Wound Care Flashcards
Venous reflux
Venous valves do not close properly
Varicose veins
Walls enlarge so valves cannot funciton properly, causing blood to pool
Phase 1 (wound healing)
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
Phase 2 (wound healing)
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
Angiogenesis
New blood vessel growth from endothelial cells, fragile capillary buds grow into wound bed; new reddish, slightly bumpy tissue is called granulation tissue
Phase 3 (wound healing)
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.
Physical therapy role in wound care
- Identify type of wound
- Identify phase of healing
- Remove barriers to healing
- Facilitate the body’s own healing process
Acute wounds
- Laceration: tearing of soft tissue
- Abrasion: road rash
- Skin tear
- Blister
Chronic wounds
- Venous stasis ulcer
- Diabetic neuropathy
- Arterial insufficiency
- Pressure injury (decubitus injury)
- Infected incision
Venous stasis ulcer
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
CVI clinical presentation
- 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
Diabetic neuropathy
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
Clinical presentation of diabetic neuropathy
- 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)
Arterial insufficiency
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
Clinical presentation of arterial insufficiency
- 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
Arteriosclerosis
Thickening, hardening and loss of elasticity of arterial walls
Atherosclerosis
Type of arteriosclerosis
- damage to endothelial lining of vessels and formation of lipid deposits, eventually leading to plaque formation
Arteriosclerosis obliterates
Peripheral manifestation of atherosclerosis characterized by intermittent claudication, rest pain, and tropic changes.
- leads to ulceration
- smoking, DMII, HTN, hyperlipidemia, and hyperhomocysteinemia
Thromboangiitis obliterans
Buerger’s disease
- inflammation leads to arterial occlusion and tissue ischemia (esp young men who smoke)
Raynauds
Vasomotor disease of small arteries and arterioles that is most often characterized by pallor and cyanosis of fingers (and feet)
Ulceration
Peripheral sign of long-standing disease process associated with arterial insufficiency
Pressure ulcers
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
Pressure ulcers clinical presentation
- 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
Phases of wound healing
- Hemostasis/coagulation
- Inflammation
- Proliferation (angiogenesis/epithelialization)
- Maturation/remodeling
Pic
Pic
Chronic wound
- not proceeding through normal healing stages
- longer than ~4wks to heal (combo of time { observations)
Intrinsic factors affecting wound healing
- circulation
- nutrition
- sensation
- age
- comorbidities (immunosupression, HIV, DMII, PVD, cancer, smoking, obesity, pain)
Extrinsic factors affecting wound healing
- mechanical stress
- chemical stress
- infection
- meds (steroids, anti-inflammatory)
Wound assessment
Wound bed tissue (want to get % viable)
- black necrotic - yellow slough (resultant waste of healing process) - red granulation - tendon - mm - bone
Drainage (exudate)
What kind and how much
- serous (yellow or thin, clear)
- sanginous (bloody)
- purlent (yellow or green, thick)
- *none < scant < mod < heavy < copious
Periwound skin
The good stuff
- periwound: dry, moist, edema, friable
- wound edge: intact or macerated, attached or undermining, epibole (rolled edge)
Data collection- measurement
Clock method 12 = head Length * width * depth - when wound is angled, ensure perpendicular measurement longest-widest - trace then count boxes - photography NOT recommended
