An immature scar is red, slightly elevated and may be pruritic or tender. With time, it will usually become mature. A mature scar is flat and usually slightly paler, but occasionally darker than the surrounding skin. A linear hypertrophic scar is red, raised and confined to the original borders of the incision. It usually occurs weeks after surgery and can continue to increase in size over the next few months. It will often become less raised with time.
A widespread hypertrophic scar, such as a burn scar, is red, raised and confined to the original borders of injury. Minor keloids are raised and usually pruritic. They extend beyond the borders of original injury, over the normal skin. They can develop up to a year post injury. They do not regress spontaneously, and if excised, usually return. Major keloids are over 5 mm in diameter. They can be painful, and often will continue to spread over years. Keloids have a familial predilection. They are much more common in blacks and Asians than in whites.
Hypertrophic scarring and keloid formation are the result of excess collagen accumulation in a healing wound. The collagen is largely Type III, the form found in normal immature scars. Causes include excessive skin tension, wound infection, delayed healing, abnormal fibroblast metabolism, and an array of hereditary abnormalities.
The importance of excess tension cannot be overemphasized. Hypertrophic scars tend to form in areas of high tension, such as the anterior chest and upper back. All measures for reducing tension on a healing scar should be employed. The molecular mechanisms for pathological scarring are under intense investigation.
Many studies have shown that levels of various cytokines are elevated in hypertrophic scars and keloids. For example, the transforming growth factor-beta (TGF-ß) superfamily has been implicated in hypertrophic scarring. Other cytokines, such as tumor necrosis factor and interleukin-1, show decreased levels in keloids. Research is ongoing, and several active clinical trials are evaluating agents that inhibit or increase key mediators in the process of excessive scarring.
Surgery alone is not recommended for keloids due to the very high rate of recurrence (50-100%). It should be combined with additional treatment modalities such as steroid injection or silicone sheeting. For hypertrophic scars, excision alone may be indicated if it is felt that the abnormal scarring was due to excessive tension or wound complications. In such cases, excision should be accompanied by a measure to decrease tension. Splinting of the incision is most effectively accomplished by intradermal sutures left in place for 6 weeks to 6 months, depending on the degree of tension. Z-plasties and other techniques of reorienting the direction of tension can be used as well.
This modality has become standard of care for the treatment of hypertrophic scars. It should be used as a first-line agent for linear hypertrophic scars. Numerous randomized, double-blind studies have shown that it is efficacious for treating hypertrophic scars and small keloids. The benefits of silicone sheeting have not been demonstrated with other types of semi- or total occlusive dressings.
Since this treatment is painless, it is an excellent option for children or adults unwilling to tolerate more painful options. For prophylaxis in those at risk for hypertrophic scarring, treatment should begin a few days postoperatively. Silicone sheeting should be worn a minimum of 12 hours a day, and preferably the entire day. It should be continued for several weeks postoperatively.
Years of clinical experience and many randomized, prospective trials have shown that triamcinolone injected into the scar is efficacious at decreasing scarring. Response rates range from 50-100%, with a recurrence rate of 10-50%. It should be the first-line therapy for keloids and second-line for hypertrophic scars. In combination with other therapies such as surgery and cryotherapy, corticosteroid injections can be even more effective.
Side effects are common and include skin atrophy, telengiectasias and pigment changes. The exact mechanism by which steroids diminish scarring is still largely unknown. What has been shown is that topical steroids are not effective in reducing scarring.
Compression is the first-line treatment for post-burn, widespread hypertrophic scars. In order to be effective, pressure must be maintained between 24-30 mm Hg for at least 6 months duration. The longer the treatment, the more efficacious pressure therapy has been shown to be.
Adhesive microporous paper tape applied to fresh incisions for several weeks postoperatively is moderately useful in preventing hypertrophic scaring. The mechanism is not entirely clear. It is likely a combination of occlusion and splinting of the incision.
Radiotherapy should be reserved for adults with keloids resistant to other treatment modalities. Monotherapy is controversial, and most surgeons recommend using it following surgical excision. Response rates range from 10-90% for radiotherapy alone, and in combination with surgery it is more likely to be effective. Recurrence is very common, ranging from 50-100%.
This modality has shown benefit in acne-induced scarring. It should not be used for large scars. Side effects are common and include hypo- or hyperpigmentation, skin atrophy and pain.
Various lasers have been used in an attempt to treat hypertrophic scars and keloids, and the results have been largely disappointing. The flashlamp-pumped pulsed-dye laser appears promising, but more studies are needed. In combination with other modalities, such as corticosteroid injection, it has been shown to be effective. Its primary role is in reducing scar erythema and flattening mildly atrophic and hypertrophic scars. At this point, it is largely an emerging technology.
A number of chemotherapeutic agents have demonstrated efficacy in treating hypertrophic scarring and keloids. These include intralesional injections of interferon, 5-fluorouracil, and bleomycin, as well as topical administration with retinoic acid. Other emerging novel treatments focus on interfering with collagen synthesis and the cytokines involved in scarring, such as inhibitors of TGF-B.
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Note: This article was sent to us by: Patricia Phillips at 02102011
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