Skin Anatomy and Assessment PDF

Skin Facts Largest external organ Skin covers >20 ft2, weighs 6-8 lbs Skin thickness: 0.5-6 mm Skin receives ⅓ of the body’s circulating blood volume Normal pH: 4 to 6.5 (acid mantle-protective barrier against bacterial and fungal infections Skin Functions Protection From:...

Skin Facts Largest external organ Skin covers >20 ft2, weighs 6-8 lbs Skin thickness: 0.5-6 mm Skin receives ⅓ of the body’s circulating blood volume Normal pH: 4 to 6.5 (acid mantle-protective barrier against bacterial and fungal infections Skin Functions Protection From: Provide: Fluid and electrolyte loss thermoregulation Mechanical injury Excretion of sweat UV injury sensation Pathogens Vitamin D synthesis Epidermis Description Function Outermost avascular layer Protection (sun, H2O loss) Regenerates ~28 days Vitamin D synthesis 0.06-1.5mm thickness Division & mobilization Plantar surface of foot & palms thickest Maintains contact w/ dermis 5 layers pigmentation Made up of primarily keratinocyte cells Allergen recognition 5 Layers Epidermis Stratum Corneum-dead keratinocyte cells, flakes and sheds Stratum Lucidum-found on palms and soles of feet Stratum granulosum Stratum spinosum Stratum basale-attached to the dermis by the thin basement membrane & responsible for the mitotic activity of keratinocyte cells Basement Membrane Zone B/w epidermis and dermis Rete ridges that interlock so stays in place Aging-flattening of rete ridges=>tears in older adults Dermis Description Function Thickest Layer of skin Supports epidermis (matrix) Major proteins-collagen and elastin Mechanical strength Contains nerve endings, blood vessels, Supplies nutrition lymphatics, capillaries, sweat and sebaceous glands, hair follicles 2 Layers: Resists shearing forces -Papillary: unique pattern allows fingerprint Moisture retention identification, capillaries and pain/touch receptors -Reticular: dense collagen for shape and Lubricates skin (sebaceous glands) firmness-anchors skin to subcutaneous tissue; contains sweat glands, hair follicles, nerve and blood vessels Inflammatory response Hypodermis: Subcutaneous Tissue Description Function Primarily composed of adipose and Attaches dermis to underlying structure connective tissue Promotes an ongoing blood supply to the Largest layer dermis for regeneration Contains major blood vessels,nerves, and Thermal insulation lymphatic vessels Storage of calories (energy) Controls body shape Mechanical “shock absorber”-cushion b/w skin layers, muscles, and bones Promotes skin mobility  Hypodermis Effects of Aging 20% loss of dermal thickness (paper thin appearance) Proportional reduction in collagen fibers, blood vessels, nerve endings (altered sensation, thermoregulation, moisture retention, sagging skin) 5 Elements of a Basic Skin Assessment Temperature Normally warm; perform bilaterally using back of hand -warmer: r/o inflammation or infection -cooler: r/o poor vascularization Color Intensity/Normal color tones=>Fitzpatrick Skin Type Moisture Dry (xerosis) or moisture associated skin damage (MASD) (incontinence,perspiration, periwound maceration) or edema (moisture beneath surface) Turgor Normally returns to original state quickly=>slow return-aging or dehydration Integrity No open areas Color Meaning Paleness r/o poor circulation Erythema varies w/ natural skin color Hyper- or Hypo- pigmentation may reflect variations in melanin deposits or blood flow Blue/Gray cyanosis=>low oxygen saturation Pallor Anemia, arterial insufficiency Yellow Jaundice (biliary tract disease or liver problems) Liver Spots Aging; exposure to UV radiation FitzPatrick Skin Type Skin Type Typical Features Tanning Ability I Pale white skin, blue/green eyes, blonde hair Always burns, does not tan II Fair skin, blue eyes Burns easily, tans poorly III Darker white skin Tans after initial burn IV Light brown skin Burns minimally, tans easily V Brown skin Rarely burns, tans darkly easily VI Dark brown or black skin Never burns, always tans darkly  Comprehensive Skin Assessment Inspection Normally smooth, slightly moist and same general tone throughout -pigmentation, pallor, cyanosis (nail beds), jaundice, hyperpigmentation, hypopigmentation, scars and bruises (location, color, length, and width) Palpation Moisture, edema, tenderness, elasticity, texture Olfaction smell Observation of hair and nail beds Clubbing, texture,color, shape Skin alterations Previous scars, graft sites, healed ulcer sites Dermatitis Inflammatory skin response to an agent Red, scaly, and itchy; may blister, ooze, develop a crust or flake off Ex) atopic dermatitis (eczema), dandruff, rash caused by contact w/ poison ivy or certain metals Vasculitis Inflammation and necrosis of the blood vessels Associated w/ many conditions (malignancies, connective tissue and inflammatory diseases, medications, chemicals, infections) Usually bilateral and below knees Variable-erythema to widespread purpura, necrosis and ulceration Tx: elevation, compression, antihistamines, NSAIDs, steroids Basal Cell Carcinoma Most common form of skin cancer Limited capacity to metastasize Arise in the basal cells of the epidermis Appearance: open sore, red patch, pink growth, shiny bump Cause: UV