Bacterial infections are a leading cause of hospitalization and mortality in patients with decompensated cirrhosis. Antibiotic prophylaxis in cirrhotic patients has demonstrated significant short-term reductions in bacterial infections in randomized controlled trials, but at the cost of drug resistance and with uncertain survival benefits.

This review examines antibiotic use in cirrhosis, focusing on patients most likely to benefit from antibiotic prophylaxis, management strategies for infections through risk-based antibiotic selection and timely treatment initiation, challenges posed by the emergence of multidrug-resistant organisms, and principles of antimicrobial stewardship.

The efficacy of prophylaxis has decreased over time, and current registry data have questioned its use, emphasizing the need for better risk-based individualized strategies. When bacterial infections occur, the efficacy of antimicrobial therapies depends heavily on local epidemiological patterns and individual patient risk factors, necessitating tailored antibiotic selection based on regional resistance data and specific clinical scenarios. Nosocomial infections, colonization with multidrug-resistant organisms, and prior exposure to systemic antibiotics are key risk factors that should guide empirical therapy selection. Until evidence-based algorithms are available, clinicians should continue to adopt individualized approaches, guided by available evidence, local specificities, and antimicrobial stewardship principles to optimize patient outcomes.

Antibiotic prophylaxis can reduce the incidence of the first episode and recurrent episodes of spontaneous bacterial peritonitis (SBP) in high-risk cirrhotic patients. However, recent data suggest that SBP prophylaxis may be underused. It is unclear how many cases of cirrhosis that develop SBP might actually be prevented with antibiotic prophylaxis.

To determine the number of "preventable" cases of SBP and the adherence to standard guidelines for the use of antibiotic prophylaxis.

A retrospective analysis of our patients diagnosed with SBP was performed. AASLD Guidelines (2004) for SBP prophylaxis include prior SBP, gastrointestinal (GI) hemorrhage, ascitic fluid (AF), protein ≤ 1 g/dl, or serum bilirubin ≥ 2.5 mg/dl. "Preventable (P) SBP" was defined as SBP occurring where prophylaxis was indicated but was not administered. "Non-preventable (NP) SBP" was defined as SBP that occurred despite proper adherence to the guidelines. "Inevitable (I) SBP" were those cases of SBP occurring in the absence of a documented indication for prophylaxis.

A total of 259 patients with cirrhosis underwent paracentesis; 29 had confirmed SBP. Eighteen of the 29 patients (62%) had "P-SBP", one (3%) had "NP-SBP", and ten (34%) had "I-SBP". In the P-SBP cases, the overlooked indications for prophylaxis were GI hemorrhage (n, %) (8, 44%), serum bilirubin ≥ 2.5 mg/dl (6, 33%), prior SBP (2, 11%) and AF protein ≤ 1 g/dl (2, 11%). Of the P-SBP, 78% were community-acquired; 22% were nosocomial. In-hospital mortality in the P-SBP was 16% (n = 3). Only one-third of patients who survived SBP received long-term outpatient prophylaxis after discharge.

Many cases of SBP could be prevented by adhering to the AASLD guidelines. GI hemorrhage is the most frequently overlooked indication for SBP prophylaxis. Studies identifying the reasons for non-adherence to guidelines and developing interventions to increase utilization are warranted.

Patients with cirrhosis of liver are at risk of developing serious bacterial infections due to altered immune defenses. Despite the widespread use of broad spectrum antibiotics, bacterial infection is responsible for up to a quarter of the deaths of patients with liver disease. Cirrhotic patients with gastrointestinal bleed have a considerably higher incidence of bacterial infections particularly spontaneous bacterial peritonitis. High index of suspicion is required to identify infections at an early stage in the absence of classical signs and symptoms. Energetic use of antibacterial treatment and supportive care has decreased the morbidity and mortality over the years; however, use of antibiotics has to be judicious, as their indiscriminate use can lead to antibiotic resistance with potentially disastrous consequences. Preventive strategies are still in evolution and involve use of antibiotic prophylaxis in patients with gastrointestinal bleeding and spontaneous bacterial infections and selective decontamination of the gut and oropharynx.

