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CHAMP Chronic Wounds. Miriam B. Rodin, MD, PhD, CMD University of Chicago. Learning objectives. Perform a competent bedside physical examination for discovery and diagnosis of wounds Incorporate knowledge of pathophysiology and wound healing into diagnostic and therapeutic assessments
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CHAMPChronic Wounds Miriam B. Rodin, MD, PhD, CMD University of Chicago
Learning objectives • Perform a competent bedside physical examination for discovery and diagnosis of wounds • Incorporate knowledge of pathophysiology and wound healing into diagnostic and therapeutic assessments • Appreciate the magnitude of the cost and care burden of chronic wounds • Incorporate evidence-based knowledge for primary prevention and clinical management of wounds
Assess Learner’s Outcome • Attitudinal • Believes that chronic wound care is an internal medicine competency • Behavioral • Performs wound evaluation at bedside on teaching rounds • Puts wound care in the problem list and management plan • Assists team to formulate an effective plan of care, including prognosis for healing • Cognitive • Recognizes inappropriate, harmful or ineffective wound management
Outline • Scope of the problem • Pathophysiology • Differential diagnosis • Management • Prevention • Geropardy: Name That Wound
Most pressure ulcers (PU) begin in acute care hospitals. • Estimates of the scope of the problem flawed by methodological barriers • Incomplete ascertainment • Confusion of incidence and prevalence • Incomparable study designs • Local institutional/population variability • CMS guidelines define PU a reportable hospital patient safety event; quality indicator.
Incidence 2.7% - 29.5% • Prevalence 4% - 69% per bed-day or 3.5% - 29.5% per patient per bed-day • High risk patients: • Quadriplegics • Neurosurgery • Orthopedic..post-op hips..up to 66% • Critical care MICU/CCU/SICU…33% - 41% • Prolonged anaesthesia time • Debilitated AND age > 70
Scope of the Problem • Chronic wound care products: a $14B industry. • Ischemic and diabetic leg ulcers are the leading indication for revascularization and amputation. • Litigation against nursing homes: #1 Falls #2 Pressure ulcers. Largest settlements for PU (FL $92m, TX $300m) and recently, hospitals.
Human cost easier to appreciate • Pain • Amputation • Disablement • Social costs (disfigurement, odors, institutionalization) • Risk management
Outline • Scope of the problem • Pathophysiology • Differential diagnosis • Management • Prevention • Geropardy: Name That Wound
Site of the injury Capillary closing pressure 32 mm/Hg Venule closing pressure 6mm/Hg
Common pathway Tissue ischemia and cell death due to • Extrinsic pressure >>Pressure (Decubitus) Ulcer • Capillary closing pressure <30mm/Hg x 15 min • Stasis >> Ulceration or Dermatitis • Obstructed outflow (venous insufficiency) • Obstructed clearance of extracellar fluid and debris (lymphatic insufficiency, sclerosis) • Arterial occlusive disease • Tissue hypoxia • Acute TE in small or terminal arterioles gangrene • Chronic PAD medium and large vessels ischemic ulcers.
