Michael R. Markiewicz and R. Bryan Bell

Outline

Soft Tissue Wound Healing

A basic understanding of wound healing is needed because of its relevance to scar formation and subsequent effects on revision.3–5 Wound healing is classified into three main phases (Fig. 22-1). These include the immediate inflammatory phase (1 to 3 days), which is characterized by a vascular and inflammatory response including local vasoconstriction for the first 5 to 10 minutes followed by a local vasodilatory response. The inflammatory phase takes place the first few days after injury, during which wound strength relies mainly on the fibrin clot. The second phase, the proliferation phase (3 to 12 days), begins within 24 hours after injury and is characterized by the recruitment of blood vessels and fibroblasts, resulting in granulation tissue. Epithelialization may be completed in 24 to 48 hours in primarily closed wounds or be delayed for as long as 3 to 5 days in wounds healing by secondary intention The final phase of wound healing is the maturation phase, during which the scar gains strength and volume and erythema decreases. Complete scar maturation and final tensile strength generally take 12 to 18 months (Fig. 22-2).

In any wound, even one with adequate primary closure, the gap between wound edges is temporarily repaired in the form of a clot consisting of platelets engrossed in a mesh of cross-linked fibrin fibers derived from fibrinogen cleaved by thrombin. The platelet clot serves as a reservoir of cytokines and growth factors that are released as platelets degranulate. Growth factors and cytokines recruit inflammatory cells, fibroblasts, and capillary ingrowth to the wound site, which invade the clot to form granulation tissue, leading to contraction of wound margins. A connective tissue scar remains when wounds are closed by secondary intention—the larger the wound gap, the wider the connective tissue scar.

Scar consists of a poorly constructed collagen matrix in dense parallel bundles, which is contrasted to the efficiently cross-linked meshwork of collagen in the native dermis. It occurs in three phases—epithelialization migration, collagenization, and angiogenesis–granulation tissue formation. Epithelialization occurs by migration of keratinocytes over the dermis and under the clot (Fig. 22-3), which is facilitated by growth factors such as epidermal growth factor (EGF) and transforming growth factor α (TGF-α).^6–8 Once a monolayer of keratinocytes covers the denuded wound surface, epithelial migration ceases and a new stratified epidermis with underlying basal lamina is reestablished from the margins of the wound inward. All aspects of a skin flap rarely touch along all the length of the wound; migration is aided by contraction of the underlying connective tissue. Within 3 to 4 days of injury, dermal fibroblasts around the wound begin to proliferate and lay down a collagen-rich matrix, a process modulated by platelet-derived growth factor (PDGF) and transforming growth factor β (TGF-β).^9–12 Finally, angiogenesis of the wound and the incorporation of pink, capillary-filled granulation tissue is mediated by fibroblast growth factor 2 (FGF2) and vascular endothelial growth factor (VEGF) released at the site of the wound.¹³ Connective tissue contraction ultimately closes embryonic and adult wounds. The major difference between scar-free healing and scar formation is that a scar-free wound site has significantly less inflammation present.⁵

Principles of Wound Management

General principles of wound management should always be followed in the traumatic setting. These include an initial thorough removal of foreign bodies, débridement, and cleansing of the wound with copious pulsatile irrigation. Formal scrubbing of the wound may be undertaken if necessary but should be done sparingly to spare further damage to soft tissues. All devitalized soft tissue should be débrided and excised and sharp healthy wound margins should be obtained to facilitate closure, with minimal scarring.¹⁴ Devitalized tissue increases the local inflammatory response and subsequent scarring. Undiluted hydrogen peroxide use in open wounds should be avoided because it inhibits wound healing and may cause tissue necrosis. Normal saline with or without bacitracin is the preferred irrigant for soft tissue trauma. Although delayed closure may be necessary in some wounds caused by edema and/or high-velocity injuries such as gunshot wounds, in wounds with a significant amount of devitalized tissue, or because of other, more urgent medical and surgical interventions that precede the treatment of head and neck injuries, primary closure should be attempted, if feasible. In the case of avulsed tissue or the inability to reapproximate local tissue under minimal tension, local flaps, regional flaps, or free tissue transfer may be needed to restore tissues adequately to previous form and function.¹⁵ Wounds should be closed in layers, if possible, to place minimum tension on the superficial skin closure and aid in the eversion of skin edges to minimize scar widening.¹⁶ Tension across a wound decreases blood flow, which leads to necrosis of wound edges and increased connective tissue growth in the proliferation phase, and to elongation of scars in the remodeling phase.^17,18 Skin flaps should be appropriately undermined so that wound edges can be everted, which will minimize scar depression.¹⁹

