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MultiSystem Management > Exam 2-wound care > Flashcards

Exam 2-wound care Flashcards

1
Q

What’s special about the first month of wound healing?

A

Their immune system is suppressed, and they have an increased risk of infection

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2
Q

What kinds of wounds do we stage?

A

Only pressure ulcers. The others are superficial, partial, deep, etc.

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3
Q

repair vs. regeneration

A
  • repair: new stuff; worse
  • -heal by granulation, contraction, epithelialization; wounds surgically repaired; full thickness
  • regeneration: fill in with old stuff; better
  • -partial thickness; heal by epithelialization
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4
Q

What considerations should be made for wounds and the acid mantle of the skin?

A
  • pH should be 4-5.5
  • use a low pH lotion
  • urine is alkaline, so incontinence can change the acid mantle
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5
Q

What are the phases of CT repair?

***

A
  • inflammation: injury to 2 weeks
  • proliferation: 48 hrs to 2-4 weeks
  • maturation: 2-4 weeks to 1-2 years
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6
Q

What does healing time depend on?

A
  • type of wound
  • size of wound: partial vs full
  • type of closure
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7
Q

What direction do wounds heal in?

A

outside-in

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8
Q

What are local factors affecting wound healing?

A
  • primary: blood supply, tissue oxygen tension

- secondary: tissue damage, mechanical stress (over a jt), pain, radiation, infection, surgical and suture techniques

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9
Q

What are systemic factors affecting would healing?

A
  • hemodynamic conditions

- age, smoking (vasoconstriction->decreased wound healing), meds, disease, nutrition anemia, alcoholism

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10
Q

Phase of hemostasis

A
  • process of clotting
  • blood flows into wound
  • immediate vasoconstriction, vasocongestion, blood coagulation and platelet aggregation
  • fibrin-rich clot seals disrupted vessels and fills tissue
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11
Q

What effects hemostatis?

A
  • anticoagulant therapy
  • coagulation dx
  • long term corticosteroids
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12
Q

Inflammatory phase

A
  • mast cells release histamines-increase vasodilation
  • migration of leukocytes: polymorphic neutrophils, monocytes
  • -phagocytosis, release of growth factors to initiate repair process, matrix for cell migration
  • stimulation of nociceptive receptors
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13
Q

What are clinical considerations for inflammation?

A
  • wound care (if present)-topical tx, occlusive dressings, debridement, RICE/positioning
  • protection, rest
  • NSAIDs, corticosteroids, aspirin
  • pain inhibitory technique (Grade I/II)
  • PAINFREE exercise for edema reduction
  • nutritional concerns
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14
Q

Proliferative phase

A
  • collagen phase
  • deposition of collagen (cross-linking): fibroblast proliferation, type 3 collagen synthesis
  • vascular integrity restored: neoangiogenesis (new capillary and arterial production results in development of granulation tissue)
  • -don’t use a gauze dressing-rips out sprouts!
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15
Q

Proliferation

A
  • granulation: primary closure (palpable healing ridge under suture; not a lot of inflammation on the sides), secondary closure (red, vascular, granulated wound bed)
  • contraction: fibroblasts and myofibroblasts create closure, defect shrinks; limited by tension in surrounding tissues
  • epithelialization: proliferation of keratinocytes (put smooth layer over wound), differentiation
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16
Q

What parts of proliferation happen in repair? Regeneration?

A
  • granulation, contraction, epithelialization

- epithelialization

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17
Q

What kind of ROM should you do in the proliferation phase?

A

AROM or gentle isometrics; no PROM-type 3 collagen doesn’t provide tensile strength, granulation tissue is fragile

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18
Q

How long does maturation take?

A

may take up to 1 year in a normal healthy adult, up to 2 years in a child, elderly, or immunocompromised patient

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19
Q

Maturation

A
  • tensile strength may increase up to 80%
  • matrix remodeling: collagen synthesis/degradation, bond conversion (type 3 to type 1/2)
  • scar tissue compaction/contraction
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20
Q

What happens if collagen degradation is disrupted?

A

hypertrophic or keloid scars

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21
Q

Properties of normal, hypertrophic, and keloid scars

A
  • normal: white/pink, indented below skin surface
  • hypertrophic: white, pink, red; slightly raised, firm, follow wound borders
  • keloid: deep red or purple; very raised, firm, extend beyond wound borders
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22
Q

Hypertrophic scars: when do they happen, do they go away, how can they be treated?

A
  • most common with deep injuries involving delayed wound closure (infection)
  • follow wound borders
  • regress spontaneously
  • reconstructive surgery and scar management can improve function and cosmesis
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23
Q

Keloid scars: why do they happen, what do they look like, can they go away, how do they feel?

