While acute and chronic wounds are different, all chronic wounds start as an acute wound.
In acute wounds, there is an orderly progression from injury to coagulation, inflammation, cell and matrix proliferation, cell migration, and tissue remodeling.
In the initial phases, a wide range of growth factors, including platelet-derived growth factor and transforming growth factor-β1, play an important role. In the proliferation/migration and modeling phases, tissue matrix metalloproteinases (MMPs), integrins, basic fibroblast growth factor, and epidermal growth factor are critical. MMP-1, MMP-9, and MMP-10 are essential for remodeling.
For acute wounds, moist wounds heal faster, and a variety of wound dressings are available, including hydrogels, polyurethane films, hydrocolloids, foams, alginates, superabsorbent dressings, and collagen-based products.
In chronic wounds, the linear progression between the sequential phases of acute wound healing is lost. Chronic wounds are often the result of ischemia, pressure, and infection; healing, in part, is dependent on addressing these factors.
Healing after skin grafting is also different, as it depends on revascularization, either neovascularization or inosculation.
Wound healing involves a complex but overlapping sequential series of events aimed at barrier restoration, from hemostasis to inflammation, proliferation, and remodeling. Many mediators, such as platelets, neutrophils, macrophages, cytokines, growth factors, matrix metalloproteinases, and their inhibitors regulate these events.1 Some wounds fail to move through these stages in an orderly and timely fashion and become chronic wounds. All these components play a role in healing, and alteration in one or more of these components may impair healing and/or lead to abnormal scar formation, such as a hypertrophic scar or keloid.2 Wounds can be categorized by the depth of the wound, which helps predict the amount of scarring that will occur. Greater scarring occurs in full-thickness versus partial or spilt-thickness wounds. Figure 149-1 outlines these differences.
Diagrammatic representation of the skin, with 2 inverted triangles representing either a split-thickness or full-thickness wound. Extending the injury below the reservoir of keratinocytes present in skin appendages (full-thickness wound) removes the capability of the keratinocytes to populate the defect from within the wound bed, which means healing has to occur from the wound edges and more scarring takes place.
DIFFERENT TYPES OF WOUND HEALING
Primary healing, also called healing by primary or first intention, is the closure of the wound soon after wound creation, as seen in surgical wounds and clean lacerations. Wound closure is aided by approximation of the wound edges using sutures, glues, tapes, or mechanical devices, and in side-to-side closure and with grafts and flaps.
Delayed primary healing is the slightly delayed closure of a wound, typically by a few days. As an example, a contaminated wound may first be treated with antimicrobials to assure eradication of bacteria that might delay healing.