Mechanisms of sepsis in acute pancreatitis in opossums

Runkel, N.; Rodriguez, Liliana F.; Moody, Frank G.

doi:10.1016/s0002-9610(99)80142-1

Cited by 40 publications

(26 citation statements)

References 22 publications

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“…Beger et al [10]and many others [8, 11]have documented the offending organisms recovered from infected necrotizing pancreatitis (table 1) virtually all of which have been gram-negative enteric bacteria, most commonly Escherichia coli. Experimentally, Runkel et al [12]confirmed a similar bacterial spectrum in the opossum model of AP under controlled conditions. The implications of a major breakdown of the gut mucosal defense barrier with subsequent bacterial/endotoxin translocation are not controversial.…”

Section: Mechanisms Of Development Of Bacteriemia/sepsis In Apmentioning

confidence: 85%

“…For years, investigators have proposed that translocation plays the major role in bacterial infections in critically ill patients and in those with severe acute pancreatitis [12, 13, 14, 15]. Runkel et al [5, 12], demonstrated in animal models of AP that there is a substantial loss of gut mucosal integrity with subsequent translocation of bacteria and/or endotoxin as the primary source of infection and sepsis in acute pancreatitis. Enteric bacteria have been consistently recovered from lymph nodes and pancreatic tissue in animals with pancreatitis [12].…”

Section: Mechanisms Of Development Of Bacteriemia/sepsis In Apmentioning

confidence: 99%

“…Runkel et al [5, 12], demonstrated in animal models of AP that there is a substantial loss of gut mucosal integrity with subsequent translocation of bacteria and/or endotoxin as the primary source of infection and sepsis in acute pancreatitis. Enteric bacteria have been consistently recovered from lymph nodes and pancreatic tissue in animals with pancreatitis [12]. Three major mechanisms promote bacterial translocation and the resultant secondary infections: (1) derangement of the indigenous intestinal microflora; (2) damage or dysfunction of the intestinal mucosa causing increased permeability, and (3) impairment of host immunity [13, 14, 16].…”

Section: Mechanisms Of Development Of Bacteriemia/sepsis In Apmentioning

confidence: 99%

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Early Enteral Feeding in Severe Acute Pancreatitis: Can It Prevent Secondary Pancreatic (Super) Infection?

Lehocky

Sarr

2000

Dig Surg

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Sepsis continues to account for a second peak in mortality in patients with severe acute pancreatitis. The prevention of these septic complications and subsequent development of multiple organ dysfunction syndrome remains a major focus for investigators, yet despite considerable clinical and experimental work addressing its etiology, septic complications remain high. Several studies have been designed to demonstrate the mechanism of origin of these septic complications with an attempt to define strategies for their prevention to improve patient outcomes. There is clear evidence that the origin of this secondary bacterial infection arises from enteric bacterial translocation secondary to disruption of the gut mucosal barrier during acute pancreatitis. Strategies designed to prevent secondary pancreatic infection include aggressive fluid resuscitation to maximize organ perfusion, early systemic antibiotic treatment or selective gut decontamination, and recently attempts to block mediators of the systemic inflammatory response. This discussion will summarize our present understanding of the etiopathogenesis of secondary bacterial ‘superinfection’ of necrotizing pancreatitis and how the initiation of enteral feeding early in the course of acute pancreatitis may prove to be an effective means of preventing and/or reversing the breakdown of the gut mucosal defense barrier.

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Section: Mechanisms Of Development Of Bacteriemia/sepsis In Apmentioning

confidence: 85%

Section: Mechanisms Of Development Of Bacteriemia/sepsis In Apmentioning

confidence: 99%

Section: Mechanisms Of Development Of Bacteriemia/sepsis In Apmentioning

confidence: 99%

See 1 more Smart Citation

Early Enteral Feeding in Severe Acute Pancreatitis: Can It Prevent Secondary Pancreatic (Super) Infection?

