Wound Healing

Wounds involving the scalp can be life-threatening, but in many cases they are manageable with a thorough understanding of the basics of wound healing. Recent advances in research have outlined significant events that take place in wound healing at both the gross tissue and molecular levels.

There are three indistinct, yet overlapping phases of wound healing: the inflammatory, proliferative, and maturation phases. A physical stimulus, such as an incision, initiates a nonspecific inflammatory response in local tissue, which marks the beginning of the inflammatory phase. Factors released from activated platelets, complement components, and prostaglandins induce local changes in the vasculature. The initial transient vasoconstriction establishes hemostasis and is subsequently followed by vasodilation with increased permeability, which further facilitates the influx of leukocytes needed for débridement. Polymorphonuclear leukocytes are the first cells to migrate into the wound, followed by local macrophages and mononuclear leukocytes. Monocytes are essential for normal wound healing by triggering invasion of fibroblasts into the wound and initiating the proliferative or fibroblastic phase of wound healing. Systemic and topical steroids have been demonstrated to retard wound-healing processes, including collagen synthesis, by reducing cell immigration.¹ Fibroblasts migrate into the wound at approximately day 4 after injury and deposit disorganized collagen, which produces a scar. Collagen cross-linking prevents degradation of collagen by collagenase and matrix metalloproteinases, thereby increasing wound tensile strength. Vitamin C is a cofactor needed for hydroxylation of lysine residues on collagen, the process by which cross-linking occurs and wounds strengthen. Closed incisional wounds regain about 20% of the original skin tensile strength after 3 weeks and up to 70% at 6 weeks, with the maximal tensile strength of 80% of the original skin strength regained after a year.¹ The increase in tensile strength is intimately related to the collagen remodeling that occurs over time. Radiation impairs the ability of fibroblasts to replicate and deposit collagen, which often results in hyperpigmented, ischemic, and sometimes ulcerated wounds vulnerable to infection.¹ In contrast, fetuses of certain gestational ages have been shown to heal with complete restoration of original skin tensile strength and epidermal appendages, without scarring. Unique differences in fetal fibroblasts, cellular infiltration, growth factor expression, and other processes have been identified, but little success has been gained in applying these principles to adult patients.¹

The protective, moisturizing epidermal layer is restored within 48 hours of closing a wound as marginal basal cells migrate from the wound edge along the extracellular matrix (largely fibrinogen). Epidermal appendages that lie deep within the dermis aid in re-epithelialization of deep wounds that extend beyond the epidermis by contributing basal stem cells capable of division and proliferation. Radiation inhibits the division of basal cells, thereby prolonging re-epithelialization and increasing the risk for bacterial penetration and infection.¹ Placing suture to reapproximate wound edges facilitates re-epithelialization of the protective barrier by providing “tracks along which keratinocytes can migrate into the wound.”¹ Suture material is also a foreign body, however, and therefore initiates a variable inflammatory response, depending on the suture material involved.

Appropriate suture selection allows the surgeon to have greater control of wound healing and the resultant cosmetic outcome. When selecting suture, the surgeon must take into account the specifics of the wound, in particular, the stress and strain of the wound site, growth potential of the wounded area, the need for permanent mechanical support, and the rate of healing.¹ Suture can be categorized as absorbable and nonabsorbable, with further subcategorization depending on suture design. Specific suture characteristics, including tensile strength, rate of infection, and rate of absorption, have been defined to allow surgeons the ability to select the appropriate suture specific for each wound. An open wound after incision is colonized with few bacteria and can therefore be closed primarily with either multifilament or monofilament resorbable suture. Using multifilament suture to close traumatic, heavily contaminated wounds may, however, potentiate a wound infection.

