Hepatic Hydrothorax: An Independent Predictor of Mortality in Cirrhosis? Is the MELD-Na Score Worth Its Salt?

Excerpt

Although pleural effusion associated with liver disease was first described by Laennec in the nineteenth century, it was not until 1958 that the term “hepatic hydrothorax” (HHT) was first used [1]. HHT refers to a transudative pleural effusion (typically exceeding 500 ml) in patients with cirrhosis in the absence of underlying cardiac or pulmonary disease [2]. HHT is considered to be a manifestation of advanced cirrhosis complicated by portal hypertension, occurring in 5–10% of patients with decompensated cirrhosis (Fig. 1) [3]. Using terms extrapolated from describing ascites, HHT is considered refractory when it is diuretic-resistant (recurs despite dietary sodium restriction and maximal diuretics) or diuretic-intractable (diuresis limited by electrolyte imbalance, hemodynamic instability, renal insufficiency, or precipitation of hepatic encephalopathy) [2, 4]. Work over the past several decades has attempted to illuminate the complex pathophysiologic processes underlying HHT. The most widely accepted mechanism posits that the negative intrathoracic pressure of the pleural space promotes migration of ascitic fluid from the peritoneal cavity into the pleural cavity through microscopic or macroscopic diaphragmatic fenestrations. Other proposed mechanisms include hypoalbuminemia, decreased colloidal (oncotic) pressure, increased azygous vein pressure and flow with consequent plasma leakage, among others [3]. Since most of these proposed mechanisms lack substantial supportive data, this topic continues to be of academic interest and debate. What remains irrefutable in the past few decades is that HHT, especially when refractory, portends a poorer prognosis in patients with cirrhosis (Table 1).

…