Sunburn

INTRODUCTION — Sunburn is an acute, transient, inflammatory response of the skin to excessive exposure to ultraviolet (UV) radiation from natural sunlight or artificial sources (eg, tanning beds, phototherapy devices) (picture 1A-B). Both ultraviolet B (UVB; 280 to 320 nm) and ultraviolet A (UVA; 320 to 400 nm) can cause sunburn, but the wavelengths that are the most effective at inducing erythema are in the UVB range [1,2].

Sunburn is a self-limited condition. The acute manifestations usually resolve in three to seven days. However, susceptibility to sunburn is a marker of genetic susceptibility to skin cancer and is associated with an increased risk of melanoma at all ages [3,4]. It is very important that clinicians counsel patients with increased susceptibility to sunburn about sun protection.

This topic will discuss the pathogenesis, clinical manifestations, and management of sunburn. Photosensitivity, photoprotection, and photosensitivity disorders are discussed separately. (See "Overview of cutaneous photosensitivity: Photobiology, patient evaluation, and photoprotection" and "Selection of sunscreen and sun-protective measures" and "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment".)

EPIDEMIOLOGY — Sunburn is common and occurs in individuals with all skin types. In the United States, the estimated sunburn prevalence (≥1 sunburn in the past 12 months) among all adults was approximately 34 percent in 2005, 37 percent in 2010, and 31 percent in 2015 [5]. Prevalences ranging from 20 to 70 percent have been reported in cross-sectional studies in Europe and Australia [6-9].

In the United States, the one-year prevalence of sunburn in African Americans and Hispanic Americans was 13 and 30 percent, respectively [10]. Higher rates of sunburn have been reported in Black people living in the United Kingdom and in Black Africans [11]. In fact, sunburn in Black skin is probably more common than realized. In a study on people of Black African or Black Caribbean heritage living in the United Kingdom, over 50 percent reported a lifetime history of sunburn [12].

Sunburn occurs more frequently among adolescents and young adults. In nation-wide surveys in the United States, approximately 70 percent of adolescents aged 11 to 18 years and 50 percent of adults aged 18 to 29 years reported at least one sunburn in the previous year [13,14].

The risk of sunburn is inversely related to latitude and is therefore greatest near the equator, where ultraviolet B (UVB) intensity is highest. The time of day is also important, and sunburn is more likely to occur at noon than earlier or later in the day. Cloud cover when the sun is high offers some protection, but significant quantities of ultraviolet (UV) radiation still reach the earth's surface [15]. Additional factors that increase the risk of sunburn include altitude (higher altitude and greater risk of sunburn as UV radiation intensity reaching the skin is greater) and reflection from snow (approximately 90 percent), sand (15 to 30 percent), and water (5 to 20 percent) [16]. There is also evidence that wet skin is more susceptible to erythema than dry skin [17].

Excessive consumption of alcohol may be a risk factor for sunburn [18,19]. In a study of beachgoers in Texas, participants reporting alcohol drinking on the beach had a greater body surface area with sunburn and blisters than nondrinkers [20].

PATHOGENESIS

Individual susceptibility — The susceptibility to sunburn is highly variable among individuals. Phenotypic characteristics that confer high susceptibility to sunburn include fair skin, blue eyes, and red or blond hair [21]. An increased susceptibility to sunburn is also a marker of increased risk of melanoma and nonmelanoma skin cancer [3,22,23]. (See "Melanoma: Epidemiology and risk factors", section on 'Ultraviolet radiation' and "Basal cell carcinoma: Epidemiology, pathogenesis, clinical features, and diagnosis", section on 'Ultraviolet radiation'.)

An individual's susceptibility to sunburn can be assessed by determining the minimum erythema dose (MED), which is the lowest dose of ultraviolet (UV) radiation delivered to the skin that produces a clearly marginated erythema in the irradiated site 24 hours after a single exposure (picture 1D). The MED is considered the threshold for sunburn and is widely used as a dose unit in phototherapy, experimental photobiology, and for the determination of a sunscreen's sun protection factor.

