|
 
 |
| REVIEW ARTICLE |
|
| Year : 2016 | Volume
: 21
| Issue : 1 | Page : 8-11 |
|
Nutrition in burn patient
Prabhu Dayal Sinwar
Department of General Surgery, Sardar Patel Medical College Bikaner, Bikaner, Rajasthan, India
| Date of Web Publication | 4-Mar-2016 |
Correspondence Address:
Prabhu Dayal Sinwar
New PG Hostel, Room No. 28, Sardar Patel Medical College Bikaner, Bikaner, Rajasthan
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0971-9903.178072
Burn injury continues to be a significant cause of morbidity and mortality. Nutritional support has become an essential element of burn care. Failure to meet the increased substrate requirements may result in impaired wound healing, multi organ dysfunction, increased susceptibility to infection, and death. Therefore, aggressive nutrition support is essential to ensure adequate burn care, attenuate the hypermetabolic response, optimize wound healing, minimize devastating catabolism, and reduce morbidity and mortality. Failure to adequately address the increased levels of inflammatory mediators, catecholamines, and corticosteroids central to the hypermetabolic response postburn injury can lead to catastrophic results. One of the most important perturbations is provision of adequate and early nutrition. The provision of the right balance of macro and micronutrients, along with additional antioxidants is essential to mitigate the hypermetabolic and hypercatabolic state that results following a burn injury. Keywords: Burns, enteral nutrition, nutrition, parenteral nutrition
How to cite this article:
Sinwar PD. Nutrition in burn patient
. J Mahatma Gandhi Inst Med Sci 2016;21:8-11 |
| Introduction | |  |
Nutrition has been recognized as a critical component of acute burn care and ultimate wound healing. Debate remains over the appropriate timing of enteral nutrition and the benefit of supplemental trace elements, antioxidants, and immunonutrition for critically ill burn patients. Enteral nutrition in burned patients should begin within few hours of burn onset. Such approach leads to better clinical outcomes for patients, reduces infections, and improves nutritional profile. The assurance of the needs of nutritional factors and energy is essential for patients having more than 20% of the body surface (BS) burned. Burn patients with >20% BS area injury suffer a long and severe response to injury, including a hyperdynamic and hypermetabolic response with lipolysis, proteolysis, glycolysis, and fever. This catabolic state ultimately results in a profound reduction of lean body mass. Poor wound healing, immune dysfunction, multiorgan failure (MOF), and even death can ensue. [1]
| Methods | | |
We performed a MEDLINE database search using the PubMed search engine with the Medical Subject Heading words such as "nutrition in burn patients," "enteral nutrition in burn patient," "parenteral nutrition in burn patient" of systematic reviews of full text article written in English and they were taken into account.
| Review and Discussion | | |
Severe burn injury is associated with metabolic alterations that persist up to 2 years postburn. [2] Immediately after injury, patients enter a period of attenuated metabolism and decreased tissue perfusion, also referred to as the "ebb" phase. Shortly after, they enter a phase of hypermetabolic rates and hyperdynamic circulation, known as the "flow" state. [3] A 10% loss of total body mass leads to immune dysfunction; 20% to decreased wound healing; 30% to severe infections; and 40% to death. [4] The protein loss is directly related to increases in metabolic rate and may persist for up to 24 months postburn, often resulting in significantly negative whole-body and cross-leg nitrogen balances. [5],[6],[7] Severely burned patients have a nitrogen loss of 20-25 g/m 2 total BS area (TBSA)/day, [6] which - if unattended - results in lethal cachexia in <30 days.
