L7 Wound Care Flashcards
Overlapping phases of healing in chronic wounds
Inflammatory (clean it up)
Proliferative (fill the void)
Maturation (remodel it)
Inflammatory phase steps summary
Vasoconstriction
Fibrin blood clot
vasodilation
neutrophils
macrophages
removal of bacteria and debris
Inflammatory phase
processes begin immediately upon tissue injury
simultaneously, several players work together to initiate and maintain this phase and the sequence of cells involved
includes coagulation cascade, AA pathways, creation/release GF, cytokines
Purpose of inflammation
clean wound of debris and stimulate fibroblast cells to produce collagen
Inflammation is clinically characterized by
redness, heat, swelling, pain, loss of function
Proliferative phase summary of steps
Macrophages release cytokines that signal endothelial cells, growth factors, epithelial cells
Causes new blood vessel growth, re-epithelization, fibroblasts–> collagen–> granulation tissue
Proliferative phase
- begins 2-3 days after wound, signaled by fibroblasts
- Fibroblasts migrate from wound margins using fibrin matrix (from inflammatory)
- Fibroblasts become dominant cell type, reaching peak at 7-14 days
- Collagen is a major component of acute wound connective tissue
- With cellular proliferation, angiogenesis in granulation occurs b/c of budding vessels
Results of proliferative phase
granulation tissue
contraction, epithelialization of wound
Granulation tissue
red, bumpy, doesn’t bleed easily
made of collagen, capillaries, ECM
Maturation phase summary steps
Collagen
Deposition
Remodeling
Increase tensile strength
scar reduction
Maturation phase
- Collagen production begins in 6 weeks
- Collagen is depostied randomly in acute wound granulation tissue, but remodeling into more organized structure occurs during maturation, increasing strength
- During scar formation, collagen 3 is replaced by type 1
- Wound eventually closes by migration of epithelial cells from wound edge. Once fibroblasts contact each other, causes myofibroblast formations
2 year post injury, tensile strength is
80% of normal strength
wound strength will never exceed this
Wound Exam
- Location
- Behavior of symptoms
- wound cultured
- wound type
- Size/depth
- signs of infection
- dry or draining
- swelling
- skin discoloration
- vascular exam
- skin nutrition
Hypergranulation tissue
also called proud flesh
extends above the surface of surrounding epithelium
has to be removed
Inflammatory exudates
- Hemorrhagic = surgery
- Seosanguinous = yellow, 2-3 days after injury
- Serous = watery, early stage of inflammations
- Purulent = cloudy pus, indicates infection
Wound eval steps
- hx of current wound
- pertinent medical history
- subjective and objective exam
Pertinent medical history
what impacts wound healing? what are the barriers to healing?
diabetes
PVD
hypertension
smoking
meds (glucoco, immunosupp)
last tetanus shot
allergies
nutritional status
activity level
wound culture
Best glucose level for best healing
<180 mg/dl
Methods to measure size/depth of wound
- plnimetry = wound tracing
- ruler method
no gold standard!
