Inflammation and Tissue Wound Repair PDF

Inflammation, Tissue Repair & Wound Healing Chris Garrison, PhD, RN, CNE, CHSE Objectives Learners will be able to: Describe the role of inflammation in wound healing Differentiate acute and chronic inflammation Explain the roles of different types of white blood cells and...

Inflammation, Tissue Repair & Wound Healing Chris Garrison, PhD, RN, CNE, CHSE Objectives Learners will be able to: Describe the role of inflammation in wound healing Differentiate acute and chronic inflammation Explain the roles of different types of white blood cells and chemical mediators in immune response Analyze the clinical factors that impact wound healing Differentiate types of wounds including their etiology and clinical management Types of Immunity Innate Immunity Physical, Chemical Barriers & Microbiome Includes skin, mucosa and substances like mucus, cilia, skin secretions Loading… Inflammatory Response Non-specific Natural Killer Cells (type of lymphocyte) WBC Adaptive Immunity Inflammation Inflammation is the physiological response to tissue injury, infection, or the presence of a foreign body Mediated by inflammatory chemicals dead Purpose is to remove microorganisms, necrotic tissue, and initiate tissue repair Cardinal signs of inflammation: Redness Swelling Heat Pain Loss of Function Acute Inflammation Vascular Phase Vasodilation at site of injury Increases blood flow to area Loading… Scause Produces heat and redness Increased capillary permeability Outflow of protein rich fluid into interstitial spaces Protein in exudate pulls in additional fluid by osmosis Produces swelling, pain, loss of function Churts use) to causeddrelation  Acute Inflammation Cellular Phase Activated platelets release inflammatory mediators Neutrophils migrate to area of injury wa Typically within 6-12 hours Phagocytosis ingest and destroy infected > - area Lifespan of 10 hours Monocytes become Macrophages Secrete additional inflammatory mediators 1- - Macrophages can engage in phagocytosis for several days  (chemicals) Key Inflammatory Mediators Arachidonic Acid Metabolites Bradykinin Histamine Complement Cytokines Chemical Mediators Involved in Inflammation Arachidonic Acid Metabolites Synthesized from Neutrophils and Macrophages Examples: ama se tubes Prostaglandins makes worse constriction - Induces vasodilation and bronchoconstriction - Leukotrienes increase Induces bronchoconstriction and microvascular permeability Chemical Mediators Involved in Inflammation Bradykinin Activated from plasma proteins (synthesized in liver) Increases vascular permeability constriction broncho Loading… Induces smooth muscle contraction of bronchioles ~ Dilates blood vessels Increases pain sensitivity Histamine Released by mast cells Results in transient vasodilation in acute phase of inflammatory reactions Binds to H-1 receptors Chemical Mediators Involved in Inflammation Complement System Plasma Proteins (synthesized in liver) Activated either by antibodies (classical pathway) or substances found on cell surfaces of infectious microorganisms (alternative pathway or lectin pathway) Functions: Opsonization Coating with protein that facilitates phagocytosis Recruitment of inflammatory cells Cell lysis destruction of > - cell don't- need · fil knowspeci Chemical Mediators (Cytokines) Involved in Inflammation Cytokines are signaling molecules that promote or inhibit inflammation IL-I & TNF-α lining Released from activated macrophages e'of new bloodset Stimulates neutrophils to adhere to endothelial cells Stimulates phagocytosis by macrophages Initiates acute phase response Fever, release of more neutrophils, hypotension, tachycardia, anorexia, malaise, release of cortisol Increased synthesis of inflammatory protein in the liver (i.e. complement and bradykinin) Chronic Inflammation Results from unresolved injury, infection, or foreign body Macrophages, lymphocytes, and fibroblasts predominate instead of neutrophils Presence of fibroblasts increases the risk of scarring and deformity sellssyntesize collagen Examples of Chronic Inflammation Granuloma Macrophages surrounded by lymphocytes “wall off” the foreign protein (i.e. latent tuberculosis) Abscess Fibroblasts wall off area of infection Antibiotics will not penetrate Requires incision and drainage (I&D) Abscess Inflammation & Disease Uncontrolled or inappropriate inflammation can cause tissue damage: ↑ Rheumatoid Arthritis Sepsis Inflammatory