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Please enable it to take advantage of the complete set of features!This clinical practice guideline gives evidence-based recommendations for the use of ONS and TF in these patients. It was developed by an interdisciplinary expert group in accordance with officially accepted standards and is based on all relevant publications since 1985. The guideline was discussed and accepted in a consensus conference. In mild acute pancreatitis enteral nutrition (EN) has no positive impact on the course of disease and is only recommended in patients who cannot consume normal food after 5-7 days. In severe necrotising pancreatitis EN is indicated and should be supplemented by parenteral nutrition if needed. In the majority of patients continuous TF with peptide-based formulae is possible. The jejunal route is recommended if gastric feeding is not tolerated. In chronic pancreatitis more than 80 of patients can be treated adequately with normal food supplemented by pancreatic enzymes. 10-15 of all patients require nutritional supplements, and in approximately 5 tube feeding is indicated. Please enable it to take advantage of the complete set of features!Both should be done on admission and at frequent intervals thereafter. The indication for nutritional support in AP is actual or anticipated inadequate oral intake for 5-7 days. This period may be shorter in those with pre-existing malnutrition. Substrate metabolism in severe AP is similar to that in severe sepsis or trauma. Parenteral amino acids, glucose and lipid infusion do not affect pancreatic secretion and function. If lipids are administered, serum triglycerides must be monitored regularly. The use of intravenous lipids as part of parenteral nutrition (PN) is safe and feasible when hypertriglyceridemia is avoided. PN is indicated only in those patients who are unable to tolerate targeted requirements by the enteral route. As rates of EN tolerance increase then volumes of PN should be decreased.
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When PN is administered, particular attention should be given to avoid overfeeding. When PN is indicated, a parenteral glutamine supplementation should be considered. In chronic pancreatitis PN may, on rare occasions, be indicated in patients with gastric outlet obstruction secondary to duodenal stenosis or those with complex fistulation, and in occasional malnourished patients prior to surgery. This clinical practice guideline gives evidence-based recommendations for the use of ONS and TF in these patients. It was developed by an interdisciplinary expert group in accordance with officially accepted standards and is based on all relevant publications since 1985. The guideline was discussed and accepted in a consensus conference. In severe necrotising pancreatitis EN is indicated and should be supplemented by parenteral nutrition if needed. In the majority of patients continuous TF with peptide-based formulae is possible. The jejunal route is recommended if gastric feeding is not tolerated. The full version of this article is available at www.espen.org. Previous article in issue Next article in issue Keywords Guideline Clinical practice Enteral nutrition Oral nutritional supplements Tube feeding Pancreatitis Undernutrition Malnutrition Abbreviations EN enteral nutrition (both oral nutritional supplements and tube feeding) IU international units PEG percutaneous endoscopic gastrostomy MCT medium chain triglycerides ONS oral nutritional supplements TF tube feeding Recommended articles Citing articles (0). For further information on methodology see Schutz et al. 77 For further information on definition of terms see Lochs et al. 78 ?? The authors of the DGEM (German Society for Nutritional Medicine) guidelines on enteral nutrition in pancreatitis are acknowledged for their contribution to this article. Published by Elsevier Ltd. All rights reserved. Recommended articles No articles found.
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Citing articles Article Metrics View article metrics About ScienceDirect Remote access Shopping cart Advertise Contact and support Terms and conditions Privacy policy We use cookies to help provide and enhance our service and tailor content and ads. By continuing you agree to the use of cookies. In the latter case, pleaseHow are we doing. Europe PMC is part of the ELIXIR infrastructureEurope PMC is a service of the. In general, wherever pancreatitis appears in vivas or in hot cases, nutrition is asked about. This chapter is a summary of the ASPEN and ESPEN guidlines for severe acute pancreatitis. In short, the population of severe pancreatitis patients benefits from early enteral nutrition, whereas for the mild cases there is no specific evidence to guide you (there does not seem to be a difference in outcome, whatever you do with their nutrition).Early studies suggested (correctly) that jejunal administration of food will bypass the cells that secrete cholecystokinin, and thus prevent pancreatic exocrine secretion. There may or may not be such an effect, but it has not been well studied. However, the mild pancreatitis patients don't need to be fed for the first few days, and this means the whole question can be avoided. One can wait for the pancreatitis to improve, and start feeding them 5-7 days after admission. For the very severe patients (i.e. those who one expects to be critically ill for many days) enteral nutrition should be commenced early. It is apparently safe to starve these mildly-moderately severe pancreatitis patients. If they fail to progress to oral diet within the week, then one may consider some form of nutritional support. The counter-argument to nasojejunal feeding is that the necrotic pancreas is probably not very responsive to the normal secretory stimuli, and will not become more necrotic if the nearby duodenum is exposed to some sort of nutritional supplement.