Experimental evidence has demonstrated that enteral nutrition influences the physiologic response to injury. Animal models using guinea pigs demonstrate that early enteral nutrition significantly reduces the hypermetabolic response to injury. [8],[9] Rat models show that enteral nutrition can decrease the levels of proinflammatory cytokines, such as tumor necrosis factor alpha, when compared with parenteral routes. [10]
Bacterial translocation and loss of gut mucosal integrity has also been shown in the host response to burn injury. [11],[12] The resulting intestinal injury may influence systemic injury and MOF. [13] Enteral nutrition helps to maintain gut mucosa viability and decreases bacterial translocation. [14] Introduction of nutrients to enhance the immune response shows promise in blunting the inflammatory response and improving the intestinal immune response. [15],[16],[17],[18] Finally, even in the acute phase of the injury, the bowel tolerates enteral feeding despite slower transit times. [19] Over the past decade, numerous studies have been conducted to clarify the role of the gastrointestinal system as an immune organ. [20] The presence of food in the gut is important for intestinal cells' nutrition by diffusion from the lumen: 50% enterocytes and 70% cells in colon meet energy needs from the lumen. In addition, the food in the intestine is a stimulus for the secretion of digestive enzymes, for the establishment of intestinal motility, and for satisfactory intestinal circulation. [21]
Gudaviciene et al. [22] in a retrospective study confirmed that incidence of inflammatory complications of burn disease is lower when introducing enteral nutrition within 24 h of the occurrence of burns. Lam et al., [23] in a prospective randomized study, demonstrated that early enteral nutrition contributed to increased cellular and humoral immunity in burned patients. Multi organ failure is the most serious complication of burn disease with high mortality rate of 45%. [24] Burned patients have increased level of mortality, possibly due to late introduction of enteral feeding, namely, the absence of food in the intestinal lumen leads to impaired function of the immune system and the development of the inflammatory response, the state described with expression endogenous sepsis or gut derived sepsis. [25] This kind of nutrition is called trophic intestinal feeding (feeding the gut). [26] The early initiation of enteral nutrition support in the burn population is of utmost importance for survival. [27]
The composition of this enteral nutrition support is equally important. The provision of the right balance of macro and micronutrients, antioxidants, and energy is essential for mitigating the hypermetabolic and hypercatabolic state that results following a burn injury. [27] While there are no definitive trials that indicate clear superiority of early nutrition, clinical practice guidelines recommend starting enteral nutrition in critically ill patients within 24 h in burns and 24-48 h in mixed Intensive Care Unit populations. [28],[29],[30]
Since the early 1900s, it has been recognized that burn patients require an increased caloric intake. High caloric feeding was advocated by Shaffer et al. in 1909 [31] and more recently by Wilmore et al. in 1979. [32] Several formulas are used to calculate caloric requirement in burned patients. One formula multiplies the basal energy expenditure (BEE) determined by the Harris-Benedict formula by two in burns >40% TBSA, assuming a 100% increase in total energy expenditure (TEE). [33] TEE was 1.33 ± 0.27 times predicted BEE was measured by doubly labeled water method, and in studies where resting energy expenditure (REE) was simultaneously measured, TEE was 1.18 ± 0.17 times REE, which in turn was 1.16 ± 0.10 times predicted BEE. [34]
The macronutrients in the formulation of burn nutrition include carbohydrates, proteins, and lipids. Some research suggests that given the inhibition of lipolysis in the acute response to injury, lipids should be limited as a source of calories. [35] Comparison of high carbohydrate, high protein, low fat enteral feeds with low carbohydrate, high protein, and high fat formulas in a systematic way showed no clear benefit to either formula, although the risk of pneumonia appeared lower with the high carbohydrate formula. [36]
Increased catabolism of protein leads to losses of over 1 kg of skeletal muscle and visceral proteins a day. [37] Despite repletion with apparently adequate amounts of dietary protein and calories, protein catabolism exceeds anabolism, and weight loss following burn injury is inevitable. [38] Severely burned children who were fed 5 g/kg/day had better immune function, fewer days of bacteremia and antibiotics, and higher survival rates than similarly-injured children randomized to 3.8 g/kg/day. [39] Current recommendations are for 1.5-2 g/kg/day in adults and 3 g/kg/day in children. [40] Overfeeding can result in fluid and electrolyte imbalances, hyperglycemia, and hepatic steatosis. [41] Protein appears to be an essential macronutrient for wound healing, and protein requirements in burn patients may be 50% higher than in healthy individuals. [42]
