Spontaneous Bacterial Peritonitis: An Update

Subspecialty Clinics: Gastroenterology Spontaneous Bacterial Peritonitis: An Update JORGE

A. GILBERT, M.D., AND PATRICK S. KAMATH, M.D.

• Objective: To describe spontaneous bacterial peritonitis (SBP) in the context of currently accepted criteria for diagnosis, treatment, and prevention. • Design: A review of SBP and its associated etiopathogenic factors is presented. • Material and Methods: Numerous studies on mechanisms of disease, diagnosis, treatment, and prevention are discussed. Diagnostic and therapeutic algorithms are presented. • Results: Peritonitis in patients with ascites in the absence of secondary causes, such as perforation of a viscus, occurs primarily in patients with end-stage liver disease. Enteric organisms, mainly gram-negative bacilli, probably translocate to regional lymph nodes to produce bacteremia and seeding of ascitic fluid. Signs and symptoms of peritonitis are usually

subtle. The ascitic fluid polymorphonuclear leukocyte count is the best determinant for early diagnosis and treatment of SBP. Third-generation cephalosporins such as cefotaxime are considered the drugs of choice for treatment, whereas quinolones such as norfloxacin are used to decrease recurrence. • Conclusion: Despite increased awareness, early diagnosis, and prompt and effective antimicrobial therapy, SBP recurs frequently and is associated with a high mortality rate. Patients with SBP should be assessed for candidacy for liver transplantation. (Mayo Clin Proc 1995; 70:365-370)

=

Spontaneous bacterial peritonitis (SBP) is defined as bacterial peritonitis that occurs in patients with ascites in the absence of recognized, secondary causes such as bowel perforat ion or intra-abdominal abscess. Although SBP has been reported to occur in several conditions associated with ascites, it is noted primarily in patients with cirrhosis and poor hepatic synthetic function. Rarely, SBP occurs in noncirrhotic liver disease such as viral or alcoholic hepatitis.' Since the description of 30 case s of SBP by Conn and Fessel? in 1971, this entity has been increasingly recognized in clinical practice. Although reviews during the 1970s estimated the mean prevalence of SBP in patients with cirrhosis and ascites to be 7%, analy sis of results of routine paracentesis shows a current prevalence of about 15%.1.3 Moreover, SBP is a frequent infection in hospitalized patient s with cirrhosis. Caly and Strau ss" prospecti vely assessed 170 such patients. Bacteri al infections developed in 47% of those patients, 31% of whom had confirmed SBP. The clinical manifestation of SBP may be subtle, and a high index of suspicion is usually necessary for the diagnosis. Despite prompt and effective antim icrobial therapy, SBP continues to be associated with a high mortality rate and a From the Division of Gastroenterology and Intern al Medicine, May o Clin ic Rochester, Rochester, Minnesota. Addr ess reprint requests to Dr. P. S. Kamath, Division of Gastroenterology , Mayo Clinic Rochester, 200 First Stre et SW , Rochester, MN 55905.

Mayo Clin Proc 1995; 70:365-370

=

BA bacterascites; CNNA culture-negative neutrocytic ascites ; PMNs = polymorphonuclear leukocytes; SBP = spontaneous bacterial peritonitis

365

high rate of recurrence. Most patients who survive the first episode of SBP will die of liver failure and complications of portal hypertension rather than of sepsis complicating SBP.5

MICROBIOLOGY AND PATHOGENESIS The bacteria isolated from the ascitic fluid in patients with SBP are usually those of the normal intestinal flora. More than 92% of all cases of SBP are monomicrobial, with aerobic gram -negative bacilli being responsible for more than two-thirds of all cases . Escherich ia coli organisms account for nearly half of these cases, followed by Kleb siella species and other gram-negative bacteria. Gram-positive organi sms are the etiologic agents in almost 25% of all cases, with streptococcal species being the most common. Anaerobic infection is rare; it probably represents no more than 5% of all cases, and, as with polymicrobial bacteria or fungi , clinicians should consider a diagnosis of secondary peritonitis.) As with other bacterial infection s associated with cirrhosis, the mechanisms involved in the development of SBP reflect the severity of the underlying liver disease. Impaired activity of the reticuloendothelial system , decreased serum and ascitic complement levels, and a low ascitic protein level are some of the mechanisms responsible for the entrance of enteral organisms into the ascitic fluid in patients with SBP.6 Previously, investigators thought that bacteria reach the peritoneal cavity by direct transmural migration from the gut. If this concept were correct, bacteria isolated from ascitic fluid © 1995 Mayo Foundation / or Medical Education and Research

For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.

