Tag: pseudohyponatremia

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July 1st approaches, it’s new fellow season

I remember the first days of nephrology fellowship. It was exhilarating. It was terrifying. All through residency, when you came across a patient that had you stumped you could just call the consultant. Now I was the last line of defense. I was on the receiving end of that phone call and I did not feel up to the task. I remember those months as being among the most stressful of my career. I started carrying around a small bottle of Pesto-Bismol to fight the stress induced gastritis.

I felt like a drunk, walking out of the ICU to take little nips from “my little helper.” It’s a lot of self induced pressure to battle the imposter syndrome inherent in being a new fellow, especially one coming from an outside institution.

One of my first consults was a transplant patient. The patient had acute kidney injury (AKI) and hyponatremia. She had recently received IVIG and I was so excited that I figured out that her hyponatremia was due to pseudohyponatremia from the IVIG. (See

this letter to the NEJM). So it was particularly disheartening when the transplant surgeon was not impressed pseudohyponatremia diagnosis especially since I had not been able to make any heads or tails regarding the AKI. He made his displeasure quit clear. I felt pertty humbled going to my attending, Patrick Cunningham, but he said, “Let’s walk through the case” and quickly, and humanely, pointed out the possibility of osmotic nephrosis from the same IVIG I had already blamed for the hyponatremia.

Fellowship is hard. Be humble. Try hard. Read as much as you can. Ask for help. Every person we graduate is a competent nephrologist. You will be one too. Trust the system. Together we’ll get you there.

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A couple of new Tweetorials

The first was in response to Robert Centor’s excellent description of how he uses reciprocal creatinine. Honestly I had not thought about reciprocal creatinine in a long time. It was fun diving into some of the literature around it. Here is the tweetorial:

Today I did a second tweetorial on hyperosmotic hyponatremia

Here I had some technical problems. I wrote the entire tweetorial using chained tweets in Safari on MacOS. When I went to upload all tweets, Twitter hung and failed to upload more than the first 8. I had to then go through and re-post the remainder of the tweetorial. I was frustrated and failed to attach two of the animated gifs I made. I added them as additional tweets but they break the flow. Tweetorials are like writing email newsletters, once you publish the tweets (or hit send on the newsletter) there is no opportunity for editing.

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OUWB Question about pseudohyponatremia

First catch of the year.

I have a question regarding your OUWB lectures. I’m trying to grasp why hyperglycemia causes an increase in serum tonicity and decrease in serum sodium, but hyperlipidemia causes no change in serum tonicity and a decrease in serum sodium. For hyperglycemia, I understand that the glucose contributes to the serum osmolarity and can’t passively cross the membrane so causes water to move. However, I’m confused with the situation with lipids and was wondering if you could clarify. Thank you so much!

I may have over indexed on false hyponatremia stuff. This is something you need to be familiar with but a detailed understanding of the mechanism of pseudohyponatremia.

The student had perfect knowledge of the mechanism behind hyperglycemia induced hyponatremia associated with hyperglycemia.

The lipid situation is just a lab error. The lipids fool the lab machine into thinking the sodium is low. It is not low. That is why the osmolality is normal. The osmolality detector is not fooled by the high fats (or proteins) in the blood.

You will not need to know the mechanism for the lab error. I tried to explain it but that may be a situation where I causes more confusion than provided clarity.

The unexpectedly high protein or lipid fraction results in the sample being over diluted resulting in a false report of hyponatremia. The serum sodium is normal. Only about a third of clinical labs are susceptible to this error.

 

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OUWB Sodium and Water Questions

For the sixth year I have had the privledge of teaching at OUWB. When I teach I get e-mail questions from the students. I respond to the students by e-mail but also post the questins and answers here so all the students get the advantages of the questions.

Caller one you are on the line…
“Long time listener; First time caller. Some of the M3s were telling us that last year, they were confused on this Team Based Learning exercise because they learned hyponatremic means low water/volume but originally they thought it meant low salt, and hypovolemic means low salt but they thought it meant low water/volume. 
 
Could you explain? A lot of us are confused now…”
The conflation of volume and osmolality is always confusing.
Hyponatremia means a low sodium concentration.
Hypovolemia means a low total body sodium (literally the total number of grams of sodium in the body). Hypovolemia does not say anything about the concentration of that sodium.
That low total body sodium may be at a high a high or low concentration depending on what the total body water is.
For example heart failure is a common cause of hyponatremia. These patients have edema and other evidence of volume overload. This is a combination of volume overload and hyponatremia. Increased total body sodium, but even great increase in total body water.
Patients with severe diarrhea also can develop hyponatremia. In this case they are volume depleted, decreased total body sodium.
And lastly, patients with SIADH, say from small cell lung cancer, are euvolemic and have a normal total body sodium*.
You can’t equate the two, just like saying that a bowl of soup is salty doesn’t explain how big the bowl is. If the soup is salty but you have only a spoonful, there is not much salt.
Hope this is helpful.
Next caller…
“Hi Dr. Topf,
 
I hope your day has been going well! I was reading over the TBL preparatory material for tomorrow and came across a point that was slightly confusing. 
 
Could you please clarify what exactly was meant by the following: 
 
“Clinicians often characterize hyponatremia by the volume status, hypovolemic hyponatremia versus hypervolemic hyponatremia. It should be clear that both of those two seemingly different causes of hyponatremia, share a single patho- physiologic explanation.”
 
I’ll hang up and take my answer off the line.”
 
Thanks for calling. Great question. This was covered in this slide from my second lecture:
The point of the slide and that both hypovolemic (on the left) and hypervolemic (on the right) cause hyponatremia by the same physiologic mechanism:
1. decreased perfusion (from heart failure in hypervolemic and volume depletion in hypovolemic)
2. Release of ADH (due to the low perfusion, not a high osmolality)
3. Decreased urine output
4. Water intake > urine output
Is that clear?
Next caller…
Hello Dr. Topf,
Please, call me @Kidney_Boy.
Hope you’re doing well. I really enjoyed your lectures today. I was studying for our upcoming class on Friday where we are going to be quizzed on a lot of the same information and I became a little confused. In the TBL article (pg 12) there is a figure and a paragraph that says glucose induced hyponatremia is a type of pseudo-hyponatremia. However it also defines pseudo-hyponatremia as a decreased serum sodium with a normal serum osmolality. 
 
Is the glucose induced factitious hyponatremia is a kind of pseudo-hyponatremia ? If so how can it be a pseudo-hyponatremia when the glucose causes an osmolality imbalance?
 
Thank you so much. 
This one is one me. The TBL document needs to be updated This is just a nomenclature issue.
There is some ambiguity on whether glucose induced hyponatremia can be called pseudohyponatremia, there is some support for it and I used to be in that camp (in fact I wrote a whole book about fluid electrolytes waving the glucose induced pseudohyponatremia flag) but most people limit the term pseudohyponatremia to just the high protein and high lipids causing the lab error (sometimes called a lab artifact), and separate out the high osmolar causes under a different category (factitious hyponatremia).
So I would study what I taught in lecture today. Understanding concepts is more important than knowing the specific names.
Obligatory blog post about the subject (see the segment after the Update):
Hope that helps.
That really clears things up for me! Thank you so much! 
That’s all we have time for. Until next time…