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SYMPTOMATIC PLANT INGESTION

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) This management includes general information regarding an approach to handling ingestions of plant material of unknown toxicity or identity.

Specific Substances

    A) TOXIC PLANT CONSTITUENTS
    1) ESSENTIAL OILS
    2) ALKALOIDS
    a) QUINOLIZIDINE ALKALOIDS
    b) INDOLE ALKALOIDS
    c) ISOQUINOLINE ALKALOIDS
    d) PYRIDINE/PIPERIDINE ALKALOIDS
    e) STEROIDAL ALKALOIDS
    f) TERPENOID ALKALOIDS
    g) TROPANE ALKALOIDS
    3) AMINO ACIDS
    4) CYANOGENIC GLYCOSIDES
    5) CARDIOACTIVE GLYCOSIDES
    6) FURANOCOUMARINS
    7) PLANT ACIDS
    8) POLY-ACETYLENE COMPOUNDS
    9) PROTEINS AND PEPTIDES
    10) SAPONINS
    11) TERPENES
    a) MONOTERPINES
    b) SESQUITERPINES
    c) DITERPINES
    d) DITERPINES
    e) TRITERPINES

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) GENERAL INFORMATION: This document is used for plants about which there is little or no information about the effects of human exposure. It may also be used if the plant that has been ingested cannot be identified.
    B) EPIDEMIOLOGY: Ingestion of plant material is common, especially among young children, but severe toxicity is unusual. Inadvertent ingestions of intact plant parts rarely cause more than mild toxicity. More severe toxicity is generally associated with deliberate ingestion (eg, for medicinal or recreational use), long-term use (eg, as part of an herbal preparation), or using processes that concentrate the toxic alkaloids (eg, brewing teas, making decoctions).
    C) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Nausea, vomiting, diarrhea, and oral irritation are common.
    2) SEVERE TOXICITY: Some common toxidromes associated with plant ingestions include:
    a) CARDIAC GLYCOSIDES: Local irritation and emesis are common early signs. Conduction defects, atrial and ventricular dysrhythmias, and complete heart block may occur.
    b) CYANOGENIC GLYCOSIDES: Cyanogenic glycosides release hydrocyanic acid upon ingestion. Effects include vomiting, ataxia, dyspnea, muscular weakness, coma, and seizures. Cyanhemoglobin is diagnostic.
    c) ANTICHOLINERGIC: Common effects include hyperthermia, flushing, dry mucous membranes, mydriasis, tachycardia, decreased gastrointestinal motility, urinary retention, delirium, hallucinations, and mental status depression.
    d) GASTROINTESTINAL IRRITANTS: Many plants are gastrointestinal irritants. Symptoms may be abrupt in onset or delayed and may include irritation of the oral or gastrointestinal mucosa, nausea, vomiting, or diarrhea.
    e) NICOTINE-LIKE TOXICITY: Nausea, vomiting, salivation, and abdominal cramps are early symptoms. These are followed by headache, confusion, tachycardia, mydriasis, fever, and ataxia. Early CNS stimulation, including seizures, may be followed by CNS depression resulting in respiratory failure.

