Prevention and Treatment of Pressure Ulcers

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PREVENTION AND TREATMENT
OF PRESSURE ULCERS
By
Holly Ferguson, PT, WCC
PURPOSE
The purpose of this self-learning module is to help guide
nurses performing skin assessment and care according to
best practice.
At the end of the module, the nurse will be able to:
• Identify skin assessment protocol
• Identify risk factors for developing pressure ulcers
• Identify at least 3 things to help prevent pressure
ulcers
• Identify the SJH nursing and interdisciplinary team
resources
• Identify ways to manage and treat pressure ulcers
What is skin?
Skin Structure and Function
NPUAP DEFINITION
(National Pressure Ulcer Advisory Panel)
a localized injury to the skin and/or underlying
tissue usually over a bony prominence, as a
result of pressure, or pressure in combination
with shear and/or friction.
PRESSURE ON VESSELS
Unrelieved
pressure on the
skin squeezes tiny
blood vessels,
which supply the
skin with nutrients
and oxygen. When
the skin is starved
for too long, the
tissue dies, and a
pressure ulcer
develops
BONY PROMINENCES
COMMON SITES
CLINICAL PRESENTATION
1. Rounded, crater like shapes with regular edges
2. Over bony prominences, but can take on the shape of
the bone (malleoli vs sacrum)
3. Usually dark regular base that do not bleed easily
4. 95% over sacrum/coccyx, trochanter, IT, heel and
lateral malleoli
STATISTICS
• 70% occur in people over 65
• Most common sites SACRUM AND HEELS
• Shoulder, heel, and ear were the favorite sites
of newly developed PrUs
EPIC ORDER SET:
PRESSURE ULCER PREVENTION
STAGES/PROGRESSION
4 stages depending on amount and time of ischemia
1. Hyperemia (redness) will occur within 30 minutes of
sustained pressure. If the Pressure is removed the
hyperemia will disappear in approximately 24-36 hours
2. Depending on a number factors (including general health)
ischemia begins in 2-6 hours of sustained pressure
3. Texture usually feels hard
4. Necrosis begins ~6 hours after sustained pressure.
5. At this stage skin appears blue or greyish and may be
indurated. Recovery at this stage is variable.
6. Finally, if pressure continues, ulceration occurs.
STAGES
Pressure Ulcer Staging
STAGE 1: Skin is intact and shows
a non blanchable, localized redness
over a bony prominence. Redness
remains after pressure is released.
Signs and symptoms may include
pain, firm, soft, warm or cool
compared to adjacent tissue. –
EPIDERMIS
STAGE 3: Skin break with deep tissue
involvement down to subcutaneous
layer. Full thickness tissue loss.
Subcutaneous fat may be visible. Bone,
tendon or muscle is not exposed. Slough
may be present but does not obscure the
depth of tissue loss. May include
undermining and tunneling.
STAGE 2: Considered partial thickness
wound. Superficial break in the epidermis or
partial thickness loss of dermis. Presents as a
shiny or dry shallow ulcer without slough or
bruising. This stage should not be used to
describe skin tears, tape burns, perineal
dermatitis, maceration or excoriation. Bruising
indicates suspected deep tissue injury.
STAGE 4: Skin break with deep tissue
involvement down to the bone, tendon, or
muscle. Full thickness tissue loss with
exposed bone, tendon or muscle. Slough or
eschar may be present on some parts of the
wound bed. Often include undermining and
tunneling. Stage 3 and 4 are considered Full
Thickness wounds.
15
STAGES
Pressure Ulcer Staging
 Unstageable: Full thickness tissue
loss in which the base of the ulcer
is covered by slough (yellow, tan,
gray, green or brown) and/or
eschar (tan, brown or black)
in the wound bed.
 Suspected Deep Tissue Injury (SDTI):
Skin is purple. Level of tissue
necrosis is suspected to be deep.
