Harvey's Garden

Spontaneous bacterial peritonitis

3 min read

  • Pathophysiology/Etiology

    • Infection of ascitic fluid without an intra-abdominal source.
    • Primarily occurs in patients with advanced cirrhosis and portal HTN. Other causes of ascites (e.g., heart failure, Budd-Chiari) are less common.
    • Bacterial translocation from the gut is the key mechanism. Impaired gut motility, bacterial overgrowth, and decreased immune function (e.g., low complement) in cirrhosis facilitate this process.
    • Most common organisms are gut flora: E. coli (most common), Klebsiella pneumoniae, and Streptococcus spp. It is typically a monomicrobial infection.

  • Clinical Presentation

    • Can be subtle or asymptomatic (~13% of cases).
    • Fever (most common sign), diffuse abdominal pain/tenderness, and worsening ascites.
    • May present with altered mental status (new or worsening hepatic encephalopathy), hypotension, or new-onset renal failure.

  • Diagnosis

    • Diagnostic paracentesis is the gold standard. Perform in any cirrhotic patient with ascites on hospital admission or with signs/symptoms of infection.
    • Ascitic Fluid Analysis:
      • PMN count ≥ 250 cells/mm³ is diagnostic.
      • Positive bacterial culture (often negative, but inpatient treatment should not be delayed). Inoculate fluid into blood culture bottles at the bedside to increase yield.
      • Serum-ascites albumin gradient (SAAG) ≥ 1.1 g/dL is consistent with portal HTN.
      • Ascitic fluid protein < 1.0 g/dL is a major risk factor for developing SBP.

  • DDx (Differential Diagnosis)

    • Secondary bacterial peritonitis: Perforated viscus (e.g., ulcer, diverticulitis). Look for multiple organisms on culture, frank peritoneal signs, or failure to improve on therapy.
      • Ascitic fluid in secondary peritonitis often shows ≥2 of the following: protein >1 g/dL, glucose <50 mg/dL, LDH > upper limit of normal for serum.
      • Requires abdominal imaging (CT scan) and surgical consult.
    • Other causes of fever in cirrhosis: UTI, pneumonia, cellulitis.

  • Management/Treatment

    • Empiric antibiotics should be started immediately after paracentesis if SBP is suspected (PMN ≥ 250).
    • First-line: Intravenous 3rd-generation cephalosporin (e.g., cefotaxime, ceftriaxone) for 5-7 days.
    • IV Albumin: Administer albumin (1.5 g/kg on day 1, 1.0 g/kg on day 3), especially if serum creatinine > 1 mg/dL, BUN > 30 mg/dL, or total bilirubin > 4 mg/dL. This reduces the risk of hepatorenal syndrome and mortality.
    • Prophylaxis:
      • Secondary prophylaxis: Lifelong antibiotics (e.g., daily ciprofloxacin or TMP-SMX) are indicated for ALL patients who survive an episode of SBP to prevent recurrence.
      • Primary prophylaxis: Indicated for high-risk patients, such as those with ascitic fluid protein < 1.5 g/dL plus impaired renal or liver function, or in the setting of acute GI hemorrhage.

  • Key Associations/Complications

    • Hepatorenal syndrome (HRS): A major cause of mortality in SBP. Albumin administration helps prevent this.
    • High mortality and recurrence: SBP is an ominous sign in cirrhosis. Recurrence is high (~70% at 1 year) without prophylaxis.
    • The development of SBP is an indication to consider referral for liver transplantation.

Graph View