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PLANTS-STIMULANTS

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) In general, this management discusses plants that may cause CNS stimulation following exposure. When appropriate see individual managements if a specific plant is suspected.

Specific Substances

    A) CONSTITUENTS OF THE GROUP
    1) Cicuta species (Water Hemlock)
    2) Conium species (Poison Hemlock)
    3) Oenanthe species (Hemlock Water Dropwort)
    4) Anamirta cocculus (Fish Berries)
    5) Coriaria species (Coriaria myrtifolia)
    a) Myrtle-leaved coriaria
    b) Currier's sumach
    c) Redoul sumach
    6) Coriaria arborea (or tree tutu)
    7) Calycanthus species (Spice Bush)
    8) Cocculus carolinus (Carolina Moonseed)
    9) STIMULANTS - PLANTS

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: In general, this management discusses plants that may cause CNS stimulation following exposure. When appropriate see individual managements if a specific plant is suspected. CICUTA SPECIES: The most prominent of this group are the water hemlocks (Cicuta species) which should not be confused with poison hemlock (Conium maculatum). Water hemlocks are weeds found along streams, swamps, and wetlands in the US and Canada and flowers from June to September. It can be mistaken for parsnips, turnips, and wild carrots. CORIARIA ARBOREA (Tutu Berry): It is a deciduous shrub found in grasslands and is native to New Zealand. OEANTHE SPECIES: It is found along ditches, streams/rivers, marshes, and meadows in Eurasia, and around Washington DC and Ohio. CORIARIA MYRTIFOLIA (Family Coriariaceae): It is a small shrub or tree which grows to 2 to 3 meters in height. It grows in the woods or along paths and hedges in the southern US and California, and outside the US in western Mediterranean, France, Spain and Morocco. CONIUM MACULATUM: Poison hemlock is an herb, widespread in Europe and the US, and grows along roadsides and fences. It can be confused with parsley, while the root looks like a parsnip or wild carrot. Fruit is present in August and September. The plant has a musty or mousy odor when bruised. The initial symptoms of poison hemlock are CNS stimulation followed by depression including coma (See PLANTS-CONIINE management for further information).
    B) TOXICOLOGY: ANAMIRTA COCCULUS: This plant, which produces fish berries, contains picrotoxin (See PICROTOXIN management for further information). CORIARIA MYRTIFOLIA: The toxin is present in the leaves and berries, which can resemble blackberries, and are present from June to September. CORIARIA ARBOREA: This plant is a picrotoxin-like toxin which can act as an antagonist at GABA A receptors within the CNS. The whole plant is toxic, except for the black or purple petals (also known as "berries"; the seeds are highly toxic). OENANTHE SPECIES: Hemlock water dropwort contains oenanthotoxin which is concentrated in the roots. Poisoning occurs when the roots are ingested after they are mistaken for parsnips (See PLANTS-OENANTHE management for further information).
    C) EPIDEMIOLOGY: CORIARIA MYRTIFOLIA: Ingestion of 5 berries in adults and 2 to 3 berries in children can cause neurologic toxicity. Unintentional ingestions have occurred when eating snails that have been picked off the plant and eating honey made from the nectar of a similar Coriaria species. CORIARIA ARBOREA: Historical cases of exposure reported vomiting, giddiness, delirium, seizures, coma and death. Of those that survived, long-term memory impairment often occurred. CICUTA MACULATA: Exposure has occurred. Historically, the case-fatality rate for poisonings reported from 1900 through 1975 was 30%.
    D) WITH POISONING/EXPOSURE
    1) OVERDOSE: SUMMARY: It is important to identify any stimulant plants, berries, roots or other plant material found near the victim. A specific history can also help to determine the course of events. SEIZURES: Onset of seizures following ingestion of these plants is usually 5 minutes to 1 to 2 hours. Postictal states following seizures may lead to the suspicion that a depressant drug has been ingested. CORIARIA ARBOREA: Historical cases of exposure reported vomiting, giddiness, delirium, seizures, coma and death. Long-term memory impairment can occur. DURATION: Dose-dependent. Symptoms may last 24 hours to 5 days.
    2) SYMPTOMS: Clinical effects that can develop after an ingestion of these plants include: acidosis, hypertension and tachycardia, orthostatic hypotension (may result from significant GI loss), cardiac arrest (infrequent), vomiting, diarrhea, salivation, elevated serum creatinine, acute renal failure (rare), myoglobinuria, rhabdomyolysis (secondary to seizure activity), muscle rigidity, mydriasis, seizures, altered level of consciousness, hallucinations, delirium, drowsiness, apnea and bronchorrhea.
    3) MILD TOXICITY: CICUTA MACULATA: Nausea, abdominal and epigastric pain are likely to develop within 15 to 90 minutes of ingestion.
    4) SEVERE TOXICITY: CICUTA MACULATA (Water Hemlock): Severe intoxication can result in profuse salivation, perspiration, bronchial secretions and respiratory distress that may lead to cyanosis. In fatal cases, severe seizure activity is likely to occur and death usually results from status epilepticus. In fatal cases, severe seizure activity is likely to occur and death usually results from status epilepticus.
    0.2.3) VITAL SIGNS
    A) WITH POISONING/EXPOSURE
    1) HYPOTHERMIA (CORIARIA MYRTIFOLIA): In one study, 4% of 83 (58 children and 25 adults) patients developed hypothermia after ingesting Coriaria myrtifolia berries or leaves (80 patients ingested berries; 3 patients ingested leaves).
    2) TACHYCARDIA (CICUTA SPECIES, OENANTHE SPECIES, CONIUM SPECIES): Tachycardia, including ventricular tachycardia, has been reported after ingestion of stimulant plants.
    3) HYPOTENSION: Hypotension can be seen if the patient has severe vomiting and diarrhea, or serious poisonings.
    0.2.4) HEENT
    A) Mydriasis and excessive salivation can occur. Lacrimation may also develop.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) All patients should be placed on a cardiac monitor and pulse oximetry.
    C) Monitor fluids and electrolytes in patients with prolonged vomiting and/or diarrhea.
    D) Evaluate for metabolic acidosis, elevated CPK, myoglobin in the urine, as well as elevated BUN and creatinine.
    E) Strychnine alkaloids can usually be identified in the urine of affected patients. Identification of other alkaloids is usually more difficult, quantitative evaluation is seldom beneficial.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive; patients may only require observation. Monitor vital signs and mental status. Tachycardia may be observed. Monitor fluid status and electrolytes in patients that develop significant vomiting. Intravenous fluids may be indicated, if the patient develops significant nausea and vomiting. Reassure the patient.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Seizures following the ingestion of these plants may occur within 5 minutes to 1 to 2 hours. Seizures are often recurrent and status epilepticus can develop. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Benzodiazepines (first-line therapy) are indicated to treat seizure activity or control agitation. Provide a supportive environment. Orotracheal intubation is indicated for airway protection in cases of severe agitation, coma or seizure activity.
    C) DECONTAMINATION
    1) PREHOSPITAL: GI decontamination is generally not recommended as spontaneous vomiting can occur. Patients may also be at risk for aspiration secondary to seizure activity.
    2) HOSPITAL: Activated charcoal may be considered upon arrival to the hospital. It is most effective when administered within one hour of ingestion. Activated charcoal should not be administered if the patient is felt to be at risk for the abrupt onset of seizures or depressed mental status (unless the airway is secured) because of the risk of aspiration in the event of spontaneous emesis.
    D) AIRWAY MANAGEMENT
    1) Monitor airway and respiratory function following exposure. Multiple seizures may result in aspiration pneumonitis and severe anoxia with cerebral edema. Supportive care for these patients should include aggressive airway management in patients with seizures or loss of consciousness, which could result in serious injury following a stimulant plant ingestion.
    E) ANTIDOTE
    1) There is no specific antidote.
    F) ENHANCED ELIMINATION
    1) Limited data. Hemodialysis may be useful in the presence of acute renal failure or as indicated by clinical symptoms.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: Adults with mild symptoms following an inadvertent exposure may be monitored at home. Monitoring at home is not indicated in children since a minor exposure (eg, several berries of Coriaria Myrtifolia) has produced neurological symptoms. Early symptoms of exposure usually include nausea and vomiting and can occur within an hour and may be followed by neurologic changes (eg, seizures) within several hours (average 3 to 6 hours). Children should be monitored for up to 8 hours for symptoms. Children that remain asymptomatic may be discharged with clear instructions provided to the parent/family to return if any symptoms develop.
    2) OBSERVATION CRITERIA: Patients with mild or ongoing symptoms may need to be observed for up to 12 hours due to the potential risk for delayed significant symptoms (ie, seizures) that has been reported in a limited number of patients exposed to the Coriaria species.
    3) ADMISSION CRITERIA: Patients with significant persistent central nervous system effects (ie, agitation, seizures), or other persistent clinical symptoms should be admitted. Patients with serious poisonings including CNS stimulation or respiratory events (ie, apnea, bronchorrhea or excessive bronchial secretions) should be admitted to an intensive care setting.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear

