Secondary peritonitis pathophysiology: Difference between revisions
Jump to navigation
Jump to search
(→Flora) |
|||
Line 17: | Line 17: | ||
==References== | ==References== | ||
{{Reflist|2}} |
Revision as of 22:35, 4 February 2017
Secondary Peritonitis Microchapters |
Diagnosis |
Treatment |
Secondary peritonitis pathophysiology On the Web |
American Roentgen Ray Society Images of Secondary peritonitis pathophysiology |
Directions to Hospitals Treating Spontaneous bacterial peritonitis |
Risk calculators and risk factors for Secondary peritonitis pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2]
Overview
Pathophysiology
- Bacteria can reach the peritoneal cavity by a variety of pathologic processes:
- Transmural inflammation with luminal obstruction,
- Perforation of the GI tract, and
- Intestinal ischemia.
- The initial inoculum of bacteria is determined by the normal flora in the involved portion of the GI tract.
Flora
Microbial cause of secondary peritonitis depends on the site of the gut perforation.[1]
- Small bowel perforation: Consist mainly of enterococci and Escherichia coli
- Distal small bowel lumen perforation: Mostly Enterobacteriaceae and anaerobic organisms, including the Bacteroides sps.
- Colon: Mostly anaerobes (e.g. Peptostreptococcus, Clostridium, and most commonly Bacteroides sps)
References
- ↑ Wong PF, Gilliam AD, Kumar S, Shenfine J, O'Dair GN, Leaper DJ (2005). "Antibiotic regimens for secondary peritonitis of gastrointestinal origin in adults". Cochrane Database Syst Rev (2): CD004539. doi:10.1002/14651858.CD004539.pub2. PMID 15846719.