A 44–year–old woman with 30–pack year smoking history, diabetes and non–alcoholic fatty liver disease presented with shortness of breath since two months and recurrent right sided pleural effusion on chest radiographs. Prior to admission, computed tomography scanning (CT scan) of the chest showed pleural effusion without pulmonary masses or pulmonary embolism. Thoracentesis revealed exudative effusion, which was attributed to furosemide therapy. Exam revealed stable vitals and dullness to percussion with decreased breath sounds on the right base. Abdomen was soft with no palpable masses or signs of ascites. Labs revealed normal complete blood counts, comprehensive metabolic panel, thyroid panel and cardiac enzymes. Repeat thoracentesis showed transudative effusion with no malignant cells on cytology, negative gram stain and cultures for bacteria, fungus and acid–fast bacilli. Repeat CT scan of the chest revealed unchanged right pleural effusion, no pulmonary embolism and 1cm nodule on the right lower lobe. Bronchoscopy revealed no endobronchial lesions. Pelvic and abdominal CT scans showed diffusely enlarged liver with mild fluid accumulation above the liver. Positron emission tomography did not show a significant uptake. Scitingraphic abdomino–thoracic examination revealed unidirectional transdiaphragmatic communication between the peritoneal and right pleural cavities. Liver biopsy showed stage four liver cirrhosis, confirming the diagnosis of hepatic hydrothorax. Treatment was started with fluid and salt restriction.
Hepatic hydrothorax is defined as a pleural effusion, usually >500 ml,in patients with cirrhosis without cardiopulmonary disease. Hepatic hydrothorax without clinical ascites is rare with only 10 reported cases. It is a diagnosis of exclusion in cirrhotic patients with recurrent pleural effusions. Once alternative diagnosis have been excluded, to confirm the diagnosis, intraperitonial injection of 99m Tc–sulfur colloid of 99m Tc–human serum albumin can be performed to illustrate migration of material from abdomen to the pleural space. Postulated mechanism is trans–diaphragmatic flow of ascites fluid to the pleural space through small diaphragmatic defects commonly found in the tendinous portion of the diaphragm. Direct visualization of the diaphragmatic defect can be done with either video–assisted thoracoscopy or thoracotomy but these are associated with significant mortality. Most important aspect of management is candidacy for liver transplantation. While awaiting transplant, mainstay of treatment is salt restriction and diuretics. Other modalities include therapeutic thoracentesis or transjugular intrahepatic portosystemic shunt(TIPS). TIPS has 80% control rate and can be a useful bridge to liver transplant. Pleurodesis in difficult due to rapid reaccumulation of fluid and chest tubes are contraindicated in these patients.
Hepatic hydrothorax without ascites is a rare presentation.