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Welcome back to the tasty morsels of critical care podcast.
Today we cover an incredibly common inpatient issue – hypnatraemia. We’ll often find 1 or 2 of these in our high dependency unit at any given time, mainly due to the requirement for frequent testing of Na levels that seems beyond the remit of normal ward level care. The approach I describe here is neither comprehensive or especially robust but it is how I approach it. Caveat emptor and all that.
The over bearing demyelinating elephant in the room in hyponatraemia is the risk of osmotic demyelinating syndrome (the pathology formerly known as central pontine myelinolysis). If we correct the Na too fast will our patients end up with a severe brain injury? This is rare but is a very real phenomenon.The brain is actually quite good at adapting to sodium levels that have lowered over a few days or weeks. Hence why the slow developing sodium of 120 often causes minimal or no symptoms. However once the patient is in this adapted state (as mentioned this probably is after a few days at a minimum) then a rapid return to baseline sodium can cause ODS. By contrast a rapid drop in sodium, eg over a few hours drinking litres of unnecessary water during a marathon, is poorly tolerated but the plus side is it can be corrected fairly rapidly without harm.
Most of the hyponatraemia we see admitted through the ED will be hypoosmotic hyponatraemia. The bucket here will include heart failure, cirrhosis, SIADH, tea and toast and beer potomania. I’m going to put these common ones to one side for a minute and look at some of the niche exam ones.
For example, i said hypoosmotic hyponnatraemia there, so presumably there could be an isotonic and a hypertonic verison. There is indeed. The isotonic hyponatraemias are usually from spurious results. For example, when you have high lipids (super high, like high enough to cause pancreatitis high) or high proteins (eg high paraproteins like myleoma) the measurement method can underestimate the sodium. You can work this out by always sending a serum osmolality. If this is normal but the Na is 125 and your calculated osmolality is low, then you have an isoosmotic hyponatraemia. You should then check the lipids and the protein. Hypertonic hyponatraemia is another strange beast. This time the tonicity is high from something else such as high glucose or mannitol drawing water from cells into plasma. Again a mix of clinical context and a serum osm will help you out here.
Let’s go back to the bread and butter (or should i say the “tea and toast”) hyponatraemia, the hypotonic or hypoosmotic hyponatraemia. Context as always will give you lots of clues, if the patient has consumed nothing but beer for weeks then the likely causes is beer potomania. If the patient has a new cancer then SIADH is high up your list.
I confess I lean heavily on the approach you can see on Deranged Physiology and have Alex Yartsev’s flow diagram saved on my phone and i look at it almost every time i’m trying to work this out. The first test (assuming you’ve confirmed this is hypotonic hyponatraemia) in this algorithm is urinary osm, the question you are asking here is whether the kidneys are doing what they’re meant to be doing in the face of a low sodium. A normal sane and functioning kidney will try and lose water to conentrate the plasma in order to bring the sodium back up to normal, in other words the kidney should be producing a dilute urine with a low osm. Next step is to check the concentration of sodium in this dilute urine. If the kidney is doing what it should be doing it should be holding onto to all the sodium it can and urine sodium should be low. The problem here is too much water, not enough solute. Think, beer potomania, tea and toast, and polydipsia. If the urine is dilute but the sodium is high then you know something has gone wonky in the kidney itself, typically AKI or resolving ATN.
On the other side of the algorithm we have a concentrated urine, in other words, a high urine osm. The kidney is holding onto water and concentrating the urine. This may be a very sane and sensible response by the kidney if you are frankly hypovolaemic from eg gastroenteritis. The kidney also gets tricked by a few conditions into thinking its hypovolaemic, things like CHF or cirrhosis where the kidney itself just mightn’t be being perfused very well. In this scenario you should have a concentrated urine with a high osm and a low urinary Na as the kidney holds onto Na for all its worth in an effort to maintain effective circulating volume. On the other hand you might find a concentrated urine with a high osm but a high sodium also. This tells us that the kidney is handling water reabsorption OK but has lost the run of itself when it comes to regulating sodium. Something may be strong arming the kidney into losing more sodium than it should, like thiazides or an external actor like ADH, in this case it would be inappropriate ADH, hence the syndrome of inappropriate ADH. In addition a lack of steroid (and in particular the mineralocorticoid part) or a dodgy thyroid may cause the kidney to lose sodium when you shouldn’t. Or of course this scenario could be due to intrinsic renal disease.
So that’s 8 or 900 hundred words running through the deranged physiology algorithm and you can imagine that simply looking at the algorithm would probably be a better use of your time so go do that.
Next time we’ll have a look at how we might manage hyponatraemia
Reading
Deranged Physiology – Wonderfully titled ” A Lazy Man’s Classification”
Oh Chapter 95