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Spontaneous Bacterial Peritonitis

  • Author: Thomas E Green, DO, MPH, FACOEP, FACEP; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
 
Updated: Jun 15, 2016
 

Background

Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection of ascitic fluid. Generally, no source of the infecting agent is easily identifiable, but contamination of dialysate can cause the condition among those receiving peritoneal dialysis (PD).

Spontaneous bacterial peritonitis occurs in both children and adults and is a well-known and ominous complication in patients with cirrhosis.[1]  Of patients with cirrhosis who have spontaneous bacterial peritonitis, 70% are Child-Pugh class C. In these patients, the development of spontaneous bacterial peritonitis is associated with a poor long-term prognosis.

Once thought to occur only in those individuals with alcoholic cirrhosis, spontaneous bacterial peritonitis is now known to affect patients with cirrhosis from any cause. In addition, spontaneous bacterial peritonitis can occur as a complication of any disease state that produces the clinical syndrome of ascites, such as heart failure and Budd-Chiari syndrome. Children with nephrosis or systemic lupus erythematosus who have ascites have a high risk of developing spontaneous bacterial peritonitis.

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Pathophysiology

The mechanism for bacterial inoculation of ascites has been the subject of much debate since Harold Conn first recognized the disorder in the 1960s. Enteric organisms have traditionally been isolated from more than 90% of infected ascites fluid in spontaneous bacterial peritonitis, suggesting that the GI tract is the source of bacterial contamination.

The preponderance of enteric organisms, in combination with the presence of endotoxin in ascitic fluid and blood, once favored the argument that spontaneous bacterial peritonitis was due to direct transmural migration of bacteria from an intestinal or hollow organ lumen, a phenomenon called bacterial translocation. However, experimental evidence suggests that direct transmural migration of microorganisms might not be the cause.

An alternative proposed mechanism for bacterial inoculation of ascites is hematogenous transmission in combination with an impaired immune system. Nonetheless, the exact mechanism of bacterial displacement from the GI tract into ascites fluid remains controversial.

A variety of factors contributes to peritoneal inflammation and bacterial growth in ascitic fluid. A key predisposing factor may be the intestinal bacterial overgrowth found in people with cirrhosis, mainly attributed to delayed intestinal transit time. Intestinal bacterial overgrowth, along with impaired phagocytic function, low serum and ascites complement levels, and decreased activity of the reticuloendothelial system, contributes to an increased number of microorganisms and decreased capacity to clear them from the bloodstream, resulting in their migration into and eventual proliferation within ascites fluid.

Interestingly, adults with spontaneous bacterial peritonitis typically have ascites, but most children with spontaneous bacterial peritonitis do not have ascites. The reason for and mechanism behind this is the source of ongoing investigation.

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Etiology

Traditionally, three fourths of spontaneous bacterial peritonitis infections have been caused by aerobic gram-negative organisms (50% of these being Escherichia coli). The remainder has been due to aerobic gram-positive organisms (19% streptococcal species). E coli is displayed in the image below.

Gram-negative Escherichia coli. Gram-negative Escherichia coli.

However, some data suggest that the percentage of gram-positive infections may be increasing.[2, 3] One study cites a 34.2% incidence of streptococci, ranking in second position after Enterobacteriaceae.[3] Viridans group streptococci (VBS) accounted for 73.8% of these streptococcal isolates.

Anaerobic organisms are rare because of the high oxygen tension of ascitic fluid.

A single organism is noted in 92% of cases, and 8% of cases are polymicrobial.

Risk factors

Patients with cirrhosis who are in a decompensated state are at the highest risk of developing spontaneous bacterial peritonitis.[4] Bacterial translocation (viable microorganism passage from the intestinal lumen to mesenteric lymph nodes) is a key factor in the development of spontaneous bacterial peritonitis.[5] Low complement levels are associated with the development of spontaneous bacterial peritonitis. Patients at greatest risk for spontaneous bacterial peritonitis have decreased hepatic synthetic function with associated low total protein level or prolonged prothrombin time (PT).

Patients with low protein levels in ascitic fluid (< 1 g/dL) have a 10-fold higher risk of developing spontaneous bacterial peritonitis than those with a protein level greater than 1 g/dL.