The cause of the injury explains the chronicity of the injury • Increased duration of extrinsic pressure: • Debilitated patients do not spontaneously adjust position: neuropathy, sedation, restraints, weakness • Loss of dermal collagen and fat support of microcirculation • Inflammation • Poor drainage inhibits clearance of bacteria, pro-inflammatory factors, necrotic tissue • Tissue hypoxia • Poor perfusion and anemia limit delivery of
Outline • Scope of the problem • Pathophysiology • Differential diagnosis • Management • Prevention • Geropardy: Name That Wound
Differential diagnosis directs • Choice of therapy • Choice of consultation • Prognostication for healing
Pressure Ulcer • The usual pressure points: sacrum, trochanters, heels, coccyx • Can develop on ANY part of the body: nostrils from nasal cannula, DHT; scalp from immobilization on ventilator • In joint spaces of contracted limbs • Where body parts “kiss” (knees, buttocks)
PRESSURE ULCERS: • Hypoxia induced cell death releases cytosolic factors into the microcirculation • Provokes circulating macrophages to the wound, produce PMN chemotactic, proflammatory substances, collagenases and proteases. • Tissue bound macrophages do not produce tissue growth factors in the presence of these substances. • Fibroblasts will not migrate into the wound bed; cell differentiation and proliferation will not occur
PRESSURE ULCER THERAPY • Relieve pressure • Remove necrotic tissue • Protect clean wound base • Be alert for secondary infection
Bedside Approach • Trigger: Pressure points? Risk factors? Immobility? ICU? Post-op? • Pressure ulcer • Stage it: • Inspect • Palpate • Debride UNLESS IT IS A DRY HEEL • Probe for depth and tunneling
Staging • Stage 0 red, blanching “post ischemic hyperemia” • Stage 1 red, non-blanching, indurated* • …Dark-skinned patients: no erythema, blue or purple discoloration and boggy feel on palpation • *Apoptotic cells are lysing, releasing chemotactic signals into interstitium, attracting macrophages. • Macrophages release collagenases, proteases and additional inflammatory intermediates (TNF, IL-2, IL-6). • Keratinized layer intact. Intradermal edema.
Staging cont’d • Stage 2 • Cell lysis extends into the dermis, a shallow crater appears. “Partial thickness.” • Dermal thickness varies over body surface, decreases with advancing age, photoaging • FULL THICKNESS WOUNDS: • Stage 3 Injury extends into the subdermal tissue • Stage 4 Injury extends into muscle, bone, internal structures (scrotum, rectum, visible tendons) • Unstageable: Depth of wound cannot be determined and is presumably 3 or 4: Eschar, heels
A decubitus ulcer in an elderly patient is seen on the left. The ulcer is covered by fibrino-purulent exudate. The picture on the right shows the same wound after it has healed. Note the puckering scar
Stage 3 sacral PU with residual eschar, slough and secondary necrotic tissue
Heel Unstageable, probable 4 Stage 2 Sacral Pressure Ulcer
ICEBERG principle • Pressure is distributed in a roughly upright cone, expanding outward and down through the subdermal tissues: • Eschar indicates Stage 3 or higher • Subcutaneous wound is larger than the visible area of eschar
Outline • Scope of the problem • Pathophysiology • Differential diagnosis • Management • Prevention • Geropardy: Name That Wound
Management of pressure ulcers • Explore open wound manually or with probe to determine extent of undermining and tunneling • Closed wound must be visually inspected daily for progression • Eschar: leathery black or brown covering is NOT a scab • MUST be opened.. sharply scored and excised.* • Failure to do so will result in rapid wound extension, anaerobic seeding and sepsis. • *Except hard, dry eschar on heel
A pressure ulcer is not an infection. • Foul, smelly gray and yellow gunk is what macrophages make while they are cleaning up dead tissue. It is NOT a sign of infection. • Signs of infection: • Expanding red, warm, indurated halo around wound • Visible bone with disrupted periosteal membrane • Exposed bone with surrounding granulation that will not cover the bone after 10-14 days • Deep tissue biopsy is confirmatory. Assume skin flora, staph species for empiric treatment. • NEVER swab a wound for culture.
Non-healing PU • Should improve within 14 d. If not: • Heavy “purulent” exudate: • gm+ colonization: absorbent dressing • Clean no exudate: • gram-neg colonization: silvadene, other Ag+ impregnated dressing • Recurrent necrosis: • consider pressure ischemia: air fluidized bed (Level 3 device). • Visible bone: • Periosteum disrupted: bone bx for culture • Terminal ulcer: • multiple non-healing ulcers of various ages: (pre-death marker, “Kennedy ulcer.” Medicare approved hospice diagnosis
Decubitus Do’s Stage 0 1 2 3 4 Relieve pressure x x x x x Avoid friction x x x x x Inspect daily x x x x x Occlusive dressings1x Sharp debridement2 x x Enzymatic debrider3 x x Moist gauze/gel packing x x Absorbent dressings4 x x “Wet-to-dry” 5 1. e.g. Hydrocolloid occlusive dressing 2. Remove eschar, soft debris 3. Removes adherent slough: yellow, brown, black material, e.g. collagenases enzymatic debriders 4. Removes non-adherent exudate, e.g. Ca.alginate, Aquacel 5. Not recommended.
