Wound risk and prevention in obesity: The role of nutrition

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Scientific Communication
adrid · Spain
EWMA n GNEAUPP 2014
Submitted to the EWMA
Journal, based on a presentation given at
The European Society for
Clinical Nutrition
and Metabolism (ESPEN)
Guest Session: Obesity and
wound management:
The role of nutrition at the
EWMA - GNEAUPP 2014,
Madrid
Wound risk and
prevention in obesity:
The role of nutrition
INTRODUCTION
Obesity is a worldwide problem, not only because of its serious medical
comorbidities but also due to its increasing prevalence. It has recently been
estimated that the prevalence of obesity has nearly doubled since 1980; 35%
and 11% of adults older than 20 years of age are now overweight or obese,
respectively, and 65% of the world’s population live in nations in which
people who are overweight or obese are more likely to die than people who
are underweight1. Therefore, a growing number of obese people will need
medical assistance. The purpose of this short review is to address the nutritional aspects of wound risk and prevention in obese people.
WOUND RISK FACTORS IN OBESE PEOPLE
Obese people often have several wound risk factors, as shown in Table 1.
Some of these may be preventable, but others are not. In addition, obesity
may impair the body’s normal reaction to the effects of gravity. Pressure causes
the brain to order a positional change to relieve ischemia, but positional
changes may be challenging for obese people and their caregivers, leading
to increased susceptibility to pressure sores2.
María D. Ballesteros-Pomar
MD, PhD
Endocrinology and Nutrition
Department, Clinical Nutrition Unit.
Complejo Asistencial
Universitario de León
Altos de Nava s/n 24008
León, Spain.
Correspondence:
mdballesteros@telefonica.
net
Conflicts of interest: None
SKIN DISORDERS IN OBESE PEOPLE
Obesity and associated comorbidities increase the likelihood of impaired
skin integrity and slow-to-heal wounds. Therefore, obese people are at risk
of developing pressure ulcers, perigenital irritant dermatitis due to urinary
and/or fecal incontinence, benign (e.g., candidal intertrigo, erythrasma) or
more serious (e.g., cellulitis, necrotizing fasciitis) skin infections, venous
ulcers, diabetic foot ulcerations, and surgical site infections3.
Obese people face numerous challenges in maintaining their skin integrity4 due to many pathogenic factors5, as shown in Figure 1. Obese people
are at risk of delayed wound healing due to reduced oxygen and nutrient
perfusion as a result of cardiovascular changes. Furthermore, adipose tissue
has a relatively reduced blood supply, leading to inadequate oxygenation.
Hypoventilation is also common in obese individuals, which reduces tissue
oxygenation4.
Furthermore, moisture and microorganism collection in the skin folds
of obese individuals can also increase the risk of infection and decrease skin
integrity. Immobility, friction, and shear due to substantial weight stress
the skin’s barrier function. Nutritional aspects also have a central role in the
pathogenesis of skin disorders in obese people. In particular, obese people
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TABLE 1.
WOUND RISK FACTORS IN OBESE PEOPLE.
• Advanced age
• Cognitive impairment/altered sensory
perception
• Hypoxia, infection/sepsis
• Intensive care unit experience,
especially vent-dependency
• Hyperglycemia/diabetes
• Inadequate perfusion/oxygenation/
circulation
• Reduced mobility and difficult positional
changes
• Multiple trauma/burns
• Pre-operative illnesses/co-morbidities
(e.g., cardiovascular disease)
Figure 1. Pathogenic mechanisms
of wound risk in obese people
(adapted from Pierpoint et al.5).
may be malnourished despite their physical appearance.
This issue will be addressed in the present overview, as
malnutrition can lead to inadequate protein, vitamins,
and nutrients that are essential to wound repair4.
THE ROLE OF VASCULARITY AS A WOUND RISK
FACTOR IN OBESE PEOPLE
Some recent reviews and studies have addressed the role of
vascularity as a wound risk factor in obese people5-7. An
inherent decreased vascularity of adipose tissue has been
described in obese people, and increased adiposity induces
a signalling cascade that positively feeds back to impair
angiogenesis and cause chronic low-grade inflammation.
