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ARTICLE IN PRESS Clinical Nutrition (2006) 25, 275–284 http://intl.elsevierhealth.com/journals/clnu ESPEN GUIDELINES ESPEN Guidelines on Enteral Nutrition: Pancreas$ a, b c d e f R. Meier , J. Ockenga , M. Pertkiewicz ,A.Pap, N. Milinic , J. MacFie , DGEM:$$C.Lo¨ser, V. Keim aDepartment of Gastroenterology, Kantonsspital Liestal, Liestal, Switzerland bDepartment of Gastroenterology, CCM, Charite´-Universita¨tsmedizin Berlin, Berlin, Germany cDepartment of Nutrition and Surgery, Central Clinical Hospital, Warsaw, Poland d1st. Department of Gastroenterology, MAV Hospital, Budapest, Hungary e Department of Gastroenterology, University Hospital ‘‘Bezanijska kosa,’’ Belgrade, Serbia-Montenegro fDepartment of Surgery, Scarborough Hospital, Scarborough, UK Received 21 January 2006; accepted 21 January 2006 KEYWORDS Summary The two major forms of inflammatory pancreatic diseases, acute and Guideline; chronic pancreatitis, require different approaches in nutritional management, which Clinical practice; are presented in the present guideline. This clinical practice guideline gives Enteral nutrition; evidence-based recommendations for the use of ONS and TF in these patients. It was Oral nutritional developed by an interdisciplinary expert group in accordance with officially supplements; accepted standards and is based on all relevant publications since 1985. The Tube feeding; guideline was discussed and accepted in a consensus conference. Pancreatitis; In mild acute pancreatitis enteral nutrition (EN) has no positive impact on the Undernutrition; course of disease and is only recommended in patients who cannot consume normal Malnutrition 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. The full version of this article is available at www.espen.org. &2006 European Society for Clinical Nutrition and Metabolism. All rights reserved. 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 $ 77 78 For further information on methodology see Schu¨tz et al. For further information on definition of terms see Lochs et al. Corresponding author. Tel.: +41619252187; fax: +41619252804. E-mail address: remy.meier@ksli.ch (R. Meier). $$ The authors of the DGEM (German Society for Nutritional Medicine) guidelines on enteral nutrition in pancreatitis are acknowledged for their contribution to this article. 0261-5614/$-see front matter & 2006 European Society for Clinical Nutrition and Metabolism. All rights reserved. doi:10.1016/j.clnu.2006.01.019 ARTICLE IN PRESS 276 R. Meier et al. Summary of statements: Acute pancreatitis Subject Recommendations Grade77 Number Indications Mild acute Enteral nutrition is unnecessary, if the patient can B 1.3 pancreatitis consume normal food after 5–7 days. Enteral nutrition within 5–7 days has no positive A 1.6 impact on the course of disease and is therefore not recommended. Give tube feeding, if oral nutrition is not possible due C 1.6 to consistent pain for more than 5 days. Severe Enteral nutrition is indicated if possible. A 1.3 necrotising Enteral nutrition should be supplemented by C 1.3 pancreatitis parenteral nutrition if needed. In severe acute pancreatitis with complications 1.8 (fistulas, ascites, pseudocysts) tube feeding can be performed successfully. Application Tubefeedingispossibleinthemajorityofpatientsbut A 1.4 may need to be supplemented by the parenteral route. Oral feeding (normal food and/or oral nutritional C 1.10 supplements) can be progressively attempted once gastric outlet obstruction has resolved, provided it does not result in pain, and complications are under control. Tube feeding can be gradually withdrawn as intake improves. Severe Use continuous enteral nutrition in all patients who C 1.7 pancreatitis tolerate it. Route Try the jejunal route if gastric feeding is not C 1.4 tolerated. In case of surgery for pancreatitis an intraoperative C 1.7 jejunostomy for postoperative tube feeding is feasible. In gastric outlet obstruction the tube tip should be C 1.8 placed distal to the obstruction. If this is impossible, parenteral nutrition should be given. Type of formula Peptide-based formulae can be used safely. A 1.5 Standard formulae can be tried if they are tolerated. C 1.5 Grade: Grade of recommendation; Number: refers to statement number within the text. Summary of statements: Chronic pancreatitis Subject Recommendations Grade77 Number General Adequate nutritional therapy as well as pain C 2.4 treatment may have a positive impact on nutritional status. Caloric intake is increased after an attenuation of postprandial pain. ARTICLE IN PRESS ESPEN Guidelines on Enteral Nutrition 277 Indications More than 80% of patients can be treated adequately B 2.4 with normal food supplemented by pancreatic enzymes. 