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, despite the absence of an obvious source for the infection.[1] It is specifically an infection of the ascitic fluid – an increased volume of peritoneal fluid.[2] Ascites is most commonly a complication of cirrhosis of the liver.[1] It can also occur in patients with nephrotic syndrome.[3][4] SBP has a high mortality rate.[5]

The diagnosis of SBP requires paracentesis, a sampling of the peritoneal fluid taken from the peritoneal cavity.[6] If the fluid contains large numbers of white blood cells known as neutrophils (>250 cells/µL), infection is confirmed and antibiotics will be given, without waiting for culture results.[7] In addition to antibiotics, infusions of albumin are usually administered.[7]

Other life-threatening complications such as kidney malfunction and increased liver insufficiency can be triggered by spontaneous bacterial peritonitis.[8][9] 30%of SBP patients develop kidney malfunction and is one of the strongest predictors for mortality. Where there are signs of this development albumin infusion will also be given.[10]

Spontaneous fungal peritonitis (SFP) can also occur and this can sometimes accompany a bacterial infection.[11]

Signs and symptoms[edit]

Signs and symptoms of spontaneous bacterial peritonitis (SBP) include fevers, chills, nausea, vomiting, abdominal pain and tenderness, general malaise, and worsening ascites.[1] Thirteen percent of patients have no signs or symptoms.[12] In cases of acute or chronic liver failure SBP is one of the main triggers for hepatic encephalopathy, and where there is no other clear causal indication for this, SBP may be suspected.[10]

These symptoms can also be the same for a spontaneous fungal peritonitis (SFP) and therefore make a differentiation difficult. Delay of diagnosis can delay antifungal treatment and lead to a higher mortality rate.[11]

Causes[edit]

SBP is most commonly caused by gram-negative E. coli, followed by Klebsiella. Common gram-positive bacteria identified, include species of Streptococcus and Staphylococcus. The percentage of gram-positive bacteria responsible has been increasing.[7]

A spontaneous fungal infection can often follow a spontaneous bacterial infection that has been treated with antibiotics.[11] The use of antibiotics can result in an excessive growth of fungi in the gut flora which can then translocate into the peritoneal cavity.[13][11] Although fungi are much larger than bacteria, the increased intestinal permeability resulting from advanced cirrhosis makes their translocation easier.[11] SFP is mostly caused by species of Candida and most commonly by Candida albicans.[13]

Pathophysiology[edit]

H2 antagonists and proton-pump inhibitors are medications that decrease or suppress the secretion of acid by the stomach. Their use in treating cirrhosis is associated with the development of SBP.[14][15][16] Bacterial translocation is thought to be the key mechanism for the development of SBP.[12][17] Small intestinal bacterial overgrowth which may be implicated in this translocation, is found in a large percentage of those with cirrhosis.[18] 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.[19]

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.[20] It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.[21] Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.[19]

In nephrotic syndrome SBP can frequently affect children but only very rarely can it affect adults.[22]

Diagnosis[edit]

Infection of the peritoneum causes an inflammatory reaction with a subsequent increase in the number of neutrophils in the fluid.[5] 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][10] 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%.[10]

Prevention[edit]

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

  • Ascitic fluid protein <1.0 g/dL.[20] Patients with fluid protein <15 g/L and either Child-Pugh score of at least 9 or impaired renal function may also benefit.[23]
  • Previous SBP[24]

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

Studies on the use of rifaximin in cirrhotic patients, have suggested that its use may be effective in preventing spontaneous bacterial peritonitis.[26][9]

Treatment[edit]

Antibiotics[edit]

Although there is no high-quality evidence, the third generation cephalosporins are considered the standard empirical treatment for spontaneous bacterial peritonitis in people with cirrhosis.[27] In practice, cefotaxime is the agent of choice for treatment of SBP. After confirmation of SBP, hospital admission is usually advised for observation and intravenous antibiotic therapy. Where there is a risk of kidney malfunction developing in a syndrome called hepatorenal syndrome intravenous albumin is usually administered too. Paracentesis may be repeated after 48 hours to ensure control of infection. After recovery from a single episode of SBP, indefinite prophylactic antibiotics are recommended.[10]

Prokinetics[edit]

The addition of a prokinetic drug to an antibiotic regimen reduces the incidence of spontaneous bacterial peritonitis possibly via decreasing small intestinal bacterial overgrowth.[28]

Intravenous albumin[edit]

A randomized controlled trial found that intravenous albumin on the day of admission and on hospital day 3 can reduce kidney impairment.[29]

Epidemiology[edit]

Patients with ascites underwent routine paracentesis, the incidence of active SBP ranged from 10% to 27% at the time of hospital admission.[30]

History[edit]

SBP was first described in 1964 by Harold O. Conn.[31]

References[edit]

