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PLANTS-PHILODENDRON

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Philodendron species are members of the Araceae family. These plants are some of the most common houseplants in the United States. Philodendrons contain oxalate crystals in raphides.

Specific Substances

    A) PHILODENDRON ANGUSTISECTUM
    1) Philodendron elegans
    PHILODENDRON BARROSOANUM
    1) Philodendron deflexum
    PHILODENDRON BIPENNIFOLIUM
    1) Fiddle Leaf Philodendron
    2) Horsehead Philodendron
    3) Panda Plant Philodendron
    4) Philodendron panduriforme
    PHILODENDRON CORDATUM
    1) Heart Leaf Philodendron
    PHILODENDRON CRUENTUM
    1) Redleaf Philodendron
    PHILODENDRON DOMESTICUM
    1) Philodendron hastatum
    2) Spade Leaf Philodendron
    PHILODENDRON EICHLERI
    1) Philodendron undulatum
    PHILODENDRON ERUBESCENS
    1) Redleaf Philodendron
    2) Blushing Philodendron
    PHILODENDRON FENDLERI
    1) Philodendron Duisbergii
    14. PHILODENDRON GIGANTEUM
    1) Giant Philodendron
    PHILODENDRON GRAZIELAE
    1) Philodendron fibrillosum
    PHILODENDRON GUTTIFERUM
    1) Leatherleaf Philodendron
    PHILODENDRON IMBE
    1) Philodendron Sellowianum
    PHILODENDRON INAEQUILATERUM
    1) Philodendron coerulescens
    2) Philodendron guatemalense
    PHILODENDRON INSIGNE
    1) Philodendron calophyllum
    PHILODENDRON LINNAEI
    1) Philodendron nobile
    PHILODENDRON MARTIANUM
    1) Philodendron cannifolium
    2) Philodendron crassum
    PHILODENDRON MELANOCHRYSUM
    1) Philodendron Andreanum
    2) Black Gold Philodendron
    PHILODENDRON ORNATUM
    1) Philodendron imperiale
    2) Philodendron Sodiroi
    PHILODENDRON PEDATUM
    1) Philodendron laciniatum
    2) Philodendron laciniosum
    PHILODENDRON PINNATIFIDUM
    1) British Guiana Philodendron
    PHILODENDRON PINNATILOBIUM
    1) Fernleaf Philodendron
    PHILODENDRON RADIATUM
    1) Philodendrum dubium
    2) Dubia Philodendron
    PHILODENDRON SAGITTIFOLIUM
    1) Philodendron sagittatum
    PHILODENDRON SCANDENS subspecies OXYCARDIUM
    1) Philodendron scandens cordatum
    2) Philodendron scandens cardatum
    PHILODENDRON SELLOUM
    1) Philodendron Johnsii
    2) Maybe Philodendron bipinnatifidum
    3) German Selloum
    4) Minature Selloum
    5) Seaside
    6) Uruguay
    7) Golden Selloum
    PHILODENDRON VERRUCOSUM
    1) Philodendron triumphans

Available Forms Sources

    A) SOURCES
    1) There are over 200 different species and many cultivars and varieties. Specific identification is often difficult because there are only minor differences.
    B) USES
    1) Philodendrons are common houseplants found throughout the world.
    2) ANNUAL CALLS TO POISON CENTERS: Annual calls to US poison centers by plant species documented in the AAPCC database during the years 2000 to 2008, ranked philodendron as the second most common plant exposure (Petersen, 2011).

