Wound care

Question 1

Difference b/t acute and chronic wounds?

Answer 1

• 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

Question 2

examples and characteristics of chronic wounds?

Answer 2

• 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

Question 3

Advantage of doppler eval?

Answer 3

• 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

Question 4

Difference betweem arterial ulcer and venous ulcer?

Answer 4

• arterial: look dry, have black eschar, may not be painful

- venous: moist, red, oozing, usually always painful

Question 5

surgical options for macrovascular disease?

Answer 5

• 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)

Question 6

Most common etiologies of chronic leg ulcers?-

Answer 6

• venous insufficiency: 60-80%
• arterial insufficiency: 20%
• diaebtes/neurpathic: a lot

Question 7

etiology of venous insufficiency?

Answer 7

• blood becomes hypoxic so skin breaks down

Question 8

Venous ulcer location and appearance?

Answer 8

• 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

Question 9

What are venous perforators?

Answer 9

• back flow from deep vein back into superficial vein

Question 10

Tx of venous ulcer?

Answer 10

• compression therapy: multilayer, short stretch
• debridement
• trental/doxy: inhibit breakdown of collagen
• closure: skin graft, skin substitutes
• endo-venous closure

Question 11

Types of compression?

Answer 11

• ace wraps
• support hose
• prescription support hose
• UNNA boots
• coban dressings
• cirAides
• tubigrip

Question 12

If compression fails, what is the next step in venous ulcer care?

Answer 12

• 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

Question 13

Why does wound healing decrease as we age?

Answer 13

• 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

Question 14

Diabetes effects on feet?

Answer 14

• neuropathy
• vascular disease
• hammertoes, bunions, corns and calluses
• dystrophic, fungal toenails
• ulcers
• infection
• amputation

Question 15

Pefect storm of diabetic foot?

Answer 15

• foot deformity
• neuropathy
• microvascular disease
• immune impairment (if blood sugar above 200 WBCs won’t work)

Question 16

Where do diabetic ulcers occur on the foot?

Answer 16

• plantar aspect of foot beneath bony prominence

- appearance: ill defined borders, prominent callus, and palpable pulses

Question 17

Factors that contribute to charcot’s foot?

Answer 17

• collapse of arch of midfoot, replaced by bony prominence. Factors: small muscle wasting, decreased sensation, and maldistribution of wt bearing

Question 18

Why should you debride a diabetic foot ulcer?

Answer 18

• 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

Question 19

offloading tx?

Answer 19

• TCC
• fracture boots
• surgical shoes
• diabetic shoe/inserts
• foam/felt padding

Question 20

3 main tx of DFUs?

Answer 20

• control blood sugar
• debride
• offload

Question 21

WHat is the gold standard for DFU offloading?

Answer 21

• TCC (total contact cast)

- isn’t applicable to all DFUs

Question 22

Failure to use TCC?

Answer 22

• pt tolerance
• time to apply cast
• supplies and cost
• reimbursement issues
• familiarity

Question 23

Bone involvement of DFU?

Answer 23

• ulcer that is present for more than 30 days
• its more than 3 mm deep
• ulcer probes to the bone

Question 24

Dx osteomyelitis?

Answer 24

• C reactive protein, greater than 3.2
• ESR greater than 70
• MRI
• bone scan
• best dx: bone biopsy and culture/sensitivity

Question 25

Primary risk factors for pressure ulcers?

Answer 25

• age
• immobility
• malnutrition
• prolonged moisture exposure
• impaired mental status

Question 26

staging of pressure ulcers?

Answer 26

• 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

Question 27

surgical repair of pressure ulcers?

Answer 27

• stage 3 to 4 don’t respond to optimal care

- procedures: direct closure, skin grafts, skin flaps, free flaps, and myocutaneous flaps

Question 28

Adjunctive therapy for pressure ulcers?

Answer 28

• hyperbaric oxygen therapy
• negative pressure wound therapy
• biological therapy

Question 29

Pressure ulcer care?

Answer 29

• 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

Question 30

9 steps of chronic wound healing eval?

Answer 30

• 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?

Question 31

Is nonviable tissue present?

Answer 31

• 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)

Question 32

Mechanical nonselective debridement - wet to dry (moist)?

Answer 32

• removes borth nonviable as well as viable tissue
• antimicrobial - vasche wash
• lowest cost
• labor intensive
• painful
• desiccation may do more harm than good

Question 33

Why is nutrition so impt in wound healing?

Answer 33

• because malnutrition decreases:

wound tensile strength and WBC function and ab levels

Question 34

factors to wound healing?

Answer 34

• nutrition
• diabetics require good glycemic control (less than 200 for optimal healing)
• renal function
• cardiac disease
• mobility
• psychosocial issues