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NUTRITIONAL SUPPORT IN ACUTE PANCREATITIS
PRAVIN AMIN
Physician and Intensivist, Bombay Hospital Institute of Medical Sciences, Mumbai.
Acute pancreatitis is an acute inflammatory process of the pancreas that can involve peri-pancreatic tissues or remote organ systems, or both. The first phase is a clinical response resulting from systemic effects of proinflammatory medicators called SIRS (systemic inflammatory response syndrome) that may lead to multiple organ failure and death. The second phase, may lead to local complications such as infected pancreatic necrosis. The most commonly used classification system for acute pancreatitis distinguishes between mild and severe disease. Severe disease is characterized by organ failure or local complications such as necrosis, pseudocysts, or fistulae. The severity of the disease must be established early to identify patients requiring intensive monitoring and support. Ranson score is about 80% accurate at 48 hours but is erroneous before this time. The APACHE II system has the sensitivity to predict severe pancreatitis in 61% patients on admission. The prognostic systems of severity remain better than clinical reasoning.
SIRS followed by local complications is associated with an increased energy requirement and, with the absence of oral intake, a persistently negative nitrogen balance and mineral and micronutrient deficiencies. Thus, early nutritional support is indicated. Formerly, total parenteral nutrition was the benchmark practice for providing exogenous nutrients to avert pancreatic stimulation. The use of early enteral feeding has recently been assessed. In two recent randomized, prospective studies, patients with severe acute pancreatitis received either total parenteral nutrition or enteral feeding (through a nasoenteric feeding tube radiographically placed beyond the ligament of treitz) within 48 hours of the onset of illness. [1] , [2] Enteral feeding was well tolerated, had no adverse clinical effects, and resulted in significantly fewer total and infectious complications. Gastric atony and obstruction of the duodenum due to pancreatic oedema or necrosis have been overcome by delivering enteral nutrition to the jejunum, distal to the ligament of treitz. At this position, regular diets do not stimulate pancreatic secretions. The efficiency, acceptance, clinical outcome and cost of enteral nutrition indicate that this feeding route should be favoured in patients with severe acute pancreatitis.
Parenteral or enteral nutrition support has not consistently improved disease activity in patients with pancreatitis and therefore cannot be considered as primary therapy for this disorder.[1] , [2] Acute, mild, and moderate pancreatitis are usually of short duration and require no specialized nutrition support. Nutrition support for patients with severe pancreatitis may prevent nutrient deficiencies and preserve lean body mass and functional capacity when nutrient intake falls below needs. Severe necrotizing pancreatitis is often complicated by fistula, pseudocyst, and abscess formation. [3] , [5] Nutritional compromise may arise from any of the following : poor oral intake due to pain, nausea, vomiting, or malabsorption; increased protein losses; requirements of fistulae or infection; or surgery. Nutrition support can improve the nutritional status of these patients. [5] , [7]
The role, if any, of intravenous lipid emulsion in influencing the natural history of pancreatitis, is not defined, despite the well-documented induction of pancreatitis by endogenous circulating triglycerides in genetic and secondary hyperlipidaemias. [4] , [8] However, because of this consideration, lipid emulsion is contraindicated as a calorie source for patients receiving nutrition support who have hyperlipidaemia and who may have impaired clearance of lipid particles. Monitoring serum triglycerides and maintaining levels of < 400 mg/dL during infusion should be a routine part of management. Lipid administration to patients with normal serum lipid levels has no adverse effects on clinical course.
Nutritional strategies in acute pancreatitis
1.Nutritional support in patients with severe necrotizing pancreatitis should be utilized when food intake is deficient for more than one week.
2.Enteral feeding is the preferred route to prevent nutritional deficits in patients with acute pancreatitis. Abdominal pain, ascites, or an increase in serum amylase may restrict the use of the gastrointestinal tract.
3.TPN should be used when enteral feeding aggravates abdominal pain, ascites, or fistulous output in patients with pancreatitis and when nutritional demands are not met by enteral route.
4.Nutritional support is unlikely to benefit patients with mild, acute, or chronic relapsing pancreatitis when the condition lasts less than 1 week.
5.Lipid emulsions can be used safely as a source of calories and essential fatty acids for patients with pancreatitis if serum triglyceride levels are monitored and remain below 400 mg/dL. Intravenous lipid emulsion could be harmful as a calorie source for patients with acute pancreatitis if lipid is not cleared adequately from the blood.
REFERENCES
1.Kalfarentzos F, Kehagias J, Mead N, Kokkinis K, Gogos CA. Enteral nutrition is superior to parenteral nutrition in severe acute pancreatitis : results of a randomized prospective trial. Br J Surg 1997; 84 : 1665-9.
2.Windsor AC, Kanwar S, Li AG, et al. Compared with parenteral nutrition, enteral feeding attenuates the acute phase response and improves disease severity in the acute phase response and improves disease severity in acute pancreatitis. Gut 1998; 42 : 431.
3.Kirby DF, Craig RM. The value of intensive nutritional support in pancreatitis. JPEN 1985; 9 : 353-7.
4.Grant JP, James S, Grabowski V, et al. Total parenteral nutrition in pancreatic disease. Ann Surg 1984; 200 : 627-31.
5.Kalfarentzos FE, Karavias DD, Karatzas TM, et al. Total parenteral nutrition in severe acute pancreatitis. J Am Coll Nutr 1991; 10 : 156-62.
6.Sax HC, Warner BW, Talamini MA, et al. Early total parenteral nutrition in acute pancreatitis : Lack of beneficial effects. Am J Surg 1987; 153 : 117-24.
7.Voitk A, Brown RA, Echave V, et al. Use of an elemental diet in the treatment of complicated pancreatitis. Am J Surg 1973; 125 : 223-7.
8.Brunzell JD, Bierman EL. Chylomicronemia syndrome. Interaction of genetic and acquired hypertriglyceridemia. Med Clin North Am 1982; 662 : 455-68.
9.Adamkin DH, Gelke KN, Andrews BF. Fat emulsions and hypertriglyceridemia. JPEN 1984; 8 : 563-7.
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