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All show a mortality benefit, thought to be the result of a decreased SIRS response, which in turn is due to diminished rates of bacterial translocation from the healthier gut. Its recommendations include the following: Its recommendations include the following: Additional insight into what the examiners expect (and who's been reading which literature) can be derived from the college answer to Question 16 from the second paper of 2017. Oh's Manual suggests that these patients need no feeding whatsoever until the disease settles (i.e. for 5-7 days), but the 2017 college answer recommends immediate feeding.Bakker et al (2014) found that enteral nutrition is no better than oral. Only progress to enteral nutrition of the patient is not tolerating oral diet after 5-7 days After pruning the evidence tree the authors found only two trials to analyse, with a total of 70 patients. They were forced to conclude that the data were insufficient for any firm recommendation, but that the trend was in the direction of better outcomes with enteral nutrition.Neither found any benefit in jejunal feeding unless you've got clearly demonstrated impaired gastric emptying. A randomized study of early nasogastric versus nasojejunal feeding in severe acute pancreatitis. Am J Gastroenterol. 2005 Feb;100(2):432-9. Compared with parenteral nutrition, enteral feeding attenuates the acute phase response and improves disease severity in acute pancreatitis. Gut. 1998;42: 431-435. Studies in dog and man..Am J Surg. 1973 Nov;126(5):606-14. The indication for nutritional support in AP is actual or anticipated inadequate oral intake for 5-7 days. This period may be shorter in those with pre-existing malnutrition. Working Group on Nutrition and Metabolism, ESICM. Thessaloniki, Greece Journal of the Pancreas Approximately 75 of patients with acute pancreatitis have mild disease with a mortality rate below 1.
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Mortality increases up to 20 if the disease progresses to its severe necrotizing form and, in the most severe cases, mortality can increase to 30-40. Severe acute pancreatitis is usually accompanied by systemic inflammatory response syndrome (SIRS) which results in hypermetabolism with prominent protein catabolism.The morphological changes include edema, parenchymatous hemorrhage in the pancreas and the intestine, necrosis of the peripancreatic fat and parenchymatous necrosis of the pancreatic tissue. The metabolic status is similar to that observed in sepsis and is characterized by a hyperdynamic condition, hypermetabolism and hypercatabolism. In severe necrotizing acute pancreatitis, 80 of all patients are catabolic, with high energy expenditure and enhanced protein catabolism. An increase in resting energy expenditure (REE), measured using indirect calorimetry, was found in patients with acute pancreatitis. They found that, in 10 of the patients with acute pancreatitis, the REE measured was 90 of the estimated one, in 38, it was 90-100 of the estimated and in 52, it was greater than the estimated by 11. The authors concluded that the Harris-Benedict equation usually underestimates energy consumption in patients with acute pancreatitis. Clinical studies have shown that, in patients with acute pancreatitis, protein catabolism and proteinolysis of skeletal muscles increase by 80 as compared to the control population. The plasma levels of aromatic amino acids increase and the levels of lateral chain amino acids decrease.As a result, about 81 of patients require extrinsic insulin administration. They found relatively low levels of lateral chain amino acids (isoleucine, leucine, and valine), but increased levels of aromatic amino acids (phenylalanine, tyrosine).The lowest calcium levels were observed in the first three days after the onset of the disease.
