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PLANTS-GASTROINTESTINAL IRRITANTS

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) This management deals with general issues involved with exposures to gastrointestinal irritant plants.

Specific Substances

    1) Varies
    2) GASTROINTESTINAL, PLANTS

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) Plants which cause gastrointestinal irritation may be grouped into 5 general categories, based on the presenting symptomatology. Before using this management, check the product index to make sure there is not a more specific management.
    1) Immediate irritation, chiefly of the mouth produced after the plants are chewed, may result from exposure to plants containing insoluble calcium oxalate, eg, Dieffenbachia, Philodendron. Please refer to the PLANTS-OXALATES management for further information.
    2) Emesis, with minimal diarrhea, following ingestion may result 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 CNS emetic zone. Examples are the bulbs of the daffodil, jonquil, and narcissus or the Wisteria seeds and flowers.
    3) Irritation of the intestinal mucosa by known chemical irritants may produce rapid onset of emesis, abdominal pain, and diarrhea. Examples are pokeweed, holly, elderberry, and baneberry.
    4) 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. Plants containing these toxins are discussed in separate managements.
    5) A fifth group includes numerous plants that have been shown to produce gastroenteritis, but the causative agent has not yet been identified.

Laboratory Monitoring

    A) Laboratory determination of serum electrolytes or serum enzymes should be performed on all seriously ill patients. It is unlikely that the plant toxins will be identifiable by fluid analysis.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) If significant spontaneous emesis has already occurred as a result of a toxin ingested, decontamination may not be necessary.
    B) ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.
    C) Maintenance of fluid and electrolyte balance is important as the degree of vomiting and diarrhea may lead to dehydration and shock. Use of cathartics is NOT indicated with this ingestion, due to the frequent occurrence of diarrhea.

Range Of Toxicity

    A) The range of toxicity is extremely variable depending upon plant species, plant part, and time of ingestion.

