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PLANTS-DIEFFENBACHIA

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Dieffenbachia species, commonly known as dumbcane, are native to tropical areas and are often found as houseplants. Most exposures are unintentional, but some have tried chewing on the plant because of a superficial resemblance to banana or sugar cane (Kingsbury, 1964).

Specific Substances

    A) Dieffenbachia maculata - Lodd
    1) Dieffenbachia picta - Schott
    2) Dieffenbachia brasiliense - Hort
    3) Spotted dieffenbachia
    Dieffenbachia exotica
    1) Dieffenbachia exotica
    Dieffenbachia amoena
    1) Dieffenbachia amoena
    Dieffenbachia memoria-Corsii - Fenzi
    1) Dieffenbachia picta var memoria - Hort
    2) Dieffenbachia maculata crossed with
    3) Dieffenbachia wallisii
    Dieffenbachia seguine - Schott
    1) Mother-in-law's tongue plant
    SYNONYMS FOR THE GROUP
    1) Dumbcane
    2) Dumb plant
    3) Tuftroot
    4) Comida de culebra - Costa Rica
    5) Hoja de puerco - Honduras
    6) Giftiger Aron - Germany
    7) Poisonous arum - England

Available Forms Sources

    A) USES
    1) Dieffenbachia plants are natives to tropical America and are primarily used as houseplants (Evans, 1987).
    2) They have been used as a means of punishment and torture in the slave days of the West Indies (Barnes & Fox, 1953) (Everitt, 1944).
    3) It has been used by Brazilian Indians and some Caribbean residents to produce sterility (usually mixed with meals) (Barnes & Fox, 1953).
    4) D. seguine was used in combination with curare as an arrow poison in the upper portions of the Amazon river valley (Remington & Wood, 1918).
    5) Some historical medical uses included slicing the plant and boiling it with wine for treatment of gout, mixing it with fat and using it as an ointment for dropsy, and preparation as a tincture for use in sexual frigidity and impotency (Fochtman et al, 1969).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Dieffenbachia is a common household plant. It has no known medicinal use.
    B) TOXICOLOGY: The leaves contain calcium oxalate crystals called raphides. Raphides can cause irritation and microtrauma with ingestion or topical mucosal exposures. The calcium oxalate crystals are insoluble; therefore not absorbed and do not cause systemic toxicity.
    C) EPIDEMIOLOGY: Dieffenbachia is a common household plant and readily available. Thus, it is a very common inadvertent exposure, especially in young children. Toxicity is mild and serious effects are rare.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Common symptoms include oral-pharyngeal pain with a chewed or ingested plant. Swelling can occur. Ocular exposures can lead to corneal abrasions and conjunctivitis. Local dermal exposures can cause dermatitis, erythema, pruritus and localized swelling and edema. After ingestion, gastrointestinal symptoms can include vomiting, nausea, abdominal pain, esophagitis, and dysphagia.
    2) SEVERE TOXICITY: Very rarely, oropharyngeal swelling can lead to airway edema and compromise.
    0.2.20) REPRODUCTIVE
    A) Chronic ingestion has caused transient sterility in animals.

