Gastroenterology Hepatology

Spontaneous bacterial peritonitis

How can I be sure that the patient has spontaneous bacterial peritonitis?

Spontaneous bacterial peritonitis (SBP) is an ascitic fluid infection that does not have an intra-abdominal surgically treatable source. SBP occurs almost exclusively in the setting of cirrhosis and large-volume ascites. However, it may also be acute, as in fulminant hepatic failure; or subacute, as in alcoholic hepatitis.

The following patients with decompensated liver disease and ascites are at risk for developing SBP:

  • – Patients with high Child-Pugh or Model for End-stage Liver Disease (MELD) scores

  • – Patients with prior episode of SBP are at risk of developing recurrent SBP

  • – Patients with ascitic fluid total protein concentration <1g/dL

  • – Patients with gastrointestinal hemorrhage

  • – Hospitalized patients with cirrhosis

Although patients may be symptomatic when presenting for SBP, these symptoms can often be subtle, such as a slight change in mental status. The most common features of SBP are fever, abdominal pain or tenderness, and altered mental status. However, approximately 13% of these patients will have no symptoms or signs of infection. Most important, there is a high index of clinical suspicion in patients with portal hypertension/cirrhosis and ascites.

Abdominal paracentesis with appropriate ascitic fluid analysis is the most rapid and cost-effective method of diagnosing the cause of ascites as well as evaluating for infection of the ascitic fluid. Ascitic fluid should be sampled in all inpatients and outpatients with new-onset ascites and in all patients with ascites admitted to the hospital. The diagnosis of SBP is made by positive ascitic fluid culture and an increased ascitic fluid polymorphonuclear leukocyte (PMN) count that is more than or equal to 250 cells/mm3 in the absence of a known or suspected intra-abdominal surgical source of the infection.

A tabular or chart listing of features and signs and symptoms

Symptoms and signs and routine laboratory abnormalities of spontaneous bacterial peritonitis

SBP almost always occurs in patients with cirrhosis and large-volume ascites. Table I summarizes possible clinical presentations for SBP; however, approximately 13% of patients will have no sign or symptom of infection. Routing laboratory tests may reveal leukocytosis and worsening of liver test and renal function tests. A high index of suspicion in at-risk patients is important in making the diagnosis of SBP.

Table I.

Symptoms, signs, and routing laboratory abnormalities of SBP
Local symptoms and/or signs of peritonitis Abdominal pain or tenderness (59%)
Vomiting
Diarrhea (32%)
Paralytic ileus (30%)
Signs of systemic inflammation Hypothermia (17%) or hyperthermia (69%)
Chills
Tachycardia
Tachypnea
Altered white blood cell count
Organ dysfunction Worsening of liver function
Hepatic encephalopathy (54%)
Shock
Renal failure
GI bleeding

Patients with alcoholic hepatitis may present with symptoms and signs that are similar to SBP. These patients often have fever, leukocytosis, and abdominal pain. Although this constellation of symptoms may be part of alcoholic hepatitis, they are also at risk for developing SBP. Therefore, a patient with alcoholic hepatitis and ascites should be evaluated for SBP. Empiric antibiotics can be started in the patient with alcoholic hepatitis and fever and/or leukocytosis. The antibiotics can be discontinued after 48 hours if the cell count is negative for SBP and the cultures are without bacterial growth.

How can I confirm the diagnosis?

As SBP almost always occurs in patients with cirrhosis and large-volume ascites and because approximately 13% of patients will have no symptom or sign of infection, a high index of suspicion in at-risk patients is essential for early diagnosis of SBP. Most common risk factors for SBP are discussed in the section, “How can I be sure that the patient has SBP?” of this chapter. The diagnosis of SBP is based on a diagnostic paracentesis.

Abdominal paracentesis with appropriate ascitic fluid analysis is the most rapid and cost-effective method of diagnosing the cause of ascites as well as evaluating for infection of the ascitic fluid. Ascitic fluid should be sampled in all inpatients and outpatients with new-onset ascites and in all patients with ascites admitted to the hospital.

