Risk Factors for Malnutrition in the Elderly Patient
Weight loss BMI
Serum albumin Serum zinc Lymphocyte count
18.5 to 24.9 4.5 to 3.5 g/dl 11 to 33 nmol/l 5000 to 1500/ml
with calcium and vitamin D can reduce the risk of long bone fractures,8586 and protein supplementation appears to reduce postoperative rehabilitation time in elderly patients with hip fractures.87 The administration of protein-calorie supplements to hospitalized elderly patients has been shown to increase rates of weight gain and significantly reduce mortality in the most undernourished subgroup.88
The timing and route of nutritional supplementation is still somewhat controversial. Enteral nutrition is generally favored and can be given in various forms, including thickened beverages, shakes, or tube feeds. However, when considering elderly patients, one needs to be realistic in determining how capable the patient is of consuming the proposed diet as well as the potential risks and discomforts of a feeding tube. In addition, enteral feeds are frequently interrupted due to diagnostic and therapeutic procedures requiring that the patient be fasted. Achieving adequate caloric delivery can therefore be problematic.89 Regardless, some patients will benefit from short courses of supplemental tube feeds, but the use of chronic tube feeds in hospitalized or nursing home patients is not clearly beneficial.90 Although there are significant risks associated with TPN, it is an option for those malnourished patients who cannot tolerate enteral intake. In a study by Mullen et al., malnourished patients who were given at least 7 d of preoperative TPN were less likely to develop postoperative complications.91 Finally, in a multicenter Veteran's Administration cooperative study, 395 preoperative patients with malnutrition by clinical screening were randomized to receive preoperative parenteral nutrition or the standard hospital diet. This study found that severely malnourished subjects in the preoperative TPN arm of the study had a decreased incidence of postoperative complications when compared to patients who did not receive TPN as well as a control group of well-nourished patients.92 These studies suggest that the nutritional state of the elderly patient has a direct influence on clinical outcome, and that severe malnutrition can be reversed with aggressive preoperative nutritional supplementation.
wound healing and nutritional support in the pediatric patient
Wound healing in the infant is thought to follow the same basic physiologic principles as in the adult patient. In general, pediatric wound healing adheres to distinct stages and requires the coordination of multiple anatomic and physiologic systems. In many ways, children have a greater capacity for wound healing given the fact that they often have fewer and less serious medical comorbidities.
However, wound healing in the pediatric patient is also characterized by the immaturity of the multiple systems involved in the healing process.93 For example, the neonate has an underdeveloped immune system at birth that gradually acquires full immunocompetence with antigenic exposure over time. The newborn child, and in particular the premature infant, relies upon passive immunity early in life. Thus the infant may have difficulty mobilizing the immune and inflammatory mediators required for the initial coordination of the wound healing process. The young child may also have difficulty overcoming bacterial and secondary infections that frequently complicate healing, not only because of an immature immune system but also because the skin is a less protective barrier during the early stages of life.94
The infant has a skin structure that is relatively weak but increases in strength over time.95 For example, the neonate's skin has weaker intercellular attachments than that of older children and adults. Thus, minimal injury or friction to the skin surface can result in separation of the epidermis from the dermis. In addition to being thin, infant skin is also characterized by fewer hair follicles and sebaceous glands.95 These changes in infant skin are confined primarily to the epidermis, while the dermis is well developed even in the extremely premature neonate. When considering protecting a hospitalized infant's skin from breakdown, it is also important to consider the differences in weight distribution among young infants, children, and adults. Infants need the most protection on the occiput that bears the majority of weight while in the supine position. The sacrum becomes the point of maximal weight bearing as we age.96
The skin of the neonate, and in particular premature neonates less than 33 weeks gestation, may not be an effective barrier to permeable fluids and the external environment.97 Although it is unclear whether this contributes to an increased degree of skin injury when traumatized, it can make the young child more susceptible to wound formation. It is also known that the infant has a relatively large skin surface-to-body-volume ratio, thereby increasing the risk of wound formation.95 While there has been much discussion in the pediatric and fetal literature about the phenomenon of scarless wound closure in the fetus, there is clear scar formation in the third gestation of pregnancy and thereafter.98 Pediatric patients may be more prone to forming keloids and hypertrophic scars than adults due to abundant collagen forma-tion.99