In clinical practice, the self-reported tendency to develop sunburn or tanning after sun exposure is used to determine an individual's skin phototype (table 1). Darker skin types (IV to VI) typically require higher doses of UV radiation to develop a visible erythema. On average, the MED of a skin type IV that tans well is about twice the MED of a skin type I that does not tan [24]. However, there is considerable overlap of MED values between different skin types. Individuals with skin types I and II may develop a sunburn with daily repeated suberythemal exposures (eg, 0.5 MED) [25].

Action spectra — An action spectrum indicates which wavelengths most effectively produce a skin response and usually corresponds to the absorption spectrum for the chromophore (molecule that absorbs UV radiation photons) that initiates the response. The action spectrum for erythema indicates that the most effective wavelengths present in sunlight are in the ultraviolet B (UVB) range. Ultraviolet A (UVA) also can cause erythema, but doses nearly 1000 times higher than UVB are required [1,2].

The sun is primarily a UVA source, with UVB representing up to approximately 5 percent of the UV radiation reaching the earth's surface [1], although this contributes to over 80 percent of the erythemally effective energy [26]. Thus, the risk of sunburn is highest when the UVB to UVA ratio is high, as occurs between 11 AM and 3 PM in the summer months in temperate climates and particularly at latitudes approaching the equator [27].

Mechanism of ultraviolet B-induced inflammation — In the sunburn response, many biochemical and cellular changes occur in the epidermis and dermis before the erythema becomes evident. However, the initiating events are incompletely understood, and the nature of the chromophore(s) (molecule absorbing the UV light) for erythema is still uncertain. The observation that the action spectrum for erythema is very similar to that for the induction of cyclobutane pyrimidine dimers (CPDs) suggests that DNA photodamage may be the trigger of the inflammatory cascade in sunburn [1]. UVB-mediated pigmentation (delayed tanning) can also be triggered by CPD, suggesting that inflammation and sunburn are also important in the tanning response [28].

Early events include vasodilation and increased blood flow, endothelial cell activation, formation of "sunburn cells" (ie, keratinocytes undergoing p53-dependent apoptosis), and release of inflammatory mediators [29-33]. Vasodilation of dermal small blood vessels and edema of endothelial cells occur within 30 minutes of sun exposure and peak at 24 hours [34]. Dyskeratotic "sunburn cells" may appear in the epidermis within hours of exposure [35].

Erythema becomes clinically apparent 3 to 6 hours after exposure, reaches a peak at 12 to 24 hours, and usually subsides at 72 hours. Neutrophilic infiltration starts approximately 3 hours after UVB exposure, peaks at 24 hours, and continues up to 48 hours later [36-38].

Prostaglandins and nitric oxide (NO) appear to be the major mediators of UVB-induced inflammation [30,31]. Numerous proinflammatory and anti-inflammatory eicosanoids have been identified in suction blister fluid over a 72-hour period after UVB exposure [30]. Vasodilatory prostaglandins (PG) PGE2, PGF2a, and PGE3 appear in the first 24 to 48 hours and are associated with increased COX-2 expression at 24 hours. Chemoattractant prostaglandins (11-, 12-, and 8-monohydroxy-eicosatetraenoic acid [HETE]) appear at 4 to 72 hours, whereas the anti-inflammatory 15-HETE is maximally present at 72 hours.

Several proinflammatory cytokines, including TNF-alpha, IL-1, IL-6, and IL-8, are elevated after UVB exposure. Cytokines may play several roles in UVB-induced inflammation, including activation of transcription factors, upregulation of endothelial adhesion molecules, and recruitment of neutrophils to the skin [27].

HISTOPATHOLOGY — The extent and time course of the histological changes observed after ultraviolet B (UVB) exposure varies with the magnitude of the exposure dose. Epidermal changes include spongiosis, parakeratosis, and "sunburn cells" (apoptotic keratinocytes with condensed nuclear chromatin and eosinophilic cytoplasm). Sunburn cells may be present in the epidermis within hours of exposure and increase in number over the following 24 hours and form a band at the stratum corneum at 72 hours [21].

Dermal changes include endothelial cell swelling, perivenular edema, and presence of degranulated mast cells. A perivascular infiltrate of neutrophils appears shortly after the exposure and peaks at about 14 hours. A later mononuclear infiltrate persists for at least 48 hours.

