education
Nutrition and wound healing
Continued research and development in the field of wound healing holds the
potential to affect both quality of life and incidence of mortality. For the health
care provider to promote successful wound healing, an understanding of the
function of nutrients in inflammation and tissue growth is helpful. The intent of
this paper is to discuss the metabolic and cellular pathways crucial to wound
healing and identify appropriate nutritional interventions and clinical applications.
macro- and micronutrients; nutrition therapy; wound healing
W
ound healing results from a com-
plex series of events that involves
the immune system working with
many other physiological systems.
Digestion, absorption, caloric
needs, protein synthesis, protein degradation and
hormonal control are all parameters that play a role
in enabling the body to heal itself.1–3 Any suboptimal
step can affect the outcome of the healing process.
Nutritional status often sets the limits for wound
healing in a healthy individual by providing the
necessary macro- and micronutrients required for
energy utilisation, protein synthesis and immune
responses. The recommended daily allowances
(RDA) for nutrients are based on the requirements
of a healthy population;4 as such, the added
demands for wound healing often exceed the RDA.
In addition, on hospital admittance, roughly 30% of
the elderly population is malnourished. Key nutri-
ents, such as zinc, iron, folate, thiamine, vitamin
B12 and water, are often deficient in otherwise
healthy elderly individuals. Since protein-energy
malnutrition (PEM) prior to and during a wounding
situation can prolong and prevent healing, timely
nutritional assessment of the patient is important in
order to apply nutritional therapy for the best pos-
sible outcome.
Underlying conditions, including age, lean body
mass, wound type and disease state, also affect the
outcome of the healing process. In addition, comor-
bidities, such as cancer and inflammation, can lead
to malnutrition and result in delayed wound heal-
ing. Given the complexity of this process, it is
important that health professionals recognise the
importance of nutritional assessment. Comorbidi-
ties, patient history, and prior nutritional status
may provide important clues for the timing and
choice of medical nutrition therapy to promote
effective wound healing.
j o u r n a l o f wo u n d c a r e v o l 2 0 , n o 8 , A u g u s t 2 0 1 1
Journal of Wound Care.Downloaded from magonlinelibrary.com by 165.193.178.076 on January 13, 2015. For personal use only. No other uses without permission. . All rights reserved.
Anatomy of a wound — profiling macro- A.R. Sherman,1 PhD;
and micronutrient needs during the M. Barkley,1 BS;
1 Department of
different stages of wound healing
Nutritional Sciences,
Wound healing is characterised by the inflammato- Rutgers, State University
ry, proliferative and remodelling phases, each of of New Jersey, USA.
which accomplishes a step in the healing process Email: asherman@aesop.
(Fig 1). These phases involve specific cellular and rutgers.edu.
humoral processes and have individual profiles for
macro- and micronutrient involvement (Table 1). In
understanding both the nutrient needs and timing
of each phase, beneficial therapeutic approaches
can be designed to optimise wound healing.
Inflammatory phase — the clean-up phase
The inflammatory phase is preceded by haemosta-
sis, which involves the initial trauma to the tissue
area by surgery, trauma, or shear. Typically, the
inflammatory phase lasts 4–6 days, depending on
the aetiology of the wound, infection, nutritional
status and comorbidities.
l Roles of macro- and micronutrients  The
processes involved in haemostasis and removal of
debris and foreign invaders from the initial wound
are dependent on several key vitamins and minerals.
Vitamin  K and calcium are required for proper
formation of fibrin clots. Vitamin K is a co-factor for
enzyme activation of prothrombin VII, IX and  X
clotting factors, which result in fibrin formation,
while calcium is necessary for binding these clotting
factors to membranes at the site of injury.
The term ‘inflammatory’ is used for this phase
because of the increased fluid and cell influx found at
the wound location. Although frequently painful for
the patient, fluid influx carries needed oxygen and
nutrients into the area. Albumin shifts from the
blood into the extracellular space, serving as a carrier
protein for vitamins, minerals, hormones, and fatty
acids. Movement of the different cell types into
wounded areas requires increased cell proliferation,
s
357
 education
Fig 1. Phases of wound healing
Inflammatory Proliferative Remodelling
4–6 days 3 days–3 weeks 2 weeks–2 years
Epithelium
Papillary
dermis
Reticular
dermis
•Loose Ends Studio
Subcutis
especially when foreign antigens are present during
infection. Increases in protein, energy and fluid are
required to meet these proliferative needs.
The amino acids arginine and glutamine are sub-
strates utilised in biochemical pathways responsible
for mediating the immune response and collagen
synthesis. Arginine’s role in inflammation influences
subsequent wound healing in the proliferation phase.
Arginine is a substrate for nitric oxide, ornithine, and
proline, which result in vasodilation as well as colla-
gen synthesis and deposition. As well as functioning
as a cytotoxin, arginine, a potent vasodilator, increas-
es permeability and regulates cytokines and the
immune response during the inflammatory phase.
Arginine is a conditionally essential amino acid
required during stress, diabetes and active growth
phases, such as wound healing. It can be converted
into nitric oxide in the nitric oxide synthase pathway
or to ornithine/proline in the arginase pathway. In
the inflammatory phase, the enzymatic pathway
responsible for this is inducible nitric oxide synthase
(iNOS), induced by cytokines, endotoxins, inter-
leukin-1 (IL-1) and tumour necrosis factor-α (TNF-α)
and calcium dependent. A correlation between
decreased nitric oxide synthesis and impaired wound
healing has been reported.5,6 Macrophages secrete
TNF-α early in wound healing and may initiate nitric
oxide synthesis. Animal models have demonstrated
that increased dietary arginine, utilised in the iNOS
pathway, is responsible for increased collagen syn-
thesis, tensile and breaking strength in wounds.7
Vitamin C also enhances nitric oxide synthesis.8
Glutamine is a source of glucose and a precursor to
DNA/RNA and the glutathione antioxidant used in
wound healing. Glutamine represents 30–50% of free
amino acids in the body and is primarily synthesised
in skeletal muscle, which contains 90% of the
358
Journal of Wound Care.Downloaded from magonlinelibrary.com by 165.193.178.076 on January 13, 2015. For personal use only. No other uses without permission. . All rights reserved.
glutamine pool. It is used in acid/base balance in the
kidney, transport and excretion of nitrogen, and is a
required fuel source for pancreatic and gastrointesti-
nal cells. During metabolic stress, glutamine is condi-
tionally essential. Neutrophils, macrophages and
lymphocytes prefer glutamine as an energy source
and as a precursor for nucleotides needed in rapidly
dividing cells. During the inflammatory phase,
phagocytosis, superoxide formation and antigen pres-
entation require glutamine.9,10 Cytotoxic reactive
oxygen species (ROS) need to be quenched by antioxi-
dants and glutamine is an important component of
the powerful endogenous antioxidant glutathione,
which detoxifies peroxides and other compounds.11
l Vitamin and mineral roles as antioxidants  The
influx of increased cell numbers in the inflammatory
phase, although beneficial, has the potential to
damage healthy cells in surrounding tissue.