17
*difference between stage II and stage III – stage
II will never have slough
*Never back stage a PrU; document a “healing
stage III” not a “stage II”
HEELS
• Second most common site for PrU’s, and most
common site of DTI
• Color reflects the degree of DTI:
– Red - hyperemia and ischemia
– Purple – infarction
– Black - necrosis
UNAVOIDABLE PRESSURE ULCERS
• According to NPUAP: An individual develops a
PrU even thought the provider had evaluated the
individual’s clinical condition and pressure ulcer
risk factors’ defined and implemented
interventions that are consistent with individual
needs, goals and recognized standards practice;
monitored and evaluated the impact of the
interventions; and revised the approaches as
appropriate
• “Kennedy Terminal Ulcers”
KENNEDY TERMINAL ULCERS
•
•
•
•
•
•
•
Ulcers that some people get as they are dying
Usually on the sacrum
Usually pear shaped
Colors vary
Irregular borders
Come on suddenly
Geriatric phenomenon
KENNEDY TERMINAL ULCERS
CONTINUED
• Often confused for dirt or dried stool in the
beginning, and providers try to wash it off
only to find it is under the skin
• In the beginning it can look like the skin got
scraped off in a bad abrasion
• Progresses rapidly (over a matter of hours)
KENNEDY TERMINAL ULCER
KENNEDY TERMINAL ULCER
KENNEDY TERMINAL ULCER
DOCUMENTATION FOR UNAVOIDABLE
END OF LIFE ULCERS
• Complete wound closure may not be realistic goal, wound
may improve but due to progressive or irreversible
underlying medical condition, complete healing is not
expected.
• The wound represents an additional body systems failure
for a person who is progressing towards death
• Patient has been losing weight despite appropriate
nutritional interventions
• A treatment plan emphasizing minimizing pain and odor
related to the dying process
• Repeated hospitalizations or ED visits in past 6 months may
indicate overall decline or instability
*from Clinical Practice Guidelines, American Medical Directors Association, CMS guidelines
TIP OF THE ICEBERG
MORE TO IT THAN MEETS THE EYE….
MUSCLE RESPONSE
1. Muscle damage is more significant than skin
damage because muscle is more sensitive to
the effects of ischemia
2. Pressure is highest where the muscle or
fascia contacts the bone
3. The ulcer starts at the bone-soft tissue
interface and extends towards the skin
4. An ulcer is like an iceberg – has a small visible
surface with a more extensive unknown base
“Assess the whole person; not just the hole
in the person”. ~ Gary Sibbold
29
EXTRINSIC FACTORS
FRICTION
1. Rubbing 2 surfaces against another
2. Friction without pressure causes damage to
only the epidermis and upper dermal layer
(think sheet burn)
SHEAR
1. Friction + Gravity = Shear
2. Think elevation of head of bed and person
sliding down in bed or sliding down in reclining
chair
3. Shear stretches and tears vessels, which reduces
the amount of pressure necessary to cause
ischemia and deep tissue injury
4. Shearing can cause undermining and tunneling
*blisters
DRYNESS
• Stratum corneum normally has 10-15% moisture
• When the moisture drops below 10% skin
becomes cracked and fissured, compromising
barrier function and increasing susceptibly to
injury
• Lotions/creams that have urea or lactic acid can
increase kin surface water-binding capacity
• Best to apply immediately after bathing when
skin is damp because the creams trap moisture
under the skin
MOISTURE
• 65% Of patients with PrUs are incontinent
• If a person is incontinent of feces, the chances
of getting a PrU increases by 3X
• Continued exposure causes maceration –
tissue softening
• Exposure to sweat or incontinent brief raises
skin pH to 7.1
• Exposure to urine or stool increases pH to 8+
Moisture continued…
• Acid Mantle of the skin –
– A slightly acidic film of the skin that acts as a
barrier to bacteria, viruses and other potential
contaminants that might penetrate the skin
– Skin has a normal pH of 4.5-6.2
– Slightly acidic
– Sweat, urine, stool, some soaps are alkaline and
decrease the acidity of the skin making it more
prone for skin breakdown and dermatitis
PERINEAL DERMATITIS
• Not to be confused with Pressure Ulcers (but
in the presence of friction, sheer or pressure
easier to cause tissue damage)
• Also called incontinence related dermatitis.