Clinical Effects

Summary Of Exposure

    A) Plants which cause gastrointestinal irritation may be grouped into 5 general categories, based on the presenting symptomatology. Before using this management, check the product index to make sure there is not a more specific management.
    1) Immediate irritation, chiefly of the mouth produced after the plants are chewed, may result from exposure to plants containing insoluble calcium oxalate, eg, Dieffenbachia, Philodendron. Please refer to the PLANTS-OXALATES management for further information.
    2) Emesis, with minimal diarrhea, following ingestion may result 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 CNS emetic zone. Examples are the bulbs of the daffodil, jonquil, and narcissus or the Wisteria seeds and flowers.
    3) Irritation of the intestinal mucosa by known chemical irritants may produce rapid onset of emesis, abdominal pain, and diarrhea. Examples are pokeweed, holly, elderberry, and baneberry.
    4) 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. Plants containing these toxins are discussed in separate managements.
    5) A fifth group includes numerous plants that have been shown to produce gastroenteritis, but the causative agent has not yet been identified.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) HYPOTENSIVE EPISODE
    1) WITH POISONING/EXPOSURE
    a) SUMMARY: Hypotension may develop in patients that develop significant gastrointestinal volume loss (eg, vomiting and/or diarrhea) (Ho et al, 2014; Puri et al, 2011).
    b) LAGENARIA SICERARIA: In an observational study of bitter bottle gourd toxicity in 15 adults, all patients developed symptoms of gastrointestinal toxicity and 8 patients developed hypotension. Of those patients, 6 had persistent hypotension. Inotropic support (dopamine and/or noradrenaline) was required for 2 to 3 days. There were no reports of significant ECG changes suggesting that the hypotension was not cardiac in origin. No permanent sequelae occurred (Puri et al, 2011).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) LAGENARIA SICERARIA (CASE REPORTS): A first generation Chinese American family consisting of older adults, ingested a meal containing bitter bottle gourd that was grown in one of the adults backyard from seeds purchased in a craft store. Everyone observed the bitter taste and within 3 to 25 minutes all 5 individuals developed gastric symptoms including fullness and nausea, followed by abdominal cramping and diarrhea. Two developed vomiting that progressed to hematemesis. All improved with supportive care and IV fluid therapy and were discharged a few hours later. The next day they all returned to the ED, due to persistent watery diarrhea, nausea and dehydration. Of the 5 patients, 4 received 2 to 3 L of IV fluids and were able to tolerate a liquid diet; the remaining patient was severely dehydrated with hypotension and required hospitalization. He ate the largest portion of the dish as to not insult his family member. He required a total of 6 L of IV fluids and potassium supplementation. He was discharged on day 2 and advised to take a 2-week course of omeprazole (Ho et al, 2014).
    b) LAGENARIA SICERARIA: In an observational study of bitter bottle gourd toxicity in 15 adults, all patients developed vomiting and abdominal pain after ingesting bitter bottle gourd (L siceraria) juice used as a traditional medicine in tropical countries. Symptoms developed within 15 minutes to 6 hours after ingestion. Reportedly when the bottle gourd becomes bitter it is considered toxic (Puri et al, 2011).
    c) ELDERBERRY: The usual concern with elderberry is the possible generation of cyanide toxicity, but a more common symptom is nausea and vomiting from ingestion of uncooked berries, leaves, or twigs. Eleven patients developed nausea and vomiting, with 8 of the 11 patients also reporting abdominal cramps, weakness, numbness, and dizziness 15 minutes after ingesting up to 5 glasses of juice pressed from the fruits, leaves, and twigs of Sambucus mexicana (elder tree of the western United States). The mixture was not cooked. Cyanide levels in these patients were normal (Anon, 1984; Anon, 1984a).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) LAGENARIA SICERARIA (CASE REPORTS): A first generation Chinese American family consisting of older adults, ingested a meal containing bitter bottle gourd that was grown in one of the adults backyard from seeds purchased in a craft store. Everyone observed the bitter taste and within 3 to 25 minutes all 5 individuals developed gastric symptoms including fullness and nausea, followed by abdominal cramping and diarrhea. Two developed vomiting that progressed to hematemesis. All improved with supportive care and IV fluid therapy and were discharged a few hours later. The next day they all returned to the ED, due to persistent watery diarrhea, nausea and dehydration. Of the 5 patients, 4 received 2 to 3 L of IV fluids and were able to tolerate a liquid diet; the remaining patient was severely dehydrated with hypotension and required hospitalization. He ate the largest portion of the dish as to not insult his family member. He required a total of 6 L of IV fluids and potassium supplementation. He was discharged on day 2 and advised to take a 2-week course of omeprazole (Ho et al, 2014).
    b) LAGENARIA SICERARIA: In an observational study of bitter bottle gourd toxicity in 15 adults, most patients (n=11) developed diarrhea after ingesting bitter bottle gourd (L siceraria) juice used as a traditional medicine. Symptoms developed within 15 minutes to 6 hours after ingestion. Reportedly when the bottle gourd becomes bitter it is considered toxic (Puri et al, 2011).
    C) HEMATEMESIS
    1) WITH POISONING/EXPOSURE
    a) LAGENARIA SICERARIA (CASE REPORTS): A first generation Chinese American family consisting of older adults, ingested a meal containing bitter bottle gourd that was grown in one of the adults backyard from seeds purchased in a craft store. Everyone observed the bitter taste and within 3 to 25 minutes all 5 individuals developed gastric symptoms including fullness and nausea, followed by abdominal cramping and diarrhea. Two developed vomiting that progressed to hematemesis. All improved with supportive care and IV fluid therapy and were discharged a few hours later. The next day they all returned to the ED, due to persistent watery diarrhea, nausea and dehydration. Of the 5 patients, 4 received 2 to 3 L of IV fluids and were able to tolerate a liquid diet; the remaining patient was severely dehydrated with hypotension and required hospitalization. He ate the largest portion of the dish as to not insult his family member. He required a total of 6 L of IV fluids and potassium supplementation. He was discharged on day 2 and advised to take a 2-week course of omeprazole (Ho et al, 2014).
    b) LAGENARIA SICERARIA: In an observational study of bitter bottle gourd toxicity in 15 adults, most patients (n=12) developed hematemesis after ingesting bitter bottle gourd (L siceraria) juice used as a traditional medicine in tropical countries. All patients underwent an endoscopy and the findings included hyperemic lesions, erosions and ulcerations in the esophagus, stomach and duodenum. Patients required IV fluid support and blood transfusion and patients were discharged with 3 to 5 days. A repeat endoscopic exam was normal after 2 weeks (Puri et al, 2011).
    D) HEMORRHAGIC DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) COLOCYNTH: Five patients developed severe bloody diarrhea after ingesting a wild fruit called Colocynth (also known as "Handal" in Arabic). One patient also inserted a walnut-sized fruit into his rectum. All patients recovered following supportive therapy within 48 hours of exposure (Khan et al, 2003).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Laboratory determination of serum electrolytes or serum enzymes should be performed on all seriously ill patients. It is unlikely that the plant toxins will be identifiable by fluid analysis.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Laboratory determination of serum electrolytes and serum enzymes should be performed in all seriously ill patients. It is unlikely that plant toxins will be identifiable in body fluid analysis.
    2) Since different toxins have different onset times, the patient should be monitored for several hours after an ingestion. Knowing the time from ingestion to symptom onset may aid in diagnosis.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Monitoring

