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Gastroenterology – Guidelines on Parenteral Nutrition, Chapter 15

Gastroenterologie – Leitlinie Parenterale Ernährung, Kapitel 15

Review Article Special Issue

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  • R. J. Schulz - Clinic for Geriatrics, St. Marien-Hospital, Cologne, Germany
  • S. C. Bischoff - Dept. Nutritional Medicine and Prevention, University Stuttgart-Hohenheim, Germany
  • B. Koletzko - Dept. Metabolic Diseases & Nutritional Medicine, Dr. von Hauner Children's Hospital, University of Munich, Germany
  • Working group for developing the guidelines for parenteral nutrition of The German Association for Nutritional Medicine

GMS Ger Med Sci 2009;7:Doc13

doi: 10.3205/000072, urn:nbn:de:0183-0000724

Received: January 14, 2009
Published: November 18, 2009

© 2009 Schulz et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.en). You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.


Abstract

In patients with Crohn's disease and ulcerative colitis parenteral nutrition (PN) is indicated when enteral nutrition is not possible or should be avoided for medical reasons. In Crohn's patients PN is indicated when there are signs/symptoms of ileus or subileus in the small intestine, scars or intestinal fistulae. PN requires no specific compounding for chronic inflammatory bowel diseases. In both diseases it should be composed of 55–60% carbohydrates, 25–30% lipids and 10–15% amino acids. PN helps in the correction of malnutrition, particularly the intake of energy, minerals, trace elements, deficiency of calcium, vitamin D, folic acid, vitamin B12, and zinc. Enteral nutrition is clearly superior to PN in severe, acute pancreatitis. An intolerance to enteral nutrition results in an indication for total PN in complications such as pseudocysts, intestinal and pancreatic fistulae, and pancreatic abscesses or pancreatic ascites. If enteral nutrition is not possible, PN is recommended, at the earliest, 5 days after admission to the hospital. TPN should not be routinely administered in mild acute pancreatitis or nil by moth status <7 days, due to high costs and an increased risk of infection. The energy requirements are between 25 and 35 kcal/kg body weight/day. A standard solution including lipids (monitoring triglyceride levels!) can be administered in acute pancreatitis. Glucose (max. 4–5 g/kg body weight/day) and amino acids (about 1.2–1.5 g/kg body weight/day) should be administered and the additional enrichment of TPN with glutamine should be considered in severe, progressive forms of pancreatitis.

Keywords: inflammatory bowel disease, Crohn's disease, ulcerative colitis, pancreatitis

Zusammenfassung

Eine parenterale Ernährung (PE) ist indiziert bei Patienten mit Morbus Crohn oder Colitis ulcerosa, wenn eine enterale Ernährung nicht möglich ist bzw. aus medizinischen Gründen vermieden werden sollte. Bei Morbus Crohn Patienten kann eine PE bei Manifestation im oberen Dünndarm und Ileus- und Subileussymptomatik, Narben oder Darmfisteln indiziert sein. Die PE bedarf keiner speziellen Zusammensetzung für chronisch entzündliche Darmerkrankungen. In beiden Erkrankungen sollte sich die PE aus 55–60% Kohlenhydraten, 25–30% Fett und 10–15% Aminosäuren zusammensetzen. Die PE unterstützt die Korrektur der Mangelernährung, vor allem die Aufnahme von Energie, Mineralstoffen, Spurenelementen, Mangel an Kalzium, Vitamin D, Folsäure, Vitamin B 12, Zink. Im Falle einer notwendigen künstlichen Ernährung bei einer schweren akuten Pankreatitis ist eine enterale Ernährung einer parenteralen Ernährungsform eindeutig überlegen. Eine Unverträglichkeit der enteralen Ernährung führt bei Komplikationen, wie Pseudozysten, intestinale und pankreatische Fisteln, pankreatische Abszesse oder pankreatischem Aszites zum Einsatz der TPE. Sollte eine enterale Ernährung nicht möglich sein, ist eine PE erst nach frühestens 5 Tagen nach Klinikeintreffen zu empfehlen. Die TPE sollte bei milder akuter Pankreatitis, Nahrungskarenz <7 Tage, nicht routinemäßig verabreicht werden, aufgrund steigender Kosten und erhöhtem Infektionsrisiko. Der Energiebedarf liegt zwischen 25 und 35 kcal/kg KG/Tag. Bei akuter Pankreatitis kann eine Standardlösung inklusive Fett verabreicht werden (Monitoring der Triglyzeridspiegel!).

