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Spontaneous bacterial peritonitis

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Spontaneous bacterial peritonitis
SpecialtyGastroenterology Edit this on Wikidata

Spontaneous bacterial peritonitis (SBP) is the development of a bacterial infection in the peritoneum causing peritonitis, despite the absence of an obvious source for the infection.[1] It occurs almost exclusively in people with portal hypertension (increased pressure over the portal vein), usually as a result of cirrhosis of the liver.[1] It can also occur in patients with nephrotic syndrome.[2][3]

The diagnosis of SBP requires paracentesis (aspiration of fluid with a needle) from the abdominal cavity.[4] If the fluid contains bacteria or large numbers of neutrophil granulocytes (>250 cells/µL) (a type of white blood cells), infection is confirmed and antibiotics are required to avoid complications. In addition to antibiotics, infusions of albumin are usually administered.

Signs and symptoms

Symptoms include fevers, chills, nausea, vomiting, abdominal tenderness and general malaise.[1] Patients may complain of abdominal pain and worsening ascites.[1] Thirteen percent of patients have no signs or symptoms.[5] Hepatic encephalopathy may be the only manifestation of SBP; in the absence of a clear precipitant for the encephalopathy, all patients should undergo paracentesis, or sampling of the ascites fluid, in order to assess for SBP.

Pathogenesis

SBP is thought to result from a combination of factors inherent in cirrhosis and ascites, such as prolonged bacteremia secondary to compromised host defenses, intrahepatic shunting of colonized blood, and defective bactericidal activity within the ascitic fluid.[6] Pharmacologic acid suppression has also been associated with SBP in patients with advanced cirrhosis.[7][8][9] Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.[10]

With respect to compromised host defenses, patients with severe acute or chronic liver disease are often deficient in complement and may also have malfunctioning of the neutrophilic and reticuloendothelial systems.[11]

As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations.[12] It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.[13] Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.[11]

Diagnosis

Diagnosis is made by paracentesis (needle aspiration of the ascitic fluid). SBP is diagnosed if the fluid contains neutrophils (a type of white blood cell) at greater than 250 cells per mm³ (equals a cell count of 250 x106/L) fluid in the absence of another reason for this (such as inflammation of one of the internal organs or a perforation).[1][14] The fluid is also cultured to identify bacteria. If the sample is sent in a plain sterile container 40% of samples will identify an organism, while if the sample is sent in a bottle with culture medium the sensitivity increases to 72-90%.[14]

Prevention

All people with cirrhosis might benefit from antibiotics (oral fluoroquinolone norfloxacin) if:

  • Ascitic fluid protein <1.0 g/dL.[12] Patients with fluid protein <15 g/L and either Child-Pugh score of at least 9 or impaired renal function may also benefit.[15]
  • Previous SBP[16]

People with cirrhosis admitted to the hospital should receive prophylactic antibiotics if:

Treatment

Antibiotics

After confirmation of SBP, patients need hospital admission for intravenous antibiotics. They will often also receive intravenous albumin. A repeat paracentesis in 48 hours is sometimes performed to ensure control of infection. Once patients have recovered from SBP, they require regular prophylactic antibiotics as long as they still have ascites.[citation needed]

Prokinetics

The addition of a prokinetic drug to an antibiotic regime reduces the incidence of spontaneous bacterial peritonitis possibly via decreasing small intestinal bacterial overgrowth.[18]

Intravenous albumin

A randomized controlled trial found that intravenous albumin on the day of admission and on hospital day 3 can reduce renal impairment.[19]

Epidemiology

Patients with ascites underwent routine paracentesis, the incidence of active SBP ranged from 10% to 27% at the time of hospital admission.[20]

History

SBP was first described in 1964 by Prof Harold O. Conn.[21]

