PRESSURE ULCERS- surgery I march 2019

by kausya

objectives: tobe able to

i. Define terms
ii. State aetiology
iii. Explain epidemiology
iv. Discuss pathophysiology
v. Do staging
vi. Diagnose
vii. Manage
viii. Prevent
ix. Explain complications
Definition

 Ulcer: A lesion through the skin or a mucous membrane resulting from loss of tissue, usually with
inflammation
 Pressure ulcer: These are ischemic necrosis and ulceration of tissues overlying a bony prominence that has
been subjected to prolonged pressure against an external object (e.g. bed, wheelchair, cast, and splint).
 They are also referred to as :Pressure sores, bedsores, decubitus ulcers, trophic ulcers
 Pressure sores occur most often in patients with diminished or absent sensation or who are debilitated,
emaciated, paralyzed, or long bedridden.
 Tissues over the sacrum, ischia, greater trochanters, external malleoli, and heels are especially susceptible;
other sites may be involved depending on the patient's position.
 Pressure sores can also affect muscle and bone.
 Pressure ulcers are the visible evidence of pathologic changes in dermal blood flow caused by pressure.
Pressure Ulcers
Definition
 Pressure Ulcers are localized areas of tissue necrosis that tend to occur when
soft tissue is compressed between a bony prominence and an external surface
for a prolonged period.
 These lesions are also called bedsores, decubitus ulcers and pressure sores
Pressure Ulcers
Epidemiology
 1-3 million Americans are affected
 Health care expenditures: $ 5 billion/year
 More than 17,000 lawsuits related to pressure Ulcers are filed annually
 1 in 4 persons in the USA who died in 1987 had a dermal ulcer
 Pressure Ulcers develop primarily in elderly patients
Pressure Ulcers
Epidemiology
 Setting
 Hospital 60%
 Nursing homes 18%
 Home 18%

 1/3 of patients undergoing surgery for hip

fracture develop a pressure ulcer
 The longer the patient stays in a nursing home,
the greater the likelihood of developing a
pressure ulcer
 Etiology
1. Intrinsic factors
 They include loss of pain and pressure sensations (which ordinarily prompt the patient to shift position and
relieve the pressure) and minimal fat and muscle padding between bony weight-bearing prominences and
skin.
 Disuse atrophy, malnutrition, anemia, and infection contribute.
 In a paralyzed patient, loss of vasomotor control leads to lowered tone in the vascular bed and lowered
circulatory rate.
 Spasticity, especially in patients with spinal cord injuries, can place a shearing force on the blood vessels to
further compromise circulation.
 2. Extrinsic factors
 The most important is pressure due to infrequent shifting of the patient's position; friction, irritation, and
pulling of skin from ill-adjusted supports or wrinkled bedding or clothing contribute.
 The force and duration of pressure directly determine the extent of the ulcer.
 In an immobilized patient, severe pressure can impair local circulation in < 3 h, causing local tissue anoxia
that, if unrelieved, progresses to necrosis of the skin and subcutaneous tissues.
 Moisture (e.g. from perspiration or incontinence) leads to tissue maceration and predisposes to pressure sores.
 The stages of pressure sore formation correspond to tissue layers
THERMODYNAMICS, METABOLISM AND
PRESSURE
 Thermodynamic factors - skin/surface interface
 As temperature increases, skin becomes more metabolically active and 0 2
demands increase
 With increased pressure, metabolic demands not able to be met and skin
becomes hypoxic
 Hypoxic skin more susceptible to breakdown
 Adding friction and shear to already fragile skin is “perfect storm”
THE 4 FORCES

1. Pressure: Force applied to soft tissue between hard surface and bony
prominence. When skin and the underlying tissues are trapped between bone
and a surface such as a wheelchair or bed, blood flow is restricted. This
deprives tissue of oxygen and other nutrients -> tissue death.
2. Friction: Resistance of one body sliding or rolling over another. Making skin
more susceptible to pressure sores.
PRESSURE AND FRICTION
3. Shear: This occurs when skin moves in one direction, and the underlying
bone moves in another. Sliding down in a bed or chair or raising the head
of bed more than 30 degrees is especially likely to cause shearing, which
stretches and tears cell walls and tiny blood vessels. Especially affected
are areas such as tailbone where skin is already thin and fragile.
4. Strain: Tissue deformation in response to pressure
Pathophysiology