The etiology of hypocalcaemia is multifactorial and is attributed to the saponification of the calcium with free fatty acids, hypoalbuminemia and hypomagnesemia as well as to the increased calcitonin release and decreased parathormone secretion. A decrease in the secretion of proteinic enzymes seems to be the most important factor in the reduction of the inflammatory activity in the pancreas. In addition, the reduction of proteinic enzyme secretion is not necessarily required to reach levels below the basic excretion level for the recovery of the pancreas.The administration of nutrition distally to the first helix of the jejunum stimulates the secretion of multiple inhibitory factors. These factors include the inhibitory polypeptide, the polypeptide YY, somatostatin, various intraluminal proteases, and even biliary salt.Long chain fatty acids are also more stimulating than medium chain fatty acids. Whole proteins stimulate pancreatic secretion more than simple amino acids while oligopeptides (dipeptides and tripeptides) seem to have even less stimulating action.The gastrointestinal tract is the biggest immunological organ of the human body.The physiological motility decreases, the intestinal villus atrophy, the intestinal wall blood flow is reduced, especially at the mucosa, and the strong intercellular and endothelial conjunctions are destroyed. Furthermore, the local secretion of immunoglobulins and the production of biliary salts are reduced due to nutrient deficiency. The final results are the loss of intraluminal The explanation of these pathophysiological mechanisms is based mainly on animal studies.
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Although animal studies have suggested mechanisms by which lack of enteral stimulation can have a negative impact, and review articles have made a case for this gut-connection in TPN complications, there is little experimental data in humans with acute pancreatitis to support the idea that the lack of gut stimulation is the primary source of complications in humans with acute pancreatitis receiving TPN. The results of this event are the production of free oxygen radicals in the intestinal lumen and the activation of local macrophages. In conclusion, the activated macrophages link the disruption of the intestinal mucosal barrier, caused by the functional inactivity of the intestine, with the systemic manifestations of the acute pancreatitis which negatively affect its course. Review articles have made a case for ischemia-reperfusion injury in severe shock, but there is little data to support that this routinely occurs in acute pancreatitis while receiving TPN. On the contrary, patients with severe acute pancreatitis (greater than 3 Ranson criteria) need long hospitalization and have increased complications and mortality rates.Even though nutritional deficits are frequent in severe acute pancreatitis, nutrition, as a part of the therapy, was neglected for a long time. There is accumulating clinical evidence that enteral nutrition can improve survival and reduce the complications accompanying the severe acute pancreatitis. Topical nutrients are the most potent stimulators of mucosal regeneration through their stimulation of the release of growth factors and of mucosal blood flow, probably due to the presence of the amino acid arginine which is a precursor of nitric oxide and growth factors. In addition to its mucosal protective and immunomodulatory effects, enteral nutrition is the most effective way of supporting the intestinal metabolism. Duodenal outputs of pancreatic enzymes were measured by aspiration using a recovery marker.
The distal opening was used for the continuous administration of a mixed liquid meal and was located at either the ligament of Treitz or 60 cm further distally. They reported that during proximal jejunal feeding, pancreatic enzyme output increased significantly over basal levels while no significant increase over basal levels was observed during distal jejunal feeding. The authors concluded that continuous feeding in the distal jejunum does not stimulate exocrine pancreatic secretion. They found that, in comparison to basal fasting trypsin secretion rates, duodenal feeding with the polymeric and elemental formulae stimulated trypsin secretion whereas intravenous feeding and mid-distal jejunal did not. The authors suggested that enteral feeding can be administered without stimulating pancreatic trypsin secretion provided it is delivered into the mid-distal jejunum. The mechanism may involve activation of the ileal brake mechanism. Diets were matched for protein and energy. They found that, compared with the placebo, all oroenteral diets stimulated amylase, lipase, trypsin and bile acid secretion, and increased plasma concentrations of gastrin and cholecystokinin whereas intravenous feeding did not. The complex formula produced a similar response whether given as drinks or duodenal infusions. Changing the duodenal formula to an elemental formula reduced enzyme secretion by 50, independently of cholecystokinin. Higher increases in plasma insulin, glucose, and amino acids were noted with intravenous feeding. The authors concluded that delivering food directly to the intestine by a feeding tube does not reduce pancreaticobiliary secretion. Intravenous administration impairs metabolic clearance. Intravenous infusions were labeled with 1-13C-leucine and enterals were labeled with 2H-leucine. The results demonstrated that, compared to fasting, enteral feeding increased the rate of appearance and secretion of newly labeled trypsin and expanded zymogen stores.