Range Of Toxicity

    A) TOXICITY: The amount required to produce toxicity varies by plant species. Strychnine containing plants produce toxicity after ingesting a small amount of plant material, while an ingestion of plants such as evergreens requires a very large ingestion.
    B) FATALITIES: WATER HEMLOCK (Oenanthe species): Fatal ingestions have been reported in the literature. CICUTA DOUGLASSII: A 1 by 1-inch piece of a root was fatal in a 16-year-old. CICUTA MACULATE: A 23-year-old man died after only 3 bites from the root of a Cicuta maculate. CORIARIA MYRTIFOLIA: In one study, 11 of 83 patients died after ingesting Coriaria myrtifolia berries or leaves.
    C) SURVIVAL: CORIARIA MYRTIFOLIA: Ingestion of 5 berries (2 to 3 for children) can cause neurological signs and symptoms. CORIARIA ARBOREA: Of 3 young adults, 2 developed seizures following the ingestion of "hundreds" of berries from the Coriaria arborea plant; all recovered completely. The ingestion of plant roots from Cicuta species (eg, Cicuta Virosa, Cicuta Douglasii) produced seizures, coma, mydriasis, renal failure and acidosis. All patients recovered following supportive care.

Summary Of Exposure

    A) BACKGROUND: In general, this management discusses plants that may cause CNS stimulation following exposure. When appropriate see individual managements if a specific plant is suspected. CICUTA SPECIES: The most prominent of this group are the water hemlocks (Cicuta species) which should not be confused with poison hemlock (Conium maculatum). Water hemlocks are weeds found along streams, swamps, and wetlands in the US and Canada and flowers from June to September. It can be mistaken for parsnips, turnips, and wild carrots. CORIARIA ARBOREA (Tutu Berry): It is a deciduous shrub found in grasslands and is native to New Zealand. OEANTHE SPECIES: It is found along ditches, streams/rivers, marshes, and meadows in Eurasia, and around Washington DC and Ohio. CORIARIA MYRTIFOLIA (Family Coriariaceae): It is a small shrub or tree which grows to 2 to 3 meters in height. It grows in the woods or along paths and hedges in the southern US and California, and outside the US in western Mediterranean, France, Spain and Morocco. CONIUM MACULATUM: Poison hemlock is an herb, widespread in Europe and the US, and grows along roadsides and fences. It can be confused with parsley, while the root looks like a parsnip or wild carrot. Fruit is present in August and September. The plant has a musty or mousy odor when bruised. The initial symptoms of poison hemlock are CNS stimulation followed by depression including coma (See PLANTS-CONIINE management for further information).
    B) TOXICOLOGY: ANAMIRTA COCCULUS: This plant, which produces fish berries, contains picrotoxin (See PICROTOXIN management for further information). CORIARIA MYRTIFOLIA: The toxin is present in the leaves and berries, which can resemble blackberries, and are present from June to September. CORIARIA ARBOREA: This plant is a picrotoxin-like toxin which can act as an antagonist at GABA A receptors within the CNS. The whole plant is toxic, except for the black or purple petals (also known as "berries"; the seeds are highly toxic). OENANTHE SPECIES: Hemlock water dropwort contains oenanthotoxin which is concentrated in the roots. Poisoning occurs when the roots are ingested after they are mistaken for parsnips (See PLANTS-OENANTHE management for further information).
    C) EPIDEMIOLOGY: CORIARIA MYRTIFOLIA: Ingestion of 5 berries in adults and 2 to 3 berries in children can cause neurologic toxicity. Unintentional ingestions have occurred when eating snails that have been picked off the plant and eating honey made from the nectar of a similar Coriaria species. CORIARIA ARBOREA: Historical cases of exposure reported vomiting, giddiness, delirium, seizures, coma and death. Of those that survived, long-term memory impairment often occurred. CICUTA MACULATA: Exposure has occurred. Historically, the case-fatality rate for poisonings reported from 1900 through 1975 was 30%.
    D) WITH POISONING/EXPOSURE
    1) OVERDOSE: SUMMARY: It is important to identify any stimulant plants, berries, roots or other plant material found near the victim. A specific history can also help to determine the course of events. SEIZURES: Onset of seizures following ingestion of these plants is usually 5 minutes to 1 to 2 hours. Postictal states following seizures may lead to the suspicion that a depressant drug has been ingested. CORIARIA ARBOREA: Historical cases of exposure reported vomiting, giddiness, delirium, seizures, coma and death. Long-term memory impairment can occur. DURATION: Dose-dependent. Symptoms may last 24 hours to 5 days.
    2) SYMPTOMS: Clinical effects that can develop after an ingestion of these plants include: acidosis, hypertension and tachycardia, orthostatic hypotension (may result from significant GI loss), cardiac arrest (infrequent), vomiting, diarrhea, salivation, elevated serum creatinine, acute renal failure (rare), myoglobinuria, rhabdomyolysis (secondary to seizure activity), muscle rigidity, mydriasis, seizures, altered level of consciousness, hallucinations, delirium, drowsiness, apnea and bronchorrhea.
    3) MILD TOXICITY: CICUTA MACULATA: Nausea, abdominal and epigastric pain are likely to develop within 15 to 90 minutes of ingestion.
    4) SEVERE TOXICITY: CICUTA MACULATA (Water Hemlock): Severe intoxication can result in profuse salivation, perspiration, bronchial secretions and respiratory distress that may lead to cyanosis. In fatal cases, severe seizure activity is likely to occur and death usually results from status epilepticus. In fatal cases, severe seizure activity is likely to occur and death usually results from status epilepticus.