Critical illness and injury result in increased oxidative stress and release of reactive oxygen species (ROS). These molecules have been associated with MOF and acute respiratory distress syndrome. ROS may produce tissue injury through oxidation of enzymes and structural proteins, peroxidation of cell plasma membranes, and induction of apoptosis. [43] Immunonutrition refers to the use of nutrients that modify a patient's immune response during critical illness. Nutrients that have been used in burn patients include omega-3 fatty acids (fish oil), glutamine, and arginine. Glutamine is thought to be a conditionally essential amino acid in burns. It provides a nitrogen source, a fuel for immune cells, fuel for enterocytes, serves as a precursor for the antioxidant glutathione, and potentially reduces insulin resistance. [44] Arginine, another conditionally essential amino acid in burns, serves as a precursor proline and glutamate, promotes T-cell proliferation, stimulates insulin, insulin-like growth factor 1, and pituitary growth hormone, as well as promoting wound healing. Omega-3 fatty acids replace omega-6 fatty acids in cell membranes and decreases inflammation due to less inflammatory breakdown products. [44]
| Conclusion | | |
Enteral nutrition support should be used in preference to parenteral nutrition support and should be provided in acute phase of recovery. For patients with burns covering more than 20% of their BS area, a high protein diet should be used with provision of adequate calories to meet energy needs. Adults should receive 1.5-2 g/kg/day and children should receive 3 g/kg/day.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Jeschke MG, Gauglitz GG, Kulp GA, Finnerty CC, Williams FN, Kraft R, et al. Long-term persistance of the pathophysiologic response to severe burn injury. PLoS One 2011;6:e21245.  |
| 2. | Hart DW, Wolf SE, Mlcak R, Chinkes DL, Ramzy PI, Obeng MK, et al. Persistence of muscle catabolism after severe burn. Surgery 2000;128:312-9. |
| 3. | Cuthbertson D. Post-shock metabolic response. Lancet 1942;2:433-6. |
| 4. | Chang DW, DeSanti L, Demling RH. Anticatabolic and anabolic strategies in critical illness: A review of current treatment modalities. Shock 1998;10:155-60. |
| 5. | Hart DW, Wolf SE, Chinkes DL, Gore DC, Mlcak RP, Beauford RB, et al. Determinants of skeletal muscle catabolism after severe burn. Ann Surg 2000;232:455-65. |
| 6. | Herndon DN, Tompkins RG. Support of the metabolic response to burn injury. Lancet 2004;363:1895-902. |
| 7. | Jahoor F, Desai M, Herndon DN, Wolfe RR. Dynamics of the protein metabolic response to burn injury. Metabolism 1988; 37:330-7. |
| 8. | Mochizuki H, Trocki O, Dominioni L, Brackett KA, Joffe SN, Alexander JW. Mechanism of prevention of postburn hypermetabolism and catabolism by early enteral feeding. Ann Surg 1984;200:297-310. [ PUBMED] |
| 9. | Dominioni L, Trocki O, Fang CH, Mochizuki H, Ray MB, Ogle CK, et al. Enteral feeding in burn hypermetabolism: nutritional and metabolic effects of different levels of calorie and protein intake. JPEN J Parenter Enteral Nutr 1985;9:269-79. [ PUBMED] |
| 10. | Cui XL, Iwasa M, Kuge H, Sasaguri S, Ogoshi S. Route of feeding influences the production and expression of tumor necrosis factor alpha in burned rats. Surg Today 2001;31:615-25. |
| 11. | Carter EA, Tompkins RG, Schiffrin E, Burke JF. Cutaneous thermal injury alters macromolecular permeability of rat small intestine. Surgery 1990;107:335-41. |
| 12. | Deitch EA. Intestinal permeability is increased in burn patients shortly after injury. Surgery 1990;107:411-6. |
| 13. | Deitch EA, Shi HP, Lu Q, Feketeova E, Skurnick J, Xu DZ. Mesenteric lymph from burned rats induces endothelial cell injury and activates neutrophils. Crit Care Med 2004;32: 533-8. |
| 14. | Peng YZ, Yuan ZQ, Xiao GX. Effects of early enteral feeding on the prevention of enterogenic infection in severely burned patients. Burns 2001;27:145-9. |
| 15. | Berger MM, Binnert C, Chiolero RL, Taylor W, Raffoul W, Cayeux MC, et al. Trace element supplementation after major burns increases burned skin trace element concentrations and modulates local protein metabolism but not whole-body substrate metabolism. Am J Clin Nutr 2007;85:1301-6. |
| 16. | Cui XL, Iwasa M, Iwasa Y, Ogoshi S. Arginine-supplemented diet decreases expression of inflammatory cytokines and improves survival in burned rats. JPEN J Parenter Enteral Nutr 2000;24:89-96. |
