Photodermatitis

Photodermatitis is an inflammatory skin reaction triggered by ultraviolet or visible light acting on an exogenous photosensitiser, and it is either phototoxic or photoallergic. It presents as an exaggerated sunburn like or eczematous eruption confined to light exposed skin.

Phototoxic reactions are common and dose related, and can occur on first exposure. Photoallergic reactions are less frequent and need prior sensitisation. Medication is the main cause in adults.

Systemic causes include doxycycline and other tetracyclines, fluoroquinolones, amiodarone, thiazides, voriconazole, naproxen and other non-steroidal anti-inflammatory drugs, phenothiazines and retinoids. Topical and contact causes include furocoumarin containing plants (celery, parsnip, lime, giant hogweed), perfume containing bergamot oil, tar, and some sunscreen filters and topical anti-inflammatory drugs.

Pathophysiology.

A photosensitiser absorbs light, mostly ultraviolet A, and generates reactive oxygen species or forms photoproducts that damage cells directly (phototoxicity) or act as haptens that sensitise T cells (photoallergy). Window glass transmits ultraviolet A, so reactions can occur indoors or in a car.

• Erythema, oedema and blistering within hours of sun exposure in a phototoxic reaction, followed by hyperpigmentation.
• Sharp margins on exposed skin: face, V of the neck, dorsal hands and forearms, with sparing of the upper eyelids, under the chin and behind the ears.
• Photoallergic reactions are eczematous and delayed by 24 to 72 hours, and may spread to covered skin.
• Specific patterns: photo onycholysis (tetracyclines), pseudoporphyria with fragile blisters (naproxen, furosemide), and slate grey pigmentation (amiodarone).

Red flags.

• Widespread blistering or facial swelling with systemic upset.
• Blistering with skin fragility and scarring, suggesting porphyria.
• Persistence for weeks after stopping the drug, suggesting persistent light reaction or chronic actinic dermatitis.

• Detailed drug, topical product and plant history, with the timing of exposure and the pattern of sparing.
• Withdrawal of the suspected agent, with improvement over days to weeks.
• Phototesting (minimal erythema dose to ultraviolet A and B) and photopatch testing in persistent or recurrent disease.
• Plasma fluorescence scanning, and urine and faecal porphyrins, when blistering is present.
• Antinuclear and anti-Ro antibodies if lupus is considered. Skin biopsy for unclear cases.

Differential diagnosis. Sunburn, polymorphic light eruption, photoallergic contact dermatitis, cutaneous lupus erythematosus, porphyria cutanea tarda, pellagra, airborne contact dermatitis, phytophotodermatitis and chronic actinic dermatitis.

• Stop or replace the photosensitiser where possible, and avoid sun exposure until the eruption settles. If the drug is essential, use strict protection.
• Photoprotection: broad spectrum sunscreen with a high sun protection factor (50 or more) and strong ultraviolet A protection, protective clothing, hats and shade, with reapplication every 2 hours.
• Cool compresses and emollients. Potent corticosteroid (betamethasone valerate 0.1%) once daily for 5 to 7 days for inflamed areas, avoiding the face where possible and using moderate potency (clobetasone butyrate 0.05%) on the face.
• Prednisolone 0.5 mg/kg/day (usually 30 to 40 mg) for 5 to 7 days for severe, extensive reactions.
• Analgesia: paracetamol 1 g every 4 to 6 hours (maximum 4 g daily) for pain.
• Persistent light reactivity: strict photoprotection, and narrowband ultraviolet B or psoralen with ultraviolet A hardening under specialist supervision.

Monitoring. Review at 1 to 2 weeks and again after stopping the agent. Persistent eruption beyond 6 weeks needs specialist assessment.

Referral and escalation. Refer to a photodermatology service for suspected photoallergy, persistent reactions, or when the diagnosis is unclear.