Solar dermatitis L55.-

Author: Prof. Dr. med. Peter Altmeyer

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Last updated on: 09.11.2023

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dermatitis photoelectrica; Erythema solaris; phototoxic dermatitis; Phototoxic dermatitis; Sunburn

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Frequent, acute, toxic dermatitis as a result of excessive exposure to ultraviolet radiation. It occurs mainly in children and adolescents who are accustomed to the sun and have fair skin and lack experience in exposure to the sun. More than 75% of all sunburns are observed in the age group up to 20 years.

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About 41% of all Germans suffer from dermatitis solaris once a year. In the group of 18-29 year olds the frequency/year was 71%, in the >60 year olds 16%. In the group of <30-year-olds about 25% more than 1x/year had dermatitis solaris.

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Phototraumatic reaction with cytotoxic process by the UVB fraction of light. Although the pathophysiology of thermal burns and dermatitis solaris is similar, the time curve is different. In burns, erythema occurs within a few minutes, in dermatitis solaris this is observed with a time delay within 3-5 hours after UV irradiation with a reactive maximum after 12-24 hours.

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Children and adolescents preferentially affected

Especially for persons with low pigmentation(skin types I and II).

It is more common in spring and summer or after a first stronger exposure to the sun after a longer, missing exposure.

Frequently also when staying in high mountain areas and at the sea (lack of UV-absorbing dust and mist particles). In addition, in these regions, UV reflection by sand, water and snow.

Clinical features
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Dermatitis begins within the first 6 hours, reaches its peak after 12-24 hours and, depending on the intensity of the toxic reaction, subsides after 72 hours.

At the beginning, the skin shows flat (usually large) erythema that is sharply limited to the area of exposure, itchy and painful erythema and sometimes also extensive swelling due to oedema formation and a feeling of heat.

In the case of more severe skin damage, intensive pain symptoms.

Depending on the extent of the damage, formation of small and larger subepithelial blisters.

Healing with crust formation, coarse lamellar desquamation and possibly permanent hyperpigmentation; scarring only in the case of severe damage.

In case of infestation of large skin areas system signs such as: fever, general feeling of illness, desiccation, drop in blood sugar levels.

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Increased risk for the development of epithelial (see carcinoma of the skin below) and melanocytic malignancies (see melanoma malignes)

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Hospitalization is necessary for patients with 2nd degree burns (blistering) of > 10-15% of the KO, for children 5-10% KO. S.u. burns.

External therapy
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In the erythematosus stage: moist compresses, cooling external agents such as creams, lotions and foam sprays (e.g. 0.1% hydrocortisone-17-butyrate cream [e.g. Laticort cream]). In a domestic environment, tap water compresses (moisten a clean cotton cloth) can also be applied. Never use ice or cold packs, as there is a risk of local cold damage. Cooling has an important function in reducing pain.

For severe burns: Short-term medium to strong glucocorticoids as cream or lotion such as 0.1% betamethasone lotio R030, 0.1% hydrocortisone butyrate (e.g. Alfason), 0.25% prednicarbate cream (e.g. Dermatop), 0.1% methylprednisolone cream (e.g. Advantan). This therapeutic approach is based on clinical experience. There is no assured knowledge regarding a positive effect of this therapy!

In the vesiculosum stage: Medium-strength glucocorticoids (see above). Moist compresses, if necessary with antiseptic additives, e.g. polihexanide (Prontosan) or octenidine (Octenisept) to avoid secondary infections, see also burn.

Internal therapy
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Immediately after sun exposure, acetylsalicylic acid (e.g. ASS) once 1 g and vitamin C (e.g. Cebion Tbl.) 400-1000 mg. NSAIDs are no longer generally recommended due to lack of study results. They probably only have an analgesic effect! In severe cases glucocorticoids, systemic p.o. in medium dosage like Prednisolon 40-60 mg/day (e.g. Decortin H), quickly balance out.

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According to a Forsa survey in 2015, 17% never use a sunscreen product, men use it less often than women (14%/21%). 70% of those surveyed do not use intensive sunbathing. 63% protect themselves with clothing or headgear. 36% consistently avoid the sun at lunchtime.

Phytotherapy external
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It is important to know about drugs and products that increase photosensitivity (see phototoxicity below).

Dermatitis solaris can act as a trigger factor for other diseases (see also light dermatoses) - e.g. psoriasis vulgaris, systemic lupus erythematosus.

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  1. Amelot A et al (2014) Phototoxic reaction associated with Malarone (atovaquone/proguanil) antimalarial prophylaxis. J Dermatol 41:346-348
  2. DAK press release: Sunburn. DAK press release 2016
  3. Jaworski K et al (2014) Cutaneous adverse reactions of amiodarone. Med Sci Monit 20: 2369-2372
  4. Lamp HP (2015) Acute phototoxic reaction in a century cyclist. Clin J Sport Med 25:e28
  5. Proksch E et al. (2007) Rational treatment of patients with 1st degree burns. dermatologist 58: 604-610
  6. Zinc A et al (2014) Images in clinical medicine. Phototoxic dermatitis. N Engl J Med 371:559


Please ask your physician for a reliable diagnosis. This website is only meant as a reference.


Last updated on: 09.11.2023