You should have seen the volume climb because, even though osmolality is normal, there is a constant small amount of ADH always being secreted, which increases pure water content in the body. The volume stabilises at a certain level when the normal feedback system, which is working hard to increase the osmolality by reducing pure water, balances out against the small constant ADH secretion which is increasing pure water. This results in an equilibrium state.

Once it has stabilised, according to the simulation, the body would be in a hypervolaemic state, as the water level is higher than normal, and with a lower osmolality than normal. On first thoughts, it would make sense that because of this, SIADH should be a hypervolaemic condition. After all, SIADH is a condition in which there is slightly more pure water than sodium. And yet anyone who has seen a standard hyponatraemia algorithm flowchart will tell you that it is listed as a euvolaemic condition, so how can this be?

The key is that, despite having a malfunctioning osmolality regulation system, the body still has a perfectly good volume regulation system.

Now turn on the volume system, and watch what happens.

Remember that the volume system detects volume and changes amount of sodium, and as long as there is a working osmolality system, water will follow sodium either in or out of the body. In SIADH the osmolality system is working - it's just slightly malfunctional. Thus, you see the sodium amount drop, water follow it out of the body, and volume therefore stabilise at the normal volume level, while osmolality remains lower than normal due to the lower total body sodium.

This is the state at which the body of a person with SIADH stabilises, and this is the reason why SIADH is not a hypervolaemic state. (Although these two steps don't happen separately in real life of course. The two feedback systems are always working simultaneously)

If needed, take some more time to explore how SIADH causes hyponatraemia before moving on. E.g. you could try turning SIADH on and off and see what happens.

Now that we have SIADH and its related conditions under our belts, we can add this set of scenarios to our hyponatraemia algorithm.

We've got quite far in our algorithm, and the end is in sight. But let's take some time to fill in some blanks and make note of a few things.

From what we've filled in, a glaring question might be "How do you know if the body perceives a hypovolaemic state?". If we once again refer back to our basic principles and think of how the body regulates volume, the answer should come to light. Remember that when the body, or more accurately the kidneys, senses a low volume, it increases sodium. One way it does this is by conserving more sodium which it would have otherwise excreted. This produces a lower than normal sodium concentration in the urine.

This is why we send off a urine sample for urinary sodium concentration in hyponatraemia. If this is normal/high, then the body is excreting sodium normally. However, if it comes back low, then it means the kidneys are conserving sodium by not excreting as much of it, and this in turn means that the kidneys are sensing low perfusion and thus inferring a low volume status. The exact threshold for low urinary sodium differs between sources, but we will use a level of 40mmol/l.

So we can make this clearer in our algorithm. Press the button below to make the necessary changes.

There are some drug-related caveats to this:

All diuretics work by increasing sodium excretion. Thus, patients who are currently taking diuretics may have an elevated urine sodium regardless of whatever volume status their kidneys perceive. When this is the case, ideally a urine sample should be taken once diuretics are no longer in effect.

There is also another option. With inappropriate ADH release, serum uric acid is reduced, whereas it is normal to high otherwise. Thus, we can use this to distinguish between the different states. However, this can only be used if the patient is not taking allopurinol or other uric acid-lowering medication.

Let's add these details to our algorithm too.

Some important points to take away at this point:

• In all 3 scenarios so far, the hyponatraemia is driven completely by ADH - i.e. ADH is what is actively causing hyponatraemia, specificially by increasing pure water. However, only in this last case is the ADH release inappropriate. In hypovolaemic and hypervolaemic hyponatraemia there is still an increase in ADH, but this is happening as an appropriate response due to perceived hypovolaemia. Thus it is not correct to diagnose SIADH simply based on a high urine osmolality.
• Unlike in many other algorithms you may see, this mechanism-based approach means that the first step in the algorithm is not to differentiate between hypo-, eu-, or hypervolaemia clinically at the bedside. In fact, studies have revealed that even experts do not accurately differentiate between hypo- and eu-volaemia or between hyper- and eu-volaemia. Even if these studies are flawed, it certainly makes sense not to go down a completely different route of an algorithm based on something that is quite subjective, especially when urinary sodium is a great objective measure. While hyponatraemia in an obviously fluid-deplete patient is likely to be due to hypovolaemia, one should wait for a urinary sodium to be sure.

Next, we're going to look at the last set of conditions, in which hyponatraemia is not being driven by ADH at all.