Neutrophils and macrophages generate bacteriocidal
hydroxyl radicals, superoxide, and hydrogen peroxide.
These ROS are generated in large quantities during the
inflammatory phase. Vitamin C, the principal water-
soluble antioxidant, has the ability to detoxify ROS
both intra- and extracellularly. Intracellular vitamin C,
which is concentrated in neutrophils through SVCT-1
and GLUT 1 and 4 receptors, protects neutrophils by
quenching cytosolic ROS.12 Extracellular vitamin C
facilitates the transition from the inflammatory to
proliferative phase by protecting surrounding
fibroblasts and collagen, responsible for differentiating
into granulation tissue.13–15
Vitamin C prevents lipid peroxidation, which has
the potential to damage phospholipid membranes.
This role has been demonstrated, as vitamin C inhibits
the oxidation of low-density lipoproteins, implicated
in initiating atherogenesis. Vitamin  C also reduces
oxidised vitamin  E, a lipid-soluble antioxidant that
protects cellular membranes, protein and DNA. Lastly,
vitamin C suppresses chemotactic recruitment of leu-
cocytes into vascular walls when responding to free
radical inflammatory mediators.16 The combined roles
of vitamin  C in ROS protection, both directly and
through vitamin E, along with the regulation of
chemotactic adhesion, may provide the necessary bal-
ance to facilitate the inflammatory phase while limit-
ing tissue damage and prolonged inflammation.
Cytosolic enzymes protect intracellular proteins
from oxidative damage during the inflammatory
phase. When available in the appropriate physiologi-
cal concentrations, zinc and copper are co-factors for
superoxide dismutase, and iron and selenium are co-
factors for catalase and glutathione peroxidase. Cata-
lytic conversion of superoxide and hydrogen perox-
ide protects cells from ROS damage. Protection
provided by these enzymes can be compromised by
preexisting mineral deficiencies. It has been suggested
that too high a concentration of zinc can interfere
with calcium-dependent haemostasis, by altering cal-
j o u r n a l o f wo u n d c a r e v o l 2 0 , n o 8 , A u g u s t 2 0 1 1
 education

References
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3 Molnar, J.A. Overview of
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Nutrition and Wound
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4 Escott-Stump, S., Earl, R.
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5 Rizk, M., Witte, M., Barbul,
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6 Schwentker, A.,Vodovotx,
Y., Weller, R., Billiar, T. Nitric
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8 Heller, R., Unebehaun, A.,
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L-ascorbic acid potentiates
endothelial nitric oxide
synthesis via a chemical
stabilization of
tetrahydrobiopterin. J Biol
Chem. 2001; 276: 1, 40–47.
9 Furukawa, S.
Supplemental glutamine
augments phagocytosis and
reactive oxygen
intermediate production by
neutrophils and monocytes
from postoperative
patients. Nutrition. 2000;
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10 Newsholme, P. Why is
L-glutamine metabolism
important to cells of the
immune system in health,
post injury, surgery or
infection? J Nutr. 2001; 131:
9 (Suppl.), 2515S–2522S.
11 Watford, M. Glutamine
metabolism and function in
relation to proline
synthesis and the safety of
glutamine and proline
supplementation. J Nutr.
2008; 138: 10, 2003S–2007S.
12 Levine, M., Padayatty, S.,
Wang,Y. et al.Vitamin C. In:
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Biochemical, Physiological,
Molecular Aspects of
Human Nutrition (2nd
edn). Saunders, 2006.
Table 1. Summary of the roles of macro- and micronutrients during the inflammatory and
proliferative phases of wound healing
Biochemical and functional pathways utilised during the wound healing process
Macro- and micronutrients Inflammation Proliferation
Protein and energy Increased need for acute phase proteins Increased need for collagen and
and proliferation of neutrophils, lymphocytes extracellular-matrix proteins (collagen,
and macrophages. elastin), angiogenesis, fibroblast and
epithelial proliferation
Arginine Nitric oxide synthase: permeability, Arginase I and II: collagen formation
vasodilation, cytotoxic and cell growth
Glutamine Acute phase protein synthesis, immune cell Preferred energy source for fibroblasts
energy source, DNA replication, phagocytosis,
superoxide and glutathione formation, anti­-
gen presentation
Vitamin C Antioxidant, chemotaxis Prolyl and lysyl hydroxylases
Zinc and copper B and T lymphocyte and neutrophil Epithelialisation and granulation tissue
proliferation, protein synthesis and superoxide formation
dismutase
Iron immune response, catalase Prolyl and lysyl hydroxylases.
cium concentrations, and retard healing.17 The calci- for wound healing. The extracellular matrix (ECM)
um dependence of iNOS further underscores the proteins, fibronectin, laminin, hyaluronan, dermatan
importance of calcium homeostasis in the inflamma- sulphate and keratan sulphate, are synthesised by
tory response. Zinc requirements appear to be fibroblasts. Myofibroblasts contract tissue for wound
increased during the formation of granulation tissue, closure. In order to support cell hypertrophy and
scar tissue and epithelialisation in the proliferative increase production of functional proteins in the
stage. Awareness of the wound’s stage is beneficial in ECM, energy and protein needs are increased. The
determining a specific nutrient profile that can pro- additional increase in enzymatic processes in turn
mote healing, and further research linking specific increases the need for vitamin and mineral co-factors.
outcomes of healing with the timing of nutrients.18,19 Studies have demonstrated increased need for vita-
Cellular and humoral immunity, principally during min  C in the physiological stress that accompanies
the inflammatory stage, provide both phagocytosis of wounds, trauma, burns, and major surgery.22 While
bacteria/debris and protection afforded from humoral the focus here is on the vitamins and minerals
immunity. Zinc deficiencies reduce the number of required for connective tissue synthesis, it is impor-
B and T lymphocytes, with total lymphocyte counts tant to note that the RDAs for all vitamins and miner-
of less than 200 shown to correlate with poor wound als should be maintained during tissue regeneration.
healing.20 Furthermore, copper deficiencies reduce Protein synthesis requires all nine essential amino
the number of neutrophils and T lymphocytes.21 acids, as well as conditionally essential amino acids
Since it is not uncommon for total lymphocyte arginine and glutamine. In addition to arginine’s role
counts and intradermal skin tests to be utilised as as a substrate in the iNOS pathway in the inflamma-
screening tools for adequate immune response in tory phase, it is also a substrate in the arginase I and
wound healing, nutritional status should be taken II pathway present in fibroblasts during the prolifera-
into consideration when interpreting results. tive phase. Arginase I is expressed in hepatocytes and
fibroblasts, while arginase II is expressed in macro-
Proliferative phase — the building phase phages. Arginase catalyses the formation of orni-
Once the inflammatory phase has provided the nec- thine, which generates both proline and polyamines,
essary clean-up and cytokine signalling, the substrates for collagen formation and cell growth.