Meticulous attention to detail and gentle tissue handling are important to optimize wound healing and minimize scarring.¹ A multivariate analysis has shown that characteristics associated with suboptimal cosmetic appearance following laceration and surgical incision closure are associated tissue trauma, use of electrocautery, incomplete wound edge apposition, and increased wound width (healing by secondary intention).²⁰ If permanent sutures are used for wound closure, they should be removed in 5 days or less to prevent track marks. Another option is to use fast, resorbing plain gut suture (5.0 to 6.0). In a study that compared 5.0 or 6.0 nylon sutures versus plain gut sutures for skin closure in a population of pediatric patients who suffered lacerations, no difference in infection or wound dehiscence was found between the two groups; however, slightly better cosmesis was found in the plain gut suture group.²¹ Similar studies,²² including a meta-analysis,²³ have confirmed these results, demonstrating no difference in long-term cosmesis, scar hypertrophy, infection rate, wound dehiscence, and wound erythema or edema between lacerations closed with nylon versus plain gut suture. For scalp incision and laceration repair, the use of staples as an alternative to suturing has been demonstrated in a randomized control trial to reduce procedure time significantly while not demonstrating any difference in cosmesis by a blinded physician at 1 week and 6 to 18 months postrepair.²⁴

Adhesive bandages such as Steri-Strips (3M, Maplewood, Minn) should be used to reduce wound tension at the time of closure and to reduce the need for long-term suture placement in those wounds under increased tension. The use of 2-octyl cyanoacrylate–based fast-acting skin adhesives has been shown to be just as effective as Steri-Strips in reducing hypertrophic scar formation,²⁵ although other study results have demonstrated superior cosmesis in wounds dressed with Steri-Strips.²⁶ A review comparing the use of tissue adhesives versus standard wound closure in patients with traumatic lacerations found that pain and procedure time were significantly reduced in the tissue adhesive group and wound dehiscence and erythema were significantly reduced in the standard wound closure group; however, there was no difference in final cosmesis or scar appearance between the two groups.²⁷

Desiccated and crusted wounds heal slower than those kept moist.²⁸ Epithelial migration follows a path of moisture and humidity, even if this route is longer (Fig. 22-4). This often requires more energy expenditure by the cell. In addition, an apoptosis-mediated decrease in granulation tissue has been shown to occur in vitro in flaps that are covered postoperatively.²⁹ Therefore, occlusive dressings and antibiotic ointment use are recommended so that epithelial migration proceeds in a direct and efficient manner. The use of occlusive or semiocclusive dressings has also been advocated as a means of promoting wound healing. Commercially available dressings, such as Tegaderm (3M), Opsite (Smith & Nephew, London), or similar polyurethane dressings minimize the amount of atmospheric oxygen that is absorbed directly through an open wound^30,31 and have been shown to decrease epithelial closure time by as much as 50%.^28,31–33 The moist environment is optimal for epithelial migration, with minimization of connective tissue formation, therefore expediting healing and reducing scar formation. These effects, however, have not been verified in a randomized control trial.³⁴ Antibiotic ointment should be applied to the wound until epithelialization occurs. Bacteria delay healing by direct cell damage, prolonging the inflammatory phase of wound healing by competing for oxygen; therefore, in addition to providing a moist environment, antibiotic ointment is beneficial for reducing bacterial colonization.³⁵

