Profound hyponatremia of around 100mEq/L or less is a double-edged sword- it’s got to be treated but can be terrifying to treat. The University of Rochester shared their protocol for controlled correction of severe hyponatremia with AJKD in October of 2010.
Hyponatremia with neurologic symptoms needs to be treated promptly but cautiously to avoid overcorrection with associated risk of osmotic demyelination. The most efficient and rapid way to raise sodium levels is to use 3% saline, but this carries a high risk of overcorrection.
The cause of hyponatremia and its reversibility must also be considered when deciding a course of action. In hypovolemia-induced hyponatremia, vasopressin levels decline and sodium levels rise as volume status is restored to normal. When medications such as thiazides and SSRI are discontinued, their effect on sodium levels goes away and sodium levels will begin to rise as the medications are cleared from the body. Similarly, in patients with beer potomania, sodium levels will rise as they begin to take in increased concentrations of solutes.
As reversible causes of hyponatremia are eliminated, vasopressin levels rapidly fall to undetectable levels- causing polyuria. Patients can excrete massive quantities of maximally dilute urine that can increase sodium levels at an unsafe rate of up to 2mEq/L/h. Most patients who present with profoundly low sodium are at higher risk of osmotic demyelination- chronic hyponatremia, sodium less than 105mEq/L, hypokalemia, alcoholism, malnutrition and liver disease all place patients in danger of this complication.
Desmopressin administered q6-8 hours has been shown by this same Rochester group to be effective and more practical than hypotonic fluids in preventing overcorrection of hyponatremia. They administer desmopressin immediately without waiting for the onset of water diuresis, and concurrently administer 3% saline solution. The goal of the use of desmopressin is to maintain constant antidiuresis and a more predictable response to 3% saline. The downside is that it takes longer to correct sodium, leaving the patient on hypertonic saline for a longer time. During this time, water intake needs to be restricted to avoid decreasing serum sodium concentrations. Desmopressin has also been used in a few cases to re-decrease serum sodium concentrations after neurologic symptoms have developed, which was effective in reversing the symptoms.
They recommend correction of no faster than 6mEq/day for patients with severe chronic hyponatremia, with 6mEq in 6 hours on the first day if symptoms are severe. This has led to the rule of 6s.
- 6 a day makes sense for safety
- 6 in 6 hours for severe symptoms and stop (no more correction that first 24 hours)
Also remember:
Potassium administration also has to be taken into account when correcting sodium with the formula:
Serum [Na+] = {Total body exchangeable (Na+ + K+)} / total body water
* Solve for {Total body exchangeable (Na+ + K+)} by multiplying total body water by serum sodium.
* Determine the amount of solute to give to correct to a goal serum sodium level by solving for the goal serum [Na+]
For example:
Current serum Na+ = 100 mEq/L
Goal serum Na+ = 105 mEq/L
Total body water = 50L
100 mEq/L=5000 mEq/ 50L
105 mEq/L= ? mEq/ 50L
105 mEq/L= 5250 mEq/ 50L
To correct sodium to 105mEq/L, 250mEq of combined sodium and potassium should be administered over an appropriate time period (6 or 24 hours based on the rule of sixes above)
Emily Petersen, MD
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