A
  • overabundant ECM deposition (collagen)
  • abnormally raise, firm, deep red/purple, extend beyond wound borders
  • don’t regress spontaneously
  • painful and itchy; change with barometric pressure
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24
Q

How can keloid scars be treated?

A
  • surgical excision
  • laser
  • anti-histamines, corticosteroids
  • cryotherapy with liquid nitrogen
  • radiation
  • respond poorly to reconstructive surgery
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25
Q

What are the 4 parts of the Vancouver scar scale?

A
  • vascularity
  • pliability
  • pigmentation
  • hieght
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26
Q

How do you score vascularity on the VSS?

A

0: normal
1: pink-increase in blood supply
2: red-greater increase in blood
3: purple-significant vascularity

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27
Q

How do you score pliability on the VSS?

A

0: normal
1: supple
2: yielding
3: firm
4: banding
5: contracture

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28
Q

How do you score pigmentation on the VSS?

A

0: normal
1: hypo
2: mixed pigmentation
3: hyper

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29
Q

How do you score height on the VSS?

A

0: flat
1: 5mm

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30
Q

What are two other scar scales?

A
  • Visual Analog Scale: photo based, doesn’t include pt; simpler and easier to conduct than VSS
  • Patient and observer scar assessment scale: includes itching, stiffness, relief, etc; may not adequately express pt perceptions and concerns; focuses on scar severity from pt and clinician perspective
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31
Q

What is an adheremeter?

A
  • measures adherence of post surgical scar; pull scar in different directions to measure adherence (mm)
  • good validity when compared to VSS at initial exam, but less after rehab
  • good to excellent interrater reliability, excellent intrarater reliability
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32
Q

What are effects of aging on wound healing?

A
  • delayed wound contraction
  • decreased tensile strength, epithelialization, inflammatory response, pain perception, mast cells, capillary growth
  • increase in wound dehiscence
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33
Q

What can cause dehiscence?

A
  • increase in tension
  • infection
  • obesity
  • age
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34
Q

When do kids have integumentary maturity?

A

33 weeks

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35
Q

Why is epidermal stripping a concern for kids?

A
  • decreased epidermal to dermal cohesion
  • tape, splints can pull epidermis off
  • infection risk
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36
Q

What should you think about with premies and wounds?

A
  • don’t have developed integumentary system: careful handling, swadling
  • IV leak can cause edema that can completely damage skin
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37
Q

What is aplasia cutis?

A
  • absence of epidermis and part of dermis in certain parts of body
  • -partial or full thickness
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38
Q

What is epidermolysis bullosa?

A
  • blisters all over body with minor friction (clothing, rubbing against someone)
  • avoid tight clothes, tape; safe handling
  • -gauze netting instead of tape
  • systemic infection usually is mode of death
  • do have it their whole lives
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39
Q

What do sickle cell wounds kind of remind you of?

A

venous wounds

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40
Q

How can lymphedema effect wounds?

A
  • increased cellulitis risk

- and you know the vascular stuff

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41
Q

How can chemo and HIV/AIDS effect wounds?

A
  • increase infection risk
  • -cellulitis
  • -sepsis
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42
Q

How can obesity effect wounds?

A
  • impaired skin barrier repair, higher pH, increase sweat gland activity
  • impeded lymph flow
  • insulin resistance syndrome
  • decreased vascularity of adipose tissue
  • excess tension on wound edges-dehiscence
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43
Q

When does dehiscence usually happen?

A

3-11 days after injury

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44
Q

How can you tx dehiscence?

A
  • abdominal binder

- Montgomery strap

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45
Q

What skin diseases can be aggravated by obesity?

A
  • irritant dermatitis
  • lymphedema
  • chronic venous insufficiency
  • plantar hyperkeratosis
  • diabetic foot ulcers
  • pressure ulcers
  • psoriasis (impaired blood flow->immature skin)
  • gout
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46
Q

What is plantar hyperkeratosis?

A
  • keratotic scar tissue on feet
  • brown, scaly
  • increased risk of wounds on feet
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47
Q

What is necrotizing fasciitis?

A
  • A strep or staph aureus-rapidly growing anaerobic bacterial infection
  • appears red, swollen, hot, painful
  • full thickness skin loss
  • high mortality
  • Fournier’s gangrene affects perineum: dead tissue has to be removed, skin grafts-don’t take welll on obese pts
  • -blisters
  • -fast growing
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48
Q

How does radiation effect wounds?

A
  • can set up fibrotic tissue due to injury of fibroblasts
  • decreased collagen production
  • destruction of cells in mitosis
  • vascular damage
  • decreased tolerance to bacterial burned, increased infection risk
  • decreased healing ability-stuck in proliferation phase
  • may have to stop radiation to heal
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49
Q

What meds can effect wounds?