Overview

Life Support

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

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: Philodendron species are members of the Araceae family. These plants are some of the most common houseplants in the United States. There are over 200 species of Philodendron. They are epiphytic herbs, primarily with climbing stems that are mostly climbing vines with aerial roots. Identification is difficult because of the many different sizes and shapes of the leaves.
    B) TOXICOLOGY: Philodendrons contain insoluble calcium oxalate crystals in raphides. However, the oxalate crystals are not well organized and do not cause significant systemic toxicity. Oxalates are found in the leaves of philodendron plants.
    C) EPIDEMIOLOGY: A common houseplant. Annual calls to US poison centers by plant species documented in the AAPCC database during the years 2000 to 2008, ranked philodendron as the second most common plant exposure. Exposure can occur but most cases do not result in significant symptoms unless a substantial ingestion has occurred.
    D) WITH POISONING/EXPOSURE
    1) INGESTION: Generally, oxalates produce gastrointestinal symptoms. Edema of the lips may occur after chewing. Systemic symptoms are unusual; local reactions such as laryngeal irritation, dysphagia, tongue edema, and pain of the mouth, lips, and throat are more common. Dysphagia, nausea, vomiting, oral pain, and perioral swelling may occur. Dehydration and electrolyte imbalance are unlikely unless excessive vomiting has occurred. One case of esophageal erosion and dyspnea was reported in an infant following ingestion; the infant had an acute respiratory arrest which lead to cardiorespiratory arrest and death about 2 weeks after exposure.
    2) DERMAL: Allergic contact dermatitis may develop. Edema and erythema of the eyelids due to an allergic reaction has occurred.
    0.2.4) HEENT
    A) Edema and erythema of the eyelids due an allergic reaction was reported. Edema of the lips may occur after chewing.
    0.2.20) REPRODUCTIVE
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.

Laboratory Monitoring

    A) Most cases of ingestion will require no laboratory work. If large amounts have been ingested the urine may be examined for oxalate crystals, but crystals have not been reported after philodendron ingestion.
    B) Patients who experience extensive vomiting should be monitored for fluid or electrolyte imbalance.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treatment is symptomatic and supportive. INGESTION: Dilution with milk or water may clear the material from the mouth and provide some demulcent action. Pain relief may be accomplished by ice or analgesics, if necessary. Correct fluid and electrolyte abnormalities in patients that develop significant vomiting. DERMAL: Allergic contact dermatitis is treated as other allergic phenomena, using corticosteroids and/or antihistamines as necessary.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Treatment is symptomatic and supportive. Severe toxicity is not anticipated due in part to the pain associated with ingesting the plant material.
    C) DECONTAMINATION
    1) PREHOSPITAL: Decontamination is seldom required. The amount ingested is usually limited by the pain associated with ingesting the plant material.
    2) HOSPITAL: Decontamination is unlikely to be necessary. Following a significant ingestion, vomiting may develop due to the irritant effects of the plant.
    D) AIRWAY MANAGEMENT
    1) Airway support is unlikely to be necessary following a "taste" or minor exposure. Assess airway following a significant ingestion due to the irritant effects of the plant that may produce esophageal erosion, swelling of the tongue and excessive salivation. Ensure adequate ventilation in patients that develop signs of significant respiratory symptoms (ie, coughing, dyspnea) or as indicated.
    E) ANTIDOTE
    1) There is no specific antidote.
    F) ENHANCED ELIMINATION
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this plant.
    G) PATIENT DISPOSITION
    1) HOME CRITERIA: A child with a minor or "taste" ingestion, that remains asymptomatic can be managed at home.
    2) OBSERVATION CRITERIA: Patients with an intentional ingestion, children who are symptomatic may require monitoring for several hours to assess for oropharyngeal pain and/or blistering, gastrointestinal symptoms or electrolyte and fluid imbalance. Patients that improve or remain asymptomatic can be discharged.
    3) ADMISSION CRITERIA: Patients should be admitted for persistent severe vomiting, dehydration, electrolyte abnormalities or significant respiratory symptoms.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    H) TOXICOKINETICS
    1) The leaves contain oxalates and can produce injury. Philodendron contains oxalate raphides (needle-like crystals) in ampoule-like cells that, when ruptured by chewing or crushing, eject their contents into tissue. However, the oxalate content of various philodendron, species is not known. Oxalates can be absorbed orally. Brief sucking or licking of a philodendron leaf is usually not associated with toxicity.
    I) DIFFERENTIAL DIAGNOSIS
    1) Exposure to other plant species (eg, Dieffenbachia species) that contain oxalates and may cause similar symptoms. The Dieffenbachia species reportedly causes more serious toxicity compared to philodendron species.
    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: Determining a toxic dose is difficult to estimate because the oxalate content of various philodendron species can vary. The estimated lethal dose of oxalates is 15 to 30 g, but as little as 5 g may be fatal. However, the oxalate content of various philodendron species is not known. In one study, philodendron may have as much as 0.7% oxalates in the form of oxalate crystals.
    B) INGESTION: In general, a substantial ingestion would be necessary to produce gastrointestinal symptoms.
    C) LOCAL REACTION: Generally, crushing, cutting, or mastication of the plant is necessary to produce a significant local reaction due to the calcium oxalate crystals; brief sucking or licking of a leaf is usually not associated with toxicity.