Nutrition plays a significant role in the wound healing process in the infant. It is well established that amino acid substrate is required for several stages in wound healing, including clot formation, fibroblast proliferation, neovascularization, wound remodeling, and immunologic-mediated phagocytosis.100101 Proteins also have a significant role in wound healing, contributing to both structure and essential enzyme synthesis. In addition, collagen synthesis may be delayed by hypoproteinemia.102 Given the limited protein reserves of the neonate and the associated net increase in protein loss with critical illness and traumatic injury, protein becomes a vital macro-nutrient. Adequate carbohydrate calories are also essential for infants with wounds because of their limited glycogen reserve. Efficient delivery can be monitored by daily weight gain (15 to 20 g/kg/d for newborns and 12 g/kg/d for 1 to 2 year olds). However, caution must be used, because excessive carbohydrates can overwhelm the neonatal bowel and result in osmotic diarrhea.103
Certain subsets of pediatric patients will need close surveillance of nutritional provision during times of wound healing. For example, the child with short bowel syndrome represents a unique anatomic and physiologic challenge to growth and nutrient absorption. A working definition for short bowel syndrome in the pediatric age group is a requirement for parenteral nutrition for at least 3 months due to inadequate intestinal absorptive capacity. These children usually have undergone a massive intestinal resection at an early age, and many are missing the terminal ileum, which is vital to normal nutrient absorption. Children with short bowel syndrome often have difficulty attaining adequate levels of the fat-soluble vitamins (A, D, E, K), vitamin B12, folate, iron, and zinc. Many of these micronutrients play important roles in the wound healing process, and thus patients with short bowel syndrome may be at increased risk for poor or delayed wound healing.
In much the same way, children with respiratory difficulty have a unique relationship between nutritional intake and wound healing. This subset of pediatric patients includes premature infants with bronchopulmonary dysplasia and babies born with congenital diaphragmatic hernia (CDH). The increased work of breathing associated with these conditions may result in an elevation of the resting energy expenditure. In contrast to the pediatric metabolic response to critical illness, in which the baby generally does not increase his energy requirements, these conditions provide a physical basis for an increase in energy needs. Therefore these children may require a greater allotment of caloric intake to maintain normal growth and wound healing parameters.
Given the unique nature of the young infant's metabolism and its limited body macronutrient stores, healing of large wounds must be followed closely in the clinical setting. Difficulties with adequate wound healing, such as poor granulation, fistula formation, or recurrent infection, should raise the possibility of insufficient nutritional intake. In this setting, a formal dietary evaluation should be performed, including assessment of micronutrient serum levels (vitamins A, B12, D, E, iron, zinc, and folate). Pediatric patients who are refractory to basic nutritional supplementation will benefit from objective determination of resting energy expenditure. This can be performed with indirect calorimetry or validated stable isotopic techniques.
wound healing and nutritional support in the elderly patient
Wound healing can pose a significant problem in elderly patients. In order to heal a wound in an efficient manner, the body needs to mount an effective inflammatory response, mobilize the appropriate resources for angiogenesis, ground substance production and collagen deposition, and eventually remodel the collagen and contract the scar.104 Elderly patients are at a disadvantage compared to younger adults, because they have lower rates of protein synthesis, are often mildly immunosup-pressed, and frequently suffer from micro- and macronutrient deficiencies. Elderly patients are also more likely to have comorbid conditions that interfere with healing wounds. Diabetes, which occurs in over 10% of patients over the age of 60,102 has serious consequences for wound healing. Not only does hyperglycemia increase the risk of infection and interfere with fibroblast and leukocyte function, but the absence of or insensitivity to insulin has also been shown to impair healing.105 Peripheral vascular disease and cardiovascular compromise are both common problems in elderly patients and can significantly affect oxygen delivery to the site of injury, prolonging the time required for healing and predisposing to chronic ulceration and skin breakdown.106 In addition, both chronic renal and hepatic disease are associated with wound healing delays due to problems with managing fluid volume and clotting factor production as well as amino acid metabolism.106 However, surprisingly, even with numerous factors that could potentially negatively impact upon healing, most simple wounds heal without significant delay.
