Diagnosis and treatment of solar dermatitis in dogs


Canine solar dermatitis, or chronic sun damage to the skin, is a common dermatologic disorder in hot, sunny climates.

Canine solar dermatitis, or chronic sun damage to the skin, is a common dermatologic disorder in hot, sunny climates. It can also affect animals that live in high altitudes or that spend a great deal of time outside, even in temperate zones.

Unfortunately, solar dermatitis can sometimes mimic other skin diseases such as allergies or pyoderma and, thus, go unrecognized and untreated until irreversible damage or sun-induced skin cancers have developed. This article reviews the pathogenesis, clinical signs, diagnosis, and treatment of solar dermatitis.

1. Severe solar dermatitis with scarring and furunculosis on the medial hock of a pit bull.


The solar spectrum is composed of about 40% visible light rays (400 to 700 nm), 50% infrared light rays (700 to 20,000 nm), and 9% ultraviolet (UV) light rays (100 to 400 nm).1 UVA rays (320 to 400 nm) penetrate more deeply into the skin than UVB rays do, and UVA rays are associated with photosensitivity reactions.2,3 Prolonged exposure to shorter wavelength UVB solar rays (290 to 320 nm) causes phototoxicity (sunburn), directly damaging keratinocytes and causing superficial skin blood vessel dilatation and leakage. Sun damage of epithelial structures subsequently leads to increases in inflammatory cytokines, prostaglandins, and leukotrienes as well as toxic oxygen intermediates that perpetuate and amplify tissue injury.2,4-6 Prolonged and repeated sun damage leads to keratinocyte proliferation, mutagenesis, atypia, and premalignant actinic keratoses, which can progress to invasive squamous cell carcinoma.2

2. Solar dermatitis causing erythematous, scaly hypotrichotic bullae on the dorsolateral trunk of a pit bull. Note the pigmented areas are normal. In this case, this dog's lesions mimicked those of seasonal allergies, as they occurred seasonally in the warm months and initially seemed to improve with glucocorticoids and antibiotics, but occurred more severely each summer. The key to the diagnosis was the lack of marked pruritus and the distribution of the lesions, sparing pigmented areas. A biopsy confirmed solar dermatitis.

Melanin present in pigmented skin absorbs UV rays, which in most cases helps prevent deeper UV light penetration and actinic damage.1 Black skin absorbs about 45% more solar radiation than white skin does.1 UV light contributes little in terms of thermal or heat burden, whereas visible radiation can penetrate into the skin and create thermal injury and necrosis.1 Sunlight-induced burns and necrosis affecting black spots in Dalmatians have been reported,7 but this uncommon type of sun-induced thermal burn has a different pathogenesis than that of canine solar dermatitis.

3. Solar dermatitis causing erythema, scaling, crusts, and hypotrichosis on the lateral trunk of a pit bull. A contributing factor to the truncal hypotrichosis was iatrogenically induced hyperadrenocorticism after 1.5 years of daily administration of 20 to 40 mg prednisone for erroneously diagnosed allergic dermatitis.


Solar dermatitis most commonly affects the white-haired and nonpigmented skin of short-coated breeds such as pit bull terriers, Staffordshire bull terriers, bull terriers, boxers, Dalmatians, American bulldogs, and whippets, but any dog with white or lightly pigmented hair and skin is at risk. Sun damage usually occurs on nonpigmented thinly haired areas such as the flank, inguinal and axillary areas, and the dorsal nose, but it can occur on the dorsal and lateral trunk and lateral limbs as well as other areas (Figures 1-4).2 In dogs that prefer to lie on one side of their body, lesions may be worse on the more chronically sun-exposed side.

4. More subtle solar-induced lesions of patchy erythema, alopecia, and fibrosis with comedones and scattered small bullae on the dorsolateral trunk of an American bulldog.

The duration and intensity of sun exposure influence the degree of skin damage. The initial signs of actinic damage are erythematous, scaly lesions, which may be tender. With repeated sun exposure, actinic folliculitis, follicular cyst formation, and dermal fibrosis occur.8 In dogs with pigmented areas on their skin, there is often sharp demarcation between areas of normal skin with protective pigment and damaged nonpigmented skin (Figure 2).2 With chronic sun exposure, damaged areas become thickened and scarred with comedones, erosions, ulcers, crusts, and draining tracts.2 Secondary bacterial pyoderma is common.9 Sun-induced skin tumors such as squamous cell carcinoma (Figure 5), hemangioma, and cutaneous hemangiosarcoma may occur. Although affected dogs may lick damaged areas, the pruritus associated with solar dermatitis is usually otherwise minimal, unlike that in dogs with allergic dermatitis. However, some dogs can have solar dermatitis and concurrent allergies.

5. Solar dermatitis on the inguinal area of an American bulldog. After years of sun damage, a large squamous cell carcinoma has formed.


