Hemostasis is initiated at the time of injury. Tissue and vascular smooth muscle contraction compresses small bleeding vessels. Activation of platelets and the coagulation cascade produce a fibrin clot within the lumens of the severed vessels and within the exposed wound.
Inflammation is stimulated by chemotactic factors released by activated platelets and the complement cascade, which initially attract neutrophils followed by macrophages. Neutrophils and macrophages phagocytose dead tissue, foreign material, and bacteria, providing physiologic debridement and preventing infection. Neutrophils perform this function for the first 72 h after injury, and macrophages perform this task for up to 30 days after a traumatic wound.
Epithelialization reaches a peak about 24 h after the injury as the inflammatory response stimulates cell division in the stratum germinativum. Epithelial cells migrate across a closed traumatic wound during the first 24 to 48 h, making the wound impervious to water. Eschar and surface debris impede this process.
Angiogenesis is vital to wound repair. New vessel growth is detectable at 72 h and reaches its peak at 7 to 10 days, accounting for the often-marked erythema seen at this time. As the wound matures, vascularity decreases nearly back to baseline at 30 days.
Fibroplasia, with collagen synthesis, reaches a peak by 7 days and essentially replaces the inflammatory mass in the wound by 3 weeks. At the same time as increasing collagen synthesis, hydrolysis and breakdown of old and damaged collagen are also taking place. The period between 7 and 10 days is the vulnerable time when the balance between collagen synthesis and breakdown is most tenuous and unwanted wound separation occurs.
Wound contraction and scar remodeling occur over the next several months. Contraction significantly modifies the cosmetic appearance of treated wounds. An important principle of wound repair is to take this expected contraction into account and repair lacerations with everted edges. Remodeling is such a powerful process that, at the time of suture removal, it is impossible to predict the ultimate appearance of wounds.8
During wound healing, excess fibroblastic activity can create excess tissue, developing either a hypertrophic scar or a keloid. Hypertrophic scars are excess collagen confined to the original boundaries of the wound and are more common in areas of increased tissue tension. Keloids have excess scar tissue from the wound extending beyond the original borders. Keloids are most often seen in African Americans but can occur in any dark-pigmented skin area.
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