Wound Assessment and Management Slides
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Minnesota HomeCare Association Agenda • Physiology of Wound Healing, Wound Types and Appropriate Dressings • Lower Extremity Wound Assessment and Differentiation: Venous and Arterial Insufficiency Acute vs. Chronic Wounds • Acute wounds occur in a sudden manner (penetrating or blunt trauma; surgery) • Chronic wounds are an acute wound that fails to heal and/or wound that results from some impediment to healing such as: – Not identifying and addressing etiology (pressure, vascularity, neuropathy, etc.) – Poor O2, Edema, Inflammation/Infection – Comorbid conditions, Repeated trauma Acute vs. Chronic Wounds Acute Chronic Acute Traumatic Wounds Chronic, non-healing Wounds Venous Pressure Neuropathic Infection PAD Categories of Wound Closure • Acute Wounds – Primary intention involves closure of a wound within hours of its creation. Wound is cleansed and edges are approximated and closed by way of sutures, staples, wound glue, butterfly, etc. • Chronic Wounds – Secondary intention involves no formal wound closure; the wound follows the three phases of healing. – Tertiary wound closure, also known as delayed primary closure, involves initial debridement of the wound for an extended period and then formal closure with suturing or by another mechanism. Physiology of Wound Healing Regeneration Scar Tissue Formation Tissue Repair by Layers • Epidermis: regenerates (includes epidermal cells that line the hair follicles, sweat glands, and sebaceous glands). • Dermis: most components regenerate. The epidermal appendages located deep in the dermal layer do not regenerate if they are lost. Total dermal loss involving epidermal appendages heals by scar formation. • Subcutaneous tissue: does not regenerate. Heals by scar formation. • Muscle: does not regenerate. Heals by scar formation • Bone: traumatic injuries regenerate. Necrotic processes usually require resection. Wound Tissue Layers Wound Healing : Partial-Thickness WOUNDS Inflammatory (BRIEF) Proliferation of epidermis Reestablishment of the normal skin layers and skin thickness Closure is by REGENERATION OF EPITHELIAL TISSUE Partial-Thickness Wounds • Involve partial skin loss of the epidermis and possibly upper dermis. Partial-thickness wounds appear very shallow/superficial but can be very PAINFUL. • Repair process: Brief inflammatory response, followed by epithelial cell proliferation (reproduction) and migration across the wound surface, which is then followed by reestablishment of the normal skin layers/thickness typically in 2-3 days. Partial Thickness Wound Examples: • Skin tears • Stage 2 Pressure injury • MASD- Moisture Associated Skin Damage • MARSI- Medical Adhesive Related Skin Injury Wound Healing : Full Thickness Wounds Inflammatory ( MAY be extended timeframe) Proliferative Remodeling- scar formation CLOSE BY MEANS OF SCAR TISSUE FORMATION Full Thickness Wounds • Involves full skin loss of the epidermis and extends minimally into the lower dermis. Full- thickness wounds may appear shallow or deep based upon the tissue layers involved and is not necessarily painful. • Repair process: Inflammatory response (may be extended), proliferation and remodeling/scar formation Full Thickness Wounds Examples: • Skin tears • Stage 3 or 4 Pressure Injury • Venous wounds Phases of Wound Healing Hemostasis and Inflammatory (Defensive) Phase • Hemostasis-clotting 1-2 days. • Inflammation- “clean-up” 3rd and 4th day. • Prolongation of the inflammatory phase is associated with increased risk of surgical dehiscence-because prolongation of the inflammatory phase means a delay in the proliferative phase, i.e., granulation tissue formation.* • In addition, prolonged inflammatory phase is also associated with increased risk of hyperproliferative scarring. Proliferation (Rebuilding) Phase • Granulation tissue formation: 5-15 days and complete by 21 days. • Contraction: Involves mobilization of wound edges to reduce the size of the wound. There are conflicting theories regarding the mechanism. • Note: Contraction only occurs in open granulating wounds not primary intention (sutures, butterfly). Remodeling (Maturation) Phase • Lysis of established collagen fibers • Synthesis of new collagen fibers • Normal time frame 1-2 years. • Strength of scar tissue: 20% of normal within 3 weeks and 80% within 3 months. • Note: Scar tissue is NEVER as strong as original tissue. • This is when recurrence occurs! Factors Associated with Chronicity • Failure to bleed- poor or altered tissue integrity • Systemic issues and co-morbidities- unmanaged Diabetes, poor perfusion, poor vascularity, CAD, COPD, etc. • Persistent Injury-continued pressure on a pressure ulcer, continued walking on a neuropathic wound • Prolonged inflammation and occurrence of Infection