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Author: admin | 01.03.2015 | Category: Relieve Tinnitus

Scar contractures, hypertrophic scars, and keloids are all examples of abnormal tissue response to the processes of wound healing.
The rigid, firm, erythematous scar contracture commonly causes sig­nificant cosmetic and functional abnormalities. 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. 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. The avoidance of wound contracture starts with the judicious plan­ning of surgical incisions. 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. 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.
Histologic differentiation between keloids and hypertrophic scars is extremely difficult, especially in the early phases of formation.
What can be said with certainty is that the bulk of tissue excess pres­ent in both conditions is overabundant extracellular matrix. Collagen production, degradation, total amount, and types present are all variable, depending on the study quoted. We hypothesize that the fibroblast, or the myofibroblast, or both are the key cells responsible for keloid and hypertrophic scar formation.
The treatment of hypertrophic scars and keloids begins with proper application of basic soft tissue handling techniques at primary wound repair.
Corticosteroids play a prominent role in the therapy of both hyper­trophic scars and keloids. Treatment of the active or mature keloid demands a more aggressive approach than that utilized with the hypertrophic scar (Table 1). The effectiveness of topical silicone gel sheeting in the treatment of hypertrophic scars and keloids has been demonstrated. One further therapeutic modality that shows promise for the treat­ment of keloids is the use of intralesional interferon gamma. Although wound healing has been studied extensively for years, the true pathogenesis of keloids, hypertrophic scars, and scar contractures remains elusive. Craig RDP, Schofield JD, Jackson DS: Collagen biosynthesis in normal and hypertrophic scars and keloid as a function of the duration of the scar. Davey RB: The use of silicone gel and Silastic foam in burn scar management: How does it work? Diegelmann RF, Cohen IK, McCoy BJ: Growth kinetics and collagen synthesis of normal skin, normal scar, and keloid fibroblasts in vitro. Gold MH: A controlled clinical trial of topical silicone gel sheeting in the treatment of hypertrophic scars and keloids.
Henderson DL, Cromwell TA, Mes LG: Argon and CO, laser treatment of hypertrophic and keloid scars. Larrabee WF, East CA , Jaffe HS, et al: Intralesional interferon gamma treatment for keloids and hypertrophic scars. RN, Siegel HW, Gillooley JF, et al: Treatment of keloids by combination surgical excision and immediate postoperative x-ray therapy.
Peacock EE, Madden JW, Trier WC: Biologic basis for the treatment of keloids and hypertrophic scars. Hello, my name* is and I am interested in scheduling an appointment with you and would like to receive information about . 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.
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). Incisions made parallel to relaxed skin tension lines heal with a smaller chance of scar contracture. For in-stance, long-term splinting of oral commissure burns helps to promote favorable healing.
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.
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. These cell types produce the bulk of extracellular matrix components during normal wound healing. When incisions are planned, they should be parallel to relaxed skin tension lines so as to lessen the wound's closing tension. Topical and intralesional glucocorticoids have been used for many years to alter cutaneous healing. Direct excision of favorably oriented hypertrophic scars, combined with postoperative dermabrasion 4 to 8 weeks postop­eratively, is commonly all that is necessary.

The skin is closed with the minimal acceptable subcutaneous dissolvable suture clo­sure combined with subcuticular monofilament suture skin closure. The recurrence rates quoted in the literature as 0 more than likely represent series with insufficient long-term follow-up. 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. Evidence is accumulating that this compound down-regulates collagen synthesis and may be useful in disease states characterized by fibrosis.
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.
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 major difference between the two theories of wound contracture is that the myofibroblast theory is based on the action of the myofibroblast (Fig. 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.
Likewise, pressure garments worn during the healing phase of significant body burns help prevent scar contracture formation. 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.
Much of this variability stems from the fact that studies of abnormal scar formation are based on tissue obtained from various human subjects. Both planned and traumatic wounds should be cleansed well and handled gently dur­ing closure.
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. 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). Most recurrences appear within the first year after surgery, although we have seen recur­rences as long as 2 years or more postoperatively.
B, Ear 1.5 years after treatment with the keloid treatment protocol of preoperative steroid injection, surgical incision, and post-operative steroid injection. 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.
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. 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. In both cases, the con­tracture results in functional and cosmetic deformity associated with this serious problem.
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.
Certain anatomic areas, such as the deltoid region, sternum, and upper back, have high skin tension. The lack of a re-liable animal model for abnormal scar formation makes the study of hy­pertrophic scar and keloid pathogenesis difficult. Most likely these changes are a direct result of the effect of wound tension on the metabolism of the fibroblast or myofibroblast.
Care should be taken to close in layers to avoid formation of dead space formation and further decrease closing tension. In addition, these effects can be exploited to lower the chances of keloid or hypertrophic scar recurrence after surgical treatment. 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. These maneuvers both reorient the scar in a more favorable direction and bring in new tissue to relieve the relative shortage. The wound is then monitored biweekly for the first month after suture removal, and every 4 to 6 weeks thereafter. 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. Intralesional interferon gamma therapy alone and in combination with surgical excision deserves further study.
Be-cause of the close relationship between hypertrophic scars and keloids, these entities are considered together. Using irregular incisions (Z-shaped, gullwing-shaped) or placing incisions in joint creases increases the chance of normal healing significantly.
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. The myofibroblast has been found to be more prevalent in either the keloid or the hypertrophic scar, depending on the study.
Two or three injections are usually suffi­cient, although occasionally, injections continue for 6 months or more.

Again, dermabrasion should be utilized 4 to 8 weeks postop­eratively to maximize the result.
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. Once the presurgical regimen has been completed, surgical excision is planned for the fourth monthly visit. If tolerable, pres­sure dressing application at this time can be helpful to lessen the chance of recurrence. The myofibroblast is a fibroblast with many morphologic and functional characteristics of smooth muscle, including the ability to contract.
Full-thickness skin grafts (FTSGs), flaps, and, to a lesser extent, split-thickness skin grafts (STSGs) decrease wound contraction.
Z-plasty, multiple Z-plasties, and flap reconstruction are often necessary to adequately release persistent contractures. The upper lip, probably because of constant muscle action, is a common site of hyper­trophic scar formation in young patients. 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.
We are currently studying the effects of mechanical tension on wound healing at the biochemical level. 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. We excise the entire keloid with the knife, taking care to minimize disruption of local normal tissue.
Subsequent monthly visits are used to monitor the firmness of the scar and to perform further injections.
Some authors advocate low-dose radiation therapy com­bined with surgery for recurrent lesions. This finding may be secondary to the life cycle of the myofibroblast in each of these settings. Webbing of the medial can-thus, oral commissure, and neck is especially amenable to single or mul­tiple Z-plasty reconstruction (Fig. In the head and neck, the most common sites of keloid formation are the ear lobule and the neck. 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. 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. 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.
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.
A minimum of three postoperative injections is given, even when there is no evidence of keloid recurrence.
Both the surgeon and the pa­tient must consider the risks associated with this aggressive therapy be-fore its utilization.
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. Local tissue un­dermining is sometimes necessary for tension-free wound closure but is kept to a minimum. If the patient remains asymptomatic, the interval between vis­its can be extended to every 3 months, with self-monitoring by the patient (Fig. We do not routinely advocate radiation therapy for recurrent keloids, because of the risk of radiation-induced malignancy in this predominantly young patient population. 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.
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. If feasible, splinting, pressure dressing, and range-of-motion exercises are all beneficial during the healing phase in preventing recontracture.
Extravasation into the normal tissue causes tissue atrophy, telangiectasia formation, and hypopigmentation.

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