Spontaneous Bacterial Peritonitis — Diagnosis & Treatment

Key Points

• Perform diagnostic paracentesis promptly in hospitalized cirrhotic patients with ascites and any clinical deterioration.
• Ascitic PMN count at least 250 cells/mm3 establishes the treatment threshold even if culture is negative.
• Inoculate ascitic fluid directly into blood-culture bottles at the bedside to improve culture yield.
• Use ceftriaxone or cefotaxime for many community-acquired cases, but broaden based on health care exposure and resistant-organism risk.
• IV albumin reduces renal complications in higher-risk SBP and is commonly given as 1.5 g/kg day 1 and 1.0 g/kg day 3.
• Poor response, polymicrobial culture, focal peritoneal signs, or atypical fluid chemistry should raise concern for a secondary surgical source.
• Routine plasma or platelet correction is not required solely to perform most diagnostic paracenteses in cirrhosis.
• Survivors generally need secondary prophylaxis and liver-transplant evaluation.

Algorithm

1. Perform diagnostic paracentesis before antibiotics when feasible without delaying treatment in an unstable patient.
2. Send cell count with differential and bedside-inoculated culture; obtain blood cultures if systemically ill.
3. If PMN count is at least 250 cells/mm3, start empiric antibiotics immediately.
4. Give IV albumin according to renal-risk criteria and manage sepsis, kidney injury, and circulatory status.
5. Assess for secondary peritonitis using examination, fluid profile, culture pattern, and abdominal imaging when indicated.
6. Repeat paracentesis when response is poor or resistant/nosocomial infection is a concern.
7. Narrow or modify antibiotics using cultures and clinical response.
8. After recovery, institute secondary prophylaxis and address transplant eligibility and cirrhosis care.

Clinical Synopsis & Reasoning

Any hospitalized patient with cirrhosis and clinically significant ascites should have a low threshold for diagnostic paracentesis, especially with abdominal pain, fever, encephalopathy, kidney injury, hypotension, GI bleeding, leukocytosis, or unexplained decompensation. SBP can be minimally symptomatic. Send ascitic cell count with differential and inoculate culture bottles at the bedside to improve yield. A PMN count of at least 250 cells/mm3 is sufficient to treat, even with a negative culture. Culture-positive ascites with a lower PMN count requires interpretation based on symptoms and repeat testing. Consider secondary bacterial peritonitis from perforation, abscess, ischemic bowel, or another surgical source when the patient has focal peritoneal signs, very high PMN count, multiple organisms, high ascitic protein or LDH, low ascitic glucose, or poor response to appropriate antibiotics. Kidney function is central because SBP can precipitate hepatorenal syndrome. Blood cultures are appropriate in systemic illness. Diagnostic paracentesis is generally safe despite elevated INR or thrombocytopenia in cirrhosis, and routine correction of coagulation tests before a low-risk paracentesis is usually unnecessary.

Treatment Strategy & Disposition

Start empiric therapy as soon as the PMN threshold is met or clinical suspicion is high. Cefotaxime or ceftriaxone is commonly used for community-acquired SBP, while hospital-acquired infection, recent broad antibiotics, prior resistant organisms, or septic shock requires broader initial coverage guided by local susceptibility patterns. Give IV albumin to reduce renal failure and mortality in patients with SBP, particularly when creatinine or bilirubin is elevated; the classic regimen is 1.5 g/kg on day 1 and 1.0 g/kg on day 3 using dry body weight or an institutionally standardized approach. Stop nonessential nephrotoxins and manage circulatory dysfunction. Repeat paracentesis after about 48 hours when response is uncertain, infection is nosocomial or resistant, or secondary peritonitis is a concern; an inadequate decline in PMNs should trigger reassessment. After recovery from an SBP episode, long-term antibiotic prophylaxis is generally indicated because recurrence risk is high. Patients with acute GI bleeding and cirrhosis also receive short-course infection prophylaxis. Evaluate for liver transplantation because SBP marks advanced decompensated liver disease.

Epidemiology / Risk Factors

• SBP occurs mainly in cirrhosis with low-protein ascites and advanced portal-hypertensive decompensation.
• A previous SBP episode strongly predicts recurrence without prophylaxis.
• GI bleeding increases bacterial translocation and infection risk in cirrhosis.
• Gram-negative enteric organisms and streptococci are common community pathogens, while resistant gram-positive and gram-negative organisms are more frequent in health care-associated disease.
• SBP often precipitates kidney injury, encephalopathy, and acute-on-chronic liver failure.

Investigations

Key Diagnostic Cutoffs

Pharmacology

Prognosis / Complications

• In-hospital mortality has improved with early paracentesis, antibiotics, and albumin but remains significant in advanced cirrhosis.
• Kidney injury, shock, resistant infection, and acute-on-chronic liver failure predict worse outcomes.
• Recurrence after a first episode is common, supporting long-term secondary prophylaxis.
• An SBP episode is a major decompensation event and should prompt transplant assessment when otherwise appropriate.
• Failure of ascitic PMN count and clinical status to improve should trigger urgent evaluation for resistant infection or a surgically treatable secondary source.

Patient Education / Counseling

• Explain that SBP can recur without obvious abdominal pain, so fever, confusion, reduced urine, or sudden weakness in cirrhosis warrants urgent assessment.
• Review the purpose and adherence requirements of long-term antibiotic prophylaxis after recovery.
• Avoid NSAIDs and other nephrotoxic medications unless specifically approved by the cirrhosis care team.
• Discuss ascites care, sodium intake, diuretics, encephalopathy prevention, and transplant evaluation as part of the same advanced-liver-disease plan.
• Advise patients to seek urgent care for GI bleeding because cirrhosis with bleeding requires infection prophylaxis and rapid endoscopic management.

Notes

The practical rule in cirrhosis with ascites is that unexplained deterioration deserves a paracentesis. Waiting for classic abdominal pain or fever misses many cases. Once the PMN count reaches 250 cells/mm3, treatment begins, culture or no culture. The two major additional decisions are whether albumin is needed to protect renal circulation and whether the process might actually be secondary peritonitis requiring source control. Surviving SBP also changes long-term management because recurrence prophylaxis and transplant evaluation become central.

References

1. AASLD Practice Guidance: Ascites, Spontaneous Bacterial Peritonitis and Hepatorenal Syndrome — Link