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ISSN 1007-9327 CN 14-1219/R  World J Gastroenterol  2009 March 7; 15(9): 1042-1049


Spontaneous bacterial peritonitis

Anastasios Koulaouzidis, Shivaram Bhat, Athar A Saeed

Anastasios Koulaouzidis, Endoscopy Unit, Centre of Liver & Digestive Disorders, Royal Infirmary of Edinburgh, 51 Little France Crescent, Edinburgh, Scotland, EH16 4SA, United Kingdom

Shivaram Bhat, Gastroenterology, Belfast Trust Matter Hospital, 47-51 Crumlin Road, Belfast, Northern Ireland, BT14 6AB, United Kingdom

Athar A Saeed, Gastroenterology Department, Queen Elizabeth Hospital, Gateshead, Tyne & Wear, NE9 6SX, United Kingdom

Author contributions: Koulaouzidis A, Bhat S and Saeed AA contributed equally to this work; Koulaouzidis A designed the review, wrote the introduction, pathogenesis, laboratory diagnosis, and variants, and had overall supervision; Bhat S wrote management; Saeed AA wrote clinical manifestations.

Correspondence to: Anastasios Koulaouzidis, MD, MRCP, Endoscopy Unit, Centre of Liver & Digestive Disorders, Royal Infirmary of Edinburgh, 51 Little France Crescent, Edinburgh, Scotland, EH16 4SA, United Kingdom.

Telephone: +44-131-2421603   Fax: +44-131-2421618

Received: December 24, 2008  Revised: January 8, 2009

Accepted: January 15, 2009

Published online: March 7, 2009



Since its initial description in 1964, research has transformed spontaneous bacterial peritonitis (SBP) from a feared disease (with reported mortality of 90%) to a treatable complication of decompensated cirrhosis, albeit with steady prevalence and a high recurrence rate. Bacterial translocation, the key mechanism in the pathogenesis of SBP, is only possible because of the concurrent failure of defensive mechanisms in cirrhosis. Variants of SBP should be treated. Leucocyte esterase reagent strips have managed to shorten the ‘tap-to-shot’ time, while future studies should look into their combined use with ascitic fluid pH. Third generation cephalosporins are the antibiotic of choice because they have a number of advantages. Renal dysfunction has been shown to be an independent predictor of mortality in patients with SBP. Albumin is felt to reduce the risk of renal impairment by improving effective intravascular volume, and by helping to bind pro-inflammatory molecules. Following a single episode of SBP, patients should have long-term antibiotic prophylaxis and be considered for liver transplantation.


© 2009 The WJG Press and Baishideng. All rights reserved.


Key words: Spontaneous bacterial peritonitis; Infection; Ascites; Leucocyte reagent strips; Portal hypertension; Ascites


Peer reviewer: Diego Garcia-Compean, MD, Professor, Faculty of Medicine, University Hospital, Department of Gastroenterology, Autonomous University of Nuevo Leon, Ave Madero y Gonzalitos, 64700 Monterrey, N.L. Mexico


Koulaouzidis A, Bhat S, Saeed AA. Spontaneous bacterial peritonitis. World J Gastroenterol 2009; 15(9): 1042-1049  Available from: URL:  DOI:



It seems that all diseases or syndromes that comprise our routine differential diagnoses were, not so long ago, obscure clinical entities, at least until an astute clinician came across them. It was not any different for spontaneous bacterial peritonitis (SBP).

    Although Laënnec’s name had been connected with cirrhosis since the early 1800s, it was only much later that SBP was diagnosed as a separate entity. The papers of Kerr et al[1] and Conn[2], which were published within a year of each other, describe the infection of ascitic fluid in the absence of a contiguous source of infection or an intra-abdominal inflammatory focus. Although similar reports had been published in the French literature since 1893, Conn[2] was the one who eventually coined the term (SBP) in his 1964 paper.

    Since then, further research has made the once-feared disease (early reported mortality of 90%)[2] a treatable complication of decompensated cirrhosis[3], albeit with a steady prevalence and high recurrence rate[4,5]. The plethora of publications has also led to national/international guidelines and recommendations over the last 10 years[5-11].



The importance of the liver as a bacterial filter is well established. However, it was Conn[2] who hypothesized that intestinal bacteria escaping into the blood stream cause prolonged bacteremia, and in turn, a greater chance of ascitic fluid invasion[3]. Other early reports have emphasized the possibility of abdominal paracentesis-induced SBP[1,3], and certainly, prior to the use of stringent skin disinfection and protective clothing, the incidence of paracentesis-induced peritonitis would have been higher. The negative impact of this thinking created generations of clinicians who were hesitant and unsure about dealing with infective ascites. The persistence of researchers has helped to assuage concerns and has led to a more liberal and appropriate paracentesis protocol[12-14].

    Bacterial translocation (BT), the key mechanism in the pathogenesis of SBP, is only possible because of the concurrent failure of defensive mechanisms in cirrhosis[15-19]. Since the early 1990s, on-going research has confirmed the intensity of BT in cirrhotic rats[15-18,20,21]. Investigators have also demonstrated pronounced impairment of gastrointestinal tract motility in cirrhosis[22-24]. The disturbance of gut flora microecology that follows, in association with changes in the (ultra)structure of the gastrointestinal tract[25-27] and reduced local and humoral immunity paves the way for the relatively free flow of microorganisms and/or endotoxins to the mesenteric lymph nodes[25-27].



The clinical manifestations of SBP are subtle and require a high index of suspicion (Table 1). Previously, there was often delay in diagnosis, which led to considerable mortality and morbidity[28].

