Acute pancreatic necrosis complicated by infection and gastro-intestinal translocation: pathogenesis correlation and therapeutic implication

The authors define pathogenetics correlations as a acute necrotizing pancreatitis complicated by infection and bacterial translocation. Acute necrotizing pancreatitis infection occurs for gastrointestinal bacterial translocation due to structural and functional modifications of intestinal mucosa. These modifications are results of mucosa ischemic-reperfusion system caused by systemic emodynamic instability in micro- and macro-circulation of splanchnic district. Emodynamic systemic instability has a central role in different multiple physiopathologic phenomena (ipovolemic shock; pancreatic shock, SIRS), which is caused by acute pancreatic necrosis and carries to common way established by severe systemics emodinamics modifications; these changes promote growth of adverse events which conduce by means of process previously described to bacterial translocation and infection of acute pancreatic necrosis. Indeed, emodynamic systemic instability of any etiology, can determine for one way bacterial translocation and on the other acute ischemic pancreatitis; both phenomena concur lead to cause beginning of acute necrotizing pancreatitis complicated by infection. The authors confirm that improved knowledge of acute pancreatic necrosis complicated by infection and own pathogenetic correlations with bacterial translocation, allows the realization of therapeutic measures aimed to prophylaxis of infection of acute pancreatic necrosis. Central emodynamic stability regularization of splanchnic perfusion and antibiotic prophylaxis, have a central role in prophylaxis of infection of acute pancreatic necrosis. Antibiotic is given by systemic (imipenem e.v.) and selective decontamination of gastrointestinal tract (SDD). SDD provides for oral antibiotic prophylaxis (PTA protocol) and systemic antibiotic prophylaxis (cefotaxime and gentamicin), in addition to microbiologic and gastrointestinal monitoring. If on the one hand the role of SDD about mortality reduction is not clear, however, on the other it is well recognized capacity of reduction the intercurrents and pulmonary infections. Other Authors think that SDD is insignificant on early mortality, whereas, is a good option to reduce late and overall mortality of acute pancreatic necrosis complicated by infection.     

Effect of early and late antibiotic treatment in experimental acute pancreatitis in rats

Background The clinical course in acute necrotizing pancreatitis is mainly determined by bacterial infection of pancreatic and peripancreatic necrosis. The effect of two antibiotic regimens for early and late treatment was investigated in the taurocholate model of necrotizing pancreatitis in the rat. Materials and methods Seventy male Wistar rats were divided into five pancreatitis groups (12 animals each) and a sham-operated group (10 animals). Pancreatitis was induced by intraductal infusion of 3% taurocholate under sterile conditions. Animals received two different antibiotic regimes (20 mg/kg imipenem or 20 mg/kg ciprofloxacin plus 20 mg/kg metronidazole) early at 2, 12, 20, and 28 h after induction of pancreatitis or late at 16 and 24 h after induction of pancreatitis or no antibiotics (control). Animals were examined after 30 h for pancreatic and extrapancreatic infection. Results Early and late antibiotic treatment with both regimes could significantly reduce pancreatic infection from 58 to 8–25%. However, extrapancreatic infection was only reduced by early antibiotic therapy. While quinolones also reduced bacterial counts in small and large bowel, imipenem did not. Conclusions In our animal model of necrotizing pancreatitis, early and late treatment with ciprofloxacin/metronidazole and imipenem reduce bacterial infection of the pancreas. Extrapancreatic infection, however, is reduced significantly only by early antibiotic treatment. The effectivity of early antibiotic treatment in the clinical setting should be subject to further investigation with improved study design and sufficient patient numbers.     

