NSG-300 Topic 4 Lecture Video:Skin Integrity and Wound Care: Notes
Foundation: Skin Integrity and Wound Care
Skin is the largest organ; acts as a protective barrier, a sensory organ, and synthesizes vitamin D. Injury poses safety risks; wound healing is a complex cellular/biochemical process influenced by systemic and local factors (underlying disease, wound cause, wound condition).
Clinician reasoning: integrate scientific nursing knowledge with clinical judgment to assess skin integrity, identify at-risk clients, monitor for actual impairment, and plan/implement/evaluate interventions.
Skin structure:
Epidermis (top layer) contains multiple sublayers; the outermost stratum corneum is a thin layer of flattened dead keratinized cells.
Desquamation (shedding) replaces surface cells; stratum corneum protects from dehydration and chemical entry; allows water evaporation and some topical absorption.
Dermis (inner layer) provides tensile strength and protection; mainly connective tissue with fewer skin cells; supports underlying tissues; responds to injury with repair processes.
Normal aging alters skin characteristics, increasing vulnerability to damage.
Key terminology for altered skin integrity:
Pressure injury (current preferred term) = localized damage to skin/underlying soft tissue, usually over a bony prominence or related to a device; may present with intact skin, a blister, or an open ulcer. Caused by intense/prolonged pressure or pressure with shear; influenced by microclimate (temperature, humidity, airflow) and patient factors (nutrition, perfusion, comorbidities).
Pressure injury risk factors include decreased mobility, decreased sensory perception, incontinence (fecal/urinary), poor nutrition, and overall tissue tolerance.
Pressure injury pathophysiology:
Pressure reduces tissue perfusion, causing ischemia and cell death; tissue tolerance is affected by microclimate and local factors.
Two conceptual models of damage:
Top-down: surface damage progressing inward (due to superficial shear/friction).
Bottom-up: deeper tissue damage initiating at muscle/bone interface progressing outward.
Primary causes: prolonged/intense pressure and shear; friction (surface drag) can contribute, especially with moisture.
Role of moisture and microenvironment:
Excess moisture (urine, stool, wound drainage, perspiration) lowers tissue resistance to pressure/friction/shear and promotes skin breakdown.
Nutrition, perfusion, and comorbidities:
Adequate oxygen and nutrient delivery via blood is essential for cellular metabolism and wound healing.
Malnutrition and comorbidities (e.g., diabetes) impair healing and increase risk.
Prevention strategy goals:
Early identification of at-risk individuals and implementation of prevention strategies.
Multidisciplinary planning to maintain skin integrity and promote wound healing.
Anatomy of the Skin and Wound Healing Concepts
Skin layers and function:
Epidermis: barrier function, desquamation, hydration control.
Dermis: structural integrity, support, contains connective tissue and relatively few skin cells.
Wounds: open vs closed
Closed wounds: surface intact; underlying tissues may be damaged (contusions, hematomas, Stage I pressure injuries).
Open wounds: skin disrupted; greater infection risk; classified by depth and tissue loss.
Wound depth classifications:
Partial-thickness wounds: epidermis and possibly superficial dermis; heal by regeneration.
Full-thickness wounds: involve epidermis and dermis and deeper structures; heal by scar formation.
Wound color assessment (color-coded wound bed descriptions):
Red: granulation tissue; viable, moist tissue indicating healing progress.
Yellow: slough; non-viable tissue needing removal.
Black/Brown/Eschar: necrotic tissue; requires debridement to visualize wound bed.
Mixed colors: combination of the above.
Wound healing phases:
Hemostasis (immediate): blood vessel constriction, platelet aggregation, coagulation; forms a fibrin matrix.
Inflammatory phase (days 0–4): histamine release, vasodilation, edema, warmth, and leukocyte infiltration; prepares wound for repair.
Proliferative phase (days 3–14, can extend up to 2 weeks): wound contraction and formation of new tissue; epithelial proliferation and migration; re-epithelialization of the wound bed.
Remodeling/Maturation phase (weeks to months): collagen fiber reorganization, scar strengthening; scar tissue often lighter/pigmented differently than surrounding skin.
Wound healing determinants:
Adequate hemostasis, infection control, and a moist wound healing environment support healing.
Oxygen delivery and nutrient availability are critical for cellular function during healing.
Pressure Injuries: Pathophysiology, Risk, and Prevention
Definitions and concepts:
Pressure injury is localized skin/soft tissue damage over bony prominences or related to medical devices.
Causes: sustained pressure, or pressure combined with shear; tissue tolerance depends on perfusion and microclimate.
Mechanisms of tissue damage:
Prolonged pressure reduces capillary blood flow leading to ischemia and cellular death.
Surface damage can begin at the skin or progress from deeper tissues depending on causation.
