Paracentesis and Ascitic Fluid analysis in context of SBP

Indications for diagnostic paracentesis:


  1. Cirrhotic patients with ascites at admission
  2. Cirrhotic patients with ascites and signs or symptoms of infection: fever, leukocytosis, abdominal pain
  3. Cirrhotic patients with ascites who present with a clinical condition that is deteriorating during hospitalization: renal function impairment, hepatic encephalopathy, gastrointestinal bleeding
  4. Patients with new-onset ascites

Peritoneal Fluid Analysis:

Test and Ascitic-Fluid Container Comments
Albumin Differential diagnosis of ascites according to the serum ascites albumin gradient
Cell Cell count and differential count
Culture Aerobic- and anaerobic-culture

Additional Analyses of Ascitic Fluid

Test and Ascitic-Fluid Container Comments
Tube without additives
Total protein Values >1 g/dl suggest secondary peritonitis instead of SBP
Lactate dehydrogenase Values greater than the upper limit of normal for serum suggest secondary peritonitis instead of SBP
Glucose Values <50 mg/dl suggest secondary peritonitis instead of SBP
Carcinoembryonic antigen Values >5 ng/ml suggest hollow viscus perforation
Alkaline phosphatase Values >240 U/liter suggest hollow viscus perforation
Amylase Values markedly elevated (often >2000 U/liter or five times serum levels) in patients with pancreatic ascites or hollow viscus perforation
Triglyceride Values >200 mg/dl suggest chylous ascites
Syringe or evacuated container
Cytology Sensitivity increased if three samples submitted and promptly evaluated
Mycobacterial culture Sensitivity only 50%

Differential Diagnosis of Ascites According to the Serum Ascites Albumin Gradient

Gradient >1.1 g/dl (portal hypertension) Gradient <1.1 g/dl

Alcoholic hepatitis

Cardiac ascites

Portal-vein thrombosis

Budd-Chiari syndrome

Liver metastases

Peritoneal carcinomatosis

Tuberculous peritonitis

Pancreatic ascites

Biliary ascites

Nephrotic syndrome


The diagnosis of SBP is suggested by a polymorphonuclear (PMN) cell count in excess of 250 cells per cubic millimeter in the absence of evidence of an alternative source of infection (secondary peritonitis), such as viscus perforation or intraabdominal abscess.

Determination of total protein, lactate dehydrogenase, and glucose levels in ascitic fluid may aid in the differentiation between SBP and secondary peritonitis. Culture is used to confirm the diagnosis of SBP.

Ascitic fluid infections


  1. Spontaneous bacterial peritonitis (SBP). Most common infection in patients with ascites and cirrihosis. Ascitic fluid infection with positive bacterial culture, neutrophil count ?250/ml and no surgically treatable source of infection. Bacterial cultures almost invariably yield a single growth. The presence of >1 organism suggests secondary peritionitis.
  2. Culture negative neutrocytic ascites. Diagnostic criteria as for SBP but cultures are negative. Other causes of raised ascitic fluid neutrophil count need to be excluded (eg peritoneal carcinomatosis, pancreatitis, TB peritonitis). Clinical, prognostic and therapeutic characteristics are similar to those of SBP and this condition should be treated in a similar fashion to SBP.
  3. Mononmicrobial non-neutrocytic bacterascites. Positive culture but neutrophils <250/ml. Clinical course is dependent on the presence/absence of clinical features. Those with clinical features of ascitic fluid infection have similar morbidity/mortality to those with SBP.
  4. Secondary bacterial peritonitis. Positive cultures (usually polymicrobial), neutrophils 250/ml, and surgically treatable source of infection. Clinical features do not distinguish SBP from secondary bacterial peritonitis. Ascites usually meets 2 of the following: total protein >1g/dL, glucose <50 mg/dL, LDH >225 U/ml (or higher than the upper limit of normal for serum)
  5. * Polymicrobial bacterascites. Gram stain or culture reveals multiple organisms but neutrophils <250/ml. Usually due to inadvertent puncture of intestine during paracentesis (risk: 1/1000). If ascitic fluid protein >1g/dL colonization usually resolves spontaneously

