CHAMP Chronic Wounds Miriam B. Rodin, MD, Ph. D, 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 $14 B 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 $92 m, TX $300 m) 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 6 mm/Hg
Common pathway Tissue ischemia and cell death due to • Extrinsic pressure >>Pressure (Decubitus) Ulcer – Capillary closing pressure <30 mm/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, proinflammatory 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: • Clean no exudate: absorbent dressing – 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 Relieve pressure x Avoid friction x Inspect daily x Occlusive dressings 1 Sharp debridement 2 Enzymatic debrider 3 Moist gauze/gel packing Absorbent dressings 4 “Wet-to-dry” 5 1 2 3 4 x x x x x x 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
Non-healing ischemic ulcer
Gangrene
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.
Diabetic foot ulcer
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.
Ulceration due to rheumatoid vasculitis
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
Hospital acquired pressure ulcer
High Transmetatarsal Amputation with pressure ulceration of protuberance
Gangrene with surrounding cellulitis
Ischemic foot ulcer
Stage 3 with surrounding cellulitis
Unstageable heel
AHCPR Clinical Guideline Pressure Ulcer Prevention • A level recommendations*: – Education of staff, patient, family (content is B or C level) *SEE AHCPR APPENDIX • B level recommendations: – Avoid massage – Q 2 hr repositioning in bed, q 1 hr sitting (Recent Swedish RCT does not support) – Bed pressure reducing devices…see Lyder reference • C level recommendations: – Inspect – Clean with mild soap – Dry (absorbent, barrier) – Body mechanics, friction – Nutritional supplements (macro or micro) – Mobilization – Documentation Braden or Norton score – Specific positioning devices, bunny boots etc. – NO donut cushions
References 1. 2. 3. 4. 5. Lyder CH. Pressure ulcer prevention and management. JAMA 2003; 289(2): 223 -6. Perneger TV et al. Hospital-acquired pressure ulcers: risk factors and use of preventive devices. Arch Internal Med 1998; 158 (17): 1940 -1945. Schoonhoven L. Prospective cohort study of routine use of risk assessment scales for prediction of pressure ulcers. BMJ 2002; 325(7368): 797. Bates-Jensen BM. Quality indicators for prevention and management of pressure ulcers in vulnerable elders. Annals Internal Med 2001; 135(8 pt 2): 744 -51. Lyder CH et al. Quality of care for medicare patients at risk for pressure ulcers. Arch Internal Med. 2001; 161(12): 1549 -54.
Appendix • Wound care vocabulary • AHCPR Clinical Guideline for PU Prevention • AHCPR Clinical Guideline for PU Treatment
Wound vocabulary • Eschar • Slough • Granulation • Undermining • Necrotic • Colonization • Cellulitis • Abcess Shear Excoriation Gangrene Collagenase Debride (Hydro)Colloid Occlusive
AHCPR Clinical Guideline Pressure Ulcer Prevention • A level recommendations: – Education of staff, patient, family (content is B or C level) • B level recommendations: – Avoid massage – Q 2 hr repositioning in bed, q 1 hr sitting (Recent Swedish RCT does not support) – Bed pressure reducing devices…see Lyder reference • C level recommendations: – – – – – Inspect Clean with mild soap Dry (absorbent, barrier) Body mechanics, friction Nutritional supplements (macro or micro) Mobilization Documentation Braden or Norton score Specific positioning devices, bunny boots etc. NO donut cushions
AHCPR Clinical Guideline Pressure Ulcer Treatment • A level recommendations: – Minimize bacterial colonization with recommended cleaning and debridement – Consider a 2 wk trial of topical triple Abx or Silvadene for a clean non -healing wound or one that continues to produce think exudate. – Systemic Abx only for cellulitis, sepsis, osteomyelitis – Assess daily for recurrent PU • B level recommendations: – Prevent malnutrition – Avoid –cidal topical agents (povidone, betadine, Dakin’s, peroxide) – Irrigation with NS 4 -15 psi for cleaning – Continuously moist dressing…no demonstrated difference among many competing products and just NS and fluff gauze. – NO wet-to-dry on clean wounds. – Consider nursing labor time needed for dressing plan – Trial of low voltage electro stimulant therapy for refractory wounds
AHCPR PU Guidelines Cont’d. • C level recommendations: – Initial standardized assessment, weekly reassessment – Reassess management if no healing of a clean wound within 2 -4 weeks – Complete H&P – Q 3 mo nutritional assessment, if p. o. intake is inadequate, consider TF – Vitamin and mineral supplements if deficiency confirmed or suspected. – Assess and manage pain – Psychosocial (caregiver availability) – Set treatment goals – Positioning schedules, devices, Air-fluidized bed if Stage 3 or 4 non-healing – Debride, sharp or chemical as appropriate – Moist dressings – Whirlpool – Loose packing of all wound cavities – No evidence for miscellaneous topical or systemic agents, hyperbaric, UV, IR, zinc, Vit C or US. – Quantitative soft and bone biopsy culture for non-healing wounds – Observe clean body substance precautions, not sterile
Скачать презентацию CHAMP Chronic Wounds Miriam B Rodin MD Ph
67ce86b965c5cea090f316349eacda52.ppt