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S5 PTA Special Topics > Wound Care > Flashcards

Wound Care Flashcards

1
Q

Venous reflux

A

Venous valves do not close properly

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2
Q

Varicose veins

A

Walls enlarge so valves cannot funciton properly, causing blood to pool

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3
Q

Phase 1 (wound healing)

A

Inflammation (day 1-10)

  • temporary repair initiated by coagulation and short-term decreased blood flow
  • spread of pathogens is slowed (edema, erythema, and drainage)
  • increased blood flow to oxygenate phagocytes
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4
Q

Phase 2 (wound healing)

A

Proliferation (day 3-20)

  • new tissue fills in wound as fibroblasts secrete collagen
  • skin integrity is restored by re-epithelialization and/or contraction
  • angiogenesis occurs
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5
Q

Angiogenesis

A

New blood vessel growth from endothelial cells, fragile capillary buds grow into wound bed; new reddish, slightly bumpy tissue is called granulation tissue

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6
Q

Phase 3 (wound healing)

A

Maturation/Remodeling (day 9-2 years)

  • granulation tissue is forming during phase 2
  • epithelial cells continue to differentiate into type 1
  • new skin has tensile strength that is 15% normal. Scar tissue is rebuilding but at best reaches 80% of original tensile strength.
  • underlying granulation tissue is replaced by less vascular tissue
  • DEEP WOUNDS: dermal appendages are rarely repaired (hair follicles, sebaceous and sweat glands, nerves) but instead are replaced by fibrous tissue.
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7
Q

Physical therapy role in wound care

A
  1. Identify type of wound
  2. Identify phase of healing
  3. Remove barriers to healing
  4. Facilitate the body’s own healing process
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8
Q

Acute wounds

A
  1. Laceration: tearing of soft tissue
  2. Abrasion: road rash
  3. Skin tear
  4. Blister
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9
Q

Chronic wounds

A
  1. Venous stasis ulcer
  2. Diabetic neuropathy
  3. Arterial insufficiency
  4. Pressure injury (decubitus injury)
  5. Infected incision
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10
Q

Venous stasis ulcer

A

Chronic venous insufficiency (CVI)

  • inadequate drainage of venous blood from a body part usually resulting in edema/skin abnormalities/ulcerations
  • majority of PVD also have CVI
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11
Q

CVI clinical presentation

A
  • swelling of LE relieved in early stages by elevation
  • itching, fatigue, aching, hot, heaviness in LE
  • skin changes (hemosiderin staining and lipodermatosclerosis)
  • fibrosis of dermis
  • wounds below medial malleolus with granulation and v wet tissue
  • s&s of lymphedema
  • nonpainful wounds
  • *compression
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12
Q

Diabetic neuropathy

A

Any diabetes-mellitus-related disorder of the peripheral or autonomic nervous system or cranial nerves.

  • many have arterial disease also
  • diabetic condition slows healing process
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13
Q

Clinical presentation of diabetic neuropathy

A
  • ulceration on WB surfaces of foot
  • usually anesthetic, round, over bony prominences
  • sensory neuropathy (pt unable to sense pain/pressure, risk of skin breakdown w/out pt awareness, and mechanical, repetitive stresses are most commmon causative factors of wounds)
  • motor neuropathy (loss of intrinsic mm, hammer-toe, claw-toe deformities due to poor weight distribution, foot drop)
  • autonomic neuropathy (decreased sweat.oil production, increased susceptibility to skin breakdown, heavy callus formation)
  • dysvascular symptoms (arterial disorders and reduced cardiac fxn, ischemia, impaired healing time, impaired transport of O2, antibiotics, and nutrients for healing)
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14
Q

Arterial insufficiency

A

Lack of adequate blood flow

  • PVD: any disorder that interferes with arterial or venous blood flow of the extremities caused by arterial insufficiency related to smoking, cardiac disease, diabetes, hypertension, renal disease, and high cholesterol/triglycerides, obesity
  • damaged in structure of arterial walls
  • more frequently lead to loss of limb and death
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15
Q

