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The Sodium Trap

Today at 1405 CST I will be presenting at the ICON2021 online conference put on by IA Med. My favorite talks at a conference are ones that update my mental model and practice. My goal with today's talk and this blog is to do exactly that.

Our story today takes place downtown at a little cafe. A couple sees a man stumbling with a bottle of something in his hand. Initial optics says this dude is intoxicated and upon further evaluation, you recognize him. This is Murphy and he is can be found 7 days a week at the local tavern.

Murphy eventually trips and hits his head on the sidewalk. Bystanders report what they believed to be ~30 seconds of seizure activity after the fall. EMS is called and patient is making purposeful movements but is combative and not coherent. EMS decides to intubate with the suspicion that this patient has a traumatic brain injury (TBI).

Flight is requested for suspected TBI. When they enter the back of the ambulance they find the patient is hypertensive, pupils equal and reactive but tearing, and a blood glucose of 100 mg/dl. After EMS states they intubated with etomidate and roc, flight provides a 100 mcg bolus of fentanyl and starts propofol at 50mcg/kg/min with a 0.5mg/kg bolus.

The patient is loaded into the helicopter and placed on a mechanical ventilator. The conversation with the flight team goes like this:

Clinician 1: So they reported seizure activity, should we grab some labs?

Clinician 2: Yah, the police officer said there was a beer bottle broken on the ground next to where he fell.

Clinician 1: Alright, let's grab some labs and see what his sodium is.

The labs come back and just as suspected, the sodium is super low.. like critically low. As a matter of fact, there are a lot of "low" readings.

Clinician 1: So we have a dude who had a reported seizure, is now paralyzed, and now has a sodium of 113 meq/l. Should we give him 100ml bolus of 3% saline?

Clinician 2: Yikes, I get so eerie when we start messing with sodium levels. It's never a problem with the sodium, it's almost always a problem with free water.

Clinician 1: Very true, that low creatinine and his appearance makes me feel like this dude does not necessarily check all the boxes on the food pyramid when it comes to nutrition.

The diagnostic momentum is pushing you towards correcting the sodium. Why? Because typically in medicine when something is low, we replenish it (glucose, potassium, magnesium, etc.) However, when it comes to sodium, it pays to slow our trigger reaction to replenish. This is why I call it..

I think the majority of us are aware that sodium is a little bit different when it comes to correction of low values. I think of this like the common mouse trap that commonly does not work. The mouse is "in the know" and avoids making a fatal error.

We had a mouse at my base that was a frackin genius...was being the keyword. My pilot said he was going to bring in "ole faithful." This was a trap that slowly led the mouse along with peanut butter. Little by little the mouse would be led to the ultimate trap.

The reason this trap works is because it uses a sequence of bait that creates a momentum. "The last bite didn't kill me, so maybe the next one won't either."

This is how I view the predicament the flight team is in right now. The diagnostic momentum is pushing you to believe 3% saline is the fix. But is it? To answer this question we first need to answer another question. How fast should we correct sodium and what happens if we elevate it too fast?

The correct answer is that we do not want to raise the serum sodium concentration above 6-8 meq/l over a 24 hour period of time. If we do, we run the risk of causing osmotic demyelination syndrome. This is a denaturing of the myelin sheath which insulates the nervous system and destruction to the pons. This can lead to irreversible neurological damage commonly known as "locked-in syndrome."

So how do we over correct? If we agree that the majority of hyponatremia is a problem of free water and not actually sodium, attention should be focused on avoiding the rapid diuresis of water resulting in rapid correction of sodium. An example of a situation in which a prehospital intervention could lead to a rapid correction in sodium, is something called beer drinker's potomania or tea & toast syndrome.

As much as we want to believe our urine output is predicated on how much water we drink, fluid intake is actually a dependent variable. What does it depend on? It depends on solute and ADH secretion. The reason we don't think of solute regulating our output is because we normally take in enough solute (10 mOsm/kg/day) to maintain a normal urine output.

However, if an individual takes in more water (solvent) than solute (nutrition), they will begin to retain free water which will in turn create a dilution hyponatremia. Alcohol is broken down into water and carbon dioxide. Neither of these contribute to solute and without solute, the kidneys will retain fluid.

So how do we muck this up? Imagine these kidneys that are retaining volume because their owners diet sucks. The sodium along with everything else is getting diluted with free water. We come along and decide we are going to fix it by starting 0.9% saline or maybe even 3% as illustrated above. This introduction of solute will cause a massive diuresis that leads to rapid correction. One liter of 0.9% saline can create up to 6 liters of urine output.. eek!

So the issue is not that we GAVE too much sodium, it's that we are trying to mix an old fashion in a cup with a leak. The kidneys got the solute they want and now want to get rid of the free water that is messing up the electrolyte concentration. This is why you will see some physicians administer a drug called desmopressin to stop the kidneys from producing urine. This turns the patient into a closed system and allows more control over the rate of correction.

Does this mean we should withhold any IV fluids if we suspect beer drinkers potomania or tea & toast syndrome? If a patient requires volume resuscitation, give them volume. But just starting fluids for the sake of starting fluids is probably not the best idea. If you give 0.9% saline, it is likely that the patient won't start urinating 6 liters right into their pants, but the hospital may see this occur. Passing on suspicion of a dilution hyponatremia from solute deficiency can put this on the providers radar and may cause them to correct the rapid correction with D5W.

In the end, the crew opted to not give 3% saline and to fluid restrict until further investigation could be done and urine osmolality could be assessed. The patient ended up having chronic hyponatremia is their history and the follow up debrief agreed that unnecessarily administering saline was the correct move. If this patient ended up needing volume resuscitation, they would have received 250ml boluses of 0.9% saline until hemodynamics improve and the information and prehospital sodium would be passed along to the receiving provider.

I hope you enjoyed this free upgrade to your mental model.


Kujubu, D. A., & Khosraviani, A. (2015). Beer Potomania--An Unusual Cause of Hyponatremia. The Permanente journal, 19(3), 74–76.

Lodhi, M. U., Saleem, T. S., Kuzel, A. R., Khan, D., Syed, I. A., Rahim, U., Iqbal, H. I., & Rahim, M. (2017). "Beer Potomania" - A Syndrome of Severe Hyponatremia with Unique Pathophysiology: Case Studies and Literature Review. Cureus, 9(12), e2000.

If you enjoyed this case study and would like to hang out with the FOAMfrat team on a regular basis, check out our online EMS refresher by clicking on the link below.

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