A
  • NSAIDs: decrease inflammation; longer than 72 hrs-can’t move to proliferation
  • immunosuppressives: prostaglandins decreased (epithelialization-wound can’t close), WBC decreased (infection)
  • steroids: inhibit collagen synthesis (proliferation), topical steroids effect epidermal resurfacing; keep sutures in longer, protect skin longer
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50
Q

A1C and wounds

A

under 6.5-bad healing

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51
Q

pre-albumin an wounds

A

risk for pressure, venous, arterial, and diabetic wounds

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52
Q

How is malnutrition diagnosed?

***

A
  • serum albumin below 3.5 mg/dL
  • total lymphocyte count is less than 1800 mm
  • body weight decreases by 15%
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53
Q

diagnositc tests for arterial wounds

A
  • capillary refill >5 seconds
  • ABI
  • tcPO2
  • Doppler (should be triphasic, mono/bi means they don’t have good blood flow)
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54
Q

diagnostic tests for venous wounds

A

Duplex US

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55
Q

What are 5 instruments to monitor wound healing?

A
  • Sussman wound healing tool
  • wound healing scale
  • pressure sore status tool
  • wound healing scale
  • national pressure ulcer advisory panel pressure ulcer scale for healing
  • -only for pressure ulcers, in case you didn’t catch that
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56
Q

Wound assessment

A
  • cause, location (tissue function/structure), shape
  • pt concerns
  • place pt in same position each time
  • local wound characteristics (location, size, wound bed, exudate, wound edge, periwound, odor)
  • clinical signs of critical colonization/local infection
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57
Q

What are examples of:

  • clean wounds
  • clean-contaminated wounds
  • contaminated wounds
  • dirty and infected wounds
A
  • hernia repair
  • appendectomy
  • laceration, open fracture
  • perforated viscera, abscess, devitalized tissue
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58
Q

Primary intention

A
  • closure by direct approximation: sutures, steri strips, dermabond, stitches, staples
  • ex-surgical incisions and lacerations
  • within 6-8 hrs of injury
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59
Q

Suture removal

A
  • anywhere from 4-14 days
  • shortest: ear, face
  • longer: back, fingertip
  • can be delayed by age, mobility of part, steroids
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60
Q

pt education for wound sutures

A
  • protection, elevation
  • minimize direct sun, sunscreen for 1 year
  • hand hygiene, showers preferable, maybe gentle soap and rinsing, pat dry
  • keep covered with antibiotic ointment and dressing
  • visual inspection
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61
Q

wound cleaning techniques

A
  • linear: wipe top to bottom, start over wound and move out

- circular: wipe in concentric circles, starting over wound and moving outward

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62
Q

Secondary intention

A
  • wound left open to heal spontaneously

- ex-contaminated wounds, partial-thickness wounds

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63
Q

Delayed primary intention

A
  • delayed healing after several days: surgical closure after granulation tissue is present in the wound bed or spontaneous healing
  • primary and secondary combo
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64
Q

Who’s at risk for skin tears?

A
  • elderly
  • immunosuppressed
  • premies
  • renal insufficiency
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65
Q

How do you classify skin tears?

A

Payne-Martin

  • 1: skin tears w/out tissue loss; flap covers dermis within 1mm of wound margin
  • 2: skin tears with partial tissue loss
  • 3: complete tissue loss; epidermal flap is absent
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66
Q

How do you treat skin tears?

A
  • prevention: avoid sheering, proper transfers, remove leg rests from WCH, use paper tape, hold down skin as you remove tapes, slowly peel tapes
  • dressing
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67
Q

How do you assess pressure ulcer risk?

A

Braden Scale

  • sensory perception, moisture, activity, mobility, nutrition, friction and shear
  • low score=higher risk
  • but studies show Braden has insufficient predictive validity, poor accuracy in ICU; not effective for obese patients
68
Q

Staging ulcers

A
  • based on depth of soft tissue
  • must have complete visualization for accurate staging
  • long term care facilities are federally required to reverse stage
69
Q

How to not confused secondary lesions with pressure ulcers

A
  • excoriation: loss of epidermis, linear erosion, destruction by mechanical means-scratch, abrasion
  • denuded: loss of epidermis; urine, feces body fluids, wound exudate or friction
70
Q

Stage 1

A
  • nonblanchable erythema
  • epidermis and dermis intact
  • no tissue loss
71
Q

Stage 2

A
  • partial thickness skin loss involving epidermis and partial loss of dermis
  • superficial ulcer
  • presents clinically as an abrasion, blister, shallow crater
72
Q

Stage 3

A
  • complete loss of epidermis and dermis down to but not through underlying fascia
  • presents clinically as a deep crater with or without undermining of adjacent tissue
  • superficial full-thickness wound
73
Q

Stage 4

A
  • deep full thickness wound
  • extensive loss of epidermis, dermis, tissue necrosis, damage to muscle, bone or joint involvement
  • undermining and sinus tracts may be present
  • -between fascial plans
  • slough
74
Q

Deep tissue injury

A
  • “pressure related DTI”
  • skin usually intact
  • outcomes; healing without ulceration, eschar formation, subcutaneous necrosis under intact skin, infection of necrotic tissue
75
Q

Neuropathic ulcers: typical location, pain

A
  • plantar aspect of foot; areas of trauma on the foot

- painless-lack of protective sensation

76
Q

What do neuropathic ulcers usually look like?

