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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
arterial insufficiency dysfunction
occlusive vasomotor inflammatory
26
arterial ulceration - occlusive
95% of cases are PAD, arteriosclerosis obliterans arteriosclerosis - hardening atherosclerosis - plaque formation intermittent claudication - "cramping"
27
intermittant claudication
"hallmark sign of arterial insufficiency:"
28
Art. ulceration
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
Art. Ulcer. Tx
``` 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
hyperglycemia
catabolic state protein breakdown occurring starvation at cellular level toxic to cellular elements greater infection susceptibility
31
ideal blood glucose to stay under
<200 mg/dL helps promote normal protein synthesis
32
A1C goals
less than 6.5%
33
neuropathy
affects 3 different areas distal to proximal loss of protective sensation occurs in 80% of ulcer
33
neuropathy
affects 3 different areas distal to proximal loss of protective sensation occurs in 80% of ulcer
34
poly neuropathy
sensory, motor, and autonomic function
35
sensory neuropathy
generally symmetrical stocking and glove distribution hyperglycemia is cause direct injury to nerve by reduced blood flow
36
ROM needs in foot
25 deg PF 7 deg of DF for normal gait
37
autonomic neuropathy
should lube feet 1x per day regulate moisture, blood flow, skin integrity, hair and nail growth
38
local factors that lead to diabetic ulcers
infections osteomyelitis increased pressure due to foot shape changes improper footwear presence of previous injury neuropathic Fx
39
greatest risk for DFU? Amputation?
neuropathy for DFU DFU for amputation
40
gold standard for DFU offloading
Total Contact Cast
41
contraindications for TCC
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
pt ed for diabetes
soaking is bad no alcohol rubs no epsom salt dryness is due to autonomic dysfunction
43
hypertrophic scarring
raised, red, rigid
44
keloid
raised, red, rigid, spreads beyond surrounding tissue
45
primary closure
closed with suture
46
secondary closure
edges cannot be approximated granulation tissue filling in scar
47
delayed primary closure
tertiary closure combo of primary and secondary wound left open a few days and surgeon closes the site
48
hyperemia
occur in 15-30 minutes redness goes away in an hour or less
49
ischemia
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
necrosis
6+ hours obvious color change, lasting temperature change, induration increased pain
51
ulceration/ tissue death
2 days - 1 week depends on depth of injury, time, and status
52
pediatric skin
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
stage 1 pressure injury
localized intact skin with non blanchable redness
54
stage 2 pressure injury
partial thickness loss of skin with exposed dermis visible wound bed with pink or red, moist, and potentially SEROUS FILLED BLISTER
55
stage 3 pressure injury
full thickness loss of skin in which adipose is visible in the ulcer, and epiboly is often present
56
stage 4 pressure injury
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
suspected Deep tissue injury
intact OR non-intact skin with localized area of persistent nonblanchable deep red, maroon, purple discoloration or epidermal separation
58
unstageable pressure injury
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
TIPSS for pressure injury prevention
turning incontinence pad bony surfaces support surfaces support nutrition

Integ (3 decks)

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