Laboratory Monitoring

    A) Routine laboratory evaluation is not indicated.
    B) Laboratory monitoring is rarely indicated in the normal exposure where symptoms are limited to the oral mucosa.
    C) Serum analysis for hypocalcemia, or the urine for oxalates are only indicated following a significant ingestion.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MILD TO MODERATE TOXICITY
    1) Dilute with small amounts of water or milk to reduce irritation. Wash skin with soap and water. Irrigate exposed eyes with water.
    B) SEVERE TOXICITY
    1) Severe toxicity is very uncommon. If severe oral-pharyngeal reaction occurs, airway protection may be indicated.
    C) ANTIDOTE
    1) There is no antidote for exposure.
    D) ENHANCED ELIMINATION
    1) There is no role for enhanced elimination
    E) PATIENT DISPOSITION
    1) HOME CRITERIA: The vast majority of exposures can be managed at home.
    2) OBSERVATION CRITERIA: Patients with oropharyngeal swelling respiratory symptoms, or severe irritation should be referred to a healthcare facility.
    3) ADMISSION CRITERIA: If patients become severely symptomatic requiring IV pain control, or concerns about airway protection, then hospital admission may be required.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity. Ophthalmology consultation may be needed for ocular exposures.
    F) PITFALLS
    1) Failure to recognize worsening oral-pharyngeal swelling after oral exposure.
    G) DIFFERENTIAL DIAGNOSIS
    1) Other oxalate raphide containing household plants such as Philodendron species, Narcissus bulbs, Brassaia, Epipremnum aurem, Spathiphyllium, and Scheflera.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    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: Toxicity is extremely variable and is usually dependent on the part of the plant that has been broken, crushed or cut and may relate to the amount ingested. Acute upper airway edema requiring emergent tracheostomy developed in a man who chewed dieffenbachia stem mistaking it for sugar cane. An adolescent developed diffuse grade 2 esophagitis and a subsequent aorto-esophageal fistula after deliberately ingesting a dieffenbachia leaf. Exploratory ingestions in young children rarely cause significant toxicity.

Clinical Effects

Summary Of Exposure

    A) USES: Dieffenbachia is a common household plant. It has no known medicinal use.
    B) TOXICOLOGY: The leaves contain calcium oxalate crystals called raphides. Raphides can cause irritation and microtrauma with ingestion or topical mucosal exposures. The calcium oxalate crystals are insoluble; therefore not absorbed and do not cause systemic toxicity.
    C) EPIDEMIOLOGY: Dieffenbachia is a common household plant and readily available. Thus, it is a very common inadvertent exposure, especially in young children. Toxicity is mild and serious effects are rare.
    D) WITH POISONING/EXPOSURE
    1) MILD TO MODERATE TOXICITY: Common symptoms include oral-pharyngeal pain with a chewed or ingested plant. Swelling can occur. Ocular exposures can lead to corneal abrasions and conjunctivitis. Local dermal exposures can cause dermatitis, erythema, pruritus and localized swelling and edema. After ingestion, gastrointestinal symptoms can include vomiting, nausea, abdominal pain, esophagitis, and dysphagia.
    2) SEVERE TOXICITY: Very rarely, oropharyngeal swelling can lead to airway edema and compromise.

