Spontaneous Bacterial Peritonitis
Spontaneous bacterial peritonitis (SBP) is a serious infection of ascitic fluid that occurs without an obvious intra-abdominal source. It is a common and life-threatening complication of advanced liver disease and portal hypertension. SBP reflects a breakdown in gut barrier function, immune defence, and bacterial clearance. Because symptoms can be subtle or atypical, SBP is frequently under-recognised.
What You Need to Know
Spontaneous bacterial peritonitis is a serious infection of ascitic fluid that occurs without an obvious intra-abdominal source such as perforation or trauma. It develops most commonly in people with cirrhosis and ascites, where portal hypertension and intestinal congestion disrupt the normal gut barrier. This disruption allows bacteria and bacterial products to translocate across the intestinal wall into mesenteric lymph nodes and the bloodstream, eventually seeding the ascitic fluid. The process is driven by altered gut permeability and impaired immune surveillance rather than a single focal breach.
Ascitic fluid itself creates conditions that favour infection. Low protein concentrations reduce opsonisation, meaning bacteria are less effectively marked for immune clearance. At the same time, cirrhosis is associated with systemic immune dysfunction, including impaired neutrophil function and reduced complement activity. Together, these changes mean that even small numbers of bacteria entering the peritoneal cavity can establish infection, explaining why spontaneous bacterial peritonitis can occur in the absence of any intra-abdominal injury.
Several interacting factors increase susceptibility and help explain why SBP is both common and recurrent in advanced liver disease:
increased gut permeability and bacterial translocation related to portal hypertension
low-protein ascitic fluid with reduced antibacterial activity
cirrhosis-associated immune dysfunction that limits effective host defence
Alcohol plays an important role in amplifying this risk. Chronic alcohol exposure accelerates progression of cirrhosis, worsens portal hypertension, and further impairs immune function. Alcohol also alters gut microbiota and increases intestinal permeability, increasing bacterial load and translocation. Ongoing alcohol intake is therefore associated with higher rates of first-time and recurrent spontaneous bacterial peritonitis, while abstinence reduces ascites severity and lowers infection risk over time.
Beyond the Basics
Gut barrier dysfunction and bacterial translocation
Portal hypertension leads to increased venous pressure within the intestinal circulation, causing bowel wall oedema and congestion. This interferes with the integrity of tight junctions between enterocytes, the specialised epithelial cells that normally form a selective barrier within the gut. When these junctions are disrupted, bacteria and endotoxins can move from the gut lumen across the intestinal wall into mesenteric lymph nodes and the systemic circulation. This process, referred to as bacterial translocation, is a central mechanism in the development of spontaneous bacterial peritonitis.
Once bacteria enter the circulation, ascitic fluid provides an accessible compartment for seeding. Unlike secondary peritonitis, this process does not require bowel perforation or direct contamination. Instead, infection arises from repeated low-level bacterial exposure combined with impaired clearance, explaining why SBP can develop insidiously in patients who otherwise appear clinically stable.
Impaired host defence in cirrhosis
Cirrhosis is associated with immune paresis, meaning immune responses are present but functionally ineffective. Neutrophils demonstrate reduced chemotaxis and impaired phagocytosis, while macrophage activity is blunted. Complement levels are often reduced due to impaired hepatic synthesis, limiting the ability to opsonise bacteria and facilitate immune clearance.
Ascitic fluid compounds this problem when protein concentrations are low. Opsonins, including immunoglobulins and complement proteins, are present in insufficient quantities to support antibacterial defence. As a result, even small bacterial inocula that would normally be cleared can proliferate within the peritoneal cavity, leading to infection.
Ascitic fluid characteristics
The biochemical composition of ascitic fluid plays a key role in determining SBP risk. Low-protein ascites is strongly associated with infection because reduced immunoglobulin and complement concentrations limit intrinsic antibacterial activity. Protein concentration therefore serves as a marker of vulnerability rather than infection itself.
Ascites volume also contributes to risk. Large-volume or long-standing ascites increases the peritoneal surface area exposed to potential bacterial seeding and often reflects more advanced portal hypertension. Patients with refractory ascites, where fluid reaccumulates despite therapy, are particularly susceptible to SBP due to the combination of high bacterial exposure and impaired immune defence.
Systemic inflammation and circulatory dysfunction
Spontaneous bacterial peritonitis triggers a systemic inflammatory response characterised by cytokine release and further vasodilation within the splanchnic circulation. This worsens the already reduced effective circulating volume seen in advanced cirrhosis. The resulting drop in arterial pressure can impair renal perfusion and precipitate acute kidney injury.
This inflammatory and haemodynamic cascade explains why SBP is a major precipitant of hepatorenal syndrome. Even when infection is treated promptly, the associated circulatory dysfunction can have lasting consequences, contributing to high morbidity and mortality.
Alcohol and recurrence risk
Alcohol increases the risk of both first-time and recurrent SBP through several reinforcing mechanisms. Ongoing alcohol intake sustains liver inflammation and fibrosis, accelerating progression to decompensated cirrhosis. It also increases gut permeability and promotes bacterial overgrowth, raising the burden of translocating organisms.
In addition, alcohol worsens immune dysfunction and contributes to progressive ascites accumulation, increasing the volume of fluid at risk of infection. Recurrence rates of SBP are significantly higher in individuals who continue drinking, while sustained abstinence reduces ascites severity, lowers bacterial translocation, and improves long-term outcomes.
Clinical Connections
Spontaneous bacterial peritonitis often presents with non-specific or subtle clinical features, which makes early recognition challenging. Fever, abdominal pain or tenderness, worsening ascites, and deterioration in mental status are common, but some patients may have minimal symptoms or no abdominal pain at all. Hepatic encephalopathy may be the first or only sign, particularly in older adults or those with advanced cirrhosis. Because of this variability, any clinical deterioration in a person with cirrhosis and ascites should prompt consideration of SBP, even when classic signs of infection are absent. Diagnosis is established by diagnostic paracentesis demonstrating an elevated ascitic neutrophil count, with or without positive culture, and should not be delayed while awaiting imaging or laboratory confirmation.
Clinical assessment focuses on identifying early changes that suggest infection or systemic involvement, as progression can be rapid. SBP commonly triggers circulatory dysfunction, which may manifest as hypotension, rising creatinine, or reduced urine output, and is a recognised precipitant of acute kidney injury and hepatorenal syndrome. Untreated infection carries a high mortality rate, but timely antibiotic therapy and supportive management significantly improve survival, underscoring the importance of early evaluation.
Key clinical features that should prompt urgent investigation include:
new or worsening encephalopathy, fatigue, or confusion
fever, abdominal discomfort, or increasing abdominal distension
signs of circulatory or renal compromise, such as hypotension, oliguria, or rising creatinine
Management extends beyond treatment of the acute episode. After recovery, the risk of recurrence remains high, particularly in those with low-protein ascites or advanced liver disease. Secondary prophylaxis with antibiotics is commonly indicated, and ongoing follow-up is essential to monitor renal function, ascites control, and overall disease progression. Early recognition of recurrence, adherence to diagnostic protocols, and prompt escalation of care are central to improving long-term outcomes in people with a history of spontaneous bacterial peritonitis.
Concept Check
What is meant by bacterial translocation?
Why is low-protein ascites associated with increased SBP risk?
How does portal hypertension contribute to gut barrier dysfunction?
Why can SBP precipitate hepatorenal syndrome?
How does alcohol increase the risk of SBP and recurrence?