proliferative phase begins. This second stage of Transforming growth factor-β (TGF-β), secreted by
wound healing can commence as early as 3 days and macrophages and fibroblasts, promotes the arginase
has a duration of approximately 3 weeks. II pathway while downregulating the iNOS pathway
Fibroblasts, which synthesise collagen, reticulin in inflammation. This suggests arginine may play a
and elastin, are considered the critical cells necessary regulatory role in wound healing.23

360 j o u r n a l o f wo u n d c a r e v o l 2 0 , n o 8 , A UGUST 2 0 1 1

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 education
13 Wang,Y., Russo, T., Kwon,
O. et al. Ascorbate recycling
in human neutrophils:
Induction by bacteria. Proc
Natl Acad Sci U S A. 1997;
94: 25, 13816–13819.
14 Long, C., Maull, K.I.,
Krishnan, R.S. et al.
Ascorbic acid dynamics in
the seriously ill and injured.
J Surg Res. 2003; 109: 2,
144–148.
15 Polidori, M., Mecocci, P.,
Levine, M., Frei, B.
Short-term and long-term
vitamin C supplementation
in humans dose-
dependently increases the
resistance of plasma to ex
vivo lipid peroxidation. Arch
Biochem Biophys. 2004;
423: 1, 109–115.
16 Lehr, H., Weyrich, A.S.,
Saetzler, R.K. et al.Vitamin
C blocks inflammatory
platelet-activating factor
memetics created by
cigarette smoking. J Clin
Invest. 1997; 99: 10,
2358–2364.
17 Lansdown, A.B.G. Zinc
in the healing wound.
Lancet. 1996; 347: 9003,
706–707.
18 Heng, M., Song, M., Heng,
M. Reciprocity between
tissue calmodulin and
CAMP levels; modulation by
excess zinc. Br J Dermatol.
1993; 129: 3, 280–285.
19 Lansdown, A.B.G.
Physiological and
toxicological changes in the
skin resulting from the
action and interaction of
metal ions. Crit Rev Toxicol.
1995; 25: 5, 397–462.
20 Walsh, C.T., Sandstead,
H.H., Prasad, A.S. et al. Zinc:
health effects and research
priorities for the 1990s.
Environ Health Perspect.
1994; 102: (Suppl. 2), 5–46.
21 Percival, S.S.
Neutropenia caused by
copper deficiency: possible
mechanisms of action. Nutr
Rev. 1995; 53: 3, 59–66.
22 Tanaka, H., Molnar, J.A.
Vitamin C and wound
healing. In: Molnar, J.A. (ed).
Nutrition and Wound
Healing (1st edn). CRC
Press, 2007.
23 Stechmiller, J.K.,
Childress, B., Cowan, L.
Arginine supplementation
and wound healing. Nutr
Clin Pract. 2005; 20: 1,
52–61.
24 Ahuja,V., Rizk, M., Barbul,
A. Arginine and wound
healing. In: Molnar, J.A. (ed).
Nutrition and Wound
Healing (1st edn). CRC
Press, 2007.
362
Journal of Wound Care.Downloaded from magonlinelibrary.com by 165.193.178.076 on January 13, 2015. For personal use only. No other uses without permission. . All rights reserved.
Increased collagen synthesis in fibroblasts has been
demonstrated in response to arginine in murine cell
cultures;24 however, other studies have demonstrated
low rates of conversion of ornithine to proline in
wound plasma.24 Further research is needed to define
the utilisation of this pathway during the proliferative
phase in wound healing. Glutamine is also utilised by
fibroblasts, and it may be the preferred energy source.11
l Collagen formation — a‘team’ approach  Synthesis
of collagen and ECM proteins by fibroblasts to
generate new connective tissue is central to the
proliferative phase. Collagen type I represents 80–90%
of the connective tissue found in the skin. The
collagen molecule is a right-handed triple helix, and
each polypeptide α-chain has uninterrupted repeats
of the amino acid glycine every three amino acids,
with proline or hydroxyproline representing up to
20–25% of the molecule. Collagen synthesis involves
modifications to the collagen molecule both intra-
and extracellularly. Post-translational hydoxylation
of proline and lysine via prolyl and lysyl hydroxylases
are dependent on vitamin C and iron. These
modifications are crucial for stabilising pro-collagen
α-helix structure through hydrogen bonding. In the
event of a vitamin C or iron deficiency, unstable helix
structure results in a non-functional collagen
molecule. This is evidenced in the clinical
manifestations of haemorrhagic lesions, capillary
weakness, petechiae and wound reopening in scurvy.
Vitamin C supplementation in both animal models
and humans has been shown to increase collagen
synthesis and tensile strength, as well as to increase
stabilisation of collagen type I mRNA.3,22
Adequate availability of tissue iron is required
since prolyl hydroxlyases are non-haem iron pro-
teins. Iron is also incorporated in iron-sulphur pro-
teins utilised for energy and ribonucletide reductas-
es, which assist in DNA synthesis, with both
processes increased in the proliferative phase.25
ECM proteins provide a roadmap for migration of
key cells into the area, as well as immobilising
cytokines such as TGF-β. The increased nutrient
needs that support synthesis of both collagen and
ECM proteins have the potential to become limiting
during deficiencies.
Remodelling phase — wound maintenance
The remodelling phase can begin as early as 2 weeks
and continue for several years. Upon completion of
new tissue growth, protein and energy needs readjust
to normal homeostatic levels. Maintenance of tissue
synthesis and degradation involves proteolytic deg-
radation by a variety of matrix metalloproteinases
(MMPs) secreted by fibroblasts, chondrocytes, mono-
cytes, neutrophils, and macrophages. Over time, a
net decrease is observed in collagen synthesis in com-
parison to the proliferative phase. Collagen strength
is eventually maximised and it is linked to adjacent
tissues.26 Since MMPs are utilised, sufficient concen-
trations of magnesium and zinc should be available.
The role of vitamin C and collagen synthesis under
non-proliferative conditions is evident, since wound
reopening is documented in scurvy.
Medical nutrition therapy and physiological
considerations with wounds
Energy and protein
Increased energy needs exist in the inflammatory
and proliferative phases to support the immune
response and regeneration of new tissue. Within the
home-care setting, a variety of predictive equations
are available to calculate energy requirements.