Heent

    3.4.3) EYES
    A) WITH POISONING/EXPOSURE
    1) Ocular exposure to the milky latex are likely to cause burning pain, photophobia, blepharospasm, edema of the eyelids (can be severe), conjunctival chemosis, lacrimation, a temporary decrease in visual acuity and corneal abrasions (Hsueh et al, 2004; Lim, 1977; Ellis et al, 1973). Symptoms are generally temporary, subsiding over 3 to 4 weeks.
    2) Permanent corneal opacification may result after eye exposure to the sap of these plants (Lampe & Fagerstrom, 1968). Calcium oxalate crystals may be visible on the corneal epithelium (Morton, 1971).
    3) Keratoconjunctivitis with the presence of needle-like calcium oxalate crystals in the cornea developed in an adult following eye contact with Dieffenbachia sap. Mild pain which progressed over a few hours to severe ocular pain, chemosis, and visual blurring occurred. Chloramphenicol and dexamethasone were administered. Conjunctival injection and chemosis resolved in 1 week and the crystals disappeared over several weeks (Seet et al, 1995).
    4) IRRITATION IN ANIMALS
    a) When tested in rabbit eyes, D. exotica showed mild irritation (mostly conjunctival) and D. picta produced severe irritation (conjunctival and corneal) (Manno et al, 1967; Fochtman et al, 1969).
    b) Keratoconjunctivitis was seen in rabbits who had the free flowing sap placed in their eyes. There was no evidence of corneal crystals. When the juice was obtained by squeezing the stalk, corneal lesions were seen, and numerous crystals were found on the cornea (Ellis et al, 1973).
    c) The eye irritant is thought to be due to an unidentified protein substance which is destroyed by treatment with trypsin and storage at room temperature for 24 hours. Eye irritation may also be due to the release of the calcium oxalate crystals in the raphides(Grant, 1986; Manno et al, 1967).
    3.4.6) THROAT
    A) WITH POISONING/EXPOSURE
    1) ORAL PAIN
    a) Oral burning or pain is the most common symptom after chewing or biting into a plant part. The pain may be mild to severe, but usually starts within a few minutes of exposure (Cumpston et al, 2003; Evans, 1987; Ladeira et al, 1975; Kuballa et al, 1981; Drach & Maloney, 1963; Mrvos et al, 1991). Since the active substance from D. picta juice is inactivated by stomach enzymes, the toxic effects of the juice are not usually observed following the ingestion of the juice; these effects are observed by the direct contact of juice with the oral cavity, or the unintentional inhalation (Dip et al, 2004).
    b) In one study of 61 cases of dieffenbachia chewing where the integrity of the leaf was broken, only 4.9% of the cases developed minor symptoms. The onset was within 5 minutes and the duration was short (Mrvos et al, 1991).
    c) Cases have also been reported where simply placing a cut stem in the mouth may cause severe pain, edema, and dysphagia for several hours (Evans, 1987). Sucking on the juice of a 1.5 cm stalk produced oral pain as well as inflammation of the oral cavity and throat (Wiese et al, 1996).
    d) Severe acute toxicity can result in symptoms within a few minutes and edema lasting for up to 12 days (Lampe & Fagerstrom, 1968).
    2) EDEMA
    a) Edema is a common effect after oral exposure. Common sites are the tongue, lips, and buccal mucosa; swelling may be minor or significant (Drach & Maloney, 1963; Mrvos et al, 1991). The tongue has been so swollen in some cases that it has protruded from the mouth for 3 days (Rizzini & Occhioni, 1957).
    1) Because of buccal and lingual swelling, speech may be difficult to understand or unintelligible (Cumpston et al, 2003; Wiese et al, 1996; Gardner, 1994; Drach & Maloney, 1963). There may be temporary paralysis of the vocal chords (Grant, 1986).
    b) Pharyngeal or laryngeal edema are rare (Mack, 1982).
    3) SALIVATION
    a) Excessive salivation may be present during the acute phase of irritation (Wiese et al, 1996; Drach & Maloney, 1963).
    4) ULCERATION
    a) Simply touching a cut stalk to the tongue (not chewing or swallowing it) resulted in an immediate tingling sensation, superficial ulceration, and oral pain (Evans, 1987). Symptoms gradually subsided over the next 5 days.
    b) Bullae formation and superficial necrosis may occur after biting a stalk (Delph, 1937). In one case, these symptoms resolved in 11 days (Drach & Maloney, 1963). In another case conservative therapy was continued for 14 days which included tube feedings and topical anti-inflammatory treatment to the oral mucosa until inflammation and necrosis had healed (Wiese et al, 1996).
    5) DYSPHAGIA
    a) Dysphagia may occur for several hours after only minor exposures (Evans, 1987).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) RESPIRATORY OBSTRUCTION
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Laryngeal and epiglottal edema requiring emergency tracheostomy occurred in a 69-year-old man one hour after arrival to the ED. The patient mistakenly bit a dieffenbachia stem thinking it was "sugar cane". Initial symptoms of dysphagia, sialorrhea, and glossitis progressed to dyspnea and stridor, with swelling of the lips, soft palate, uvula and tongue. His course was complicated by bilateral pneumothoraces following tracheostomy and bilateral chest tubes were placed. However, the patient progressed well with a course of methylprednisolone, albuterol, and diphenhydramine. His tracheostomy was capped on the 3rd hospital day. The patient was discharged on an albuterol inhaler and antibiotic therapy (Cumpston et al, 2003).
    b) Tracheostomy was required in one case where lingual edema was so severe that maintenance of an airway became difficult (Manoguerra, 1975).
    B) EDEMA OF LARYNX
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: A 70-year-old man presented with aphasia, dysphagia, sialorrhea, a wound on his lips and tongue, and swelling of the face after a taste exposure of white extract of Dieffenbachia from the leaves of the plant. Shortly after exposure, he developed severe oral pain. Upon examination, the patient had a cyanotic appearance and slight edema of the upper and lower lips. Severe edema, ulceration, and necrosis developed in the oropharyngeal area followed by widespread swelling in the neck region. Slight respiratory distress and stridor were present along with hoarseness and incomprehensible speech. However, the airway remained patent with no airway support needed. Treatment included a 9-day regimen of pheniramine hydrogen maleate, oxygen therapy, analgesics, and parenteral clarithromycin. Lamipril and furosemide were added for hypertension. Improvement in edema of the neck, oropharynx and larynx occurred by the fifth day and recovery from the lesions in the mouth and mucosa in the epiglottis occurred by the eighth day. The patient was discharged a short time later with no permanent sequelae noted at follow-up (Altin et al, 2013).
    C) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Dyspnea or stridor may occur if swelling becomes so extensive that airway obstruction occurs (Cumpston et al, 2003; Manoguerra, 1975).
    3.6.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) APNEA
    a) Animals who were force fed extract or juice developed salivation, lacrimation, bradycardia, CNS depression, occasionally seizures, and death due to respiratory failure (Walter & Khanna, 1972).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Vomiting may occur, but generally does not (Mack, 1982). A burning sensation of the esophagus and stomach was reported in one case of chewing on a stem (Faivre & Barral, 1974).
    B) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea does not commonly occur, but has been reported after an adult chewed on a stem (Faivre & Barral, 1974).
    C) ESOPHAGITIS
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Esophagitis has been reported in a 12-year-old girl who intentionally ingested leaves in a suicide attempt. Grade 2 esophagitis was found on endoscopy. Approximately 5 weeks later, the patient reported hematemesis and melena and was readmitted with a massive gastrointestinal bleed due to an aortoesophageal fistula. Fluid resuscitation preoperatively and intraoperatively included 11 units of packed red blood cells, 12 units of fresh frozen plasma, 3 units of thrombocytes, 4 L of synthetic colloids and 2.5 L of crystalloids. She progressed well after surgical repair and was discharged 3 weeks later with no permanent sequelae (Snajdauf et al, 2005).

