Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - 45
CLINICAL PRACTICE GUIDELINE
original volume. Ulcers treated with 100 µg/mL of
PDGF had a mean ulcer volume reduction of
71%, and placebo-treated ulcer volume only
decreased a mean of 17%.
Autologous Platelet-Rich Plasma
Blood platelets adhere, aggregate, and
release numerous growth factors, adhesion
molecules, and lipids that regulate the migration,
proliferation, and functions of keratinocytes,
fibroblasts, and endothelial cells. Platelet-rich
plasma contains is an autologous preparation of
platelets in concentrated plasma, rich in growth
factors that promote tissue regeneration.
Although there is some limited evidence that
platelet-rich plasma may be effective, the
evidence is not strong enough to recommend
its use as a therapy.
Modification of
Treatment Plan
18. Modify the treatment plan if the ulcer
shows no evidence of healing within 2 to 4
weeks. Review individual factors associated
with non-healing of pressure ulcers, such as
the following:
Incontinence
Infection
Carcinoma
Abnormal wound healing
Nutrition
Medication
Support surfaces
Transfer
Noncompliance
(Scientific evidence-I, III, V; Grade of recommendation-A;
Strength of panel opinion-Strong)
Pressure ulcers receiving effective/adequate
treatment should show signs of healing within
2 to 4 weeks. Inadequate healing should prompt
a reassessment of the treatment plan,
compliance with treatment recommendations,
and other sources of treatment failure
(Bergstrom et al., 1994).
I N C O N T I N E N CE
Urine and stool contamination of pressure
ulcers interferes with their healing (Wilczweski
et al., 2012). If there is urinary incontinence, a
reevaluation of the bladder management program
must be performed and use of an external catheter,
indwelling catheter, more frequent intermittent
catheterization, or change in medication should be
entertained. If there is bowel incontinence, a
reevaluation of the bowel program must be
performed. Causes of incontinence can include
bowel impaction, infection, inadequate evacuation,
and loose stool due to colonic denervation.
Persistent incontinence of stool that is unable to
be controlled and which contaminates a nonhealing pressure ulcer is a strong indication for
a colostomy.
I NFECTI ON
Most chronic pressure ulcers become
colonized with bacteria. When the number of
bacteria reaches a critical threshold on the wound
bed, they are thought to inhibit wound healing
and damage wound tissues. This can be
considered local infection. At this point it is
thought that biofilm is present which harbors
bacterial colonies within the wound. The signs of
infection may be subtle manifesting as only a lack
of healing progress or with increased wound
drainage, epithelial bridging, malodor, a color
change of the wound bed, or friable granulation
tissue (Leaper 2012).
To treat local infection, clinicians need to
control the bacteria burden and the biofilm must
be removed (see recommendation 14). Cleansing
the wound adequately is the mainstay of
treatment; however, topical antibiotics and
antiseptics such as silver sulfadiazine cream,
honey, polyhexamethylene biguamide, cadexomer
iodine are often useful adjunct treatments if
progress in healing is not being made (Kucan et
al., 1981; Leaper DJ 2012). Mupirocin calcium
cream 2% may be applied for pressure ulcers
infected or colonized with staphylococcus aureus
and streptococcus pyogenes resistant to other
topical agents. Prolonged use, however, may
result in overgrowth of nonsusceptible
microorganisms, including fungi.
If the infection spreads into deeper tissues,
the signs of infection become more overt with
erythema, induration, purulence, and foul odor.
Cellulitis and osteomyelitis may occur. Swab
cultures of wound surfaces are not be useful in
determining the presence of deep tissue infection
related to pressure ulcers as they typically reflect
the surface bacteria and not the particular
bacteria within the tissue (Rousseau, 1989). Deep
tissue biopsy is the commonly used method for
obtaining a culture of bacteria within tissue
(Sapico et al., 1986). Results may vary depending
on the site of the lesion biopsied.
Poor wound healing and recurrence of
pressure ulcers may result from underlying
osteomyelitis. In a prospective blind trial involving
45
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury
Table of Contents for the Digital Edition of Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury
Contents
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - Cover1
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - Cover2
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - i
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - Contents
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - iii
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - iv
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - v
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - vi
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - vii
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - viii
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - ix
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - x
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - xi
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - xii
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - xiii
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - xiv
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