Emergency medicine updates: Spontaneous bacterial peritonitis

a b s t r a c t

Introduction: Spontaneous bacterial peritonitis (SBP) is a common infection in patients with cirrhosis and ascites and is associated with significant risk of mortality. Therefore, it is important for emergency medicine clinicians to be aware of the current evidence regarding the diagnosis and management of this condition.

Objective: This paper evaluates key evidence-based updates concerning SBP for the emergency clinician. Discussion: SBP is commonly due to Gram-negative bacteria, but infections due to Gram-positive bacteria and multidrug resistant bacteria are increasing. The typical presentation of SBP includes abdominal pain, worsening ascites, fever, or altered mental status in a patient with known liver disease; however, some patients may be asymptomatic or present with only mild symptoms. Paracentesis is the Diagnostic modality of choice and should be performed in any patient with ascites and concern for SBP or Upper gastrointestinal bleeding, or in those being admitted for a complication of cirrhosis. Ultrasound should be used to optimize the procedure. An ascites absolute Neutrophil count (ANC) >= 250 cells/mm3 is diagnostic of SBP. Ascitic fluid should be placed in blood cul- ture bottles to improve the culture yield. Leukocyte esterase reagent strips can be used for rapid diagnosis if available. While many patients will demonstrate coagulation panel abnormalities, routine transfusion is not rec- ommended. Management traditionally includes a third-generation cephalosporin, but specific patient popula- tions may require more broad-spectrum coverage with a carbapenem or piperacillin-tazobactam. Albumin infusion is associated with reduced risk of Renal impairment and mortality.

Conclusions: An understanding of literature updates can improve the care of patients with suspected SBP.

Published by Elsevier Inc.

  1. Introduction

end-stage liver disease resulting in cirrhosis and ascites is a major cause of death worldwide and is associated with a variety of complica- tions [1-9]. One of the most common complications is bacterial infection due to the decreased humoral and cell-mediated immunity, abnormal gastrointestinal (GI) function and microbiome, reduced hepatic protein production, and Bacterial translocation worsened by portal hyperten- sion [4-10]. Infections account for 25-46% of admissions in those with decompensated cirrhosis, and infection increases mortality four-fold [4-6,10-13]. The most common infection in patients with cirrhosis is primary spontaneous bacterial peritonitis (SBP), which is an infection of the peritoneal ascitic fluid without an intra-abdominal focus of infec- tion [4-7,10]. SBP accounts for over 30% of all infections in those with cirrhosis and is present in 5-30% of cirrhotic patients admitted with ascites [7,14-23]. Mortality associated with SBP is significant,

* Corresponding author.

E-mail address: [email protected] (B. Long).

1 Present Address: 3551 Roger Brooke Dr. Fort Sam Houston, TX 78234

with mortality rates per episode of SBP ranging from 15 to 40% [16-27]. Literature suggests a 40% survival rate at one year following an episode of SBP [10,28]. Older age, Recurrent episodes of SBP, hepatorenal syndrome, Hepatic encephalopathy, Acute kidney injury , concurrent GI bleeding, and higher Model for End-Stage Liver Dis- ease (MELD) scores are predictors of worse outcomes [4-7,29-31].

SBP is most commonly a monomicrobial infection. The most common microbes involved include Gram-negative bacteria such as

E. coli (48-90% of cases) [32-44]. However, Gram-positive bacteria are becoming more common, as well as infections with multidrug resistant (MDR) bacteria, particularly among those with Nosocomial infections [21,32-46]. Studies suggest SBP due to MDR bacteria or Klebsiella is associated with worse outcomes [47-49]. One study with over 1300 patients with cirrhosis found that half of infections were community acquired, while 25% were nosocomial and another 25% were healthcare associated [11,12].

While emergency clinicians regularly manage patients with cirrhosis, there have been several literature updates concerning primary SBP. The following questions will highlight some of these key updates, but this paper is not intended to serve as a review of SBP in its entirety. 0735-6757/Published by Elsevier Inc.

  1. Discussion
    1. What are the major risk factors for SBP?

There are several risk factors for development of SBP in those with known cirrhosis and ascites. Major risk factors include upper GI bleed- ing, low ascitic protein concentration (< 1.5 g/dL), history of prior SBP, serum total bilirubin >2.5 mg/dL, and malnutrition [4-8,50-56]. Many patients with these risk factors are placed on antibiotic prophy- laxis such as norfloxacin [5-8]. SBP can occur in up to 25-65% of patients with ascites and GI bleeding [4-8,57]. A low ascitic protein concentra- tion < 1.5 g/dL is also a significant risk factor for SBP, particular when combined with Child-Pugh score >= 9, Serum bilirubin level >= 3 mg/dL, creatinine >=1.2 mg/dL or Blood urea nitrogen level >= 25 mg/dL, or serum sodium <=130 mEq/L [4-8,53,57-60]. Prior history of SBP also predicts greater risk, as the recurrence rate of SBP after an initial episode approaches 70% if prophylaxis is not provided [61]. Other risk factors include use of proton pump inhibitors (PPIs), refractory ascites, older age, and endoscopic management of esophageal varices [5-8]. PPIs may increase the risk of SBP by reducing gastric pH and impairing nat- ural host defenses [62,63]. However, the literature is controversial, with some studies demonstrating increased infection and mortality with PPIs and others demonstrating no association [16,39,64-66].

    1. When should SBP be suspected?

The classic presentation of SBP is fever, abdominal pain or tender- ness, and altered mental status in a patient with ascites. However, 10-33% of cases are asymptomatic or demonstrate only mild symptoms [4-9,67,68]. SBP is rare in those with ascites caused by alternate etiologies (e.g., end-stage renal disease, heart failure, peritoneal carcino- matosis, pancreatic disease) in the absence of cirrhosis, though it may still rarely occur [4-6,69]. Clinical deterioration, including altered mental status, AKI, or worsening jaundice, may be suggestive of infec- tion in patients with cirrhosis. Abnormal temperature is a common finding, including both fever and hypothermia. One study found that fever at the time of presentation was 90% specific but only 18% sensitive for the diagnosis [70]. This same study found fever within 24 h of presentation had a sensitivity of 35.5% with a specificity of 81.1% [70]. Importantly, Mild hypothermia is normal in patients with advanced cirrhosis. Thus, a lower threshold for fever is often recommended (i.e., 37.8 ?C) [4-9]. SBP may also present with marked hypothermia (specificity of 93.4%), which is a marker of more severe disease and associated with poor outcome [70].

