Spontaneous Bacterial Peritonitis

Introduction

Spontaneous bacterial peritonitis (SBP) is defined as an ascitic fluid infection without an evident source.
It is one of the most common bacterial infections in patients with cirrhosis and has a poor prognosis if it’s missed.
Classically, patients present with the classic triad of FBI: fever, belly pain, and increasing ascites.

One key concept to get your head around is the SAAG score.

Usually, a SAAG score, or a serum-ascites albumin gradient, should be considered for a first episode of ascites. This is simply the difference between the serum albumin concentration and the ascites albumin concentration.

A high SAAG score is above 11g/L and means there is a large difference between two. This occurs when the hydrostatic pressure in the blood is high due to portal hypertension from cirrhosis and heart failure.

A low saag score means the albumin level in the blood and the ascites is similar. This occurs in malignancy and secondary peritonitis.

the spread of intestinal bacteria into the portal circulation and then the ascitic fluid.

The most common pathogen is E.Coli, accounting for 50% of cases.

Liver cirrhosis predisposes people to this bacterial translocation because of three reasons:

1. Cirrhosis can trigger bacterial overgrowth in the gut

2. Portal hypertension causes increased intestinal permeability to enteric bacteria

3. Cirrhosis causes an acquired immune deficiency as it reduces the production of proteins in the complement system

Key risk factors for SBP include varices, advanced cirrhosis, a prior episode of SBP, malnutrition, and the use of proton pump inhibitors.

bedside testing, bloods, and imaging.

Point of care tests might help you rule out other sources of infection like a urine dipstick, but they might also help to assess how sick the patient is. An ECG, Blood glucose level and venous blood gas are three quick point of care tests to help immediately risk stratify the patient.

Standard blood tests might include an FBC to check for neutrophilia and anaemia from bleeding varies, UECs will help you identify a kidney injury, LFT’s and coagulation studies are vital as they will quantify hepatic decompensation, and finally, blood cultures may assist in identifying the pathogenic organism.

Imaging might include an ultrasound and a CT abdomen. The USS is the definitive test for the detection of ascites. Sonography can determine adequacy of fluid for paracentesis and can help localise the procedure. A CT abdomen should only be considered if you have findings suggestive of secondary peritonitis which is caused by a surgically treatable intraabdominal source.

Let’s now move to the diagnostic algorithm for spontaneous bacterial peritonitis that is suggested by BMJ Best Practice.

If our initial tests are suggestive of SBP, we need to perform a diagnostic paracentesis. This is a procedure that removes fluid from the abdomen through a slender needle and is both diagnostic and therapeutic. As mentioned before, the standard of care is now via ultrasound guidance.

With this specimen, we should send it for cell culture and cell counts.

This is the important part: if the total white cell count is more than 0.5 or the neutrophil count is more than 250 cells/mm^3; this is diagnostic of spontaneous bacterial peritonitis and should prompt immediate management. If it is lower than this, SBP can usually be ruled out.

While bacteria are rarely detected on gram stain, a polymicrobial growth from the peritoneal fluid culture is highly indicative of secondary peritonitis.

You should always examine the sample appearance as subjective descriptions of the fluid being “hazy” or “cloudy” indicate SBP with relatively high sensitivity.

acute treatment and prevention.

In the acute setting, consider early resuscitation with fluids, empirical broad spectrum antibiotic therapy, and managing other complications of cirrhosis.

Fluid resuscitation is important, especially if patients have features of sepsis. You should also consider intravenous albumin at 20%. This reduces the rate of acute kidney injury and improves survival.

Antibiotics should always be based on your local guidelines. In Australia, ceftriaxone 2 g IV daily is often used empirically. A good benchmark is to provide this within an hour of presentation.

Complication management is case dependent. For example, if a patient presents with hepatic encephalopathy, consider using oral lactulose to help reduce the absorption of toxic amines by lowering the colonic pH.

Secondary prophylaxis should be considered after the first episode of spontaneous bacterial peritonitis. This reduces the risk of subsequent episodes and improves mortality. Consider daily Trimethoprim and Sulfamethoxazole. Primary prophylaxis is only recommended for patients at very high risk.

The main clinical features of spontaneous bacterial peritonitis include abdominal pain, fever, diarrhoea, and features of decompensated cirrhosis.

Diffuse abdominal pain is the hallmark of SBP. Unlike the classic presentation of secondary peritonitis from something like a perforation which results in a rigid abdomen, the pain in SBP is more diffuse and subtle. This is because the ascites separates the visceral and parietal peritoneal surfaces.

Fever is the most common clinical manifestation of SBP. As people with advanced cirrhosis are usually slightly hypothermic, any increase in temperature should be taken seriously.

Diarrhoea is thought to be caused by the bacterial overgrowth associated with cirrhosis. Its important to note that this might herald the onset of ascitic fluid infection.

Other clinical manifestations associated with decompensated cirrhosis are plentiful but consider

The following key A to D features:

Altered mental state from hepatic encephalopathy, bleeding from anorectal or oesophageal varices, colour change from jaundice, and distension from the ascites.

To remember this, I think that spontaneous bacterial peritonitis is caused by the CIA, it presents with the FBI, and it can only be managed with cats.

SBP occurs in cirrhosis because of the overgrowth and crowding of bacteria, increased intestinal permeability, and an acquired immune deficiency.

It presents with fever, belly pain, and increasing ascites and can be managed with antibiotics like ceftriaxone, albumin, and then prevented with prophylactic Trimethoprim and sulfamethoxazole.