Laboratory Monitoring

    A) Monitor vital signs and mental status.
    B) Attempt to identify the plant in question; a nursery, botanist or poison center may be helpful.
    C) Patients with minor irritant symptoms after small exposures generally do not require laboratory evaluation.
    D) Monitor serum electrolytes, renal function, and hepatic enzymes in patients with significant symptoms.
    E) Institute continuous cardiac monitoring and obtain serial ECGs if ingestion of cardiac glycoside-containing plants is suspected.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) SUPPORT
    1) Care is symptomatic and supportive.
    B) DECONTAMINATION
    1) PREHOSPITAL: Because toxic effects of these plants are unknown; prehospital GI decontamination is generally not recommended.
    2) HOSPITAL: Most plant alkaloids are well adsorbed by activated charcoal. Consider activated charcoal for recent, large ingestions of a plant with the potential for significant toxicity if the patient is alert, not vomiting and can protect the airway. Gastric lavage is generally not warranted and is not useful for removing plant pieces. Whole bowel irrigation may be useful after extremely large ingestions.
    C) HYPOTENSION
    1) Administer intravenous fluids; add vasopressors if hypotension persists.
    D) VENTRICULAR DYSRHYTHMIAS
    1) Institute continuous cardiac monitoring, obtain an ECG, and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders. Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Amiodarone should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require immediate cardioversion. Consider using digoxin antibodies for suspected cardiac glycoside poisoning with significant dysrhythmias. Optimal dose is not known, but an initial dose of 10 vials is suggested for patients with severe dysrhythmias.
    E) COMA
    1) Aggressively treat and evaluate coma regardless of suspected cause. Intubate and ventilate as needed. Comatose patients should receive oxygen, naloxone, thiamine (adults), and either D50 or rapid bedside determination of glucose concentration. Check core temperature to evaluate for hypo- or hyperthermia. Consider evaluation for CNS lesion or infection with CT and lumbar puncture.
    F) SEIZURES
    1) Treat with benzodiazepines; add propofol or barbiturates if seizures persist.
    G) GASTROENTERITIS
    1) Severe gastroenteritis may require full electrolyte monitoring and replacement.
    H) HALLUCINATIONS
    1) May require sedation with benzodiazepines.
    I) OTHER
    1) Perform serial examinations to determine whether the patient is improving or deteriorating.
    J) PITFALLS
    1) Exploratory plant ingestions by children rarely cause significant toxicity, do not overtreat. Herbal and plant preparations may contain unidentified medications or toxins such as heavy metals that contribute to toxicity.
    K) PATIENT DISPOSITION
    1) HOME CRITERIA: Patients with only mild irritant symptoms after inadvertent ingestion can probably be observed at home.
    2) OBSERVATION CRITERIA: Symptomatic patients, or those with large or deliberate ingestions, use over a long period of time or use in a form that concentrates the plant alkaloids (teas, decoctions) should be referred to healthcare facility for evaluation and observation for 6 hours.
    3) ADMISSION CRITERIA: Patients with persistent signs or symptoms or laboratory abnormalities should be admitted.
    4) CONSULT CRITERIA: A botanist, nursery or poison center may be useful to help identify an unknown plant. Consult a poison center or medical toxicologist for patients with significant toxicity or in whom the diagnosis is unclear.

Range Of Toxicity

    A) TOXICITY: Toxicity is extremely variable in the plant world. Serious symptoms may result with as few as 1 or 2 beans or seeds of some plants, whereas large amounts of other plants must be ingested for symptoms to develop. Inadvertent ingestions of intact plant parts rarely cause more than mild toxicity. More severe toxicity is generally associated with deliberate ingestion (eg, for medicinal or recreational use), long term use (eg, as part of an herbal preparation), or using processes that concentrate the toxic alkaloids (eg, brewing teas, making decoctions).