    SBP almost always occurs in large volume ascites, in patients with liver cirrhosis. Ascites of other causes or low volume rarely gives rise to SBP. Patients with cirrhosis usually have hypothermia; therefore, any temperature > 37.8 should be investigated, unless it is clearly caused by flu-like symptoms. The necessary investigations are full blood count (FBC), urinalysis, ascitic fluid cell count, and ascites, blood and urine culture. Fever caused by SBP is differentiated from that of alcoholic hepatitis, in which the ascitic fluid neutrophil count is normal[28]. Alterations in mental status may be subtle and only apparent to someone close to the patient. A connect-the-number test, e.g. Reitan trail test, is preferable to testing serum ammonia levels[29]. Abdominal pain can be continuous and is different from tense ascites. Tenderness is a common feature. Paralytic ileus, hypotension and hypothermia are seen in advanced illness, where prognosis may be dire. Thirteen percent of patients have no signs or symptoms[28]. A ‘diagnostic tap’ should be performed in all patients with ascites admitted to hospital. SBP in outpatients with cirrhotic ascites is less frequent, occurs in patients with less advanced liver disease, and may have a better outcome than its counterpart in hospitalized patients[30]. A retrospective review of 916 outpatient AF samples from the United States showed that abnormal AF appearance had a sensitivity of 98.1% [(95% confidence interval (CI): 95.3%-99.5%] and a specificity of 22.7% (95% CI: 19.4%-26.3%) in the detection of SBP[31]. For out- and inpatients, laboratory abnormalities such as leukocytosis, metabolic acidosis and azotemia, should prompt investigations for SBP, even in the absence of other clinical features.



The process of ascitic fluid analysis has come a long way. Inspections for color and transparency (as first evidence of infection) will probably always be carried out. Practice from this point forward, however, varies between regions and to a lesser extent, between hospitals. Over the last decade, it seems that a selective, possibly common-sense approach has started to prevail over the light-hearted dictum “send it (AF) for everything”.

    The diagnostic algorithm proposed by Runyon[28] (Figure 1) remains the most logical and cost-effective way to handle an abdominal paracentesis specimen, and we recommend that every gastrointestinal (GI) ward should have a laminated copy readily available in the doctors’ office or protocol folder. Diagnostic paracentesis is now regarded as a safe procedure. Undoubtedly, there are complications inherent with the test, but the incidence rate of these is low[32-34]. The reported risks of diagnostic paracentesis include bleeding (hemoperitoneum or abdominal wall hematoma), visceral perforation, local infection at the site of paracentesis, or peritonitis. However, the most common complication is persistent leak. Post-procedural bleeding risk is very low, not only for diagnostic, but also for therapeutic taps[33-36]. Runyon has suggested that the practice of attempting to correct any coagulopathy prior to paracentesis is not cost-effective[28]. The use of trans-abdominal ultrasound (TUS) assists in a more accurate AF tap; therefore, it is an appealing alternative to the blind technique[37-39].

    The majority of the inpatient diagnostic AF taps are performed with a blind technique. The accepted area of preference is away from the midline, at the point of maximal dullness, and ideally in the left iliac fossa, two fingerbreadths medial and two ventral to the anterior superior iliac spine (“Runyon’s spot”)[28]. We advise that after two dry taps, TUS should be used to mark the best insertion spot. Equipment required for the tap comprises: 10-mL syringe; 1.5-inch, 22-gauge metal (or 18-gauge) needle; pack of sterile gloves and a galipot with skin disinfectant[34,40]. Thirty milliliters of ascitic fluid should be aspirated and distributed between two blood culture bottles (aerobic and anaerobic, ideally 5-10 mL
in each after replacement of the paracentesis green needle by a sterile one), a purple top tube and a brown top one for the necessary biochemistry.

    The biochemical tests required for every ascitic fluid sample are for protein, albumin, glucose and lactate dehydrogenase, while other tests are graded between optional and unnecessary. Further expansion on AF biochemistry is beyond the scope of this review and the reader is advised to consult relevant textbooks/reviews[28]. Reference will only be made to AF tests used for the diagnosis of SBP.

    A review of the laboratory diagnosis of SBP would not be complete without alluding to the most recent and practical change in protocol. Following aspiration of the AF sample, after inoculating the culture bottles and prior to splitting the rest of the sample into the purple- and brown-topped tubes, a small amount should be poured over a leukocyte esterase reagent strip (LERS) (any urine dipstick has the relevant reagent square), in order to detect any color change in the respective square. The colorimetric scale reference chart can be viewed on the side of the storage container. Results are obtained by direct optical comparison of the LERS with the scale, or, when available, by spectrophotometric analysis. Hepatologists, gastroenterologists and internists have developed an interest in this new addition (at least for AF analysis), especially as satisfactory sensitivity and specificity for SBP detection have been reported in small French and Spanish studies[41-43]. Further studies have been conducted worldwide[44-48]. However, initial enthusiasm and suggestions that LERSs may be used as the sole method of detection of AF infection have been tempered by the latest reports and two systematic reviews[49-51]. It appears that enthusiasm alone replaced structured, evidence-based approaches for LERSs in the presumptive diagnosis of SBP[50,51].

    In rural, remote and smaller hospitals and in developing countries, LERSs shrink the ‘tap-to-shot’ time i.e. the time between paracentesis and first antibiotic dose, to only a few minutes. LERSs bear no resemblance to pH, lactate, lactoferrin or other difficult-to-measure infection indices. However, they are cheap and readily available. Moreover, no diagnosis is made in a clinical vacuum and in the right clinical context, the use of a single ‘stat’ dose prompted by a positive LERS can potentially lessen the burden of infection[51-53].

    Eventually, the AF sample will find its way to the bench of a busy clinical laboratory. It is known that in SBP, the number of polymorphonuclear neutrophils (PMNs) in the ascitic fluid is 250/mL[6,28]. Despite numerous publications emphasizing the contrary[13,28,54,55], many AF samples are prioritized inappropriately by clinical laboratories, giving rise to a significant delay in results. The manual count (performed by the traditional hematological method utilizing a microscope and Bucker chamber) is laborious and, in many instances, subjective. Angeloni et al[56] have produced clinical evidence that manual and automated PMN counting is equally efficient[57]. Cereto et al[58] have confirmed these results. Two years later, Link and colleagues (prompted by the statement of the International Ascites Club consensus document) examined the use of automated counters in detecting the total leucocyte count in ascitic fluid and diagnosing SBP[59]. It is surprising that such a crucial issue in expediting the diagnosis of SBP remained unaddressed for so long by many laboratories, which, despite the above evidence, continued to employ the old-fashioned manual technique over the automated one. At this point, it is necessary to highlight an important caveat when determining AF PMN count: an accurate PMN count may only be determined after non-traumatic paracentesis. If the tap is traumatic or the fluid is a priori hemorrhagic (red cells 10000/mL), the PMN count should be corrected as follows: subtract (from the measured PMN count) 1 PMN for every 250 red cells[7].

