Are You Confident of the Diagnosis?

What you should be alert for in the history

Be alert for an eruption that is localized to photodistributed areas, but not diffuse. Patients typically describe pain more than itch. Upon focused questioning, the patient will report topical plant exposure occurring one to two days prior to the onset of the reaction. The reaction can occur after a single such plant exposure.

Common offending plants include:

  • – lime, lemon, bergamot, burning bush, bitter orange, gas plant, common rue (Rutacease) (Figure 1)

    Continue Reading

  • – carrots, cow parsley, wild chervil, fennel, dill, parsnip, celery (Umbelliferae)

  • – figs (Moraceae)

  • – mustard (Cruciferae)

  • – buttercup (Ranunculceae)

  • – St. John’s wort

Figure 1.

Member of rutacea plant family.

Characteristic findings on physical examination


– Unusual, linear and spotty patches or plaques in areas of sun exposure (Figure 2).

Figure 2.

Phytophotodermatitis of the arm after exposure to rue.

– Lesions are routinely present on the dorsum of the hands, but can be anywhere on sun-exposed skin.


– Early lesions are typically erythematous patches, papules and plaques, with or without vesicles and bullae (Figure 3).

Figure 3.

Phytophotodermatitis of fingers after exposure to lime skin.

– Resolving lesions may only have hyperpigmentation, often in linear configuration, and hyperpigmentation alone may also occur.

Expected results of diagnostic studies

This is a clinical diagnosis. If a biopsy is necessary, it will show necrotic keratinocytes and mild spongiosis in the epidermis, variable edema and an infiltrate of neutrophils, lymphocytes and/or macrophages (depending on stage of lesions) in the dermis, with or without subepidermal blistering. Serologic, genetic, and patch testing are not required to make the diagnosis but may be used to exclude other diseases in the differential diagnosis.

Diagnosis confirmation

The diagnosis is purely clinical, using the distribution, morphology and history. Histology may support the diagnosis, but usually is not necessary. The differential diagnosis includes phototoxicity secondary to other exposures or drugs, profound sun or thermal burn, airborne contact dermatitis, irritant or allergic contact dermatitis, porphyria cutanea tarda, child abuse and herpes simplex virus. Patch and photopatch testing may be used to diagnose or exclude allergic contact dermatitis and photoallergic contact reactions, respectively. Porphyrin levels may be used to exclude porphyria cutanea tarda.

Who is at Risk for Developing this Disease?

Anyone may be at risk, since this is a toxic (not allergic) reaction. However, some occupations have an increased association, particularly those with increased exposure to plants, such as bartenders, gardeners, farmers, grocery store employees, and chefs.

What is the Cause of the Disease?

In phototoxic or photoirritant contact dermatitis, the major chemicals involved are furocoumarins, particularly 8-methoxypsoralen, 4,5,8-trimethylpsoralen, and 5-methoxypsoralen (Bergapten).


Psoralens intercalate into DNA of skin cells and absorb radiation in the ultraviolet A (UVA) range, resulting in DNA cross-linking, ultimately leading to phototoxic damage of keratinocytes.

Systemic Implications and Complications

There are no associated systemic complications.

Treatment Options

– Blisters may be opened sterilely

– Cool soaks and/or compresses as needed.

– Acetaminophen as needed

– Nonsteroidal anti-inflammatory agents as needed

– Opioid pain relievers as needed

– Photoprotection routinely, including protective clothing and broad spectrum sunscreen

– Low to mid-potency topical corticosteroids twice a day as needed; eg, hydrocortisone 2.5% ointment, desonide ointment, hydrocortisone valerate 0.2% ointment (Westcort), triamcinolone 0.1% ointment

– Hydroquinone 2% or 4% cream twice a day for pigmentation

Optimal Therapeutic Approach for this Disease

Since the disease is a toxic reaction, cellular damage and keratinocyte necrosis have irreversibly been initiated by the time of presentation. Therefore, all treatment is aimed at symptomatic relief and prevention of future occurrences. Blisters may be opened sterilely and cool soaks and/or compresses employed as needed for alleviation of pain. Severe pain may be managed with round-the-clock and/or as needed acetaminophen, non-steroidal anti-inflammatory agents, and/or opioid pain relievers.

Prevention involves avoidance of furocoumarin exposures when exposed to sunlight and ample washing of skin after exposure. Photoprotection with protective clothing and broad spectrum sunscreen is necessary for prevention of future occurrences. Photoprotection and sometime bleaching agents are useful for treatment of residual hyperpigmentation.

There is no role for systemic corticosteroids, since the toxic reaction already occurred. However, low to mid-potency topical corticosteroids may be of some benefit to accelerate clearance of lesions.

Patient Management

The patient can be followed up as needed for treatment of residual hyperpigmentation.

Education should be provided for avoidance of future exposures to phytophototoxic agents in the setting of sun exposure and various approaches to photoprotection.

Unusual Clinical Scenarios to Consider in Patient Management

Rarely, systemic phytophotodermatitis has been reported to have occurred from eating celery root via absorption of substantial amounts of psoralens.

What is the Evidence?

Deleo, VA. “Photocontact dermatitis”. Dermatol Ther. vol. 17. 2004. pp. 279-88. (Review of photo-allergic and photo-irritant contact dermatitis, phytophotodermatitis, and photo-patch testing.)

Lugovic, L, Situm, M, Ozanic-Bulic, S, Sjerobabski-Masnec, I. “Phototoxic and photoallergic skin reactions”. Coll Antropol. vol. 31. 2007. pp. 63-7. (Review of drug-induced photosensitivity, photo-allergic and photo-toxic reactions.)

Carlsen, K, Weismann, K. “Phytophotodermatitis in 19 children admitted to hospital and their differential diagnoses: Child abuse and herpes simplex virus infection”. J Am Acad Dermatol. vol. 57. 2007. pp. S88-91. (Case series of phytophotodermatitis that describes clinical features and its differential diagnosis.)

Wagner, AM, Wu, JJ, Hansen, RC, Nigg, HN, Beiere, RC. “Bullous phytophotodermatitis associated with high natural concentrations of furanocoumarins in limes”. Am J Contact Dermat. vol. 13. 2002. pp. 10-4. (Case report of a severe bullous presentation of phytophotodermatitis and the identification of the offending furocoumarins.)

Klaber, RE. “Phytophotodermatitis”. Arch Dis Child. vol. 91. 2006. pp. 385(Case report of a child with widespread blistering phytophotodermatitis after playing in undergrowth.)

(Report of a cross-sectional study of employees at a grocery with high rates of phytophotermatitis, and brief editorial review of phytophotodermatitis.)

Ljunggren, B. “Severe phototoxic burn following celery ingestion”. Arch Dermatol. vol. 126. 1990. pp. 1334-6. (Case report of a severe generalized phytophotodermatitis in a woman that went to a tanning salon 1 hour after eating a large amount of celery.)