366

Mayo Clin Proc, April 1995, Vol 70

SPONTANEOUS BACTERIAL PERITONITIS

in patients with SBP would be polymicrobial and not predominantly monomicrobial due to aerobic gram-negative baciIli. A current consideration is that portal hypertension increases bacterial translocation to the lymphatic system and portal vein. The potential mechanisms responsible for this action are bacterial overgrowth due to impaired gastrointestinal transit, impaired host defense, or, most likely, morphologic and functional damage to the bowel mucosa. Two studies 7,8 in rats have determined the degree of translocation in surgically induced portal hypertension. Sorell and associates 7 clearly showed that the increase in bacterial translocation to lymph nodes and blood in portal hypertension is significant. The degree of translocation is further increased in the presence of hemorrhagic shock. Whether the direct effect of portal hyperten sion or the underlying liver disease is responsible for this phenomenon is still, however , a matter of debate. In a similar rat model, Wang and colleagues" compared the degree of bacterial translocation in rats that underwent partial and subtotal hepatectomy with rats that had portal hyperten sion produced by portal vein ligation. Although translocation occurred in the group that had portal vein ligation, the degree of translocation was higher in the group that had major liver resection s. Of importance, these studies on surgically induced portal hypertension or hepatic resection do not accurately reflect the clinical situation in which SBP develops in patients with parenchymal liver disease. Thus, animal models with no liver parenchymal disease might not be the best model for studying translocation and SBP. In a rat model with cirrhosis induced by carbon tetrachloride, Runyon and coworkers? recently showed that translocation, defined by culture positivity in lymph nodes, could be demonstrated in 78% of cirrhotic rats in comparison with only 4% of noncirrhotic rats. SBP occurred in approxi mately two-thirds of animals in which translocation could be demonstrated. Of interest, E. coli and other gram-negative enteric organisms were cultured in most cases. Although the exact sequence of events is not entirely clear, microorganisms may translocate to mesenteric lymph nodes, reach the circulation through the thoracic duct, and produce transient bacteremia. Impaired peripheral clearance of bacteria has also been demonstrated in patients with cirrho sis. In such patients, bacteria persist longer in the circulation and eventually gain access to the ascitic fluid as a result of decreased opsonic activity in serum and other neutroph il defects including chemotaxis." Macrophage function has been shown to be impaired in patients with alcoholic cirrhosis. Macrophage Fcy receptors participate in the clearance of IgG-coated microorganisms and thus are important in host defense . The functional integrity of Fcy receptors has been shown to be impaired in patients with autoimmune disease and end-stage

renal disease who are receiving hemodial ysis. Recently, Gomez and associates 11 showed that clearance of IgG-coated erythrocytes by macrophag e Fcy receptors is significantly impaired in patients with alcoholic cirrhosis. Patients with cirrhosis who had this defect had more severe infection s than did patients with cirrhosis without this defect. Moreover, ascitic fluid complement, normally needed for opsonization and phagocytosis, has been shown to be significantly decreased in patients with cirrhosis , a situation that allows bacterial proliferation. Thus, primary bacteremia in conjunc tion with secondary seeding of the ascitic fluid is the most likely explanation for the development of SBP in patients with cirrhosi s.

