eMedicine Specialties > Emergency Medicine > Toxicology

Plant Poisoning, Resins: Treatment & Medication

Author: Hagop A Isnar, MD, FACEP, Associate Medical Director, Consulting Staff, Department of Emergency Medicine, Auburn Memorial Hospital
Coauthor(s): Charles McKay, MD, Chief, Toxicology Section, Department of Traumatology and Emergency Medicine, Hartford Hospital
Contributor Information and Disclosures

Updated: Mar 2, 2009

Treatment

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 Media files 3-4), poison oak (see Media file 5), and poison sumac (see Media file 6).

Poison ivy. Photo from the Centers for Disease Co...

Poison ivy. Photo from the Centers for Disease Control and Prevention.

Poison ivy. Photo from the Centers for Disease Co...

Poison ivy. Photo from the Centers for Disease Control and Prevention.


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 indiv...

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.

Poison oak rash. This photograph depicts an indiv...

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 Media file 1).

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 Media file 2).

Daphne. Photo by Cornell University Poisonous Pla...

Daphne. Photo by Cornell University Poisonous Plants Informational Database.

Daphne. Photo by Cornell University Poisonous Pla...

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.

Medication

Medical care of poisoning is primarily symptomatic in nature. Gastric decontamination may benefit by reducing the absorbed dose.

GI decontaminants

These agents are the preferred method when GI decontamination is desired. They are generally mixed and given with a cathartic (eg, 70% sorbitol), except in young pediatric patients in whom electrolyte disturbances may be of concern.


Activated charcoal (Liqui-Char)

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. Does not dissolve in water.
For maximum effect, administer within 30 min of ingesting poison.

Adult

1 g/kg (30-100 g) PO

Pediatric

1-2 g/kg (15-30 g) PO

May inactivate ipecac syrup if used concomitantly; effectiveness of other medications decreases with coadministration; do not mix charcoal with sherbet, milk, or ice cream (decreases adsorptive properties)

Documented hypersensitivity; poisoning or overdosage of mineral acids and alkalies; unprotected airway with absent gag reflex

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not very effective in poisonings of ethanol, methanol, and iron salts; induce emesis before administering activated charcoal; after emesis with ipecac, patient may not tolerate activated charcoal for 1-2 h; can administer in early stages of gastric lavage; without sorbitol, gastric lavage returns are black; monitor for presence of bowel sounds to minimize risk of charcoal ileus

Antihistamines

Competitive histamine antagonists minimize severity of hypersensitivity response.


Diphenhydramine (Benadryl)

For symptomatic relief of symptoms caused by release of histamine in allergic reactions.

Adult

25-50 mg PO q4-6h

Pediatric

5 mg/kg/d PO 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; anticholinergic plant toxicity

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May exacerbate angle-closure glaucoma, hyperthyroidism, peptic ulcer, and urinary tract obstruction; may cause drowsiness


Hydroxyzine (Vistaril, Atarax)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS. Sedating, alternative to diphenhydramine.

Adult

25-50 mg PO q4-6h

Pediatric

2-4 mg/kg/d PO divided q6h

CNS depression may increase with alcohol or other CNS depressants

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Associated with clinical exacerbations of porphyria (may not be safe for patients with porphyria); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness

Benzodiazepines

These agents are used to abort seizures, if present.


Diazepam (Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.

Adult

5-10 mg IV q10-15min until symptoms resolve; not to exceed 30 mg

Pediatric

>30 days to 5 years: 0.2-0.5 mg IV (slowly) q2-5min until symptoms resolve; not to exceed 5 mg
>5 years: 1 mg IV (slowly) q2-5min until symptoms resolve; not to exceed 10 mg

Increases toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohols, and MAOIs

Documented hypersensitivity; acute narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)


Lorazepam (Ativan)

Sedative hypnotic with short onset of effects and relatively long half-life.
By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.
Monitoring patient's blood pressure after administering dose is important. Adjust prn.

Adult

2-8 mg IV/IM; titrate to effect

Pediatric

0.05 mg/kg IV/IM

Toxicity in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates, and MAOIs

Documented hypersensitivity; preexisting CNS depression; hypotension; narrow-angle glaucoma

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease

Corticosteroids

These agents are useful for contact dermatitis.


