Nutrition
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Studies have shown that protein catabolism increases by 80% and energy expenditure by 20% in acute pancreatitis, indicating that nutritional requirements are elevated. Other studies have associated the resolution of negative nitrogen balance by nutrition support with improved outcome. Consequently, the need for effective nutrition is one cornerstone of management of acute pancreatitis. ⋯ No study has shown that jejunal feeding exacerbates the disease. Further, jejunal feeding is associated with fewer infectious and metabolic complications. These observations and the fact that enteral feeding is one-tenth the cost of TPN has resulted in the general acceptance of jejunal feeding as the preferred mode for maintaining nutrition in patients with acute pancreatitis.
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The catabolic response to sepsis, severe injury, and burn is characterized by whole-body protein loss, mainly reflecting increased breakdown of muscle proteins, in particular myofibrillar proteins. Glucocorticoids and various proinflammatory cytokines are important regulators of muscle proteolysis in stressed patients. There is evidence that breakdown of proteins by the ubiquitin-proteasome pathway plays an important role in muscle cachexia, although other mechanisms may participate, such as calcium- and calpain-dependent release of myofilaments from the sarcomere. ⋯ In addition to nutrition support, various hormones, including insulin, growth hormone, and insulin-like growth factor-1, may blunt the catabolic response in patients with stress. Experimental studies have indicated that other treatments may become available in the future, including cytokine antibodies, calcium antagonists, and induction of heat shock response. Methods to prevent or reduce the catabolic response to stress are important considering the significant clinical consequences of muscle cachexia.
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Cirrhotic patients may become candidates for elective and emergency surgery. This may be due to conditions requiring operations such as cholecystectomy, herniotomy, or gastrointestinal malignancies, more common in cirrhotics when compared with the general population, or to complications of the liver disease such as resectable hepatocellular carcinomas or surgical portosystemic shunts to treat portal hypertension. It has been estimated that 10% of cirrhotics undergo at least one operative procedure during the final 2 y of their lives. ⋯ Few data are available concerning the perioperative nutrition support in surgical cirrhotic patients. The results of these studies are sometimes encouraging in reporting that the nutrition therapy may improve the clinical outcome in cirrhotic patients undergoing general surgery and/or liver transplantation. The limited number of patients and their heterogeneity, however, do not allow definitive conclusions, and more research on this issue is needed.
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Hypercatabolism after trauma may lead to acute protein malnutrition, ultimately resulting in multiple organ failure. Nutrition support may prevent this sequence. This review addresses the need for early nutrition support, the preferred route of substrate delivery, and the potential advantages of "immune-enhancing" diets.
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This review analyzes the literature and the historical concerns (restrictions, traditions, nasogastric tube) and pathophysiologic factors (postoperative ileus, risk of anastomotic dehiscence, nausea and vomiting, loss of appetite) invoked for not instituting early oral feeding after major abdominal procedures. It appears that several factors may promote postoperative oral feeding such as thoracic epidural analgesia, multimodal anti-emetic treatment, opioid-sparing analgesia, selective peripheral opioid antagonists, and enforced oral nutrition. Recent data from multimodal fast-track rehabilitation surgical programs in abdominal surgery provide a rational basis for future studies to investigate and facilitate enforced oral feeding after major abdominal procedures.