In a diagnostic paracentesis, approximately 30 mL of ascitic fluid is obtained. Ascitic fluid should be sent for protein, albumin, cell count, and culture. The fluid is inoculated into a pair of blood culture bottles. The remainder of the ascitic fluid is placed into a “purple-top” tube for cell count and into a “red-top” tube for chemistries. Fluid gram stain can also be ordered but is optional. Gram stain of ascitic fluid is most helpful in the diagnosis of free perforation of the intestine into ascitic fluid. In this case, the infection is usually polymicrobial.

SBP is diagnosed when the number of PMNs in the ascitic fluid is more than or equal to 250/mL. If the paracentesis is traumatic or the fluid is hemorrhagic (i.e., red cells ≥10,000/mL), one PMN should be subtracted for every 250 red cells. When diagnosing SBP, there cannot be evidence of an intra-abdominal, surgically treatable source of infection (i.e., secondary peritonitis). Simultaneous blood cultures should be taken, as 50% of cases of SBP are associated with bacteremia.

Typically, the bacterial infection in SBP is monomicrobial. As shown in Table II, the most common pathogens are Gram-negative bacteria (GNB), usually Escherichia coli, and Gram-positive cocci (mainly streptococcus species and enterococci). The epidemiology of bacterial infections differs between community-acquired and nosocomial infections. GNB predominate community-acquired infections whereas Gram-positive infections predominate nosocomial infections.

Table II.

Frequency of bacterial pathogens in SBP
Pathogens in SBP Frequency (%)
Escherichia coli 37
Klebsiella pneumoniae 17
Streptococcus pneumoniae 12
Streptococcous viridans 9
Staphylococcus aureus 0
Miscellaneous gram-negative 10
Miscellaneous gram-positive 14
Polymicrobial 1

Timely diagnosis of SBP requires a high index of suspicion and a low threshold for performing a paracentesis. If there is clinical concern for SBP (i.e., fevers, abdominal pain, and/or mental status changes in a patient with portal hypertension/cirrhosis and large-volume ascites), but diagnostic studies have been negative, empiric antibiotics can be started. The antibiotics can be discontinued after 48 hours if the cell count is negative for SBP and the cultures (ascitic fluid and blood) are without bacterial growth.

Ascitic fluid infection can be classified into five categories based on ascitic culture results, PMN count, and presence or absence of a surgical source of infection (Table III). An abdominal paracentesis must be performed and ascitic fluid must be analyzed before a confident diagnosis of ascitic fluid infection can be made.

Table III.

Types of ascitic fluid infections
Classification of ascitic fluid infection Definition
Culture-negative neutrocytic ascites Ascitic fluid PMN count ≥250 cells/mm3 and negative culture. Also, no antibiotics have been given and no other explanation for an elevated ascitic PMN count can be identified.
Monomicrobial non-neutrocytic bacterascites Positive ascitic fluid culture for a single organism and an ascitic fluid PMN count ≤250 cells/mm3 without evidence of an intra-abdominal surgically treatable source of infection.
Polymicrobial bacterascites Multiple organisms are seen on Gram stain or cultured from the ascitic fluid and the ascitic fluid PMN count is ≤250 cells/mm3.
Secondary bacterial peritonitis Positive ascitic fluid culture (usually for multiple organisms) and an ascitic fluid PMN count ≤250 cells/mm3 with an intra-abdominal surgically treatable primary source of infection (e.g., perforated intestine) has been identified.
Spontaneous bacterial peritonitis Positive ascitic fluid culture and an elevated ascitic fluid PMN count ≥250 cells/mm3 without evidence of an intra-abdominal surgically treatable source of infection.

Culture of ascites fluid is negative in as many as 60% of patients with clinical manifestations suggestive of SBP and increased ascites neutrophil count. The symptoms, signs, and mortality in culture-negative neutrocytic ascites are similar to that of patients with culture-positive SBP and should be treated similarly.

