View clinical trials related to Hepatic Hydrothorax.
Filter by:Hepatic hydrothorax (HH) is a pleural effusion that develops in a patient with cirrhosis and portal hypertension in the absence of cardiopulmonary disease (Lv et al., 2018). Several factors are known to contribute to the development of effusion; the most accepted mechanism of which is the direct delivery of ascitic fluid from the peritoneal cavity to the pleural cavity by "positive" intra-abdominal pressure and a "negative" intrathoracic pressure of the pleural cavity through microscopic congenital diaphragmatic defects (Han et al., 2022).
In cirrhotic patients with recurrent hepatic hydrothorax liver transplantation is a definitive treatment. But a significant number of individual are ineligible for liver transplantation. In these patients to ameliorate the symptoms various treatment modalities such as TIPS, serial thoracocentesis, pigtail catheter drainage and pleurodesis are used. We are doing this study to assess the safety and efficacy of serial thoracocentesis verus pigtail catheter drainage.
Hepatic hydrothorax is defined with accumulation of transudate fluid (500 ml) in the pleural cavity in patients with decompensated liver cirrhosis but without cardiopulmonary and pleural diseases. The Prevalence is 5-12% The treatment for hydrothorax is diuretics, repeated thoracocentensis, TIPS and liver transplant.. Midodrine increases effective arterial blood volume and also increases renal perfusion.It has also been used in Refractory ascitis .It has been shown to mobilise ascitis. In patients who are ineligible for TIPS and Liver transplant there is no data on Midodrine and its effects on Hydrothorax in cirrhotics.There are also no guidelines on the use of albumin during Pleural fluid tapping and the dose to be used. This study is being done to assess the safety and efficacy of Midodrine in hydrothorax.
Transjugular intrahepatic portosystemic shunt (TIPS) is the first-line therapy for patients with cirrhosis and refractory ascites. However, mental changes known as hepatic encephalopathy (HE) frequently occur after TIPS. There is no effective method to predict HE after TIPS. Oral glutamine challenge (OGC) and psychometric tests have been used to assess the risk for HE, but never in patients undergoing TIPS. Severe muscle loss may also predispose patients to HE. The aim of the present study is to assess if both the OGC and psychometric tests can accurately predict the development of overt HE after TIPS. Patients will be studied before TIPS and followed after TIPS for the development of HE. The role of muscle loss in favoring HE, as well as is possible reversibility after TIPS will also be investigated.