Ultraviolet Light Reactions

My-Linh T. Nguyen

Sunburn is acute inflammation of the skin in response to ultraviolet (UV) damage. Its characteristic erythema and pain are well known to many patients. Sunburns present a problem not only because of their immediate symptomatology, but also because they are a marker of excessive sun exposure and thus cancer risk. Patients with a history of sunburn carry a twofold relative risk of developing melanoma versus patients with no sunburn history. Treatment for sunburns involves symptomatic relief, fluid replacement, prophylaxis for possible infection, and preventative counseling.

There are many other reactions to the sun that may mimic sunburn or have more of an eczematous nature. Commonly encountered conditions would include polymorphous light reaction, photoallergic contact dermatitis, and phytophotodermatitis. These will be discussed in further detail.

Sunburn

Background/Epidemiology

For lighter-skinned individuals, most have experienced sunburn as a result of prolonged sunlight exposure. In the United States, 30% to 40% of adults and 83% of children report at least one sunburn in the preceding year. Individuals with darker skin types are less likely to burn, but occasionally may experience sunburn while on a photosensitizing medication or in some cases as a result of a systemic illness that includes photosensitivity. In general, sunburns are classified as a superficial or first-degree burn. Sunburns are more common in men and, in general, children are burned more frequently than adults.

Key Features

Sunburn is caused by excessive UV radiation causing delayed, sharply demarcated, uniform edema in exposed skin with possible pain, pruritus, edema, and vesicles/bullae.
Predisposing factors include: light skin, light hair, and photosensitizing medications.
Treatment:
- Symptomatic therapy (cold compress, moisturizing lotion, nonsteroidal anti-inflammatory drugs [NSAIDs], corticosteroids).
- Fluid replacement.
- Infection prophylaxis (topical antibiotic if vesicles/bullae present).
- Sun avoidance during healing.
- Preventative counseling.

Pathogenesis

The exact mechanisms leading to the sunburn reaction are not fully known. Current evidence suggests that UV irradiation leads to cutaneous vasodilation, causing erythema, edema, and neutrophilic infiltration. UVB radiation causes apoptosis through a variety of pathways, including DNA mutagenesis, direct activation of membrane-bound death receptors, and generation of intracellular reactive oxygen species.

Table 22-1 Fitzpatrick’s Skin Phototypes

SKIN TYPE	BASELINE COLOR BEFORE SUN EXPOSURE	RESPONSE TO SUN EXPOSURE AS ESTIMATED BY PATIENT
I	Pale white	Does not tan; burns easily
II	White	Tans with difficulty; burns easily
III	White to olive	Tans gradually; burns minimally
IV	Light brown	Tans easily; burns minimally
V	Brown	Tans easily; rarely burns
VI	Black	Becomes darker; never burns

Clinical Presentation

Manifestation

The presentation of sunburn can range from mild (sharply demarcated, uniform erythema on sun-exposed areas with sparing of covered skin [Fig. 22-1]) to severe (erythema accompanied by edema, vesicles, bullae, pain, and/or pruritus). Erythema typically arises 6 hours after sun exposure, peaks at 12 to 24 hours, and resolves after 72 hours. In severe cases, fever, fatigue, headache, and tachycardia may be present.

Figure 22-1 Acute sunburn on the neck. Note the sharp cutoff where the shirt protected the skin.

History and Risk Factors

UV exposure: the amount of UV exposure correlates with severity of sunburn. Low latitude, high altitude, and midday exposure (11 AM to 4 PM) represent the greatest risk for skin damage. Sunburns can occur on cloudy days, as UV radiation penetrates cloud cover, and in the shade, because UV can reflect off of snow, water, and concrete to reach skin.
Skin type: the Fitzpatrick skin phototypes scale (Table 22-1) classifies skin based on its baseline color and reaction to sun exposure. Skin types I and II are at greatest risk for sunburns.
Hair color: lighter hair such as blonde, red, or light brown is associated with increased risk of sunburns.
Photosensitizing medications: summarized in Table 22-2.

Table 22-2 Medications Associated With Photosensitivity

Amiodarone
Antifungals (itraconazole, voriconazole)
Diltiazem
Furosemide
NSAIDs (ibuprofen, diclofenac, piroxicam, naproxen)
Phenothiazines
Psoralens
Quinolones
Retinoids (isotretinoin, acitretin)
Sulfonylureas (glipizide, glyburide)
Tetracyclines (tetracycline/doxycycline)
Thiazides

Table 22-3 Differential Diagnosis of Sunburn Reactions

CONDITION	NOTES
Systemic lupus erythematosus	Obtain antinuclear antibody (ANA) level if suspected. Often presents as malar (“butterfly”) rash.
Drug-induced photosensitivity	Reaction may be more severe with limited sun exposure. History reveals exposure to photosensitizing drugs or other chemicals. See Table 22-2 for a summary of important causes of photosensitivity. Systemic photosensitizing drugs cause an exaggerated sunburn reaction in all areas of sun-exposed skin, whereas topical drugs cause the reaction in areas where the drug was applied.
Photoallergic contact dermatitis	Occurs due to reaction between a topically applied products (such as sunscreen) which is modified by UV exposure, subsequently causing a delayed type hypersensitivity
Phototoxic reaction	Most commonly caused by plant exposures, as discussed in the following section.
Polymorphous light eruption	Presents as rash rather than uniform erythema.
Solar urticaria	Wheals/erythema after minutes of sun exposure
Xeroderma pigmentosum	Presents in early childhood after minimal sun exposure.
Erythropoietic protoporphyria	Rare autosomal dominant disease that presents in early childhood after minimal sun exposure.