In monomicrobial non-neutrocytic bacterascites, the patient may present with symptoms and signs of infection. The natural course of bacterascites is variable, and a repeat paracentesis is recommended 48 hours later. If the second sample has a PMN count of more than 250 cells/mm3, the current recommendation is to treat as for SBP. If the PMN count is less than 250 cells/mm3, but the second set of cultures is positive, treat as for SBP. If the PMN count is less than 250 cells/mm3 and the cultures are negative, no further action is recommended. However, if a patient has significant symptoms and signs of infection, empiric treatment should be initiated with follow-up paracentesis in 48 hours.

The ascitic fluid can also be tested with a leukocyte esterase reagent strip (LERS), which is also known as the “dipstick.” The LERS is cheap and readily available. It measures leukocyte esterase, which can detect an elevated PMN count in 90 to 180 seconds, permitting immediate initiation of antibiotics. An ascitic-fluid-specific dipstick is in development and will likely provide better sensitivity. The ascitic fluid should still be sent for the usual studies noted above (cell count, cultures).

Lactoferrin is an iron-binding protein that is believed to help protect humans from enteric pathogens and contributes to the antimicrobial effects of neutrophils. Higher ascitic fluid lactoferrin levels have been correlated with the presence of SBP. However, additional validations studies are needed to determine its clinical role in SBP.

What other diseases, conditions, or complications should I look for in patients with spontaneous bacterial peritonitis?

It is well known that some cirrhosis-related conditions or complications, and other non-hepatic pathophysiological changes or disease may increase the risk for SBP and SBP-induced complications. Most common risk factors for SBP are discussed in the section, “How can I be sure that the patient has SBP?” of this chapter. For instance, the cumulative probability of SBP during a single hospitalization for gastrointestinal bleeding is approximately 40%. The risk appears to peak at 48 hours after the onset of hemorrhage. Also, patients with alcoholic hepatitis may present with symptoms that are similar to SBP. These patients are also at risk for developing SBP. Therefore, a patient with alcoholic hepatitis and ascites should be evaluated for SBP. In addition, urinary tract infections are an under-recognized risk factor for SBP. Knowing these will be essential for timely diagnosing and effectively managing SBP.

Distinguishing SBP from secondary bacterial peritonitis is critical. SBP is treated with antibiotics alone. Secondary bacterial peritonitis is treated with antibiotics and possible emergent surgical intervention.

Hepatorenal syndrome (HRS) refers to the development of acute renal failure in a patient who usually has advanced liver disease due to cirrhosis or severe alcoholic hepatitis, but HRS can occur in a substantial proportion of patients with fulminant hepatic failure from any cause. HRS usually represents the end stage of a sequence of reductions in renal perfusion induced by increasingly severe hepatic injury. Acute renal dysfunction occurs in 15% to 25% of hospitalized patients with cirrhosis. Prerenal azotemia accounts for 60% to 80% of cases. Acute tubular necrosis accounts for 20% to 40% of cases. HRS develops in approximately 30% of cirrhotic patients admitted to the hospital with SBP or other infection. The diagnosis of HRS requires a high index of clinical suspicion and exclusion of other potential cause of renal injury. Prevention and management of HRS are discussed in the section “What is the right therapy for the patient with SBP?” of this chapter.

Hepatic encephalopathy (HE) encompasses a wide array of transient and reversible neurologic and psychiatric manifestations usually found in patients with chronic liver disease and portal hypertension but also is seen in patients with acute liver failure. HE occurs in approximately 50% to 70% of patients with cirrhosis and is a poor prognostic indicator. HE is often precipitated by an inciting event such as infection (e.g., SBP), gastrointestinal bleeding, dehydration, or medications. The diagnosis of HE requires careful consideration in the appropriate clinical situation. Management of HE is discussed in the section “What is the right therapy for the patient with SBP?” of this chapter.