Although the healing of acute surgical or traumatic wounds is usually not problematic for elderly patients, chronic wounds and, specifically, decubitus pressure ulcers, are particularly concerning. Pressure ulcers are associated with poor nutritional status, with malnourished patients being twice as likely to develop these wounds compared to well-nourished elderly patients.107 It is estimated that as many as 65% of malnourished elderly people in chronic care facilities have pressure ulcers.108 Even adequately nourished patients are at risk for developing these wounds. Up to 10% of hospitalized geriatric patients will develop decubitus ulcers during their hospital stay.106 In addition to ensuring that patients are rotated frequently and physical pressure is eliminated as much as possible, ensuring maximal blood flow, a full nutritional assessment is necessary in the setting of decubitus ulcers and, in fact, is prudent in the elderly population whenever wound healing is problematic.109 One of the most important factors for proper wound healing is the ability to channel adequate energy to the wound. The body tends to place a high priority on wound healing, but if there is an infection or abscess elsewhere, requiring additional energy, wound healing can be delayed.100 The most energy-consuming aspect of wound healing is collagen synthesis and deposition. The estimated caloric requirement is 0.9 kcal/g of collagen. Small wounds do not usually pose a significant metabolic burden, but large wounds can.88 Generally, an appropriate balance of protein, carbohydrates, and lipids is essential for proper nutrition and the best chances of uneventful wound healing. Deficiencies in protein can lead to problems with skin cell proliferation, tissue reorganization, and collagen synthesis; inadequate intake of carbohydrates can impair fibroblast proliferation;110 and too few lipids can result in problems with cell membrane and intracellular matrix synthesis, as well as dampened inflammatory reactions.111112 There has also been extensive research into the roles of specific single nutrients in the healing process in the hopes that providing supplementation of these components will enhance healing. These nutrients include single amino acids, vitamins, and trace elements.
Two amino acids of special interest are arginine and glutamine. Arginine, although not considered an essential amino acid under normal conditions, when given as a supplement in experimental conditions has been shown to improve collagen deposition and strength.104 One of the metabolic pathways for arginine includes conversion to ornithine, which is a proline precursor and therefore may directly stimulate collagen production.113 Arginine is also thought to reduce protein breakdown during catabolic conditions, mainly by stimulating the release of insulin, glucagon, and growth hormone. Glutamine is another potentially useful amino acid for wound healing. It is the most abundant amino acid in the body and is used by many inflammatory cells for fuel as well as for nucleotide synthesis needed for cellular replication.114 However, despite encouraging findings for both arginine and glutamine, there is little evidence to support routine supplementation in the elderly, and neither amino acid has had a significant effect on preventing pressure ulcers in susceptible patients.115
The vitamins of most benefit in wound healing are vitamins C and A. Vitamin C is historically known to be a crucial cofactor for proper collagen cross-linking,116 and although deficiencies are rare in elderly patients, it is important to provide supplementation if inadequate intake is anticipated. The recommended daily dietary allowance is 60 mg, except for women over the age of 51, who should get 62 mg/d. Vitamin A is also important for wound healing and is particularly effective as a supplement in patients who are being treated with steroids, radiotherapy, or who have diabetes. At supplemental doses of 25,000 U/d in this patient population, healing may be accelerated secondary to an increased inflammatory response and increased collagen synthesis.80
