Chylous Ascites in Cirrhotics - An Ominous Sign!

Abstract

Purpose: To make the clinician aware of chylous ascites as a rare complication of cirrhosis and its presence as an indicator of poor prognosis. A 42 year old male with alcoholic cirrhosis presented with progressively worsening shortness of breath, increasing abdominal girth and weakness. Vitals were stable. He appeared pale, thin and in mild respiratory distress. He had diminished breath sounds and dullness over the left lung. Abdominal exam revealed shifting dullness and normal bowel sounds. Moderate pedal edema was noted. Significant labs include creatinine of 2.4 mg/dl (0.7-1.3), INR=1.3(0.8-1.1), total protein= 6.5 g/dl, ALP=233 IU/L (25-100), AST=83 IU/L (8-40), ALT= 68 IU/L (10-40), total bilirubin= 1.3 mg/dl (0.3-1.2), alpha-feto protein = 2 ng/ml. CT showed a large left pleural effusion and liver cirrhosis with massive ascites. Ultrasound Doppler ruled out portal vein thrombosis. Large volume paracentesis and analysis of the milky-white ascitic fluid demonstrated: SAAG >1, protein <2 g/dl and triglyceride of 219 mg/dl consistent with portal hypertension and chylous ascites. The pleural fluid analysis was consistent with a transudative effusion and triglycerides were elevated at 260 mg/dl consistent with chylothorax. This patient with Child's class C cirrhosis and a MELD score of 18 developed hepato-renal syndrome, and was given albumin, octreotide and midodrine. The ascites was refractory to diuretics. A chest tube was placed for the chylothorax but he did not improve and subsequently died. Chylous ascites is the accumulation of milky peritoneal fluid, rich in triglycerides (>110 mg/dl) due to the presence of lymph in the abdomen. It is a rare complication that presents in 0.5-1% of cirrhotics. Hemodynamic changes cause increase in lymph flow (from 1L to roughly 20 L) and this leads to the dilatation of lymphatics making them susceptible to rupture. Transformation from clear to chylous ascitic fluid indicates a poorer prognosis compared to patients in whom ascites was chylous from the onset. The mortality rates exceed 70% during the first year of diagnosis of chylous ascites in cirrhosis. Treatment aims at improving nutrition to decrease chyle production. Diets rich in medium chained triglycerides decrease flow of chyle because they are directly absorbed from intestinal cells and transported to the liver via the portal vein. Management of cirrhosis with a low sodium diet, diuretics and evaluation for liver transplant are important. TPN and TIPS are therapeutic options tried in refractory patients but offer minimum benefit. TIPS in these patients have a high occlusion and complication rates. Somatostatin and octreotride have also been used but current data is lacking in their efficacy.