Clinical Effects

Summary Of Exposure

    A) BACKGROUND: Philodendron species are members of the Araceae family. These plants are some of the most common houseplants in the United States. There are over 200 species of Philodendron. They are epiphytic herbs, primarily with climbing stems that are mostly climbing vines with aerial roots. Identification is difficult because of the many different sizes and shapes of the leaves.
    B) TOXICOLOGY: Philodendrons contain insoluble calcium oxalate crystals in raphides. However, the oxalate crystals are not well organized and do not cause significant systemic toxicity. Oxalates are found in the leaves of philodendron plants.
    C) EPIDEMIOLOGY: A common houseplant. Annual calls to US poison centers by plant species documented in the AAPCC database during the years 2000 to 2008, ranked philodendron as the second most common plant exposure. Exposure can occur but most cases do not result in significant symptoms unless a substantial ingestion has occurred.
    D) WITH POISONING/EXPOSURE
    1) INGESTION: Generally, oxalates produce gastrointestinal symptoms. Edema of the lips may occur after chewing. Systemic symptoms are unusual; local reactions such as laryngeal irritation, dysphagia, tongue edema, and pain of the mouth, lips, and throat are more common. Dysphagia, nausea, vomiting, oral pain, and perioral swelling may occur. Dehydration and electrolyte imbalance are unlikely unless excessive vomiting has occurred. One case of esophageal erosion and dyspnea was reported in an infant following ingestion; the infant had an acute respiratory arrest which lead to cardiorespiratory arrest and death about 2 weeks after exposure.
    2) DERMAL: Allergic contact dermatitis may develop. Edema and erythema of the eyelids due to an allergic reaction has occurred.

Heent

    3.4.1) SUMMARY
    A) Edema and erythema of the eyelids due an allergic reaction was reported. Edema of the lips may occur after chewing.
    3.4.2) HEAD
    A) LIP EDEMA may occur after ingestion (McIntire et al, 1990).
    3.4.3) EYES
    A) DERMATITIS of the eyelids, with erythema, scaling, and edema was attributed to a delayed hypersensitivity reaction (Harris, 1942; Lampe & McCann, 1985).
    B) CONJUNCTIVITIS was reported after exposure (Mitchell & Rook, 1979).
    3.4.6) THROAT
    A) IRRITATION: Oral irritation and throat irritation were reported in 30.1% and 11.1% of patients, respectively, following a philodendron ingestion, according to the AAPPCC Toxic Exposure Surveillance System (TESS) from 1992 through 1999 (Mrvos et al, 2001).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) APNEA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Respiratory arrest due to vagotonia secondary to esophageal damage, leading to a cardiorespiratory arrest and death was reported 17 days after an 11-month-old chewed on philodendron leaves (McIntire et al, 1990).
    B) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) CASE REPORT: Difficulty with breathing was noted in a child more than 12 hours after chewing on philodendron leaves (McIntire et al, 1990).
    C) COUGH
    1) WITH POISONING/EXPOSURE
    a) INCIDENCE: Coughing was reported in 13.9% of patients following a philodendron ingestion, according to the AAPCC TESS from 1992 through 1999 (Mrvos et al, 2001).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH POISONING/EXPOSURE
    a) Dysphagia, nausea, vomiting, oral pain, and perioral swelling may occur.
    b) Vomiting may occur with ingestion (McIntire et al, 1990). Philodendron is one of the most common plants associated with vomiting; however, the incidence can be variable (Krenzelok et al, 2002).
    c) INCIDENCE: According to the AAPCC TESS from 1992 through 1999, 4.1% and 21.8% of patients reported the occurrence of nausea and vomiting, respectively, following a philodendron ingestion (Mrvos et al, 2001).
    B) ESOPHAGITIS
    1) WITH POISONING/EXPOSURE
    a) Esophageal erosions have been seen after chewing on philodendron leaves (McIntire et al, 1990).
    C) DYSPHAGIA
    1) WITH POISONING/EXPOSURE
    a) Dysphagia and oropharyngeal lesions were noted several hours to days after ingestion of philodendron leaves in one case (McIntire et al, 1990).
    D) INFLAMMATORY DISEASE OF MUCOUS MEMBRANE
    1) WITH POISONING/EXPOSURE
    a) Stomatitis, swelling of the tongue, and excessive salivation may occur after ingestion (Spoerke & Smolinske, 1990).
    E) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea was reported in 2.3% of patients following a philodendron ingestion, according to the AAPCC TESS from 1992 through 1999 (Mrvos et al, 2001).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) CONTACT DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) Originally thought to be non-sensitizing (Rook et al, 1972), philodendrons are now known to cause allergic contact dermatitis (de Corres et al, 1984; Fisher, 1973) (Zina & Bonu, 1960). Symptoms are not related to season. The reactions may be mild to severe (Dorsey, 1962), and may resemble the rash seen with poison oak (Ayres & Ayres, 1958).
    b) Dermatitis is more common when the plants are handled frequently, like in a greenhouse, and if the plants are wet. Allergic dermatitis to philodendron is not uncommon in workers of commercial greenhouses (Dorsey, 1962).
    c) Dermatitis of the eyelids was reported in a housewife who frequently washed the leaves of her philodendron (Harris, 1942). Ayres and Ayres (1958) reported several cases of erythematovesicular eruptions that occurred in workers exposed to philodendron or in housewives who handled the plants often (Ayres & Ayres, 1958).
    d) The specific allergen is thought to be an alkyl resorcinol (Reffstrup et al, 1982).
    e) The species involved with theses cases are often not known (Andrews, 1954), but there is some cross-reactivity between species (Hammershoy & Verdich, 1980). Several reports of dermatitis have involved:
    SPECIESREFERENCE
    Philodendron consanguineumSchwartz et al, 1957 Weber, 1930 Engel & Horn, 1972 Pardo-Castello, 1923
    Philodendron scandens subspecies oxycardium Philodendron scandens cordatumHammershoy & Verdich, 1980
    Philodendron sellaumAyres & Ayres, 1958
    Philodendron cordatumAyres & Ayres, 1958
    Philodendron speciosumAyres & Ayres, 1958