CLINICAL MANIFESTATIONS — Clinical manifestations of sunburn range from mild erythema to highly painful erythema with edema, vesiculation, and blistering (picture 1A-D and table 2). Blistering indicates superficial partial-thickness or, rarely, deep partial-thickness burn. (See "Assessment and classification of burn injury".)

Erythema is usually first noted 3 to 5 hours following sunlight exposure, peaks at 12 to 24 hours, and in most cases subsides at 72 hours [27]. The skin areas that were covered or shaded are typically spared (picture 1B). In individuals with highly pigmented skin, erythema may not be evident, and sunburn may manifest with skin peeling in the following days.

Increased skin sensitivity to heat and mechanical pressure are characteristic and present even in mild cases [39]. In severe cases, systemic symptoms, including headache, fever, nausea, and vomiting, may develop.

Clinical course — The erythema typically resolves in three to seven days. Blisters heal without scarring in 7 to 10 days. Peeling of the skin, desquamation, and tanning are noted four to seven days after exposure.

In individuals with lightly pigmented skin, multiple permanent, brown macules, often with irregular borders, may occur after sunburn (sunburn-induced solar lentigines (picture 2A-B)). (See "Benign pigmented skin lesions other than melanocytic nevi (moles)", section on 'Solar lentigo'.)

DIAGNOSIS — The diagnosis of sunburn is usually straightforward, based upon the clinical findings of painful erythema with or without vesiculation and blistering (picture 1A-C, 1E) in exposed areas and a history of exposure to sunlight. Additional elements of history that may be helpful for the diagnosis include:

●Exposure to photosensitizing drugs (table 3).

●Contact with topical photosensitizers (table 4). Topical retinoids and alpha-hydroxy acids strip the top stratum corneum and can reduce the threshold for burning.

●Use of indoor tanning equipment.

●Exposure to ultraviolet B (UVB) phototherapy or ultraviolet A (UVA) photochemotherapy (PUVA).

DIFFERENTIAL DIAGNOSIS

Exaggerated sunburn reactions — Exaggerated sunburn reactions may occur as a result of exposure to phototoxic drugs or topical photosensitizer substances and in individuals with genetic disorders conferring an increased sensitivity to ultraviolet (UV) radiation:

●Drug-induced phototoxic reactions – Phototoxic agents include drugs and other compounds that reduce the dose threshold for UV radiation-induced erythema when ingested or applied to the skin (table 3). Phototoxic reactions appear as exaggerated sunburns, starting with a stinging or burning sensation associated with redness and swelling in exposed skin within minutes of sun exposure (picture 3A-C). (See "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment", section on 'Phototoxicity'.)

●Phytophotodermatitis – Phototoxic reactions may be induced by topical exposure to plants containing furocoumarins (table 4). Patients with phytophotodermatitis typically present with erythema, edema, and bullae in linear or bizarre configurations that reflect the manner in which they have come in contact with the plant (picture 4A-B). (See "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment", section on 'Phytophotodermatitis'.)

●Xeroderma pigmentosum – Xeroderma pigmentosum (XP) is an autosomal recessive disorder resulting from mutations in one of seven genes (XPA to XPG) involved in the nucleotide excision repair of UV radiation-induced photoproducts in DNA [40,41]. Infants with XP often experience severe sunburns after minimal sun exposure. Older children present with premature skin aging, pigmentary changes, and early development of skin cancers. (See "The genodermatoses: An overview", section on 'Xeroderma pigmentosum'.)

●Erythropoietic protoporphyria – Erythropoietic protoporphyria (EPP) is an inherited autosomal porphyria characterized by acute, painful, nonblistering photosensitivity episodes usually first noted in early childhood. The measurement of total and free erythrocyte protoporphyrin is necessary to confirm the diagnosis. (See "Erythropoietic protoporphyria and X-linked protoporphyria".)

Nonsunburn reactions — Several idiopathic photodermatoses may mimic sunburn. However, they can be easily differentiated from sunburn based upon their clinical presentation and time course:

●Polymorphous light eruption – Polymorphous light eruption (PLE) is an idiopathic photodermatosis characterized by erythematous, itchy papules and vesicles occurring hours to days after sun exposure and persisting for several days (picture 5A-B) [42]. (See "Polymorphous light eruption".)