exposure Squamous Cell Carcinoma Second most common skin malignancy Uncontrolled growth of abnormal cells arising in the squamous cells of epidermis Scaly red patches or open sores, elevated growths w/ a central depression Can metastasize; mostly on areas exposed to sun Major cause: UV exposure Malignant Melanoma: begins in melanocytes Types of Infections Viral Herpes 1&2, Herpes Zoster (shingles) and warts Fungal Ringworm, athletes foot, yeast infection Bacterial Abscess, cellulitis, impetigo Immune Disorders Lupus, psoriasis, scleroderma Cellulitis Bacterial skin infection Swollen, red, hot and tender, fever Lower legs most commonly affected May affect skin surface or underlying tissues and can spread to lymph nodes and bloodstream Can lead to antibiotic resistant infection such as MRSA (life-threatening) Management: antibiotics, elevation, cooling Differential diagnosis from DVT  Scleroderma Chronic connective tissue disease classified as an autoimmune rheumatic disease; excessive collagen production Skin appears hard, shiny w/ loss of mobility, usually hx of raynaud’s Sx: mild to life threatening -localized: more common in children; waxy patches on skin and skin under patches may thicken and affect joint motion -systemic: more common in adults; may affect connective tissue (becomes hard and fibrous) in the skin, esophagus, GI tract, lungs, kidneys, heart, blood vessels, muscles, and joints Female: male=>4:1; most common onset 25-55 y/o No cure, tx sx Shingles/Herpes Zoster Viral disease caused by reactivation of the varicella virus responsible for chickenpox -contagious of not had chicken pox Affects the cutaneous nerves usually in a single dermatome Pain, itching and burning precede lesions 3-5 days Pain may be severe Tx with antiviral agents Ocular complications may occur Candidiasis/Yeast Infection Fungal overgrowth cause by candida-albicans or other candida species=>typically affecting skin, genitals, throat, mouth or blood Presents as red pinpoint papules frequently w/ satellite lesions Overgrowth of normally present flora due to: -antibiotics -diabetes -topical steroids -skin maceration -immune deficiencies 4 Phases of Wound Healing Hemostasis Inflammatory Phase Proliferation (Regeneration or Remodeling Phase Granulation) Phase (Maturation) 0-24 hrs 1-10 days 3 days-21 days 7 days-2 years -lasts up to 1 yr for normal health adults and 2 yrs for children, elderly, or immunocompromised pts  Phase 1: Hemostasis What happens? Epinephrine is released in an attempt to minimize bleeding into the soft tissue What cells are involved ? Platelet cells are responsible for clot formation and releasing cytokines Process Tissue injury causes hemorrhage into the wound⇒platelets aggravates eventually resulting in fibrin clot formation and hemostasis⇒fibrinolysis to break down fibrin clot Phase 2: Inflammatory Infiltration of Mount an acute inflammatory response neutrophils and -Neutrophils: clear invading microbes (bacteria) and cellular debris in the wound area macrophages by phagocytosis -Macrophages: like neutrophils, but also rich source of biological regulators (cytokines, growth factors, bioactive lipid products, proteolytic enzymes) Clinical Observations -erythema -warmth -edema -pain Goals -Contain exudate (in wound) -Reduce edema (in tissues) -Remove necrotic tissues -Promote granulation -Prevent maceration (periwound) Phase 3: Proliferation Granulation, Migration over the matrix within the wound contraction, & -In the dermis, fibroblasts and endothelial cells support capillary growth (angiogenesis), epithelialization collagen formation, and the formation of granulation tissue at the site of injury -Within the wound bed, fibroblasts produce collagen, glycosaminoglycans and proteoglycans (major components of the extracellular matrix) Clinical Observations Beefy red granulation, epithelialization Goals -Stimulate angiogenesis -Promote epithelialization -Prevent epiboly -Protect wound -Prevent maceration -Maintain moist wound environment Epithelialization Epithelial cells migrate in a single layer across a granulated wound surface towards the middle and proliferate Contact inhibition-occurs when new epithelial cells cover the wound -Rolled or curled edges (epiboly) frequently occur in wounds that have no granular tissue to cross A wound is closed when epithelial integrity is restored however it is not healed  Phase 4: Remodeling/Maturation Wound is now closed. This phase can last for years! Regression of newly formed capillaries High fibroblast activity with extracellular matrix remodeling Shrinking, thinning, paling of scars -Scar tissue is only 80% as strong as original tissue Goals: -Educate pt in pressure relief, skin inspection -Mobilize soft tissue -Gradual/incremental stress of tissue How wounds heal In order of increasing complexity Superficial Wound Healing (often included under primary intention) Primary Intention Secondary Intention Tertiary Intention Skin Graft Local Flap/Free Flap Primary Intention Closed by approximation of wound margins-immediately closed Best choice for recent, clean wounds, well-vascularized areas, minimal tissue loss (surgical incision, laceration, puncture, superficial and partial-thickness wounds Typically