Spontaneous Bacterial Peritonitis Interpreter
Spontaneous Bacterial Peritonitis Interpreter
An ascitic neutrophil count of 250 or more is spontaneous bacterial peritonitis and is treated on the count. The harder question is the one underneath it: a perforated viscus produces exactly the same count, needs an operation rather than antibiotics, and is separated from SBP by Runyon’s three ascitic fluid criteria. This page does both, and names culture-negative neutrocytic ascites and bacterascites as the separate entities they are.
Is this SBP — and is it actually secondary peritonitis?
Ascitic tap → which entity, and who needs a surgeonA 61-year-old with alcohol-related cirrhosis presents with abdominal pain and fever. A diagnostic paracentesis gives an ascitic neutrophil count of 1,400 cells/mm³, total protein 32 g/L, glucose 1.8 mmol/L and an LDH above the laboratory’s serum upper limit of normal. The serum-ascites albumin gradient is 14 g/L. The culture is not back.
Four entities from two numbers, and one question underneath all of them
Neutrophils ≥ 250/mm³, culture negative → culture-negative neutrocytic ascites. Same disease, same treatment.
Neutrophils < 250/mm³, culture positive with one organism → bacterascites. Treat if symptomatic, otherwise re-tap.
Neutrophils < 250/mm³, culture negative → no SBP on this sample.
Underneath all four: Runyon’s criteria. Two or more of — total protein above 10 g/L, glucose below 2.8 mmol/L, LDH above the serum upper limit of normal — means secondary bacterial peritonitis until a perforation has been excluded. So does a polymicrobial culture.
Worked example
A 61-year-old with alcohol-related cirrhosis presents with abdominal pain and fever. A diagnostic paracentesis gives an ascitic neutrophil count of 1,400 cells/mm³, total protein 32 g/L, glucose 1.8 mmol/L and an LDH above the laboratory's serum upper limit of normal. The serum-ascites albumin gradient is 14 g/L. The culture is not back.
Neutrophils 1,400/mm³ — far above 250, so this is a neutrocytic ascites and antibiotics start regardless
Gradient 14 g/L, so the ascites is portal hypertensive and SBP is on the table
Now Runyon: protein 32 g/L is above 10 g/L — criterion one met
Glucose 1.8 mmol/L is below 2.8 mmol/L (50 mg/dL) — criterion two met
LDH above the serum upper limit of normal — criterion three met. Three of three, where two is enough
A protein of 32 g/L is the finding that should stop you. Spontaneous bacterial peritonitis arises in protein-poor ascites; this fluid is protein-rich, glucose-depleted and LDH-high, which is what a perforation into the peritoneum looks like
Action: broad-spectrum antibiotics with anaerobic cover, urgent cross-sectional imaging, surgical referral, ascitic CEA and alkaline phosphatase, and a repeat tap at 48 hours. Treating this as ordinary SBP would be antibiotics alone for a perforated viscus
Change one entry and the page changes with it. Drop the protein to 8 g/L and the glucose to 3.5 mmol/L, leaving only the LDH criterion, and the same 1,400 cells read as straightforward spontaneous bacterial peritonitis
The four entities, and what separates them
| Entity | Neutrophils | Culture | Treatment |
|---|---|---|---|
| Spontaneous bacterial peritonitis | ≥ 250/mm³ | One organism | Cefotaxime or equivalent plus albumin; secondary prophylaxis on recovery |
| Culture-negative neutrocytic ascites | ≥ 250/mm³ | No growth | Identical. A negative culture is not a reason to stop |
| Monomicrobial non-neutrocytic bacterascites | < 250/mm³ | One organism | Treat if symptomatic; otherwise repeat the tap and treat if the count has risen |
| Polymicrobial bacterascites | < 250/mm³ | More than one organism | Broad-spectrum cover and imaging — usually perforation, or a needle injury at the tap |
| Secondary bacterial peritonitis | ≥ 250/mm³ | Often polymicrobial | Surgery. Antibiotics alone will not treat a perforation |
Runyon’s criteria, and why each one points where it does
| Criterion | Threshold | Why a perforation does this |
|---|---|---|
| Ascitic total protein | Above 1 g/dL (10 g/L) | SBP arises in protein-poor ascites — low protein is itself a risk factor for it. A perforation spills protein-rich intestinal content into the peritoneum |
| Ascitic glucose | Below 50 mg/dL (2.78 mmol/L; this page uses 2.8) | A large bacterial and leucocyte load consumes glucose far faster than the single translocated organism of SBP |
| Ascitic LDH | Above the upper limit of normal for serum | Released from the mass of dying neutrophils and from devitalised tissue. Stated against your own laboratory’s serum limit, not as a fixed number |
| Two or more of the three | — | Suspect secondary bacterial peritonitis. Image and refer |
| Supporting: ascitic CEA | Above 5 ng/mL | Wu 2001 — supports gut perforation specifically |
| Supporting: ascitic alkaline phosphatase | Above 240 U/L | Wu 2001 — same |
| Supporting: repeat tap at 48 hours | Count has not fallen | In SBP on appropriate antibiotics the count falls substantially. In secondary peritonitis it does not |
Treated on the count — except when the count is the wrong question
Spontaneous bacterial peritonitis is diagnosed and treated on the ascitic neutrophil count rather than on the culture, because the culture is frequently silent and the mortality is not. A count of 250 cells per mm³ or more in a cirrhotic with portal hypertensive ascites is the diagnosis, and a negative culture gets the condition a different name — culture-negative neutrocytic ascites — rather than a different treatment. That much is settled and is covered in detail by the record that computes the count. What this page adds is the part that the count cannot answer.
