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Endocrinology > Chronic wound care > Flashcards

Chronic wound care Flashcards

1
Q

Many suffer for years with wounds such as?

4

A
  1. Venous stasis
  2. Pressure ulcer
  3. Soft tissue radionecrosis
  4. Diabetic ulcer
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2
Q

Acute Wounds heal in a predictable fashion

Three Phases?

A
  1. Inflammatory,
  2. Proliferative,
  3. Remodeling
    Wounds heal in 4-6 weeks
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3
Q

Chronic wounds are characterized by what?

4

A

by

  1. wound hypoxia causing
  2. bacterial colonization and 3. persistent inflammation which leads to
  3. wound stasis

Wounds are unhealed after 6-12 weeks

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4
Q

Acute would characteristics?

4

A
  1. heal in an expected time
  2. cause is transient
  3. usually lack significant impediments to healing
  4. repair is sustained
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5
Q

Chronic wounds/ulcer characteristics?

4

A
  1. nonhealing, slow healing
  2. cause is ongoing
  3. multiple systemic and local impediments to healing
  4. wound often recurs
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6
Q

First step of would healing?

Steps?

A

Is there adequate perfusion?

  1. Vascular history
  2. Pulse Exam
  3. Ankle Brachial Index (ABI) – Requires Doppler
    Normal ABI 0.9-1.2 (beware > 1.2)
  4. Intermittent Claudication 0.5-0.9
  5. Critical Ischemia > 0.4
  6. Transcutaneous Oxygen Pressure Measurement
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7
Q

Transcutaneous Oxygen Pressure Measurements for the following conditions: (TcpO2 or TCOM)

PAD?
DM+PAD?
Critical limb ischemia?

A

PAD>40 mm Hg,

DM+PAD >50 mm Hg Critical Limb Ischemia less than 30 mm Hg

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8
Q

Whats the normal ABI?
PAD?
Severe IC?
Rest pain/ulceration?

A

Normal–0.95-1.2
PAD–less than 0.9
Severe IC –0.4-0.9
Rest pain/ulceration–less than 0.40

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9
Q

How specific and sensitive is ABI for PAD?

When are pulse volume recordings useful?

A

95% sensitive and 99% specific

Useful when systolic blood pressures falsely increased

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10
Q

Advantage of doppler evaluation

4

A
  1. Requires minimal equipment (continuous wave doppler)
  2. Minimal time
  3. Gives reasonable evaluation of arterial supply to limb prior to debridement
  4. Not quantitaive but qualitative and helpful in screening patients with severe arterial insufficiencies
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11
Q

Arterial ulcer appearance?

A

dry, darker, crusty, eschar, outside sometimes painfull and sometimes not

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12
Q

Surgical Options for Macrovascular Disease

6

A
  1. Open with multiple by pass options
    Endo
  2. Angioplasty with or without drug coated balloons
  3. Stenting
  4. Atherectomy (even tibial vessels)
  5. Laser
  6. Cell therapy (now in controlled trials)
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13
Q

Where is the most common spot for venous ulcers?

NOnvenous?

A

ankle and lower shin

mid shin down to all of the foot

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14
Q

Venous ulcers causes?

3

A
  1. Impaired valve funtion- not circulating blood. low oxygen. blood just sitting there
  2. thrombosis
  3. impaired muscle (cant push the blood through) paralyzed pts
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15
Q

Venous ulcers?

A

hyperpigmentation, swelling, shiny, bright and bloody

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16
Q

Location of venous ulcers?

Appearance?

Origin?
5

A

midcalf to heel (gaitor area)

shallow, irregular, exudate is common, painful

  1. venous valve incompetence
  2. venous hypertension
  3. extravascular blood loss/edema
  4. RBC’s > hemosiderin staining?
  5. WBC’s > enzyme-mediated tissue destruction
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17
Q

Venous ulcer treatment?

5

A
  1. Compression therapy
  2. Debridement
  3. Trental/Doxycycline
  4. Closure (skin graft and skin substitutes)
  5. Endo-venous closure (laser ablation)
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18
Q

Types of compression

A
  1. ACE wraps
  2. Over the counter support hose
  3. Prescription support hose with graduated pressure
  4. UNNA boots (zinc and calamine)
  5. 2, 3, and 4 layer Coban dressings
  6. CirAides
  7. Tubigrip
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19
Q

What is the usually mechanism of advanced wound intervention?

A

Endogenous laser ablation of saphenous vein (ELVT)

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20
Q

Most chronic wounds occur in patients of what age?

A

over 60

21
Q

Decline in wound healing rates associated with comorbidities (PAD, DM,VSD, infection) superimposed on an injury. Why?
4

A

Decline in molecular processes important for tissue repair –

  1. accelerated senescence of cells,
  2. decreased production of growth factors,
  3. decreased ability to survive hypoxia or toxins,
  4. decreased production of collagen and other matrix molecules
22
Q

What is the perfect storm for a diabetic ulcer?