●Solar urticaria – Solar urticaria is a form of physical urticaria that presents with wheals or, less commonly, erythema alone after only minutes of exposure to sunlight and resolves within several hours (picture 6). Phototesting can confirm the diagnosis. (See "Physical (inducible) forms of urticaria", section on 'Solar urticaria'.)

●Chronic actinic dermatitis – Chronic actinic dermatitis is a rare, persistent photo-induced eczema that typically affects men over 60 years (picture 7A-B). Many patients have a history of atopic dermatitis or a coexisting allergic contact dermatitis. (See "Photosensitivity disorders (photodermatoses): Clinical manifestations, diagnosis, and treatment", section on 'Chronic actinic dermatitis'.)

●Systemic lupus erythematosus — The classic butterfly rash of systemic lupus erythematosus (picture 8A-B), which usually appears after exposure to sunlight, is frequently mistaken for a sunburn. (See "Overview of cutaneous lupus erythematosus", section on 'Acute cutaneous lupus erythematosus'.)

MANAGEMENT

Mild to moderate sunburn — Sunburn is a self-limiting condition that usually resolves in a few days. There are no specific therapies to reverse the skin damage and hasten the healing time. Management involves the symptomatic treatment of skin inflammation and control of pain:

●Cool compresses or soaks, calamine lotion, or aloe vera-based gels provide some relief of pain and discomfort. Bland emollients (eg, liquid paraffin/white soft paraffin 50/50) can be used on intact skin as tolerated. Ruptured blisters should be gently cleaned with mild soap and water and covered with wet dressings (eg, saline or petrolatum impregnated gauzes). Blisters should have the roof left on and the fluid inside extruded.

●For the treatment of skin pain and inflammation, we suggest oral nonsteroidal anti-inflammatory drugs (NSAIDs). We generally use ibuprofen at a dose of 400 to 800 mg per dose three to four times per day in adults and children >12 years and 4 to 10 mg/kg per dose every six to eight hours in children 6 months to 12 years. Treatment should be initiated as soon as the first symptoms become apparent and continued for 24 to 48 hours.

The efficacy of oral NSAIDs for the symptomatic treatment of sunburn has not been adequately evaluated in randomized trials. In a few small observational studies of experimentally induced ultraviolet B (UVB) erythema, aspirin, ibuprofen, and indomethacin were reported as effective in reducing UVB-induced erythema if initiated before or immediately after the irradiation [43-45].

In a double-blind crossover study, psoriatic patients receiving UVB phototherapy were given ibuprofen or placebo immediately after irradiation and for the following 24 hours [46]. Ibuprofen was more effective than placebo only in reducing technician-observed erythema, whereas no difference was noted for other endpoints (patient-observed erythema, pruritus, skin pain, general discomfort, and nocturnal restlessness).

Topical diclofenac gel has been reported as effective in reducing pain and inflammation from sunburn [47]. However, topical diclofenac may induce allergic contact dermatitis and photoallergic contact dermatitis [48-50].

●We do not use topical corticosteroids for the treatment of sunburn. Although they are frequently used in clinical practice, there is little evidence that they are beneficial in reducing the symptoms and healing time of sunburn.

In a study of patients with naturally acquired sunburn, participants reported similar pain, redness, and healing time for skin areas treated with topical fluocinolone acetonide or placebo [51]. In a randomized study of patients with experimentally induced UVB erythema, irradiated skin areas were treated with moderate- or high-potency topical corticosteroids (table 5) 30 minutes before, 6 hours after, or 23 hours after exposure [52]. A clinically significant reduction of erythema was noted only in areas treated with high-potency corticosteroids before the irradiation.

Patients with severe sunburn — Patients with extensive blistering sunburn, severe pain, and systemic symptoms (eg, fever, headache, vomiting, dehydration) may require hospitalization for fluid replacement and parenteral analgesia (table 6). (See "Treatment of superficial burns requiring hospital admission", section on 'Assessment for inpatient care'.)

Blistered areas should be gently cleaned with mild soap and water and covered with sterile dressings. Topical antimicrobials or antibiotics (eg, silver sulfadiazine or mupirocin 2% ointment) may be used to prevent bacterial superinfection. (See "Treatment of superficial burns requiring hospital admission", section on 'Burn wound dressings and topical therapy' and "Topical agents and dressings for local burn wound care".)

