This was an actual case I saw and thought it generated a multitude of interesting dilemmas. When I initially examined the patient she was in status epilepticus. This, by itself, mandated the immediate correction of her serum sodium. But what was the best way to achieve the correction without adversely affected the patient? This was my thought process…
The patient is 100kg women, so her TBW should be 50 Liters. (using the Watson Formula)
I decided to separate her water and solute gains/losses to determine what her total body sodium was at that instance.
She had already received 2L of normal saline but lost 3L in urine, so net water loss of 1L. 1L of free water loss would cause that serum sodium to rise 2.5meq/L.
Calculation: 120 (desired Na)-115 (actual Na)/120 (desired Na) times 50L (TBW) is equal to roughly 2L. Therefore, 2L of free water loss would raise serum sodium 5 meq/L.
Therefore, for each 1L of water loss, the serum sodium would rise 2.5 meq/L. (5meq/L divided by 2)
So, just based on water loss, her serum sodium has risen 2.5 meq/L already, so the serum sodium is 117.5 meq/L. Next, I calculated the impact of solute gain. Total solute for a 100kg woman with a serum sodium of 115 would be 5750 (50L times 115meq/L). I estimated that she gained 133 meq of solute… INPUT: 2L of normal saline 388meq KCL 80meq Total input 468 meq solute input LOSS: Urine sodium of 75 meq/L times 3L urine output is 225 meq Urine potassium of 10 meq/L times 3L urine output is 30 meq Total loss: 255meq
So, total solute input (388)-total solute output (255) equals a gain of 133meq of solute.
How does this impact the serum sodium? Total body solute 5750 plus gain of 133 equals 5865 5865 meq (New Total Body Solute) divided by TBW (50 L) equals 117.3 Therefore, serum sodium rose 2.3 based on solute gain alone.
If you add the affect of free water loss and solute gain, I anticipated that the serum sodium at that instance was 120 meq/L (2.5 meq/L from water loss and 2.3 from solute gain plus starting sodium of 115). So, I thought that the serum sodium was already in the “safe” zone and that the seizures were related to alcohol withdrawl.
I decided NOT to use 3% saline, and continue with gentle potassium repletion at that time (depite the intensivist’s insistence). What this physician failed to realize was that KCl has the same osmotic potential as sodium!
In fact, there are case reports of central pontine myelinosis induced by rapid correction of hyponatremia via potassium repletion alone.
The patient’s repeat sodium was 121! Her serum sodium stabilized over the coarse of a few days with mere potassium repletion. Her seizures persisted and patient eventually required anti-epileptic therapy.
Given the complexities of this case, there is not a perfect strategy for management. The purpose was to generate thoughts and discussions on the intricacies of hyponatremia management. Would you have managed her differently? Let me know your thoughts…
Michael Lattanzio, DO