4

A
  1. foot deformity
  2. neuropathy
  3. microvascular disease (do damage on the cellular level and not the tissue level)
  4. immune impairment
23
Q

Diabetic ulcers are commonly located where?

Appearance? 3

A

plantar aspect of the foot beneath a bony prominence

ill-defined borders, prominent callus, and palpable pulse

24
Q

Charcot is characterized by what?

A

collapse of the arch of the midfoot which is replaced by a bony prominance

25
Q

Why should we debride an ulcer?

A

to control excessive or abnormal bacterial load and biofilm.

Necrotic tissue becomes a petri dish for higher bacterial count
–May lead to clinical infection and delayed healing

26
Q

When can you not debride?

A

if you dont have a pulse on the foot (cannot debride an ischemic/hypoxic foot)

27
Q

Debridement may allow for improved availability of what?

Goal?

What kind of meds does it support?

A

endogenous growth factors

To manage and control the pathology (painful wounds are difficult to manage)

To enhance the effectiveness of topical products and therapies (dressings, growth factors, tissue grafts etc)

28
Q

What kind of cells are need to be removed from the wound bed?

A

senescent cells (these cells have a sluggish response to advanced healing agents)

29
Q

What is the DFU gold standard treatment?

A

Pressure relief -TCC

total contact cast

30
Q

Bone involvement usual occurs when the ulcer is present for how long?
How deep?

A

more than 30 days

3 mm deep

31
Q

Where does osteomyelitis occur most commonly?

A

Plantar 1st and 5th metatarsal head

1st toe

32
Q

How do we diagnose osteomyelitis? 5

Whats the best diagnosis tool?

A
  1. C-reactive protein of more than 3.2
  2. ESR more than 70mm/Hr
  3. MRI
  4. Bone scan
  5. Bone biopsy with culture for sensitivity*****
33
Q

Primary risk factors for a pressure ulcer?

5

A
  1. age
  2. immobility
  3. malnutrition (protein)
  4. prolonged moisture exposure
  5. impaired mental status
34
Q

What are the most common places for pressure ulcers?

5

A
  1. head
  2. shoulder
  3. sacrum
  4. buttock
  5. heel
35
Q

reducing pressure ulcer risk?

3

A
  1. positioning devices
    - pillows
    - foam wedges
  2. Pressure reducing devices like mattress overlays, low air loss mattresses, air-fluidized beds, multimodes splints
  3. Turning schedule
36
Q

Describe stage 1 pressure ulcer?

A

Intact skin with nonblanchable redness of a localized area

37
Q

Describe pressure ulcer stage 2?

A

Partial thickness loss of dermis presenting as a shallow open ulcer with a red or pink wound bed without slough (may also present as a serum filled blister)

38
Q

Describe a stage 3 pressure ulcer?

A

full thickness tissue loss. Subq fat might be visible but bone tendon and muscle are not exposed.

39
Q

Describe stage 4 pressure ulcer?

A

Full thickness tissue loss with exposed bone tendon or muscle. Slough or eschar may be present.

40
Q

Describe an unstagable pressure ulcer?

A

Full thickness tissue loss in which the base of the ulcer is covered by slough and/or eschar in the wound bed.

41
Q

What should we do if eschar is on the wound?

A

leave eschar on there, it serves as a bandaid.

42
Q

If there is a wound that is stably healing and it starts to get pain or stops getting better then what is happening?

A

its infected

43
Q

Indications for surgical repair of ulcers?

What are our options for procedures?
5

A

Stage 3 to 4 pressure ulcers that do not respond to optimal care

Direct closure
skin grafts
skin flaps
free flaps
myocutaneous flaps
44
Q

79

A

79

45
Q

Pressure ulcer care begins with what?

What three things follow?

A

pressure relief!

  1. debridement
  2. would cleansing
  3. appropriate dressing application
46
Q

The Nine Steps of Chronic Wound Healing Evaluation

A
  1. Adequate Perfusion?
  2. Nonviable Tissue Present?
  3. Infection and/or Inflammation?
  4. Edema?
  5. Microenvironment conducive to healing?
  6. Tissue Growth Optimized?
  7. Offloading or Pressure Relief Appropriate?
  8. Pain Controlled?
  9. Host Factors Optimized?
47
Q

Is nonviable tissue present what do we do:
Perfusion adequate?
Perfusion is inadequate?

A

If perfusion is adequate and/or infection is present – sharp surgical (excisional) or selective debridement

If perfusion is inadequate and/or no infection and minimal necrosis – mechanical nonselective (wet to dry), autolytic, enzymatic, or biological debridement

48
Q

Malnutrition decreases what for slower would healing?

2

A
  1. Wound tensile strength

2. WBC function and antibody levels

Endocrinology (23 decks)

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