Ascites, hepatic encephalopathy and variceal hemorrhage are three major complications of portal hypertension. The diagnostic evaluation of ascites involves an assessment of its etiology by determining the serum-ascites albumin gradient and the exclusion of spontaneous bacterial peritonitis. Ascites is primarily related to an inability to excrete an adequate amount of sodium into urine, leading to a positive sodium balance. Sodium restriction and diuretic therapy are keys of ascites control. But, with the case of refractory ascites, large volume paracentesis and transjugular portosystemic shunts are required. In hepatorenal syndrome, splanchnic vasodilatation with reduction in effective arterial volume causes intense renal vasoconstriction. Splanchnic and/or peripheral vasoconstrictors with albumin infusion, and renal replacement therapy are only bridging therapy. Liver transplantation is the only definitive modality of improving the long term prognosis.

To review relevant studies for both primary and secondary antibiotic prophylaxis of spontaneous bacterial peritonitis (SBP) in patients with cirrhosis without gastrointestinal bleeding.

A search of PubMed (1980-July 2010) was conducted using the terms prophylaxis, SBP, and antibiotics. A manual review of bibliographies was conducted for inclusion of relevant articles.

Prospective studies and meta-analyses published in English were included.

Ten trials and 3 meta-analyses were included. Of the 10 trials, 2 examined the use of secondary prophylaxis for prevention of subsequent episodes of SBP, 4 examined the use of primary prophylaxis to prevent an initial SBP episode, and 4 examined the use of antibiotic prophylaxis in a mixed population. Seven trials evaluated the use of an antibiotic compared to placebo or no treatment. Only 1 trial evaluated norfloxacin versus trimethoprim/sulfamethoxazole. Trial duration varied from 24 days to 12 months. In general, trials examining norfloxacin as secondary prophylaxis found significantly decreased occurrence of SBP but no significant difference in mortality rates. Primary prophylaxis studies found no significant difference in the incidence of infections, including SBP, with norfloxacin or ciprofloxacin treatment but significantly lower incidence of gram-negative infections. Mixed population studies found a significantly decreased incidence of SBP but no significant difference in mortality. In the 3 meta-analyses, a significant decrease in mortality and an overall decrease in SBP incidence in the treatment groups were noted.

Based on currently available data, the use of prophylactic antibiotic therapy is warranted for the prevention of recurrent SBP in patients with cirrhosis and ascites. In patients with low ascetic fluid protein and at least 1 more risk factor, primary prophylaxis may be considered. Further studies with improved methodology are needed to determine whether prophylactic antibiotic therapy has an impact on mortality.

Spontaneous bacterial peritonitis is frequent among cirrhotic patients, associated with significant morbidity and mortality. Selective intestinal decontamination employing antibiotics is a proposed prophylactic measure. While data regarding this modality among cirrhotic patients with gastrointestinal bleeding exist, there is insufficient data synthesis regarding cirrhotic patients with ascites and no gastrointestinal bleeding.

To assess whether antibiotic prophylaxis decreases spontaneous bacterial peritonitis and mortality among cirrhotic patients with ascites and no gastrointestinal bleeding.

We identified relevant randomised trials by searching trial registries of The Cochrane Hepato-Biliary Group and The Cochrane Collaboration, medical literature search engines, and reviewing all literature we found on the topic until February 2009.

We searched for randomised clinical trials assessing prophylactic treatment among adult cirrhotic patients with ascites and no gastrointestinal bleeding, comparing antibiotic therapy with no intervention, placebo, or with another antibiotic regimen.

Three independent authors searched for and collected the trials and extracted relevant data. Four other independent authors validated the findings and assessed them. The studies were assessed for design, patient and intervention characteristics, and quality. A meta-analysis was performed to estimate measures of association between antibiotic prophylaxis and spontaneous bacterial peritonitis or mortality.

Nine trials were included in the review. Seven trials, comparing antibiotics to placebo or no treatment, were meta-analysed. Systematic bias in design or publication is suggested by trial results. The randomisation results suggest that the probability that true randomisation took place in all trials is very small and the report of most trials regarding design was poor. The proportion of participants with spontaneous bacterial peritonitis varied between the trials from 15% to 50%. The calculated relative risks (95% confidence interval) of spontaneous bacterial peritonitis and mortality among patients treated with antibiotics compared with no treatment/placebo were 0.20 (0.11 to 0.37) and 0.61 (0.43 to 0.87). There were very few reports of adverse events.