Abdominal pain or tenderness is the most sensitive finding (94.1%) for SBP, but it is not specific (15.1%) [70]. However, pain and tenderness may be subtle due to the presence of ascites [4-7]. Most patients will demonstrate diffuse abdominal pain, but this will often be different than the pain due to stretching of the abdominal wall associated with worsening ascites. Approximately 50% of patients with SBP will present with some form of altered mental status, with a specificity of 95.3% [6,9,70,71]. However, Mental status changes can be subtle and may best be detected by those who know the patient well (e.g., family, significant other). Diarrhea is also common in those with SBP due to alteration in gut flora [4-7]. Nausea and vomiting have a sensitivity ap- proaching 30% and a specificity of 70% [70]. severe illness can present with hypotension, paralytic ileus, and hypothermia, which are markers of critical illness and associated with increased mortality [4-7]. Exami- nation may reveal abdominal tenderness, but abdominal rigidity does not typically develop even in those with critical illness. Vital sign abnor- malities such as tachycardia may be present, and patients may demon- strate altered mental status. There may be stigmata of liver disease including jaundice, scleral icterus, spider angiomas, palmar erythema, and asterixis [4-9,70]. Unfortunately, clinician gestalt is not reliable in excluding the diagnosis of SBP. One study of ED patients with suspected SBP found that clinician gestalt for the diagnosis of SBP had a sensitivity

of 76% and specificity of 34% [70]. Another study of 43 patients with SBP found that physician clinical suspicion had a sensitivity of 42% for SBP [72]. Of the 43 patients diagnosed with SBP, 25 had a pretest clinical suspicion of “none” or “low” by the emergency clinician [72]. Thus, clin- ical gestalt is not adequate to exclude the diagnosis of SBP without peritoneal fluid testing, and a low threshold for paracentesis is recom- mended, even in well-appearing patients with ascites [4-9,70,72].

    1. Do patients with SBP routinely require blood product transfusion to address coagulation panel or platelet abnormalities?

The majority of patients with Liver dysfunction have thrombocyto- penia and abnormal coagulation panel testing. Literature suggests 70% of patients have an abnormal prothrombin time, and up to 84% have thrombocytopenia [73-77]. However, current evidence suggests that patients with cirrhosis have a balanced coagulopathy, with hypo- and Hypercoagulable states [5,6,8,9,75]. This is primarily due to hepatic synthetic dysfunction with reduced production of procoagulant and an- ticoagulant factors. Studies suggest that patients have a low overall risk of bleeding with paracentesis and that the procedure is safe even in the setting of coagulopathy [5-9,75]. One study of 1100 patients receiving paracentesis found no Bleeding complications requiring transfusion, even in patients with International normalized ratio > 8 and platelet counts of 19,000/microL [78]. A 1991 study found a 0.25% rate of bleeding after paracentesis [73]. A 2005 study found severe bleeding occurred in only 9 of 4729 paracenteses (0.19%), though neither INR nor platelet count were predictive of bleeding risk [79]. A separate study found a bleeding rate of 1% in those with platelet count <50,000/microL, while another study including 304 paracenteses performed on patients with platelet counts <50,000/microL found an overall event rate of 0.99% [80,81]. Another 2009 study of patients undergoing diagnostic paracenteses reported no bleeding complications among patients with an abnormal INR [82]. Based on current evidence, neither elevated INR nor thrombocytopenia is a contraindication to paracentesis, and guide- lines state that routine assessment of prothrombin time and platelet count before paracentesis is unnecessary [5,6]. Transfusion to correct coagulation panel abnormalities is also not recommended by current guidelines, as it increases the risk of adverse events and is not associated with a reduced risk of bleeding or complications [5-9].

    1. What diagnostic testing should be obtained?

The diagnostic modality of choice for SBP is ascitic fluid sampling via paracentesis, and an ascites absolute neutrophil count (ANC) >= 250 cells/mm3 is diagnostic of SBP [4-9]. Paracentesis should be performed when SBP is suspected, with ascites fluid sent for cell count and culture [4-9]. Other testing, including serum laboratory assessment, may be helpful but should not be used to exclude the condition in isolation. Guidelines recommend performing paracentesis in patients with clini- cal suspicion for SBP or in a patient with cirrhosis and ascites who is being admitted for a complication of cirrhosis [5,6]. This includes those with worsening renal or liver function, encephalopathy, and GI bleeding [5,6,8]. Early diagnosis is critical, with one study suggesting that each hour of delay in obtaining ascitic fluid was associated with a 3.3% increase in mortality [83]. This same study found that paracentesis performed within 12 h was associated with lower in-hospital mortality and shorter length of stay when compared to paracentesis performed within 12-72 h (13% compared to 27%) [83]. Another study found a mortality rate of 8.9% for patients with ascites who did not undergo paracentesis versus 6.3% for those who did [84].

Of note, paracentesis is a relatively safe procedure with a low com-

plication rate (iatrogenic infection 0.2%, hemorrhage 0.4%, bowel perfo- ration 0.8%) [82,85,86]. A site that provides access to a deep pocket of fluid while avoiding vasculature is recommended. We recommend using ultrasound to confirm ascites and evaluate for the optimal site of drainage, starting the evaluation in the left lower and right lower

quadrants, lateral to the rectus sheath. Ultrasound can also be used to measure abdominal wall thickness and evaluate for the presence of any vessels running through the abdominal wall [87,88]. One study evaluating fluid depth and abdominal wall thickness found the left lower quadrant was superior to the infraumbilical midline site [89]. Once obtained, diagnosis of SBP only requires cell count to obtain the ANC, though culture and Gram stain should also be sent [5,6,9]. Other ascites fluid testing such as total protein and albumin, glucose, and lac- tate dehydrogenase (LDH) may be used to evaluate for other aspects of clinical importance, such as the patient with new onset ascites, but they are not necessary for diagnosis of SBP [5-9]. Approximately 1 mL of as- citic fluid should be injected into a purple top EDTA blood tube for cell count, with 2-3 mL sent for Gram stain in a red-top tube or sterile urine container [90,91]. Additional ascitic fluid should be inoculated into blood culture bottles, with at least 10 mL per bottle, which increases the sensitivity to over 90% [90]. In contrast, the sensitivity of cultures obtained in other types of containers is approximately 50% [91]. Blood cultures should be obtained around the same time as the ascitic fluid culture and prior to receiving antibiotics, to raise the likeli- hood of isolating the organism [61]. A different needle than the one used to obtain the ascitic fluid should be used to transfer the fluid to the blood culture bottle in order to reduce the risk of contamination.

