Clinical meaning
Wound healing proceeds through four overlapping phases: hemostasis (platelet aggregation, fibrin clot formation within minutes of injury, mediated by the coagulation cascade with thrombin converting fibrinogen to fibrin), inflammation (neutrophil and macrophage infiltration clearing debris and bacteria through phagocytosis and reactive oxygen species production, peak 24-48 hours, mediated by pro-inflammatory cytokines IL-1, IL-6, TNF-alpha), proliferation (fibroblast migration and collagen deposition forming granulation tissue, angiogenesis creating new capillary networks through VEGF signaling, epithelial cell migration across the wound bed from wound margins and skin appendages, wound contraction by myofibroblasts -- days 4-21), and remodeling/maturation (collagen reorganization from type III to type I collagen through matrix metalloproteinase activity, scar tissue formation reaching maximum 80% of original tensile strength -- 3 weeks to 2 years).
Wound classification guides nursing assessment and management: acute wounds heal predictably through the above phases, while chronic wounds (present greater than 30 days without healing progress) are stalled in the inflammatory phase due to persistent infection, biofilm formation, ischemia, repeated trauma, or systemic factors. Wound assessment follows a systematic approach: location, size (length x width x depth in centimeters), wound bed characteristics (granulation tissue -- beefy red, healthy; slough -- yellow or tan, devitalized but viable tissue requiring debridement; eschar -- black or brown, necrotic tissue), exudate (serous, sanguineous, serosanguineous, purulent -- noting amount, color, and odor), wound edges (approximated, rolled/epibole indicating stalled epithelialization, undermining indicating tissue destruction beneath intact skin, tunneling), and periwound skin (maceration from excessive moisture, erythema, induration suggesting cellulitis).