In addition, increased expression of 11β-hydroxysteroid
dehydrogenase type 1 (11βHSD1), an intracellular glucocorticoid-amplifying enzyme, has been observed in obese
people. As glucocorticoids suppress angiogenesis, the elevated level of 11βHSD1 serves to amplify the inhibitory effects of glucocorticoids. As adipose tissue becomes
hypoxic from impaired angiogenesis, hypoxia-inducible
factor 1 alpha (HIF1β) levels increase and initiate local
inflammation and fibrosis, which further impair the angiogenic process and wound healing. Other microvascular
abnormalities linked to obesity include reduced nitrogen
oxide availability, which impairs microvascular rarefaction,
and prolonged elevation of free fatty acids in the blood due
to increased fat mass, which impairs capillary recruitment5.
In surgical wounds, the increased tension on wound
edges that frequently occurs in obese people contributes
72
• Some disease states that cause hyper metabolism and increase nutritional risk
to wound dehiscence8. Wound tension increases tissue
pressure, reducing microperfusion and the availability of
oxygen to the wound. The increase in pressure ulcers or
pressure-related injuries in obese individuals is also influenced by hypovascularity, as poor perfusion makes tissue
more susceptible to this type of injury. Venous insufficiency is another vascular factor associated with the development of chronic wounds and delayed wound healing5.
OTHER PATHOGENIC MECHANISMS OF WOUND
RISK IN OBESE PEOPLE
Beyond impaired angiogenesis and vascularity, chronic
low-grade inflammation associated with obesity is another
important pathogenic mechanism of skin disorders and
impaired wound healing. Obesity-related microangiopathy and alterations in immune mediators may lengthen
the inflammatory stage of wound healing and leave obese
individuals more susceptible to infections.
Oxidative stress has also been linked to obesity, especially abdominal obesity, through a deficiency in adiponectin, an adipocytokine that protects against oxidative
stress and inflammation. Low adiponectin levels impair
wound healing via two mechanisms: impaired angiogenesis
and impaired keratinocyte proliferation and migration,
which is a critical process in the re-epithelialisation phase
of wound healing4,5. Another aspect of wound healing that
is potentially affected by a hypoxic environment in obesity is the capability of fibroblasts to synthesise collagen5.
EWMA Journal 2015 vol 15 no 1
Scientific Communication
DIABETES AND WOUND HEALING
IN OBESE PEOPLE
Obesity is often associated with metabolic complications,
with diabetes being one of the most relevant complications
that also has an important role in wound risk and impaired
healing. Poor blood glucose control impairs wound healing
and increases risk of infection, and the metabolic stress
caused by the wound further increases blood glucose.
In diabetic patients, foot ulcers and pressure-related
chronic non-healing wounds are always accompanied by
hypoxia9, resulting from insufficient perfusion and angiogenesis8. Hypoxia may further increase the early inflammatory response, which prolongs injury by increasing levels of oxygen radicals. Hyperglycemia also increases
the production of oxygen radicals, thereby contributing
to oxidative stress. The formation of advanced glycation
end products under hyperglycemic conditions is associated
with impaired wound healing. High levels of metalloproteases found in diabetic foot ulcers and chronic wounds are
also associated with tissue destruction and inhibit normal
repair processes. Diabetic patients exhibit dysregulated
cellular functions leading to inadequate bacterial clearance
and delayed or impaired repair, such as defects in T-cell
immunity, leukocyte chemotaxis, phagocytosis, bactericidal capacity, and dysfunctional fibroblasts and epidermal
cells10. Diabetic neuropathy also contributes to impaired
wound healing. Figure 2 shows factors that contribute to
impaired healing in individuals with diabetes.
MALNUTRITION AND WOUND HEALING
As previously mentioned, obesity does not necessarily imply a good nutritional status. Obese people are sometimes
malnourished because of bad nutritional habits or fad diets, but malnutrition is difficult to detect. This paradoxical
malnutrition results from a calorie-dense diet that is high
in carbohydrates and fats and low in vitamins and minerals5. Many micronutrient and macronutrient deficiencies
have been described in obese people11. Among 232 obese
individuals studied by Ernst et al12. before bariatric surgery, 12.5% were deficient for albumin, 8.0% for phosphate, 4.7% for magnesium, 6.9% for ferritin, 6.9% for
hemoglobin, 24.6% for zinc, 3.4% for folate, 18.1% for
vitamin B12, 32.6% for selenium, 5.6% for vitamin B3,
2.2% for vitamin B6, 2.2% for vitamin E, and 25.4% for
25-OH vitamin D. Albumin deficiency and anemia were
positively correlated with body mass index (BMI), and
48.7% of the obese people included in the study showed at
least one nutritional deficiency. As proper wound healing
requires adequate levels of vitamins and minerals5, obese
people may be at risk of impaired wound repair.