While the most specific marker for SBP is an ascites ANC >= 500 cells/mm3,a threshold of >=250 cells/mm3 is recommended for diagnosis of SBP [4-9,92,93]. Recent studies have evaluated the use of leukocyte esterase reagent strips for rapid diagnosis of SBP at the bedside [94]. There are several reagent strips available, including Aution Sticks, Combur, Multistix, and Periscreen reagent strips. These colorimetric strips typically provide readings ranging between 0 and 4. A 2021 meta-analysis found the Aution stick was the most sensitive but is the least studied, while the Multistix strip was the most specific (Table 1) [94]. Of note, the Periscreen reagent strip is not a urine testing strip but was developed as a high sensitivity screening test to evaluate peri- toneal fluid for SBP in Peritoneal dialysis patients. Reagent strip testing can be helpful in institutions where cell count is not rapidly available.

Serum laboratory abnormalities are common in patients with SBP, including anemia (due to GI bleeding, malnutrition, hypersplenism, al- cohol use), thrombocytopenia (portal hypertension, hypersplenism), elevated total bilirubin and prothrombin time, hyponatremia (excess water intake), elevated aspartate and alanine aminotransferases, and elevated creatinine and blood urea nitrogen (BUN) [5,6,8,9,76,95]. However, these findings are neither sensitive nor specific for SBP [5,6,8,9,76,95]. C-reactive protein (CRP) and procalcitonin have been evaluated in those with SBP [76,96-99]. A 2022 meta-analysis found an area under the receiver operating curve (AUROC) for procalcitonin using a cut-off >2.0 ng/mL was 0.75 (95% CI 0.61-0.88), and

CRP > 3.0 mg/L demonstrated an AUROC of 0.55 (95% CI 0.43-0.68)

Table 1

Reagent strips test characteristics [94].

Test Sensitivity (95% CI) Specificity (95% CI) Aution Stick

[98]. The combination of elevated procalcitonin with CRP demonstrated an AUROC of 0.76 (95% CI 0.61-0.90) for diagnosing all-cause SBP [98]. Another meta-analysis found procalcitonin had a pooled sensitivity of 79% (95% CI 64-89%) and specificity of 89% (95% CI 82-94%), while

CRP had a sensitivity of 77% (95% CI 69-84%) and specificity of 85%

(95% CI 76-90%) [99]. A separate 2022 meta-analysis evaluated neutrophil-to-lymphocyte ratio for diagnosis of SBP and reported a sensitivity of 92.1% and a specificity of 72.6% [100]. However, the NLR thresholds ranged from 2.4 to 9.2, and there was significant heterogene- ity in the included studies [100]. Blood cultures should be obtained, and positive blood cultures are associated with increased mortality [4-6,61,101].

    1. Antibiotics for SBP

Antibiotics are a cornerstone of treatment and should be adminis- tered immediately after paracentesis is performed if the patient has ab- dominal pain/tenderness, altered mental status, temperature > 37.8 ?C (100? F), or if the ascitic fluid ANC is >=250 cells/mm3 [4-9]. Patients can rapidly progress to septic shock and multisystem organ failure, so rapid diagnosis and treatment with antibiotics are essential [4-9]. Mortality increases by 8-10% for every hour delay in antibiotics for those with cirrhosis in septic shock [11,13,102,103]. Antibiotics should not be with- held pending Bacterial culture results [4-9].

Traditionally, a third-generation cephalosporin(e.g., ceftriaxone 2 g IV daily or cefotaxime 2 g IV every 8 h) is given for SBP and is effective in locations with local patterns of antimicrobial susceptibility [4-9,46]. However, cephalosporins have become less effective due to the increas- ing rates of nosocomial infections and MDR bacteria. Recent studies suggest MDR bacteria are present in 11-50% of patients with SBP [21,43-49,104-111]. One study found that a third-generation cephalo- sporin would have adequately covered 70% of community-acquired cases of SBP and 56% of nosocomial infections [109]. Current data demonstrate that the initial use of carbapenems may result in greater resolution of SBP and reduced mortality in patients with nosocomial in- fections or critically ill patients [21,110-114]. One study found carba- penem therapy in critically ill patients was associated with a reduction in mortality compared to third-generation cephalosporins (23% vs. 39%, odds ratio 0.84, 95% CI 0.75-0.94) [110], while another found carbapenem therapy reduced mortality and AKI in those with recurrent SBP [112]. Piperacillin-tazobactam may be utilized in place of a carba- penem [113,114]. Thus, patients with shock, critical illness, end-organ injury, recurrent SBP, or recent hospitalization and receipt of antibiotics should receive broad-spectrum coverage with piperacillin-tazobactam or a carbapenem (e.g., ertapenem, imipenem, meropenem) [4,5,7,21]. There is also an increasing prevalence of Staphylococcus aureus as the causative agent in those with nosocomial SBP, accounting for 19-48% of infections [115]. If risk factors for methicillin resistant Staphylococcus aureus (MRSA) are present or the patient has recent healthcare exposure, coverage for MRSA should be considered (e.g., vancomycin, linezolid) [4,5,7,21].

    1. What is the role of albumin in SBP?

– Overall

96.2% (92.6-99.8%)

94.0% (90.4-97.6%)

– Visual

97.3% (94.5-1.00%)

93.5% (89.0-98.1%)

Combur 10

– Overall

89.2% (84.6-93.8%)

92.2% (87.4-97.0%)

– Threshold >=1

86.6% (81.5-91.7%)

87.1% (81.1-93.1%)

– Threshold >=2

81.4% (68.9-93.9%)

97.0% (94.9-99.1%)


– Overall

80.6% (73.8-87.4%)

93.8% (96.2-98.5%)

– Visual

80.1% (72.9-87.2%)

97.6% (96.5-98.6%)

– Threshold >=1

84.7% (77.1-92.3%)

96.4% (94.4-98.5%)

– Threshold >=2

77.5% (59.8-95.2%)

97.6% (96.2-99.0%)

– Threshold >=3

62.2% (49.2-75.3%)

99.2% (98.9-99.6%)


– Overall

93.9% (90.0-97.9%)

67.2% (38.1-96.3%)

CI – confidence interval.

