Part 1- wound care intro.pptx

Part I: Wound Care Intro Joy Gonzalez MPT, CWS, FACCWS & Greg Ernst, PT, PhD Photo credit: Wound Care Essentials Practice Principles Second Edition 2008, Quick Reference To Wound Care Second Edition 2005, Misty Vaughn, PT, CWS Anatomy & Physiology of the Skin  The skin is the largest organ in...

Part I: Wound Care Intro Joy Gonzalez MPT, CWS, FACCWS & Greg Ernst, PT, PhD Photo credit: Wound Care Essentials Practice Principles Second Edition 2008, Quick Reference To Wound Care Second Edition 2005, Misty Vaughn, PT, CWS Anatomy & Physiology of the Skin  The skin is the largest organ in the body, 10% of BW  Healthy skin is tough, pliable, elastic, and hydrated  The skin acts to protect from water loss, shearing, toxic irritants, and mechanical injury  The skin functions in thermal regulation, synthesis of vitamin D, and sensation Skin pH  Skin is acidic: pH: 4.2 – 5.6 ◦ Normal flora ◦ More neutral = susceptible to pathologic organisms like staph, strep, and yeast Layers of the Skin The Skin Epidermis  Protective layer  No blood supply (avascular)  Lines hair follicles, sweat glands, and sebaceous glands  Divided into 5 layers 1. 2. 3. 4. 5. Stratum Stratum Stratum Stratum Stratum Corneum Lucidum Granulosum Spinosum Basale First Four Layers 1. 2. 3. 4. Stratum Corneum “horny layer”, comprised of dead keratinized cells (insoluble fibrous protein), shed as a result of mechanical force Stratum Lucidum replaces the shed Stratum corneum (most readily seen in the thick skin of soles and palms) Stratum Granulosum “granular layer” Stratum Spinosum “spiny layer” comprised of multisided cells Stratum Basale  Contains keratinocytes and melanocytes, Merkel cells (touch receptors), Langerhan cells (important in immune function)  Stratum Basale migrates upwards to the Stratum Corneum where it is sloughed off (takes 30-45 days) Basement Membrane Zone (BMZ)  Separates the epidermis from the dermis  This is the layer affected in blister formation  Rete ridges are epidermal protrusions which point down to connect to the dermis and are partially responsible for skin integrity Dermis  Gives skin its bulk  Vascular (supplies nourishment to epidermis through capillary bed diffusion)  Innervated  Comprised of collagen ( 4 main types) and elastin I. II. III. IV. 90% tendons, ligaments, bone, skin Major component of cartilage Arteries, intestine, uterus Found in the basement membrane  Divided into 3 layers 1. Papillary Dermis 2. Reticular dermis 3. Hypodermis Layers of the Dermis 1. 2. 3. Papillary Dermis lies below BMZ forms structures with Rete ridges called dermal papillae which contain capillary loops to supply oxygen and nutrients to the epidermis and contain pain/touch receptors Reticular Dermis contains a complex of cutaneous blood vessels Hypodermis attaches the dermis to the underlying structures, is comprised of loose connective tissue and fat cells (nutritional storage) and is well supplied with blood vessels and nerve endings Layers of the Skin Age Related Changes  Decreased         Dermal thickness (causing thinning of skin) Fatty layers (bony prominences less protected) Collagen & Elastin Sensation Sweat Glands (leading to dry skin) Circulation Epidermal regeneration Decrease in number of Rete ridges Thin skin Normal skin Skin and Incontinence Urinary: 50% of nursing home residents have some type of incontinence  Combined urinary and fecal incontinence raise skin pH  Irritates the epidermis and can cause dermatitis and skin erosion.  Key Cells in Wound Healing Platelet: smallest cell in blood  Erythrocyte: major cellular element of circulating blood, contains hemoglobin, major function is to transport oxygen  Leukocyte: white blood cell  Monocyte: large circulating leukocyte which differentiates into a macrophage  Macrophage: phagocytic cell, produces MMP’s and growth factors  Matrix Metalloproteases: protein degrading enzymes, mediates tissue destruction, overactive in RA, OA, Atherosclerosis  Key Cells in Wound Healing  Fibroblast: synthesis collagen and other ECM substances, depending on need of surrounding tissues  Myofibroblast: Modified fibroblast found at periphery of wound and is responsible for contraction  Neutrophils: small white blood cell, hundreds of thousands circulating, begin process of clean up until macrophages arrive Key Cells in Wound Healing  Endothelial Cells: line vessels; particularly capillaries, migrate and form new vessels Growth Factors Also called Cytokines (cell-activity)  Stored in platelets  Regulate/coordinate healing process  Complex proteins released by cells and stimulate:  Cell Migration Cell Proliferation Angiogenesis Production and degradation of extracellular matrix (ECM)  Growth factor production by other cells  Apoptosis (programmed cell death)     Integrins  Cell surface receptors  Enable cells to detect and interact with components of ECM  Have ability for reversible binding (can attach, then un-attach) Integrins  When      are they used?? Platelet interactions with collagen during hemostasis Leukocyte merging during early inflammation Endothelial cell budding and growth during angiogenesis Epithelial cell migration Fibroblast movement through granulation tissue Phases of Wound Healing 1. 