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PLANTS-POKEWEED

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) The pokeweed plant is found throughout the United States, Northern America, and Southern Europe. It has been used as a pot herb and in herbal medicine. It is toxic to both animals and humans and the toxin is thought to be due to oxalic acid, saponins and an alkaloid. The root and leaves are poisonous; mature berries are relatively nontoxic.

Specific Substances

    1) American Cancer
    2) American Nightshade
    3) American Spinach
    4) Bear's grape
    5) Bledo
    6) Cancer Root
    7) Cokan
    8) Coakum
    9) Crow Berry
    10) Garget
    11) Ink Berry
    12) Ink weed
    13) Phytolacca americana
    14) Phytolacca decandra
    15) Pigeon Berry
    16) Pocan
    17) Pocon
    18) Poke
    19) Poke Salad Plant
    20) Pokeberry
    21) Pokeroot
    22) Red Ink Plant
    23) Red Weed
    24) Scoke berry
    25) Txiu Kub Nyug (Laotian)
    26) Virginia Poke
    27) POKEWEED - PLANTS

Available Forms Sources

    A) FORMS
    1) TOXICITY: Pokeweed is considered toxic to both animals and humans. The highest concentration of toxic principles is in the roots; leaves and stems have intermediate toxicity, and berries are the least toxic (2:11A). Mature berries are considered to be relatively nontoxic (Nelson et al, 2007).
    2) Ingestion often occurs after eating uncooked leaves in salads and mistaking the pokeweed root for other root vegetables (ie, parsnips or horseradish) (Nelson et al, 2007).
    B) USES
    1) The pokeberry plant has been recommended as a pot herb and poisonings have resulted from eating the leaves, or mistaking the roots for horseradish, parsnip, or Jerusalem artichoke. The leaves, even if boiled, drained and reboiled, a method that reputedly renders the plant nontoxic, appear to have still caused poisonings (Anon, 1991).
    2) Other folk medicine uses include treatment for rheumatism and arthritis, and as an emetic and purgative (Anon, 1991).
    3) The Herb Trade Association has adopted a policy stating that poke ROOT is toxic and should not be sold as an herbal food or beverage, or in any other form that could represent a danger to an uninformed consumer (Anon, 1991).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) DESCRIPTION: Pokeweed is a shrub which grows to 8 feet tall. It has white flowers which develop into juicy, dark, purple berries. It has a large fleshy root system with thick, light purple stems. The pokeweed plant is found throughout the United States, Northern America, and Southern Europe.
    B) USES: It has been used as a pot herb and in herbal medicine.
    C) TOXICOKINETICS: It is toxic to both animals and humans and the toxin is thought to be due to oxalic acid, saponins and an alkaloid. The root is the most toxic component of the plant, but all parts are considered toxic.
    D) EPIDEMIOLOGY: Exposure is uncommon.
    E) WITH POISONING/EXPOSURE
    1) ADVERSE EFFECTS: Patients who ingest the root, leaves, or berries develop primarily a self-limited but severe gastroenteritis and headache. In some cases, intense vomiting, abdominal pain, hemorrhagic gastritis, and foamy diarrhea can be caused by saponins.
    2) ONSET: 0.5 to 5.5 hours.
    3) DURATION: Symptoms last 1 to 48 hours (mean 24 hours).
    4) FATALITY: An adult died within 2 hours of inadvertently ingesting the root.
    5) PHYSICAL FINDINGS: Signs which may aid in the diagnosis include purple stains on the hands and face caused by the berry juice. Lab analysis may reveal plasmacytosis/leukocytosis caused by pokeweed mitogen.
    0.2.4) HEENT
    A) Headache is a common symptom. Blurred vision, excessive salivation, and sore throat have also been seen.
    0.2.5) CARDIOVASCULAR
    A) Tachycardia and hypotension are rare complications that occur due to prolonged nausea, vomiting, and diarrhea.
    B) Ventricular fibrillation was observed in a young man that collapsed within 2 hours of ingesting pokeweed root. Aggressive resuscitation efforts failed.
    0.2.6) RESPIRATORY
    A) Respiratory depression may occur.
    0.2.7) NEUROLOGIC
    A) Weakness and dizziness can occur; seizures and coma may occur in severe cases.
    0.2.8) GASTROINTESTINAL
    A) A self-limited but severe gastroenteritis characterized by a burning sensation in the mouth, intense vomiting, abdominal cramping, hemorrhagic gastritis, and frothy diarrhea may occur.
    0.2.13) HEMATOLOGIC
    A) Mitogenic cell changes have been seen in children after ingestion of berries or exposures to cuts to the juice of berries.

