What are the diagnostic criteria and treatment options for Spontaneous Bacterial Peritonitis (SBP)?

Diagnosis of Spontaneous Bacterial Peritonitis (SBP)

SBP is diagnosed when ascitic fluid polymorphonuclear (PMN) leukocyte count exceeds 250 cells/mm³, regardless of culture results, and empiric antibiotics must be started immediately without waiting for culture confirmation. 1, 2

Diagnostic Paracentesis: When and How

Indications for Diagnostic Paracentesis

• Perform diagnostic paracentesis on all cirrhotic patients with ascites at hospital admission, even without symptoms of infection 1, 2
• Ascitic fluid infection occurs in approximately 12-16% of hospitalized cirrhotic patients, with many cases being completely asymptomatic 1, 2
• Urgent paracentesis is also required when patients develop fever, shock, gastrointestinal bleeding, hepatic encephalopathy, worsening liver or renal function, abdominal pain, or any signs of systemic inflammation 1, 2

Proper Specimen Collection Technique

• Inoculate at least 10 mL of ascitic fluid into aerobic and anaerobic blood culture bottles at the bedside immediately after paracentesis 1, 2
• This bedside inoculation technique increases culture sensitivity to >90% 1, 2
• Obtain blood cultures simultaneously before initiating antibiotics to increase organism isolation rates 1, 2
• Never administer antibiotics before obtaining specimens—even a single dose causes cultures to be negative in 86% of cases 1

Diagnostic Criteria

Primary Diagnostic Threshold

• PMN count >250 cells/mm³ establishes the diagnosis of SBP and mandates immediate empiric antibiotic therapy 1, 2
• This threshold was deliberately chosen lower than 500 cells/mm³ to avoid missing true cases, as each hour of treatment delay increases in-hospital mortality by 3.3-10% 2
• The greater clinical risk lies with underdiagnosing SBP rather than overdiagnosing it 2

Culture-Negative Neutrocytic Ascites

• Patients with PMN >250/mm³ but negative cultures have "culture-negative neutrocytic ascites" and should be treated identically to culture-positive SBP 1, 2
• These patients have similar signs, symptoms, and mortality as culture-positive SBP 1
• Culture-negative cases represent 30-40% of SBP cases and occur when prior antibiotics were given or when organisms are difficult to culture 1

Bacterascites (Special Consideration)

• Bacterascites is defined as positive culture but PMN <250/mm³ 2
• If the patient is symptomatic, treat as SBP 2
• If asymptomatic, repeat paracentesis as 38% will progress to frank SBP 2

Microbiological Profile

Common Organisms

• Approximately 60% of SBP cases are caused by gram-negative bacteria, with Escherichia coli being most common, followed by Klebsiella pneumoniae 1, 3
• Gram-positive organisms include Staphylococcus aureus, Enterococcus faecalis, and Enterococcus faecium 1
• Fungi represent less than 5% of infections 1

Emerging Resistance Patterns

• There has been a significant shift toward gram-positive and multidrug-resistant organisms (MDRO), particularly in nosocomial and healthcare-associated SBP 1
• MDROs now represent 35% of overall infections in cirrhotic patients 1
• This shift has decreased response rates to traditional first-line empirical antibiotics 1

Treatment Initiation

Empiric Antibiotic Therapy

• Start IV antibiotics empirically before obtaining culture results in all patients with ascites PMN count >250/mm³ 1, 2
• For community-acquired SBP, cefotaxime 2g IV every 8-12 hours is first-line therapy with 77-98% resolution rates 1, 2
• A 5-day course is as effective as 10 days of treatment 2
• Oral ofloxacin 400mg twice daily can be used in uncomplicated SBP without shock, hepatic encephalopathy, or renal impairment 2

Nosocomial and Healthcare-Associated SBP

• For nosocomial SBP, recent hospitalization, or critically ill patients in the ICU, use broader-spectrum antibiotics such as carbapenems or piperacillin-tazobactam 1, 4
• Inappropriate initial antimicrobial therapy in septic shock increases mortality risk by 10-fold 1
• Initial carbapenems may lead to higher resolution rates and lower mortality in nosocomial cases 1

Albumin Therapy

• Administer IV albumin 1.5 g/kg body weight within 6 hours of diagnosis, followed by 1.0 g/kg on day 3 1, 2, 4
• This regimen reduces mortality from 29% to 10% and decreases type 1 hepatorenal syndrome from 30% to 10% 1, 2
• Albumin is particularly critical in patients with creatinine ≥1.0 mg/dL or bilirubin ≥5 mg/dL 4

Monitoring Treatment Response

Follow-Up Paracentesis

• Perform repeat diagnostic paracentesis at 48 hours after initiating antibiotics to assess treatment response 2, 4
• Treatment success is defined as a decrease in ascitic PMN count to <25% of the pre-treatment value with clinical improvement 1, 2
• If PMN count fails to decrease by at least 25%, suspect treatment failure 2

Management of Treatment Failure

• Consider resistant bacteria requiring antibiotic modification based on culture sensitivities or empiric escalation to broader-spectrum agents 2
• Obtain CT imaging and surgical consultation to exclude secondary bacterial peritonitis from a surgically treatable intra-abdominal source 2

Antibiotic Stewardship

• Narrow antibiotic coverage as soon as culture results are available and give for as short a time as possible 1
• Do not use quinolones in patients already taking them for prophylaxis, in areas with high quinolone resistance, or in nosocomial SBP 2

Critical Pitfalls to Avoid

• Never make a "clinical diagnosis" of SBP without paracentesis—this is inadequate and delays appropriate therapy 1
• Do not wait for culture results to initiate treatment—the PMN count alone is sufficient 1, 2
• Patients with focal intra-abdominal inflammatory conditions (diverticulitis, cholecystitis) may have PMN >250/mm³ but should be treated for the specific condition, not SBP 1
• Do not place a chest tube in patients with spontaneous bacterial empyema (pleural fluid PMN >250/mm³)—treat with antibiotics only 1

Prognosis

• SBP carries approximately 20% hospital mortality despite infection resolution 2
• Early appropriate antibiotic treatment combined with albumin therapy significantly improves survival 2
• Delaying antibiotic therapy increases mortality by 10% for every hour's delay in cirrhotic patients with septic shock 2