N.Karthika Priyatharshini,M.

Sc(N)
Assistant Professor
KVCN
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
PROMINENCE
S
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. Risk assessment
2. Systematic skin assessment
3. Reduction of risk factors
4. 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 VENOUS ARTERIAL

ULCERS ULCERS ULCERS
A1C Hemoglobin X X
Albumin X X
CBC X X
Cholesterol X
Glucose X X X
Hematocrit X X
Hemoglobin X X
Pre-albumin X X
Total lymphocyte 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 10-16 5-9 <5
mg/dL
Transferrin, mg/dL 150-200 100-149 <100
Total lymphocyte <1500 <1200 <800
count/mm3
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