Indications for Antibiotics

The benefit and use of antimicrobials to prevent wound infection have been a controversial subject for years. Infection has been defined quantitatively as greater than 10⁵ bacteria per gram of tissue.¹ The time interval between wounding and administration of antibiotics is influential in preventing infection. Three hours from the time of injury to the time of antibiotic administration is critical in preventing infection of contaminated wounds.² Traumatic wounds benefit from immediate high-pressure irrigation (use of jet lavage or a 35-mL syringe with an 18-gauge needle) and débridement. A 6-hour delay in cleansing and débridement leads to higher rates of infection and is therefore a relative indication for antibiotic administration.² The anatomic location of the wound has also been shown to have an impact on the incidence of infection, with head and scalp wounds exhibiting the lowest rate of infection and the foot the highest rate. This is probably due to the inherent colonization of bacteria and difference in tissue vascularity that characterizes the foot and the face. Trauma incurred by repeatedly passing the scalpel through tissue has also been shown to limit local defense mechanisms, reduce tissue vascularity, and thereby increase the incidence of infection.² Studies have demonstrated that stellate lacerations or crush injuries have higher rates of infection than do linear lacerations with less tissue damage, probably secondary to the relative hypovascularity of traumatic wounds. Wounds that have been neglected for more than 6 hours warrant antibiotic administration with or without primary closure in some cases. Wounds in anatomic locations with a higher incidence of infection and wounds contaminated with saliva, feces, or vaginal secretions meet the criteria for the use of antibiotics.² Infection delays wound healing and often leads to a poor functional and cosmetic outcome.

Preoperative hair removal and its impact on reducing surgical site infection have previously been the subject of much debate. There is little statistically significant evidence supporting hair removal before the day of surgery. However, there is sufficient evidence in the literature and support by the Centers for Disease Control and Prevention in 1999 to advocate clipping hair over shaving or using depilating cream.³

Incision

Appropriate technical skill has a significant impact on the functional and cosmetic outcome. Appropriate lighting and equipment, detailed examination of the wound and surrounding tissue, planning of incisions, atraumatic tissue handling, appropriate suture selection, closure technique, and timely suture removal are the basic principles of wound repair that surgeons can manipulate to reduce the possibility of unfavorable healing and scarring. In general, incisions are optimally placed parallel to skin tension lines, referred to as “lines of election” or “Langer’s lines.” These lines lie perpendicular to the direction of underlying muscular contraction. Langer’s lines are directed circumferentially along the occiput and the temporoparietal regions and directed anteroposteriorly on the vertex of the scalp, as displayed in Figure 29-1. Circular scalp defects can be converted to an elliptical shape with the length at least twice as long as the width to avoid skin redundancy or “dog-ears.”⁴ Elliptical excisions placed along Langer’s lines achieve the greatest width of tissue removal and heal with minimal tension and scarring. Atraumatic tissue handling and appropriate technique also reduce unfavorable healing. Care should be taken when handling the scalpel to make the incision perpendicular to the skin and avoid scything or undermining the adjacent epidermis. The skin edge should be held at the dermal level to avoid damaging the epidermis. The needle should then be inserted perpendicular to the skin edge at an equal depth and distance on each side of the wound, as displayed in Figure 29-2.⁴ Unequal “bites” create inversion of the wound edges, which results in an inverted scar that casts a shadow and draws more visual attention once healed.⁴ Unique to the scalp is the ability to conceal the scar within the hairline. The adolescent hairline lies along the superior border of the frontalis muscle, whereas the adult male hairline recedes to about one fingerbreadth superior to the adolescent hairline, or 1.5 cm superior to the upper brow crease.⁵ The hairline is not a fixed point but rather a transition zone with fine hairs growing anteriorly and coarser hairs growing more posteriorly. The angle of an incision is just as aesthetically important as the location of an incision involving the scalp. Incisions should be placed parallel to hair follicles to avoid transecting the bulb of the follicles and causing cicatricial alopecia.⁶ The direction of hair growth is typically in the forward direction on the anterior part of the scalp, more radial near the crown, and more inferior along the temples. The direction of hair growth can be used to hide incisions when appropriately placed.⁵ In general, with scar visibility as the only consideration, the scar line should be oriented perpendicular to the “fall pattern” of the adjacent hair follicles so that the hair covers the scar line.

FIGURE 29-1 Langer’s lines of the scalp. Place incisions parallel to Langer’s lines for minimal tension and optimal healing.

(Adapted from Seery GE. Surgical anatomy of the scalp. Dermatol Surg. 2002;28:581-587.)

FIGURE 29-2 Suture technique. Insert the needle perpendicular to the skin surface. Take “bites” of equal depth and distance.

