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8 The Role of Nutrition in the Management and Prevention of Pressure Ulcers
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pressure ulcer surface area showed more decrease (−4.2 cm 2 vs. −2.1 cm 2 ) in surface
area in patients fed with the enteral formula containing 24 % protein compared to a
formula containing 14 % protein. However, changes in body weight or in biochemical parameters of nutritional status did not differ between groups. The study was
limited by a small sample size (only 28 patients completed the study), nonrandom
assignment to treatment groups, confounding effects of air-fl uidized beds, and the
use of two different feeding routes [ 52 ].
In a study of enteral tube feedings in a long-term care setting, 49 patients were
followed for 3 months [ 53 ]. Patients received 1.6 times basal energy expenditure
daily, 1.4 g of protein/kg/day, and 85 % or more of their total recommended daily
allowance. At the end of 3 months, there was no difference in number or healing of
pressure ulcers.
A concentrated, fortifi ed, collagen protein hydrolysate supplement was evaluated
in 44 subjects with 75 pressure ulcers and compared to 27 subjects with 33 pressure
ulcers who received a noncaloric control. At 8 weeks there was a small but statistically signifi cant difference in the Pressure Ulcer Scale for Healing score (3.55 intervention vs. 3.22 control) [ 54 ]. The randomization process did not produce equal
group size, and the number and severity of the pressure ulcers at baseline was not
balanced between groups, potentially biasing the study.
In a long-term care setting, 93 tube-fed residents with a wound were compared
to 57 tube-fed residents without a wound. Persons with a wound were started on an
enteral tube feeding formula containing 1.25 g/protein/day, and persons without a
wound were started on an enteral tube feeding formula containing 1.0 g/protein/day.
At admission, only 12 % of persons with a wound and 21 % of persons without a
wound had normal prealbumin levels. Over a mean follow-up of about 1 month, the
amount of protein in the feeding formula was maintained or increased based on
serum prealbumin levels. The serum prealbumin level normalized or increased by 8
points in 42 % of persons with a wound and in 46 % of persons without a wound.
However, there was no correlation between persons who improved their serum prealbumin and those who did not based on protein intake. There was also no correlation observed between the PUSH score and improvement in serum prealbumin [ 55 ].
These data suggest that increasing protein intake, in some cases to greater than
2 g/protein/day, is not associated with greater healing of pressure ulcers. It also
indicates that serum prealbumin is a poor marker of nutritional status.
Forty-three non-malnourished subjects with stage 3 or 4 pressure ulcer were
evaluated in a multisite, randomized, controlled, double-blind trial. Subjects were
screened to exclude malnutrition, defi ned as a body mass index less than 18.5 kg/m 2
for those younger than 70 years or 21 kg/m 2 for those older than 70 years. Other
exclusion criteria were severe medical conditions, life expectancy shorter than 6
months, receiving palliative care, use of corticosteroids, and/or dietary restrictions
such as a protein-restricted diet. Subjects were offered 200 mL of a high energy
supplement enriched with arginine, antioxidants, and other micronutrients (not
specifi ed) three times daily for a maximum of 8 weeks or a non-caloric placebo,
similar in taste and appearance, over the same timeframe. In the supplemented
group, the mean change in wound size was 0.26 cm 2 /day compared to 0.14 cm 2 /day
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in the control group over the fi rst 3 weeks. By 8 weeks, the mean healing rate in the
supplemented group was similar to the control group (0.16 cm 2 /day vs. 0.15 cm 2 /day,
respectively). In this population screened to exclude undernutrition, complete healing was observed in 6 ulcers in the supplemented group, compared to 5 ulcers in the
control group by 8 weeks. No change was observed in body mass index [ 56 ].