Laboratory Monitoring

    A) No toxic serum concentration for pokeberry, its mitogens, or saponins has been established.
    B) Fluid and electrolytes should be monitored in cases of severe vomiting and diarrhea.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. The leaves and roots of the pokeweed plant are toxic. Nausea and vomiting may be delayed 2 to 3 hours after ingestion and include nausea, vomiting and diarrhea. Monitor fluid status and electrolyte balance as necessary. Administer IV fluids to replace significant gastrointestinal loss. Treat significant diarrhea with antidiarrheals.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Hypotension may occur secondary to fluid and electrolyte loss. Fluid replacement should be initiated before pharmacologic intervention. Severe toxicity is not anticipated. In significant exposures, the central nervous system should be monitored. Historically, there have been rare reports of seizure activity.
    C) DECONTAMINATION
    1) PREHOSPITAL: Gastrointestinal decontamination may not be needed because vomiting may present following ingestion. CNS depression is a rare finding. Activated charcoal is unlikely to be necessary following a minor or "taste" exposure.
    2) HOSPITAL: Consider activated charcoal following a significant recent exposure if the patient is alert and the airway is protected.
    D) AIRWAY MANAGEMENT
    1) Airway management is unlikely to be necessary following minor or taste exposure of the leaves or roots. Assess airway and respiratory effort as indicated, if a patient shows signs of CNS toxicity.
    E) ANTIDOTE
    1) No known antidote.
    F) ENHANCED ELIMINATION
    1) There is no information regarding the benefits of enhanced elimination. It is also unlikely that enhanced elimination would be needed following an exposure to pokeweed.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: A patient with an inadvertent minor exposure, that remains asymptomatic can be managed at home. Symptoms may be delayed several hours following exposure.
    2) OBSERVATION CRITERIA: Patients with a deliberate overdose, and those who are symptomatic, need to be monitored to assess fluid and electrolyte balance. Clinical (gastrointestinal) events may last up to 48 hours. Once the patient is stable and if the patient has only mild gastrointestinal symptoms, the patient may be safely managed at home with adequate outpatient care and follow-up as needed.
    3) ADMISSION CRITERIA: Patients should be admitted for severe vomiting, profuse diarrhea, severe abdominal pain, dehydration, electrolyte abnormalities and if alterations in CNS function are present.
    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.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: A minimum lethal dose has not been established. ROOT: A young adult collapsed and died within 2 hours of inadvertently ingesting a 4 to 5 inch piece of pokeweed root. Initially, epigastric pain and gastrointestinal symptoms were reported within 45 to 90 minutes of exposure. LEAVES/BERRIES: Ingestion of the leaves or berries usually results in self-limited, but severe gastroenteritis and headache. Onset is 0.5 to 5.5 hours. Symptoms usually last 1 to 48 hours (mean 24 hours).

Clinical Effects

Summary Of Exposure

    A) DESCRIPTION: Pokeweed is a shrub which grows to 8 feet tall. It has white flowers which develop into juicy, dark, purple berries. It has a large fleshy root system with thick, light purple stems. The pokeweed plant is found throughout the United States, Northern America, and Southern Europe.
    B) USES: It has been used as a pot herb and in herbal medicine.
    C) TOXICOKINETICS: It is toxic to both animals and humans and the toxin is thought to be due to oxalic acid, saponins and an alkaloid. The root is the most toxic component of the plant, but all parts are considered toxic.
    D) EPIDEMIOLOGY: Exposure is uncommon.
    E) WITH POISONING/EXPOSURE
    1) ADVERSE EFFECTS: Patients who ingest the root, leaves, or berries develop primarily a self-limited but severe gastroenteritis and headache. In some cases, intense vomiting, abdominal pain, hemorrhagic gastritis, and foamy diarrhea can be caused by saponins.
    2) ONSET: 0.5 to 5.5 hours.
    3) DURATION: Symptoms last 1 to 48 hours (mean 24 hours).
    4) FATALITY: An adult died within 2 hours of inadvertently ingesting the root.
    5) PHYSICAL FINDINGS: Signs which may aid in the diagnosis include purple stains on the hands and face caused by the berry juice. Lab analysis may reveal plasmacytosis/leukocytosis caused by pokeweed mitogen.