    Opinion is still divided on the issue of automated vs manual testing, but utilization of culture bottles in SBP diagnosis is now the well-established gold standard. SBP is a low-colony-count, monomicrobial infection of the AF and, in this context, is very similar to bacteremia. The use of blood culture bottles can increase the yield of AF culture from 40% to > 80%[7].

    Although initially attractive[60], pH testing of the AF, has now fallen into obscurity[28,34]. This is partly attributable to limited clinical accessibility and partly to increased investigator interest in newer measurements, i.e. procalcitonin and lactoferrin[4,60]. pH was last used in a clinical study in 1995[34]. In their systematic review, Wong et al[34] have found that ascitic fluid pH 7.35 and blood-ascitic fluid odds ratio (OR) 0.10 had the highest diagnostic OR for SBP, and it may be reasonable to suggest a return to pH testing combined with LERSs as an appropriate means to diagnose SBP. The majority of urine dipsticks include a pH reagent square and the latest study on the subject has demonstrated that combination of LERSs with nitrite offers no additional benefit in SBP detection[48]. As far as we are aware, no study has investigated the combination of pH squares with LERSs. We can, however, envisage similar problems to those experienced by investigators in LERS studies occurring in this instance, namely, the lack of specificity of the reagents used for the usual pH values of AF (urine pH reference range is 6.75-7.5).

    The use of procalcitonin should also be mentioned. Procalcitonin is the pro-hormone of calcitonin. It is synthesized in many different tissues of infected organs and has been hailed as a novel index of inflammation. Initial interest in its use in SBP[61] was eventually dampened by another study a year later[62]. Lactoferrin seems far more promising to serve as a rapid and reliable screening tool for SBP in patients with cirrhosis, and a recent study has suggested the need to develop an AF-specific dipstick[63].



Bacterascites (monomicrobial non-neutrocytic bacterascites) is the term used to describe the colonization of ascitic fluid by bacteria, in the absence of an inflammatory reaction in the bacterial fluid. By definition, the PMN count is < 250/mm3 and bacterial culture is positive, while the patient may present with symptoms and signs of infection. The natural course of bacterascites, if untreated, is variable. Diagnosis of bacterascites can only be made 2-3 d after initial paracentesis (the time necessary for culture growth), and a repeat ascitic tap is recommended on day 3. If the second sample has a PMN count > 250/mm3, the current recommendation is to treat as for SBP. If the PMN count is < 250/mm3, but the second set of cultures is positive, treat again as for SBP. If the PMN count is < 250/mm3 and the second set of cultures is negative, no further action is recommended[7,28].

    Culture-negative neutrocytic ascites is the term used to describe the clinical situation in which the ascitic PMN count is > 250/mm3 but fluid cultures fail to grow any bacteria. It is considered to represent the expected 20% failure rate of culture to isolate microorganisms, and it requires antibiotic treatment as if it were SBP. However, the term is now considered obsolete[28,55].



Appropriate antibiotic therapy should achieve resolution of infection in most cases of SBP[64]. However, the management of SBP is complex and not just a matter of empirical therapy. Important issues include: (1) identification of the underlying organism; (2) choice of safe and appropriate antibiotics; (3) preservation of renal function and treatment of renal dysfunction; (4) duration of antibiotic therapy; and (5) subsequent antibiotic prophylaxis.

    Whilst clarifying the diagnosis of SBP with paracentesis, an attempt should be made at identification of the underlying organism with inoculation of ascitic fluid into blood culture bottles. This vastly improves the identification of the responsible organism and, therefore, allows improved treatment of atypical or resistant organisms. Inoculation into blood culture bottles improves diagnostic yield from 40% to around 80%[65]. Simultaneous blood cultures should be taken as 50% of cases of SBP are associated with bacteremia[66].

    The common causative organisms of SBP are Gram-negative bacteria such as Escherichia coli and other coliforms such as Klebsiella spp. These account for at least 50% of cases. Other causative organisms include pneumococci, streptococci and miscellaneous Gram-positive and -negative organisms[28,55,65,66] (Table 2).

    Empirical therapy should not be delayed (beyond the first few minutes needed for LERS reading) while awaiting identification of the exact organism. Third generation cephalosporins are the antibiotic of choice as they have a number of advantages: (1) relatively safe and well tolerated; (2) broad spectrum activity; and (3) effectiveness, with many studies confirming high levels of SBP resolution.

    Cefotaxime 2 g every 12 h is often used intravenously for at least 5 d[67-69]. A 5-d course of treatment has been shown to be equally effective as 10 d[70]. Other third generation cephalosporins (e.g. ceftriaxone) are felt to be equally effective[3,71-73]. Alternative antibiotic regimens include amoxycillin/clavulanic acid, fluoroquinolones or piperacillin/tazobactam[74-77] (Table 3). Regional resistance patterns should be accounted for with early communication with a microbiologist if necessary[11,77]. According to the International Ascites Club, it is important to perform a second tap 48 h after the start of therapy. If there is a less than a 25% drop in PMN count from baseline, a change of antibiotic should be considered[4,5].