A
  • round, punched out lesion
  • callus rim-dead tissue
  • granular bed
  • if they have vascular disease it may not look so red and granular
  • -amputation risk
77
Q

Neuropathic ulcers: glucose, basement membrane, ischemia

A
  • poor control; impaired immune response, poor tissue oxygenation; wounds love sugar; can’t due ABIs with hardened arteries
  • thickening-can’t close wound efficiently, no epithelialization; need skin substitute; defects in leukocyte function
  • regional; PVD
78
Q

Neuropathic ulcers: motor and sensation, ANS, risks

A
  • Charcot foot, claw toes, poor footwear can contribute; glycolization on tendons-not as flexible, elastic, lose mobility, risk for spontaneous rupture
  • dysfunction: anhydrous skin
  • osteomyelitis, fungal infections in nails, ulceration/amputation, potential for silent infection
  • -don’t see it, smell it or see blood/pus
79
Q

Charcot foot

A
  • painless, progressive, degenerative
  • microtraumas cause microfractures in joints
  • increased blood flow and bone reabsorption
  • osteoporosis
  • clinically appears painless, swollen, red
  • usually heal by casting
  • 10-15degree temp difference between feet (Charcot hot)
  • -offload and cast until temp difference is gone
  • risk for ulcers especially in mid and hind foot
80
Q

Other foot deformities with neuropathy

A
  • claw toe: stress on MT heads, dorsal aspect of PIP
  • hammer and mallet toes: pressure on distal end of toe
  • hallux limitus: decreased MTP extension causes great toe ulceration in neuropathic foot due to increased pressure during toe off
  • equinus: limitation of DF; increased stress of forefoot during gait
  • foot drop: peroneal nerve palsy; extended bed rest, adaptive shortening of Achille’s
81
Q

How do you classify neuropathic ulcers?

A

Wagner
-0-5
-based on depth from pre-ulcerative lesion to gangrene of foot requiring amputation
University of Texas-San Antonio: more detailed than Wagner, harder to work with? Stages A-D, Grades 0-3

82
Q

What does a monofilament of 4.17 mean? 5.07?

A
  • normal

- lose of protective sensation if they can’t feel 5.07 over 1 or 2 points

83
Q

How do you use the tuning fork for diabetic sensation exam?

A
  • 128 Hz fork
  • perpendicular to dorsal side of distal phalanx of first toe
  • do twice, but alternate with one mock application where the fork isn’t vibrating
  • at risk for ulceration with 2 out of 3 incorrect answers
  • -loss of protective sensation
84
Q

Describe arterial ulcers

A
  • commonly with gangrene
  • distal ends of toes; toes, feet, anterior tib
  • well circumscribed shape
  • no vascularization-pale granulation, little drainage
  • absense of hair, cold, low ABIs, weak or absent pulses
  • limited treatment options because they don’t have good oxygenation and nutrients
  • moderate to severe pain
  • skin shiny, dry, pale
85
Q

Describe venous ulcers

A
  • can’t pull drainage back up to heart-lots of exudate
  • hemosiderin staining
  • lipodermatosclerosis; edema
  • brigth red granulation
  • medial malleolus or above
  • minimal pain
  • irregular shape
  • warm foot
86
Q

What is hemosiderin staining?

A

brown staining on legs because of frequent ulcerations and injury; broken down RBCs that stain the skin
ONLY IN VENOUS ULCERS

87
Q

What is lipodermatosclerosis?

A
  • upside down champagne bottle
  • small around ankle, big around calf
  • edema that penetrates through skin that causes plaques of protein along skin
88
Q

How do we classify venous ulcers?

A

CEAP Classification of Chronic Venous Disease

89
Q

How do we score edema?

A

1+ barely perceptible depression

2+ easily identified depression, 30 secs

90
Q

How do we score ischemic pain with ambulation?

A

-indicates degree of circulatory inadequacy; graded exercise test at 2 mph with grade increases
>150m=mild impairment
50-150m=moderate impairment
<50m=severe impairment

91
Q

What are 2 methods to measure wounds?

A
  • linear measurements

- clock method

92
Q

How do you linearly measure wounds?

A
  • lenghtxwidthxdepth
  • greatest length x greatest width
  • wound edge to wound edge in a straight line in cm
  • depth: visible surface to deepest area
  • perpendicular lines, straight lines
93
Q

How do you measure using the clock method?

