General Considerations
With advances in the knowledge of wound healing, as well as the development of better materials and techniques, many options have become available in the treatment of patients with unsightly scars. Nevertheless, no technique has been devised to allow for total and permanent elimination of scars. Patients should be counseled to understand that the goal of scar revision is to replace one scar for another to improve the appearance and the acceptability of the scar.
The wound healing process is divided into three stages. In the inflammatory phase, the release of inflammatory mediators results in migration of fibroblasts into the wound. During the proliferative phase, an extracellular matrix is formed that comprises proteoglycans, fibronectin, hyaluronic acid, and collagen secreted by fibroblasts. Angiogenesis and re-epithelialization of the wound also occur during the proliferative phase. Collagen and the extracellular matrix mature in the remodeling phase, and the wound contracts. Wound strength reaches 20% of its preinjury strength at 3 weeks. The ultimate tensile strength of the wound is 70–80% of that of the uninjured skin.
Pathogenesis
Genetic factors contributing to poor scar formation are likely to be present in patients with Fitzpatrick skin Types III and above. Darker skins tend to form postinflammatory hyperpigmentation and are more likely to form keloids or hypertrophic scars. Younger skin has more tensile strength, which can lead to widening of the scar, whereas older skin tends to scar better because of a lesser amount of tension on the wound.
Iatrogenic causes of poor scar formation include excessive soft tissue trauma while handling the skin, failure to reapproximate and evert the wound edges properly, and closure under excessive tension. Failure to evert the wound edges at the time of closure leads to formation of a depressed scar. Lack of deep support of the wound can lead to excessive tension on wound edges, resulting in a widened scar. Sutures from facial wounds should be removed after 5–7 days. Removing sutures too early or too late may lead to a wide scar or unsightly tracking, respectively. Early treatment with steroids or isotretinoin (Accutane) can adversely affect wound healing. It is recommended that laser resurfacing procedures or elective surgery, especially on the face, be delayed for at least 12–18 months after completing a course of isotretinoin.
Hypertrophic scars are self-limited scars, which hypertrophy within the limits of the wound but above the skin level. Hypertrophic scars are more common than keloids and occur without race predilection and in any age group. Initially, these scars are red, raised, pruritic, and occasionally painful, but they tend to flatten over time. They appear worse at 2 weeks to 2 months after wound closure. In general, hypertrophic scars are more responsive to steroid injections than are keloids.
Keloid scars can be distinguished from hypertrophic scars by spreading beyond the original wound. Keloids have a distinct race predilection to darker skins and occur most often in patients who are 10–30 years old. In contrast to hypertrophic scars, keloid scars remain raised, red, pruritic, and occasionally painful rather than regressing at a few months.
Widened scars are typically flat and depressed and do not have an erythematous or pruritic phase. They occur without race or age tendency and occur most frequently on the body. Wound color typically improves to match the uninjured skin with time.
Histologically, the collagen in both keloids and hypertrophic scars is organized in discrete nodules, frequently obliterating the rete pegs in the papillary dermis of the lesions. While collagen in normal dermis is arranged in discrete fascicles separated by considerable interstitial space, collagen nodules in keloids and in hypertrophic scars appear avascular and unidirectional and are aligned in a highly stressed configuration. Collagen synthesis is greater in keloids than hypertrophic scars. Collagen synthesis is three times greater in keloids than hypertrophic scars and 20 times greater than in normal scars. Keloids immunochemically demonstrate a greater tissue concentration of immunoglobulin G (IgG) relative to hypertrophic scars and normal skin. Disagreement exists about whether hypertrophic scars can be differentiated from keloids using light microscopy. Blackburn and Cosman described eosinophilic refractile hyaline collagen fibers, an increase in mucinous ground substance, and a lack of fibroblasts in keloids. Scanning electron microscopy findings clearly demonstrate the randomly organized sheets of collagen with no obvious relationship to the skin surface in keloid scar formation.
Clinical Findings
Skin is anisotropic and nonlinear and has time-dependent properties. The term anisotropic indicates that the mechanical properties of skin vary with direction. The relaxed skin tension lines (RSTLs) are the lines of minimal tension of the skin; incisions parallel with these lines are under the least possible tension while healing. Perpendicular to the RSTLs are the lines of maximal extensibility. A fusiform excision parallel with the RSTLs and closed in the direction of the lines of maximal extensibility heals under minimal closing tension and results in the best scar.
Complications
Complications of scar revision vary according to the method used. These include local infection, graft or flap necrosis, and further scarring after the revision. Viral reactivation of the herpes zoster virus is a potential complication after dermabrasion or laser resurfacing. Laser resurfacing can also cause postinflammatory hyperpigmentation, which may last several months, or hypopigmentation, which may be difficult to treat. Resurfacing methods that go beyond the deep reticular dermis can cause further scarring instead of improving a scar.
Treatment
For many years, corticosteroid injection has been established in the reduction of hypertrophic scars and keloids. Common preparations include triamcinolone acetonide (Kenalog) and triamcinolone diacetate (Aristocort). Steroids decrease fibroblast proliferation, reduce blood vessel formation, and interfere with fibrosis by inhibiting extracellular matrix protein gene expression (downregulates pro-α1 collagen gene). By decreasing the production of collagen, a smaller scar is created. Doses ranging from 5 mg/mL to 40 mg/mL are injected at 3- to 6-week intervals. Typically, multiple injections are required to obtain the desired benefit. Complications of steroid injection include atrophy of the subcutaneous layer, granuloma formation, pigmentary changes, and development of telangiectasias.
New intralesional treatments have included the use of antimitotic agents such as bleomycin and 5-fluorouracil (5-FU). Small doses of these drugs may be injected into hypertrophic scar tissue with good results. Intralesional injections of 5-FU in combination with triamcinolone acetonide plus concomitant use of a pulsed-dye laser have had good results. Injections can be performed as frequently as three times per week. Injections of bleomycin into a keloid using a multipuncture technique have also shown some promise in scar flattening and preventing recurrence. Antimitotic medications should not be administered to pregnant women.
Atrophic and depressed scars may also be treated with injectable fillers in an attempt to provide bulk in areas of tissue deficiency. The most commonly used agents include nonanimal stabilized hyaluronic acid (Restylane, Juvederm, Captique, Elevess), animal based hyaluronic acid (Hylaform), hydroxyapatite (Radiesse), bovine collagen (Zyderm, Zyplast), pooled human collagen (micronized AlloDerm or Cymetra, CosmoDerm, CosmoPlast), autologous dermis, and fat. These biologically derived materials provide temporary correction (2–12 months). Synthetic materials such as expanded polytetrafluoroethylene (e-PTFE, GoreTex, SoftForm, UltraSoft, Advanta) may also be used to provide a filling effect in depressed areas. Injectable Fibrel and silicone are no longer in widespread use.