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DOI: 10.1055/s-2001-11716
J.A.Barth Verlag in Medizinverlage Heidelberg GmbH & Co.KG
Pankreatitis und Ernährung
Bedeutung des Gastrointestinaltraktes und der Ernährung für die septischen KomplikationenPublication History
Publication Date:
31 December 2001 (online)
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Pancreatitis and nutrition. The role of the gut and nutrition for septic complications
Summary
Septic complications are an important factor for the morbidity and mortality of acute pancreatitis. The gut has been identified as a source of infection early in the course of the disease allowing intestinal bacteria to translocate into pancreatic necrosis and other organs. Bacterial translocation is promoted by an impaired intestinal mucosal barrier which can be attributed to the reduced oxygen and substrate supply of the intestine during the early systemic response to the pancreatic injury. A rat model of severe acute pancreatitis has been used to confirm the hypothesis that an impaired mucosal barrier can be stabilized by supplying certain nutritients, vitamins and trace elements. Following a discussion of the many aspects of bacterial translocation and gut derived sepsis, the role of the gut and nutrition for the development of septic complications in acute pancreatitis is summarized as follows: Early in the course of acute pancreatitis the gut is a target organ of the primary systemic inflammatory response (SIRS) to pancreatic injury. SIRS-induced gut barrier dysfunction promoting bacterial translocation makes the gut the motor for secondary (septic) complications. As a septic focus the gut becomes a target for therapeutic measures aimed at stabilizing the impaired gut barrier. Nutritive factors demonstrated to improve impaired gut barrier function include early enteral feeding and specific factors like glutamine which are essential for enterocytes and colonocytes in stress. Experimental data are presented to underline the significance of these nutritive factors and subsequent randomized multicenter trials performed to verify the positive experimental results are introduced. The effect of other nutritive factors (e. g. omega-3-fatty acids) has not yet been systemically investigated. Thus, experimental and clinical studies need to be performed for evaluating their effect on bacterial translocation and the disease course in acute pancreatitis.
Zusammenfassung
Septische Komplikationen sind die Hauptursache der Morbidität und Mortalität in der postakuten Phase der akuten Pankreatitis. Ausgangspunkt der Infektionen ist der Darm, von wo Bakterien in der Frühphase der Erkrankung in die Pankreasnekrosen und andere Organe translozieren. Wegbereiter der bakteriellen Translokation ist die Beeinträchtigung der intestinalen Mukosabarriere, die u. a. auf eine Minderversorgung des Darmes mit Sauerstoff und Substraten zurückzuführen ist. Die Frage, ob sich die gestörte Mukosabarriere durch die Zufuhr bestimmter Nährstoffe, Vitamine und Spurenelemente bzw. eine frühzeitige enterale Ernährung stabilisieren läßt, wird anhand der Literaturdaten und eigener Untersuchungen am Rattenmodell der akut nekrotisierenden Pankreatitis diskutiert. Die Bedeutung des GI-Traktes und der Ernährung für die Entwicklung septischer Komplikationen wird wie folgt zusammengefaßt: Der Darm ist primär Zielorgan der initialen systemischen Entzündungsreaktion (SIRS) auf die Pankreasschädigung. Dadurch kommt es zu einer Störung der Mukosabarriere, die den Übertritt von Bakterien aus dem Darm in den Organismus begünstigt. Der Darm wird somit zum Motor des sekundären (septischen) Multiorganversagens. Als septischer Fokus wird der Darm damit ein wichtiges Zielorgan für therapeutische Maßnahmen. Diese schließen nutritive Faktoren ein. Nutritive Faktoren, die die gestörte Darmbarrierefunktion verbessern können, sind eine frühzeitige enterale Ernährung und die Substitution von Substraten, die für den Darm in Streßsituationen essentiell sind, wie z. B. Glutamin. Dies wird durch experimentelle Daten belegt. Laufende klinische Studien, die die Effizienz dieser Therapieformen auch in der Praxis belegen sollen, werden vorgestellt. Zum Nachweis des Effektes anderer nutritiver Faktoren (z. B. Omega-3-Fettsäuren) auf die bakterielle Translokation und den Krankheitsverlauf bei der akuten Pankreatitis werden vergleichbare experimentelle und klinische Studien gefordert.
