Wound Care for the Primary Care Physician

Transcription

1 Saturday General Session Wound Care for the Primary Care Physician Ana Catalina Macias, MD Assistant Professor of Medicine, Geriatrics Section Baylor College of Medicine Houston, Texas Educational Objectives By the end of this activity, the participant should be better able to: 1. Discuss the stages in the wound healing cascade and define the four major types of wounds and the characteristics of each. 2. Examine the most common factors that affect wound healing and differentiate the effect of each of the overall healing of wounds. 3. Assess the wounds for signs of infections. 4. Discuss management priorities and treatment plans based on proper wound assessment, including specific treatments, topical preps, dressings, etc. Speaker Disclosure Dr. Catalina Macias has disclosed that she has no actual or potential conflict of interest in relation to this topic. 10

2 Speaker Disclosure Dr. Macias has disclosed that she has no actual or potential conflict of interest in relation to this topic. Ana Catalina Macias, MD Assistant Professor, Section of Geriatrics, Department of Medicine Baylor College of Medicine Geriatric Medicine and Wound Care Michael E. DeBakey VA Medical Center Objectives By the end of this activity, the participant should be better able to: Discuss the cascade of normal wound healing. Examine the most common factors that affect wound healing. Discuss the TIME principle of wound healing. Review 4 major types of wounds. Wound Healing Physiology Phases of Wound Healing Hemostasis 0 3 hours Inflammatory 0 3 days Proliferative 3 21 days Remodeling/Maturation 21 days 1.5 years Yamaguchi Y, Yoshikawa K. Cutaneous wound healing: an update. J Dermatol Oct;28(10): Hemostasis Occurs within minutes of the initial injury unless there are underlying clotting disorders. 1

3 Inflammation Vasodilation increase in blood flow erythema, swelling and warmth Neutrophils phagocytize debris and micro organisms (first line of defense) Monocytes then release intracellular enzymes to further digest tissue Fibrin is broken and attracts fibroblasts and epithelial cells which are aided by local mast cells Cytokines and growth factors are released Inflammation Monocytes differentiate into macrophages and secrete extracellular enzymes, paving the way to resolving inflammation MMPs (Matrix metalloproteinases) Responsible for removal of devitalized tissue Repair of lost or damaged tissue Remodeling MMPs are balanced by TIMPs Tissue inhibitors of metalloproteinases Released locally by cells TIMPs bind to MMPs and deactivate them Uncontrolled MMPs cause degradation of newly formed tissue or destruction of growth factors prolonging inflammatory phase and delay in wound healing Chronic wound Proliferation Characterized by angiogenesis, collagen deposition, granulation tissue formation, wound contraction and epithelialization Wound bed must fill in from the bottom up with collagen and must be maintained in an optimal environment (moisture balance) before the epithelial cells will begin to proliferate and migrate across the wound surface to close the wound. Balance between MMPs and TIMPs result in net production of new tissue. Remodeling Healing process involves the remodeling and realignment of collagen Tensile strength 70 80% of what it was before the injury Main cells Fibroblasts Chronic Wounds Factors Affecting Wound Healing Stalled with suppressed cell division and migration Due to: High levels of inflammatory cytokines and MMPs Low levels of TIMPs and growth factors In this environment cells are senescent and unresponsive to growth factors Local Growth factors Edema Ischemia Low oxygen Infection Arterial insufficiency Venous insufficiency Neuropathy Systemic Inadequate perfusion Metabolic disease Chronic disease Nutrition Smoking Exposure to radiation 2

4 Wound Infection Overgrowth of Microorganisms Resultant Tissue Destruction Local symptoms Wound deterioration Erythema, edema, drainage (purulent), tenderness, warmth, induration and/or crepitus Systemic symptoms Fever, leukocytosis, confusion, tachycardia, hypotension, malaise Wound Infection Prolongs the inflammatory stage Induces additional tissue destruction Delays collagen synthesis Prevents epithelialization Colonization vs. Infection Colonization Bacteria in wound bed, not affecting the environment Critical Colonization Suspect bacterial burden if a clean wound shows no improvement after 14 DAYS of topical therapy Infection Invasion of the soft tissues Chronic Wound Infection Wound Culture Traditional swab culture Not recommended Detects only surface bacterial colonization/contamination May not reflect the invasive organism causing infection Quantitative Wound Culture Recommended Documents bacterial burden Identifies bacteria actually invading wound tissue Tissue Biopsy, Needle Aspiration or Quantitative Swab Technique Topical Antimicrobial Therapy Silver dressings Cadexomer iodine Others used just for short periods Acetic acid Hydrogen peroxide Chlorpactin Dakin s Povidone iodine TIME Principle Structured approach to wound bed preparation Tissue Infection/inflammation Moisture balance Edge of wound Optimizes the management of chronic wounds Should be done with every wound assessment 3