Glutamine stabilizes intestinal permeability and reduces pancreatic infection in acute experimental pancreatitis

Intestinal barrier failure and subsequent translocation of bacteria from the gut play a decisive role in the development of systemic infections in severe acute pancreatitis. Glutamine (GLN) has been shown to stabilize gut barrier function and to reduce bacterial translocation in various experimental settings. The aim of this study was to evaluate whether GLN reduces gut permeability and bacterial infection in a model of acute necrotizing pancreatitis. Acute necrotizing pancreatitis was induced in 50 rats under sterile conditions by intraductal infusion of glycodeoxycholic acid and intravenous infusion of cerulein. Six hours after the induction of pancreatitis, animals were randomly assigned to one of two groups: standard total parental nutrition (TPN) or TPN combined with GLN (0.5 g/kg⁻¹/day⁻¹). After 96 hours, the animals were killed. The pancreas was prepared for bacteriologic examination, and the ascending colon was mounted in a Ussing chamber for determination of transmucosal resistance and mannitol flux as indicators of intestinal permeability. Transmucosal resistance was 31% higher in the animals treated with GLN-supplemented TPN compared to the animals given standard TPN. Mannitol flux through the epithelium was decreased by 40%. The prevalence of pancreatic infections was 33% in animals given GLN-enriched TPN as compared to 86% in animals receiving standard TPN (P < 0.05). Adding GLN to standard TPN not only reduces the permeability of the colon but decreases pancreatic infections in acute necrotizing pancreatitis in the rat. This confirms previous reports that GLN decreases bacterial translocation by stabilizing the intestinal mucosal barrier. The present findings provide the first evidence suggesting that stabilizing the intestinal barrier can reduce the prevalence of pancreatic infection in acute pancreatitis and that GLN may be useful in preventing septic complications in clinical pancreatitis.     

急性坏死性胰腺炎并发感染的机理研究

目的观察急性坏死性胰腺炎时肠屏障损伤与细菌移位情况,探讨急性胰腺炎继发感染的机理。方法１５只犬于肠道内定植ＰＵＣ１８质粒菌ＪＭ１０９后,分对照组（ｎ＝７）和急性坏死性胰腺炎组（ＡＮＰ,ｎ＝８）。ＡＮＰ组经主胰管注入牛磺胆酸钠和胰蛋白酶制作ＡＮＰ模型。结果ＡＮＰ组较对照组血胰淀粉酶显著升高（Ｐ＜０．０１）;尿中乳果糖／甘露醇比值高出对照组２～１２倍;空、回、盲肠粘膜及肠内容物中大肠杆菌明显增加（Ｐ＜０．０１）,双歧杆菌、乳酸杆菌明显减少（Ｐ＜０．０１、Ｐ＜０．０５）。对照组犬血培养阴性,除２只犬肠系膜淋巴结培养出细菌外,其余脏器培养均阴性。ＡＮＰ组犬血和脏器细菌培养阳性率均为１００％,且每只犬都能检出术前定植于肠道的质粒菌ＪＭ１０９;胰腺腺泡出血、坏死;肠粘膜绒毛破坏;血浆、回肠组织二胺氧化酶活性下降。结论ＡＮＰ时肠粘膜屏障功能严重受损,发生肠道细菌移位,成为继发性胰腺感染的潜在根源。     

Early enteral feeding in severe acute pancreatitis: can it prevent secondary pancreatic (super) infection?

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.     

Modification of intestinal flora with multispecies probiotics reduces bacterial translocation and improves clinical course in a rat model of acute pancreatitis

BACKGROUND: Infection of pancreatic necrosis by gut bacteria is a major cause of morbidity and mortality in patients with severe acute pancreatitis. Use of prophylactic antibiotics remains controversial. The aim of this experiment was assess if modification of intestinal flora with specifically designed multispecies probiotics reduces bacterial translocation or improves outcome in a rat model of acute pancreatitis. METHODS: Male Sprague-Dawley rats were allocated into 3 groups: (1) controls (sham-operated, no treatment), (2) pancreatitis and placebo, and (3) pancreatitis and probiotics. Acute pancreatitis was induced by intraductal glycodeoxycholate and intravenous cerulein infusion. Daily probiotics or placebo was administered intragastrically from 5 days prior until 7 days after induction of pancreatitis. Tissue and fluid samples were collected for microbiologic and quantitative real-time PCR analysis of bacterial translocation. RESULTS: Probiotics reduced duodenal bacterial overgrowth of potential pathogens (Log(10) colony-forming units [CFU]/g 5.0 +/- 0.7 [placebo] vs 3.5 +/- 0.3 CFU/g [probiotics], P < .05), resulting in reduced bacterial translocation to extraintestinal sites, including the pancreas (5.38 +/- 1.0 CFU/g [placebo] vs 3.1 +/- 0.5 CFU/g [probiotics], P < .05). Accordingly, health scores were better and late phase mortality was reduced: 27% (4/15, placebo) versus 0% (0/13, probiotics), respectively, P < .05. CONCLUSIONS: This experiment supports the hypothesis that modification of intestinal flora with multispecies probiotics results in reduced bacterial translocation, morbidity, and mortality in the course of experimental acute pancreatitis.     