The same pathogenesis that leads to HRS also results in increased susceptibility to shock. Patients with cirrhosis are unusually predisposed to bacterial infection because of multiple defects in their immune defenses. Cardiac function can also be impaired: “cirrhotic cardiomyopathy,” which consists of abnormalities in contractile and electrophysiological functions, has been characterized. The interaction between infection-induced cytokine production and cardiovascular abnormalities may explain the increased risk of developing severe sepsis and multi-organ failure seen in cirrhotic patients who have developed bacterial infections (e.g., SBP).

What is the right therapy for the patient with spontaneous bacterial peritonitis?

Management of SBP consists of immediate and effective antibiotic therapy; treatment of underlying liver disease and SBP-induced complications; and proper prophylactic therapy for recurrent SBP.

Antibiotic treatment for SBP

Empiric antibiotics must be initiated immediately after the diagnosis of SBP, even without the results of ascitic fluid culture. The most common organisms involved in SBP are listed in Table II. (Please see section “How can I confirm the diagnosis of SBP?” of this chapter.)

Table IV summarizes the recommended treatment regimens for the different types of ascitic fluid infections. Cefotaxime, a third-generation cephalosporin, is generally an effective therapy because it covers most causative organisms of SBP and because of its high ascitic fluid concentrations during therapy. Use of cefotaxime in SBP has not resulted in superinfection or nephrotoxicity. A 5-day therapy regimen is as effective as a 10-day treatment. Therefore, the recommended treatment is cefotaxime 2 grams intravenously every 8 hours for 5 days. In patients with creatinine higher than 3 mg/dL, the dosing interval may be extended to 12 hours. Anaerobic coverage is usually not needed nor is coverage for Pseudomonas or Staphylococcus.

Table IV.

Recommended treatment regimens
Diagnosis Treatment
Culture-negative neutrocytic ascites 5 days of IV* third-generation cephalosporin
Monomicrobialnon-neutrocytic bacterascites 5 days of IV antibiotic to which the organism is highly susceptible, if the patient is symptomatic of persistently culture-positive; not all patients with bacterascites require treatment.
Polymicrobial bacterascites IV third-generation cephalosporin plus an antianaerobic drug such as metronidazole. Duration is determined by clinical response and serial ascitic fluid PMN counts and cultures.
Secondary bacterial peritonitis Surgical intervention plus approximately 2 weeks of IV cephalosporin plus an antianaerobic drug such as metronidazole
Spontaneous bacterial peritonitis 5 days of IV antibiotic to which the organism is highly susceptible (e.g., cefotaxime 2 g every 8 hours empirically followed by more specific therapy after susceptibility results are available)

Potentially nephrotoxic antibiotics, such as aminoglycosides, should not be used as empiric therapy. For example, gentamicin has been shown to have an unpredictable volume of distribution in patients with ascites.

Managing underlying liver disease and SBP-induced complications

As discussed in section “What other diseases, conditions, or complications should I look for in patients with SBP?” of this chapter, renal failure develops in 30% to 40% of patients with SBP. The diagnosis of HRS requires a high index of clinical suspicion and exclusion of other potential causes of renal injury. Intravascular volume depletion, nephrotoxins, and infection should be avoided or addressed if present. The risk of renal failure may be decreased with intravenous albumin. It is recommended that patients diagnosed with SBP receive intravenous albumin at a dose of 1.5 g/kg of body weight on day 1 and 1 g/kg of body weight on day 3.

As discussed in the section “What other diseases, conditions, or complications should I look for in patients with SBP?” of this chapter, HE encompasses a wide array of transient and reversible neurologic and psychiatric manifestations. HE is often precipitated by an inciting event such as infection (e.g., SBP), gastrointestinal bleeding, dehydration, or medications. These precipitating factors should be identified and treated. Patients with significant liver dysfunction are susceptible to many causes of encephalopathy other than HE. These other causes should be excluded or, if present, treated accordingly. Initial treatment for HE is often lactulose.