5 Schultz GS, Sibbald RG, Falanga V, et al. Wound bed preparation: a systematic approach to wound management. Wound Repair Regen Mar;11 Suppl 1:S1 28. T Tissue Necrotic tissue Prolongs the inflammatory phase Delays wound healing Medium for bacterial growth Debridement Facilitates visualization of wound base Transforms the chronic wound by creating an acute wound Creates a viable wound bed Autolytic, Sharp/surgical, Mechanical, Biotherapy, Enzymatic (chemical) I Infection/Inflammation Biofilms Complex microbial community bacteria embedded in a protective matrix of sugars and proteins Provide protection for microorganisms embedded within them, improving tolerance to the host s immune system, antimicrobials and environmental stresses Major contributing factor to chronic inflammatory changes in the wound bed Treatment Removed by sharp debridement Antibiofilm agents silver, iodine and honey dressings I Infection/Inflammation Manage bacterial load Contamination, colonization or critical colonization Treat infection Local or systemic Manage inflammation from chronic diseases Autoimmune diseases SLE, RA, Vasculitis Inflammatory conditions Inflammatory bowel disease M Moisture Imbalance Excess Tissue maceration Edema of the tissue Dry Slows epithelial cell migration Eschar formation E Edge of Wound Impairment of keratinocyte migration Epibole rolled or curled under wound edges Aggressive debridement 4

6 Major Types of Wounds Pressure Injury Vascular Ulcers Arterial Ulcers Venous Stasis Ulcers Neuropathic/Diabetic Foot Ulcers Others Pyoderma gangrenosum, malignancies, calciphylaxis Pressure Injury Localized damage to the skin and/or underlying soft tissue usually over a bony prominence or related to a medical or other device Result of intense and/or prolonged pressure or pressure in combination with shear Tolerance of soft tissue for pressure and shear are affected by: microclimate, nutrition, perfusion, co morbidities and condition of the soft tissue Common Sites of Pressure Injury Occiput (<1%) Scapula (<1%) Spine (<1%) Elbow (<1%) Sacrum & Coccyx (65%) Trochanter (9%) Ischium (4%) Knee (3%) Tibia (2%) Heel & Ankle (15%) Pressure Injury By 2030, 20% of the world s population will be over the age of 65 Fastest growing segment of the population Individuals over the age of 80 70% of pressure injuries occur in people over the age of 70 NPUAP (2001) Prevalence 15.1%, incidence of 7% in US hospitals U.S. Census Bureau. Population Projections Program, Population Division, U.S. Census Bureau. Washington, DC, Thomas DR. Issues and dilemmas in the prevention and treatment of pressure ulcers. J Gerontol 2001; 56A:M Pressure Injury in the Elderly Frailty Malnutrition Co morbidities Immobility Dementia Halfens RJ, et al. Int J Nurs Stud 2000;37(4): Lindgren M, el al. Scand J Caring Sci 2004;18(1): Nixon J, et al. Health Technol Assess 2006;10(22):iii iv, ix x, Nixon J, et al. Int J Nurs Stud 2007;44(5): Schoonhoven L, et al. Qual Saf Health Care 2006;15(1): Anthony D, el al. Clin Rehabil 2000;14(1): Pernerger TV, et al. J Clin Epidemiol 2002; 55(5):

7 Pressure Injury How are we doing? 503,300 admissions with PI as related diagnosis (2006) Total increase of 78.9% since % increase for primary diagnosis of pressure ulcer 15% increase in total hospitalizations Compared to stays for all other conditions, hospitalizations due to pressure ulcers were: More likely discharge to nursing home More likely to result in death 72% of patients admitted with a secondary diagnosis of pressure ulcers were 65 and older Russo, C.A. (Thomson Reuters), Steiner, C. (AHRQ) and Spector, W. (AHRQ). Hospitalizations Related to Pressure Ulcers, HCUP Statistical Brief #64. December Agency for Healthcare Research and Quality, Rockville, MD. us.ahrq.gov/reports/statbriefs/sb64.pdf Pressure Ulcers in America: prevalence, incidence and implications for the future. NPUAP us.ahrq.gov/reports/statbriefs/sb64.jsp Pressure Injury Cost Overall impact US 1.2% of total health care expenditure 2006 Cost Data Estimated cost to heal a single pressure ulcer range from $3,500 to $60,000 Legal Issues More than 17,000 lawsuits filed annually Average $250,000 per judgment Centers for Medicare and Medicaid. Fed Regist 2007 Aug 22;72(162): Bennett G et al. Age Aging. 2004;33(3): Severens JL, et al. Adv Skin Wound Care. 2002; 15(2): Bennet RG, et al. J AM Geriatric Soc. 2000; 48(1): Pressure Injury Changes NPUAP changed terminology from Pressure ulcer to Pressure injury This more accurately describes pressure injuries to both intact and ulcerated skin Also, Arabic numbers are now used instead of Roman numerals The term suspected has been removed from the Deep Tissue Injury label Pressure Injury Staging Staged to indicate the extent of tissue damage Only used for pressure ulcers Stage all pressure ulcers at the deepest level of damage Once a pressure ulcer is staged, it remains at that stage Reverse staging/back staging should never be used to describe the healing of a pressure ulcer Pressure Injury Stage 1 Non blanchable erythema of intact skin Presence of blanchable erythema or changes in sensation, temperature, or firmness may precede visual changes. Color changes do not include purple or maroon discoloration 6