Wounds should be cleaned daily during the immediate postoperative period using a mixture of 50% hydrogen peroxide and 50% water. Sunblock should be applied to the area of wound closure to reduce irritation and minimize the inflammatory response. The patient should be instructed to massage the wound once epithelialization occurs using a simple base cream twice a day, 10 minutes at a time.36,37 The effects of scar massage, however, have been questioned.³⁸ In addition, silicone sheets or gels may be used after epithelialization occurs and may assist in better scar maturation of hypertrophic and keloid scars.^39–44 Although a barrier, silicone sheets do allow the passage of oxygen. It has been shown in an animal model that silicone sheets cause hydration of keratinocytes within the stratum corneum of the epidermis, which has a suppressive effect on the metabolism of underlying fibroblasts and results in decreased capillary activity, hyperemia, and collagen deposition, and therefore decreases dermal thickness and subsequent scar hypertrophy.⁴⁵ Oxygen tension, pressure, or silicone leakage into dermis, however, has not been shown to be mechanisms for silicone effectiveness.^46–49 Furthermore, silicone sheets have been found to improve pigmentation, vascularity, and reduce the height of scars after 3 months of postoperative use.^50,51 Reduction of pain and pruritus has also been demonstrated to be a benefit of silicone sheets, but these benefits are not seen until after 6 months of use.⁵² In a study that used the Vancouver Scar Scale to assess the effects of silicone gel, silicone gel sheets, and allantoin in improving postburn scarring less than 6 months from injury, the investigators found no significant difference in the silicone gel and gel sheet group, but there was a significant difference in improvement when comparing the allantoin groups with the silicone sheet and silicone gels group.⁵³ All three groups showed a significant improvement 6 months from baseline. The effects of silicone sheet use have been shown to last up to 6 months after removal; therefore, their benefits are maintained once they are discontinued⁵⁴ Onion extract, another popular topical treatment for scars, has shown only to improve scar color while not having an effect on scar height.⁵⁵

Preoperative Consultation

Detailed explanation of possible and realistic outcomes at the initial encounter will help circumvent any unreasonable expectations that the patient might have and prepare the patient for the reality that further procedures will be needed. Although the surgeon may have a good idea of which scar revision procedure the patient will need at the time of initial repair, it may not be until weeks to months later, after scar maturation occurs, that the surgeon will be able to formulate a definitive treatment plan. Depressed scars tend to contract initially and then relax as they mature, whereas hypertrophic scars and keloids will often grow as the patient ages. On follow-up examination, the surgeon should note scar tension and adjacent tissue laxity of the scar while attempting to predict the outcome of tissue rearrangement. In addition, the patient’s medical history should be revisited because much may be left out in the emergent setting. Hereditary, vascular, metabolic, and immune deficiencies may be detrimental to wound healing. Finally, the patient must be compliant with postoperative care. This not only includes local care to the wound, but maintaining proper nutrition, because vitamin and trace mineral deficiencies such as deficiencies of vitamin A, C, E, zinc, and iron can be detrimental to wound healing.31,56

Scar Analysis

The purpose of scar analysis is to use a reliable and valid measure for quick and efficient scar assessment, which requires that the surgeon have a firm understanding of scar terminology (Table 22-1).⁵⁷ Documentation of a standardized assessment is necessary for developing a treatment plan and for serial evaluations. Photographic assessment using standardized lighting, spacing, positioning, camera settings, and background is beneficial for initially assessing and serially tracking the progress of the scar maturation.^58–65 Imaging software can be used to analyze, measure, and follow scars and can aid in surgical planning by almost performing the surgery before the actual procedure.⁶⁶ Immediate preoperative and postoperative photographs should be taken.⁶⁷ It is useful to review photographs after the patient has left. It is then that the surgeon will often notice subtle abnormalities that could affect the management of the scar. Also, photographs will document changes in following appointments often overlooked by the patient and surgeon.

Several factors must be considered when developing a treatment plan for scar revision, such as scar width, length, relationship to relaxed skin tension lines (RSTLs), neighboring anatomic landmark distortion, tissue loss, scar type, patient age and race, scar location (visible versus nonvisible with clothing), skin type (Fitzpatrick), tissue tension and laxity, and local tissue reservoirs (Box 22-1). Figure 22-5 illustrates a basic template for the surgeon to use for scar revision, but this must be tailored to the specific patient and scar.

The most widely used scarring index is the Vancouver Scar Scale, which gives the surgeon an objective measure of burn scars and assists in prognosis and management. Although some have described it as a valid research tool with good interrater reliability (Table 22-2),⁶⁸ others have not.⁶⁹ Another scale, the patient and observer scar assessment, has an objective component comparable to the Vancouver scale, but relies on patient opinion (Table 22-3).⁷⁰ A number of other subjective and objective assessment tools and devices have been reported in the literature.^71–76 Most indices include the clinical assessment of vascularization, pigmentation, thickness, surface, pliability, size, reflection, distortion, texture, functional deficits, and pain. These characteristics are often a clue to the cause of the scar. For example, postinflammatory hyperpigmentation is often seen in scars associated with acne, inherited and acquired diseases, temperature extremes, sites of allergic reaction, radiation, and sun exposure.⁷⁷ Hypopigmentation often has iatrogenic causes, such as chemical peel, dermabrasion, laser resurfacing or, with burns, trauma and infection.^78,79