Heent

    3.4.1) SUMMARY
    A) Headache is a common symptom. Blurred vision, excessive salivation, and sore throat have also been seen.
    3.4.3) EYES
    A) VISUAL DISTURBANCES including blurred vision and transient blindness have been seen (Goldfrank & Kirstein, 1976; Jaeckle & Freemon, 1981).
    B) IRRITATION: The dried root, when powdered, is an eye irritant (Mitchell & Rook, 1979).
    3.4.5) NOSE
    A) SNEEZING: The dried root has been made into a dust and used to produce sneezing (Mitchell & Rook, 1979).
    3.4.6) THROAT
    A) SALIVATION: Excessive salivation, sore throat, and yawning have been reported (Lampe & Fagerstrom, 1968; Jaeckle & Freemon, 1981).
    B) SORE THROAT has been reported (French, 1900).
    C) YAWNING has been reported (French, 1900).

Cardiovascular

    3.5.1) SUMMARY
    A) Tachycardia and hypotension are rare complications that occur due to prolonged nausea, vomiting, and diarrhea.
    B) Ventricular fibrillation was observed in a young man that collapsed within 2 hours of ingesting pokeweed root. Aggressive resuscitation efforts failed.
    3.5.2) CLINICAL EFFECTS
    A) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) Tachycardia was seen in one patient, possibly secondary to prolonged nausea, vomiting, and diarrhea (Lewis & Smith, 1979).
    B) VENTRICULAR FIBRILLATION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT/FATALITY: An 18-year-old man inadvertently ingested a 4 to 5 inch piece of pokeweed root thought to be parsnip. He initially developed epigastric pain and vomiting 45 minutes after exposure, and within 2 hours of ingestion he collapsed at home. He was found in ventricular fibrillation and resuscitation efforts were unsuccessful. The root was identified postmortem (Brooker et al, 2001).
    C) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) Hypotension was seen in several patients, possibly secondary to prolonged nausea, vomiting, and diarrhea (Lewis & Smith, 1979; Roberge et al, 1986). Mild hypotension (74/54) was seen in a 68-year-old after drinking poke leaf tea (Jaeckle & Freemon, 1981).
    D) HEART BLOCK
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 46-year-old man ingested uncooked pokeweed leaves and subsequently developed a type I Mobitz heart block, later followed by first degree heart block (PR interval 224 msec). The patient experienced severe vomiting, diarrhea, and lethargy at this time. The patient gradually recovered following administration of intravenous promethazine and decontamination with activated charcoal. ECG 36 hours after presentation was normal (Hamilton et al, 1995).

Respiratory

    3.6.1) SUMMARY
    A) Respiratory depression may occur.
    3.6.2) CLINICAL EFFECTS
    A) ACUTE RESPIRATORY INSUFFICIENCY
    1) WITH POISONING/EXPOSURE
    a) Respiratory depression as well as difficulty in breathing may occur (2:11A).

Neurologic

    3.7.1) SUMMARY
    A) Weakness and dizziness can occur; seizures and coma may occur in severe cases.
    3.7.2) CLINICAL EFFECTS
    A) MUSCLE WEAKNESS
    1) WITH POISONING/EXPOSURE
    a) Paresthesias, weakness, and dizziness may be seen (French, 1900; 2:11A).
    b) CASE REPORT: A 68-year-old who drank 100 mL of tea became too weak to stand within 15 minutes (Jaeckle & Freemon, 1981).
    B) SEIZURE
    1) WITH POISONING/EXPOSURE
    a) Seizures may occur in severe cases but, is generally more of a tremor than seizures (2:11A; French, 1900). A gross tremor was reported in one patient (Jaeckle & Freemon, 1981). No clear evidence has shown a correlation between pokeweed exposure and seizures.
    C) COMA
    1) WITH POISONING/EXPOSURE
    a) In severe poisonings with large amounts, coma is possible. This plant has been listed by some as a "narcotic plant" used to produce CNS depression, but this CNS depression is not usually present in acute poisonings (Emboden, 1979).
    b) CASE REPORT: A patient who ingested 100 mL of "tea" became unconscious for about 10 to 15 minutes (Jaeckle & Freemon, 1981).
    D) HEADACHE
    1) WITH POISONING/EXPOSURE
    a) Headache has been a commonly reported symptom (2:11A).

