Karen L. Krok; Andrés Cárdenas


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

In This Article


The etiology of hepatic hydrothorax is not completely understood. It is believed that 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. Ascites formation involves the combination of portal hypertension and splanchnic arterial vasodilation. These two events modify the intestinal microcirculation and result in excess lymph formation relative to absorptive capacity in the peritoneal cavity. Increased capillary pressure and permeability secondary to splanchnic arterial vasodilation is the predominant mechanism in this process.

Several observations indicate that the most likely cause of pleural effusions in patients with cirrhosis is the passage of a large amount of ascites from the peritoneal to the pleural cavity through diaphragmatic defects.[8–12] This mechanism was first suggested following the observation of a pneumothorax after injection of air into the peritoneal cavity; when air is infused intraperitoneally in patients with hepatic hydrothorax, a chest x-ray performed within 48 hours can detect air above the diaphragmatic surface in the right side of the chest.[8] Diaphragmatic defects can be demonstrated both grossly and microscopically in patients with hepatic hydrothorax. Microscopic examination of these defects reveals discontinuities in the collagen bundles that make up the tendinous portion of the diaphragm.[8] Typically, the defects are smaller than 1 cm and tend to occur on the right side. This right-sided predominance likely occurs due to the close anatomical relationship of bare areas of the liver with the diaphragm as well as the fact that the left side of the diaphragm is thicker and more muscular than the right. Huang and colleagues[13] have classified the diaphragmatic defects into four morphological types:

  • Type 1: No obvious defect

  • Type 2: Blebs lying in the diaphragm

  • Type 3: Broken defects (fenestrations) in the diaphragm

  • Type 4: Multiple gaps in the diaphragm

Diaphragmatic defects occur in up to 20% of the noncirrhotic population; interestingly, despite the prevalence of these defects, a pneumothorax only rarely develops following laparoscopic procedures.[14–16] Obviously the presence of ascites alters the pressure gradient between the intrathoracic and intraabdominal regions. In patients with ascites, the increasing abdominal pressure and the diaphragmatic thinning secondary to malnutrition in some cirrhotic patients enlarge these defects. When intraabdominal pressure increases, gaps can develop between the muscle fibers of the diaphragm and lead to small herniations of the peritoneum into the pleural space. These herniations, called pleuroperitoneal blebs, may rupture and therefore facilitate passage of fluid. The negative intrathoracic pressure favors the one-way transfer of fluid across these defects, possibly with a valvular mechanism.[6,17,18] Interestingly, up to 20% of patients with hepatic hydrothorax have no clinically significant ascites.[19–24] Ascites develops in patients with hepatic hydrothorax when the formation of ascitic fluid exceeds its absorption by the peritoneal lymphatics and transfers into the pleural space.

The valvular mechanism of hepatic hydrothorax development has been corroborated with nuclear medicine studies using 99mTc-human albumin or 99mTc-sulfur colloid and dye studies that show a unidirectional passage of these markers from the abdominal to the pleural cavity in the first 24 hours after administration.[23,25–27] Also, radioactive isotope scans confirm communication between the peritoneal cavity and the pleural space, even in the absence of sonographic evidence of ascites.[25] Fluid can also leak directly from the liver into the pleural space when bare areas of the liver are in contact with the defects in the diaphragm.