Negatives of planimetry
difficult to race wound edges
doesn’t measure wound depth
Ruler method
dimensions with a ruler using clock method
12 to 6, 3 to 9
depth is done with q-tip
Signs of infection
- Odor
- Colored Drainage
- Fever
- Cellulitis
in a nonhealing wound, you must consider infection
Odor
pseudomonas smells sweet
proteus smells like urine
Colored drainage
pseudomonas is greenish
proteus is yellowish
Cellulitis
diffuse infection of subcutaneous layer of skin, usually spreads rapidly
caused by bacteria
Types of chronic wounds
pressure injuries
venous stasis ulcers
arterial insufficiency ulcers
neuropathic ulcers
Purpose of wound care (no matter the type)
remove infection
remove devitalized tissue
promote healing
Pressure Injuries
localized areas of cellular necorsis resulting from prolonged, unrelieved pressure between any bony prominence and an external obkect, injury can present as intact skin or open ulcer
the unrelieved pressure results in ischemic hypoxia and damage to underlying tissue
Incidence of pressure injuries
1.5 million a year
in long term care, regulatory agencies use development of pressure injuries as an indicator of QOC to patients
Tip of the iceberg effect
Begins with ischemia first in
tendon, then subcutaenous, dermis, epidermis
Contributory factors to pressure injuries
prolonged pressure, shear forces, friction, maceration, repetitive stress and nutritional deficiencies
RF for pressure injuries
elderly, debilitated, immobilized
sitting for long periods
inability to reposition every 20 to 30 min
sitting in commode chair >20 min
exposure to unrelieved pressure during operation
decreased blood flow from hypotension
decrease sensation
cognitive impairment
loss of bowel/bladder control
Maceration
skin changes due to excessive moisture
For pressure injury prevention, do not raise HOB
> 30°
CP of Pressure Injuries
occurs over bony prominences
most common in sacrum, buttocks, hips, heels
color: red, brown, yellow
infection
painful if sensation is intact
inflammatory response with necrotic tissue
Stage 1 Pressure Injuries
nonblanchable erythema of intact skin whose indicators as compared to an ajacent or opposite area on the body
Stage 1 may include changes:
skin temp
tissue consistency-firm or boggy
sensation
persistent redness, NOT purple or maroon
Stage 2 Pressure Injuries
partial thickness skin loss with exposed dermis,
shallow open ulcer with red or pink wound bed without slough.
may also present as intact or open serum filled blister. no bruising
Stage 3 pressure injury
full thickness skin loss
adipose is visible
granulation tissue and rolled edges are present
can include undermining and tunneling
no fascia/muscle present
slough/eschar are present
Stage 4 pressure injury
full thickness skin and tissue loss
exposed muscle, bone, tendon
includes sinus tracts or tunneling
Epibole
rolled wound edges
Osteomyelitis
inflammation that occurs in the bone
Undermining
deeper wound than surface edge depth
Sinus tracts
most common in surgical or neuropathic wounds
present in stage 4
measured with q-tip
Unstageable pressure ulcer
obscured full-thickness skin and tissue loss
covered by slough and/or eschar
the true depth cannot be determined until slough is removed
Stable eschar on heel
serves as body’s natural cover and should not be removed
Deep tissue pressure injury
persistent non-blanchable deep red, maroon, or purple localized area
intact or non intact skin or epidermal separation revealing dark wound bed or blood filled blister
damage of underlying soft tissue
often an evolution of stage 3/4 ulcer
must document color
educate about wound evolution
Vascular Ulcers Types
Venous
Arterial
Neuropathic
Mixed
not the same staging as pressure injuries
Venous ulcers
Associated with chornic venous insufficiency, valvular incompetence, venous HTN. Most common chronic wound
RF: HF, LE muscle weakness, prolonged standing, pregnancy, obesity, LE trauma, immobility, family hx, advancing age
Location of venous ulcers
can occur anywhere in leg, most common site is area over medial mallelous
usually bilateral
How does heart failure lead to venous ulcers?
the heart fails, right ventricle backs up into the body, leading to a lot of edema, and tehn venous stasis ulcers
Dynamic insufficiency
problems with:
capillary filtration
osmotic uptake of fluid
Mechanical insufficiency
problems with lymphatic drainage
CP of venous stasis ulcers
- normal pulses b/c arterial system is intact
- no pain to aching/throbbing, especially when body part is below heart
- Color is normal or bluish
- Temperature is normal
- Edema is usually marked
- Many skin changes like pigmentation from dying hemoglobin, drying skin, thickening of skin
- Ulceration: especially over medial ankle, WET
- Gangrene is absent
Common looks of venous ulcers
usually present as shallow, irregular, or oval in shape, with macerated borders. Wet/moist skin
color is red, brown, purple. Edema and scally
Treatment of venous insufficiency ulcers
- CONTROL EDEMA with leg elevation and compression therapy
- Topical therapy
Prevention of venous ulcers
no smoking, adequate nutrition, skin care, optimize venous return , compliance with meds like digitalis and diuretics
Topical therapy for venous ulcers
bandages, pressure garments, unna boot, mechanical pump
helps to promote favorable healing environment by removing exudate, infection, necrosis. also protects surrounding skin to avoid maceration
Whenis a Wound culture required?
