Spontaneous bacterial peritonitis (SBP) is a serious infection of the ascitic fluid, which accumulates in the abdominal cavity, typically due to advanced liver disease like cirrhosis. SBP is defined by its spontaneous development, meaning it occurs without an obvious source of contamination, such as a perforated bowel or an abscess. This infection represents a life-threatening complication for patients with ascites, and if left untreated, it carries a high mortality rate, requiring swift medical intervention.
Understanding the Causes and Risk Factors
The primary cause of SBP is the breakdown of the body’s natural defenses in people with advanced liver disease. The core mechanism is bacterial translocation, where bacteria from the gut move across the intestinal wall into the bloodstream or surrounding tissue. Because the cirrhotic liver cannot effectively filter these bacteria, they colonize the ascitic fluid.
Ascites, a sign of severe portal hypertension, creates a stagnant environment ideal for bacterial growth. This process is worsened by a dysfunction of the local immune system in the abdominal cavity. The ascitic fluid often lacks sufficient levels of protective proteins, such as complement and immunoglobulins, necessary to fight infection.
A major risk factor for a first SBP episode is a low protein concentration in the ascitic fluid, usually defined as less than 1.5 grams per deciliter (g/dL). This low protein level reflects a lack of the natural immune factors needed to prevent bacterial proliferation. Other factors that increase the likelihood of SBP include acute gastrointestinal bleeding and the use of certain medications, such as proton pump inhibitors, which can alter the gut’s bacterial environment.
Advanced liver failure, indicated by a high Model for End-Stage Liver Disease (MELD) score or Child-Pugh stage C, also significantly increases the risk. These markers reflect the overall severity of the underlying liver dysfunction and the resulting immune impairment. Patients who have previously experienced an SBP episode face a very high risk of recurrence, with rates reported to be as high as 70% within a year.
Recognizing the Symptoms
Recognizing the signs of SBP can be challenging because the symptoms are often non-specific or subtle. The most common indicators that should prompt immediate medical evaluation are the sudden onset of fever and new or worsening abdominal pain. The pain is typically diffuse across the abdomen, and the area may feel tender during a physical exam.
A change in mental status, often presenting as new or worsening confusion or disorientation, is another significant sign of SBP, sometimes referred to as hepatic encephalopathy. This occurs because the infection can trigger a systemic inflammatory response, further impairing brain function. Other signs include a reduction in urine output, signaling worsening kidney function, or a general feeling of being unwell.
SBP can sometimes present with no abdominal symptoms at all, making awareness of non-abdominal signs like fever or confusion particularly important. Up to 13% of patients may not show any overt symptoms. For anyone with known ascites, any unexplained deterioration in their overall condition should be treated as a potential SBP until proven otherwise.
How SBP is Diagnosed and Treated
The definitive diagnosis of SBP requires a procedure called diagnostic paracentesis, which involves using a fine needle to withdraw a sample of the ascitic fluid from the abdomen. This procedure is mandatory for all patients with cirrhosis and ascites who are admitted to the hospital, even if they have no clear signs of infection. The fluid sample is immediately analyzed, and a portion is placed into blood culture bottles to identify the causative bacteria.
The diagnosis is confirmed by measuring the number of polymorphonuclear leukocytes (PMNs) in the fluid. A PMN count equal to or greater than 250 cells per cubic millimeter (cells/mm³) is the diagnostic threshold for SBP, regardless of whether the bacterial culture comes back positive. Delaying this diagnostic tap is strongly associated with increased mortality.
Treatment must begin immediately after the fluid is collected, without waiting for the culture results, which can take several days. Initial therapy involves administering broad-spectrum intravenous antibiotics, typically a third-generation cephalosporin like cefotaxime or ceftriaxone, to target the most likely gut-derived bacteria. The standard duration of antibiotic therapy is typically five to seven days.
In addition to antibiotics, patients at high risk of developing kidney failure often receive intravenous albumin. Albumin is given on the day of diagnosis and again on the third day of treatment, as this has been shown to reduce the risk of a severe complication called hepatorenal syndrome and improve survival rates. A follow-up paracentesis is often performed about 48 hours after starting antibiotics to ensure the PMN count is dropping.
Preventing Future Episodes (Prophylaxis)
Preventing SBP is a major focus of long-term management for patients with cirrhosis and ascites. This prevention strategy, known as prophylaxis, is divided into primary (for high-risk patients who have never had SBP) and secondary (for those who have already recovered from an SBP episode).
Secondary prophylaxis is highly recommended for all survivors of an SBP episode, involving long-term oral antibiotics to prevent recurrence. The goal is to continuously suppress the growth of bacteria in the gut and minimize translocation into the ascitic fluid. Common regimens involve daily, low-dose oral antibiotics like norfloxacin or trimethoprim-sulfamethoxazole, and this treatment typically continues indefinitely until the patient undergoes a liver transplant or the ascites resolves.
Primary prophylaxis is considered for patients with ascites who meet specific high-risk criteria, such as having a low ascitic fluid protein level (less than 1.5 g/dL) or acute gastrointestinal bleeding. Patients experiencing an acute gastrointestinal bleed are given a short, seven-day course of antibiotics to prevent SBP. For those with low ascitic fluid protein, long-term oral antibiotics may be used, though this strategy is reserved for the most vulnerable patients due to concerns about antibiotic resistance.