Nathan Monhian, MD and Anil R. Shah, MD
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 total and permanent removal or effacement 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 is comprised of 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 pre-injury strength at three weeks. The ultimate tensile strength of the wound is 70–80% of that of the uninjured skin.
A. Genetic Factors
Genetic factors contributing to poor scar formation are likely to be present in patients with Fitzpatrick skin Types III and above, typically transmitted as either an autosomal dominant or recessive trait. Darker skins tend to form post-inflammatory 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, while older skin tends to scar better due to a lesser amount of tension on the wound.
Keloid and hypertrophied scars result from increased collagen production and decreased collagen degradation. Propyl hydroxylase is elevated in keloid forming skin versus normal skin. Propyl hydroxylase is responsible for hydroxylation of proline during collagen synthesis, creating a relative collagen overproduction.
B. Iatrogenic Causes
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 elective surgery, especially on the face, be delayed for at least 12–18 months after completing a course of isotretinoin.
C. Hypertrophic Scar, Keloids, and Widened Scars
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 can occur in any age group. Initially, hypertrophic scars are red, raised, pruritic, and occasionally painful, but they tend to gradually flatten over time. They appear worst at 2 weeks to 2 months after wound closure. In general, hypertrophic scars are more responsive to steroid injections than keloids.
Keloids 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 aged 10-30 years. 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 in normal scars. 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.
Skin is anisotropic, 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 to these lines are under the least possible tension while healing. Perpendicular to the RSTLs are the lines of maximal extensibility (LME). A fusiform excision parallel to the RSTLs and closed in the direction of the lines of maximal extensibility will heal under minimal closing tension and results in the best scar.
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 post-inflammatory hyperpigmentation, which may last several months. Resurfacing methods that go beyond the deep reticular dermis can cause further scarring instead of improving a scar.
A. Nonsurgical Measures
1. Intralesional agents—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 (down regulates pro-alpha 1 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 Kenalog 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.
2. Soft tissue fillers—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 bovine collagen (Zyderm, Zyplast), pooled human collagen, (micronized AlloDerm or Cymetra, CosmoDerm, CosmoPlast), hyaluronic acid (Hylaform, Restylane), hydroxyapatite (Radiesse), autologous dermis, and fat. These biologically derived materials provide temporary correction (2–12 months). Synthetic materials such as expanded polytetrafluoroethylene (e-PTFE, Goretex, SoftForm, or Ultrasoft) may also be used to provide a filling effect in depressed areas. Injectable Fibrel and silicone are no longer in widespread use.
3. Silicone sheeting, hydration, and compression—Silicone has been used with relative success in the management of hypertrophic scars, although its mechanism of action is not clearly understood. Although it was initially hypothesized to work through pressure over the scar tissue, the efficacy of silicone has been demonstrated even in non-pressure dressings. It appears that hydration, or rather, the ability of silicone to prevent wound desiccation, is a contributing mechanism. Hydration inhibits the in vitro production of collagen and glycosaminoglycans by fibroblasts. Silicone sheeting can be worn daily for as long as 12–24 hours daily, though its application is somewhat cumbersome. An alternative to silicone sheeting, silicone gel can be applied to the scar. Both silicone gel and silicone sheeting have shown positive results in the reduction of scar size and erythema.
The use of continuous pressure at 80 mm Hg provided by tight-fitting dressings has been shown to prevent and modify scar formation. The potential mechanisms of action are local tissue hypoxia and reduction of the intralesional population of mast cells, which may affect fibroblast growth.
4. Pulsed dye laser—The pulsed-dye 585 nm wavelength laser can be effective in reducing scar erythema by reducing neovascularization. Several treatments are usually required using a low to moderate fluence (5.0–7.0 J/cm2) with no overlap. Hypertrophic scars may also shrink with this treatment as a result of a reduction in the number and activity of fibroblasts.
5. Dermabrasion—Raised, depressed, or hyperpigmented scars may benefit from superficial abrasion of the skin, which blends the scar with its surrounding tissue by changing the texture, color, and depth of the scar. The technique of resurfacing depends on the nature of the deformity. The goal of this technique is to even out any uneven surfaces. The depth of the dermabrasion depends of the depth of the scar. However, dermabrasion should not go beyond the reticular dermis or greater scarring or hypopigmentation will result.