Prophylactic antibiotic treatment for SBP

Studies have identified several risk factors associated with new-onset or recurrent SBP, making it possible to use prophylactic antibiotics in patients at high risk of SBP. Three high-risk patient populations have been identified: (1) cirrhotic patients with acute gastrointestinal hemorrhage; (2) patients with low total protein content (<1 g/dL) in ascitic fluid and no prior history of SBP (primary prophylaxis); and (3) patients with previous histories of SBP (secondary prophylaxis).

SBP occurs in 25% to 65% of patients with gastrointestinal bleeding. The incidence of bacterial infection is high in patients with advanced cirrhosis and/or severe hemorrhage. Bacterial infection in patients with variceal hemorrhage is associated with increased rate of failure to control bleeding, rebleeding, and hospital mortality. Antibiotic prophylaxis in patients with gastrointestinal bleeding significantly decreases both the incidence of severe infections and mortality.

Ceftriaxone is the prophylactic antibiotic of choice in patients with gastrointestinal bleeding and severe liver disease. In patients with less severe liver disease, a quinolone can be given to prevent the development of SBP. For more information on SBP prophylaxis, please refer to the section “How should I monitor the patient with SBP?” of this chapter.

What is the most effective initial therapy?

As discussed in section “What is the As discussed in section “What is the right therapy for the patient with SBP?” and in Table IV of this chapter, third-generation cephalosporins are the antibiotic of choice for SBP. They are relatively safe and well tolerated. They also offer broad-spectrum activity.

Cefotaxime is an effective first-line therapy. Infection resolution is obtained in 77% to 98% of patients with SBP. Five days of treatment is as efficacious as 10 days and is significantly less expensive. Cefotaxime, 2 grams intravenously every 8 hours, is the preferred starting dose. Nephrotoxic antibiotics should be avoided.

The risk of renal failure in SBP may be decreased with intravenous albumin. It is recommended that patients diagnosed with SBP receive intravenous albumin at a dose of 1.5 g/kg of body weight on day 1 and 1 g/kg of body weight on day 3.

Listing of usual initial therapeutic options, including guidelines for use, along with expected result of therapy.

As discussed in section “What is the right therapy for the patient with SBP?” and in Table IV of this chapter, third-generation cephalosporins are the first-line antibiotic of choice for SBP. They are relatively safe and well tolerated. They also offer broad-spectrum activity. Infection resolution is obtained in 77% to 98% of patients with SBP.

Amoxicillin/clavulanic acid is an alternative to a cephalosporin. First, given intravenously then, orally, it has similar results with respect to SBP resolution and mortality and has a lower cost. Ciprofloxacin for 7 days intravenously or for 2 days intravenously followed by 5 days orally results in a similar SBP resolution rate and hospital survival compared to cefotaxime. Quinolones should not be used in patients who are taking this class of medications for prophylaxis against SBP, in areas where there is a high prevalence of quinolone-resistant bacteria, or in nosocomial SBP.

Failure of antibiotic therapy should be suspected if there is worsening of clinical signs and symptoms and/or the ascitic fluid neutrophil count fails to decrease to less than 25% of the pretreatment value after 2 days of antibiotics. This should raise the suspicion of an infection caused by bacteria resistant to antibiotic therapy or secondary bacterial peritonitis. Therefore, modification of antibiotic treatment according to culture sensitivity results or on an empiric basis is necessary.

A listing of a subset of second-line therapies, including guidelines for choosing and using these salvage therapies

As discussed in sections “What is the right therapy for the patient with SBP?” and “Listing of usual initial therapeutic options, including guidelines for use, along with expected result of therapy for SBP,” and in Table IV of this chapter, third-generation cephalosporins are the first-line antibiotic of choice for SBP, and amoxicillin/clavulanic acid and ciprofloxacin could be alternative regimens.