have minimal scarring and heal quickly Specific Techniques: sutures, staples, adhesives Dehiscence: Surgical complication in which the wound ruptures along the suture line Risk Factors: age, diabetes, obesity, poor knotting or grabbing of stitches, increased abdominal pressure (lifting)  Secondary Intention Wound closes on own w/o superficial closure Wounds-significant tissue loss or necrosis, irregular or non viable wound margins that cannot be re-approximated, infection or debris contamination (ex. Venous ulcer or pressure injury) Granulation tissue gradually fills the wound bed to the levels of surrounding skin w/ closure occurring by wound contraction and scar formation Typically, larger scars Tertiary Intention/Delayed Primary Intention Wound left open, then sutured closed 4-7 days after signs of infection diminished -usually, traumatic wounds Occurs when a wound -Heavily contaminated -High risk for infection Skin Graft Type of medical grafting involving transplantation of skin Used to treat; -Extensive wounds -Burns Chronic Wounds Chronic wound fail to progress in a timely manner through the normal phases of healing Time frame of >30 days duration for complete healing Wound gets stuck in inflammatory phase Presence of infection and biofilm are common -Biofilm: complex microbial community embedded in an extracellular polymeric substance; the EPS attaches the biofilm to a living surface and prevents the immune system from recognizing the microorganism Failure to respond to interventions Risk Factors: -comorbid conditions=>diabetes, poor circulation, nutritional deficiencies, adverse pressure, advanced age  Causes of Delayed Healing Local Factors (Wound) Systemic Factors (Individual) -Oxygenation -Age -Infection -Stress -Foreign Body -Comorbidities -Desiccation (extremely dry) -Obesity -Maceration (wet) -Smoking -Mechanical stresses -Medications -Nutrition Oxygenation The early wound is typically hypoxic due to vascular disruption and high oxygen consumption by metabolically active cells. Hypoxia initially stimulates wound healing such as the release of growth factors and angiogenesis Oxygen is then needed to sustain the healing process Age Associated w/ decreased: Associated w/ increased: -dermal thickness, causing thinning of the skin -Time for epidermal regeneration -amount and flexibility of collagen and elastin causing skin wrinkling (leading to slower healing) -size of rete ridges, thus increasing the risk of skin tears -Damage to skin from sun -sensation and metabolism -sweating due to atrophy of the sweat glands=>leading to dry skin -subcutaneous tissue leading to less padding over bony prominences Obesity Local wound conditions Wound complications -decreased vascularity in adipose tissue -infections -skin folds harbor microorganisms -dehiscence -friction from skin-on-skin contact -hematoma and seroma formation -increased wound tension -pressure and venous ulcers -increased tissue pressure -venous hypertension -decreased ability to reposition self Smoking Post-operatively, pts who smoke show delayed wound healing and an increase in infections, wound rupture, wound and flap necrosis, and a decrease in the tensile strength of the wound  Nutrition Malnutrition or specific nutrient deficiencies impact wound healing Patients w/ chronic or non-healing wounds and nutrition deficiency often require nutritional supplementation Carbohydrate, protein, fat, vitamin and mineral metabolism affect the healing process -carbohydrates: primary source of energy in the wound-healing process -fatty acids: used as nutritional support for surgical or critically ill patients to help meet energy demands and provide essential building blocks for wound healing and tissue repair Medications Commonly used medications that have a significant impact on healing -Glucocorticoid steroids: anti-inflammatory agents -Non-steroidal Anti-inflammatory drugs (NSAIDs): long term use -Chemotherapeutic Drugs Verified Burn Care Centers Requirements Comprehensive care within 24 hrs of admission At least one full-time equivalent burn PT and one OT, more depending on center volume (1 FTE/6pts), w/ qualified therapists available 7 days/week Inpatients should receive a minimum of daily therapy services Competency-based burn therapy orientation program for all therapists assigned to the burn center -Recert a minimum of once every two years Hospitalization for Burns Full thickness burns or partial Circumferential burns suspected/confirmed inhalation thickness >10% total body surface injury area Children ( necrotic stringy Black-eschar=> necrotic, dry, hard,thick,leathery adherent or nonadherent Color Chart Color Description Goal Red -Beefy red is healthy granulating base -Protect from harsh environment -Light pink=>poor circulation -Maintains moist wound environment -Dusky red=>impending necrosis Black -necrotic tissue -Remove dead tissue -eschar is dead tissue covering wound like a lid Yellow -fibrin=>hardened sheet -Remove dead tissue -slough=>necrotic inside wound (not always yellow)  Assessment: Epithelialization Growth of the epithelium over the wound bed Will look white or silvery along the edges (do not rub off) Watch for hypergranulation which will prevent