Case Presentation: A 62-year-old with End Stage Liver Disease (ESLD) secondary to autoimmune hepatitis presented with 2 days of dyspnea and cough. In the ED, vital signs were notable for tachypnea and mild hypoxia. Labs revealed an elevated B-type natriuretic peptide of 123. Physical exam demonstrated crackles at the right lung base and bilateral lower extremity edema. Chest x-ray showed recurrent right-sided pleural effusion for which the patient had been admitted several times over the span of a few months. A thoracentesis yielded 1.2 liters of yellow fluid which met criteria for a transudative effusion. Despite her history of ESLD, there was initially low concern for hepatic hydrothorax as our patient had only minimal ascites on abdominal imaging. Her unilateral pleural effusion was attributed to a new diagnosis of congestive heart failure. Despite optimization of home diuretics, our patient’s pleural effusion continued to reoccur. Cardiology, Pulmonology, and Gastroenterology were all consulted to consider alternate causes. Subsequent work-up revealed an unremarkable transthoracic echocardiogram, CT angiogram without evidence of pulmonary embolism, and a cardiac catheterization with normal right-sided pressures despite evidence of hypervolemia on physical exam and minimal preceding diuresis.Hepatic hydrothorax was considered to the most likely etiology of the pleural effusion. Our patient was offered serial thoracentesis and her diuretic regimen was further optimized. She was scheduled for outpatient transjugular intrahepatic portosystemic shunt (TIPS) placement.
Discussion: Hepatic hydrothorax is a diagnosis of exclusion. It is a pleural effusion in an ESLD patient without evidence of cardiopulmonary disease [1]. Diagnosis is supported by chest radiography and a pleural fluid aspirate suggestive of a transudative process from portal hypertension. The pathogenesis is not entirely understood but is likely due to damaged diaphragmatic muscles from increased intraabdominal pressure [1]. Defects are often right-sided given proximity to the congested liver and the relative weakness of the right hemidiaphragm.First-line treatment for hepatic hydrothorax is sodium restriction and oral diuresis [1]. If symptoms persist, serial thoracentesis can be considered. Refractory cases may necessitate escalating therapies such as TIPS placement, pleurodesis, surgical repair of diaphragmatic defects, or liver transplantation [1]. Hepatic hydrothorax mostly occurs in patients with large-volume ascites from portal hypertension. Our patient had minimal ascites, which suggests that portal hypertension alone is sufficient to cause hepatic hydrothorax. Given their experience managing pleural effusions and caring for other complications of decompensated cirrhosis, hospitalists are well-poised to diagnose and treat hepatic hydrothorax.
Conclusions: Hepatic hydrothorax typically occurs as a result of diaphragmatic tissue damage from longstanding ascites and portal hypertension. Our patient had only trace ascites and developed a significant hepatic hydrothorax, suggesting that this process can occur in the absence of traditional findings. Hospitalists should consider a diagnosis of hepatic hydrothorax in ESLD patients with unilateral pleural effusions, especially when cardiopulmonary workup is otherwise unrevealing. Hepatic hydrothorax is predominately treated with diuretics and diet modification. Refractory cases may necessitate TIPS placement or other advanced interventions.