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PLANTS-PEYOTE/MESCALINE

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Mescaline (3,4,5 trimethoxyphenylethylamine), a methoxylated amphetamine, is the active ingredient of the peyote cactus (Lophophora Williamsii). At least 8 other alkaloids have been identified. Lophophora Williamsii (the peyote cactus) contains over 60 alkaloids including pellotine and tyramine derivatives.
    B) Mescaline is similar in structure and activity to the hallucinogenic amphetamines and similar in activity to LSD (lysergic acid diethylamide), psilocybin/psilocin, and the hallucinogenic indoles. Cross-tolerance occurs between all hallucinogens, especially between LSD, mescaline, and psilocybin.

Specific Substances

    1) Mescaline (3,4,5 trimethoxyphenylethylamine)
    2) Lophophora Williamsii (the peyote cactus)
    3) Trichocercus pachanoi
    4) Trichocercus tersscheckii
    5) PLANTS-MESCALINE
    6) PLANTS-PEYOTE

Available Forms Sources

    A) FORMS
    1) Mescaline is available from illicit sources in both natural (peyote) and synthetic forms.
    2) Peyote is available as whole dried cactus tops ("buttons"), chopped buttons, ground powder, capsules, or a brownish-gray liquid extract. The green or brown bitter-tasting buttons may be blended with liquids, boiled to make tea, or eaten whole.
    3) Synthetic mescaline is available as a white or brown crystalline powder or as tablets or capsules. Peyote contains 1% to 6% mescaline; each button contains an average of 45 mg of mescaline (Koupilova et al, 1986), and 6 to 12 buttons is the usual hallucinogenic dose. Synthetic mescaline is sold in 200 to 500 mg doses. A variety of chemical procedures are available for producing mescaline and are discussed by Nieforth (1971).
    4) The pill form of mescaline, which must be taken in milligram quantities, is aspirin-sized or larger, or a large capsule.
    5) Mescaline substitutes: Tiny, brightly colored "microdots" are sold as mescaline but actually contain small amounts of LSD (Schwartz, 1988).
    B) SOURCES
    1) Medical personnel should be skeptical in diagnosing mescaline exposures from patient history because two studies done in Canada and the East coast revealed that none of the samples contained mescaline. LSD, PCP, amphetamines, ASA, STP and strychnine were assayed in these samples. Of 563 samples submitted to an anonymous laboratory over a 10-year period, 76% contained adulterants or no active drugs. The most frequent adulterants were LSD and PCP (Messinger, 1984). "Street" buys are probably not mescaline or peyote unless the cactus button is intact.
    C) USES
    1) Mescaline is an FDA schedule I controlled substance (high potential for abuse and no currently accepted medical use in the US).
    2) Some Native Americans ingest peyote in their religious ceremonies (Halpern, 2004).

