Gastrointestinal Diseases Related to Nutrition


Pancreatitis

Acute pancreatitis is an example of a disease process possibly affected by method of feeding (total parenteral nutrition [TPN] versus total enteral nutrition [TEN]). In a prospective study of 54 patients with acute mild pancreatitis, catheter sepsis was 10 times higher in the TPN group than in control subjects who received intravenous fluids only. In the same study, pneumothorax occurred only in the TPN group, and length of hospital stay was longer in the TPN group. This study suggests a significant risk associated with giving TPN to patients with mild pancreatitis.

Based on recent recommendations from the American Society of Parenteral and Enteral Nutrition, patients with mild pancreatitis, who typically resume eating within 7 to 10 days of leaving the hospital, should not receive TEN or TPN unless they have lost significant weight, defined as greater than 10% of usual weight, in the previous 6 months. A study compared complications in 38 patients with severe acute pancreatitis treated with either TEN or TPN. Septic complications, hyperglycemia, peripancreatic necrosis, and cost were all greater in those patients who had received TPN. Mortality rate was similar in the two groups.

Another prospective study of 34 patients with severe pancreatitis compared outcomes with TEN and TPN and found that multiorgan failure, abdominal sepsis, and mortality were greater in the TPN group. In addition, markers of disease severity—including C-reactive protein, Acute Physiology and Chronic Health Evaluation II score, and immunoglobulin M endotoxin—were all higher in patients receiving TPN. Although bacterial translocation was not formally evaluated, TEN might have reduced bacterial translocation compared with TPN, explaining why outcomes were better with TEN. Another study of 156 patients with pancreatitis reported that hypocaloric feeding with TEN resulted in fewer septic and metabolic complications than TPN feeding. More than 50% of the TPN patients were hyperglycemic versus only 15% of TEN patients. Despite fewer complications in the TEN group, mortality rates were the same in both groups. Current data support the superiority of TEN over TPN in managing patients with acute severe pancreatitis.

In patients with chronic pancreatitis, the cause of malnutrition is multifactorial, including fear of postprandial abdominal pain (sitophobia), steatorrhea, anorexia, and often coexistent alcoholism. Steatorrhea and azotorrhea (fecal protein loss) occur when lipase and trypsin secretion are reduced by 90%. Nutritional management first begins with appropriate management of a patient's abdominal pain. Analgesics should be given at least 30 minutes before meals to prevent postprandial exacerbation of pain. Meta-analysis failed to show a beneficial effect of exogenous pancreatic enzyme replacement in relieving abdominal pain. Treatment of exocrine insufficiency focuses on giving adequate pancreatic enzymes. The minimal dose of lipase required is 28,000 IU/meal. Enzymes should be given with meals to ensure adequate mixing with food. Weight maintenance, symptomatic improvement of diarrhea, and decreased 72-hour fecal fat excretion are the goals of therapy. Dietary fat intake should not be restricted. Fat-soluble vitamins and vitamin B 12 should be replaced if necessary.

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