Sandbox:peritonitis: Difference between revisions
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=== Primary or Spontaneous Peritonitis === | === Primary or Spontaneous Peritonitis === | ||
Primary peritonitis is defined as the presence of polymorphonuclear cells >250/mm3 in ascitic fluid in the absence of an intra-abdominal source of infection or malignancy. | Primary peritonitis is defined as the presence of polymorphonuclear cells >250/mm3 in ascitic fluid in the absence of an intra-abdominal source of infection or malignancy.<ref name="pmid22147550">Wiest R, Krag A, Gerbes A (2012) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=22147550 Spontaneous bacterial peritonitis: recent guidelines and beyond.] ''Gut'' 61 (2):297-310. [http://dx.doi.org/10.1136/gutjnl-2011-300779 DOI:10.1136/gutjnl-2011-300779] PMID: [https://pubmed.gov/22147550 22147550]</ref> | ||
==Classification== | ==Classification== | ||
Revision as of 19:07, 6 January 2017
Definition
Peritonitis defined as the inflammation of the peritoneum from any cause.
Primary or Spontaneous Peritonitis
Primary peritonitis is defined as the presence of polymorphonuclear cells >250/mm3 in ascitic fluid in the absence of an intra-abdominal source of infection or malignancy.[1]
Classification
Peritonitis is classified based on the etiology as follows:[2]
| Peritonitis | |||||||||||||||||||||||||||||||||||||||||
| Primary peritonitis | Secondary peritonitis | Tertiary peritonitis | |||||||||||||||||||||||||||||||||||||||
| ❑ Spontaneous peritonitis ❑ Peritonitis in patients with CAPD ❑ Tuberculous peritonitis | ❑ Peritonitis without evidence for pathogens ❑ Peritonitis with fungi ❑ Peritonitis with low-grade pathogenic bacteria | ||||||||||||||||||||||||||||||||||||||||
| Acute perforation peritonitis ❑ Gastrointestinal perforation ❑ Intestinal ischemia ❑ Pelviperitonitis and other forms | Postoperative peritonitis ❑ Anastomotic leak ❑ Accidental perforation and devascularization | Post-traumatic peritonitis ❑ After blunt abdominal trauma ❑ After penetrating abdominal trauma | |||||||||||||||||||||||||||||||||||||||
Pathogenesis
Peritonitis can be regarded as the localized event after any trigger of inflammation similar to the systemic inflammatory response(SIRS).[3]
Primary peritonitis
As the primary disease (e.g. cirrhosis) progresses, gram negative bacteria increase in numbers in the gut.[4] Once bacteria reach a critical concentration in the gut lumen, they will translocate into the mesenteric lymphatic system because of the failure of the gut to contain bacteria and failure of the immune system to kill the virulent bacteria once they have escaped the gut result in bacteremia and endotoxinemia.
Secondary peritonitis develops perforation of intra abdominal organs when bacteria contaminate the peritoneum as a result of spillage from an intraabdominal viscus. The organisms found almost always constitute a mixed flora in which facultative gram-negative bacilli and anaerobes predominate, especially when the contaminating source is colonic.
Epidemiology
SBP is the most frequent bacterial infection in cirrhosis, accounting for 10-30% of all reported bacterial infections in hospitalised patients.[5][6]
Diagnosis
Identification of risk factors and individualisation of timing and selection of prophylactic measures are the key to success without major development of resistant bacteria.
Prevention
Prophylaxis is of crucial relevance when trying to improve survival.
References
- ↑ Wiest R, Krag A, Gerbes A (2012) Spontaneous bacterial peritonitis: recent guidelines and beyond. Gut 61 (2):297-310. DOI:10.1136/gutjnl-2011-300779 PMID: 22147550
- ↑ Wittmann DH, Schein M, Condon RE (1996). "Management of secondary peritonitis". Ann Surg. 224 (1): 10–8. PMC 1235241. PMID 8678610.
- ↑ Marshall J, Sweeney D (1990) Microbial infection and the septic response in critical surgical illness. Sepsis, not infection, determines outcome. Arch Surg 125 (1):17-22; discussion 22-3. PMID: 2294878
- ↑ Guarner C, Runyon BA, Young S, Heck M, Sheikh MY (1997) Intestinal bacterial overgrowth and bacterial translocation in cirrhotic rats with ascites. J Hepatol 26 (6):1372-8. PMID: 9210626
- ↑ Fernández J, Navasa M, Gómez J, Colmenero J, Vila J, Arroyo V et al. (2002) Bacterial infections in cirrhosis: epidemiological changes with invasive procedures and norfloxacin prophylaxis. Hepatology 35 (1):140-8. DOI:10.1053/jhep.2002.30082 PMID: 11786970
- ↑ Pinzello G, Simonetti RG, Craxì A, Di Piazza S, Spanò C, Pagliaro L (1983) Spontaneous bacterial peritonitis: a prospective investigation in predominantly nonalcoholic cirrhotic patients. Hepatology 3 (4):545-9. PMID: 6862365