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Mescaline is a hallucinogen found in peyote (lophophora williamsii). Peyote is a spineless cactus found in northern Mexico and the southwestern United States. In the United States, the legal use of Peyote is restricted to members of the Native American Church. It is used by some members of the Native American Church for religious ceremonies and as a treatment for various physical and psychological ailments. Peyote/mescaline is also abused as a hallucinogen.
    B) TOXICOLOGY: Mescaline is naturally occurring exogenous phenylethylamine. Endogenous phenylethylamines include dopamine, norepinephrine, and tyrosine. Due to this structural similarity, mescaline can be expected to produce CNS stimulation and sympathomimetic effects. Exogenous phenylethylamine are also known to produce hallucinations. The degree of hallucinogenicity is largely determined by the presence of a methyl group in the side chain of the phenylethylamine.
    C) EPIDEMIOLOGY: Peyote intoxication is not common, but causes mild to moderate clinical effects frequently requiring medical treatment. Life threatening toxicity is not expected. A review of the California Poison Control System database in 2010, revealed 31 exposures in the previous 12 years. Most (n=30/31) exposures were oral, one was by powder insufflation. Most patients (n=26/31) required management in a healthcare facility. In another study, a survey of Navajo adolescents enrolled in an inpatient substance abuse program revealed that only 1 in 9 participants had used peyote.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Vomiting is very common after ingestion. Tachycardia, mydriasis, agitation and hallucinations are also common. Vomiting generally precedes the hallucinatory effects and resolves within 2 hours. CNS effects can last 6 to 12 hours.
    2) SEVERE TOXICITY: High doses of peyote/mescaline produce more pronounced sympathomimetic effects such as tachycardia and hypertension. Hallucinations may be associated with homicidal, suicidal, or psychotic behavior. There have been no reported deaths due to the physiologic effects of peyote/mescaline. Traumatic death has occurred secondary to hallucination.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) Increased pulse, blood pressure, temperature, and respiratory rate may be noted.
    0.2.4) HEENT
    A) WITH POISONING/EXPOSURE
    1) Mydriasis, salivation, and blurred vision often present.
    0.2.5) CARDIOVASCULAR
    A) WITH POISONING/EXPOSURE
    1) Increases in heart rate and blood pressure may occur. Palpitations may occur.
    0.2.6) RESPIRATORY
    A) WITH POISONING/EXPOSURE
    1) Respiratory rate may be increased.
    0.2.7) NEUROLOGIC
    A) WITH POISONING/EXPOSURE
    1) Headache, dizziness, ataxia, drowsiness, feelings of hot or cold, tremors, weakness, malaise, agitation, hallucinations and paresthesias have been reported.
    0.2.8) GASTROINTESTINAL
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and abdominal cramps frequently precede hallucinatory effects.
    0.2.10) GENITOURINARY
    A) WITH POISONING/EXPOSURE
    1) An antidiuretic effect may be noted.
    0.2.14) DERMATOLOGIC
    A) WITH POISONING/EXPOSURE
    1) Flushing, diaphoresis, and piloerection may occur.
    0.2.15) MUSCULOSKELETAL
    A) WITH POISONING/EXPOSURE
    1) Shivering, tremors, weakness, increased muscle tone, and hyperreflexia have been noted.
    0.2.18) PSYCHIATRIC
    A) WITH POISONING/EXPOSURE
    1) Visual and auditory hallucinations, abnormal sensory perception, and anxiety are common. Suicidal thoughts, emotional instability, fear, anxiety, paranoia, and flashbacks may occur.
    0.2.20) REPRODUCTIVE
    A) It is considered a potential teratogen. Congenital malformations have been noted in fetuses of hamsters treated with mescaline. An increased incidence of fetal deaths and low birth weight has been reported in fetuses of hamsters.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Routine laboratory studies are not indicated; unless otherwise indicated. Monitor CK in patients with prolonged agitation, seizures or coma.
    C) Routine urine toxicology screens do not detect mescaline.
    D) Qualitative analysis of a urine sample is sufficient to confirm the presence of mescaline, but the assay is not widely available. Blood levels have not been correlated with clinical toxicity.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. AGITATION: Treat agitation and/or hallucinations with a benzodiazepine (lorazepam 1 to 2 mg in an adult) or an antipsychotic (haloperidol: 5 to 10 mg in an adult).
    B) MANAGEMENT OF SEVERE TOXICITY
    1) High doses of peyote/mescaline can produce more pronounced sympathomimetic effects such as tachycardia and hypertension. Hallucinations may be associated with homicidal, suicidal, or psychotic behaviors. there have been no reported deaths due to the physiologic effects of peyote/mescaline. Traumatic deaths have occurred secondary to hallucinations.
    C) DECONTAMINATION
    1) PREHOSPITAL: Spontaneous emesis may occur and usually always precedes CNS and sympathetic signs and symptoms. Activated charcoal may be considered in patients that are alert and able to protect their airway.
    2) HOSPITAL: Consider activated charcoal in patients that are alert and able to protect their airway.
    D) ANTIDOTE
    1) There is no specific antidote.
    E) PATIENT DISPOSITION
    1) HOME CRITERIA: An adult with mild symptoms with an ingestion that was not a self-harm attempt can be observed at home as long as a sober responsible adult is present. Referral for substance abuse counseling should be considered.
    2) OBSERVATION CRITERIA: Patients with a self-harm ingestion, and those with more than mild symptoms (eg, intractable vomiting, severe agitation or hallucinations) should be referred to a healthcare facility for treatment. Any child with a peyote ingestion should be referred to a healthcare facility.
    3) ADMISSION CRITERIA: Patients with persistent agitation or hallucinations or vomiting should be admitted.
    4) CONSULT CRITERIA: Consult a medical toxicologist or poison center for patient with severe toxicity or in whom the diagnosis is unclear. Refer for substance abuse counseling as appropriate.
    F) PHARMACOKINETICS
    1) Peyote is rapidly absorbed with peak serum concentrations of mescaline occurring 2 to 4 hours after an oral dose. Symptoms onset is usually 30 minutes to 2 hours postingestion. Symptoms may last 6 to 12 hours. Mescaline is not bound to plasma proteins and has a large volume of distribution. About 60% of a mescaline dose is excreted unchanged in urine, about 40% undergoes hepatic metabolism.