Bacterial translocation and its prevention in acute pancreatitis

In recent years, bacterial translocation from the gut onto pancreatic necrosis has been proposed as the main cause of pancreatic infection and the consequent sepsis. Failure of the intestinal barrier, together with bacterial overgrowth due to motility changes and immunosuppression, constitute the pathways of the continuous pancreatic contamination from bacterial translocation in patients with severe acute pancreatitis. Selective decontamination, by using a combination of oral and intravenous antibiotics, has been reported to decrease the incidence of sepsis and the related mortality. Immunostimulation is another action to be taken to enhance the ability of the immune system to prevent bacterial translocation, by the entrapment and killing, by enterocytes, of the bacteria trying to translocate through the bowel wall. To keep the mucosal barrier function intact is one of the main issues in the prevention of bacterial translocation. This could be achieved by the adequate delivery of oxygen and nutrient supplementation. Enteral nutrition is a key factor, as it has been proven to maintain mucosal integrity, along with preventing deterioration of the immune function of the intestine.     

急性坏死性胰腺炎时肠屏障损害及肠源性细菌和内毒素移位的实验研究

目的 观察急性坏死性胰腺炎（ANP）时肠粘膜屏障的改变和肠源性细菌和内毒素移位。方法 将Wistar大鼠随机分为正常对照组（n=6)、假手术组（n=30)和ANP组（n=39)。采用人工胆汁胰管逆行灌注法制作ANP模型。观察胰腺、小肠病理改变和小肠粘膜上皮细胞间紧密连接（冷冻蚀刻电镜）变化。动态测定血浆D-乳酸、内毒素水平,以及腹腔脏器细菌移位率。结果 ANP后小肠粘膜损伤,皮皮细胞间紧密连接破坏甚至消失,血浆D-乳酸水平上升,发病早期即出现内毒素血症;ANP发生后72h脏器细菌移位率达到59.5%。结论 ANP早期肠粘膜屏障功能受损。导致肠道细菌和内毒素移位,成为全身炎症反应和胰腺继发感染的根源。     

急性坏死性胰腺炎并发感染防治方法的实验研究

目的 观察不同方法对急性坏死性胰腺炎（ＡＮＰ）并发感染的防治效果。方法 用胰管逆行注入法复制犬和大鼠ＡＮＰ模型,将大鼠随机分为非治疗组和中药、微生态、导泻、选择性肠道脱污染（ＳＤＤ）和生长抑素５个治疗组,观察胰、肠组织学、肠上皮细胞间连接结构、肠通透性、肠道菌群、脏器细菌移位率和病死率的变化。结果 中药清胰汤、双歧杆菌合剂和ＳＤＤ能明显改善肠道屏障的肠通透性,减轻细菌移位,降低病死率,单纯导泻效果     

Frequency and time course of pancreatic and extrapancreatic bacterial infection in experimental acute pancreatitis in rats