A
  • wound as a the face of a clock
  • 12 is head, 6 towards feet, 3 and 9 on the sides
  • on feet: heel is 12, toes are 6
94
Q

What are other ways to measure wounds?

A
  • trace shape on film
  • photography
  • computer digitalization of wound description
95
Q

What is tunneling?

A
  • channel/pathway extending in any direction from wound through subcutaneous tissue or muscles resulting in dead space with potential for abscess formation
  • most often seen with pressure ulcers
  • between fascial sheaths
  • caused by shearing
96
Q

What is undermining?

A
  • tissue destruction underlying intact skin around the wound margins/edges
  • caused by shearing
  • shelves
  • could be due to dressing in the wound
  • have to fill in undermining before the wound heals
97
Q

How do you measure tunneling/undermining?

A
  • measure at 12, 3, 6, 9
  • if there’s no undermining at those positions you don’t have to measure
  • measure depth/length with a qtip
98
Q

What’s the rule for wound healing time?

A

You want to see 40% wound healing in 4 weeks.

99
Q

What is a sinus tract?

A
  • blind ended rarct from surface of skin to underlying area or abscess cavity
  • caused by degradation of subcutaneous tissue in a linear manner
  • pack a sinus; dressing
  • -iodine string things
  • can used pulsed lavage
100
Q

What is a fistula?

A
  • abnormal communication between 2 or more structures or spaces
  • -rectum->skin
  • -skin->bladder
  • caused by dehisced wound or surgical incision; shearing forces
  • -infection
  • treat with surgery, negative pressure wound tx
  • drain a fistula
101
Q

What is periwound?

A

4cm of wound edge

102
Q

How do you inspect periwound?

A
  • color
  • induration: hardness; infection, scar tissue
  • warmth
  • edema-venous
  • hypo/hyper pigmentation
  • palpation: moisture, temp, turgor (dehydration, edema), pulses, mobility
103
Q

What does agranular tissue look like?

A
  • shiny with red bumps
  • infection cooking
  • want bumps=new capillaries sprouting
104
Q

Documenting periwound color

A 
1 pink or normal for ethnic group
2 bright red or blanches to touch
3 white, grey pallor, or hypopigmented (maceration, callous-both have to be removed)
4 dark red, purple, and/o non-blanchable
5 black or hyperpigmented
105
Q

Documenting induration

A

1 none present
2 50% around wound
5 >4cm in any area around wound

106
Q

What is granulation tissue?

A
  • growth of small blood vessels and CT into the wound cavity
  • bright, beefy, red, shiny, granular
  • may bleed easily
  • agranular
107
Q

What do you do for exposed structures?

A
  • tendons and bones

- keep tendon shiny and moist; grey, brittle, dry=dead tendon

108
Q

How do you document granulation?

A

-divide by quarters
1 skin intact or partial thickness wound
2 bright, beefy red; 75% to 100% of wound filled &/or tissue overgrowth
3 bright, beefy red; 25% of wound filled
4 pink, &/or dull, dusky re &/or fills <25% of wound
5 no granulation tissue present

109
Q

What is hypergranulation?

A
  • over healing; granulation tissue pops out
  • bad dressing, no health care
  • won’t heal-have to cross borders over so it can epithelialize
  • silver nitrate, foam dressing, silver stick thing
110
Q

How do you assess the base of the wound?

A
  • look for necrosis, eschar, slough, etc
  • adherance of tissue
  • document % of tissue type and location
111
Q

What do would base colors mean?

A
  • red: clean, healing, granulation-good
  • yellow: possible infection, needs cleaning, necrotic
  • black: needs cleaning, necrotic
112
Q

How do you assess wound edges?

A
  • contraction (want)
  • adherence (want)
  • epibole (don’t want): rolled edge, usually to undermining; due to bad dressing usually
113
Q

How do you document epithelialization?

A

1 100% wound covered, surface intact
2 75-100% covered and/or epithelial tissue extends >0.5cm into wound bed
3 50-75% wound covered and/or epithelial tissue extends to <25% wound covered

114
Q

Types of drainage

A
  • serous: clear, shiny, can be yellow; healthy
  • sanguineous: red, bloody; healthy
  • serosanguineous: pinkish-red; healthy
  • seropurulent: bright yellow, slight odor; infected
  • purulent: thick cloudy or opaque exudate; odor; infected
115
Q

Amount of drainage

A
  • none
  • scant
  • small/minimal: 75% bandage
  • ODOR: strong, foul, pungent, fecal, musty, sweet
116
Q

wound assessment: infection

A
  • classic s/s: induration, fever, edema, erythema
  • can include foul odor, viscous drainage, pain
  • interferes with collagen production (chronic inflammatory state)
  • cultures performed to determine treatment
  • quantity of bacteria/bioburden: quantitative culture (SOC), swab
  • -10 to the 5th
  • depends on number of organisms, virulence, host resistance
  • lab values: increased WBC (>10000), increased ESR (>15, >20), elevated quatitative ounts
117
Q