Diagnosing solar dermatitis involves considering a patient's signalment and clinical signs and ruling out other causes of scaly, erythematous dermatitis or folliculitis (e.g. bacterial, Demodex species, and dermatophyte infections). Lack of resolution of skin lesions with empiric therapy should raise your suspicion of solar dermatitis and the need for further investigation.

Ultimately, skin biopsy and histology are used to diagnose solar dermatitis and solar-induced neoplasia. Depending on the degree of secondary bacterial infection, systemic antibiotics may be indicated for two to three weeks before biopsy to ensure that infection does not alter histologic interpretation. Additionally, clearing secondary skin infection also increases the likelihood of correctly selecting solar-induced rather than infection-induced skin lesions for biopsy.10 However, if an obviously neoplastic skin mass is noted on physical examination, perform a biopsy immediately to expedite treatment. Biopsy can be performed by administering lidocaine locally and obtaining multiple skin punch or excisional biopsy samples of different lesions (Figure 6).

6. Inguinal erythema, scarring, and furunculosis caused by chronic sun damage in the same dog as in Figure 1. The circled areas indicate biopsy sites.

Since some of the histologic changes can be seen with other conditions such as bacterial folliculitis, one key to a definitive histologic diagnosis is to include a complete history with the biopsy submission form, including signalment, degree of sun exposure, distribution of lesions, clinical description of lesions, response or lack of response to prior therapies, and current medications (including glucocorticoids) that could affect the histologic findings. Requesting a full histologic description and seeking interpretation by a veterinary dermatopathologist are recommended.

In early cases of solar dermatitis, histologic examination shows variable degrees of perivascular dermatitis, folliculitis, and dermal fibrosis or increased collagen accumulation or collagen damage. Solar elastosis (linear bands of degenerated basophilic elastin accumulation arranged parallel to the skin surface) may be seen. In chronic cases, histologic examination may show follicular cysts, pyogranulomatous inflammation, and precancerous actinic keratosis or neoplastic cells.2,9,10


The best treatment for canine solar dermatitis is prevention. Educate owners of at-risk dogs about the need for sun avoidance starting at a young age. Also tell owners of affected and at-risk dogs that oral and topical medications cannot replace sun avoidance in treating and preventing solar dermatitis.

Reduce sun exposure

The main treatment recommendation for solar dermatitis is restricting sun exposure by keeping the dog indoors during the day, especially between 9 a.m. and 3 p.m., which is considered the most intense UV radiation time.2 If some sun exposure is unavoidable, then frequent (twice a day11) topical application of a waterproof, high-SPF sunscreen (a product with an SPF > 15 absorbs more than 92% of UVB rays12 ) that is labeled as safe for babies and that protects against UVA and UVB rays is indicated.2 Having the dog wear a T shirt may help decrease sun exposure2; however, it is often impossible to cover all at-risk areas of the skin. A dog sun suit is available at www.designerdogwear.com, or clients may be able to sew a sun suit for their pets by using sun-blocking fabric available for people.

Beta-carotene or acetretin

To decrease sun damage, beta-carotene (30 mg orally b.i.d. for 30 days then 30 mg/day for life) in combination with anti-inflammatory doses of oral glucocorticoids may be effective in early cases.2,13 Skin damage may also be reduced by administering oral retinoids (synthetic vitamin A analogues, which are more potent and less toxic than vitamin A2,14 ) such as acitretin at a dosage of 0.5 to 1 mg/kg orally every 24 hours.2 The potential side effects of retinoids include keratoconjunctivitis sicca, mucocutaneous lesions, vomiting, diarrhea, musculoskeletal abnormalities, triglyceride elevations, and hepatotoxicity,2,11 so careful monitoring is necessary. Additionally, retinoids are highly teratogenic.2 A positive clinical response to retinoids should be noted within four to six weeks. At that point, the frequency of medication can be reduced to an alternate-day basis.11

Vitamin A

Because of the expense of retinoids, oral vitamin A has been used anecdotally for canine solar dermatitis, but controlled clinical trials and published studies elucidating doses or side effects are not available. The dosage of oral vitamin A in dogs should not exceed 400 IU/kg/day, and patients should be monitored for the same potential side effects as listed for retinoids.2


Actinic keratosis in people may be helped by using a topical immunomodulator such as imiquimod (Aldara—3M Pharmaceuticals), but studies in dogs are lacking. Imiquimod's mechanism of action involves inducing local antitumor and antiviral immune responses by stimulating lymphocytes, dendritic cells, and macrophages. In people, imiquimod cream is applied to affected areas two to three times a week for four to 16 weeks.15-18 According to the Aldara package insert, the size of the treated area should be no larger than 2 x 2 in, and the cream should not be used near the eyes, lips, or nostrils. The cream is left on the skin for eight hours before being washed off with mild soap and water. Side effects include localized redness, crusting, burning, and pruritus at the site of application. In dogs with more extensive lesions of solar dermatitis, the expense of Aldara (about $245 for a box of 12 individual 250-mg single-use packets) may preclude its use.

