Patients with advanced cirrhosis and portal hypertension have abnormal extracellular fluid volume regulation that in most cases results in accumulation of fluid, typically in the abdominal cavity (ascites) or lower extremities (edema). In approximately 5 to 10 percent of cirrhotic patients, fluid accumulates in the pleural space [1-3]. Hepatic hydrothorax is defined as a pleural effusion, usually greater than 500 mL, in patients with cirrhosis and without primary cardiac, pulmonary, or pleural disease [1,4].
While patients with ascites can often tolerate up to 5 to 10 L of fluid with only mild symptoms, those with a pleural effusion can have severe symptoms (such as shortness of breath, cough, and hypoxemia) with as little as 1 to 2 L of fluid. This topic review will summarize issues related to hepatic hydrothorax while other complications of cirrhosis are presented separately.
The underlying mechanisms leading to fluid retention in patients with hepatic hydrothorax are similar to those leading to other forms of fluid accumulation in patients with cirrhosis. (See "Pathogenesis of ascites in patients with cirrhosis".)
Although the exact mechanisms involved in the development of hepatic hydrothorax are incompletely understood, it probably results from the passage of ascites from the peritoneal to the pleural cavity through small diaphragmatic defects. These are typically less than 1 cm (and may be microscopic) and are generally located in the tendinous portion of the diaphragm [5-10].
The negative intrathoracic pressure generated during inspiration favors the passage of fluid from the intra-abdominal to the pleural space. Thus, many patients have only mild or no clinically detectable ascites [2,11-13]. Hepatic hydrothorax develops when the absorptive capacity of the pleural space is exceeded. This theory is supported by studies using 99mTc-human albumin or 99mTc-sulphur colloid, which demonstrate unidirectional passage of these markers from the abdominal to the pleural cavity [14-19].