Comorbidities, such as renal and liver disease, dia-
betes and obesity, can alter energy requirements;
therefore, modifications are evaluated under the
management of a dietitian. Typically, the provision
of sufficient energy spares amino acids for protein
synthesis, needed for acute phase proteins and gen-
eration of new tissue. Provisions in the range of
23–35kcal/kg are prescribed.27 The Mifflin-St Jeor
equation can also be applied to healthy individuals
with appropriate activity and injury factors.28
Protein requirements for wound healing can vary
depending on the type and severity of the wound.
Current clinical applications suggest 1–1.5g/kg body
weight for trauma, surgical and pressure ulcer
wounds. Burns and severe wounds may require
upwards of 1.5–2.0g/kg,29 while a normal, healthy
adult requires 0.8g/kg body weight.
A full complement of all amino acids is necessary
for protein synthesis. Animal proteins, such as eggs,
milk and meat, provide complete proteins. If vegeta-
ble proteins are the only source of nutrition, use of
complementary plant foods, such as beans and rice,is
necessary. Soy is the exception, since it has an amino
acid score, which is adequate to meet requirements.30
Current protein supplements provide a range of
formulations, from specific amino acids to complete
proteins. With the variety of supplements currently
marketed, an awareness of matching the protein
needs of the individual to the supplement may
become crucial to home-health care providers.31 For
example, a patient that has existing PEM would not
benefit from a supplement that provides just arginine
and vitamin C, since preexisting protein malnutrition
would require all the essential amino acids.
Albumin and prealbumin — nutrition status and
predictor of mortality
The most abundant plasma protein is albumin, which
is synthesised in the liver and functions as a carrier for
fatty acids, vitamins, minerals, bilirubin, cortisol, thy-
roxine and drugs. It also maintains osmotic balance
between the extra and intravascular compartments of
the body. Historically, albumin was used as a marker
to assess protein status, since a decrease in availability
j o u r n a l o f wo u n d c a r e v o l 2 0 , n o 8 , A UGUST 2 0 1 1

of amino acids can result in the decreased synthesis of
albumin. However, it is now known that specific
physiological conditions can shift albumin to the
extravascular space, resulting in a decrease in plasma
albumin independent of overall nutritional status.32
Illness, stress, inflammation, trauma and surgery
all trigger this extravascular shift due to hormone
and cytokine signalling. Other disease states, such as
diabetes-induced glomerulosclerosis, lupus ery-
thematosus, renal vein thrombosis, drugs, burns, cir-
rhosis, rheumatoid arthritis and multiple myeloma,
decrease albumin levels directly. The measurement of
albumin levels is also dependent on the hydration
state of the patient and administration of anabolic
hormones.33 Given the long list of physiological con-
ditions that affect albumin, its use as a marker of
nutritional status can lead to misinterpretation.
In the event of decreased albumin due to inflam-
mation or trauma, biochemical signalling directs bio-
chemical pathways to utilise lean body mass (mainly
muscle tissue) as a protein source and provides the
additional protein needs required. Lean body mass
provides the amino acid glutamine, which is utilised
for both energy and protein. Glucose is synthesised
j o u r n a l o f wo u n d c a r e v o l 2 0 , n o 8 , A UGUST 2 0 1 1
Journal of Wound Care.Downloaded from magonlinelibrary.com by 165.193.178.076 on January 13, 2015. For personal use only. No other uses without permission. . All rights reserved.
education
through gluconeogenesis in the liver, and amino
acids, specifically glutamine, can be utilised for acute
phase protein synthesis. This reduction in plasma
albumin levels, along with increased utilisation of
lean body mass for protein, has been causally linked
with increased morbidity and mortality. A 10%
decrease in lean body mass level is connected to 10%
mortality, with increased infection and decreased
immunity, whereas a 20% loss in lean body mass is
associated with decreased wound healing and 30%
mortality.1 Decreased albumin, prealbumin, transfer-
rin, and total lymphocyte counts have repeatedly
been linked to increased morbidity and mortality.
Current clinical protocols identify that patients
are at high risk of malnutrition when plasma albu-
min levels are less than 3.0g/dl accompanied by 3–5
additional altered lab values.34 Decreased albumin
levels beyond 26 weeks in long-term care have also
been predictive of low healing rates in patients with
pressure ulcers.29,32,35
Prealbumin (transthyretin), a carrier protein for
vitamin  A, is also used as a marker to identify
patients at risk of malnutrition. Similar to albumin,
it is a negative acute phase protein that decreases in
363
 education
25 Crichton, R. Iron. In:
Stipanuk, M. (ed).
Biochemical, Physiological,
Molecular Aspects of
Human Nutrition (2nd
edn). Saunders, 2006.
26 Ross, M.H., Pawlina, W.
Connective tissue. In:
Histology - A Text and Atlas
(5th edn). Lippincott
Williams & Wilkins, 2006.
27 Escott-Stump, S. Dietary
practices and miscellaneous
conditions. In: Escott-
Stump, S. (ed). Nutrition
and Diagnosis-Related Care
(6th edn). Lippincott
Williams & Wilkins, 2008.
28 Mifflin, M., St Jeor, S.T.,
Hill, L. et al. A new
predictive equation for
resting energy expenditure
in healthy individuals. Am J
Clin Nutr. 1990; 51: 2,
241–247.
29 Charney, P., Malone, A.
Nutrition Assessment (2nd
edn). American Dietetic
Association, 2009.
30 Gallagher, M.L. The
nutrients and their
metabolism. In: Mahan, L.K.,
Escott-Stump, S. (eds).
Krause’s Food & Nutrition
Therapy (12th edn).
Saunders, 2008.
31 Castellanos,V.H.,
Litchford, M.D., Campbell,
W.W. Modular protein
supplements and their
application to long-term
care. Nutr Clin Pract. 2006;
21: 5, 485–504.
32 Fuhrman, P., Charney, P.,
Mueller, C. Hepatic proteins
and nutrition assessment. J
Am Diet Assoc. 2004; 104:
8, 1258–1264.
33 Nelms, M.N. Assessment
of nutrition status and risk.
In: Nelms, M., Sucher, K.,
Long, S. (eds). Nutrition
Therapy and
Pathophysiology.
Wadsworth/Cengage
Learning, 2007.
34 Nutrition Care Manual.
American Dietetic
Association; c2011 [cited
20 July 2011]. Available
from: http://www.
nutritioncaremanual.org.
35 Ek, A.C., Unosson, M.,
Larsson, J. et al. The
development and healing of
pressure sores related to
the nutritional state. Clin
Nutr. 1991; 10: 5, 245–250.
36 Bernstein, L., Ingenbleek,
Y. Transthyretin: its
response to malnutrition
and stress injury. clinical
usefulness and economic
implications. Clin Chem
Lab Med. 2002; 40: 12,
1344–1348.
