Case Presentation: An 84 year old female with a past medical history of stroke, hypertension, hyperlipidemia, hypothyroidism, cataracts, glaucoma and recent diagnosis of autoimmune hepatitis presented with shortness of breath and abdominal pain. Three months prior to admission, the patient had been admitted and found to have acute liver failure secondary to autoimmune hepatitis and was discharged on a steroid taper. However, subsequent liver biopsy showed submassive liver tissue necrosis consistent with new cirrhosis. On admission, the patient was found to have severe sepsis with lactic acidosis secondary to Escherichia coli bacteremia. The patient underwent right thoracentesis twice and a paracentesis. Imaging and fluid studies indicated that the patient had spontaneous bacterial peritonitis complicated by secondary right empyema in the setting of right hepatic hydrothorax. The patient was treated with broad spectrum antibiotics which were eventually narrowed to ceftriaxone. Initially, the work of breathing improved, but unfortunately the patient’s condition continued to deteriorate despite maximal medical therapy with worsening confusion, agitation, and dyspnea requiring continuous BiPAP. The decision was made to transition the patient to inpatient hospice.
Discussion: Autoimmune hepatitis has a variety of potential phenotypes. Classically, it presents as a chronic necro-inflammatory liver disease and up to 25% of the patients present with acute liver injury. If left untreated, the more severe phenotypes can progress to hepatocellular injury, inflammatory infiltrate, and ultimately liver cirrhosis. An uncommon complication in cirrhotic patients is hepatic hydrothorax, which is estimated to occur in 5-15% of cirrhotic patients. It is hypothesized that ascitic fluid, through small diaphragmatic defects, transports from the abdominal cavity into the thoracic cavity and exceeds the resorptive capacity of the pleural space. In our patient, E. Coli likely translocated from the gut into the bloodstream and eventually into the abdominal ascitic fluid, where it percolated through the diaphragm and caused the empyema in the setting of hepatic hydrothorax, with autoimmune hepatitis and steroid therapy contributing to ascites formation and immunosuppression that predisposed the patient to severe infection.
Conclusions: We present a rare case of a cirrhotic patient with acute autoimmune hepatitis complicated by hepatic hydrothorax who presented with E. coli septicemia and developed secondary spontaneous bacterial peritonitis and empyema.