Spontaneous bacterial peritonitis

I. What every physician needs to know.

Spontaneous bacterial peritonitis (SBP) is an infection of ascites that occurs in the absence of an identified intra-abdominal source of infection, such as intestinal perforation or abscess. Bacteria are felt to translocate across the bowel wall, seeding lymph nodes and ultimately ascites, and host factors such as low complement and protein levels in ascitic fluid contribute to the infectious risk. Bacterial translocation is more common as cirrhosis becomes more advanced, and patients without portal hypertension (HTN), and specifically those without cirrhosis, are unlikely to develop SBP.

II. Diagnostic Confirmation: Are you sure your patient has spontaneous bacterial peritonitis?

SBP is confirmed by performing a paracentesis, and SBP is defined as a polymorphonuclear (PMN) cell count in the ascitic fluid ≥ 250 cells/mm3 (cubic millimeter) in conjunction with a positive ascitic fluid culture and/or gram stain. If the paracentesis sample is bloody, subtract 1 PMN from every 250 red blood cell/mm3 to obtain a corrected PMN count. An elevated PMN count in the absence of a positive culture often represents infection and is usually treated identically to SBP; this entity is usually called culture-negative neutrocytic ascites or culture-negative SBP.

Bacterascites refers to a positive culture and/or gram stain with a PMN count below 250 cells/mm3; most cases resolve spontaneously, but antibiotics should be given to symptomatic patients. Repeat paracentesis may also be considered to document the change in the PMN count. Secondary peritonitis, in which a perforated viscus or abscess results in infected ascitic fluid, is discussed in more detail below.

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A. History Part I: Pattern Recognition:

All patients presenting with new onset ascites should undergo diagnostic paracentesis to determine the cause. Additionally, patients with known ascites should undergo paracentesis if there is clinical suspicion for SBP. Many authors advocate performing a diagnostic paracentesis in all inpatients with cirrhosis and ascites regardless of symptoms, given the risk of asymptomatic infection.

Signs, symptoms, and associated conditions of SBP include:

  • abdominal pain

  • fever (or hypothermia)

  • leukocytosis

  • altered mental status (encephalopathy)

  • ileus

  • diarrhea

  • acidosis

  • hypotension

  • acute renal failure

  • gastrointestinal (GI) bleeding.

Fever and abdominal pain are the most sensitive symptoms of SBP, but none are sufficiently specific to rule in the condition prior to paracentesis.

B. History Part 2: Prevalence:

Though SBP can occur in patients with ascites from any cause, it is nearly always seen in cirrhotics with portal HTN. The incidence of SBP in cirrhosis ranges from 3.5% in asymptomatic outpatients to 10-30% in hospitalized patients. About half of the cases of SBP are present at time of admission, while half are acquired in the hospital.

C. History Part 3: Competing diagnoses that can mimic spontaneous bacterial peritonitis.

Other intraabdominal processes, such as perforation or abscess, can also cause infected ascites. Clinical findings and results from paracentesis will help to distinguish SBP from secondary peritonitis (see below). Additionally, patients with worsening ascites may complain of increased abdominal pain and exhibit significant abdominal tenderness on exam without having SBP. Patients with cirrhosis are at increased risk for a variety of infections which can all cause fever and altered mental status.

D. Physical Examination Findings.

Patients with SBP may present with abdominal distention, pain, fever (or hypothermia), tachycardia, hypotension, or altered mental status. Physical exam findings suggestive of ascites include dullness to percussion over the flanks or shifting dullness. A fluid wave may also be present. Patients with ascites secondary to liver dysfunction may also have stigmata of liver disease, including jaundice, palmar erythema, spider angiomata, and caput medusae. It is important to remember that a diagnosis of SBP cannot be made by physical exam alone; a paracentesis must be performed to make this diagnosis. Finally, SBP is often difficult to distinguish from secondary peritonitis based solely on historical and physical exam findings.

E. What diagnostic tests should be performed?

SBP is diagnosed by paracentesis. Paracentesis should be performed in the lateral left lower quadrant or lateral right lower quadrant. The use of fresh frozen plasma or platelets prior to paracentesis is almost never needed since the bleeding risk from paracentesis, even in the setting of coagulopathy (elevated international normalized ratio [INR]) or thrombocytopenia is low (~1/1000). Paracentesis has been safely performed with an INR as high as 8.7 or a platelet count as low as 19,000 cells/mm3.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Ascitic fluid obtained from paracentesis should be sent for cell count, differential, gram stain, and culture (both aerobic and anerobic). All cultures (blood and ascitic fluid) should be sent prior to the initiation of antibiotics when possible. Inoculating fluid at the bedside directly into blood culture bottles may improve sensitivity but may also lead to false positive results, and some microbiology laboratories discourage this practice.