Lehocky

Sarr

2000

Dig Surg

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“…Increased pancreatic exocrine secretion, 23 increased bile acid concentrations in pancreatic juice, 24 decreased myoelectric activity of the duodenum and the sphincter of Oddi, 25 and increased bacterial translocation from the gut and endotoxemia 26,27 are among the changes that follow biliary obstruction. Interestingly, none of these isolated factors caused severe necrotizing pancreatitis when it was experimentally combined with PDO.…”

Section: Discussionmentioning

confidence: 99%

Reticuloendothelial System Blockade Promotes Progression from Mild to Severe Acute Pancreatitis in the Opossum

Schleicher¹,

Baas²,

Elser³

et al. 2001

Annals of Surgery

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ObjectiveTo examine the relation between hepatic reticuloendothelial system (RES) dysfunction and the development of acute biliary pancreatitis. In an opossum model, the authors tested the hypothesis that RES blockade can turn the mild pancreatitis seen after pancreatic duct obstruction (PDO) into the severe form. Summary Background DataBiliary obstruction is considered the decisive event in gallstone pancreatitis. Suppression of the RES occurs during biliary obstruction. MethodsEighteen opossums were placed into three groups of six animals each: group A, RES blockade with -carrageenan; group B, PDO; and group C, PDO and RES blockade with carrageenan. The severity of pancreatitis was evaluated by enzyme serum levels and percentage of pancreatic tissue necrosis. RES capacity was measured by dynamic liver scintigraphy, and hepatic blood flow was documented using the hydrogen clearance technique. ResultsNo changes in hepatic blood flow occurred in groups A to C. RES capacity was suppressed in groups A and C; in group B, RES function remained unchanged. In group A, amylase and lipase levels remained normal, 3 Ϯ 1.9% of pancreatic tissue were necrotic. The animals in group B developed mild edematous pancreatitis with an increase in amylase and lipase levels and 15 Ϯ 10% of pancreatic necrosis. In group C, amylase and lipase increased significantly and histology revealed severe necrotizing pancreatitis, with 72 Ϯ 11% of necrotic areas. ConclusionsArtificial RES blockade can promote the progression from mild pancreatitis as observed after PDO to the severe necrotizing form of the disease. Thus, RES dysfunction resulting from biliary obstruction might be an important cofactor in the pathogenesis of bile-induced pancreatitis.Acute biliary pancreatitis is an inflammatory disease that varies in severity and outcome. Mild edematous pancreatitis usually results in morphologic and functional recovery, whereas severe necrotizing pancreatitis is often associated with multisystemic complications and a death rate of 10% to 50%. 1 The reason for this variety in manifestation is not known. The identification of factors determining the severity of acute pancreatitis is essential to improve the understanding of the pathophysiology of bile-induced pancreatitis and its complications.Obstruction of the terminal biliopancreatic ductal system is considered to be the triggering event in human gallstone pancreatitis. Opie, 2 in 1901, postulated that reflux of bile, caused by a gallstone impacted in a common terminal biliopancreatic duct, initiates the process of pancreatic inflammation. Today, most authors disagree with this socalled common channel theory, and not reflux of bile but simultaneous obstruction of the biliary and the pancreatic ducts and their pathophysiologic consequences are considered to be the determining factors in the development of severe pancreatitis.

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“…Bár tény, hogy a hasnyálmirigyet érintő másodlagos infekciók fő forrását a bélből származó, transz lokálódott baktériumok jelentik, mind a mai napig ismeretlen, hogy a mikroorganizmusok pontosan milyen útvonalon jutnak a hasnyálmirigybe. A klinikai és kísérle-tes eredmények szerint az intestinalis baktériumok haematogen [39], lymphogen [40], kontaminálódott epén keresztül vagy transmuralis úton is a hasnyálmirigybe kerülhetnek [41]. Ezt a megfi gyelést megerősíti, hogy a hasnyálmirigy fertőzéseit okozó baktériumok között elsősorban enteralis mikroorganizmusok találhatóak, pél-dául Escherichia coli és Klebsiella speciesek [40,42].…”

