eMedicine Specialties > Emergency Medicine > Toxicology
Plant Poisoning, Phytophototoxins: Treatment & Medication
Updated: Sep 23, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Emergency Department Care
- Limit or avoid contact with the specific plant.
- Avoid sun exposure.
- In most cases, history identifies plant exposure.
- Treat inflammatory condition based on severity of symptoms.
- Treat mild reactions with cool wet dressings, topical steroids, and nonsteroidal anti-inflammatory drugs (NSAIDs).
- Severe reactions may require systemic steroids.
- Topical application of 4% hydroquinone cream once or twice daily for several weeks may lessen hyperpigmentation. This is best done in conjunction with a dermatologist.
Consultations
Consultation with a dermatologist may be helpful.
Medication
The goals of pharmacotherapy are to reduce morbidity and prevent complications.
Depigmenting agents
These agents have been shown to be useful in the treatment of phytophototoxins plant poisoning.
Hydroquinone (Claripel, Eldoquin-Forte, Solaquin-Forte)
Suppresses melanocyte metabolic processes, especially enzymatic oxidation of tyrosine to 3,4-dihydroxyphenylamine. Exposure to sun reverses effects and causes repigmentation.
Adult
Apply sparingly bid and rub in
Pediatric
<12 years: Not recommended
>12 years: Administer as in adults
None reported
Documented hypersensitivity; sunburns
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
Application area should not exceed that of face, neck, hands, or arms; protection from the sun with sunscreen concomitantly is essential; sunscreens containing benzophenones preparations appear to afford better protection; may cause burning or stinging sensation after application
Corticosteroids
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Hydrocortisone (Cortaid, Cortizone)
Applied to skin and mucus membranes provides general anti-inflammatory activity via intracellular mechanisms. Absorption from skin and potency depend on modifications to drug structure, vehicle of application, and condition of exposed skin.
Adult
Apply 1-2.5% cream or ointment sparingly bid/qid to affected areas
Pediatric
Apply 0.5-1% cream or ointment to affected areas bid/qid; limit use to least potent agent (eg, 0.5%)
None reported
Documented hypersensitivity; viral, fungal, and bacterial skin infections
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
Prolonged use, application over large surface areas, application of potent steroids, and use of occlusive dressings may increase systemic absorption of corticosteroids and may cause Cushing syndrome, reversible HPA-axis suppression, hyperglycemia, and glycosuria
Prednisone (Deltasone, Meticorten, Orasone)
Immunosuppressant for treatment of autoimmune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and also suppresses lymphocyte and antibody production.
Adult
0.5-2 mg/kg/d PO; taper as condition improves; single morning dose is safer for long-term use, but divided doses have more anti-inflammatory effect
Pediatric
Administer as in adults
Coadministration with estrogens may decrease 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, connective tissue, or tubercular skin infections; peptic ulcer disease; hepatic dysfunction; GI bleeding or ulceration
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
Nonsteroidal anti-inflammatory agents
Although most NSAIDs are used primarily for their anti-inflammatory effects, they are effective analgesics and are useful for the relief of mild to moderate pain.
Indomethacin (Indocin)
Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis.
Adult
25-50 mg PO bid/tid
75 mg SR/PO bid; not to exceed 200 mg/d
Pediatric
1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d
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; may increase PT when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; GI bleeding or renal insufficiency
Pregnancy
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
Precautions
Acute renal insufficiency, hyperkalemia, hyponatremia, interstitial nephritis, and renal papillary necrosis may occur; increases risk of acute renal failure in patients with preexisting renal disease or compromised renal perfusion; reversible leukopenia may occur, (discontinue if leukopenia, granulocytopenia, or thrombocytopenia persists)
More on Plant Poisoning, Phytophototoxins |
| Overview: Plant Poisoning, Phytophototoxins |
| Differential Diagnoses & Workup: Plant Poisoning, Phytophototoxins |
Treatment & Medication: Plant Poisoning, Phytophototoxins |
| Follow-up: Plant Poisoning, Phytophototoxins |
| References |
| « Previous Page | Next Page » |
References
Bansal I, Kerr H, Janiga JJ, Qureshi HS, Chaffins M, Lim HW. Pinpoint papular variant of polymorphous light eruption: clinical and pathological correlation. J Eur Acad Dermatol Venereol. Apr 2006;20(4):406-10. [Medline].
