What is the etiopathogenesis and clinical presentation of Spontaneous Bacterial Peritonitis (SBP)?

Etiopathogenesis and Clinical Presentation of Spontaneous Bacterial Peritonitis

Etiopathogenesis

SBP develops through bacterial translocation from the gut to the bloodstream and ascitic fluid, facilitated by portal hypertension-induced intestinal permeability and impaired host defenses in cirrhotic patients. 1

Pathogenic Mechanisms

• Bacterial translocation is the primary mechanism, where bacteria pass from the intestinal lumen through the gut wall to mesenteric lymph nodes and then to the bloodstream and ascitic fluid 1

• Portal hypertension increases intestinal permeability and promotes bacterial overgrowth in the jejunum, creating conditions favorable for translocation 1, 2

• Cirrhosis-associated immune dysfunction impairs the reticuloendothelial system's ability to clear translocated bacteria, allowing infection to establish 1, 3

• Decreased antimicrobial capacity of ascitic fluid, particularly when protein concentration is <10-15 g/L, reduces local defense mechanisms 4, 3

• Genetic factors contribute to susceptibility—patients carrying NOD2 variants with impaired bacterial recognition have higher SBP risk 1

Microbiology

• Gram-negative bacteria account for approximately 60% of cases, with Escherichia coli being most common, followed by Klebsiella pneumoniae 1, 5

• Gram-positive cocci (mainly Staphylococcus aureus, Enterococcus faecalis, and Enterococcus faecium) represent an increasing proportion of infections 1, 6

• Infections are characteristically monomicrobial, distinguishing SBP from secondary bacterial peritonitis 1, 5

• Multidrug-resistant organisms are increasingly prevalent, particularly in nosocomial and healthcare-associated infections 1, 2

Clinical Presentation

Up to one-third of patients with SBP are completely asymptomatic, making routine diagnostic paracentesis essential in all hospitalized cirrhotic patients with ascites. 1

Classic Symptoms and Signs

• Abdominal pain and tenderness (with or without rebound tenderness) are the most specific findings when present 1

• Ileus with nausea, vomiting, or diarrhea may occur 1, 5

• Fever or hypothermia with chills suggests systemic inflammation, though these may be absent 1

Nonspecific Presentations

• Hepatic encephalopathy may be the sole presenting feature in many patients 1

• Acute kidney injury (AKI) develops in approximately 20% of cases and signals poor prognosis 1, 7

• Worsening jaundice or deteriorating liver function without obvious cause 1, 8

• Hemodynamic instability or shock in severe cases 1

• Gastrointestinal bleeding may coexist or precipitate SBP 1

Critical Clinical Pitfall

Any patient with cirrhosis who deteriorates clinically should be suspected of having bacterial infection, particularly SBP, regardless of the absence of classic symptoms. 1 Each hour of delay in diagnostic paracentesis after hospital admission increases in-hospital mortality by 3.3% after adjusting for MELD score, and in septic shock, mortality increases by 10% for every hour's delay in initiating antibiotics 4, 1

Epidemiology

• Prevalence is 1.5-3.5% in outpatients and 10-11.3% in hospitalized cirrhotic patients with ascites 4, 8

• Half of SBP episodes are present at hospital admission, while the remainder develop during hospitalization 1, 4

• Spontaneous infections account for 36% of all infections in cirrhosis, making SBP one of the most common infection types in this population 1