370
Correspondence / Nutrition 30 (2014) 369–371
first concrete product of this workshop. We believe that as selected participants, and thus, as potential young nutrition leaders we have much more to give; converting efforts into real benefits for the entire population, but with a special focus on the most socioeconomically vulnerable groups. We acknowledge all those who made this workshop possible, and those who offered us the chance to be part of this meeting in a country as wonderful as Cuba. In gratitude we hope to harvest and share the best fruits from this sowing. Note: This letter reflects the opinions of all workshop participants. References 1 Rivera JA. Improving nutrition in Mexico: the use of research for decision making. Nutr Rev 2009;67:S62–5. 2 Monteiro CA, Gomes FS, Cannon G. The snack attack. Am J public Health 2010; 100:975. 3 Gomes FS. Marketing of unhealthy food to young children. Brazilian David and multinational Goliath. Public Health Nutr 2009;12:1024–5. 4 Gomes FS, Lobstein T. Food and beverage transnational corporations and nutrition policy. SCN News; 2011:57–65.
Alex Brito, M.S. Analay Cabrera, M.S. Fabio da Silva Gomes, Ph.D. Sandra P. Crispim, M.S., Ph.D. uregui, M.S. Alejandra Ja Rebecca Kanter, Ph.D. Rodrigo Chamorro, M.S. € ssel, Ph.D. Michael Maia Schlu vez, M.D. Rimsky Cha Israel Rıos-Castillo, M.S. Marıa F. Kroker , Ph.D. Maria D. Defago n, M.S. Ana V. Chaco Giovanna Gatica, M.S. Marıa V. Natero, M.S. Catalina Arango Ana G. Mejicano, M.S. Celia A. Masi, M.S. Evelyn I. Rold an, M.S. ndez, M.S. Marıa E. Herna R. Lo pez, M.S. Jose Miluska Carrasco, M.S. ~ a, M.S. Liz A. Pen Carlos Viera Selected participants of the VI Latin American Workshop on Leadership in Nutrition, Cuba 2012 http://dx.doi.org/10.1016/j.nut.2013.08.020
Pressure ulcers and malnutrition: A devastating and common association Pressure ulcers (PU) are a major health-care challenge, not just in developing countries but in the United States as well. The Joint Commission estimated that in 2007 between 1.3 and 3 million people were diagnosed with PUs in the United States [1]. The estimated annual cost of care in 2008 was $3.3 billion [2,3], with PUs being one of the most devastating nosocomial complications behind the ballooning of health care costs not
only in the United States [3] but worldwide [4]. The association between nutritional status, specifically malnutrition, and PU has been established and validated by multiple authors [1,5], including the work by Brito et al. appearing in this issue of Nutrition. The above-mentioned work portrays a very grim picture, as does a previous multicenter study from Brazil published in 2001, which reported the incidence of malnutrition in Brazilian hospitals at 48% [6]; in this new cohort, the incidence of malnutrition has increased to 52%, and the incidence of severe malnutrition has gone from 12.6% to 22.4%. Beyond reporting the association between malnutrition and PUs, this work highlights the difficulty in recognizing and treating malnutrition in institutionalized patients even in an environment of heightened awareness such as the one in these Brazilian hospitals. Similarly, a high incidence (>20%) of malnutrition has been reported from industrialized countries [7]. An Australian paper from 2010 [1] reports the incidence of PUs in malnourished patients was 36% versus 16% in nonmalnourished patients, indicating how widespread this problem is. It is important to recognize that the success of the nutritional care of institutionalized patients depends not only on the exclusive work of a nutrition support team, but also on the work of the nursing staff, who, as the closest providers to the patients, are in the best position to provide and care for them. This success will lead to a safer and higher quality care with a positive impact on the patients’ outcomes. Finally, in order to truly have an impact on the incidence of malnutrition and PUs, home care, nursing