NERDS and STONES

A
  • NERDS: superficial increased bacterial
  • -nonhealing, exudating, red and bleeding, debris (yellow or black necrotic tissue), small
  • -topic, antimicrobial
  • STONES: deep compartment infection
  • -size is bigger, temp increased, probe to exposed bone, new satellite areas for breakdown, exudate erythema edema, smell
  • -topic, antimicrobial with systemic infection
118
Q

most common pathogens

A
  • staph: pt or health care providers skin
  • escherichia coli: contamination from intestinal contents
  • pseudomonas aeruginosa: anaerobes; contamination from whirlpool, hospital environment
119
Q

What are biofilms?

A
  • common cause of persistent infection
  • slimy
  • can’t get off with debridement
  • mist tx
120
Q

Cellulitis

A
  • lymphedema, vascular insufficiency, elderly at risk
  • -but anyone can get it
  • infection under dermis
  • can become septic
  • lymphanginitis: in lymphatic system; red streaking
  • IV antibiotics
121
Q

Osteomyelitis

A
  • probing to bone has better sensitivity and specificity than an MRI
  • can see infection on bone in radiographs
122
Q

infection vs inflammation

A
  • both are warm
  • infection: pus, odor, trauma, immunosuppressed,diabetic, pain increases with spread, asymmetric, usually single site, pain, swelling, erythema, advancing margin; IV antibiotics
  • inflammation: CV disease, RA, IBD origin; constant pain with onset of lesion; symmetric, multiple lesions, satellite breakdown, palpable purpura, local; should go through cycle in 3-4 days (infection takes longer)
123
Q

VTE vs cellulitis vs CHF

A
  • VTE: one leg bigger than other, recent surgery, throbbing/burning, sudden onset
  • cellulitis: streaking, red, patchy, irregular borders
  • CHF: pitting edema B, weight gain >10lbs , dyspnea
124
Q

contamination/colonization

A
  • in every wound
  • no local pain, no fever, normal smell, healthy granulation, minimal exudate, normal wound margin, healing wound
  • topical antimicrobial if risk of infection
  • no healing in 2 weeks: consider adding topical antimicrobial-could be a biofilim
125
Q

critical colonization/ocal infection

A
  • new or increased pain, may have odor,abnormal/absent granulation, increased serous exudate, possible tunneling or pocketing, static wound
  • no fever
  • topical antimicrobial
126
Q

infection

A
  • severe, systemic
  • severe or increased pain at wound and surrounding tissues; fever, systemic symptoms; foul or excessive odor; abnormal granulation or necrotic tissue; excessive or purulent exudate; tunneling, pocketing, warmth,maceration, edema, erythema; increased wound size
  • systemic antibiotics, topical antimicrobial for added benefit
127
Q

What is an antimicrobial?

A

-agent that kills or inhibits microorganisms

128
Q

What are the kinds of antimicrobials?

A
  • antibacterials
  • antiseptics
  • antifungals
129
Q

antibacterials

A
  • destroy or stop bacterial growth
  • narrow spectrum
  • bacitracin/neomyocin; gentamicin cream; sulfamyelon; silver sulfadiazine cream
130
Q

antiseptics

A

prevent or arrest growth by preventing replication, inhibiting activity or killing bacteria

  • broadly toxic, kills healthy cells
  • only used for infected or critically colonized wounds; inflammatory phase
  • reassess after 7 days
  • povidine iodine, acetic acid, hdrogen peroxide, Dakin’s solution
  • cytotoxicity-very cytotoxic
  • excessive use can result in allergies, superinfection
  • recheck frequently
  • can increase periwound if used on dressings
131
Q

antifungals

A
  • inhibits or kills fungi
  • diabetic pts, obese pts
  • nystatin, ketoconazole, miconazole nitrate
  • fungicidal vs fungistatic
  • limited absorption
  • need physician referrals
  • don’t work well with hyperhydrosis: obese pts
132
Q

bacitracin

A
  • petroleum based ointment
  • gram negative/positive cocci and bacilli; superficial and partial thickness wounds
  • can cause hypersensitivity reactions
133
Q

gentamicin cream

A
  • gram negative bacteria, strep and staph, folliculitis, impetigo
  • resistance is common
  • can cause hypersensitivity, ototoxicity, nephrotoxicity
134
Q

sulfamyelon

A
  • broad spectrum
  • partial and full thickness burns and wounds
  • may develop fungal growth; may inhibit keratinocytes and fibroblasts; potential systemic reactions
  • -use in inflammatory phase, not proliferation
  • pain with removal and application
  • not very successful
135
Q

