eMedicine Specialties > Emergency Medicine > Toxicology

Plant Poisoning, Phytophototoxins

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
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

Updated: Sep 23, 2008

Introduction

Background

Phytophotodermatitis (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.

Pathophysiology

PPD 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.

Frequency

United States

Incidence 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.

International

No difference exists between US and international occurrence.

Mortality/Morbidity

Significant long-term skin changes (hyperpigmentation, scarring) can occur with chronic exposure.

Race

No racial predisposition is demonstrated. Fair-skinned individuals are more frequently reported.

Clinical

History

PPD often occurs in linear and odd patterns, including "handprints."

• A phototoxic reaction can result from contact with a specific plant via skin exposure, or less commonly, ingestion, followed by exposure to sunlight.
• Symptoms usually occur within 24-48 hours following sunlight exposure.
• Symptoms are frequently described as an initial burning pain and erythema, followed by blistering. Blistering may occur within 10 minutes.
• Pruritus is uncommon, distinguishing PPD from allergic phytodermatitis (eg, toxicodendron dermatitis).

Physical

• A usually sharp demarcation between normal covered and abnormal exposed skin
• Initial nonpruritic erythema of exposed areas
• Development of edema, leading to vesicles and/or bullae
• Possible desquamation
• Resultant dense hyperpigmentation from melanocytic response

Causes

PPD 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.

Differential Diagnoses

Dermatitis, Atopic
Dermatitis, Contact
Sunburn

Other Problems to Be Considered

Actinic prurigo
Allergic contact dermatitis to airborne substances
Hydroa aestivalis and vacciniforme
Chronic actinic dermatitis
Porphyria cutanea tarda
Protoporphyria
Polymorphous light eruption
Solar urticaria

Workup

Laboratory Studies

• PPD is a clinical diagnosis. No serum level for psoralens is available or appropriate. Clinical presentation is delayed and systemic clearance of psoralens is complete.

Other Tests

• With yeast inhibition technique, plant extract is used to evaluate for presence of psoralens.
• In individuals in whom the diagnosis is in question, referral to a dermatologist for photo-patch testing may be warranted. Testing should include sunscreens, pesticides, and plant allergens.

Procedures

• In individuals in whom the diagnosis is in question, referral to a dermatologist for a skin biopsy may be warranted. A skin biopsy may demonstrate epidermal hyperkeratosis, "sunburn cells," and an inflammatory cell infiltrate. An increase in melanocytes is seen.

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.

Dosing

Adult

Apply sparingly bid and rub in

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity; sunburns

Precautions

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.

Dosing

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%)

Interactions

None reported

Contraindications

Documented hypersensitivity; viral, fungal, and bacterial skin infections

Precautions

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.

Dosing

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

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

Contraindications

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

Precautions

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.

Dosing

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

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

Contraindications

Documented hypersensitivity; GI bleeding or renal insufficiency

Precautions

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)

Follow-up

Further Inpatient Care

• In general, a phototoxic exposure is self-limited and subsides within a week if further insult is avoided.
• If symptoms persist or worsen instead of improving, other illnesses, such as the primary light disorders, should be considered and further evaluation is warranted by a dermatologist.

Deterrence/Prevention

• Limit or avoid contact with the specific plant.
• Limit sun exposure.

Complications

• Long-term exposure and severe reactions may result in hyperpigmentation requiring continued topical steroid treatment.

Prognosis

• Significant long-term skin changes (hyperpigmentation, scarring) can occur with chronic exposure.

Patient Education

• Patients should be educated regarding plants that produce phytophototoxicity in order to avoid skin exposure. Patients may be counseled to wear gloves and skin coverings when their work necessitates ongoing exposure to these plant oils and to the sun.

Miscellaneous

Medicolegal Pitfalls

• Failure to recognize systemic photosensitization caused by exposure to plant furocoumarins and the use of common drugs (eg, tetracycline, minocycline, doxycycline, chlorpromazine, chlorothiazide diuretics, sulfonamides, nalidixic acid, griseofulvin, sulfonylureas)
• Once possibility of an exogenous light photosensitizer has been ruled out, failure to consider primary light disorders such as porphyria and collagen vascular disorders with polymorphous light eruption

References

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Keywords

phytophotodermatitis, PPD, photosensitization, phytophotosensitivity, photosensitive reaction, furocoumarins, psoralens, Umbelliferae, Rutaceae, Moraceae, Compositae, Ranunculaceae, perfume-induced berloque dermatitis, ultraviolet light, UV, UVA , UV-A

Contributor Information and Disclosures

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, MD, MS, DTM&H, FACEP, FAAEM 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
Disclosure: Nothing to disclose.

Coauthor(s)

Thomas Joseph Lydon, MD, PhD, Consulting Staff, Section of Emergency Medicine, Dartmouth-Hitchcock Medical Center
Disclosure: Nothing to disclose.

William H Shoff, MD, DTM&H, Director, PENN Travel Medicine, Associate Professor, Department of Emergency Medicine, Hospital of the University of Pennsylvania
William H Shoff, MD, DTM&H is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene, International Society of Travel Medicine, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Glaxo Smith Kline Consulting fee Consulting; Glaxo Smith Kline Honoraria Speaking and teaching

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, ABAT, Director of Pharmacy, Sacred Heart Hospital
John T VanDeVoort, PharmD, ABAT is a member of the following medical societies: American Academy of Clinical Toxicology and 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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