A perforated viscus in a patient with ascites produces exactly the same neutrophil count. It is not rare, it is not obvious on examination in a patient who already has a tense abdomen and encephalopathy, and the treatments diverge completely: spontaneous bacterial peritonitis needs a cephalosporin and albumin, while secondary bacterial peritonitis needs an operation. Giving antibiotics alone to someone with a perforation is close to uniformly fatal. Operating on someone with uncomplicated SBP is also harmful. So the two have to be separated on the fluid, and Runyon and Hoefs published the way to do it in 1984: at least two of an ascitic total protein above 1 g/dL, an ascitic glucose below 50 mg/dL, and an ascitic LDH above the upper limit of normal for serum.
Each of those three has a mechanism behind it, which is why they hold up. Spontaneous bacterial peritonitis arises in protein-poor ascites — a low ascitic protein is one of the accepted indications for primary prophylaxis — so protein-rich fluid is already the wrong setting for it, and a perforation spills protein-rich intestinal content directly into the peritoneum. The glucose falls because a perforation delivers a bacterial and leucocyte load that consumes it far faster than the single translocated organism of an SBP does. And the LDH rises from the mass of dying neutrophils and devitalised tissue. A polymicrobial culture points the same way for the same reason: SBP is monomicrobial because it comes from translocation of one organism, and gut contents are not.
Two further tests support the same question and are worth sending when it is live. Ascitic carcinoembryonic antigen above 5 ng/mL and ascitic alkaline phosphatase above 240 U/L both favour gut perforation. And the simplest discriminator of all is time: repeat the paracentesis at 48 hours. In spontaneous bacterial peritonitis treated with an appropriate antibiotic the neutrophil count falls substantially; in secondary bacterial peritonitis it does not, because the source is still open. A count that has not fallen is a prompt to image and to call a surgeon, not to change the antibiotic and wait another two days.
Frequently asked questions
What ascitic neutrophil count diagnoses spontaneous bacterial peritonitis?
250 cells/mm³ or more, which is 0.25 × 10⁹/L, applied to the absolute polymorphonuclear count after correction for a blood-stained tap — not the total white cell count and not the percentage. The diagnosis is made on that number with or without a positive culture, and treatment starts on it. The ascitic fluid neutrophil count calculator computes the corrected count and shows how large the correction for red cells can be.
What are Runyon’s criteria for secondary bacterial peritonitis?
At least two of three findings in the ascitic fluid: total protein above 1 g/dL (10 g/L), glucose below 50 mg/dL (which converts to 2.78 mmol/L), and lactate dehydrogenase above the upper limit of normal for serum. Two or more in a patient with a neutrocytic ascites means a perforated or inflamed intra-abdominal organ until imaging says otherwise, and it needs a surgeon rather than antibiotics alone. A polymicrobial culture points the same way, as do an ascitic carcinoembryonic antigen above 5 ng/mL and an alkaline phosphatase above 240 U/L.
Is culture-negative neutrocytic ascites a milder form of SBP?
No — it is the same disease with a silent culture, and it is treated identically. The culture is negative for procedural reasons far more often than because there is no organism: conventional processing of ascitic fluid grows something in roughly two thirds of true cases, bedside inoculation into blood culture bottles raises that to around nine in ten, and a single dose of antibiotic before the tap sterilises the great majority. Complete the full antibiotic course, give albumin where indicated, and start secondary prophylaxis on recovery.
The culture grew an organism but the neutrophil count is under 250. What now?
That is monomicrobial non-neutrocytic bacterascites, a separate entity from SBP. Roughly half of these episodes resolve spontaneously and the other half progress. The patient decides the management, not the culture: if there is fever, abdominal pain, encephalopathy or deteriorating renal function, treat as SBP now. If the patient is well, repeat the paracentesis and treat if the count has risen to 250 or more or the same organism grows again. If the growth is polymicrobial rather than a single organism, the differential changes entirely — that is usually a perforation or a needle injury to bowel at the tap, and it needs imaging.
Why does a high ascitic protein argue against spontaneous bacterial peritonitis?
Because SBP arises in protein-poor ascites. A low ascitic protein reflects poor opsonic activity in the fluid and is itself a risk factor for the condition — an ascitic protein below 15 g/L with organ dysfunction is an accepted indication for primary prophylaxis. Protein-rich ascites is the wrong setting for spontaneous infection and the right setting for something that has spilled intestinal content into the peritoneum, which is why ascitic protein above 10 g/L is the first of Runyon’s three criteria.
How useful is repeating the tap at 48 hours?
It is the most useful single thing after the initial chemistry. In spontaneous bacterial peritonitis treated with an appropriate antibiotic, the ascitic neutrophil count falls substantially over 48 hours. In secondary bacterial peritonitis it does not, because the source is still open, and in an SBP with a resistant organism it also does not. So a count that has not fallen is a prompt to image the abdomen and involve surgery, or to reconsider the antibiotic — and either of those is better done at 48 hours than at five days.
Related calculators
References
- Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 practice guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021;74(2):1014–1048.
- Runyon BA, Hoefs JC. Ascitic fluid analysis in the differentiation of spontaneous bacterial peritonitis from gastrointestinal tract perforation. Hepatology. 1984;4(3):447–450.
- Runyon BA, Hoefs JC. Culture-negative neutrocytic ascites: a variant of spontaneous bacterial peritonitis. Hepatology. 1984;4(6):1209–1211.
- Wu SS, Lin OS, Chen YY, et al. Ascitic fluid carcinoembryonic antigen and alkaline phosphatase levels for the differentiation of primary from secondary bacterial peritonitis with intestinal perforation. J Hepatol. 2001;34(2):215–221.
- European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018;69(2):406–460.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.