silver sulfadiazine cream

A
  • broad spectrum, wounds of all types and sizes
  • resistance is rare
  • transient leukopenia, medication eschar, may be toxic to cells
  • -leukopenia: increased healing times, infection risk
136
Q

betadine

A
  • aqueous solution of povidone-iodine
  • -dilute it
  • fast acting, broad spectrum; kills gram positive/negative, MRSA, fungi,viruses
  • can effect fibroblasts, only use in inflammatory phase if critically colonized or infected
  • dries out wound bed
  • not usually recommended unless the pt is in hospice, or they have dry gangrene (autolytic debridement)
137
Q

hypochlorite solution

A
  • bleach; Dakin’s solution
  • 1/4 strength
  • effective against gram positive and microorganisms known to infect burns
  • whirlpools
  • infected, systemic infection
138
Q

Acetic acid

A
  • vinegar
  • bactericidal against gram positive and negative, esp pseudomonas
  • diluted
  • don’t use more than 7 days
139
Q

Hydrogen peroxide

A
  • Kim does not like this one at all; don’t use!
  • 3% solution provides effervescent cleansing through release oxygen; cytotoxic at 3%
  • doesn’t decrease bacteria levels
140
Q

What are iatrogenic factors?

A
  • the way the wound is physically managed
  • ex-poor wound management, removal of dressings, wound cleansing
  • poor use of topical antiseptics
141
Q

Types of debridement

A
  • mechanical
  • enzymatic
  • sharp
  • autolytic
  • bio-surgical
142
Q

Things you should never debride ever.

A
  • dry, stable eschar with no signs of infection
  • pyoderma gangrenosum: rare chronic inflammatory disease; if you debride it it keeps getting bigger and bigger (reintroducing inflammatory process)
  • -irregular jagged wound margins, halo erythema; most common on legs, dorsal hands, extensor forearm or face
  • -see with other illnesses: 75% w/ malignancy; RA, Crohn’s, ulcerative colitis, IBD; pts between 40-60
143
Q

ABI and debridement

A
  • assess before doing sharps debridement

- 1 calcified vessels if diabetic

144
Q

transcutaneous oxygen

A
  • tcPO2
  • pressure reflects amount of o2 coming out through skin, which in turn reflects amount of o2 delivered o skin by blood
  • 50-60 normal; 30 good healing
145
Q

Mechanical debridement

A 
NONSELECTIVE
-wet to dry dressings
-whirlpool
-pulsed lavage
-wound irrigation: after whirlpool, after some dressings, granulation tissue
SELECTIVE: blunt/sharp
146
Q

hydrotherapy indications: whirlpool

A
  • burns, traumatic, removal of adherent dressings, psoriasis, greater than 50% necrotic tissue, stage 3 or 4 ulcers with heavy amounts of necrotic tissue
  • not our favorite
147
Q

hydrotherapy indications: pulsed lavage

A
  • preferred
  • pressure ulcers, diabetic foot ulcers, venous insufficiency ulcers, deep or tunneling wound, infected surgical sites, heavily contaminated wounds, burns, multiple wounds
  • suction will stimulate wound healing
  • shown to be very effective
148
Q

pulsed lavage: what does it do?

A
  • cleanses and reduces bacteria and infection
  • promotes granulation-negative pressure suction
  • safe, effective ranges from 4-15 PSI (above that pushes bacteria back into dermis)
  • used for tunnels and undermining (special tips)
  • can put hot backs, but use even heating or you’ll burn the pt
  • change tips every time
  • no family, wipe everything down; gloves, gown, the works
149
Q

enzymatic debridement

A
  • enzymtic ointments to remove dead tissue (collagenase)
  • santyl
  • requires physician’s order
  • wound surface must be kept moist
  • burning sensation or erythema with application
  • selective
  • NOT antibacterial or antimicrobial
  • less painful than sharps debridement
  • make sure it’s not infected
  • cross-hatching
150
Q

Autolytic debridement

A
  • can use with enzymatic; decreased ABIs, decrease PCO2
  • in combo with sharps to speed up
  • breakdown of necrotic tissue by body’s own WBCs
  • moisture retentive dressings: hydrocolloids, hydrogels, nonadherent/contact layer, transparent films, hydrophillic/hydrofiber/speciality absorptives
  • ex-ripping off a bandaid
  • can have increased odors, exudate; lowers cost
  • very slow; selective, less painful
151
Q

Biologic/maggot debridement

A
  • processed maggot dressing
  • very selective
  • diabetic neuropathy does best
152
Q

Dry vs moist wound healing

A
  • dry: forms scab, eschar; inhibits epithelial cell migration; food for pathogens, increased infection risk; affects blood flow, cools off wound; increased pt discomfort
  • moist: facilitates autolytic debridement (WBCs); promotes angiogenesis; bathes cells in protein, enzyme rich environment; enhances epidermal cell migration; optimizes immune function; increases pt comfort, decreases dressing changes
153
Q

How to select the ideal wound dressing:

A
  • moisture balance
  • semi occlusive vs occlusive (minimize contamination from outside wound-barrier, pretend skin)
  • thermally insulate (takes 20-30 mins to heat up again)-stops angiogenesis if cold
  • nontraumatic
  • compatible with wound characteristics: infected wound, debridement
154
Q

What should you consider for the pt?

