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Management Of Scar Contractures, Hypertrophic Scars, And Keloids


David A. Sherris, MD, Wayne F. Larrabee, Jr, MD, and Craig S. Murakami, MD

Scar contractures, hypertrophic scars, and keloids are all examples of abnormal tissue response to the processes of wound healing. By definition, a scar contracture is the result of contractile wound healing processes oc­curring in a scar that has already been re-epithelialized and adequately healed.25 A scar contracture typically appears as a fixed, rigid scar that causes functional or cosmetic deformities. Hypertrophic scars and keloids produce a clinical picture of an erythematous, tender, elevated, unsightly scar that may itch, become hyperpigmented, or produce a contraction cicatrix. The clinical difference between the two rests in the fact that a hypertrophic scar that persists for more than 12 months, and whose mar-gins extend beyond the confines of the original wound, is a keloid.22 In this article, the clinical appearance, etiology, pathogenesis, and treatment of scar contractures, hypertrophic scars, and keloids are discussed. Be-cause of the close relationship between hypertrophic scars and keloids, these entities are considered together.

The rigid, firm, erythematous scar contracture commonly causes sig­nificant cosmetic and functional abnormalities. The medial canthus, nasal ala, oral commissure, and neck are the most common sites for scar con­tractures on the head and neck, although any area can be affected.

PATHOGENESIS
Wound contraction is a normal phase in cutaneous wound healing by which the edges of a wound are pulled toward the center of the wound itself. This phenomenon has been extensively studied, and two predom­inant theories about its etiology deserve mention, the myofibroblast the­ory and the fibroblast locomotion theory. The major difference between the two theories of wound contracture is that the myofibroblast theory is based on the action of the myofibroblast (Fig. 1). This specialized fibroblast is found predominantly in granulating wounds but also is iden­tified in burn scars, contractures around silicon implants, the palmar fascia in Dupuytren's contracture, keloids, and hypertrophic scars. The myofibroblast is a fibroblast with many morphologic and functional characteristics of smooth muscle, including the ability to contract.

Electron microscopic examination of the myofibroblast
Figure 1. Electron microscopic examination of the myofibroblast demonstrates the cytoplas­mic filaments (small arrows), the rough endoplasmic reticulum (long arrows), and the multiple indentations of the wall of the nucleus (thin arrows), characteristic of this cell type (original magnification x 1500).

According to the myofibroblast theory, myofibroblasts act as a contractile multicellular unit analogous to a muscle, thereby generating rearrange­ment of the surrounding connective tissue matrix. In contrast, the fibro­blast locomotion theory is based on the premise that the motion of indi­vidual fibroblasts through the wound causes local rearrangement of the surrounding connective tissue matrix.25,29 Most likely, both phenomena take place in vivo and combine to cause the wound contraction necessary for normal wound healing. Presumably, scar contracture represents either a derangement in these systems or a normal contracture in a region that cannot structurally resist the forces of contracture. In both cases, the con­tracture results in functional and cosmetic deformity associated with this serious problem.

TREATMENT
The avoidance of wound contracture starts with the judicious plan­ning of surgical incisions. Incisions made parallel to relaxed skin tension lines heal with a smaller chance of scar contracture. Likewise, incisions planned longitudinally across concave surfaces (e. g., the medial canthus) or joint spaces are more likely to form hypertrophic scars and scar con­tracture. Using irregular incisions (Z-shaped, gullwing-shaped) or placing incisions in joint creases increases the chance of normal healing significantly.

Large open wounds with associated tissue loss present a unique prob­lem. These wounds heal by scar contracture. Depending on the location of the wound, distortion may or may not be significant. For instance, a wound of the central forehead heals by second intention with significant wound contracture but minimal distortion secondary to the underlying bony structure. Conversely, a similar wound of the neck heals secondarily by contracture with significant distortion and associated morbidity of re­stricted head movement and cosmetic deformity; in these cases, it may be advantageous to prevent healing by second intention with either a skin graft or flap. Full-thickness skin grafts (FTSGs), flaps, and, to a lesser extent, split-thickness skin grafts (STSGs) decrease wound contraction. This finding may be secondary to the life cycle of the myofibroblast in each of these settings. Namely, in granulating wounds, the myofibroblast is present the longest, whereas in STSG-treated wounds, it is present an intermediate period, and in FTSG-treated wounds, it is present the short­est time.25 This finding suggests that by shortening the time the myofi­broblast is present in the healing area, one can limit scar contracture.

