wound healing and wound care.pptx

wound healing and wound care

1. Wound healing and wound care Dr Thana Ram Patel Assistant Professor Department of General Surgery Dr SN medical college jodhpur

2. Wound Healing BASIC PRINCIPLES A. Healing is initiated when inflammation begins. B. Occurs via a combination of regeneration and repair

3. regeneration A. Replacement of damaged tissue with native tissue; dependent on regenerative capacity of tissue B. Tissues are divided into three types based on regenerative capacity: labile, stable, and permanent.

4. Labile tissues Labile tissues possess stem cells that continuously cycle to regenerate the tissue. 1. Small and large bowel (stem cells in mucosal crypts, Fig. 2.5) 2. Skin (stem cells in basal layer in epidermis, Fig. 2.6) 3. Bone marrow (hematopoietic stem cells)

5. Stable tissues Stable tissues are comprised of cells that are quiescent (G0 ) , but can reenter the cell cycle to regenerate tissue when necessary. 1. Classic example is regeneration of liver by compensatory hyperplasia after partial resection. Each hepatocyte produces additional cells and then reenters quiescence. stable cells (e.g., fibroblasts, smooth muscle cells ) can replicate.

6. Permanent tissues Permanent tissues lack significant regenerative potential (e.g., myocardium/ cardiac muscle and striated / skeletal muscle, and neurons).

7. Repair (fibrosis/ scar) A. Replacement of damaged tissue with fibrous scar B. Occurs when regenerative stem cells are lost (e.g., deep skin cut) or when a tissue lacks regenerative capacity (e.g., healing after a myocardial infarction, Fig. 2.7) C. Granulation tissue formation is the initial phase of repair (Fig. 2.8). 1. Consists of fibroblasts (deposit type III collagen), capillaries (provide nutrients), and myofibroblasts (contract wound) D. Eventually results in scar formation, in which type III collagen is replaced with type I collagen 1. Type III collagen is pliable and present in granulation tissue, embryonic tissue, uterus, and keloids . 2. Type I collagen has high tensile strength and is present in skin, bone, tendons, and most organs. 3. Collagenase removes type III collagen and requires zinc as a cofactor.

8. The main components of connective tissue repair are angiogenesis, migration and proliferation of fibroblasts, collagen synthesis, and connective tissue remodeling.

9. 1 haemostasis 2 inflammation 3 profliferation 4 remodelling .

10. Mechanism of tissue generation and repair MECHANISMS OF TISSUE REGENERATION AND REPAIR A. Mediated by paracrine signaling via growth factors (e.g., macrophages secrete growth factors that target fibroblasts) B. Interaction of growth factors with receptors (e.g., epidermal growth factor with growth factor receptor) results in gene expression and cellular growth. C. Examples of mediators include 1. TGF-α - epithelial and fibroblast growth factor 2. TGF-β - important fibroblast growth factor; also inhibits inflammation 3. Platelet-derived growth factor - growth factor for endothelium, smooth muscle, and fibroblasts 4. Fibroblast growth factor - important for angiogenesis; also mediates skeletal development 5. Vascular endothelial growth factor (VEGF) - important for angiogenesis

11. repair Repair by connective tissue (fibrosis) 1. Repair by connective tissue occurs when injury is severe or persistent. Tissue in a third-degree burn cannot be restored to normal, owing to loss of skin, basement membrane, and connective tissue infrastructure. 2. Steps in normal connective tissue repair a. Repair requires neutrophil transmigration (see previous discussion) to liquefy injured tissue and then macrophages to remove the debris. b. Repair requires formation of granulation tissue, the precursor of scar tissue . Granulation tissue accumulates in the ECM and eventually produces dense fibrotic tissue (scar). c. Repair requires the initial production of type III collagen. Type III collagen has poor tensile strength; hence, the wound can easily be reopened d. Dense scar tissue produced from granulation tissue contains type III collagen (weak collagen) that must be remodeled. (1) Remodeling increases the tensile strength of scar tissue. (2) Metalloproteinases ( collagenases containing zinc) replace type III collagen with type I collagen (strong collagen), which increases the tensile strength of the wound to ≈70% to 80% of the original after ≈3 months. Scar tissue after 3 months is primarily composed of acellular connective tissue that is devoid of inflammatory cells and adnexal structures and is surfaced by an intact epidermis

12. Factors influencing B. Delayed wound healing occurs in Extrinsic causes 1. Infection (most common cause; S aureus is the most common offender) 2. foreign body

13. 3. Other causes include, ischemia, diabetes.

14. Systemic factors Intrinsic causes Nutritional deficiencies

15. Nutritional deficiencies that impair wound healing Nutritional deficiencies that impair wound healing a. Protein deficiency (e.g., malnutrition) b. Vitamin C deficiency - Vitamin C is an important cofactor in the hydroxylation of proline and lysine procollagen residues; hydroxylation is necessary for eventual collagen cross-linking. c. Trace metal deficiency (1) Copper deficiency leads to decreased cross-linking in collagen (also in elastic tissue). Copper is a cofactor for lysyl oxidase , which cross-links lysine and hydroxylysine to form stable collagen. (2) Zinc deficiency leads to defects in removal of type III collagen in wound remodeling. Type III collagen has decreased tensile strength, which impairs wound healing. Zinc is a cofactor for collagenase , which replaces the type III collagen of granulation tissue with stronger type I collagen.