Vital Signs

    3.3.1) SUMMARY
    A) WITH POISONING/EXPOSURE
    1) HYPOTHERMIA (CORIARIA MYRTIFOLIA): In one study, 4% of 83 (58 children and 25 adults) patients developed hypothermia after ingesting Coriaria myrtifolia berries or leaves (80 patients ingested berries; 3 patients ingested leaves).
    2) TACHYCARDIA (CICUTA SPECIES, OENANTHE SPECIES, CONIUM SPECIES): Tachycardia, including ventricular tachycardia, has been reported after ingestion of stimulant plants.
    3) HYPOTENSION: Hypotension can be seen if the patient has severe vomiting and diarrhea, or serious poisonings.
    3.3.3) TEMPERATURE
    A) WITH POISONING/EXPOSURE
    1) HYPOTHERMIA (CORIARIA MYRTIFOLIA): In one study, 4% of 83 (58 children and 25 adults) patients developed hypothermia after ingesting Coriaria myrtifolia berries or leaves (80 patients ingested berries; 3 patients ingested leaves) (de Haro et al, 2005).
    3.3.4) BLOOD PRESSURE
    A) WITH POISONING/EXPOSURE
    1) HYPOTENSION: Hypotension can be seen if the patient has severe vomiting and diarrhea, or serious poisonings (Downs et al, 2002; Landers et al, 1985).
    3.3.5) PULSE
    A) WITH POISONING/EXPOSURE
    1) TACHYCARDIA (CICUTA SPECIES, OENANTHE SPECIES, CONIUM SPECIES): Tachycardia, including ventricular tachycardia, has been reported after ingestion of stimulant plants (Downs et al, 2002; no authors listed, 1994).