DIAGNOSIS Although by definition ascites is present in all cases of SBP (Table 1), it may not always be detectable on physical examination. If the diagnosis of SBP is being considered in such situations, an ultrasound study should be done for detection and diagno stic aspiration of ascitic fluid . Fever and abdomin al pain are the most common clinical finding s. Onset or worsening of hepatic encephalopathy, rebound tenderness, and decreased bowel sounds have a varied frequency of occurrence. Occasionally, SBP may manifest as a fulminant variant in conj unction with septic shock. Subtle clinical findings such as mild hepatic encephalopathy, diarrhe a, back pain, hypothermia, and refractoriness to diuretic s have also been observed. Therefore, SBP should be considered in patients with ascites in whom there is clinical deterioration, either in the presence or in the absence of peritoneal signs. A few cases of spontaneous bacterial empyema have recently been described in patients with cirrhosis and SBP. 12 This situation is thought to occur by hematogenous seeding of the pleural fluid or by transfer of infected ascites through the diaphragm. In addition, SBP may be entirely asymptomatic Table I.-Clinical Features of Spontaneous Bacterial Peritonitis Feature

%

Ascites Fever Abdominal pain Onset or worsening of encephalopathy Absence of abdominal findings Rebound tenderness None Hypoten sion

100 50-80 60 60 50 50 10-33 5-15

Data from Correia JP, Conn HO. Spontaneous bacterial peritonitis in cirrhosis: endemic or epidemic? Med Clin North Am 1975 Jul; 59:963-981 and Wilcox CM, Dismukes WE. Spontaneous bacterial peritonitis: a review of pathogenesis, diagnosis, and treatment. Medicine 1987; 66:447-456.

For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.

Mayo Clin Proc, April 1995, Vol 70

SPONTANEOUS BACTERIAL PERITONITIS

in up to 10% of patients; 13 therefore, a high index of suspicion is needed for the diagnosis. Several parameters of ascitic fluid have been studied to provide a rapid and accurate diagnosis of SBP. 14- I6 Ascitic fluid pH seems to be an indirect measurement of the presence of neutrophils, and a large number of them (more than 250 polymorphonuclear leukocytes [PMNs]/mm 3) must be present before the pH decreases. Gram staining of ascitic fluid may help identify peritonitis due to gut perforation, but it infrequently detects bacteria in SBP. Consequently, in that clinical setting, a Gram stain of ascitic fluid should not be routinely ordered. Special smears and cultures for tuberculosis are reserved for specific clinical situations, such as those in which a high fluid cell count has a predominance of lymphocytes. Cytologic tests for malignant lesions should be performed during the initial assessment of patients with ascites but are probably not routinely necessary in a subsequent paracentesis. The PMN count in ascitic fluid is thought to be the single best predictor of SBp I5 (Fig. 1). A PMN count of more than 500/mm 3 has been shown to have a sensitivity of more than 80% and a specificity of 98%. A PMN count of more than 250/mm3 is considered to have a slightly higher sensitivity of about 85% but a mild decrease in specificity to about 93%. Both cell counts have a diagnostic accuracy of more than 90%. Patients with more than 500 PMNs/mm 3 are considered to have SBP even in the absence of clinical signs and symptoms of peritonitis. Patients with an ascitic fluid PMN count between 250 and 500/mm 3 and signs and symptoms of infection presumably have SBP; if the patient is asymp-

tomatic, paracentesis should be repeated in 24 to 48 hours. A cell count of less than 250/mm 3, in the setting of sterile fluid, rules out SBP. For bacterial cultures, 10 mL of ascitic fluid should be routinely inoculated at the bedside in blood-culture bottles. This technique decreases the time for culture positivity and, more importantly, increases the yield of positive cultures in comparison with inoculation by conventional culture techniques. 17

DIFFERENTIAL DIAGNOSIS AND VARIANTS OF SBP Although spontaneous peritonitis is the most frequent cause of bacterial peritonitis in patients with ascites and cirrhosis, a small group of patients with secondary bacterial peritonitis may not have classic peritoneal signs. In an initial specimen of ascitic fluid, a leukocyte count of more than I0,OOO/mm3, a protein concentration of more than I g/dL, and the finding of polymicrobials, particularly in the setting of anaerobic bacteria or fungi, raise suspicion of secondary rather than primary peritonitis. 15.18 Likewise, a low ascitic fluid glucose level and a high concentration of lactate dehydrogenase, although not helpful in distinguishing bacterial peritonitis from sterile ascites, may be of value in recognizing secondary from spontaneous peritonitis." In addition, if, after 48 hours of antibiotic therapy, a diagnostic paracentesis shows an increase in PMNs, we believe that abdominal roentgenography, computed tomography, or water-soluble contrast studies of the upper and lower gastrointestinal tract must be performed to exclude bowel perforation or intra-abdominal abscess. Distinguishing secondary from spontaneous perito-