Gastrointestinal

    3.8.1) SUMMARY
    A) A self-limited but severe gastroenteritis characterized by a burning sensation in the mouth, intense vomiting, abdominal cramping, hemorrhagic gastritis, and frothy diarrhea may occur.
    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Nausea and vomiting may be delayed up to 2 to 3 hours after exposure; symptoms may last for as long as 48 hours (Nelson et al, 2007).
    b) There have been outbreaks of gastrointestinal illness due to this plant (Callahan, 1981) including nausea, intense vomiting, and stomach cramps. Vomiting may be persistent and bloody (Lewis & Smith, 1979; Hamilton et al, 1995).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Diarrhea may be delayed up to 2 to 3 hours after exposure; symptoms may last for as long as 48 hours (Nelson et al, 2007).
    b) Frothy diarrhea is another commonly seen symptom (2:11A). Diarrhea may be very watery and foamy, and possibly bloody (Lewis & Smith, 1979; Roberge et al, 1986; Hamilton et al, 1995).
    C) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Abdominal cramping may be delayed up to 2 to 3 hours after exposure; symptoms may last for as long as 48 hours (Nelson et al, 2007).
    D) INFLAMMATORY DISEASE OF MUCOUS MEMBRANE
    1) WITH POISONING/EXPOSURE
    a) There may be a bitter and burning sensation in the mouth as well as in the throat (Jaeckle & Freemon, 1981; Kell et al, 1982). Excessive salivation may occur (French, 1900).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) URINARY INCONTINENCE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Urinary incontinence was reported in a 68-year-old man (Jaeckle & Freemon, 1981).

Hematologic

    3.13.1) SUMMARY
    A) Mitogenic cell changes have been seen in children after ingestion of berries or exposures to cuts to the juice of berries.
    3.13.2) CLINICAL EFFECTS
    A) WHITE BLOOD CELL ABNORMALITY
    1) WITH POISONING/EXPOSURE
    a) MITOGENIC CELL CHANGES have been seen in children after ingestion of berries or exposure of cuts to the juice of berries.
    1) Cells morphologically similar to plasmablasts and proplasmacytes were found on peripheral blood smears for up to 2 weeks (Barker et al, 1966; Barker et al, 1967).
    b) CASE REPORT: A patient described by Roberge et al (1986) had a 4-fold increase in her lymphocyte count within one week of ingesting poke.
    c) LYMPHOBLASTOID CELLS are often seen with symptomatic cases. In Virginia plant samples, peak mitogenic activity appeared in the berries in September (Kell et al, 1982).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) EXCESSIVE SWEATING
    1) WITH POISONING/EXPOSURE
    a) Sweating has been reported in a number of cases (Guthrie, 1887; French, 1900).
    B) SKIN IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Both the root and the green plant may produce dermal irritation, a sense of heat, or smarting. An eschar may form (Mitchell & Rook, 1979).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No toxic serum concentration for pokeberry, its mitogens, or saponins has been established.
    B) Fluid and electrolytes should be monitored in cases of severe vomiting and diarrhea.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) No toxic serum concentration for pokeberry, berry mitogens, or saponins have been established. Fluid and electrolytes should be monitored in cases of severe vomiting and diarrhea.

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 should be admitted for severe vomiting, profuse diarrhea, severe abdominal pain, dehydration, electrolyte abnormalities and if alterations in CNS function are present.
    6.3.1.2) HOME CRITERIA/ORAL
    A) A patient with an inadvertent minor exposure, that remains asymptomatic can be managed at home. Symptoms may be delayed several hours following exposure.
    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 a deliberate overdose, and those who are symptomatic, need to be monitored to assess fluid and electrolyte balance. Clinical (gastrointestinal) events may last up to 48 hours (Nelson et al, 2007). Once the patient is stable and the patient has only mild gastrointestinal symptoms, the patient may be safely managed at home with adequate outpatient care and follow-up as needed.

Monitoring

    A) No toxic serum concentration for pokeberry, its mitogens, or saponins has been established.
    B) Fluid and electrolytes should be monitored in cases of severe vomiting and diarrhea.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Gastrointestinal decontamination may not be needed because vomiting may present following ingestion. CNS depression is a rare finding.
    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) Gastrointestinal decontamination may not be needed because vomiting may present following ingestion or CNS depression.
    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) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Aggressive replacement of fluids and/or electrolytes is necessary in patients who have prolonged vomiting and diarrhea (Guthrie, 1887; Jaeckle & Freemon, 1981).
    B) SEIZURE
    1) Historically, seizures only occurred in serious cases, and are not a frequent presentation. At the time of this review, there have been no recent cases of serious toxicity.
    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, 2009; 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).
    C) HYPOTENSIVE EPISODE
    1) Hypotension may occur secondary to fluid and electrolyte loss. Fluid replacement should be initiated before pharmacologic intervention.
    2) 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.
    3) 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).
    4) 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).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DERMAL DECONTAMINATION
    1) The mitogenic agents in pokeberry may be absorbed by abraded skin, so decontamination is important.
    2) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Enhanced Elimination

    A) SUMMARY
    1) There is no information regarding the benefits of enhanced elimination. It is also unlikely that enhanced elimination would be needed following an exposure to pokeweed.