Heent

    3.4.1) SUMMARY
    A) Mydriasis and excessive salivation can occur. Lacrimation may also develop.
    3.4.3) EYES
    A) MYDRIASIS: Dilated pupils may be noted (Ball et al, 1987; Knutsen & Paszkowski, 1984).
    B) CORIARIA MYRTIFOLIA: In one study, 22% of 83 (58 children and 25 adults) patients developed mydriasis after ingesting Coriaria myrtifolia berries or leaves (80 patients ingested berries; 3 patients ingested leaves) (de Haro et al, 2005).
    C) CICUTA MACULATA: Variable dilation and constriction of the pupils has been reported in a patient with an apparent water hemlock poisoning that was lethal (Heath, 2001). Another case report of a 22-year-old man that died presented with dilated pupils (no authors listed, 1994).
    D) OENANTHE CROCATA: In 2 case series with a total of 12 patients, hemlock water dropwort poisoning produced dilated pupils (Downs et al, 2002; O'Mahony et al, 1987).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) HEMLOCK WATER DROPWORT: Tachycardia (eg, cicuta, oenanthe and conium species) may be noted (Downs et al, 2002; no authors listed, 1994; Knutsen & Paszkowski, 1984).
    B) HYPERTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypertension may be noted rarely (Knutsen & Paszkowski, 1984).
    C) ORTHOSTATIC HYPOTENSION
    1) WITH POISONING/EXPOSURE
    a) HEMLOCK WATER DROPWORT: Orthostatic hypotension may occur, secondary to fluid loss (ie, emesis and/or diarrhea) (Downs et al, 2002; Applefeld & Caplan, 1979; Landers et al, 1985; Mutter, 1976).
    D) CARDIAC ARREST
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Abrupt cardiac arrest may develop, sometimes within minutes after ingestion (Heath, 2001).
    b) CICUTA SPECIES: From 1985 to 1994 only 19 plant-related fatalities were reported in the AAPCC TESS database; 5 of these involved the ingestion of water hemlock (Cicuta) (Krenzelok et al, 1996).
    1) WATER HEMLOCK: A 22-year-old man suffered a cardiopulmonary arrest after ingesting water hemlock and experiencing 6 seizures (Landers et al, 1985). Death also occurred in a 23-year-old man after he mistakenly ingested water hemlock instead of wild ginseng. He developed ventricular fibrillation; resuscitation efforts were unsuccessful (no authors listed, 1994).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) WITH POISONING/EXPOSURE
    a) CORIARIA MYRTIFOLIA: In one study, 7% of 83 (58 children and 25 adults) patients developed apnea after ingesting Coriaria myrtifolia berries or leaves (80 patients ingested berries; 3 patients ingested leaves) (de Haro et al, 2005).
    B) BRONCHORRHEA
    1) WITH POISONING/EXPOSURE
    a) CICUTA SPECIES: Patients with serious poisonings may develop bronchorrhea or excessive bronchial secretions. Symptoms can progress to include respiratory distress and cyanosis (no authors listed, 1994; Landers et al, 1985).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures following the ingestion of these plants may occur within 5 minutes to 1 to 2 hours (Robson, 1965; Ball et al, 1987; Heath, 2001). Seizures are often recurrent and status epilepticus can develop (Carlton et al, 1979).
    b) CHINESE STAR ANISE (ILLICIUM VERUM): A 3-month-old infant developed an episode of vomiting followed by "twitching" of her extremities and "rolling" eye movement approximately 3 to 4 hours after being given formula containing a tea brewed from star anise (the dried fruit is a spice used in teas) for colic. These symptoms were followed by lethargy. Upon admission the patient appeared gray and ashen with normal vital signs and pulse oximetry (100% on room air). Her skin color and activity level improved with stimulation and oxygen therapy. Laboratory studies, a toxicology screen and a head CT were normal. She was admitted for observation and discharged the following day alert with no sequelae; follow-up at one month was normal (Madden et al, 2012).
    c) CORIARIA MYRTIFOLIA: CASE REPORT: An 8-year-old boy presented with a drunken-like state, vomiting, loss of consciousness, and generalized recurrent seizures after ingesting an unknown quantity of Coriaria myrtifolia berries. Following supportive therapy and treatment with benzodiazepines, he recovered and was discharged the next day (de Haro et al, 2005).
    1) In a study, 31% of 83 (58 children and 25 adults) patients developed seizures after ingesting Coriaria myrtifolia berries or leaves (80 patients ingested berries; 3 patients ingested leaves) (de Haro et al, 2005).
    d) WATER HEMLOCK: A 16-year-old boy mistook water hemlock for wild carrots while spending a night camping in the woods. Within an hour of ingestion, nausea and vomiting developed. He also had diaphoresis and reported a feeling of confusion. A short time later the patient experienced a 1-minute tonic-clonic seizure that was witnessed by his friend. Three hours after exposure, the teen arrived at an Emergency Department after walking with his friend to get medical help. He recovered completely following supportive care and was discharged to home within 48 hours (French & Hendrickson, 2010).
    e) CICUTA VIROSA: A 23-year-old man developed grand mal seizures after ingesting water hemlock and he subsequently died (no authors listed, 1994).
    f) OENANTHE CROCATA: After mistakenly ingesting hemlock water dropwort instead of water parsnips, two young adults had generalized tonic-clonic seizures (Downs et al, 2002). In another case series, 2 of 4 adults having eaten a soup made with hemlock water dropwort suffered seizures (O'Mahony et al, 1987).
    g) CORIARIA ARBOREA: Of 3 young adults, 2 developed seizures following the ingestion of the berries from the C arborea plant. The first patient was a 26-year-old man who had a tonic-clonic seizure 5.5 hours after ingestion. Onset was sudden and unexpected. The patient was treated with diazepam but a second seizure occurred approximately 4 hours later. He was monitored overnight with no further seizure activity. The second patient was a 21-year-old woman who had a self-resolving tonic-clonic seizure approximately 6.5 hours after exposure. She developed anxiety and slight tachycardia prior to the seizure. All 3 adults were monitored overnight, and had normal ECGs; the third patient remained well except for nausea. All 3 were discharged the following day with no further symptoms (Belcher & Morton, 2013).
    B) DROWSINESS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: An 11-year-old boy ingested an unknown amount of the root of Hemlock Water Dropwort mistaking the root for wild carrots and developed confusion, drowsiness, headache, as well as GI symptoms an hour after ingestion. Upon admission, clinical signs and symptoms included myosis and ophthalmoplegia along with laboratory evidence of moderate rhabdomyolysis (creatinine kinase 464 International Units/L). Following supportive care, symptoms resolved completely (Durand et al, 2008).
    C) DISTURBANCE OF CONSCIOUSNESS
    1) WITH POISONING/EXPOSURE
    a) WATER HEMLOCK: A 16-year-old boy mistook water hemlock for wild carrots while spending a night camping in the woods. Within an hour of ingestion, nausea and vomiting developed. He also had diaphoresis and reported a feeling of confusion. A short time later the patient experienced a 1-minute tonic-clonic seizure that was witnessed by his friend. Three hours after exposure, the teen arrived at an Emergency Department after walking with his friend to get medical help. He recovered completely following supportive care and was discharged to home within 48 hours (French & Hendrickson, 2010).
    D) HALLUCINATIONS
    1) WITH POISONING/EXPOSURE
    a) Hallucinations and amnesia may occur. During the convalescent period, patients may complain of nightmares and anxiety.
    E) PARESTHESIA
    1) WITH POISONING/EXPOSURE
    a) Paresthesias were reported after ingestion of the root of Oenanthe crocata (Ball et al, 1987).
    F) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) CORIARIA MYRTIFOLIA: In one study, 83 cases (58 children and 25 adults) of Coriaria myrtifolia poisoning (80 cases of berries ingestion; 3 cases of leaves) were identified. The interval between ingestion and onset of manifestations were obtained in 27 symptomatic cases; the mean delay was 150 minutes (range, 10 to 360 minutes). The following neurological symptoms were reported (de Haro et al, 2005):
    SYMPTOMS% (N=83)
    Drowsiness14%
    Hyperreflexia13%
    Malaise and lypothimia11%
    Coma10%
    Disorientation10%
    Severe headache6%
    Dizziness4%
    Agitation4%