homes, hospitals, long-term acute-care facilities, and other health-care institutions must include clear parameters for screening for nutritional risk and comprehensive recommendations for the treatment of malnutrition in their guidelines for the prevention and management of PUs. References [1] Banks MD, Graves N, Bauer JD, Ash S. The costs arising from pressure ulcers attributable to malnutrition. Clin Nutr (Edinburgh, Scotland) 2010; 29:180–6. [2] Pham B, Stern A, Chen W, Sander B, John-Baptiste A, Thein HH, et al. Preventing pressure ulcers in long-term care: a cost-effectiveness analysis. Arch Intern Med 2011;171:1839–47. [3] Van Den Bos J, Rustagi K, Gray T, Halford M, Ziemkiewicz E, Shreve J. The $17. 1 billion problem: the annual cost of measurable medical errors. Health Aff (Millwood) 2011;30:596–603. [4] Dealey C, Posnett J, Walker A. The cost of pressure ulcers in the United Kingdom. J Wound Care 2012;21:261–6. [5] Volkert D, Pauly L, Stehle P, Sieber CC. Prevalence of malnutrition in orally and tube-fed elderly nursing home residents in Germany and its relation to health complaints and dietary intake. Gastroenterol Res Pract 2011; 2011:247315. [6] Waitzberg DL, Caiaffa WT, Correia MI. Hospital malnutrition: the Brazilian national survey (IBRANUTRI): a study of 4000 patients. Nutrition 2001;17: 573–80. Epub 2001/07/13. [7] Alvarez-Hernandez J, Planas Vila M, Leon-Sanz M, Garcia de Lorenzo A, Celaya-Perez S, Garcia-Lorda P, et al. Prevalence and costs of malnutrition in hospitalized patients: the PREDyCES(R) Study. Nutr Hosp 2012;27: 1049–59.
Jose M. Pimiento, M.D. Sonia Echeverri, R.N., M.Sc.* Surgical Oncologes/Mercy Health Lacks Cancer Center, Michigan State University College of Human Medicine, Grand Rapids, MI, USA Corresponding author. Tel. þ1 571 620 3580; fax: þ1 571 620 3580. E-mail address: [email protected] (S. Echeverri) http://dx.doi.org/10.1016/j.nut.2013.08.007
Correspondence / Nutrition 30 (2014) 369–371
Sepsis, critical illness, host defense, autocannibalism, and nutritional support During wars, church bells often were melted down to yield metal to forge cannons. War strategy was fine-tuned by evolution long before military strategists appeared, and in sepsis muscle proteins are “melted down” to yield the amino acids (AAs) to fight invaders. Protein catabolism maintains an autotransfusion of AAs to support synthesis of immunocompetent cells, immunoglobulins, acute-phase proteins, new tissue for repair, and so on. Moreover, through hepatic gluconeogenesis, AAs yield glucose to fuel combating cells (plus brain and other cells). The support of combating cells, commonly reflected by moderate hyperglycemia, is recognized as a priority by the injured and septic host; while in history inefficiency in supporting winning soldiers contributed to defeat. The review by Hartl and Jauch [1] in this issue explains how, in injury and sepsis, many features that a physician may consider “abnormal” turn out to be critical expressions of host defense, selected during evolution. Their insight into the real war strategy engaged by the host has important nutritional implications, apart from the obvious need to eradicate sepsis and support organ functions. In fact, it is true that in desperate and preterminal septic illness there is “bad” autocannibalism (or self-destruction) with useless waste of endogenous resources, massive proteolysis, and inability to use exogenous substrates [2]. However, and most importantly, in earlier and more balanced stages of sepsis there is “good” hypercatabolism supporting host defense and tissue repair. Experience has shown that in these stages the body may not tolerate large doses of glucose, but tolerates and makes advantageous use of exogenous AAs. Awareness of this effect has led to progressively increasing the dose of AAs in the artificial nutrition of septic and other critically ill adult patients to even more than 1.5 g/kg daily [3–7], also considering