic Toxicology - Drugs and Chemicals\nA Suicide Attempt in a 28-Year-Old Man\nForensic Investigation - Motor Vehicle Accidents and Motor Vehicle-Pedestrian Accidents\nAltered Mental Status in a Young Man Picked Up On the Street\nThe Autopsy Report\nSeizures, Coma More Common With Synthetic Cannabinoids in Adolescents\nKetamine Promising in Cocaine Addiction\nSuicidal Bupropion Overdosing in Teens Has Worse Outcomes Than SSRI Overdosing\n9 Bug Bites You Need to Know\nAccording to Emergency Physicians\nMore Emergency 'MacGyver' Tips for Physicians\nEscalating Workplace Violence Rocks Hospitals\nAvoiding the 'H Bombs' in Traumatic Brain Injury\nVisits to the Emergency Department Reach New High in CDC Data\nChallenging the One-Hour Sepsis Bundle\n2001 /viewarticle/888040 Journal Article\nJournal Article Deaths Involving Fentanyl, Fentanyl Analogs, and U-47700 — 10 States, July–December 2016\nNews Largest Animal Study of Cell Phone Radiation and Cancer Risk\nJournal Article Newly Emerging Drugs of Abuse and Their Detection Methods\nNews Cancer Fears Over Cell Phones, Again, but FDA Disagrees"