16. glucocorticoids a. Interfere with collagen formation and decrease tensile strength b. Clinically useful in preventing excessive scar formation (1) Dexamethasone is used along with antibiotics to prevent scar formation in bacterial meningitis. Dexamethasone reduces the amount of cytokines (e.g., TNF-α and IL-1 in the cerebrospinal fluid) and has been associated with decreased inflammation, decreased cerebral edema, and lower rates of hearing loss. (2) Plastic surgeons inject high-potency steroids into wounds to prevent excessive scar tissue formation. c. Other effects of glucocorticoids (1) Inhibit production of cytokines (including IL-1, IL-6, and TNF) and other inflammatory mediators (e.g., histamine, prostaglandins) (2) Reduce vasodilation in response to inflammatory mediators, which reduces the accumulation of cells and fluid in the interstitial space (reduces swelling). (3) Reduce the immune cell response by inducing apoptosis of lymphocytes.

17. Cutaneous wound NORMAL AND ABERRANT WOUND HEALING A. Cutaneous healing occurs via primary or secondary intention. 1. Primary intention-Wound edges are brought together (e.g., suturing of a surgical incision); leads to minimal scar formation 2. Secondary intention-Edges are not approximated. Granulation tissue fills the defect; myofibroblasts then contract the wound, forming a scar.

18. Abnormal wound healing excessive formation of the repair components, deficient scar formation, formation of contractures .

19. Excessive Scarring Excessive formation of the components of the repair process can give rise to hypertrophic scars and keloids . The accumulation of excessive amounts of collagen may give rise to a raised scar known as a hypertrophic scar. These often grow rapidly and contain abundant myofibroblasts , but they tend to regress over several months (Fig. 3.31A). If the scar tissue grows beyond the boundaries of the original wound and does not regress, it is called a keloid (Fig. 3.31B, C). Keloid formation seems to be an individual predisposition, and for unknown reasons it is somewhat more common in African Americans. Hypertrophic scars generally develop after thermal or traumatic injury that involves the deep layers of the dermis.

20. Normal and aberrant wound healing C. Dehiscence is rupture of a wound; most commonly seen after abdominal surgery D. Hypertrophic scar is excess production of scar tissue that is localized to the wound (Fig. 2.9). E. Keloid is excess production of scar tissue that is out of proportion to the wound (Fig.2.10). 1. Characterized by excess type III collagen 2. Genetic predisposition (more common in African Americans) 3. Classically affects earlobes, face, and upper extremities

21. Defects in healing – chronic wounds These are seen in numerous clinical situations, as a result of local and systemic factors. The following are some common examples. • Venous leg ulcers (Fig. 3.30A) develop most often in elderly people as a result of chronic venous hypertension, which may be caused by severe varicose veins or congestive heart failure. Deposits of iron pigment ( hemosiderin ) are common, resulting from red cell breakdown, and there may be accompanying chronic inflammation. These ulcers fail to heal because of poor delivery of oxygen to the site of the ulcer. • Arterial ulcers (Fig. 3.30B) develop in individuals with atherosclerosis of peripheral arteries, especially associated with diabetes. The ischemia results in atrophy and then necrosis of the skin and underlying tissues. These lesions can be quite painful. • Diabetic ulcers (Fig. 3.30C) affect the lower extremities, particularly the feet. There is tissue necrosis and failure to heal as a result of vascular disease causing ischemia, neuropathy, systemic metabolic abnormalities, and secondary infections. Histologically , these lesions are characterized by epithelial ulceration (Fig. 3.30E) and extensive granulation tissue in the underlying dermis

22. Pressure sores (Fig. 3.30D) are areas of skin ulceration and necrosis of underlying tissues caused by prolonged compression of tissues against a bone, e.g., in elderly patients with numerous morbidities lying in bed without moving. The lesions are caused by mechanical pressure and local ischemia. When a surgical incision reopens internally or externally it is called wound dehiscence. The risk factors for such an occurrence are obesity, malnutrition, infections, and vascular insufficiency. In abdominal wounds it can be precipitated by vomiting and coughing.

23. Parenchymal wound Parenchymal fibrosis

24. Wound care The aim of wound management is to prevent the build-up of unwanted tissues types (necrotic tissue , slough tissue) on the wound bed, while encouraging the growth of granulation and epithelial (healing) tissue in order to repair the wound.

25. dressing Hydrating / moisturisinng dressings - Hydrocolloids – these are hydrating products that can be used on dry wounds with little or no moisture in order to raise the exudate levels to a moist environment Absorbent dressings - Foams – these are absorbent dressings intended to reduce exudate levels. Films – these products neither absorb moisture nor hydrate wounds. Used on their own they can only be used on vulnerable but unbroken skin (e.g. a Grade 1 pressure damage, areas vulnerable to friction, or on healed wounds that require some protection for a while).

26. Absorbent primary dressings Alginates – these are absorbent primary dressings Hydrofibre – this is an absorbent primary dressing absorbent primary dressings that require one of the aforementioned insulating secondary dressings applied over them. Failure to ‘insulate’ this type of dressing will cause it to dry and adhere to the wound bed, thereby causing trauma on removal. This type of dressing is required for deeper wounds

27. Non-adherent – these are dressings that don’t insulate the wound, hydrate nor absorb moisture and are commonly used for superficial wounds under other dressing types to prevent them from adhering to the wound. Many wound experts consider these dressing types have little usefulness in wound care and are therefore most frequently used with vacuum-assisted closure treatments (topical negative pressure)