You are in: eMedicine Specialties > Emergency Medicine > TOXICOLOGY Plant Poisoning, PhytophototoxinsArticle Last Updated: Sep 23, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 10
  Author: Suzanne Moore Shepherd, MD, MS, DTM&H, FACEP, FAAEM, Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania; Director of Education and Research, PENN Travel Medicine Suzanne Moore Shepherd is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, and Wilderness Medical Society Coauthor(s): Thomas Joseph Lydon, MD, PhD, Consulting Staff, Section of Emergency Medicine, Dartmouth-Hitchcock Medical Center; William H Shoff, MD, DTM&H, Director, PENN Travel Medicine, Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania Editors: 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; John T VanDeVoort, PharmD, ABAT, Director of Pharmacy, Sacred Heart Hospital; Michael Hodgman, MD, Assistant Clinical Professor of Medicine, Department of Emergency Medicine, Bassett Healthcare; 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; 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 Author and Editor Disclosure Synonyms and related keywords: phytophotodermatitis, PPD, photosensitization, phytophotosensitivity, photosensitive reaction, furocoumarins, psoralens, Umbelliferae, Rutaceae, Moraceae, Compositae, Ranunculaceae, perfume-induced berloque dermatitis, ultraviolet light, UV, UVA , UV-A INTRODUCTIONSection 2 of 10
  BackgroundPhytophotodermatitis (PPD) is a photosensitive dermal reaction induced by exposure to certain plants with subsequent exposure to sunlight. Both components (plant and light) are required; neither agent alone can cause PPD. PathophysiologyPPD can occur through ingestion of the plant or, more commonly, through topical contact. Furocoumarins (psoralens) are the major photoreactive essential plant oils involved in PPD reaction. Plants are thought to produce furocoumarins for disease resistance. Members of plant families Apiaceae, Rutaceae, Moraceae, Rosaceae, Asteraceae, Brassicaceae, Clusiaceae, Convolvulaceae, Anacardiaceae, Fabaceae, and Ranunculaceae are noted to cause PPD reaction. Common plants implicated in these families include celery, giant hogweed, angelica, parsnip, fennel, dill, anise, parsley, lime, lemon, rue, fig, mustard, scurf pea, and chrysanthemums. Oil of bergamot, extracted from the rind of fresh bergamot oranges (Citrus bergamia), is commonly used to scent commercial perfumes and colognes. Perfume-induced berloque dermatitis is a specific form of PPD reaction; areas of skin reaction correspond to areas exposed to perfume. Exposure to certain wavelengths of ultraviolet A (UV-A) light enables furocoumarin to absorb the energy, thereby altering reactivity of the molecule and causing the molecule to attain a high-energy state. The activated molecules form photoaddition products with DNA pyrimidine bases and result in epidermal cell nucleic acid damage (type I reaction). Activated furocoumarins can also produce oxygen, superoxide, and hydroxy radicals, which cause cellular membrane damage (type II reaction). Both mechanisms result in cellular dysfunction and tissue destruction. When acute, the process is phototoxic. Chronic presentation of PPD involves a photoallergic response; light-activated plant products act as haptens and produce a cell-mediated hypersensitivity response. Psoralens may not be primarily involved in this mechanism of injury. Phytophototoxicity is amplified by humidity and perspiration. The phototoxic inflammatory eruption usually appears 24 hours after exposure and peaks within 48-72 hours. Initial burning erythema is followed by blistering. FrequencyUnited StatesIncidence varies per population and exposure. Individuals who handle produce or receive significant sunlight exposure (eg, field workers, farmers, gardeners, grocery workers, bartenders, vegetarians, persons who use tanning salons) are at an increased risk. Cases of PPD more commonly occur in late spring and summer when furocoumarins are found in increased concentration in plants and when individuals experience increased UV exposure. InternationalNo difference exists between US and international occurrence. Mortality/MorbiditySignificant long-term skin changes (hyperpigmentation, scarring) can occur with chronic exposure. RaceNo racial predisposition is demonstrated. Fair-skinned individuals are more frequently reported. CLINICALSection 3 of 10
HistoryPPD often occurs in linear and odd patterns, including "handprints."
Physical
CausesPPD is induced by exposure to certain plants with subsequent exposure to sunlight. PPD can occur through ingestion of the plant or, more commonly, through topical contact. DIFFERENTIALSSection 4 of 10
Dermatitis, Atopic Dermatitis, Contact Sunburn
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| Drug Name | Hydroquinone (Claripel, Eldoquin-Forte, Solaquin-Forte) |
|---|---|
| Description | Suppresses melanocyte metabolic processes, especially enzymatic oxidation of tyrosine to 3,4-dihydroxyphenylamine. Exposure to sun reverses effects and causes repigmentation. |
| Adult Dose | Apply sparingly bid and rub in |
| Pediatric Dose | <12 years: Not recommended >12 years: Administer as in adults |
| Contraindications | Documented hypersensitivity; sunburns |
| Interactions | None reported |
| 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 |
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
| Drug Name | Hydrocortisone (Cortaid, Cortizone) |
|---|---|
| Description | 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 Dose | Apply 1-2.5% cream or ointment sparingly bid/qid to affected areas |
| Pediatric Dose | Apply 0.5-1% cream or ointment to affected areas bid/qid; limit use to least potent agent (eg, 0.5%) |
| Contraindications | Documented hypersensitivity; viral, fungal, and bacterial skin infections |
| Interactions | None reported |
| 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 |
| Drug Name | Prednisone (Deltasone, Meticorten, Orasone) |
|---|---|
| Description | 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 Dose | 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 Dose | Administer as in adults |
| Contraindications | Documented hypersensitivity; viral, fungal, connective tissue, or tubercular skin infections; peptic ulcer disease; hepatic dysfunction; GI bleeding or ulceration |
| Interactions | 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 |
| 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 |
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.
| Drug Name | Indomethacin (Indocin) |
|---|---|
| Description | Rapidly absorbed; metabolism occurs in liver by demethylation, deacetylation, and glucuronide conjugation; inhibits prostaglandin synthesis. |
| Adult Dose | 25-50 mg PO bid/tid 75 mg SR/PO bid; not to exceed 200 mg/d |
| Pediatric Dose | 1-2 mg/kg/d PO divided bid/qid; not to exceed 4 mg/kg/d or 150-200 mg/d |
| Contraindications | Documented hypersensitivity; GI bleeding or renal insufficiency |
| Interactions | 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 |
| 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) |
Plant Poisoning, Phytophototoxins excerpt
Article Last Updated: Sep 23, 2008