There is no evidence that oral corticosteroids are useful in severe sunburn. In a small study, participants received prednisone 80 mg or placebo immediately after UVB irradiation and for the following three days [53]. Prednisone was not more effective than placebo in reducing erythema, edema, and pain of the irradiated sites.

PREVENTION — Prevention of sunburn involves sun avoidance, wearing protective clothing, and liberal use of broad spectrum sunscreens. It is important that clinicians counsel patients with sun-sensitive skin types about sun protection, because susceptibility to sunburn is a marker of genetic susceptibility to skin cancer and is associated with an increased risk of melanoma at all ages [3,4]. Patients using regular sunscreen experience less sunburn than those who occasionally use it, although this effect may be in part due to safer sun behavior among regular sunscreen users [54,55]:

●Seeking shade – Individuals should be advised to seek shade or reduce exposure particularly in the summer months and between 10:00 AM and 4:00 PM, when sunlight intensity is greatest. Infants younger than six months should be kept out of direct sunlight.

●Wear protective clothing – Protective clothing such as long sleeves and broad brim hats should be worn while outdoors. Fabrics that are tightly woven, thick, or dark colored are useful for protection. Clothing developed for photosensitive individuals is commercially available from specialty companies. (See "Selection of sunscreen and sun-protective measures", section on 'Photoprotective clothing'.)

●Use broad spectrum sunscreen – Broad spectrum sunscreens with sun protection factor (SPF) 30 or higher should be regularly used when performing outdoor activities in sunny weather, especially in regions with high levels of insolation. Sunscreens should be applied 15 to 30 minutes before sun exposure to allow the formation of a protective film on the skin and reapplied at least every two hours. (See "Selection of sunscreen and sun-protective measures" and "Selection of sunscreen and sun-protective measures", section on 'Proper use of sunscreens'.)

For infants younger than six months, the American Academy of Pediatrics recommends using a minimal amount of sunscreen with an SPF of ≥15 on small areas (eg, face, back of hands) when adequate clothing and shade are not available.

Intentional tanning by using ultraviolet A (UVA) tanning beds does not protect against the risk of sunburn. Although suberythemal repetitive exposures to UVA induce a visible increase in skin pigmentation (immediate tanning, due to oxidation and redistribution of existing melanin), they do not increase melanin production and provide little or no photoprotection against subsequent UV exposures [56].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Care of the patient with burn injury".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topics (see "Patient education: Sunburn (The Basics)")

●Beyond the Basics topics (see "Patient education: Sunburn (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Pathogenesis – Sunburn is an acute, delayed, and transient inflammatory response of the skin to excessive exposure to ultraviolet (UV) radiation from natural sunlight or artificial sources. Both ultraviolet B (UVB) and ultraviolet A (UVA) can cause sunburn; however, the wavelengths that are most effective in inducing erythema are in the UVB range (290 to 320 nm). (See 'Introduction' above and 'Action spectra' above.)

●Clinical manifestations – Clinical manifestations of sunburn include painful erythema with or without edema, vesiculation, and blistering (picture 1A-D and table 2). Erythema is usually first noted 3 to 5 hours following sunlight exposure, peaks at 12 to 24 hours, and usually subsides at 72 hours. (See 'Clinical manifestations' above.)

●Diagnosis – The diagnosis of sunburn is usually straightforward, based upon the clinical findings (picture 1A-C, 1E) and a history of exposure to sunlight or artificial sources of UV radiation. (See 'Diagnosis' above.)

●Management – Sunburn is a self-limiting condition that in most cases resolves in a few days. There are no specific therapies to reverse the skin damage and hasten the healing time:

•Mild to moderate sunburn – Cool compresses or soaks, calamine lotion, or aloe vera-based gels may be used for the relief of skin discomfort. For the treatment of skin pain and inflammation, we suggest oral nonsteroidal anti-inflammatory drugs (NSAIDs) (Grade 2C). (See 'Management' above.)

•Severe sunburn – Patients with extensive blistering sunburn, severe pain, and systemic symptoms may require hospitalization for fluid replacement and parenteral analgesia (table 6). Wound care is similar as for superficial burns. (See 'Patients with severe sunburn' above and "Treatment of superficial burns requiring hospital admission".)