Risk factors and populations at risk:
Impaired mobility or sensation; inability to reposition; altered mental status or confusion; incontinence (urinary/fecal); poor nutrition.
Higher risk in elderly and medically complex patients.
Mediating factors:
Microclimate: temperature, humidity, airflow near the skin.
Nutrition and perfusion status; comorbidities such as diabetes or vascular disease.
Injury progression concepts:
Top-down model: superficial damage from shear/friction over time.
Bottom-up model: deeper tissue injury from force at the bone-muscle interface; may progress rapidly once started.
Common sites and device-related risk:
Sacral area, heels, and other bony prominences; medical devices (e.g., ETT ties, masks, nasal cannula) can cause device-related injuries.
Medical adhesive-related skin injury: erythema or other skin changes persisting 30 minutes or more after device removal.
Prevention strategies:
Early risk assessment; use predictive tools like the Braden Scale; tailor prevention to risk level.
Mechanical loading strategies: move/turn patients regularly; use pressure-relieving surfaces (mattress overlays, specialized bed systems, seat cushions).
Microclimate management: keep skin dry; manage moisture from incontinence, wound drainage, sweating.
Nutrition optimization: ensure adequate caloric and protein intake to support tissue repair.
Education of patients and families; involvement in prevention and care.
Braden Scale for risk assessment:
Six subscales: sensory perception, moisture, activity, mobility, nutrition, friction & shear.
Score range: 6 ext{ to } 23; lower scores indicate higher risk.
The Braden score is widely used in hospitals, long-term care, and home care.
Other risk considerations:
Age-related changes, diabetes-related circulatory issues, cognitive or sensory impairments, and the presence of medical devices increase risk.
Prevention and wound-care planning principles:
Skin care and incontinence management; maintaining skin integrity with barrier creams; avoid drying soaps; use non-ionic surfactants.
Repositioning every 1.5–2 hours as a baseline; adjust frequency based on patient needs.
Use of appropriate support surfaces; ensure microclimate control around bony prominences.
Nutrition-focused interventions: adequate calories, protein (protein needs often elevated in wound healing); vitamins A/C; zinc and copper as supportive cofactors.
Calculations and guidance:
Pressure is defined as P = \frac{F}{A}, where P is pressure, F is the applied force, and A is the contact area.
Nutrition/calorie targets: increased protein intake (often up to 1.8\ ext{g/kg/day}) and overall caloric intake to support healing; Joint Commission recommends nutrition assessment within 24 hours of admission.
Wound Assessment and Documentation
Core assessment components for skin wounds:
Wound location, type, and stage of healing (depth, tissue loss).
Wound bed appearance: color (red granulation tissue, yellow slough, black eschar).
Wound size: measured length, width, and depth.
Exudate: amount, color, consistency, odor.
Peri-wound skin: redness, warmth, maceration.
Pain: location, intensity, quality, aggravating/relieving factors.
Surrounding skin integrity and signs of infection.
Staging and depth considerations:
Stage 1: non-blanchable erythema of intact skin; changes in sensation, temperature, or firmness may precede color changes; do not include purple or maroon discoloration.
Stage 2: partial-thickness skin loss with exposed dermis; wound bed is viable pink/red, moist; may present as intact or ruptured serum-filled blister.
Stage 3: full-thickness skin loss with adipose tissue visible; granulation tissue and epibole (rolled edges) may be present; undermining or tunneling may occur; slough/eschar may obscure depth.
Stage 4: full-thickness skin and tissue loss with exposed fascia, muscle, tendon, ligament, cartilage, or bone; undermining/tunneling common.
Deep tissue injury: intact or non-intact skin with localized area of non-blanchable deep red/maroon/purple discoloration or epidermal separation revealing a dark wound bed; may evolve rapidly.
Unstageable: full-thickness tissue loss where depth cannot be assessed due to slough/eschar obscuring the wound bed.
Wound infection signs:
Erythema, increased drainage, change in drainage color/odor, peri-wound warmth, pain, edema, fever, leukocytosis.
Wound cultures or tissue biopsy may be used to determine causative organisms.
Wound healing mechanisms and classification:
Partial-thickness wounds heal by regeneration of epidermis and possible dermal layers.
Full-thickness wounds heal by scar formation; deeper structures do not regenerate.
Wound color assessment aids determination of need for debridement and healing trajectory.
Wound Healing Process: Phases and Clinical Implications
Hemostasis:
Vascular constriction; platelets aggregate; fibrin clot forms a matrix for repair.
Hemostasis may be impaired by anticoagulants or clotting disorders.
Inflammatory phase:
Histamine release causes vasodilation; white blood cells migrate to the wound site; redness, warmth, edema occur.
Proliferative phase:
Begins around day 3–4 and can last up to 2 weeks; wound contraction and formation of granulation tissue; epithelial proliferation/migration.