6. Laser resurfacing—Laser resurfacing has replaced mechanical dermabrasion in many practices. One advantage of laser resurfacing over mechanical dermabrasion is that the depth of penetration is easier to control. Another advantage is that there is no aerosolization of skin and blood, thereby lowering the risk of viral transmission. The thermal damage that results from laser resurfacing is advantageous in that it produces collagen contracture of 20–60%. However, the postoperative period of laser resurfacing is marked by prolonged erythema. The most common lasers in use for resurfacing are the high-energy pulsed CO2 laser, which produces photothermal injury, and the Erbium:YAG laser, which results in photomechanical injury to the skin. Combining different laser modalities, such as the pulsed dye and CO2 lasers, may provide an added advantage in scar improvement.
7. Camouflage— Many patients who seek scar revisions may not be able to camouflage the scar or have minimal knowledge of available camouflage techniques. Makeup, hair, and accessories can sometimes offer excellent coverage of the scar. Newer makeup materials and techniques allow for better and more complete coverage of unsightly defects. Opaque cosmetics with a slightly low tone, which disguises the erythema of scars, generally provide better results.
B. Preoperative Considerations
1. Patient expectations—As with any cosmetic procedure, the patient’s motivations and expectations for seeking corrective surgery should be carefully considered. In general, well-informed patients with realistic expectations will have better overall outcomes. A patient should understand that scar revision is a process to improve the appearance of the scar by adjusting, repositioning, or narrowing the scar and that complete elimination of the scar is impossible at this point. However, the physician should be sensitive to the fact that the scar may represent a traumatic experience to the patient. If the revision does not meet the patient’s expectations, the patient may suffer additional trauma. Occasionally, psychological counseling should be recommended in conjunction with scar revision.
2. Timing of scar revision—Scars in the inflammatory phase are prone to hypertrophy. The initial scar can be expected to change due to collagen remodeling and collagen fiber reorientation. While collagen remodeling continues for 1–3 years, most significant changes occur in the first 4–6 months, and an average of 6 months’ delay before revision is reasonable. Nevertheless, in clinical situations, where skin edges are grossly misaligned or the scar lies in an unfavorable direction, scar revision may prove beneficial as early as 2 months.
3. Scar analysis—Before embarking on a revision, the primary scar, and its desired location when revised, should be carefully analyzed. Scars can be classified according to their location, etiology, size, shape, contour, and color. Cosmetically favorable scars are similar in color to the surrounding tissue. They are also fine, flat, and well positioned in the face. Scars that are located in the periphery of the face, at a transition line between two cosmetic subunits, or directly in the midline are less conspicuous. The lack of one or more of these qualities results in an unsightly scar. Noticeable scars are wide, raised, or depressed, or are often hyperpigmented or hypopigmented compared to the adjacent skin. They may cut across different subunits or lie in an unfavorable direction. A scar contracture in sensitive areas—for example, at the vermilion or the eyelid—can distort adjacent structures and create cosmetic or functional deformities.
C. Surgical Measures
Appropriate scar management begins at the time of injury. Good surgical technique is essential for normal wound healing. Crushing the skin edges, tying sutures too tightly, and cauterizing too excessively may result in local tissue inflammation, necrosis, and poor scarring. Adequate wound humidity and coverage is also important for minimizing scar formation. Studies suggest that epithelial cells migrate more readily with adequate surface moisture. If the wound is kept moist, particularly with an occlusive dressing, migration proceeds more directly and efficiently. Local tissue ischemia caused by infection, hematoma, foreign bodies, anemia, or poor surgical technique may slow wound healing. In addition, local wound infection prolongs wound healing. Bacteria delay normal healing phases by directly damaging cells of wound repair by prolonging the inflammatory phase as well as competing for oxygen and nutrients within the tissue. Surgical excision of hypertrophic scars or keloids may lead to recurrence rates of 45–100%.