SBP commonly results in multiorgan failure, with the kidneys most commonly affected [4-9,116-119]. Literature suggests renal dysfunction occurs in 30-50% patients with SBP [116-119]. Acute kidney injury is the primary predictor of mortality in patients with SBP [4,5,7,118-122], with one study finding a 30% increase in mortality among patients with SBP and concomitant AKI [123]. A separate systematic review found in-hospital mortality for those with SBP and AKI was 67% versus 11% for those without AKI [119].

A meta-analysis found administration of albumin IV is associated with a 22.3% absolute reduction in risk of developing renal impairment (number-needed-to-treat [NNT] 5) and a 19.4% absolute reduction in risk of mortality (NNT 6) [124,125]. A meta-analysis published in 2022

found albumin infusion reduced all-cause mortality and renal impair- ment [126]. Guidelines recommend administering albumin in those with a bilirubin >4 mg/dL, creatinine >1 mg/dL, or BUN >30 mg/dL [5,6,127,128]. The regimen includes 1.5 g/kg of 20% albumin IV at the time of diagnosis, with 1 g/kg IV 48 h later.

If renal failure has developed, mortality significantly increases [4-9,127]. Renal failure in those with cirrhosis is associated with re- duced effective arterial volume and activation of the renin-angiotensin system. Volume expansion with albumin is an integral component of therapy for these patients.

  1. Conclusions

SBP is associated with significant risks of morbidity and mortality. There are a variety of causative organisms, including Gram-negative bacteria, Gram-positive bacteria, and MDR bacteria. The disease should be suspected in those with known liver disease and abdominal pain, worsening ascites, fever, and altered mental status. Paracentesis is recommended for diagnosis in any patient with ascites and concern for SBP, upper GI bleeding, or in those being admitted for a complication of their cirrhosis. Ultrasound can assist in locating the optimal site for paracentesis. Ascites ANC >= 250 cells/mm3 is diagnostic. Further testing of ascitic fluid with leukocyte esterase reagent strips may be considered in settings in which peritoneal fluid testing is not available. Routine transfusion is not recommended to correct coagulation panel abnormal- ities. Management includes antibiotics depending on the patient and local sensitivities. Albumin infusion should also be considered for patients with SBP.

CRediT authorship contribution statement

Brit Long: Writing – review & editing, Writing – original draft, Visu- alization, Resources, Conceptualization. Michael Gottlieb: Writing – review & editing, Validation, Supervision, Resources, Conceptualization.

Declaration of Competing Interest



BL and MG conceived the idea for this manuscript and contributed substantially to the writing and editing of the review. This manuscript did not utilize any grants, and it has not been presented in abstract form. This clinical review has not been published, it is not under consideration for publication elsewhere, its publication is approved by all authors and tacitly or explicitly by the responsible authorities where the work was carried out, and that, if accepted, it will not be published elsewhere in the same form, in English or in any other language, including electroni- cally without the written consent of the copyright-holder. This review does not reflect the views or opinions of the U.S. government, Depart- ment of Defense, U.S. Army, U.S. Air Force, or SAUSHEC EM Residency Program.