A
  • user friendly; family
  • minimal dressing changes
  • cost
  • minimal need for secondary dressing
  • remain in place for their lifestyle
155
Q

What are composite dressing?

A
  • combo of 2 or more distinct dressings
  • autolytic debridement
  • primary or secondary dressing, minimal to heavy exudate, granulation tissue, necrotic tissue
  • molds well, easy to apply and remove, but requires border of intact skin
  • ex- bandaid: had adherent part and non-adherent part
  • -foam dressing with silver
  • combines adhesive, wicking, antimicrobials
  • -easier for pt to use
156
Q

What do active dressings do?

A
  • stimulate and accelerate wound repair: brings in cytokines and growth factors to bring in collagen, etc to move into proliferative phase
  • -platelet derived growth factors
  • -epidermal growth factors: dermal substitute (delivers growth factor to wound via scaffold), recombinant growth factor via gel, freeze dried collagen to improve functionality of growth factors
  • not for infected or critically colonized wounds
  • can help biofilm
  • donor sites
157
Q

What are active dressings and what wounds are they used for?

A
  • promogran: pressure and venous ulcers
  • oasis: venous ulcer, recalcitrant sinus tracts
  • apligraf: diabetic foot, venous ulcers
  • dermagraft: diabetic foot ulcers
  • all made in a lab, MD applies
158
Q

What are absorbent antimicrobials?

A
  • Ag
  • Cadexomer iodine: slowly releases over 3-5 days; shown to be effective
  • Iodosorb, Acticoat
  • wound exudate reacts w/ gel or properties in dressing; provide moist healing environemtn; highly absorbent
  • concern with overuse of antibiotics
  • only with infected or critically colonized
  • vertical wicking>lateral wicking
159
Q

Caclium alginate

A
  • seaweed
  • highly exudating wounds; controls exudate-hemostasis
  • gel mixture formed when exudate reacts with dressing; provides moist healing environment
  • requires secondary dressing
  • be sure to wash out wound during dressing changes
  • -sheet better than fibers
160
Q

Foam dressings

A
  • absorb exudate; don’t use for dry wounds; moderate to heavy exudate
  • cushioning (stage 1 ulcers), insulation, semiocclussive (allows oxygen in), autolytic debridement
  • with or without adhesive border
  • curafoam, flexzan, allevyn
161
Q

Hydrocolloids

A
  • adhesive, occlusive, conformable
  • low to moderate exudate
  • moist healing environment; autolytic debridement; can increase reisk of maceration, more debridement->more exudate
  • don’t use if infected
  • angiogenesis
  • duoderm, tegasorb, curaderma
  • 3-5 days; remove when edges roll
  • rub to warm up first; not much cushion, doesn’t absorb much, odorous, can’t see wound bed
162
Q

Hydrogel

A
  • hydrate a dry wound bed-gives moisture back to wound
  • autolytic debridement for wounds with slough/eschar
  • minimal absorptive capabilities
  • cooling effec
  • requires secondary dressing
163
Q

Hydrophilic fiber dressing

A
  • synthetic
  • highly absorbent; provide moist environment
  • decreased maceration risk because it absorbs a lot
  • -lateral wicking; depends, diapers
  • not indicated for dry wounds
164
Q

nonadherent/contact layers

A
  • thin, nonadherent sheet, porous
  • protects wound base from trauma; protect tendon
  • primary dressing for partial and full thickness wounds, exudative wounds, donor sites, skin grafts
  • not recommended for dehydrated or eschar covered wounds
  • impregnated gauze: reduces adherence to wound bed, vaseline; adds moisture to wound
  • only greater than 50% necrotic, frequent dressing changes
  • in wound bed
165
Q

transparent films

A
  • maintain moist environment
  • can see wound
  • semiocclussive: oxygen in
  • waterproof
  • not absorbent, minimal exudate
  • IVs, secondary dressings-bioclusive, blister film, polyskin
166
Q

Medihoney

A
  • used in all stages, hard to heal wounds/burns
  • 100% active leptospermum honey
  • dry to light exudate, hard to dress areas
  • honeycolloid: light to moderate exudate
  • impregnated alginate pad: moderate to heavy exudate
  • -w/ calcium alginate
  • Cochrane report says no

MultiSystem Management (6 decks)

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