Spontaneous bacterial peritonitis complicating decompensated cirrhosis

Clinical History

Patient with history of alcohol abuse and hepatitis B-related liver cirrhosis with portal hypertension, splenomegaly and oesophageal varices, currently hospitalized because of progressive, nontender abdominal distension from massive ascites refractory to medical treatment.
At admission, physical examination and laboratory detected oedematous ankle swelling, oliguria, anaemia and impaired renal function.

Imaging Findings

Following abdominal ultrasound (not shown) severely limited by abdominal distension, multidetector CT (Fig.1) was performed hours after admission, without intravenous contrast medium due to impaired renal function (35 ml/min estimated glomerular filtration). Massive fluid-attenuation ascites was confirmed, with small-sized cirrhotic liver, moderate splenomegaly, normal-sized kidneys with preserved parenchymal thickness and no hydronephrosis, absent abscesses and perforated viscera. In the pelvis, some hyperattenuating (28-30 Hounsfield Units) dependent effusion was detected, raising suspicion of haemoperitoneum.
Paracentesis drained turbid yellowish peritoneal effusion, with increased (900/mmc, 300 neutrophils) cell count allowing to diagnose spontaneous bacterial peritonitis.
Intensive treatment including paracentesis, albumin, blood transfusions, antibiotics (ceftriaxone) improved clinical conditions and laboratory data, including renal function. Two days later contrast-enhanced multiphasic CT showed minimally decreased ascites, excluded portomesenteric venous thrombosis, hepatocellular carcinoma, peritoneal thickening, omental soft-tissue masses, other neoplastic or bleeding abdominal lesions.
The patient was discharged on norfloxacin prophylaxis in severe clinical conditions.

Discussion

Cirrhotic patients suffer from acquired immune deficiency and therefore increased susceptibility for bacterial infections, including ascitic fluid and urinary infections, pneumonia, and bacteraemia in descending order of frequency. Defined by infected ascites without an intra-abdominal surgically treatable source of infection, spontaneous bacterial peritonitis (SBP) represents a common, life-threatening although treatable complication of decompensated cirrhosis. Most usually diagnosed in Child C liver disease with large-volume ascites, SBP reaches 3.5-5% prevalence in outpatients and 10-30% in hospitalized cirrhotic patients. With prompt diagnosis and treatment, mortality recently dropped to 20-40%. However, long-term prognosis remains poor due to severe underlying liver disease and SBP represents a common cause of death in the cirrhotic population [1-4].
Mechanisms involved in SBP pathophysiology include intestinal bacterial overgrowth plus structural and functional abnormalities of the intestinal mucosal barrier leading to microbial translocation from the small bowel lumen, combined with an impaired immune response [2-4].
Clinical manifestations are unspecific and often insidious, such as fever (in nearly 70% of patients), abdominal distension, diarrhoea, hepatic encephalopathy, worsening renal function. Abdominal tenderness and peritonitis are uncommon; at least 10% of patients are asymptomatic. The diagnosis is established by paracentesis, which is suggested in all cirrhotics at hospitalization, with new-onset or increasing ascites, unexplained clinical deterioration, hepatic encephalopathy or gastrointestinal bleeding. SBP is a monomicrobial infection caused in 60-70% of cases by Gram-negative bacteria such as Escherichia coli and Klebsiella, and is diagnosed on the basis of increased (>250 cells/mmc) polymorphonuclear leukocytes count in ascites. Culture-negative neutrocytic ascites (nearly 50% of patients) is regarded and treated as SBP [1-5].
As this case exemplifies, the finding of higher-than-water attenuation peritoneal effusion in cirrhosis may strengthen clinical suspicion or suggest SBP. Furthermore, CT allows differentiation exclusion of haemoperitoneum due to bleeding hepatocellular carcinoma, and differentiation from alternative causes of dense or neutrocytic ascites, including secondary bacterial peritonitis which is an uncommon polymicrobial infection characterized by increased protein and decreased glucose levels in ascites, secondary to perforation, inflammation or abscess of an intra-abdominal organ [1-4].
Empirical antibiotics (third-generation cephalosporins) plus plasma expansion with albumin should be started immediately after SBP diagnosis, which currently resolves in almost 80% of cases. Additionally, oral antibiotic prophylaxis is recommended in patients with risk factors such as previous SBP episode (due to the 40-70% chance of recurrence within a year), ascitic fluid protein level above 1 g/dl, severe liver disease and gastrointestinal bleeding [1, 2, 4].

Differential Diagnosis List

Final Diagnosis

Spontaneous bacterial peritonitis in decompensated liver cirrhosis.

URL:	https://eurorad.org/case/11587
DOI:	10.1594/EURORAD/CASE.11587
ISSN:	1563-4086