Karen L. Krok; Andrés Cárdenas

Disclosures

Semin Respir Crit Care Med. 2012;33(1):3-10. 

In This Article

Abstract and Introduction

Abstract

Hepatic hydrothorax is defined as a transudative pleural effusion, usually greater than 500 mL, in patients with portal hypertension without any other underlying primary cardiopulmonary cause. It develops most likely because of diaphragmatic defects that allow for passage of fluid from the peritoneal space to the pleural space. Because of the mechanical constraints of the thoracic cavity, this complication of portal hypertension can be challenging to treat because patients will become symptomatic when as little as 500 mL of fluid is present in the pleural space. Treatments include salt restriction, diuretics, thoracentesis, transjugular intrahepatic portosystemic shunt, video-assisted thoracoscopy, and pleurodesis. It is important to note that a chest tube is not a potential treatment option; a hepatic hydrothorax should not be treated with a chest tube unless there is frank pus in the pleural fluid or a pneumothorax is present. The ultimate treatment is a liver transplant; the development of a hepatic hydrothorax thus warrants a referral to a liver transplant center.

Introduction

Patients with end-stage liver disease often suffer from complications of portal hypertension. In these patients, 50% ultimately will develop ascites and 25% will develop a variceal hemorrhage. Hepatic hydrothorax is a less common complication of portal hypertension occurring in 5 to 10% of patients with cirrhosis. Despite its infrequency, it remains a challenging problem for clinicians, and its development warrants a liver transplant evaluation.

Hepatic hydrothorax is defined as a transudative pleural effusion, usually greater than 500 mL in patients with portal hypertension without any other underlying primary cardiopulmonary cause. The presence of portal hypertension and not cirrhosis is the sine qua non for the development of hepatic hydrothorax; it should be noted, however, that most patients (> 80%) with portal hypertension have cirrhosis. Although patients with ascites can often tolerate 5 to 8 L of fluid in their abdomen before becoming significantly symptomatic, a patient with a hepatic hydrothorax will develop dyspnea, shortness of breath, and/or hypoxia when only 1 to 2 L of fluid accumulate in the pleural space. This is expected given the structural characteristics of the thoracic cavity. As a result, this complication of portal hypertension is challenging for both patients and clinicians.

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