These differences persisted whether the feedings were polymeric or elemental, duodenal, or jejunal. In contrast, intravenous feeding had no effect on basal rates. The authors concluded that all common forms of enteral feeding stimulate the synthesis and secretion of pancreatic trypsin, and only parenteral nutrition avoids it. The nasojejunal tube was placed by endoscopy. Twenty out of 21 patients (95) tolerated the entire estimated energy load well, without any specific problems of reflux and aspiration. Progressive improvement of the clinical condition was observed without recurrence of the disease or a fatal course. Five of these patients showed progressive improvement and one of them died from corrosion of the splenic artery by a large pancreatic pseudocyst. Five of these patients had undergone surgery within 48 hours from the onset of the disease and were fed immediately postoperatively. No complications were observed which could be attributed to enteral nutrition, and the clinical condition of these patients had not deteriorated. They found that the secretion of pancreatic enzymes, especially trypsin and lipase, was significantly lower in the patients with acute pancreatitis. The writers suggested that, in acute pancreatitis, the stimulating action of food is noticeably decreased. All patients had 3 or more Glasgow criteria, more than 6 criteria of the APACHE II score, and the Balthazar severity index was at least five. The jejunal administration of enteral nutrition was well tolerated by 22 patients (88), without any signs of clinical deterioration. They did not find any differences in morbidity and mortality in these two groups of patients. Several trials have now proven that TPN should be avoided in the management of patients with acute pancreatitis. Seventy-five percent of the patients improved during the 48 h observation and were discharged within 4 days, eating normally.
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Of the 53 remaining patients (average Ranson criteria 3), 26 were randomized to jejunal elemental diet feeding (mainly radiological placement) and 27 to TPN. Seven patients in the TPN group developed pancreatic complications in comparison to only 2 in the enteral nutrition group, and the incidence of total septic events and total complications were significantly more common in the TPN group (P All clinical outcome parameters improved in the enteral nutrition group, but not in the TPN group: SIRS presented in 11 enteral nutrition patients prior to feeding and only in 2 after the 7 days (P et al. Markers of systemic inflammation and oxidative stress were compared between the two groups. Three patients in the TPN group developed respiratory failure and 3 developed nonrespiratory single organ failure. None in the enteral nutrition group developed such complications. Hospital stay was shorter in the enteral nutrition group (7 vs. 10 days). Although limited by a small sample size, this trial demonstrates the importance of starting enteral nutrition early in the clinical outcome of severe acute pancreatitis. They concluded that enteral nutrition should be the preferred route of nutritional support in patients with acute pancreatitis because it was associated with a significantly lower incidence of infection and a reduced length of hospital stay. There were no significant differences in mortality and non-infectious complications. There is also a need to study the best time to begin nutritional support in severe acute pancreatitis. The placement of the jejunal feeding tubes, accidental removal and proximal migration of the tube can contribute to reduction or delay in providing adequate nutrition Forty-nine consecutive patients with objectively graded severe acute pancreatitis, were randomized to receive either nasogastric (27 patients) or nasojejunal (23 patients) feeding.