  1. Nader LA, Mattos AA, Bastos GA. Burden of liver disease in Brazil. Liver Int. 2014;34:


  1. Blachier M, Leleu H, Peck-Radosavljevic M, et al. The burden of liver disease in Europe: a review of available epidemiological data. J Hepatol. 2013;58:593-608.
  2. Asrani SK, Larson JJ, Yawn B, et al. Underestimation of liver-related mortality in the United States. Gastroenterology. 2013;145:375-82.
  3. Mattos AA, Wiltgen D, Jotz RF, et al. Spontaneous bacterial peritonitis and extraperitoneal infections in patients with cirrhosis. Ann Hepatol. 2020 Sep-Oct; 19(5):451-7.
  4. Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 prac- tice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021 Aug;74(2):1014-48.
  5. Aithal GP, Palaniyappan N, China L, et al. Guidelines on the management of ascites in cirrhosis. Gut. 2021 Jan;70(1):9-29.
  6. Marciano S, Diaz JM, Dirchwolf M, Gadano A. Spontaneous bacterial peritonitis in patients with cirrhosis: incidence, outcomes, and treatment strategies. Hepat Med. 2019 Jan 14;11:13-22.
  7. Angeli P, Bernardi M, Villanueva C, et al. EASL clinical practice guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018;69: 406-60.
  8. Long B, Koyfman A. The emergency medicine evaluation and management of the patient with cirrhosis. Am J Emerg Med. 2018 Apr;36(4):689-98.
  9. Arvaniti V, D’Amico G, Fede G, et al. Infections in patients with cirrhosis increase mortality four-fold and should be used in determining prognosis. Gastroenterol- ogy. 2010;139:1246-56.
  10. Piano S, Singh V, Caraceni P, et al. Epidemiology and effects of bacterial infections in patients with cirrhosis worldwide. Gastroenterology. 2019;156:1368-80. e10.
  11. Fernandez J, Acevedo J, Castro M, et al. prevalence and risk factors of infections by multiresistant bacteria in cirrhosis: a prospective study. Hepatology. 2012;55: 1551-61.
  12. Piano S, Bartoletti M, Tonon M, et al. Assessment of Sepsis-3 criteria and quick SOFA in patients with cirrhosis and bacterial infections. Gut. 2018;67:1892-9.
  13. Ubhi N, Mourad A, Tausan M, et al. Outcomes after hospitalisation with spontane- ous bacterial peritonitis over a 13-year period: a retrospective cohort study. Eur J Gastroenterol Hepatol. 2023 Apr 1;35(4):384-93.
  14. Fiore M, Maraolo AE, Gentile I, et al. Current concepts and future strategies in the antimicrobial therapy of emerging gram-positive spontaneous bacterial peritonitis. World J Hepatol. 2017;9:1166-75.
  15. Shizuma T. Spontaneous bacterial and fungal peritonitis in patients with liver cir- rhosis: a literature review. World J Hepatol. 2018;10:254-66.
  16. Musskopf MI, Fonseca FP, Gass J, et al. Prognostic factors associated with in-hospital mortality in patients with spontaneous bacterial peritonitis. Ann Hepatol. 2012;11: 915-20.
  17. Coral GP, Mattos AA, Damo DF, Viegas AC. Prevalence and prognosis of spontaneous bacterial peritonitis. Experience in patients from a general hospital in Porto Alegre, RS, Brazil (1991-2000). Arq Gastroenterol. 2002;39:158-62.
  18. Caly WR, Strauss E. A prospective study of bacterial infections in patients with cir- rhosis. J Hepatol. 1993;18:353-8.
  19. Rostkowska KA, Szymanek-Pasternak A, Simon KA. Spontaneous bacterial peritoni- tis – therapeutic challenges in the era of increasing drug resistance of bacteria. Clin Exp Hepatol. 2018 Dec;4(4):224-31.
  20. De Mattos AA, Costabeber AM, Liono LC, Tovo CV. Multi-resistant bacteria in spon- taneous bacterial peritonitis: a new step in management? World J Gastroenterol. 2014;20:14079-86.
  21. Oliveira AM, Branco JC, Barosa R, et al. Clinical and microbiological characteristics associated with mortality in spontaneous bacterial peritonitis: a multicenter cohort study. Eur J Gastroenterol Hepatol. 2016;28(10):1216-22.
  22. Oladimeji AA, Temi AP, Adekunle AE, et al. Prevalence of spontaneous bacterial peritonitis in liver cirrhosis with ascites. Pan Afr Med J. 2013;15:128.
  23. Devani K, Charilaou P, Jaiswal P, et al. Trends in hospitalization, acute kidney injury, and mortality in patients with spontaneous bacterial peritonitis. J Clin Gastroenterol. 2019 Feb;53(2):e68-74.
  24. Niu B, Kim B, Limketkai BN, et al. Mortality from spontaneous bacterial peritonitis among hospitalized patients in the USA. Dig Dis Sci. 2018 May;63(5):1327-33.
  25. Santoiemma PP, Dakwar O, Angarone MP. A retrospective analysis of cases of spon- taneous bacterial peritonitis in cirrhosis patients. PloS One. 2020 Sep 28;15(9): e0239470.
  26. Iogna Prat L, Wilson P, Freeman SC, et al. Antibiotic treatment for spontaneous bac- terial peritonitis in people with decompensated liver cirrhosis: a network meta- analysis. Cochrane Database Syst Rev. 2019 Sep 16;9(9):CD013120.