The pooled estimates suggest that antibiotic prophylaxis might be prudent among cirrhotic patients with ascites and no gastrointestinal bleeding. However, poor trial methodology and report coupled with findings suggesting systematic bias in publication and design reflect the fragility of these findings. Potential hazard to society and the patients themselves from resistant pathogens should be considered when promoting long-lasting antibiotic prophylaxis. It seems that recommending antibiotic prophylaxis is still far from being a substantiated prevention strategy. Trials of better design, well reported, and of longer follow-up are greatly needed.

The use of antibiotics in the primary prophylaxis for spontaneous bacterial peritonitis (SBP) in patients with cirrhosis is controversial. Our purpose was to determine the beneficial effect of fluoroquinolones as compared with placebo in primary prophylaxis of SBP in high-risk patients with cirrhosis by using meta-analysis.

Medline, Embase, Cochrane, and Web of Science databases were searched in all languages until August 2008 for randomized placebo-controlled studies evaluating the role of fluoroquinolones in primary prevention of SBP in patients with low protein ascites (total ascitic protein, <1.5 g/dL) and without history of SBP. Two investigators independently performed literature search and data extraction, and then another investigator independently reviewed whether the studies met prespecified criteria and rechecked data extraction. Odds ratios (Peto method) for the risk reduction with fluoroquinolones were calculated for each study and combined by using a random-effects model.

Four randomized controlled studies met predefined criteria. The odds ratios for developing first episode of SBP, serious infections, and mortality with fluoroquinolone prophylaxis (n = 194) versus placebo (n = 190) were 0.18 (95% confidence interval [CI], 0.09-0.35), 0.18 (95% CI, 0.10-0.32), and 0.60 (95% CI, 0.37-0.97), respectively. All studies were unidirectional in showing the beneficial effect of fluoroquinolone prophylaxis. We were limited by finding few studies with relatively small sample sizes.

Daily oral fluoroquinolone prophylaxis reduces the risk of development of first episode of SBP and mortality in cirrhotic patients with low total protein in the ascitic fluid. Fluoroquinolones might be advisable for the primary prophylaxis of SBP in selected high-risk patients with cirrhosis.

Although norfloxacin (N) is widely accepted as the drug of choice for spontaneous bacterial peritonitis (SBP) prophylaxis, there is data to suggest that trimethoprim-sulfamethoxazole (TS) may be similarly effective. However, no studies have compared the efficacy and safety of N and TS in SBP prophylaxis. The aim of this retrospective analysis was to compare outcomes in patients who received either N or TS for the prevention of SBP.

Records of all cirrhotic patients prescribed either N or TS for SBP prevention between April 2001 and May 2004 were reviewed. Data collected included age, sex, Child-Pugh score, ascitic protein concentration, etiology of liver disease, infections (SBP, bacteremia, and extraperitoneal infections), side-effects, and survival.

Sixty-nine patients (18 female, 51 male), mean age 53.9 +/- 10.6 years, were prescribed N (n = 37) or TS (n = 32). The Child-Pugh score, model for end-stage liver disease score, and the prevalence of a low ascitic protein (<15 g/L) were similar between the groups (12.0 vs 12.4, 19.7 vs 18.2, and 78% vs 84%, respectively, P > 0.05). Fourteen (38%) infections occurred in the N group and 16 (50%) in the TS group (P > 0.05). Eight patients (21.6%) in the N group and nine (28%) in the TS group developed SBP (P > 0.05). The rates of liver transplantation (10 vs 13), adverse events (two in each group) and death (13 vs 14) were similar in the two treatment groups.

Our findings suggest N and TS have similar efficacy in preventing SBP. This has significant implications for both the cost of SBP prophylaxis and the prevalence of fluoroquinolone resistance in patients with cirrhosis.

Spontaneous bacterial peritonitis (SBP) is the infection of ascitic fluid in the absence of any intra-abdominal, surgically treatable source of infection. Despite timely diagnosis and treatment its reported incidence in ascitic patients varies between 7-30%. Ascitic paracentesis remains the chief diagnostic procedure. Automated cell counters have the same diagnostic accuracy as the manual measurement of white cells. Lately, the use of leucocyte reagent strips (dipsticks) has emerged as a useful alternative. Examination of the fluid is not complete unless the sample is inoculated in blood culture bottles. Treatment is currently with third-generation cephalosporins or oral quinolones. Following a single episode of SBP patients should have long term antibiotic prophylaxis.

