1. Epidemiology and Impact

The development of ascites marks the critical transition from compensated to decompensated cirrhosis, a turning point that dramatically worsens prognosis. Spontaneous bacterial peritonitis (SBP) is a frequent and life-threatening complication in this population, contributing significantly to both short- and long-term mortality.

Key Data Points

• The annual incidence of new-onset ascites in patients with compensated cirrhosis is 5–10%. Its appearance causes the 5-year survival rate to plummet from approximately 80% to just 30%.
• SBP complicates 10–30% of hospital admissions for patients with cirrhosis and ascites, with a one-year mortality rate approaching 40%.
• In the outpatient setting, the incidence of SBP is lower but still significant, at around 3.5% per year for decompensated cohorts.
• Multidrug-resistant (MDR) pathogens are a growing concern, accounting for 20–25% of community-acquired SBP cases and rising to 35–40% in nosocomial SBP.
• Timeliness of diagnosis is critical: delaying diagnostic paracentesis by more than 12 hours after admission increases in-hospital mortality by approximately 3.3% for every hour of delay.

2. Pathophysiology of Ascites Formation

Ascites formation is a complex process driven by severe portal hypertension and profound splanchnic vasodilation. This combination creates a state of effective arterial underfilling, which activates powerful neurohormonal systems that command the kidneys to retain sodium and water, eventually leading to the accumulation of fluid in the peritoneal cavity.

3. Pathogenesis of Spontaneous Bacterial Peritonitis

SBP is an infection of the ascitic fluid that occurs without an evident intra-abdominal source. It arises from gut-derived bacteria that translocate across a compromised intestinal barrier into ascitic fluid, which has severely impaired local immune defenses.

Key Pathways

• Bacterial Translocation: Portal hypertension leads to intestinal bacterial overgrowth, gut dysbiosis, and increased mucosal permeability. This allows bacteria and their byproducts (e.g., endotoxin) to escape the gut lumen and seed the mesenteric lymph nodes and, ultimately, the peritoneal cavity.
• Impaired Ascitic Fluid Defenses: The ascitic fluid in cirrhosis is a prime culture medium. A low total protein concentration (<1.5 g/dL) is a major risk factor because it correlates with low levels of complement and other opsonins, which are crucial for phagocytosis and bacterial clearance.
• Common Pathogens: The most frequent culprits are enteric Gram-negative bacteria, such as Escherichia coli and Klebsiella species. However, Gram-positive cocci (e.g., Staphylococcus, Enterococcus) are increasingly identified, especially in nosocomial cases.

4. Risk Factors for SBP

The risk of developing SBP is not uniform among patients with ascites. It can be stratified based on the characteristics of the ascitic fluid itself, a history of prior infections, comorbid conditions, and certain medications.

1. Clinical and Laboratory Factors

• Low Ascitic Fluid Protein: A concentration <1.5 g/dL is the single strongest predictor, increasing SBP risk by at least five-fold.
• Prior SBP: Patients who have survived one episode of SBP have a 70% chance of recurrence within one year if they do not receive antibiotic prophylaxis.
• Recent Upper GI Bleeding: Variceal hemorrhage increases SBP risk due to mucosal ischemia and enhanced bacterial translocation.

2. Comorbidities

• Renal Dysfunction: A baseline serum creatinine ≥1 mg/dL is a significant risk factor.
• Advanced Liver Disease: Indicated by severe hyponatremia (serum Na⁺ ≤130 mmol/L) or high bilirubin.
• Other Conditions: Diabetes mellitus and congestive heart failure also increase risk.

3. Medications

• Proton Pump Inhibitors (PPIs): Data are conflicting, but some studies suggest that by reducing gastric acid, PPIs may promote bacterial overgrowth and increase SBP risk. Their use should be regularly re-evaluated.
• Nonselective β-blockers: While essential for variceal prophylaxis, they may worsen circulatory dysfunction and increase mortality risk in patients with refractory ascites.

5. Clinical Presentation

The signs and symptoms of ascites can be subtle initially but become more obvious as fluid accumulates. SBP often presents with classic signs of peritonitis, but its presentation can be occult, especially in critically ill or elderly patients, where it may manifest only as a change in mental status or hemodynamic stability.

Ascites Findings

• Physical Exam: Shifting dullness on percussion is the most sensitive physical sign. A fluid wave and flank dullness are more specific but appear later. Ultrasound can detect as little as 100 mL of fluid.
• Tense Ascites: Large volumes can cause significant abdominal distention, leading to dyspnea from diaphragmatic elevation, early satiety, and umbilical hernias.

SBP Presentation

• Classic Triad: Fever, diffuse abdominal pain, and rebound tenderness. However, all three are present in less than half of patients.
• Occult Presentation: In the ICU or in elderly patients, SBP may present without localizing signs. The only clues may be worsening hepatic encephalopathy, acute kidney injury, hypotension, or unexplained acidosis.
• Laboratory Clues: Peripheral leukocytosis, rising serum creatinine, and an elevated procalcitonin (>0.5 ng/mL) can suggest an underlying infection.