Ascitic fluid cell count

I

> 500 PMNslmm3

1250-500 PMNslmm31

I

I

I

----,

-No treatment -Follow-up paracentesis mandatory

-No treatment -Follow-up paracentesis not required

L.....-

""----------1

367

Treat as SSP

Fig. 1. Algorithm of utility of ascitic fluid cell counts and ascitic fluid cultures in patients with ascites. PMNs = polymorphonuclear leukocytes; SBP =spontaneous bacterial peritonitis.

For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.

368

SPONTANEOUS BACTERIAL PERITONITIS

nitis is extremely important because secondary peritonitis is best treated surgically. On the basis of the ascitic cell count and culture results, two variants of SBP have been described: culture-negative neutrocytic ascites (CNNA)19-21 and bacterascites (BA).22,23 CNNA is a term used when, in the absence of secondary causes of peritonitis, the ascitic fluid neutrophil count is more than 25D/mm3 but the fluid is sterile. This situation is thought to occur because of inadequate culture techniques or because SBP is resolving. CNNA has a mean prevalence of about 4% in patients with ascites due to cirrhosis; however, in patients with increased PMNs in the absence of secondary causes of peritonitis, about a fifth have CNNA. Studies have shown that this entity probably does not differ from its culture-positive variant relative to severity of liver disease and clinical or laboratory findings. Although the prognosis associated with CNNA in comparison with that of culturepositive cases is unknown, CNNA should be considered and treated as SBP. BA is diagnosed when ascitic fluid cultures are positive in the absence of a substantial ascitic neutrophilic response (PMNs, less than 25D/mm3 ) . Asymptomatic cases of BA may represent the transient passage of bacteria into the ascitic fluid. In contrast to patients with SBP, patients with BA have a tendency toward less severe liver disease and thus a lower incidence of complications such as hepatic encephalopathy and gastrointestinal bleeding. BA may have a higher incidence of gram-positive organisms. In addition, investigators have shown that, if BA is truly asymptomatic, it rarely progresses to SBP and that, in most asymptomatic cases, treatment is unnecessary. Nonetheless, close surveillance is necessary, and diagnostic paracentesis should be repeated promptly if the suspicion of SBP persists. Signs and symptoms of infection in the setting of BA seem to correlate with a high frequency of progression to SBP, and such situations warrant antibiotic therapy.

PROGNOSIS During the past 20 years, the mortality associated with SBP has decreased considerably. When initially described, this entity had a mortality rate between 80 and 90%.2 Currently, most studies show a mortality rate of about 30 to 40%.6 Increased awareness and early diagnosis are probably responsible for this observed decrease in mortality. Factors that have been associated with a poor outcome include a bilirubin level of more than 8 mg/dL, a serum albumin level of less than 2.5 g/dL, a serum creatinine value of more than 2.1 mg/dL, hepatic encephalopathy, hepatorenal syndrome, and upper gastrointestinal bleeding, all indicators of poor liver function (Table 2).24-26 Fever and bacteremia probably do not cause a worse prognosis. A prospective study by Tito and associates" showed that, after an initial episode of SBP,

Mayo CliD Proc, April 1995, Vol 70

Table 2.-Factors Associated With a Poor Outcome in Patients With Spontaneous Bacterial Peritonitis Bilirubin >8 mgldL Albumin <2.5 g/dL Creatinine >2.1 mg/dL Hepatic encephalopathy Hepatorenal syndrome Upper gastrointestinal bleeding

the probability of a recurrence at 1 year is almost 70%. Recurrent episodes are associated with a high mortality rate and are most likely to occur in patients with an ascitic fluid protein level of less than 1 g/dL and a prolonged prothrombin time. Longitudinal assessment of patients who have recovered from an episode of SBP showed that SBP was the cause of death in no more than a third of cases, and, in most patients, the severity of the liver disease dictated the prognosis.' Thus, most patients with SBP are candidates for liver transplantation.