Glukose von max. 3–6 g/kg KG/Tag und Aminosäuren von 1,2–1,5 g/kg KG/Tag sollten zugeführt werden sowie eine zusätzliche Anreicherung durch Glutamin von TPE sollte bei schweren Verlaufsformen einer Pankreatitis erwogen werden.

Schlüsselwörter: chronisch entzündliche Darmerkrankungen, Morbus Crohn, Colitis ulcerosa, Pankreatitis


Crohn's disease

Indication and time of parenteral nutrition (PN)

  • PN is indicated when enteral nutrition is not possible or should be avoided for medical reasons (A).
  • PN is indicated when there are signs/symptoms of ileus or subileus in the small intestine, scars or intestinal fistulae (C).

Substrate intake

  • PN requires no specific compounding for chronic inflammatory bowel diseases.
  • It should be composed of 55–60% carbohydrates, 25–30% lipids and 10–15% amino acids (A). No conclusive data is available on the use of admixtures in the form of polyunsaturated fatty acids (C).
  • PN helps in the correction of malnutrition, particularly the intake of energy, minerals, trace elements, deficiency of calcium, vitamin D, folic acid, vitamin B12, and zinc (A).

Commentary

Once the use of PN has been decided upon, a PN solution should be used due to the high incidence of malnutrition in chronic inflammatory bowel disease. PN should be administered via central venous access for osmolarity over 800 mosmol/l and continuously over 24 hours.

The daily parenteral energy intake in well-nourished adult patients should amount to 25–30 kcal/kg body weight. During the first 24–48 hours, the PN administration should be slowly started with a phase of an “up-titration”, starting with about 50% of the energy amount. The volume should be adjusted to 30–40 ml/kg body weight, depending on the loss of fluid. Concentrations of 4–6 g glucose/kg body weight, 1.5–2 g lipids per kg body weight and 1.5–2 g amino acids per kg body weight are recommended [1].

PN is indicated in cases of toxic megacolon, malabsorption syndrome, particularly short bowel syndrome, insufficient growth and disturbance of growth in children as well as when enteral nutrition is not tolerated [2], [3], [4], [5], [6], [7], [8], [9], [10].

PN presents no advantage if the disease is chronically active (A). An increased rate of remission is not achieved with PN, according to the official recommendations of the American Gastroenterological Association (AGA). PN has no influence on the surgical intervention rate. According to these recommendations, it is not necessary to bypass the intestinal passage to attain clinical remission.

An optimal supply of nutrients improves bowel motility, intestinal permeability and nutritional status, and lowers inflammatory reactions [8], [11]. Malnutrition often occurs in patients with inflammatory bowel diseases. There are extensive differences in the parameters for malnutrition between Crohn’s disease and ulcerative colitis. Malnutrition is diagnosed in 80% of Crohn's disease patients [5], [9], [10], [11]. The severity of malnutrition depends on the duration of the illness, activity of the inflammation, the function of the small intestine and extent of the diseased sections in the small intestine, and results in a higher incidence of protein energy malnutrition as well as specific substrate deficiency.

Clinical symptoms, inflammatory and nutritional parameters in Crohn's disease can improve under enteral/oral nutrition [2], [6], [10], [12], [13], [14]. There is no standardised data available regarding the remission rate with PN. It was found that in complicated cases, remission could be more easily attained through PN than with enteral nutrition [15].

Total PN is an important therapy in children and teenagers [5].

In terms of wound healing and reconstitution of the small intestine, PN shows no advantages as compared to enteral nutrition. It is assumed that oral/enteral nutrition provides faster stability in organ function of the small intestine.

Complications like venous thromboses, occlusion of the central venous vessels, sepsis, cholestasis/cholangitis/cholecystitis, cholestatic liver dysfunction are associated with TPN [16], [17], [18], [19], [20], [21], [22], [23], [24], [25], [26], [27]. Acute elevation in transaminases, overall bilirubin and albumin are characteristics of PN metabolic complications [16], [17], [18], [19], [20], [21], [22], [24], [25].