Twenty-eight subjects older than 65 years with a stage 3–4 pressure ulcer which
was present for less than 1 month were randomized to receive a standard hospital
diet with no supplement ( N = 15) or a standard hospital diet plus a supplement con-
taining 500 kcal with 34 g protein, 6 g arginine, 500 mg vitamin C, and 18 mg zinc
( N = 13). Nine subjects who were tube fed in the treatment group (69 %) received a
formula containing 1,000 kcal, 55 g protein (20 %), 8 g arginine, 380 mg vitamin C,
and 20 mg zinc. Nine subjects who were tube fed in the control group (60 %)
received an enteral formula containing 16 % protein. All subjects were adjusted to a
target of 30 Kcal/kg/day. After 12 weeks, complete pressure ulcer healing was documented for only one person in the treatment group. The PUSH score between groups
was different only at week 12. The was no difference in ulcer area measured in
square millimeters at any time point. The percentage of decrease in pressure ulcer
area in the treatment group was greater compared to the control group at week 8 and
12. No nutritional parameter was different between groups except for the treatment
group having a higher zinc level. Surprisingly, reaching a target of 30 kcal/kg/day
did not affect wound healing, and no benefi t from increased protein intake or independent effect of arginine or zinc was observed. These fi ndings call into question
empirically derived recommendations. In addition, no effect on wound healing measured by change in PUSH score or change in ulcer area was observed despite an
increase in energy intake and protein intake over a 12 week period (controls 4.6 kcal/
kg/day vs. treatment 3.1 kcal/kg/day). This data suggest that a specifi c nutritional
formula may produce small benefi ts in improving pressure ulcer size. However, no
specifi c supplemental nutritional component could account for the variation [ 57 ].
D.R. Thomas
Nutrition and Prevention of Pressure Ulcers
Increasing knowledge of the complexity of wound healing has led to hypothesis that
providing hypercaloric feeding in the form of nutritional supplements to patients at
risk for undernutrition might lead to reversal of undernutrition and the prevention of
pressure ulcers. Despite the observed epidemiological association, results of trials
of nutritional intervention in prevention of pressure ulcers has been disappointing.
Controversy exists about the ability of nutritional support to reduce complications or improve wound healing [ 58 ]. Although correction of poor nutrition is part
of total patient care and should be addressed in each patient, only one nutritional
intervention has shown effectiveness in prevention of pressure ulcers in published
studies [ 59 ].
In that trial, 672 persons older than 65 years, in the acute phase of a critical illness, received 2 oral supplements per day in addition to the standard hospital diet
8 The Role of Nutrition in the Management and Prevention of Pressure Ulcers
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135
compared to a group receiving a standard hospital diet alone. After 15 days of follow- up, the incidence of pressure ulcers (stages 1–4) was 40 % in the nutritional
intervention group compared to 48 % in the control group (relative risk 0.83, 95 %
CI 0.70–0.99). The groups were randomized by ward, rather than individually, and
were not comparable at baseline, with the nutritional intervention group having a
lower initial pressure ulcer risk [ 60 ].
In another trial, oral nutrition supplements were given to 33 % of one group
compared to 87 % of another group. There was no difference in pressure ulcer incidence (26 % vs. 20 %), pressure ulcer prevalence at discharge (15 % vs. 10 %),
mortality (16 % vs. 14 %), length of stay (17.3 days vs. 17.4 days), or nosocomial
infections (26 % vs. 19 %) between groups [ 61 ]. This observational study of hospi-
talized, critically ill patients given nutritional supplements suggests no effect on
pressure ulcer incidence.
The effect of overnight supplemental enteral feeding in patients with a fracture
of the hip and a high pressure ulcer risk score has been evaluated. Of the 62 patients
randomized for enteral feeding, only 25 tolerated their tube for more than 1 week,
and only 16 tolerated their tube for 2 weeks. No difference was found for the development of a pressure ulcer, total serum protein, serum albumin, or the severity of
pressure sores after 1 and 2 weeks. Comparison of the actually tube-fed group
( n = 25 at 1 week, n = 16 at 2 weeks) and the control group showed two to three times
higher protein and energy intake ( p < 0.0001) and a signifi cantly higher total serum
protein and serum albumin after 1 and 2 weeks in the actually tube-fed group
(all p < 0.001). However, the development of pressure ulcers and severity were not
signifi cantly infl uenced in the per protocol tube-fed group [ 62 ]. It is possible
that the lack of effect on supplemental enteral feeding was due to poor tolerance of
the feedings.