Patients with cirrhosis have altered immune defenses and are considered immunocompromised individuals. Changes in gut motility, mucosal defense and microflora allow for translocation of enteric bacteria into mesenteric lymph nodes and the blood stream. Additionally, the cirrhotic liver is ineffective at clearing bacteria and associated endotoxins from the blood thus allowing for seeding of the sterile peritoneal fluid. Thus, hospitalised cirrhotic patients, particularly those with gastrointestinal hemorrhage, are at high risk of developing bacterial infections, the most common being spontaneous bacterial peritonitis. Given the significant morbidity and mortality associated with spontaneous bacterial peritonitis and the fact that half of the cases are community acquired, all hospitalised cirrhotic patients should have a diagnostic paracentesis to exclude infection. Those admitted with gastrointestinal bleed and a negative paracentesis require short-term prophylaxis with norfloxacin. A third generation cephalosporin is the treatment of choice for spontaneous bacterial peritonitis and, once the acute infection is resolved, secondary prophylaxis with oral norfloxacin is warranted. Patients who develop renal dysfunction at the time of active infection have the highest mortality and require adjunctive albumin therapy. This article reviews the pathogenesis of SBP, the evidence behind the antibiotics used, the rationale for adjunctive albumin therapy in the setting of acute renal failure, and the role of prophylactic antibiotics in specific high-risk populations.

Spontaneous bacterial peritonitis (SBP) is one of the main infectious complications of cirrhosis and occurs in 8-30% of hospitalized patients with ascites. SBP is characterized by infection of the ascitic fluid (AF) in the absence of any primary focus of intra-abdominal infection. The main route by which the AF becomes infected is the hematogenous route. The pathogenic mechanism by which infection develops is bacterial translocation from the intestinal flora to the mesenteric lymph nodes and from there to the bloodstream. Contributing factors are an increased growth of Gram-negative aerobic bacilli in the jejunum, changes in the intestinal barrier and in addition factors which could reduce the local flow of blood. For clinical diagnosis, patients with SBP may present signs of peritoneal irritation and pain, together with changes in gastrointestinal motility, sometimes with nausea, vomiting, diarrhea or ileus. Many patients, however, may not present any symptoms or signs as a result of the presence of SBP. Diagnostic paracentesis of the AF must be performed for every patient with cirrhosis, hospitalized with ascites. Laboratory diagnosis of SBP is carried out by polymorphonuclear count in the AF, together with a positive culture from the AF, which is characteristically monomicrobial. Escherichia coli has been the main bacterium isolated from AF as well as other Gram-negative bacteria from the Enterobacteriaceae family and Streptococcus genus. A more rapid diagnosis of SBP can be obtained via the use of leukocyte esterase, which is present in biological fluids and reacts with a component of the dipstick, changing its color. During the acute phase of SBP, antibiotics should be initiated promptly once the clinical and laboratory diagnosis of SBP has been made, before the result of AF culture. Cefotaxime or other third-generation cephalosporins have been considered the first-choice empirical antibiotics in the treatment of cirrhotic patients with SBP, and is efficacious in approximately 90% of cases. Broad-spectrum quinolones, which are almost completely absorbed after oral administration and diffuse rapidly through the AF, are currently used for oral treatment of uncomplicated SBP. Patients who have already had a previous episode of SBP, with a 69% probability of recurrence within a year, will benefit from prophylactic treatment. Cirrhotic patients with a high risk of SBP and other infections, such as those with gastrointestinal bleeding, also benefit from primary prophylaxis and norfloxacin has been used with success.

Spontaneous bacterial peritonitis is a serious complication of cirrhotic ascites, arising most frequently in those with advanced liver disease. Its development leads to a further reduction in the effective arterial blood volume, and it has a mortality rate equivalent to that of a variceal bleed. However, problems remain with regard to the identification and optimal treatment of spontaneous bacterial peritonitis. Several important studies and consensus documents on the condition have recently been published which aid in the identification of patients at risk and help to guide therapy. In this review, we discuss these publications and address the issues of diagnosis, treatment and both primary and secondary prophylaxis of spontaneous bacterial peritonitis in the light of recent data.