A 2012 review by Siple et al[6] and a 2013 study by Deshpande et al[7] show several case studies and cohorts of patients with cirrhosis and chronic liver disease who were on proton pump inhibitors (PPIs) for a prolonged duration who were at significantly increased risk for the development of spontaneous bacterial peritonitis. While prospective studies are needed on this subject, there appears to be a direct correlation between a lack of an acidic environment and portal hypertension to put these patients at increased risk for spontaneous bacterial peritonitis. Thus, in patients on long-term PPI therapy, the suspicion for infection should be heightened and the benefit of long-term PPI therapy should outweigh the risk for the development of spontaneous bacterial peritonitis.

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Epidemiology

In patients with ascites, the frequency may be as high as 18%. This number has grown from 8% over the past 2 decades, most likely secondary to an increased awareness of spontaneous bacterial peritonitis and a lowered threshold to perform diagnostic paracentesis.

No race predilection is known for spontaneous bacterial peritonitis. In patients with ascites, both sexes are affected equally.

Although the etiology and incidence of hepatic failure differ between children and adults, in those individuals with ascites, the incidence of spontaneous bacterial peritonitis is roughly equal. Two peak ages for spontaneous bacterial peritonitis are characteristic in children: the first in the neonatal period and the second at age 5 years.

According to a 2015 study by Ge and Runyon, when the initial infection was spontaneous bacterial peritonitis, subsequent infections were more likely to be caused by drug-resistant organisms. The risk of subsequent infections was increased in older patients and in patients taking proton-pump-inhibitors (PPIs) or spontaneous bacterial peritonitis prophylaxis (ie, selective intestinal decontamination).[8]

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Prognosis

The mortality rate in patients with spontaneous bacterial peritonitis ranges from 40-70% in adult patients with cirrhosis. Rates are lower in children with nephrosis. Patients with concurrent renal insufficiency have been shown to be at a higher risk of mortality from spontaneous bacterial peritonitis than those without concurrent renal insufficiency. Mortality from spontaneous bacterial peritonitis may be decreasing among all subgroups of patients because of advances in its diagnosis and treatment. In addition, nonselective beta-blockers increase the risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis.[9]

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Contributor Information and Disclosures
Author

Thomas E Green, DO, MPH, FACOEP, FACEP Associate Dean for Clinical Affairs, Des Moines University College of Osteopathic Medicine; Attending Physician, Emergency Department, Emergency Practice Associates; Associate Professor of Emergency Medicine, Midwestern University, Chicago College of Osteopathic Medicine

Thomas E Green, DO, MPH, FACOEP, FACEP is a member of the following medical societies: American College of Emergency Physicians, American College of Osteopathic Emergency Physicians, American Association for Physician Leadership, American Osteopathic Association

Disclosure: Nothing to disclose.

Coauthor(s)

Steven M Bandy, MD, FACEP Staff Physician, Department of Emergency Medicine, Johnston Memorial Hospital; Adjunct Clinical Professor of Emergency Medicine, Virginia College of Osteopathic Medicine

Steven M Bandy, MD, FACEP is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Chief Editor

Jeter (Jay) Pritchard Taylor, III, MD Assistant Professor, Department of Surgery, University of South Carolina School of Medicine; Attending Physician, Clinical Instructor, Compliance Officer, Department of Emergency Medicine, Palmetto Richland Hospital

Jeter (Jay) Pritchard Taylor, III, MD is a member of the following medical societies: American Academy of Emergency Medicine, South Carolina Medical Association, Columbia Medical Society, South Carolina College of Emergency Physicians, American College of Emergency Physicians, American Medical Association, Society for Academic Emergency Medicine

Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Chief Editor for Medscape.

References
  1. Lata J, Stiburek O, Kopacova M. Spontaneous bacterial peritonitis: a severe complication of liver cirrhosis. World J Gastroenterol. 2009 Nov 28. 15 (44):5505-10. [Medline].

  2. Bert F, Noussair L, Lambert-Zechovsky N, Valla D. Viridans group streptococci: an underestimated cause of spontaneous bacterial peritonitis in cirrhotic patients with ascites. Eur J Gastroenterol Hepatol. 2005 Sep. 17(9):929-33. [Medline].

