Spontaneous bacterial peritonitis overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Shivani Chaparala M.B.B.S [2] Ahmed Younes M.B.B.CH [3]


Spontaneous bacterial peritonitis (SBP) is a form of peritonitis that occurs in most of the patients with advanced cirrhosis, in 10-30% of hospitalized patients with ascites and in various other clinical settings, such as nephrotic syndrome, heart failure, tuberculous infection, continuous ambulatory peritoneal dialysis for chronic renal failure.[1] [2] SBP is diagnosed with a positive bacterial culture for a single organism and an AF ( ascitic fluid) : polymorphonuclear (PMN) cell count of > 250/mm3, in the absence of a surgically treatable intra-abdominal source of infection. More than 60% of SBP episodes are caused by enteric gram-negative organisms such as Escherichia coli and Kleibsella. Selective intestinal decontamination (SID) with fluorinated quinolones suppresses the gram-negative intestinal flora and is known to reduce the incidence of SBP.[3][4] SBP results due to the inability of the gut to contain bacteria and failure of the immune system to eradicate the organisms once they have escaped into the blood stream. Clinical signs and symptoms are non specific and indistinguishable from secondary peritonitis. Ascitic fluid analysis is helpful in differentiating SBP from secondary peritonitis. Because of the lack of specificity and sensitivity of clinical signs and symptoms, cirrhotic patients with unexplained deterioration should undergo a diagnostic paracentesis. Once diagnosed, patients with SBP should receive prompt empiric antibiotic treatment ( Cephalosporins) without waiting for the ascitic fluid culture. Failure of prompt initiation of antibiotics results in significant and potentially fatal deterioration in the clinical status of the patient. Patients who survive an episode of SBP are at high risk of recurrence. Patients with cirrhosis and ascites developing abdominal pain and/or temperature >100F are more prone to have SBP and should receive empiric antibiotic treatment. Early detection and treatment improve outcome and prevent complications such as shock and renal failure.[5]

To see a comprehensive video about SBP, click here.

Historical Perspective

Kerr and colleagues (1963) described 11 episodes of ascitic fluid infection in 9 cirrhotic patients while Harold O.Conn , M.D, a world-renowned hepatologist (1964) introduced the term “spontaneous bacterial peritonitis” for the first time in English literature. Later in the history, SBP was studied extensively by many renowned researchers and health care professionals as this condition was seen among many patients with cirrhosis, which has lead to the thorough understanding and recognition of SBP.


Spontaneous bacterial peritonitis is one of the variants of ascitic fluid infections.[6]. Classification of ascitic fluid infections is based on neutrophil count and culture report.[7][8]. Asymptomatic bacterascites is usually the transient residence of bacteria in ascitic fluid without clinical features of peritonitis or increased ascitic fluid polymorphonuclear cells.[9]. SBP is also classified based on the routes of infection and the clinical setting as follows Health care-associated, Nosocomial, Community acquired, Multi-drug resistant, Recurrent.


Spontaneous bacterial peritonitis is thought to result from a combination of factors related to cirrhosis and ascites such as: altered microbial flora, hypo-motility of the intestine, intestinal bacterial overgrowth, increased intestinal mucosal permeability, bacterial translocation to lymph nodes. Presence of ascites is an important risk factor for the development of bacterial translocation. In healthy individuals, bacteria that colonize lymph nodes are killed by local immune defenses. However, in the setting of cirrhosis, an acquired state of immunodeficiency there is: malfunctioning of the reticulo-endothelial and neutrophilic system, reduced cellular and humoral bactericidal function which favor the spread of bacteria to the blood stream.[10][11][12]


Spontaneous bacterial peritonitis is a blood-borne infection caused by Enteric organisms in 70% of cases (Mono-microbial origin in 90% of cases). Aerobic gram-negative bacteria like Escherichia coli account for half of the cases. Gram-positive cocci Streptococcus species in 20% cases with enterococcus accounting for 5% of the cases. Staphylococcus aureus and Streptococcus salivarius are less frequent causes. Poly-microbial infection is Iatrogenic (more likely associated with abdominal paracentesis) or intra-abdominal source of infection. The cause of SBP has not been established definitively but is believed to involve hematogenous spread of organisms in a patient with a diseased liver and altered portal circulation resulting in defect in the usual filtration function. In adults, spontaneous bacterial peritonitis occurs most commonly in conjunction with cirrhosis of the liver and portal hypertension (frequently as a result of alcoholism and hepatitis).

