Hey everyone, this is Jessica, and welcome to CritIC.
Today I want to talk about hyponatremia.
And if you ask any internist to talk about hyponatremia, you'd get a lecture of about
36 hours, so I'll do my best to keep this short.
So what I want to do in this video is give a short, practical approach to the analysis
of hyponatremia in the clinic.
Let's get started.
Hyponatremia occurs when there is an imbalance between the amount of bodily water and the
amount of bodily salt, or sodium.
An important concept to remember is that in extreme circumstances volume regulation trumps
osmoregulation.
Obviously, when your leg gets bitten off by a lion, it’s more important to keep an adequate
blood pressure (volume regulation) than it is to maintain electrolyte homeostasis (osmoregulation).
Of course, one cannot go without the other: sodium is the most abundant ion in our body,
responsible for tonicity.
By retaining sodium (through the renin-angiotensin-aldosterone system), the body also retains water.
Another hormone responsible for volume regulation is ADH, or anti-diuretic hormone, also known
as vasopressin.
The end product of the renin angiotensin aldosterone system or RAAS-system is aldosterone.
Aldosterone is made in the adrenal gland, and has as effect the retention of sodium
at the expense of potassium.
In other words: when the RAAS system is activated, sodium is resorbed back in the distal tubulus
and collecting ducts of the kidney, causing little sodium to be excreted in urine.
So if your RAAS system is “on”, the urine sodium is low.
Usually it is defined as lower than 30 millimoles per liter, but it’s more accurate to calculate
the fractional excretion of sodium, because the excretion of sodium and creatinine in
urine is variable.
Anti-diuretic hormone (ADH or vasopressin) is made in the pituitary gland.
It acts on the collecting ducts of the kidney, where it opens aquaporin channels.
This leads to the resorption of water.
By resorbing water, the urine will be very concentrated, which means there will be lots
of particles in urine as compared to water.
So if your ADH is “ON”, the urine osmolality is high (being, higher than in serum).
An actual hyponatremia is a hypotonic hyponatremia.
This means that the tonicity or osmolality in serum is lowered, because sodium is the
most important contributor to serum osmolality.
Hyponatremia can also be isotonic or hypertonic, which is caused by either lab errors (in pseudohyponatremia)
or by other osmoles (like in hyperglycemia).
These types of hyponatremia are not discussed in this video.
The hypotonic hyponatremia can easily be systematically evaluated when taken into account the effect
of the RAAS and ADH systems on the urine.
In other words, for the analysis of hyponatremia, the very least you need to know is the serum
sodium, osmolality and creatinin, as well as the urine sodium, osmolality and creatinin.
So what if a patient has hyponatremia because of dehydration.
Obviously, the serum sodium is low because we’re talking about hyponatremia.
The serum osmolality is low as well, it’s a hypotonic hyponatremia.
What can be expected of the urine sodium and osmolality?
Well, dehydration means that the body wants to retain water, and it does this by retaining
sodium.
In other words, the RAAS system is on, so the urine sodium is low.
The ADH system is also on, it’s called anti-diuretic hormone for a reason!
So the urine is very concentrated, meaning the urine osmolality is high.
What if a patient has hyponatriemia due to SIADH (syndrome of inappropriate ADH secretion).
The exact pathophysiology of SIADH is something for another video, but the approach to hyponatremia
is the same as in any other hypotonic hyponatremia.
The problem of SIADH is primarily ADH itself.
There is inappropriate ADH secretion, so ADH is (inapproprately but still) on; urine osmolality
is high.
The body is retaining water, which leads to a slight intravascular overload.
The RAAS-system will sense this and will switch off.
Urine sodium is high.
What if a patient has hyponatremia due to heart failure or decompensated liver cirrhosis.
The main problem is that there is an extravascular volume overload, but an intravascular volume
depletion.
So the body detects dehydration: the RAAS system will be on (low urine sodium) as well
as the ADH system (high urine osmolality).
Treatment of hyponatremia due to dehydration or heart failure is however the exact opposite!
Dehydration means rehydration, and heart failure means treatment with diuretics.
- Fun fact: in Dutch we call this "to dewater" or "drain" the patient -
So how do we separate the two when the laboratory results are exactly the same?
By looking at the patient and assessing volume status: blood pressure, postural hypotension,
edema, central venous pressure, skin turgor, etc.
What if a patient has hyponatremia due to polydipsia.
These people drink lots and lots of water.
Dispite the fact that their RAAS system is switched off (they aren’t dehydrated), their
urine sodium is low.
This is because they are relatively sodium deficient when compared to their waterstores:
they just don’t have enough sodium to pee out.
Because they keep on drinking water, all they pee out is water, so it’s very unconcentrated.
Therefore urine osmolality is low.
The same principle goes for the so called “tea and toast” hyponatremia.
The classical example is an old lady drinking solely tea (i.e. water) and only eating toast
(which has no salt).
They have an absolute salt deficiency, resulting in a low urine sodium and low urine osmolality.
What if a patient uses diuretics.
Well, they have an intravascular volume depletion, so their RAAS system will want to switch on.
However, because of the diuretic they cannot retain sodium, so the urine sodium will be
high for this reason.
The ADH system will be on of course because of the intravascular volume depletion; urine
osmolality is high.
In other words: when you have a patient with hyponatremia that uses diuretics, stop the
diuretic and repeat the analysis.
Only then can you analyze the hyponatremia properly, and usually the hyponatremia will
(partially) resolve itself.
So, to wrap things up: when you encounter a patient with hyponatriemia, do a history
and exam, focusing on medication (especially diuretics) and assess volume status.
Next, get a urine sample on sodium and osmolality, and use these to assess whether or not the
RAAS and ADH systems are switched on or off, to figure out the cause of the hyponatremia.
I hope that this video was helpful.
Please let me know what you think in the comments below.
Be a critic ;) Or if you have suggestions for a next video.
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