    f) CASE REPORT: A 23-year-old was seen one week after the start of pruritic, papulovesicular eruptions on the back of both hands, the inner wrists and forearms, and the outer surfaces of the upper arms. There was also erythema and edema of the eyelids, face, and neck. The patient was occupationally exposed to Philodendron scandens on a daily basis. Patch testing with dried, crushed leaves and stems was negative at 24 hours. The material was moistened and re-examined at 48 hours and a papulovesicular dermatitis was observed (Dorsey, 1958).
    g) INCIDENCE: Dermal irritation, erythema, and rash were reported in 3.8%, 1.9%, and 1.4% of patients, respectively, following ingestion of philodendrons, according to the AAPCC TESS from 1992 through 1999 (Mrvos et al, 2001).

Reproductive

    3.20.1) SUMMARY
    A) At the time of this review, no data were available to assess the potential effects of exposure to this agent during pregnancy or lactation.
    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) Most cases of ingestion will require no laboratory work. If large amounts have been ingested the urine may be examined for oxalate crystals, but crystals have not been reported after philodendron ingestion.
    B) Patients who experience extensive vomiting should be monitored for fluid or electrolyte imbalance.
    4.1.2) SERUM/BLOOD
    A) BLOOD/SERUM CHEMISTRY
    1) Fluid and electrolyte abnormalities are unlikely but should be monitored if vomiting is excessive.
    2) Hypocalcemia and tetany are unlikely unless large amount have been ingested.
    4.1.3) URINE
    A) URINALYSIS
    1) It is unlikely that oxalate crystal would be found in the urine. Generally insufficient amounts are ingested (Lampe & McCann, 1985).

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients should be admitted for persistent severe vomiting, dehydration, electrolyte abnormalities or significant respiratory symptoms.
    6.3.1.2) HOME CRITERIA/ORAL
    A) A child with a minor or "taste" ingestion, that remains asymptomatic 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 or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with an intentional ingestion, children who are symptomatic may require monitoring for several hours to assess for oropharyngeal pain and/or blistering, gastrointestinal symptoms or electrolyte and fluid imbalance. Patients that improve or remain asymptomatic can be discharged.