MANAGEMENT Initial studies showed that the combination of ampicillin and an aminoglycoside was associated with a cure rate of at least 75%.1 In subsequent studies, however, aminoglycosides were associated with a high rate of nephrotoxicity and thus should be avoided. Third-generation cephalosporins are currently considered the drugs of choice for SBP (Fig. 2). Cefotaxime, 2 g administered intravenously every 8 hours, has been shown to have a cure rate of at least 85% and has been proved in controlled studies to be more effective than ampicillin-tobramycin; it has a superior safety profile." Other therapeutic alternatives include agents with extended antimicrobial spectrum such as amoxicillin-clavulanic acid, which, in one uncontrolled study," had a cure rate of 85%. In light of the high mortality associated with SBP, intravenous administration of antibiotics for 10 to 14 days has been considered the standard treatment; however, studies have shown that one dose of cefotaxime sterilizes the ascitic fluid in more than 85% of cases, probably because the ascitic fluid bacterial concentration is 10w.IS,1? A study by Runyon and colleagues" showed no difference in infection or hospital-related mortality, bacteriologic cure, or recurrence of infection between patients treated for 10 days versus those treated for 5 days with intravenously administered cefotaxime. No difference was noted between the two groups relative to mortality, even in the patients with bacteremia. Consequently, a brief course of therapy is generally safe. We advocate a repeat paracentesis 48 hours after therapy has been initiated to confirm that cell counts have decreased and that the fluid has become sterile in culture-

For personal use, Mass reproduce only with permission from Mayo Clinic Proceedings,

SPONTANEOUS BACTERIAL PERITONITIS

Mayo Clio Proc, April 1995, Vol 70

369

Cefotaxime,29 I.V. 8h Repeat paracentesis in 48 hr

Decrease in PMNs I

I

I Exclude bowel perforation or intra-abdominal abscess

<250PMNs

Stop treatment after total of 5-7 days

Continue treatment until PMNs <250

Fig. 2. Management algorithm for patients diagnosed with spontaneous bacterial peritonitis. I. V. = intravenous; PMNs = polymorphonuclear leukocytes.

posiuve cases. Generally, we recommend 5 to 7 days of cefotaxime therapy and verify that the PMN count is lower than 250/mm 3 at the completion of treatment. PREVENTION Because of the high mortality and recurrence rates associated with SBP, both primary and secondary preventions have been attempted. Selective decontamination of the digestive tract, a concept introduced by van der Waaij and colleagues" in 1971 and mainly attempted in patients with leukemia receiving chemotherapy, aims at eliminating potentiaIly pathogenic aerobic gram-negative microorganisms from the bowel without affecting the anaerobic microflora responsible for the colonization resistance. In primary prophylaxis, antibiotics such as norfloxacin are used in patients thought to have a high risk for the development of SBP but who as yet do not have the infection. Such high-risk patients include those with a low ascitic fluid protein level, increased bilirubin level, gastrointestinal bleeding, and acute liver failure.":" Studies have shown a significantly decreased incidence of SBP in such groups, primarily due to a reduction in gram-negative bacilli, but have failed to show a significant decrease in mortality or in the number of readmissions to a hospital. Likewise, routine use of intravenous cefotaxime therapy before emergency endoscopic variceal sclerotherapy does not decrease the risk of SBP in patients with variceal hemorrhage." Secondary prophylaxis, which is used to prevent recurrent SBP, was clearly shown by Gines and coworkers" to be effective. In that study, 400 mg of norfloxacin per day decreased the l-year probability of recurrence from 68% to 20%. This reduction was exclusively caused by a substantial