 Prolong weight bearing and mechanical shear forces act on areas of soft tissue
overlying bony prominence ―> when this pressure exceeds normal capillary
perfusion pressure (32 mm Hg) ―> occlusion & tearing of small blood vessels
―> reduced tissue perfusion ―> ischaemic necrosis ―> Pressure sore.
Staging
1. Stage I: Non-blanching erythema, warmth, tenderness
2. Stage II: Skin breakdown limited to dermis, excoriation, blistering, drainage, more sharply defined erythema, variable
skin temperature, local swelling or edema
3. Stage III: Ulcer formation into subcutaneous tissues, crater formation, slough, eschar, and/or drainage
4. Stage IV: Ulcers extend beyond deep fascia into muscle or bone, decayed area may be larger than visibly apparent
wound, osteomyelitis or sepsis may be present, granulation tissue and epithelialization may be present at wound
margins
Risk factors
 Age. Older adults tend to have thinner skin, making them more
susceptible to damage from minor pressure. They have less natural
cushioning over their bones. And poor nutrition, delays wound
healing.

 Lack of pain perception. Spinal cord injuries and some diseases

cause a loss of sensation ―> bedsore is forming.
 Natural thinness or weight loss. Muscle atrophy
and wasting are common in people living with
paralysis. If you lose fat and muscle there is no
cushion over your bones.
 Malnutrition. Pressure sores develops if you have
a poor diet, especially one deficient in protein,
zinc and vitamin C.
 Urinary or fecal incontinence. Problems with
bladder control can greatly increase risk of
pressure sores because skin stays moist, making
it more likely to break down. And bacteria from
fecal matter not only can cause serious local
infections but also can lead to life-threatening
systemic complications such as sepsis, gangrene
and, rarely, necrotizing fasciitis, a severe and
rapidly spreading infection.
 Other medical conditions. diabetes and vascular disease affect
circulation ―> tissue damage.
 Smoking. Smokers tend to develop more severe wounds and heal
more slowly, mainly because nicotine impairs circulation and reduces
the amount of oxygen in blood.
 Decreased mental awareness. People whose mental awareness is
lessened by disease, trauma or medications are often less able to
take the actions needed to prevent or care for pressure sores.
Risk Factors

 Spinal cord injuries  Chronic systemic illness

 Traumatic brain injury  Fractures
 Neuromuscular disorders  Aging skin
 Immobility  decreased epidermal turnover
  dermoepidermal junction flattens
Malnutrition
 fewer blood vessels
 Fecal and urinary incontinence
 Decreased pain perception
 Altered level of consciousness
Site
 Pressure ulcers
commonly occur
over the :
 Sacrum
 Greater
trochanter
 Ischial tuberosity
 Malleolus
 Heel
 Fibular head
 Scapula
While on a wheelchair a pressure sore develop on:
- tailbone or buttocks
- shoulder blades and spine
- The backs of arms and legs where they rest against the
chair
Stages/ classification
Classification
 Stage I
1. 1. most superficial,
 2. non blanchable redness, does not subside
after pressure is relieved.
 3. The skin may be hotter or cooler than
normal
 4. have an odd texture, or
 5. perhaps be painful to the patient.
STAGE I
• Stage II is damage to the epidermis extending into, but no deeper
than, the dermis. In this stage, the ulcer may be referred to as a blister or
abrasion.

• The ulcer is superficial and manifest clinically

as an abrasion, blister or shallow crater
STAGE II
STAGE II
• Stage III involves the full thickness of the skin and may extend
into the subcutaneous tissue layer. This layer has a relatively poor blood
supply and can be difficult to heal.