Failure of antibiotic therapy should be suspected if there is worsening of clinical signs and symptoms and/or the ascitic fluid neutrophil count fails to decrease to less than 25% of the pretreatment value after 2 days of antibiotics. This should raise the suspicion of an infection caused by bacteria resistant to antibiotic therapy or secondary bacterial peritonitis. Therefore, modification of antibiotic treatment according to culture sensitivity results or on an empiric basis is necessary.

Listing of these, including any guidelines for monitoring side effects of spontaneous bacterial peritonitis treatment

Re-analysis of ascitic fluid is generally not needed in many patients with infected ascites. Repeat paracentesis can be performed to document sterility of culture and dramatic decrease in PMN count in patients with SBP; however, it is generally not necessary. If the clinical setting, patient’s symptoms, fluid analysis, organism(s), or patient’s response is atypical, repeat paracentesis can be helpful.

As discussed in the section “What is the right therapy for a patient with SBP?” of this chapter, HRS refers to the development of acute renal failure in a patient who usually has advanced liver disease due to cirrhosis, severe alcoholic hepatitis, or (less often) metastatic tumor; however, it can occur in a substantial proportion of patients with fulminant hepatic failure from any cause.

Cefotaxime 2 grams intravenously every 8 hours is the preferred starting dose for treatment of SBP. However, in patients with a serum creatinine level greater than 3 mg/dL, the dosing interval may be extended to every 12 hours. The risk of renal failure may be decreased with intravenous albumin. It is recommended that patients diagnosed with SBP receive intravenous albumin at a dose of 1.5 g/kg of body weight on day 1 and 1 g/kg of body weight on day 3.

How should I monitor the patient with spontaneous bacterial peritonitis?

Managing and monitoring the patients diagnosed with SBP may include the following aspects: (1) assessing antibiotic treatment response; (2) managing SBP-induced complications; (3) preventing recurrent SBP; and (4) managing underling liver disease, including ascites.

Assessing antibiotic treatment response

As discussed in the section “Listing of these, including any guidelines for monitoring side effects of SBP treatment” of this chapter, re-analysis of ascitic fluid is generally not needed in many patients with infected ascites. However, if the clinical setting, patient’s symptoms, fluid analysis, organism(s), or patient’s response is atypical, repeat paracentesis can be helpful.

Managing SBP-induced complications

The annual frequency of HRS in patients with cirrhosis and ascites is approximately 8% but has been reported to be as high as 40%. HRS develops in approximately 25% of patients hospitalized with severe alcoholic hepatitis and 10% who require serial large-volume paracentesis. HRS occurs in approximately 30% of patients with SBP, treated with antibiotics alone and is associated with a poor survival. The concurrent administration of albumin decreases the frequency of HRS and improves survival. Please see section “What is the right therapy for the patient with SBP?” of this chapter for more information on HRS. The diagnosis of HRS requires a high index of clinical suspicion and exclusion of other potential cause of renal injury. Intravascular volume depletion, nephrotoxins, and infection should be avoided or addressed if present.

SBP without septic shock may precipitate deterioration of circulatory function with severe hepatic insufficiency, hepatic encephalopathy, and type 1 HRS and has an approximately 20% hospital mortality rate despite infection resolution.

Preventing recurrent SBP

Patients with prior episodes of SBP have high risks of developing recurrent SBP and prophylactic antibiotics may be warranted (i.e., secondary prevention). For the indications of primary prevention for SBP in patients without prior histories of SBP, please refer to the section “What is the right therapy for the patient with SBP?” of this chapter. The treatment regimens are the same for both primary and secondary prevention. However, the treatment duration is short for primary prevention but indefinite until liver transplantation for secondary prevention.

Norfloxacin 400 mg/day orally has the strongest evidence and is the treatment of choice. However, alternative treatments include ciprofloxacin 750 mg orally once weekly or sulfamethoxazole 800 mg and trimethoprim 160 mg orally once daily. In cirrhotic patients with gastrointestinal hemorrhage, prophylactic antibiotics should be started immediately and continued for 7 days. Prophylactic antibiotics should be used only in patients with the greatest risk of SBP because of increased resistance to antibiotics and increased likelihood of Gram-positive bacterial infections in patients who have received long-term SBP prophylaxis.

