Chapter 39: Tissue and Wound Healing PDF
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This chapter discusses wound healing, covering various types of wounds and the processes involved in healing, from homeostasis to remodeling. It also mentions factors affecting healing and different methods of treatment for wounds.
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HAPTER 39: TISSUE AND WOUND HEALING C Epidermis is upper layer with stratified squamous epithelial cells, keratinocytes as well as melanocytes, T lymphocytes, dendritic (langerhans) cells, and tactile (merkel) cells (NO BLOOD, AVASCULAR and NO lymphatic vessels) ermis is the thicker layer w...
HAPTER 39: TISSUE AND WOUND HEALING C Epidermis is upper layer with stratified squamous epithelial cells, keratinocytes as well as melanocytes, T lymphocytes, dendritic (langerhans) cells, and tactile (merkel) cells (NO BLOOD, AVASCULAR and NO lymphatic vessels) ermis is the thicker layer with two layers papillary (superficial), and reticular (thicker and deeper) containing blood vessels, D appendages, sensory receptors, smooth and skeletal muscle cells cute wound occurs suddenly or over a brief period resulting from physical trauma or medical interventions A Heals in organized and timely manner with restoration of structural and functional integrity in four to six weeks hronic wound occurs over long period with healing not being organized or in timely manner and can/does impair structural and C functional integrity Partial thickness wound Full thickness wound Damage extends through epidermis, dermis is intact Damage extends through epidermis and dermis Reepithelialization ossible extends into subcutaneous tissue, P muscle, bone Scar formation Wound healing 1. Hemostasis 2. Inflammation 3. proliferation/granulation 4. Remodeling maturation Clinical mediators are neutrophils, macrophages, lymphocytes, platelets, keratinocytes, fibroblasts, endothelial cells, growth factors, and cytokines Depends on type of injury, extent of tissue loss, infection, necrotic tissue, or secondary tissue breakdown, type of cells involved rimary intention (primary P closure) S econdary intention (secondary/spontaneous closure) Tertiary intention (delayed primary closure) S urgical closure Repair 0 formation of new ECM Regeneration - reepithelialization Little granulation tissue F ull thickness wound healed without closure attempt Large amount of granulation tissue or exudate Longer healing time so larger scar Skin grafting, skin substitutes ombination of primary and secondary C intention Contaminated wound cleaned, left open drainage Scarring > primary intention and < secondary ypoxia delays or stops wound healing process with greatest at center or wound and can lead to wound infection (infection H amplifies it) It inhibits fibroblast activity, collagen deposition in matric Stimulus for angiogenesis Reepithelialization occurs only when wound covered with granulation tissue adly contaminated wounds may overwhelm host defenses and can be largely caused by inappropriate surgical wound handling B such as inappropriate suture material increases likelihood of body reaction, break in asepsis, duration of surgery or open time, spill of intestinal contents into peritoneum, failure to proper prepare skin preoperatively Nutrition plays a major role in wound healing especially carbohydrates and fats M alnutrition decreases immune and inflammatory responses, delays wound healing, increases wound infection, diminished angiogenesis, reduces matrix formation and remodeling Vitamins and mineral deficiencies are associated with chronic, nonhealing wounds in nutritionally debilitated individuals Medications can also affects wound healing Corticosteroids promote breakdown of carbohydrates, fats, and proteins and anti inflammatory action impedes inflammatory phase wound healing Antineoplastic drugs are potent immunosuppressants that impair reepithelialization, granulation tissue formation, angiogenesis Abnormal wound healing - deficient, is insufficient deposition of dermal connective tissue matrix weakens tissue to wound failure Clinical manifestations include signs of infection, absence of healing ridge by fifth to ninth postoperative day, seroma or hematoma formation, increase in serous discharge hronic non healing wound do not processed through healing process or does but cannot maintain structural and functional C integrity characterized by an arrest in the inflammatory phase Can harbor bacteria, imbalance between neutrophilic proteolytic enzymes and their inhibitors, increases levels of inflammatory mediators, chronic inflammation, necrosis, fibrosis ressure injuries are localized ischemic lesions of skin and underlying tissue most commonly over bony prominences because P external pressure impair flow of blood and lymph Causes can be immobility, reactive hyperemia, microthrombi, shearing forces Risk factors as immobility or inactivity, poor perfusion, and skin status Clinical manifestations include pressure decreases from boney area toward periphery, discoloration to blisters or areas of denuded superficial skin to deep tissue damage with necrosis, graded or staged to classify degree of tissue damage Treatment is surgical debridement, autolytic debridement, skin grafting, topical and systemic antibiotics, hydrocolloid and transparent film dressing, alginate, foam, iodine dressing