8 Pressure Injury Stage 1 Pressure Injury Stage 1 Pressure Injury Stage 2 Partial thickness skin loss with exposed dermis Wound bed is viable, pink or red, moist May also present as an intact or ruptured serum filled blister Adipose (fat) is not visible and deeper tissues are not visible Pressure Injury Stage 2 Granulation tissue, slough and eschar are not present. Usually result from adverse microclimate and shear in the skin This stage should not be used to describe moisture associated skin damage (MASD) or traumatic wounds (skin tears, burns, abrasions Pressure Injury Stage 2 Pressure Injury Stage 2 7

9 Pressure Injury Stage 3 Full thickness skin loss Adipose (fat) is visible in the ulcer Granulation tissue and epibole (rolled wound edges) are often present Slough and/or eschar may be visible Pressure Injury Stage 3 Depth of tissue damage varies by anatomical location Areas of significant adiposity can develop deep wounds Undermining and tunneling may occur Fascia, muscle, tendon, ligament, cartilage and/or bone are not exposed If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury Pressure Injury Stage 3 Pressure Injury Stage 3 Pressure Injury Stage 4 Full thickness skin and tissue loss Exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone in the ulcer Slough and/or eschar may be visible Pressure Injury Stage 4 Epibole (rolled edges), undermining and/or tunneling often occur Depth varies by anatomical location If slough or eschar obscures the extent of tissue loss this is an Unstageable Pressure Injury 8

10 Pressure Injury Stage 4 Pressure Injury Stage 4 Unstageable Pressure Injury Unstageable Pressure Injury Full thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar If slough or eschar is removed, a Stage 3 or Stage 4 pressure injury will be revealed Stable eschar on the heel or ischemic limb should not be softened or removed Unstageable Pressure Injury Unstageable Pressure Injury 9

11 Deep Tissue Pressure Injury Persistent non blanchable deep red, maroon or purple discoloration Pain and temperature change often precede skin color changes Discoloration may appear differently in darkly pigmented skin Deep Tissue Pressure Injury Results from intense and/or prolonged pressure and shear forces at the bone muscle interface It may evolve rapidly to reveal the actual extent of tissue injury, or may resolve without tissue loss Do not use DTPI to describe vascular, traumatic, neuropathic, or dermatologic conditions Deep Tissue Pressure Injury Deep Tissue Pressure Injury Other Definitions Medical Device Related Pressure Injury Result from the use of devices designed and applied for diagnostic or therapeutic purposes The resultant pressure injury generally conforms to the pattern or shape of the device The injury should be staged using the staging system. Other Definitions Mucosal Membrane Pressure Injury Found on mucous membranes with a history of a medical device in use at the location of the injury Due to the anatomy of the tissue these ulcers cannot be staged 10

12 Pressure Injury Treatment Treatments: Wound Debridement if appropriate Appropriate dressing and frequency of change Main Remove pressure Venous Insufficiency Ulcers Result from disorders of the deep venous system 1% of the population 3.5% of persons >65 Recurrence rate 70% Venous ulcers account for 90% of all chronic wounds on the lower leg Venous Insufficiency Ulcers Predisposing factors: Thrombophlebitis Deep Vein Thrombosis (DVT) Prior pregnancy Leg trauma Cardiac disease Poor nutrition Absence of/or poor calf muscle pumps Venous Insufficiency Ulcers Most are located in the medial aspect of leg superior to medial malleolus Granulation tissue usually present Irregular wound margins Exudation varies Degree of pain varies greatly from painless to extremely painful Venous Insufficiency Ulcers Venous Insufficiency Ulcers Assessment Edema Hemosiderin deposits Pulses present Ankle flaring Lipodermatosclerosis subcutaneous tissue fibrosis Dermatitis Scarring from previous ulcer 11