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) EXCESSIVE SALIVATION
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Salivation may occur with Cicuta, Oenanthe, and Conium poisoning.
    b) CICUTA MACULATA (Water Hemlock): A severe intoxication can result in profuse salivation, perspiration, bronchial secretions and respiratory distress that may lead to cyanosis (no authors listed, 1994).
    B) VOMITING
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Vomiting and abdominal pain may occur (de Haro et al, 2005; Ball et al, 1987; Carlton et al, 1979). Vomiting is an early symptom of exposure (no authors listed, 1994).
    b) CICUTA MACULATA: Mild symptoms of Cicuta maculata exposure can include abdominal pain, nausea, and epigastric pain within 15 to 90 minutes (no authors listed, 1994).
    c) CORIARIA MYRTIFOLIA: In one study, 63% of 83 (58 children and 25 adults) patients developed digestive signs (eg; abdominal pain, vomiting) after ingesting Coriaria myrtifolia berries or leaves (80 patients ingested berries; 3 patients ingested leaves) (de Haro et al, 2005).
    d) WATER HEMLOCK: A 16-year-old boy mistook water hemlock for wild carrots while spending a night camping in the woods. Within an hour of ingestion, nausea and vomiting developed. He also had diaphoresis and reported a feeling of confusion. A short time later the patient experienced a 1-minute tonic-clonic seizure that was witnessed by his friend. Three hours after exposure, the teen arrived at an Emergency Department after walking with his friend to get medical help. He recovered completely following supportive care and was discharged to home within 48 hours (French & Hendrickson, 2010).
    e) OENANTHE CROCATA: In 8 patients, nausea and vomiting developed after eating a curry made with the roots of hemlock water dropwort (Downs et al, 2002).
    f) OEANTHE CROCATA: An 11-year-old boy ingested an unknown amount of the root of Hemlock Water Dropwort mistaking the root for wild carrots and developed confusion, drowsiness, headache, as well as abdominal pain, vomiting and diarrhea an hour after ingestion. Upon admission, clinical signs and symptoms included myosis and ophthalmoplegia along with laboratory evidence of moderate rhabdomyolysis. Following supportive care, all symptoms resolved completely (Durand et al, 2008).
    g) CICUTA MACULATA: Six patients experienced nausea and vomiting after eating water hemlock mistaken as wild parsnips during a rafting trip (Landers et al, 1985).
    h) CORIARIA ARBOREA: Two hours after ingestion of Coriaria arborea berries, 3 young adults developed nausea. Two reported moderate nausea and one had mild symptoms (Belcher & Morton, 2013).
    C) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Diarrhea may occur following ingestion.
    b) OEANTHE CROCATA: An 11-year-old boy ingested an unknown amount of the root of Hemlock Water Dropwort mistaking the root for wild carrots and he developed confusion, drowsiness, headache, as well as abdominal pain, vomiting and diarrhea an hour after ingestion. Upon admission, clinical signs and symptoms included myosis, ophthalmoplegia along with laboratory evidence of moderate rhabdomyolysis. Following supportive care, all symptoms resolved completely (Durand et al, 2008).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ACUTE RENAL FAILURE SYNDROME
    1) WITH POISONING/EXPOSURE
    a) CICUTA MACULATA: Acute oliguric renal failure secondary to rhabdomyolysis was reported in a 26-year-old man who ingested a thumb-sized piece of a Cicuta root (Carlton et al, 1979).
    b) WATER HEMLOCK: Elevated serum creatinine was reported in a 14-year-old who developed seizures and cardiac arrest after ingesting presumed water hemlock. The patient developed multi-organ system failure (ie. acute lung injury, hypotension, and DIC) and died 20 hours after ingestion (Heath, 2001).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ACIDOSIS
    1) OENANTHE CORCATA: Metabolic acidosis was seen in 2 patients who ingested Oenanthe crocata roots (Ball et al, 1987).
    2) CICUTA: It also developed in patients with multiple seizures after Cicuta ingestion (Heath, 2001; Knutsen & Paszkowski, 1984).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) SWEATING
    1) WITH POISONING/EXPOSURE
    a) CICUTA MACULATA (Water Hemlock): A severe intoxication can result in profuse salivation, perspiration, bronchial secretions and respiratory distress that may lead to cyanosis (no authors listed, 1994).

Musculoskeletal

    3.15.2) CLINICAL EFFECTS
    A) INCREASED MUSCLE TONE
    1) WITH POISONING/EXPOSURE
    a) Muscular rigidity may be noted. Fasciculations and increased muscle tone may be seen with ingestion of Conium species due to its nicotinic effects.
    b) CORIARIA MYRTIFOLIA: In one study, 12% of 83 (58 children and 25 adults) patients developed hypertonia and muscle cramping after ingesting Coriaria myrtifolia berries or leaves (80 patients ingested berries; 3 patients ingested leaves) (de Haro et al, 2005).
    B) RHABDOMYOLYSIS
    1) WITH POISONING/EXPOSURE
    a) Rhabdomyolysis has been reported (Carlton et al, 1979).
    b) OEANTHE CROCATA: An 11-year-old boy ingested an unknown amount of the root of Hemlock Water Dropwort mistaking the root for wild carrots and developed confusion, drowsiness, headache, as well as abdominal pain, vomiting and diarrhea an hour after ingestion. Upon admission, clinical signs and symptoms included myosis and ophthalmoplegia along with laboratory evidence of moderate rhabdomyolysis (creatinine kinase 464 International Units/L). Following supportive care, all symptoms resolved completely (Durand et al, 2008)

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) All patients should be placed on a cardiac monitor and pulse oximetry.
    C) Monitor fluids and electrolytes in patients with prolonged vomiting and/or diarrhea.
    D) Evaluate for metabolic acidosis, elevated CPK, myoglobin in the urine, as well as elevated BUN and creatinine.
    E) Strychnine alkaloids can usually be identified in the urine of affected patients. Identification of other alkaloids is usually more difficult, quantitative evaluation is seldom beneficial.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Blood levels for each plant toxin is not useful. However, it is beneficial to evaluate electrolyte status after multiple episodes of vomiting and diarrhea and to evaluate for elevated creatine kinase and urinalysis for myoglobin after prolonged or multiple seizures (to evaluate for rhabdomyolysis, and renal insufficiency or failure).
    2) Monitor liver enzymes as indicated. Elevated aspartate transaminase (AST), creatine kinase, and lactate dehydrogenase were reported for 10 days after seizures caused by Oenanthe crocata exposure (Ball et al, 1987)
    3) Elevated CPK has also been observed in cases of Cicuta ingestion (Carlton et al, 1979).

Methods

    A) MULTIPLE ANALYTICAL METHODS
    1) Oenanthotoxin may be identified by HPLC or absorption spectroscopy but is difficult to find in the serum of poisoned patients (Ball et al, 1987).

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 significant persistent central nervous system effects (ie, agitation, seizures), or other persistent clinical symptoms should be admitted. Patients with serious poisonings including CNS stimulation or respiratory events (ie, apnea, bronchorrhea or excessive bronchial secretions) should be admitted to an intensive care setting.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Adults with mild symptoms following an inadvertent exposure may be monitored at home. Monitoring at home is not indicated in children since a minor exposure (eg, several berries of Coriaria Myrtifolia) has produced neurological symptoms. Early symptoms of exposure usually include nausea and vomiting and can occur within an hour and may be followed by neurologic changes (eg, seizures) within several hours (average 3 to 6 hours). Children should be monitored for up to 8 hours for symptoms. Children that remain asymptomatic may be discharged with clear instructions provided to the parent/family to return if any symptoms develop.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with mild or ongoing symptoms may need to be observed for up to 12 hours due to the potential risk for delayed significant symptoms (ie, seizures) that has been reported in a limited number of patients exposed to the Coriaria species.
    B) CORIARIA ARBOREA (Tutu Berry): Of three cases of tutu berry exposure in young adults, 2 developed tonic-clonic seizures 5.5 and 6.5 hours, respectively after exposure. Based on the late onset of symptoms or only mild symptoms, the observation period should be 12 hours or longer in patients that are admitted with mild symptoms (Belcher & Morton, 2013).