Renal function

One third of patients with SBP will develop renal failure. The renal dysfunction is thought to occur as a result of a reduced effective circulating volume[7,78]. Renal dysfunction has been shown to be an independent predictor of mortality in patients with SBP[79]. Therefore, close attention to renal function and the avoidance of nephrotoxic medication is paramount. On the other hand, diuretic therapy and large-volume paracentesis should not be necessarily withheld (they potentially exacerbate the reduction in effective circulating volume and contribute to renal deterioration) if albumin is administered[80,81]. The benefit of human albumin solution for treating renal dysfunction has been studied in randomized controlled trials[82,83]. Albumin is thought to reduce the risk of renal impairment by improving effective intravascular volume and by helping to bind pro-inflammatory molecules[7,8,11]. Studies have shown an improvement in short-term survival and a reduction in renal impairment in patients with SBP treated with albumin. Although these studies have been subject to criticism[84,85], most authors agree that infusion of 1.5 g/kg on day 1 and 1 g/kg on day 3 is beneficial in patients that have developed, or are developing renal dysfunction[7,61]. Patients with normal renal function are unlikely to benefit from albumin therapy.



Unfortunately, the long-term prognosis of patients with cirrhosis who have had a prior episode of SBP is poor. Mortality rates of 50%-70% have been reported at 1 year follow-up[7,11]. This is largely a result of the advanced stage of liver cirrhosis in these patients, along with the associated complications[86]. The recurrence rate of SBP following a first episode is up to 70% at 1 year[7,86]. Given the high recurrence rate, it seems sensible to recommend prophylaxis to this group of patients and referral for transplant assessment. This therapy is backed up by evidence showing a reduction in recurrence of SBP from 68% to 20% in one study[87].

    Norfloxacin 400 mg/d or ciprofloxacin 500 mg/d orally appear to be the most studied and commonly recommended regimes[87-92]. Levofloxacin or antibiotic cycling may be used as an alternative[93-95]. There is debate over the use of antibiotics as primary prophylaxis against SBP. Some studies have shown reduced rates of SBP in selected patients deemed at high risk of developing SBP (those with low ascitic total protein)[79,91,96]. However, there are various criticisms of these studies, and at present, primary prophylaxis is not recommended. Further studies may help clarify this issue.

    The last group of patients that are felt to benefit from antibiotic prophylaxis are those with known cirrhosis admitted with GI bleeding. Infection rates are high in this group regardless of whether they have ascites. The infection rates are also higher than those in patient with cirrhosis admitted for other reasons[61]. Several studies have shown a clear benefit from initiating antibiotic prophylaxis in this group[97-100]. Reductions in infection rate and mortality have been noted. Once again, the choice of antibiotic should be broad spectrum and guided by local policy; either oral norfloxacin or ciprofloxacin have been suggested[7,61].



1      Kerr DN, Pearson DT, Read AE. Infection of ascitic fluid in patients with hepatic cirrhosis. Gut 1963; 4: 394-398  

        PubMed    DOI

2      Conn HO. Spontaneous peritonitis and bacteremia in laennecs cirrhosis caused by enteric organisms. A relatively

        common but rarely recognized syndrome. Ann Intern Med 1964; 60: 568-580   PubMed

3      Garcia-Tsao G. Spontaneous bacterial peritonitis: a historical perspective. J Hepatol 2004; 41: 522-527   PubMed    DOI

4      Angeloni S, Leboffe C, Parente A, Venditti M, Giordano A, Merli M, Riggio O. Efficacy of current guidelines for the

        treatment of spontaneous bacterial peritonitis in the clinical practice. World J Gastroenterol 2008; 14: 2757-2762  

        PubMed    DOI

5      Wong F, Bernardi M, Balk R, Christman B, Moreau R, Garcia-Tsao G, Patch D, Soriano G, Hoefs J, Navasa M. Sepsis in

        cirrhosis: report on the 7th meeting of the International Ascites Club. Gut 2005; 54: 718-725   PubMed    DOI

6      Salerno F, Angeli P, Bernardi M, Laffi G, Riggio O, Salvagnini M. Clinical practice guidelines for the management of

        cirrhotic patients with ascites. Committee on Ascites of the Italian Association for the Study of the Liver. Ital J

        Gastroenterol Hepatol 1999; 31: 626-634   PubMed

7      Rimola A, García-Tsao G, Navasa M, Piddock LJ, Planas R, Bernard B, Inadomi JM. Diagnosis, treatment and prophylaxis

        of spontaneous bacterial peritonitis: a consensus document. International Ascites Club. J Hepatol 2000; 32: 142-153  

        PubMed    DOI

8      Runyon BA. Management of adult patients with ascites due to cirrhosis. Hepatology 2004; 39: 841-856   PubMed    DOI

9      WGO practice guideline: Condition: Management of ascites complicating cirrhosis in adults. Available from:


10    Peck-Radosavljevic M, Trauner M, Schreiber F. Austrian consensus on the definition and treatment of portal

        hypertension and its complications. Endoscopy 2005; 37: 667-673   PubMed    DOI

11    Moore KP, Aithal GP. Guidelines on the management of ascites in cirrhosis. Gut 2006; 55 Suppl 6: vi1-v12   PubMed           DOI

12    Hoefs JC, Runyon BA. Spontaneous bacterial peritonitis. Dis Mon 1985; 31: 1-48   PubMed

13    Runyon BA. Spontaneous bacterial peritonitis: an explosion of information. Hepatology 1988; 8: 171-175   PubMed

14    Runyon BA. Strips and tubes: improving the diagnosis of spontaneous bacterial peritonitis. Hepatology 2003; 37: 745-

        747   PubMed    DOI

15    Runyon BA, Squier S, Borzio M. Translocation of gut bacteria in rats with cirrhosis to mesenteric lymph nodes partially

        explains the pathogenesis of spontaneous bacterial peritonitis. J Hepatol 1994; 21: 792-796   PubMed

16    Llovet JM, Bartolí R, Planas R, Cabré E, Jimenez M, Urban A, Ojanguren I, Arnal J, Gassull MA. Bacterial translocation in

        cirrhotic rats. Its role in the development of spontaneous bacterial peritonitis. Gut 1994; 35: 1648-1652   PubMed    DOI