required after 2-4 weeks of failing to respond to therapy or if it appears infected
Unna Boot
medication-impregnated dressing containing zinc oxide paste, calamine lotion, glycerin, gelatin
purpose is edema control, skin care, protection
less effective in non-ambulatory patients, espeically uncomfortable in hot weather
changed every 7-10 days
can help stop scratching and itching
Unna boot technique
Reduce local edema
apply unna boot with 4 layers w/overlapping spiral technique
last ace bandage layer applied firmly from foot to knee
Compression pump
goal to decrease edema, ideally would do this prior to unna boot
intermittent compression unit designed to reduce swelling in lower extremity
Arterial insufficiency ulcers
associated with chronic arterial insufficiency, arteriosclerosis obliterans, atheroembolism, hx of minor non healing trauma
most worrisome because of threat of limb loss
RF for Arterial ulcers
smoking, HTN, hyperlipidemia, diabetes, advanced age
Location of arterial ulcers
can occur anywhere in leg, most common in small toes, feet, on boney areas of trauma
CP of arterial ulcers
- Poor/absent pulses
- Severe pain; intermittent claudication that often progresses to pain at rest
- Color is pale on elevation, dusky rubor on dependency
- Cool temperature
- Trophic skin changes, loss of hair in feet/toes, thickened toenails
- Gangrene may be present adjacent to ulcer
Dusky rubor
redness below heart
due to increases in vasodilation
Arterial ulcers treatment
Patient ed
Control underlying medical problem of BP, A1c, diet, and weight
topical therapy
Prevention for Arterial ulcers
no smoking
diabetes control
compliance w/meds
proper fitting footwear
Patient ed for arterial
neutral or dependent position for legs
avoid sitting w/crossed legs, exposure to cold/friction/tight clothing, stop moisture between toes, don’t walk barefoot
Topical therapy for arterial ulcer
promote favorable healing environment by removing excessive exudate, infection, necrosis
wound cleansing with saline
some debridement may be contraindicated for necrotic
non-necrotic require topical dressings
protect surrounding skin
When peripheral pulses are present (with alterial ulcers)
hydrogels, collagens, alginates, medicated creams
occlusive dressings should be used with caution
When should you get a vascular consult?
ABI <.5
pain is increasing
ulcer fails to respond to treatment in 2-4 weeks
Complications of arterial ulcer treatment
infection, gangrene, osteomyelitis, amputation
clinical manifestations of infection are likely to be subtle, due to reduced blood flow
Tests for vascular ulcers
PTs must use tests to detect and quantify peripheral arterial disease (PAD)
- LE pulses: palpate or doppler
- Dependent rubor
- ABI
Dependent Rubor/redness
- position patient supine with lower extremity elevate 45° for 1 min or until foot blanches
- Observe color of foot
- Instruct patient to sit up and dangle leg
- Record time for color to return to foot
Capillary filling time
normal = 10-15 s
mod ischemia = 15-25 s
Severe ischemia = 25-40 s
Very severe ischemia = 40s+
ABI Method
- position patient supine w/hips in slight ER, knees slightly flexed and lateral borders of foot in contact with table/bed
- Record brachial SBP
- Place BP cuff around leg just above malleoli and record SBP
- Calculate ABI: Ankle SBP (higher value)/ Arm SBP (higher value). Choose the smaller ratio for the ABI
> 1.4 ABI
vessel calcification/hardening
refer to vascular specialist/surgeon
1.0-1.4 ABI
normal
.9-1.0 ABI
acceptable
.8-.9 ABI
some arterial disease/occlusion
treat risk factors
.5-.8 ABI
moderate arterial disease/occlusion
refer to vascular specialist
<.8 ABI
No LE compression for wound healing
refer out
<.5 ABI
severe arterial disease/occlusion. usually pain at rest, wounds may need to be revascularized heal
refer out
Neuropathic ulcers
caused by diabetes, associated with arterial disease and peripheral neuropathy, caused by repetitive trauma on insensitive skin
Location of neuropathic ulcers
occurs where arterial ulcers usually appear, or where peripheral neuropahty appears (plantar aspect of foot)
CP of Neuropathic ulcers