  27. D’Amico G, Garcia-Tsao G, Pagliaro L. Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies. J Hepatol. 2006;44(1): 217-31.
  28. Melcarne L, Sopena J, Martinez-Cerezo FJ, et al. Prognostic factors of liver cirrhosis mortality after a first episode of spontaneous bacterial peritonitis. A multicenter study. Rev Esp Enferm Dig. 2018 Feb;110(2):94-101.
  29. Bal CK, Daman R, Bhatia V. Predictors of fifty days in-hospital mortality in decom- pensated cirrhosis patients with spontaneous bacterial peritonitis. World J Hepatol. 2016 Apr 28;8(12):566-72.
  30. Elzouki AN, Hamad A, Almasri H, et al. Predictors of short-term mortality following first episode of spontaneous bacterial peritonitis in hospitalized cirrhotic patients. Cureus. 2021 Oct 23;13(10):e18999.
  31. Ariza X, Castellote J, Lora-Tamayo J, et al. Risk factors for resistance to ceftriaxone and its impact on mortality in community, healthcare and nosocomial spontaneous bacterial peritonitis. J Hepatol. 2012;56:825-32.
  32. Poca M, Alvarado E, Concepti NM, et al. P0190: predictive model of mortality in cir- rhotic patients with high risk spontaneous bacterial peritonitis. J Hepatol. 2015;62: S375.
  33. Tandon P, Kumar D, Seo YS, et al. The 22/11 risk prediction model: a validated model for predicting 30-day mortality in patients with cirrhosis and spontaneous bacterial peritonitis. Am J Gastroenterol. 2013;108(9):1473-9.
  34. Sreenivasulu V, Bheemasenachari M. Study of prevalence of spontaneous bacterial peritonitis in cirrhosis of liver with ascites. J Evol Med Dent Sci. 2016;5(44): 2720-4.
  35. Malik R, Mookerjee RP, Jalan R. Infection and inflammation in Liver failure: two sides of the same coin. J Hepatol. 2009;51(3):426-9.
  36. Huang CH, Lin CY, Sheen IS, et al. Recurrence of spontaneous bacterial peritonitis in cirrhotic patients non-prophylactically treated with norfloxacin: serum albumin as an easy but reliable predictive factor. Liver Int. 2011;31(2):184-91.
  37. Elfert A, Abo Ali L, Soliman S, et al. Randomized controlled trial of rifaximin versus norfloxacin for secondary prophylaxis of spontaneous bacterial peritonitis. Eur J Gastroenterol Hepatol. 2016;28(12):1450-4.
  38. O’Leary JG, Reddy KR, Wong F, et al. Long-term use of antibiotics and proton pump inhibitors predict development of infections in patients with cirrhosis. Clin Gastroenterol Hepatol. 2015.;13(4) 753e1-759e2.
  39. Pimentel R, Leitao J, Gregorio C, et al. Spontaneous bacterial peritonitis in cirrhotic patients: a shift in the microbial pattern? A retrospective analysis. GE Port J Gastroenterol. 2021 Aug 24;29(4):256-66.
  40. Elshamy RM, Oda MS, Saeed MA, Ramadan RA. A comparative study on nosocomial and community-acquired spontaneous bacterial peritonitis in patients with liver cirrhosis at a university hospital. Eur J Gastroenterol Hepatol. 2022 Jun 1;34(6): 655-63.
  41. Abu-Freha N, Michael T, Poupko L, al.. Spontaneous bacterial peritonitis among cir- rhotic patients: prevalence, clinical characteristics, and outcomes. J Clin Med. 2021 Dec 31;11(1):227.
  42. Sunjaya DB, Lennon RJ, Shah VH, et al. Prevalence and predictors of third- generation cephalosporin resistance in the Empirical treatment of spontaneous bacterial peritonitis. Mayo Clin Proc. 2019 Aug;94(8):1499-508.
  43. Oliveira JC, Carrera E, Petry RC, et al. High prevalence of multidrug resistant bacteria in cirrhotic patients with spontaneous bacterial peritonitis: is it time to change the standard antimicrobial approach? Can J Gastroenterol Hepatol. 2019 May 13;2019: 6963910.
  44. Sofjan AK, Musgrove RJ, Beyda ND, et al. Prevalence and predictors of spontaneous bacterial peritonitis due to ceftriaxone-resistant organisms at a large tertiary Cen- tre in the USA. J Glob Antimicrob Resist. 2018 Dec;15:41-7.
  45. Fiore M, Gentile I, Maraolo AE, et al. Are third-generation cephalosporins still the empirical antibiotic treatment of community-acquired spontaneous bacterial peri- tonitis? A systematic review and meta-analysis. Eur J Gastroenterol Hepatol. 2018 Mar;30(3):329-36.
  46. Ding X, Yu Y, Chen M, et al. Causative agents and outcome of spontaneous bacterial peritonitis in cirrhotic patients: community-acquired versus nosocomial infections. BMC Infect Dis. 2019 May 23;19(1):463.
  47. Alexopoulou A, Vasilieva L, Agiasotelli D, et al. Extensively drug-resistant bacteria are an independent predictive factor of mortality in 130 patients with spontaneous bacterial peritonitis or spontaneous bacteremia. World J Gastroenterol. 2016 Apr 21;22(15):4049-56.
  48. Furey C, Zhou S, Park JH, et al. Impact of bacteria types on the clinical outcomes of spontaneous bacterial peritonitis. Dig Dis Sci. 2023 Mar 7. s10620-023-07867-8.
  49. Salerno F, La Mura V. Treatment of spontaneous bacterial peritonitis. Dig Dis. 2015;