Monitoring

    A) Monitor vital signs and mental status.
    B) All patients should be placed on a cardiac monitor and pulse oximetry.
    C) Monitor fluids and electrolytes in patients with prolonged vomiting and/or diarrhea.
    D) Evaluate for metabolic acidosis, elevated CPK, myoglobin in the urine, as well as elevated BUN and creatinine.
    E) Strychnine alkaloids can usually be identified in the urine of affected patients. Identification of other alkaloids is usually more difficult, quantitative evaluation is seldom beneficial.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Induced emesis is NOT recommended. Spontaneous emesis may occur.
    B) ACTIVATED CHARCOAL
    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) 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) EMESIS/NOT RECOMMENDED
    1) Induced emesis is NOT recommended. Plants in this group are likely to produce seizures. Seizures can occur rapidly, within 30 to 60 minutes after ingestion (Heath, 2001; Litovitz et al, 1986; Litovitz et al, 1988; Knutsen & Paszkowski, 1984) or may delayed up to several hours after exposure (Belcher & Morton, 2013).
    B) ACTIVATED CHARCOAL
    1) Activated charcoal may be considered upon arrival to the hospital. It is most effective when administered within one hour of ingestion. Activated charcoal should not be administered if the patient is felt to be at risk for the abrupt onset of seizures or depressed mental status (unless the airway is secured) because of the risk of aspiration in the event of spontaneous emesis.
    2) 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.
    3) 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) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive; patients may only require observation. Monitor vital signs and mental status. Tachycardia may be observed. Monitor fluid status and electrolytes in patients that develop significant vomiting. Intravenous fluids may be indicated, if the patient develops significant nausea and vomiting. Reassure the patient.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Seizures following the ingestion of these plants may occur within 5 minutes to 1 to 2 hours. Seizures are often recurrent and status epilepticus can develop. Treat seizures with IV benzodiazepines; barbiturates or propofol may be needed if seizures persist or recur. Benzodiazepines (first-line therapy) are indicated to treat seizure activity or control agitation. Provide a supportive environment. Orotracheal intubation is indicated for airway protection in cases of severe agitation, coma or seizure activity.
    B) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Monitor cardiac function closely. Although infrequently reported (Krenzelok et al, 1996), abrupt cardiac arrest may develop, sometimes within minutes after ingestion (Heath, 2001; no authors listed, 1994; Landers et al, 1985).
    3) Monitor fluid and electrolytes in patients with prolonged vomiting and/or diarrhea.
    4) Monitor liver enzymes and renal function following a significant exposure.
    5) Serum testing is not available in the hospital setting for these plants.
    C) HYPOTENSIVE EPISODE
    1) SUMMARY
    a) Infuse 10 to 20 milliliters/kilogram of isotonic fluid and keep the patient supine. If hypotension persists, administer dopamine or norepinephrine. Consider central venous pressure monitoring to guide further fluid therapy.
    2) DOPAMINE
    a) DOSE: Begin at 5 micrograms per kilogram per minute progressing in 5 micrograms per kilogram per minute increments as needed (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). If hypotension persists, dopamine may need to be discontinued and a more potent vasoconstrictor (eg, norepinephrine) should be considered (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    b) CAUTION: If ventricular dysrhythmias occur, decrease rate of administration (Prod Info dopamine hcl, 5% dextrose IV injection, 2004). Extravasation may cause local tissue necrosis, administration through a central venous catheter is preferred (Prod Info dopamine hcl, 5% dextrose IV injection, 2004).
    3) NOREPINEPHRINE
    a) PREPARATION: 4 milligrams (1 amp) added to 1000 milliliters of diluent provides a concentration of 4 micrograms/milliliter of norepinephrine base. Norepinephrine bitartrate should be mixed in dextrose solutions (dextrose 5% in water, dextrose 5% in saline) since dextrose-containing solutions protect against excessive oxidation and subsequent potency loss. Administration in saline alone is not recommended (Prod Info norepinephrine bitartrate injection, 2005).
    b) DOSE
    1) ADULT: Dose range: 0.1 to 0.5 microgram/kilogram/minute (eg, 70 kg adult 7 to 35 mcg/min); titrate to maintain adequate blood pressure (Peberdy et al, 2010).
    2) CHILD: Dose range: 0.1 to 2 micrograms/kilogram/minute; titrate to maintain adequate blood pressure (Kleinman et al, 2010).
    3) CAUTION: Extravasation may cause local tissue ischemia, administration by central venous catheter is advised (Peberdy et al, 2010).
    D) SEIZURE
    1) Seizures following the ingestion of these plants may occur within 5 minutes to 1 to 2 hours (Robson, 1965; Ball et al, 1987; Heath, 2001). Seizures are often recurrent and status epilepticus can develop (Carlton et al, 1979).
    2) SUMMARY
    a) Attempt initial control with a benzodiazepine (eg, diazepam, lorazepam). If seizures persist or recur, administer phenobarbital or propofol.
    b) Monitor for respiratory depression, hypotension, and dysrhythmias. Endotracheal intubation should be performed in patients with persistent seizures.
    c) Evaluate for hypoxia, electrolyte disturbances, and hypoglycemia (or, if immediate bedside glucose testing is not available, treat with intravenous dextrose).
    3) DIAZEPAM
    a) ADULT DOSE: Initially 5 to 10 mg IV, OR 0.15 mg/kg IV up to 10 mg per dose up to a rate of 5 mg/minute; may be repeated every 5 to 20 minutes as needed (Brophy et al, 2012; Prod Info diazepam IM, IV injection, 2008; Manno, 2003).
    b) PEDIATRIC DOSE: 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).
    c) Monitor for hypotension, respiratory depression, and the need for endotracheal intubation. Consider a second agent if seizures persist or recur after repeated doses of diazepam .
    4) NO INTRAVENOUS ACCESS
    a) DIAZEPAM may be given rectally or intramuscularly (Manno, 2003). RECTAL DOSE: CHILD: Greater than 12 years: 0.2 mg/kg; 6 to 11 years: 0.3 mg/kg; 2 to 5 years: 0.5 mg/kg (Brophy et al, 2012).
    b) MIDAZOLAM has been used intramuscularly and intranasally, particularly in children when intravenous access has not been established. ADULT DOSE: 0.2 mg/kg IM, up to a maximum dose of 10 mg (Brophy et al, 2012). PEDIATRIC DOSE: INTRAMUSCULAR: 0.2 mg/kg IM, up to a maximum dose of 7 mg (Chamberlain et al, 1997) OR 10 mg IM (weight greater than 40 kg); 5 mg IM (weight 13 to 40 kg); INTRANASAL: 0.2 to 0.5 mg/kg up to a maximum of 10 mg/dose (Loddenkemper & Goodkin, 2011; Brophy et al, 2012). BUCCAL midazolam, 10 mg, has been used in adolescents and older children (5-years-old or more) to control seizures when intravenous access was not established (Scott et al, 1999).
    5) LORAZEPAM
    a) MAXIMUM RATE: The rate of intravenous administration of lorazepam should not exceed 2 mg/min (Brophy et al, 2012; Prod Info lorazepam IM, IV injection, 2008).
    b) ADULT DOSE: 2 to 4 mg IV initially; repeat every 5 to 10 minutes as needed, if seizures persist (Manno, 2003; Brophy et al, 2012).
    c) PEDIATRIC DOSE: 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, if seizures continue (Brophy et al, 2012; Loddenkemper & Goodkin, 2011; Hegenbarth & American Academy of Pediatrics Committee on Drugs, 2008; Sreenath et al, 2010; Chin et al, 2008).
    6) PHENOBARBITAL
    a) ADULT LOADING DOSE: 20 mg/kg IV at an infusion rate of 50 to 100 mg/minute IV. An additional 5 to 10 mg/kg dose may be given 10 minutes after loading infusion if seizures persist or recur (Brophy et al, 2012).
    b) Patients receiving high doses will require endotracheal intubation and may require vasopressor support (Brophy et al, 2012).
    c) PEDIATRIC LOADING DOSE: 20 mg/kg may be given as single or divided application (2 mg/kg/minute in children weighing less than 40 kg up to 100 mg/min in children weighing greater than 40 kg). A plasma concentration of about 20 mg/L will be achieved by this dose (Loddenkemper & Goodkin, 2011).
    d) REPEAT PEDIATRIC DOSE: Repeat doses of 5 to 20 mg/kg may be given every 15 to 20 minutes if seizures persist, with cardiorespiratory monitoring (Loddenkemper & Goodkin, 2011).
    e) MONITOR: For hypotension, respiratory depression, and the need for endotracheal intubation (Loddenkemper & Goodkin, 2011; Manno, 2003).
    f) SERUM CONCENTRATION MONITORING: Monitor serum concentrations over the next 12 to 24 hours. Therapeutic serum concentrations of phenobarbital range from 10 to 40 mcg/mL, although the optimal plasma concentration for some individuals may vary outside this range (Hvidberg & Dam, 1976; Choonara & Rane, 1990; AMA Department of Drugs, 1992).
    7) OTHER AGENTS
    a) If seizures persist after phenobarbital, propofol or pentobarbital infusion, or neuromuscular paralysis with general anesthesia (isoflurane) and continuous EEG monitoring should be considered (Manno, 2003). Other anticonvulsants can be considered (eg, valproate sodium, levetiracetam, lacosamide, topiramate) if seizures persist or recur; however, there is very little data regarding their use in toxin induced seizures, controlled trials are not available to define the optimal dosage ranges for these agents in status epilepticus (Brophy et al, 2012):
    1) VALPROATE SODIUM: ADULT DOSE: An initial dose of 20 to 40 mg/kg IV, at a rate of 3 to 6 mg/kg/minute; may give an additional dose of 20 mg/kg 10 minutes after loading infusion. PEDIATRIC DOSE: 1.5 to 3 mg/kg/minute (Brophy et al, 2012).
    2) LEVETIRACETAM: ADULT DOSE: 1000 to 3000 mg IV, at a rate of 2 to 5 mg/kg/min IV. PEDIATRIC DOSE: 20 to 60 mg/kg IV (Brophy et al, 2012; Loddenkemper & Goodkin, 2011).
    3) LACOSAMIDE: ADULT DOSE: 200 to 400 mg IV; 200 mg IV over 15 minutes (Brophy et al, 2012). PEDIATRIC DOSE: In one study, median starting doses of 1.3 mg/kg/day and maintenance doses of 4.7 mg/kg/day were used in children 8 years and older (Loddenkemper & Goodkin, 2011).
    4) TOPIRAMATE: ADULT DOSE: 200 to 400 mg nasogastric/orally OR 300 to 1600 mg/day orally divided in 2 to 4 times daily (Brophy et al, 2012).