Clinical Effects

Summary Of Exposure

    A) GENERAL INFORMATION: This document is used for plants about which there is little or no information about the effects of human exposure. It may also be used if the plant that has been ingested cannot be identified.
    B) EPIDEMIOLOGY: Ingestion of plant material is common, especially among young children, but severe toxicity is unusual. Inadvertent ingestions of intact plant parts rarely cause more than mild toxicity. More severe toxicity is generally associated with deliberate ingestion (eg, for medicinal or recreational use), long-term use (eg, as part of an herbal preparation), or using processes that concentrate the toxic alkaloids (eg, brewing teas, making decoctions).
    C) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Nausea, vomiting, diarrhea, and oral irritation are common.
    2) SEVERE TOXICITY: Some common toxidromes associated with plant ingestions include:
    a) CARDIAC GLYCOSIDES: Local irritation and emesis are common early signs. Conduction defects, atrial and ventricular dysrhythmias, and complete heart block may occur.
    b) CYANOGENIC GLYCOSIDES: Cyanogenic glycosides release hydrocyanic acid upon ingestion. Effects include vomiting, ataxia, dyspnea, muscular weakness, coma, and seizures. Cyanhemoglobin is diagnostic.
    c) ANTICHOLINERGIC: Common effects include hyperthermia, flushing, dry mucous membranes, mydriasis, tachycardia, decreased gastrointestinal motility, urinary retention, delirium, hallucinations, and mental status depression.
    d) GASTROINTESTINAL IRRITANTS: Many plants are gastrointestinal irritants. Symptoms may be abrupt in onset or delayed and may include irritation of the oral or gastrointestinal mucosa, nausea, vomiting, or diarrhea.
    e) NICOTINE-LIKE TOXICITY: Nausea, vomiting, salivation, and abdominal cramps are early symptoms. These are followed by headache, confusion, tachycardia, mydriasis, fever, and ataxia. Early CNS stimulation, including seizures, may be followed by CNS depression resulting in respiratory failure.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Ocular exposure to the juice from Ecballium elaterium (squirting cucumber a plant endemic to the Mediterranean basin and used for its cathartic, analgesic, and anti-inflammatory properties) has caused eye pain, tearing, conjunctival injection, yellowish discharge, and in one patient corneal edema and erosion (Raikhlin-Eisenkraft & Bentur, 2000).
    3.4.6) THROAT
    A) IRRITATION: Buccal and respiratory irritation accompanied by a sore throat, drooling, dysphagia, edema, and dyspnea occurred in 4 patients within minutes of intranasal or oral administration of the undiluted juice of Ecballium elaterium, a plant endemic to the Mediterranean basin and used for its cathartic, analgesic, and anti-inflammatory properties. All patients recovered following treatment with antihistamines, corticosteroids, beta2-agonists, and oxygen. Biochemical analysis of the plant revealed mixtures of alkaloids containing triterpenes and elaterins (Raikhlin-Eisenkraft & Bentur, 2000).

