To consider this final scenario, we don't need to add any more buttons to represent any more diseased states. This is because, in this set of scenarios, there is nothing actually wrong with the body - the kidneys, the osmolality system, the volume system are all working perfectly fine.
We've been able to cause this kind of hyponatraemia on any of the pages so far, and you may have already seen it without realising if you happen to have experimented enough!
To simulate this kind of hyponatraemia, you need to keep the osmolality at a high level and not let it come back to normal. You can do this by doing either of the following:
On the water slider below the beaker, pick a certain spot which, when clicked, increases the volume level. Then keep clicking on this spot repeatedly, so that even as the volume tries to equalise, your clicks mean it immediately shoots back up again.
On the water slider below the beaker, pick a certain spot which, when clicked, increases the volume level. Then drag the slider to that amount and keep moving your mouse up and down ever so slightly so that you're continuously setting the water level to a high amount.
Once you're able to consistently keep doing one of these, pay close attention to the sodium amount number above the beaker, the sodium molecules in the water, and the osmolality number below the beaker.
What you were doing was to simulate a constant high volume from excessive water intake. It may have been hard to do. But then so is drinking so much water that your kidneys can't handle it!
When you do this, the kidneys are constantly sensing a low serum osmolality. The body tries to increase osmolality by reducing pure water content, which it is doing successfully by excreting its maximal amount, but the kidneys can only excrete so much pure water per day. The constant water intake exceeds the maximal amount which the kidneys can excrete, and this results in hyponatraemia.
Note that unlike in all the scenarios before this, hyponatraemia due to excessive water intake is not driven by ADH - it is ADH-independent. The fact that water is being excreted by the kidneys at their maximal rate tells you that ADH is in fact low, which is a completely appropriate response to the low serum osmolality produced by excessive water intake.
You may have noticed that if you do this long enough, you can cause the sodium to go incredibly low. In fact, in keeping with real life, these kinds of patients can be extremely sick.
Excessive water intake isn't the only situation in which hyponatraemia occurs despite maximal water excretion by the kidneys.
While it is still true that the body attempts to change osmolality by changing water (not sodium), it turns out that in order to excrete pure water, the kidneys actually need to have a minimum amount of sodium present. If someone's oral intake of salt is extremely low, then they may be drinking normal amounts of water, but their kidneys can't excrete enough water to match their poor salt intake, resulting in hyponatraemia. Another simpler way of looking at this scenario is that water intake is normal, but sodium intake is low. This means that eventually, hyponatraemia will occur. But as the kidneys have nothing wrong with them, they respond appropriately by continually excreting maximal amounts of pure water. It just happens that this isn't enough to increase serum osmolality. This is what happens in tea and toast syndrome, and beer drinker's potomania.
There is a final condition in which ADH isn't actually relevant, but it belongs on this page because it is an ADH-independent cause of hyponatraemia. In severe renal insufficiency, if there is very little urine output but water intake is normal, then there will eventually be an excess of water compared to sodium.
If needed, take some more time to explore these conditions before moving on.
Hooray! We can now fill in the final scenario in our hyponatraemia algorithm:
In most commonly encountered cases of hyponatraemia, the hyponatraemia is driven by ADH, and your main dilemma within the diagnostic process will be deciding if this is appropriate or inappropriate. If you ever see hyponatraemia with a low ADH, it should immediately stand out in your mind as a rare situation. (The treatment of ADH-independent hyponatraemia is also completely different)
This brings us to the question of "How do you know if ADH is high, i.e. ADH is driving the hyponatraemia?" We'll once again use the patient's urine to answer this question.
What does ADH affect? ADH affects water, and water only. So if ADH is high, then more water is conserved, less water is present in the urine, urine water content is low, and so urine osmolality will be high.
If ADH is low, then less water is conserved, more water is present in the urine, urine water content is high, and so urine osmolality will be low.
Thresholds differ, and some sources use a hard threshold such as 100mOsm or 300mOsm. But in order to stress that we are separating cases based on mechanism, what is important is whether this osmolality is lower or higher than the serum osmolality (which may differ based on how severe the hyponatraemia is). Thus, we will use serum osmolality as the threshold rather than any fixed numerical value.
In ADH-driven causes of hyponatraemia, urine osmolality is usually much higher than serum osmolality (e.g. 850mOsm). In ADH-independent causes of hyponatraemia, urine osmolality is usually much lower than serum osmolality (e.g. 100mOsm). In severe renal insufficiency, ADH can be anything, but the kidney has completely lost its ability to concentrate or dilute the urine, and so urine osmolality will be very similar to serum osmolality (e.g. 280mOSm).