10–15% of all patients require oral nutritional C 2.4 supplements. Tube feeding is indicated in approximately 5% of C 2.4 patients with chronic pancreatitis. Specific Stenosis of duodenum C 2.5 contraindications Grade: Grade of recommendation; Number: refers to statement number within the text. 1. Acute pancreatitis (AP) tional requirements in such cases by whatever means are most appropriate. Preliminary remarks: The management of acute Both specific and non-specific metabolic altera- pancreatitis (AP) differs according to its severity. tions occur in AP 9 (Ib). Basal metabolic rate Classified by the Atlanta criteria1 approximately increases due to inflammatory stress and pain, 75% of the patients have mild disease with a leading to enhanced total energy expenditure.9 In mortality rate below 1%.2 Mortality increases up severe necrotising pancreatitis, 80% of all patients to 20% if the disease progresses to its severe are catabolic9 (Ib), with high energy expenditure necrotizing form3–8 and in the most severe cases and enhanced protein catabolism10 (IIa). The mortality can rise to 30–40%.7,8 Severe AP with its negative nitrogen balance can be as much as related systemic inflammatory response (SIR) 40g/day11,12 and can have a deleterious effect on causes increased metabolic demands and may both nutritional status and disease progression. In progress to multiorgan disease (MOD). Using ima- onetrial, patients with a negative nitrogen balance ging methods and laboratory parameters, progres- had a ten-fold higher mortality than those with a sion can be predicted. Until recently, EN, either normal balance.13 This conclusion has to be treated orally or by tube, was believed to have a negative with caution since no study has been stratified impact on the progression of the disease due to according to disease severity, and the relation stimulation of exocrine pancreatic secretion and between nitrogen balance and progression might, the consequent worsening of the autodigestive therefore, merely reflect the severity of disease. processes of the pancreas. Even though nutritional Starvation for more than seven days should deficits are frequent in severe pancreatitis, nutri- always be avoided, since protein and energy tion as a part of therapy was neglected for a long catabolism induces undernutrition—and probably time. Even now, few nutritional studies in this worsens the prognosis. It has been shown, that as condition have been published. little as five days of conservative therapy without nutritional support in previously healthy men 1.1. What influence does acute pancreatitis suffering from severe pancreatitis results in severe exert on nutritional status and on energy and undernutrition, water retention and decreased substrate metabolism? muscle function proportional to decreased protein stores.14 Mild pancreatitis has little impact on nutritional Hyperlipidaemia occurs frequently in acute pan- status or metabolism. In severe necrotising 15,16 pancreatitis energy expenditure and protein creatitis. It is not clear whether this is a catabolism are increased (IIa). consequence of disease or due to pathogenic factors or a combination of both17 (Ib). The latter Comment: In mild acute pancreatitis the clinical seems more likely, since serum lipids normalize course is usually uncomplicated and patients can during recovery from AP. Severe hyperlipidaemia consume normal food, low in fat (o30% of total itself may be the sole cause of AP. It is a particular energy intake [vegetable fat are preferred]), with- problem in the most severe cases, reflecting severe in three to seven days. The disease has little impact disturbances of fat metabolism secondary to sepsis on nutritional status or on energy and substrate and treatment. metabolism. It is not clear whether this is also true The enhanced metabolic rate and protein cata- in the presence of pre-existing undernutrition, bolism necessitate an increased energy intake from although it is probably important to meet nutri- both fat (30%) and carbohydrates (50%). 