Monitor for disease progression

Even with future sun avoidance, prior skin damage can still progress to skin neoplasia months or years after exposure (Figure 7). Once skin neoplasia has occurred, aggressive surgical resection or laser therapy should be performed. In addition, if large or invasive masses are present, screening for metastasis to draining lymph nodes and internal structures is necessary.

7. The same dog as in Figures 1 and 6 after six weeks of antibiotic therapy and three months of sun avoidance. Although scarring is still present, the prior lesions of erythema and bullae have resolved. However, note the persistent scaly, erythematous erosive lesion on the prepuce, which is likely a precancerous or early cancer lesion. A biopsy is indicated.

Kimberly S. Coyner, DVM, DACVD

Dermatology Clinic for Animals

5231 W. Charleston Blvd.

Las Vegas, NV 89146


1. Scheuplein RJ. Mechanism of temperature regulation in the skin. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al., eds. Dermatology in general medicine. 3rd ed. New York: McGraw-Hill Book Co, 1987;347-357.

2. Scott DW, Miller WH, Griffin CE. Muller and Kirk's small animal dermatology. 6th ed. Philadelphia, Pa: WB Saunders Co, 2001;1073-1080.

3. Bernhard JD, Pathak MA, Kochevar IE, et al. Abnormal responses to ultraviolet radiation. In: Fitzpatrick TB, Eisen AZ, Wolff K, et al., eds. Dermatology in general medicine. 3rd ed. New York: McGraw-Hill Book Co, 1987;1481-1507.

4. Freedberg IM, Eisen AZ, Wolff, K, et al. Fitzpatrick's dermatology in general medicine . 5th ed. New York: McGraw-Hill Book Co, 1999.

5. Hruza LL, Pentland AP. Mechanisms of UV-induced inflammation. J Invest Dermatol 1993;100:35S-41S.

6. Kimura T, Doi K. Responses of the skin over the dorsum to sunlight in hairless descendants of Mexican hairless dogs. Am J Vet Res 1994;55:199-203.

7. Hargis AM, Lewis TP. Case report: Full thickness cutaneous burn in black-haired skin on the dorsum of the body of a Dalmatian puppy. Vet Dermatol 1999;10:39-42.

8. Mason K. Actinic dermatosis in dogs and cats, in Proceedings. Annu Meet Eur Soc Vet Dermatol Eur Coll Vet Dermatol 1997;67.

9. Medleau LM, Hnilica KA. Small animal dermatology: A color atlas and therapeutic guide . Philadelphia, Pa: WB Saunders Co, 2005.

10. Gross TL, Ihrke PJ, Walder EJ, et al. Skin diseases of the dog and cat: Clinical and histopathologic diagnosis. 2nd ed. Oxford: Blackwell Science, 2005;399-401.

11. Rosenkrantz WS. Solar dermatitis. In: Griffin CE, Kwochka KW, MacDonald JM, eds. Current veterinary dermatology. St. Louis, Mo: Mosby-Year Book, 1993;309.

12. Kimura T, Doi K. Protective effects of sunscreens on sunburn and suntan reactions in cross-bred Mexican hairless dogs. Vet Dermatol 1994;5:175-187.

13. Mason KV. The pathogenesis of solar induced skin lesions in bull terriers, in Proceedings. Annu Member Meet Am Acad Vet Dermatol Am Coll Vet Dermatol 1987;12.

14. Keller KL, Fenske NA. Use of vitamins A, C, and E and related compounds in dermatology: a review. J Am Acad Dermatol 1998;39:611-625.

15. Alomar A, Bichel J, McRae S. Vehicle-controlled, randomized, double-blind study to assess safety and efficacy of imiquimod 5% cream applied once daily 3 days per week in one or two courses of treatment of actinic keratoses on the head. Br J Dermatol 2007;157:133-141.

16. Lebwohl M, Dinehart S, Whiting D et al. Imiquimod 5% cream for the treatment of actinic keratosis: results from two phase III, randomized, double-blind, parallel group, vehicle-controlled trials. J Am Acad Dermatol 2004;50:714–721.

17. Szeimies RM, Gerritsen MJ, Gupta G, et al. Imiquimod 5% cream for the treatment of actinic keratosis: results from a phase III, randomized, double-blind, vehicle-controlled, clinical trial with histology. J Am Acad Dermatol 2004;51:547–555.

18. Korman N, Moy R, Ling M, et al. Dosing with 5% imiquimod cream 3 times per week for the treatment of actinic keratosis: results of two phase 3, randomized, double-blind, parallel-group, vehicle-controlled trials. Arch Dermatol 2005;141:467–473.

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