Review Article

Spontaneous Bacterial Peritonitis – Bacteriology, Diagnosis, Treatment, Risk Factors and Prevention

J. B. Dever; M. Y. Sheikh

Disclosures

Aliment Pharmacol Ther. 2015;41(11):1116-1131. 

In This Article

Abstract and Introduction

Abstract

Background Spontaneous bacterial peritonitis (SBP) is a severe and often fatal infection in patients with cirrhosis and ascites.

Aim To review the known and changing bacteriology, risk factors, ascitic fluid interpretation, steps in performing paracentesis, treatment, prophylaxis and evolving perspectives related to SBP.

Methods Information was obtained from reviewing medical literature accessible on PubMed Central. The search term 'spontaneous bacterial peritonitis' was cross-referenced with 'bacteria', 'risk factors', 'ascites', 'paracentesis', 'ascitic fluid analysis', 'diagnosis', 'treatment', 'antibiotics', 'prophylaxis', 'liver transplantation' and 'nutrition'.

Results Gram-positive cocci (GPC) such as Staphylococcus,Enterococcus as well as multi-resistant bacteria have become common pathogens and have changed the conventional approach to treatment of SBP. Health care-associated and nosocomial SBP infections should prompt greater vigilance and consideration for alternative antibiotic coverage. Acid suppressive and beta-adrenergic antagonist therapies are strongly associated with SBP in at-risk individuals.

Conclusions Third-generation, broad-spectrum cephalosporins remain a good initial choice for SBP treatment. Levofloxacin is an acceptable alternative for patients not receiving long-term flouroquinolone prophylaxis or for those with a penicillin allergy. For uncomplicated SBP, early oral switch therapy is reasonable. Alternative antibiotics such as pipercillin–tazobactam should be considered for patients with nosocomial SBP or for patients who fail to improve on traditional antibiotic regimens. Selective albumin supplementation remains an important adjunct in SBP treatment. Withholding acid suppressive medication deserves strong consideration, and discontinuing beta-adrenergic antagonist therapy in patients with end-stage liver disease and resistant ascites is standard care. Liver transplant evaluation should be undertaken for patients who develop SBP barring contraindications.

Introduction

Spontaneous bacterial peritonitis (SBP) is a common and frequently fatal bacterial infection of ascites occurring in patients with cirrhosis who have diverse symptomatology. The diagnosis is distinct from secondary peritonitis and hence is made in the absence of an intra-abdominal source of infection or inflammatory process. SBP was first described in 1907 by Krencker followed by Caroli in 1958 and Kerr and colleagues in 1963.[1–3] Conn coined the term 'spontaneous bacterial peritonitis' in 1964 to depict a syndrome of peritonitis and bacteremia in Laennec's cirrhosis without an apparent cause of infection.[4] SBP occurs in cirrhotic patients with varied aetiologies, not just alcohol, and further research has uncovered causal factors such as translocation of gut bacteria to lymph nodes making the aetiology less elusive.

Portal hypertension, splanchnic vasodilation and activation of the renin–angiotensin cascade leads to sodium and water retention and fluid overflow into the peritoneal cavity.[5] Ascites is primarily a transudative fluid with poor opsonic activity which provides a favourable environment for growth of bacteria. SBP rarely occurs without cirrhosis, but cardiac,[6] renal,[7] malignancy,[8,9] portal vein thrombosis[10] and autoimmune[11,12]-related infection of ascites has been reported.

Ascitic fluid infection is classified into five types based on polymorphonuclear cell count, ascitic fluid culture results and clinical circumstances: classic culture-positive SBP, culture-negative SBP also known as culture-negative neutrocytic ascites (CNNA), monomicrobial and polymicrobial bacterascites, and secondary peritonitis (Table 1).

Intestinal Gram-negative flora are the major cause of SBP. A variety of factors are associated with the development of SBP including the pathophysiological hallmark: bacterial translocation in an immunocompromised host. The incidence of SBP ranges from 10% to 30%[13] and mortality from 10% to 46%[14,15] in hospitalised patients. Clinical acumen, prompt diagnosis and appropriate treatment remain the most important tools for physicians when caring for patients who acquire SBP in various clinical settings.

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