Once a defect is present in an unfavorable region, the application of splinting, range-of-motion exercises, and pressure dressings during the healing phase helps prevent the formation of scar contractures. For in-stance, long-term splinting of oral commissure burns helps to promote favorable healing. Likewise, pressure garments worn during the healing phase of significant body burns help prevent scar contracture formation. The mechanism by which each of these methods prevents scar contracture is unclear. Most likely, the mechanism is mechanical, because discontinuation of the splint or pressure while granulation tissue is still present leads to rapid wound contracture Six to 12 months after initial tissue injury and utilization of previously mentioned treatment modalities, surgical intervention is appropriate. Z-plasty, multiple Z-plasties, and flap reconstruction are often necessary to adequately release persistent contractures. Webbing of the medial can-thus, oral commissure, and neck is especially amenable to single or mul­tiple Z-plasty reconstruction (Fig. 2). In the head and neck, the limbs of the Z-plasty should be limited to 1.5 cm. in length. If feasible, splinting, pressure dressing, and range-of-motion exercises are all beneficial during the healing phase in preventing recontracture. Intralesional injection of triamcinolone acetonide, 10 mg/mL (Kenalog 10) at intervals of 4 to 6 weeks can also help decrease scar contracture. Care must be taken to keep the injection within the scar tissue. Extravasation into the normal tissue causes tissue atrophy, telangiectasia formation, and hypopigmentation.

Patient with scar contracture and hypertrophy on the neck
Figure 2. A, Patient with scar contracture and hypertrophy on the neck. B, The upper end of the scar was excised and repaired with multiple Z-plasties. The lower end of the scar under-went multiple 10 mg/mL intralesional injections of triamcinolone acetonide. C, Patient appears 1 year postoperatively with improved neck mobility and appearance.

The hypertrophic scar is familiar to every surgeon as a raised, ery­thematous, pruritic lesion that, although unsightly, remains within the confines of the original scar. Typically, hypertrophic scars regress with time and may eventually result in widened, depressed scars." Conversely, keloids initially develop as hypertrophic scars but soon extend beyond the confines of the initial wound and rarely regress on their own. Both keloids and hypertrophic scars are more common in younger, darker-skinned patients.' These lesions also occur more commonly in wounds closed under tension. Certain anatomic areas, such as the deltoid region, sternum, and upper back, have high skin tension. These regions are es­pecially vulnerable to hypertrophic scar formation. The upper lip, probably because of constant muscle action, is a common site of hyper­trophic scar formation in young patients. In the head and neck, the most common sites of keloid formation are the ear lobule and the neck.

Histologic differentiation between keloids and hypertrophic scars is extremely difficult, especially in the early phases of formation. Numerous pathologists have described parameters to distinguish these two fibrous tumors. The most consistent differences are the presence of abun­dant mucin and brightly eosinophilic bundles of collagen in the keloid, which are not present in the hypertrophic scar. Evaluation with electron microscopy has yielded contradictory results. The myofibroblast has been found to be more prevalent in either the keloid or the hypertrophic scar, depending on the study. We believe that the myofibroblast is impor­tant in the formation of both entities, and that its abundance is related to the maturity, rather than the type, of keloid or scar examined. Possibly, the myofibroblast is present for the shortest time in the normal scar, for an intermediate time in the hypertrophic scar, and for the longest time in the keloid scar.

PATHOGENESIS
At the biochemical level, keloids and hypertrophic scars are difficult to distinguish. Depending on the maturity of lesions studied, researchers have found both keloid and hypertrophic scars to exhibit variable levels of certain cell types, collagen synthesis rates, collagen degradation rates, and so on, in comparison with normal scar tissue. Much of this variability stems from the fact that studies of abnormal scar formation are based on tissue obtained from various human subjects. The lack of a re-liable animal model for abnormal scar formation makes the study of hy­pertrophic scar and keloid pathogenesis difficult.

