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 EWMA Journal 2015 vol 15 no 1 71 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. EWMA Journal 2015 vol 15 no 1 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. REFERENCES World Health Organization. Obesity and Overweight. Fact sheet N°311. Reviewed May 2014. Available at:http://www.who.int/mediacentre/factsheets/fs311/en/ Accessed July 20,2014. pathy, hypertension, and insulin resistance. Circulation. 2004;109(21):2529-35. Epub 2004 May 10. Levy BI, Schiffrin EL, Mourad JJ, Agostini D, Vicaut E, Safar ME, Struijker-Boudier HA. Impaired tissue perfusion: a pathology common to hypertension, obesity, and diabetes mellitus. Circulation. 2008;118(9):968-76. Lowe JR. Skin integrity in critically ill obese patients. Crit Care Nurs Clin North Am 2009;21(3):311-22. Beitz JM. Providing quality skin and wound care for the bariatric patient: an overview of clinical challenges. Ostomy Wound Manag. 2014;60(1):12-21. Trans Tasman Dietetic Wound Care Group - Professional Association. Evidence based practice guidelines for the nutritional management of adults with pressure injuries. 2011. NGC:008729. Available at: http://daa. asn.au/wp-content/uploads/2011/09/Trans-TasmanDietetic-Wound-Care-Group-Pressure-Injury-Guidelines-2011.pdf . Accesssed July 21, 2014. Guo S, Dipietro LA. Factors affecting wound healing. J Dent Res. 2010;89(3):219-29. Epub 2010 Feb 5. Tandara AA, Mustoe TA. Oxygen in wound healing— more than a nutrient. World J Surg 2004; 28:294-300. Sibbald RG, Woo KY. The biology of chronic foot ulcers in persons with diabetes. Diabetes Metab Res Rev 2008;24(Suppl 1):25-30. Moizé V, Deulofeu R, Torres F, de Osaba JM, Vidal J. Nutritional intake and prevalence of nutritional deficiencies prior to surgery in a Spanish morbidly obese population. Obes Surg. 2011;21(9):1382-8. Pierpont YN, Dinh TP, Salas RE, Johnson EL, Wright TG, Robson MC, Payne WG. Obesity and surgical wound healing: a current review. ISRN Obes. 2014 Feb 20;2014:638936. de Jongh RT, Serné EH, IJzerman RG, de Vries G, Stehouwer CD. Impaired microvascular function in obesity: implications for obesity-associated microangio 74 Ernst B, Thurnheer M, Schmid SM, Schultes B. Evidence for the necessity to systematically assess micronutrient status prior to bariatric surgery. Obes Surg. 2009;19(1):66-73. Epub 2008 May 20. Mathison CJ.Skin and wound care challenges in the hospitalized morbidly obese patient. J Wound Ostomy Continence Nurs. 2003;30(2):78-83. Clark M, Schols JM, Benati G, Jackson P, Engfer M, Langer G, Kerry B, Colin D; European Pressure Ulcer Advisory Panel. Pressure ulcers and nutrition: a new European guideline. J Wound Care. 2004;13(7):26772. Dorner B, Posthauer ME, Thomas D and National Pressure Ulcer Advisory Panel. The Role of Nutrition in Pressure Ulcer Prevention and Treatment: National Pressure Ulcer Advisory Panel White Paper. 2009 NPUAP Nutrition White Paper. Available at: http:// www.npuap.org/wp-content/uploads/2012/03/NutritionWhite-Paper-Website-Version.pdf. Accessed July 24, 2014. Braden B. The Braden Scale for Pressure Ulcer Prediction. Available at: http://www.bradenscale.com/ images/bradenscale.pdf. Accesed July 25, 2014. Stratton RJ, Ek AC, Engfer M, Moore Z, Rigby P, Wolfe R, Elia M. Enteral nutritional support in prevention and treatment of pressure ulcers: a systematic review and meta-analysis. Ageing Res Rev. 2005;4(3):422-50. EWMA Journal 2015 vol 15 no 1