| 17. | Falder S, Silla R, Phillips M, Rea S, Gurfinkel R, Baur E, et al. Thiamine supplementation increases serum thiamine and reduces pyruvate and lactate levels in burn patients. Burns 2010;36:261-9. |
| 18. | Fan J, Meng Q, Guo G, Xie Y, Li X, Xiu Y, et al. Effects of early enteral nutrition supplemented with arginine on intestinal mucosal immunity in severely burned mice. Clin Nutr 2010;29:124-30. |
| 19. | Sallam HS, Kramer GC, Chen JD. Gastric emptying and intestinal transit of various enteral feedings following severe burn injury. Dig Dis Sci 2011;56:3172-8. |
| 20. | Kang W, Kudsk KA. Is there evidence that the gut contributes to mucosal immunity in humans? JPEN J Parenter Enteral Nutr 2007;31:246-58. |
| 21. | Kudsk KA. Current aspects of mucosal immunology and its influence by nutrition. Am J Surg 2002;183:390-8. |
| 22. | Gudaviciene D, Rimdeika R, Adamonis K. Influence of enteral nutrition on the frequency of complications in case of major burns. Medicina (Kaunas) 2004;40:957-61. |
| 23. | Lam NN, Tien NG, Khoa CM. Early enteral feeding for burned patients - An effective method which should be encouraged in developing countries. Burns 2008;34:192-6. |
| 24. | Ryan CM, Schoenfeld DA, Thorpe WP, Sheridan RL, Cassem EH, Tompkins RG. Objective estimates of the probability of death from burn injuries. N Engl J Med 1998;338:362-6. |
| 25. | Sanderson IR, Croft NM. The anti-inflammatory effects of enteral nutrition. JPEN J Parenter Enteral Nutr 2005;29 4 Suppl:S134-8. |
| 26. | Wildhaber BE, Yang H, Spencer AU, Drongowski RA, Teitelbaum DH. Lack of enteral nutrition - Effects on the intestinal immune system. J Surg Res 2005;123:8-16. |
| 27. | Rodriguez NA, Jeschke MG, Williams FN, Kamolz LP, Herndon DN. Nutrition in burns: Galveston contributions. JPEN J Parenter Enteral Nutr 2011;35:704-14. |
| 28. | Jacobs DG, Jacobs DO, Kudsk KA, Moore FA, Oswanski MF, Poole GV, et al. Practice management guidelines for nutritional support of the trauma patient. J Trauma 2004;57:660-78. |
| 29. | Kreymann KG, Berger MM, Deutz NE, Hiesmayr M, Jolliet P, Kazandjiev G, et al. ESPEN guidelines on enteral nutrition: Intensive care. Clin Nutr 2006;25:210-23. |
| 30. | Heyland DK, Schroter-Noppe D, Drover JW, Jain M, Keefe L, Dhaliwal R, et al. Nutrition support in the critical care setting: Current practice in canadian ICUs - Opportunities for improvement? JPEN J Parenter Enteral Nutr 2003;27:74-83. |
| 31. | Shaffer PA, Coleman W, Somogyi M, Reinoso EA, Cutler E. Protein metabolism in typhoid fever. Arch Intern Med 1909;IV:538-600. |
| 32. | Wilmore DW, Curreri PW, Spitzer KW, Spitzer ME, Pruitt BA Jr. Supranormal dietary intake in thermally injured hypermetabolic patients. Surg Gynecol Obstet 1971;132: 881-6. [ PUBMED] |
| 33. | Curreri PW. Nutritional support of burn patients. World J Surg1978;2:215-21. [ PUBMED] |
| 34. | Goran MI, Peters EJ, Herndon DN, Wolfe RR. Total energy expenditure in burned children using the doubly labeled water technique. Am J Physiol Endocrinol Metab 1990;259:E576-85. |
| 35. | Williams FN, Branski LK, Jeschke MG, Herndon DN. What, how, and how much should patients with burns be fed? Surg Clin North Am 2011;91:609-29. |
| 36. | Masters B, Aarabi S, Sidhwa F, Wood F. High-carbohydrate, high-protein, low-fat versus low-carbohydrate, high-protein, high-fat enteral feeds for burns. Cochrane Database Syst Rev 2012;1:CD006122. |
| 37. | Wolfe RR, Goodenough RD, Wolfe MH. Isotopic approaches to the estimation of protein requirements in burn patients. Adv Shock Res 1983;9:81-98. [ PUBMED] |
| 38. | Prelack K, Cunningham JJ, Sheridan RL, Tompkins RG. Energy and protein provisions for thermally injured children revisited: An outcome-based approach for determining requirements. J Burn Care Res 1997;18:177-81. |
| 39. | Alexander JW, MacMillan BG, Stinnett JD, Ogle CK, Bozian RC, Fischer JE, et al. Beneficial effects of aggressive protein feeding in severely burned children. Ann Surg 1980;192: 505-17. [ PUBMED] |
| 40. | Bell SJ, Molnar JA, Krasker WS, Burke JF. Weight maintenance in pediatric burned patients. J Am Diet Assoc 1986;86:207-11. [ PUBMED] |
| 41. | Klein CJ, Stanek GS, Wiles CE 3 rd . Overfeeding macronutrients to critically ill adults: Metabolic complications. J Am Diet Assoc 1998;98:795-806. |
| 42. | Stroud M. Protein and the critically ill; do we know what to give? Proc Nutr Soc 2007;66:378-83. |
| 43. | Nathens AB, Neff MJ, Jurkovich GJ, Klotz P, Farver K, Ruzinski JT, et al. Randomized, prospective trial of antioxidant supplementation in critically ill surgical patients. Ann Surg 2002;236:814-22. |
| 44. | Kurmis R, Parker A, Greenwood J. The use of immunonutrition in burn injury care: Where are we? J Burn Care Res 2010;31:677-91. |
|
Search Pubmed for