Therefore, obese people may have depleted lean body
mass and protein stores while maintaining high levels of
adipose mass and may be deficient in many vitamins and
minerals needed for healing. Furthermore, detecting malnutrition is not easy in these individuals, as many nutrition
screening tools rely on BMI or percentage weight loss,
making it difficult to assess malnutrition. 
Figure 2. Potential effects of diabetes
on wound healing. MMPs, matrix metalloproteases; ROS, reactive oxygen
species; AGEs, advanced glycation
end products (adapted from Guo et
al.8.
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73
PREVENTION OF WOUNDS IN OBESE PEOPLE
Some preventative measures might decrease the risk of skin
breakdown and maximise wound healing in obese people13. It is very important to maintain skin integrity using
cleansers, lotions, moisture barrier ointments, and sealants.
Also, patient independence and mobility should be promoted through the use of supplies, equipment, adaptive
devices, and rooms designed for obese patients. Special
attention should be paid to tube site care, positioning,
and stabilisation. Leg elevation and external compression
to encourage fluid recirculation is also important to avoid
pressure sores. Furthermore, an adequate staff-to-patient
ratio significantly helps to prevent sores13.
ROLE OF NUTRITION IN PREVENTING
PRESSURE SORES
Evidence-based guidelines on pressure ulcer prevention
and treatment that have been developed by the European
Pressure Ulcer Advisory Panel (EPUAP)14 and the American National Pressure Ulcer Advisory Panel (NPUAP)15
specifically address the role of nutrition in preventing pressure sores. First, general recommendations are made for
the screening and assessment of nutritional status of every
individual at risk for pressure ulcers, as the early identification and management of undernutrition can prevent
pressure ulcer development. The guidelines suggest using
any valid, reliable, and practical tool for nutritional screening that is quick and easy to use and acceptable to both
the individual and health care worker as well as having
a nutritional screening policy in place in all health care
settings. The Braden Risk Assessment Scale for predicting
pressure ulcer risk includes a nutrition subscale that can be
used in the nutrition screening and assessment process16.
The problem for obese people is that any tool based on
body weight may underestimate malnutrition, and there is
currently no screening tool validated for obese individuals.
Second, the guidelines propose providing nutritional
support to each individual with nutritional and pressure
ulcer risks by performing nutritional assessment, estimating nutritional requirements, comparing nutrient intake
with estimated requirements, providing appropriate nutrition intervention based on an appropriate feeding route,
and monitoring and evaluating nutritional outcome. Individuals with nutritional and pressure ulcer risks should
receive at least 30-35 kcal per kg body weight per day,
with 1.25-1.5 g/kg/day protein and 1 ml/kcal/day fluid
intake. Obese individuals should not be underfed when
at wound risk. When estimating their energy needs, the
use of adjusted body weight or specific formulae should
be considered. In obese people, beware of calories, but
maintain or increase protein supply.
Third, a specific recommendation is to offer highprotein mixed oral nutritional supplements and/or tube
feeding in addition to the usual diet to individuals with
nutritional and pressure ulcer risks. This recommendation
is based on a systematic review and meta-analysis showing
a 25% reduction in pressure ulcer development in at-risk
patients with high-protein oral nutritional supplements
(250-500 kcal/day) compared to routine care17. Obese
people should not be excluded from this recommendation
when they are either malnourished or at high nutritional
risk. A decision tree on nutrition in pressure ulcers prevention and treatment has been published by EPUAP14.
In conclusion, obesity itself should be recognised as a relevant risk factor for wounds, even more so if complicated
by diabetes or cardiovascular disease. Also, as obese people
may be malnourished, nutritional assessment and management, as in any other at-risk patient, is vital for wound
prevention.
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EWMA Journal 2015 vol 15 no 1
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