decrease in the incidence of infections caused by aerobic gram-negative bacteria but not by gram-positive organisms. As in primary prevention, this study on prevention of recurrence failed to show a decrease in the number of hospitalizations or in mortality. A recent study by Ukah and assoelates" on the early outcome of liver transplantation in 25 patients with a history of SBP showed that 35% of all postoperative infections were due to an organism identical to the one that caused the episode of SBP before transplantation. Such patients had a higher postoperative morbidity and mortality rate than did those with no peritonitis before transplantation. Thus, prospective studies are needed on the shortand long-term outcome of liver transplantation to assess the efficacy of selective intestinal decontamination. CONCLUSION SBP is a clinical entity noted primarily in patients with endstage liver disease. Aerobic gram-negative bacilli are the predominant organisms involved. Primary bacteremia, which occurs as a consequence of impaired function of the reticuloendothelial system along with an increase in bacterial translocation from the bowel, is probably followed by secondary seeding of the ascitic fluid. Although fever and abdominal pain are the most frequent clinical manifestations, the signs and symptoms may be subtle, or the patient may be asymptomatic. The ascitic fluid PMN count is the best determinant for the diagnosis of SBP; however, its clinical variants should be closely monitored for appropriate management of patients with SBP. Currently, cefotaxime is considered the drug of choice for treatment, whereas nonabsorbable antibiotics such as norfloxacin are used to decrease the recurrence of SBP.

For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.

370

SPONTANEOUS BACTERIAL PERITONITIS

REFERENCES 1. Garcia-Tsao G. Spontaneous bacterial peritonitis. Gastroenterol Clin North Am 1992 Mar; 21:257-275 2. Conn HO, Fessel JM. Spontaneous bacterial peritonitis in cirrhosis: variations on a theme. Medicine 1971; 50: 161-197 3. Kline MM, McCallum RW, Guth PH. The clinical value of ascitic fluid culture and leukocyte count studies in alcoholic cirrhosis. Gastroenterology 1976; 70:408-412 4. Caly WR, Strauss E. A prospective study of bacterial infections in patients with cirrhosis. J Hepatol 1993; 18:353-358 5. Tito L, Rimola A, Gines P, L1ach J, Arroyo V, Rodes J. Recurrence of spontaneous bacterial peritonitis in cirrhosis: frequency and predictive factors. Hepatology 1988; 8:27-31 6. Runyon BA. Spontaneous bacterial peritonitis: an explosion of information. Hepatology 1988; 8: 171-175 7. Sorell WT, Quigley EM, Jin G, Johnson TJ, Rikkers LF. Bacterial translocation in the portal-hypertensive rat: studies in basal conditions and on exposure to hemorrhagic shock. Gastroenterology 1993; 104:1722-1726 8. Wang X, Andersson R, Soltesz V, Wang L, Bengmark S. Effect of portal hypertension on bacterial translocation induced by major liver resection in rats. Eur J Surg 1993; 159:343-350 9. 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; 21:792796 10. Rajkovic lA, Williams R. Abnormalities of neutrophil phagocytosis, intracellular killing and metabolic activity in alcoholic cirrhosis and hepatitis. Hepatology 1986; 6:252-262 II. Gomez F, Ruiz P, Schreiber AD. Impaired function of macrophage Fey receptors and bacterial infection in alcoholic cirrhosis. N Engl J Med 1994; 331:1122-1128 12. Xiol X, Castellote J, Baliellas C, Ariza J, Gimenez Roca A, Guardiola J, et al. Spontaneous bacterial empyema in cirrhotic patients: analysis of eleven cases. Hepatology 1990; 11:365-370 13. Pinzello G, Simonetti RG, Craxi A, Di Piazza S, Spano C, Pagliaro L. Spontaneous bacterial peritonitis: a prospective investigation in predominantly nonalcoholic cirrhotic patients. Hepatology 1983; 3:545-549 14. Runyon BA. Care of patients with ascites. N Engl J Med 1994; 330:337-342 15. Akriviadis EA, Runyon BA. Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis. Gastroenterology 1990; 98:127-133 16. Runyon BA, Antillon MR. Ascitic fluid pH and lactate: insensitive and nonspecific tests in detecting ascitic fluid infection. Hepatology 1991; 13:929-935 17. Runyon BA, Canawati HN, Akriviadis EA. Optimization of ascitic fluid culture technique. Gastroenterology 1988; 95: 1351-1355 18. Runyon BA, Hoefs JC Ascitic fluid analysis in the differentiation of spontaneous bacterial peritonitis from gastrointestinal tract perforation into ascitic fluid. Hepatology 1984; 4:447-450 19. Runyon BA, Hoefs JC. Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis. Hepatology 1984; 4:1209-1211 20. Pascual J, Sureda A, Boixeda D. Culture-negative neutrocytic ascites is a variant of spontaneous bacterial peritonitis [letter]. Am J Gastroenterol 1990; 85: 101-102 21. Pelletier G, Salmon D, Ink 0, Hannoun S, Attali P, Buffet C, et al. Culture-negative neutrocytic ascites: a less severe variant of spontaneous bacterial peritonitis. J Hepatol 1990; 10:327-331

Mayo Clio Proc, April 1995, Vol 70

22. 23. 24. 25.