Genitourinary

    3.10.2) CLINICAL EFFECTS
    A) URINARY SYSTEM FINDING
    1) WITH POISONING/EXPOSURE
    a) LACK OF EFFECT
    1) Renal damage is not expected with Dieffenbachia (Lampe & Fagerstrom, 1968).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Skin irritation can occur with dermal exposure (Rizzini & Occhioni, 1957; Pohl, 1961; Pohl, 1964; Bruneton, 1999). Contact dermatitis was confirmed by a patch test in a woman working as a housekeeper following ongoing dermal exposure (every 2 to 3 days) to a dieffenbachia plant (Sanchez-Morillas, 2005).
    B) BULLOUS ERUPTION
    1) WITH POISONING/EXPOSURE
    a) Severe burning, itching, and occasional blistering may last many hours after handling Dieffenbachia plants (Barnes & Fox, 1953).

Immunologic

    3.19.3) ANIMAL EFFECTS
    A) ANIMAL STUDIES
    1) ALLERGIC REACTION
    a) Rats treated with Dieffenbachia juice had circulating histamine concentrations higher than the control group (Fochtman et al, 1969).

Reproductive

    3.20.1) SUMMARY
    A) Chronic ingestion has caused transient sterility in animals.
    3.20.2) TERATOGENICITY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the teratogenic potential of this agent.
    3.20.3) EFFECTS IN PREGNANCY
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Carcinogenicity

    3.21.3) HUMAN STUDIES
    A) LACK OF INFORMATION
    1) At the time of this review, no data were available to assess the carcinogenic potential of this agent.

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Routine laboratory evaluation is not indicated.
    B) Laboratory monitoring is rarely indicated in the normal exposure where symptoms are limited to the oral mucosa.
    C) Serum analysis for hypocalcemia, or the urine for oxalates are only indicated following a significant ingestion.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Hypocalcemia is rarely seen with Dieffenbachia. Calcium concentrations should be examined when it is thought that significant amounts may have been ingested. Since hypocalcemia is unusual, there are no good data on the amount of Dieffenbachia necessary to produce this effect.
    4.1.3) URINE
    A) URINALYSIS
    1) In general, oxalates are not absorbed in sufficient quantities to cause oxalate crystals to be found in the urine, and examination of the urine for these crystals is not necessary.

