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C. Pucheu-Haston1
1Louisiana State University School of Veterinary Medicine, Veterinary Clinical Sciences, Baton Rouge, USA
CM Pucheu-Haston, DVM, PhD, DACVD
Department of Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA
Solar dermatitis (photodermatitis, actinic dermatitis) is a broad term referring to acute or chronic dermatitis resulting from exposure to ultraviolet (UV) light. High- energy, shorter wavelength light (UVB, 280-320nm) is responsible for acute phototoxic reactions (sunburn), while longer wavelengths (UVA, 320-400 nm) penetrate deeply into the skin and are responsible for the permanent damage associated with chronic solar dermatitis.
Clinical appearance:
Solar dermatitis is typically seen on lightly or non- pigmented skin with minimal or no hair cover. While affected animals typically spend considerable time outdoors, chronic solar dermatitis may even be seen in indoor-only animals, as much UVA light is not stopped by standard window glass. In dogs, affected areas typically include the planum nasale, dorsal and rostral muzzle, ventrum and ventrolateral thorax, especially
in “sunbathers” that like to lay on their sides or backs.
In cats, affected areas typically include the pinnae, preauricular skin, eyelid margins and planum nasale. Involvement of the bridge of the nose and rostral muzzle may also be seen.
Acute phototoxicity is characterized by erythematous, thickened and painful skin. Severe cases may develop vesicles, erosions, or frank necrosis with the later development of post-inflammatory scaling. Chronic
solar dermatitis is characterized by palpably thickened skin, erythema, erosions, ulcerations, scarring, comedones (often grossly dilated and filled with paste- like debris). Secondary bacterial infection and neoplastic transformation (squamous cell carcinoma, hemangioma / hemangiosarcoma) are common.
Acute solar dermatitis:
Cases of acute solar dermatitis are expected to be self-limiting if further solar exposure can be avoided. Specific therapy is similar to that used for any minor burn.
The discomfort associated with this condition may be considerable, and short term analgesic therapy with non-steroidal anti-inflammatory drugs (NSAIDS) or tramadol is indicated. Very inflamed cases may benefit from prednisone (1.1mg/kg once daily for 7-10 days) in conjunction with an appropriate analgesic agent, such as tramadol.
Topical care:
Cool baths may help to decrease some of the discomfort. If erosion or ulceration is present, use of an antiseptic shampoo or spray will help to prevent the development of secondary infection. Topical glucocorticoids (1% hydrocortisone spray or gel; hydrocortisone-containing shampoos) may help to decrease discomfort and inflammation.
If infection is already present, systemic antibiotic therapy (such as cephalexin 22mg/kg twice daily, cefpodoxime 5-10mg/kg once daily or amoxicillin/clavulanate at 22mg/ kg twice daily) is appropriate.
Chronic solar dermatitis:
Therapy of chronic dermatitis is more challenging, as much of the damage associated with chronic solar exposure is permanent.
Irreversible damage and dilation of hair follicles may be seen in the affected area, and patients may develop follicular impaction, furunculosis, cellulitis and severe secondary bacterial infection as a result. Long-term courses of antibiotics (6-8 weeks or more, ideally selected by antibiotic sensitivity testing) may be necessary to resolve these infections. These patients will benefit from frequent baths with antiseptic agents such as chlorhexidine to help minimize the frequency of subsequent bacterial infections. Nonetheless, recurring bacterial folliculitis may become a long term issue for many patients.
Lesions of canine solar dermatitis have been demonstrated to have increased production of COX- 2, and some cases will respond at least partially to
An Urban Experience

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