that commonly used mixed parenteral AA solutions and elemental enteral formulas provide about one-sixth less protein substrate than the sum of their constituent AAs [3]. As obvious as this may appear to well-updated nutrition specialists, in clinical practice it seems to be largely disattended [4,5] and critically ill patients often are subjected to protein (and calorie) underfeeding, also because of poor knowledge of pathophysiology. This enhances the value of the work by Hartl and Jauch [1], which further provides hints on the adaptive nature of hyperglycemia and selective insulin resistance, at least in well-balanced septic states, and on some drawbacks of intensive insulin therapy [1,8]. Other implications concern the lipid component of nutrition. In addition to being in general a main stem of nutritional sup-
371
port, it offers the possibility of moderating the inflammatory response through the administration of fish oil, of mixed fat emulsions with reduced doses of linoleic acid, or of newly developed mixed fat emulsions with soybean oil, medium chain triglycerides, and fish oil, with or without olive oil [9]. This possibility still needs to be better evaluated. The most challenging issue in sepsis concerns the turning point at which the defensive-reparative response turns into a selfdamaging process, with uncontrolled inflammation, extreme metabolic dysregulation, wasteful proteolysis (“bad” autocannibalism), and lethal organ failure [1,2,10,11]. This condition has been allowed to appear only recently, due to powerful cardiorespiratory and pharmacologic therapies that permit survival after insults that a few decades ago would have been rapidly lethal [1]. This accounts for our still poor knowledge of the issue, with inability to recognize individual predisposition to the self-damaging response (which also has genetic components) [12], and inability to predict in timely fashion its occurrence, so as to accelerate aggressive measures for the quickest possible eradication of sepsis. References [1] Hartl WH, Jauch KW. Metabolic self-destruction in critically ill patients. Origins, mechanisms and therapeutic principles. Nutrition; 2013; 2013;30: 261–7. [2] Cerra FB, Siegel JH, Coleman B, Border JR, McMenamy RR. Septic autocannibalism. A failure of exogenous nutritional support. Ann Surg 1980;192:570–80. [3] Hoffer LJ. How much protein do parenteral amino acid mixtures provide? Am J Clin Nutr 2011;94:1396–8. [4] Hoffer LJ, Bistrian BR. Appropriate protein provision in critical illness: a systematic and narrative review. Am J Clin Nutr 2012;96:591–600. [5] Hoffer LJ, Bistrian BR. Why critically ill patients are protein deprived. JPEN J Parenter Enteral Nutr 2013;37:300–9. [6] Singer P, Cohen JD. To implement guidelines: the (bad) example of protein administration in the ICU. JPEN J Parenter Enteral Nutr 2013;37:294–6. [7] Hoffer LJ, Bistrian BR. Why critically ill patients are protein deprived. JPEN J Parenter Enteral Nutr 2013;37:441. [8] Kuppinger D, Hartl WH. In search of the perfect glucose concentration for hospitalized patients: a brief review of the meta-analyses. Nutrition 2013;29:708–12. [9] Chiarla C, Giovannini I, Giuliante F, Ardito F, Vellone M, De Rose AM, et al. Parenteral nutrition in liver resection. J Nutr Metab 2012;2012:508103. [10] Siegel JH, Cerra FB, Coleman B, Giovannini I, Shetye M, Border JR, et al. Physiological andmetabolic correlations inhuman sepsis. Surgery 1979;86:163–93. [11] Chiarla C, Giovannini I, Giuliante F, Zadak Z, Vellone M, Ardito F, et al. Severe hypocholesterolemia in surgical patients, sepsis, and critical illness. J Crit Care 2010;25:361.e7–361.e12. [12] Cavaillon J-M, Adrie C. Genetic polymorphism and other parameters that affect predisposal to infection and outcome. In: Cavaillon J-M, Adrie C, editors. Sepsis and non-infectious systemic inflammation. From biology to critical care. Weinheim: Wiley-VCH Verlag GmbH & Co. KGaA; 2009. p. 315–46.