Differentiating Spontaneous bacterial peritonitis from Other Diseases

SBP has to be differentiated from other abdominal conditions presenting with fever and abdominal pain. It also has to be differentiated from secondary peritonitis, chemical peritonitis, peritoneal dialysis peritonitis, chronic tuberculous peritonitis.

Epidemiology and Demographics

Spontaneous bacterial peritonitis (SBP) is a potentially life threatening complication in patients with cirrhosis and is seen in hospitalized patients. The prevalence of SBP in cirrhotic patients with ascites admitted to the hospital ranges from 10%-30%.[14]. Studies have demonstrated a 12% incidence of spontaneous bacterial peritonitis in patients admitted with decompensated cirrhosis. 2 studies examining asymptomatic patients presenting for a therapeutic paracentesis showed a combined 2.5% incidence of spontaneous bacterial peritonitis. Overall one-year mortality rate after a first episode of SBP is 30%-93% regardless of its recurrence. The mean age of presentation of SBP was 49 years. There is no gender difference in the incidence of SBP in patients with ascites.

Risk Factors

Common risk factors in cirrhotic patients with ascites include: Low protein level in ascitic fluid (<1 g/dL), upper GI bleeding, low complement concentration (complement 3) in ascitic fluid, renal failure, Elevated serum bilirubin level (>4 mg/dL), use of Proton pump inhibitors (PPI) in cirrhotic patients, Child-Pugh stage C, Model For End-Stage Liver Disease MELD ≥ 22.[15]


There is no definitive screening test for spontaneous bacterial peritonitis. According to Liver International journal, it has been demonstrated that fecal calprotectin concentrations (FCCs) are significantly elevated in cirrhotic patients and are dependent on the severity of liver disease. Assessing FCCs may help to identify cirrhotic patients with hepatic encephalopathy and SBP as a significant correlation emerged between elevated fecal calprotection and these complications.[16] However, there is insufficient evidence to recommend routine screening for SBP.

Natural History, Complications, and Prognosis

Early diagnosis and initiating treatment is the most important factor for improving the survival and avoiding the complications of SBP. The sooner the diagnosis, the better the outcome. Mortality due to SBP remains high probably due to associated advanced liver disease.


According to the 2010 European Association for the Study of the Liver clinical practice guidelines the diagnosis of SBP is based on:[17]

  • Diagnostic paracentesis:
    • A diagnostic paracentesis should be carried out in all patients with cirrhosis and ascites at hospital admission to rule out SBP.[18][19]
    • A diagnostic paracentesis should also be performed in patients with gastrointestinal bleeding, shock, fever, or other signs of systemic inflammation, gastrointestinal symptoms, as well as in patients with worsening liver and/or renal function, and hepatic encephalopathy.
  • Ascitic fluid cell analysis
    • The diagnosis of SBP is based on neutrophil count in ascitic fluid of >250/mm3 as determined by microscopy.
    • At present there are insufficient data to recommend the use of automated cell counters or reagent strips for the rapid diagnosis of SBP.
  • Ascitic fluid culture
    • Ascitic fluid culture is frequently negative even if performed in blood culture bottles and is not necessary for the diagnosis of SBP, but it is important to guide antibiotic therapy.
    • Blood cultures should be performed in all patients with suspected SBP before starting antibiotic treatment.
    • Some patients may have an ascitic neutrophil count less than 250/mm3 but with a positive ascitic fluid culture. This condition is known as bacterascites.
    • If the patient exhibits signs of systemic inflammation or infection, the patient should be treated with antibiotics.
    • Otherwise, the patient should undergo a second paracentesis when culture results come back positive.
    • Patients in whom the repeat ascitic neutrophil count is >250/mm3 should be treated for SBP, and the remaining patients (i.e., neutrophils <250/mm3) should be followed up .

Diagnostic Criteria

The diagnosis of SBP is based on two of the following criteria from guidelines:[20]

History and Symptoms

80-90% of patients with spontaneous bacterial peritonitis are symptomatic, in many cases the presentation is subtle. Spontaneous bacterial peritonitis may be present in 10–20% of patients hospitalized with chronic liver disease, sometimes in the absence of any suggestive symptoms or signs. Patients with SBP most often present with: abdominal pain, fever, altered mental status (hepatic encphalopathy).[21][22]

Physical Examination

The clinical examination findings in spontaneous bacterial peritonitis are usually unpredictable, so there should be a low threshold to consider SBP in any patient with cirrhosis. Fever, acute abdominal and altered mental status are the physical findings. Physical examination typically demonstrates signs of chronic liver disease with ascites. Abdominal tenderness is present in less than 50% of patients, and its presence suggests other processes.

