Disorders of ECF Volume: Cirrhosis of the Liver

Abstract

Na⁺ and water retention, and extracellular fluid (ECF) volume expansion, leading to formation of edema and ascites are the most common clinical findings in patients with severe liver disease. The initiating process for these clinical manifestations is hepatic cell death. Pathologically, in cirrhosis, the liver is characterized by fibrosis and nodular regeneration. Liver function tests (aminotransferases, bilirubin, alkaline phosphatase) are abnormal. Similar to congestive heart failure (CHF), retention of Na⁺ and water occurs in cirrhosis as a result of activation of salt and water-retaining mechanisms rather than intrinsic abnormalities of the kidney. As in CHF, there is a decrease in effective arterial blood volume (EABV) due to arterial vasodilation in the splanchnic circulation prior to edema formation. This decrease in EABV, in turn, activates the neurohumoral vasoconstrictors and antidiuretic hormone (ADH) release. As a result, Na⁺ reabsorption is increased in the proximal and distal tubules. Water reabsorption is promoted by ADH. Resistance to atrial natriuretic peptide (ANP) also seems to contribute to Na⁺ retention. When these mechanisms persist despite adequate plasma volume, alterations in Starling forces promote edema formation. The mediators of the splanchnic vasodilation seem to be nitric oxide, endotoxin, and prostaglandins.