In another observational trial of nursing home residents referred to the hospital
for a percutaneous endoscopic gastroscopy (PEG), persons who did not have a pressure ulcer at the time of PEG insertion ( n = 1,124) were 2.3 times more likely to
develop a new pressure ulcer (95 % CI, 2.0–2.7). In those subjects who had a pressure ulcer at the time of PEG insertion ( n = 452), the ulcer was 30 % less likely to
heal (odds ratio 0.70, 95 % CI, 0.55–0.89) compared to controls [ 63 ]. There are
several possibilities for this unexpected observation, but the data suggest that incidence or healing of pressure ulcers is independent of enteral tube feeding.
In 59 older hospitalized patients after a hip fracture, subjects were randomized
to receive either a standard hospital diet alone or standard hospital diet with one
additional oral nutrition supplement daily. The number of pressure ulcers during
hospitalization, during rehabilitation, and after 6 months was not different between
groups [ 64 ].
In 103 hospitalized patients with a hip fracture, the intervention group received
one supplement daily in addition to the standard hospital diet, and the control group
received the standard hospital diet plus a noncaloric water-based placebo. The incidence of stage 1–2 pressure ulcers at 2 weeks was not different between groups
(55 % versus 59 % control). At 28 days, the incidence of stage 2 or higher pressure
ulcer was not different in the nutritional intervention group (18 % vs. 28 %) [
65 ].
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In a study of survival among residents in long-term care with severe cognitive
impairment, 135 residents were followed for 24 months [ 66 ]. The reasons for the
placement of a feeding tube included the presence of a pressure ulcer. Having a
feeding tube was not associated with increased survival; in fact the risk was slightly
increased (OR 1.09). There was no apparent effect of the prevalence of pressure
ulcers in this group of enterally fed persons.
These trials are limited by small sample size, short durations, and methodological
fl aws. Although limited in the power to detect important clinical differences between
groups, the studies to date have not suggested an effect of nutritional interventions
on the prevention of pressure ulcers.
D.R. Thomas
Factors Contributing to the Nutritional Paradox
Historically, hypoalbuminemia has been a hallmark of the pediatric syndrome of
kwasiokor. Until recently, serum albumin and other acute phase reactants (e.g., prealbumin) have been used to defi ne undernutrition. Increasingly, serum albumin and
prealbumin are now recognized as acute phase reactants [ 67 ]. Physiological stress
(such as surgical operations), cortisol excess, and hypermetabolic states reduce
serum albumin even in the presence of adequate protein intake. Serum albumin has
poor correlation with objective measures of nutritional status, suggesting that serum
albumin is measuring a nonnutritional construct [ 68 ].
Infl ammatory cytokines are well known for producing decreases in albumin, prealbumin, cholesterol, transferrin, and hemoglobin. The use of these acute-phase
reactants as nutritional markers could lead to overdiagnosis of undernutrition [ 69 ].
Poor nutritional status defi ned by these variables may indicate poor health rather
than poor nutrient intake [ 70 ].
In chronic disease, cachexia is recognized as a major cause of weight loss [ 71 ].
Cachexia is a complex metabolic syndrome associated with underlying illness and
characterized by loss of muscle with or without loss of fat mass. Anorexia, infl ammation, insulin resistance, and increased muscle protein breakdown are frequently
associated with cachexia. Moreover, cachexia is distinct from starvation, agerelated loss of muscle mass, or primary medical illnesses and is associated with
increased mortality [ 72 ]. Cachexia is associated with cancer [ 73 ], end-stage renal
disease [ 74 ], congestive heart failure [ 75 ], AIDS [ 76 ], and rheumatoid arthritis [ 77 ],
among others.
