Early Diagnosis of Hepatic Hydrothorax with Associated Occlusion of a Peritoneo-Venous Shunt with Tc-99m MAA: Early Diagnosis of Hepatic Hydrothorax with Tc-99m MAA.

A 53-year-old man with pancreatic adenocarcinoma and status post subtotal pancreaticoduodenectomy was referred to evaluate patency of a peritoneovenous shunt (Denver shunt), which was placed for refractory ascites. The patient was injected with Tc-99m macroaggregated albumin (Tc-99m MAA) radiotracer, and immediate (30 min) and 4-h delayed scintigraphic images of the chest and abdomen obtained (Fig. 1a, b). Whereas a normal peritoneal scintigraphy would show radiotracer accumulation within the peritoneal cavity and further flow through the Denver shunt to the system circulation, in this case there was nonvisualization of the Denver shunt or cardiac and/or blood pool activities on both early and delayed images, suggesting obstruction of Denver shunt. Meanwhile, tracer uptake in the right hemithorax was observed on the 4-h delayed image, which led to suspicion for hepatic hydrothorax. Of note, at the time of the nuclear medicine study, there was only a minimal right-sided pleural effusion on a chest X-ray obtained 2 h earlier (Fig. 1c, arrows). Fig. 1 After the intraperitoneal injection of 5.2 mCi Tc-99m MAA, anterior images of the chest and abdomen were obtained at 30 min (a) and 4 h (b). A chest X-ray obtained after 2 h (c) The patient received a new Denver shunt replacement. However, a computed tomography (CT) scan of the chest obtained 2 weeks later demonstrated persistence of large ascites, and progression of hydrothorax into bilateral pleural spaces despite replacement of a new Denver shunt (Fig. 2a). In addition, portal venous thrombosis was also noted (Fig. 2b). Despite replacement, no significant improvement in the ascites was observed; thus, the severe hepatic hydrothorax likewise recurred and was classified as refractory hydrothorax. In past studies, the peritoneovenous shunt had been used successfully for recurrent hepatic hydrothorax and ascites, but in this instance, it was unsuccessful [1]. The patient had persist large amount ascites and worsening bilateral pleural effusions, which were refractory to various treatments including thoracentesis and paracentesis, and died from septic shock 2 months later. Fig. 2 CT of the chest obtained 2 weeks later demonstrated persistence of large ascites (a, dashed white arrow), and progression of hydrothorax into bilateral pleural spaces (a, block white arrows) despite replacement of a new Denver shunt (a, dashed ... Hepatic hydrothorax is the development of a pleural effusion in the setting of liver cirrhosis and portal hypertension, in the absence of cardiopulmonary disease [2]. Some cases have reported a hepatic hydrothorax without appreciable ascites [3, 4]. Although the exact mechanisms are not fully understood, hepatic hydrothorax probably results from the passage of ascites from the peritoneal cavity into the pleural cavity through small diaphragmatic defects [5, 6]. Though peritoneal scintigraphy with Tc-99m sulfur colloid can be used for detection of hepatic hydrothorax [7], our case demonstrated that Tc-99m MAA also can be used for this purpose, and was able to detect a minimal pleural effusion in the setting of severe uncontrolled ascites resulting from portal venous thrombosis. Though not as effective as replacing shunt, urokinase has been reported to be able to restore shunt patency [8]. Other treatment options for recurrent hydrothorax besides thoracentesis are transjugular intrahepatic portosystemic shunt (TIPS), pleurodesis, and thoracoscopic surgery to repair the diaphragmatic defect [9, 10].