Range Of Toxicity

    A) TOXICITY: 3.75 mg/kg can cause moderate to severe intoxication. Twenty to 60 mg/kg doses caused hypotension, bradycardia, vasodilation, and respiratory depression in experimental animals.

Clinical Effects

Summary Of Exposure

    A) USES: Mescaline is a hallucinogen found in peyote (lophophora williamsii). Peyote is a spineless cactus found in northern Mexico and the southwestern United States. In the United States, the legal use of Peyote is restricted to members of the Native American Church. It is used by some members of the Native American Church for religious ceremonies and as a treatment for various physical and psychological ailments. Peyote/mescaline is also abused as a hallucinogen.
    B) TOXICOLOGY: Mescaline is naturally occurring exogenous phenylethylamine. Endogenous phenylethylamines include dopamine, norepinephrine, and tyrosine. Due to this structural similarity, mescaline can be expected to produce CNS stimulation and sympathomimetic effects. Exogenous phenylethylamine are also known to produce hallucinations. The degree of hallucinogenicity is largely determined by the presence of a methyl group in the side chain of the phenylethylamine.
    C) EPIDEMIOLOGY: Peyote intoxication is not common, but causes mild to moderate clinical effects frequently requiring medical treatment. Life threatening toxicity is not expected. A review of the California Poison Control System database in 2010, revealed 31 exposures in the previous 12 years. Most (n=30/31) exposures were oral, one was by powder insufflation. Most patients (n=26/31) required management in a healthcare facility. In another study, a survey of Navajo adolescents enrolled in an inpatient substance abuse program revealed that only 1 in 9 participants had used peyote.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Vomiting is very common after ingestion. Tachycardia, mydriasis, agitation and hallucinations are also common. Vomiting generally precedes the hallucinatory effects and resolves within 2 hours. CNS effects can last 6 to 12 hours.
    2) SEVERE TOXICITY: High doses of peyote/mescaline produce more pronounced sympathomimetic effects such as tachycardia and hypertension. Hallucinations may be associated with homicidal, suicidal, or psychotic behavior. There have been no reported deaths due to the physiologic effects of peyote/mescaline. Traumatic death has occurred secondary to hallucination.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Increased pulse, blood pressure, temperature, and respiratory rate may be noted.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) PYREXIA: A rise in body temperature of 0.5 to 1.0 degrees Celsius may be noted (Kapadia & Fayez, 1970).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) Mild increases in blood pressure (10 to 20 mmHg), pulse (10 to 20 beats/min), respirations, and temperature (0.5 to 1 degree Celsius) are frequent. A reflex bradycardia may occasionally be noted (Jacobsen, 1963).

Heent

    3.4.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Mydriasis, salivation, and blurred vision often present.
    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) MYDRIASIS and blurred vision are common. Neck cramps have been reported (Kapadia & Fayez, 1970; Hollister & Hartman, 1962).
    a) INCIDENCE: In a retrospective review of the California Poison Control System database from the years 1997 to 2008 for all cases of peyote or mescaline alone exposures, a total of 31 cases were identified. Mydriasis was one of the most common adverse effects reported. Of the 31 cases, 9 (29%) patients developed mydriasis (Carstairs & Cantrell, 2010).
    2) PERMANENT INJURY: No permanent injury or visual alterations result from mescaline (Grant, 1986).