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) If patients become severely symptomatic requiring IV pain control, or concerns about airway protection, then hospital admission may be required.
    6.3.1.2) HOME CRITERIA/ORAL
    A) The vast majority of exposures can be managed at home.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity. Ophthalmology consultation may be needed for ocular exposures.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with oropharyngeal swelling respiratory symptoms, or severe irritation should be referred to a healthcare facility.

Monitoring

    A) Routine laboratory evaluation is not indicated.
    B) Laboratory monitoring is rarely indicated in the normal exposure where symptoms are limited to the oral mucosa.
    C) Serum analysis for hypocalcemia, or the urine for oxalates are only indicated following a significant ingestion.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Decontamination is generally not necessary because the amount ingested is small.
    2) Dilution with milk or water may clear the material from the mouth and provide some demulcent action.
    3) In large scale chart review of plant exposures to the Dieffenbachia spp. and Philodendron spp., decontamination therapy was not found to alter outcome; most exposures were asymptomatic (Krenzelok et al, 1996).
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Dilution with milk or water may clear the material from the mouth and provide some demulcent action. Activated charcoal is generally not required.
    2) In large scale chart review of plant exposures to the Dieffenbachia spp. and Philodendron spp., decontamination therapy was not found to significantly alter patient outcome (Krenzelok et al, 1996).
    6.5.3) TREATMENT
    A) GASTROINTESTINAL IRRITATION
    1) Ice or cold packs may be of some assistance. A cold popsicle, ice cream, or a cold beverage may be of some relief (Mack, 1982).
    2) Local anesthetics such as viscous lidocaine have been prescribed for topical treatment. The viscous lidocaine should be swished in the mouth, but not swallowed (Evans, 1987).
    3) Systemic opioids may be required in some severe cases for pain relief (Drach & Maloney, 1963).
    4) A soft diet may be recommended in cases of significant oral pain and edema (Evans, 1987; Lampe & Fagerstrom, 1968).
    5) Milk and an ordinary sugar cube have been anecdotally reported to produce some relief from the pain (Anon, 1978).
    6) Antacids, such as an aluminum-magnesium hydroxide mixture (one ounce in adults), given once every 2 hours, may have some benefit (Drach & Maloney, 1963; Lampe & Fagerstrom, 1968).
    B) ANTIHISTAMINE
    1) SUMMARY: Based on animal studies, histamine appears to have some part in the reaction to Dieffenbachia. Animals pretreated with antihistamines had reduced symptomatology (Fochtman et al, 1969).
    2) DIPHENHYDRAMINE: A test dose of 50 mg of diphenhydramine given to one patient with a serious reaction resulted in no reduction of edema (Drach & Maloney, 1963).
    3) ANIMAL DATA: Chlorpheniramine was administered to poisoned guinea pigs and it did not stop the development of edema (Ladiera et al, 1975).
    C) CORTICOSTEROID
    1) ANIMAL DATA: Animals pretreated with corticosteroids had reduced symptoms initially, but the steroids only seemed to delay the reaction (Fochtman et al, 1969).
    D) FLUID/ELECTROLYTE BALANCE REGULATION
    1) There is usually insufficient vomiting and diarrhea to cause dehydration or electrolyte imbalance. Should extensive fluid loss occur, monitor patients for electrolytes abnormalities.
    E) AIRWAY MANAGEMENT
    1) Rare cases of airway obstruction following severe cases of dieffenbachia poisoning have been reported (Cumpston et al, 2003). In the event of airway compromise, supportive measures including endotracheal intubation, cricothyrotomy or emergent tracheostomy, and mechanical ventilation may be necessary.