Section: áBraunclassified

Bacterial translocation: gap in the shield

et al. 2014

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A gastrointestinalis traktus a táplálék feldolgozásában betöltött emésztő-, illetve felszívófunkcióján túl kiemelkedő jelentőséggel bír a béllumenben lévő patogénekkel szemben, megakadályozva azok keringésbe jutását, és fontos szerepet játszik az immunhomeosztázis fenntartásában. Bakteriális transzlokáció alatt a gyomor-bél rendszer életképes baktériumainak vagy bakteriális termékeinek különböző, extraintestinalis szövetekbe jutása értendő. A kóros jelensé-get számos klinikai kórkép kapcsán azonosították. A bakteriális transzlokáció kialakulására prediszponáló, alapvető feltételek közé tartozik a bél mikrofl órájának megváltozása, a nyálkahártya-integritás sérülése, valamint a gazdaszervezet immunhiányos állapota. A bakteriális transzlokáció fellépése megnövekedett szövődményekkel és mortalitási rátával párosul, ezért a jövőben fontos mérlegelendő szempontot kell képeznie a kockázati csoportba tartozó betegek terápiás algoritmusának felállítása során Orv. Hetil., 2014, 155(8), 304-312.Kulcsszavak: bélfl óra, bakteriális transzlokáció, szepszis, bélrendszer Bacterial translocation: gap in the shieldThe gastrointestinal tract is not only regarded as a system where nutrient absorption takes place, but also as a vital barrier against intraluminal pathogens entering the circulation and the maintenance of immune homeostasis. Bacterial translocation is defi ned as the penetration of viable bacteria or bacterial compounds from the gastrointestinal tract to extraintestinal sites. This disorder has been described in several clinical conditions. The main promoting factors for bacterial translocation have been proposed to be changes in the intestinal microfl ora, mucosal barrier failure and defects in host immunity. The presence of bacterial translocation has been associated with higher complications and mortality rates; therefore it should be taken into account in the therapeutic strategies of patients with predisposing factors. Keywords: intestinal fl ora, bacterial translocation, sepsis, gutRosero, O., Kovács, T., Ónody, P., Harsányi, L., Szijártó, A. [Bacterial translocation: gap in the shield]. Orv. Hetil., 2014, 155(8), 304-312. (Beérkezett: 2013 elfogadva: 2014. január 9.) Rövidítések AKI = (acute kidney injury) akut vesekárosodás; ARDS = (acute respiratory distress syndrome) akut légzési elégtelenség; CARS = (compensatory anti-infl ammatory response syndrome) kompenzatorikus antiinfl ammatorikus válasz; GALT = (gut associated lymphoid tissue) bélhez kapcsolódó limfoid szövet; MODS = (multiple organ dysfunction syndrome) több-szervi működészavar; MOF = (multiple organ failure) több-szervi elégtelenség; NO = nitrogén-monoxid; SIRS = (sistemic infl ammatory response syndrome) szisztémás gyulladásos vá-lasz szindróma; TPN = (total parenteral nutrition) teljes parenteralis táplálás A gastrointestinalis traktus a tápanyagok felszívódásán túl alapvető szerepet játszik az endokrin, az anyagcsereés az immunológiai homeosztázis biztosításában. A táplálék számos komponensű mikrofl órája révén az emésztőtraktus és nyirok...

show abstract

Mechanisms of sepsis in acute pancreatitis in opossums

Cited by 40 publications

References 22 publications

Early Enteral Feeding in Severe Acute Pancreatitis: Can It Prevent Secondary Pancreatic (Super) Infection?

Early Enteral Feeding in Severe Acute Pancreatitis: Can It Prevent Secondary Pancreatic (Super) Infection?

Reticuloendothelial System Blockade Promotes Progression from Mild to Severe Acute Pancreatitis in the Opossum

Bacterial translocation: gap in the shield

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