13 Venous Insufficiency Ulcers Treatments: Wound Debridement if appropriate Appropriate dressing and frequency of change depending on exudate Compression Leg elevation Venous Insufficiency Ulcers Treatments: Exercise Weight loss Appropriate nutrition Consider use of adjunctive therapies Lymphedema pump Compression Goal Reduce venous hypertension and improve venous return Necessary for healing ABI must be >0.8 to apply compression Explain to patient that compression therapy is lifelong Consider if patient will be able to apply them Compression Different types Graded elastic compressive stockings Paste gauze boots Layered bandaging Adjustable layered compression garments Garments should be changed every 6 9 months if worn daily Noncompliance is the primary cause of compression therapy failure Compression Contraindications Severe PVD Uncontrolled CHF Cutaneous infection Pulmonary edema Active DVT (OK once anticoagulation initiated) Arterial Insufficiency Ulcers Impairment of arterial blood flow leading to tissue ischemia, necrosis or ulceration Most common disorder associated with compromised wound healing 12

14 Arterial Insufficiency Ulcers Risk Factors: Peripheral Vascular Disease (PVD) Diabetes Mellitus Hypertension Advanced age Smoking Arterial Insufficiency Ulcers Most are located in the distal toes, heel, pretibial area Painful Pale wound bed lacking granulation, may be necrotic Minimal drainage desiccated and dry Appearance punched out Peri wound skin pale Arterial Insufficiency Ulcers Arterial Insufficiency Ulcers Assessment: Weak/absent pulses, Cool feet Pain and Claudication Dependent rubor Elevation pallor Absence of leg hair Skin shiny, dry, pale Thickened nails Arterial Insufficiency Ulcers Treatments: Maximize blood flow and tissue perfusion Surgical revascularization Angioplasty Pharmacotherapy agents Lifestyle changes Judicious debridement Neuropathic Ulcers Annual incidence 1% to 6.84% Lifetime risk 15% to 25% Associated with amputations 14% to 24% Death 5% to 13% of cases After an amputation 50% risk of contralateral amputations within 2 years Boulton AJ, Kirsner, RS, Vileikyte L. N Engl J Med. 2004; 351 (1): Boulton AJ, et al. Lancet. 2005;366(9498): Sanders LF. J Am Podiatric Med Assoc. 1994;84(7):

15 Neuropathic Ulcers Hospital admissions in diabetic patients related to foot ulcers is 6% to 25% Diabetic foot ulcers are a contributing factor in >85% of all diabetes related lower extremity amputations Relative 5 year mortality rates of for patients with neuropathic and ischemic diabetic foot ulcers were 45% and 55% respectively Apelqvist J, Larson J. Diabetes Metab Res Rev. 2000;16:S75 83 Pecoraro RE, Reiber GE, Burgess EM. Diabetes Care. 1990;13(5): Neuropathic Ulcers Predisposing factors: Noncompliance with diabetes management/uncontrolled Peripheral vascular disease Peripheral neuropathy Motor leads to excessive callus build up and Charcot joint Sensory Diminished or absent sensation to pain, temperature and position. Loss of protective sensation Autonomic reduced or absent sweating, dry skin Cuts or trauma can go unnoticed Neuropathic Ulcers Neuropathic Ulcers Systemic factors: Uncontrolled hyperglycemia Duration of diabetes Peripheral vascular disease Visual impairment Older age Local factors: Peripheral neuropathy Structural foot deformity Trauma Improperly fitted shoes History of prior ulcer Pressure Limited joint mobility Painless Even wound margins with propensity to form callous Deep wound bed Granular tissue Neuropathic Ulcers Neuropathic Ulcers Wagner Classification System 0 No open lesions; may have deformity or cellulitis 1 Superficial diabetic ulcer (partial or full thickness) 2 Ulcer extension to ligament, tendon, joint capsule, or deep fascia without abscess or osteomyelitis 3 Deep ulcer with abscess, osteomyelitis, or joint sepsis 4 Gangrene localized to portion of forefoot or heel 5 Extensive gangrenous involvement of the entire foot Adapted from Wagner FW Jr. The Diabetic Foot. Orthopedics 1987;10:

16 Neuropathic Ulcers Assessment: Neuropathy Diminished or no sensation in foot Arterial evaluation Foot deformities Neuropathic Ulcers Treatment Wound Debridement necrotic tissue and hyperkeratotic rim Appropriate dressing and frequency of change Control serum glucose levels Offloading and Orthotics Monitor for infection Take Home Points The basic principles of wound healing apply to almost all types of wounds Accurate assessment of each type of wound is needed Refer to a wound care specialist when the wound is complicated or not healing Thank You! In what phase of wound healing are most chronic wounds likely stalled? 1. Proliferative phase 2. Hemostasis phase 3. Inflammatory phase 4. Remodeling/Maturation phase Which is the most common pressure injury site? 1. Shoulder 2. Heel 3. Elbow 4. Sacrum 15

17 After wound is healed, the skin tensile strength is % of what it was before the injury % % % % Noncompliance is the primary cause of compression therapy failure. 1. True 2. False 16

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