Key words
Pancreatitis - bacterial translocation - sepsis - nutrition - glutamine
Schlüsselwörter
Pankreatitis - bakterielle Translokation - Sepsis - Ernährung - Glutamin
Literatur
- 1 Alexander J W. Bacterial translocation during enteral and parenteral nutrition (review). Proc Nutr Soc. 1998; 57 389-393
- 2 American College of Chest Physicians and Society of Critical Care Medicine Consensus Conference . Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med. 1992; 20 864-871
- 3 Ammori B J, Leeder P G, King R F G J, Barclay G R, Martin I G, Larvin M, McMahon M J. Early failure of intestinal barrier function and endotoxaemia in severe acute pancreatitis. Int J Pancreatol 1998; 23: 210 (abstract)
- 4 Bahrami S, Redl H, Schlag G. The intestine as the cause of infection and multiple organ failure. Wien Klin Wochenschr (Suppl). 1998; 1 2-10
- 5 Bai M X, Jiang Z M, Liu Y W, Wang W T, Li D M, Wilmore D W. Effects of alanyl-glutamine on gut barrier function. Nutrition. 1996; 12 793-796
- 6 Beger H G, Block S, Bittner R. The significance of bacterial infection in acute pancreatitis. In: Beger HG, Büchler M (Hrsg). Acute pancreatitis. Springer, Berlin, Heidelberg 79-86
- 7 Bradley E L. A clinically based classification system for acute pancreatitis. Arch Surg. 1993; 128 586-590
- 8 De Beaux A C, Palmer K R, Carter D C. Factors influencing morbidity and mortality in acute pancreatitis. Gut. 1995; 37 121-126
- 9 Deitch E A. Bacterial translocation. The influence of dietary variables. Gut (Suppl). 1994; 1 23-27
- 10 Eibl G, Foitzik T, Forgacs B, Wagner J, Kirchengast M, Buhr H J. Reduktion sekundärer Pankreasinfektionen bei auter Pankreatitis durch Verbesserung der intestinalen Mikrozirkulation. Langenbecks Arch Chir Suppl 1 (Forumsbd) 1999; 33-36
- 11 Foitzik Th, Eibl G, Kirchengast M, Buhr H J. Comparison of delayed therapy with ICAM-1 antibodies and a specific endothelin-1 antagonist in severe experimental pancreatitis. J Gastrointest Surg . 2000; 4 240-246
- 12 Foitzik Th, Fernandez-del Castillo C, Rattner D W, Ferraro M J, Warshaw A L. Pathogenesis and prevention of early pancreatic infection in experimental acute cecrotizing pancreatitis. Ann Surg. 1995; 222 179-185
- 13 Foitzik Th, Eibl G, Hotz H G, Faulhaber J, Kirchengast M, Buhr H J. Endothelin receptor blockade in severe acute pancreatitis leads to systemic enhancement of microcirculation, stabilization of capillary permeability, and improved survival rates. Surgery. 2000; 128 399-407
- 14 Foitzik Th, Klar E, Buhr H J. Umsetzung experimenteller Forschungsergebnisse in der Behandlung der akut nekrotisierenden Pankreatitis. Chirurg. 1998; 69 423-431
- 15 Foitzik Th, Kruschewski M, Kroesen A J, Hotz H G, Eibl G, Buhr H J. Does glutamin reduce bacterial translocation. Int J Colorect Dis. 1999; 14 143-149
- 16 Foitzik Th, Mithöfer K, Fernandez-del Castillo C, Lewandrowski K B, Rattner D W, Ferraro M J, Warshaw A L. Time course of bacterial infection of the pancreas and its relation to disease severity in a rodent model of acute necrotizing pancreatitis. Ann Surg. 1994; 220 193-198
- 17 Foitzik Th, Stufler M, Hotz H G, Klinnert J, Wagner J, Warshaw A L, Schulzke J D, Fromm M, Buhr H J. Glutamine stabilizes intestinal permeability and reduces pancreatic infection in acute experimental pancreatitis. J Gastrointest Surg. 1997; 1 40-47
- 18 Forgacs B, Wudel E, Franke J, Eibl G, Faulhaber J, Kahrau S, Buhr H J, Foitzik T. Impairment of RES-function early in acute pancreatitis. Pancreas 1998; 17: 433 (abstract)