These evolving concepts have led to proposals for redefi nition of nutritional
constructs. Current understanding of undernutrition defi nes three categories: pure
chronic starvation without infl ammation, acute disease or major injury with infl ammation, and chronic diseases or conditions that impose sustained infl ammation of a
mild to moderate degree [ 78 ]. One of the chief distinguishing factors is that starva-
tion without infl ammation is amenable to hypercaloric feeding in all but the terminally undernourished patients, while acute and chronic infl ammatory conditions are
remarkably resistant to hypercaloric feeding [
79 , 80 ].
8 The Role of Nutrition in the Management and Prevention of Pressure Ulcers
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Cytokine-mediated anorexia and weight loss are common in the population that
develop pressure ulcers. A preliminary study of cytokines in patients with pressure
ulcers indicates that serum interleukin-6 was not different between subjects with a
pressure ulcer ( N = 23) and those without pressure ulcers ( N = 17) within 5 days of
acute hospitalization. Serum interleukin-1β is elevated in patients with pressure
ulcers [ 81 ].
Elevated cytokines, particularly interleukin-1α, interleukin-1β, and interleukin 6, have been observed in persons with pressure ulcers. Whether these levels change
with healing, or are predictive of healing are not known. These cytokines are known
to also increase in severe undernutrition. Existing studies are not clear whether the
elevation is due to the presence of a pressure ulcer or due to underlying severe
undernutrition. Alternatively, the elevation of cytokine levels may be a common
pathway for both conditions.
Circulating serum levels of interleukin-6, interleukin-2, and interleukin-2R are
higher in spinal cord injured patients compared to normal controls and highest in
subjects with pressure ulcers ( N = 19). The highest concentration of cytokines were
in subjects with the slowest healing pressure ulcers [ 82 ]. Among spinal injury
patients with pressure ulcers ( N = 19), interleukin-6 blood levels were increased,
but interleukin-1 and tumor necrosis factor were not elevated [ 83 ]. Levels of
interleukin-1α are elevated in chronic wounds but low in acute wound fl uid [ 84 ].
Cytokines regulate appetite directly through the central feeding drive.
Interleukin-1 concentrations are elevated in elderly patients with severe undernutrition of unknown etiology [ 85 ]. Levels of interleukin-1β and interleukin-6 are
increased in elderly persons without evidence of infection or cancer [ 86 ].
Interleukin-1, interleukin-6, tumor necrosis factor, interferon-γ, leukemia inhibitory
factor (D-factor), and prostaglandin E 2 have all been implicated in cancer-induced
severe undernutrition [ 87 , 88 ]. Leptin, a central regulator of food intake and body
fat mass, increases under the stress of hip operations [ 89 ], but is low in undernour-
ished men [ 90 ].
The lack of effect of hypercaloric feeding in pressure ulcers may refl ect that
the underlying pathophysiology is cytokine-induced cachexia rather than simple
starvation.
137
Conclusions
Nutritional support is a cornerstone of clinical care and should be provided to all
persons, including persons with pressure ulcers, consistent with medical goals and
patient wishes. Whether nutrition can improve the outcome of pressure ulcers
remains disputable.
Energy requirements for persons with pressure ulcers are estimated empirically
between 25 and 30 kcal/kg/day and has been confi rmed in studies using nutritional
formulas such as the Harris–Benedict equation. The optimum amount of protein
intake is not known but likely lies between 1.2 and 1.5 g/kg/day. Higher protein
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D.R. Thomas
intakes may be harmful and have not been associated with higher rates of healing.
Supplemental amino acids and supertherapeutic supplements of vitamins and minerals
have not been shown to have much effect on the healing of pressure ulcers.
Clinical nutritional intervention trials suffer from small sample sizes and poor
methodological design, but in general have not shown exceptional benefi t in
improving complete healing of pressure ulcers. Improvements in nutritional markers,
such as serum protein concentrations, nitrogen balance, and weight gain, have not
usually been accompanied by clinical wound healing [ 91 , 92 ].
Nutritional therapy will improve starvation due to lack of food, but cachexia
associated with infl ammatory conditions has been remarkably resistant to hypercaloric feeding [ 93 ]. Additional interventions besides providing adequate nutrients
may be required in persons with cachexia [ 94 ] .
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D.R. Thomas
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