Cardiovascular

    3.5.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Increases in heart rate and blood pressure may occur. Palpitations may occur.
    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Mild increases in heart rate (10 to 20 beats per minute) and in blood pressure (10 to 20 mmHg) are often noted. Palpitations, mild bradycardia, and chest tightness have been reported. Mescaline doses of 1 to 20 mg/kg generally produce the mild tachycardia, while doses of 50 to 240 mg/kg induce bradycardia (Aboul-Enein, 1973).
    b) INCIDENCE: In a retrospective review of the California Poison Control System database from the years 1997 to 2008 for all cases of peyote or mescaline alone exposures, a total of 31 cases were identified. Tachycardia was commonly reported. Of the 31 cases, 16 (52%) patients developed tachycardia. Heart rate ranged from 101 to 190 beats/min (mean 127 bpm, median 120 bpm) in 12 documented cases (Carstairs & Cantrell, 2010).
    3.5.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) VASODILATATION
    a) Animal studies suggest that large doses (greater than 20 mg/kg) of mescaline may cause bradycardia, hypotension, and vasodilation as well as pressor responses. The response is both dose-related and species dependent (Orzechowski & Goldstein, 1973; Kapadia & Fayez, 1970).

Respiratory

    3.6.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Respiratory rate may be increased.
    3.6.2) CLINICAL EFFECTS
    A) HYPERVENTILATION
    1) WITH POISONING/EXPOSURE
    a) The respiratory rate may be increased.
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) RESPIRATORY DEPRESSION
    a) Large doses produce respiratory depression in experimental animals, and respiratory arrest associated with seizures is the terminal event in animals given a lethal overdose (Kapadia & Fayez, 1970).

Neurologic

    3.7.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Headache, dizziness, ataxia, drowsiness, feelings of hot or cold, tremors, weakness, malaise, agitation, hallucinations and paresthesias have been reported.
    3.7.2) CLINICAL EFFECTS
    A) HALLUCINATIONS
    1) WITH POISONING/EXPOSURE
    a) Auditory, gustatory, olfactory, tactile, and visual hallucinations, abnormal perception of space and time, and anxiety are common. Suicidal thoughts, emotional instability, fear, sexual feelings, paranoia, and violent behavior have been reported (Kapadia & Fayez, 1970; Ludwig & Levine, 1965; Jacobsen, 1963; Hollister & Hartman, 1962).
    b) In a volunteer study psychotomimetic effects included thought disorder, delusions, anxiety and depression (Hermle et al, 1992). Psychotomimetic effects were most pronounced 3.5 to 4 hours after mescaline intake and had resolved by 15 hours.
    c) INCIDENCE: In a retrospective review of the California Poison Control System database from the years 1997 to 2008 for all cases of peyote or mescaline alone exposures, a total of 31 cases were identified. Hallucinations were one of the most common adverse effects reported. Of the 31 cases, 18 (58%) patients developed hallucinations (Carstairs & Cantrell, 2010).
    d) FLASHBACKS have occurred (Teitelbaum & Wingeleth, 1977; Kapadia & Fayez, 1970; Jacobsen, 1963; Hollister & Hartman, 1962).
    B) FEELING AGITATED
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a retrospective review of the California Poison Control System database from the years 1997 to 2008 for all cases of peyote or mescaline alone exposures, a total of 31 cases were identified. Agitation was one of the most common adverse effects. Of the 31 cases, 11 (35.5%) patients developed agitation (Carstairs & Cantrell, 2010).
    C) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache, dizziness, ataxia, drowsiness, feelings of hot or cold, tremors, weakness, malaise, and paresthesias have been reported.
    D) COMA
    1) WITH POISONING/EXPOSURE
    a) Coma has been reported following the ingestion of methadone and alcohol with mescaline (Chaikin, 1980).
    E) INSOMNIA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 54-year-old man with a history of alcohol abuse and combat-related posttraumatic stress disorder presented with a 2-week history of sleep deprivation and psychosis with visual and auditory hallucinations. His symptoms began a few hours after drinking peyote juice during a healing ceremony. Following treatment with 50 mg of trazodone, he had 15 hours of uninterrupted sleep, that resulted in complete resolution of his psychotic symptoms (Lu et al, 2004).
    F) CEREBROVASCULAR DISEASE
    1) WITH POISONING/EXPOSURE
    a) In a volunteer study SPECT scanning after mescaline ingestion revealed increased cerebral blood flow and metabolism in the frontal cortical regions, particularly in the right brain (Hermle et al, 1992).
    3.7.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) SEIZURES
    a) Seizures and CNS depression are preterminal events in animals given lethal overdoses of mescaline (Kapadia & Fayez, 1970).
    2) CNS EFFECTS
    a) Rats given mescaline into various parts of the brain showed a decreased ability to successfully negotiate a T-maze (Koupilova et al, 1999).