Numerous studies show that catheter-related sepsis occur on an average once or twice every two years in patients on long-term PN who are suffering from a functional short bowel syndrome, as a result of chronic inflammatory bowel diseases. Recurring catheter infections with septic components occur during hospital stays in dependence of central access catheter models and in dependence of training and care standards in the hospital in patients who are not receiving long-term PN [28]. There are no advantages of PN therapy over enteral nutrition therapy regarding fistula healing. No differences can be seen in the rate of survival.


Ulcerative colitis

Indication and time of PN

  • PN is indicated when enteral nutrition is not possible or should be avoided for medical reasons (A).

Substrate intake

  • PN requires no specific compounding for chronic inflammatory bowel diseases (A).
  • It should be composed of 55–60% carbohydrates, 25–30% lipids and 10–15% amino acids (A). No conclusive data is available on the use of admixtures in the form of polyunsaturated fatty acids (C).
  • PN helps in the correction of malnutrition, particularly the intake of energy, minerals, trace elements, deficiency of calcium, vitamin D, folic acid, vitamin B12, and zinc (A). In addition, the intake of vitamins, trace elements and minerals can be orally or intravenously substituted irrespective of PN.

Commentary

No significant improvement in clinical parameters was observed in patients with ulcerative colitis with the use of PN [2], [29]. There is no standardised data available regarding the remission rate with PN. It was also observed that, in complicated cases, remission could be more easily attained with PN than with enteral nutrition [15].

Total PN is an important therapy in children and teenagers [5].

In terms of wound healing and the reconstitution of the small intestine, PN shows no advantages compared to enteral nutrition. It is assumed that oral/enteral nutrition provides faster stability in organ function of the small intestine.

Complications like venous thrombosis, occlusion of the central venous vessels, sepsis, cholestasis/cholangitis/cholecystitis, cholestatic liver dysfunction are associated with TPN [16], [17], [19], [20], [21], [22], [24], [25], [30].

Acute increase in transaminases, overall bilirubin and albumin are characteristics of metabolic complications of PN [16], [17], [19], [20], [21], [22], [24], [25], [30].

There are no advantages of PN therapy over enteral nutrition therapy regarding fistula healing. No differences can be seen in the rate of survival.


Acute pancreatitis

Indication and time of PN

  • Enteral nutrition is clearly superior to PN in severe, acute pancreatitis (A).
  • An intolerance to enteral nutrition results in an indication for total PN in complications such as pseudocysts, intestinal and pancreatic fistulae, and pancreatic abscesses or pancreatic ascites (B).
  • If enteral nutrition is not possible, PN is recommended, at the earliest, 5 days after admission to the hospital (C).
  • TPN should be not be routinely administered in mild acute pancreatitis or nil by moth status <7 days, due to high costs and an increased risk of infection (C).

Commentary

The nutritional therapy of acute pancreatitis depends on the severity of the disease, presence of any complications and nutritional state of the patient. Enteral transduodenal feeding should be started once acute pancreatitis is suspected. There is a clear benefit with enteral nutrition in numerous studies [31], [32], [33], [34], [35], [36], [37], [38], [39], [40], [41] regarding LOS, infection-related morbidity and possible organ failures. Total PN should be started only when there are contraindications to enteral nutrition or no possible access.

The time to start should be after the resolution of the acute phase in acute, complicated forms of pancreatitis [42], [43]. A prospective, controlled and randomised study on acute pancreatitis [44] shows that exclusive TPN results in a longer LOS and increase in costs with no improvement regarding the course of disease.

Recent studies have shown that enteral nutrition through a jejunal tube can be of an advantage in specific patient groups [45], [46], [47], [48]. A similarly positive effect is also achieved by using nasogastric tubes, but in a smaller study [49].

Jejunal feeding is assessed to be safe and effective in the postoperative stage in severe forms of pancreatitis, according to the study by Pupelis [45]. TPN is presumed to prevent stimulation of the exocrine pancreas as well as help in the maintenance of metabolic homeostasis in severe forms of pancreatitis [17], [30]. In severe cases (presence of ileus), the task of TPN is to compensate for the increased protein expenditure, as well as to maintain the nutrition state of the patient. PN reduces mortality and improves the nutritional situation in such circumstances [50], [51], and is to be continued until a stable, haemodynamic state is achieved [52], [53].

