Hyponatremia in patients with cirrhosis
- Richard H Sterns, MD
Richard H Sterns, MD
- Editor-in-Chief — Nephrology
- Section Editor — Fluid and Electrolytes
- Professor Emeritus
- University of Rochester School of Medicine and Dentistry
- Bruce A Runyon, MD
Bruce A Runyon, MD
- Section Editor — Cirrhosis and Its Complications
- Clinical Professor of Medicine
- University of New Mexico, Division of Gastroenterology and Hepatology
- Special Hepatology Consultant to the Indian Health Service
- Northern Navajo Medical Center, Shiprock, New Mexico
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 . (See "Pathogenesis of ascites in patients with cirrhosis", section on 'Water retention'.)
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 .
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 . 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 .
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".)To continue reading this article, you must log in with your personal, hospital, or group practice subscription. For more information on subscription options, click below on the option that best describes you:
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- Systemic vasodilation
- - Activation of endogenous vasoconstrictors
- Water retention
- PREDICTOR OF ADVERSE PROGNOSIS
- Decision to treat
- Therapeutic modalities
- - Fluid restriction
- - Correction of hypokalemia
- - Vasopressin receptor antagonists
- Do not use tolvaptan in patients with cirrhosis
- - Other
- Hypertonic saline, osmotic demyelination, and liver transplantation
- INFORMATION FOR PATIENTS
- SUMMARY AND RECOMMENDATIONS