The ulcer manifests clinically as a deep crater

with or without undermining of adjacent
tissue
STAGE III
STAGE III
Stage IV is the deepest, extending into the muscle, tendon or even
bone.
 “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/or tunneling”
 Depth varies according to anatomic location
 Exposed bone/tendon usually directly visible and/or palpable
STAGE IV
Stage 4

B
STAGE IV
 Treatment
Stage I pressure ulcer treatment options
 Manage incontinence, keeping area clean and dry.
 Use moisture barrier as needed.
 Off load area were pressure ulcer is – pressure reducing surfaces
 Stage II pressure ulcer treatment options
 Dry wound bed: cleanse with normal saline, apply small amount of hydrogel and cover with dd everyday.
 Off load area were pressure ulcer is – pressure reducing or relieving surfaces.
 Minimal drainage: cleanse with normal saline, apply hydrocolloid dressing every three days and prn soiling or
dislodging. Monitor placement every day.
 Off load area were pressure ulcer is – pressure reducing or relieving surfaces.
Stage iii pressure ulcer treatment options
 Minimal drainage and clean wound bed: cleanse with normal saline, apply small
amount of hydrogel and cover with dd every day.
 Off load area were pressure ulcer is – pressure relieving surfaces.
 Presence of slough: cleanse with normal saline, apply accuzyme and cover with dd
everyday.
 Use foam dressing instead of dd for heavy drainage.
 Off load area were pressure ulcer is – pressure relieving surfaces.
 Heavy drainage and clean: cleanse with normal saline, apply foam dressing every
two days and prn soiling or dislodging. monitor placement every day.
 load area were pressure ulcer is – pressure relieving surfaces –preferable a low aOff
ir loss mattress replacement.
 Stage IV pressure ulcer treatment options
 Minimal drainage and clean wound bed: cleanse with normal saline, apply small amount of hydrogel and
cover with dd every day.
 Off load area were pressure ulcer is – pressure relieving surfaces.
 Presence of slough: cleanse with normal saline, apply accuzyme and cover with dd everyday.
 Use foam dressing instead of dd for heavy drainage.
 Off load area were pressure ulcer is – pressure relieving surfaces –preferable a low air loss mattress
replacement.
 Heavy drainage and clean: cleanse with normal saline, apply foam dressing every two days and prn soiling
or dislodging. Monitor placement every day.
 Off load area were pressure ulcer is – pressure relieving surfaces –preferable a low air loss mattress
replacement.
 General
 The ulcer is analogous to an iceberg; it has a small visible surface with a more extensive unknown base.
 There is no good method to determine the extent of tissue damage.
 Incipient pressure sores (stages 1 and 2) require all the prophylactic measures above to prevent necrosis.
 The area should be kept exposed, free from pressure, and dry.
 Stimulating the circulation by gentle massage can accelerate healing.
 Ulcers that have not advanced beyond stage 3 may heal spontaneously if the pressure is removed and the
area is small.
 New hydrophilic gels and hydrocolloid dressings speed healing.
 Stage 4 ulcers require debridement or more extensive surgery.
 When the ulcers are filled with pus or necrotic debris, dextranomer beads or newer hydrophilic polymers
may hasten debridement without surgery.
 Conservative debridement of necrotic tissue with forceps and scissors should be instituted.
 Some ulcers may be debrided by cleansing with 1.5% hydrogen peroxide
 Whirlpool baths may assist debridement.
 Contnued--
 More advanced ulcers with fat and muscle involvement require surgical debridement and closure.
 Affected bony tissue may require surgical removal; disarticulation of a joint may be needed.
 The granulation tissue formation that follows debridement may provide a satisfactory base for
skin grafts to cover small areas.
 A sliding full-thickness skin flap graft is the closure of choice, especially over large bony
prominences (e.g. sacrum, ischia, and the trochanters); because scar tissue cannot develop the
tolerance to pressure that is needed.
 For adequate healing, the patient may need to be placed on a bed that redistributes weight, such as
one using a forced-air system.
 For cellulitis, penicillinase-resistant penicillin or a cephalosporin is necessary.
 Many new dressings and topical agents are becoming available.
 No powder, gel, or dressing is universally superior because some are hydrophilic and highly
occlusive; prolonged use increases the risk of infections such as Pseudomonas.
 Others are painful, all are expensive, and controlled clinical trials evaluating the advantages and
disadvantages of various dressings often are not available.
 Valuable advice on the care of decubiti can often be obtained from geriatric nurse practitioners.
 Plastic surgery consultation is sometimes needed.
 Treatment and Management
 Pain Management
 A primary goal of wound assessment should be to relieve pain. Except in neurologically
impaired patients, chronic ulcers may be painful.
 Nutrition
 One of the most important reversible host factors contributing to wound healing is nutritional
status.
 Dressings
 Moist wound healing allows experimentally induced wounds to resurface up to 40%faster than
air-exposed wounds
 Debridement
 Necrotic debris increases the possibility of bacterial infection and delays wound healing
 Growth Factors
 Acute wound healing proceeds in a carefully regulated fashion that is reproducible from wound
to wound. A number of growth factors have been demonstrated to mediate the healing process.
 Infection
 Quantitative microbiology alone is a poor predictor of clinical infection in chronic wounds
 Pressure-Relieving Devices
 Pressure-relieving devices have a therapeutic role
 Assessment of pressure ulcer
Assess and document:
 cause
 site/location
 dimensions
 stage orAssess and document:
 cause
 site/location
 dimensions
 stage or grade
 necrosis or slough
 exudate amount and type
 local signs of infection
 pain
 wound appearance
 surrounding skin – including erythema, maceration, moisture damage
 undermining/tracking, sinuses, tunnelling or fistulae
ssessment cont