BACKGROUND: Infectious complications in severe pancreatitis are the main factors determining clinical course and outcome. The taurocholate model for acute necrotizing pancreatitis was evaluated for frequency and time course of pancreatic and extrapancreatic bacterial infection. METHODS: Sixty-five male Wistar rats were divided into 5 groups of 13 animals each. Specimens for bacteriologic examination were taken, and pancreatitis was induced by intraductal infusion of 3% taurocholate under sterile conditions. Animals were killed 8, 16, 24, or 32 hours thereafter, and bacteriologic examination was performed. A control group of animals with intraductal infusion of 0.9% saline solution were killed after 32 hours. RESULTS: There was no significant pancreatic infection in the control group and in the 8-hour group (1 of 13 rats). Sixteen and 24 hours after induction of pancreatitis, infection and inflammation of the pancreas were found in 77% (10 of 13 rats), and after 32 hours pancreatic infection occurred in 69% (9 of 13 rats). Extrapancreatic bacterial infection after 16 hours occurred in the liver (62%), spleen (62%), and mesenteric lymph nodes (46%). Bacteria infecting the pancreas reflected the bacterial spectrum of the large bowel and terminal ileum before induction of pancreatitis (Escherichia coli [77%], Proteus [43%], Enterococcus [37%], and Staphylococcus [23%]). CONCLUSIONS: Pancreatic infection is an early and frequent finding in the taurocholate model of acute necrotizing pancreatitis. Infection occurs between 8 and 16 hours after induction of pancreatitis. The source of infecting bacteria seems to be the large bowel or the terminal ileum. We present a useful model of severe pancreatitis in which to study bacterial translocation, the further route of spread, and therapeutic approaches.     

雷公藤多甙联合生长抑素治疗对大鼠急性坏死性胰腺炎肠道细菌移位的影响

目的 探讨雷公藤多甙联合生长抑素治疗对大鼠急性坏死性胰腺炎(ANP)肠道细菌移位的影响. 方法 逆行胰胆管穿刺注射3.5%牛磺胆酸钠(0.2 ml/100 g)诱导ANP大鼠模型.分为5组:假手术组(SO)、坏死组(ANP)、生长抑素治疗组(ANP+S)、雷公藤多甙治疗组(ANP+T)、雷公藤多甙+生长抑素治疗组(ANP+T+S).术后禁食12 h,不禁水.各组均随机标记6只观察术后生存时间.术后24h,观察血清淀粉酶、血清脂肪酶活性,血浆内毒素水平,脏器细菌培养结果,胰腺和回肠黏膜病理学变化及大鼠存活率. 结果 雷公藤多甙与生长抑素联合治疗ANP大鼠,可以显著降低血清淀粉酶、血清脂肪酶活性;减轻胰腺组织和肠黏膜炎症细胞浸润、水肿;降低血浆内毒素水平和脏器细菌培养阳性率;提高ANP大鼠存活率. 结论 ANP大鼠存在肠道细菌移位;雷公藤多甙联合生长抑素的治疗可减轻ANP大鼠胰腺和肠道损伤,加强肠道的生物学屏障,降低肠源性细菌及内毒素移位发生率,阻止ANP的发展.     

Controlled clinical trial of selective decontamination for the treatment of severe acute pancreatitis.

OBJECTIVE: A randomized, controlled, multicenter trial was undertaken in 102 patients with objective evidence of severe acute pancreatitis to evaluate whether selective decontamination reduces mortality. SUMMARY BACKGROUND DATA: Secondary pancreatic infection is the major cause of death in patients with acute necrotizing pancreatitis. Controlled clinical trials to study the effect of selective decontamination in such patients are not available. METHODS: Between April 22, 1990 and April 19, 1993, 102 patients with severe acute pancreatitis were admitted to 16 participating hospitals. Patients were entered into the study if severe acute pancreatitis was indicated, on admission, by multiple laboratory criteria (Imrie score > or = 3) and/or computed tomography criteria (Balthazar grade D or E). Patients were randomly assigned to receive standard treatment (control group) or standard treatment plus selective decontamination (norfloxacin, colistin, amphotericin; selective decontamination group). All patients received full supportive treatment, and surveillance cultures were taken in both groups. RESULTS: Fifty patients were assigned to the selective decontamination group and 52 were assigned to the control group. There were 18 deaths in the control group (35%), compared with 11 deaths (22%) in the selective decontamination group (adjusted for Imrie score and Balthazar grade: p = 0.048). This difference was mainly caused by a reduction of late mortality (> 2 weeks) due to significant reduction of gram-negative pancreatic infection (p = 0.003). The average number of laparotomies per patient was reduced in patients treated with selective decontamination (p < 0.05). Failure of selective decontamination to prevent secondary gram-negative pancreatic infection with subsequent death was seen in only three patients (6%) and transient gram-negative pancreatic infection was seen in one (2%). In both groups of patients, all gram-negative aerobic pancreatic infection was preceded by colonization of the digestive tract by the same bacteria. CONCLUSION: Reduction of gram-negative colonization of the digestive tract, preventing subsequent pancreatic infection by means of selective decontamination, significantly reduces morbidity and mortality in patients with severe acute necrotizing pancreatitis.     