What can be said with certainty is that the bulk of tissue excess pres­ent in both conditions is overabundant extracellular matrix. Glycopro­teins (especially chondroitin 4-sulfate) and water are both significantly increased in the extracellular matrix of keloids and hypertrophic scars."

Collagen production, degradation, total amount, and types present are all variable, depending on the study quoted. The variability in these param­eters is merely a reflection of the heterogeneity of the lesions studied, especially as related to the maturity of the lesion.

We hypothesize that the fibroblast, or the myofibroblast, or both are the key cells responsible for keloid and hypertrophic scar formation. These cell types produce the bulk of extracellular matrix components during normal wound healing. In fact, experimental evidence suggests that hy­pertrophic scars and keloids result from excessive amounts of collagen and proteoglycan production or from lack of remodeling of these moie­ties.''-" We also hypothesize that wound tension is a major factor in the formation of both the hypertrophic scar and the keloid, which occurs sec­ondary to direct biochemical changes induced by this mechanical factor. Most likely these changes are a direct result of the effect of wound tension on the metabolism of the fibroblast or myofibroblast. Fibroblasts have been shown to increase cell proliferation in response to mechanical tension in vitro.4 Mechanical stretch alone has been shown to raise the number of myofibroblasts in mouse dermis in vivo.28 Presumably, mechanical ten­sion is also responsible for a positive balance in the collagen and proteo­glycan production-degradation cycle in the wound healing under exces­sive tension. We are currently studying the effects of mechanical tension on wound healing at the biochemical level. The cause-effect relationship between hypertrophic scar and keloid formation as well as other etiologic factors, such as the age and race of the patient, remain more highly spec­ulative and are not discussed here.

TREATMENT
The treatment of hypertrophic scars and keloids begins with proper application of basic soft tissue handling techniques at primary wound repair. When incisions are planned, they should be parallel to relaxed skin tension lines so as to lessen the wound's closing tension. Both planned and traumatic wounds should be cleansed well and handled gently dur­ing closure. Care should be taken to close in layers to avoid formation of dead space formation and further decrease closing tension. Appropriate splints and dressings should be utilized in the postoperative period. Pres­sure dressing applied during the healing process of high-risk wounds or wounds demonstrating early hypertrophic scar, keloid scar, or scar con­tracture formation arrests progression and causes regression of the ab­normal scarring process. Pressure-treated scars have been demonstrated to have decreases in intercollagen cohesiveness, total chondroitin 4-sulfate content, and fibroblast content, presumably secondary to local hypoxia accentuated by the mechanical pressure. When applied, pressure dressings and splints should be used whenever possible for 4 to 6 months, to lessen the risk of contracture and scar hypertrophy after removal of the apparatus.

CORTICOSTEROIDS
Corticosteroids play a prominent role in the therapy of both hyper­trophic scars and keloids. Topical and intralesional glucocorticoids have been used for many years to alter cutaneous healing. The effects of exces­sive glucocorticoids on cutaneous wound healing include decreasing col­lagen synthesis, glycosaminoglycan synthesis, the inflammatory process in the wound, and fibroblast proliferation and increasing wound hy­poxia." Clinically, these effects translate to inhibition of fibroplasia, which is especially advantageous in the early hypertrophic scar and keloid. In addition, these effects can be exploited to lower the chances of keloid or hypertrophic scar recurrence after surgical treatment. Because of their rel­atively poor tissue absorption through intact or sutured skin, topical ster­oids help to prevent abnormal scar development in only relatively super­ficial lesions, such as dermabrasion or laser wounds." In these cases, topical fluorinated corticosteroid preparations may be useful in the pre­vention of abnormal scarring before the process has been established." We typically use 1% hydrocortisone or flurandrenolide-impregnated (Cordran) tape for such situations until clinical signs of abnormal scarring disappear.