Bowel Disease White Blood Cell (WBC) Count Differential Normal White Blood Cell Count 5,000-11,000/ ml3 Neutrophils 40-70% of WBCs under normal conditions Primary initial phagocytosis in acute injury or infection Short life span Eosinophils 1-6% of total WBC count Associated with an increase in number during allergic reactions and infection by intestinal parasites Release inflammatory chemicals in areas of inflammation Primary function is to kill parasitic helminths (worms) Basophils 0-2% of total WBC count Release vasoactive substances (heparin, histamine) during inflammation Macrophages & Monocytes Monocytes Immature macrophages 5% of total WBC count Circulate in the blood stream for about 3 days prior to entering tissue and becoming macrophage Macrophages & Monocytes Macrophages Life span from months to years Functions Phagocytosis Repair of injured tissue Secretion of cytokines to help control the immune system Secrete growth factors to stimulate angiogenesis and fibroblasts Lymphocytes NK cells Innate immune cells Can kill tumor cells and virally infected cells without previous exposure T Cells Major cells of cell-mediated immunity T-helper cells stimulate B-cell proliferation and antibody production B Cells Major cells of antibody-mediated immunity Able to produce antibodies Require help from T helper cells to respond Differential white blood cell response to infection Bacterial infection Increase in neutrophils If severe may include immature neutrophils “bands” “Left shift” Viral infection Decrease in neutrophils Increase in lymphocytes Tissue Regeneration Tissue varies in ability to replace itself with functional cells Labile Cells Continuously divide and can be replaced rapidly Mucosal linings, bone marrow Stable Cells Stop dividing when growth ceases but can regenerate if needed Parenchymal cells of liver and kidney, vascular endothelium Permanent Cells Cannot divide Nerve cells, myocardial cells Wound Healing Process Phase I: Hemostasis Purpose is to stop blood loss Phase II: Inflammatory Phase Purpose is to clean out debris Localized inflammation Neutrophils arrive Begin phagocytosis of bacteria and debris Macrophages Arrive after 24 hours Continue phagocytosis Release growth factors that stimulate epitheliazation, angiogenesis and attract fibroblasts and prepare for proliferative phase Wound Healing Process Phase III: Proliferate Phase Purpose is to build new tissue Granulation Fibroblasts synthesize collagen and growth factors which induce angiogenesis Possible complications Loading… For granulation to occur necrotic tissue must be removed Hypergranulation Excessive granulation tissue that extends above the wound edges and prevents healing Epitheliazation Migration of epithelial cells to close surface of wound Hypergranulation Wound Healing Process Phase IV: Remodeling Phase Purpose is to strengthen new tissue Collagen scar reorganizes and strengthening Continues for up to 2 years Scars never regain full tensile strength Complication Keloid Abnormal scar tissue formation More common in African-Americans Keloid Types of Wound Healing Primary Intention Edges approximated Surface epitheliazation Secondary Intention Deeper wounds Heals bottom up by granulation Things needed for effective wound healing Removal of necrotic tissue Control of infection Moist wound bed Adequate nutrition Adequate oxygen delivery Oxygenation Perfusion Hemoglobin Causes of Impaired Wound Healing Malnutrition Protein, carbohydrate, Vitamin A, Vitamin C, Zinc Vascular Disease Diabetes Decreased O2 release, Microvascular Disease, Impaired Leukocyte function Hypoxia Smoking Decreased oxygenation and hypercoagulability Medications Corticosteroids, Chemo Critical Thinking Question Why would corticosteroids impair wound healing? Types of Wounds Surgical Wounds Traumatic Wounds Pressure Ulcers Burns Arterial Ulcers Venous Stasis Ulcers Wound Dehiscence Separation of a surgical wound Sensation of “giving way” Risk factors obesity, diabetes, malnutrition Precipitating factors Sudden straining Splint incision to prevent Management Cover wound Notify surgeon Evisceration Protrusion of organs through an open surgical wound Surgical Emergency Cover with sterile saline towels or dressings Keep NPO Prep for surgery Surgical Wound Dehiscence Traumatic Wounds Laceration Tearing of tissue May require suturing Abrasion Scraping of superficial layer Contusion Blunt trauma Bruising/hematoma Puncture Deep