Wound categorization
- superficial: epidermis only
- partial thickness: epidermis and dermis
- full thickness: epidermis, dermis, and subcutaneous tissues
Pressure injury staging
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
Payne-Martin Skin Tear Classification
I. (Ia) linear no tissue loss. (Ib) skin flap completely covers dermis within 1mm
II. (IIa) <25% skin loss. (IIb) >25% skin loss
III. ?
Treatment of chronic wounds
- debridement of non-viable tissue
- moisture balance
- assessment of big picture (education, prevention, biomechanics, activity)
Selective debridement
- 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
Non-selective debridement
- mechanical: using physical modalities such as whirlpool or pulsed lovage to loosen and remove tissue
- low frequency ultrasound, MIST
Sharp debridement
Use of nonsterile scalpel, scissors, or forceps to remove non-viable tissue
- not surgical debridement, which may also remove viable tissue
Primary dressings
placed directly on the wound, must be absorbent and non adherent
- alginates - foam - collagen - gauze - hydrogel - hydrocolloid - transparent film - silver or honey
Secondary dressings
placed over the primary dressing to secure to body
- gauze - transparent dressing - compression - tape - coben
Gauze
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
Foam
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
Alginate
Highest absorption (seaweed)
- heavily draining wounds
- can be placed on or in wound
- decreases frequency of dressing changes
Silver dressing
Antimicrobial (more expensive)
Collagen
Absorb MMPs, for slow healing wounds
Hydrogel
Low absorbing, add moisture to wound by sheet or gel
- dry wound bed
- faster healing time with wet vs dry
hydrocolloid
occlusive dressings for autolytic debridement (contraindicated with infection)
- very thick, occludes air and holds in the heat
- moisture aides to remove slough
non-stick dressing
- need to minimize irritation when removing
- telfa - adaptic - silicone based
collagen
naturally occurring proteins in all three phases of wound healing
- main component of connective tissue (lower layer of skin or dermis and scar tissue
primary intention
wound edges are approximated by sutures, staples, etc (surgical incision)
- heals by epithelialization
secondary intention
unable to approximate edges due to too much skin loss
- heals by granulation, contraction, and re-epithelializaition (chronic wound or pressure ulcer)
wound contraction
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
hypergranulation
occurs when the new tissue grows up above the plane of the skin
- proud flesh
epibole
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
tunneling
can be caused by infection but wound is open underneath the skin.
contamination
presence of non-replicating organisms, host controls bacteria
- every wound is contaminated
colonization
presence of replicating organisms, no injury to host
critical colonization
presence of replicating organisms, host injury, healing stopped
infection
presence of replicating organisms, host invades tissue, blocks healing
- bacteria count greater than 1 x 105 organisms per gram of tissue
degrees of infection
- acute local infection
- chronic local infection
- systemic dissemination (sepsis)
bacterial infection
- cellulitis: hot, subcutaneous edema redness, widespread, poorly defined edges
- impetigo: contagious, staph or strep, itching
- abscess: pus filled cavity that needs to be drained
fungal infection
- ringworm: involves hair, nails, or skin. Ring shaped patches of scales/vesicles
- athlete’s foot: typically between toes, red, itching, pain
parasitic infection
from insect/animal contact
- scabies: mites that burrow into skin and itch
- lice: affect head, body, or genitals
viral infection
- herpes 1: simplex (cold sore)
- herpes 2: vesicular genital eruptions
- herpes zoster: shingles, chicken pox, virus in ganglia
- warts
wound cultures- swab
- least reliable
- detect surface contaminants
wound cultures- levine method
- swab placed on healthy granulation tissue
- enough pressure applied to extract fluid
- swab rotated 360 degrees, placed in transport media
wound cultures- quantitative biopsy
- most accurate
- often performed in OR bedside by MD
- method of hemostasis required
limitations to wound cultures
- > 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
inflammation purpose - duration - characteristics
- bring inflammatory cells to wound site - control bacteria and debris
- 1-3 days post injury (3-5)
- erythema - heat- edema - pain
diabetic wound treatment
- offloading: pressure MUST be removed before any healing can occur
- blood sugar control: MUST be maintained. The HA1C number tells us the long-range control, not just the snapshot of a blood sugar reading
venous wounds
- compression dressings: edema is contributing to the delayed healing. due to compromised valves and veins, the patient will ALWAYS need to wear the garments.
diabetic wound
- 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
CVI (from slides)
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
characteristics of CVI (slides)
- 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
CVA ulcers PTA role (slides)
- MIST - compression (multiple layers, higher, elastic)/pneumatic - EDUCATION venous anatomy, daily compression
PAOD (slides)
peripheral arterial occlusive disease (PAD/PVD)
- most adults have atherosclerosis by middle age
- 4% w/claudication
PAOD characteristics (slides)
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
PAOD PTA role (slides)
- clean wound environment - offload heels - NO debridement - optimize blood flow NO COMPRESSION - - exercise 3x/wk - rooke boot - wound vac - anodyne - hyperbaric o2
ankle brachial index
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