    A) Laboratory determination of serum electrolytes or serum enzymes should be performed on all seriously ill patients. It is unlikely that the plant toxins will be identifiable by fluid analysis.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Spontaneous emesis may occur as a result of the toxin ingested. Decontamination may not be necessary.
    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) If significant spontaneous emesis has already occurred as a result of the toxin ingested, decontamination may not be necessary.
    B) ACTIVATED CHARCOAL
    1) CHARCOAL ADMINISTRATION
    a) Consider administration of activated charcoal after a potentially toxic ingestion (Chyka et al, 2005). Administer charcoal as an aqueous slurry; most effective when administered within one hour of ingestion.
    2) CHARCOAL DOSE
    a) Use a minimum of 240 milliliters of water per 30 grams charcoal (FDA, 1985). Optimum dose not established; usual dose is 25 to 100 grams in adults and adolescents; 25 to 50 grams in children aged 1 to 12 years (or 0.5 to 1 gram/kilogram body weight) ; and 0.5 to 1 gram/kilogram in infants up to 1 year old (Chyka et al, 2005).
    1) Routine use of a cathartic with activated charcoal is NOT recommended as there is no evidence that cathartics reduce drug absorption and cathartics are known to cause adverse effects such as nausea, vomiting, abdominal cramps, electrolyte imbalances and occasionally hypotension (None Listed, 2004).
    b) ADVERSE EFFECTS/CONTRAINDICATIONS
    1) Complications: emesis, aspiration (Chyka et al, 2005). Aspiration may be complicated by acute respiratory failure, ARDS, bronchiolitis obliterans or chronic lung disease (Golej et al, 2001; Graff et al, 2002; Pollack et al, 1981; Harris & Filandrinos, 1993; Elliot et al, 1989; Rau et al, 1988; Golej et al, 2001; Graff et al, 2002). Refer to the ACTIVATED CHARCOAL/TREATMENT management for further information.
    2) Contraindications: unprotected airway (increases risk/severity of aspiration) , nonfunctioning gastrointestinal tract, uncontrolled vomiting, and ingestion of most hydrocarbons (Chyka et al, 2005).
    6.5.3) TREATMENT
    A) SUPPORT
    1) The goal of therapy is primarily to replace fluid and electrolyte losses. Other treatment is symptomatic and supportive. There are no specific antidotes.
    B) FLUID/ELECTROLYTE BALANCE REGULATION
    1) Maintenance of fluid and electrolyte balance is important as the degree of vomiting and diarrhea may produce dehydration and shock.