The results showed that nasogastric feeding was safe, with no differences in pain score, analgesic requirement, serum C-reactive protein concentrations or clinical outcome. Nasogastric feeding was equally well tolerated and the outcome was no different from nasojejunal feeding. They concluded that, when compared to nasojejunal feeding, nasogastric feeding is considered simpler, cheaper and easier to use, and is as good as nasojejunal feeding in patients with severe acute pancreatitis. A total of 31 patients with severe acute pancreatitis were randomized to receive feeding by either nasogastric (15 patients) or nasojejunal (16 patients). The authors reported no difference in the outcome measures (discharge, surgery, death) and satisfactory toleration of enteral nutrition by both nasojejunal and nasogastric routes. Neither nasojejunal nor nasogastric feeding led to recurrence or worsening of pain in acute pancreatitis. They reported that, in predicted severe acute pancreatitis, early nasogastric enteral nutrition was feasible and resulted in a better control of blood glucose levels, although the overall complication rate was higher in the enteral nutrition group. No beneficial effects on the intestinal permeability or on the inflammatory response were seen by enteral nutrition treatment. The hospital stay also seemed longer in the patients with a nasogastric tube. However, this was a single centre study with a small sample size. This was probably due to the development of a severe retroperitoneal inflammatory process. For the determination of the severity of acute pancreatitis, and in an attempt to predict morbidity and mortality, the use of the APACHE II grading system was proven more accurate than clinical evaluation of the patient at the time of admission.
In two prospective randomized comparative studies, the sensitivity of the clinical evaluation in predicting the development of severe acute pancreatitis was 34-44 while the sensitivity of the APACHE II grading system was 63- 82 (severe acute pancreatitis; APACHE II score greater than 9).These patients usually have pancreatic necrosis in more than 30 of the organ, mortality is about 19 and morbidity about 38, and it is usually not feasible to feed them normally per os for a period of 7-10 days from the onset of the disease.In patients with severe acute pancreatitis, who are candidates to be supported by enteral nutrition, a special silicone nasojejunal tube should be placed immediately by endoscopy or radiological control. The end of the tube should be at a distance of 25-30 cm after the Treitz ligament. With the administration of a fat-free elemental diet minimum stimulation of the pancreatic secretion is ensured while oligopeptide diets in which 70 of the contained fat is in the form of moderate chain triglycerides are better absorbed in the intestine, although they cause relatively greater stimulation of the pancreatic secretion. However, this is still theoretical and is not based on randomized controlled trials. Oral refeeding can usually be a problem (pancreatitis from refeeding). Usually, food per os is given after 3-4 days after the patient last complained about pain, and the levels or serum amylase and lipase have returned to almost normal.However, the majority of the studies were nonrandomized and retrospective, with a limited number of patients and relatively few data regarding the consequences of artificial nutrition on the final outcome of the disease. Thus, they recommended the use of intravenous nutritional support for all patients with acute pancreatitis. They did not observe any significant positive effect on the course of the disease. On the contrary, they found an increase in infectious complications from the catheter in 14.
8 of patients with acute pancreatitis and in 17.4 of patients with chronic pancreatitis. They also stated that TPN may have some beneficial results in patients with complications which prolong the course of the disease, such as fistulas or pancreatic ascites.These abnormalities lead to immunosuppression and to an increase in the severity and duration of systemic inflammatory response syndrome. Escherichia coli endotoxin was then intravenously administered. The people who received TPN had higher levels of glycogen, epinephrine, Creactive protein and tumor necrosis factor (TNFa). In addition, they presented a greater loss of amino acids and lactic acid from the skeletal muscles.Thirteen patients completed the study protocol and there was a trend for the glutamine fed group to show improved lymphocyte proliferation, increased T-cell DNA synthesis and decreased release of the proinflammatory cytokine IL-8. In a recent study, Halley et al.A possible explanation could be that the administration of probiotics might increase the local oxygen demand in the small bowel mucosa and that the presence of probiotics caused local inflammation at the level of the mucosa. The authors concluded that the administration of probiotics must be regarded as unsafe especially in patients at risk for non-occlusive mesenteric ischemia.There is no evidence that nutritional support (enteral or parenteral) has a beneficial effect on the clinical outcome in patients with mild acute pancreatitis. In mild acute pancreatitis, the clinical course is usually uncomplicated and patients can consume a low-fat oral diet within 3-7 days. The disease does not have a major impact on nutritional status, energy or substrate metabolism. It is not clear whether this is true in cases with pre-existing malnutrition. It is crucial for patients with signs of malnutrition that their requirements are met by providing artificial nutrition. If upper gastric intolerance occurs, small bowel feeding should be preferred.