Enhanced Elimination

    A) HEMODIALYSIS
    1) Limited data. Hemodialysis may be useful in the presence of acute renal failure or as indicated by clinical symptoms.
    2) CASE REPORT: Hemodialysis for 2 hours, followed by charcoal hemoperfusion for 2 hours, was performed in a 30-year-old man who ingested Cicuta virosa. The patient regained consciousness one hour after the start of this therapy. The amount of cicutoxin removed was not calculated (Knutsen & Paszkowski, 1984).

Case Reports

    A) ADULT
    1) CICUTA SPECIES
    a) CICUTA MACULATA: A man in his twenties was reported to develop seizures one hour after ingestion of Cicuta maculata. He became comatose, and was tachycardic, with labored breathing. Anticonvulsants were not available, and he died one hour after seizures began (Litovitz et al, 1986).
    b) CICUTA DOUGLASII: A 16-year-old boy ingested a 1 inch by 1 inch piece of a Cicuta douglasii root. After 45 minutes, he became diaphoretic, faint, frothed at the mouth, seized, and had a cardiac arrest. He was pronounced dead within 2 hours of ingestion (Litovitz et al, 1988).
    c) CICUTA ROOT: A 26-year-old man ingested a thumb-sized piece of a root of Cicuta (species unknown) and vomited within 15 minutes, followed by coma and seizures. Diazepam controlled the seizures, and he remained obtunded for 24 to 48 hours. Acute renal failure, rhabdomyolysis, and myoglobinuria ensued (CPK greater than 10,000). He recovered with supportive care and hemodialysis (Carlton et al, 1979).
    d) CICUTA MACULATA: A 23-year-old man ingested 3 bites from the root of a Cicuta maculate plant. Within 30 minutes he developed vomiting and seizures. He had tachycardia, mydriasis, salivation, and seizures. In the emergency department, he developed ventricular fibrillation and was unable to be resuscitated (no authors listed, 1994).
    e) CICUTA DOUGLASII: A 27-year-old man ingested Cicuta douglasii and developed multiple generalized tonic-clonic seizures within 45 minutes of the ingestion. He was lethargic upon arrival to the hospital and had a creatinine of 1.8 mg/dL and a urinalysis had 2+ blood. On hospital day 2, and EEG was obtained and was consistent with a toxic-metabolic process. His lethargy improved and upon discharge from the hospital, he had amnesia of the seizure period and sometimes had difficulty finding words (Landers et al, 1985).
    2) HEMLOCK WATER DROPWORT
    a) CASE REPORTS: Eight adults developed nausea, vomiting, sweating, and lethargy after ingesting a curry made of hemlock water dropwort. Two of the eight had grand mal seizures. One of the seizure patients also had visual hallucinations and tachycardia in the emergency department. With symptomatic and supportive care all 8 patients recovered with no long term effects (Downs et al, 2002).
    b) CASE REPORTS: Four adults presented to the emergency department with nausea and diaphoresis as well as mydriasis after ingesting a soup mistakenly made from hemlock water dropwort. All four recovered with supportive care. None of these four patients developed seizures (O'Mahony et al, 1987).
    3) OENANTHE CROCATA
    a) A 26-year-old man ingested the roots of O. crocata and within 40 minutes developed nausea, abdominal pain, increased respiratory rate, and seizures. Upon admission, bradycardia and acidosis were observed. The patient was treated for seizure control and acidosis and given respiratory support. After 30 hours of treatment with anticonvulsants, no further seizures were seen, although EEG tracings showed bilateral slow wave abnormalities. No neurological sequelae were seen, but elevated creatine kinase, lactate dehydrogenase, and aspartate transaminase were seen for 10 days (Ball et al, 1987).

