Spontaneous bacterial peritonitis

Spontaneous bacterial peritonitis (SBP) is the development of peritonitis (infection in the abdominal cavity) despite the absence of an obvious source for the infection.^[1] It occurs almost exclusively in people with portal hypertension (increased pressure over the portal vein), usually as a result of cirrhosis of the liver.^[1] It can also occur in patients with nephrotic syndrome.^[2][3]

The diagnosis of SBP requires paracentesis (aspiration of fluid with a needle) from the abdominal cavity.^[4] If the fluid contains bacteria or large numbers of neutrophil granulocytes (>250 cells/µL) (a type of white blood cells), infection is confirmed and antibiotics are required to avoid complications. In addition to antibiotics, infusions of albumin are usually administered.

Symptoms

Symptoms include fevers, chills, nausea, vomiting, abdominal tenderness and general malaise.^[1] Patients may complain of abdominal pain and worsening ascites.^[1] Thirteen percent of patients have no signs or symptoms.^[5] Hepatic encephalopathy may be the only manifestation of SBP; in the absence of a clear precipitant for the encephalopathy, all patients should undergo paracentesis, or sampling of the ascites fluid, in order to assess for SBP.

Pathogenesis

SBP is thought to result from a combination of factors inherent in cirrhosis and ascites, such as prolonged bacteremia secondary to compromised host defenses, intrahepatic shunting of colonized blood, and defective bactericidal activity within the ascitic fluid.^[6] Pharmacologic acid suppression has also been associated with SBP in patients with advanced cirrhosis.^[7][8][9] Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.^[10]

With respect to compromised host defenses, patients with severe acute or chronic liver disease are often deficient in complement and may also have malfunctioning of the neutrophilic and reticuloendothelial systems.^[11]

As for the significance of ascitic fluid proteins, it was demonstrated that cirrhotic patients with ascitic protein concentrations below 1 g/dL were 10 times more likely to develop SBP than individuals with higher concentrations.^[12] It is thought that the antibacterial, or opsonic, activity of ascitic fluid is closely correlated with the protein concentration.^[13] Additional studies have confirmed the validity of the ascitic fluid protein concentration as the best predictor of the first episode of SBP.^[11]

Diagnosis

Diagnosis necessitates paracentesis (needle drainage of the ascitic fluid) and laboratory confirmation of ascitic neutrophils > 250/mm³.^[1]

Treatment

Antibiotics

After confirmation of SBP, patients need hospital admission for intravenous antibiotics (most often cefotaxime 2g IV Q8-12H for at least 5 days or ceftriaxone 2g IV Q24H). They will often also receive intravenous albumin. A repeat paracentesis in 48 hours is sometimes performed to ensure control of infection. Once patients have recovered from SBP, they require regular prophylactic antibiotics as long as they still have ascites.

Prokinetics

The addition of a prokinetic drug to an antibiotic regime reduces the incidence of spontaneous bacterial peritonitis possibly via decreasing small intestinal bacterial overgrowth.^[14]

Intravenous albumin

A randomized controlled trial found that intravenous albumin on the day of admission and on hospital day 3 can reduce renal impairment.^[15]

Prevention/screening

All cirrhotic patients might benefit from antibiotics (oral fluoroquinolone norfloxacin) if:

• Ascitic fluid protein <1.0 g/dL.^[12] Patients with fluid protein <15 g/L and either Child-Pugh score of at least 9 or impaired renal function may also benefit.^[16]
• Previous SBP^[17]

Cirrhotic patients admitted to the hospital should receive prophylactic antibiotics if:

• They have bleeding esophageal varices^[18]

Epidemiology

Patients with ascites underwent routine paracentesis, the incidence of active SBP ranged from 10% to 27% at the time of hospital admission.^[19]

History

SBP was first described in 1964 by Prof Harold O. Conn.^[20]

References