Remodeling/Maturation phase:
Begins weeks after injury and can continue >1 year depending on wound depth; collagen reorganizes; scar tissue gains strength but remains less elastic than original tissue.
Complications to monitor:
Hemorrhage: early post-trauma bleeding; post-healing hemorrhage may indicate suture disruption, infection, or erosion by devices.
Infection: signs include erythema, warmth, edema, purulent drainage, fever, elevated WBC.
Dehiscence: partial or total separation of wound layers; risk is higher with poor nutrition, infection, or comorbidities.
Evisceration: protrusion of visceral organs through a wound opening; emergency; manage with sterile saline-covered dressings and immediate surgical consult; NPO status advised.
Surgical and Traumatic Wounds: Practical Aspects
Wound types by causation and healing approach:
Clean surgical incisions heal by primary intention when edges are well-approximated; risk of infection is low; rapid healing.
Wounds with tissue loss (burns, Stage II pressure injuries, severe lacerations) heal by secondary intention; longer healing, higher infection risk, potential for more scarring.
Wounds can heal by tertiary intention when left open for observation before closure due to contamination risk.
Wound cleansing and debridement:
Use non-cytotoxic cleaners (e.g., normal saline) to avoid harming healthy tissue.
Debridement removes non-viable tissue to reduce infection risk and reveal the wound bed.
Maintain a moist wound environment to facilitate epithelial migration and healing.
Assessing wound drainage and infection:
Drainage types and amounts are documented; purulent drainage is a sign of infection.
Closed surgical wounds: minimal drainage early post-op; any change in drainage amount/color may indicate complications.
Wound care plan elements:
Establish nursing diagnoses (e.g., impaired skin integrity related to pressure/infection).
Define SMART outcomes (specific, measurable, achievable, relevant, time-bound).
Plan interventions with consideration of comorbidities, nutrition, infection risk, and mobility.
Prevention and Management: Practical Interventions
Core prevention principles for pressure injuries:
Prevention is prioritized for all patients with mobility limitations or at risk for skin breakdown.
Skin care routines: avoid harsh soaps; use non-drying cleansers; dry thoroughly; apply moisturizers appropriately.
Incontinence management: gentle cleansing and application of moisture barriers to protect skin.
Repositioning: standard interval 1.5–2 hours; adjust based on patient needs and risk; use assistive devices to minimize shear.
Mechanical loading and support devices: therapeutic mattresses, overlays, cushions to distribute pressure and manage shear.
Nutrition and hydration:
Adequate protein and calories are essential; protein needs may rise to support tissue repair (commonly up to 1.8\ ext{g/kg/day}); ensure sufficient calories and micronutrients (vitamins A & C, zinc, copper).
Nutritional assessment recommended within 24 hours of admission; reassess as status changes.
Education and caregiver involvement:
Teaching patients and families about wound prevention, dressing changes, and signs of deterioration.
Plan for home care with a skin/wound care team when appropriate; ensure caregiver competency with return demonstrations.
Dressings and topical care:
Dressings should maintain a moist environment, control exudate, and protect surrounding skin.
Dressings are selected based on wound stage, exudate level, and presence of necrotic tissue.
When a wound is healing by secondary intention, dressings help maintain moisture and assist in debridement as needed.
Advanced therapies:
Negative pressure wound therapy (vacuum-assisted therapy) helps draw wound edges together and remove exudate; used for acute and chronic wounds.
Dressings and wound containment:
Anchoring dressings with tape or other securement methods requires careful attention to skin sensitivity; non-allergenic options reduce irritation.
Drains and drains care:
Drains remove accumulated wound fluid; assess drain type, placement, and drainage characteristics; monitor for infection or obstruction.
Skin barriers may be used around drain sites to protect surrounding skin.
External supports and movement:
Binders and bandages for immobilization or support; select material considering patient comfort and skin condition.
Pain management during wound care:
Use techniques to minimize discomfort during dressing changes (gentle tape removal, careful cleaning, minimizing movement of the wound area).
Wound assessment and documentation:
Regular wound measurement and documentation on progression or regression;
Note location, stage, size (length × width × depth), tissue type, exudate, color, odor, and peri-wound conditions.
Case Study: Mr. Omar Ahmed
Patient profile:
76-year-old with recent pneumonia; prior coronary artery bypass (3 years ago) as a precaution; hypertension; type 2 diabetes mellitus; limited mobility; malnourished with >20 lb weight loss over 2 months.
In the hospital, he reports bottom painful from lying in bed; he is on telemetry.
Risk factors for pressure injury identified:
Advanced age, limited mobility, possibly reduced sensation, nutritional deficit, diabetes, comorbidities.
Risk increases with incontinence and moisture exposure; he is described as lying in bed for prolonged periods.
