From the Guidelines
Hyponatremia due to cirrhosis should be managed based on the severity of the condition, with mild cases (sodium 126-135 mEq/L) requiring monitoring and water restriction, while more severe cases (sodium <120 mEq/L) may necessitate hospitalization, fluid restriction, and the use of vasopressin receptor antagonists or hypertonic saline in select cases, as recommended by the American Association for the Study of Liver Diseases in 2021 1.
Management of Hyponatremia in Cirrhosis
The management of hyponatremia in cirrhosis depends on the severity of the hyponatremia and the presence of symptoms.
- For mild hyponatremia (sodium 126-135 mEq/L), no specific management is required apart from monitoring and water restriction 1.
- For moderate hyponatremia (sodium 120-125 mEq/L), water restriction to 1,000 mL/day and cessation of diuretics is recommended 1.
- For severe hyponatremia (sodium <120 mEq/L), a more severe restriction of water intake with albumin infusion may be necessary 1.
Use of Vasopressin Receptor Antagonists
Vasopressin receptor antagonists, such as tolvaptan, can be used for short-term treatment of severe hyponatremia, but should be used with caution due to the risk of rapid sodium correction 1.
Use of Hypertonic Saline
Hypertonic saline is reserved for short-term treatment of patients with symptomatic or severe hyponatremia, or those with imminent liver transplantation 1.
Goal of Sodium Correction
The goal of sodium correction is to increase serum sodium by 4-6 mEq/L per 24-hour period, not to exceed 8 mEq/L per 24-hour period, to minimize the risk of osmotic demyelination syndrome 1.
Long-term Management
Long-term management of hyponatremia in cirrhosis focuses on treating the underlying liver disease, including alcohol abstinence, viral hepatitis treatment, and nutritional support 1.
From the Research
Pathophysiology of Hyponatremia in Cirrhosis
- Hyponatremia in cirrhosis is characterized by excessive renal retention of water relative to sodium due to reduced solute-free water clearance 2.
- The primary cause is increased release of arginine vasopressin, which leads to impaired free water generation and avid retention of sodium and water 3, 4.
- Splanchnic vasodilation and activation of compensatory mechanisms such as renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system, and antidiuretic hormone (ADH) also contribute to the development of hyponatremia 3.
Clinical Implications and Complications
- Hyponatremia is associated with increased mortality in cirrhotic patients, those with end-stage liver disease (ESLD) on transplant waiting lists, and posttransplantation patients 2.
- Hyponatremia is also associated with numerous complications, including severe ascites, hepatic encephalopathy, infectious complications, renal impairment, and increased severity of liver disease in cirrhosis 2, 4.
- Clinical features of hyponatremia are often nonspecific and depend on the acuity of onset, and may include nausea, lethargy, weakness, or anorexia, as well as confusion, seizures, psychosis, or coma in severe cases 4.
Management and Treatment
- Treatment of hyponatremia in cirrhosis includes discontinuation of diuretics, beta-blockers, and albumin infusion, as well as hypertonic saline infusion in patients with very low serum sodium or severe symptoms 4, 5.
- Vasopressin (V2) receptor antagonists, such as tolvaptan, may be used to normalize sodium levels, but their efficacy in patients with severe hyponatremia is limited 6.
- Liver transplantation remains the definitive treatment for patients with cirrhosis and hyponatremia to improve survival 4.
- Fluid restriction should be avoided during the first 24 hours of treatment to prevent overly rapid correction of hyponatremia, and tolvaptan should not be used in patients who cannot sense/respond to thirst, anuric patients, hypovolemic patients, and/or those requiring urgent intervention to raise serum sodium acutely 2.