Newsletter

[ Vol. 9 No. 3 ] (September - December 2008 )
Nutrition support in acute pancreatitis: What is the score?

Rakesh K Tandon
Head, Dept of Gastroenterology, Pushpawati Singhania Research Institute for
Liver, Renal and Digestive Diseases, New Delhi, India.

Acute pancreatitis is an abdominal emergency that requires immediate attention to provide the patient relief from pain and do aggressive fluid replacement. Further management depends on the severity of the disease. Those with mild to moderate disease (70-80%) tend to settle down within 3-5 days and are fed orally a gradually advancing diet. The remaining 20-30% suffering from severe acute pancreatitis (SAP) may continue to have systemic inflammatory response syndrome (SIRS) for several weeks and suffer rapid weigh loss and high mortality.^1,2 It is this group of patients that requires special nutritional support.³

SIRS in AP is caused initially because of the inflammation in the pancreas, stimulation of exocrine enzyme secretion as a result of feeding and loss of gut integrity and is greatly responsible for the subsequent course of the disease.³ Whilst factors causing inflammation, such as a stone in the common bile duct, ethanol ingestion, infection, should be removed, proper nutritional management is required to control the other two factors. To avoid stimulation of the exocrine pancreas, the patients were kept nil orally and given pareneral nutrition (PN) in the past. This approach however, did not show any benefit in outcome in at least two prospective studies in mild acute pancreatitis.^4,5 The major factor that possibly contributed to this poor outcome was the increased intestinal permeability. Enteral feeding (EN) was thus introduced by placing a nasojejunal tube. That indeed led to a better outcome. Of 6 prospective randomized controlled trials (PRCTs) of EN vs PN in AP randomized within 48 hours, five showed significant impact on clinical outcome.^5-10 In these five studies, EN was associated with decreased infectious morbidity, shorter length of hospital stay, less overall complications, reduced duration of the disease process and length of nutritional therapy and faster resolution of SIRS. Futhermore, the cost of therapy was much lower in the EN group.⁷ This should not be surprising as similar experience exists with use early enteral feeding in critically ill patients. In 15 PRCTs and 2 metaanalyses, early vs delayed feeding in such patients has been shown to reduce infection, length of hospital stay as well as mortality.³

In studies on patients with AP, it is notable that two factors were crucial in determining a favourable outcome with enteral feeding. Firstly, only patients with severe AP benefitted. One study that enrolled patients with AP of much milder severity (Ranson’s criteria 1.1) early EN failed to show any benefit.⁵ Secondly, if the introduction of EN was delayed to 4 full days in patients with SAP the expected benefit from EN over PN did not occur.¹¹ Delays in initiating EN in SAP lead to prolonged ileus and reduced chances for tolerance. In a prospective nonrandomized study of 102 patients with AP, it has been shown that it feeding could be started within 2 days tolerance to feeding was achieved in 92% of the patients.¹² If however the start of enteral feeding got delayed to 5 days or beyond the tolerance rate was reduced to 50% and if delayed to beyond 6 days the tolerance to EN was down to 0%.¹² On the other hand, early start of enteral feeding within 48 hours of admission served to maintain gut function and improve tolerance. Fewer problems were encountered with ileus and gastric stasis with this aggressive approach.

Most groups have used naso-jejunal feeding although there are problems with regard to maintenance of the position of the tube and the patency of the tube. There is at least one group of investigators who suggest that naso-gastric feeding may be tolerated by patients with acute pancreatitis as well as naso-jejunal feeding.¹³ A group of 26 patients with prognostically severe AP were fed by fine-bore naso-gastric tube soon after admission. This was shown to be both practical and safe in 22 of the 26 patients. Feeding began within 48 hours of hospital admission starting with 30 ml/hr in most of these patients, increasing gradually within a further 36-48 hours of treatment. Subsequently, a randomized study of naso-gastric versus naso-jejunal feeding in severe AP has shown little difference in terms of c-reactive protein response, pain, analgesic requirement or clinical outcome from these two approaches of early naso-enteric feeding.¹⁴