Assessment findings (case-specific):
Pressure injury over the sacral area described as Stage 2, 1 in × 2 in in size, depth 1/8 in, with red/moist wound bed and no necrotic tissue.
Wound is a partial thickness wound with granulation tissue indicating healing potential.
Interventions in the case:
Assess the risk factors and determine an appropriate support surface/compression-relief device to reduce sacral pressure.
Evaluate and address caloric intake and nutrition; consider a calorie count; Mr. Ahmed has been consuming fewer calories, with a plan to increase intake.
Use of a pressure-relieving strategy (turning schedule, skin care, barrier creams as needed).
Wound care: gentle cleansing with non-cytotoxic solutions (e.g., normal saline); maintain a moist wound environment; avoid overpacking if used for a packing dressing; debridement only if non-viable tissue is present.
Wound measurement and monitoring: track size change (e.g., 1 in × 2 in area and depth changes over time); document tissue type (red moist tissue) and absence of necrotic tissue.
Outcomes and follow-up:
After care, wound size and tissue appearance improved; no new areas of non-blanchable erythema noted; patient reported no new pain indicating no progression of tissue damage.
Nutrition improved with increased caloric intake.
Family teaching involved Mrs. Ahmed (wife) in wound care at home; a plan for home care, education, and follow-up with home health services was developed.
Teaching and home care planning:
Teach the family member to perform dressing changes, with a goal of return demonstration.
Use visual aids (pictorial guides) and demonstrations; include patient and spouse in teaching sessions; plan two sessions: observation/demonstration and return demonstration.
Assess patient and family satisfaction, comfort, and confidence during wound care.
Broader implications from the case:
Emphasizes home care planning, caregiver education, nutrition optimization, and ongoing wound assessment as critical components of wound healing and prevention of recurrence.
Practical Nursing Skills: Dressing Changes, Cleaning, and Devices
Cleaning and dressing basics:
Clean wounds with normal saline or other non-cytotoxic cleansers; avoid harsh soaps; ensure skin around wound is dry before applying dressings.
Dressings: select based on wound stage, exudate level, and need to maintain moisture; remove dressings when drainage stops for primary healing wounds, or maintain moisture for wounds healing by secondary intention.
Debridement may be required for necrotic tissue to allow wound bed exposure for assessment.
Negative pressure therapy: indication and use
Vacuum-assisted closure (VAC) therapy can accelerate wound closure by applying localized negative pressure, drawing edges together, and removing exudate.
Drains and drain care:
Drains help remove wound exudate/blood; secure drains and monitor drainage volume/color.
Use skin barriers around drain sites to prevent skin maceration and protect surrounding tissue.
Immobilization and supports:
Bandages, binders, and slings provide additional protection, reduce edema, and secure dressings.
Heat and cold therapy:
Consider heat/cold for inflammation or pain management; assess contraindications (e.g., active bleeding, impaired circulation, neuropathy).
Warm applications improve circulation and tissue relaxation; cold reduces edema and pain; avoid applying heat/cold to an area with open wounds or compromised sensation.
Important Formulas and Numerical References
Pressure injury risk and mechanics:
Pressure on tissue: P = \dfrac{F}{A} where P is pressure, F is the force (e.g., body weight), and A is surface area.
Braden Scale:
Score range: 6 \leq \text{Braden score} \leq 23; lower scores indicate higher risk for pressure injuries.
Nutrition and healing considerations:
Protein needs for wound healing are increased; general targets range up to 1.8\ \text{g/kg/day} depending on clinical status.
Caloric requirements should support healing; micronutrients (e.g., vitamins A, C, zinc, copper) support collagen synthesis, immune function, and wound repair.
Key Takeaways for Exam Preparation
Know the differences between epidermal and dermal injuries, and between partial-thickness vs full-thickness wounds.
Be able to describe all stages of pressure injuries, including what differentiates Stage 1 from Deep Tissue Injury and Unstageable injuries, and why necrotic tissue complicates staging.
Understand the pathophysiology of pressure injuries, including how shear, friction, moisture, nutrition, perfusion, and age contribute to risk.
Recognize clinical signs of infection, dehiscence, and evisceration, and the appropriate immediate responses.
Be familiar with prevention strategies: assessment tools (especially the Braden Scale), repositioning schedules, use of pressure-relieving surfaces, moisture management, and nutritional optimization.
Master wound assessment components: location, stage, size, tissue type, exudate, peri-wound skin, pain, and presence of drains.
Understand general wound care principles: cleansing with non-cytotoxic solutions, debridement when indicated, moist wound environment, and appropriate dressing selection.
Know nursing roles in patient and family education, home care planning, and interdisciplinary collaboration for wound care.
Review Mr. Ahmed’s case as a practical example of risk identification, wound assessment, intervention planning, and caregiver education.
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