Clinical presentation of arterial insufficiency

A
  • LE wounds on lateral malleolus, dorsum of feet and toes
  • diabetes
  • abnormal nail growth, decrease leg and foot hair, dry skin
  • cool skin
  • painful wounds
  • necrotic and pale wound base lacking granulation tissue
  • skin around the wound may be black, mummified (dry gangrene)
  • decreased pulse, pallor on leg elevation, rubor when dependent
  • *no compression, bypass graft, exercise
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16
Q

Arteriosclerosis

A

Thickening, hardening and loss of elasticity of arterial walls

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17
Q

Atherosclerosis

A

Type of arteriosclerosis

- damage to endothelial lining of vessels and formation of lipid deposits, eventually leading to plaque formation

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18
Q

Arteriosclerosis obliterates

A

Peripheral manifestation of atherosclerosis characterized by intermittent claudication, rest pain, and tropic changes.

  • leads to ulceration
  • smoking, DMII, HTN, hyperlipidemia, and hyperhomocysteinemia
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19
Q

Thromboangiitis obliterans

A

Buerger’s disease

- inflammation leads to arterial occlusion and tissue ischemia (esp young men who smoke)

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20
Q

Raynauds

A

Vasomotor disease of small arteries and arterioles that is most often characterized by pallor and cyanosis of fingers (and feet)

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21
Q

Ulceration

A

Peripheral sign of long-standing disease process associated with arterial insufficiency

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22
Q

Pressure ulcers

A

Caused by unrelieved pressure to dermis and underlying vascular structures, usually between bone and support surfaces

  • decreased blood flow leads to cell death, tissue necrosis, and finally a visible wound
  • dermis can tolerate ischemia for 2-8hours, deep tissue only 2 hours
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23
Q

Pressure ulcers clinical presentation

A
  • first sign is blanchable erythema along with increased skin temp
  • progression to superficial abrasion, blister, or shallow crater indicates involvement of dermis
  • deep crater ulcer with minimal bleeding and infuriated and warm tissues. Escher formation marks full0thickness skin loss. Tunneling or undermining is often present
  • majority form over sacrum, coccyx, greater trochanter, ischial tuberosity, calcaneus, and lateral malleolus
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24
Q

Phases of wound healing

A
  1. Hemostasis/coagulation
  2. Inflammation
  3. Proliferation (angiogenesis/epithelialization)
  4. Maturation/remodeling
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25
Q

Pic

A

Pic

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26
Q

Chronic wound

A
  • not proceeding through normal healing stages

- longer than ~4wks to heal (combo of time { observations)

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27
Q

Intrinsic factors affecting wound healing

A
  • circulation
  • nutrition
  • sensation
  • age
  • comorbidities (immunosupression, HIV, DMII, PVD, cancer, smoking, obesity, pain)
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28
Q

Extrinsic factors affecting wound healing

A
  • mechanical stress
  • chemical stress
  • infection
  • meds (steroids, anti-inflammatory)
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29
Q

Wound assessment

A

Wound bed tissue (want to get % viable)

- black necrotic - yellow slough (resultant waste of healing process) - red granulation - tendon - mm - bone

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30
Q

Drainage (exudate)

A

What kind and how much

  • serous (yellow or thin, clear)
  • sanginous (bloody)
  • purlent (yellow or green, thick)
  • *none < scant < mod < heavy < copious
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31
Q

Periwound skin

A

The good stuff

  • periwound: dry, moist, edema, friable
  • wound edge: intact or macerated, attached or undermining, epibole (rolled edge)
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32
Q

Data collection- measurement

A 
Clock method 12 = head 
Length * width * depth 
- when wound is angled, ensure perpendicular measurement longest-widest 
- trace then count boxes 
- photography NOT recommended
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33
Q

Wound categorization

A
  • superficial: epidermis only
  • partial thickness: epidermis and dermis
  • full thickness: epidermis, dermis, and subcutaneous tissues
34
Q

Pressure injury staging

A

I. Red, non-blanchable, intact skin, warmer or cooler than near-by skin
II. Blister, epidermis is gone, like abrasion
III. Full-thickness damage of dermis, with necrotic tissue or slough
IV. Down to subcutaneous tissue (mm, tendon, bone)
Unstagable: can’t see wound bed d/t necrosis
DTI: deep tissue injury

35
Q

Payne-Martin Skin Tear Classification

A

I. (Ia) linear no tissue loss. (Ib) skin flap completely covers dermis within 1mm
II. (IIa) <25% skin loss. (IIb) >25% skin loss
III. ?