The lack of utilisation of the intestine in acute pancreatitis seems to worsen the metabolic stress situation, lengthen the LOS and increase the risk of complications [31], [34], [40], [46], [54], [55]. Further evidence indicates that not only enteral nutrition, but also specific nutritional components in enteral nutrition such as probiotics, arginine, glutamine and antioxidants have a positive influence on LOS and the rate of complications [56], [57].

Energy intake

  • The energy requirements lie in a range between 25 and 35 kcal/kg body weight/day [16] (A).

Substrate intake

  • A standard solution including lipids can be administered in acute pancreatitis (C). Lipids can be administered to meet energy requirements and should be subject to regular monitoring (triglycerides).
  • Carbohydrates are the most important energy source. Glucose administration (max. 4–5 g/kg body weight/day) counteracts intrinsic gluconeogenesis, and prevents protein degradation. Administering glucose instead of lipids, as an energy supplier, lowers the potential risk of hyperlipidemia, but lipid administration cannot be avoided in most cases (B).
  • An even nitrogen balance can be achieved and maintained with amino acids. The intake of amino acids should be about 1.2–1.5 g/kg body weight/day (A).
  • The additional enrichment of TPN with glutamine should be considered in severe, progressive forms of pancreatitis, thereby improving the clinical progression (B).
  • The intravenous administration of lipid emulsions is safe, as long as triglyceride levels (<400 mg/dl) are monitored (C). Statements on particularly beneficial fatty acid admixtures cannot be made regarding pancreatitis.

Commentary

McClave et al. [44] carried out a study in 1997, in which 30 patients received either total PN or total enteral nutrition. No differences between the two groups were observed with regards to mortality, level of pain in the period until amylase levels normalised, serum albumin levels and the frequency of nosocomial infections. Significantly more hyperglycaemia occurred in the total PN group [34].

Tests on fatty acid admixtures are at present only available for “Intralipid” solutions and are deemed safe for administration [58].

The glucose admixture was modified in 2 studies [58], [59] based on the clinical picture of stress-induced hyperglycaemia. In the study carried out by Wu [58], initial hyperglycaemia was reported in 64% of patients, which was easier to control with a lipid/glucose admixture than in a pure glucose admixture. Hypertriglyceridemia, or negative effects on the liver function, were not reported. Significant differences regarding the glucose levels, cholesterol levels or uric acid levels were also not reported in Martinez' work [59].

De Beaux et al. [60] carried out a study of 14 patients with acute pancreatitis, where one group received standardised PN and the other group received nutrition enriched with glutamine. The glutamine group showed increased lymphocyte proliferation, an increase in T-cell DNA as well as a drop in an interleukin 8 concentration. The administration of glutamine could be beneficial in preventing complications. A lower rate of complications and significantly lower rates of pancreatic infections were also described with glutamine in the papers by Ockenga et al. [61] and Xian et al. [62]. Patients with acute pancreatitis show an increased rate of catheter-sepsis and metabolic dysfunctions. The administration of thiamine, folic acid, magnesium and zinc is recommended in patients with a history of alcohol abuse [17], [63].

Patients with severe diseases and complications require early enteral nutritional therapy to prevent detrimental effects caused by nutritional losses (especially proteins) [32], [36], [64]. Some authors recommend early jejunal nutrition with an elementary diet and others recommend TPN combined with enteral nutrition [65]. PN should only be used in complicated cases when ileus is present or probable with regular checks for glucose, triglycerides and serum pH.


Notes

This article is part of the publication of the Guidelines on Parenteral Nutrition from the German Society for Nutritional Medicine (overview and corresponding address under http://www.egms.de/en/journals/gms/2009-7/000086.shtml).

English version edited by Sabine Verwied-Jorky, Rashmi Mittal and Berthold Koletzko, Univ. of Munich Medical Centre, Munich, Germany.