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) BRADYCARDIA
    1) WITH POISONING/EXPOSURE
    a) CARDIOACTIVE GLYCOSIDES: A marked bradycardia with varying first-, second-, and third-degree heart block may occur with these glycosides (Driggers et al, 1989). Ventricular dysrhythmias and asystole may also occur (Pearn, 1987).
    B) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) CARDIOACTIVE GLYCOSIDES: Hypotension may result from the bradycardia or dysrhythmias (Haynes et al, 1985).
    C) ATRIAL FIBRILLATION
    1) WITH POISONING/EXPOSURE
    a) CARDIOACTIVE GLYCOSIDES: With nonspecific sinus tachycardia segment changes and intraventricular conduction, delays were seen more than 12 hours after ingestion of an oleander tea (Driggers et al, 1989).
    D) ELECTROCARDIOGRAM ABNORMAL
    1) WITH POISONING/EXPOSURE
    a) CARDIOACTIVE GLYCOSIDES: Decreased QRS-T interval, T-wave flattening or inversion, and an increased PR interval have been noted (Driggers et al, 1989).
    E) TACHYARRHYTHMIA
    1) WITH POISONING/EXPOSURE
    a) HYPERTENSION may occur, inconsistently (Rosen & Lechner, 1962).
    b) SINUS TACHYCARDIA is a common anticholinergic finding, particularly in children and young adults (Belton & Gibbons, 1979; O'Grady et al, 1983).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Dyspnea of varying degrees of severity was reported in 4 patients within minutes of receiving the undiluted juice of Ecballium elaterium, an herb used for its cathartic, analgesic, and anti-inflammatory properties. All patients recovered following supportive treatment. Biochemical analysis of the plant revealed mixtures of alkaloids containing triterpenes and elaterins (Raikhlin-Eisenkraft & Bentur, 2000).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM DEFICIT
    1) WITH POISONING/EXPOSURE
    a) CNS depression may occur in various forms with differing onset, severity, and duration. Some of the different types of CNS depression, as caused by different types of plants, are listed below. Some of these have more specific managements that should be consulted for additional information.
    b) SUDDEN ONSET: Unconsciousness of sudden onset can be produced by all parts, including the nectar, of certain species of rhododendron, monkshood (genus Aconitum), hellebore or corn lily (genus Veratrum), and death camas (genus Zigadenus).
    c) DEPRESSION WITH DELIRIUM: Depression of consciousness, often mixed with delirium, mania, or hallucinations, may be produced by plants containing the belladonna alkaloids, such as jimson weed (Datura stramonium), belladonna (Atropa belladonna), henbane (Hyoscyamus niger), and chalice vine (Solandra guttata).
    d) DELAYED DEPRESSION: Unconsciousness is a late, and usually ominous, sign in poisoning by ackee (Blighia sapida); nicotine-, anabasine-, or cytisine-containing plants, such as cultivated and native tobacco plants (genus Nicotiana); or cytisine- (or similar quinolizidine alkaloid-) containing plants, such as golden chain (Laburnum anagyroides) and perhaps large quantities of mescal bean (Sophora secundiflora) or golden banner (genus Thermopsis). Ingestion of the unripe fruit of the lantana (Lantana camara) may cause delayed CNS depression.
    B) CENTRAL STIMULANT ADVERSE REACTION
    1) WITH POISONING/EXPOSURE
    a) SEIZURES following the ingestion of certain plants may occur within 5 minutes to 1 to 2 hours (Robson, 1965; Ball et al, 1987). Seizures are often recurrent (Carlton et al, 1979).
    b) HALLUCINATIONS and amnesia may occur. During the convalescent period, patients may complain of nightmares and anxiety.
    1) Patients suffering from hallucinations following the ingestion of a plant may also demonstrate anticholinergic, cholinergic, nicotinic, or other findings, so the treatment may be specific. Plants may also produce hallucinations because of unknown agents. Treatment should be conservative and supportive.
    c) PARESTHESIA was reported after ingestion of the root of Oenanthe crocata (Ball et al, 1987).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) GASTROINTESTINAL IRRITATION
    1) WITH POISONING/EXPOSURE
    a) Plants that cause gastrointestinal irritation may be grouped into four general categories based on symptomatology.
    b) Irritation, chiefly of the mouth and produced immediately after the plants are chewed, results from exposure to plants containing insoluble calcium oxalate (eg, genera Dieffenbachia, Philodendron).
    B) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Emesis with minimal diarrhea following ingestion results from exposure to plants containing a toxic principle that has only a limited and direct action on the gastric mucosa. It may also act on the emetic zone of the CNS. These symptoms may be produced by the bulbs of the daffodil, jonquil, and narcissus or the seeds and flowers of wisteria.
    C) GASTRITIS
    1) WITH POISONING/EXPOSURE
    a) Irritation of the intestinal mucosa producing rapid onset of emesis, abdominal pain, and diarrhea results from exposure to such plants as pokeweed, holly, baneberry, and others.
    D) GASTROENTERITIS
    1) WITH POISONING/EXPOSURE
    a) Delayed gastroenteritis, occurring 1 hour to 2 days following exposure, results from absorption of the toxins from potato sprouts, Jerusalem cherry, horsenettle, crocus, castor bean, and rosary pea.