36
Q

Treatment of chronic wounds

A
  • debridement of non-viable tissue
  • moisture balance
  • assessment of big picture (education, prevention, biomechanics, activity)
37
Q

Selective debridement

A
  • surgical: performed under anesthesia by MD able to remove viable/non-viable tissue
  • sharp: sterile procedure to remove only non-viable tissue with topical anesthesia
  • enzymatic: use of prescriptin ointment (Santyl) to remove necrotic tissue/slough
  • autolytic: use of body’s heat using occlusive dressing
  • maggot: placement of sterile, medically prepared bottle fly larva
38
Q

Non-selective debridement

A
  • mechanical: using physical modalities such as whirlpool or pulsed lovage to loosen and remove tissue
  • low frequency ultrasound, MIST
39
Q

Sharp debridement

A

Use of nonsterile scalpel, scissors, or forceps to remove non-viable tissue
- not surgical debridement, which may also remove viable tissue

40
Q

Primary dressings

A

placed directly on the wound, must be absorbent and non adherent
- alginates - foam - collagen - gauze - hydrogel - hydrocolloid - transparent film - silver or honey

41
Q

Secondary dressings

A

placed over the primary dressing to secure to body

- gauze - transparent dressing - compression - tape - coben

42
Q

Gauze

A

Common, inexpensive, low absorbing

  • primary or secondary or used to clean wounds
  • pros: cheap
  • cons: can stick to wound causing pain and removal of healing tissue
43
Q

Foam

A

Moderate absorption, cushioning

  • ideal dressing / max protection
  • moderate absorption
  • minimizes maceration by wicking up rather than having absorbed drainage come in contact with intact skin
44
Q

Alginate

A

Highest absorption (seaweed)

  • heavily draining wounds
  • can be placed on or in wound
  • decreases frequency of dressing changes
45
Q

Silver dressing

A

Antimicrobial (more expensive)

46
Q

Collagen

A

Absorb MMPs, for slow healing wounds

47
Q

Hydrogel

A

Low absorbing, add moisture to wound by sheet or gel

  • dry wound bed
  • faster healing time with wet vs dry
48
Q

hydrocolloid

A

occlusive dressings for autolytic debridement (contraindicated with infection)

  • very thick, occludes air and holds in the heat
  • moisture aides to remove slough
49
Q

non-stick dressing

A
  • need to minimize irritation when removing

- telfa - adaptic - silicone based

50
Q

collagen

A

naturally occurring proteins in all three phases of wound healing
- main component of connective tissue (lower layer of skin or dermis and scar tissue

51
Q

primary intention

A

wound edges are approximated by sutures, staples, etc (surgical incision)
- heals by epithelialization

52
Q

secondary intention

A

unable to approximate edges due to too much skin loss

- heals by granulation, contraction, and re-epithelializaition (chronic wound or pressure ulcer)

53
Q

wound contraction

A

characterized by myofibroblasts at wound periphery

  • appear 4-6 days post injury
  • generate strong contractile forces on wound edges
  • wound edges draw closer to each other at rate that varies by location
54
Q

hypergranulation

A

occurs when the new tissue grows up above the plane of the skin
- proud flesh

55
Q

epibole

A

when the raw wound edge curls down to the wound bed

  • the wound thinks it closed and wound closure is delayed/stopped.
  • can be treated with sliver nitrate to re-open and detach the rolled edge
56
Q

tunneling

A

can be caused by infection but wound is open underneath the skin.