Ivo Giovannini, M.D.* Carlo Chiarla, M.D. CNR-IASI Center for the Pathophysiology of Shock, Department of Surgical Sciences, Catholic University of the Sacred Heart Rome, Italy Corresponding author. Tel.: þ39 06 3015 4082; fax: þ39 06 3057845. E-mail address: [email protected] (I. Giovannini) http://dx.doi.org/10.1016/j.nut.2013.08.018
Correspondence / Nutrition 30 (2014) 369–371
first concrete product of this workshop. We believe that as selected participants, and thus, as potential young nutrition leaders we have much more to give; converting efforts into real benefits for the entire population, but with a special focus on the most socioeconomically vulnerable groups. We acknowledge all those who made this workshop possible, and those who offered us the chance to be part of this meeting in a country as wonderful as Cuba. In gratitude we hope to harvest and share the best fruits from this sowing. Note: This letter reflects the opinions of all workshop participants. References 1 Rivera JA. Improving nutrition in Mexico: the use of research for decision making. Nutr Rev 2009;67:S62–5. 2 Monteiro CA, Gomes FS, Cannon G. The snack attack. Am J public Health 2010; 100:975. 3 Gomes FS. Marketing of unhealthy food to young children. Brazilian David and multinational Goliath. Public Health Nutr 2009;12:1024–5. 4 Gomes FS, Lobstein T. Food and beverage transnational corporations and nutrition policy. SCN News; 2011:57–65.
Alex Brito, M.S. Analay Cabrera, M.S. Fabio da Silva Gomes, Ph.D. Sandra P. Crispim, M.S., Ph.D. uregui, M.S. Alejandra Ja Rebecca Kanter, Ph.D. Rodrigo Chamorro, M.S. € ssel, Ph.D. Michael Maia Schlu vez, M.D. Rimsky Cha Israel Rıos-Castillo, M.S. Marıa F. Kroker , Ph.D. Maria D. Defago n, M.S. Ana V. Chaco Giovanna Gatica, M.S. Marıa V. Natero, M.S. Catalina Arango Ana G. Mejicano, M.S. Celia A. Masi, M.S. Evelyn I. Rold an, M.S. ndez, M.S. Marıa E. Herna R. Lo pez, M.S. Jose Miluska Carrasco, M.S. ~ a, M.S. Liz A. Pen Carlos Viera Selected participants of the VI Latin American Workshop on Leadership in Nutrition, Cuba 2012 http://dx.doi.org/10.1016/j.nut.2013.08.020
Pressure ulcers and malnutrition: A devastating and common association Pressure ulcers (PU) are a major health-care challenge, not just in developing countries but in the United States as well. The Joint Commission estimated that in 2007 between 1.3 and 3 million people were diagnosed with PUs in the United States [1]. The estimated annual cost of care in 2008 was $3.3 billion [2,3], with PUs being one of the most devastating nosocomial complications behind the ballooning of health care costs not
only in the United States [3] but worldwide [4]. The association between nutritional status, specifically malnutrition, and PU has been established and validated by multiple authors [1,5], including the work by Brito et al. appearing in this issue of Nutrition. The above-mentioned work portrays a very grim picture, as does a previous multicenter study from Brazil published in 2001, which reported the incidence of malnutrition in Brazilian hospitals at 48% [6]; in this new cohort, the incidence of malnutrition has increased to 52%, and the incidence of severe malnutrition has gone from 12.6% to 22.4%. Beyond reporting the association between malnutrition and PUs, this work highlights the difficulty in recognizing and treating malnutrition in institutionalized patients even in an environment of heightened awareness such as the one in these Brazilian hospitals. Similarly, a high incidence (>20%) of malnutrition has been reported from industrialized countries [7]. An Australian paper from 2010 [1] reports the incidence of PUs in malnourished patients was 36% versus 16% in nonmalnourished patients, indicating how widespread this problem is. It is important to recognize that the success of the nutritional care of institutionalized patients depends not only on the exclusive work of a nutrition support team, but also on the work of the nursing staff, who, as the closest providers to the patients, are in the best position to provide and care for them. This success will lead to a safer and higher quality care with a positive impact on the patients’ outcomes. Finally, in order to truly have an impact on the incidence of malnutrition and PUs, home care, nursing homes, hospitals, long-term acute-care facilities, and other health-care institutions must include clear parameters for screening for nutritional risk and comprehensive recommendations for the treatment of malnutrition in their guidelines for the prevention and management of PUs. References [1] Banks MD, Graves N, Bauer JD, Ash S. The costs arising from pressure ulcers attributable to malnutrition. Clin Nutr (Edinburgh, Scotland) 2010; 29:180–6. [2] Pham B, Stern A, Chen W, Sander B, John-Baptiste A, Thein HH, et al. Preventing pressure ulcers in long-term care: a cost-effectiveness analysis. Arch Intern Med 2011;171:1839–47. [3] Van Den Bos J, Rustagi K, Gray T, Halford M, Ziemkiewicz E, Shreve J. The $17. 1 billion problem: the annual cost of measurable medical errors. Health Aff (Millwood) 2011;30:596–603. [4] Dealey C, Posnett J, Walker A. The cost of pressure ulcers in the United Kingdom. J Wound Care 2012;21:261–6. [5] Volkert D, Pauly L, Stehle P, Sieber CC. Prevalence of malnutrition in orally and tube-fed elderly nursing home residents in Germany and its relation to health complaints and dietary intake. Gastroenterol Res Pract 2011; 2011:247315. [6] Waitzberg DL, Caiaffa WT, Correia MI. Hospital malnutrition: the Brazilian national survey (IBRANUTRI): a study of 4000 patients. Nutrition 2001;17: 573–80. Epub 2001/07/13. [7] Alvarez-Hernandez J, Planas Vila M, Leon-Sanz M, Garcia de Lorenzo A, Celaya-Perez S, Garcia-Lorda P, et al. Prevalence and costs of malnutrition in hospitalized patients: the PREDyCES(R) Study. Nutr Hosp 2012;27: 1049–59.
Jose M. Pimiento, M.D. Sonia Echeverri, R.N., M.Sc.* Surgical Oncologes/Mercy Health Lacks Cancer Center, Michigan State University College of Human Medicine, Grand Rapids, MI, USA Corresponding author. Tel. þ1 571 620 3580; fax: þ1 571 620 3580. E-mail address: [email protected] (S. Echeverri) http://dx.doi.org/10.1016/j.nut.2013.08.007
Correspondence / Nutrition 30 (2014) 369–371
Sepsis, critical illness, host defense, autocannibalism, and nutritional support During wars, church bells often were melted down to yield metal to forge cannons. War strategy was fine-tuned by evolution long before military strategists appeared, and in sepsis muscle proteins are “melted down” to yield the amino acids (AAs) to fight invaders. Protein catabolism maintains an autotransfusion of AAs to support synthesis of immunocompetent cells, immunoglobulins, acute-phase proteins, new tissue for repair, and so on. Moreover, through hepatic gluconeogenesis, AAs yield glucose to fuel combating cells (plus brain and other cells). The support of combating cells, commonly reflected by moderate hyperglycemia, is recognized as a priority by the injured and septic host; while in history inefficiency in supporting winning soldiers contributed to defeat. The review by Hartl and Jauch [1] in this issue explains how, in injury and sepsis, many features that a physician may consider “abnormal” turn out to be critical expressions of host defense, selected during evolution. Their insight into the real war strategy engaged by the host has important nutritional implications, apart from the obvious need to eradicate sepsis and support organ functions. In fact, it is true that in desperate and preterminal septic illness there is “bad” autocannibalism (or self-destruction) with useless waste of endogenous resources, massive proteolysis, and inability to use exogenous substrates [2]. However, and most importantly, in earlier and more balanced stages of sepsis there is “good” hypercatabolism supporting host defense and tissue repair. Experience has shown that in these stages the body may not tolerate large doses of glucose, but tolerates and makes advantageous use of exogenous AAs. Awareness of this effect has led to progressively increasing the dose of AAs in the artificial nutrition of septic and other critically ill adult patients to even more than 1.5 g/kg daily [3–7], also considering that commonly used mixed parenteral AA solutions and elemental enteral formulas provide about one-sixth less