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).
    6.8.2) TREATMENT
    A) DEXAMETHASONE
    1) A dexamethasone ophthalmic ointment was used to treat one case of eye exposure which had resulted in pain, photophobia, and corneal and stromal crystals. The crystals gradually cleared over 2 months; the effect of the dexamethasone was difficult to determine (Ellis et al, 1973).
    B) INFECTIOUS CRYSTALLINE KERATOPATHY
    1) Chloramphenicol eyedrops, followed by a combined treatment of chloramphenicol and dexamethasone, have been used to treat crystalline keratopathy. The ocular effects resolved within several months. It is not known if treatment with chloramphenicol and dexamethasone influenced the outcome (Seet et al, 1995).
    C) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) 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).
    6.9.2) TREATMENT
    A) SKIN IRRITATION
    1) Removal of calcium oxalate raphides from the skin by application and removal of adhesive tape ameliorated skin irritation from a different oxalate containing plant, but the usefulness of this treatment with Dieffenbachia has not been determined (Snyder et al, 1979).
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) SUMMARY
    1) There is no role for enhanced elimination.

Abstracts

Case Reports

    A) ADULT
    1) A 40-year-old woman bit into the stalk of a Dieffenbachia without swallowing any of the material. Within 6 hours she had excessive salivation, severe edema of the side of the face, pain in the mouth and tongue, dysphagia, and bullae on the swollen surfaces of the tongue and mucosa. Her speech was almost unintelligible. The patient was admitted for observation and given meperidine for oral pain, aluminum-magnesium hydroxide every 2 hours, and intravenous fluids. The day after admission she was able to start on a diet of soft foods, and was discharged 19 hours post admission. The patient continued to experience pain and developed superficial necrosis of areas of the tongue and buccal mucosa, which gradually resolved over the next 11 days (Drach & Maloney, 1963).
    B) PEDIATRIC
    1) An 8-year-old boy splashed some squeezed juice from a stem into his left eye. He immediately experienced pain and photophobia. When seen by a physician, conjunctivitis an corneal and stromal crystals were seen. His visual acuity was normal. He was treated with an dexamethasone ophthalmic ointment. Within 11 days half of the crystals were gone. The rest disappeared over a 2 month period (Ellis et al, 1973).
    2) A 12-year-old girl intentionally ingested leaves of a Dieffenbachia plant in a suicide attempt. She was diagnosed with Grade 2 esophagitis and treated with antibiotics and steroids. Her clinical course was complicated by a massive GI bleed about 5 weeks after exposure and an aortoesophageal fistula that required surgical repair. Upon follow-up, she had no permanent sequelae (Snajdauf et al, 2005).

Range Of Toxicity

Summary

    A) TOXICITY: Toxicity is extremely variable and is usually dependent on the part of the plant that has been broken, crushed or cut and may relate to the amount ingested. Acute upper airway edema requiring emergent tracheostomy developed in a man who chewed dieffenbachia stem mistaking it for sugar cane. An adolescent developed diffuse grade 2 esophagitis and a subsequent aorto-esophageal fistula after deliberately ingesting a dieffenbachia leaf. Exploratory ingestions in young children rarely cause significant toxicity.

Minimum Lethal Exposure

    A) SUMMARY
    1) A minimum lethal dose has not been determined. Fatalities may occur if the airway were obstructed due to excessive swelling (Manoguerra, 1975).