Laboratory Findings

Early Diagnostic paracentesis (< 72hrs) is recommended in all cirrhotic patients with ascites. Paracentesis reveals an ascitic fluid with a total white cell count of up to 500 cells/mcL with a high polymorphonuclear (PMN) cell count (250/mm3 more). Ascitic fluid analysis and culture should be performed before initiating antibiotic therapy by bedside inoculation of ascitIc fluid ≥ 10 mL into blood culture bottles. Ascitic fluid analysis is the gold standard for the confirmation of the diagnosis of spontaneous bacterial peritonitis.[23][18]


Medical Therapy

Empiric treatment


The AASLD guidelines suggest using long term antibiotic prophylaxis in patients with: Ascitic fluid total protein less than 1.5 g/dL and with at least one of the following: Serum creatinine greater than or equal to 1.2 mg/dL, Blood urea nitrogen greater than or equal to 25 mg/dL, serum sodium less than or equal to 130 mEq/L, or Child-Turcotte-Pugh greater than or equal to 9 points (with bilirubin greater than or equal to 3 mg/dL). Daily oral norfloxacin in patients with more advanced liver disease has shown to prevent the development of spontaneous bacterial peritonitis and hepatorenal syndrome and improved survival rates at 3 months. Norfloxacin also reduced SBP recurrence rates from 68% to 20%.[4]





