Secondary peritonitis pathophysiology: Difference between revisions
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{{Secondary peritonitis}} | {{Secondary peritonitis}} | ||
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==Overview== | ==Overview== | ||
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* [[Bowel perforation|Distal small bowel lumen perforation]]: Mostly [[Enterobacteriaceae]] and [[Anaerobic organism|anaerobic organisms]], including the [[Bacteroides]] spp. | * [[Bowel perforation|Distal small bowel lumen perforation]]: Mostly [[Enterobacteriaceae]] and [[Anaerobic organism|anaerobic organisms]], including the [[Bacteroides]] spp. | ||
* [[Colon]]: Mostly anaerobes (e.g. [[Peptostreptococcus]], [[Clostridium|Clostridium,]] and most commonly [[Bacteroides|Bacteroides sis]]) | * [[Colon]]: Mostly anaerobes (e.g. [[Peptostreptococcus]], [[Clostridium|Clostridium,]] and most commonly [[Bacteroides|Bacteroides sis]]) | ||
[[Bacteria]] and [[digestive enzymes]] act on the [[peritoneal]] [[Serosa|serosal]] surface resulting in [[Digestion|enzymatic digestion]], [[necrosis]] and an outpouring of serum [[protein]] and [[Electrolyte|electrolytes]] from the blood into the [[peritoneal cavity]], together with the formation of an exudate rich in [[granulocytes]]. The [[inflammatory process]] may be diffuse or confined to an abscess. Systemically, there is [[Paralytic ileus|paralysis of the bowel]], [[hemoconcentration]], and decrease in the [[cardiac output]] due to the shift of fluids and later [[acidosis]]. Intrapulmonary shunting, [[Hypocapnia|hypo]]/[[hypercapnia]], [[hypoxemia]], [[Azotemia|progressive azotemia]], [[acute tubular necrosis]], [[weight loss]] by [[protein]] consumption, fall of [[body temperature]], loss of heat production, and exhaustion are other complications that may lead to the death of the patient if the process is not interrupted. | [[Bacteria]] and [[digestive enzymes]] act on the [[peritoneal]] [[Serosa|serosal]] surface resulting in [[Digestion|enzymatic digestion]], [[necrosis]] and an outpouring of serum [[protein]] and [[Electrolyte|electrolytes]] from the blood into the [[peritoneal cavity]], together with the formation of an exudate rich in [[granulocytes]]. The [[inflammatory process]] may be diffuse or confined to an [[abscess]]. Systemically, there is [[Paralytic ileus|paralysis of the bowel]], [[hemoconcentration]], and decrease in the [[cardiac output]] due to the shift of fluids and later [[acidosis]]. Intrapulmonary shunting, [[Hypocapnia|hypo]]/[[hypercapnia]], [[hypoxemia]], [[Azotemia|progressive azotemia]], [[acute tubular necrosis]], [[weight loss]] by [[protein]] consumption, fall of [[body temperature]], loss of heat production, and exhaustion are other complications that may lead to the death of the patient if the process is not interrupted. | ||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
[[Category:Emergency mdicine]] | |||
[[Category:Disease]] | |||
[[Category:Up-To-Date]] | |||
[[Category:Infectious disease]] | |||
[[Category:Gastroenterology]] | |||
[[Category:Surgery]] |
Latest revision as of 00:07, 30 July 2020
Secondary Peritonitis Microchapters |
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Secondary peritonitis pathophysiology On the Web |
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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
Secondary bacterial peritonitis is caused by inoculation of bacteria from the (GI lumen or during surgical procedures) in the peritoneal cavity.
Pathophysiology
- Bacteria can reach the peritoneal cavity by a variety of pathologic processes:
- The initial inoculum of bacteria is determined by the normal flora in the involved portion of the GI tract.
Flora
Microbial organisms causing 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 spp.
- Colon: Mostly anaerobes (e.g. Peptostreptococcus, Clostridium, and most commonly Bacteroides sis)
Bacteria and digestive enzymes act on the peritoneal serosal surface resulting in enzymatic digestion, necrosis and an outpouring of serum protein and electrolytes from the blood into the peritoneal cavity, together with the formation of an exudate rich in granulocytes. The inflammatory process may be diffuse or confined to an abscess. Systemically, there is paralysis of the bowel, hemoconcentration, and decrease in the cardiac output due to the shift of fluids and later acidosis. Intrapulmonary shunting, hypo/hypercapnia, hypoxemia, progressive azotemia, acute tubular necrosis, weight loss by protein consumption, fall of body temperature, loss of heat production, and exhaustion are other complications that may lead to the death of the patient if the process is not interrupted.
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.