epithelialization Assessment: Odor Assess after dressing removed and wound debrided and rinsed Odor being present does not guarantee infection -If necrotic tissue, usually has a mild odor -Odor is present when automatically debriding Examples: -Pseudomonas: smells strongly sweet, fruity -Malignancy: wet cardboard Assessment: Wound Drainage Type (Color and Consistency) Amount (subjective-correlated to #s of dressing changes) -Serous (clear) -None, minimal (normal), moderate -Sanguinous (bloody) -Desiscation=>drying out of a wound -Serosanguinous (clear and bloody) -Purulent (green/yellow/brown) Assessment: Undermining, tunneling/sinus tract Undermining -area “under” wound edge that erodes (wound looks smaller than it is from the outside) -use clock terms to describe location Sinus Tract or Tunnel -channel that extends from wound -Potential for abscess formation Assessment: Pitting Edema Palpate at ankle and medial aspect of tibia -1+ indentation barely detectable -2+ slight indentation, 15 seconds to rebound -3+ deeper indentation, 30 seconds to rebound -4+ indentation lasts >30 seconds  Assessment: Edema Circumferential measurements noting landmarks are most commonly done but volumetric measurement is the most accurate Cellulitis: swelling localized to affected area, erythema, fever, diffuse tenderness Congestive Heart Failure: bilateral lower extremity pitting edema Lymphedema: spongy consistency, thickened skin, mild relief w/ elevation Venous Insufficiency: edema, pigmentation, relief w/ elevation Ankle Brachial Index Vascular test for arterial involvement using Doppler stethoscope Use cuff to find brachial and ankle systolic Divide ankle/brachial 0.9-1.3=>blood pressure at ankle is > pressure at arm; indicating no significant narrowing or blockage of blood flow 0.75-0.9=>moderate peripheral arterial disease 0.5-0.75=>severe disease rest pain or gangrene Assessment: Circulation and Sensation Pulses (peripheral) Capillary Refill Time Light Touch Sensation -0=>no pulse felt -Apply pressure until -Gold Standard: -1+=>barely felt blanches Semmes-Weinstein -2+=>diminished -Normal=> ~normal pulse -Arterial compromise -5.07 protective sensation -4+=>bounding indicated if >4.5 sec if elderly -4.17 normal senation Assessment: Pain Intensity-use pain scale Characteristics Location When does the pain occur -time of day, position of extremity -location  Pressure Sore Risk Assessment Tool Braden Norton -Six subscales, scored 1-4 greatest to least -Five categories scored 1-4 worse to better impaired -Physical condition,mental condition, activity, -Sensory perception, moisture, activity, mobility, incontinence mobility, nutrition, friction/shear -relieved w/ legs in dependent position -intermittent claudication -minimal exudate -pallor w/ elevation -periwound tissue shiny and tight -usually, dorsum of foot or toes -gangrene -irregular shape -dry necrotic eschar -temperature decreased in extremities -absence of palpable pulses -atrophy below level of occlusion Test and Pulses exam Measures -dorsalis pedis and posterior tibial -present vs. absent Capillary Refill -apply pressure until blanches; normal refill is revascularization -NO COMPRESSION!! -Don’t debride nonviable in the presence of ischemia -Ulcers w/o adequate arterial inflow must be kept dry and protected (moisture will increase bacterial growth)=>ulcers w/ adequate blood supply and expected to heal-use moist wound healing principles Goals -Improve and/or restore arterial flow to the lower extremity -Prevent and treat infection -Prevent osteomyelitis and moist gangrene -If no surgery, prevent deterioration and infection -Pt education is key=>proper foot care, decreased friction, no compression, behavior modification, signs and symptoms of infection and gangrene Rubor of Dependency Evaluates presence of LE ischemia Supine, examine the sole of the foot for color Elevate one leg about 45-60°x1 minute, examine color -normal=>little or no color change on elevation -pale,chalky white or painful=>arterial insufficiency Lower to dependent position, note time for color to return -normal=>pink within >20-30 sec + dark red (rubor)=arterial compromise  Venous Filling Time Another way to assess arterial flow Supine: elevate one leg for 60 seconds -Instead of sole of foot you examine dorsal veins of foot (superficial dorsal veins will collapse) Lower legs to dependent position Time the filling of the dorsal vein -venous reflux, incompetent valves - ~15 sec=>normal - >15 sec=arterial compromise Pressure Injury Staging Stage 1 Non-blanchable -Intact skin w/ a localized area of non-blanchable erythema, which may erythema of intact skin appear differently in darkly pigmented 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; these may indicate deep tissue pressure injury Stage 2 Partial-thickness skin -the wound bed is viable, pink or red, moist and may also present as an loss w/ exposed intact or ruptured serum-filled blister dermis -adipose is not visible and deeper tissues are not visible; granulation tissue, slough and eschar are not present -these injuries commonly result from adverse microclimate and shear in the skin over the pelvis and shear in the heel Stage 3 Full-thickness skin loss -adipose is visible in the ulcer and granulation tissue and epibole are often present -slough and/or eschar may be visible -the 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 ar not exposed Stage 4 Full-thickness and -exposed or directly palpable fascia, muscle tendon, ligament, cartilage, tissue loss or bone in the ulcer -slough and/or eschar may be visible -epibole, undermining and/or tunneling often occur; depth varies by anatomical location Unstageable Obscured full -extent of tissue damage within the ulcer cannot be confirmed b/c it is thickness and tissue obscured by slough or eschar loss -if slough or eschar is removed, a stage 3 or 4 pressure injury will be revealed -stable eschar (dry, adherent, intact w/o erythema or fluctuance) on the heel or ischemic limb should not be softened or removed Deep Tissue Persistent -Intact or non-intact w/ localized area of persistent non-blanchable deep Pressure Non-blanchable deep red, maroon, purple discoloration or epidermal separation revealing a Injury red, maroon or purple dark wound bed or blood-filled blister discoloration -Pain and temperature change often precede skin color changes -this injury results from intense and/or prolonged pressure and shear forces at the bone-muscle interface; the wound may evolve rapidly to reveal the actual extent of tissue injury or may resolve w/o tissue loss Pressure Injury Etiology Treatment -Debride necrotic tissue -clean, moist wound environment -prevention of infection -positioning -pt education -use draw sheet for repositioning -assess need for supportive device Positioning in Supine -Turn ~ every 2 hours/individualized per patient -HOB 2 hrs) Treatment Compression -long term therapy -compression stockings, multilayer compression wraps Elevation above level of heart exercise to improve muscular pump=>ankle pumps Goals -decrease venous hypertension=>address LE edema -remove necrotic debris -control exudate -stimulate fibrinolysis and angiogenesis -educate in prevention and using compression for the remainder of life Ceap Classification System Class 0 No sign of venous disease Class 1 Telangiectasias “spider veins” or reticular veins (blue lines, smaller than varicose veins) Class 2 Varicose veins=>distention veins Class 3 edema Class 4a Pigmentation and eczema Class 4b Lipodermatosclerosis and atrophie blanche (white, patchy scarring at site of prior ulcer) Class 5 Healed venous ulcer Class 6 Active venous ulcer Neuropathic Ulcers Risk Factors Previous Peripheral neuropathy Peripheral vascular Diabetic Cigarette amputation disease nephropathy smoking** Past foot ulcer Foot deformity Visual impairment Poor glycemic history control** Neuropathic Ulcer Mechanics Internal Stressors External Stressors -High pressures -tissue breakdown -high pressures -tissue breakdown -foot deformities -charcot foot -shoes -gait speed/step length -intrinsic and extrinsic muscle weakness -Environment -walking barefoot -open toe shoes/sandals  Neuropathies Sensory Loss of protective sensation=>decrease in awareness of trauma Delay in intervention and increased risk of infection Autonomic Decreased perspiration and sebaceous secretions so prone to dryness, crack, and calluses Motor Weakness in intrinsic muscles w/ resultant muscle imbalances and foot deformities -microfractures and ligamentous laxity (spring) -charcot foot=>rocker bottom Impairments in ROM at foot and ankle Diabetes Foot Screen Section 1 12 Y/N questions Section 2 Drawings and Sensory Exam Section 3 Placement into a risk category and management category Foot Evaluation As needed Risk Classification/Referral/Follow-Up 0 Diabetes, but no loss of protective sensation in feet 1 Diabetes, loss of protective sensation in feet 2 Diabetes, loss of protective sensation in feet with high pressure (callous/deformity) or poor circulation 3 Diabetes, history of plantar ulceration or neuropathic fracture Risk Stratification 0 Very low No LOPS and no signs of PAD Once a year 1 Low LOPS or PAD Once every 6-12 months 2 Moderate LOPS + PAD OR LOPS+foot deformity OR Once every 3-6 months PAD + foot deformity 3 Hgh LOPS or PAD & one or more of the following: Once every 1-3 months -hx of a foot ulcer -lower extremity amputation (minor or major) -end-stage renal disease Examination-Neurological 10g-Semmes Weinstein monofilaments Apply to hands or forehead first Test 3 sites on feet Pt cannot watch testing Perpendicular to skin until buckles 2 seconds for approach, contact and removal Do they feel pressure and where? Alternate w/ mock applications Protective sensation=> correct ⅔ at each site 128-Hz tuning forks: test of vibration sensation; test over distal phalanx of great toe bilaterally -abnormal response: pt loses vibration sensation but examiner still perceives it ⅔ attempts Pinprick sensation: proximal to toenail on both hallux; need to perceive pinprick Ankle reflexes: stretch achilles tendon to neutral; strike w/ hammer; absence of ankle reflex at rest or when hooking fingers together and pulling is abnormal Deformity Hammertoe Extension of the MP joint and flexion of the PIP joint caused by muscle imbalance, poor fitting shoes-usually only 1 toe Clawtoe Extension of the MP joint/flexion of IP joints caused by insufficiency