1.3.3 Sunburn

Acute phototoxic dermatitis caused by electromagnetic radiation in the UVB range (280-315/320 nm). Unphysiologically high UVA doses can elicit an erythema by reactive oxygen release too.

It is an acute dermatitis caused by erythematogenic doses of UVB radiation, which is more common in fair-skinned subjects (Fitzpatrick skin types I-II). Highest erythematogenic dose is with 313 nm. More severe cases result in release of pro-inflammatory cytokines (IL-6), prostaglandins (PGE2), isoprostans and leucotrienes (LTB4) into systemic circulation and leading also to systemic symptoms incl. fever. Acute overdosing of UVA (315–400 nm) for example by artificial tanning studio exposure can stimulate release of free oxygen radicals and damage DNA.

In areas direct exposed to UVB light energy the erythema develops.

Unremarkable. Increase of CRP or mild leucocytosis with involvement of large body surface areas.

Apoptosis and necrosis of epidermal keratinocytes is a remarkable sign. Langerhans cells show disfiguring in their cytology by immunostaining (dysfunction) and a decrease in numbers. Edema of the upper dermis and widening of capillaries is typical. Submicroscopically, mutations by cyclobutan dimers develop. Incomplete DNA repair can lead to mutations and persisting clones of keratinocytes which later may develop into in situ carcinoma (actinic keratoses).

It shows a highly variable clinical appearance (just as in acute contact dermatitis): erythema, vesicles or blisters, weeping, crusts, scales. When the exposure was high and the body surface involved large, fever and malaise are to be observed. Complete spontaneous healing is the regular course with some pityriasiform desquamation after a couple of days and hyperpigmentation. In more severe courses, small or large blisters may require special care.

Frequent sunburns and continuous suberythomatogenic doses of UVB, especially in childhood, lead to increased numbers of melanocytic naevi and an increased risk of malignant melanoma and non-melanoma skin cancer later in life. After chronic repeated overexposure of natural or artificial UVB/UVA skin becomes mottled and shows atrophy, discolouring with hyper-and hypopigmentation, teleangiectasia and roughness as well as wrinkling.

• Acute contact dermatitis

• photoallergic or phototoxic reactions (several drugs, natural substances, i.e. Ammi majus and visnaga, Pastinaca sativa, Ruta graveolens)

• diseases provoked by light such as porphyrias

• all types of lupus erythematosus and dermatomyositis

• Erythroderma in psoriasis, atopic dermatitis, ichthyosis, pityriasis rubra pilaris

Prevention: Sun protection factor of > 25, UV protecting glasses, UV protecting dress, sunscreen and shadow, avoiding of exposure between 11 am to 15 pm. Consider light sensitization by drugs and natural substances taken orally or applied to the skin.

Therapy: Immediate removal from solar exposure is essential, shade alone is not enough. Within the first 12 hours, oral non-steroidal anti-inflammatory drugs and class 3 antihistamines with effects on the release of prostaglandines and leukotrienes should be combined. Cooling topical agents (lotions, cold creams) and wet dressings at the beginning, later after 12 to 24 hours topical corticosteroids should be applied. Sometimes a systemic corticosteroid dose single dose of 50 to 100 mg will be helpful. Systemic replacement of fluid loss is recommended.