57
Q

contamination

A

presence of non-replicating organisms, host controls bacteria
- every wound is contaminated

58
Q

colonization

A

presence of replicating organisms, no injury to host

59
Q

critical colonization

A

presence of replicating organisms, host injury, healing stopped

60
Q

infection

A

presence of replicating organisms, host invades tissue, blocks healing
- bacteria count greater than 1 x 105 organisms per gram of tissue

61
Q

degrees of infection

A
  • acute local infection
  • chronic local infection
  • systemic dissemination (sepsis)
62
Q

bacterial infection

A
  1. cellulitis: hot, subcutaneous edema redness, widespread, poorly defined edges
  2. impetigo: contagious, staph or strep, itching
  3. abscess: pus filled cavity that needs to be drained
63
Q

fungal infection

A
  • ringworm: involves hair, nails, or skin. Ring shaped patches of scales/vesicles
  • athlete’s foot: typically between toes, red, itching, pain
64
Q

parasitic infection

A

from insect/animal contact

  • scabies: mites that burrow into skin and itch
  • lice: affect head, body, or genitals
65
Q

viral infection

A
  • herpes 1: simplex (cold sore)
  • herpes 2: vesicular genital eruptions
  • herpes zoster: shingles, chicken pox, virus in ganglia
  • warts
66
Q

wound cultures- swab

A
  • least reliable

- detect surface contaminants

67
Q

wound cultures- levine method

A
  • swab placed on healthy granulation tissue
  • enough pressure applied to extract fluid
  • swab rotated 360 degrees, placed in transport media
68
Q

wound cultures- quantitative biopsy

A
  • most accurate
  • often performed in OR bedside by MD
  • method of hemostasis required
69
Q

limitations to wound cultures

A
  • > 90% bacterial species do not grow under standard cultivation conditions
  • culturing favors lab weeds no necessarily the most dominant or influential species
  • excludes microbes that rely on community interactions, esp important in biofilms
70
Q

inflammation purpose - duration - characteristics

A
  1. bring inflammatory cells to wound site - control bacteria and debris
  2. 1-3 days post injury (3-5)
  3. erythema - heat- edema - pain
71
Q

diabetic wound treatment

A
  1. offloading: pressure MUST be removed before any healing can occur
  2. blood sugar control: MUST be maintained. The HA1C number tells us the long-range control, not just the snapshot of a blood sugar reading
72
Q

venous wounds

A
  1. compression dressings: edema is contributing to the delayed healing. due to compromised valves and veins, the patient will ALWAYS need to wear the garments.
73
Q

diabetic wound

A
  • typically planter surface, round shape
  • callus is formed from pressure
  • wound bed is clean but not the good granulation tissue needed fro next stage of healing
  • periwound skin has signs of maceration,
  • **sharp debridement, offloading, absorptive dressing
74
Q

CVI (from slides)

A

venous insufficiency - venous stasis disease - venous reflux disease

  • NEVER goes away
  • 500,000-1,000,000 have venous leg ulcers
  • ~50% americans have venous disease
75
Q

characteristics of CVI (slides)

A
  • shallow - irregular borders - heavily draining, weeping - firm edema - hemosidrin staining, hyperpigmentation - palpable pulses - usually located at medial lower leg and ankle “gaiter” - dull, aching pain relieved with elevation
76
Q

CVA ulcers PTA role (slides)

A
  • MIST - compression (multiple layers, higher, elastic)/pneumatic - EDUCATION venous anatomy, daily compression
77
Q

PAOD (slides)

A

peripheral arterial occlusive disease (PAD/PVD)

  • most adults have atherosclerosis by middle age
  • 4% w/claudication
78
Q

PAOD characteristics (slides)

A

well defined boarders - punched out - minimal drainage - trophic changes (hair, adipose, sweat gland loss) - toe tips, non-plantar surface of foot, lateral ankle - pain with elevation

79
Q

PAOD PTA role (slides)

A
  • clean wound environment - offload heels - NO debridement - optimize blood flow NO COMPRESSION - - exercise 3x/wk - rooke boot - wound vac - anodyne - hyperbaric o2
80
Q

ankle brachial index

A

systolic bp of dorsalis pedis artery or posterior tibialis artery OVER systolic bp of brachial artery
>1.0 normal
<0.8 arterial involvement (no compression)
<0.5 urgent referral
<0.45 no wound healing

S5 PTA Special Topics (13 decks)

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