Abstract
Although there are a limited number of quality studies, appropriate peri-operative management of serum electrolytes seems to reduce adverse outcomes in liver transplantation. Hyponatremia is defined as the presence of serum concentration of sodium equal ≤130 mmol/L and it is detected in approximately 20% of patients with end stage liver disease waiting for a liver transplant (LT). This paper will focus on the pathogenesis of dilutional hyponatremia and its significance in terms of both candidacy for LT and post-operative outcomes.
Highlights
Pathogenesis of Hyponatremia in Cirrhotic PatientsA variety of factors can contribute to the development of hyponatremia in patients with end stage liver disease [1]
There are a limited number of quality studies, appropriate peri-operative management of serum electrolytes seems to reduce adverse outcomes in liver transplantation
The Model for End Stage Liver Disease (MELD) is a scoring system used to measure the severity of chronic liver disease [9]
Summary
A variety of factors can contribute to the development of hyponatremia in patients with end stage liver disease [1]. AVP acts via V2 receptors on the renal collecting tubules triggering movement of aquaporin-2 water channels to the apical membranes causing re-absorption of water [1]. These changes altogether lead to a decrease in serum sodium concentration despite the existence of increased renal sodium reabsorption and high total body sodium content [2]. This type of hyponatremia is referred to as “dilutional” hyponatremia. Reduction in the delivery of filtrate to the distal nephron and decreased renal prostaglandin synthesis are known to participate in the impairment of solute-free water excretion in cirrhotic patients with subsequent development of dilutional hyponatremia [2]
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