1. Primary excision and straight-line closure—The most common technique in the revision of scars 2 cm or shorter is primary excision and linear closure. Typically with this procedure, a small margin of normal skin in the periphery of the scar is excised with the scar in a fusiform fashion and the defect is closed in a linear fashion. The optimal length-to-width ratio to prevent standing cone deformities while maintaining the minimum length of the new scar is 3:1. The wound edges should be undermined to reduce the tension on the closure line. The defect is then closed in two layers, with subdermal absorbable sutures to minimize tension and fine monofilament sutures, such as 5.0 or 6.0 nylon or polypropylene, for the superficial layer. Wound eversion should be meticulously achieved.
With large scars, where total excision of the scar is not practical, serial excisions of the central portion of the scar with advancement of the peripheral tissue can be useful. A minimum period of 6 weeks should be allowed between each two excisions.
Small and pitted or depressed scars, such as deep acne scars, can be revised by punch excision and primary closure with wound eversion. As an alternative, small, full-thickness skin grafts can be placed into the defects and secured in position with sutures, bolstering techniques, or both.
2. W-Plasty—The W-plasty is a series of connected, triangular advancement flaps mirrored along the length of the scar. A W-plasty, unlike a Z-plasty, incorporates shorter limbs and does not result in an overall change in the length of the scar. Unfavorable scars that are short and located in forgiving locations, such as the forehead or cheeks, scars that lie perpendicular to RSTLs, pretrichial scars, and scars over curved surfaces such as the inferior mandibular border are particularly good indications of W-plasty. This procedure can make the scar less conspicuous by making it irregular, thus making it more difficult for the observing eye to track. It also disrupts wound contracture with its irregular pattern.
In designing a W-plasty, dots representing the apices of the triangles are placed 3–5 mm from the scar edge. These dots should be spaced 5–6 mm apart, and each limb of the triangle should be 3–5 mm in length. The angle of the apex of each triangle should be determined by its relationship to the RSTLs, making one of the limbs of the triangle parallel to these lines. The ends of the W-plasty should be less than 30° to avoid standing cone deformities. Alternately, an M-plasty can be utilized at the ends to prevent extending the excision. The scar is excised, the adjacent tissue is undermined, and the wound is closed with a two-layer closure. Horizontal mattress sutures can be used to enhance wound eversion.
3. Geometric broken-line closure—Geometric broken-line closure (GBLC) differs from W-plasty in that instead of using a series of triangles, it includes other alternating geometric shapes, such as squares and semicircles, along with triangles (Figure 70–1). Scars that respond well to GBLC are those that are relatively long and 45° or greater from RSTLs. Scars that are perpendicular to these lines have the best cosmetic result using GBLC. GBLC is slightly more challenging than W-plasty, but the principles and techniques are otherwise identical.
4. Z-Plasty—The Z-plasty consists of two transposition-advancement flaps designed to accomplish three goals: (1) change scar direction, (2) interrupt scar linearity, and (3) lengthen scar contracture (Figure 70–2). Z-pasty is particularly beneficial if it can reorient a scar with RSTLs or in a natural junction between facial esthetic units. Similarly, with this technique, a long scar can be broken up into several smaller components to allow better camouflage (Figure 70–3). Finally, scars that cause distortion of facial features due to scar contracture are good candidates for revision using Z-plasty.
A main advantage of Z-plasty over other techniques, such as W-plasty, is that usually no additional normal skin needs to be removed. A properly planned Z-plasty results in minimal distortion of surrounding structures. Moreover, it can counter the forces of scar contracture, thus correcting webbed or contracted scars that distort anatomic landmarks.
Precise preoperative planning of this technique is an essential requirement for its success. In its classic description, Z-plasty consists of one central and two peripheral limbs in the shape of a Z, such that two triangular flaps of equal size are created. All three limbs are of equal length, and the central limb consists of the scar that is to be lengthened and realigned. The orientation of the final scar can be determined by the direction in which the lateral limbs are placed and by varying the angles of the lateral limbs in relation to the central limb. The most commonly used angles are 30°, 45°, and 60°, which produce lengthening of the scar of 25%, 50%, and 75%, respectively. For long scars, where a single Z-plasty may produce long, linear scars, multiple Z-plasties can be used along the scar.