364
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response to metabolic stress. It has a half-life of
2  days, in contrast to the 20-day half-life of albu-
min. Monitoring of nutritional interventions
through prealbumin’s quick recovery has demon-
strated improved treatment outcomes and has been
incorporated into assessment protocols in several
health-care settings.36–38 Consideration of dietary
consumption, weight loss, serum proteins, wound
healing and changes in medical status provide a
more accurate assessment of nutritional status than
reliance on serum proteins alone.
Vitamin C
Vitamin C is the principal, water-soluble antioxi-
dant in plasma. Dietary intake of vitamin  C is
reflected mainly in plasma levels. Body stores are
more accurately reflected in leucocytes, which pro-
vide a recycling pathway for oxidised vitamin C.
As wound healing stages are dependent upon vita-
min C in a number of cell types and enzymes, tissue
levels would be a more appropriate assay for body
stores.12 Body pool vitamin C can be depleted within
30 days in the absence of adequate intake. Deficiency
symptoms include petechial haemorrhage, bleeding
gums, ecchymoses, hyperkeratosis and arthralgia.
Fatigue is an early symptom preceding all others.
Populations at risk of deficiency are individuals with
cancer, cachexia, drug and alcohol addiction, elderly
men and low socioeconomic status.
Vitamin C intakes of 100–200mg/day are sufficient
to maximise both plasma and tissue levels in healthy
adults.39,40 These concentrations are equivalent to the
consumption of five servings of fruits and vegetables
daily. Many studies show benefits of the consump-
tion of vitamin C-rich foods, with decreased risk of
stroke, diabetic complications, heart attack, and low-
er risk of gastrointestinal and lung cancer. The Behav-
ioral Risk Factor Surveillance System (BRFSS) reported
only 32.6% of the US adult population surveyed con-
sumed fruit two or more times per day.41
Intestinal vitamin C uptake studies indicate that
its bioavailability maximises at 200mg; therefore,
divided doses are indicated above this level. The low
toxicity risk of vitamin  C in light of deficiencies
existing in malnourished and elderly population
has led practitioners to prescribe vitamin  C for
wound healing in elective small to moderate sur-
gery, and to promote pressure ulcer healing. It is
typically administered in doses of 500–1000mg dai-
ly, in divided doses of 250mg each. Vitamin C also
increases iron absorption by reducing iron to the
more bioavailable, ferrous state; as such, it is con-
traindicated in iron overload patients, such as sickle
cell sideroblastic anaemia and thalassaemia major.
Limits of 200mg/day are also indicated in patients
with renal failure and/or a history of renal stones.
Excessive vitamin C supplementation can result in
false positives on occult blood stool tests.
j o u r n a l o f wo u n d c a r e v o l 2 0 , n o 8 , A u g u s t 2 0 1 1
The trace elements — iron, zinc, copper
Zinc, iron, and copper are three trace elements that
have been assigned relevant roles in wound healing.
Plasma levels of these minerals are difficult to assess
and generally cannot be directly linked to nutrition-
al status or wound healing. Comorbidities, meta-
bolic stress, and metabolic balance all affect plasma
and tissue localisation of each mineral.
Zinc absorption and status is influenced by a
number of factors. Dietary zinc absorption is mainly
in the jejunum and is inhibited by high dietary
phytate and calcium. Since 57% of plasma zinc is car-
ried on albumin and 40% on alpha-2 macroglobulin,
a low albumin level leads to an inaccurate estimate of
total zinc body pools. Acute phase responses to infec-
tion and inflammation also sequester zinc within the
liver, lowering plasma zinc levels. Deficiency symp-
toms include delayed wound healing, loss of appe-
tite, diarrhoea, hair loss, sexual impotence, atopic
dermatitis, psoriasis, taste abnormalities, white spots
on fingernails and depression. Populations at risk of
zinc deficiency are vegetarians, alcoholics, and indi-
viduals with malabsorptive disease and chronic diar-
rhoea. At the other end of the zinc spectrum, high
dietary zinc interferes with copper absorption and
can result in copper deficiency.
Clinical evidence supports a benefit of zinc supple-
mentation in wound healing only in zinc-deficient
individuals. The timing of zinc requirements during
the different phases of wound healing may be more
relevant. New granulation tissue in the proliferative
phase of wound healing has increased zinc require-
ments, which corroborates its functional role as a
transcriptional regulator and a mediator of insulin-
like growth factor.17,42,43 Guidelines from the National
Pressure Ulcer Advisory Panel White Paper suggest
supplementation of no more than 40mg elemental
zinc per day in deficient individuals.44 Current clini-
cal dosing is generally given as zinc sulphate 220mg
PO daily/10 days, which delivers close to RDA of
15mg per day, assuming a 30% bioavailability of zinc.
Longer durations of zinc supplementation can result
in copper deficiencies, which can result in aortic rup-
ture and abnormal bone collagen cross-linking.45
The literature on copper status in wound healing
seems to be secondary to other trace minerals, per-
haps because severe copper deficiency is rare. Cop-
per deficiencies are usually a result of over-supple-
mentation with zinc, inadequate supplementation
with total parenteral nutrition, and decreased
absorption with intestinal resection.21 Deficiency
usually presents clinically with neutropenia.
Plasma copper is incorporated into ceruloplasmin
in the liver, which increases in the presence of infec-
tion and inflammation. Past studies have demon-
strated that deficiencies resulted in increased infec-
tions in patients with Menkes’ disease, a
neurodegenerative disease of impaired copper trans-
 education

port, and pre-term infants, while supplementation wound healing additional iron is recommended. The 37 Brugler, L., DiPrinzio,
decreased infection in infants with Marasmus, a form level and timing of iron supplementation during M.J., Bernstein, L. The
of severe protein-energy malnutrition.46 It is hard to wound healing has not yet been determined. Symp- five-year evolution of a
malnutrition treatment
elucidate copper’s specific role in immunity, since toms of deficiency include fatigue, impaired physical program in a community
copper is utilised in numerous enzymes and its func- work, difficulties in mental concentration and com- hospital. Jt Comm J Qual
Improv. 1999; 25: 4,
tion in ceruloplasmin can indirectly affect iron sta- promised immune function. Supplemental iron is 191–206.
tus. Elastin cross-linking and angiogenesis are two best absorbed from ferrous fumarate, ferrous sulphate 38 Mears, E. Outcomes of
key steps in the formation of granulation tissue and and ferrous gluconate. continuous process
improvement of a nutritional
ECM in the proliferative phase of healing, both of
care program incorporating
which are dependent on copper. Current literature Conditionally essential amino acids — glutamine serum prealbumin
suggests that angiogenesis may be copper sensitive and arginine measurements. Nutrition.
