Updated: May 27, 2009
Plant exposures are some of the most frequent poisonings reported to poison control centers. Exposures to plants containing oxalate crystals, such as Philodendron and Dieffenbachia, are among the most common toxic plant exposures reported in the US.
For the past 200 years, the irritant properties of the Dieffenbachia plant have had various uses, including punishing slaves and treating gout, impotence, and frigidity. Today, plants containing oxalate are admired for their ornamental beauty and found in public places and homes.
The following plants contain oxalates:
Nonsoluble calcium oxalate crystals are found in plant stems, roots, and leaves. The stalk of the Dieffenbachia plant produces the most severe reactions. These needlelike crystals produce pain and edema when they contact lips, tongue, oral mucosa, conjunctiva, or skin.1 Edema primarily is due to direct trauma from the needlelike crystals and, to a lesser extent, by other plant toxins (eg, bradykinins, enzymes).2,3
Philodendron and Dieffenbachia exposures are among the most common plant exposures reported to poison control centers.
According to the 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS), 7368 single exposures were documented for oxalate plant poisonings.4
In most cases, nonsoluble oxalate plants produce self-limited symptoms and clinical manifestations. Significant morbidity or mortality is extremely rare. One case report of an infant fatality attributed to airway obstruction after exposure to Dieffenbachia exists.
The 2007 Annual Report of the American Association of Poison Control Centers' NPDS reported 1145 minor outcomes, 81 moderate outcomes, 3 major outcomes, and no deaths from oxalate plant exposures.4
The majority of oxalate plant exposures occur in children younger than 5 years while sampling houseplants in the home.
The 2007 Annual Report of the American Association of Poison Control Centers' NPDS reported 6020 oxalate plant exposures in those younger than 6 years, 762 exposures in those aged 6-19 years, and 455 exposures in those older than 19 years.4
Symptoms, if they develop, occur rapidly and may include the following:
No physical findings exist in the majority of oxalate exposures.
| Angioedema | Plant Poisoning, Hypoglycemics |
| Conjunctivitis | Plant Poisoning, Licorice |
| Corneal Abrasion | Plant Poisoning, Resins |
| Dermatitis, Contact | Stevens-Johnson Syndrome |
| Plant Poisoning, Glycosides - Cardiac | |
| Plant Poisoning, Glycosides - Coumarin | |
| Plant Poisoning, Herbs |
Caustic ingestions
Most exposures are self-limited and only require analgesics for patient comfort.
Nearly all cases of houseplant exposures involving oxalate-containing plant species are managed at home in consultation with a regional poison control center. Poison control centers may be helpful with plant identification, particularly if a fax copy or digital picture of the plant can be transmitted.
Analgesics may be required for pain.
Pain control is essential to quality patient care. Analgesics ensure patient comfort, which is beneficial for patients who have sustained trauma or sustained injuries.
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.
650 mg PO/PR q4h prn
15 mg/kg/dose PO/PR q4h prn
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in patients with chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate serious illness; APAP is contained in many OTC products and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose (4 g/d)
DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
200-600 mg PO qid prn
5-10 mg/kg PO q6h prn
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Category D in third trimester of pregnancy; caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
Treatment for significant oral and/or laryngeal edema.
For symptomatic relief of symptoms caused by release of histamine.
25-50 mg PO/IV/IM q6h
5 mL of diphenhydramine elixir as oral swish q2h prn
5 mg/kg/d PO/IV/IM divided qid
Potentiates effect of CNS depressants; because of alcohol content, do not give syrup dosage form to patient taking medications that can cause disulfiramlike reactions
Documented hypersensitivity; MAOIs
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction; first trimester of pregnancy
Gardner DG. Injury to the oral mucous membranes caused by the common houseplant, dieffenbachia. A review. Oral Surg Oral Med Oral Pathol. Nov 1994;78(5):631-3. [Medline].
Lin TJ, Hung DZ, Hu WH, Yang DY, Wu TC, Deng JF. Calcium oxalate is the main toxic component in clinical presentations of alocasis macrorrhiza (L) Schott and Endl poisonings. Vet Hum Toxicol. Apr 1998;40(2):93-5. [Medline].
Zhong LY, Wu H. [Current researching situation of mucosal irritant compontents in Araceae family plants]. Zhongguo Zhong Yao Za Zhi. Sep 2006;31(18):1561-3. [Medline].
Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057. [Medline]. [Full Text].
