Wound healing is a continuum of overlapping stages comprising inflammation, debridement, repair, and maturation. During the inflammatory stage, hemorrhage occurs immediately, followed by small vessel constriction and clot formation to attenuate hemorrhage. Plasma leaks from dilated permeable vessels, and leukocytes escape the vessels by diapedesis. The fibrinous clot in the wound aids in hemostasis and maintains homeostasis as the surface dries to a scab, serving as a biologic bandage. During this stage, the wound area is hyperemic, edematous, and painful.
Early in the healing process, neutrophils and macrophages in the wound begin the debridement process. In addition, macrophages produce cytokines and growth factors essential for healing progression. They work in concert with lymphocytes to activate the local immune response in the wound. The wound fluid, degenerating leukocytes, and dead tissue comprise the purulent inflammatory exudate associated with this stage of healing. At this time, the appearance of the wound will generally deteriorate before it begins to improve.
The repair stage is manifested by proliferation of fibroblasts, capillary infiltration, and epithelial proliferation and migration. Proliferation of fibroblasts and capillary infiltration manifest as granulation tissue. This tissue is a barrier to infection, causes wound contraction, incorporates collagen production by fibroblasts, and provides a surface over which epithelium can migrate. In open wounds, the tissue has a bright reddish-pink appearance and is associated with decreased fluid production. The granulation bed of healthy wounds progressively decreases in size.
During maturation, the wound gains strength. Early in this stage, strength results from collagen production by fibroblasts. Later, strength comes from inter- and intramolecular cross-linking of collagen fibers.
Wound healing can be complicated by many factors-one of the most notable is pressure applied to the tissues. Pressure both causes wounds and prevents healing.