History and exam
Key diagnostic factors
common
presence of risk factors
Patients with end-stage liver disease presenting with hepatic encephalopathy, decompensated cirrhosis, increase in ascites volume and/or frequency, or gastrointestinal bleeding are at particularly high risk.
Patients who have recently had a therapeutic endoscopy are also at risk.
Malignant ascites also carries a risk, albeit one that is less well-described than the risk in patients with end-stage liver disease.[78]
abdominal pain or tenderness
signs of ascites
Clinical manoeuvres for the detection of ascites include examining for flank dullness, shifting dullness, fluid wave, and auscultatory percussion.
The sensitivities and specificities of these signs for ascites vary widely. Percussion of the abdominal wall is the most sensitive of the manoeuvres for ascites, with a sensitivity of 84%.[83]
nausea/vomiting
Caused by the intestinal hypomotility and bacterial overgrowth associated with cirrhosis and SBP.
diarrhoea
Caused by the intestinal hypomotility and bacterial overgrowth associated with cirrhosis and SBP.
altered mental status
In patients admitted to the hospital with hepatic encephalopathy, there was an 18% prevalence of SBP in 1 series.[5]
Other diagnostic factors
common
hypothermia
Signs of sepsis may be present.
hypotension
Signs of sepsis may be present.
tachycardia
Signs of sepsis may be present.
Risk factors
strong
decompensated hepatic state (usually cirrhosis)
In patients with advancing cirrhosis (increasingly frequent episodes of tense ascites, gastrointestinal bleeding, hepatic encephalopathy), there can be worsening bacterial intestinal overgrowth with increased haematogenous spread, as well as decreased ascitic protein content and opsonic activity to fight off infection.
low ascitic protein/complement
A randomised, placebo-controlled trial found that patients with a total ascitic protein concentration <15 g/L (<1.5 g/dL) were at increased risk for development of SBP compared with those with a higher protein concentration.[55] However, subsequent cohort studies have failed to replicate this finding.[56][57]
gastrointestinal bleeding
weak
ascites due to malignancy, renal insufficiency, or congestive heart failure
There are no studies that describe whether patients with ascites due to end-stage liver disease are at higher risk for SBP than those with ascites not due to liver disease. However, there is some suggestion that mechanisms in cirrhosis that cause increased susceptibility to infection may not be present in patients without cirrhosis.[58]
extra-intestinal infection
Respiratory and urinary tract infections may seed to the ascitic fluid; in these cases, the organisms causing the SBP may not be part of the normal intestinal flora.
invasive procedures
Invasive procedures, such as central venous catheterisation, urinary catheterisation, paracentesis, and transjugular intrahepatic portosystemic shunt placement, have been associated with SBP.
use of proton-pump inhibitors (PPIs)
PPIs facilitate enteric colonisation, overgrowth, and translocation into the peritoneum, which might increase the risk for SBP. Meta-analyses demonstrate PPI use as an independent predictor of increased SBP risk in cirrhotic patients.[59] One recent meta-analysis looking at over 10,000 patients demonstrated a weak but statistically significant association between SBP and PPI use.[60] The decision to prescribe a PPI for a patient with cirrhosis should be made carefully.
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