Case Presentation: A 57-year-old male with history of non-alcoholic steatohepatitis (NASH) cirrhosis complicated by recurrent hepatic hydrothorax (requiring approximately 15 thoracenteses) presented with dyspnea. Admission chest x-ray and subsequent computed tomography (CT) scan revealed a large pleural effusion with collapse of the right lower lobe. He underwent thoracentesis with removal of two liters of pink, milky fluid, different in appearance than his prior thoracenteses. Initial pleural fluid analysis was consistent with transudative chylothorax based on Light’s criteria with pleural-to-serum lactate dehydrogenase (LDH) ratio of < 0.6, pleural-to-serum protein ratio of < 0.5, low pleural fluid LDH 44 U/L, pleural fluid triglycerides 205 mg/dL, and nucleated cell count of 90 cells/μL. Follow-up chest CT and abdominal ultrasound showed rapid re-accumulation of pleural fluid (without abdominal ascites) and no evidence of lymphadenopathy, malignancy, or thoracic duct abnormality. The patient received treatment with subcutaneous octreotide three times daily for five days and was placed on a low-fat diet. After multidisciplinary discussion, he was considered high-risk for transjugular intrahepatic portosystemic shunt (TIPS) procedure (due to baseline diastolic dysfunction) and ultimately underwent partial splenic artery embolization (SAE) with interventional radiology to reduce portal pressure.

Discussion: Patients with decompensated cirrhosis have a wide range of complications. Transudative pleural effusions, most often due to hepatic hydrothorax, occur in only 5-10% of cirrhotic patients, often due to diaphragmatic defects allowing abdominal ascitic fluid to travel to the pleural space. Chylothorax, usually exudative, contains high triglycerides and chylomicrons, and commonly occurs in the setting of damage to the thoracic duct from trauma or obstruction. However, our patient’s chylothorax was transudative, and imaging revealed no thoracic duct abnormalities. The mechanism of transudative chylothorax is not well understood; however, in cirrhosis, increased pressure in the splanchnic lymphatic vessels and the thoracic duct due to increased portal venous pressure might cause transudative ascites and chylothorax. This rare complication of cirrhosis is managed conservatively with dietary modifications (low-fat, high protein diet with medium-chain fatty acids), somatostatin analogues (octreotide), and thoracenteses; some patients require total parenteral nutrition. Lymphangiogram is generally avoided in the absence of traumatic injury due to low likelihood of identifying anatomic defects of the thoracic duct and increased risk of causing injury to the duct. Interventions targeting reducing portal or splanchnic pressures (e.g. pleurodesis, thoracic duct surgical ligation or embolization, SAE, and TIPS) might help patients refractory to conservative management, but efficacy data is scarce.

Conclusions: We are reporting one of under twenty cases of transudative chylothorax in a patient with cirrhosis. Chylothorax in patients with cirrhosis confers increased morbidity and mortality; therefore, prompt recognition and therapies are indicated.