17    Garcia-Tsao G, Lee FY, Barden GE, Cartun R, West AB. Bacterial translocation to mesenteric lymph nodes is increased in

        cirrhotic rats with ascites. Gastroenterology 1995; 108: 1835-1841   PubMed

18    Guarner C, Runyon BA, Young S, Heck M, Sheikh MY. Intestinal bacterial overgrowth and bacterial translocation in

        cirrhotic rats with ascites. J Hepatol 1997; 26: 1372-1378   PubMed    DOI

19    Cirera I, Bauer TM, Navasa M, Vila J, Grande L, Taurá P, Fuster J, García-Valdecasas JC, Lacy A, Suárez MJ, Rimola A,

        Rodés J. Bacterial translocation of enteric organisms in patients with cirrhosis. J Hepatol 2001; 34: 32-37   PubMed

20    Runyon BA, Sugano S, Kanel G, Mellencamp MA. A rodent model of cirrhosis, ascites, and bacterial peritonitis.

        Gastroenterology 1991; 100: 489-493   PubMed

21    Sánchez E, Casafont F, Guerra A, de Benito I, Pons-Romero F. Role of intestinal bacterial overgrowth and intestinal

        motility in bacterial translocation in experimental cirrhosis. Rev Esp Enferm Dig 2005; 97: 805-814   PubMed    DOI

22    Chesta J, Lillo R, Defilippi C, Jouanee E, Massone MA, Maulén M, Zavala A. [Patients with liver cirrhosis: mouth-cecum

        transit time and gastric emptying of solid foods] Rev Med Chil 1991; 119: 1248-1253   PubMed

23    Madrid AM, Cumsille F, Defilippi C. Altered small bowel motility in patients with liver cirrhosis depends on severity of

        liver disease. Dig Dis Sci 1997; 42: 738-742   PubMed    DOI

24    Madrid AM, Brahm J, Antezana C, González-Koch A, Defilippi C, Pimentel C, Oksenberg D, Defilippi C. Small bowel

        motility in primary biliary cirrhosis. Am J Gastroenterol 1998; 93: 2436-2440   PubMed

25    Chiva M, Guarner C, Peralta C, Llovet T, Gómez G, Soriano G, Balanzó J. Intestinal mucosal oxidative damage and

        bacterial translocation in cirrhotic rats. Eur J Gastroenterol Hepatol 2003; 15: 145-150   PubMed

26    Ramachandran A, Prabhu R, Thomas S, Reddy JB, Pulimood A, Balasubramanian KA. Intestinal mucosal alterations in

        experimental cirrhosis in the rat: role of oxygen free radicals. Hepatology 2002; 35: 622-629   PubMed    DOI

27    Karahan OI, Dodd GD 3rd, Chintapalli KN, Rhim H, Chopra S. Gastrointestinal wall thickening in patients with cirrhosis:

        frequency and patterns at contrast-enhanced CT. Radiology 2000; 215: 103-107   PubMed

28    Runyon BA. Ascites and spontaneous bacterial peritonitis. In: Feldman M, Friedman LS, Sleisenger MH, eds. Sleisenger

        and Fordran’s gastrointestinal and liver disease, 8th ed. Philadelphia: Saunders, 2006: 1935-1964

29    Conn HO. Trailmaking and number-connection tests in the assessment of mental state in portal systemic

        encephalopathy. Am J Dig Dis 1977; 22: 541-550   PubMed

30    Evans LT, Kim WR, Poterucha JJ, Kamath PS. Spontaneous bacterial peritonitis in asymptomatic outpatients with

        cirrhotic ascites. Hepatology 2003; 37: 897-901   PubMed    DOI

31    Chinnock B, Hendey GW. Can clear ascitic fluid appearance rule out spontaneous bacterial peritonitis? Am J Emerg Med

        2007; 25: 934-937   PubMed    DOI

32    Runyon BA. Paracentesis of ascitic fluid. A safe procedure. Arch Intern Med 1986; 146: 2259-2261   PubMed

33    McGibbon A, Chen GI, Peltekian KM, van Zanten SV. An evidence-based manual for abdominal paracentesis. Dig Dis Sci

        2007; 52: 3307-3315   PubMed    DOI

34    Wong CL, Holroyd-Leduc J, Thorpe KE, Straus SE. Does this patient have bacterial peritonitis or portal hypertension?

        How do I perform a paracentesis and analyze the results? JAMA 2008; 299: 1166-1178   PubMed

35    Pache I, Bilodeau M. Severe haemorrhage following abdominal paracentesis for ascites in patients with liver disease.

        Aliment Pharmacol Ther 2005; 21: 525-529   PubMed    DOI

36    Grabau CM, Crago SF, Hoff LK, Simon JA, Melton CA, Ott BJ, Kamath PS. Performance standards for therapeutic

        abdominal paracentesis. Hepatology 2004; 40: 484-488   PubMed    DOI

37    Bard C, Lafortune M, Breton G. Ascites: ultrasound guidance or blind paracentesis? CMAJ 1986; 135: 209-210   PubMed

38    Nazeer SR, Dewbre H, Miller AH. Ultrasound-assisted paracentesis performed by emergency physicians vs the

        traditional technique: a prospective, randomized study. Am J Emerg Med 2005; 23: 363-367   PubMed    DOI

39    Sakai H, Sheer TA, Mendler MH, Runyon BA. Choosing the location for non-image guided abdominal paracentesis. Liver

        Int 2005; 25: 984-986   PubMed    DOI

40    Thomsen TW, Shaffer RW, White B, Setnik GS. Videos in clinical medicine. Paracentesis. N Engl J Med 2006; 355: e21           PubMed

41    Vanbiervliet G, Rakotoarisoa C, Filippi J, Guérin O, Calle G, Hastier P, Mariné-Barjoan E, Schneider S, Piche T,

        Broussard JF, Dor JF, Benzaken S, Hébuterne X, Rampal P, Tran A. Diagnostic accuracy of a rapid urine-screening test

