Newsletter

[ Vol. 7 No. 3 ] (September - December 2006 )
Nutritional support in acute and chronic pancreatitis

Rakesh K. Tandon
E-154, Saket, New Delth, India
Email: rakesh_tandon@hotmail.com

 

Acute Pancreatitis:
Acute pancreatitis is a hypercatabolic state resulting in rapid loss of body weight, fat and protein1,2. The patients are in a hyper-dynamic state manifested by a fall in systemic resistance and rise in cardiac output. This is associated with a marked increase in visceral and muscle blood flow and oxygen consumption. Total caloric need rises as the oxygen consumption increases. Protein catabolism and ureagenesis increase as amino-acids are utilized as substrates for peripheral oxidized and gluconeogenesis. Nitrogen losses as high as 40 gm/day have been noted. Branched-chain amino acids are oxidized preferentially by skeletal muscles and serve as important fuel during the hyper-metabolic state3. Mortality and morbidity increase markedly, particularly if appropriate nutritional support is not given to the patients in such a state.

In patients with severe acute pancreatitis (10%-20% of all pancreatitis patients) parenteral nutrition may have to be given as a supplement, especially if the patient develops multiorgan failure or remains haemodynamically unstable and has ileus or is unable to take by mouth. The best parenteral solution is a mixture of all the three substrates, viz. carbohydrates, proteins and fat. The calorie and fuel requirements of the individual patients may be calculated using Harris-Benedict equation with appropriate additions for stress factors4 or, better still, by using indirect calorimetry. In general, patients with severe acute pancreatitis require 2000-2500kg/day of calories, of which 50%-60% may come from glucose, 15%-20% from protein and 20%-30% from lipids. Before infusing lipids however, it should be ensured that the patient does not have hypertriglyceridaemia. If the serum triglyceride levels are raised, fats should be avoided in the infusate.

As soon as the patient stabilizes, the attempt should be switched to enteral feeding. A naso-enteral tube is inserted under endoscopic guidance on the second or third day of hospitalization and a semi-elemental diet is started through it. This should have a concentration of one calorie per ml. If the enteral feeding is tolerated within the next 2-3 days the feeding is advanced to using a polymeric formula or a house diet.

There is a dearth of supporting evidence for any benefit of total parenteral nutrition (TPN) in acute pancreatitis. In fact, no benefit of TPN could be demonstrated in two prospective studies in mild acute pancreatitis5,6. That should not be surprising as such patients improve rapidly and are able to tolerate oral feeding within 2-3 days of acute pancreatitis and the initial 2-3 days can be covered well with simple intravenous glucose saline. In fact, a USA based study in patients with mild or moderate AP found that naso-jejunal feeding was better than TPN in that there was no significant difference in clinical outcome but a considerable reduction in cost and morbidity associated with naso-enteral feeding6. Proper studies in severe acute pancreatitis are lacking, but one recent randomized prospective study comparing the efficacy of enteral nutrition and TPN showed that enteral nutrition was well tolerated and was as effective as TPN but was associated with fewer complications7. In this study the mean APACHE II score was over 11.5 and CRP values were over 280 mg/L. The total number of days in intensive care and overall hospital stay showed no statistical differences. Mortality was similar in both groups but the cost of therapy was US$ 45 per day in the naso-jejunal feeding group and more than three times this in the TPN group. Another study suggested that total enteral nutrition modulated the inflammatory and septic response in acute pancreatitis and this was clinically beneficial8. This UK-based study was much smaller, comprising only 13 patients with severe AP. They were more or less equally divided between the TPN group and enteral nutrition group. There was a tendency to poor results in the TPN group; they had a higher morbidity and mortality. There was a lower systemic inflammatory response syndrome (SIRS) scoring in the group fed enterally and also lower IgM anticore endotoxin antibody level in those fed enterally. Enteral feeding is therefore being increasingly favoured in severe acute pancreatitis.

The leading groups in the UK and continental Europe now employ early enteral nutrition in preference to intravenous feeding in patients with severe AP. 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 as well as naso-jejunal feeding by patients with acute pancreatitis9,10. 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 treatmet9. 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 to early naso-enteric feeding10.

All these studies are still rather small, but the clinical practice, particularly in Europe and the UK, is moving increasingly to early use of naso-enteric feeding with a lowering of the risk to the patient that is associated with TPN. The limited randomized studies that are available do point to enteral deeding being cheaper and safer than intravenous feeding. Certain nutrients may be particularly useful in specific conditions. For example, immuno-nutrition provided parenterally has been show to result in earlier resolution of severe AP. Similarly, addition of probiotics (Lactobacillus plantarum) to enteral feeding may prevent the occurrence of infection in pancreatic necrosis11.