  1. Gines P, Rimola A, Planas R, et al. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in cirrhosis: results of a double-blind, placebo-controlled trial. Hepatology. 1990;12(4 Pt 1):716-24.
  2. de Franchis R, Faculty BVI, Faculty Baveno VI. Expanding consensus in portal hyper- tension: report of the Baveno VI consensus workshop: Stratifying risk and individ- ualizing care for portal hypertension. J Hepatol. 2015;63(3):743-52.
  3. Runyon BA. Low-protein-concentration ascitic fluid is predisposed to spontaneous bacterial peritonitis. Gastroenterology. 1986;91(6):1343-6.
  4. Llach J, Rimola A, Navasa M, et al. Incidence and predictive factors of first episode of spontaneous bacterial peritonitis in cirrhosis with ascites: relevance of ascitic fluid protein concentration. Hepatology. 1992 Sep;16(3):724-7.
  5. Rimola A, Bory F, Teres J, et al. Oral, nonabsorbable antibiotics prevent infection in cirrhotics with gastrointestinal hemorrhage. Hepatology. 1985 May-Jun;5(3): 463-7.
  6. Andreu M, Sola R, Sitges-Serra A, et al. Risk factors for spontaneous bacterial peri- tonitis in cirrhotic patients with ascites. Gastroenterology. 1993 Apr;104(4): 1133-8.
  7. Bernard B, Cadranel JF, Valla D, et al. Prognostic significance of bacterial infection in bleeding cirrhotic patients: a prospective study. Gastroenterology. 1995;108(6): 1828-34.
  8. Fernandez J, Tandon P, Mensa J, Garcia-Tsao G. antibiotic prophylaxis in cirrhosis: good and bad. Hepatology. 2016;63(6):2019-31.
  9. Schwabl P, Bucsics T, Soucek K, et al. Risk factors for development and mortality of spontaneous bacterial peritonitis in cirrhotic patients with ascites. Z Gastroenterol. 2013.;51(05).
  10. Fernandez J, Navasa M, Planas R, et al. Primary prophylaxis of spontaneous bacte- rial peritonitis delays hepatorenal syndrome and improves survival in cirrhosis. Gastroenterology. 2007;133(3):818-24.
  11. Rimola A, Garc A-Tsao G, Navasa M, et al. Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: a consensus document. International Ascites Club. J Hepatol. 2000;32(1):142-53.
  12. Miura K, Tanaka A, Yamamoto T, et al. Proton pump inhibitor use is associated with spontaneous bacterial peritonitis in patients with liver cirrhosis. Intern Med. 2014; 53(10):1037-42.
  13. Zhang M, Liu W, Xu X, et al. Association between proton pump inhibitor therapy and spontaneous bacterial peritonitis occurrence in cirrhotic patients: a clinical re- view. Curr Med Sci. 2022 Aug;42(4):673-80.
  14. Kwon JH, Koh SJ, Kim W, et al. Mortality associated with proton pump inhibitors in cirrhotic patients with spontaneous bacterial peritonitis. J Gastroenterol Hepatol. 2014;29(4):775-81.
  15. Dam G, Vilstrup H, Watson H, Jepsen P. Proton pump inhibitors as a risk factor for hepatic encephalopathy and spontaneous bacterial peritonitis in patients with cirrhosis with ascites. Hepatology. 2016;64(4):1265-72.
  16. Terg R, Casciato P, Garbe C, et al. Proton pump inhibitor therapy does not increase the incidence of spontaneous bacterial peritonitis in cirrhosis: a multicenter pro- spective study. J Hepatol. 2015;62(5):1056-60.
  17. Runyon BA. Monomicrobial nonneutrocytic bacterascites: a variant of spontaneous bacterial peritonitis. Hepatology. 1990 Oct;12(4 Pt 1):710-5.
  18. Koulaouzidis A, Bhat S, Saeed AA. Spontaneous bacterial peritonitis. World J Gastroenterol. 2009 Mar 7;15(9):1042-9.
  19. Manzo M, Desai P. Spontaneous bacterial peritonitis in a patient with nonportal hypertensive ascites. Ochsner J. 2022 Spring;22(1):100-3.
  20. Chinnock B, Afarian H, Minnigan H, et al. Physician Clinical impression does not rule out spontaneous bacterial peritonitis in patients undergoing emergency depart- ment paracentesis. Ann Emerg Med. 2008;52:268-73.
  21. Ge PS, Runyon BA. Preventing future infections in cirrhosis: a battle cry for stew- ardship. Clin Gastroenterol Hepatol. 2015 Apr;13(4):760-2.
  22. Chinnock B, Hendey GW, Minnigan H, et al. Clinical impression and ascites appear- ance do not rule out bacterial peritonitis. J Emerg Med. 2013 May;44(5):903-9.
  23. McVay PA, Toy PT. Lack of increased bleeding after paracentesis and thoracentesis in patients with mild coagulation abnormalities. Transfusion. 1991 Feb;31(2): 164-71.
  24. Sigal SH, Sherman Z, Jesudian A. Clinical implications of thrombocytopenia for the cirrhotic patient. Hepat Med. 2020 Apr 14;12:49-60.
  25. Tripodi A, Primignani M, Mannucci PM, Caldwell SH. Changing concepts of cirrhotic coagulopathy. Am J Gastroenterol. 2017;112(2):274-81.
  26. Wehmeyer MH, Krohm S, Kastein F, et al. Prediction of spontaneous bacterial peritonitis in cirrhotic ascites by a simple scoring system. Scand J Gastroenterol. 2014;49:595-603.
  27. Runyon BA. Paracentesis of ascitic fluid. A safe procedure. Arch Intern Med. 1986 Nov;146(11):2259-61.
  28. Grabau CM, Crago SF, Hoff LK, et al. Performance standards for therapeutic abdom- inal paracentesis. Hepatology. 2004 Aug;40(2):484-8.
  29. Pache I, Bilodeau M. Severe haemorrhage following abdominal paracentesis for ascites in patients with liver disease. Aliment Pharmacol Ther. 2005 Mar 1;21(5): 525-9.
  30. Gines A, Fernandez-Esparrach G, Monescillo A, et al. Randomized trial comparing albumin, dextran 70, and polygeline in cirrhotic patients with ascites treated by paracentesis. Gastroenterology. 1996;111:1002-10.
  31. Kurup AN, Lekah A, Reardon ST, et al. Bleeding rate for ultrasound-guided paracentesis in thrombocytopenic patients. J Ultrasound Med. 2015;34(10): 1833-8.
  32. De Gottardi A, Thevenot T, Spahr L, et al. Risk of complications after abdominal paracentesis in cirrhotic patients: a prospective study. Clin Gastroenterol Hepatol. 2009;7:906-9.
  33. Kim JJ, Tsukamoto MM, Mathur AK, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis. Am J Gastroenterol. 2014 Sep;109(9):1436-42.
  34. Gaetano JN, Micic D, Aronsohn A, et al. The benefit of paracentesis on hospitalized adults with cirrhosis and ascites. J Gastroenterol Hepatol. 2016;31:1025-30.
  35. Hibbert R, Atwell T, Lekah A, et al. Safety of ultrasound-guided thoracentesis in pa- tients with abnormal preprocedural coagulation parameters. Chest. 2013;144: 456-63.
  36. Mallory A, Schaefer JW. Complications of diagnostic paracentesis in patients with liver disease. JAMA. 1978;239:628-30.
  37. Mercaldi CJ, Lanes SF. Ultrasound guidance decreases complications and improves the cost of care among patients undergoing thoracentesis and paracentesis. Chest. 2013;143:532-8.
  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;23:363-7.
  39. Sakai H, Sheer TA, Mendler MH, et al. Choosing the location for non-image guided abdominal paracentesis. Liver Int. 2005;25:984-6.
  40. Runyon BA, Canawati HN, Akriviadis EA. Optimization of ascitic fluid culture tech- nique. Gastroenterology. 1988 Nov;95(5):1351-5.
  41. Runyon BA, Antillon MR, Akriviadis EA, McHutchison JG. Bedside inoculation of blood culture bottles with ascitic fluid is superior to delayed inoculation in the de- tection of spontaneous bacterial peritonitis. J Clin Microbiol. 1990 Dec;28(12): 2811-2.
  42. Runyon BA, AASLD Practice Guidelines Committee. Management of adult patients with ascites due to cirrhosis: an update. Hepatology. 2009;49:2087-107.
  43. Albillos A, Cuervas-Mons V, Millan I, et al. Ascitic fluid polymorphonuclear cell count and serum to ascites albumin gradient in the diagnosis of bacterial peritoni- tis. Gastroenterology. 1990;98:134-40.
  44. Patel KP, Gallagher JP, Korbitz PM, et al. Performance of leukocyte esterase reagent strips in the detection of spontaneous bacterial peritonitis in cirrhotic patients: a systematic review and meta-analysis. J Clin Exp Hepatol. 2022 Mar-Apr;12(2): 519-32.
  45. Baraldi O, Valentini C, Donati G, et al. Hepatorenal syndrome: update on diagnosis and treatment. World J Nephrology. 2015;4:511-20.
  46. Yang Y, Li L, Qu C, et al. Diagnostic accuracy of serum procalcitonin for spontaneous bacterial peritonitis due to end-stage liver disease: a meta-analysis. Medicine (Bal- timore). 2015 Dec;94(49):e2077.
  47. Lesinska M, Hartleb M, Gutkowski K, Nowakowska-Dulawa E. Procalcitonin and macrophage inflammatory protein-1 beta (MIP-1?) in serum and peritoneal fluid