More useful is the direct intralesional placement of corticosteroids. Numerous studies have demonstrated the efficacy of intralesional corti­costeroid therapy alone and in combination with surgery for the treatment of keloids and hypertrophic scars.7, 11,12,14,20,22,26 In both situations, care must be taken to avoid the extravasation of steroid into surrounding nor­mal soft tissue, which would cause tissue atrophy, telangiectasia forma­tion, hypopigmentation, and possible worsening of the original problem. For the treatment of developing hypertrophic scars, we start therapy with triamcinolone acetonide, 10 mg/mL (Kenalog 10), injected intralesionally with a 25- or 27-gauge needle at 4- to 6-week intervals. Treatment is stopped (1) when there is significant clinical regression of the scar, (2) when surgical treatment seems eminent, or (3) when the previously men­tioned adverse effects appear. Two or three injections are usually suffi­cient, although occasionally, injections continue for 6 months or more.

Treatment of Hypertrophic Scars

Mature hypertrophic scars are typically amenable to surgical excision and reconstruction. Direct excision of favorably oriented hypertrophic scars, combined with postoperative dermabrasion 4 to 8 weeks postop­eratively, is commonly all that is necessary. When a hypertrophic scar is unfavorably oriented in relation to relaxed skin tension lines, aesthetic unit boundaries, or local anatomic structures or is associated with a rel­ative tissue deficiency, Z-plasty, multiple Z-plasty, or other flap recon­struction is usually necessary. These maneuvers both reorient the scar in a more favorable direction and bring in new tissue to relieve the relative shortage. Again, dermabrasion should be utilized 4 to 8 weeks postop­eratively to maximize the result.

Treatment of Keloids

Treatment of the active or mature keloid demands a more aggressive approach than that utilized with the hypertrophic scar (Table 1). The lit­erature supports the use of intralesional corticosteroids alone or in com­bination with surgical excision to minimize the chance of recurrence. Various authors have advocated the use of laser excision or cryosurgical excision in combination with corticosteroid therapy, al-though none of these studies has established the superior efficacy of these approaches over knife excision combined with corticosteroid therapy. Like Farrior and Stambaugh/ we utilize a regimen of preex­cisional intralesional steroid injection even when the keloid appears so large and mature that eventual surgical excision is inevitable. Our ration-ale is that the affected patients, who are notoriously noncompliant, must understand and accept the need for continued intralesional corticosteroid therapy, especially after surgery, to prevent the recurrence of the keloid. If a patient cannot comply with the presurgical injection schedule, the chance of successful therapy over the long term is significantly dimin­ished, and surgical excision is deferred.

Table 1. KELOID TREATMENT PROTOCOL

Time* Treatment Regimen
0 Injection 1: Equal parts triamcinolone acetonide, 40 mg/mL, and 2% lidocaine with 1:100,000 epinephrine.
1 month Injection 2: same as injection 1.
1 month Injection 3: same as injection 1.
1 month Surgical excision of keloid and injection 4: triamcinolone acetonide, 10 mg/mL.
5-7 days Suture removal.
1-3 weeks Injection 5: 1 part triamcinolone acetonide, 40 mg/mL, to 3 parts 1% lidocaine with 1:100,000 epinephrine.
4-6 weeks Injection 6: same as injection 5.
4-6 weeks Injection 7: same as injection 5.
4-12 weeks Continue injections as needed to prevent recurrence. Consider pressure dressing at signs of recurrence. Follow patients at least 2 years postoperatively.
Each time given is counted from the previous step of the protocol.

The presurgical injection schedule consists of three monthly injections of triamcinolone acetonide, 40 mg/mL (Kenalog 40), mixed with equal parts of 2% lidocaine and 1:100,000 epinephrine (see Table 1). The solution is injected with either a 25- or 27-gauge needle directly into the lesion. Overlying tissue commonly blanches, and the injections can be somewhat uncomfortable. Care is taken to avoid steroid extravasation into the sur­rounding soft tissues. Once the presurgical regimen has been completed, surgical excision is planned for the fourth monthly visit. We excise the entire keloid with the knife, taking care to minimize disruption of local normal tissue. Some surgeons advocate leaving a cuff of keloid tissue in situ, though there is not significant support in the literature to indicate that this practice decreases the chances of recurrence. Local tissue un­dermining is sometimes necessary for tension-free wound closure but is kept to a minimum. In cases associated with tissue loss not amenable to a low-tension primary closure, the wound bed is left open to heal by second intention. We do not use flap reconstruction in cases of keloid surgery, for fear of worsening the problem in the long term.