Although sometimes forgotten, the trace element zinc has an important role in wound healing because of its role in DNA and protein synthesis. After injury, there is a redistribution of zinc with increased uptake in the wound, liver, and spleen, resulting in a relative decrease in plasma and skin levels.117 When deficient (levels less than 100 ^g/100 ml), wound strength and epithelialization can be affected.74 Although there is no proven benefit to supplementing patients who are not deficient, if the serum level is low it should be brought to adequate levels. The recommended daily dose for elderly patients is 15 mg.88 Hospitalized patients are particularly at risk for low serum zinc levels due to decreased oral intake and increased zinc losses through diarrhea or malabsorption.118 There is also some benefit to using topical zinc ointments, because zinc is absorbed percutaneously and enhances cell division within the epidermal layer. In addition, the topical zinc formulations have mild antibacterial properties.101
It is important to remember that a nutritional evaluation for an elderly patient who is critically ill or injured requires ongoing assessment. Elderly adults, similarly to infants and children, are at risk of becoming malnourished while in the hospital because they are not always able to adequately nourish themselves. Although elderly patients do have some nutritional reserve, they can become deficient in both macro-and micronutrients during times of illness due to ongoing catabolism. The sooner nutritive deficiencies are detected and corrected, the more the patient will benefit and the better the chance of uncomplicated wound healing.
The dramatic increase in protein breakdown during critical illness coupled with the known association between protein loss and patient mortality and morbidity has stimulated a wide array of research efforts. The measurement of whole body nitrogen balance through urine and stool was once the only way to investigate changes in protein metabolism, but now validated nonradioactive stable isotope tracer techniques exist to measure the precise rates of protein turnover, breakdown, and synthesis.119
However, the modulation of protein metabolism in critically ill patients has proved difficult. Dietary supplementation of amino acids increases protein synthesis but appears to have no effect on protein breakdown rates. Thus investigators have recently focused on the use of alternative anabolic agents to decrease protein catab-olism. To achieve this goal, researchers have used various pharmacologic tools, including growth hormone, insulin-derived growth factor I (IGF-I), and testosterone with varying degrees of success.120122 One of the most promising agents, however, may be the anabolic hormone insulin.
Multiple studies have used insulin to reduce protein breakdown in healthy volunteers and adult burn patients.123125 In children with extensive burns, intravenous insulin has been shown to increase lean body mass and mitigate peripheral muscle catabolism.126 A recent prospective, randomized trial of over 1500 adult postoperative patients in the intensive care unit demonstrated significant reductions in mortality and morbidity with the use of intravenous insulin.127 Preliminary stable isotopic studies demonstrate that an intravenous insulin infusion may reduce protein breakdown by 32% in critically ill neonates on ECMO.128 The use of insulin and other hormonal modalities to modulate the protein metabolic response to systemic illness will continue to be an active area of clinical investigation in critically ill adults and children. It is likely that interventions that promote net protein accretion will augment the wound healing process, as additional protein substrate will be available for the various mechanisms involved in wound healing.
1. Forbes, G.B. and Bruining, G.J., Urinary creatinine excretion and lean body mass, Am. J. Clin. Nutr., 29, 1359-1366, 1976.
2. Foman, S.J., Haschke, F., Zeigler, E.E. et al., Body composition of reference children from birth to age 10 years, Am. J. Clin. Nutr., 35, 1169-1175, 1982.
3. Munro, H.N., Nutrition and muscle protein metabolism, Fed. Proc., 37, 2281-2282, 1978.
4. Long, C.L., Spencer, J.L., Kinney, J.M. et al., Carbohydrate metabolism in normal man and effect of glucose infusion, J. Appl. Phys., 31, 102-109, 1971.
5. Herrera, E. and Amusquivar, E., Lipid metabolism in the fetus and the newborn, Diabet./Metab. Res. Rev., 16, 202-210, 2000.
6. Reichman, B., Chessex, P., Vercellen, G. et al., Dietary composition and macronutrient storage in preterm infants, Pediatrics, 72, 322-328, 1983.
