Solar Keratoses

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Solar (actinic) keratoses present as scaling hyperkeratotic plaques or papules on skin exposed to light. They are most commonly seen on elderly subjects with fair skin who have had high levels of ultraviolet exposure over many years. They may be associated with other signs of photodamage such as yellowing, coarsening, and wrinkling of the skin. Individuals with large numbers of solar keratoses are at increased risk of developing nonmelanoma skin cancer. Histologically, the lesions show epidermal thickening, with abnormal epidermal differentiation and scaling. Solar keratoses are common, and up to 20% of individuals over the age of 60 are affected. Some solar keratoses may resolve spontaneously, but a small proportion may develop into squamous cell carcinoma. Solar keratoses may respond to topical 5% 5-fluoro-uracil cream (Efudix) an antimetabolite that inhibits DNA synthesis. This should be applied once or twice daily for 10-14 days, and may cause the lesions and the surrounding skin to become sore and inflamed. Alternatively, the 5% 5-fluorouracil cream can be applied twice daily for 2 days each week and the frequency increased until the level of the patient's tolerance is reached, but it is probable that some degree of irritation is necessary for the treatment to be effective. The accompanying irritation and soreness may be treated with topical corticosteroids. Topical 5-fluorouracil has also been claimed to be effective for superficial basal cell carcinoma and for Bowen's disease. Topical tretinoin 0.05% and isotretinoin 0.1% have also been used to treat multiple solar keratoses.


Sunscreens are preparations that filter out or reflect harmful ultraviolet radiation. Various disorders may be precipitated or aggravated by exposure to ultraviolet light. These include polymorphic light eruption, Hutchinson's summer prurigo, cutaneous porphyria, rosacea, and lupus erythematosus. Exposure to ultraviolet radiation is also a major risk factor for both malignant melanoma and nonmelanoma skin cancer as well as photoaging. Recurrent attacks of herpes simplex may also be precipitated by ultraviolet exposure. Sunscreens differ greatly in their protective capacity and some of the newer sunscreens also offer some degree of protection against ultraviolet A.


Ulcers may be seen at any body site, but are most commonly seen on the legs, probably caused by a combination of trauma and impaired circulation. The venous return of blood from the legs depends on efficient working of the calf muscles to act as a pump coupled with the action of valves in the deep veins preventing the reflux of blood. Damage to the valves of the deep veins following deep vein thrombosis may be associated with pregnancy. Injury or immobilization may also lead to valvular incompetence.

The most common types of ulcer are venous ulcers caused by leaking valves in the deep veins, resulting in venous hypertension, and edema of the subcutaneous tissue. An extravascular accumulation of fibrinous material leaked from dermal blood vessels results in a fibrous cuff around the capillaries that prevents diffusion of oxygen and other nutrients through the blood vessel wall as well as causing fibrosis, and sclerosis of the dermal capillaries. Venous ulcers are more common in women than men and result from inadequate provision of nutrients and oxygen to the skin. Venous ulcers are most commonly seen on the medial aspect of the lower leg usually above the medial malleolus (inner aspect of the ankle) (Fig. 7). Large ulcers may encircle the leg.

On examination, the lower leg and ankle and foot may be edematous, there may be prominent varicose veins present. Leakage of blood into the skin may cause deposition of hemosiderin. The ulcers may heal spontaneously or may become chronic and indolent. The ulcers may be complicated by infection, bleeding or by eczema. Varicose eczema, surrounding the ulcer, is common, and in many patients, it may be due to allergic contact hypersensitivity to medicaments, such as neomycin clioquinal (Vioform), lanolin, or ethylene diamine, used in treating the leg ulcer or eczema. Rarely, in long-standing ulcers, malignant change with the development of squamous cell carcinoma may occur, and patients with long-standing ulcers may become anemic. It is important to try and improve venous return (drainage) by

1. Elevation of the legs for regular periods

2. Compression bandaging with elasticated stockings or bandages (which should be graduated so that pressure is greatest at the ankle and least at the top of the dressing)

Figure 7 A large venous ulcer on the medial (inner) aspect of the leg.

3. Regular exercise

4. Weight reduction

Exudate and slough should be removed and ulcers may be cleaned with normal saline, sodium hypochloride solution, Eusol, or 5% hydrogen peroxide. Topical antiseptics, such as povidone iodine or potassium permanganate, may help reduce the bacterial load. Crust may be loosened by the application of saline- or potassium permanganate-soaked dressings. Local surgical debridement may be necessary for a thick eschar. Hydrogen peroxide cream 1.5%, streptokinase/streptodornase solution (Varidase) may also be useful in helping remove thick slough.

Numerous dressings are available to treat leg ulcers, including nonadherent gauze, paraffin gauze, silver sulfadiazine (Flamazine), and absorbent hydrocolloid dressings. Any ulcerated area of skin will rapidly become colonized with numerous different bacteria, and these should be treated only if they are causing local cellulitis. The main function of leg ulcer dressings should be to provide comfort, protection for the wound, and an optimum local environment to allow reepithelization. Hydro-colloid dressings have the advantage that they may be left in situ for several days before changing. They have the disadvantages of an unpleasant odor and an unpleasant fluid may collect beneath the dressing. Surrounding (varicose) eczema may be treated with topical corticosteroids.

Ischemic leg ulcers are due to reduced circulation secondary to atherosclerosis, vasculitis, or other causes of arterial obstruction. Arterial ulcers tend to be more sharply defined and painful than venous ulcers. In the leg, they are more common on the anterior aspect of the shin, rather than the medial aspect of the ankle. Compression bandaging will impair arterial blood supply further and thus it is important that arterial pulses are examined and if necessary Doppler ultrasound or other investigations are performed so that arterial ulcers are not incorrectly treated with compression. Ulcers may also occur in diabetes, and vasculitis, or may be due to pyoderma gangrenosum, as well as secondary to infection, trauma, or malignant disease.

Decubitus ulcers (pressure sores) are the result of localized ischemia secondary to prolonged pressure in patients who are immobile. They are most common over the sacrum ischial tuberosities, heels, occiput, shoulders, and elbows. The ulcers are often deep and sloughy. Neuropathic ulcers result from decreased cutaneous innervation, resulting in diminished sensation, and are most commonly seen on the feet. Leg ulcers may also be due to sickle cell disease, idopathic thrombocytopenic purpura, tuberculosis, syphillis, and deep fungal infections.

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