ICD-9: 692.70 ○ ICD-10: L56.8
The term photosensitivity describes an abnormal response to sunlight. Cutaneous photosensitivity reactions require absorption of photon energy by molecules in the skin. Energy is either dispersed harmlessly or elicits chemical reactions that lead to clinical disease. Absorbing molecules can be (1) exogenous agents applied topically or systemically, (2) endogenous molecules either usually present in skin or produced by an abnormal metabolism, or (3) a combination of exogenous and endogenous molecules that acquire antigenic properties and thus elicit a photoradiation-driven immune reaction. Photosensitivity disorders occur only in body regions exposed to solar radiation (Fig. 10-1).
Acute photosensitivity; three types:
A sunburn-type response with skin changes simulating a normal sunburn such as in phototoxic reactions to drugs or phytophotodermatitis (PPD).
A rash response with macules, papules, or plaques, as in eczematous dermatitis. These are usually photoallergic in nature.
Urticarial responses are typical for solar urticaria; but urticarial lesions can also occur in erythropoietic porphyria.
Chronic photosensitivity: chronic repeated sun exposures over time result in polymorphic skin changes that have been termed dermatoheliosis (DHe), or photoaging. A classification of skin reactions to sunlight is shown in Table 10-1.
Basics of Clinical Photomedicine
TABLE 10-1SIMPLIFIED CLASSIFICATION OF SKIN REACTIONS TO SUNLIGHT |Favorite Table|Download (.pdf) TABLE 10-1 SIMPLIFIED CLASSIFICATION OF SKIN REACTIONS TO SUNLIGHT
Metabolic and nutritional
Other rare syndromesa
Variations in solar exposure on different body areas.
The main culprit of solar radiation-induced skin pathology is the ultraviolet (UV) portion of the solar spectrum. Ultraviolet radiation (UVR) is divided into two principal types: UVB (290–320 nm), the “sunburn spectrum,” and UVA (320–400 nm) that is subdivided into UVA-1 (340–400 nm) and UVA-2 (320–340 nm). The unit of measurement of sunburn is the minimum erythema dose (MED), which is the minimum UV exposure that produces an erythema 24 h after a single exposure. UVB erythema develops in 6–24 h and fades within 72–120 h. UVA erythema develops in 4–16 h and fades within 48–120 h.
Variations in Sun Reactivity in Normal Persons: Fitzpatrick Skin Phototypes
(Table 10-2). Sunburn is seen most frequently in individuals who have pale white or white skin and a limited capacity to develop inducible, melanin pigmentation (tanning) after exposure to UVR. Basic skin color is divided into white, brown, and black. Not all persons with white skin have the same capacity to develop tanning, and this fact is the principal basis for the classification of “white” persons into four skin phototypes (SPT). The SPT is based on the basic skin color and on a person’s own estimate of sunburning and tanning (Table 10-2).
TABLE 10-2CLASSIFICATION OF FITZPATRICK’S SKIN PHOTOTYPES (SPT) |Favorite Table|Download (.pdf) TABLE 10-2 CLASSIFICATION OF FITZPATRICK’S SKIN PHOTOTYPES (SPT)
|SPT ||Basic Skin Color ||Response to Sun Exposure |
|I ||Pale white ||Burn easily, do not tan |
|II ||White ||Burn easily, tan with difficulty |
|III ||White ||May burn initially but tan easily |
|IV ||Light brown/olive ||Hardly burn, tan easily |
|V ||Brown ||Usually do not burn, tan easily |
|VI ||Black ||Do not burn, become darker |
SPT I persons usually have pale white skin color, blond or red hair, and blue eyes; but, in fact, they may have dark brown hair and brown eyes. SPT I persons sunburn easily with short exposures and do not tan. SPT II persons sunburn easily but tan with difficulty, while SPT III persons may have some sunburn with short exposures but can develop marked tanning. SPT IV persons tan with ease and do not sunburn with short exposures. Persons with constitutive brown skin are termed SPT V and with black skin SPT VI. Note that sunburn depends on the amount of UVR energy absorbed. Thus, with excessive sun exposure, even SPT VI person can have a sunburn.
Acute Sun Damage (Sunburn)
ICD-9: 692.71 ○ ICD-10: L55
Sunburn is an acute, delayed, and transient inflammatory response of normal skin after exposure to UVR from sunlight or artificial sources.
By nature, it is a phototoxic reaction.
Sunburn is characterized by erythema (Fig. 10-2) and, if severe, by vesicles and bullae, edema, tenderness, and pain.
Acute sunburn Painful, tender, bright erythema with mild edema of the upper back with sharp demarcation between the sun-exposed and sun-protected white areas.
Sunburn depends on the amount of UVR energy delivered and the susceptibility of the individual (SPT). It will therefore occur more often around midday, with decreasing latitude, increasing altitude, and decreasing SPT. Thus, the “ideal” setting for a sunburn to occur would be an SPT I individual (highest susceptibility) on Mt. Kenya (high altitude, close to the equator) at noon (UVR is highest). Of course, sunburn can occur at any latitude, but the probability for it to occur decreases with increasing distance from the equator.