7. Schulze, K.F., Stefanski, M., Masterson, J. et al., Energy expenditure, energy balance and composition of weight gain in low birth weight infants fed diets of different protein and energy content, J. Pediatr., 110, 753-759, 1987.
8. Whyte, R.K., Haslam, R., Vlainic, C. et al. Energy balance and nitrogen balance in growing low birthweight infants fed human milk or formula, Pediatr. Res., 18, 891898, 1983.
9. Food and Nutrition Board, Recommended Dietary Allowances, 10th ed., National Academy of Science — National Research Council, Washington, D.C., 1989.
10. Kashyap, S., Schulze, K.F., Forsyth, M. et al., Growth, nutrient retention, and metabolic response in low birth weight infants fed varying intakes of protein and energy, J. Pediatr, 113, 713-721, 1988.
11. Denne, S.C., Karn, C.A., Ahlrichs, J.A. et al., Proteolysis and phenylalanine hydrox-ylation in response to parenteral nutrition in extremely premature and normal new-borns, J. Clin. Invest., 97, 746-754, 1996.
12. Hay, W.W., Lucas, A., Heird, W.C. et al., Workshop summary: nutrition of the extremely low birth weight infant, Pediatrics, 104, 1360-1368, 1999.
13. Keshen, T., Miller, R.G., Jahoor, F. et al., Stable isotopic quantitation of protein metabolism and energy expenditure in neonates on and post extracorporeal life support, J. Pediatr. Surg., 32, 958-963, 1997.
14. Jaksic, T., Wagner, D.A., Burke, J.F. et al., Proline metabolism in adult male burned patients and healthy control subjects, Am. J. Clin. Nutr., 54, 408-413, 1991.
15. Cogo, P.E., Carnielli, V.P., Rosso, F. et al., Protein turnover, lipolysis, and endogenous hormonal secretion in critically ill children, Crit. Care Med., 30, 65-70, 2002.
16. Coss-Bu, J.A., Klish, W.J., Walding, D. et al., Energy metabolism, nitrogen balance, and substrate utilization in critically ill children, Am. J. Clin. Nutr, 74, 664-669, 2001.
17. Bilmazes, C., Klein, C.L., Rorbaugh, D.K. et al., Muscle protein catabolism after injury in man, as measured by urinary excretion of 3-methyl-histidine, Clin. Sci., 52, 527-533, 1977.
18. Pierro, A., Metabolism and nutritional support in the surgical neonate, J. Pediatr. Surg., 37, 811-822, 2002.
19. Long, C.L., Kinney, J.M., and Geiger, J.W., Non-suppressability of gluconeogenesis by glucose in septic patients, Metabolism, 25, 193-201, 1976.
20. Keshen, T., Miller, R., Jahoor, F. et al., Glucose production and gluconeogenesis are negatively related to body weight in mechanically ventilated, very low birthweight neonatos, Pediatr. Res., 31, 132-138, 1997.
21. Meszaros, K., Bojta, J., Bautista, A.P. et al., Glucose utilization by Kupffer cells, endothelial cells, and granulocytes in endotoxemic rat liver, Am. J. Phys., 267, G7-G12, 1994.
22. Denne, S.C., Karn, C.A., Wang, J. et al., Effect of intravenous glucose and lipid on proteolysis and glucose production in normal newborns, Am. J. Phys, 269, E361-E366, 1995.
23. Mitton, S.G. and Garlick, P.J., Changes in protein turnover after the introduction of parenteral nutrition in premature infants: comparison of breast milk and egg protein-based amino acid solutions, Pediatr. Res., 32, 447-454, 1992.
24. Pencharz, P., Beesley, J., Sauer, P. et al., Total-body protein turnover in parenterally fed neonates: effects of energy source studied by using [15N]glycine and [1-13C]leu-cine, Am. J. Clin. Nutr., 50, 1395-1400, 1989.