Summary

    A) TOXICITY: The amount required to produce toxicity varies by plant species. Strychnine containing plants produce toxicity after ingesting a small amount of plant material, while an ingestion of plants such as evergreens requires a very large ingestion.
    B) FATALITIES: WATER HEMLOCK (Oenanthe species): Fatal ingestions have been reported in the literature. CICUTA DOUGLASSII: A 1 by 1-inch piece of a root was fatal in a 16-year-old. CICUTA MACULATE: A 23-year-old man died after only 3 bites from the root of a Cicuta maculate. CORIARIA MYRTIFOLIA: In one study, 11 of 83 patients died after ingesting Coriaria myrtifolia berries or leaves.
    C) SURVIVAL: CORIARIA MYRTIFOLIA: Ingestion of 5 berries (2 to 3 for children) can cause neurological signs and symptoms. CORIARIA ARBOREA: Of 3 young adults, 2 developed seizures following the ingestion of "hundreds" of berries from the Coriaria arborea plant; all recovered completely. The ingestion of plant roots from Cicuta species (eg, Cicuta Virosa, Cicuta Douglasii) produced seizures, coma, mydriasis, renal failure and acidosis. All patients recovered following supportive care.

Minimum Lethal Exposure

    A) CASE REPORTS
    1) CICUTA DOUGLASII: Death occurred in a 16-year-old who ingested a 1-inch piece of Cicuta douglasii root (Litovitz et al, 1988), and in an 8-year-old who ate a small piece of this root (Withers et al, 1969).
    2) WATER HEMLOCK: Fatal ingestions are reported in the US from water hemlock every few years (Landers et al, 1985).
    3) CICUTA MACULATE: A 23-year-old man died after only 3 bites from the root of a Cicuta maculate (no authors listed, 1994).
    4) CORIARIA MYRTIFOLIA: In one study, 11 of 83 patients (58 children and 25 adults) died after ingesting Coriaria myrtifolia berries or leaves (80 patients ingested berries; 3 patients ingested leaves) (de Haro et al, 2005).

Maximum Tolerated Exposure

    A) CASE REPORTS
    1) ADULT
    a) CICUTA VIROSA: Ingestion of a whole root of Cicuta virosa resulted in seizures, coma, mydriasis, and acidosis, with survival in a 30-year-old man (Knutsen & Paszkowski, 1984).
    b) CICUTA ROOT: Ingestion of a thumb-sized piece of a root of Cicuta by an adult resulted in multiple seizures, complicated by renal failure with eventual recovery (Carlton et al, 1979).
    c) CICUTA DOUGLASII: Ingestion of 5 roots of Cicuta douglasii by a 13-year-old boy resulted in coma, vomiting, seizures, and periods of apnea. He was promptly brought to a hospital and treated with diazepam. He recovered fully (Mutter, 1976).
    d) CORIARIA MYRTIFOLIA: Five berries (2 to 3 for children) can cause neurological signs and symptoms (de Haro et al, 2005).
    e) CORIARIA ARBOREA: Of 3 young adults, 2 developed seizures following the ingestion of "hundreds" of berries from the Coriaria arborea plant. The first patient was a 26-year-old man who had a tonic-clonic seizure 5.5 hours after ingestion. Onset was sudden and unexpected. The patient was treated with diazepam but a second seizure occurred approximately 4 hours later. He was monitored overnight with no further seizure activity. The second patient was a 21-year-old woman who had a self-resolving tonic-clonic seizure approximately 6.5 hours after exposure. She developed anxiety and slight tachycardia prior to the seizure. All 3 adults were monitored overnight, and had normal ECGs; the third patient remained well except for nausea. All 3 were discharged the following day with no further symptoms (Belcher & Morton, 2013).
    2) PEDIATRIC
    a) CICUTA ROOT: Ingestion of a small piece of a Cicuta root by an 11-year-old girl resulted in vomiting and seizures, followed by complete recovery (Rork, 1969).

Toxicologic Mechanism

    A) CALYCANTHIDINE and related alkaloids are constitutents of the spice bush (Calycanthus species). These toxins resemble strychnine.
    B) CICUTOXIN is an unsaturated aliphatic alcohol polyacetylene compound found in water hemlock. It is thought to be either a GABA receptor antagonist or a potassium channel blocker (Nelson et al, 2007). It acts rapidly on the central nervous system to produce seizures, most likely by overstimulation of central cholinergic pathways (North & Nelson, 1985).
    C) OENANTHOTOXIN is an unsaturated higher alcohol (C17H22O2) found in Oenanthe species and is the cis-isomer of cicutoxin. Concentration in Oenanthe roots is greatest in the spring and winter.
    1) Pharmacologic effects in animals include tachypnea; hypotension followed by hypertension. Seizures are common.
    2) CONIINE is a nicotine-like alkaloid.
    D) STRYCHNINE is a component of Strychnos nux-vomica, a tree grown in Hawaii.
    E) OTHERS, such as thujone and other essential oils, which are contained in some of the evergreens (Thuia species), may also produce seizure episodes shortly after ingestion of concentrated teas made from the needles (Lampe & Fagerstrom, 1968).

Clinical Effects

    11.1.2) BOVINE/CATTLE
    A) Cattle fatally poisoned by Cicuta species may have evidence of roots in the esophageal groove, with no obvious signs in the rumen (Smith & Lewis, 1987).

General Bibliography

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