Chronic, non-healing Wounds Venous Pressure Neuropathic Infection PAD Wet Wounds Wet Wounds • Are inflamed • May be infected • May be associated with edema • May become macerated • May cause hyper- granulation tissue • May have dressing with inadequate absorption Dry Wounds Dry Wounds • Are inflamed • May be infected • May be associated with PAD • May become desiccated • Gauze dressings • May have been “left open to air” Wet & Dry Wound By Wound Type Wet Wound Types Dry Wound Types • Venous insufficiency (CVI) • Arterial Insufficiency • Lymphedema (PAD) • Road Rash-massive skin • Muscle wasting loss • Sub Q loss • Stage 4 Pressure Injury • Traumatic injury- • Blisters bony prominences • Any infected wound • Unstageable Pressure • Can be DFU, skin tear, Injury abscess Dressing Options – Wet Wounds Wet Wounds- Absorbers • Dense foam • Hydrofiber • Calcium alginate • Hydrofiber • Self adaptive dressings • NPWT Dressing Options – Dry Wounds Dry Wounds • Hydrogel • Tube • Sheet • Impregnated gauze • Self-adaptive dressings Wound Etiology • Wound etiology refers to the wound type and can often identify causative factors • Essential to identify at onset of care • Wound etiology drives the plan of care • Represents a variety of skin disruption types Predicting Success of Conventional Wound Management at Week 4 <40% VLU’s Closure reduction unlikely at in wound 24 size weeks¹˴² DFU’s <50% Closure reduction unlikely at in wound 12 weeks³ size 1. GelfanInvest Dematol. 2002;119:1420-1425; 2. Phillips TJ, et al. J Am Acad Dematol. 2000;43:627-630; d JM. J 3. Sheehan P. Diabetes Care. 2003;26:1879-1882. Wound Bed Preparation • The process of identifying common impediments to healing chronic wounds and implementing corrective management strategies to promote closure. • The process is orderly and based upon well demonstrated scientific evidence, using the TIME Model. (Tissue integrity, Inflammation/Infection, Moisture balance, Edge progression) Wound Bed Preparation • T- Tissue Viability: wound bed free of necrotic debris • I- Inflammation/Infection: decrease inflammation, eliminate infection • M- Moisture Balance: not wet, not dry wound tissue • E- Edge progression: skin and wound edge are attached Debridement is an Essential First Step of Wound Bed Preparation • Initial debridement is required to remove the necrotic tissue, excessive bacterial burden, and cellular burden of dead and senescent cells • Early step for venous, pressure,and diabetic neuropathic ulcers • Arterial insufficiency ulcers should only be debrided after arterial inflow has been re- established • Continuous, ongoing debridement is necessary to keep the wound free of ingrowth of nonviable micro-debris between episodic debridement sessions Debridement Methods • Surgical /Sharp Debridement • Mechanical – Wet to Dry Gauze – Monofilament pads – Ultrasonic cavitation – Whirlpool / Pulse Lavage Debridement Methods • Biologic Agents- Blow Fly Larvae • Autolytic Agents- hydrocolloids, films, manuka honey, hydrogels • Enzymatic Debriders- Santyl Collagenase Appropriate Use of Betadine In the presence of PAD in particular: • Eliminate source of pressure • Paint stable, closed eschar (or blister) with betadine and allow to air dry (1-2 times daily) • Refer for Vascular follow up, if consistent with management goals Microbial Continuum Model Contamination (host control) Colonization (established microbial Host Resistance population, host control, microbial balance) Critical Colonization Topical Antiseptic (established microbial population, Agents wound not progressing, microbial imbalance, no signs of infection) Microorganism (load x virulence) Infection Systemic Antibiotics & Topical (microbial control) Antiseptic Agents Colonized vs. Infected • There is no question that clinical infection must be treated • Evidence shows that bacterial burden of 106 organisms or more per gram of tissue seriously impairs healing (Robson 1997) When to Culture • Erythema, warmth at peri- • Delayed healing, wound non-healing • Unusual or foul odor • Poor granulation tissue- friable, dull color • Edema, induration • New breakdown or slough • Drainage – change in color and consistency, increase • Pocketing at base of the wound • Pain and tenderness • Correlate with labs • Wound deterioration Chronic Wounds – often subtle Wound Culture Methods • Wound biopsy: Gold Standard • Swab cultures- correlation with reasonable accuracy to biopsy if done with Levine technique • Wound fluid aspiration What to Culture Obtaining Swap Cultures • Cleanse and flush wound extensively with NS X 3 • Using aseptic technique, firmly place sterile cotton tip applicator over 1cm area of GRANULATION tissue and push to express exudate into cotton swab • Process for lab assessment Levine Technique • Quantitative assessment is optimal Management of Wound Infection