Saudi Journal of Gastroenterology
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Year : 1995  |  Volume : 1  |  Issue : 3  |  Page : 169-172
Spontaneous bacterial peritonitis


Department of Medicine. Gastroenterology Division, College of Medicine, King Saud University, Riyadh, Saudi Arabia

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   Abstract 

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.

How to cite this article:
Al Amri SM. Spontaneous bacterial peritonitis. Saudi J Gastroenterol 1995;1:169-72

How to cite this URL:
Al Amri SM. Spontaneous bacterial peritonitis. Saudi J Gastroenterol [serial online] 1995 [cited 2020 Oct 27];1:169-72. Available from: https://www.saudijgastro.com/text.asp?1995/1/3/169/34055



   Definition and Classification Top


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].


   Pathogenesis Top


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 Top


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 Top


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].


   Prophylaxis Top


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 Top


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.

 
   References Top

1.Crossley IR, Williams R. Spontaneous bacterial peritonitis. Gut 1985;26:325-31.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Runyon BA. Spontaneous bacterial peritonitis: an exp­losion of information. Hepatology 1988;8(1):171-5.  Back to cited text no. 2    
3.AI Amri SM, Allam AR, AI Mofleh IA. Spontaneous bacterial peritonitis and culture-negative neutrocytic ascites in patients with non-alcohol liver cirrhosis. J Gas­troenterol Hepatol 1994;9:433-6.  Back to cited text no. 3    
4.Pelletier G, Salmon D, Ink 0, et al. Culture-negative neutrocytic ascites: a less severe variant of spontaneous bacterial peritonitis. J Hepatol 1990;10:327-31.  Back to cited text no. 4    
5.Bhuva M, Ganger D, Jensen D. Spontaneous bacterial peritonitis: an update on evaluation, management and prevention. Am J Med 1994;97:169-75.  Back to cited text no. 5  [PUBMED]  
6.Runyon BA. Ascites and spontaneous bacterial peritonitis. In: Sleisenger MH, Fordtran JS, editors. Gastrointestinal disease: pathophysiology/diagnosis/ management. Philadelphia: Saunders 1993;1988-95.  Back to cited text no. 6    
7.Runyon BA. Monomicrobial non-neutrocytic bacteras­cities: a variant of spontaneous bacterial peritonitis. Hepatology 1990;12:71;.  Back to cited text no. 7    
8.Runyon BA, Hoefs JC. Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis. Hepatology 1984;4:1209-11.  Back to cited text no. 8  [PUBMED]  
9.Terg R, Levi D, Lopez P, et al. Analysis of clinical course and prognosis of culture-positive spontaneous bacterial peritonitis and neutrocytic ascites. Evidence of the same disease. Dig Dis Sci 1992;37:1499-504.  Back to cited text no. 9    
10.Hoefs JC, Canawati H, Sapico FL, Hopkins RR, Weiner J, Montgomerie JZ. Spontaneous bacterial peritonitis. Hepatology 1982;2(4):399-407.  Back to cited text no. 10    
11.Runyon BA, Umland ET, Merlin T. Inoculation of blood culture bottles with ascitic fluid: improved detection of spontaneous bacterial peritonitis. Arch Intern Med 1987;147:73-5.  Back to cited text no. 11  [PUBMED]  
12.Rajkovic IA, Williams R. Abnormalities of neutrophil phagocytosis, intracellular killing and metabolic activity in alcoholic cirrhosis and hepatitis. Hepatology 1986;6:252-62.  Back to cited text no. 12  [PUBMED]  
13.Rimola A, Soto R, Borly F, Arroyo V, Piera C, Rodes J. Reticuloendothelial system phagocytic activity in cir­rhosis and its relation to bacterial infections and prog­nosis. Hepatology 1984;4:53-8.  Back to cited text no. 13    
