Wound care Flashcards
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
characteristics:
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
- endo:
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
- debridement
- 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
- cirAides
- tubigrip
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?
- neuropathy
- vascular disease
- hammertoes, bunions, corns and calluses
- dystrophic, fungal toenails
- ulcers
- infection
- amputation
Pefect storm of diabetic foot?
- foot deformity
- neuropathy
- 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
offloading tx?
- TCC
- fracture boots
- surgical shoes
- diabetic shoe/inserts
- foam/felt padding
3 main tx of DFUs?
- control blood sugar
- debride
- offload
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
- familiarity
Bone involvement of DFU?
- ulcer that is present for more than 30 days
- its more than 3 mm deep
- ulcer probes to the bone
Dx osteomyelitis?
- C reactive protein, greater than 3.2
- ESR greater than 70
- MRI
- bone scan
- best dx: bone biopsy and culture/sensitivity
Primary risk factors for pressure ulcers?
- age
- immobility
- malnutrition
- 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?
- edema?
- 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
- painful
- 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
factors to wound healing?
- nutrition
- diabetics require good glycemic control (less than 200 for optimal healing)
- renal function
- cardiac disease
- mobility
- psychosocial issues
