This common discomfort occurs principally in the early summer after exposure on the bathing beaches. Blonds are more susceptible than brunets. The individual reaction varies: in some persons a redness begins rapidly upon exposure and in a few hours assumes a scarlet tint and is associated with local burning and heat, or bleb formation; in others the reaction does not appear until the day following exposure. Mild burns provoke a hot drawn uncomfortable feeling in the skin, which is dry and erythematous. These symptoms will disappear in about twenty-four to thirty-six hours, followed by the deposition of variable amounts of pigment. Severe burns engender great discomfort, of a peculiarly insufferable character, intensely augmented by the slightest body movement. Contact with clothing or bedding is unbearable. The integument is parched and of an angry-red hue. Shock, chills, fever, nausea, tachycardia and a sense of impending dissolution may be present. This syndrome, more or less in its entirety, may persist for a day or two. Toxemia and pain will then begin to subside. Blister formation and a firm edema of the ankles, legs, face and other parts of the body may appear. Sometimes herpes simplex, solar urticaria, or lesions that resemble erythema multiforme appear repeatedly at the same site following each exposure. When the acute symptoms disappear the epidermis desquamates and the pigmentation in the skin is increased. After repeated exposures brunets develop so much pigmentation that they are protected by it against sunburn. Indeed the formation of pigment and hyperkeratosis may be so rapid and give such complete protection that tanning may be the only effect. Sunburn is caused by the ultraviolet
rays from the sun and not by the heat rays, chiefly by
wavelengths between 2970 and 3030 Å. Ultraviolet sensitivity is increased by
heat.
Solar urticaria
has been extensively studied by Kesten and Slatkin. Whereas the erythematogenic
rays of the sun are between 2,900 and 3,200 Å.U., certain bands of the spectrum
in the range of ultraviolet (2,900— .3,900), visible light (3,900-7,700), and
infrared ( 7,700-14,000 Å.U.) may specifically produce solar urticaria. The
symptoms at first are limited to the exposed portions of the body, but later
may become widespread or generalized. Syncope may supervene.
A
variety of substances are known to be photosensitizers. Louis Schwartz lists
the following: coal tar, pitch, asphalt, creosote oil, fluorescein, rhodamine
H., bergamot, figs, buckwheat, India wheat, wild carrot, puncture weed, alsike
clover, St. John's wort, bur clover, bunch grass, lady's thumb, and rabbit
bush.
Although
sunburn is common it cannot be regarded other than as a severe injury of the
skin. It is sometimes the precursor of vitiligo, telangiectasia, herpes
simplex, and lupus erythematosus, whereas infection of the blisters by pyogenic
microorganisms may lead to impetigo, and infection of the hair follicles to
furunculosis.
Some
individuals have strange polymorphic reactions to strong sunlight. One of my
patients develops nodules that last for weeks and show histologic features of
lymphosarcoma. Samuel F. Rosen has a patient who regularly develops a large
patch of herpes simplex on one shoulder that is followed in ten days by an
attack of erythema multiforme. John Lamb described persistent indurated plaques
of erythema that had the histologic features of mycosis fungoides. Papular
prurigo-like eruptions and verrucous changes also occur. Arnold and Brunsting
have reported changes clinically and histologically similar to colloid milium.
Jessner has called attention to lymphocytic infiltrations that clinically
simulate lupus erythematosus but pathologically do not show any liquefaction
degeneration of the basal cell layer, follicular hyperkeratosis or other signs
of lupus erythematosus. Swelling of one ear or vesiculation of the forearm may
result from riding in an automobile with the window open and the forearm
resting on the car door. Repeated exposures cause hyperpigmentation (tanning)
and hyperkeratosis which are protective.
The prevention
of sunburn is accomplished by the application of creams, ointments, oils or
lotions containing physical or chemical parasols. The most effective chemical
parasols are the esters of para-aminobenzoic acid, particularly the glyceryl
ester, the naphthol sulfonates, benzyl salicylate, menthyl salicylate, phenyl
salicylate, sodium salicylate, quinine derivatives, the ester of anthranilic
acid (orthoaminobenzoic acid), and tannic acid. Zinc oxide and bismuth
subcarbonate are examples of physical parasols. There is a definite
relationship between chemical structure and sun-screening efficiency. The best
vehicle is mineral oil or a combination of mineral, sesame and peanut oils.
Glycerol monostearate and cetyl alcohol are valuable emulsifying agents. The
above ingredients absorb ultraviolet radiation, and although their action is
insufficient to prevent the effects of prolonged exposure to the sun
completely, they do materially diminish them. Insoluble pigments in face powders
are also preventive. Large hats and veils are protective, especially if the
latter are red or light in color.
Treatment. The application of an
effective anesthetic cold cream, such