of intrinsics Neuropathic insidious, chronic destruction of bones and joint (osteolysis) (Charcot) result in pathologic fractures, discocations, subluxation, and/or Arthropathy instabilities Neurotraumatic Theory Conditions Peripheral neuropathy with LOPS and proprioception An unrecognized injury (Ex. fall, MVA, bumped foot into table leg or overuse or minor repetitive trauma) Continued repetitive after the unrecognized initial injury Adequate blood supply; continued trauma in setting of peripheral neuropathy can lead to abnormal regulation of blood flow with a significant increase in blood flow to the foot  Eichenholz Stage 1st Dissolution=>fragmentation of bone, dislocation of joints, and loss of bone mass due to increased blood flow; days to weeks Foot/ankle swollen, red, and warm Difficult to distinguish from infection Tx: offloading in a TCC for 4-6 months 2nd Coalescence/Healing: bony fragments healing, new bone formation, less red and swollen Tx: CROW=>offloads, custom-molded, fully padded device that is a combined AFO and custom walking boot; bivalve or clamshell w/ a rocker bottom 3rd Resolution=>bone fragments smooth over and bony density increases (evolves over several months) foot/ankle displays permanent enlargement and fixed deformity due to bone fragments and joint dislocation healing in a displaced position; skin color and temperature normalize Tx: accommodative shoes w/ custom insert or brace Total Contact Cast Indications: Grade 1,2 plantar ulcers; Charcot Arthropathy Contraindications: acute infections, marked edema, marked exudate, severe vascular disease Alternatives: pneumatic walkers/prefabricated boots, healing shoe -Keys to effective design: fixed ankle, rocker sole, soft insert Wagner Ulcer Classification 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 w/o abscess or osteomyelitis 3 Deep ulcer w/ abscess, osteomyelitis, or joint sepsis 4 Gangrene localized to portion of forefoot or heel  Moist Wound Environment Increases breakdown of dead tissue and fibrin Accelerates angiogenesis Prevents tissue dehydration and cell death Enhances wound re-epithelialization Decreases cost (fewer dressing changes) Decreases or eliminate pain Increases quality of life Wound Bed Preparation Definition Best Practices DIME acronym Provides optimal foundation for -Identify and treat the cause -D=>Debridement preparing the wound bed for (healable, maintenance, -I=>Infection or Inflammation healing and removing the most non-healable) -M=>Moisture Balance common type of barriers -Address patient-centered concerns -E=>Edge-nonhealing -Provide local wound care -Provide organizational support-interprofessional teams Debridement Definition When to When not to Removal of necrotic tissue, -Enhance wound assessment: determine if -Arterial Insufficiency exudate, bacteria, & viable tissue present -Stable heel ulcers metabolic waste from -Promote growth and healing: creates an -Wound w/ pyoderma wound to improve the acute wound within a chronic wound, gangrenosum-large, painful ulcers healing process restores nutrient supply from underlying usually on legs-disorder of the circulation, facilitates optimal oxygen immune system delivery to wound site -Decrease risk of infection: reduces biological burden of the wound  Tissue Types Fat -Normal is shiny and yellow -Devitalized is grey or brown and appears dull Fascia -White and tough Muscle -Normally very vascular and a deep color red Blood Vessels -Red or purple dependent on oxygen level Tendon -White, shiny, and appears rope-like -Color will change from white to yellow or black if necrotic Bone -White and hard -Becomes darker if necrotic Joint Capsule -Covered with white capsule Cartilage Normally white What to Debride Slough Soft, moist, stringy, yellow, loose or adherent non-viable tissue Eschar Dry, leathery, thick, hard necrotic tissue Callus Thickened skin (hyperkeratosis) Debridement Methods Mechanical Nonselective Wet-to-dry dressings, whirlpool, pulsed lavage Surgical Semi-selective; fast and effective Scalpels, scissors, forceps, tweezers Autolytic Selective; use body’s endogenous Transparent film or hydrocolloid enzymes to liquefying necrotic tissue; Contraindicated in presence of infection, slow and easy extensive necrotic tissue, undermining Enzymatic Selective; eats through necrotic tissue Collagenase Indicated for adherent or gel-like slough Biological Selective; produce powerful proteolytic Maggots enzymes that destroy dead tissue by Contraindications: exposed blood vessels, ingesting acute infections, necrotic bone or tendons, vascular issues-cannot heal Topical Systemic antibiotics Silver and Cadexomer Iodine Agents  Mechanical Debridement Wet-to-Dry dressings Whirlpool Pulsed Lavage -Limited use=>insensate -Limited use=>large wounds to -Use when large amounts of population, moderate to large aggressively clean or soften necrotic tissue and other amount of necrotic tissue, necrotic tissue debridement options not an surgical intervention is not an -Contraindications: clean, option immediate option granulating wound -Contraindications: clean, -Contraindications: clean, -Precautions: venous granulating wound granulating wound insufficiency, neuropathy Surgical Debridement