Range Of Toxicity

Summary

    A) The range of toxicity is extremely variable depending upon plant species, plant part, and time of ingestion.

Minimum Lethal Exposure

    A) ANIMAL STUDIES
    1) COLOCYNTH - Animal studies reported that the fruit causes organ damage in the liver, kidney, and gastrointestinal tract. Approximately 60% of treated rats were killed after ingesting a dose of 800 mg/kg of the ethanolic extract of the leaves (Khan et al, 2003).

Maximum Tolerated Exposure

    A) GENERAL/SUMMARY
    1) Toxicity varies from essentially harmless to life-threatening (rosary pea) and is dependent upon plant species, plant part, and time of ingestion.

Pharmacology Toxicology

Toxicologic Mechanism

    A) Gastrointestinal irritation may be the result of physical irritation to the stomach by a plant and its constituents or by stimulation of the CNS emetic center.

References

General Bibliography

    1) Alaspaa AO, Kuisma MJ, Hoppu K, et al: Out-of-hospital administration of activated charcoal by emergency medical services. Ann Emerg Med 2005; 45:207-12.
    2) Anon: Poisoning from elderberry juice - California. MMWR 1984a; 33:173-174.
    3) Anon: Poisoning from elderberry juice. JAMA 1984; 251:2075.
    4) Chyka PA, Seger D, Krenzelok EP, et al: Position paper: Single-dose activated charcoal. Clin Toxicol (Phila) 2005; 43(2):61-87.
    5) Dagnone D, Matsui D, & Rieder MJ: Assessment of the palatability of vehicles for activated charcoal in pediatric volunteers. Pediatr Emerg Care 2002; 18:19-21.
    6) Elliot CG, Colby TV, & Kelly TM: Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest 1989; 96:672-674.
    7) FDA: Poison treatment drug product for over-the-counter human use; tentative final monograph. FDA: Fed Register 1985; 50:2244-2262.
    8) Golej J, Boigner H, Burda G, et al: Severe respiratory failure following charcoal application in a toddler. Resuscitation 2001; 49:315-318.
    9) Graff GR, Stark J, & Berkenbosch JW: Chronic lung disease after activated charcoal aspiration. Pediatrics 2002; 109:959-961.
    10) Guenther Skokan E, Junkins EP, & Corneli HM: Taste test: children rate flavoring agents used with activated charcoal. Arch Pediatr Adolesc Med 2001; 155:683-686.
    11) Harris CR & Filandrinos D: Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med 1993; 22:1470-1473.
    12) Ho CH, Ho MG, Ho SP, et al: Bitter bottle gourd (Lagenaria siceraria) toxicity. J Emerg Med 2014; 46(6):772-775.
    13) Khan SA, Shelleh HH, Bhat AR, et al: Colocynth toxicity. A possible cause of bloody diarrhea. Saudi Med J 2003; 24(8):904-906.
    14) Lampe KF & Fagerstrom R: Plant Toxicity and Dermatitis, Williams & Wilkins Co, Philadelphia, PA, 1968.
    15) None Listed: Position paper: cathartics. J Toxicol Clin Toxicol 2004; 42(3):243-253.
    16) Pollack MM, Dunbar BS, & Holbrook PR: Aspiration of activated charcoal and gastric contents. Ann Emerg Med 1981; 10:528-529.
    17) Puri R, Sud R, Khaliq A, et al: Gastrointestinal toxicity due to bitter bottle gourd (Lagenaria siceraria)--a report of 15 cases. Indian J Gastroenterol 2011; 30(5):233-236.
    18) Rau NR, Nagaraj MV, Prakash PS, et al: Fatal pulmonary aspiration of oral activated charcoal. Br Med J 1988; 297:918-919.
    19) Spiller HA & Rogers GC: Evaluation of administration of activated charcoal in the home. Pediatrics 2002; 108:E100.
    20) Thakore S & Murphy N: The potential role of prehospital administration of activated charcoal. Emerg Med J 2002; 19:63-65.