Clinical meaning
Wound healing progresses through four overlapping phases: hemostasis (platelet aggregation, fibrin clot formation), inflammation (neutrophil and macrophage infiltration, cytokine release), proliferation (angiogenesis, granulation tissue formation, epithelialization), and remodeling (collagen cross-linking and scar maturation over 6-24 months). Chronic wounds become arrested in the inflammatory phase due to persistent bacterial biofilms, elevated matrix metalloproteinase (MMP) activity that degrades extracellular matrix and growth factors, and cellular senescence of fibroblasts and keratinocytes. Pressure injuries develop when sustained mechanical loading compresses tissue between bone and an external surface, causing ischemia-reperfusion injury, lymphatic obstruction, and tissue necrosis — staging follows the NPUAP classification from Stage 1 (non-blanchable erythema) to Stage 4 (full-thickness tissue loss with exposed bone/tendon).
Exam relevance
Risk factors: - Venous insufficiency (most common cause of lower extremity ulcers) - Arterial insufficiency (peripheral arterial disease) - Diabetic neuropathy with repetitive microtrauma - Pressure from immobility or medical devices - Radiation therapy (radiation dermatitis and fibrosis) - Immunosuppressive medications - Biofilm formation in wound bed