The evaluation of ascites includes a directed history, focused physical examination, and diagnostic paracentesis with ascitic fluid analysis. Dietary sodium restriction and oral diuretics are the mainstay of therapy for the majority of patients with cirrhotic ascites. Transjugular intrahepatic portocaval shunt has emerged as the treatment of choice for selected patients with refractory ascites, although serial large-volume paracenteses should be attempted first. Early diagnosis, broad-spectrum antibiotics, and albumin infusion contribute to the successful management of spontaneous bacterial peritonitis (SBP). Referral for liver transplant evaluation should be considered at the first sign of decompensation and should not be delayed until development of ominous clinical features, such as refractory ascites and SBP.

Spontaneous bacterial peritonitis (SBP) is a frequent complication in cirrhotic patients with ascites. Diagnosis of SBP is established by a polymorphonuclear cell count in ascitic fluid > or =250 cells/mm(3). The organism responsible for the infection is isolated in 60-70% of the cases. The remaining cases are considered to have a variant of SBP (culture-negative SBP) and are treated in the same way as those with a positive culture. The SBP resolution rate ranges between 70 and 90%, and hospital survival between 50 and 70%. An early diagnosis and the use of a more adequate antibiotic therapy are the most probable reasons for the improvement in prognosis for SBP in recent decades. Despite the resolution of the infection, SBP may trigger severe complications such as renal impairment, gastrointestinal bleeding and accentuation of hepatic insufficiency which are responsible for the associated mortality. Patients recovering from an episode of SBP should be considered as potential candidates for liver transplantation.

Although only the expansion of the donor pool will have a major impact on the survival of patients with decompensated cirrhosis awaiting OLT, anticipation of complications such as SBP may improve the likelihood of a patient surviving until OLT, and may ameliorate some of the major causes of morbidity of cirrhosis, such as osteoporosis. Close communication between the treating physicians and the transplant center is crucial to ensure that the patients' UNOS status can be appropriately adjusted if additional complications of cirrhosis, such as intractable ascites, have occurred.

The pathophysiology of circulatory and renal dysfunction in cirrhosis and the treatment of ascites and related conditions (hepatorenal syndrome and spontaneous bacterial peritonitis) have been research topics of major interest during the last two decades. However, many aspects of these problem remain unclear and will constitute major areas of investigation in the next millennium. The pathogenesis of sodium retention, the most prevalent renal function abnormality of cirrhosis, is only partially known. In approximately one third of patients with ascites, sodium retention occurs despite normal activity of the renin-aldosterone and sympathetic nervous systems and increased circulating plasma levels of natriuretic peptides and activity of the so-called natriuretic hormone. These patients present an impairment in circulatory function which, although less intense, is similar to that of patients with increased activity of the renin-aldosterone and sympathetic nervous systems, suggesting that antinatriuretic factors more sensitive to changes in circulatory function that these systems may be important in the pathogenesis of sodium retention in cirrhosis. The development of drugs that inhibit the tubular effect of antidiuretic hormone and increase renal water excretion without affecting urine solute excretion has opened a field of great interest for the management of water retention and dilutional hyponatremia in cirrhosis. Two families of drugs, the V2 vasopressin receptor antagonists and the kappa-opioid agonists, have been shown to improve free water clearance and correct dilutional hyponatremia in human and experimental cirrhosis with ascites. The first type of drugs blocks the tubular effect of antidiuretic hormone and the second inhibits antidiuretic hormone secretion by the neurohypophysis. On the other hand, two new treatments have also been proved to reverse hepatorenal syndrome in cirrhosis. The most interesting one is that based on the simultaneous administration of plasma volume expansion and vasoconstrictors. The second is transjugular intrahepatic porto-systemic shunt. The long-term administration (1-3 weeks) of analogs of vasopressin (ornipressin or terlipressin) or other vasoconstrictors together with plasma volume expansion with albumin is associated with a dramatic improvement in circulatory function and normalization of serum creatinine concentration in patients with severe hepatorenal syndrome. Of interest is the observation that in many of these patients, hepatorenal syndrome does not recur following discontinuation of the treatment, thus raising important questions about the mechanism by which hepatorenal syndrome follows a progressive course in most untreated cases. The pathogenesis of circulatory dysfunction in cirrhosis and the role of local mechanisms in the development of the splanchnic arteriolar vasodilation associated with portal hypertension will continue as important topics in clinical and basic research in Hepatology. Of special interest is the study of the mechanism by which circulatory function further deteriorates following complications such as severe bacterial infection or therapeutic interventions such as therapeutic paracentesis, and the adverse consequences of the impairment in circulatory function on renal and hepatic hemodynamics. Finally, although major advances have been made concerning the treatment and secondary prophylaxis of spontaneous bacterial peritonitis in cirrhosis, many aspects of the pathogenesis of this infection remain unclear. The mechanism of bacterial translocation and of the colonization of bacteria in the ascitic fluid are particularly important to design adequate measures for primary prophylaxis of this severe bacterial infection.