Scar contour exists on a continuum, from the depressed scar to the hypertrophic scar and keloid. Hypertrophic scars typically remain confined to the borders of the inciting injury and usually retain their shape, whereas keloids are defined as scars that extend beyond the borders of the original wound, do not regress spontaneously, and tend to recur following excision.⁸⁰ Keloids present a special problem in treatment (see later). Scar depression often results from excessive tension across the wound. Scar texture and reflection are mainly concerns of aesthetics. Scar contracture may have functional and aesthetic ramifications in the head and neck. Pertinent to the craniomaxillofacial skeleton, scar tethering to underlying fascia, muscle, or bone may occur, resulting in aesthetic and functional deficits, mainly the failure to animate or move the face and neck.

Painful scars, especially those associated with burns, can severely debilitate the patient. The patient may present with allodynia, hyperesthesia, hypoesthesia, or dysesthesia, often caused by tissue adhesion, surround soft tissue damage, underlying skeletal damage, or neuroma or perineural scar formation. An increase in nociceptive nerve fibers following burn injury is associated with increased cutaneous innervation and increased density of certain neuropeptides, and may be responsible for chronic pain in patients with burns.81–83 Excision of this tissue, in addition to reconstruction using local, regional, or distant flaps, may relieve pain in some patients. Scars in the midline are less likely to produce pain, but may cause more scarring because of increased tension.⁸⁴

Elevated scars present in different patterns, depending on the thickness and integrity of the remaining dermal wound edges. Hypertrophic scars are dome-shaped and have a thin epidermis, whereas partially avulsive or oblique wounds result in contraction at the base of the wound, creating an elevated and inclined scar. As the scar matures, wound edges of different dermal thickness and elevation result in elevated scars with gradual step-offs; misaligned wound edges of the same dermal thickness produce elevated scars with abrupt step-offs. Depressed scars may be related to underlying tissue loss or to increased tension across the wound, resulting in atrophy of the underlying dermis, which results in a smooth and shiny scar.

Timing of Scar Revision

Experience has shown that in general, the appearance of most scars tends to improve spontaneously after a period of maturation during the first year after injury, after which time the appearance of the scar stabilizes and surgical revision may be considered.112,113 However, scars oriented perpendicular to RSTLs or those associated with functional impairment may be revised earlier than 1 year on an individualized basis.^114,115

Early scar revision may be undertaken as early as 4 weeks when there is severe functional impairment, such as salivary and lacrimal gland obstruction, lip incompetence, or lagophthalmos with corneal exposure. Early scar revision may also be advisable in well-localized scars sustained from low-energy injuries in which adjacent skin damage is minimal. Although a delay in scar revision of at least 6 months is generally recommended for most adult scars, high-energy injuries may continue to remodel and mature over a longer period of time, and delay for 12 months may be advisable.¹¹⁶

Interventions such as dermabrasion and shave excision may be performed as soon as 4 weeks from the initial wound repair, based on the high level of fibroblastic activity during this period. Because dermabrasion itself causes erythema, early intervention may overlap with erythema from initial repair, leading to less total time of erythema for the patient. For hypertrophic scars and keloids, steroid injections may be considered as early as 3 weeks and may be given at the time of scar revision. Cigarette smoking, isotretinoin, and vitamin E use are injurious to wounds and scar revision should be delayed until they have been discontinued.¹¹⁷

Surgical Options

Scar revision can be broken down into three different treatment modalities—scar excision, tissue rearrangement, and surface treatment (Box 22-2). The selection of treatment should be based on the individual scar and on the needs and expectations of the patient. For example, conservative treatment may be warranted for a demanding patient with unrealistic expectations. Narrow scars parallel to RSTLs may have distracting features such as surface discoloration and texture irregularities. These scars will often benefit from surface treatments. Longer scars, which vary more than 35 degree from neighboring RSTLs and have a local tissue reservoir, may be improved with tissue rearrangement such as W-plasty or geometric broken line excision and closure (GBLC). Z-plasty, local or regional flaps, or free tissue transfer may be indicated if neighboring tissue reservoirs are deficient or if anatomic structures and landmarks would be distorted by closure.