Common Decubitus Errors • Staging errors: • Occlusive dressing on a 3, 4 or closed unstageable: creates anaerobic environment, prevents daily inspection. • Overly aggressive debridement: • Sharply debride hard, dry eschar OR fluid-filled blister on a heel • Recurrent trauma to a healing wound: e.g. wet-to-dry • Use of –cidal agents on granulation tissue: • Topical iodine, Dakin’s, peroxide on any clean wound. • Overuse of antibiotics: • Creates multiply resistant organisms • Encouraged by inappropriate swab wound cultures • Systemic antibiotics without evidence of systemic infection (cellulitis, osteo, bacteremia)
ISCHEMIC ULCER • Arterial occlusion prevents macrophage, fibroblast, growth factor migration to the wound. • Ischemic ulcer paradoxically clean and dry. • Gangrene is not an infection: Necrosis of fleshy soft tissue. • Treatment of wet vs dry gangrene: • Wet early surgery for odors or painted with betadine as a desiccant • Dry allowed to auto-amputate.
Ischemic Ulcers: Epidemiologic Risk Factors • Classic CVD RF multiple longitudinal studies: Framingham, Chicago Heart, Honolulu Heart, CHS, Rotterdam, Whitehall • Smoking • HTN • DM • Older age • Male sex • Hypercholesterolemia • Black race • HHC • CRP • D-dimer.
ISCHEMIC ULCER • Approach to therapy: • Protect at-risk watershed tissue • Restore perfusion • Manage pain
Physical Diagnosis • End arterial location, typically feet • Non-healing lower leg trauma. • Clean (more or less), dry, no granulation tissue, edge may be heaped up. • Signs of chronic ischemia • Muscle wasting • Cool extremities • Dopplers ABI’s • Blanching or incr pain on elevation • Arterial ischemic ulcer
Diabetic Ulcers • Typically on the ball of the foot or other weight-bearing pressure point. • Characteristic hard keratinized margin with a small deep open center. • Small vessel disease, neuropathy • Debridement superficial only for comfort. • Probe for bone. • Infection is more likely, empiric ABX warranted .
Stasis Ulceration and Dermatitis • Pro-inflammatory cells and substances trapped in the tissue by venous, lymphatic incompetence • Back pressure impedes fibroblast and growth factor penetration of superficial dermal layers. • Unrelieved, eventually exceeds arteriolar, lymphatic closing pressures, lymphatic capillaries sclerose.
Physical Diagnosis • Lower leg circumferential or • Localized: perforator vein syndrome • Pain improves with elevation • Extensive: chronic edema, elephantiasis (Milroy’s disease). • Rarely extends completely through the dermis • Weeping. Bubbling. Secondary inflammation. • May be visible, palpable varicosities.
Stasis Ulceration and Dermatitis • Approach to therapy: • Reduce interstitial edema by compression • Clean superficial slough with dressings, gentle debridement e.g. 4-layer dressing NO WET-TO-DRY • Treat co-existent cellulitis
Wound Consultation • Ostomy RN St 0-2; 3-4 after sharp debridement. • Advantage: Will inspect & dress wound daily. • General surgery: • Advantage: Debride large wounds • Vascular surgery for ischemic wounds • Advantage: Will take patient for revascularization • Ortho for wounds with visible bone • Advantage: Can get bone and deep tissue biopsy • Plastics if a possible candidate for flap or skin graft • Derm for chronic stasis dermatitis, “unkowns” • Advantage: Outpatient follow up if ambulatory • PT • 4 layer & compression dressings, some sharp debridements • Dawn Piech 2-6891
Outline • Scope of the problem • Pathophysiology • Differential diagnosis • Management • Prevention • Geropardy: Name That Wound
Prevention • No A level recommendations (ACHPR) • No A level evidence (ACHPR)
Outline • Scope of the problem • Pathophysiology • Differential diagnosis • Management • Prevention • Geropardy: Name That Wound
High Transmetatarsal Amputation with pressure ulceration of protuberance