Resin Poisoning Treatment & Management
- Author: Hagop A Isnar, MD, FACEP; Chief Editor: Asim Tarabar, MD more...
Prehospital Care
- Plant parts or information regarding surroundings obtained by prehospital providers may be helpful in identifying the suspected toxin.
- Rinse mouth in cases of mucosal irritation to help alleviate symptoms.
- Generally, induced vomiting with ipecac syrup is not encouraged, particularly in cases with potential for altered mental status.
Emergency Department Care
Airway, breathing, and circulation must, above all else, be ensured. Remove any remaining toxin. Ipecac syrup is not recommended. Gastric lavage is unlikely to be effective for removal of plant parts. Activated charcoal may be of benefit, particularly if administered within the first several hours; however, it may be of little benefit with rapidly absorbed substances such as teas.
Hemodialysis has not been proven clinically effective in removing any plant toxin.
Carefully monitor urine output in systemically ill patients because many plant toxins result in GI fluid losses and/or third-spacing of fluid.
Toxicodendron species
An estimated 70% of the population are sensitized to allergens found in the Toxicodendron species, which include poison ivy (see first and second images below), poison oak (see third image below), and poison sumac (see last image below).
Poison ivy. Photo by Cornell University Poisonous Plants Informational Database.
Poison ivy. Photo from the Centers for Disease Control and Prevention.
Poison oak. Photo by Cornell University Poisonous Plants Informational Database.
Poison sumac. Photo by Cornell University Poisonous Plants Informational Database. These plants cause potentially severe contact dermatitis. The allergenic substance of Toxicodendron species is found in the milky white sap that is distributed throughout the plant, seed, flowers, and berries. A unique characteristic of the emulsion found in all Toxicodendron species is the color change from milky white to black lacquer upon exposure to air for several minutes. This spot test is not recommended for routine identification because of inherent risk of exposure (see Plant Poisoning, Toxicodendron).
Contact dermatitis develops within 48 hours for most exposures. Highly sensitized individuals develop eruptions within 8 hours. Eruptions often appear in a linear pattern, indicating that a portion of bruised plant was rubbed across the skin when handled or trampled.
Poison oak rash. This photograph depicts an individual's arm with a blistering poison oak rash. Note the linear pattern to the lesions. Hardin Library for the Health Sciences, University of Iowa Public Domain Picture (http://www.lib.uiowa.edu/haRDIN/MD/cdc/4484.html) and Centers for Disease Control and Prevention. Symptoms at presentation range from mild erythema to papules, vesicles, and bullae. Although once believed to contain the allergen, vesicular fluid cannot transmit contact dermatitis. Systemic distribution of toxin may cause diffuse urticaria or erythema multiforme.
In mild cases involving only erythema and papules, a topical lotion of calamine or steroid cream and an oral antihistamine may be used.
Severe cases require more aggressive therapy. Topical therapy for such cases includes the following:
- Aluminum sulfate (1:10 diluted in water) compressed for 30 minutes 3 times a day to dry blisters and relieve itching
- Potassium permanganate soaks to dry blisters (one-half tablespoon in a tub of water for 20 min/d)
In severe cases, oral corticosteroids may be required and should be tapered over 2-3 weeks. A shorter duration of therapy is associated with rebound dermatitis.
Symptoms in severe cases should be cleared within 3 weeks; symptoms in milder cases may last only 10 days.
Possible sequelae include hyperpigmentation over the area of eruption.
After contact with poison ivy, washing the exposed area as well as hands and clothes with soap and water within 30 minutes of exposure greatly reduces the risk of developing contact dermatitis.
Water hemlock
Cicuta maculate and most other species of Cicuta are similar in appearance and grow to heights of 6 ft. The sap is a yellow oily compound with a parsnip scent and contains cicutoxin, a long chained aliphatic alcohol. Cicutoxin is distributed throughout the plant, with the highest concentration in the tuberous roots. One mouthful of root is sufficient to kill a grown man, and toxicity has been documented after dermal contact. These plants are found in wet swamplands throughout the United States and are the most toxic plants in Alaska (see image below).
Hemlock. Photo by Cornell University Poisonous Plants Informational Database. Cicutoxin has a parasympathomimetic action when ingested and produces symptoms in 15-60 minutes. Muscarinic actions manifest as abdominal pain, vomiting, diarrhea, trismus, and hypersalivation. More central effects manifest as central nervous system depression, respiratory distress, and possibly tonic-clonic seizures. Death is usually secondary to respiratory arrest.
Pay particular attention to the patient's airway and respiratory status. Treatment is mostly supportive. Benzodiazepines are recommended for control of seizures. Treatment with anticholinergics has not been proven effective in animal models.
Consider creatine kinase measurements; the combination of seizures with resultant rhabdomyolysis and gastrointestinal fluid losses place the patient at risk for oliguric renal failure.
Given the GI losses, closely monitoring the patient's fluid balance is needed.