Hepatic

    3.9.2) CLINICAL EFFECTS
    A) TOXIC LIVER DISEASE
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 15-year-old girl had taken an herbal product purchased over the internet containing gotu kola developed acute liver failure about 6 weeks later. She had been on lymecycline the previous 8 weeks. Her symptoms included a short history of abdominal pain and vomiting. Her initial laboratory studies included a bilirubin of 31 mol/L (range: 5 to 21); ALT 319 International Units/L (less than 45); GGT 39 International Units/L (less than 25) and albumin 35 g/L (34 to 48). Prothrombin time was 31 s (9 to 14) and an INR of 2.7. The patient was treated with N-acetylcysteine (100 mg/kg/24 hr) as a continuous infusion for a total of 54 hours. Vitamin K (10 mg once daily) was also given for 4 days. She improved quickly and her liver enzymes and coagulation studies normalized. Serology for viral hepatitis was negative; ultrasound revealed a mild echogenic liver. A temporal association with an herbal product containing gotu kola inducing acute hepatitis and immediate resolution of symptoms was observed in this case (Dantuluri et al, 2011).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) ABNORMAL RENAL FUNCTION
    1) WITH POISONING/EXPOSURE
    a) SOLUBLE OXALATES: Renal damage may be noted following ingestion of plants containing soluble oxalates (Reig et al, 1990; Tallqvist & Vaananen, 1960). Renal damage is uncommon, but careful follow-up is indicated (Farre et al, 1989; Franceschi & Horner, 1980).
    1) Nephritis is more common among people who use plant species within genera Colocasia and Xanthosoma as a food crop (Kasilo, 1990).
    2) Severe renal lesions may produce proteinuria, oliguria, albuminuria, and anuria (Sanz & Reig, 1992).
    3) Renal lesions appear as small hemorrhages, congestion, cellular cloudy swelling, sclerosis and hyaline degeneration of the tubules, and lesions associated with interstitial tubular glomerulonephrosis (Bottarelli, 1968).
    4) HEMATURIA and oxaluria were seen several hours after a 16-year-old boy ingested 3 enormous servings of red currants. Oxalate crystals were seen in the urine. No sequelae occurred (Vicary, 1977).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor vital signs and mental status.
    B) Attempt to identify the plant in question; a nursery, botanist or poison center may be helpful.
    C) Patients with minor irritant symptoms after small exposures generally do not require laboratory evaluation.
    D) Monitor serum electrolytes, renal function, and hepatic enzymes in patients with significant symptoms.
    E) Institute continuous cardiac monitoring and obtain serial ECGs if ingestion of cardiac glycoside-containing plants is suspected.
    4.1.2) SERUM/BLOOD
    A) Because of the wide range of existing poisonous plants and the limitations of standard toxicological screening, it is difficult to investigate deaths associated with possible plant toxin ingestion. In addition, it is difficult to obtain specific signs of poisoning at autopsy. One author proposed that it is crucial to identify plant material at the scene of a suspected poisoning to help with toxicological identifications (Byard et al, 2002).

Methods

    A) Microscopic examination of plant fragments by a botanist or other expert may be of benefit.
    B) CHROMATOGRAPHY
    1) Unless a laboratory is specifically set up to assay plant alkaloids, they are usually unidentifiable, although detectable on many thin layer systems.
    2) Mass spectroscopy coupled with gas chromatography can sometimes identify specific plant chemicals in a laboratory with experience.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with persistent signs or symptoms or laboratory abnormalities should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) Patients with only mild irritant symptoms after inadvertent ingestion can probably be observed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) A botanist, nursery or poison center may be useful to help identify an unknown plant. Consult a poison center or medical toxicologist for patients with significant toxicity or in whom the diagnosis is unclear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Symptomatic patients, or those with large or deliberate ingestions, use over a long period of time or use in a form that concentrates the plant alkaloids (teas, decoctions) should be referred to healthcare facility for evaluation and observation for 6 hours.

