Saudi Journal of Gastroenterology

: 1995  |  Volume : 1  |  Issue : 3  |  Page : 169--172

Spontaneous bacterial peritonitis

Saleh M Al Amri 
 Department of Medicine. Gastroenterology Division, College of Medicine, King Saud University, Riyadh, Saudi Arabia

Correspondence Address:
Saleh M Al Amri
Assistant Professor and Consultant Physician Division of Gastroenterology (59) P.O. Box 2925, Riyadh 11461
Saudi Arabia


Spontaneous bacterial peritonitis (SBP) is an infection of the ascitic fluid without obvious intra-abdominal source of sepsis; usually complicates advanced liver disease. The pathogenesis of the disease is multifactorial: low ascitic protein-content, which reflects defi­cient ascitic fluid complement and hence, reduced opsonic activity is thought to be the most important pathogenic factor. Frequent and prolonged bacteremia has been considered as another pertinent cause of SBP. This disease is associated with high mortality and recurrence. Therefore, orompt recognition and institution of therapy and plan of prophylaxis is vital.

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Al Amri SM. Spontaneous bacterial peritonitis.Saudi J Gastroenterol 1995;1:169-172

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 Definition and Classification

Spontaneous bacterial peritonitis (SBP) is defined as infection of the ascitic fluid without any obvious intra-abdominal source of sepsis. The prevalence of the disease ranges between 8% and 25% in cirrhotic patients and is associated with a high in-hospital mortality [1],[2],[3].

Ascitic fluid infection is classified into three types based on the polymorphonuclear count and culture. Classically, SBP is defined when ascitic fluid neutrophil count is ≥ 250 cells/mm 3 , positive ascitic fluid culture in the absence of intra-abdom­inal source of infection [3],[4]. The second variant of peritonitis is culture- negative neutrocytic ascites (CNNA), which is defined as ascitic fluid neutrophil count of ≥ 250 cell/mm 3 , negative asci­tic fluid culture and no history of antibiotics in the last 30 days [3],[4]. The third subtype is monomic­robial non-neutrocytic bacter ascites (MNB), defined as positive ascitic fluid culture, but the ascitic fluid polymorph count is less than 250 cells/ mm 3 [5],[6],[7],[8][Table 1].

Several studies compared the clinical picture of SBP and CNNA [3],[4],[8],[9]. Both groups presented with similar clinical and biochemical picture with no significant statistical difference. As for the out­come in two studies, CNNA was found to carry the same prognosis, with similar mortality and recurrence rate as SBP[8],[9]; while another two studies came to a conclusion that CNNA is a less severe variant of SBP[3],[4].

Negative ascitic fluid culture in CNNA may reflect insensitive culture technique or delay in ascitic fluid transportation to laboratory, as the bacterial concentration in ascitic fluid is low [2],[11].

Runyon found in his prospective study that 31.9% of patients with positive ascitic fluid culture had a polymorphonuclear count of less than 250 cells/mm 3 . Clinically, almost half of the patients presented with fever, while minority had abdomi­nal pain [5],[7]. In general majority of patients with bacterial peritonitis were reported to be symptomatic at the time of diagnosis. The com­monest presenting symptoms were: fever, abdom­inal pain and change in mental status[7].


The exact mechanism of infecting ascitic fluid is not well known. However, it may be related to severe complement deficiency and dysfunction of the neutrophils and reticuloendothelial system [12],[13]. Furthermore, intrahepatic and portosys­temic shunting of blood may be an important mechanism for frequent spontaneous bacteremia [1],[16]. This leads patients with liver cirrhosis to have frequent and prolonged bacteremia.

Recently-published data in animal models showed the occurrence of bacterial translocation in 88% of cirrhotic animals compared to zero per­cent in controls [14]. It appears that the gut mucosa in cirrhotic patients is abnormally perme­able, and therefore facilitates the migration of bacteria from gut wall to mesenteric lymph nodes, from which it gains access into the circulation [15],[16]. Moreover, lymphatic rupture and direct bacteria leak into ascitic fluid have been described[6]. It has been found that more than 50% of patients with SBP grew the same organism from blood and ascitic fluid, which supports the importance of bacteremia as a pathogenic factor in SBP [17],[18].

Not all cirrhotic ascites develop SBP; the preva­lence of the disease is 8-25% [1],[2],[3]. So, which patients are at risk of getting this serious complica­tion?

Patients with low ascitic protein concentration (≤1 gram/dl) are prone to develop SBP. This has been documented by Runyon [19] and confirmed by other investigations [18],[20].

