2002
DOI: 10.1159/000064712
|View full text |Cite
|
Sign up to set email alerts
|

Gastric colonisation, intestinal permeability and septic morbidity in acute pancreatitis

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
27
1
5

Year Published

2004
2004
2020
2020

Publication Types

Select...
6
3
1

Relationship

0
10

Authors

Journals

citations
Cited by 40 publications
(33 citation statements)
references
References 32 publications
0
27
1
5
Order By: Relevance
“…In the 1990s, several authors observed a positive correlation between bacterial translocation and IAP in animal models, even when IAP was raised for less than 1 h. This result was caused by increased gut permeability induced by splanchnic ischemia with and without reperfusion [27,28] . The mechanism by which the necrotic pancreas becomes infected is unclear, but experimental and clinical data suggest that the gastrointestinal tract is the likely source of organisms, since intestinal colonization by pathogens often precedes pancreatic infection [29][30][31][32][33] . The gut clearly plays a major role in the development of MODS.…”
Section: Discussionmentioning
confidence: 99%
“…In the 1990s, several authors observed a positive correlation between bacterial translocation and IAP in animal models, even when IAP was raised for less than 1 h. This result was caused by increased gut permeability induced by splanchnic ischemia with and without reperfusion [27,28] . The mechanism by which the necrotic pancreas becomes infected is unclear, but experimental and clinical data suggest that the gastrointestinal tract is the likely source of organisms, since intestinal colonization by pathogens often precedes pancreatic infection [29][30][31][32][33] . The gut clearly plays a major role in the development of MODS.…”
Section: Discussionmentioning
confidence: 99%
“…First, there is compelling evidence that in severe acute pancreatitis gut barrier function is compromised resulting in greater intestinal permeability to bacteria (which may lead to infected necrosis) and endotoxins (which stimulate nitric oxide and cytokine production that contribute to organ failure) (98-100, 179). There is also evidence that there is a higher incidence of gastric colonization with potentially pathogenic enteric bacteria in severe disease that may also contribute to septic complications (130). Because enteral feeding stabilizes gut barrier function, there has been considerable interest in the ability of enteral feeding not only to provide appropriate nutritional support, but also to prevent systemic complications and improve morbidity and mortality.…”
Section: Level Of Evidence: IImentioning
confidence: 99%
“…Microbial contamination of the injured pancreatic tissues is thought to be a consequence of the translocation of viable organisms across the mucosa of the gastrointestinal tract (63). The development of infection may be suggested by fever, leukocytosis, or evidence of persistent or evolving organ dysfunction; however, these manifestations are nonspecific.…”
Section: Grade Cmentioning
confidence: 99%