protein substrate than the sum of their constituent AAs [3]. As obvious as this may appear to well-updated nutrition specialists, in clinical practice it seems to be largely disattended [4,5] and critically ill patients often are subjected to protein (and calorie) underfeeding, also because of poor knowledge of pathophysiology. This enhances the value of the work by Hartl and Jauch [1], which further provides hints on the adaptive nature of hyperglycemia and selective insulin resistance, at least in well-balanced septic states, and on some drawbacks of intensive insulin therapy [1,8]. Other implications concern the lipid component of nutrition. In addition to being in general a main stem of nutritional sup-
371
port, it offers the possibility of moderating the inflammatory response through the administration of fish oil, of mixed fat emulsions with reduced doses of linoleic acid, or of newly developed mixed fat emulsions with soybean oil, medium chain triglycerides, and fish oil, with or without olive oil [9]. This possibility still needs to be better evaluated. The most challenging issue in sepsis concerns the turning point at which the defensive-reparative response turns into a selfdamaging process, with uncontrolled inflammation, extreme metabolic dysregulation, wasteful proteolysis (“bad” autocannibalism), and lethal organ failure [1,2,10,11]. This condition has been allowed to appear only recently, due to powerful cardiorespiratory and pharmacologic therapies that permit survival after insults that a few decades ago would have been rapidly lethal [1]. This accounts for our still poor knowledge of the issue, with inability to recognize individual predisposition to the self-damaging response (which also has genetic components) [12], and inability to predict in timely fashion its occurrence, so as to accelerate aggressive measures for the quickest possible eradication of sepsis. References [1] Hartl WH, Jauch KW. Metabolic self-destruction in critically ill patients. Origins, mechanisms and therapeutic principles. Nutrition; 2013; 2013;30: 261–7. [2] Cerra FB, Siegel JH, Coleman B, Border JR, McMenamy RR. Septic autocannibalism. A failure of exogenous nutritional support. Ann Surg 1980;192:570–80. [3] Hoffer LJ. How much protein do parenteral amino acid mixtures provide? Am J Clin Nutr 2011;94:1396–8. [4] Hoffer LJ, Bistrian BR. Appropriate protein provision in critical illness: a systematic and narrative review. Am J Clin Nutr 2012;96:591–600. [5] Hoffer LJ, Bistrian BR. Why critically ill patients are protein deprived. JPEN J Parenter Enteral Nutr 2013;37:300–9. [6] Singer P, Cohen JD. To implement guidelines: the (bad) example of protein administration in the ICU. JPEN J Parenter Enteral Nutr 2013;37:294–6. [7] Hoffer LJ, Bistrian BR. Why critically ill patients are protein deprived. JPEN J Parenter Enteral Nutr 2013;37:441. [8] Kuppinger D, Hartl WH. In search of the perfect glucose concentration for hospitalized patients: a brief review of the meta-analyses. Nutrition 2013;29:708–12. [9] Chiarla C, Giovannini I, Giuliante F, Ardito F, Vellone M, De Rose AM, et al. Parenteral nutrition in liver resection. J Nutr Metab 2012;2012:508103. [10] Siegel JH, Cerra FB, Coleman B, Giovannini I, Shetye M, Border JR, et al. Physiological andmetabolic correlations inhuman sepsis. Surgery 1979;86:163–93. [11] Chiarla C, Giovannini I, Giuliante F, Zadak Z, Vellone M, Ardito F, et al. Severe hypocholesterolemia in surgical patients, sepsis, and critical illness. J Crit Care 2010;25:361.e7–361.e12. [12] Cavaillon J-M, Adrie C. Genetic polymorphism and other parameters that affect predisposal to infection and outcome. In: Cavaillon J-M, Adrie C, editors. Sepsis and non-infectious systemic inflammation. From biology to critical care. Weinheim: Wiley-VCH Verlag GmbH & Co. KGaA; 2009. p. 315–46.
Ivo Giovannini, M.D.* Carlo Chiarla, M.D. CNR-IASI Center for the Pathophysiology of Shock, Department of Surgical Sciences, Catholic University of the Sacred Heart Rome, Italy Corresponding author. Tel.: þ39 06 3015 4082; fax: þ39 06 3057845. E-mail address: [email protected] (I. Giovannini) http://dx.doi.org/10.1016/j.nut.2013.08.018