Diagnosis

Diagnosis is relatively straightforward given a history of recent sun exposure and physical exam showing characteristic skin reaction in sun-exposed areas.

History: UV exposure 3 to 6 hours before onset of erythema
Physical exam:
- Skin: uniform erythema in sun-exposed areas with sharp demarcation versus nonexposed areas. In severe sunburn, erythema may be accompanied by edema, vesicles, and bullae.
- General: in severe cases, fever, malaise, and rapid pulse may be present.
- Mucous membranes: rarely, tongue may be sunburned if mouth is open during physical activity

The differential diagnosis of sunburn reactions is broad. Causes range simply from prolonged UV exposure to systemic illnesses, which cause increased sensitivity to the sun. This differential is summarized in Table 22-3.

Treatment

Sunburn is managed through symptomatic treatment, fluid replacement, prophylaxis for infection if needed, and avoidance of sun exposure during recovery. Currently, there are no recommended therapies that significantly shorten recovery time or reduce epithelial injury.

For hyperpigmentation following phytophotodermatitis, hydroquinone 4% cream may be useful in lightening the dark pigment.

Symptomatic Treatment

The patient may find moisturizing lotion, aloe vera gel, cool water soaks, and/or cold compresses helpful in relieving discomfort.
Topical or oral NSAIDs decrease erythema if used before or immediately after UV exposure, but their benefits drop off 24 hours after UV exposure. One exception is topical diclofenac 0.1% gel (5 mg/cm²), which, when applied 6 and 10 hours after UV exposure, can relieve pain and erythema for up to 48 hours.
Topical corticosteroids may boost the benefits of NSAIDs if applied shortly after UV exposure. They do not provide clinically significant benefit after 30 hours post-UV exposure or when used without NSAIDs.
Antihistamines are not recommended, as they have not been shown to produce clinically significant benefits.
Although there is little published evidence documenting the efficacy of topical anesthetics in sunburn, some patients may find relief with agents such as benzocaine. Benzocaine may cause allergic contact dermatitis.

Fluid replacement: oral rehydration is recommended to compensate for increased fluid loss through the injured skin.
Infection prophylaxis: if vesicles/bullae are present, a topical antibiotic such as silver sulfadiazine or bacitracin may be used to decrease the risk of infection.
Sun avoidance during healing: further sun exposure should be avoided for 1 to 2 weeks, as the injured skin is more susceptible to sunburns during this time. See “Prevention” below.

“At a Glance” Therapy

Symptomatic Treatment

Moisturizing lotion, aloe vera gel, cool water soaks, and/or cold compresses
Topical (diclofenac 0.1% gel applied 6 and 10 hours after UV exposure) or oral NSAIDs
Topical corticosteroids should be used in conjunction with topical NSAIDs
Antihistamines produce clinically significant benefits.
Although there is little published evidence documenting the efficacy of topical anesthetics in sunburn, some patients may find relief with agents such as benzocaine. Benzocaine use may cause allergic contact dermatitis.

Prevention

To avoid further sunburns as well as to reduce chronic sun damage and cancer risk, UV exposure should be limited using the following techniques:

Avoid sun exposure between 10 AM to 4 PM, and especially between 11 AM to 2 PM. This should be done even on cloudy days, as UV radiation penetrates cloud cover.
Wear sunglasses, a wide-brimmed hat, and dark, loose-fitting clothing.
Wear sunscreen with at least an SPF (sun protection factor) of 30. SPF is the factor by which a substance prolongs the minimal duration of UV exposure required to produce erythema. If a patient normally develops erythema after 10 minutes of exposure, for instance, then with SPF-15 sunscreen, he/she would theoretically develop erythema after 150 minutes of UV exposure. However, this is an overestimate, as most people significantly under-apply sunscreen (recommended application is 2 mg/cm² or 30 to 35 mL/body application) and realistically achieve only 20% to 50% of the expected SPF. Sunscreen should be applied 15 to 30 minutes before sun exposure and re-applied every 2 to 3 hours.
Oral and topical antioxidants such as vitamins A, C, and E help protect against sunburns. However, antioxidants should be used in conjunction with sunscreen, not as a replacement.
Although tanning through gradual sun exposure or tanning beds can decrease the risk of sunburn, it is not recommended as a preventative technique, because tanning may not prevent chronic sun damage and skin cancer and may carry its own negative risks. Artificial “sunless” tanning uses dyes to give the appearance of tanned skin and does not confer sunburn protection.

Course and Complications

Rupturing of vesicles and bullae can lead to infection.
Severe sunburns can damage melanocytes, leading to mottled depigmentation, or induce melanocyte proliferation, causing solar lentigines.
Sunburns are a marker of excessive UV exposure and indicate increased risk of dermatoheliosis, actinic keratoses, and skin cancer. A history of sunburn confers a 2.0 relative risk of developing melanoma versus no sunburn history.