Monitoring

    A) Monitor vital signs and mental status.
    B) Attempt to identify the plant in question; a nursery, botanist or poison center may be helpful.
    C) Patients with minor irritant symptoms after small exposures generally do not require laboratory evaluation.
    D) Monitor serum electrolytes, renal function, and hepatic enzymes in patients with significant symptoms.
    E) Institute continuous cardiac monitoring and obtain serial ECGs if ingestion of cardiac glycoside-containing plants is suspected.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Because toxic effects of these plants are unknown; prehospital GI decontamination is generally not recommended.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) HOSPITAL: Most plant alkaloids are well adsorbed by activated charcoal. Consider activated charcoal for recent, large ingestions of a plant with the potential for significant toxicity if the patient is alert, not vomiting and can protect the airway. Gastric lavage is generally not warranted and is not useful for removing plant pieces. Whole bowel irrigation may be useful after extremely large ingestions.
    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).
    C) WHOLE BOWEL IRRIGATION
    1) INDICATIONS: Whole bowel irrigation may be useful for ingestions of very large amounts of toxic plants.
    a) WHOLE BOWEL IRRIGATION/INDICATIONS: Whole bowel irrigation with a polyethylene glycol balanced electrolyte solution appears to be a safe means of gastrointestinal decontamination. It is particularly useful when sustained release or enteric coated formulations, substances not adsorbed by activated charcoal, or substances known to form concretions or bezoars are involved in the overdose.
    1) Volunteer studies have shown significant decreases in the bioavailability of ingested drugs after whole bowel irrigation (Tenenbein et al, 1987; Kirshenbaum et al, 1989; Smith et al, 1991). There are no controlled clinical trials evaluating the efficacy of whole bowel irrigation in overdose.
    b) CONTRAINDICATIONS: This procedure should not be used in patients who are currently or are at risk for rapidly becoming obtunded, comatose, or seizing until the airway is secured by endotracheal intubation. Whole bowel irrigation should not be used in patients with bowel obstruction, bowel perforation, megacolon, ileus, uncontrolled vomiting, significant gastrointestinal bleeding, hemodynamic instability or inability to protect the airway (Tenenbein et al, 1987).
    c) ADMINISTRATION: Polyethylene glycol balanced electrolyte solution (e.g. Colyte(R), Golytely(R)) is taken orally or by nasogastric tube. The patient should be seated and/or the head of the bed elevated to at least a 45 degree angle (Tenenbein et al, 1987). Optimum dose not established. ADULT: 2 liters initially followed by 1.5 to 2 liters per hour. CHILDREN 6 to 12 years: 1000 milliliters/hour. CHILDREN 9 months to 6 years: 500 milliliters/hour. Continue until rectal effluent is clear and there is no radiographic evidence of toxin in the gastrointestinal tract.
    d) ADVERSE EFFECTS: Include nausea, vomiting, abdominal cramping, and bloating. Fluid and electrolyte status should be monitored, although severe fluid and electrolyte abnormalities have not been reported, minor electrolyte abnormalities may develop. Prolonged periods of irrigation may produce a mild metabolic acidosis. Patients with compromised airway protection are at risk for aspiration.
    6.5.3) TREATMENT
    A) SUPPORT
    1) Care is symptomatic and supportive; most patients recover uneventfully after plant ingestions.
    B) MONITORING OF PATIENT
    1) Monitor vital signs and mental status.
    2) Attempt to identify the plant in question; a nursery, botanist or poison center may be helpful.
    3) Patients with minor irritant symptoms after small exposures generally do not require laboratory evaluation.
    4) Monitor serum electrolytes, renal function, and hepatic enzymes in patients with significant symptoms.
    5) Institute continuous cardiac monitoring and obtain serial ECGs if ingestion of cardiac glycoside-containing plants is suspected.
    C) COMA
    1) Aggressively treat and evaluate coma regardless of suspected cause. Intubate and ventilate as needed. Comatose patients should receive oxygen, naloxone, thiamine (adults), and either D50 or rapid bedside determination of glucose concentration. Check core temperature to evaluate for hypo- or hyperthermia. Consider evaluation for CNS lesion or infection with CT and lumbar puncture.
    D) 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).
    E) CONDUCTION DISORDER OF THE HEART
    1) VENTRICULAR DYSRHYTHMIAS SUMMARY
    a) Obtain an ECG, institute continuous cardiac monitoring and administer oxygen. Evaluate for hypoxia, acidosis, and electrolyte disorders (particularly hypokalemia, hypocalcemia, and hypomagnesemia). Lidocaine and amiodarone are generally first line agents for stable monomorphic ventricular tachycardia, particularly in patients with underlying impaired cardiac function. Amiodarone should be used with caution if a substance that prolongs the QT interval and/or causes torsades de pointes is involved in the overdose. Unstable rhythms require immediate cardioversion.
    2) Consider using digoxin antibodies for suspected cardiac glycoside poisoning with significant dysrhythmias. Optimal dose is not known, but an initial dose of 10 vials is suggested for patients with severe dysrhythmias.
    3) LIDOCAINE
    a) LIDOCAINE/INDICATIONS
