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Hyponatremia in patients with cirrhosis

Authors
Richard H Sterns, MD
Bruce A Runyon, MD
Section Editor
Michael Emmett, MD
Deputy Editor
John P Forman, MD, MSc

INTRODUCTION

Hyponatremia is a common problem in patients with advanced cirrhosis. The pathogenesis of hyponatremia in these patients is directly related to the hemodynamic changes and secondary neurohumoral adaptations that occur, resulting in an impaired ability to excrete ingested water. The severity of the hyponatremia is related to the severity of the cirrhosis [1]. (See "Pathogenesis of ascites in patients with cirrhosis", section on 'Water retention'.)

PATHOGENESIS

A variety of factors can contribute to the development of hyponatremia in patients with cirrhosis. The most important factor is systemic vasodilation, which leads to activation of endogenous vasoconstrictors including antidiuretic hormone (ADH); ADH promotes the water retention that is responsible for the fall in serum sodium.

Systemic vasodilation — Systemic vasodilation plays a central role in the pathogenesis of hyponatremia in patients with cirrhosis and ascites. These patients usually have a marked reduction in systemic vascular resistance (SVR) and in mean arterial pressure and an increase in cardiac output [2-4]. The vascular territory in which the reduced SVR is most obvious is the splanchnic circulation [5].

The presence of vasodilation in other vascular territories is less obvious and the subject of controversy [6,7]. As an example, the factors that cause splanchnic vasodilatation may have a biphasic effect on the renal circulation. Early in the course of the disease – stable cirrhosis without ascites – the dilating substances also may influence the renal vasculature and the glomerular filtration rate may be greater than normal (150 versus 105 mL/min in one study) at this stage [8]. With more severe disease, the splanchnic vasodilatation becomes more marked, resulting in a fall in mean arterial pressure and decreased renal perfusion, leading in some patients to the hepatorenal syndrome [6].

The precise mechanisms of vasodilation in cirrhosis have become better understood, with increased generation of nitric oxide and prostaglandins appearing to play an important role (algorithm 1). Nitric oxide production may be stimulated by absorbed endotoxin from the gastrointestinal tract, which is less efficiently cleared due to portal-systemic shunting and decreased reticuloendothelial cell function in cirrhosis [9,10]. (See "Pathogenesis of ascites in patients with cirrhosis".)

               

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Literature review current through: Nov 2016. | This topic last updated: Fri Apr 15 00:00:00 GMT+00:00 2016.
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