Effect of platelet-activating factor antagonists (BN-52021, WEB-2170, and BB-882) on bacterial translocation in acute pancreatitis

Bacterial translocation is an important source of pancreas infection in acute pancreatitis. The effect of platelet-activating factor (PAF) in the pathogenesis of acute pancreatitis has been proved in various studies. The aim of this study was to determine whether potent PAF antagonists influence bacterial translocation in acute pancreatitis. Acute pancreatitis was induced in 62 Wistar rats by injection of 2.5% sodium taurocholate into the biliopancreatic duct. The rats treated with PAF factor antagonists received intravenous injection of WEB-2170 (10 mg/kg), lexipafant (5 mg/kg), and BN-52021 (5 mg/kg) 30 minutes before induction of acute pancreatitis. Six hours after induction of acute pancreatitis, bacteriologic cultures and histologic scoring of tissues were performed. There was a statistically significant reduction in bacterial translocation to the mesenteric lymph nodes and liver but not to the pancreas of the rats treated with PAF antagonists. No significant increase in the intestinal bacterial population of any group was found. There were no statistical differences between the pancreatic histologic scores of the groups. PAF antagonists reduced bacterial translocation to distant sites other than the pancreas, preventing the bacterial dissemination that occurs in the early phase of acute pancreatitis and may have beneficial effects on the evolution of this disease.     

Effect of early antibiotic prophylaxis with ertapenem and meropenem in experimental acute pancreatitis in rats

Background  The clinical course in acute necrotizing pancreatitis is mainly influenced by bacterial infection of pancreatic and peripancreatic necrosis. The effect of two antibiotic treatments for early prophylaxis was studied in the taurocholate model of necrotizing pancreatitis in the rat. Methods  Sixty male Sprague-Dawley rats were divided into three pancreatitis groups (15 animals each) and a sham-operated group (15 animals, control group). Pancreatitis was induced by intraductal infusion of 3% taurocholate under sterile conditions. Animals were placed on one of two different antibiotic regimens (15 mg/kg ertapenem or 20 mg/kg meropenem, one shot) after the induction of pancreatitis or received no antibiotics (control). All animals were sacrificed after 24 h to study pancreatic and extrapancreatic infection. Results  Early antibiotic prophylaxis with either erapenam or meropenem significantly decreased pancreatic infection from 12/15 (control group) to 4/15 (ertapenem antibiotic group) and 3/15 (meropenem antibiotic group) (P < 0.05). Conclusions  In our animal model of necrotizing pancreatitis, early antibiotic prophylaxis with ertapenem and meropenem reduced bacterial infection of the pancreas. The efficacy of early antibiotic prophylaxis with ertapenem in the clinical setting should be subject to further research.     

Bacterial translocation and infected pancreatic necrosis in acute necrotizing pancreatitis derives from small bowel rather than from colon

Background

The clinical course of acute necrotizing pancreatitis (ANP) is determined by the superinfection of pancreatic necrosis. To date, the pathophysiology of the underlying bacterial translocation is poorly understood. The present study investigated the bacterial source of translocation.

Methods

A terminal loop ileostomy was applied in rats. Selective digestive decontamination (SDD) of either the small bowel or the colon was performed. After 3 days of SDD, severe ANP was induced. At 24 hours, bacterial translocation was assessed by cultures of bowel mucosa, mesenteric lymph nodes, and pancreas using a scoring system (0-4).

Results

Without SDD, pancreatic infection was present in all cases with an average score of 2.67. Colon SDD reduced pancreatic superinfection to 1.67 (not significant). SDD of the small bowel significantly reduced superinfection to 1.0 (P < .005).

Conclusions

Bacterial translocation from the colon is less frequent than translocation from the small bowel. Thus, the small bowel seems to be the major source of enteral bacteria in infected pancreatic necrosis.     