14.Runyon BA, Squier SU. Translocation of gut bacteria of cirrhotic rats to mesenteric lymph nodes may partially explain the pathogenesis of spontaneous bacterial peritonitis. Hepatology 1991;14:91A.  Back to cited text no. 14    
15.Berg RD, Gaslington AW. Translocation of certain indi­genous bacteria from the gastrointestinal tract to the mesenteric lymph nodes and other organs in a gnotobio­tic mouse model. Infect Immun 1979;23:403.  Back to cited text no. 15    
16.Deitch EA, Wintertonn J, Li M, et al. The gut as a portal of entry of bacteria. Ann Surg 1987;205:681.  Back to cited text no. 16    
17.Graudal N, Milman N, Kirkegaard E, et al. Bacteremia in cirrhosis of the liver. Liver 1986;6:297.  Back to cited text no. 17  [PUBMED]  
18.Hoefs JC, Runyon BA. Spontaneous bacterial peritonitis. Dis Mon 1985;31:1.  Back to cited text no. 18    
19.Runyon BA. Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis. Gas­troenterology 1986;91:1343-6.  Back to cited text no. 19    
20.Mal F, Huu TP, Bendahou M, Trinchet JC, Gamier M, Hakim J, Beaugrand M. Chemoattractant and opsonic activity in ascitic fluid. J Hepatology 1991;12:45-9.  Back to cited text no. 20    
21.Runyon BA, Morrissey RL, Hoefs JC, Wyle FA. Opsonic activity of human ascitic fluid: a potentially­important protective mechanism against spontaneous bacterial peritonitis. Hepatology 1985;5:634-7.  Back to cited text no. 21  [PUBMED]  
22.Kurtz RC, Bronzo RL. Does spontaneous bacterial peritonitis occur in malignant ascites ? Am J Gastroen­terol 1982;77:146-8.  Back to cited text no. 22    
23.Runyon BA. Spontaneous bacterial peritonitis associated with cardiac ascites. Am J Gastroenterol 1984;79:796.  Back to cited text no. 23  [PUBMED]  
24.Reynolds TB. Rapid presumptive diagnosis of spontane­ous bacterial peritonitis. Gastroenterology 1986;90:1294-7.  Back to cited text no. 24  [PUBMED]  
25.Wilcox CM, Dismukes WE. Spontaneous bacterial peritonitis: a review of pathogenesis, diagnosis and man­agement. Medicine 1987;66:447-56.  Back to cited text no. 25  [PUBMED]  
26.Weinstein MP, lannini PB, Stratton CW, et al. Spon­taneous bacterial peritonitis: a review of 28 cases with emphasis on improved survival and factors influencing prognosis. Am J Med 1978;64:592-8.  Back to cited text no. 26    
27.Felisart J, Rimola A, Arroyo V, Perez-Ayuso RM, Quin­tero E, Gines P, Rodes J. Cefotaxime is more effective than is ampicillin-tobramycin in cirrhotics with severe infections. Hepatology 1985;5(3):457-62.  Back to cited text no. 27    
28.Tito L, Rimola A, Gines P, Llach J, Arroyo V, Rodes J. Recurrence of spontaneous bacterial peritonitis in cir­rhosis: frequency and predictive factors. Hepatology 1988;8:27-31.  Back to cited text no. 28    
29.Runyon BA, Antillon MR, McHutchison JG. Diuresis increases ascitic fluid opsonic activity in patients who sur­vive spontanous bacterial peritonitis. J Hepatol 1992;249-52.  Back to cited text no. 29    
30.Rimola A, Bory F, Teres J, Perez-Ayuso RM, Arroyo V, Rodes J. Oral, nonabsorbable antibiotics prevent infec­tion in cirrhotics with gastrointestinal hemorrhage. Hepatology 1985;593):463-7.  Back to cited text no. 30    
31.Soriano G, Guarner C, Teixido M, Such J, Barrios J, Enriquez J, Vilardell F. Selective intestinal decontami­nation prevents spontaneous bacterial peritonitis. Gas­troenterology 1991;100:477-81.  Back to cited text no. 31    
32.Gines P, Rimola A, Planas R, et al. Antibiotic prophylaxis for prevention of spontaneous bacterial peritonitis. Gastroenterology 1991;101:550-1.  Back to cited text no. 32    

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Correspondence Address:
Saleh M Al Amri
Assistant Professor and Consultant Physician Division of Gastroenterology (59) P.O. Box 2925, Riyadh 11461
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


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