Molecules that absorb UVR for UVB sunburn erythema are not known, but damage to DNA may be the initiating event. The mediators that cause the erythema include histamine for both UVA and UVB. In UVB erythema, other mediators include TNF-α, serotonin, prostaglandins, nitric oxide, lysosomal enzymes, and kinins. TNF-α can be detected as early as 1 h after exposure.
Onset depends on intensity of exposure. Pruritus may be severe even in mild sunburn; pain and tenderness occur with severe sunburn.
Some SPT I and II persons develop headache and malaise even after short exposures. In severe sunburn, the patient is “toxic”—with fever, weakness, lassitude, and a rapid pulse rate.
Confluent bright erythema always confined to sun-exposed areas and thus sharply marginated at the border between exposed and covered skin (Fig. 10-2). Develops after 6 h and peaks after 24 h. Edema, vesicles, and even bullae; always uniform erythema and no “rash,” as occurs in most photoallergic reactions. As edema and erythema fade vesicles and blisters dry to crusts, which are then shed.
Distribution. Strictly confined to areas of exposure; sunburn can occur in areas covered with clothing, depending on the degree of UV transmission through clothing, the level of exposure, and the SPT of the person.
Sunburn is frequent on the vermilion border of the lips and can occur on the tongue in mountain climbers who stick their tongue out panting.
“Sunburn” cells in the epidermis (apoptotic keratinocytes); exocytosis of lymphocytes, vacuolization of melanocytes, and Langerhans cells. Dermis: endothelial cell swelling of superficial blood vessels.
Diagnosis and Differential Diagnosis
History of UVR exposure and sites of reaction on exposed areas. Phototoxic erythema: history of medications that induce phototoxic erythema. SLE can cause a sunburn-type erythema. Erythropoietic protoporphyria (EPP) causes erythema, vesicles, edema, and purpura.
Sunburn, unlike thermal burns, cannot be classified on the basis of depth, i.e., first-, second-, and third-degree because 3° burns after UVR do not occur—therefore, there is no scarring. A permanent reaction from severe UV burns is mottled depigmentation, probably related to the destruction of melanocytes, and eruptive solar lentigines (see Fig. 10-23).
SPT I or II should avoid sunbathing, especially between 11 am and 2 pm. Clothing: UV-screening cloth garments. There are now many highly effective topical chemical filters (sunscreens) in lotion, gel, and cream formulations.
Topical. Cool wet dressings and topical glucocorticoids.
Systemic. Acetylsalicylic acid, indomethacin, and NSAIDs.
Bed rest. If very severe, a “toxic” patient may require hospitalization for fluid replacement, prophylaxis of infection.
ICD-9: 692.79 ○ ICD-10: L56.0
Interaction of UVR with a chemical or drug within the skin.
Two mechanisms: phototoxic reactions, which are photochemical reactions and photoallergic reactions, where a photoallergen is formed that initiates an immunologic response and manifests in skin as a type IV immunologic reaction.
The difference between phototoxic and photoallergic eruptions is that the former manifests like an irritant (toxic) contact dermatitis or sunburn and the latter like an allergic eczematous contact dermatitis (see Table 10-3).
TABLE 10-3CHARACTERISTICS OF PHOTOTOXICITY AND PHOTOALLERGY |Favorite Table|Download (.pdf) TABLE 10-3 CHARACTERISTICS OF PHOTOTOXICITY AND PHOTOALLERGY
| ||Phototoxicity ||Photoallergy |
|Clinical presentation ||Sunburn reaction: erythema, edema, vesicles and bullae burning smarting; frequently resolves with hyperpigmentation ||Eczematous lesions, papules, vesicles, scaling, crusting; usually pruritic |
|Histology ||Apoptotic keratinocytes, sparse dermal infiltrate of lymphocytes, macrophages, and neutrophils ||Spongiotic dermatitis, dense, dermal lymphohistiocytic infiltrate |
|Pathophysiology ||Direct tissue injury ||Type IV delayed hypersensitivity response |
|Occurrence after first exposure ||Yes ||No |
|Onset of eruption after exposure ||Minutes to hours ||24–48 h |
|Dosage of agent needed for eruption ||Large ||Small |
|Cross-reactivity with other agents ||Rare ||Common |
|Diagnosis ||Clinical + phototests ||Clinical + phototests + photopatch tests |
Phototoxic Drug-/Chemical-Induced Photosensitivity
ICD-9: 692.79 ○ ICD-10: L56.0
An adverse reaction of the skin that results from simultaneous exposure to certain drugs (via ingestion, injection, or topical application) and to UVR or visible light or chemicals that may be therapeutic, cosmetic, industrial, or agricultural.
Two types of reaction: (1) systemic phototoxic dermatitis, occurring in individuals systemically exposed to a photosensitizing agent (drug) and subsequent UVR, and (2) local phototoxic dermatitis, occurring in individuals topically exposed to the photosensitizing agent and subsequent UVR.
Both are exaggerated sunburn responses (erythema, edema, vesicles, and/or bullae).
Systemic phototoxic dermatitis occurs in all UVR-exposed sites; local phototoxic dermatitis only in the topical application sites.