Keloids are dermal hyperproliferative growths with excessive accumulation of dense fibrous tissue that may appear in areas of trauma. By definition, keloids are scars that extend beyond the borders of the original wound and do not regress spontaneously. In addition to the cosmetic disfigurement and negative psychological impact that keloids may cause the patient, these scars can often present with intense pain and pruritus.
The therapeutic options for keloids are numerous; however, there is no one modality that is considered to be universally safe and effective. Prevention of recurrence should be the main determinant in treatment selection. The initial rule of treatment involves prevention and patient education. It is of the utmost importance to close wounds with minimal tension and inflammation. Non-essential cosmetic surgery should be avoided in patients predisposed to developing keloids. These scars commonly develop in high-tension areas of the body. Incision sites in the skin of the mid-chest and skin overlying joints should be avoided, and surgical wounds should parallel skin creases.
Common therapeutic modalities include occlusive dressings, compression therapy, intralesional corticosteroid injections, intralesional interferon injections, intralesional 5-fluorouracil injections, cryosurgery, surgical excision, radiation therapy, and laser therapy. As no single therapy is vastly superior or universally efficacious, combination therapies have led to the best success rates.
Intralesional corticosteroids have been the mainstay of treatment for keloids. The most commonly used is triamcinolone acetonide in concentrations of 10–40 mg/mL administered intralesionally with a 25–27-gauge needle at 4- to 6-week intervals. Topical corticosteroids and topically applied corticosteroid-impregnated tape are also used frequently; the basis for the latter involves recent data demonstrating that occlusion enhances percutaneous penetration of steroid by the formation of a drug reservoir within the stratum corneum. Silicone gel sheets and silicone occlusive dressings have anti-keloidal effects, which appear to be a result of hydration.
Pressure devices are thought to induce local tissue hypoxia and have been shown to have a thinning effect on keloids. A novel idea in the treatment of keloids and hypertrophic scars is the use of intralesional interferon-α2b, which has been used successfully to reduce scar height and postoperative recurrences, via a mechanism of collagen synthesis inhibition. Interferon-γ has also been evaluated in the treatment of keloids, with modest results.
Cryotherapy can be used as monotherapy or in conjunction with other treatment modalities, most commonly triamcinolone, with reported efficacy. Its mechanism of action involves the induction of vascular damage and tissue anoxia that ultimately leads to necrosis. However, some reported side effects have included hypopigmentation and postoperative pain. A specialized intralesional needle cryoprobe method has been recently reported to result in better efficacy and fewer side effects.
Radiation therapy has been used as monotherapy or as an adjuvant to surgical excision. The carcinogenesis risks of radiotherapy are extremely small; however, the concept of using potentially harmful radiation to treat benign lesions is a persistent and important issue.
Surgical excision alone yields widely varying results with high (55–100%) recurrence rates. The combination of surgical excision with other modalities, such as intralesional corticosteroids or with pressure dressing, X-ray therapy, interstitial radiation, and brachytherapy, reduces recurrence rates to a range of 10–50%.
CO2 and argon lasers have been used in the past in the treatment of keloids, but have recently been replaced by the Nd:YAG and 585 nm pulsed dye laser because of their better efficacy and fewer adverse effects. Intralesional injection of 5-fluorouracil has been beneficial for hypertrophic scars and for keloids. Bleomycin, retinoic acid, intralesional verapamil, and mitomycin C have all been reported to have good efficacy in small clinical trials, but more clinical experience with these agents is needed.
Dermatofibrosarcoma protuberans can be easily misdiagnosed as a keloid. Histopathology may help differentiate the two, but expression of CD34 by tumor cells occurs only in dermatofibrosarcoma protuberans.
A new uniform protocol of combined corticosteroid injections and ointment application reduces recurrence rates after surgical keloid/hypertrophic scar excision.
Twenty-one keloids were treated with surgical excision, then corticosteroid injections after removal of the sutures and every 2 weeks (for five more times) thereafter. In addition, all postsurgical wounds received self-administered steroid ointment application twice daily for 6 months after suture removal. Recurrence occurred in three of the 21 keloid cases (14.3%) and one of the six hypertrophic scar cases (16.7%).
Keloids treated with topical injections of triamcinolone acetonide. Immediate and long term results.
In a prospective clinical trial of 52 patients, intralesional injections of triamcinolone acetonide alone resulted in significant flattening and reduction of pruritus in 93% of the keloids. One-third had partial recurrence at 1 year, and at 5 years more than 50% had recurred. All recurrences were successfully treated with further triamcinolone acetonide injections.