Peritonitis Bakterial Spontan (SBP)

01Pathophysiology

Spontaneous bacterial peritonitis is an infection of the ascitic fluid that occurs without a surgically treatable intra-abdominal source. It arises almost exclusively in patients with portal hypertension and cirrhotic ascites, and understanding the chain of events from liver disease to infected ascites is essential for recognizing why this population is vulnerable.
Cirrhosis causes portal hypertension, which drives fluid transudation into the peritoneal cavity. The resulting ascitic fluid is characteristically low in total protein and complement, meaning it has poor opsonic and bactericidal activity. In a healthy peritoneal cavity, opsonins tag bacteria for destruction by phagocytes. When these opsonins are deficient, even a small bacterial inoculum can survive and multiply.
The bacteria themselves reach the ascitic fluid through a process called bacterial translocation. Cirrhotic patients develop small intestinal bacterial overgrowth due to impaired gut motility and mucosal edema from portal hypertension. Bacteria migrate across the intestinal epithelium into mesenteric lymph nodes, enter the portal circulation, and bypass hepatic clearance because the reticuloendothelial system (Kupffer cell function) is severely impaired in advanced cirrhosis. Once bacteria reach the systemic circulation or the peritoneal fluid directly, the protein-poor ascites serves as an ideal culture medium.
This explains why the infection is monomicrobial: it results from hematogenous seeding of a single organism rather than perforation of a viscus, which would introduce a polymicrobial flora. It also explains why low ascitic fluid protein () is the strongest independent risk factor, as it directly reflects the opsonic deficiency that permits bacterial survival.

02Classification and Clinical Manifestation

Not all infected ascites qualifies as classic SBP. The classification depends on the combination of ascitic fluid PMN count and culture result.

The clinical presentation itself ranges from overt to subtle. The following table outlines the key manifestations.

The critical teaching point here is that any clinical deterioration in a cirrhotic patient with ascites should raise suspicion for SBP, even when classic signs of peritonitis are absent. The classic exam finding of rigid abdomen with rebound and guarding is often blunted because the large volume of ascites separates the inflamed peritoneal surfaces.

03Diagnostic Workup

Diagnostic paracentesis is the single most important step. Every patient admitted to the hospital with cirrhotic ascites should undergo paracentesis, and every cirrhotic patient with ascites who develops fever, abdominal pain, encephalopathy, renal failure, or any unexplained clinical decline should be tapped. The PMN count is the cornerstone of diagnosis: a value $\ge 250{\text{cells/mm}}^3\backslash geq\; 250\backslash \; \backslash text\{cells/mm\}^3$ in the ascitic fluid is diagnostic and treatment must begin immediately, without waiting for culture results. This is a commonly tested principle.
The ascitic fluid culture serves as the most accurate confirmatory test, but it has practical limitations. Conventional culture methods yield positive results in only about half of cases. Bedside inoculation of ascitic fluid directly into aerobic and anaerobic blood culture bottles at the time of paracentesis raises the sensitivity to roughly 80%. On the exam, if a vignette describes a patient with PMN $\ge 250\backslash geq\; 250$ but negative cultures, this is culture-negative neutrocytic ascites and is still treated as SBP.
When the ascitic fluid analysis reveals polymicrobial organisms on Gram stain, glucose , LDH greater than the upper limit of normal for serum, or total protein $>1\text{ g/dL}>\; 1\backslash \; \backslash text\{g/dL\}$, suspect secondary bacterial peritonitis (a surgically treatable source such as a perforated viscus). These are Runyon's criteria for distinguishing secondary from spontaneous peritonitis and frequently appear in vignettes designed to test whether you can identify the patient who needs imaging and surgical consultation rather than antibiotics alone.