- typically not painful due to sensory loss
- pulses may be present or dimished
- absent ankle jerks common
- sepsis common, gangrene may develop
- surrounding calluses are typical
Prevention of neuropathic ulcers
no smoking
control A1C ,7%
diabetic foot screen
routine professional foot care
compliance with meds
proper-fitting footwear
control underlying medical problem
Patient ed for neuropathic ulcers
exposure to cold, friction, moisture between toes, walking barefoot, external use of heat
Topical therapy for neuropathic ulcers
- promote favorable healing
- WOund cleansing with saline
- Necrotic tissue–surgical consul, autolysis, mechanical
- Non-necrotic ulcers–absorptive dressings
- Shallow ulcers–hydrocolloid, moist gauze
- Protect surrounding skin to avoid maceration
Complications of neuropathic ulcers
infection, gangrene, osteomyelitis
Infection control
ABX tx is prescribed if indicated
oral meds: antimicrobials, anti-inflammatories, analegesics
Topic meds: NSAIDs, lidocaine, silver nitrate (anti-inflamm, anesthetics, antimicrobials)
VAC
Vacuum assisted closure
open-cell foam dressing placed into wound
also called negative pressure wound therapy
provides controlled subatmospheric pressure
helps control edema, increase local blood flow, remove infectious material
you can mobilize with the patient
Surgical intervention for chronic wound care
indicated for excising an ulcer, enhancing vascularity and for resurfacing wounds, preventing sepsis and osteomyelitis
may be indicated for Stage 3 and stage 4 pressure ulcers
revascularization procedures may be done for neuropathic and arterial ulcers
Hyperbaric Oxygen Therapy
patient breathes 100% O2 in seated, full body chamber with elevated atmospheric pressure
helps reverse tissue hypoxia and facilitates wound healing due to enhacned solubility of O2 in blood
Used for nonhealing wounds that do not have adequate oxygenation
should NOT be used for untreated pneumothorax, some antineoplastic medications
Is HBOT effective for chronic wounds?
-Ulcer healing and rate of minor amputation were not affected HBOT
-significant reduction in risk of major amputation with HBOT
-HBOT improved healing rate short term in diabetic foot ulcers
-helps with mixed ulcers
-possible decrease in venous ulcers
Wound cleansing
removal of loose cellular debris, metabolic wastes, bacteria and topical agents that may slow healing
goal = obtain clean wound without trauma to new granulation tissue
wound should be cleaned initially and at each dressing change
Do not use the following on chronic wounds
some common topical cleansing agents are cytotoxic to healing tissues
1.iodine
2. hydrogen peroxide
3. weak bleach solution
4. dakin’s
5. acetic acid
You should NOT use ____ for wound cleaning
harsh soaps
alcohol based products
harsh antiseptics
Use ____ for most ulcers
saline
Even if a wound does not look dirty, it needs regular cleaning because
bacteria can form a biofilm
biofilm = layer of bacteria bound together by compounds they secrete that protect the colony and help it grow
bacteria are more resistant to antibiotics when living in a biofilm
Methods of wound cleansing
- minimal mechanical force
- irrigation
- Hydrotherapy
Minimal mechanical force
cleanse with gauze, cloth, or sponge
clean wound enough to enhance healing w/out causing trauma
Irrigation
can use a syringe, squeezable bottle with tip or battery powered irrigation device (pulsatile lavage)
Pulsatile lavage is usually with suction; Safe and effective pressures are 4-15 psi. goal is to loosen wound debris and remove it by suction
Hydrotherapy
not gold standard
indications: wounds/ulcers with large amounts of exudate, slough, and necrotic tissue
increases circulation, assists in wound debridement, and/or removal dressings
must be discontinued when ulcer is clean
Wound Debridement
removal of necrotic or infected tissue that interferes with wound healing
allows exam of ulcer and determination of wound extent. Decreases bacterial contamination in wound. Decreases spread of infection
5 methods
Autolytic
selective method of natural debridement that occurs under occlusive or semiocclusive moisture retentive dressings