Chronic Pancreatitis:
The 3 major manifestations of chronic pancreatitis are pain, diabetes and steatorrhoea. Whereas the first 2 manifestations are treated mainly by drugs the correction of steatorrhoea requires a judicious use of dietary components and pancreatic enzymes.

Since the pancreatic lipase is deficient in chronic pancreatitis, a low fat diet is advocated to minimize loss of water and energy through loose stools. Administration of pancreatic lipase enterally should correct the fat absorption and it does partly, but the amount of lipase required with each meal is 30,000 units of lipase in the duodenum and that poses certain practical difficulties. Firstly, the enzyme gets destroyed by the acid secreted in the stomach and hence the gastric acid is to be suppressed by a heavy dose of proton pump inhibitor. Secondly, to achieve proper mixing of lipase with the chime lipase is to be delivered in the duodenum along with the chime movement from the stomach into the duodenum and that is achieved partly by providing lipase in microshere form (eg, Creon 10000).

Another way of getting some fat absorbed despite lipase deficiency is to administer medium chain triglycerides as they get absorbed directly into the portal venous system without going through the normal intraluminal and intramucosal digestion.

Overall, however, maintaining nutrition in chronic pancreatitis is not such a problem as is controlling pain and diabetes.

*Head; Dept. of Gastroenterology, Pushpawati Singhania Research Institute for Liver, Renal and Digestive Diseases, New Delhi – 110029


 
The leading groups in the UK and continental Europe now employ early enteral nutrition in preference to intravenous feeding in patients with severe AP. 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 as well as naso-jejunal feeding by patients with acute pancreatitis9,10. 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 treatmet9. 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 to early naso-enteric feeding10.

All these studies are still rather small, but the clinical practice, particularly in Europe and the UK, is moving increasingly to early use of naso-enteric feeding with a lowering of the risk to the patient that is associated with TPN. The limited randomized studies that are available do point to enteral deeding being cheaper and safer than intravenous feeding. Certain nutrients may be particularly useful in specific conditions. For example, immuno-nutrition provided parenterally has been show to result in earlier resolution of severe AP. Similarly, addition of probiotics (Lactobacillus plantarum) to enteral feeding may prevent the occurrence of infection in pancreatic necrosis11.

Chronic Pancreatitis:
The 3 major manifestations of chronic pancreatitis are pain, diabetes and steatorrhoea. Whereas the first 2 manifestations are treated mainly by drugs the correction of steatorrhoea requires a judicious use of dietary components and pancreatic enzymes.

Since the pancreatic lipase is deficient in chronic pancreatitis, a low fat diet is advocated to minimize loss of water and energy through loose stools. Administration of pancreatic lipase enterally should correct the fat absorption and it does partly, but the amount of lipase required with each meal is 30,000 units of lipase in the duodenum and that poses certain practical difficulties. Firstly, the enzyme gets destroyed by the acid secreted in the stomach and hence the gastric acid is to be suppressed by a heavy dose of proton pump inhibitor. Secondly, to achieve proper mixing of lipase with the chime lipase is to be delivered in the duodenum along with the chime movement from the stomach into the duodenum and that is achieved partly by providing lipase in microshere form (eg, Creon 10000).

Another way of getting some fat absorbed despite lipase deficiency is to administer medium chain triglycerides as they get absorbed directly into the portal venous system without going through the normal intraluminal and intramucosal digestion.

Overall, however, maintaining nutrition in chronic pancreatitis is not such a problem as is controlling pain and diabetes.

*Head; Dept. of Gastroenterology, Pushpawati Singhania Research Institute for Liver, Renal and Digestive Diseases, New Delhi – 110029


REFERENCES

 

1. Blackburn GL. 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. Blackburn GL, Moldawer LIFELONG, Usui S, et al. Branched chain amino acid administration and metabolism during starvation, injury and infection. Surgery 1979, 86: 307-10
4. Harris JA, Benedict FG. Biometric studies of Basal metabolism in Man. Washington DC, Carnegic Institute at Wastington, publication no 279, 1919
5. 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
6. 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
7. Kalfarentzos F, Kehagis J, Kokkinis 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
8. Windsor ACJ, 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
9. Eatock FC, hnog PS, Menezes, Imrie CW, McKay CJ, Carter R. Naso-gastric feeding in severe acute pancreatitis is safe and avoids the risks associated with the naso-jejunal route: A randomized controlled trial, (Abstract) Digestive Disease Week 2001.
10. Eatock FC, Brombacher GD, Steven A et al. Naso- gastric feeding in severe acute pancreatits may be practical and safe. Int J Pancreatol 2000; 28: 23-9
11. Olah A, Belagyi T, Issekutz 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 Surg 2002; 89: 1163-7

From
The 11th PENSA Congress
October 1-4 2005
Sheraton Grande Walkerhill Hotel, Seoul, Korea
Page: 132-134