Resin Poisoning Treatment & Management

  • Author: Hagop A Isnar, MD, FACEP; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Feb 1, 2011
 

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.
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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 Poison ivy. Photo by Cornell University Poisonous Plants Informational Database. Poison ivy. Photo from the Centers for Disease ConPoison ivy. Photo from the Centers for Disease Control and Prevention. Poison oak. Photo by Cornell University Poisonous Poison oak. Photo by Cornell University Poisonous Plants Informational Database. Poison sumac. Photo by Cornell University PoisonouPoison 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 indiviPoison 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 PlaHemlock. 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 PlanDaphne. 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.

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Consultations

Consult a medical toxicologist and/or regional poison center for further assistance.

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Contributor Information and Disclosures
Author

Hagop A Isnar, MD, FACEP  Department of Emergency Medicine, Crouse Hospital

Hagop A Isnar, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Charles McKay, MD  Chief, Toxicology Section, Department of Traumatology and Emergency Medicine, Hartford Hospital

Charles McKay, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, and American College of Medical Toxicology

Disclosure: Nothing to disclose.

Specialty Editor Board

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT  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 Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Clinical Toxicologists, 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.

Chief Editor

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

References
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  17. 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].

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Hemlock. Photo by Cornell University Poisonous Plants Informational Database.
Daphne. Photo by Cornell University Poisonous Plants Informational Database.
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.
Poison ivy rash. This photograph shows an individual's arm with a blistering poison ivy rash. Hardin Library for the Health Sciences, University of Iowa Public Domain Picture (http://www.lib.uiowa.edu/haRDIN/MD/cdc/4483.html) and Centers for Disease Control and Prevention.
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.
 
 
 
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