Sandbox:peritonitis: Difference between revisions

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| '''SBP culture postive'''
| '''SBP culture postive'''
| PMNs ≥250 cells/mm3 and culture positivity Patients with cirrhosis and ascites in the presence or absence of symptoms and signs
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* PMNs ≥250 cells/mm3 and culture positivity  
 
* Patients with cirrhosis and ascites in the presence or absence of symptoms and signs
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|'''Culture-negative neutrocytic ascites'''(CNNA) or culture-negative SBP
|'''Culture-negative neutrocytic ascites'''(CNNA) or culture-negative SBP
| PMNs ≥250 cells/mm3 Poor culture technique and negative culture prior antibiotics or low opsonic activity in ascitic fluid. Commonly encountered phenotype and requires antibiotic therapy
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* PMNs ≥250 cells/mm3 and culture negativity
* Poor culture technique and prior antibiotics or low opsonic activity in ascitic fluid. Commonly encountered phenotype and requires antibiotic therapy
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| '''Monomicrobial bacterascites'''
| '''Monomicrobial bacterascites'''
| PMNs <250 cells/mm3 and Positive culture Ascitic fluid infection which may resolve spontaneously or progress to SBP. Similar mortality to SBP and should be treated the same
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* PMNs <250 cells/mm3 and culture positivity
* Ascitic fluid infection which may resolve spontaneously or progress to SBP. Similar mortality to SBP and should be treated the same
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Revision as of 02:58, 9 January 2017


Definition

Peritonitis defined as the inflammation of the peritoneum from any cause which lines abdominal cavity and the internal organs as a serosal membrane. Contrast to peritonitis, Intrabdominal infection is defined as the inflammation of peritoneum due to infectious cause.

Primary or Spontaneous Peritonitis

Primary peritonitis is defined as the infection of the peritoneal cavity which is spontaneous and often associated with liver disease and ascites. It is also known as spontaneous bacterial peritonitis.[1] Primary peritonitis lacks an identifiable anatomical derangement.[2]

Secondary Peritonitis

Secondary peritonitis is defined as the infection of the peritoneum due to spillage of organisms into the peritoneal cavity resulting from hollow viscus perforation, anastomotic leak, ischemic necrosis, or other injuries of the gastrointestinal tract.[3]

Tertiary Peritonitis

Tertiary peritonitis is defined as the persistant or recurrent intra-abdominal infection that occur in ≥48 hours following the successful and adequate surgical source control of primary or secondary peritonitis.[3][4][5]


Bacterascitis

Bacterascites is defined as the presence of culture positivity without increase in PMN count in the ascitic fluid.[6]

Historical Perspective

The first reports describing this entity appeared in the German and French literatures between 1907 and 1958.

Classification

Peritonitis is classified based on the etiology as follows:[7]

 
 
 
 
 
 
 
 
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).[8]

Primary peritonitis

As the primary disease (e.g. cirrhosis) progresses, gram negative bacteria increase in numbers in the gut.[9] 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.

Causes

Common Causes

Primary Peritonitis Secondary Peritonitis Tertiary Peritonitis
  • Cirrhosis with ascitis
  • Portal hypertension with ascitis
  • Renal failure patient with continuous ambulatory peritoneal dialysis (CAPD)
  • Ruptured gastric ulcer, appendicular abscess or diverticular abscess
  • Inflamatory bowel diseases such as chron's disease or ulcerative colitis with toxic megacolon
  • Pelvic inflamatory disease
  • Recent surgical procedures
  • Recent trauma to the abdomen (e.g. Stab injury or gun shot injury)


Epidemiology

SBP is the most frequent bacterial infection in cirrhosis, accounting for 10-30% of all reported bacterial infections in hospitalised patients.[10][11]

The prevalence of SBP in outpatient setting asymptomatically is low (< 3.5% ), but the prevalence increases to 8%-36% in the nosocomial setting.[12][13]

Mortality rate for the first episode of SBP in in-patient setting varies between 10-50%, depending upon the risk factors.[11][14] One-year mortality after a first episode of SBP has been reported to be 31% and 93%.

