Pathophysiology and Clinical Manifestations

Transmitted radiation <300 nm is largely absorbed in the epidermis, whereas that >300 nm is mostly transmitted to the dermis after variable epidermal melanin absorption. Children vary in susceptibility to UV radiation, depending on their skin type (amount of pigment) (Table 648-1). Immediate pigment darkening is due to UVA radiation–induced photo-oxidative darkening of existing melanin and its transfer from melanocytes to keratinocytes. This effect generally lasts for a few hours and is not photoprotective. UVB-induced effects appear 6-12 hr after initial exposure and reach a peak in 24 hr. Effects include redness, tenderness, edema, and blistering (Fig. 648-1). Reactive oxidation species generated by UVB induce keratinocyte membrane damage and are involved in the pathogenesis of sunburn. A portion of the vasodilatation seen in UVB-induced erythema is mediated by prostaglandins E₂ and F₂. Delayed melanogenesis as a result of UVB radiation begins in 2-3 days and lasts several days to a few weeks. Manufacture of new melanin in melanocytes, transfer of melanin from melanocytes to keratinocytes, increase in size and arborization of melanocytes, and activation of quiescent melanocytes produce delayed melanogenesis. This effect reduces skin sensitivity to development of UV-induced erythema. The amount of protection afforded depends on the skin type of the patient. Additional effects and possible complications of sun exposure include increased thickness of the stratum corneum, recurrence or exacerbation of herpes simplex labialis, lupus erythematosus, and many other conditions (Table 648-2).

Table 648-1 SUN-REACTIVE SKIN TYPES

Figure 648-1 Sunburn. Well-demarcated, severe erythema.

Treatment

Acute severe sunburn should be managed with cool compresses. Topical corticosteroids and oral prostaglandin inhibitors such as ibuprofen and indomethacin may decrease erythema and pain but must be administered preradiation or early in the course of the sunburn. Once peak erythema has been reached, little help is afforded by these medications. Proprietary preparations containing topical anesthetics are relatively ineffective and potentially hazardous because of their propensity to cause contact dermatitis. A bland emollient is effective in the desquamative phase.

Prognosis and Prevention of Sequelae

The long-term sequelae of chronic and intense sun exposure are not often seen in children, but most individuals receive >50% of their lifetime UV dose by age 20 yr. Therefore, pediatricians have a pivotal role in educating patients and their parents about the harmful effects, potential malignancy risks, and irreversible skin damage that result from unduly prolonged exposure to the sun and tanning lights. Premature aging, senile elastosis, actinic keratoses, squamous and basal cell carcinomas, and melanomas all occur with greater frequency in sun-damaged skin. In particular, blistering sunburns in childhood and adolescence significantly increase the risk for development of malignant melanoma. Sun protection is best achieved by sun avoidance, which includes minimizing time in the midday sun (10 AM to 3 PM), staying in the shade, and wearing protective clothing including wide-brimmed hats. Protection is enhanced by a wide variety of sunscreen agents. Physical opaque sunscreens (zinc oxide, titanium dioxide) block UV light, whereas chemical sunscreens (para-aminobenzoic acid [PABA], PABA esters, salicylates, benzophenones, dibenzoylmethanes [avobenzone], cinnamates, terephthalylidene dicamphor sulfonic acid [ecamsule]) absorb damaging radiation. The benzophenones and dibenzoylmethanes provide protection in both the UVA and UVB ranges. Stabilizers such as octocrylene and diethyl 2,6-naphthalate increase the time of function of the dibenzoylmethanes. Ecamsule and drometrizole trisiloxane are UVA sunscreens. Vitamins C and E added to sunscreen may also be beneficial in reduction of the formation of reactive oxygen species. Children with skin types I to III (see Table 648-1) require sunscreens with a sun protection factor (SPF) of at least 15, although the higher SPF, the more protection. SPF is defined as the minimal dose of sunlight required to produce cutaneous erythema after application of a sunscreen, divided by the dose required with no use of sunscreen. SPF applies only to UVB protection. UVA rating of sunscreens should be available in the near future.