    1) Ventricular tachycardia or ventricular fibrillation (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010; Vanden Hoek et al, 2010).
    b) LIDOCAINE/DOSE
    1) ADULT: 1 to 1.5 milligrams/kilogram via intravenous push. For refractory VT/VF an additional bolus of 0.5 to 0.75 milligram/kilogram can be given at 5 to 10 minute intervals to a maximum dose of 3 milligrams/kilogram (Neumar et al, 2010). Only bolus therapy is recommended during cardiac arrest.
    a) Once circulation has been restored begin a maintenance infusion of 1 to 4 milligrams per minute. If dysrhythmias recur during infusion repeat 0.5 milligram/kilogram bolus and increase the infusion rate incrementally (maximal infusion rate is 4 milligrams/minute) (Neumar et al, 2010).
    2) CHILD: 1 milligram/kilogram initial bolus IV/IO; followed by a continuous infusion of 20 to 50 micrograms/kilogram/minute (de Caen et al, 2015).
    c) LIDOCAINE/MAJOR ADVERSE REACTIONS
    1) Paresthesias; muscle twitching; confusion; slurred speech; seizures; respiratory depression or arrest; bradycardia; coma. May cause significant AV block or worsen pre-existing block. Prophylactic pacemaker may be required in the face of bifascicular, second degree, or third degree heart block (Prod Info Lidocaine HCl intravenous injection solution, 2006; Neumar et al, 2010).
    d) LIDOCAINE/MONITORING PARAMETERS
    1) Monitor ECG continuously; plasma concentrations as indicated (Prod Info Lidocaine HCl intravenous injection solution, 2006).
    4) AMIODARONE
    a) AMIODARONE/INDICATIONS
    1) Effective for the control of hemodynamically stable monomorphic ventricular tachycardia. Also recommended for pulseless ventricular tachycardia or ventricular fibrillation in cardiac arrest unresponsive to CPR, defibrillation and vasopressor therapy (Link et al, 2015; Neumar et al, 2010). It should be used with caution when the ingestion involves agents known to cause QTc prolongation, such as fluoroquinolones, macrolide antibiotics or azoles, and when ECG reveals QT prolongation suspected to be secondary to overdose (Prod Info Cordarone(R) oral tablets, 2015).
    b) AMIODARONE/ADULT DOSE
    1) For ventricular fibrillation or pulseless VT unresponsive to CPR, defibrillation, and a vasopressor therapy give an initial dose of 300 mg IV followed by 1 dose of 150 mg IV. For stable ventricular tachycardias: Infuse 150 milligrams over 10 minutes, and repeat if necessary. Follow by a 1 milligram/minute infusion for 6 hours, then a 0.5 milligram/minute. Maximum total dose over 24 hours is 2.2 grams (Neumar et al, 2010).
    c) AMIODARONE/PEDIATRIC DOSE
    1) Infuse 5 milligrams/kilogram as a bolus for pulseless ventricular tachycardia or ventricular fibrillation; may repeat twice up to 15 mg/kg. Infuse 5 milligrams/kilogram over 20 to 60 minutes for perfusing tachycardias. Maximum single dose is 300 mg. Routine use with other drugs that prolong the QT interval is NOT recommended (Kleinman et al, 2010).
    d) ADVERSE EFFECTS
    1) Hypotension and bradycardia are the most common adverse effects (Neumar et al, 2010).
    F) BRADYCARDIA
    1) ATROPINE/DOSE
    a) ADULT BRADYCARDIA: BOLUS: Give 0.5 milligram IV, repeat every 3 to 5 minutes, if bradycardia persists. Maximum: 3 milligrams (0.04 milligram/kilogram) intravenously is a fully vagolytic dose in most adults. Doses less than 0.5 milligram may cause paradoxical bradycardia in adults (Neumar et al, 2010).
    b) PEDIATRIC DOSE: As premedication for emergency intubation in specific situations (eg, giving succinylchoine to facilitate intubation), give 0.02 milligram/kilogram intravenously or intraosseously (0.04 to 0.06 mg/kg via endotracheal tube followed by several positive pressure breaths) repeat once, if needed (de Caen et al, 2015; Kleinman et al, 2010). MAXIMUM SINGLE DOSE: Children: 0.5 milligram; adolescent: 1 mg.
    1) There is no minimum dose (de Caen et al, 2015).
    2) MAXIMUM TOTAL DOSE: Children: 1 milligram; adolescents: 2 milligrams (Kleinman et al, 2010).
    2) ISOPROTERENOL INDICATIONS
    a) Used for temporary control of hemodynamically significant bradycardia in a patient with a pulse; generally other modalities (atropine, dopamine, epinephrine, dobutamine, pacing) should be used first because of the tendency to develop ischemia and dysrhythmias with isoproterenol (Neumar et al, 2010).
    b) ADULT DOSE: Infuse 2 micrograms per minute, gradually titrating to 10 micrograms per minute as needed to desired response (Neumar et al, 2010).
    c) CAUTION: Decrease infusion rate or discontinue infusion if ventricular dysrhythmias develop(Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    d) PEDIATRIC DOSE: Not well studied. Initial infusion of 0.1 mcg/kg/min titrated as needed, usual range is 0.1 mcg/kg/min to 1 mcg/kg/min (Prod Info Isuprel(TM) intravenous injection, intramuscular injection, subcutaneous injection, intracardiac injection, 2013).
    3) A temporary pacemaker may be required for persistent bradycardia or atrioventricular block.
    G) GASTROENTERITIS
    1) In patients with persistent or severe vomiting or diarrhea, closely monitor fluid status and replace fluids and electrolytes as needed.
    H) SEIZURE
    1) 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).
    2) 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 .
    3) 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).
    4) 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).
    5) 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).
    6) 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).
    I) HALLUCINATIONS
    1) If a sedative is required, benzodiazepines are recommended.