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.[1]

Varient of Spontaneous bacterial peritonitis (SBP) Ascitic fluid analysis and other information
SBP culture postive
  • PMNs ≥250 cells/mm3 and culture positivity
  • Patients with cirrhosis and ascites in the presence or absence of symptoms and signs
Culture-negative neutrocytic ascites(CNNA) or culture-negative SBP
  • PMNs ≥250 cells/mm3 and culture negativity
  • Poor culture technique and prior antibiotics or low opsonic activity in ascitic fluid. Commonly encountered phenotype and requires antibiotic therapy
Monomicrobial bacterascites
  • PMNs <250 cells/mm3 and culture positivity
  • Ascitic fluid infection which may resolve spontaneously or progress to SBP. Similar mortality to SBP and should be treated the same


Treatment

Primary Peritonitis

The flora of primary peritonitis is typically monomicrobial.

Secondary Peritonitis

Treatment of secondary peritonitis depends on the etiological factor and effective therapy includes cause specific surgical intervention and adjunctive antibiotic therapy.[5]

Prevention

Prophylaxis is of crucial relevance when trying to improve survival.[1]

References

  1. 1.0 1.1 1.2 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
  2. Mishra SP, Tiwary SK, Mishra M, Gupta SK (2014) An introduction of Tertiary Peritonitis. J Emerg Trauma Shock 7 (2):121-3. DOI:10.4103/0974-2700.130883 PMID: 24812458
  3. 3.0 3.1 Calandra T, Cohen J, International Sepsis Forum Definition of Infection in the ICU Consensus Conference (2005) The international sepsis forum consensus conference on definitions of infection in the intensive care unit. Crit Care Med 33 (7):1538-48. PMID: 16003060
  4. Evans HL, Raymond DP, Pelletier SJ, Crabtree TD, Pruett TL, Sawyer RG (2001) Tertiary peritonitis (recurrent diffuse or localized disease) is not an independent predictor of mortality in surgical patients with intraabdominal infection. Surg Infect (Larchmt) 2 (4):255-63; discussion 264-5. DOI:10.1089/10962960152813296 PMID: 12593701
  5. 5.0 5.1 Nathens AB, Rotstein OD, Marshall JC (1998) Tertiary peritonitis: clinical features of a complex nosocomial infection. World J Surg 22 (2):158-63. PMID: 9451931
  6. Castellote J, Girbau A, Maisterra S, Charhi N, Ballester R, Xiol X (2008) Spontaneous bacterial peritonitis and bacterascites prevalence in asymptomatic cirrhotic outpatients undergoing large-volume paracentesis. J Gastroenterol Hepatol 23 (2):256-9. DOI:10.1111/j.1440-1746.2007.05081.x PMID: 17683477
  7. Wittmann DH, Schein M, Condon RE (1996). "Management of secondary peritonitis". Ann Surg. 224 (1): 10–8. PMC 1235241. PMID 8678610.
  8. 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
  9. 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
  10. 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
  11. 11.0 11.1 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
  12. Jeffries MA, Stern MA, Gunaratnam NT, Fontana RJ (1999) Unsuspected infection is infrequent in asymptomatic outpatients with refractory ascites undergoing therapeutic paracentesis. Am J Gastroenterol 94 (10):2972-6. DOI:10.1111/j.1572-0241.1999.01445.x PMID: 10520854
  13. Conn HO, Fessel JM (1971) Spontaneous bacterial peritonitis in cirrhosis: variations on a theme. Medicine (Baltimore) 50 (3):161-97. PMID: 4938274
  14. Nobre SR, Cabral JE, Gomes JJ, Leitão MC (2008) In-hospital mortality in spontaneous bacterial peritonitis: a new predictive model. Eur J Gastroenterol Hepatol 20 (12):1176-81. DOI:10.1097/MEG.0b013e32830607a2 PMID: 18941414