Maximum Tolerated Exposure

    A) SUMMARY
    1) Toxicity is extremely variable and is usually dependent on the part of the plant that has been broken, crushed or cut (Spoerke & Smolinske, 1990).
    B) CASE SERIES
    1) In large review of plant exposures reported to AAPCC TESS for the years 1985 to 1994, exposures to Dieffenbachia spp. and Philodendron spp. were examined (Krenzelok et al, 1996). The two genuses accounted for 96,659 plant exposures or 10.6% of all plant exposures (n=912,534), with Dieffenbachia representing approximately 40% of the cases. The following effects were reported for both types of exposures: minor 15.5%, moderate 0.4%, and 8 patients had major effects. Decontamination did not change outcome. The authors suggested that these exposures are not associated with significant toxicity as to require referral to a health care facility.
    2) In one study of 61 cases of Dieffenbachia exposure, the chewing of the plant where the integrity of the leaf was broken, only 4.9% of the cases had minor symptoms; onset was within 5 minutes with a short duration(Mrvos et al, 1987).
    3) In a review of 61 pediatric and adult cases reported to a Regional Poison Information Center over a 24 month period, only 3 cases were symptomatic and no significant adverse effects occurred. Reported effects resulting from chewing or tasting a dieffenbachia leaf included erythema on the lip of an infant, oral burning in a 4-year-old, and an adult with oral burning (Mrvos et al, 1991).
    4) A one year survey of exposures reported to a regional poison center resulted in 43 cases. Twelve of these had oral or gastrointestinal effects; 6 had eye or skin irritation (Spoerke & Temple, 1978).
    5) Cases have also been reported where simply placing a cut stem in the mouth may cause severe pain, edema, and dysphagia for several hours (Drach & Maloney, 1963; Evans, 1987).
    C) CASE REPORTS
    1) PEDIATRIC: A 12-year-old girl intentionally ingested leaves of a Dieffenbachia plant in a suicide attempt. She was diagnosed with Grade 2 esophagitis and treated with antibiotics and steroids. Her clinical course was complicated by a massive GI bleed about 5 weeks after exposure and an aortoesophageal fistula that required surgical repair. Upon follow-up, she had no permanent sequelae (Snajdauf et al, 2005).
    2) ADULT: Laryngeal and epiglottal edema requiring emergency tracheostomy occurred in a 69-year-old man one hour after arrival to the ED. The patient mistakenly bit a dieffenbachia stem thinking it was "sugar cane". Initial symptoms of dysphagia, sialorrhea, and glossitis progressed to dyspnea and stridor, with swelling of the lips, soft palate, uvula and tongue. His course was complicated by bilateral pneumothoraces following tracheostomy and bilateral chest tubes were placed. However, the patient progressed well with a course of methylprednisolone, albuterol, and diphenhydramine. His tracheostomy was capped on the 3rd hospital day. The patient was discharged on an albuterol inhaler and antibiotic therapy (Cumpston et al, 2003).
    3) ADULT: A 70-year-old man presented with aphasia, dysphagia, sialorrhea, a wound on his lips and tongue, and swelling of the face after a taste exposure of white extract of Dieffenbachia from the leaves of the plant. Shortly after exposure, he developed severe oral pain. Upon examination, the patient had a cyanotic appearance and slight edema of the upper and lower lips. Severe edema, ulceration, and necrosis developed in the oropharyngeal area followed by widespread swelling in the neck region. Slight respiratory distress and stridor were present along with hoarseness and incomprehensible speech. However, the airway remained patent with no airway support needed. Treatment included a 9-day regimen of pheniramine hydrogen maleate, oxygen therapy, analgesics, and parenteral clarithromycin. Lamipril and furosemide were added for hypertension. Improvement in edema of the neck, oropharynx and larynx occurred by the fifth day and recovery from the lesions in the mouth and mucosa in the epiglottis occurred by the eighth day. The patient was discharged a short time later with no permanent sequelae noted at follow-up (Altin et al, 2013).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) LD50- (ORAL)RAT:
    1) >160 mL/kg (RTECS, 2000)