In performing this technique, the scar is excised along the central limb and the peripheral limbs are incised. The two triangular flaps and the surrounding tissue are mobilized and the flaps are transposed and advanced. After meticulous hemostasis, the flaps are closed using tension-reducing techniques and eversion. A passive drain with pressure dressing may be necessary to reduce the dead space and the chance of fluid accumulation under the flaps.
5. Skin grafts—Full-thickness skin grafts can be utilized in a variety of ways in scar revision. Scars can be simply excised and grafted with a full-thickness graft. Skin grafts can also be used to fill skin defects after punch excision of deep or depressed scars. Contracted scars in the lower eyelid that lead to ectropion often require replacement of the anterior lamellar defect using a full-thickness graft. Defects in the upper eyelid causing lagophthalmos can be repaired in a similar fashion using skin grafts.
6. Flaps—Flaps can be beneficial in a variety of ways in scar revision. In general, they can be used when the best option in scar revision is complete excision of the scar and reconstruction of the defect with a local flap. For example, a small scar of the nasal tip may be excised and repaired using a bilobed flap, just as one might repair a defect after ablation of a malignant growth in the same area. (For a more comprehensive discussion of local flaps, see Chapter 75, Local & Regional Flaps in Head and Neck Reconstruction.)
Most scars may be improved using a variety of scar revision techniques. Essentials of wound care are as important after the revision in order to achieve optimal outcomes. However, a scar may require several revision procedures before an outcome acceptable to the patient is achieved. The need for multiple procedures should be clearly discussed with the patient.
Chen MA, Davidson TM. Scar management: prevention and treatment strategies. Curr Opin Otolaryngol Head Neck Surg. 2005 Aug;13(4):242-7. This review paper discusses the basic science mechanism underlying aberrant wound healing, as well as the strategies for prevention and management of keloids and hypertrophic scars.
Liu W, Wang DR, Cao YL. TGF-[beta]: a fibrotic factor in wound scarring and a potential target for anti-scarring gene therapy. Curr Gene Ther. 2004; 4:123-136. This paper provides an update on the role of TGF-[beta] in scar formation and basic science gene therapy study.
Lee KK, Mehrany K, Swanson NA. Surgical revision. Dermatol Clin 2005; 23:141-150. This review provides an excellent summary of surgical techniques for scar prevention and updates on scar revision strategies including dermabrasion, laser resurfacing, intralesional steroids, excision, and geometric closures.
Blackburn WR, Cosman B: Histologic basis of keloid and hypertrophic scar differentiation. Clinicopathologic correlation. Arch Pathol 1966 Jul; 82(1): 65-71
Brown SA, Coimbra M, Coberly D, et al. Oral nutritional supplementation accelerates skin wound healing: a randomized, placebo-controlled, double-arm, crossover study. Plast Reconstr Surg 2004; 114:237-244. This paper details one of the few well-designed studies on a prescription supplement for wound healing.
Cohen IK, McCoy BJ, Mohanakumar T, Diegelmann RF: Immunoglobulin, complement, and histocompatibility antigen studies in keloid patients. Plast Reconstr Surg 1979 May; 63(5): 689-95
Ehrlich HP, Desmouliere A, Diegelmann RF, et al: Morphological and immunochemical differences between keloid and hypertrophic scar. Am J Pathol 1994 Jul; 145(1): 105-13
Panin G, Strumia R, Ursini F. Topical [alpha]-tocopherol acetate in the bulk phase: eight years of experience in skin treatment. Ann N Y Acad Sci 2004; 1031:443-447. This paper provides a useful review of topical vitamin E utility in wound healing.
Clark JM, Wang TD. Local flaps in scar revision. Facial Plast Surg. 2001;17(4):295. [PMID: 11735064] (This article reviews common techniques employed in reconstruction of facial defects and scars and provides several cases where these techniques were successfully employed.)