Chinaberry
Melia azedarach is a tree that may grow to a height of 50 ft. The leaves are serrated with 2-inch long leaflets. The flowers are scented, purplish, and grow in clusters. Chinaberry trees produce yellow berries that persist after the leaves are shed; they contain 3-5 smooth black seeds. Chinaberry trees grow in the South from Virginia to Florida to Texas and Hawaii.
A recently identified neurotoxin (tetranortriterpene) and an unidentified gastroenteric toxin are concentrated in the berry and bark of chinaberry. Ingestion of 6-8 berries has been reported to cause fatality in a young child.
Prolonged latent period is followed by development of mental confusion, ataxia, dizziness, and stupor. Some patients may develop intense vomiting and bloody diarrhea, which results in hypovolemic shock. Reports of respiratory depression, seizures, and paralysis also exist. In some autopsies, fatty degeneration of the liver has been observed.
Supportive care with fluid and electrolyte replacement is indicated.
Given the possibility of hepatic fatty degeneration, monitoring liver function is important.
Daphne
Daphne are deciduous round shrubs growing to heights of 4-5 ft. Elliptical leaves with purple or white flowers grow in clusters before the appearance of leaves. Although most exposure is due to the yellow fruit and pits of daphne, the entire plant is poisonous. Ingestion of only a few daphne fruits can be fatal to a young child. Daphne are cultivated throughout the United States and are naturalized to the northeastern United States and Canada (see image below).
Daphne. Photo by Cornell University Poisonous Plants Informational Database. Ingestion of daphne causes vesication and edema of the mouth, lips, and pharynx with secondary hypersalivation and dysphagia. Subsequent symptoms include extreme thirst, abdominal pain, vomiting, and bloody diarrhea.
Daphnetoxin may cause organ damage, usually due to hypovolemia and electrolyte imbalance; therefore, the kidneys are particularly at risk for damage secondary to acute tubular necrosis.
Fluid and electrolyte balance is critical to prevent a potentially lethal outcome.
Consultations
Consult a medical toxicologist and/or regional poison center for further assistance.
Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol (Phila). Dec 2007;45(8):815-917. [Medline].
Watson WA, Litovitz TL, Rodgers GC. 2004 Annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 2005;23(5):589-666. [Medline].
Arena J. Plants That Poison. Emerg Med. Jun 15 1989;20-64.
Braitberg G, et al. Toxic plant ingestions. In: Wilderness Medicine. 1995:862-89.
Brodell RT, Williams L. Taking the itch out of poison ivy. Are you prescribing the right medication?. Postgrad Med. Jul 1999;106(1):69-70. [Medline].
Brook I, Frazier EH, Yeager JK. Microbiology of infected poison ivy dermatitis. Br J Dermatol. May 2000;142(5):943-6. [Medline].
DiPalma JR. Poisonous plants. Am Fam Physician. Apr 1984;29(4):252-4. [Medline].
Evans FJ, Schmidt RJ. Plants and plant products that induce contact dermatitis. Planta Med. Apr 1980;38(4):289-316. [Medline].
Geehr E. Common toxic plant ingestions. Emerg Med Clin North Am. Aug 1984;2(3):553-62. [Medline].
Guin JD. Treatment of toxicodendron dermatitis (poison ivy and poison oak). Skin Therapy Lett. Apr 2001;6(7):3-5. [Medline].
Hardin JW, Arena J. Human Poisonings from Native and Cultivated Plants. 1974:23, 93, 100, 107.
Kunkel DB, Spoerke DG. Evaluating exposures to plants. Emerg Med Clin North Am. Feb 1984;2(1):133-44. [Medline].
Lampe KF, McCann MA. AMA Handbook of Poisonous and Injurious Plants. 1985:56, 68, 115.
Lee NP, Arriola ER. Poison ivy, oak, and sumac dermatitis. West J Med. Nov-Dec 1999;171(5-6):354-5. [Medline].
Litovitz TL, Klein-Schwartz W, Caravati EM, et al. 1998 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 1999;17(5):435-87. [Medline].
Litovitz TL, Smilkstein M, Felberg L, et al. 1996 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med. Sep 1997;15(5):447-500. [Medline].
McGovern TW, LaWarre SR, Brunette C. Is it, or isn't it? Poison ivy look-a-likes. Am J Contact Dermat. Jun 2000;11(2):104-10. [Medline].
McKenzie RA, ALIA. Plant poisoning? Which plant?!. Aust Vet J. Jun 1993;70(6):201-2. [Medline].
Patterson SE, Williams JV, Marks JG Jr. Prevention of sodium lauryl sulfate irritant contact dermatitis by Pro- Q aerosol foam skin protectant. J Am Acad Dermatol. May 1999;40(5 Pt 1):783-5. [Medline].
Rondeau ES, Everson GW, Savage W, Rondeau JH. Plant nurseries: a reliable resource for plant identification?. Vet Hum Toxicol. Dec 1992;34(6):544-6. [Medline].
Tilton BR, Ryan ME, Edson LY, Martyak GG. Plant ingestions in children. Pa Med. May 1985;88(5):45-9. [Medline].