Gastrointestinal

    3.8.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Nausea, vomiting, and abdominal cramps frequently precede hallucinatory effects.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Nausea and vomiting usually precede the hallucinatory effects. Anorexia, hunger, abdominal cramps, diarrhea, and salivation have also been reported (Teitelbaum & Wingeleth, 1977).
    b) GI symptoms usually resolve within 2 hours (after vomiting) but may persist for several days and be mistaken for gastroenteritis (Teitelbaum & Wingeleth, 1977).

Genitourinary

    3.10.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) An antidiuretic effect may be noted.
    3.10.2) CLINICAL EFFECTS
    A) SUPPRESSED URINE SECRETION
    1) WITH POISONING/EXPOSURE
    a) An antidiuretic effect in man was noted at 5 mg/kg (Hollister, 1970).

Hematologic

    3.13.2) CLINICAL EFFECTS
    A) HEMATOLOGY FINDING
    1) WITH POISONING/EXPOSURE
    a) Total leukocyte and eosinophil counts were decreased 24 hours after mescaline administration (Aboul-Enein, 1973).

Dermatologic

    3.14.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Flushing, diaphoresis, and piloerection may occur.
    3.14.2) CLINICAL EFFECTS
    A) FLUSHING
    1) WITH POISONING/EXPOSURE
    a) Flushing, diaphoresis, and piloerection are common (Teitelbaum & Wingeleth, 1977; Hollister & Hartman, 1962).

Musculoskeletal

    3.15.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) Shivering, tremors, weakness, increased muscle tone, and hyperreflexia have been noted.
    3.15.2) CLINICAL EFFECTS
    A) HYPERREFLEXIA
    1) WITH POISONING/EXPOSURE
    a) Increased muscle tone and hyperreflexia have been noted. Shivering, tremors, and weakness are common (Kapadia & Fayez, 1970; Jacobsen, 1963; Hollister & Hartman, 1962).
    B) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Rhabdomyolysis associated with prolonged coma has been reported following the ingestion of mescaline with methadone and alcohol (Chaikin, 1980).