References

1.
Buchman AL, Scolapio J, Freyer J. AGA technical review on short bowel syndrome and intestinal transplantation. Gastroenterol. 2003;124(4):1111-34.
2.
Bartels M, Nagel E, Pichlmayr R. Welche Rolle spielt die Ernährung bei der Colitis ulcerosa? Ein Beitrag zum heutigen Stellenwert der diätetischen Therapie in der Behandlung entzündlicher Darmerkrankungen [What is the role of nutrition in ulcerative colitis? A contribution to the current status of diet therapy in treatment of inflammatory bowel diseases]. Langenbecks Arch Chir. 1995;380(1):4-11.
3.
Diamanti A, Gambarara M, Knafelz D, Marcellini M, Boldrini R, Ferretti F, Papadatou B, Castro M. Prevalence of liver complications in pediatric patients on home parenteral nutrition: indications for intestinal or combined liver-intestinal transplantation. Transplant Proc. 2003;35(8):3047-9. DOI: 10.1016/j.transproceed.2003.10.037 External link
4.
Iyer KR, Srinath C, Horslen S, Fox IJ, Shaw BW, Sudan DL, Langnas AN. Late graft loss and long-term outcome after isolated intestinal transplantation in children. J Pediatr Surg. 2002;37(2):151-4. DOI: 10.1053/jpsu.2002.30240 External link
5.
Keller KM, Wirth S. Parenteral nutrition in treatment of short stature in adolescents with Crohn disease. Klin Pädiatr. 1992;204:411-6. DOI: 10.1055/s-2007-1025381 External link
6.
Kelly DG, Fleming CR. Nutritional considerations in inflammatory bowel diseases. Gastroenterol Clin North Am. 1995;24(3):597-611.
7.
Kolb S. Parenterale Ernährung zu Hause bei Morbus Crohn. Ernährung. 1990;1:40-4.
8.
Ruemmele FM, Roy CC, Levy E, Seidman EG. Nutrition as primary therapy in pediatric Crohn's disease: fact or fantasy?. J Pediatr. 2000;136(3):285-91. DOI: 10.1067/mpd.2000.104537 External link
9.
Silk DB. Medical management of severe inflammatory disease of the rectum: nutritional aspects. Baillieres Clin Gastroenterol. 1992;6(1):27-41. DOI: 10.1016/0950-3528(92)90016-8 External link
10.
Stokes MA. Crohn's disease and nutrition. Br J Surg. 1992;79(5):391-4. DOI: 10.1002/bjs.1800790505 External link
11.
Greenberg GR, Fleming CR, Jeejeebhoy KN, Rosenberg IH, Sales D, Tremaine WJ. Controlled trial of bowel rest and nutritional support in the management of Crohn's disease. Gut. 1988;29:1309-15. DOI: 10.1136/gut.29.10.1309 External link
12.
Gilroy R, Sudan D. Liver and small bowel transplantation: therapeutic alternatives for the treatment of liver disease and intestinal failure. Semin Liver Dis. 2000;20:437-50. DOI: 10.1055/s-2000-13151 External link
13.
Goh J, O'Morain CA. Review article: nutrition and adult inflammatory bowel disease. Aliment Pharmacol Ther. 2003;17(3):307-20. DOI: 10.1046/j.1365-2036.2003.01482.x External link
14.
Tsujikawa T, Andoh A, Fujiyama Y. Enteral and parenteral nutrition therapy for Crohn's disease. Curr Pharm Des. 2003;9(4):323-32.
15.
Evans JP, Steinhart AH, Cohen Z, McLeod RS. Home total parenteral nutrition: an alternative to early surgery for complicated inflammatory bowel disease. J Gastrointest Surg. 2003;7(4):562-6. DOI: 10.1016/S1091-255X(02)00132-4 External link
16.
Abu-Elmagd K, Bond G. Gut failure and abdominal visceral transplantation. Proc Nutr Soc. 2003;62:727-37. DOI: 10.1079/PNS2003288 External link
17.
American Gastroenterological Association. American Gastroenterological Association medical position statement: parenteral nutrition. Gastroenterology. 2001;121(4):966-9. DOI: 10.1016/S0016-5085(01)91000-5 External link
18.