Prednisone (Deltasone)

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Adult

40-60 mg PO qd; taper over 2-3 wk

Pediatric

1-2 mg/kg PO qd; taper over 2-3 wk

Coadministration with estrogens may decrease prednisone clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity; viral, fungal, tubercular skin, or connective tissue infections; peptic ulcer disease; hepatic dysfunction; GI disease

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use


Methylprednisolone (Solu-Medrol, Depo-Medrol)

Useful to treat inflammatory and allergic reactions. By reversing increased capillary permeability and suppressing PMN activity, may decrease inflammation.
Multiple corticosteroid preparations are available. Widely available in the ED because of its other uses (ie, acute asthma, spinal cord injury) and is supplied in both parenteral and oral formulations and is therefore discussed here as a typical drug of this class.

Adult

2-60 mg PO qd
40-250 mg IV/IM q6h

Pediatric

1-2 mg/kg PO qd
1-2 mg/kg IV/IM q6h

NSAIDs may cause ulcers when taken concurrently; anticholinesterases may increase weakness in patients with myasthenia gravis when taken concurrently with steroids; risk exists of possible viral dissemination with live-virus vaccines

Documented hypersensitivity; some evidence indicates fetal harm from corticosteroids, so benefits and risks should be considered for use during pregnancy; immunosuppressed patients receiving corticosteroids are at risk for dissemination, activation, or certain infections, and this should be considered when prescribing for these patients

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Short-term use of corticosteroids, even in large doses, has minimal harmful effects; long-term usage has multiple adverse effects
Possible complications include hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections

More on Plant Poisoning, Resins

Overview: Plant Poisoning, Resins
Differential Diagnoses & Workup: Plant Poisoning, Resins
Treatment & Medication: Plant Poisoning, Resins
Follow-up: Plant Poisoning, Resins
Multimedia: Plant Poisoning, Resins
References

References

  1. 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].

  2. 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].

  3. Arena J. Plants That Poison. Emerg Med. Jun 15 1989;20-64.

  4. Braitberg G, et al. Toxic plant ingestions. In: Wilderness Medicine. 1995:862-89.

  5. 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].

  6. Brook I, Frazier EH, Yeager JK. Microbiology of infected poison ivy dermatitis. Br J Dermatol. May 2000;142(5):943-6. [Medline].

  7. DiPalma JR. Poisonous plants. Am Fam Physician. Apr 1984;29(4):252-4. [Medline].

  8. Evans FJ, Schmidt RJ. Plants and plant products that induce contact dermatitis. Planta Med. Apr 1980;38(4):289-316. [Medline].

  9. Geehr E. Common toxic plant ingestions. Emerg Med Clin North Am. Aug 1984;2(3):553-62. [Medline].

  10. Guin JD. Treatment of toxicodendron dermatitis (poison ivy and poison oak). Skin Therapy Lett. Apr 2001;6(7):3-5. [Medline].

  11. Hardin JW, Arena J. Human Poisonings from Native and Cultivated Plants. 1974:23, 93, 100, 107.

  12. Kunkel DB, Spoerke DG. Evaluating exposures to plants. Emerg Med Clin North Am. Feb 1984;2(1):133-44. [Medline].

  13. Lampe KF, McCann MA. AMA Handbook of Poisonous and Injurious Plants. 1985:56, 68, 115.

  14. Lee NP, Arriola ER. Poison ivy, oak, and sumac dermatitis. West J Med. Nov-Dec 1999;171(5-6):354-5. [Medline].

  15. 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].

  16. 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].

  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].

  18. McKenzie RA, ALIA. Plant poisoning? Which plant?!. Aust Vet J. Jun 1993;70(6):201-2. [Medline].

  19. 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].

  20. 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].

  21. Tilton BR, Ryan ME, Edson LY, Martyak GG. Plant ingestions in children. Pa Med. May 1985;88(5):45-9. [Medline].

Further Reading

Keywords

plant poisoning resins, resins, plant resins, poison ivy, poison oak, poison sumac, contact dermatitis, glycoresins, oleoresins, urushiols, poisonous plants, poisonous plant exposures, plant toxin, Toxicodendron species, Cicuta maculata, water hemlock, cicutoxin, chinaberry, Melia azedarach, tetranortriterpene, daphne, daphnetoxin, toxic plant ingestion, resin skin exposure

Contributor Information and Disclosures

Author

Hagop A Isnar, MD, FACEP, Associate Medical Director, Consulting Staff, Department of Emergency Medicine, Auburn Memorial 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.

Medical Editor

Miguel C Fernandez, 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 Fernandez, 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, Society for Academic Emergency Medicine, and Texas Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

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.

Managing Editor

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.

CME Editor

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, 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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