Bacterial analysis of infected pancreatic necrosis and its prevention (Symposium 8: Pancreatobiliary infection (IHPBA))

In severe acute pancreatitis, sepsis mainly due to pancreatic or peripancreatic infection have emerged as the most serious complications and now accounts for more than 80% of deaths. Collective review of organisms associated with secondary pancreatic infection in patients with acute pancreatitis has revealed that most of them are intestinal flora. Several experimental studies including ours have revealed that acute pancreatitis promotes bacterial translocation (BT), which in turn leads to infection of the pancreas and septic complications. Prophylactic antibiotics given intravenously have been demonstrated to be beneficial in reducing the rate of pancreatic infection, but their survival benefit remains unclear. We have demonstrated that continuous regional arterial infusion (CRAI) of an antibiotic is more effective than intravenous administration in preventing pancreatic infection and improving survival, in a canine model of acute necrotizing pancreatitis. Our recent experimental study has revealed that CRAI of an antibiotic via the superior mesenteric artery (SMA) is effective in mitigating intestinal mucosal damage and preventing BT in acute pancreatitis, thereby improving survival. BT aggravates pancreatic necrosis and remote organ damage in acute pancreatitis, and SMA infusion of antibiotics is effective in preventing BT and is practical for clinical use.     

区域动脉灌注治疗重症急性胰腺炎116例报告

目的为探讨提高重症急性胰腺炎的疗效。方法应用Ｓｅｌｄｉｎｇｅｒ法,置导管于胰腺病变供血动脉内,灌注抑酶制剂和抗生素,以提高进入胰腺组织内的药物浓度,达到控制胰腺病变和预防继发性感染的目的。结果通过１１６例区域动脉灌注的方法和综合疗法,明显减少了坏死胰腺组织的感染,降低了死亡率。结论该法是治疗重症急性胰腺炎的新疗法,特别适合于胰腺早期病变的治疗。     

Effects of combined nutritional therapy on acute necrotizing pancreatitis in rats in the early phase of the disease

The aim of this study was to investigate the influence of a small amount of enteral nutrition along with parenteral nutrition on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats in the early phase of disease. The induction of ANP resulted in a significant increase in mortality rate, intestinal permeability, bacterial infection in the pancreas and extrapancreatic organs, pancreatic necrosis and serum activity of urea and amylase, and a significant decrease in concentrations of calcium, protein and albumin. But no difference was observed between the pancreatitis groups. Significant hyperglycemia and increased liver transaminase activity were observed in rats treated with combined nutritional therapy (CNT). CNT did not improve the course of acute pancreatitis, intestinal permeability, bacterial translocation, or reduce the extent of acinar cell injury in ANP and is therefore unlikely to be of benefit in patients with pancreatitis in the early period.     

Selective bowel decontamination results in gram-positive translocation

Colonization by enteric gram-negative bacteria with subsequent translocation is believed to be a major mechanism for infection in the critically ill patient. Selective bowel decontamination (SBD) has been used to control gram-negative infections by eliminating these potentially pathogenic bacteria while preserving anaerobic and other less pathogenic organisms. Infection with gram-positive organisms and anaerobes in two multivisceral transplant patients during SBD led us to investigate the effect of SBD on gut colonization and translocation. Methods: Twenty-four rats received enteral polymixin E, tobramycin, amphotericin B, and parenteral cefotaxime for 7 days (PTA + CEF); 23 received parenteral cefotaxime alone (CEF), 19 received the enteral antibiotics alone (PTA), 21 controls received no antibiotics. Cecal homogenates, mesenteric lymph node (MLN), liver, and spleen were cultured. Results: Only 8% of the PTA + CEF group had gram-negative bacteria in cecal culture vs 52% CEF, 84% PTA, and 100% in controls. Log Enterococcal colony counts were higher in the PTA + CEF group (8.0 + 0.9) vs controls (5.4 + 0.4) P less than 0.01. Translocation of Enterococcus to the MLN was significantly increased in the PTA + CEF group (67%) vs controls (0%) P less than 0.01. SBD effectively eliminates gram-negative organisms from the gut in the rat model. Overgrowth and translocation of Enterococcus suggests that infection with gram-positive organisms may be a limitation of SBD.     

Pancreatitis and nutrition. Significance of the gastrointestinal tract and nutrition for septic complications

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.