Pharmacology Toxicology

Toxicologic Mechanism

    A) PROPOSED MECHANISMS
    1) Various mechanisms have been proposed for the toxicity of Dieffenbachia. Toxicity appears to be a combination of the amount of oxalate, the form (raphides) of the oxalate, and various proteinaceous enzymes (Walter, 1967; Gardner, 1994) Spoerke & Smolinske, 1990.
    2) The amount of oxalate is not substantial, and is in higher concentration in some food plants such as spinach (Manoguerra, 1975). The raphide form of the oxalates may contribute to mechanical damage that allows for other toxic substances to penetrate the mucosa.
    3) Low concentrations of "irritants" (unspecified) were found in alcohol and acid extracts of D. seguine and D. picta . The concentration of these substances appeared to be higher in the stems than in the leaves or leaf stems (Barnes & Fox, 1953).
    4) Saponins have been proposed as being responsible, but Barnes (1953) has discredited this theory.
    5) Alkaloids have also been proposed as the toxic agent, but work by Winek in 1967 (Fochtman et al, 1969) seems to have eliminated alkaloids.
    6) Cyanogenic glycosides have been identified in D. exotica and D. bausii (Walter, 1967; Walter & Muni, 1968; Dore, 1963). What part, if any, these glycosides appear to contribute to toxicity is uncertain. One study where mice received intraperitoneal injections of both intact juice and juice that had the cyanogenic glycosides hydrolyzed showed the intact material to be less toxic (Walter & Muni, 1968).
    B) OXALATE RAPHIDES
    1) Dieffenbachia species contain oxalate raphides (needle-like crystals) in ampoule-like cells called idioblasts (Rauber, 1985; Sakai & Nagao, 1980) reviewed in Bruneton, 1999. When ruptured by chewing or crushing, these cells eject their contents into tissue. It appears that the rupturing of these cells and the injection of the cell contents occurs at the same time (Frohne & Pfander, 1984).
    2) The exact contents of these cells is not known, but crystallographic evidence is that there is some free oxalic acid in the cells. These raphides may be coated with various proteolytic enzymes which produce additional tissue damage (Mors & Rizzini, 1966; Kuballa et al, 1981; Walter & Khanna, 1973).
    3) These cells are found in species like the Taro as well. Taro is not edible unless it has first been cooked (Sakai & Hanson, 1974).
    4) A good discussion of these cells is found in Rauber (1985). They are about 200 microns long and 10 microns wide, and have a thick, rigid, doubly refractile cell wall except for where it narrows into a "nozzle" at both ends. Because they are not connected to the surrounding leaf stroma cells, they may be easily dislodged and found floating in macerated preparations.
    C) PROTEIN SUBSTANCES
    1) These were noted by Occhioni and Rizzini (1958) who found out these agents could be digested with trypsin. Animals exposed to plant juices that had been digested with trypsin (with the trypsin being inactivated prior to administration) showed less damage than those treated with non-trypsin treated juices (Fochtman et al, 1969).
    2) A proteolytic enzyme (initially designated as dumbain) has been identified (Walter, 1967).
    3) The amino acid asparagine has been isolated from D. picta, D. seguine, and D. amoena (Walter & Khanna, 1972). The enzymatic properties were demonstrated by digesting earthworms over a 12 hour period, by inactivation similar to papain by heat and alcohol, and by reaction with egg albumin (Walter, 1967).
    4) Bradykinin and histamine release has been documented in vitro with stem juice which contains the protein fraction (Kuballa et al, 1981).

Animal Toxicology

Clinical Effects

    11.1.1) AVIAN/BIRD
    A) Budgerigars (parakeets) gavaged with frozen, powdered and rehydrated leaves of Dieffenbachia (D. seguine) developed no signs of toxicity (Shropshire et al, 1992).
    B) Canaries gavaged with frozen, powdered and rehydrated leaves of Dieffenbachia (D. seguine) developed signs of toxicity after 10 minutes and died after 90 to 120 minutes. Signs of toxicity included depression, labored open-beak breathing, progressive salivation, presence of mucous in beak, neck stretching, head shaking, agitation, and death (Arai et al, 1992).
    11.1.13) OTHER
    A) OTHER
    1) SUMMARY - Dieffenbachia poisoning in small animals may result in immediate pain and inflammation of the mouth and throat, anorexia, vomiting, extension of the tongue, head shaking, salivation, dyspnea, depression and vocalization. Diarrhea may occur (Anon, 1991; Dumonceaux, 1992).
    2) Small animals who were force-fed extract or juice developed salivation, lacrimation, bradycardia, CNS depression, occasionally seizures, and death due to respiratory failure (Walter & Khanna, 1972).

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) GENERAL
    1) It has been suggested that immediate pain limits the amount of plant ingested. Consequently death is rare (Anon, 1991).
    B) EXOTIC BIRDS
    1) BUDGERIGARS (parakeets) were gavaged with frozen, powdered and rehydrated leaves every 90 minutes for 4 doses developed no signs of toxicity. Each dose was equivalent to 250 milligrams of fresh leaves (Shropshire et al, 1992).
    2) CANARIES gavaged with a single dose of frozen, powdered and rehydrated leaves developed signs of toxicity after 10 minutes and died after 90 to 120 minutes. The dose was estimated to contain the equivalent of 120 milligrams fresh plant leaves (Arai et al, 1992).

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