1996; 12: 7–8, 479–484.
and topical copper has been shown to accelerate Glutamine and arginine are considered to be condi-
39 Gray, M.,Whitney, J.D.
murine dermal wound closure.47 Given the pivotal tionally essential since endogenous synthesis is una- Does vitamin C
mechanisms that copper is utilised in, it is warranted ble to meet metabolic requirements in times of supplementation promote
pressure ulcer healing? J
that patients should be assessed for adequate copper stress, intestinal diseases, growth and trauma. The Wound Ostomy Continence
intake and maintain a RDA level of intake.47 current theory is that arginine and glutamine sup- Nurs. 2003; 30: 5, 245–249.
There is no literature to date that supports iron plementation may be beneficial to wound healing 40 Halliwell, B.Vitamin C:
poison, prophylactic, or
supplementation for promoting wound healing. when these amino acids become essential. Increased
panacea? Trends Biochem
Although iron’s participation as a co-factor for anti- immunity and collagen deposition have been attrib- Sci. 1999; 24: 7, 255–259.
oxidants and collagen synthesis has been demon- uted to both; however, more studies are needed to 41 Behavioral Risk Factor
strated,25 causal links between iron deficiency and explore their efficacy and dosing. Most research has Assessment Survey
(BRFSS). Fruit and
wound healing outcomes have not been identified. focused on incisional wounds in animal models or vegetable consumption
The interdependency of trace elements in biochem- in vitro with fibroblast cultures.23 among adults - 2005.
MMWR. 2007 [cited 20 July
ical pathways and the complexity of the immune Arginine, lysine and ornithine share the same 2011]; 56: 10, 213–217.
response are difficult to control in study design. protein transporter in the intestine and in other Available from: http://www.
Iron is absorbed more readily from meat sources, as sites, such as the brain, leucocytes, erythrocytes and cdc.gov/mmwr/preview/
mmwrhtml/mm5610a2.htm.
haem, or by combining meat with plant sources. fibroblasts. Evidence for arginine’s efficacy in wound 42 Lewis, B. Zinc and
High-fibre supplements, phytates, and legumes and healing is scarce at best. The few human studies that vitamin C in the aetiology
beans can inhibit uptake.33 have been completed focused on incisional wounds of pressure sores. J Wound
Care. 1996; 5: 10, 483–484.
As with zinc, accurate iron status is hard to assess in a healthy population; increased collagen and pro-
43 Collins, N. Zinc
during inflammation. Hepatic mechanisms respond tein deposition was demonstrated with 17–25g free supplementation: yea or
to inflammation by decreasing intestinal uptake and arginine supplements for a 14-day period.48–50 nay? Adv Skin Wound Care.
2003; 16: 5, 226–230.
release of iron into plasma. In addition, transferrin lev- The role of arginine in chronic inflammation asso-
44 Dorner, B., Posthauer,
els decrease in response to inflammation, and ferritin ciated with pressure and diabetic ulcers has yet to be M.E., Thomas, D. The role of
levels can increase. In the absence of inflammation, a elucidated. One study demonstrating decreased nitric nutrition in pressure ulcer
prevention and treatment:
ferritin status < 12μg/dl reflects exhaustion of iron oxide in diabetics reported restored wound healing National Pressure Ulcer
stores. Beyond this point, transferrin iron begins to with arginine supplementation.24 Arginine dosing has Advisory Panel White
decrease. Less than 16% transferrin reflects functional been found to be safe at 30–60g/day, with reported Paper. Adv Skin Wound
Care. 2009; 22: 5, 212–221.
iron depletion. Transferrin receptor is a far superior mild gastrointestinal disturbances in some cases.31
45 Grider, A. Zinc, Copper,
marker of functional depletion but it is not commonly However, caution should be exercised with specific and manganese. In: Stipanuk,
used in clinical practice due to prohibitive cost. Other comorbidities. One randomised trial reported M. (ed). Biochemical,
Physiological, Molecular
measurements, such as mean corpuscular volume and increased mortality after acute myocardial infarction Aspects of Human
erythrocyte protoporphyrin, have delayed responses during arginine supplementation.31 Since arginine is Nutrition (2nd edn).
due to the 120-day duration of erythrocytes.25 utilised in the urea cycle, it may be contraindicated in Saunders, 2006.
46 Sherman, A.R. Zinc,
Despite the absence of evidence to support a ben- patients with renal and liver disease.23,31 copper, and iron nutriture
efit of iron supplementation in wound healing, it is Glutamine needs should be considered in the and immunity. J. Nutr. 1992;
important to note that iron deficiency is the most context of metabolic stress. Circulating glutamine 122: 3 (Suppl.), 604–609.
47 Sen, C.K., Khanna, S.,
common anaemia in the US, specifically among and dietary glutamate are the enterocyte’s primary
Venojarvi, M. et al.
childbearing females. Studies documenting iron defi- fuel source. In the presence of inflammatory condi- Copper-induced vascular
ciencies have demonstrated altered immune respons- tions, such as wound healing, endogenous endothelial growth factor
expression and wound
es resulting in increased infection, decreased lym- glutamine is shunted away from enterocytes to sup- healing. Am J Physiol Heart
phocyte proliferation, decreased interleukin-1 ply fuel for immune cells, substrate for gluconeo- Circ Physiol. 2002; 282: 5,
synthesis in macrophages, and impaired protein syn- genesis, and amino acids for acute phase protein H1821–H1827.
48 Barbul, A., Lazarou, S.A.,
thesis in immune tissues.46 These cellular and humor- synthesis. When attempting to increase plasma Efron, D.T. et al. Arginine
al responses are crucial steps in the inflammatory and glutamine to efficacious concentrations during met- enhances wound healing
proliferative phases of wound healing. Since current abolic stress, the increased dietary glutamine and lymphocyte immune
responses in humans.
recommendations for iron are based on replacement requirements of the entercoytes need to be met Surgery. 1990; 108: 2,
of normal losses, these authors suggest that during first.11 Metabolic stress signals biochemical path-
s

331–337.

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 education
49 Hurson, M., Regan, M.C.,
Kirk, S.J. et al. Metabolic
effects of arginine in a
healthy elderly population. J
Parenter Enteral Nutr.
1994; 19: 3, 227–230.
50 Williams, J.Z., Abumrad,
N., Barbul, A. Effect of a
specialized amino acid
mixture on human
collagen deposition. Ann
Surg. 2002; 236: 3,
369–375.
51 Wernerman, J. Clinical
use of glutamine
supplementation. J Nutr.
2008; 138: 10, 2040S–2044S.
52 Schoemann, M.B.,
Bechtold, C.D., Agarwal, S.,
Lentz, C.W. Glutamine and
wound healing. In: Molnar,
J.A. (ed). Nutrition and
Wound Healing (1st edn).
CRC Press, 2007.