References

  1. ^ a b c d e Lata J, Stiburek O, Kopacova M (November 2009). "Spontaneous bacterial peritonitis: a severe complication of liver cirrhosis". World J. Gastroenterol. 15 (44): 5505–10. doi:10.3748/wjg.15.5505. PMC 2785051. PMID 19938187.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  2. ^ Hingorani SR, Weiss NS, Watkins SL (August 2002). "Predictors of peritonitis in children with nephrotic syndrome". Pediatr. Nephrol. 17 (8): 678–82. doi:10.1007/s00467-002-0890-6. PMID 12185481.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  3. ^ Chuang TF, Kao SC, Tsai CJ, Lee CC, Chen KS (January 1999). "Spontaneous bacterial peritonitis as the presenting feature in an adult with nephrotic syndrome". Nephrol. Dial. Transplant. 14 (1): 181–2. doi:10.1093/ndt/14.1.181. PMID 10052502.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  4. ^ Rimola A, García-Tsao G, Navasa M, et al. (January 2000). "Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus document. International Ascites Club". J. Hepatol. 32 (1): 142–53. doi:10.1016/S0168-8278(00)80201-9. PMID 10673079.
  5. ^ Koulaouzidis A, Bhat S, Saeed AA (March 2009). "Spontaneous bacterial peritonitis". World J. Gastroenterol. 15 (9): 1042–9. doi:10.3748/wjg.15.1042. PMC 2655193. PMID 19266595.{{cite journal}}: CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  6. ^ Runyon BA, Hoefs JC (1984). "Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis". Hepatology. 4 (6): 1209–11. doi:10.1002/hep.1840040619. PMID 6500513.
  7. ^ Gati GA, Deshpande A (2012). "Increased rate of spontaneous bacterial peritonitis among cirrhotic patients receiving pharmacologic acid suppression". Clinical Gastroenterology and Hepatology. 4 (4): 422–27. doi:10.1016/j.cgh.2011.11.019. PMID 22155557.
  8. ^ Deshpande A, Pasupuleti V (2012). "Acid suppressive therapy is associated with spontaneous bacterial peritonitis in cirrhotic patients: a meta-analysis". Journal of Gastroenterology and Hepatology. 28 (2): 235–42. doi:10.1111/jgh.12065. PMID 23190338.
  9. ^ Bajaj JS, Zadvornova Y (2009). "Association of Proton Pump Inhibitor Therapy With Spontaneous Bacterial Peritonitis in Cirrhotic Patients With Ascites". American Journal of Gastroenterology. 104 (5): 1130–34. doi:10.1038/ajg.2009.80. PMID 19337238.
  10. ^ Runyon BA (1988). "Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis". Hepatology. 8 (3): 632–5. doi:10.1002/hep.1840080332. PMID 3371881.
  11. ^ a b Alaniz C, Regal RE (April 2009). "Spontaneous Bacterial Peritonitis: A Review of Treatment Options". P T. 34 (4): 204–210. PMC 2697093. PMID 19561863.
  12. ^ a b Runyon BA (December 1986). "Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis". Gastroenterology. 91 (6): 1343–6. PMID 3770358.
  13. ^ Runyon BA, Morrissey RL, Hoefs JC, Wyle FA (1985). "Opsonic activity of human ascitic fluid: a potentially important protective mechanism against spontaneous bacterial peritonitis". Hepatology. 5 (4): 634–7. doi:10.1002/hep.1840050419. PMID 4018735.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ a b Moore KP, Aithal GP (October 2006). "Guidelines on the management of ascites in cirrhosis". Gut. 55 Suppl 6: vi1–12. doi:10.1136/gut.2006.099580. PMC 1860002. PMID 16966752.
  15. ^ Fernández J, Navasa M, Planas R, et al. (2007). "Primary prophylaxis of spontaneous bacterial peritonitis delays hepatorenal syndrome and improves survival in cirrhosis". Gastroenterology. 133 (3): 818–24. doi:10.1053/j.gastro.2007.06.065. PMID 17854593.
  16. ^ Grangé JD, Roulot D, Pelletier G, et al. (1998). "Norfloxacin primary prophylaxis of bacterial infections in cirrhotic patients with ascites: a double-blind randomized trial". J. Hepatol. 29 (3): 430–6. doi:10.1016/S0168-8278(98)80061-5. PMID 9764990.
  17. ^ Soares-Weiser K, Brezis M, Tur-Kaspa R, Leibovici L (2002). Soares-Weiser, Karla (ed.). "Antibiotic prophylaxis for cirrhotic patients with gastrointestinal bleeding". Cochrane database of systematic reviews (Online) (2): CD002907. doi:10.1002/14651858.CD002907. PMID 12076458.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ Hiyama, T.; Yoshihara, M.; Tanaka, S.; Haruma, K.; Chayama, K. (Apr 2009). "Effectiveness of prokinetic agents against diseases external to the gastrointestinal tract". J Gastroenterol Hepatol. 24 (4): 537–46. doi:10.1111/j.1440-1746.2009.05780.x. PMID 19220673.
  19. ^ Sort P, Navasa M, Arroyo V, et al. (1999). "Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis". N. Engl. J. Med. 341 (6): 403–9. doi:10.1056/NEJM199908053410603. PMID 10432325.
  20. ^ Runyon BA (1988). "Spontaneous bacterial peritonitis: an explosion of information". Hepatology. 8 (1): 171–5. doi:10.1002/hep.1840080131. PMID 3338704.
  21. ^ CONN HO (April 1964). "Spontaneous peritonitis and bacteremia in Laennec's cirrhosis caused by enteric organisms. A relatively common but rarely recognized syndrome" (PDF). Ann. Intern. Med. 60 (4): 568–80. doi:10.7326/0003-4819-60-4-568. PMID 14138877.
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