Download Review Decubitus ulcers: A review of the literature

Review
Decubitus ulcers: A
review of the literature
Cheryl Bansal,BA, Ron Scott,MD, David Stewart,MD,
and Clay J. Cockerell,MD
International Journal of Dermatology 2005,44
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Introduction and Pathogenesis
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Constant pressure can come from lying down (“decubitus”
from the Latin decumbere, “to lie down”) or from sitting.
Decubitus ulcers, also known as bedsores and pressure
sores,are caused by impaired blood supply and tissue
malnutrition owing to prolonged pressure over skin, soft
tissue, muscle,and/or bone.
Decubitus ulcers have probably existed since the dawn
of humankind.
They have been observed in unearthed human mummies
and addressed in scientific writings of the19th century.
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Introduction and Pathogenesis
Decubitus ulcers can develop on any part of the body
where sustained pressure and compressive forces are
maintained for a sufficient period of time.
 sacrum and hips is most often affected (67%),
occiput, helices, elbows, and lower extremities (25%),
including heels and ankles.
 25% of decubitus ulcers start in the operating room
during surgery.
 83% of hospitalized patients with decubitus ulcers
developed them in the first 5 days of hospitalization.
 The prevalence rate in nursing homes is estimated to be
17–28%.
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Introduction and Pathogenesis
Impaired patients decubitus ulcers occur at an annual
rate of 5–8%, with lifetime risk estimated to be 25–85%.
 Decubitus ulcers are listed as the direct cause of death in
7–8% of paraplegics.
 Hospitalized patients have a 3–17% incidence rate, while
hospitalized surgical patients have a 12–66% incidence
rate.
 Immobilized patients in long-term care facilities have a
33% incidence rate.
 Some estimates suggest that 60,000 people die from
decubitus ulcers or their sequelae per year.
 Present treatment costs for decubitus ulcers in the US is
estimated in excess of $1 billion per year.
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Morphology
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Several classification systems for decubitus ulcers have
been described: Daniel’s,Shea’s,and the National
Pressure Ulcer Advisory Panel (NPUAP), which is a
modification of Shea’s classification.
The most widely accepted classification system for
decubitus ulcers is the NPUAP.
Stage I of the NPUAP classification represents intact
skin with signs of impending ulceration: blanching
and/or nonblanching erythema, warmth, and induration.
Stage II ulcers present clinically as a shallow ulcer
(including epidermis and possibly dermis) with
pigmentation changes.
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Morphology
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Stage II ulcers, like Stage I, can be reversible.
Stage III ulcer represents a full-thickness loss of skin
with extension through subcutaneous tissue, but not
underlying fascia.
Stage IV represents full-thickness skin and subcutaneous
tissue loss. resulting in involvement of muscle, bone,
tendon, or joint capsule.
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Histopathology
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Decubitus ulcers have many histologic stages.
Clinically, the decubitus ulcer spectrum includes
blanching erythema, nonblanching erythema,
decubitus dermatitis, early ulcer, healing ulcer,
chronic ulcer, and black eschar/gangrene.The
progression is dynamic and multiple stages are
often observed in one decubitus ulcer.
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Treatment
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Today, the treatment of decubitus ulcers is based on four
primary modalities: (1) pressure reduction and
prevention of additional ulcers, (2) wound management,
(3) surgical intervention, and (4) nutrition.
An additional way to reduce pressure involves turning
and repositioning the patient every 2 h to reduce
pressure on vulnerable areas.
Current research indicates that the 2-h interval may not
be adequate.
The key aspects of wound management to ensure
effective healing are cleaning and effective drainage and
absorption while protecting the skin adjacent to the
wound.
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Treatment
Skin adjacent to the wound may be lubricated to
decrease friction and be kept relatively dry.
 Surgical intervention for decubitus ulcers involves
debridement or flap creation for some Stage III
and Stage IV ulcers.
 Malnutrition should be addressed because the
malnourished patient has a higher susceptibility
for ulcer formation.
 Other treatment modalities that can be employed
as needed.
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Treatment
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There are several risk assessment scales:
Norton,Cubbin and Jackson, Braden,
Douglas,and Waterlow.
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Current studies show these risk assessment
scales may not as effective as nurses’ judgement
as to which atients are at risk.
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Treatment
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Table 1 Decubitus ulcer Do’s and Don’ts
Do’s
Don’ts
Move the patient or encourage the
Do not use donut-type
patient to move every 2 h
cushions and device
Keep skin clean and lubricated
Keep skin dry
Use pressure relief devices such as
pillows, foam cushions, mattresses
and gel heel protectors
Pay special attention to skin areas with
little fat padding, such as bony prominences
Put patient on a stool and urine voiding
schedule
Use incontinence devices as appropriate
Keep incline no higher than 30 degrees to
prevent sliding and friction on lower back
and buttocks
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Outcomes
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Ferrell et al . found that no pressure ulcer healed
completely or reduced in surface area greater than 50%
within 30 days and only 14% of pressure ulcers
completely healed within 79 days.
This indicates that long-term therapy may be necessary.
Yao-Chin et al . found 53% of pressure ulcers healed
within 42 days.
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Complications
Osteomyelitis
 hypercalcemia
 myonecrosis
 necrotizing fasciitis
 amyloidosis
 sepsis
 gangrene
 death
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Future Research
Growth factors and hyaluronic acid have also been
implicated in the process of wound healing.
 Becaplermin has been given FDA approval for treatment
of lower extremity diabetic neuropathic ulcers. It may
also have a place in the treatment of decubitus ulcers.
 Polyphenols such as catechin and black catechu have
been found to have scavenger effects on oxygen radicals.
 Topical vitamin E has been found to accelerate the
healing of skin wounds and ulcers.
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謝謝聆聽
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