The aim of this study was to perform a cost analysis of different strategies of long term antibiotic prophylaxis for spontaneous bacterial peritonitis (SBP) in patients with cirrhosis and ascites. The study involved a cost analysis using a decision analysis model and patients with cirrhosis and ascites who are at risk for developing SBP.

Two different strategies of antibiotic prophylaxis were compared with a "no prophylaxis" strategy in patients with cirrhosis and ascites using a decision analysis model. In strategy I, antibiotic prophylaxis was administered in all patients with cirrhosis and ascites and in strategy II, patients were stratified into a low risk and a high risk group on the basis of serum bilirubin and ascitic fluid protein levels; only patients in the high risk group received antibiotic prophylaxis. The cost per patient treated for 1 yr was the outcome measure compared in the different strategies. Clinical input probabilities and ranges used were obtained by searching the MEDLINE database for English language articles. Cost estimates were obtained from a university hospital setting. Cost analysis was done with a societal perspective, and only direct costs were taken into account. Sensitivity analyses were performed to evaluate the effect of variations in the key clinical probabilities and cost estimates ranging from a best case to a worst case scenario on the outcome measure.

The estimated cost per patient treated in strategy I, strategy II, and strategy III (the strategy of "no prophylaxis") were $1311, $1123, and $3509, respectively. Over a broad range of clinical and cost variables, the strategy of risk stratification and restriction of antibiotic prophylaxis to the subgroup of patients with cirrhosis and ascites who were at high risk for SBP (as identified by serum bilirubin >2.5 mg/dl and ascitic fluid protein <1 g/dl) was the most favored strategy. However, when the cost of prophylaxis was low or the probability of a primary episode of SBP was at the lower end of the range reported in the literature, administering antibiotic prophylaxis to all patients with cirrhosis and ascites was the least costly strategy.

This cost analysis indicates that antibiotic prophylaxis particularly when restricted to a subgroup of patients who, by simple laboratory parameters, are identified to be at high risk for SBP, is very cost-effective in the prevention of SBP in patients with cirrhosis and ascites.

Norfloxacin is useful to prevent infections in hospitalized cirrhotic patients with low ascitic fluid protein concentrations. It is also effective in preventing the recurrence of spontaneous bacterial peritonitis. The aim of our study was to determine the efficacy of norfloxacin in the primary prophylaxis of gram-negative bacilli infections in cirrhotic patients with low ascitic fluid protein levels (<15 g/l).

One hundred and seven patients were randomized to receive norfloxacin (400 mg/day; n=53) or placebo (n=54) for 6 months. The patients had no history of infection since cirrhosis diagnosis and no active infection.

The probability of gram-negative infection was significantly lower among patients treated with norfloxacin than among those treated with placebo. Six gram-negative bacilli infections occurred in the placebo group and none in the treatment group. Severe infections (spontaneous bacterial peritonitis, neutrocytic ascites and bacteremia) developed in nine patients in the placebo group (17%) and in one patient in the norfloxacin group (2%; p<0.03). There was no between-group difference in the overall rate of infection or in survival. In ten patients from the norfloxacin group, gram-negative bacilli not present in baseline stool cultures were transiently isolated in follow-up cultures.

These data show that primary prophylaxis with norfloxacin for 6 months is effective in the prevention of infections caused by gram-negative bacilli in cirrhotic patients with low ascitic fluid total protein levels.

Intraabdominal infections are commonly encountered in clinical practice and represent a major cause of morbidity and mortality. The most common etiology is contamination of the peritoneal space by endogenous microflora secondary to loss of integrity of the gastrointestinal tract which results in secondary peritonitis. Primary peritonitis or spontaneous bacterial peritonitis is less common and usually occurs in the presence of ascites without an evident source of infection. Peritonitis associated with chronic ambulatory peritoneal dialysis is not discussed in this review. This review summarizes the significant progress which has been made with regard to primary and secondary peritonitis in the last two decades. The review emphasizes the issues of etiology, pathogenesis, microbiology, diagnosis, medical treatment and prevention.