Campos FG, Waitzberg DL, Teixeira MG, Mucerino DR, Habr-Gama A, Kiss DR. Inflammatory bowel diseases: principles of nutritional therapy. Rev Hosp Clin Fac Med Sao Paulo. 2002;57(4):187-98. DOI: 10.1590/S0041-87812002000400009 External link
19.
Cucino C, Sonnenberg A. Cause of death in patients with inflammatory bowel disease. Inflamm Bowel Dis. 2001;7(3):250-5. DOI: 10.1097/00054725-200108000-00011 External link
20.
Forbes A. Review article: Crohn's disease – the role of nutritional therapy. Aliment Pharmacol Ther. 2002;16 Suppl 4:48-52. DOI: 10.1046/j.1365-2036.16.s4.7.x External link
21.
Higgens CS, Keighley MR, Allan RN. Impact of preoperative weight loss and body composition changes on postoperative outcome in surgery for inflammatory bowel disease. Gut. 1984;25:732-6. DOI: 10.1136/gut.25.7.732 External link
22.
Hwang TL, Lue MC, Chen LL. Early use of cyclic TPN prevents further deterioration of liver functions for the TPN patients with impaired liver function. Hepatogastroenterology. 2000;47(35):1347-50.
23.
Meadows N. Monitoring and complications of parenteral nutrition. Nutrition. 1998;14(10):806-8. DOI: 10.1016/S0899-9007(98)00089-6 External link
24.
Muiesan P, Dhawan A, Novelli M, Mieli-Vergani G, Rela M, Heaton ND. Isolated liver transplant and sequential small bowel transplantation for intestinal failure and related liver disease in children. Transplantation. 2000;69(11):2323-6. DOI: 10.1097/00007890-200006150-00017 External link
25.
Müller A, Neuhaus P. Dünndarmtransplantation - klinischer Stand und eigene Ergebnisse. Dtsch Ärztebl. 2004;101(1-2):A38-43. Available from: http://www.aerzteblatt.de/v4/archiv/lit.asp?id=39981 External link
26.
Seo M, Okada M, Yao T, Furukawa H, Matake H. The role of total parenteral nutrition in the management of patients with acute attacks of inflammatory bowel disease. J Clin Gastroenterol. 1999;29(3):270-5. DOI: 10.1097/00004836-199910000-00009 External link
27.
Stange EF, Schreiber S, Raedler A, Stallmach A, Schölmerich J, Loeschke K, Starlinger M, Fischbach W, Caspary WF. Therapie des Morbus Crohn – Ergebnisse einer Konsensuskonferenz der Deutschen Gesellschaft fur Verdauungs- und Stoffwechselkrankheiten [Therapy of Crohn diseases – results of a Consensus Conference of the German Society of Digestive and Metabolic Diseases]. Z Gastroenterol. 1997;35(7):541-4.
28.
Lowen CC, Greene LM, McClave SA. Nutritional support in patients with inflammatory bowel disease. Postgrad Med. 1992;91(5):407-14.
29.
González-Huix F, Fernández-Bañares F, Esteve-Comas M, Abad-Lacruz A, Cabré E, Acero D, Figa M, Guilera M, Humbert P, de León R, et al. Enteral versus parenteral nutrition as adjunct therapy in acute ulcerative colitis. Am J Gastroenterol. 1993;88(2):227-32.
30.
Bodoky G, Harsanyi L, Pap A, Tihanyi T, Flautner L. Effect of enteral nutrition on exocrine pancreatic function. Am J Surg. 1991;161(1):144-8. DOI: 10.1016/0002-9610(91)90375-N External link
31.
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. DOI: 10.1111/j.1572-0241.2002.05979.x External link
32.
Gupta R, Patel K, Calder PC, Yaqoob P, Primrose JN, Johnson CD. A randomised clinical trial to assess the effect of total enteral and total parenteral nutritional support on metabolic, inflammatory and oxidative markers in patients with predicted severe acute pancreatitis (APACHE II > or =6). Pancreatology. 2003;3(5):406-13. DOI: 10.1159/000073657 External link
33.