Opsonization, fixation of complement to bacte­rial surface is the initial and most important step in engulfing and therefore killing of bacteria by phagocytic cells [21]. The opsonic activity has been found to correlate closely with ascitic pro­tein, C 3 and C 4 concentration. Patients with low protein have opsonic activity and therefore are at risk of developing SBP[20],[21].

Mal et al demonstrated in his prospective study, that chemoattractant, as well as opsonic activity, were low in patients with ascites and SBP, com­pared to patients with ascites but who did not develop SBP[20]. Conversely, patients with high protein-content ascites are resistant to infec­tion[2],[22],[23].

 Diagnostic Approach

The diagnosis of SBP depends on a high index of suspicion in patients with ascites and clinical deterioration. Ascitic fluid analysis is the quickest method of supporting the clinical suspicion of SBP. Ascitic polymorphonuclear count is the most important initial step in diagnosis, as culture takes several days before growth is obtained[1],[24].

Conventional ascitic fluid culture is an insensi­tive method. In a prospective study comparing conventional and blood culture bottle inoculation with 10 ml ascitic fluid, Runyon demonstrated the superiority of bedside inoculation of ascitic fluid into blood culture bottle; the culture yield was 42% and 91%, respectively[2],[11]. Gram-stain rarely detects the organisms, and is of limited importance [6],[11].

 Antibiotic therapy of SBP

Gram-negative enteric organism and strepto­pneumonia are the causative pathogens in over 80% of instances of SBP[5],[25]. Hence, the choice of antibiotics should cover these most likely agents.

Early studies have used combination of ampicil­lin and aminoglycoside[1],[26]. However, amino­glycosides have a narrow therapeutic band over which nephrotoxicity occurs. Within this range, antibiotics level may not be adequate. Further­more, the volume distribution of aminoglycoside is unpredictable in ascites[1],[2].

Several studies have proved, in randomized­controlled studies that third generation cephalosporins are more effective than the combination of ampicillin and tobramycin[1],[2],[27]. This drug covers 98% of the SBP flora and resulted in no nephrotoxicity, and at the same time achieved an adequate ascitic fluid level[1],[5],[27].

Reported mortality in patients with SBP is improving with early literature reporting 100% death in SBP, while newer studies quote a figure of 50%.[2],[3],[4],[8],[9] This could be as consequence of the awareness of the physician, early performance of paracentesis and use of more effective drugs[2].


SBP is a recurrent disease, with recurrence rate of 69% at one year. Moreover the recurrence is often fatal[2],[5],[28]. Therefore, prevention of recurrence is of ultimate importance [Table 2]. It has been shown previously that the chemoattrac­tant and opsonic activity which correlates with protein concentration in ascitic fluid is signific­antly lower in patients with SBP, compared to those who do not[20]. Recently, Runyon has shown a significant increase in opsonic activity and concentration of total protein and comple­ment in 11 patients who responded to diuretics [29]. However, most patients with SBP have advanced liver disease and probably renal dys­function and therefore may not respond to diure­tic therapy[5],[20]). Rimola et al investigated the use of oral nonabsorbable antibiotic in a ran­domized-controlled study in cirrhotic patients with gastrointestinal bleeding, and found that 11 of treated patients, compared to 25 control group, developed infections (P <0.025). Another two patients in treated group vs 10 in control, developed SBP (P <0.025)[30].

Two studies reported the use of norfloxacin in the prevention of SBP in cirrhotic patients, the first by Soriano et al, who in a prospective ran­domized study treated 32 cirrhotic patients with low ascitic fluid protein, and compared the inci­dence of infection in 31 nontreated cirrhotic patients. Treated patients received norfloxacin 400 mg during their hospital stay. The incidence of infection in general, and SBP were significantly lower in treated group (P <0.005) and 0.05 respectively[31]. The second study by Gines et al who, in a double-blind, placebo-controlled group, studied the use of norfloxacin in the prevention of SBP. In the study, 40 patients received norfloxa­cin (400 mg) compared to 40 patients who received placebo. Thirty-five percent of placebo group and 13% from norfloxacin group developed recurrent SBP (P = 0.01). The overall probability of SBP recurrence at one year was decreased from 68% to 20% (P <0.01)[32] [Table 3].

 Conclusion and recommendation

SBP is a serious complication that develops in patients with severe liver disease. Low ascitic pro­tein is the most important predisposing factor. Mortality and recurrence rate is high. A high index of suspicion of SBP and early performance of paracentesis and bedside inoculation of ascitic fluid into blood culture bottle and the use of and early institution of effective drugs have reduced the mortality. Aggressive use of diuretic and prophylactic antibiotics has reduced the recurr­ence rate.


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