If there is a high suspicion for secondary peritonitis, total protein, glucose, lactate dehydrogenase (LDH), carcinoembryonic antigen (CEA), and alkaline phosphatase (AP) may also be sent. Findings which support a possible diagnosis of secondary peritonitis include two or more of the following (Runyon’s criteria):

  • Total protein > 1 g/dL (grams/deciliter)

  • Glucose < 50 mg/dL (milligrams/deciliter)

  • LDH > upper limit of normal for serum

A CEA > 5 ng/mL (nanograms/milliliter) and an alkaline phosphatase level > 250 U/L (units/liter) are sensitive and specific for perforation leading to secondary peritonitis. Lastly, a polymicrobial gram stain and/or culture should raise suspicion for perforation, with or without any of the other above findings. All cases of suspected secondary peritonitis require prompt abdominal imaging and surgical consultation.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Ultrasound (US) may be helpful in determining if a patient has ascites, how much ascites is present, and which fluid pocket can be tapped safely. The best site for paracentesis may be “marked” either in radiology or at the bedside, and ultrasound marking was found in one study to lead to higher success rates than a “blind” approach. Plain films may be quickly ordered and reviewed for perforation in suspected secondary peritonitis, and ultimately a computed tomography (CT) scan of the abdomen may be necessary to evaluate for perforation or abscess.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis.

Ascitic fluid total protein, LDH, CEA, and AP should only be sent if there is a high suspicion for secondary peritonitis.

III. Default Management.

Patients who are clinically stable should undergo paracentesis prior to administering antibiotics. However, antibiotics should be given while ascitic fluid results are pending if suspicion for infection is high. Current evidence supports the use of a third generation cephalosporin such as ceftriaxone 2 g (grams) daily or 1 g twice daily or cefotaxime 2 g every 8 hours, for empiric treatment of SBP. Alternatively, an oral or intravenous fluoroquinolone may be used, only if the prevalence of fluroquinolone-resistant organisms is low. Oral quinolones may be given to low-risk patients (those without renal failure, vomiting, or encephalopathy) after a brief initial hospitalization. Five days of treatment is sufficient provided the patient shows clinical improvement.

These antibiotics provide adequate coverage for gram negative bacilli such as E coli and Klebsiella, which are the most common cause of SBP; cephalosporins have consistently shown a cure rate of 90-95%. One randomized-controlled trial showed that giving albumin in addition to antibiotics decreased the risk of renal failure and death. Albumin was given at 1.5 mg/kg (milligram/kilogram) of body weight on day 1, followed by 1 mg/kg on day 3. Patients with a creatinine < 1 mg/dL, BUN < 30 mg/dL, and bilirubin < 4 mg/dL were shown to do well without the need for albumin infusion.

A. Immediate management.

Patients who are unstable, i.e., show signs and symptoms of sepsis, should be started on empiric, broad-spectrum antibiotics immediately (prior to paracentesis). These may be narrowed once their infectious work-up is completed.

B. Physical Examination Tips to Guide Management.

Improvement in abdominal pain and decreased tenderness to palpation, and resolution of fever and tachycardia indicates resolving infection. Development of peritoneal signs (rebound, guarding) may indicate secondary peritonitis (perforation, abscess) and should prompt immediate imaging and possible surgical consultation.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Improvement in peripheral leukocytosis and acidosis may indicate resolving infection. Also, an association between SBP and hepatorenal syndrome has been described. Thus, creatinine should also be monitored closely. A repeat paracentesis is required in the patient who fails to clinically improve or deteriorates. A rising PMN count on repeat paracentesis may require broadening of the antibiotic regimen, or a search for causes of secondary peritonitis. A declining PMN count in a patient who continues to be symptomatic warrants a longer antibiotic course.

D. Long-term management.

Please see “prophylaxis” section below.

E. Common Pitfalls and Side-Effects of Management

Albumin should only be given on hospital days 1 and 3 to help reduce renal impairment and mortality in selected patients. Five days of antibiotic treatment is sufficient in the vast majority of patients.

IV. Management with Co-Morbidities

In general, there are no significant changes that should be made to the management of SBP in the setting of various co-morbidities (see below).

A. Renal Insufficiency.

Antibiotics should be adjusted (renally-dosed) in the setting of renal insufficiency.

B. Liver Insufficiency.

No change in standard management.