1.0–1.5g ARTICLE IN PRESS 278 R. Meier et al. proteins are usually sufficient. Carbohydrates are syndrome (SIRS) was significantly attenuated in all the favoured source of calories, since administra- enterally fed patients. Sepsis and multiorgan fail- tion is easy, although hyperglycaemia, secondary to ure as well as incidence of surgery were reduced. insulin resistance and in some cases islet cell Whereas two patients died in the PN group, no damage, has to be avoided, placing a limit on the death occurred in the EN group. Major weaknesses rate of administration of glucose and, in some of this study are the small number of patients with cases, necessitating the use of insulin10 (IIa). severe pancreatitis and the marked differences in 1.2. Does nutritional status influence outcome? nutrient intake between the enteral and the parenteral groups. Although not investigated in this context, severe A further trial by Powell et al.22 (Ib) could not undernutrition is likely to affect outcome nega- confirm these findings. They compared early TF in tively. patients with severe AP to patients without nutri- Comment: Since there are no studies addressing tional support. One possible explanation could be this issue, the question cannot be properly an- the different patient populations studied. In the swered for AP. It has to be considered that under- Windsor group the mean APACHE II was 8 in the EN groupand9.5inthePNgroup.21InthePowellseries nutrition is a well-known risk factor for more APACHE II scores were 13 or more.22 complications and higher morbidity in other dis- In a randomised prospective controlled trial, eases. It also has to be considered that under- comparing EN (TF) vs. PN in patients with severe nutrition is known to occur in 50–80% of chronic pancreatitis Kalfarentzos et al.23 (Ib) scored less alcoholics and that alcohol is a major aetiological than half of those studied, but, in the remainder, factor in acute pancreatitis (30–40% of patients).18 Overweight, with a high body mass index is also mean APACHE II scores were 12.7 in the EN group associated with a poorer prognosis. and11.8inthePNgroup.ENwaswelltoleratedand was associated with fewer septic and other 1.3. Is EN indicated in acute pancreatitis? complications than PN as well as cost were more In mild acute pancreatitis EN is unnecessary, if than three times less. the patient can consume normal food after five In recent years it has become clear, that PN to seven days (B). related complications have often been the conse- In severe necrotising pancreatitis, EN is in- quence of overfeeding or even just catheter sepsis.24 Van den Berghe et al. showed, irrespective dicated if possible (A). This should be supple- of the route of nutritional support, that the control mented by parenteral nutrition if needed (C). of hyperglycemia with insulin reduced mortality in Comment: Parenteral nutrition (PN) has been the critically ill patients.25 Hyperglycaemia may occur standard way of meeting nutritional requirements with EN as well as PN. since it avoids pancreatic stimulation and improves Several studies in patients with trauma, thermal nutritional status. A positive benefit has, however, injury and major gastrointestinal surgery have not yet been confirmed in trials. There are two shown a reduction in septic complication with investigations in mild to moderate pancreatitis EN26,27 (Ib) which also helps to maintain mucosal 19 comparing parenteral to no nutritional support function and limit absorption of endotoxins and (Ib) or to TF20 (Ib). In the trial by Sax et al. no cytokines from the gut.28,29 In animals with induced difference in mortality or complication rate be- pancreatitis, EN prevented bacterial transloca- tween the two regimens could be demonstrated.19 tion,30 but whether this occurs in patients with AP Catheter induced septicaemias as well as hypergly- is still unclear.31 caemia occurred significantly more often in the PN Recent evidence has encouraged a much greater group. McClave et al., in a prospective randomised use of EN than PN in severe acute pancreatitis, controlled study, compared early EN via a jejunal whenever possible. EN, by down-regulating tube to PN in patients with mild to moderate splanchnic cytokine production and modulating pancreatitis.20 Early EN was initiated within 48h the acute phase response, reduces catabolism and after admission to hospital. No difference in the preserves protein.21 investigated parameters was found, although PN Abou-Assi et al.32 studied 156 patients with AP was found to be four times more expensive. All over 12 months. During the first 48h all patients patients in both groups survived. were treated with i.v. fluid and analgesics. 87% of Windsor et al.21 (Ib) compared PN with EN in patients had mild, 10% moderate, and 3% severe patients with mild to moderate (total peripheral PN disease. Those who improved went on to normal vs. ONS) and severe pancreatitis (total central PN food as soon as possible. The non-responders vs. TF). The systemic inflammatory response were randomized to receive nutrients either by a
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