cavity created Laceration Abrasion Traumatic Wound Management Control bleeding Cleanse wound of foreign material Assess wound Size and dimension Need for closure Update tetanus vaccine Educate patient Wound care S/S of infection Pressure Ulcers Skin breakdown caused by unrelieved pressure Also called Decubitus Ulcer/Bed Sore Pressure, usually over bony prominences, cuts off circulation to skin and underlying tissue resulting in ischemia, necrosis and breakdown Capillary pressure is 25-35 mm Hg Causative Factors Interplay between compressive pressure and tissue resilience Friction Shear Duration of pressure Decreased tissue tolerance Caused by poor nutrition, incontinence, moisture Impact of Shear Areas of greatest risk for pressure ulcers Heels Sacrum Coccyx Trochanters Ischium Factors which reduce tissue resistance to pressure Aging Diabetes Moisture/Incontinence Vascular Disease Malnutrition Albumin level Dehydration Risk Factors Paralysis/Immobility Orthopedic Surgery Confusion/Sedation Impaired sensation Heart Failure, Arterial disease, COPD, diabetes, malignancy Elderly Prevention: Initial Assessment Head to toe skin assessment with attention to pressure points Assess Mobility, Alertness, Sensation, Continence, Nutrition/Hydration, Circulation (Braden Scale or Norton Scale) Implement risk reduction plan Prevention: Pressure Reduction Reposition Q 2 hours if bedfast reposition Q 1 hour if chair fast Pressure reducing mattress and chair cushion (Check for bottoming out) Positioning Keep heels completely off the bed Do not position on trochanters Turn 30 degrees off back Keep HOB < 30 degrees unless contraindicated Use Pillows and Wedges to eliminate all areas of pressure Use turn sheet Heels Floated Off Bed Initial Presentation Non-blanching erythema Darker skinned individual Darker than surrounding skin Area of warmth Induration Boggy Skin taut, shiny, scaly Stage I Pressure Ulcer Staging Do not back stage Only stage pressure ulcers Stage I Skin intact with tissue damage Stage II Superficial ulcer, crater or blister Stage III Full-thickness into subcutaneous tissue Stage IV Extensive destruction of fascia, muscle, bone, tendon Non-Stageable Eschar covered area Pressure Ulcer Assessment Stage Size L, W, D Wound Bed Granulation, slough, eschar, necrotic tissue Drainage/ Exudate COCA Peri-wound skin Undermining Tunneling Undermining Tunneling Pressure Ulcer Treatment Maintain moist wound bed Avoid maceration Remove non-viable tissue Treat infection Avoid cytotoxic solutions in clean wounds Relieve pressure Improve nutrition Debridement Don’t debride heel eschar Mechanical Wound irrigation Wet to Dry Whirlpool Autolytic Enzymatic Collagenase (Santyl®) Surgical/Sharp Required for sepsis or advancing cellulitis Arterial Ulcers Etiology Atherosclerosis Tissue Hypoxia Trauma Location Distal Extremities Appearance Necrotic Minimal Drainage Arterial Ulcers Prevention Improve perfusion Protect from injury Assessment Wound Circulation Ankle-Brachial Index Treatment Keep wound clean Hyperbaric Therapy Re-vascularize Venous Stasis Ulcers Etiology Chronic Venous Insufficiency Edema Location Malleolus, Tibial Appearance Jagged Weeping Venous Stasis Ulcers Prevention Control edema Protect from injury Assessment Wound Circulation Ankle-Brachial Index Treatment Keep wound clean Hyperbaric Therapy Compression Critical Thinking Questions What factor is most important to heal: An arterial ulcer? A venous stasis ulcer? Review Question Which of the following chemical mediators is involved in generating a febrile response to an infection? A. Histamine B. Bradykinin OC. TNF-α D. Leukotrienes Review Question Which of the following white blood cells is the primary responder to bacterial infection? A. O Neutrophil B. Eosinophil C. Basophil D. Lymphocyte Review Question Which type of tissue is best able to be regenerated into its original condition? A. Peripheral nerves B. Myocardium C. Liver cells ②D. Oral mucosa Review Question Which of the following wounds would heal by secondary intention? A. An abrasion B. A sutured surgical wound C. A Stage I Pressure Ulcer OD. A Stage III Pressure Ulcer Review Question Which of the following conditions is likely to result in chronic inflammation? (Select all that apply) A. A surgical wound OB. Tuberculosis C. A laceration OD. An Abscess E. An Abrasion Review Question What stage is this pressure ulcer? Review Question A. Stage I OB. Stage II C. Stage III D. Stage IV