  3. Cholongitas E, Papatheodoridis GV, Lahanas A, Xanthaki A, Kontou-Kastellanou C, Archimandritis AJ. Increasing frequency of Gram-positive bacteria in spontaneous bacterial peritonitis. Liver Int. 2005 Feb. 25(1):57-61. [Medline].

  4. [Guideline] Runyon BA. Management of adult patients with ascites due to cirrhosis: an update. Hepatology. 2009 Jun. 49(6):2087-107. [Medline].

  5. Greenberger NJ et al. Ascites & Spontaneous Bacterial Peritonitis. Current Diagnosis & Treatment: Gastroenterology, Hepatology & Endoscopy. 2nd ed. 2012. Ch 45.

  6. Siple JF, Morey JM, Gutman TE, Weinberg KL, Collins PD. Proton pump inhibitor use and association with spontaneous bacterial peritonitis in patients with cirrhosis and ascites. Ann Pharmacother. 2012 Oct. 46(10):1413-8. [Medline].

  7. Deshpande A, Pasupuleti V, Thota P, Pant C, Mapara S, Hassan S. Acid-suppressive therapy is associated with spontaneous bacterial peritonitis in cirrhotic patients: a meta-analysis. J Gastroenterol Hepatol. 2013 Feb. 28(2):235-42. [Medline].

  8. Ge PS, Runyon BA. Preventing future infections in cirrhosis: a battle cry for stewardship. Clin Gastroenterol Hepatol. 2015 Apr. 13 (4):760-2. [Medline].

  9. Mandorfer M, Bota S, Schwabl P, Bucsics T, Pfisterer N, Kruzik M. Nonselective ß blockers increase risk for hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterology. 2014 Jun. 146(7):1680-90.e1. [Medline].

  10. Riggio O, Angeloni S. Ascitic fluid analysis for diagnosis and monitoring of spontaneous bacterial peritonitis. World J Gastroenterol. 2009 Aug 21. 15(31):3845-50. [Medline]. [Full Text].

  11. Chinnock B, Gomez R, Hendey GW. Peritoneal fluid cultures rarely alter management in patients with ascites. J Emerg Med. 2011 Jan. 40(1):21-4. [Medline].

  12. Gaya DR, David B Lyon T, et al. Bedside leucocyte esterase reagent strips with spectrophotometric analysis to rapidly exclude spontaneous bacterial peritonitis: a pilot study. Eur J Gastroenterol Hepatol. 2007 Apr. 19(4):289-95. [Medline].

  13. Téllez-Ávila FI, Chávez-Tapia NC, Franco-Guzmán AM, Uribe M, Vargas-Vorackova F. Rapid diagnosis of spontaneous bacterial peritonitis using leukocyte esterase reagent strips in emergency department: uri-quick clini-10SG® vs. Multistix 10SG®. Ann Hepatol. 2012 Sep-Oct. 11(5):696-9. [Medline].

  14. Runyon BA. Monomicrobial nonneutrocytic bacterascites: a variant of spontaneous bacterial peritonitis. Hepatology. 1990 Oct. 12(4 Pt 1):710-5. [Medline].

  15. [Guideline] Runyon BA. Introduction to the revised American Association for the Study of Liver Diseases Practice Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology. 2013 Apr. 57(4):1651-3. [Medline].

  16. Pande C, Kumar A, Sarin SK. Addition of probiotics to norfloxacin does not improve efficacy in the prevention of spontaneous bacterial peritonitis: a double-blind placebo-controlled randomized-controlled trial. Eur J Gastroenterol Hepatol. 2012 Jul. 24(7):831-9. [Medline].

  17. Runyon BA, Borzio M, Young S, Squier SU, Guarner C, Runyon MA. Effect of selective bowel decontamination with norfloxacin on spontaneous bacterial peritonitis, translocation, and survival in an animal model of cirrhosis. Hepatology. 1995 Jun. 21 (6):1719-24. [Medline].

  18. Fernández J, Navasa M, Planas R, Montoliu S, Monfort D, Soriano G, et al. Primary prophylaxis of spontaneous bacterial peritonitis delays hepatorenal syndrome and improves survival in cirrhosis. Gastroenterology. 2007 Sep. 133 (3):818-24. [Medline].

 
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