A46-10 Hepatic Hydrothorax With Chylous Characteristics: A Diagnostic Challenge in Decompensated Cirrhosis

Abstract Introduction Pleural effusions in cirrhosis are usually transudative hepatic hydrothoraces. While hepatic hydrothorax occurs in 5-10% of patients with cirrhosis, the presentation of a chylous-appearing fluid, particularly in the context of recent trauma, represents a significant diagnostic rarity. This presentation raises concern for thoracic duct injury, but may also represent the translocation of chylous ascites. We present a rare case of a massive left-sided effusion with chylous characteristics in decompensated cirrhosis, emphasizing the importance of biochemical differentiation between hepatic hydrothorax and true chylothorax. Case Description A 67-year-old woman with non-alcoholic cirrhosis and prior chylous ascites presented with acute dyspnea after a fall. Chest radiography revealed complete opacification of the left hemithorax. Thoracentesis drained 3 L of milky fluid, followed by re-expansion pulmonary edema requiring non-invasive ventilation. Pleural fluid analysis showed triglycerides 1116 mg/dL, protein 2.4 g/dL, and no lymphocytosis—transudative by Light’s criteria and biochemically similar to her ascitic fluid (SAAG 2). CT imaging showed no mediastinal pathology, but effusion recurred rapidly (1.3 L/day) despite prior VATS pleurodesis. The patient developed hepatorenal syndrome, prompting transfer for liver-transplant evaluation. The final diagnosis was refractory hepatic hydrothorax with chylous characteristics, not traumatic chylothorax. Discussion This case illustrates that in cirrhotic patients, a chylous-appearing effusion may reflect chylous ascitic translocation rather than thoracic-duct disruption. The diagnostic clarity rested on the transudative nature of the pleural fluid (protein 2.4 g/dL, meeting Light’s criteria for transudate) and the lack of lymphocytosis, which contrasts with the typical exudative, lymphocyte-predominant profile of a traumatic chylothorax. Elevated triglycerides in transudative pleural fluid mirror the underlying chylous ascites—a rare but recognized manifestation of portal hypertension. Local measures such as pleurodesis often fail when the driving force is persistent portal hypertension. Conclusion This case underscores that in cirrhotic patients with a chylous-appearing pleural effusion, biochemical analysis is paramount to differentiate hepatic hydrothorax from a true chylothorax, thereby preventing misguided and invasive procedures and appropriately directing care towards definitive management of portal hypertension, such as liver transplantation. This abstract is funded by: None