        (Multistix8SG) in cirrhotic patients with spontaneous bacterial peritonitis. Eur J Gastroenterol Hepatol 2002; 14: 1257-

        1260   PubMed

42    Castellote J, López C, Gornals J, Tremosa G, Fariña ER, Baliellas C, Domingo A, Xiol X. Rapid diagnosis of spontaneous

        bacterial peritonitis by use of reagent strips. Hepatology 2003; 37: 893-896   PubMed    DOI

43    Thévenot T, Cadranel JF, Nguyen-Khac E, Tilmant L, Tiry C, Welty S, Merzoug N. Diagnosis of spontaneous bacterial

        peritonitis in cirrhotic patients by use of two reagent strips. Eur J Gastroenterol Hepatol 2004; 16: 579-583   PubMed

44    Sapey T, Mena E, Fort E, Laurin C, Kabissa D, Runyon BA, Mendler MH. Rapid diagnosis of spontaneous bacterial

        peritonitis with leukocyte esterase reagent strips in a European and in an American center. J Gastroenterol Hepatol

        2005; 20: 187-192   PubMed    DOI

45    Braga LL, Souza MH, Barbosa AM, Furtado FM, Campelo PA, Araújo Filho AH. Diagnosis of spontaneous bacterial

        peritonitis in cirrhotic patients in northeastern Brazil by use of rapid urine-screening test. Sao Paulo Med J 2006; 124:

        141-144   PubMed    DOI

46    Li J, Pan Y, Bao WG, Niu JQ, Wang F. [Multistix10SG urine test in diagnosing spontaneous bacterial peritonitis] Zhonghua

        Ganzangbing Zazhi 2006; 14: 784-785   PubMed

47    Rerknimitr R, Rungsangmanoon W, Kongkam P, Kullavanijaya P. Efficacy of leukocyte esterase dipstick test as a rapid

        test in diagnosis of spontaneous bacterial peritonitis. World J Gastroenterol 2006; 12: 7183-7187   PubMed

48    Torun S, Dolar E, Yilmaz Y, Keskin M, Kiyici M, Sinirtas M, Sarandol E, Gurel S, Nak SG, Gulten M. Evaluation of leukocyte

        esterase and nitrite strip tests to detect spontaneous bacterial peritonitis in cirrhotic patients. World J Gastroenterol

        2007; 13: 6027-6030   PubMed

49    Nousbaum JB, Cadranel JF, Nahon P, Khac EN, Moreau R, Thévenot T, Silvain C, Bureau C, Nouel O, Pilette C, Paupard

        T, Vanbiervliet G, Oberti F, Davion T, Jouannaud V, Roche B, Bernard PH, Beaulieu S, Danne O, Thabut D, Chagneau-

        Derrode C, de Lédinghen V, Mathurin P, Pauwels A, Bronowicki JP, Habersetzer F, Abergel A, Audigier JC, Sapey T,

        Grangé JD, Tran A. Diagnostic accuracy of the Multistix 8 SG reagent strip in diagnosis of spontaneous bacterial

        peritonitis. Hepatology 2007; 45: 1275-1281   PubMed    DOI

50    Nguyen-Khac E, Cadranel JF, Thevenot T, Nousbaum JB. Review article: the utility of reagent strips in the diagnosis of

        infected ascites in cirrhotic patients. Aliment Pharmacol Ther 2008; 28: 282-288   PubMed    DOI

51    Koulaouzidis A, Leontiadis GI, Abdullah M, Moschos J, Gasem J, Tharakan J, Maltezos E, Saeed AA. Leucocyte esterase

        reagent strips for the diagnosis of spontaneous bacterial peritonitis: a systematic review. Eur J Gastroenterol Hepatol

        2008; 20: 1055-1060   PubMed

52    Castellote J, Xiol X. Reagent strips and spontaneous bacterial peritonitis. Aliment Pharmacol Ther 2008; 28: 660;

        author reply 661   PubMed    DOI

53    Sierra F, Torres D, Cárdenas A. The role of likelihood ratio in clinical diagnosis: applicability in the setting of

        spontaneous bacterial peritonitis. Clin Gastroenterol Hepatol 2005; 3: 85-89   PubMed

54    Koulaouzidis A, Said E, Saeed AA. Use of urine dipsticks in spontaneous bacterial peritonitis (SBP): benefit for the busy

        junior physician [abstract]. Endoscopy 2006; 38: 1187

55    Koulaouzidis A, Bhat S, Karagiannidis A, Tan WC, Linaker BD. Spontaneous bacterial peritonitis. Postgrad Med J 2007;

        83: 379-383   PubMed

56    Angeloni S, Nicolini G, Merli M, Nicolao F, Pinto G, Aronne T, Attili AF, Riggio O. Validation of automated blood cell

        counter for the determination of polymorphonuclear cell count in the ascitic fluid of cirrhotic patients with or without

        spontaneous bacterial peritonitis. Am J Gastroenterol 2003; 98: 1844-1848   PubMed    DOI

57    Riggio O, Angeloni S, Parente A, Leboffe C, Pinto G, Aronne T, Merli M. Accuracy of the automated cell counters for

        management of spontaneous bacterial peritonitis. World J Gastroenterol 2008; 14: 5689-5694   PubMed    DOI

58    Cereto F, Genescà J, Segura R. Validation of automated blood cell counters for the diagnosis of spontaneous bacterial

        peritonitis. Am J Gastroenterol 2004; 99: 1400   PubMed    DOI

59    Link BC, Ziske CG, Schepke M, Schmidt-Wolf IG, Sauerbruch T. Total ascitic fluid leukocyte count for reliable exclusion of

        spontaneous bacterial peritonitis in patients with ascites. Eur J Gastroenterol Hepatol 2006; 18: 181-186   PubMed

60    Stassen WN, McCullough AJ, Bacon BR, Gutnik SH, Wadiwala IM, McLaren C, Kalhan SC, Tavill AS. Immediate

        diagnostic criteria for bacterial infection of ascitic fluid. Evaluation of ascitic fluid polymorphonuclear leukocyte count, pH,

        and lactate concentration, alone and in combination. Gastroenterology 1986; 90: 1247-1254   PubMed