26.

27.

28.

29.

30. 31. 32. 33. 34.

35.

36.

37.

38.

Runyon BA. Monomicrobial non neutrocytic bacterascites: a variant of spontaneous bacterial peritonitis. Hepatology 1990; 12:710715 Pelletier G, Lesur G, Ink 0, Hagege H, Attali P, Buffet C, et al. Asymptomatic bacterascites: is it spontaneous bacterial peritonitis? Hepatology 1991; 14:112-115 Llovet JM, Planas R, Morillas R, Quer JC, Cabre E, Boix J, et al. Short-term prognosis of cirrhotics with spontaneous bacterial peritonitis: multivariate study. Am J Gastroenterol 1993; 88:388-392 Toledo C, Salmeron JM, Rimola A, Navasa M, Arroyo V, Llach J, et al. Spontaneous bacterial peritonitis in cirrhosis: predictive factors of infection resolution and survival in patients treated with cefotaxime. Hepatology 1993; 17:251-257 Mihas AA, Toussaint J, Hsu HS, Dotherow P, Achord JL. Spontaneous bacterial peritonitis in cirrhosis: clinical and laboratory features, survival and prognostic indicators. Hepatogastroenterology 1992; 39:520-522 Felisart J, Rimola A, Arroyo V, Perez-Ayuso RM, Quintero E, Gines P, et al. Cefotaxime is more effective than is ampicillintobramycin in cirrhotics with severe infections. Hepatology 1985; 5:457-462 Grange JD, Amiot X, Grange V, Gutmann L, Biour M, Bodin F, et al. Amoxicillin-c1avulanic acid therapy of spontaneous bacterial peritonitis: a prospective study of twenty-seven cases in cirrhotic patients. Hepatology 1990; 11:360-364 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 van der Waaij D, Berghuis-de Vries JM, Lekkerkerk-van der Wees JEC Colonization resistance of the digestive tract in conventional and antibiotic-treated mice. J Hyg 1971; 69:405-411 Andreu M, Sola R, Sitges-Serra A, Alia C, Gallen M, Vila MC, et al. Risk factors for spontaneous bacterial peritonitis in cirrhotic patients with ascites. Gastroenterology 1993; 104:1133-1138 Soriano G, Guarner C, Teixido M, Such J, Barrios J, Enriquez J, et al. Selecti ve intestinal decontamination prevents spontaneous bacterial peritonitis. Gastroenterology 1991; 100:477-481 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; 5:463-467 Soriano G, Guarner C, Tomas A, Villanueva C, Torras X, Gonzalez D, et al. Norfloxacin prevents bacterial infection in cirrhotics with gastrointestinal hemorrhage. Gastroenterology 1992; 103:12671272 Salmeron JM, Tito L, Rimola A, Mas A, Navasa MA, L1ach J, et al. Selective intestinal decontamination in the prevention of bacterial infection in patients with acute liver failure. J Hepatol 1992; 14:280285 Selby WS, Norton ID, Pokorny CS, Benn RAV. Bacteremia and bacterascites after endoscopic sclerotherapy for bleeding esophageal varices and prevention by intravenous cefotaxime: a randomized trial. Gastrointest Endosc 1994; 40:680-684 Gines P, Rimola A, Planas R, Vargas V, Marco F, Almela M, et al. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in cirrhosis: results of a double-blind, placebo-controlled trial. Hepatology 1990; 12:716-724 Ukah FO, Merhav H, Kramer D, Eghtesad B, Samimi F, Frezza E, et al. Early outcome of liver transplantation in patients with a history of spontaneous bacterial peritonitis. Transplant Proc 1993; 25:11131115

For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings.