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Integ > chronic wounds, vascular, wound vac > Flashcards

chronic wounds, vascular, wound vac Flashcards

1
Q

Acute healing characterisitics

A

progression through healing process in a timely & uncomplicated manner.

Surgical or traumatic wounds that were healed by primary intention.

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2
Q

Chronic wound healing characteristics

A

Might be a wound that fails to progress through a normal, orderly, timely sequence of repair.

Healing may have pathology & generally occurs through secondary intention.

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3
Q

intrinsic factors that affect healing (5)

A 
Age
Chronic dz
Perfusion/oxygen
Immunosupression
Neurologic Impairments
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4
Q

extrinsic wound factors

A 
Medications
Nutrition
Chemo/radiation
Stress - physical/emotional
Bioburden
The Clinician
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5
Q

local factors to wound healing

A

bacteria, perfusion defects, moisture, nutrients, oxygen

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6
Q

systemic factors for wound healing

A

comorbidities, nutritional status, obesity, age

Psychological stress- result in cellular
dysfunction- Depression

Noise- increase plasma cortisol and
adrenocorticotropic hormones.

Pain

Obesity- more complicated with surgical
procedures. Decreased blood perfusion,
immobility, intra-abdominal pressure

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7
Q

iatrogenic factors

A

“clinician induced”

dressings, medications, PT treatments

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8
Q

Does prophylactic use of antibiotics improve healing rates

A

no

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9
Q

if a wound is not colonized, can it be infected?

A

no

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10
Q

most common cause of leg ulcers

A

venous insufficiency

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11
Q

typical venous pressure in legs

A

60-90 mmHg

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12
Q

pathogenesis of venous insufficincy

A

failure of the muscle pump

pressure rises in veins

ambulatory hypertension is widely accepted as a cause of venous ulcerations

potentially: development of pericapillary fibrin cuff or leukocyte plug

failure of valves causing back flow

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13
Q

homans theory

A

concept of “stasis”

has been disproved as insufficiency instead of stasis

there is actually more oxygen present

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14
Q

4 mechanisms of venous insufficiency

A

venous thrombosis

venous obstruction

venous dilation

hemorrhage

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15
Q

venous thrombosis

A

platelets adhere to endothelial wall

becomes occluded

inflammation may occur

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16
Q

venous obstruction

A

result of ambulatory venous hypertension

determined by location and duration of obstruction

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17
Q

venous dilation

A

varicosity, dilated permanently and superficial

may be genetic

not fully understood if the defect lies in the valves or vein wall

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18
Q

hemorrhage

A

considered a concurrent problem with all previously given condition

hematoma can develop

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19
Q

venous insufficiency clinical features

A

may appear like bacterial cellulitis

hemosiderin staining

more shallow and less painful

borders of wounds are flat and may appear wet, and eczematous

medial malleoli is most common

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20
Q

tx of venous insufficiency

A

Leg elevation

wt reduction

low sodium

exercise (water aerobics is great)

unna boot or profore

wound vac

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21
Q

compression needs to treat VI

A

30-40 mmHG

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22
Q

short stretch bandage

A

low resting pressure but high working pressure

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23
Q

high stretch

A

sustains high pressure at rest and during ambulation

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24
Q

arterial insufficiency

A

PAD - supply and demand issue

50% may be asymptomatic with blockage

smoking reduction is best result

control diet, age and familial factors

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25
Q

arterial insufficiency dysfunction

A

occlusive

vasomotor

inflammatory

26
Q

arterial ulceration - occlusive

A

95% of cases are PAD, arteriosclerosis obliterans

arteriosclerosis - hardening

atherosclerosis - plaque formation

intermittent claudication - “cramping”

27
Q

intermittant claudication

A

“hallmark sign of arterial insufficiency:”

28
Q

Art. ulceration

A

generally more painful

located on anterior tib, lateral leg, or distal toes

may present on pressure areas

gangrene may present wet or dry

will appear pale, thin, little drainage, or eschar

punched out margins

skin MAY BE DRY, SCALY, LOSS OF HAIR, COOL IN TEMPERATURE

29
Q

Art. Ulcer. Tx

A 
Local wound bed care, limb protection, risk factor
reduction
Modalities
Surgical
Pharmacological management (Lipitor, Zocor,
Crestor)
Risk Factor reduction
ABI used to diagnose the issue
30
Q

hyperglycemia

A

catabolic state

protein breakdown occurring

starvation at cellular level

toxic to cellular elements

greater infection susceptibility

31
Q

ideal blood glucose to stay under

A

<200 mg/dL

helps promote normal protein synthesis

32
Q

A1C goals

A

less than 6.5%

33
Q

neuropathy

A

affects 3 different areas

distal to proximal

loss of protective sensation occurs in 80% of ulcer

33
Q

neuropathy

A

affects 3 different areas

distal to proximal

loss of protective sensation occurs in 80% of ulcer

34
Q

poly neuropathy

A

sensory, motor, and autonomic function

35
Q

sensory neuropathy

A

generally symmetrical

stocking and glove distribution

hyperglycemia is cause

direct injury to nerve by reduced blood flow

36
Q

ROM needs in foot

A

25 deg PF

7 deg of DF for normal gait

37
Q

autonomic neuropathy

A

should lube feet 1x per day

regulate moisture, blood flow, skin integrity, hair and nail growth

38
Q

local factors that lead to diabetic ulcers

A

infections

osteomyelitis

increased pressure due to foot shape changes

improper footwear

presence of previous injury

neuropathic Fx

39
Q

greatest risk for DFU? Amputation?

A

neuropathy for DFU

DFU for amputation

40
Q

gold standard for DFU offloading

A

Total Contact Cast

41
Q

contraindications for TCC

A

need to be grade 1 or 2 on Wagner scale, no infections, arterial disease, deep wounds, or fluctuating edema

be cautious about fibular head impingment

42
Q

pt ed for diabetes

A

soaking is bad

no alcohol rubs

no epsom salt

dryness is due to autonomic dysfunction

43
Q

hypertrophic scarring

A

raised, red, rigid

44
Q

keloid

A

raised, red, rigid, spreads beyond surrounding tissue

45
Q

primary closure

A

closed with suture

46
Q

secondary closure

A

edges cannot be approximated

granulation tissue filling in scar

47
Q

delayed primary closure

A

tertiary closure

combo of primary and secondary

wound left open a few days and surgeon closes the site

48
Q

hyperemia

A

occur in 15-30 minutes

redness goes away in an hour or less

49
Q

ischemia

A

redness goes away in an hour or less 1-6 hours of pressure with/ without shear

may take 24-48 hours for tissue to recover – deep redness

50
Q

necrosis

A

6+ hours

obvious color change, lasting temperature change, induration

increased pain

51
Q

ulceration/ tissue death

A

2 days - 1 week

depends on depth of injury, time, and status

52
Q

pediatric skin

A

much more friable

upper body ulcers occur more frequently in peds

most common:

head in infants and children, and sacrum in children over 10

53
Q

stage 1 pressure injury

A

localized intact skin with non blanchable redness

54
Q

stage 2 pressure injury

A

partial thickness loss of skin with exposed dermis

visible wound bed with pink or red, moist, and potentially SEROUS FILLED BLISTER

55
Q

stage 3 pressure injury

A

full thickness loss of skin in which adipose is visible in the ulcer, and epiboly is often present

56
Q

stage 4 pressure injury

A

full thickness skin and tissue loss with exposed fascia, muscle, tendon, ligament, cartilage, or bone in the ulcer

slough or eschar may be visible

57
Q

suspected Deep tissue injury

A

intact OR non-intact skin with localized area of persistent nonblanchable deep red, maroon, purple discoloration or epidermal separation

58
Q

unstageable pressure injury

A

full thickness skin and tissue loss in which the extent of tissue damage within the ulcer cannot be confirmed because it is obscured by slough or eschar

59
Q

TIPSS for pressure injury prevention

A

turning

incontinence

pad bony surfaces

support surfaces

support nutrition

Integ (3 decks)

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