Sunburn (solar erythema)

Are You Confident of the Diagnosis?

What you should be alert for in the history

Sunburn is an acute cutaneous inflammatory reaction that follows excessive exposure of the skin to sunlight or other sources of ultraviolet radiation (UVR) such as tanning beds and phototherapy lamps.

Characteristic findings on physical examination

Most sunburns are superficial or first-degree burns that present as erythema 3-4 hours after sun exposure (Figure 1). The erythema peaks at 12-24 hours, and lasts approximately 4-7 days, then typically ends with desquamation.

Figure 1.

Sunburn occurring on the back of a young female after sunbathing on the beach

Longer exposure to UVR may lead to second-degree burns and blistering. The main symptom is pain; however fever, malaise, nausea, and vomiting may occur in more severe cases. Patients on photosensitizing medications or drinking alcohol are more likely to develop severe burns.

Expected results of diagnostic studies

The histological changes following UV irradiation include thickening of stratum corneum, epidermis and dermis, as well as intercellular and perivascular edema in the dermis, and perivascular infiltration. Both epidermal keratinocytes and Langerhans cells undergo apoptotic changes as a consequence of UV-induced DNA damage. These ’sunburn’ cells can be seen in the epidermis (Figure 2).

Figure 2.

Apoptotic keratinocytes, charcteristic of so-called ‘sun-burn’ cells. (Courtesy of Miles McFarland, MD)

Who is at Risk for Developing this Disease?

Over 30% of US adults and 69% of US children obtain at least one sunburn each year. Men are more likely to obtain a sunburn, which is likely attributed to different sun protection practices.

An individual’s tendency to burn is largely genetically determined. Darker skin types are less likely to develop a sunburn, however all skin types are susceptible.

UVR, which is the cause of sunburn, is higher during the mid-day which is typically 10am to 4pm, at higher altitude, and at latitudes closer to the equator.

What is the Cause of the Disease?

Sunlight is composed of a continuous spectrum of electromagnetic radiation that is divided into three main regions of wavelengths: UV, visible, and infrared.

UV radiation comprises the wavelengths from 200 to 400nm, the span of wavelengths just shorter than those of visible light (400–700nm). UV radiation is further divided into three sections, each of which has distinct biological effects: UVA (320–400nm), UVB (280–320nm), and UVC (200–280 nm). UVC is effectively blocked from reaching the Earth’s surface by the ozone layer, although accidental exposure could occur from man-made sources. Over 95% of the mid-day UVR is composed of UVA rays. However, UVB is much more erythemogenic and is the principle cause of sunburn.

UVB rays initiate DNA damage which leads to a series of biochemical and immunologic events that cause erythema and inflammation. Inflammatory mediators include prostaglandins, histamine, substance P, lipoxygenase products, cytokines, and adhesion molecules. Local cutaneous blood flow is increased by 2-3 times leading to erythema.

Systemic Implications and Complications

UVR is a human carcinogen. Even one sunburn increases an individual’s risk to develop basal cell skin cancer, squamous cell skin cancer, and melanoma. Melanoma is a highly malignant cancer that can lead to death if not detected early. Routine skin exams are warranted for those with signs of chronic sun damage or any new or changing moles.

UVR also causes local immunosuppression by causing Langerhans cell apoptosis. Langerhans cells are the antigen-presenting cells of the skin that participate in T-cell activation. This may play a role in increasing the risk of malignancy by diminished immunosurveillence.

Treatment Options

Treatment otions are summarized in the Table I.

Table I.
Medical Treatment
NSAIDs ( example: ibuprofen, aspirin), dose dependent on patient age.
Cool baths
Emollients (example: cetaphil cream, aloe vera cream)
Topical steroid creams (example: hydrocortisone 2.5% or triamcinolone 0.1 % cream or ointment)

Optimal Therapeutic Approach for this Disease

NSAIDs, antioxidants, antihistamines and emollients are ineffective at decreasing recovery time in patients. However symptomatic relief from pain and pruritus should be addressed. Most patients will only need oral hydration, and emollients such as aloe vera or other cooling creams (menthol or other succulant herbs) for symptomatic relief.

NSAIDs may be useful to relieve pain and decrease inflammation. More severe cases may need intravenous hydration and stronger pain relievers. For blistering, silvadene ointment may be used for symptomatic relief and also help prevent secondary infection. However, secondary infection is unusual.

Topical mid to high potency steroids (see Table I) have shown minimal improvement in a few small randomized controlled trials. Combination treatment with NSAIDs and topical steroids may be more effective at decreasing pain and erythema.

Little scientific evidence supports the use of a short non-tapered course of systemic corticosteroids in severe patients.

Topical anesthetics, such as benzocaine, should be avoided due to risk of allergic contact dermatitis.

Patient Management

Most cases of sunburn resolve spontaneously over 4-7 days with scaling and desquamation without sequelae. Chronic sun exposure of the skin can lead to multiple deleterious effects, including premature aging and wrinkling of the skin and development of premalignant and malignant lesions.

Unusual Clinical Scenarios to Consider in Patient Management

Sun sensitivity, if recurrent or persistent, should alert the clinician to at least consider other diagnoses that may be photosensitive or ’photoaggravated’:

–Lupus, dermatomyositis and other connective tissue diseases


–Xeroderma pigmentosa

–PMLE, actinic prurigo, hydroia vacciniforme, solar urticaria or other idiopathic photosensitivity disorders

What is the Evidence?

Cokkinides, V, Weinstock, M, Glanz, K, Albano, J, Ward, E, Thun, M. “Trends in sunburns, sun protection practices, and attitudes toward sun exposure protection and tanning among US adolescents, 1998-2004”. Pediatrics. vol. 118. 2006. pp. 853-64. (Epidemiologic view of sun exposure and sun protective practices.)

“Sunburn prevalence among adults – United States,1999, 2003, and 2004”. MMWR Morb Mortal Wkly Rep Jun 1. vol. 56. 2007. pp. 524-8. (Epidemiologic study.)

Parrish, JA, Jaenicke, KF, Anderson, RR. “Erythema and melanogenesis action spectrum of normal human skin”. Photochem Photobiol. vol. 36. 1982. pp. 187-191. (Basic science study determining peak wavelengths leading to biological changes.)

Walsh, LJ. “Ultraviolet B irradiation of skin induces mast cell degranulation and release of tumour necrosis factor-alpha”. Immunology and Cell Biology. vol. 73. 1995. pp. 226-233. (Basic science studies about biologic effects of UVB rays.)

Driscoll, MS, Wagner, RF. “Clinical management of the acute sunburn reaction”. Cutis. vol. 66. 2000. pp. 53-8. (Review of pharmacologic agents used to treat sunburn.)

Han, A, Maibach, HI. “Management of acute sunburn”. Am J Clin Dermatol. vol. 5. 2004. pp. 39-47. (Literature review regarding pharmacologic treatment of acute sunburn reaction.)