Hernández-Aranda JC, Gallo-Chico B, Ramírez-Barba EJ. Apoyo nutricional en pancreatitis aguda grave: Ensayo clinico controlado [Nutritional support in severe acute pancreatitis: Controlled clinical trial]. Nutr Hosp. 1996;11(3):160-6.
34.
Kalfarentzos F, Kehagias J, Mead N, Kokkinis K, Gogos CA. Enteral nutrition is superior to parenteral nutrition in severe acute pancreatitis: results of a randomized prospective trial. Br J Surg. 1997;84(12):1665-9.
35.
Louie B, Noseworthy T, Hailey D, Gramlich L, Jacobs P, Warnock G. Enteral or Parenteral Nutrition for Severe Pancreatitis: A Health Technology Assessment. JPEN J Parenter Enteral Nutr. 2002;26(4):S32.
36.
Mans G. Die Ernährungstherapie der akuten Pankreatitis. Aktuel Ernaehr Med. 1997;22:276-80.
37.
Nathens AB, Curtis JR, Beale RJ, Cook DJ, Moreno RP, Romand JA, Skerrett SJ, Stapleton RD, Ware LB, Waldmann CS. Management of the critically ill patient with severe acute pancreatitis. Crit Care Med. 2004;32(12):2524-36. DOI: 10.1097/01.CCM.0000148222.09869.92 External link
38.
Olah A, Pardavi G, Belagyi T, Nagy A, Issekutz A, Mohamed GE. Early nasojejunal feeding in acute pancreatitis is associated with a lower complication rate. Nutrition. 2002;18(3):259-62. DOI: 10.1016/S0899-9007(01)00755-9 External link
39.
Powell JJ, Murchison JT, Fearon KC, Ross JA, Siriwardena AK. Randomized controlled trial of the effect of early enteral nutrition on markers of the inflammatory response in predicted severe acute pancreatitis. Br J Surg. 2000;87(10):1375-81. DOI: 10.1046/j.1365-2168.2000.01558.x External link
40.
Windsor AC, Kanwar S, Li AG, Barnes E, Guthrie JA, Spark JI, Welsh F, Guillou PJ, Reynolds JV. Compared with parenteral nutrition, enteral feeding attenuates the acute phase response and improves disease severity in acute pancreatitis. Gut. 1998;42(3):431-5.
41.
Zhao G, Wang CY, Wang F, Xiong JX. Clinical study on nutrition support in patients with severe acute pancreatitis. World J Gastroenterol. 2003;9(9):2105-8.
42.
Sax HC, Warner BW, Talamini MA, Hamilton FN, Bell RH Jr, Fischer JE, Bower RH. Early total parenteral nutrition in acute pancreatitis: lack of beneficial effects. Am J Surg. 1987;153(1):117-24. DOI: 10.1016/0002-9610(87)90211-X External link
43.
Tenner S. Initial management of acute pancreatitis: critical issues during the first 72 hours. Am J Gastroenterol. 2004;99:2489-94. DOI: 10.1111/j.1572-0241.2004.40329.x External link
44.
McClave SA, Greene LM, Snider HL, Makk LJ, Cheadle WG, Owens NA, Dukes LG, Goldsmith LJ. Comparison of the safety of early enteral vs parenteral nutrition in mild acute pancreatitis. JPEN J Parenter Enteral Nutr. 1997;21(1):14-20. DOI: 10.1177/014860719702100114 External link
45.
Pupelis G, Selga G, Austrums E, Kaminski A. Jejunal feeding, even when instituted late, improves outcomes in patients with severe pancreatitis and peritonitis. Nutrition. 2001;17(2):91-4. DOI: 10.1016/S0899-9007(00)00508-6 External link
46.
Hallay J, Kovacs G, Szatmari K, Kovács G, Szatmári K, Bakó A, Szentkereszty Z, Lakos G, Sipka S, Sápy P. Early jejunal nutrition and changes in the immunological parameters of patients with acute pancreatitis. Hepatogastroenterology. 2001;48(41):1488-92.
47.
Harsányi L, Bodoky G, Pap A. The effect of jejunal nutrition on pancreatic exocrine function. Acta Chir Hung. 1992;33(1-2):13-21.
48.
Pandey SK, Ahuja V, Joshi YK, Sharma MP. A randomized trial of oral refeeding compared with jejunal tube refeeding in acute pancreatitis. Indian J Gastroenterol. 2004;23(2):53-5.
49.