Rodgers BJ, Williams EF, Hove CR. W-plasty and geometric broken line closure. Facial Plast Surg. 2001;17(4):239. [PMID: 11735056] (W-plasty provides a regularly irregular scar and geometric broken-line closure provides an irregularly irregular scar. Both methods divert the attention of the eye by producing a nonlinear scar pattern.)
Figure 70–1. Geometric broken-line closure. (A) Random geometric patterns in mirror images are marked around the scar. (B) The scar is excised. (C) Wound edges are advanced and closed with appropriate sutures.
Figure 70–2. 60° Z-plasty.
Figure 70–3. Multiple Z-plasties at 45°.
Clinical differences become more apparent as lesions mature. The most consistent histologic difference is the presence of broad, dull, pink bundles of keloid collagen in keloids, which is not present in hypertrophic scars
The collagen fibrils in keloids are more irregular, abnormally thick, and have unidirectional fibers arranged in a highly stressed orientation. Biochemical differences in collagen content in normal hypertrophic scars and keloids have been examined in numerous studies. Collagenase activity, ie, prolyl hydroxylase, has been found to be 14 times greater in keloids than in both hypertrophic scars and normal scars. Collagen synthesis in keloids is 3 times greater than in hypertrophic scars and 20 times greater than in normal scars. Type III collagen, chondroitin 4-sulfate, and glycosaminoglycan content are higher in keloids than in both hypertrophic and normal scars. Collagen cross-linking is greater in normal scars, while keloids have immature cross-links that do not form normal scar stability.
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.
Keloids have the clinical appearance of a raised amorphous growth and are frequently associated with pruritus and pain (see Images 1-2). Scanning electron microscopy reveals a number of distinguishing features, including randomly organized collagen fibers in a dense connective tissue matrix. In normal scars, the collagen bundles are arranged parallel to the skin surface (see Image 3).
(Emedicine. Otolaryngology. Hypertrophic scars and keloids)
Hypertrophic scars are more common than keloids. Hypertrophic scars may occur in persons of any age or at any site, and they tend to spontaneously regress. In general, hypertrophic scars are more responsive to treatment. While keloids occur most frequently in black persons, they may occur in persons of any race with a proven tendency to keloid formation. Keloids are 5-15 times more common in black persons than in white persons (Alhady, 1969). This predilection for formation in persons of certain races is not observed with hypertrophic scars.
Keloids are more prevalent in persons aged 10-30 years, while hypertrophic scars occur in persons of any age. In general, the risk for either type of abnormal scar diminishes with age (Murray, 1981). Furthermore, the propensity for keloid formation can be familial, genetically transmitted as an autosomal dominant or recessive trait (Omo-Dare, 1975; Rao, 1990).
Widened scars can occur in persons of any age. Widened scar formation occurs with no predilection to sex or ethnicity. No inheritance pattern is associated with the risk for scar widening. Widened scars are most commonly found to involve the arms, legs, and abdomen.
Although multiple factors are involved in abnormal scar formation, studies indicate that keloid and hypertrophied scars result from increased collagen production and decreased collagen degradation. Cohen demonstrated that levels of the collagen-related enzyme prolyl hydroxylase are elevated in keloid-affected skin compared with normal skin (Cohen, 1971). Prolyl hydroxylase is required for the hydroxylation of proline during collagen synthesis, suggesting that collagen overproduction occurs with keloids.
Upon clinical examination, keloids and hypertrophic scars are raised above the skin level. Hypertrophic scars are self-limited; they hypertrophy within the confines of the wound. Initially, hypertrophied scars can be raised, red, pruritic, and even painful; however, over time, they become pale and flat. Hypertrophied scars appear worst at 2 weeks to 2 months.
Keloid scars can be differentiated from hypertrophic scars by their spread beyond the original wound. Keloid scars tend to remain red, pruritic, and painful for many months to years until menopause. Patients usually have a personal or familial history of keloid formation.
Different from hypertrophic and keloid scars, widened scars are flat and sometimes depressed. With adequate wound maturation, these wounds fade to the pigment of the surrounding uninjured skin. Widened scars are not usually red or pruritic.