25. Beaufrere, B., Fournier, V., Salle, B. et al., Leucine kinetics in fed low-birth-weight infants: importance of splanchnic tissues, Am. J. Physiol., 263, E214-E220, 1992.
26. Mitton, S.G., Calder, A.G., and Garlick, P.J., Protein turnover rates in sick, premature neonates during the first few days of life, Pediatr. Res., 30, 418-422, 1991.
27. Rivera, A., Jr., Bell, E.F., and Bier, D.M., Effect of intravenous amino acids on protein metabolism of preterm infants during the first three days of life, Pediatr. Res., 33, 106-111, 1993.
28. Thureen, P.J., Anderson, A.H., Baron, K.A. et al., Protein balance in the first week of life in ventilated neonates receiving parenteral nutrition, Am. J. Clin. Nutr., 68, 1128-1135, 1998.
29. Duffy, B. and Pencharz, P., The effects of surgery on the nitrogen metabolism of parenterally fed human neonates, Pediatr. Res., 20, 32-35, 1996.
30. Poindexter, B.B., Karn, C.A., Leitch, C.A. et al., Amino acids do not suppress proteolysis in premature neonates, Am. J. Physiol., 281, E472-E478, 2001.
31. Goldman, H.I., Freundenthal, R., Holland, B. et al., Clinical effects of two different levels of protein intake on low birth weight infants, J. Pediatr., 74, 881-889, 1969.
32. Goldman, H.I., Liebman, O.B., Freundenthal, R. et al., Effects of early dietary protein intake on low-birth-weight infants: evaluation at 3 years of age, J. Pediatr., 78, 126-129, 1971.
33. Tappy, L., Schwarz, J.-M., Schneiter, P. et al., Effects of isoenergetic glucose-based or lipid-based parenteral nutrition on glucose metabolism, de novo lipogenesis, and respiratory gas exchanges in critically ill patients, Crit. Care Med., 26, 860-867, 1998.
Shew, S.B., Keshen, T.H., Jahoor, F. et al., The determinants of protein catabolism in neonates on extracorporeal membrane oxygenation, J. Pediatr. Surg., 34, 1086-1090, 1999.
Forsyth, J.S., Murdock, N., and Crighton, A., Low birthweight infants and total parenteral nutrition immediately after birth. III. Randomised study of energy substrate utilization, nitrogen balance, and carbon dioxide production, Arch. Dis. Child Fetal and Neonatal Ed., 73, F13-F16, 1995.
Jones, M.O., Pierro, A., Garlick, P.J. et al., Protein metabolism kinetics in neonates: effect of intravenous carbohydrate and fat, J. Pediatr. Surg., 30, 458-462, 1995. Jeenvanandam, M., Young, D.H., and Schiller, W.R., Nutritional impact on energy cost of fat fuel mobilization in polytrauma victims, J. Trauma, 30, 147-154, 1990. Powis, M.R., Smith, K., Rennie, M. et al., Effect of major abdominal operations on energy and protein metabolism in infants and children, J. Pediatr. Surg., 33, 49-53, 1998.
Paulsrud, J.R., Pensler, L., Whitten, C.F. et al., Essential fatty acid deficiency in infants induced by fat-free intravenous feeding, Am. J. Clin. Nutr, 25, 897-904, 1972. Friedman, Z., Danon, A., Stahlman, M.T. et al., Rapid onset of essential fatty acid deficiency in the newborn, Pediatrics, 58, 640-649, 1976.
Giovannini, M., Riva, E., and Agostoni, C., Fatty acids in pediatric nutrition, Pediatr. Clin. N. Am., 42, 861-877, 1995.
Committee on Nutrition, European Society of Pediatric Gastroenterology and Nutrition, Comment on the content and composition of lipids in infant formulas, Acta Paed. Scand., 80, 887-889, 1991.