Considerations Indications Contraindications -Analgesia/anesthesia required -Gold standard for removal of -Arterial insufficiency -Fast and selective adherent necrotic tissue -Malignant wounds -Opportunity to collect tissue and -Foreign material -Dry gangrene bone cultures -be prepared for bleeding w/ silver -Impaired clotting -Adequate perfusion needed nitrate sticks -Interface b/w viable and -Not recommended in severely non-viable tissue unclear compromised pt -Septicemia (untreated) -Licensure -Changes chronic to acute wound environment Inflammation vs Infection Inflammation Infection -Is integral to microbial resistance -When the host resistance fails to control the -Release of inflammatory mediators results in growth of microorganisms localized vasodilation and increased blood flow to -Cumulative effect of the toxic substances results the area of injury in tissue injury and wound deterioration -Remove microorganisms and debris as well as -Occurs in wound tissue-not on the surface bacterial toxins Clinical Signs and Sx Inflammation Infection Erythemal Border Well-defined Poorly defined; much larger; possible red streaks Drainage Thin and proportionate to wound size Thick, copious, white, green, purulent Temperature Local increase Local increased even more, pt possibly febrile Swelling Slight Disproportionate  Bacterial Balance ALL chronic wounds are contaminated Contamination: organisms present on wound surface; no signs and sx; begins w/ injury that disrupts skin; can be washed away with irrigation Colonization: organisms multiply on wound surface; early reversible adherence; later irreversible adherence of organisms to the tissue; no signs and sx Critical colonization: organisms form biofilm on wound surface, causing local tissue damage (delayed healing, local infection) Infection: organisms invade tissue and systemic response occurs; tx w/ antibiotics Diagnostic Tests Tissue biopsy The goal standard for wound infection General Interpretation infected=>106 or greater organisms or presence of staphylococcus Determine type Organisms and number of colonies per gram of tissues Culturing -biopsy -swab Exudate Management Normal levels of exudates are good=>contain WBCs, lysosomal enzymes, lymphokines and growth factors Chronic and excessive exudate slows down the healing process -appropriate dressings -address underlying factors -compression if indicated -Bacterial Burden=>microbial management -Edema=>Compression -Breakdown of Necrotic Tissue=>Debridement Moisture Wet skin softens and breaks open more easily Wet skin can cause rashes and lead to skin breakdown Keep Dry If Fungal/Yeast Infections=>use antifungal powders Herpes=>want to scab to form b/c infectious when wet Arterial Insufficiency in LE ulcers  Wound Edge The final stage of wound Advancement of the epithelial edge of the wound healing is epithelialization Cause of edge non-healing Non-migrating keratinocytes or non-responsive wound cells; overproduction of hyperkeratosis and callus formation; undermining or rolling of a wound edge (epibole); underlying infection Actions Re-assess cause or consider corrective therapies -Debridement, skin grafts, biological agents, adjunctive therapies Outcome Advancing edge of wound Principles of Care: MEASURES Acronym M=>minimize trauma to the wound E=>eliminate dead space (tunnels, tracts, undermining) A=>assess and manage the amount of exudates S=>support the body’s tissue defense system U=>use non-toxic wound cleansers R=>remove infection, debris, and necrotic tissue E=>environment maintenance, including thermal insulation and a moist wound bed S=>Surrounding tissue, protect from injury and bacterial invasion Ideal Dressings Maintains a moist environment (not Is absorbent macerating or desiccating) Facilitates autolytic debridement Provides thermal insulation Is conformable for use needed (fill tunneling, Acts as a bacterial barrier undermining etc.) Comes in numerous shapes and sizes Is non-traumatic upon removal  Dressings Primary Dressings Secondary Dressings Comes in contact w/ the wound bed Covers a primary dressings or secures a 3 Categories dressing in place 1.​ Maintains adequate moisture Ex) gauze and tape 2.​ Absorbs excess moisture 3.​ Adds moisture NICE Dressing Decision Making Necrotic tissue to be debrided? -Dressings are a slower option than sharp/surgical -Ex) autolytic debridement Wound Infected or inflamed? -Consider antimicrobial dressings (ex. silver, iodine) Wound Characteristics? -Does location need to be considered-need to be waterproof? Exudate -Match absorbency, assess surrounding skin to evaluate for maceration Skin Cleansers Wound Cleansing=>use fluids to remove debris, remnants of prior dressings, microorganisms from wound and peri-wound Cleanse≠sterilize; cleanse=wash (no cytotoxicity) If fibrinous material and debris can’t wash out=>debride! Cleanse w/ each dressing change as needed Caution-can cause tissue damage depending on pressure and agent No difference in rates of infection & healing b/w water and saline in cleansing chronic wounds in adults/children Saline vs. water vs. wound cleansers Be cautious of cytotoxicity -Hydrogen peroxide: may act as a chemical debriding agent to lift debris and necrotic