• Most common cause of nosocomial diarrhea is
C-Diff, second is candida albicans (yeast)
• Regular use of absorptive pads or briefs raises
the pH of the skin and increases production of
perspiration
• Perineal dermatitis
• Candida
Candida
•
•
•
•
•
Usually treated topically
Remove moisture
Kerlix AMD dressings
Interdry AG (from Coloplast)
Check for other sources of infection – (thrush,
vaginitis) which requires oral treatment
(diflucan)
INTRINSIC FACTORS
•
•
•
•
•
•
•
•
•
Malnutrition and dehydration
Critical illness
Age – thinning of the skin
Low Blood pressure
Tissue Oxygenation
Smoking
Weight loss
Infection
Fever
PREVENTION
1.
2.
3.
4.
Risk assessment
Systematic skin assessment
Reduction of risk factors
Patient, family and staff education
RISK ASSESSMENT
1. Braden Scale –
a. 6 subscales that reflect the degrees of sensory
perception, moisture, activity, mobility, nutrition,
friction and shear.
b. Each subscale is rated on a scale according to risk and
the scores are totaled
c. Lower scores mean higher risk for pressure ulcer
development
POSITIONING
• For bed bound patients, perform full position
change at least every 2 hours.
• Sage Turn and Position Unit
5 PILLOW RULE
1. Pillow 1 under legs to elevate heels (or
Prevelon Heel Protectors)
2. Pillow 2 between ankles if on side
3. Pillow 3 between knees if on side
4. Pillow behind the back (unless you are using
the Turn and position unit)
5. Pillow 5 under the head
Do you need to float heels:
Can the patient lift their leg off the
bed by themselves and hold it a
few seconds?
RULE OF 30
1. Head of bed is elevated no more than 30
degrees and the body is placed in a 30 degree
laterally included position when positioned on
either side. If the HOB is raised for eating or
watching TV, return to original 30 asap
2. In the 30 degree lateral inclined position, hips
and shoulders are tilted to 30 degrees supine
position and pillows or foam wedges are used to
keep positioned without pressure on the
sacrum. Never place directly on trochanter.
(Turn and Position Unit)
MORE
• Use draw sheet and trapeze if possible to
decrease friction
• Do not position, if possible, over area of break
down
• NEVER massage reddened areas (this is
friction and will increase break down)
• Keep in mind heel pads and elbow pads
prevent FRICTION not PRESSURE
PREVENTION OF FRICTION
•
•
•
•
•
•
•
Lift sheets
Trapeze
Heel and elbow pads
Moisturizers
Hydration
Transparent dressings
Skin sealants
SEATING
• Instruct patient to self reposition, if able,
every 15 minutes
• If patient is unable to independently
reposition, place on pressure redistributing
cushion and you reposition every hour
• Check for bottoming out
PREVENTION OF SHEAR
•
•
•
•
•
Anti-shear mattress
Lift sheets
HOB 30 degrees
Use pillows or wedges
Use Turn and Position System
HAMMOCK EFFECT
• Seat sags in the middle.
• Needs replaced, placing cushion will not
correct
• Thighs roll inward, creating pressure on
trochanters
• Spine slouches, body slides forward causing
pressure on the ITs, and shear on the buttocks
thighs and spine
Support Surfaces
• Group 1 static – foam, air, water, gel
• Group 2 Dynamic – alternating pressure, low
air loss, rotational
• Group 3 Air Fluidized (clinitron) – fluidized
beds (not for pts with unstable spine or
pulmonary disease). Good for pts with
multiple PU’s, burns, flaps and grafts
51
MANAGEMENT OF INCONTINENCE
• Bowel and bladder training when appropriatite
• Loose stools – ask for bulk in diet, dietary
changes, check for c-diff
• Avoid hot water when cleansing
• Do not scrub
• Use skin barriers
• Use open system for management while in bed
and at night
TREATMENT
• Remove pressure, friction and sheer
• Stage I PrUs can be healed in one day
• Use of hydrocolloids may be helpful in increasing
the healing rate on stage II, III. May be used in
stage I if semi transparent
• Stage IV or heavily exudating stage II may need
alginate, composites, foams and transparent
films.
• Advanced wound care products (ECM, skin
grafting, wound vacs etc)
NON STERILE DRESSING CHANGE
TECHNIQUE
Refer to policy VA-76 on the Communicator
AHRQ (Agency for Healthcare
Research)RECOMMENDATIONS
• NO foam rings
• No cut outs
• No Donuts
• Why? Pressure and ischemia!