61    Viallon A, Zeni F, Pouzet V, Lambert C, Quenet S, Aubert G, Guyomarch S, Tardy B, Bertrand JC. Serum and ascitic

        procalcitonin levels in cirrhotic patients with spontaneous bacterial peritonitis: diagnostic value and relationship to pro-

        inflammatory cytokines. Intensive Care Med 2000; 26: 1082-1088   PubMed

62    Spahr L, Morard I, Hadengue A, Vadas L, Pugin J. Procalcitonin is not an accurate marker of spontaneous bacterial

        peritonitis in patients with cirrhosis. Hepatogastroenterology 2001; 48: 502-505   PubMed

63    Parsi MA, Saadeh SN, Zein NN, Davis GL, Lopez R, Boone J, Lepe MR, Guo L, Ashfaq M, Klintmalm G, McCullough AJ.

        Ascitic fluid lactoferrin for diagnosis of spontaneous bacterial peritonitis. Gastroenterology 2008; 135: 803-807  

        PubMed    DOI

64    Ghassemi S, Garcia-Tsao G. Prevention and treatment of infections in patients with cirrhosis. Best Pract Res Clin

        Gastroenterol 2007; 21: 77-93   PubMed    DOI

65    Garcia-Tsao G. Spontaneous bacterial peritonitis. Gastroenterol Clin North Am 1992; 21: 257-275   PubMed

66    Arroyo V, Bataller R, Ginès P. Spontaneous bacterial peritonitis. In: O’Grady. IG, Lake JR, Howdle PD, eds.

        Comprehensive clinical hepatology, 1st ed. Barcelona: Mosby, 2000: 153-169

67    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: 457-462   PubMed

68    Chen TA, Lo GH, Lai KH, Lin WJ. Single daily amikacin versus cefotaxime in the short-course treatment of spontaneous

        bacterial peritonitis in cirrhotics. World J Gastroenterol 2005; 11: 6823-6827   PubMed

69    Rimola A, Salmerón JM, Clemente G, Rodrigo L, Obrador A, Miranda ML, Guarner C, Planas R, Solá R, Vargas V. Two

        different dosages of cefotaxime in the treatment of spontaneous bacterial peritonitis in cirrhosis: results of a

        prospective, randomized, multicenter study. Hepatology 1995; 21: 674-679   PubMed

70    Runyon BA, McHutchison JG, Antillon MR, Akriviadis EA, Montano AA. Short-course versus long-course antibiotic

        treatment of spontaneous bacterial peritonitis. A randomized controlled study of 100 patients. Gastroenterology 1991;

        100: 1737-1742   PubMed

71    França A, Giordano HM, Sevá-Pereira T, Soares EC. Five days of ceftriaxone to treat spontaneous bacterial peritonitis in

        cirrhotic patients. J Gastroenterol 2002; 37: 119-122   PubMed

72    Angeli P, Guarda S, Fasolato S, Miola E, Craighero R, Piccolo F, Antona C, Brollo L, Franchin M, Cillo U, Merkel C, Gatta

        A. Switch therapy with ciprofloxacin vs. intravenous ceftazidime in the treatment of spontaneous bacterial peritonitis in

        patients with cirrhosis: similar efficacy at lower cost. Aliment Pharmacol Ther 2006; 23: 75-84   PubMed    DOI

73    Gómez-Jiménez J, Ribera E, Gasser I, Artaza MA, Del Valle O, Pahissa A, Martínez-Vázquez JM. Randomized trial

        comparing ceftriaxone with cefonicid for treatment of spontaneous bacterial peritonitis in cirrhotic patients. Antimicrob

        Agents Chemother 1993; 37: 1587-1592   PubMed

74    Taşkiran B, Colakoğlu O, Sözmen B, Unsal B, Aslan SL, Buyraç Z. Comparison of cefotaxime and ofloxacin in treatment         of spontaneous bacterial peritonitis. Turk J Gastroenterol 2004; 15: 34-38   PubMed

75    Navasa M, Follo A, Llovet JM, Clemente G, Vargas V, Rimola A, Marco F, Guarner C, Forné M, Planas R, Bañares R,

        Castells L, Jimenez De Anta MT, Arroyo V, Rodés J. Randomized, comparative study of oral ofloxacin versus intravenous

        cefotaxime in spontaneous bacterial peritonitis. Gastroenterology 1996; 111: 1011-1017   PubMed

76    Tuncer I, Topcu N, Durmus A, Turkdogan MK. Oral ciprofloxacin versus intravenous cefotaxime and ceftriaxone in the

        treatment of spontaneous bacterial peritonitis. Hepatogastroenterology 2003; 50: 1426-1430   PubMed

77    Soares-Weiser K, Brezis M, Leibovici L. Antibiotics for spontaneous bacterial peritonitis in cirrhotics. Cochrane

        Database Syst Rev 2001; CD002232   PubMed    DOI

78    Follo A, Llovet JM, Navasa M, Planas R, Forns X, Francitorra A, Rimola A, Gassull MA, Arroyo V, Rodés J. Renal

        impairment after spontaneous bacterial peritonitis in cirrhosis: incidence, clinical course, predictive factors and

        prognosis. Hepatology 1994; 20: 1495-1501   PubMed

79    Terg R, Gadano A, Cartier M, Casciato P, Lucero R, Muñoz A, Ro mero G, Levi D, Terg G, Miguez C, Abecasis R. Serum

        creatinine and bilirubin predict renal failure and mortality in patients with spontaneous bacterial peritonitis: a

        retrospective study. Liver Int 2008; 29: 415-419   PubMed    DOI

80    Choi CH, Ahn SH, Kim DY, Lee SK, Park JY, Chon CY, Moon YM, Han KH. Long-term clinical outcome of large volume

        paracentesis with intravenous albumin in patients with spontaneous bacterial peritonitis: a randomized prospective

        study. J Gastroenterol Hepatol 2005; 20: 1215-1222   PubMed    DOI

81    Solà R, Andreu M, Coll S, Vila MC, Oliver MI, Arroyo V. Spontaneous bacterial peritonitis in cirrhotic patients treated

        using paracentesis or diuretics: results of a randomized study. Hepatology 1995; 21: 340-344   PubMed