Surgical Anatomy

Deciding where to place the incision on the scalp warrants a detailed discussion of the surgical anatomy and blood supply of the scalp. The scalp extends anteroposteriorly from the supraorbital margin to the superior nuchal line and laterally to the zygoma. It is composed of five layers, with the outer three layers—skin, subcutaneous tissue, galea—fixed together as a unit that glides easily over the pericranium, as illustrated in Figure 29-3.

FIGURE 29-3 Layers of the scalp. The epidermis, dermis, and galea glide over the pericranium as a fixed unit. Scalp vessels travel within the subcutaneous layer superficial to the galeal layer.

(Adapted from Wells, M. Scalp reconstruction. In Mathes SJ, ed. Plastic Surgery. Philadelphia: Saunders; 2006:607-610.)

Scalp skin (epidermis and dermis) is the thickest on the body; it ranges from 3 mm at the vertex to 8 mm at the occiput, which is ideal for harvesting split-thickness skin grafts.⁷ Just deep to the skin is the subcutaneous tissue, where hair follicles, sweat glands, and rich vascular anastomotic networks lie. Dense fibrous septa within the subcutaneous tissue adhere to the adventitia and prevent retraction of arteries when severed. This is important in control of scalp hemorrhage. Manual compression with immediate suturing is a more effective means of controlling bleeding in the scalp than attempting to grasp bleeding points with a hemostat.^8,9 Scalp vessels travel within the subcutaneous layer just superficial to the galea. The galea is the aponeurotic layer that connects the frontalis to the occipitalis muscle and is contiguous with the temporoparietal fascia laterally. The superficial temporal fascia is a thin, highly vascular layer that is contiguous with the galea and lies deep to the subcutaneous tissue of the lateral aspect of the scalp.¹⁰ A plethora of confusing synonyms have been coined for identification of this layer, including (superficial) temporoparietal fascia, epicranial aponeurosis, superficial muscular aponeurotic system (SMAS), and galeal extension.¹¹ The superficial temporal artery and vein are housed within the fascia, thus rendering this layer vital to the viability of temporoparietal, pericranial flaps.

The superficial temporal fascia is contiguous with the periosteum of the zygoma and inferior to the SMAS of the face. In the temporal region, the galea becomes adherent to the underlying subgaleal fascia, but the subgaleal fascia can easily be detached from the deep temporalis fascia or the layer covering the temporalis muscle, as depicted in Figure 29-4.¹² The deep temporal fascia is a thick white fascial layer on the external surface of the temporalis muscle. Similar to the galea or superficial temporal fascia, the deep temporal fascia also has multiple synonyms in the literature: temporal fascia, middle temporal fascia, and superficial deep temporal fascia. Loose areolar tissue, often referred to as subgaleal fascia, allows the galea and overlying layers to glide as a unit over the pericranium. This subaponeurotic space is a potential pathway for the ingress of bacteria intracranially via emissary veins, which can result in meningitis or septic vein thrombosis.⁷

FIGURE 29-4 Anatomy of the temporoparietal region. The superficial temporal artery lies within the galea (temporoparietal fascia), which becomes adherent to the superficial temporal fascia overlying the temporalis muscle.

(Adapted from Abul-Hassan HS, von Drasek Ascher G, Acland RD. Surgical anatomy and blood supply of the fascial layers of the temporal region. Plast Reconstr Surg. 1986;77:17-23.)

Over the past 50 years, understanding of human anatomy has changed dramatically. Appreciating the interrelationships and three-dimensional nature of regional anatomy replaced the traditional teaching of independent body systems and tissues. The erroneous concept that the skin circulation was derived from a vascular network independent of the deeper structures has been replaced with the concept of angiosomes, or composite blocks of tissue supplied by source arteries.¹³ Source arteries are described as musculocutaneous, septocutaneous, and fasciocutaneous or “axial” vessels, depending on the path that the vessel takes from the regional artery to the subdermal plexus, as illustrated in Figure 29-5. The anterior aspect of the face is supplied by musculocutaneous perforators, whereas the scalp is supplied by fasciocutaneous perforators.¹³ The musculocutaneous and fasciocutaneous perforators pierce the deep fascia at fixed skin margins—the supraorbital rim, tragus, mastoid process, masseter, parotid, and superior nuchal line. They then radiate from these fixed regions into areas of mobile skin intimately related to the SMAS and its galeal extension.¹³

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