Range Of Toxicity

Summary

    A) TOXICITY: Toxicity is extremely variable in the plant world. Serious symptoms may result with as few as 1 or 2 beans or seeds of some plants, whereas large amounts of other plants must be ingested for symptoms to develop. Inadvertent ingestions of intact plant parts rarely cause more than mild toxicity. More severe toxicity is generally associated with deliberate ingestion (eg, for medicinal or recreational use), long term use (eg, as part of an herbal preparation), or using processes that concentrate the toxic alkaloids (eg, brewing teas, making decoctions).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Patients coming to attention of emergency departments or poison centers may have just ingested a plant and be asymptomatic or may already have become symptomatic.
    2) If the plant is unknown, then a period of observation is suggested to establish whether the patient will become symptomatic.
    3) If the patient is symptomatic, then a clinical evaluation of the symptom complex may lead to the diagnosis of a specific plant group, which may then be handled according to specialized managements for individual plants.
    B) In a review of plant ingestions reported to the AAPCC from 2000 to 2009, severity of symptoms was found to be related to the reason for exposure. In 610,017 cases of unintentional plant ingestion, 23% of patients had no effect, 5.9% had minor effects, 0.6% had moderate effect, 0.04% had major effect, and 0.002% were fatal. Of patients with inadvertent exposures, 66.8% were not followed up because no or minimal toxicity was expected. In comparison, in 23,939 cases where the exposure was deliberate (usually substance abuse), 12.3% had no effect, 17.5% had minor effect, 22.9% had moderate effect, 2.9% had major effect, and 0.1% were fatal. Of these deliberate exposure patients, 32.6% were not followed up because no or minimal toxicity was expected (Krenzelok & Mrvos, 2011).

References

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