The first step when confronted with a low sodium is to ask yourself if it is real. There are two interpretations of the word “real”. Firstly the machine at the lab may have spat out an incorrect result. This occurs if there is excess protein or lipid in the sample, because it affect the calculations made when the sample is diluted. This is not true of blood gas analysers- the blood gas sodium is accurate on a blood gas.
The other is to ask does this actually reflect a low serum osmolarity. We don’t care about hyponatremia so much because of the low sodium itself, but because we assume it reflects low serum osmolarity overall. It is this that actually causes all the troubles of cerebral oedema etc. Most of the time this is a correct assumption because serum osmolarity is
Most of the time the other components don’t play a huge role. But if the glucose is sky high, or you have another osmotically active particle such as mannitol, water will be sucked out of the cells, diluting the sodium. The sodium in this case is “real” however is doesn’t really matter because the overall plasma osmolarity is raised due to the presence of mannitol or craploads of sugar.
An easy way to eliminate this possibility is to check a serum osmolarity.
At the end of the first section we discussed people who had excessive sodium losses. Now, even though these patients might be losing a lot of sodium from the GI tract or the respiratory tract the sodium concentration of these losses is still always LESS than plasma sodium concentration. The total amount of sodium being lost is high but the sodium concentration of lost fluid is still low. So how do these patients become hyponatremic?
Well firstly one of the responses of the kidney to hypovolemia is to activate vasopressin and hold onto free water. However patients with hypovolemia also tend to hold onto sodium – a urine sodium < 20mmol/L fits with hypovolemic hyponatremia. So this doesn’t fully explain it. Even when urinary sodium reabsorption is inhibited, as you might see if the cause of hypovolemia is diuretics, the urine sodium rarely gets above 100mmol/L. So the renal response to hypovolemia of holding onto free water does not fully explain why the sodium drops.
It’s because people continue to drink water, usually from the tap, and the thirstier they feel the more they drink. In short water and sodium are both lost, the water is replaced, the sodium is not, and the renal response prevents the free water from being excreted. Voila, low sodium levels. However without an ongoing exogenous source of water, hyponatremia will not develop.
So hypovolemic hyponatremia presents with low urine sodium levels, unless the cause is diuretics, or some other form of renal loss, such as acute tubular necrosis where the tubules are damaged, cannot retain sodium and put out vast quantities of urine. One could of course examine the patient and determine that they are hypovolemic as the textbooks advise, but anyone who has worked in clinical medicine for more than 2 minutes will realise that when it comes to differentiating between hypovolemia and euvolemia, one might as well do a rain dance, summon the gods, and ask them what they think. People who are confident in their ability to clinically differentiate between the two are probably deluded.
So the treatment is to expand the plasma volume with a resuscitation fluid and remove the stimulus for vasopressin secretion. Free water will be able to be excreted and the sodium will rise. You should probably do this cautiously- dumping a lot of fluid into someone often removes the vasopressin stimulus quite rapidly and an alarming diuresis can result, one that raises the sodium by more than the 8mmol/24 hours that safety recommends.
It would actually make complete sense to volume expand someone intravenously while at the same time restricting their oral fluid intake. Given that salt water tastes disgusting we tend to drink mostly free water, so expanding someone with salty water while limiting their free water intake is perfectly logical. Maybe best avoided however as people will give you weird looks and if you’ve already induced a diuresis adding on a free water restriction might overcorrect the sodium.
The classic cause of euvolemic hyponatremia is SIADH. The same pathophysiology that we already discussed applies, except this time vasopressin release is stimulated in the absence of hypovolemia, so the kidneys will not be holding onto sodium, and the urine sodium will be > 40mmol/L. However as mentioned, renal losses of sodium from diuretics or ATN will give the same urine chemistry, and this is a common pitfall. SIADH is actually not that common in patients presenting from home. It is more common is postsurgical patients where vasopressin is released due to the surgical stimulus and in little kids who become sick.
Hypervolemia should be more obvious clinically. The pathophysiology here is once again the same except the stimulus for vasopressin release is the sympathetic response to a failing heart. Diuresis is the treatment of choice here. It probably works because frusemide induces a loss of “salty water” and “free water”, but more “free water” and the patient is prevented from taking excessive free water because we usually fluid restrict people who are overloaded. Reducing atrial stretch and the neuroendocrine response to this also probably plays a part.
In all of these conditions the urine osmolarity will be higher than serum because the kidney is reabsorbing water. If the urine osmolarity is low the patient is likely to have psychogenic polydipsia.
If your patient has acute neurological symptoms a bolus of hypertonic saline is in order, and you should ask for help on how to do this.
Lastly you may wonder why the chloride is low- given that chloride is the main anion that balances the cations in the plasma, it is inevitable that a low Na+ leads to a low Cl-.
Hopefully this gives some better understanding of why hyponatremia develops and how to manage it. The key is really understanding the difference between salty water and free water.