A higher protein intake should only be given to patients with a severe negative nitrogen balance. A lower protein intake is sometimes necessary in patients with severe renal or hepatic failure. Enteral intake by continuous feeding regimen is recommended Oral refeeding with a diet rich in carbohydrates and moderate in proteins and fat is recommended. If the diet is well-tolerated, oral nutrition can be increased continuously. The nutrient requirements depend on the severity of the disease. Patients with severe acute pancreatitis are hypermetabolic.Several studies have demonstrated that enteral nutrition via nasogastric or nasojejunal tubes is possible and beneficial in patients with severe acute pancreatitis. Further multicenter randomized trials studies are needed to confirm whether nasogastric feeding, as compared to nasojejunal feeding, is a practical and effective form of management for patients with severe acute pancreatitis. Nutritional support has shown no beneficial effect in mild acute pancreatitis. Parenteral nutrition increases complications due to uncontrolled hyperglycemia and infection, and is more expensive than enteral nutrition. Parenteral nutrition should be reserved for patients with severe pancreatitis who cannot tolerate enteral nutrition, who have an exacerbation of their disease with enteral feeding, and for those before undergoing pancreatic surgery if they have severe signs of malnutrition. Not enough information is available to make specific recommendations for the use of specific supplements of enteral nutrition. The use of probiotics is controversial in patients with acute pancreatitis. Whether any nutritional therapy for patients admitted for severe acute pancreatitis is better than no artificial nutrition support, is difficult to answer according to the limited studies available. Clinical nutrition in pancreatitis. Dig Dis Sci 1997;Milinic N, Macfie J, et al. ESPEN Guidelines on. Enteral Nutrition: Pancreas.
Clin Nutr 2006; 25:275-Feeding the injuredResting energy expenditure in patients withJL. Total parenteral nutrition and alternate energy substrates in treatment of severe acute pancreatitis.JN, Johnson CD. A randomised clinical trial to assessPancreatologyCristallo M, Bevilacqua G et al. Hemodynamic andAm J GastroenterolPrediction ofAPACHE II, clinical assessment and multiple factorPancreatic secretionPancreatitis. In: Cynober I, Moore FA (eds). NutritionPerform Programm Basel. Switzerland: Nestec Ltd,Nutrition in the patient with severe acute pancreatitis. Nutrition 1998; 4:269-75. S Afr J SurgKvale D, Rognum TO, et al. Immunobiology andMcClave SA, Greene LM, Snider HL, Makk LJ, Comparison of theThe gut's role inF. Immunologic mechanisms in intestinal diseases.Care Nutr 1994; 2:9-15. AH, Booth FV, Morgenstein-Wagner TB, et al. EarlyThe results of aEnteral andBest Pract ResHypocaloricGogos CA. Enteral nutrition is superior to parenteralBr J Surg 1997; 84:1665-JA, Spark JI, et al. Compared with parenteral nutrition,JH, Biemond I, Lamers CB, Masclee AA. Does jejunalEnteral feeding without pancreatic stimulation.Abou-Assi S, Clore J, et al. Physiological effects ofQ. Trypsin and splanchnic protein turnover duringAm J PhysiolGeubel A, Van Steenbergen W, Reynaert M. Is earlyPancreas 1998; 17:187-93.Gurd FN, Thompson AG. Use of an elemental diet inPostoperative jejunal feeding following complicatedNutrition support duringMcKay CJ, Carter R. Nasogastric feeding in severeMcKay CJ, Carter CR, Imrie CW. A randomized studyAm J Gastroenterol 2005;FN, Bell RH Jr, Fischer JE, Bower RH. Early totalMeta-analysis of parenteralYK. Early enteral nutrition in severe acute pancreatitis:J Clin GastroenterolMarignani M, Capotondi C et al. Enteral Nutrition in. Severe Acute Pancreatitis: Nasogastric (NG) vs. Nasojejunal (NJ) Tube. In: Italian Association for the. Study of the Pancreas (AISP) 31st National Congress. Naples, Italy, September 20-22, 2007. JOP. J PancreasBarton R.