Chapter 12: Inflammation & Healing Processes

Inflammation is presented as a protective vascular and cellular response to tissue injury, characterized by sequential phases involving vasodilation, increased capillary permeability, and cellular migration of neutrophils, monocytes, and lymphocytes to the injury site. Chemical mediators including histamine, cytokines, prostaglandins, and complement proteins orchestrate this response by regulating vasodilation, chemotaxis, and pain signaling. The chapter distinguishes between acute inflammation that resolves within weeks, subacute presentations with extended duration, and chronic inflammatory conditions that persist for months or years. Clinical manifestations encompass the classic signs of redness, heat, swelling, pain, and loss of function, accompanied by systemic responses such as fever through cytokine-mediated prostaglandin release in the hypothalamus. Wound healing mechanisms are explored through regeneration of identical cell types and repair via connective tissue formation, with healing classified as primary intention for approximated surgical wounds, secondary intention for large irregular wounds healing from the base upward, and tertiary intention involving delayed closure after contamination. The chapter emphasizes comprehensive wound assessment techniques, therapeutic interventions including negative pressure wound therapy and hyperbaric oxygen treatment, and the selection of appropriate dressings such as hydrogels, alginates, and antimicrobial preparations. Pressure injury prevention receives significant attention, incorporating risk assessment tools like the Braden Scale and staging systems from non-blanchable erythema to full-thickness tissue loss with bone exposure. Nursing interventions focus on repositioning protocols, pressure redistribution, moisture management, nutritional optimization, and psychosocial support throughout the healing process.