Proper wound closure techniques aid the body’s natural process of wound healing. Thus, it is important to understand the physiology of wound healing. The wound healing process occurs in three distinct phases: (1) the inflammatory phase, (2) the proliferative or granulation phase, and (3) the differentiation or maturation phase.
The inflammatory phase (days 0-5) begins immediately after wounding and within 1 to 2 hours; there is a release of vasoactive substances including histamine, serotonin, and cytokines. These substances cause an increase in local vessel permeability leading to an increased exudation of plasma. The leaky capillaries allow cells such as T lymphocytes, leukocytes, neutrophil granulocytes, monocytes, and macrophages to reach the wound area. Neutrophils (polymorphonuclear leukocytes) predominate in the wound during the first 48 hours after wounding. The polymorphonuclear leukocytes provide a nonspecific cellular defense that is the initial protection against wound infection. The nuclei of neutrophils contain proteolytic enzymes that facilitate cleaning of the wound and phagocytosis of bacteria. Following the neutrophils, macrophages start to migrate into the wounded area and predominate by day 4. The macrophages’ main role is to phagocytose debris and to digest bacteria. At the fourth day of wound healing, fibroblasts begin to appear. During this early phase of wound healing, the tensile strength of the wound is minimal and is the result of the fibrin coagulum in the wound bed.1
In parallel with the changes occurring deep within the wound, the superficial epithelium also undergoes changes. The epidermis adjacent to the wound edge begins to thicken within 24 hours after injury. Basal cells at the margin of the wound release their attachment to the dermis, enlarge, and migrate across the wound surface to cover the wound. This is possible because the cells undergo a series of rapid mitotic divisions, resulting in migration of the new cells by moving over one another until the wound bed is completely covered by epithelium. Re-epithelialization is usually complete in less than 48 hours in the case of well-approximated wounds.
When a wound becomes infected, there is a failure to progress from the first to the second stage of wound healing. Bacteria or foreign bodies within the wound promote the persistence of neutrophils. With continued neutrophil degranulation and prolonged phagocytosis, there is an accumulation of partially digested material, which is the origin of pus. Furthermore, there is delayed synthesis of critical structural proteins such as collagen. The infected wound will therefore not progress to maximum structural integrity until the infection has resolved.
In the absence of significant infection or wound contamination, the second stage of wound healing begins. The proliferative or granulation phase (days 6-14) is characterized by the formation of granulation tissue in the wound. Granulation tissue consists of a mixture of cellular elements, including fibroblasts and inflammatory cells, along with newly formed capillaries contained within a matrix of collagen, fibronectin, and hyaluronic acid. Early in the second phase, there is a rapid increase in the numbers of fibroblasts. The increase is secondary to an influx as well as in situ production of fibroblasts.2 Structural proteins required for wound repair are pri marily synthesized by fibroblasts. Most important, fibroblasts produce large quantities of collagen, which makes up the majority of the extracellular wound matrix. It is this matrix that is responsible for the tensile strength of scar tissue. The collagen is initially deposited in a disorganized fashion. Through cross-linking, the individual collagen fibrils are subsequently reorganized into regularly organized bundles. The new collagen array is oriented along the lines of mechanical stress in the healing wound. The process of fibroblast proliferation and synthetic activity is termed fibroplasia. Revascularization of the wound proceeds in parallel with fibroplasia.3 Capillary buds sprout from blood vessels adjacent to the wound and extend into the wound space. With continued growth, the new vessels eventually branch at their tips and join to form multiple capillary loops. With formation of capillary loops, blood flow recommences. New sprouts then extend from these loops to form an active capillary plexus.
The differentiation or maturation phase is the third segment of wound healing. This occurs from day 15 to 1 year postoperatively and beyond. During this period, there is a gradual egress of fibroblasts and macrophages. Overall, the wound becomes less vascular. Collagen fibers progress on the continuum from disarray to organization. As the collagen becomes more organized, wound strength continues to improve; 45% of normal wound strength is achieved by day 70 and 50% by day 120.4 In general, with optimal wound healing, scar tissue strength approaches 80% of the original tissue strength before wounding. Many factors contribute to normal wound healing; these are listed in Table 4-1. An understanding of these factors assists successful primary wound closure.
TABLE 4-1
Factors Affecting Wound Healing
Investigators have used their understanding of wound healing science to guide novel therapies. Lee et al5 showed that the use of laser therapy (intense pulsed light) or microneedle techniques could increase collagen deposition during the wound healing response. An increase in collagen deposition tended to result in improved scar appearance and overall wound healing. Other investigators have shown a decrease in the incidence of scar hypertrophy and an improvement in wound healing by use of lasers to treat scars after surgery.6 Kim et al5 showed that three postoperative treatments of suture line scars with the erbium : glass laser (1550 nm) dramatically improved the appearance of thyroidectomy scars.