Based on these studies the present trend is strongly in favour of using early naso-enteric feeding. However, judicious use of TPN in certain specific situations may still be needed in patients with AP; they include those with gastrointestinal hemorrhage or respiratory failure requiring ventilatory support. Which nutrients to feed and at what rate remain to be determined. Since fats stimulate the exocrine pancreas maximally and carbohydrates minimally, it would appear logical to start with carbohydrates. Small peptides are less stimulating than intact proteins or individual amino acids. Clearly studies need to address these issues. Similarly, the role of glutamine and other immunonutrients remains highly debatable. Addition of probiotics (Lactobacillus plantarum) to enteral feeding has also shown recently some promise of preventing the occurrence of infection in pancreatic necrosis.¹⁵

REFERNCES:

1. BlackburnGL. Williams LF, Bistrian BR, et al. New approaches to the management of severe acute pancreatitis. Am J Surg 1976, 131: 114-124.
2. Feller JH, Brown RA, Tousant GPM, and Tompson AG. Changing methods in the treatment of severe pancreatitis. Am J Surg 1974, 124: 196-201.
3. McClave SA. Nutrition support in acute pancreatitis. Gastroenterology Clinics of North America 2007; 36: 65-74.
4. Sax HC, Warner BW, Talamini MA, et al. Early total parenteral nutrition in acute pancreatitis: lack of beneficial effect. Am J Surg 1987, 153: 117-24.
5. Mc Clave S A, Snifer H. Owens Negative, et al. Comparison of the safety of early enteral VS parenteral nutrition in mild acute pancreatitis. J Parenter Enter Nutr 1997, 21: 14-20.
6. Kalfarentzos F, Kehagis J, Kokkimis K, et al. Enteral nutrition is superior to parenteral nutrition in severe acute pancreatitis: results of a randomized prospective trial. Br J Surg 1997, 84: 1665-1669.
7. WindsorACJ, Kanwar S, Li AGK, et al. Compared with parenteral nutrition, enteral feeding attenuates the acute phase response and improve disease severity in acute pancreatitis. Gut 1998, 42: 431-435.
8. Olah A, Pardavi G, Belagyi T et al. Early nasojejunal feeding in acute pancreatitis is associated with a lower complication rate. Nutrition 2002; 18: 259-62.
9. Abou-Assi S, Craig K, O’Keefe SJ. Hypocaloric jejunal feeding is better than total parenteral nutrition in acute pancreatitis: results of a randomized comparative study. Am J Gastroenterol 2002, 97: 2255-62.
10. Gupta R, Patel K, Calder PC et al. A randomized clinical trial to assess the effects of totalenteral and total parenteral nutritional support on metabolic, inflammatory and oxidative markers in patients with predicted severe acutepancreatitis (APACHE II > or =6).Pancreatology 2003; 3: 406-13.
11. Louie BE, Noseworthy T, Hailey D et al. Enteral or parenteral nutrition for severe pancreatitis: a randomized controlled trial and health technology assessment. Con J Surg 2005; 48: 298-306.
12. Cravo M, Camillo ME, Marques A et al. Early tube feeding in acute pancreatitis: a prospective study. Clin Nutri 1989; 8: 14.
13. Eatock FC, Brombacher GD, Steven A et al. Naso-gastric feeding in severe acute pancreatitis may be practical and safe. Int J Pancreatol 2000; 28: 23-9.
14. Eatock FC, Chong PS, Menezes N, Imrie CW, McKay CJ, Carter R. A randomized study of early nasogastric versus naso-jejunal feeding in severe acute pancreatitis. Am J Gastroenterol 2005; 100: 432-9.
15. Olah A, Belagyi T, Isskutz A, Gamal ME, Bengmark S. Randomized clinical trial of specific lactobacillus and fibre supplement to early enteral nutrition in patients with acute pancreatitis. Br J Sung 2002; 89: 1163-7.

From  
The 12^th PENSA Congress
October 18-20 2007, Century Park Hotel. Manila, Philippines 
Page: 33-34