2. 3. 4. Hemostasis Inflammation Proliferation Maturation Hemostasis Happens immediately and takes just minutes  Vasoconstriction  Platelet aggregation  Fibrin deposition   End result is a clot which is essential as it preserves the integrity of the high pressure circulatory system to limit blood loss . Plus the fibrin mesh material is a provisional wound matrix onto which fibroblasts and other cells migrate. Inflammatory phase Hemostatic response Functions to control blood loss  retraction and sealing off of small blood vessels  platelets aggregate, deposit fibrin  fibrin forms a lattice for clot formation  clot serves as the initial source of tensile strength in the wound  Inflammatory Phase (1-5 days)  Characterized by      Erythema Edema Heat Pain Vascular permeability Transition from vasoconstriction to vasodilatation mediated mainly by histamine  Macrophages and leukocytes migrate into wound and initiate cellular wound debridement by phagocytosing bacteria and foreign material  Inflammatory phase Cellular response Leukocytes are attracted to the injured area  Neutrophils rid the area of bacteria and debris by phagocytosis in early inflammation  In late inflammation, monocytes convert into large macrophages, which engulf large amounts of bacteria and cellular debris  Sets the stage for wound repair  Proliferative Phase (5-25 days)  Characterized by  Beefy red appearance  Cobblestone texture  Bleeds easily  Purpose     is Initiate granulation and epithelialization Synthesis of new collagen Formation of new blood vessels (angiogenesis) Wound contraction as wound edges draw together, this is cell mediated and does not require the synthesis of new collagen Proliferative/repair phase Granulation tissue Maturation Phase (1-24 months)  Characterized by scar  Shrinking  Thinning  paling Purpose is for scar to re-establish tensile strength  Immature scars contain disorganized fine collagen fibers whereas mature scars have thicker fibers arranged in an orientation paralleling skin stress  Wounds will ultimately regain only 80% of their original strength  Types of Wounds  Thickness ◦ Partial: involve the epidermis and into (but not through) the dermis  Heal by re-epithelialization ◦ Full: extends through the dermis and may involve the subcutaneous tissue, muscle, or bone  Heal by granulation, contraction, and reepithelialization Wound Closure Primary closure (first intention) 1.    Wound edges approximated by sutures, staples Heals by epithelialization Ex: surgical wound Secondary Closure (secondary intention) 2.    Not possible to approximate secondary to damage or tissue loss Heals by granulation, contraction, epithelialization Ex: pressure ulcer Delayed Primary Closure (tertiary closure) 3.  Wound edges approximated after risk of infection is controlled Abnormal Wound Healing Hypergranulation  Tunneling / Undermining  Hyperkeratosis  Hypertrophic scarring  Keloid scarring  Scar contracture  Hypergranulation Hyperkeratosis Tunneling Undermining Types of Wounds  Acute  Chronic  Arterial Ulcers  Venous Ulcers  Diabetic Ulcers  Pressure Ulcers  Skin Tears Acute Wounds  Heal within an expected time frame  Usually with little to no complications  Overreaction in healing:  Hypertrophic scaring  keloids  Examples:  Gunshot wounds  Surgical incisions  Abrasions Chronic Wounds Do not heal in the expected time frame  May be a result of:   Circulation: decreased blood flow = decreased O2, decreased nutrition, decreased immune cells  Mechanical Stress:  pressure - compression of tissue between a surface and bony prominence,  Friction - two surfaces rubbing together,  shear – disruption of connection between soft tissue and bone  Debris in wound: granulation can not occur on top of dead tissue, foreign material (dressing residue, gauze fibers) if left in a wound can slow/prevent healing  Temperature: temperature must remain constant, can take up to 5 hours for ambient temp of wound to return to homeostasis after dressing change Chronic Wounds    Maceration/Desiccation: too much moisture/too little moisture in a wound impedes the migration of epidermal cells Infection: prolongs the inflammatory stage, causes additional tissue destruction Chemical stress: Although these chemicals kill bacteria, they also kill maturing endothelial cells, they are cytotoxic to wound tissue and should not be used to clean wounds. EX: Betadine, Hydrogen Peroxide, Dakin’s solution, Alcohol, Vinegar, Iodophor Chronic Wounds  Health Status: diabetes, immunocompromised, decreased circulatory status  Nutrition: fluids, calories, proteins, carbs  Age  Body Build: obese patients higher risk for wound dehiscence and hernias, thinner patients have less adipose tissue and therefore less nutritional storage, both may be malnourished Thank you  The next presentations will talk about different types of wounds. 