Case Presentation: A 43-year-old woman with cryptogenic cirrhosis complicated by a previous episode of spontaneous bacterial peritonitis, recurrent bilateral hepatic hydrothorax, hepatic encephalopathy, and esophageal variceal bleeding presented with a three-day history of dyspnea. Her oxygen saturation was 90% on room air, but the remainder of her vital signs were within normal limits. A chest x-ray revealed a large left-sided pleural effusion (Figure 1). Point-of-care ultrasound showed a simple left-sided pleural effusion (Figure 2) and only trace ascites. Thoracentesis of the left pleural space yielded 1.5 L of yellow opaque fluid. Fluid studies revealed albumin < 1.0 g/dL, LDH 209 U/L, protein < 2.0 g/dL, and 2950 nucleated cells/uL (81% neutrophils, 17% monocytes, 1% lymphocytes, 1% mesothelial cells). The cell count was diagnostic of spontaneous bacterial empyema. Gram stain of the fluid showed 1+ neutrophils but no organisms. Ceftriaxone was administered for five days, and albumin was also administered (1.5 g/kg once followed by 1 g/kg 24 hours later) as recommended by the Hepatology consult team. The pleural fluid culture remained negative at five days. She was discharged home in good condition.
Discussion: Spontaneous bacterial empyema (SBEM) is a complication of hepatic hydrothorax with an estimated incidence of 2% in patients with cirrhosis but up to 16% in those with hepatic hydrothorax. The mortality rate may be as high as 38%. The diagnosis is made when the pleural fluid neutrophil count is > 250 cells/mL with a positive fluid culture or when the fluid neutrophil count is > 500 cells/mL with a negative fluid culture. The pathogenesis of SBEM differs from that of empyema associated with pneumonia and may stem from spontaneous transient bacteremia or from flow of infected ascites into the pleural space through a diaphragmatic defect (although up to 40% of SBEM cases are not associated with spontaneous bacterial peritonitis). Treatment consists of antibiotics directed against Enterobacteriaceae (e.g., Escherichia coli, Klebsiella pneumoniae) which are the most common causative organisms. The use of albumin in treatment of SBEM is not well-studied. In contrast to empyema associated with pneumonia, a chest tube should not be placed for drainage of SBEM unless frank pus is encountered to avoid potentially life-threatening volume depletion and renal failure. While paracentesis in all patients with cirrhosis and ascites requiring hospitalization has been shown to lead to decreased mortality rates and is formally recommended, no similar guidance exists regarding routine thoracentesis in patients with cirrhosis who require hospitalization and are found to have pleural effusions. Given the reduced risks of thoracentesis with ultrasound guidance and the significant mortality associated with SBEM, it may be time to re-evaluate the probable need to perform thoracentesis in patients with cirrhosis requiring hospitalization and found to have pleural effusions.
Conclusions: SBEM is not a rare complication of hepatic hydrothorax and is associated with a significant mortality rate. A pleural effusion in a patient with cirrhosis should never be assumed to be hepatic hydrothorax even in a patient with a history of recurrent hepatic hydrothorax. Further studies may be needed to investigate whether all patients with cirrhosis and pleural effusions who require hospitalization should routinely undergo thoracentesis.