Abstracts

Case Reports

    A) ADULT
    1) A 68-year-old man who was in good health was hospitalized complaining of syncope preceded by sweating, urinary incontinence, confusion, and weakness. Earlier that morning he had a sudden onset of salivation and vomiting, then became unconscious for 10 to 15 minutes. The man drank improperly prepared pokeweed tea 15 minutes before the initial symptoms. About 100 mL of the tea was consumed. The patient fully recovered by the next day (Jaeckle & Freemon, 1981).

Range Of Toxicity

Summary

    A) TOXICITY: A minimum lethal dose has not been established. ROOT: A young adult collapsed and died within 2 hours of inadvertently ingesting a 4 to 5 inch piece of pokeweed root. Initially, epigastric pain and gastrointestinal symptoms were reported within 45 to 90 minutes of exposure. LEAVES/BERRIES: Ingestion of the leaves or berries usually results in self-limited, but severe gastroenteritis and headache. Onset is 0.5 to 5.5 hours. Symptoms usually last 1 to 48 hours (mean 24 hours).

Therapeutic Dose

    7.2.1) ADULT
    A) GENERAL
    1) 60 to 300 milligrams of dried root were used in herbal medication; 1 gram is a recommended emetic dose (JEF Reynolds , 1989).

Minimum Lethal Exposure

    A) SUMMARY: A minimum lethal dose has not been established.
    B) CASE REPORT/FATALITY: An 18-year-old man inadvertently ingested a 4 to 5 inch piece of pokeweed root thought to be parsnip. He initially developed epigastric pain and vomiting 45 minutes after exposure, and within 2 hours of ingestion he collapsed at home. He was found in ventricular fibrillation and resuscitation efforts were unsuccessful. The root was identified postmortem (Brooker et al, 2001).

Maximum Tolerated Exposure

    A) BERRIES
    1) Cooked berries have been used in pies.
    2) Pokeweed berries have often been made into wine.
    3) Ingestion of 10 berries has caused toxicity. Mack (1982) states, without a clinical case, that as few as 10 ripe berries in a preschool aged child may produce toxicity (Mack, 1982).
    B) LEAVES
    1) Properly prepared leaves, shoots, and roots are thought to be harmless, but there have been cases reported with symptoms caused by properly prepared poke. Poke is prepared by boiling, discarding the water, and boiling again (Kunkel & Spoerke, 1984).
    2) CASE REPORT: Ten leaves eaten by a 32-year-old man produced abdominal pain, vomiting, and diarrhea within 2.5 hours of ingestion. The patient was hospitalized for 3 days, but made a very rapid recovery during the first 24 hours. He was treated with charcoal, IV fluids, and prochlorperazine for nausea (Stein, 1979).
    C) ROOTS
    1) The highest concentration of Phytolacca toxin is found in the root (Palmer & Betz, 2006).
    2) One-half teaspoon of pokeroot, made into tea, produced poisoning (Lewis & Smith, 1979).
    3) CASE REPORT: An amount of root estimated as "a thimble-full" produced visual disturbances, extensive vomiting, slight diarrhea, paresthesia, yawning, salivation, and tremors in an adult. Symptom onset was about 1.5 hours after ingestion. The vomiting lasted 12 hours (French, 1900).

Pharmacology Toxicology

Toxicologic Mechanism

    A) GASTROENTERITIS - Active components of pokeweed include phytolacca toxin (and related triterpene saponins) and mitogens. Triterpenoid saponins destroy erythrocytes via lysis, apparently via a reaction between saponin and cholesterol in the cell membrane. Given parenterally, saponins may produce marked visceral vasodilation (Kingsbury, 1974). The triterpene saponins cause a characteristic foamy, or "sudsing", diarrhea and severe vomiting. (Roberge et al, 1986; Hamilton et al, 1995). Hemorrhagic gastritis may also be seen (Palmer & Betz, 2006).
    B) AUTONOMIC EFFECTS - Severe gastroenteritis induced by pokeweed may produce autonomic effects, either vagal or sympathetic. In one case, the intense vomiting and intestinal colic from pokeweed ingestion were presumed to be the cause of a prolonged parasympathetic effect on the heart, resulting in Mobitz type I heart block due to increased vagal tone (Hamilton et al, 1995).

References

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