Monitoring

    A) Most cases of ingestion will require no laboratory work. If large amounts have been ingested the urine may be examined for oxalate crystals, but crystals have not been reported after philodendron ingestion.
    B) Patients who experience extensive vomiting should be monitored for fluid or electrolyte imbalance.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Decontamination is seldom required. The amount ingested is usually limited by the pain associated with ingesting the plant material.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Decontamination is seldom required. The amount ingested is usually limited by the pain associated with ingesting the plant material.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treatment is symptomatic and supportive. The insoluble oxalates found in philodendron are unlikely to cause any systemic symptoms. Treatment for local pain is generally all that is necessary (Lampe & McCann, 1985).
    b) INGESTION: Dilution with milk or water may clear the material from the mouth and provide some demulcent action. There is usually insufficient vomiting to cause dehydration or electrolyte imbalance, but patients should be monitored for fluid loss and oral or intravenous rehydration, if necessary. Correct electrolyte abnormalities in patients that develop significant vomiting.
    c) LOCALIZED PAIN: Pain relief may be accomplished by ice or analgesics, if necessary. Cold water or ice pack application may relieve local pain in the mouth. Popsicles can be particularly useful in children. Analgesic medication may be required if the pain is intense. There is usually insufficient vomiting to cause dehydration or electrolyte imbalance, but patients should be monitored for fluid loss and oral or intravenous rehydration performed if necessary. Correct electrolyte abnormalities in patients that develop significant vomiting.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Treatment is symptomatic and supportive. Severe toxicity is not anticipated due in part to the pain associated with ingesting the plant material.
    B) MONITORING OF PATIENT
    1) Most cases of ingestion will require no laboratory work. Patients who experience extensive vomiting should be monitored for fluid and electrolyte imbalance.

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).

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) DERMATITIS
    1) Allergic contact dermatitis is treated as other allergic phenomena, using corticosteroids and/or antihistamines as necessary.
    2) Corticosteroid dressings have been used as treatment for the dermatitis (Dorsey, 1958).
    3) Removal of calcium oxalate raphides from the skin by application and removal of adhesive tape ameliorated acute skin irritation in volunteers (Snyder et al, 1979). Usually, philodendron dermatitis is not due to oxalate crystals, but to an allergen.
    B) Treatment should include recommendations listed in the ORAL EXPOSURE section when appropriate.

Enhanced Elimination

    A) LACK OF INFORMATION
    1) No studies have addressed the utilization of extracorporeal elimination techniques in poisoning with this plant.

Abstracts

Case Reports

    A) INFANT
    1) An 11-month-old child chewed Philodendron leaves one afternoon but had no immediate symptoms. Later that evening the child received 2 bottles of milk. The next day, the child became fussy, dyspneic, had increased mucous, and would not eat. An examination by a physician could find no specific inflammation or infection. That evening the child developed blood tinged mucous and was admitted to a hospital (McIntire et al, 1990):
    a) An initial exam showed, caustic lesions of the mucous membranes of the oral pharynx, lower gingival sulcus, hard palate, posterior pharynx and lip edema. The nasal passages appeared undamaged. Intravenous fluids were started because of reduced oral intake. Endoscopy was not performed. The child was discharged 5 days after exposure with normal food and fluid intake.
    b) Fifteen days postingestion the child was again admitted with vomiting, reduced fluid intake, a persistent cough, and copious amounts of mucous. Laboratory tests indicated anisocytosis, polychromasia, hypochromasia, toxic granules, and 12% monocytes. Signs of aspiration were not seen on chest x-ray.
    c) An esophageal examination and dilation were performed without difficulty. There was a fibrinoexudative web at the esophageal end of the larynx, and slight burns in the rostral area of the posterior cricoid. On day 17, the child had an acute respiratory arrest which lead to a cardiorespiratory arrest and death.
    d) Postmortem findings showed esophageal erosions consistent with oxalate ingestion. Death was attributed to cardiorespiratory arrest secondary to vagotonia, due to esophageal erosions from ingestion of philodendron leave.
    B) ADVERSE EFFECTS
    1) Mrvos et al (1991) reported on 127 exposures to philodendron plants. Only one patient had symptoms of lip swelling, which occurred within 5 minutes and lasted for a short period (Mrvos et al, 1991).
    C) ADULT
    1) DERMAL: A 23-year-old was seen one week after the start of pruritic, papulovesicular eruptions on the back of both hands, the inner wrists and forearms, and the outer surfaces of the upper arms. There was also erythema and edema of the eyelids, face, and neck. The patient was occupationally exposed to Philodendron scandens on a daily basis. Patch testing with dried, crushed leaves and stems was negative at 24 hours. The material was moistened and re-examined at 48 hours and a papulovesicular dermatitis was observed (Dorsey, 1958).