Reproductive

    3.20.1) SUMMARY
    A) It is considered a potential teratogen. Congenital malformations have been noted in fetuses of hamsters treated with mescaline. An increased incidence of fetal deaths and low birth weight has been reported in fetuses of hamsters.
    3.20.2) TERATOGENICITY
    A) CONGENITAL ANOMALY
    1) HUMAN - Mescaline has been associated with a specific combination of abnormalities when used excessively. It is considered a potential teratogen (Gilmore, 2001).
    2) ANIMAL - Congenital malformations have been noted in fetuses of hamsters treated with mescaline (Geber, 1967). Cytogenetic study of life-long peyote users did not find evidence of increased chromosomal abnormalities (Dorrance et al, 1975).
    3.20.3) EFFECTS IN PREGNANCY
    A) ABORTION
    1) An increased incidence of fetal deaths and low birth weight has been reported in fetuses of hamsters treated with mescaline (Geber, 1967).
    B) PLACENTAL BARRIER
    1) Mescaline readily passes through the placenta of mice; mescaline levels in the placenta 1 hour after dosing were higher than maternal plasma levels. Fetal brain levels were 2 to 4 times higher than maternal brain levels at 15 minutes and 4 hours post-dosing (Shah et al, 1973).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Routine laboratory studies are not indicated; unless otherwise indicated. Monitor CK in patients with prolonged agitation, seizures or coma.
    C) Routine urine toxicology screens do not detect mescaline.
    D) Qualitative analysis of a urine sample is sufficient to confirm the presence of mescaline, but the assay is not widely available. Blood levels have not been correlated with clinical toxicity.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Blood levels of mescaline averaged 14.8 mcg/mL at 15 minutes, 4.9 mcg/mL at 1 hour, and 2.1 mcg/mL at 2 hours following an IV dose of 5 mg/kg in human volunteers (Mokrasch & Stevenson, 1959). Blood mescaline concentrations following a 500-mg oral dose averaged 3.8 mcg/mL at 2 hours and 1.5 micrograms/milliliter at 7 hours following ingestion by human subjects (Charalampous et al, 1966).
    a) These doses and levels were associated with hallucinogenic effects. Because of tolerance, lack of known correlation between blood levels and clinical toxicity, and the non-lethality of mescaline, blood levels are not necessary. The qualitative presence of mescaline is sufficient to confirm the diagnosis.
    2) Monitor creatine phosphokinase (CPK) levels in substantial overdoses for possible rhabdomyolysis, especially if prolonged seizures or coma develop.
    4.1.3) URINE
    A) URINARY LEVELS
    1) The presence of mescaline or its metabolites in urine may be used to confirm the diagnosis, but the assay is not widely available. Quantitative analysis is not of clinical value.
    4.1.4) OTHER
    A) OTHER
    1) MONITORING
    a) Continuous ECG and blood pressure monitoring is advisable following mescaline poisoning.

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Active drug and metabolites in the urine can be detected by thin layer chromatography, gas chromatography, fluorometry and mass spectrometry (Van Peteghem et al, 1980) (Teitelbaum & Wingeleth, 1977; Cohen & Vogel, 1970). Quantitative analysis of plasma or urine requires fluorometry or gas chromatography/mass spectrometry.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with persistent agitation or hallucinations or vomiting should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) An adult with mild symptoms with an ingestion that was not a self-harm attempt can be observed at home as long as a sober responsible adult is present. Referral for substance abuse counseling should be considered.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a medical toxicologist or poison center for patient with severe toxicity or in whom the diagnosis is unclear. Refer for substance abuse counseling as appropriate.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with a self-harm ingestion, and those with more than mild symptoms (eg, intractable vomiting, severe agitation or hallucinations) should be referred to a healthcare facility for treatment. Any child with a peyote ingestion should be referred to a healthcare facility.
    B) Asymptomatic patients may be discharged following a 4 hour period of observation.
    C) Symptomatic patients should be observed until they become asymptomatic. This may require admission to an ICU setting with suicide precautions if emergency department observation is not possible.
    D) Patients with suicidal intentions or psychotic behavior lasting longer than 12 to 24 hours should be transferred to the care of a psychiatrist.