Cheeke PR. Endogenous toxins and mycotoxins in forage grasses and their effects on livestock. J Anim Sci. Mar 1995;73(3):909-18. [Medline]. [Full Text].
Fochtman FW, Manno JE, Winek CL, Cooper JA. Toxicity of the genus Dieffenbachia. Toxicol Appl Pharmacol. Jul 1969;15:38-45. [Medline].
Jaspersen-Schib R, Theus L, Guirguis-Oeschger M, Gossweiler B, Meier-Abt PJ. [Serious plant poisonings in Switzerland 1966-1994. Case analysis from the Swiss Toxicology Information Center]. Schweiz Med Wochenschr. Jun 22 1996;126(25):1085-98. [Medline].
Krenzelok EP, Jacobsen TD, Aronis JM. Plant exposures: a state profile of the most common species. Vet Hum Toxicol. Aug 1996;38(4):289-98. [Medline].
Lampe KF. AMA Handbook of Poisonous and Injurious Plants. AMA; 1985:1-6, 72.
Loretti AP, da Silva Ilha MR, Ribeiro RE. Accidental fatal poisoning of a dog by Dieffenbachia picta (dumb cane). Vet Hum Toxicol. Oct 2003;45(5):233-9. [Medline].
Manríquez O, Varas J, Ríos JC, Concha F, Paris E. Analysis of 156 cases of plant intoxication received in the Toxicologic Information Center at Catholic University of Chile. Vet Hum Toxicol. Feb 2002;44(1):31-2. [Medline].
McIntire MS, Guest JR, Porterfield JF. Philodendron--an infant death. J Toxicol Clin Toxicol. 1990;28(2):177-83. [Medline].
Mitchell JC, Rook A. Botanical Dermatology: Plants and Plant Products. 1979:114-5.
Mrvos R, Dean BS, Krenzelok EP. Philodendron/dieffenbachia ingestions: are they a problem?. J Toxicol Clin Toxicol. 1991;29(4):485-91. [Medline].
Ogzewalla CD, Bonfiglio JF, Sigell LT. Common plants and their toxicity. Pediatr Clin North Am. Dec 1987;34(6):1557-98. [Medline].
Pamies RJ, Powell R, Herold AH, Martinez J III. The dieffenbachia plant. Case history. J Fla Med Assoc. Nov 1992;79(11):760-1. [Medline].
Rauber A. Observations on the idioblasts of Dieffenbachia. J Toxicol Clin Toxicol. 1985;23(2-3):79-90. [Medline].
Tagwireyi D, Ball DE. The management of Elephant's Ear poisoning. Hum Exp Toxicol. Apr 2001;20(4):189-92. [Medline].
Watson JT, Jones RC, Siston AM, Diaz PS, Gerber SI, Crowe JB. Outbreak of food-borne illness associated with plant material containing raphides. Clin Toxicol (Phila). 2005;43(1):17-21. [Medline].
plant poisoning, poisonous plant, toxic plants, oxalate crystals, oxalate exposures, Philodendron, Dieffenbachia, Anthurium, Anthurium species, Arum, Araceae, Arisaema species, Caladium, Caladium bicolor, Calla lily, Zantedeschia species, Chinese evergreen, Aglaonema species, Dieffenbachia, Dieffenbachia species, Jack-in-the pulpit, Arisaema triphyllum, Monstera, Ceriman, Monstera deliciosa, Nephthytis, Syngonium podophyllum, Philodendron, Philodendron species, Pothos or Hunter's robe, Epipremnum aureum, skunk cabbage, Symplocarpus foetidus
Jason F Kearney, MD, Consulting Staff, Department of Emergency Medicine, Emergency Medicine Associates, PC, Southwest Washington Medical Center
Jason F Kearney, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
William K Chiang, MD, Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center
William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Miguel C Fernández, MD, FAAEM, FACEP, FACMT, Associate Clinical Professor; Medical and Managing Director, South Texas Poison Center, Department of Surgery/Emergency Medicine and Toxicology, University of Texas Health Science Center at San Antonio
Miguel C Fernández, MD, FAAEM, FACEP, FACMT is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, Society for Academic Emergency Medicine, and Texas Medical Association
Disclosure: Nothing to disclose.
John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.
Michael Hodgman, MD, Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare
Michael Hodgman, MD is a member of the following medical societies: American College of Medical Toxicology, American College of Physicians, Medical Society of the State of New York, and Wilderness Medical Society
Disclosure: Nothing to disclose.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.
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