53 Collins, C.E., Kershaw, J.,
Brockington, S. Effect of
nutritional supplements on
wound healing in
home-nursed elderly: a
randomized trial.
Nutrition. 2005; 21: 2,
147–155.
54 Arnaud-Battandier, F.,
Malvy, D., Jeandel, C. et al.
Use of oral supplements in
malnourished elderly
patients living in the
community: a pharmaco-
economic study. Clin Nutr.
2004; 23: 5, 1096–1103.
55 Mini-Nutrition
Assessment – MNA.
Société des Produits Nestlé
S.A. c2004 [cited 20 July
2011]; Available from:
http://mna-elderly.com/.
56 Soriano, L.F.,Vazquez,
M.A.L., Perez-Portabella
Maristany, C. et al. The
effectiveness of oral
nutritional supplementation
in the healing of pressure
ulcers. J Wound Care. 2004;
13: 8, 319–322.
57 Heyman, H., van de
Looverbosch, D.E.J., Meijer,
E.P., Schols, J.M.G.A.
Benefits of an oral
nutritional supplement on
pressure ulcer healing in
long-term care residents. J
Wound Care. 2008; 17: 11,
476–480.
58 Milne, A.C., Avenell, A.,
Potter, J. Meta-analysis:
protein and energy
supplementation in older
people. Ann Intern Med.
2006; 144: 1, 37–48.
59 Green, S.M., Winterberg,
H., Franks, P.J. et al.
Nutritional intake in
community patients with
pressure ulcers. J Wound
Care. 1999; 8: 7, 325–330.
366
Journal of Wound Care.Downloaded from magonlinelibrary.com by 165.193.178.076 on January 13, 2015. For personal use only. No other uses without permission. . All rights reserved.
ways to upregulate net glutamine synthesis in mus-
cle tissue. This can result in decreased lean body
mass, a concern, particularly in older patients who
typically have lowered muscle mass.
No clinical studies were found demonstrating
glutamine’s efficacy with improved wound healing.
The study by Williams et al.50 did report increased
collagen deposition in vivo; however, these results
cannot be directly linked to glutamine since arginine
and β-hydroxy β-methylbutyrate were given as well
as glutamine. Some clinical studies have demonstrat-
ed that parenteral supplementation of glutamine
decreases mortality and complication rates in ICU
patients.51 Beneficial effects observed with enteral
supplementation have been limited to maintaining
the integrity of the intestines and further research is
needed to explore effects on specific pathologies.52
Typical diets provide 10g of glutamine per day. Dos-
ing studies indicate glutamine to be quite safe in the
range of 40–55g/day, with dietary requirements under
catabolic conditions as high as 20–40g/day. Dosing
near 0.6g/kg body weight in divided doses has been
reported to be beneficial.11,31 As with arginine, caution
should be exercised in glutamine supplementation in
patients with renal and liver diseases since excessive
glutamine increases blood ammonia levels.
Nutritional supplements, malnutrition and
wound healing
The evidence that nutritional deficiencies are a risk
factor for pressure ulceration and delayed healing
has prompted research and marketing focused on
nutritional intervention and its affect on wound
outcomes. This has led to the development of vari-
ous commercial nutritional supplements, adminis-
tered in acute and long-term settings accessible by
health professionals. The effects of nutritional sup-
plementation in the home-care setting are just
beginning to be examined. Collins demonstrated
improvements in cognitive and wound indices in
home-nursed older patients.53
A prospective, longitudinal, cohort study reported
an improvement in mini-nutrition assessments
(MNAs) located in geographical areas with high sup-
plement prescription rates in malnourished older
patients. The MNA, developed by Nestle, is a reliable
nutritional assessment survey composed of 18 ques-
tions, categorised into general, anthropometric, die-
tary and subjective assessment. In this study, baseline
MNA scores of community patients assessed as at-risk
or malnourished improved significantly in the test
group that was prescribed frequent oral supplemen-
tation (> 95% of group), in contrast to the group that
was prescribed less oral supplementation (10% of
group).54,55 Scarce data are available on whole food
sources, which have the potential to provide compa-
rable macro- and micronutrient levels, as well as the
additional health benefits of phytonutrients. Com-
mercial liquid nutritional supplements typically con-
sist of more than one nutrient, often combinations
of protein, vitamin C arginine, glutamine, zinc, iron
and vitamin E. Since these supplements are mixed, it
is generally not possible to assign causality to a single
micronutrient in intervention studies.
Despite claims of the beneficial outcomes of nutri-
tional supplements for wound healing, variability
among study designs has limited consistency in evi-
dence-based conclusions. Variations in age, comor-
bidities, biochemical assays, definitions of malnutri-
tion, timing and wound measurement protocol are
some study limitations. Ethical considerations, such
as withholding a nutritional supplement from a
patient, also impose severe limitations on the inter-
pretation of results. Non-existent placebo-controls
or ‘quasi’ controls from outside of the study are
often utilised in study design. In a randomised trial
in home-nursed elderly, a significant decrease in
wound exudate was reported comparing 1kcal/ml
versus 2kcal/ml supplements with intake. However,
the study had limitations due to the absence of a
placebo-control group.52,55,56
Recently, a meta-analysis evaluated 55  trials
(n=9187) that randomly assigned elderly patients pro-
tein and energy supplementation and assessed for
improvement in clinical and nutritional outcomes.58
It was found that the quality of most studies was poor
with inadequate blinding of outcome assessors. Small
sample sizes and short length of study made it diffi-
cult to draw significant conclusions. The meta-analy-
sis concluded that nutritional supplementation
results in fewer complications and reduced mortality
in individuals who received short-term care with pre-
existing malnourishment, with no evidence for ben-
efits in well-nourished individuals. This may suggest
that protein is spared for wound healing when suffi-
cient energy requirements are met. Nutritional sup-
plementation in community-based patients did not
appear to result in any significant conclusions. How-
ever, it was noted that non-concordance with supple-
mentation that often exists in home-care/community
patients could negatively affect the outcome.57,58
Study designs examine the effects of preexisting
malnutrition, as well as nutritional intervention in
the prevention of pressure ulceration and the promo-
tion of healing. The majority of studies showed that
lower intakes of protein and energy were associated
with an increase in existing or newly developed
ulcers.35,59 A review by Mathus-Vliegen,61 of nutrition-
al status and pressure ulcers, pointed out that patients
with cachexia are often not distinguished from under-
fed patients in study designs. Conclusive findings
regarding the benefits of nutritional supplementation
are subsequently weakened since increased protein
catabolism present in cachexia supersedes any
positive outcomes of supplementation. When con-
trolling the inflammatory marker C-reactive protein,
j o u r n a l o f wo u n d c a r e v o l 2 0 , n o 8 , A u g u s t 2 0 1 1
 education

a large, multicentre trial (n=672) showed a significant tered dietitian. Since low body mass index and loss of 60 Pinchcofsky-Devin, G.D.,
decrease in pressure ulcer incidence with nutritional lean body mass are risk factors for malnutrition and Kaminkski, M.V. Correlation
of pressure sores and
supplementation, from 47.2% down to 40.6%.62 increased morbidity and mortality, monitoring these nutritional status. J Am
Studies focused on individuals with similar meta- are useful. Although portable digital scales and triceps Geriatr Soc. 1986; 34: 6,
435–440.
