Thread by @rabihmgeha

Teaching Rounds Day 3/15

H2O toxicity...

Say what?

Yes...
H2O toxicity.

The Story and The Schema.
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The Story...

What is H20 toxicity?
It’s when the blood has too much H2O.

What exactly is too much?
Enough that neurons swell and
don't work well.

Cool.

The symptoms of this mysterious condition?
When severe, patients can have a seizure, and other marked neurologic symptoms.

More commonly, patients have symptoms from the underlying cause, and not so much the H20 toxicity.

Wait, what causes H20 toxicity?
Hold that thought. We'll get to it soon.

Ok, so, if patients don't have symptoms specific to H20 toxicity, how are we supposed to suspect and diagnose it?

Honestly, we get lucky...

I have never (ever!) ... been convinced a patient has H20 toxicity after the HPI.

Instead, I am often worried about them and obtain a “basic lab eval", and that is where I get lucky.

Lucky, how?
The sodium comes back low...

What does sodium have to do with water toxicity?

Here's the key fact is this tale...

When we say "too much water", too much relative to what?

Relative to the amount of dissolved substances in the blood = osms.

In most cases, sodium accounts for the majority of the solute dissolved in the serum.

Yes…in most cases, not all.

Sometimes, other substances sneak in and begin to account for a large of fraction of the osms.

In these instances, the sodium no longer becomes a reliable indicator of the presence of water toxicity.

A common example?
Hyperglycemia.

Ok…
Let’s go back to the causes H20 toxicity.

Here's how I break them down:

1.Excess H20 intake

2 Reduced renal H20 clearance

What causes reduced renal clearance of H20?

1. CKD
2. Reduced dietary osm intake
3. Thiazides
4. ADH!

OK…enough of The Story.

Time for The Schema.

How do we tease out between these 5 causes clinically?

Step 1 -
To ensure we are solving the right problem, measure the serum osms**

If the Na is low, but the osms are normal, H2O toxicity may not be the problem at hand!

Check out this amazing tweetorial from @kidney_boy that illustrates this: bit.ly/2vNdcSz

**Disclosure -
I don't measure the osmolarity with every hyponatremic patient.

If the hyponatremia is mild, and I have a working diagnosis for the cause, I often treat accordingly, and if things don't go the way I expect, I get the serum osm.

Step 2 -
Now that we’ve verified that we have true hypoosmolarity, and therefore H20 intoxication.

Let's go back to our 5 causes...

The easiest cause to tease out from these 5 is ADH.

How?

ADH is the only mechanism by which, in the setting of serum hypoosomolarity, the URINE osmolarity is be elevated.

Low serum osm + high urine osm = ADH.

If ADH is on, we then study whether
ADH switched on for physiologic reasons, or if it's inappropriately on = SIADH.

If it’s NOT ADH,

We use the
history (H20 intake, dietary osm intake),
med list (HCTZ) and
prior creatinine (CKD)

to tease out between the other causes, recognizing that multiple causes may be at play! (e.g, CKD + reduced osm intake)

The best breakdown I have heard of how to do all this?

@jackpenner's schema and video - bit.ly/3b64K0T

and

@DxRxEdu's breakdown on this @CPSolvers episode
bit.ly/2RQB3sW

Check them out!