Aetiology & Pathogenesis

– seemingly innocuous procedures can lead to transient bacteraemia and SBP in cirrhotics (eg NG tube placement, endoscopy, IV catheter insertion, bladder catheterization)
– usually develops when the volume of ascites is sizeable but can occur even when fluid is difficult to detect on physical examination
– E.coli, Strep (usually pneumococcus) and Klebsiella account for 3/4 of cases. Gram negative infection more common than gram positive. Anaerobes rarely isolated
– current view is that SBP is the result of bacterial overgrowth in the small intestine followed by bacterial translocation across the intestinal wall. Because of impaired immune response in cirrhotics and portosystemic shunts the bacteria then spread into the systemic circulation and seed in ascites.
Predisposing factors

* Severity of liver disease:
70% of cases occur in patients with Child’s grade C with most of the rest occuring in patients with Child’s grade B.
Total ascites protein <1 g/dL predisposes to SBP because it correlates with complement levels and opsonic activity
* GI bleeding
20% of patients with cirrhosis and ascites presenting with a GI bleed have SBP
* Bacteriuria
* Previous SBP
Recurrence rates: 43% by 6 months, 69% by 1 year and 74% by 2 years

Clinical features

  1. signs may be absent in up to 1/3
  2. fever/hypothermia
  3. abdominal pain and tenderness
  4. rigidity is not a feature in patients with infected ascites, even if there is a free perforation of the intestine. This is a result of the large volume of ascites preventing contact between the visceral and parietal peritoneal surfaces
  5. hepatic encephalopathy
  6. diarrhoea
  7. ileus
  8. shock
  9. important to have high index of suspicion and low threshold for diagnostic paracentesis. Unexplained deterioration in a patient with cirrhosis and ascites should lead to diagnostic paracentesis


  • diagnostic tap of ascites. Innoculate some fluid directly into blood culture bottle as well as sending fluid for gram stain (often not helpful) and cell and differential count. Suspect SBP if neutrophil count > 250/ml. Other tests which may be helpful include total protein, glucose (in malignancy or gut perforation), LDH ( in spontaneous bacterial peritonitis) , amylase ( in pancreatitis). Risk of paracentesis is small despite almost invariable impairment of clotting in these patients. Approx. 1% risk of significant abdominal wall haematoma, 0.01% risk of haemoperitoneum and 0.01% risk of iatrogenic infection
  • follow up paracentesis probably not necessary if response to treatment is dramatic, setting is typical and infection is monomicrobial. However if there are features to suggest secondary peritonitis paracentesis should be repeated (usually after 48 h)
  • peritonitis secondary to abscess or perforated viscus should be suspected if WCC >10,000/ml, ascitic protein is elevated, cultures of fluid grow anaerobes or multiple organisms, or follow-up paracentesis after 48 h of treatment reveals persistently positive cultures or a rising WCC


  1. Spontaneous bacterial peritonitis, culture negative neutrocytic ascites, symptomatic monomicrobial bacterascites
  2. 3rd generation cephalosporin (cefotaxime 2g 8 hrly) until sensitivity known. 5 day course satisfactory even for patients who are bacteraemic.
  3. Asymptomatic monomicrobial bacterascites
  4. Repeat paracentesis after 48 h.
  5. Treat with cefotaxime if symptoms develop or neutrophil count in repeat sample ?250/ml


  1. Fernandez J, Bauer TM, Navasa M, Rodes J. Diagnosis, treatment and prevention of spontaneous bacterial peritonitis. Baillieres Best Pract Res Clin Gastroenterol. 2000 Dec;14(6):975-990.
  2. Thomsen TW, Shaffer RW, White B, Setnik GS. Videos in clinical medicine. Paracentesis. N Engl J Med. 2006 Nov 9;355(19):e21.
  1. February 12, 2010
  2. February 12, 2010

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