Corticosteroid injection is started at the time of surgical excision, when the wound bed and wound margins are injected with a small amount of intradermal triamcinolone acetonide, 10 mg/mL. The skin is closed with the minimal acceptable subcutaneous dissolvable suture clo­sure combined with subcuticular monofilament suture skin closure. The skin may be further supported with taping, and sutures are removed at the appropriate time according to the wound site (5 to 7 days). The wound is then monitored biweekly for the first month after suture removal, and every 4 to 6 weeks thereafter. The wound is injected with triamcinolone acetonide, 40 mg/mL diluted to 10 mg/mL, and 1% lidocaine with 1:100,000 epinephrine at the first evidence of keloid recurrence, or at 4 weeks postoperatively. Subsequent monthly visits are used to monitor the firmness of the scar and to perform further injections. A minimum of three postoperative injections is given, even when there is no evidence of keloid recurrence. If the patient remains asymptomatic, the interval between vis­its can be extended to every 3 months, with self-monitoring by the patient (Fig. 3). Most patients who have gone through our protocol to this point are quite willing to monitor their wounds and schedule appointments when there is evidence of recurrence.

RECURRENCE

Even with aggressive follow-up and care, the rate of keloid recurrence can approach 50% after combination steroid and surgical therapy.' These rates compare favorably with all other current treatment modalities avail-able. The recurrence rates quoted in the literature as 0 more than likely represent series with insufficient long-term follow-up. Most recurrences appear within the first year after surgery, although we have seen recur­rences as long as 2 years or more postoperatively. For recurrence after the described regimen, we either repeat the protocol or defer further therapy if the recurrent lesion is smaller than the primary lesion. If tolerable, pres­sure dressing application at this time can be helpful to lessen the chance of recurrence. Some authors advocate low-dose radiation therapy com­bined with surgery for recurrent lesions. Both the surgeon and the pa­tient must consider the risks associated with this aggressive therapy be-fore its utilization. We do not routinely advocate radiation therapy for recurrent keloids, because of the risk of radiation-induced malignancy in this predominantly young patient population.

Large ear lobule keloid secondary to ear piercing
Figure 3. A, Large ear lobule keloid secondary to ear piercing. B, Ear 1.5 years after treatment with the keloid treatment protocol of preoperative steroid injection, surgical incision, and post-operative steroid injection.

Other Treatment Modalities

The effectiveness of topical silicone gel sheeting in the treatment of hypertrophic scars and keloids has been demonstrated. Although the mechanism of action has not yet been determined, it has been postu­lated to be similar to the role of the stratum corneas, i.e., restoring he­mostasis by decreasing hyperemia and fibrosis,5 possibly by decreasing evaporative water loss from the healing skin.

In a prospective randomized trial, Sproat and colleagues found sil­icone gel sheets to provide superior results compared with standard tri­amcinolone acetonide (Kenalog) injection therapy. These authors reported that the use of the sheeting was less expensive than the Kenalog protocol, allowed self-administration with painless application and without con­comitant use of pressure garments, and provided easier symptomatic re-lief. The precise role of topical silicone gel sheeting in the treatment of hypertrophic scars and keloids is still being elucidated, but preliminary findings are promising.

One further therapeutic modality that shows promise for the treat­ment of keloids is the use of intralesional interferon gamma. Evidence is accumulating that this compound down-regulates collagen synthesis and may be useful in disease states characterized by fibrosis. The single clin­ical trial of this therapy demonstrated significant regression of all hyper­trophic scars and keloids treated, with minimal adverse side effects. Intralesional interferon gamma therapy alone and in combination with surgical excision deserves further study.

CONCLUSION

Although wound healing has been studied extensively for years, the true pathogenesis of keloids, hypertrophic scars, and scar contractures remains elusive. Further basic science study is necessary to clarify the causes of these conditions, so that more effective treatment modalities can be developed in the future. Until that time, the mainstays of therapy are adherence to good soft tissue surgical technique, proper use of splinting and pressure dressings, judicious administration of intralesional cortico­steroids, and the application of established techniques of scar revision surgery when necessary.

REFERENCES

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  9. Gold MH: A controlled clinical trial of topical silicone gel sheeting in the treatment of hypertrophic scars and keloids. J Am Acad Dermatol 30:506-507, 1994
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