 odour
 grade
 necrosis or slough
 exudate amount and type
 local signs of infection
 pain
 wound appearance
 surrounding skin – including erythema, maceration, moisture damage
 undermining/tracking, sinuses, tunnelling or fistulae
 odour
Competency framework
Assessment factors1:
 Intrinsic factors: • Extremes of age.
 Reduced mobility • Vascular disease.
 Sensory impairment • Severe chronic or
 Neuropathy terminal illness.
• Previous history of
 Acute illness.
pressure damage.
 Level of consciousness. •
Malnutrition and
dehydration.
Competency framework
Assessment factors 2:

 Extrinsic factors:
 Pressure.

• Other factors:
Shearing.
 Friction.
• Medication.
• Moisture to the skin.
Tests and diagnosis

 Bedsores are usually unmistakable, even in the initial stages, but doctor is
likely to order blood tests to check nutritional status and overall health.
Depending on the circumstances, there may have other tests.
 Wound swab – C/S
 Incision biopsy – if malignancy is suspected.
Treatments and drugs
 Treating bedsores is challenging. Open wounds are slow to heal, and
because skin and other tissues have already been damaged or
destroyed, healing is never perfect.
 Requires a multidisciplinary approach – nurses, physician, social
worker, physical therapist, urologist or gastroenterologist, a
neurosurgeon, orthopedic surgeon and plastic surgeon.
TREATMENT OBJECTIVES
 Identification of problem
 Debridement of necrotic tissue
 Moist wound care without maceration
 Control of infection/bioburden
 Management of pain
 Pressure redistribution/Offloading

 Choice of wound care products is individual preference as long as above

objectives met.
 A) Conservative treatment
Although it may take some time, most stage I and stage II sores will heal
within weeks with conservative measures. But stage III and stage IV wounds,
which are less likely to resolve on their own, may require surgery.
 1. Changing positions often. Carefully follow the
schedule for turning and repositioning — approximately
every 15 minutes if in a wheelchair and at least once
every two hours when in bed. If unable to change
position on own, a family member or other caregiver
must be able to help.
 2. Using support surfaces. These are special cushions,
pads, mattresses and beds that relieve pressure on an
existing sore and help protect vulnerable areas from
further breakdown.
PRESSURE REDISTRIBUTION
 3. Cleaning. It's essential to keep wounds clean to prevent infection. A stage I
wound can be gently washed with water and mild soap, but open sores should
be cleaned with a saltwater (saline) solution each time the dressing is
changed. Avoid antiseptics such as hydrogen peroxide and iodine, which can
damage sensitive tissue and delay healing.
 4. Controlling incontinence as far as possible is crucial to helping sores
 5. Removal of damaged tissue (debridement). To heal
properly, wounds need to be free of damaged, dead or infected
tissue. This can be accomplished in several ways -
 a. Autolytic debridement is autolysis with the body's own
enzymes.
 b. Biological debridement, or maggot debridement therapy,
 c. Chemical debridement, or enzymatic debridement
 d. Mechanical debridement
 e. Sharp debridement is the removal of necrotic tissue with a
scalpel or similar instrument.
 f. Surgical debridement
 g. Ultrasound-assisted wound therapy
 6. Dressings.
 7. Oral antibiotics.
 8. Healthy diet.
 9. Muscle spasm relief
 10. Educating the caregiver
 B) Surgical repair by - tissue flap, free flap,
Negative Pressure Wound Therapy