tissue from wound surface; Need to irrigate w/ normal saline following use; do not use in sinus tracts -Goal: microbial elimination at what cost  Gauze Available in sponges, rolls, strips Disadvantages -may be impregnated w/ hydrogel -requires a secondary dressing -used as a primary or secondary dressing -may leave lint/fibers in wound -allows bacteria in -traumatic removal Transparent Films Description Thin polyurethane membrane; “see through” Indications Wounds w/ absent/low levels of exudate; stage 1,2 pressure injury, superficial wounds, minor burns or lacerations, over sutures, catheter sites, donor sites and protection of skin against friction Advantages Wound inspection, impermeable to external fluids and bacteria, conformable, promote autolytic debridement, reduces friction Disadvantages Non-absorptive, may adhere to fragile skin, not for draining wounds, fluid retention may lead to maceration Example Tegaderm Changes ~5-7 days or prn if leakage Hydrocolloids Description Occlusive or semi-occlusive dressings Indications Stage 2,3 pressure injury, partial and full thickness wounds, under compressive wraps, preventative dressings for friction areas, primary or secondary dressings, 1st, 2nd degree burns Advantages Autolytic debridement, self adherent, impermeable to fluid/bacteria, conformable, reduces wound pain, thermal insulation Disadvantages Contraindicated if muscle, bone, tendon or 3rd degree burns, infection, not recommended for heavy draining wounds, sinus tracts or fragile skin, difficult to remove -not for diabetic foot ulcers (traps bacteria) Example Duoderm Changes ~3-7 days or prn if exudate  Hydrogels Description Water or glycerin based, nonadherent (gels, sheets, strips, and gauze available) Indications Stage 2-4 pressure ulcers, partial and full thickness wounds, dermabrasion, painful wounds, 1st & 2nd degree burns, skin tears, donor sites, necrotic wounds Advantages Nonadherent, trauma-free removal, rehydrates wound bed, can be used w/ topical meds, can be used in cavities or tunnels, softens and loosens necrosis Disadvantages Some require secondary dressing to secure, may macerated periwound, not recommended for heavily draining, contraindicated for 3rd degree burns Example Aquasite Changes ~24-72 hours Foam Description Hydrophilic, polyurethane or gel-film coated foam Indications Stage 2-4 pressure ulcers, partial and full thickness wounds, surgical wounds, venous ulcers-under compression wraps, tunneling and cavity wounds Advantages Nonadherent, trauma-free removal, conformable, various shapes and forms, highly absorbent, can be used with infection Disadvantages Not recommended with non-draining wounds or dry eschar, may need secondary dressing, may macerated periwound, contraindicated for 3rd degree burns Example Optifoam Changes 3-5 days Calcium Alginate Description A nonwoven composite of fibers; manufactured from brown seaweed; forms a soft gel when in contact w/ wound exudate Indications Stage 3-4 pressure ulcers, partial and full thickness wounds, dehisced wounds, can be used w/ tunneling and undermining Advantages Trauma-free removal, can be used with tunneling and undermining Disadvantages Contraindicated for dry eschar, 3rd degree burns, heavy bleeding, may require secondary dressing; odor during dressing change Example Aquacel Changes ~24-48 hours  Composite Dressings Description Combination of 2 different dressings; provides multiple functions Indications Partial and full thickness wounds, stage 1-4 pressure injury, surgical ulcers Advantages Conformable, multiple sizes and shapes, easy to apply and remove, adhesive border Disadvantages Adhesive border may limit use on fragile skin, some contraindicated for stage 4 ulcers, may not provide moist wound environment Example CombiDERM -bacterial barrier, absorptive layer, foam, hydrocolloid, hydrogel, semi-adherent or nonadherent Changes Per package Antimicrobial Dressings Description Adjunct to systemic antibiotic therapy, variety of forms-transparent dressings, gauze, foams, absorptive fillers; active ingredients may be silver ions, cadexomer iodine Indications Cadexomer iodine=>infected wounds (pressure,venous,arterial, diabetic or surgical Advantages Decreases bacterial load in the wound and decreases the risk of infection; provide antimicrobial effect and a moist environment Disadvantages Sensitivity to product ingredients Example Iodoflex Pads, Acticoat Changes Up to 7 days Collagen Description Absorbent topical wound dressing made from 100% collagen or combined w/ alginate; derived from bovine or ovine; provides a 3D matrix for ingrowth Indications Chronic, non healing wounds, partial and full thickness wounds, stage 3 pressure ulcers, donor sites, surgical wounds Advantages Absorbent, nonadherent, biodegradable goal, conforms well, may be used in combination w/ topical agents Disadvantages Contraindicated for 3rd degree burns and sensitivity to collagen or bovine products; necrotic wounds Example DermaCol, Biostep Changes 1-3 days dressing change Dressings and Exudate Chart Films None-low levels Hydrogel None-moderate levels Hydrocolloid Low-moderate levels Alginate Moderate-heavy levels Foams Moderate-heavy levels Specialty absorbent Heavy levels