American Association for the Study of Liver Diseases (AASLD) Practice Guidelines recommend that in patients with cirrhosis and ascites, but no gastrointestinal bleeding, long-term use of norfloxacin (or trimethoprim/sulfamethoxazole) can be justified if the ascitic fluid protein is <1.5 g/dL and at least one of the following is present: serum creatinine >1.2 mg/dL, blood urea nitrogen >25 mg/dL, serum sodium <130 mEq/L, or Child-Pugh score >9 points with bilirubin >3 mg/dL.

Managing underlying liver disease, including ascites

The goals of care in a patient with decompensated cirrhosis is to prevent superimposed insults to the liver; slow or reverse or stabilize the progression of liver disease; prevent and treat complications; and determine the appropriateness and optimal timing of liver transplant.

Treatment of ascites is also important in decreasing the recurrence of SBP. Appropriate treatment of ascites depends on the etiology of fluid retention. The serum ascites-albumin gradient (SAAG) is helpful diagnostically and for therapeutic decision making. Close clinical follow-up to control ascites is recommended. Treatment of ascites can include diuretics and therapeutic paracentesis.

Cirrhosis complicated by ascites and SBP is associated with significant morbidity and mortality, related in part, to the severe underlying liver disease. In 50% of patients in whom cirrhosis is diagnosed before decompensation, ascites occurs within 10 years. When ascites appears, the expected mortality rate is approximately 50% in just 2 years. In a patient with SBP and decompensated cirrhosis, it is important to have a high index of suspicion for other possible complications of cirrhosis and to timely and effectively treat these complications. A referral for liver transplantation should be considered in those patients with progressive hepatic decompensation and high and rising MELD scores.

What is the Evidence?

"EASL clinical practice guidelines on the management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome in cirrhosis". J Hepatol. vol. 53. 2010. pp. 397-417.

(This includes the most recent clinical practice guidelines on the management of ascites as published by the European Association for the Study of the Liver (EASL). Ascites is the most common complication of cirrhosis. Also discussed is the management of spontaneous bacterial peritonitis and hepatorenal syndrome.)

Koulaouzidis, A, Bhat, S, Saeed, AA. "Spontaneous bacterial peritonitis". World J Gastroenterol. vol. 15. 2009. pp. 1042-9.

(This article offers a concise review of the pathogenesis, clinical manifestations, diagnosis, and management of SBP.)

Runyon, BA. "AASLD Practice Guidelines Committee. Management of adult patients with ascites due to cirrhosis: an update". Hepatology. vol. 49. 2009. pp. 2087-107.

(This set of clinical practice guidlines are put forth by the American Association for the Study of Liver Diseases (AASLD). These guidelines provide a data-supported approach to the diagnostic, therapeutic, and preventive care of ascites.)

Runyon, BA, Feldman, M, Friedman, LS, Brandt, LJ. "Sleisenger and Fordtran’s Gastrointestinal and Liver Disease". Elsevier. 2010.

(Sleisenger and Fordtran’s Gastrointestinal and Liver Disease is a comprehensive textbook of gastrointestinal diseases. The section on ascites and SBP is succinct but extensive.)

Hu, K-Q, Runyon, BA, Friedman, LS, Keeffe, EB. "Handbook of Liver Disease". Churchill Livingstone. 2004.

(This work displays comprehensive information on ascites and SBP in an outline format to expedite diagnostic and therapeutic decision making.)

Sort, P, Navasa, M, Arroyo, V. "Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis". N Engl J Med. vol. 341. 1999. pp. 403-9.

(This is a landmark study that showed that adding intravenous albumin to antibiotics in the treatment of SBP reduces the incidence of renal impairment and death.)
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