Range Of Toxicity

Summary

    A) TOXICITY: Determining a toxic dose is difficult to estimate because the oxalate content of various philodendron species can vary. The estimated lethal dose of oxalates is 15 to 30 g, but as little as 5 g may be fatal. However, the oxalate content of various philodendron species is not known. In one study, philodendron may have as much as 0.7% oxalates in the form of oxalate crystals.
    B) INGESTION: In general, a substantial ingestion would be necessary to produce gastrointestinal symptoms.
    C) LOCAL REACTION: Generally, crushing, cutting, or mastication of the plant is necessary to produce a significant local reaction due to the calcium oxalate crystals; brief sucking or licking of a leaf is usually not associated with toxicity.

Minimum Lethal Exposure

    A) ACUTE
    1) The estimated lethal dose of oxalates is 15 to 30 grams, but as little as 5 grams may be fatal (Farre et al, 1989).
    B) CONCENTRATION LEVEL
    1) Unfortunately the oxalate content of various philodendrons is not known. One study showed as much as 0.7% oxalate in the form of oxalate crystals (Sellers, 1978). This would be about 700 grams or 1.5 pounds of leaves.

Maximum Tolerated Exposure

    A) SUMMARY
    1) A substantial ingestion of this plant would be necessary to produce some gastrointestinal symptoms, most exposures do not produce any symptoms (Nelson et al, 2007)
    2) Generally crushing, cutting, or mastication of the plant part is necessary to produce the full local reaction due to the calcium oxalate crystals (Rauber, 1985). Briefly sucking on or licking a leaf is not generally associated with toxicity.

Pharmacology Toxicology

Toxicologic Mechanism

    A) OXALATE RAPHIDES
    1) TOXIN: Insoluble calcium oxalate crystals (Nelson et al, 2007).
    2) Philodendron contain oxalate raphides (needle-like crystals) in ampoule-like cells that (Nelson et al, 2007; McIntire et al, 1990), when ruptured by chewing or crushing, 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). However, the oxalate crystals are not well organized and do not cause as much toxicity as the Dieffenbachia species. The leaves contain oxalates and can cause injury (Nelson et al, 2007).
    3) The exact contents of these cells is not known, but crystallographic evidence indicates that there is some free oxalic acid in the cells. These raphides may be coated with various proteolytic enzymes which produce additional tissue damage (Walter & Khanna, 1973; McIntire et al, 1990).
    B) ASPARAGINE: Many of the Araceae species also contain a proteinaceous substance called asparagine (Lawrence, 1997).

Animal Toxicology

Clinical Effects

    11.1.6) FELINE/CAT
    A) General debilitation, listlessness, total loss of kidney function, CNS stimulation, seizures and death have been reported (Greer, 1961; Pierce, 1970).
    B) Thirty-five of 72 cats that became ill following ingestion died (Greer, 1961).
    11.1.13) OTHER
    A) OTHER
    1) SUMMARY: Ingestion may result in immediate local irritation and pain, excessive salivation, edema of the tongue and pharynx, dyspnea, vocalization and head shaking (Anon, 1991; Dumonceaux, 1992).

Treatment

    11.2.2) LIFE SUPPORT
    A) SUMMARY
    1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.
    11.2.5) TREATMENT
    A) CAT
    1) One group found early administration of terramycin enemas to be beneficial to cats (Greer, 1961).

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) CAT
    1) The toxic dose to cats is not known, but small amounts appear to be cumulative (Greer, 1961).

References

General Bibliography

    1) Andrews GC: Diseases of the Skin for Practitioners and Students, 4th ed, WB Saunders Company, Philadelphia, PA, 1954, pp 108.
    2) Anon: House/ornamental plants toxic to companion animals. In: Merck Veterinary Manual, Merck, Rahway, NJ, 1991, pp 1658-1664.
    3) Ayres S Jr & Ayres S III: Philodendron as a cause of contact dermatitis. Arch Dermatol 1958; 78:330-333.
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