Euvolemic Hyponatremia: Euvolemic hyponatremia, typically caused by SIADH, is characterized by a high Uosm (>100 mosm/L) and a high UNa (>30 mEq/L). All patients require free water restriction, and fluid intake should be at least 500 mL below a patient’s urine output, usually one liter or less. If this is ineffective, salt tabs can be given. Salt tabs will increase the solute load, necessitating an increase in urine output. Patients should be given approximately nine grams of salt tabs in three divided doses (equivalent to 1 L of NS). Patients with highly concentrated urine (Uosm >500 mosm/L) will not respond as well to the salt load, because the kidneys will continue to excrete much of the sodium in a concentrated urine. In such patients, a loop diuretic can be used to help excrete free water, because it decreases the Uosm to about ½ NS (154 mOsm/L). One possible regimen is 20-40 mg of oral furosemide two to three times daily.
Hypervolemic Hyponatremia: Hypervolemic hyponatremia is caused by congestive heart failure (CHF), cirrhosis, or nephrotic syndrome. In all cases, there is excess ADH as a result of the carotid baroreceptors sensing a decrease in effective circulation volume. In the case of CHF and cirrhosis, the degree of hyponatremia is a marker of disease severity, but there is no data to show that correction of hyponatremia improves outcomes. Fluid restriction is the cornerstone of therapy, but if the patient’s volume status is not optimized, then loop diuretics may improve hyponatremia through excretion of diluted urine. In addition, angiotensin-converting enzyme inhibitors can improve hyponatremia in CHF by reducing ADH levels and improving cardiac output via afterload reduction.
There has been recent interest in the use of vasopressin V2 receptor antagonists or “vaptans.” The SALT 1 and 2 trials, which included patients with CHF and cirrhosis, showed that they are effective in increasing serum sodium and improving mental function in the short term. But there are concerns about hepatotoxicity, overly rapid correction of serum sodium, lack of mortality benefit, and cost.14 The latest American Heart Association CHF guidelines recommend (class IIb) vaptans in patients with “hyponatremia that may be causing cognitive symptoms when standard measures have failed.”15 Tolvaptan, in particular, should not be used in cirrhotic patients due to concerns of hepatotoxicity.
Outcome of the Case
Because of the high UNa and Uosm and the use of a selective serotonin reuptake inhibitor (SSRI), the treating physician suspects the patient has SIADH. Given the severe symptoms, he is given 100 mL of 3% hypertonic saline and experiences improvement in his lethargy. Repeat sodium is 112 mEq/L. Using the equation above, a basal rate is calculated:
Change in serum sodium from 1 L of 3% saline= 514 mEq/L -112 mEq/L = 9.4 mEq 43 L
Because the goal correction rate is 6-8 mEq/L in 24 hours and the sodium has already increased by three, the physician elects to increase the sodium by 5 mEq/L for a total of 8 mEq/L for 24 hours:
5.0 mEq x 1000 ml = 532 ml of 3% saline ÷ 24 hours = 22 mL/hr. 9.4 mEq
Serum sodium is checked every two hours. The following day, the sodium is 115 mEq/L and the patient is fully alert. The hypertonic saline is stopped and the patient is maintained on free water restriction. Some 72 hours later, the sodium is 124 mEq/L.
Dr. Chang is co-director of the medicine-geriatrics clerkship, director of education in the division of hospital medicine, and assistant professor in the department of medicine at Mount Sinai Medical Center in New York City. Dr. Madeira is clinical instructor in the department of general internal medicine at the NYU School of Medicine and a hospitalist at the VA NY Harbor Healthcare System.