Flashcards in Wound care Deck (34):
Difference b/t acute and chronic wounds?
- acute wounds heal in pedictable fashion
3 phases: inflammatory, proliferative, and remodeling, would will heal in 4-6 weeks
- chronic wounds: characterized by wound hypoxia causing bacterial colonization and persistent inflammation which leads to wound stasis
- wounds are unhealed after 6-12 weeks
examples and characteristics of chronic wounds?
- pressure ulcers
- diabetic neuropathic ulcers
- venous insufficiency ulcers
- arterial insufficiency ulcers
- inflammatory ulcers
non healing, slow healing, cause is ongoing, multiple systemic and local impediments to healing, wound often recurs
Advantage of doppler eval?
- requires minimal equipment, continuous wave doppler
- minimal time
- gives reasonable eval of arterial supply to limb prior to debridement
- not quantitive by qualitative and helpful in screening pts with severe arterial insufficiences
Difference betweem arterial ulcer and venous ulcer?
- arterial: look dry, have black eschar, may not be painful
- venous: moist, red, oozing, usually always painful
surgical options for macrovascular disease?
- open with multiple by pass options
angioplasty with or without drug coated balloons, stenting, atherectomy (even tibial vessels), laser, cell therapy (now in controlled trials)
Most common etiologies of chronic leg ulcers?-
- venous insufficiency: 60-80%
- arterial insufficiency: 20%
- diaebtes/neurpathic: a lot
etiology of venous insufficiency?
- blood becomes hypoxic so skin breaks down
Venous ulcer location and appearance?
- midcalf to heel (gaitor area)
- appearance: shallow, irregular, exudate is common, painful
- origin: venous valve incompetence, venous HTN, extravascular blood loss, edema: RBCs hemosiderin staining, WBCs enzyme mediated tissue destruction
What are venous perforators?
- back flow from deep vein back into superficial vein
Tx of venous ulcer?
- compression therapy: multilayer, short stretch
- trental/doxy: inhibit breakdown of collagen
- closure: skin graft, skin substitutes
- endo-venous closure
Types of compression?
- ace wraps
- support hose
- prescription support hose
- UNNA boots
- coban dressings
If compression fails, what is the next step in venous ulcer care?
- want to improve arterial flow
- improve venous return: PTA, bypass
- reduce venous reflux: deep - vein valve replacements
- superficial: stripping, ablative procedures
- endoenous laser ablation of saphenous vein
- surgical excision of veins
- cover wound with skin
Why does wound healing decrease as we age?
- most chronic wounds occur in pts over 60
- decline in wound healing rates associated with comorbidities (PAD, DM, VSD, infection)
- decline in molecular processes impt for tissue repair - accelerated senescence of cells, decreased production of growth factors, decreased ability to survive hypoxia or toxins, decreased production of collagen and other matrix molecules
Diabetes effects on feet?
- vascular disease
- hammertoes, bunions, corns and calluses
- dystrophic, fungal toenails
Pefect storm of diabetic foot?
- foot deformity
- microvascular disease
- immune impairment (if blood sugar above 200 WBCs won't work)
Where do diabetic ulcers occur on the foot?
- plantar aspect of foot beneath bony prominence
- appearance: ill defined borders, prominent callus, and palpable pulses
Factors that contribute to charcot's foot?
- collapse of arch of midfoot, replaced by bony prominence. Factors: small muscle wasting, decreased sensation, and maldistribution of wt bearing
Why should you debride a diabetic foot ulcer?
- to control excessive or abnormal bacterial load and biofilm: necrotic tissue becomes petri dish for higher bacterial count, may lead to clinical infection and delayed healing
- may allow for improved availability of endogenous growth factors
- to manage and control the pathology (painful wounds are difficult to manage)
- to enhance the effectiveness of topical products and therapies
- to remove non-migratory cells from ulcer edge: sensecent cells must be removed from wound bed, senescent cells have sluggish response to advanced healing agents
- fracture boots
- surgical shoes
- diabetic shoe/inserts
- foam/felt padding
3 main tx of DFUs?
- control blood sugar
WHat is the gold standard for DFU offloading?
- TCC (total contact cast)
- isn't applicable to all DFUs
Failure to use TCC?
- pt tolerance
- time to apply cast
- supplies and cost
- reimbursement issues
Bone involvement of DFU?
- ulcer that is present for more than 30 days
- its more than 3 mm deep
- ulcer probes to the bone
- C reactive protein, greater than 3.2
- ESR greater than 70
- bone scan
- best dx: bone biopsy and culture/sensitivity
Primary risk factors for pressure ulcers?
- prolonged moisture exposure
- impaired mental status
staging of pressure ulcers?
- stage 1: intact skin with non-blanchable redness usually over bony prominence
- stage 2: partial thickness of loss of dermis presenting as shallow open ulcer with red pink around bed, w/o slough
- stage 3: full thickness tissue loss, subq fat may be visible but bone, tendon and muscle not exposed, sligh may be present, tunneling
- stage 4: full thickness tissue loss with exposed bone, tendon or muscle, slough or eschar may be present, tunneling
unstageable: full thickness tissue loss, covered by slough and eschar
surgical repair of pressure ulcers?
- stage 3 to 4 don't respond to optimal care
- procedures: direct closure, skin grafts, skin flaps, free flaps, and myocutaneous flaps
Adjunctive therapy for pressure ulcers?
- hyperbaric oxygen therapy
- negative pressure wound therapy
- biological therapy
Pressure ulcer care?
- begins with pressure relief. Debridement, wound cleansing, and appropriate dressing application follow (w/ exception of sage 1)
- infection control, pain management, nutrition and skin care also impt
- hyperbaric oxygen therapy, negative pressure wound therapy, and use of biologics are useful adjunct therapy
9 steps of chronic wound healing eval?
- adequate perfusion?
- nonviable tissue present?
- infection and/or inflammation?
- microenviro conductive to healing?
- tissue growth optimized?
- offloading or pressure relief appropriate?
- pain controlled?
- host factors optimized?
Is nonviable tissue present?
- if perfusion is adequate and or infection is present - sharp surgical (excisional) or selective debridement
- if perfusion inadequate and no infection and minimal necrosis: mechanical nonselective, autolytic, biological debridement (want to keep moisture intact)
Mechanical nonselective debridement - wet to dry (moist)?
- removes borth nonviable as well as viable tissue
- antimicrobial - vasche wash
- lowest cost
- labor intensive
- desiccation may do more harm than good
Why is nutrition so impt in wound healing?
- because malnutrition decreases:
wound tensile strength and WBC function and ab levels