Monitoring

    A) Monitor vital signs and mental status.
    B) Routine laboratory studies are not indicated; unless otherwise indicated. Monitor CK in patients with prolonged agitation, seizures or coma.
    C) Routine urine toxicology screens do not detect mescaline.
    D) Qualitative analysis of a urine sample is sufficient to confirm the presence of mescaline, but the assay is not widely available. Blood levels have not been correlated with clinical toxicity.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Spontaneous emesis may occur and usually always precedes CNS and sympathetic signs and symptoms. Activated charcoal may be considered in patients that are alert and able to protect their airway.
    B) ACTIVATED CHARCOAL
    1) PREHOSPITAL ACTIVATED CHARCOAL ADMINISTRATION
    a) Consider prehospital administration of activated charcoal as an aqueous slurry in patients with a potentially toxic ingestion who are awake and able to protect their airway. Activated charcoal is most effective when administered within one hour of ingestion. Administration in the prehospital setting has the potential to significantly decrease the time from toxin ingestion to activated charcoal administration, although it has not been shown to affect outcome (Alaspaa et al, 2005; Thakore & Murphy, 2002; Spiller & Rogers, 2002).
    1) In patients who are at risk for the abrupt onset of seizures or mental status depression, activated charcoal should not be administered in the prehospital setting, due to the risk of aspiration in the event of spontaneous emesis.
    2) The addition of flavoring agents (cola drinks, chocolate milk, cherry syrup) to activated charcoal improves the palatability for children and may facilitate successful administration (Guenther Skokan et al, 2001; Dagnone et al, 2002).
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Spontaneous emesis may occur and usually always precedes CNS and sympathetic signs and symptoms, gastric lavage is unlikely to be of benefit by the time clinical toxicity becomes evident. Activated charcoal is may be considered.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) Intoxication with peyote is rarely life-threatening. Although animal data indicate that hypotension, bradycardia, vasodilation, respiratory depression, apnea, coma, and seizures may occur following large or lethal doses of mescaline, such toxicity has not been reported in humans.
    2) It is likely that the unpleasant taste of peyote and the frequent occurrence of spontaneous emesis limits the amounts of mescaline ingested and absorbed in human intoxications.
    3) Mild increases in blood pressure, pulse, and temperature do not require specific treatment and generally resolve with treatment of anxiety, agitation, and hallucinations. Benzodiazepines are the drug of choice.
    B) MONITORING OF PATIENT
    1) No specific diagnostic testing is indicated.
    2) Careful consideration must be given to possible coingestants and contaminants. If the cause of altered mental status is unclear, basic metabolic studies and a head CT should be considered.
    3) Reference laboratories can identify mescaline in clinical samples, but they are not useful to guide therapy.
    4) An ECG should be obtained in any patient with tachycardia or chest pain.
    C) PSYCHOMOTOR AGITATION
    1) Sedate patient with benzodiazepines as necessary; large doses may be required.
    2) INDICATION
    a) If patient is severely agitated, sedate with IV benzodiazepines.
    3) DIAZEPAM DOSE
    a) ADULT: 5 to 10 mg IV initially, repeat every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) CHILD: 0.1 to 0.5 mg/kg IV over 2 to 5 minutes; up to a maximum of 10 mg/dose. May repeat dose every 5 to 10 minutes as needed (Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    4) LORAZEPAM DOSE
    a) ADULT: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed (Manno, 2003).
    b) CHILD: 0.05 to 0.1 mg/kg IV over 2 to 5 minutes, up to a maximum of 4 mg/dose; may repeat in 5 to 15 minutes as needed (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008).
    5) Extremely large doses of benzodiazepines may be required in patients with severe intoxication in order to obtain adequate sedation. Titrate dose to clinical response and monitor for hypotension, CNS and respiratory depression, and the need for endotracheal intubation.
    6) MIDAZOLAM: 0.05 to 0.1 mg/kg IV initially with additional doses every 15 to 30 minutes as needed. Cardiac monitoring and observation for hypotension and respiratory depression are necessary.
    7) If agitation is severe or unresponsive to benzodiazepines, administer haloperidol or chlorpromazine. Effects of mescaline appear to involve stimulation of both serotonin (5-hydroxytryptamine) and dopamine receptors in the CNS. In experimental studies, these effects can be blocked by either a serotonin antagonist (methysergide) or a dopamine antagonist (haloperidol) (Trulson et al, 1983).
    a) ADULT: Haloperidol 5 to 10 mg orally, IM, or IV (0.05 to 0.15 mg/kg) or chlorpromazine 25 to 100 mg orally or IM (0.5 mg/kg).
    b) PEDIATRIC: Avoid haloperidol. If 6 months or older, administer chlorpromazine 0.5 mg/kg orally or IM. Cardiac monitoring and observation for hypotension and respiratory depression are necessary when these agents are given IM or IV.
    D) FLASHBACKS
    1) Flashbacks may be exacerbated by phenothiazines. The preferred treatment is a benzodiazepine (Abraham, 1983).
    E) VASOSPASM
    1) ANIMAL DATA: In a dog model of mescaline intoxication, mescaline induced cerebral vasospasm could be blocked by verapamil (1 mcM)(Altura & Altura, 1981).