Indications = all necrotic wounds in medically stable people
Contraindications: infected wounds
Enzymatic debridement
selective method of chemical debridement that promotes liquefication of necrotic tissue by applying topical preparations of proteolytic/collagenolytic enzymes to tissues
Indications: all moist necrotic wounds, eschar after cross-hatching
Contraindications = ischemic wounds
Eschar scoring
diagonal lines
Eschar cross-hatching
creating squares with opposite lines from the scoring
enzymatic debrider is placed on top
Mechanical Debridement
nonselective method that removes foreign material and dead or contaminated tissue by physical means. May also remove healthy tissue
includes wet to dry gauze dressings, wound vac, whirlpool
indications: moist necrotic tissue
contraindications = clean, granulated wounds
Conservative sharp wound debridement
selective method using sterile instruments that sequentially removes only necrotic tissue without anesthesia, resulting in little/no bleeding induced in viable tissue
includes: scalpel, scissors, forceps, silver nitrate stick
indications: scoring, cross-hatching, excision of eschar
contraindications: clean wounds, patients with clotting disorder, sepsis
Silver nitrate uses
regenerative effect (growth of good cells)
cauterization (stop growth of bad cells)
Surgical/sharp wound debridement
more efficient method, nonselective and performed by surgeon using sterile instruments in operative procedure in which pt is usually under anesthesia, removes most/all of necrotic tissue, and some healthy
indications = advancing cellulitis with sepsis, immunocompromised, infection
Contraindications = when OWL cannot be improved, underlying systemic disorders
Wound Dressings
topical products that protect wound from trauma and contamination, absorb drainage, may debride necrotic tissue and enhance healing
GOAL is to provide warm, moist healing environment
Simple Principles for wound dressings
if wound is dry = apply a moistening dressing
if wound is too wet = apply an absorptive dressing
Transparent films
Tegaderm, opsite
minimal exudate
skin donor sites, IV sites
non absorptive
secondary dressings are not required
Hydrocolloid Dressings
Duoderm, Curaderm
-not transparent, can’t see wound
-there’s characteristic odor w/yellow exudate that looks similar to pus when removing bandage
-causes smell when removed
-maintains moist environment
-comfortable, reduces pain, easy to apply, conformable
-for partial thickness, pressure injuries
-for mild exudate
Hydrogel dressings
minimal to moderate exudate
partial and full thickness wounds
most require a secondary dressing
Foam dressings
moderate exudate
provides padding, protection, insulation
-stops maceration of wound
-sometimes has antimicrobial
-non transparent
Alginate dressings
absorbs 20x its weight in exudate
expensive
mod to large amounts of exudate
easy to apply
requires secondary dressing
Black wound
Clean = minimal mechanical force or irrigation
Debride = yes, cross hatching and forceps, enzymatic solution, or biological, mechanical methods
Dress = hydrocolloid or hydrogel. Wet to dry gauze after enzymatic solution
Yellow wound
Clean = pulsed lavage w/suction or minimal mechanical
Debride = yes, conservative sharp, mecahnical
Dress = calcium alginate, gauze, wt to dry
Red Wound
Clean = very light mechanical, low pulsed lavage
Debride = no
Dress = hydrocolloid/hydrogel, foam
Edema management
leg elevation and exercise
compression therapy w/wraps, bandages, stockings, pump therapy
Nutrition
malnutrition and dehydration impede wound healing
nutritional assessment should be performed every 3 months to ensure adequate protein and caloric intake
patients need aggressive nutritional support
some vitamin deficiencies impede wound healing (C, A, zinc)
Patients at high risk for poor wound healing
weight loss >15-25% of body weight
protein depletion = based on albumin
Injury/wound prevention and reduction
- Daily skin inspection
- Positioning to relieve pressure and allow tissue reperfusion
- skin protection techniques
- pressure-relieving devices
- avoid maceration damage
- patient/caregiver educaiton