of patients with decompensated cirrhosis and spontaneous bacterial peritonitis. Adv Med Sci. 2014 Mar;59(1):52-6.

  1. Verma R, Satapathy SK, Bilal M. Procalcitonin and C-reactive protein in the diagno- sis of spontaneous bacterial peritonitis. Transl Gastroenterol Hepatol. 2022 Oct 25; 7:36.
  2. Lin KH, Wang FL, Wu MS, et al. Serum procalcitonin and C-reactive protein levels as markers of bacterial infection in patients with liver cirrhosis: a systematic review and meta-analysis. Diagn Microbiol Infect Dis. 2014;80:72-8.
  3. Seyedi SA, Nabipoorashrafi SA, Hernandez J, et al. Neutrophil to lymphocyte ratio and spontaneous bacterial peritonitis among cirrhotic patients: a systematic re- view and meta-analysis. Can J Gastroenterol Hepatol. 2022 Sep 27;2022:8604060.
  4. Sanglodkar U, Jain M, Venkataraman J. Predictors of immediate and short-term mortality in spontaneous bacterial peritonitis. Indian J Gastroenterol. 2020 Aug; 39(4):331-7.
  5. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of ef- fective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med. 2006 Jun;34(6):1589-96.
  6. Kumar A, Ellis P, Arabi Y, Roberts D, Light B, Parrillo JE, et al. Initiation of inappro- priate antimicrobial therapy results in a fivefold reduction of survival in human septic shock. Chest. 2009;136:1237-48.
  7. Mucke MM, Mayer A, Kessel J, et al. Quinolone and multidrug resistance predicts failure of antibiotic prophylaxis of spontaneous bacterial peritonitis. Clin Infect Dis. 2020 Apr 15;70(9):1916-24.
  8. Tay PWL, Xiao J, Tan DJH, Ng C, Lye YN, Lim WH, et al. An Epidemiological Meta- Analysis on the Worldwide Prevalence, Resistance, and Outcomes of Spontaneous Bacterial Peritonitis in Cirrhosis. Front Med (Lausanne). 2021 Aug 5;8:693652.
  9. Moreau R, Jalan R, Gines P, CANONIC Study Investigators of the EASL-CLIF Consor- tium, et al. Acute-on-chronic liver failure is a distinct syndrome that develops in patients with acute decompensation of cirrhosis. Gastroenterology. 2013 Jun;144 (7):1426-37. 1437.e1-9.
  10. Fernandez J, Prado V, Trebicka J, et al. European Foundation for the Study of Chronic Liver Failure (EF-Clif). Multidrug-resistant bacterial infections in patients with de- compensated cirrhosis and with acute-on-chronic liver failure in Europe. J Hepatol. 2019 Mar;70(3):398-411.
  11. Costabeber AM, Mattos AA, Sukiennik TC. Prevalence of bacterial resistance in hos- pitalized cirrhotic patients in southern Brazil: a new challenge. Rev Inst Med Trop Sao Paulo. 2016;58:36.
  12. Friedrich K, Nussle S, Rehlen T, et al. Microbiology and resistence in first episodes of spontaneous bacterial peritonitis: implications for management and prognosis. J Gastroenterol Hepatol. 2016;31:1191-5.
  13. Kim SW, Yoon JS, Park J, et al. Empirical treatment with carbapenem vs third- generation cephalosporin for treatment of spontaneous bacterial peritonitis. Clin Gastroenterol Hepatol. 2021 May;19(5):976-986.e5.
  14. Piano S, Fasolato S, Salinas F, et al. The empirical antibiotic treatment of nosocomial spontaneous bacterial peritonitis: results of a randomized, controlled clinical trial. Hepatology. 2016;63:1299-309.
  15. Sasidharan Nair GV, Mathen PG, Pillai MG, et al. Initial choice of antibiotic in recur- rent spontaneous bacterial peritonitis: a retrospective study. Int J Crit Illn Inj Sci. 2019 Oct-Dec;9(4):187-90.
  16. Wieser A, Li H, Zhang J, et al. Evaluating the best empirical antibiotic therapy in pa- tients with acute-on-chronic liver failure and spontaneous bacterial peritonitis. Dig Liver Dis. 2019 Sep;51(9):1300-7.
  17. Quickert S, Wurstle S, Reuken PA, et al. Real-world effectiveness of piperacillin/taz- obactam with and without linezolid for spontaneous bacterial peritonitis. Dig Dis. 2022;40(6):777-86.
  18. Falcone M, Russo A, Pacini G, et al. Spontaneous bacterial peritonitis due to meth- icillin resistant S. aureus in a patient with cirrhosis: the potential role for daptomy- cin and review of the literature. Infect Dis Rep. 2015;7:56-9.
  19. Moreau R, Durand F, Poynard T, et al. Terlipressin in patients with cirrhosis and type 1 hepatorenal syndrome: a retrospective multicenter study. Gastroenterology. 2002;122(4):923-30.
  20. Marciano S, Dirchwolf M, Bermudez CS, et al. Spontaneous bacteremia and sponta- neous bacterial peritonitis share similar prognosis in patients with cirrhosis: a co- hort study. Hepatol Int. 2018;12(2):181-90.
  21. Follo A, Llovet JM, Navasa M, et al. Renal impairment after spontaneous bacterial peritonitis in cirrhosis: incidence, clinical course, predictive factors and prognosis. Hepatology. 1994;20(6):1495-501.
  22. Tandon P, Garcia-Tsao G. Renal dysfunction is the most important independent predictor of mortality in cirrhotic patients with spontaneous bacterial peritonitis. Clin Gastroenterol Hepatol. 2011;9(3):260-5.
  23. Sort P, Navasa M, Arroyo V, et al. Effect of intravenous albumin on renal impair- ment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999;341:403-9.
  24. Sohn W, Kim JH, Cho JY. Effect of acute kidney injury on long-term outcomes of spontaneous bacterial peritonitis in cirrhotic patients using the International Club of Ascites-acute kidney injury criteria. J Gastroenterol Hepatol. 2020 May;35(5): 870-6.
  25. Xiong J, Zhang M, Guo X, et al. Acute kidney injury in critically ill cirrhotic patients with spontaneous bacterial peritonitis: a comparison of KDIGO and ICA criteria. Arch Med Sci. 2019 May 17;16(3):569-76.
  26. Coral GP, Mattos AA. Renal impairment after spontaneous bacterial peritonitis: in- cidence and prognosis. Can J Gastroenterol Hepatol. 2003;17:187-90.
  27. Salerno F, Navickis RJ, Wilkes MM. Albumin infusion improves outcomes of pa- tients with spontaneous bacterial peritonitis: a meta-analysis of randomized trials. Clin Gastroenterol Hepatol. 2013;11:123-30.
  28. Long B, Gottlieb M. Albumin infusion for spontaneous bacterial peritonitis. Am Fam

Physician. 2022 Oct.;106(4) Online. PMID: 36260890.

  1. Batool S, Waheed MD, Vuthaluru K, et al. Efficacy of intravenous albumin for spon- taneous bacterial peritonitis infection among patients with cirrhosis: a meta- analysis of randomized control trials. Cureus. 2022 Dec 30;14(12):e33124.
  2. Salerno F, Gerbes A, Gines P, et al. Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Postgrad Med J. 2008;84:662-70.
  3. Sigal SH, Stanca CM, Fernandez J, et al. Restricted use of albumin for spontaneous bacterial peritonitis. Gut. 2007 Apr;56(4):597-9.