Should Hypertonic Saline Be Used to Treat a Patient With Hyponatremia?

Corey M. Slovis, MD


February 03, 2009

Should I use hypertonic saline to treat a patient with hyponatremia?

Response from Corey M. Slovis, MD
Professor and Chairman, Department of Emergency Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee; Chief of Emergency Medical Services, Vanderbilt Medical Center, Vanderbilt University Hospital, Nashville, Tennessee

Hyponatremia is defined as a serum sodium level less than 135 mEq/L. Although most hyponatremic patients have a serum sodium level of 125-135 mEq/L and are asymptomatic, severe hyponatremia can cause an osmotic shift of water from plasma into the brain cells, leading to nausea, vomiting, headache, and malaise. Worsening hyponatremia leads to confusion, diminished reflexes, convulsions, stupor, or coma.[1]

Patients with symptomatic severe hyponatremia usually have serum sodium levels less than 120 mEq/L. Causes of severe hyponatremia include water intoxication and syndrome of inappropriate antidiuretic hormone (ADH) secretion. Water intoxication can be accidental, such as a marathon runner who ingests water in excess of total body losses but does not replace the sweat losses of sodium and chloride. Another example is a user of the illicit drug MDMA (3,4-methylenedioxymethamphetamine), also known as ecstasy, who hydrates excessively. Additionally, water intoxication can occur in psychiatric patients with polydipsia.[1,2]

Generally, hyponatremia is best treated by slowly raising the patient's serum sodium level; most experts agree that the rate should be no more than 10-12 mEq/L per day. Faster rates are implicated in the rare but devastating complication of central pontine myelinosis. Patients with central pontine myelinosis can suffer flaccid paralysis, "locked-in" syndrome, and death.[1,2,3]

Patients with a serum sodium level in the 100- to 110-mEq/L range and who are symptomatic require a more rapid replacement in order to prevent permanent neurologic damage. An acute rise of 3-6 mEq/L allows brain-body solute equilibration and patient stabilization.

To date, there are no large, well-controlled studies comparing the various therapies for symptomatic hyponatremia. The current recommendations are based primarily on case series, consensus panels, and expert opinions. On the basis of the available information, hypertonic saline should be reserved for a previously well individual who is symptomatic with seizures, coma, or new focal neurologic findings and whose serum sodium level is less than 120 mEq/L. (Some experts argue that 110 mEq/L is the limit.[1,2,4,5])

I recommend that this very select group of patients receive 1.5 mL/kg of 3% hypertonic saline in less than an hour, and have this regimen supplemented with a small dose (20 mg) of intravenous furosemide to facilitate free water diuresis and block ADH secretion from the hypertonic saline infusion. This will raise the serum sodium level by 1-2 mEq/L within 1 hour. A second infusion can be given over another hour if the patient is still symptomatic. Seizures can also be treated aggressively in this routine manner with intravenous benzodiazepines.

Although a rise of 3-6 mEq/L will stabilize the patient and may occur fairly rapidly, the total rise during the first 24 hours of treatment should not exceed 10-12 mEq/L.[1,5] The level of monitoring required by these patients means admission to an intensive care unit with serum sodium measurements every 2 hours; intravenous D5W infusion may be needed if the serum sodium level rises too rapidly.


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