Abstracts

Case Reports

    A) ACUTE EFFECTS
    1) The clinical course of intoxication following peyote ingestion usually begins with disagreeable autonomic symptoms such as nausea, vomiting, abdominal cramps, diaphoresis, dizziness, headache, and general malaise. Physiological effects are usually maximal at 2 hours following ingestion at which time psychic effects begin to predominate. Psychic symptoms may last 6 to 12 hours (Kapadia & Fayez, 1970; Jacobsen, 1963).

Range Of Toxicity

Summary

    A) TOXICITY: 3.75 mg/kg can cause moderate to severe intoxication. Twenty to 60 mg/kg doses caused hypotension, bradycardia, vasodilation, and respiratory depression in experimental animals.

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) There is no therapeutic use, therefore no therapeutic dose exists. Peyote has been used for religious purposes by North American Indian tribes (Duke, 1985).

Minimum Lethal Exposure

    A) CASE REPORTS
    1) A death due to hallucinogenic effects leading to trauma has been described (Reynolds & Jindrich, 1985).
    2) Death due to Mallory-Weiss esophageal lacerations after vomiting and hemoaspiration has been reported (Nolte & Zumwalt, 1999).

Maximum Tolerated Exposure

    A) A potent mescaline intoxication is approximately 3.75 mg/kg body weight (Halpern, 2004).
    B) CASE SERIES: In a retrospective review of the California Poison Control System database from the years 1997 to 2008 for all cases of peyote or mescaline alone exposures, a total of 31 cases were identified. Of the 31 cases, 26 patients were evaluated in the Emergency Department. Commonly reported adverse events included hallucinations (58%), tachycardia (52%), agitation (35.5%) and mydriasis (29%). Clinical outcome included no clinical effects (n=1); 9 (29%) minor cases; 20 (64.5%) moderate cases and one major case. No deaths occurred. In most cases, symptoms lasted less than 24 hours. A 16-year-old boy was hospitalized for 3 days after boiling an unknown amount of peyote buttons and drinking the tea. He developed tachycardia, hypertension, and agitation. In most cases, treatment was supportive. Only one patient required intubation after being found unconscious several hours after peyote ingestion (Carstairs & Cantrell, 2010).
    C) ANIMAL DATA
    1) Doses of 20 to 60 mg/kg have produced hypotension, bradycardia, vasodilation, and respiratory depression in experimental animals (Kapadia & Fayez, 1970).

Serum Plasma Blood Concentrations

    7.5.2) TOXIC CONCENTRATIONS
    A) TOXIC CONCENTRATION LEVELS
    1) ACUTE
    a) Peak blood levels of 5 to 15 micrograms/milliliter are noted within 2 hours of an hallucinogenic dose of mescaline (Aboul-Enein, 1973). No correlation between the degree or type of response and blood levels or excretion rate has been noted (Kapadia & Fayez, 1970).

Toxicity Information

    7.7.1) TOXICITY VALUES

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Although the precise mechanism of action is unknown, the hallucinogenic and behavioral effects of mescaline appear to involve stimulation of both serotonin (5-hydroxytryptamine) and dopamine receptors in the CNS. In experimental studies, these effects can be blocked by either a serotonin antagonist (methysergide) or a dopamine antagonist (haloperidol) (Trulson et al, 1983). In another study in rats given 10 mg/kg intraperitoneally, serotonin levels increased and 5-hydroxy-indole- 3-acetic acid (5-HIAA) levels decreased. Another study showed increases in 5-HIAA, so the overall effect on 5-HIAA is unclear (Aboul-Enein, 1973).
    B) Mescaline is also known to produce cerebral vasospasm, an effect which can be blocked by verapamil (Altura & Altura, 1981).
    C) The sympathomimetic effects of mescaline are probably also centrally mediated. Peripheral effects may also be due to mescaline-induced changes in catecholamine metabolism and adrenalmedullary function (Hollister & Moore, 1968).
    D) Mescaline does NOT affect monoamine oxidase or aromatic amino acid decarboxylase activities in the brain.
    E) Mescaline, in animals, produced a decrease in nicotinamide adenine dinucleotide (NAD) synthesis in the brain (Aboul-Enein, 1973).
    F) Bradycardia induced by mescaline appears not to be due to simple adrenergic beta-receptor blockage (Morton & Malone, 1969).

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