bolic physiology may be advantageous for studying skin-fold callipers are simple and effective tools to
61 Mathus-Vliegen, E. Old
inflammatory models, such as wound healing.61 monitor nutritional status, provisions for these are age, malnutrition, and
Furthermore, adequate documentation of supple- often neglected in community health care. pressure sores: an ill-fated
alliance. J Gerontol. 2004;
ment intake assures the patient is consuming the It is not uncommon that home-care patients recent-
59A: 4, 355–360.
prescribed amount. It was found that if supplement ly discharged from the hospital are already at some 62 Bourdel-Marchasson, I.,
intake is less than prescribed, or compromised by level of nutritional deficiency. Nutritional supplemen- Barateau, M., Rondeau,V. et
diarrhoea, its efficacy in preventing pressure ulcera- tation can be provided from commercial drink prepa- al. A multi-center trial of the
effects of oral nutritional
tion is reduced.60 Lastly, high protein supplements rations and/or whole foods, and home care limitations supplementation in critically
consumed by malnourished long-term care resi- may determine which supplement will provide ill older inpatients.
Nutrition. 2000; 16: 1, 1–5.
dents display a significant decrease in wound sur- improved intake for the patient. Commercially pre-
63 Breslow, R.A., Hallfrisch,
face area in category IV pressure ulcers, when com- pared liquid supplements are favourable in the cases of J., Guy, D.G. et al. The
pared with lower protein supplements.63 poor dentition, neurological pathologies, anorexia importance of dietary
protein in healing pressure
and inability to shop for food. Preparations currently
ulcers. J Am Geriatr Soc.
Recommendations on the market specifically for wound healing have 1993; 41: 4, 357–362.
We have demonstrated that the physiology of wound varying concentrations of complete or incomplete 64 Braden Scale. Available
healing involves numerous metabolic, humoral and protein, vitamins, minerals, glutamine and arginine. from: http://www.
bradenscale.com/images/
cellular mechanisms, each dependent on a preceding Whole foods have the ability to offer these same bradenscale.pdf.
step for initiation. The awareness of the role of each nutrients along with the additional benefits of phyto­ 65 Bagley, B. Determine,
individual macro- and micronutrients in wound heal- nutrients. Choice, variety and palatability of whole Nutrition Screening
Initiative. Am Fam Phys.
ing can be advantageous, particularly when address- foods provide enjoyment and subsequently increase 1998 [cited 20 July 2011];
ing cases of delayed healing. Since it is impossible to quality of life. Therefore, exploring approaches to Available at: http://www.
aafp.org/afp/980301ap/
easily identify what specific mechanism is subopti- overcome barriers to whole-food choices is warrant- edits.html.
mal, proper nutritional supplementation should sup- ed. Numerous resources provide simple dietary tips 66 Collins, N. Best practices,
ply the patient with a broader profile of nutrients that to increase protein and vitamins in foods that are tips, and techniques for
are known to be commonly limiting in the diet of consumed on a routine basis. The addition of milk preventing unintended
weight loss and healing
patients. Complete protein, vitamin C, zinc, iron, and and dairy products, nut butters, protein powders and wounds. Ostomy Wound
copper are all required for essential metabolic and oils to foods can boost protein and energy intakes. Manage. 2009; 55: 8, 8–10.
immunological mechanisms in wound healing, and Milk used for cereals, pudding and sauces can be for- 67 Edmonds, J. Nutrition
and wound healing: putting
should be supplied in adequate amounts to alleviate tified with dry milk powders. Simple shakes can be theory into practice. Br J
deficiencies and/or meet increased requirements. blended with yogurt, milk, instant breakfast mix and Community Nurs. 2007; 12:
12, S31–S34.
Since malnutrition is a risk factor for pressure ulcers, fruits to easily provide needed protein and vita-
68 Wright, J. Maintaining
identifying patients early allows for successful inter- mins.66–68 Since whole foods have numerous benefits, optimum nutrition. J Comm
vention. There are various assessment tools for spe- research would be warranted to explore home-care Nurs. 2006; 20: 11, 44–50.
cific types of wounds, such as pressure ulcers, that protocols that utilise whole foods for prevention of 69 United States
Department of Agriculture.
usually include a nutritional risk question. The Braden pressure ulcers and promotion of wound healing. USDA National Nutrient
scale is a commonly used screen that identifies six risk Home-care dietitians, visiting nurses and home Database for Standard
factors for pressure ulcers.64 This scale lists one nutri- health aides are responsible for assessment and dis- Reference, Release 15.
c2011 [cited 20 Jul 2011];
tional risk question based on meal intake, protein semination of nutrition education, and provide Available from: http://www.
intake and fluid consumption. Screening scales also valuable observations of nutritional trends in the nal.usda.gov/fnic/foodcomp/
Data/SR15/wtrank/wt_
have been developed specifically for identifying risk community. Often these professionals have a major rank.html.
factors for malnutrition. The Nutrition Screening Ini- impact on the nutritional status of the patient.
tiative, sponsored by the American Academy of Fam- Development of home-health care nutrition train-
ily Physicians, the American Dietetic Association and ing programmes reinforced with whole-food
the National Council of the Aging, was developed to resources has the potential to alleviate malnutrition
provide a simple survey that can be utilised by home and increase quality of life in elderly populations.
health care and the public. The screen, titled ‘Deter- Challenges, such as clarification of complete/
mine’, is based on 10 questions representing risk fac- incomplete protein in over-the-counter supple-
tors for malnutrition: illness, meal intake, fruits, veg- ments, whole-food alternatives for protein and con-
etables, dairy, alcohol, dentition, isolation, sumer over-supplementation with zinc, should be
medication, weight loss and self-care.65 It may be addressed. Easily accessible web resources for nutri-
advantageous to utilise the Determine Survey or simi- ent composition are accessible to home-care provid-
lar screens for malnutrition after identification of ers. The USDA maintains an extensive databank for
nutritional deficiencies by the Braden scale. Early food composition and has a user-friendly site for
nutritional intervention can be initiated with a regis- food nutrient lists.69 n

j o u r n a l o f wo u n d c a r e v o l 2 0 , n o 8 , A u g u s t 2 0 1 1 367

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