C. Systolic and Diastolic Heart Failure

No change in standard management, though 25% albumin rather than 5% should be given to lessen the salt load.

D. Coronary Artery Disease or Peripheral Vascular Disease

No change in standard management.

E. Diabetes or other Endocrine issues

No change in standard management.

F. Malignancy

Patients with malignant ascites may have elevated ascitic fluid white cell and PMN counts, but SBP in patients with malignant ascites is rare.

G. Immunosuppression (HIV, chronic steroids, etc).

No change in standard management.

H. Primary Lung Disease (COPD, Asthma, ILD)

No change in standard management.

I. Gastrointestinal or Nutrition Issues

No change in standard management.

J. Hematologic or Coagulation Issues

No change in standard management.

K. Dementia or Psychiatric Illness/Treatment

No change in standard management.

V. Transitions of Care

A. Sign-out considerations While Hospitalized.

If a patient with SBP decompensates (becomes febrile, tachycardic, hypotensive, or has worsening abdominal pain), it is reasonable to broaden antibiotics and repeat paracentesis to rule out worsening abdominal infection. If the patient develops peritoneal signs on physical exam, the covering physician should check an abdominal x-ray and/or CT scan of the abdomen to rule out secondary peritonitis. Surgical consultation may be warranted depending on the results of imaging. Additionally, patients with ascites who are admitted for other reasons (not SBP) and decompensate should undergo paracentesis to rule out SBP.

B. Anticipated Length of Stay.

Length of stay will depend on their clinical presentation and co-morbidities. Some studies have shown that patients who develop SBP while hospitalized have a longer length of stay (may have more resistant bacteria causing the infection). Low-risk patients may be transitioned to oral antibiotics and discharged before completing the standard 5 days of treatment.

C. When is the Patient Ready for Discharge.

Patients are ready for discharge after defervescence, provided they are tolerating oral intake and encephalopathy (if present) is improved. Patients with decompensated cirrhosis (i.e., bilirubin > 4 mg/dL) or renal failure need to remain hospitalized until their labs improve or stabilize. These high-risk patients usually receive a full parenteral treatment course in the hospital. If blood or ascitic fluid cultures are positive, it would be reasonable to wait on the identification and sensitivities of the pathogen to better tailor the antibiotics.

D. Arranging for Clinic Follow-up

1. When should clinic follow up be arranged and with whom.

Patients should follow-up with their hepatologist or primary care physician within 1-2 weeks after discharge to ensure that they are continuing to improve clinically. Labs may need to be monitored sooner than the follow-up appointment.

2. What tests should be conducted prior to discharge to enable best clinic first visit.

Basic labs should be drawn prior to discharge (complete blood count [CBC], chemistry panel). Thus, if the patient presents to their follow-up appointment with infectious symptoms, the outpatient provider can repeat a CBC to check for worsening leukocytosis. Additionally, if patients are being discharged on diuretics for management of their ascites, either for the first time or on a different dose, their renal function and electrolytes should be carefully monitored.

3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

See above.

E. Placement Considerations.


F. Prognosis and Patient Counseling.

SBP is a significant cause of morbidity and mortality in patients with cirrhosis. The mortality rate is 20-40% at one year. Management of ascites can help prevent future episodes of SBP. Thus, patients with ascites who have alcoholic liver damage should be counseled on alcohol cessation. First-line treatment of patients with ascites includes sodium restriction (2000 mg/day) and diuretics. Fluid restriction is felt to be less important than salt restriction, but becomes necessary with moderate to severe hyponatremia.

VI. Patient Safety and Quality Measures

A. Core Indicator Standards and Documentation.


B. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

According to the American Association for the Study of Liver Diseases (AASLD) guidelines, patients with ascites who are admitted to the hospital with GI bleeding should be placed on SBP prophylaxis. Intravenous ceftriaxone at 1 gm daily, or a fluoroquinolone (such as norfloxacin), may be used for 7 days or until the patient is discharged, though ceftriaxone was found to be superior to norfloxacin in one study.

Patients with a history of SBP, or those with an ascitic fluid protein < 1 g/dL, benefit from antibiotic prophylaxis. Possible regimens include norfloxacin 400 mg once daily, trimethoprim/sulfamethoxazole (TMP/SMX) 160 mg/800 given 5 times/week, or ciprofloxacin 750 mg once a week. TMP/SMX and ciprofloxacin can also be given daily as intermittent dosing may increase bacterial resistance. Proton pump inhibitors may increase the risk of SBP and should only be given if there is a clear indication to do so.

What's the evidence?

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