04Management and Treatment

Acute Stabilization. The moment the ascitic fluid PMN count returns at $\ge 250{\text{cells/mm}}^3\backslash geq\; 250\backslash \; \backslash text\{cells/mm\}^3$, start empiric IV cefotaxime at 2 g every 8 hours. Do not delay treatment to await culture results. Cefotaxime is preferred because it covers the most common causative organisms (enteric gram-negatives and streptococci) and it achieves excellent ascitic fluid penetration. Ceftriaxone at 1 to 2 g once daily is an acceptable alternative.
Albumin infusion is a critical and highly testable component. The landmark trial by Sort et al. demonstrated that adding IV albumin (1.5 g/kg on the day of diagnosis and 1.0 g/kg on day 3) significantly reduces the incidence of hepatorenal syndrome and lowers mortality. On an exam, if you are asked about the next best step after starting antibiotics, the answer is albumin. Albumin is particularly indicated in patients with serum creatinine $>1\text{ mg/dL}>\; 1\backslash \; \backslash text\{mg/dL\}$, blood urea nitrogen $>30\text{ mg/dL}>\; 30\backslash \; \backslash text\{mg/dL\}$, or total bilirubin $>4\text{ mg/dL}>\; 4\backslash \; \backslash text\{mg/dL\}$, though current guidelines broadly recommend it for all SBP patients.
Response monitoring. A repeat paracentesis at 48 hours should show a PMN count that has fallen by at least 25%. If the count has not decreased or has risen, consider secondary bacterial peritonitis, a resistant organism, or an alternative diagnosis. This is the point at which imaging (CT abdomen) and surgical consultation may be warranted.
Contraindication to remember: Aminoglycosides (gentamicin, tobramycin) are contraindicated in SBP because cirrhotic patients are extremely susceptible to aminoglycoside-induced nephrotoxicity, which compounds the already elevated risk of hepatorenal syndrome.
Long-term prophylaxis. Any patient who survives an episode of SBP has a one-year recurrence rate of approximately 70% without prophylaxis. Lifelong oral fluoroquinolone (norfloxacin 400 mg daily) or TMP-SMX one double-strength tablet daily is recommended until liver transplantation or death. Primary prophylaxis is indicated for patients who have never had SBP but whose ascitic fluid total protein is in the setting of advanced liver disease (Child-Pugh $\ge 9\backslash geq\; 9$ with bilirubin $\ge 3\text{ mg/dL}\backslash geq\; 3\backslash \; \backslash text\{mg/dL\}$) or renal impairment (creatinine $\ge 1.2\text{ mg/dL}\backslash geq\; 1.2\backslash \; \backslash text\{mg/dL\}$ or BUN $\ge 25\text{ mg/dL}\backslash geq\; 25\backslash \; \backslash text\{mg/dL\}$). Finally, all cirrhotic patients presenting with gastrointestinal bleeding receive IV ceftriaxone 1 g daily for 7 days as SBP prophylaxis, regardless of the presence of ascites at admission.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most common way students lose points on SBP questions is by failing to initiate treatment based on the PMN count alone. A vignette will present a cirrhotic patient with fever, provide the ascitic fluid PMN count at or above 250, and then note that cultures are "pending." The correct next step is to start IV cefotaxime immediately. Choosing to "wait for culture results" is the designed wrong answer.
The second frequent trap involves forgetting the IV albumin. Many students correctly identify the antibiotic but do not add albumin on day 1 and day 3. Exam questions may frame this as "the patient is started on cefotaxime; what additional intervention reduces mortality?" and the answer is albumin.
A third trap is confusing SBP with secondary bacterial peritonitis. When a vignette gives you a PMN count above 250 but also mentions polymicrobial organisms, very low glucose in the ascitic fluid, or an LDH that exceeds the serum value, the question is testing whether you recognize secondary peritonitis, which requires imaging and surgery rather than antibiotics alone.
Finally, questions may test prophylaxis indications. A patient who survives SBP needs lifelong antibiotic prophylaxis. A patient who has never had SBP but has low ascitic protein with advanced liver failure needs primary prophylaxis. A cirrhotic patient admitted with a GI bleed needs short-course IV ceftriaxone. Confusing these three scenarios and their regimens is a common source of errors.
The core competency being tested across all SBP questions is the ability to act decisively on an ascitic fluid PMN count, distinguish spontaneous from secondary peritonitis using straightforward fluid parameters, and recall the complete treatment package of antibiotics plus albumin plus prophylaxis.