82    Fernández J, Monteagudo J, Bargallo X, Jiménez W, Bosch J, Arroyo V, Navasa M. A randomized unblinded pilot study

        comparing albumin versus hydroxyethyl starch in spontaneous bacterial peritonitis. Hepatology 2005; 42: 627-634  

        PubMed    DOI

83    Sort P, Navasa M, Arroyo V, Aldeguer X, Planas R, Ruiz-del-Arbol L, Castells L, Vargas V, Soriano G, Guevara M, Ginès

        P, Rodés J. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous

        bacterial peritonitis. N Engl J Med 1999; 341: 403-409   PubMed

84    Sigal SH, Stanca CM, Fernandez J, Arroyo V, Navasa M. Restricted use of albumin for spontaneous bacterial peritonitis.

        Gut 2007; 56: 597-599   PubMed    DOI

85    Wong F. Drug insight: the role of albumin in the management of chronic liver disease. Nat Clin Pract Gastroenterol

        Hepatol 2007; 4: 43-51   PubMed    DOI

86    Garcia-Tsao G. Current management of the complications of cirrhosis and portal hypertension: variceal hemorrhage,

        ascites, and spontaneous bacterial peritonitis. Gastroenterology 2001; 120: 726-748   PubMed

87    Ginés P, Rimola A, Planas R, Vargas V, Marco F, Almela M, Forné M, Miranda ML, Llach J, Salmerón JM. Norfloxacin

        prevents spontaneous bacterial peritonitis recurrence in cirrhosis: results of a double-blind, placebo-controlled trial.

        Hepatology 1990; 12: 716-724   PubMed

88    Inadomi J, Sonnenberg A. Cost-analysis of prophylactic antibiotics in spontaneous bacterial peritonitis. Gastroenterology

        1997; 113: 1289-1294   PubMed

89    Das A. A cost analysis of long term antibiotic prophylaxis for spontaneous bacterial peritonitis in cirrhosis. Am J

        Gastroenterol 1998; 93: 1895-1900   PubMed

90    Grangé JD, Roulot D, Pelletier G, Pariente EA, Denis J, Ink O, Blanc P, Richardet JP, Vinel JP, Delisle F, Fischer D,

        Flahault A, Amiot X. Norfloxacin primary prophylaxis of bacterial infections in cirrhotic patients with ascites: a double-

        blind randomized trial. J Hepatol 1998; 29: 430-436   PubMed

91    Novella M, Solà R, Soriano G, Andreu M, Gana J, Ortiz J, Coll S, Sàbat M, Vila MC, Guarner C, Vilardell F. Continuous

        versus inpatient prophylaxis of the first episode of spontaneous bacterial peritonitis with norfloxacin. Hepatology 1997;

        25: 532-536   PubMed    DOI

92    Rolachon A, Cordier L, Bacq Y, Nousbaum JB, Franza A, Paris JC, Fratte S, Bohn B, Kitmacher P, Stahl JP. Ciprofloxacin

        and long-term prevention of spontaneous bacterial peritonitis: results of a prospective controlled trial. Hepatology 1995;

        22: 1171-1174   PubMed

93    Dupeyron C, Mangeney N, Sedrati L, Campillo B, Fouet P, Leluan G. Rapid emergence of quinolone resistance in

        cirrhotic patients treated with norfloxacin to prevent spontaneous bacterial peritonitis. Antimicrob Agents Chemother

        1994; 38: 340-344   PubMed

94    Esposito S, Noviello S, Leone S, Ianniello F, Ascione T, Gaeta GB. Clinical efficacy and tolerability of levofloxacin in

        patients with liver disease: a prospective, non comparative, observational study. J Chemother 2006; 18: 33-37   PubMed

95   Assy N, Schlesinger S, Miron D, Hussein O. Cycling of antibiotics for the prophylaxis of recurrent spontaneous bacterial

        peritonitis in a cirrhotic patient. World J Gastroenterol 2005; 11: 6407-6408   PubMed

96    Fernández J, Navasa M, Planas R, Montoliu S, Monfort D, Soriano G, Vila C, Pardo A, Quintero E, Vargas V, Such J,

        Ginès P, Arroyo V. Primary prophylaxis of spontaneous bacterial peritonitis delays hepatorenal syndrome and improves

        survival in cirrhosis. Gastroenterology 2007; 133: 818-824   PubMed    DOI

97    Pauwels A, Mostefa-Kara N, Debenes B, Degoutte E, Lévy VG. Systemic antibiotic prophylaxis after gastrointestinal

        hemorrhage in cirrhotic patients with a high risk of infection. Hepatology 1996; 24: 802-806   PubMed

98    Blaise M, Pateron D, Trinchet JC, Levacher S, Beaugrand M, Pourriat JL. Systemic antibiotic therapy prevents bacterial

        infection in cirrhotic patients with gastrointestinal hemorrhage. Hepatology 1994; 20: 34-38   PubMed

99    Hsieh WJ, Lin HC, Hwang SJ, Hou MC, Lee FY, Chang FY, Lee SD. The effect of ciprofloxacin in the prevention of

        bacterial infection in patients with cirrhosis after upper gastrointestinal bleeding. Am J Gastroenterol 1998; 93: 962-

        966   PubMed    DOI

100  Hou MC, Lin HC, Liu TT, Kuo BI, Lee FY, Chang FY, Lee SD. Antibiotic prophylaxis after endoscopic therapy prevents

        rebleeding in acute variceal hemorrhage: a randomized trial. Hepatology 2004; 39: 746-753   PubMed

 S- Editor  Tian L    L- Editor  Kerr C    E- Editor  Zheng XM





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