Berkley SF, Hightower AW, Beier RC, et al. Dermatitis in grocery workers associated with high natural concentrations of furanocoumarins in celery. Ann Intern Med. Sep 1986;105(3):351-5. [Medline].
Epstein WL, Epstein JH. Plant induced dermatitis. In: Wilderness Medicine. 3rd ed. 1995:843-61.
Gross TP, Ratner L, de Rodriguez O, et al. An outbreak of phototoxic dermatitis due to limes. Am J Epidemiol. Mar 1987;125(3):509-14. [Medline].
Ivie GW, Holt DL, Ivey MC, et al. Natural toxicants in human foods: psoralens in raw and cooked parsnip root. Science. Aug 21 1981;213(4510):909-10. [Medline].
Juckett G. Plant dermatitis. Possible culprits go far beyond poison ivy. Postgrad Med. Sep 1996;100(3):159-63, 167-71. [Medline].
Klaber R. Phyto-photo-dermatitis. Br J Dermatol. 1943;54:193-211.
Lecha M. Idiopathic photodermatoses: clinical, diagnostic and therapeutic aspects. J Eur Acad Dermatol Venereol. Nov 2001;15(6):499-504; quiz 504-5. [Medline].
Ljunggren B. Severe phototoxic burn following celery ingestion. Arch Dermatol. Oct 1990;126(10):1334-6. [Medline].
Lovell CR. Phytodermatitis. Clin Dermatol. Jul-Aug 1997;15(4):607-13. [Medline].
Mark KA, Brancaccio RR, Soter NA, Cohen DE. Allergic contact and photoallergic contact dermatitis to plant and pesticide allergens. Arch Dermatol. Jan 1999;135(1):67-70. [Medline].
Maso MJ, Ruszkowski AM, Bauerle J, et al. Celery phytophotodermatitis in a chef. Arch Dermatol. Jun 1991;127(6):912-3. [Medline].
Massmanian A. Contact dermatitis due to Euphorbia pulcherrima Willd, simulating a phototoxic reaction. Contact Dermatitis. Feb 1998;38(2):113-4. [Medline].
Moller H. Contact and photocontact allergy to psoralens. Photodermatol Photoimmunol Photomed. Feb 1990;7(1):43-4. [Medline].
Pathak MA. Phytophotodermatitis. Clin Dermatol. Apr-Jun 1986;4(2):102-21. [Medline].
Pathak MA, Kramer DM. Photosensitization of skin in vivo by furocoumarins (psoralens). Biochim Biophys Acta. Nov 19 1969;195(1):197-206. [Medline].
Rhodes LE. Topical and systemic approaches for protection against solar radiation-induced skin damage. Clin Dermatol. Jan-Feb 1998;16(1):75-82. [Medline].
Sasseville D. Phytodermatitis. J Cutan Med Surg. Jul 1999;3(5):263-79. [Medline].
Sharma A, Goel HC. Some naturally occurring phytophototoxins for mosquito control. Indian J Exp Biol. Oct 1994;32(10):745-51. [Medline].
Tunget CL, Turchen SG, Manoguerra AS, et al. Sunlight and the plant: a toxic combination: severe phytophotodermatitis from Cneoridium dumosum. Cutis. Dec 1994;54(6):400-2. [Medline].
White W. Club Med dermatitis. N Engl J Med. Jan 30 1986;314(5):319-20. [Medline].
Wolf R, Oumeish OY. Photodermatoses. Clin Dermatol. Jan-Feb 1998;16(1):41-57. [Medline].
Zeller MP. Beauty with a Bite: Apiaceae (Umbelliferae) the carrot family. Regul Horticult. 1999;25:10-13.
Further Reading
Keywords
phytophotodermatitis, PPD, photosensitization, phytophotosensitivity, photosensitive reaction, furocoumarins, psoralens, Umbelliferae, Rutaceae, Moraceae, Compositae, Ranunculaceae, perfume-induced berloque dermatitis, ultraviolet light, UV, UVA , UV-A
Treatment & Medication: Plant Poisoning, Phytophototoxins