Van Aerde, J.E., Sauer, P.J., Pencharz, P.B. et al., Metabolic consequences of increasing energy intake by adding lipid to parenteral nutrition in full-term infants, Am. J. Clin. Nutr., 59, 659-662, 1994.
Cleary, T.G. and Pickering, L.K., Mechanisms of intralipid effect on polymorphonuclear leukocytes, J. Clin. Lab. Immunol., 11, 21-26, 1983.
Perriera, G.R., Fox, W.W., Stanley, C.A. et al., Decreased oxygenation and hyperlipi-demia during intravenous fat infusions in premature infants, Pediatrics, 66, 26-30, 1980. Freeman, J., Goldmann, D.A., Smith, N.E. et al., Association of intravenous lipid emulsion and coagulase-negative staphylococcal bacteremia in neonatal intensive care units, N. Engl. J. Med, 323, 301-308, 1990.
Blackburn, G.L., Bistrian, B.R., Mani, B.S. et al., Nutritional and metabolic assessment of the hospitalized patient, J. Parenter. Enteral Nutr., 1, 11-22, 1977. Jahoor, F., Desair, M., Herndon, D.N. et al., Dynamics of the protein metabolic response to burn injury, Metabolism, 37, 330-337, 1988.
Jones, M.O., Pierro, A., Hammond, P. et al., The metabolic response to operative stress in infants, J. Pediatr. Surg., 28, 1258-1263, 1993.
Shew, S.B., Keshen, T.H., Glass, N.L. et al., Ligation of a patent ductus arteriosus under fentanyl anesthesia improves protein metabolism in premature neonates, J. Pediatr. Surg, 35, 1277-1281, 2000.
Pierro, A., Carnielli, V., Filler, R.M. et al., Partition of energy metabolism in the surgical newborn, J. Pediatr. Surg., 26, 581-586, 1991.
Jaksic, T., Shew, S.B., Keshen, T.H. et al., Do critically ill surgical neonates have elevated energy expenditure? J. Pediatr. Surg., 36, 63-67, 2001. Garza, J.J., Shew, S.B., Keshen, T.H. et al., Energy expenditure in ill premature neonates, J. Pediatr. Surg., 37, 289-293, 2002.
Letton, R.W., Chwals, W.J., Jamie, A. et al., Early postoperative alterations in infant energy use increase the risk of overfeeding, J. Pediatr. Surg., 30, 988-993, 1995.
55. Weinstein, M.R. and Oh, W., Oxygen consumption in infants with bronchopulmonary dysplasia, J. Pediatr., 99, 958-961, 1981.
56. Briassoulis, G., Venkataraman, S., and Thompson, A.E., Energy expenditure in critically ill children, Crit. Care Med., 28, 1166-1172, 2000.
57. Coss-Bu, J.A., Jefferson, L.S., Walding, D. et al., Resting energy expenditure in children in a pediatric intensive care unit: comparison of Harris-Benedict and Talbot predictions with indirect calorimetry values, Am. J. Clin. Nutr., 67, 74-80, 1998.
58. Jensen, G.L., McGee, M., and Binkley, J., Nutrition in the elderly, Gastroenterol. Clin. N. Am., 30, 313-333, 2001.
59. Kinney, J.M., Energy requirements of the surgical patient, in Manual of surgical nutrition, Ballinger, W.F., Collins, J.A., Druker, W.R. et al., Eds., W.B. Saunders, Philadelphia, 1975, pp. 223-235.
60. Blumberg, J., Nutrient requirements of the healthy elderly — should there be specific RDAs? Nutr. Rev., 52, S15-S18, 1994.
61. Lau, H.C., Granick, M.S., Aisner, A.M., and Solomon, M.P., Wound care in the elderly patient, Surg. Clin. N. Am., 74, 441-463, 1994.
62. Tellado, J.M., Garcia-Sabrido, J.L., Hanley, Ja., Shizgal, H.M., and Christou, N.V., Predicting mortality based on body composition analysis, Ann. Surg., 208, 81-87,
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