- 19 Gianotti L, Alexander J W, Gennari R, Pyles T, Babcock G F. Oral glutamine decreases bacterial translocation and improves survival in experimental gut origin sepsis. JPEN. 1995; 19 69-74
- 20 Gumaste V V, Gupta R, Wasserman D, Dave P B, Vieux K. Colonic involvement in acute pancreatitis. Am J Gastroenterol. 1995; 90 640-641
- 21 Hotz H G, Foitzik T, Rohweder J, Schulzke J D, Fromm M, Runkel N S F, Buhr H J. Intestinal microcirculation and gut permeability in acute pancreatitis. J Gastrointest Surg. 1998; 2 518-525
- 22 Kalfarentzos F, Kehagias J, Mead N, Kokkinis K, Gogos C A. Enteral nutrition is superior to parenteral nutrition in severe acute pancreatitis. Results of a randomized prospective trial. Br J Surg. 1997; 84 1665-1669
- 23 Klar E, Foitzik T, Buhr H J, Messmer K, Herfarth C. Isovolemic hemodilution with Dextran 60 as a treatment of pancreatic ischemia in acute pancreatitis. Ann Surg. 1993; 217 369-374
- 24 Klar E, Messmer K, Warshaw A L, Herfarth C. Pancreatic ischemia in experimental acute pancreatitis. Mechanism, significance and therapy (review). Br J Surg. 1990; 77 1205-1210
- 25 Luiten E J T, Hop W C J, Lange F H, Bruinning H A. Controlled clinical trial of selective gut decontamination for the treatment of severe acute pancreatitis. Ann Surg. 1995; 222 57-65
- 26 McClave S A, Greene L M, Snider H L, Makk L J K, Cheadle W G, Owens N A, Dukes L G, Goldsmith L J. Comparison of the safty of early enteral versus parenteral nutrition in mild acute pancreatitis. JPEN. 1997; 21 14-20
- 27 McKay C J, Curran F, Sharples C, Baxter J N, Imrie C W. Prospective placebo-controlled randomized trial of lexipafant in predicted severe acute pancreatitis. Br J Surg. 1997; 84 1239-1243
- 28 Nakad A, Piessevaux H, Marot J C, Hoang P, Geubel A, Van Steenbergen W, Reynaert M. Is early enteral nutrition in acute pancreatitis dangerous. Pancreas. 1998; 17 187-193
- 29 Ogawa M. Acute pancreatitis and cytokines: “Second attack” by septic complications lead to organ failure. Pancreas. 1998; 16 312-315
- 30 Pederzoli P, Bassi C, Vesentini S, Campedelli A. A randomized multicenter trial of antibiotic prophylaxis of septic complications in acute necrotizing pancreatitis with imipenem. Surg Gynecol Obstet. 1993; 176 480-483
- 31 Roth E. Die Bedeutung des Glutamins in der Intensivmedizin. Intensivmed. 1997; 34 91-100
- 32 Runkel N S F, Moody F G, Smith G S. The role of the gut in the development of sepsis in acute pancreatitis. J Surg Res. 1991; 51 18-23
- 33 Sun Z, Wang X, Deng X, Lasson A, Wallen R, Hallberg E, Andersson R. The influence of intestinal ischemia and reperfusion on bidirectional intestinal barrier permeability, cellular membrane integrity, proteinase inhibitors, and cell death in rats. Shock. 1998; 10 203-212
- 34 Tenner S, Sica G, Hughes M, Noordhoeck E, Feng S, Zinner M, Banks P A. Relationship of necrosis and organ failure in severe acute pancreatitis. Gastroenterology. 1997; 113 899-903
- 35 Wernermann J, Hammarqvist F. Glutamine: a necessary nutrient for the intensive care patient. Int J Colorectal Dis. 1999; 14 137-142
- 36 Windsor A C J, Kanwar S, Li A G K, Barnes E, Guthrie J A, Spark J I, Welsh F, Guillou P J, Reynolds J V. Compared with parenteral nutriion, enteral feeding attenuates the acute response and improves disease severity in acute pancreatitis. Gut. 1998; 42 431-435
Priv.-Doz. Dr. Th. Foitzik
Chirurgische Klinik I
Universitätsklinikum Benjamin Franklin
Freie Universität Berlin
Hindenburgdamm
D-12200 Berlin
Fax: Fax: 0 30/84 45-27 40
Email: e-mail: foitzik@ukbf.fu-berlin.de