LABS
RECOMMENDED
PRESSURE ULCERS
VENOUS ULCERS
A1C Hemoglobin
X
X
Albumin
X
X
CBC
X
Cholesterol
X
X
Glucose
X
X
Hematocrit
X
X
Hemoglobin
X
X
Pre-albumin
X
X
Total lymphocyte
ARTERIAL ULCERS
X
X
X
LABS CONTINUTED
• Albumin – long term measure of protein status (18-21 days)
• Prealbumin – more current picture of protein status (1-2 days)
• Transferrin – transports iron to bone marrow. Used to measure
visceral protein status. Accurate indicator of protein stores as it
responds more readily than albumin
• Total Lymphocyte count – measures immunity to proteins (required
to elicit immune response necessary to heal)
• Glucose – elevated glucose impairs wound healing by impairing
lymphocyte function and immune response
• Hematocrit – low red blood cells= anemia= decreased oxygen
carrying capacity
• CBC – complete blood count gives overview of general health status
MARKERS OF MALNUTRITION
MILD
MODERATE
SEVERE
% usual body wt
85-95%
75-84%
<75%
*Albumin, g/dL
2.8-3.4
2.1-2.7
<2.1
Pre albumin mg/dL
10-16
5-9
<5
Transferrin, mg/dL
150-200
100-149
<100
Total lymphocyte
count/mm3
<1500
<1200
<800
Transferrin vs Ferritin
• Sick people produce less transferrin, so the
body cannot transport iron to bone marrow.
If you supplement extra iron to combat
anemia, that is converted to ferritin, which
leads to higher infection risks.
Minnesota Starvation Study
• 1944
• Showed that serum albumin was not a good
predictor of nutritional or protein status
UNINTENDED WEIGHT LOSS
1. A 5% loss of weight from the previous month
indicates a significant decline in nutritional status
2. A 10% loss in 6 months or less indicates a significant
decline in nutritional status
3. Protein energy malnutrition is the most common form
of malnutrition in people with wounds which results
in loss of lean body mass (LBI)
4. LBI results in catabolism – breakdown of muscle for
energy
***NON HEALING WOUNDS!
NUTRITIONAL NEEDS WITH PrU’s
•
•
•
•
•
•
•
•
•
•
Calorie needs increase from 1.2-2.0 times the basal energy expenditure
Protein needs increase from 1.2-1.5gm/kg body weight. Proteins are made of
amino acids are necessary to generate acute phase proteins, including collagen
and proteogycans
Fats are important for development of cell membranes
Fluid requirements are 30 ml/kg body weight or a minimum of 1500 ml/day
Arginine and Glutamine – amino acids responsible for collagan formation cannot
be metabolized at adequate rate during stress, therefore must be suplimented
Vit A – important for deposition of collagin, and fibroblasts
Vit C – cofactor in collagen formation and fibroblast
Vit B – necessary to get energy from amino acids
Copper – required for collagen linking – low = weak scars and frequent break down
Iron – important for hemoglobin and transport of oxygen
VITAMINS/MINERALS
• Copper, Zinc and Iron all compete for the
same cell receptor.
• If you have weak scar tissue or dehisced
wounds likely too much zinc and not enough
copper which is important for skin integrity
• Supplements with >30 mg zinc = too much
• New studies do not show any benefit from
supplemental Vit C, plus it can be bad for
kidney stone patients
COMPLETE VS INCOMPLETE PROTEIN
•
•
•
•
Complete have all 3 amino acids
Chicken = complete
Ground beef and lunch meat = often incomplete
Tofu = complete
*protein is most important at breakfast, because
you have all day to absorb it and make it available
for use. If not available during the day, body will
catabolize itself, and then use protein to replace
catabolized tissue. Constant deficit.
ENCOURAGE BLOOD FLOW
• Heal through blood flow
• Exercise: punching, legs kicks, isometrics etc
encourage 10X every hour
• Walking at least 4 times a day if able
• PT/OT
ARE ALL ULCERS PRESSURE ULCERS?
• NO!
• Trauma, skin tears, moisture, arterial, venous,
diabetic.
• These are often confused with Pressure ulcers.
• Pressure Ulcers are over bony prominences as
a result of pressure.
• Do not stage any other ulcer besides pressure
ulcers
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