 C) Other treatment options

Researchers are searching for more effective bedsore treatments. Under
investigation are hyperbaric oxygen, electrotherapy and the topical use of
human growth factors.
Prevention
 The best treatment is prevention by relief of pressure on sensitive areas.
 In a bedridden patient, position must be changed at least q 2 h until tolerance for longer periods can be
demonstrated (by the absence of redness).
 Air-filled alternating-pressure mattresses, sponge-rubber egg crate mattresses, and silicone gel or water mattresses
help decrease pressure on sensitive areas but do not negate the need for position changes q 2 h.
 When maximal relief of pressure is needed, other systems, including air flotation mattresses, must be used.
 A Stryker frame facilitates turning patients with spinal cord injuries.
 Protective padding (e.g. sheepskin or a synthetic equivalent) at bony prominences should be used, especially under
braces or plaster casts; a window should be cut out of the cast at potential pressure sites.
 Wheelchair-bound patients may develop pressure sores.
 Thus, they must shift position or be shifted q 10 to 15 min, even if a pressure-relieving pillow is used.
 Inspection under adequate light is important.
 Pressure points should be checked for erythema or trauma at least once/day.
 Patients and families must be taught a routine of daily visual inspection and palpation of sites for potential ulcer
formation.
 Prevention cont
 Meticulous care is necessary to prevent maceration and secondary infection.
 Lying on a sheepskin helps keep the patient's skin in good condition and minimize pressure sores.
 Protective padding, pillows, or a sheepskin can be used to separate body surfaces.
 Maintaining cleanliness and dryness helps prevent maceration.
 Bedding and clothing should be changed frequently; sheets should be soft, clean, and free from wrinkles and
particulate matter.
 Sponging the skin in hot weather and thorough drying after baths are essential.
 Special efforts are required for incontinent patients.
 Most areas may be powdered with plain talc.
 Oversedation should be avoided and activity encouraged.
 Physiotherapy, when practicable, may be carried out by means of passive and active exercises.
 Hydrotherapy is also valuable.
 A well-balanced diet, high in protein, is important.
 There is some evidence that supplemental vitamin C and zinc help healing
Prevention

 Bedsores are easier to prevent than to treat, but that doesn't mean the
process is easy or uncomplicated. Although wounds can develop in spite of the
most scrupulous care, it's possible to prevent them in many cases.
 Position changes
Changing position frequently and consistently is crucial to preventing
bedsores. Experts advise shifting position about every 15 minutes that
you're in a wheelchair and at least once every two hours, even during the
night, if you spend most of your time in bed.
 Skin inspection
Daily skin inspections for pressure sores are an integral part of prevention.
 Nutrition
A healthy diet is important in preventing skin breakdown and in aiding
wound healing
 Lifestyle changes –
-Quitting smoking,
- Exercise - Daily exercise improves circulation
Complications

 Cellulitis. This causes pain, redness and swelling, all of

which can be severe. Cellulitis can also lead to life-
threatening complications, including sepsis and
meningitis.
 Bone and joint infections. These develop when the
infection from a bedsore burrows deep into joints and
bones. Joint infections (septic or infectious arthritis) can
damage cartilage and tissue, whereas bone infections
(osteomyelitis) may reduce the function of joints and
limbs.
 Sepsis. It occurs when bacteria enters bloodstream through the broken skin
and spreads throughout the body — a rapidly progressing, life-threatening
condition that can cause shock and organ failure.
 Cancer. This is usually an aggressive carcinoma affecting the skin's squamous
cells.
End than kyou