  1. Kato A, Ohtake T, Furuya R, Nakajima T, Ohura M, Kumagai H; et al. (1993). "Spontaneous bacterial peritonitis in an adult patient with nephrotic syndrome". Intern Med. 32 (9): 719–21. PMID 8142677.
  2. Runyon BA (1984). "Spontaneous bacterial peritonitis associated with cardiac ascites". Am J Gastroenterol. 79 (10): 796. PMID 6486115.
  3. Soriano G, Guarner C, Teixidó M, Such J, Barrios J, Enríquez J; et al. (1991). "Selective intestinal decontamination prevents spontaneous bacterial peritonitis". Gastroenterology. 100 (2): 477–81. PMID 1985045.
  4. 4.0 4.1 Llovet JM, Rodríguez-Iglesias P, Moitinho E, Planas R, Bataller R, Navasa M; et al. (1997). "Spontaneous bacterial peritonitis in patients with cirrhosis undergoing selective intestinal decontamination. A retrospective study of 229 spontaneous bacterial peritonitis episodes". J Hepatol. 26 (1): 88–95. PMID 9148028.
  5. Crossley IR, Williams R (1985). "Spontaneous bacterial peritonitis". Gut. 26 (4): 325–31. PMC 1432517. PMID 3884467.
  6. Sheer TA, Runyon BA (2005). "Spontaneous bacterial peritonitis". Dig Dis. 23 (1): 39–46. doi:10.1159/000084724. PMID 15920324.
  7. Dever JB, Sheikh MY (2015) Review article: spontaneous bacterial peritonitis--bacteriology, diagnosis, treatment, risk factors and prevention. Aliment Pharmacol Ther 41 (11):1116-31. DOI:10.1111/apt.13172 PMID: 25819304
  8. Runyon BA, AASLD Practice Guidelines Committee (2009). "Management of adult patients with ascites due to cirrhosis: an update". Hepatology. 49 (6): 2087–107. doi:10.1002/hep.22853. PMID 19475696.
  9. Pelletier G, Lesur G, Ink O, Hagege H, Attali P, Buffet C; et al. (1991). "Asymptomatic bacterascites: is it spontaneous bacterial peritonitis?". Hepatology. 14 (1): 112–5. PMID 2066060.
  10. Tsiaoussis GI, Assimakopoulos SF, Tsamandas AC, Triantos CK, Thomopoulos KC (2015). "Intestinal barrier dysfunction in cirrhosis: Current concepts in pathophysiology and clinical implications". World J Hepatol. 7 (17): 2058–68. doi:10.4254/wjh.v7.i17.2058. PMC 4539399. PMID 26301048.
  11. Runyon BA, Squier S, Borzio M (1994). "Translocation of gut bacteria in rats with cirrhosis to mesenteric lymph nodes partially explains the pathogenesis of spontaneous bacterial peritonitis". J Hepatol. 21 (5): 792–6. PMID 7890896.
  12. Bauer TM, Steinbrückner B, Brinkmann FE, Ditzen AK, Schwacha H, Aponte JJ; et al. (2001). "Small intestinal bacterial overgrowth in patients with cirrhosis: prevalence and relation with spontaneous bacterial peritonitis". Am J Gastroenterol. 96 (10): 2962–7. doi:10.1111/j.1572-0241.2001.04668.x. PMID 11693333.
  13. Rimola A, Soto R, Bory F, Arroyo V, Piera C, Rodes J (1984). "Reticuloendothelial system phagocytic activity in cirrhosis and its relation to bacterial infections and prognosis". Hepatology. 4 (1): 53–8. PMID 6693068.
  14. Oladimeji AA, Temi AP, Adekunle AE, Taiwo RH, Ayokunle DS (2013). "Prevalence of spontaneous bacterial peritonitis in liver cirrhosis with ascites". Pan Afr Med J. 15: 128. doi:10.11604/pamj.2013.15.128.2702. PMC 3830462. PMID 24255734.
  15. Schwabl P, Bucsics T, Soucek K, Mandorfer M, Bota S, Blacky A; et al. (2015). "Risk factors for development of spontaneous bacterial peritonitis and subsequent mortality in cirrhotic patients with ascites". Liver Int. 35 (9): 2121–8. doi:10.1111/liv.12795. PMID 25644943.
  16. Gundling, Felix; Schmidtler, Fabian; Hapfelmeier, Alexander; Schulte, Benjamin; Schmidt, Thomas; Pehl, Christian; Schepp, Wolfgang; Seidl, Holger (2011). "Fecal calprotectin is a useful screening parameter for hepatic encephalopathy and spontaneous bacterial peritonitis in cirrhosis". Liver International. 31 (9): 1406–1415. doi:10.1111/j.1478-3231.2011.02577.x. ISSN 1478-3223.
  17. "EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis". Journal of Hepatology. 53 (3): 397–417. 2010. doi:10.1016/j.jhep.2010.05.004. ISSN 0168-8278.
  18. 18.0 18.1 Runyon BA (1986). "Paracentesis of ascitic fluid. A safe procedure". Arch Intern Med. 146 (11): 2259–61. PMID 2946271.
  19. De Gottardi A, Thévenot T, Spahr L, Morard I, Bresson-Hadni S, Torres F; et al. (2009). "Risk of complications after abdominal paracentesis in cirrhotic patients: a prospective study". Clin Gastroenterol Hepatol. 7 (8): 906–9. doi:10.1016/j.cgh.2009.05.004. PMID 19447197.
  20. "EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis". Journal of Hepatology. 53 (3): 397–417. 2010. doi:10.1016/j.jhep.2010.05.004. ISSN 0168-8278.
  21. Such J, Runyon BA (1998). "Spontaneous bacterial peritonitis". Clin Infect Dis. 27 (4): 669–74, quiz 675-6. PMID 9798013.
  22. Chinnock B, Hendey GW, Minnigan H, Butler J, Afarian H (2013). "Clinical impression and ascites appearance do not rule out bacterial peritonitis". J Emerg Med. 44 (5): 903–9. doi:10.1016/j.jemermed.2012.07.086. PMID 23473819.
  23. Orman ES, Hayashi PH, Bataller R, Barritt AS (2014). "Paracentesis is associated with reduced mortality in patients hospitalized with cirrhosis and ascites". Clin Gastroenterol Hepatol. 12 (3): 496–503.e1. doi:10.1016/j.cgh.2013.08.025. PMC 3944409. PMID 23978348.
  24. Guarner C, Runyon BA (1995). "Spontaneous bacterial peritonitis: pathogenesis, diagnosis, and management". Gastroenterologist. 3 (4): 311–28. PMID 8775093.
  25. Poca M, Concepción M, Casas M, Alvarez-Urturi C, Gordillo J, Hernández-Gea V; et al. (2012). "Role of albumin treatment in patients with spontaneous bacterial peritonitis". Clin Gastroenterol Hepatol. 10 (3): 309–15. doi:10.1016/j.cgh.2011.11.012. PMID 22094025.
  26. Salerno F, Navickis RJ, Wilkes MM (2013). "Albumin infusion improves outcomes of patients with spontaneous bacterial peritonitis: a meta-analysis of randomized trials". Clin Gastroenterol Hepatol. 11 (2): 123–30.e1. doi:10.1016/j.cgh.2012.11.007. PMID 23178229.

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