  1. ^ a b c d 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.
  2. ^ Alaniz, C; Regal, RE (April 2009). "Spontaneous bacterial peritonitis: a review of treatment options". P & T : A Peer-reviewed Journal for Formulary Management. 34 (4): 204–10. PMC 2697093. PMID 19561863.
  3. ^ 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.
  4. ^ Teo, S; Walker, A; Steer, A (December 2013). "Spontaneous bacterial peritonitis as a presenting feature of nephrotic syndrome". Journal of Paediatrics and Child Health (Review). 49 (12): 1069–71. doi:10.1111/jpc.12389. PMID 24118585.
  5. ^ a b MacIntosh, T (1 March 2018). "Emergency Management of Spontaneous Bacterial Peritonitis - A Clinical Review". Cureus. 10 (3): e2253. doi:10.7759/cureus.2253. PMC 5929973. PMID 29721399.
  6. ^ 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.
  7. ^ a b c Dever, JB; Sheikh, MY (June 2015). "Review article: spontaneous bacterial peritonitis--bacteriology, diagnosis, treatment, risk factors and prevention". Alimentary Pharmacology & Therapeutics (Review). 41 (11): 1116–31. doi:10.1111/apt.13172. PMID 25819304.
  8. ^ Fernández, J; Bauer, TM; Navasa, M; Rodés, J (December 2000). "Diagnosis, treatment and prevention of spontaneous bacterial peritonitis". Bailliere's Best Practice & Research. Clinical Gastroenterology. 14 (6): 975–990. doi:10.1053/bega.2000.0142. PMID 11139350.
  9. ^ a b Fukui, H; Kawaratani, H; Kaji, K; Takaya, H; Yoshiji, H (2018). "Management of refractory cirrhotic ascites: challenges and solutions". Hepatic Medicine : Evidence and Research. 10: 55–71. doi:10.2147/HMER.S136578. PMC 6039068. PMID 30013405.
  10. ^ a b c d e 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.
  11. ^ a b c d e Shizuma, T (27 February 2018). "Spontaneous bacterial and fungal peritonitis in patients with liver cirrhosis: A literature review". World Journal of Hepatology. 10 (2): 254–266. doi:10.4254/wjh.v10.i2.254. PMC 5838444. PMID 29527261.
  12. ^ a b Koulaouzidis, A; Bhat, S; Saeed, AA (7 March 2009). "Spontaneous bacterial peritonitis". World Journal of Gastroenterology. 15 (9): 1042–9. PMC 2655193. PMID 19266595.
  13. ^ a b Fiore, M; Leone, S (14 September 2016). "Spontaneous fungal peritonitis: Epidemiology, current evidence and future prospective". World Journal of Gastroenterology. 22 (34): 7742–7. doi:10.3748/wjg.v22.i34.7742. PMC 5016373. PMID 27678356.
  14. ^ Gati GA, Deshpande A (2012). "Increased rate of spontaneous bacterial peritonitis among cirrhotic patients receiving pharmacologic acid suppression". Clinical Gastroenterology and Hepatology. 10 (4): 422–27. doi:10.1016/j.cgh.2011.11.019. PMID 22155557.
  15. ^ 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.
  16. ^ 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.
  17. ^ Căruntu, FA; Benea, L (March 2006). "Spontaneous bacterial peritonitis: pathogenesis, diagnosis, treatment". Journal of Gastrointestinal and Liver Diseases : JGLD. 15 (1): 51–6. PMID 16680233.
  18. ^ Maslennikov, R; Pavlov, C; Ivashkin, V (4 October 2018). "Small intestinal bacterial overgrowth in cirrhosis: systematic review and meta-analysis". Hepatology international. doi:10.1007/s12072-018-9898-2. PMID 30284684.
  19. ^ 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.
  20. ^ a b Runyon BA (December 1986). "Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis". Gastroenterology. 91 (6): 1343–6. PMID 3770358.
  21. ^ 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.
  22. ^ Ruiz, S; Soto, S; Rodado, R; Alcaraz, F; López Guillén, E (September 2007). "[Spontaneous bacterial peritonitis as form of presentation of idiophatic nephrotic syndrome in a black adult]". Anales de Medicina Interna (Madrid, Spain : 1984). 24 (9): 442–4. PMID 18198954.
  23. ^ 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.
  24. ^ 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.
  25. ^ Chavez-Tapia, Norberto C.; Barrientos-Gutierrez, Tonatiuh; Tellez-Avila, Felix I.; Soares-Weiser, Karla; Uribe, Misael (2010-09-08). "Antibiotic prophylaxis for cirrhotic patients with upper gastrointestinal bleeding". The Cochrane Database of Systematic Reviews (9): CD002907. doi:10.1002/14651858.CD002907.pub2. ISSN 1469-493X. PMID 20824832.
  26. ^ Goel, A; Rahim, U; Nguyen, LH; Stave, C; Nguyen, MH (December 2017). "Systematic review with meta-analysis: rifaximin for the prophylaxis of spontaneous bacterial peritonitis". Alimentary Pharmacology & Therapeutics. 46 (11–12): 1029–1036. doi:10.1111/apt.14361. PMID 28994123.
  27. ^ Chavez-Tapia, NC; Soares-Weiser, K; Brezis, M; Leibovici, L (21 January 2009). "Antibiotics for spontaneous bacterial peritonitis in cirrhotic patients". The Cochrane Database of Systematic Reviews (1): CD002232. doi:10.1002/14651858.CD002232.pub2. PMID 19160207.
  28. ^ 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.
  29. ^ 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.
  30. ^ Runyon BA (1988). "Spontaneous bacterial peritonitis: an explosion of information". Hepatology. 8 (1): 171–5. doi:10.1002/hep.1840080131. PMID 3338704.
  31. ^ 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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