Eatock FC, Chong P, Menezes N, Murray L, McKay CJ, Carter CR, Imrie CW. A randomized study of early nasogastric versus nasojejunal feeding in severe acute pancreatitis. Am J Gastroenterol. 2005;100:432-9. DOI: 10.1111/j.1572-0241.2005.40587.x External link
50.
August D. Guidelines for the use of parenteral and enteral nutrition in adult and pediatric patients. JPEN J Parenter Enteral Nutr. 2002;26:68SA-70SA.
51.
Heyland DK, MacDonald S, Keefe L, Drover JW. Total parenteral nutrition in the critically ill patient: a meta-analysis. JAMA. 1998;280(23):2013-9. DOI: 10.1001/jama.280.23.2013 External link
52.
Kaushik N, O'Keefe SJ. Nutritional support in acute pancreatitis. Curr Gastroenterol Rep. 2004;6(4):320-6. DOI: 10.1007/s11894-004-0085-3 External link
53.
Mallampalli A, McClave SA, Snider HL. Defining tolerance to enteral feeding in the intensive care unit. Clin Nutr. 2000;19(4):213-5. DOI: 10.1054/clnu.2000.0137 External link
54.
Jabbar A, Chang WK, Dryden GW, McClave SA. Gut immunology and the differential response to feeding and starvation. Nutr Clin Pract. 2003;18:461-82. DOI: 10.1177/0115426503018006461 External link
55.
Marik PE, Zaloga GP. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ. 2004;328:1407. DOI: 10.1136/bmj.38118.593900.55 External link
56.
Lasztity N, Hamvas J, Biró L, Németh E, Marosvölgyi T, Decsi T, Pap A, Antal M. Effect of enterally administered n-3 polyunsaturated fatty acids in acute pancreatitis--a prospective randomized clinical trial. Clin Nutr. 2005;24:198-205. DOI: 10.1016/j.clnu.2004.12.008 External link
57.
Oláh A, Belágyi 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(9):1103-7. DOI: 10.1046/j.1365-2168.2002.02189.x External link
58.
Wu H, Wu Z, Wu G. [Effect of intralipid on patients with acute necrotic pancreatitis: a prospective clinical study]. Zhonghua Wai Ke Za Zhi. 1995;33(5):261-4.
59.
Martinez J, Castilla M, Velasco P, et al. Non-Glucose carbohydrates in the Parenteral Nutrition of Patients with a Systemic Inflammatory Response Syndrome. Nutr Hosp. 1999;14:41.
60.
de Beaux AC, O'Riordain MG, Ross JA, Jodozi L, Carter DC, Fearon KC. Glutamine-supplemented total parenteral nutrition reduces blood mononuclear cell interleukin-8 release in severe acute pancreatitis. Nutrition. 1998;14(3):261-5. DOI: 10.1016/S0899-9007(97)00477-2 External link
61.
Ockenga J, Borchert K, Rifai K, Manns MP, Bischoff SC. Effect of glutamine-enriched total parenteral nutrition in patients with acute pancreatitis. Clin Nutr. 2002;21(5):409-16. DOI: 10.1054/clnu.2002.0569 External link
62.
Xian H, Qing-Jiu M, Jian-Guo L, Yan-Kui C, Xi-Lin D. Effect of total parenteral nutrition (TPN) with and without glutamine dipeptide supplementation on outcome in severe acute pancreatitis (SAP). Clin Nutr Suppl. 2004;1(1):43-7. DOI: 10.1016/j.clnu.2004.07.011 External link
63.
Al Omran M, Groof A, Wilke D. Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database Syst Rev. 2003;CD002837. DOI: 10.1002/14651858.CD002837 External link
64.
Meier R, Beglinger C, Layer P, Gullo L, Keim V, Laugier R, Friess H, Schweitzer M, Macfie J; ESPEN Consensus Group. ESPEN guidelines on nutrition in acute pancreatitis. European Society of Parenteral and Enteral Nutrition. Clin Nutr. 2002;21(2):173-83. DOI: 10.1054/clnu.2002.0543 External link
65.
Sun B, Gao Y, Xu J, Zhou XL, Zhou ZQ, Liu C, Jiang HC. Role of individually staged nutritional support in the management of severe acute pancreatitis. Hepatobiliary Pancreat Dis Int. 2004;3(3):458-63.