Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - 26
26
PRESSURE ULCER PREVENTION AND TREATMENT FOLLOWING SPINAL CORD INJURY
al., 1997). Serum albumin levels have also been
inversely related to the worst category/stage
of a pressure ulcer and significantly associated
with lifetime incidence of pressure ulcers, number
of different sites, and recurrences (Salzberg et
al., 1996).
A diet rich in calories and protein is
recommended to improve serum albumin levels
instead of intravenous albumin administration
because intravenous albumin is deficient in
essential amino acids and provides only transient
increases in serum albumin (Fuoco et al., 1997).
Nutritional status as measured by serum
albumin has not been correlated with the
development or healing of pressure ulcers in
some studies (Allman et al., 1995; Day and
Leonard, 1993). No significant differences in
serum concentrations of total protein or albumin
were found between individuals with "slow"
(no healing within 5 weeks after initiating
therapy) and "fast" (healing within 5 weeks of
treatment) healing ulcers (Segal et al., 1997).
These conflicting findings could be explained by
factors other than nutritional status. Factors
associated with hypoalbuminemia include losses
of protein and albumin into the pressure ulcer
exudate (Allman et al., 1995) and the presence
of a chronic cytokine-induced inflammatory state
(Bonnefoy et al., 1995; Segal et al., 1997; Strauss
and Margolis, 1996).
Albumin and prealbumin are negative acute
phase reactants. They are inversely influenced by
inflammatory and stress responses. C-reactive
protein, a protein that increases with stress, is
useful in interpreting whether albumin and
prealbumin are being affected or decreased by
inflammation and stress.
Serum total protein levels less than 6.4 g/dL
have been associated with pressure ulcer
development (Blaylock, 1995; Salzberg et al.,
1996; Tourtual et al., 1997).
Hemoglobin and Hematocrit
Anemia, assessed by hemoglobin and
hematocrit levels, reduces oxygen supply to
tissues, thus impairing healing of pressure
ulcers. Hemoglobin levels below 12-14 g/dL are
associated with increased incidence of pressure
ulcers (Lehman, 1995; Rochon et al., 1993;
Salzberg et al., 1996; Tourtual et al., 1997).
Hematocrit levels below 36% have also been
inversely associated with lifetime total pressure
ulcers, the depth of the ulcer, and the number
of different sites (Salzberg et al., 1996). Iron
therapy is not necessarily recommended to
correct hemoglobin and hematocrit levels because
anemia could result from an inability to use iron
stores rather than from iron deficiency (Fuoco
et al., 1997).
Total Lymphocyte Count
Decreased total lymphocyte count (< 1500/
mm3) is an independent significant risk factor
associated with the development of pressure
ulcers (Allman et al., 1995; Lehman, 1995).
Lymphopenia can also result from non-nutritional
factors, such as infections and steroid use that
compromise immunocompetence.
9. Provide adequate nutritional intake to meet
individual needs, especially for calories (or
energy), protein, micronutrients (zinc,
vitamin C, vitamin A, and iron), and fluids.
(Scientific evidence- I, II, III, IV V; Grade of
,
recommendation-A; Strength of panel opinion-Strong)
CALORI ES ( ENERGY)
Calories are required to fuel basic life
processes and to spare lean body mass from
being used to meet metabolic demands.
Individuals with SCI commonly have lower energy
needs than matched individuals without SCI, in
part due to decreased metabolic demand by
denervated muscles. An estimate of the difference
in basal energy expenditure between persons with
SCI who have severe pressure ulcers and those
who do not have pressure ulcers is approximately
5 Kcal/Kg of body weight per day. This has been
demonstrated in several studies using indirect
calorimetry and has been replicated in other
populations with and without pressure ulcers
(Alexander et al. (1995); Liu et al. (1996); Sergi
(2007)). Both pressure ulcer surface area and
severity have been found to be significantly
related to percent of predicted energy expenditure
(Liu et al., 1996; Sergi 2007). One possible
explanation for the increased energy expenditure
found in those with pressure ulcers is the
underlying chronic inflammatory processes
induced by cytokines and cortisol (Bonnefoy et
al., 1995; Segal et al., 1997).
PROTEI N
Protein is essential for tissue growth,
maintenance, and repair. A high protein intake is
needed for optimal healing of pressure ulcers
(Allman et al., 1995). Breslow et al. (1993)
reported that administration of supplemental
nutritional formulas containing 24% protein
instead of 14% administered for 8 weeks in a
malnourished nursing home population can result
in a decrease in pressure ulcer surface area
correlated to both dietary protein and calorie
intake per kilogram of body weight.
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
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Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - xi
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Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - xiv
Pressure Ulcer Prevention and Treatment Following Spinal Cord Injury - 1
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