Zaven Sargsyan Profile picture
Jul 25, 2020 9 tweets 4 min read Read on X
I haven’t ordered a CK-MB in 8 years.

If you’re worried about the ❤️, it adds nothing to your troponin.

If you’re worried about 🥩💪🏽, it adds nothing to CK.

Many hospital/labs don’t even run CK-MBs, considering them too low-value.

#TipsForNewDocs
Thanks for comments, y’all. Regarding utility in detecting reinfarction:

First, I must say that I do hospital medicine and minimal ICU, so this isn’t a daily quandary for me. I was mostly imagining the “new docs” on the wards.

That being said, some thoughts/references:

1/7
First, the whole idea is that MB may have an earlier rise than troponin, and a quicker fall (especially if low GFR).

As such, in back to back events, there may be a clearer separation of humps in the MB curve.

You may have seen curves like this (Wikipedia)

2/ Image
Some try to apply these kinetics in practice. I used to, but my CCU attendings convinced me that between symptoms, ECG, and troponin, there’s little value added by CKMB in most cases.

Here’s perspective from UTD authors:

3/ Image
But even isolating the biomarkers alone, here is a nice series of 3 patients with reinfarction demonstrating that CKMB is redundant when you have access to troponin.

PMID 15563477

4/ Image
Before tweeting the original post, I texted two trusted cardiologists, who trained and practice at different institutions. Caveat, only one is an interventionalist.

5/ ImageImage
Parenthetically, troponin peak correlates with infarct size and prognosis too. Though some question even ITS practical value post-reperfusion, and choose not to trend it to peak.

PMID 16275971

6/ Image
All in all, I think routine use of CK-MB is low value, even in patients with possible reinfarction. But there may be occasional times where it’s useful (certainly if troponin not available).

What I’d very strongly discourage is this, in a patient with mild rhabdo:

7/7 Image

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More from @sargsyanz

Mar 27
Another outstanding episode to add to the IDA series.

But I am having trouble reconciling this bit with my experience with IV Fe reactions and my understanding of their mechanism.

Hoping to learn a bit more from #medtwitter and @COREIMpodcast crew

1/6
The experts and references say IgE-mediated anaphylaxis is vanishingly rare. Good.

Most IV iron reactions are thought to be complement-activation-related pseudo-allergy, the final effect of which is histamine release.

Why does this preclude serious reactions?

2/6
I've probably only given a couple hundred doses of IV iron. And yet I distinctly remember:

1 reaction with profound oropharyngeal swelling + hypotension

1 reaction with acute hypotension, abdominal cramping/vomiting/diarrhea

1 reaction with rash + severe dyspnea/wheezing

3/6
Read 6 tweets
Apr 17, 2023
How do salt tabs and urea work in treating SIADH?

They force you to excrete water that you otherwise wouldn't have excreted.

1/
A puzzle:

If this statement is true...

"You can either fluid restrict to 1 liter, or fluid restrict to 1.5 liters AND take 3 one-gram salt tabs with every meal, and achieve the same result"

That must mean that the urine osmolarity is...

2/
Ok let's see what happens. Patient with SIADH without easily reversible cause.

Mouth/gut: [eats/absorbs NaCl]

Kidneys: Thanks but we didn't need that, gonna pee it out.

But you can't pee pure salt. That would hurt. So you gotta mix it in some water.

3/
Read 11 tweets
Jan 18, 2023
Ultrasound: “no evidence of cholecystitis”

Op report: “gangrenous cholecystitis with extremely friable tissue. Purulent drainage with manipulation of gallbladder.”

I've seen this many times.

Thread

1/
Like any test, RUQUS is not perfect in detecting cholecystitis.

A systematic review in 2012 put pooled sensitivity at 81%, but as you see in plot of included studies, there's heterogeneity, with sensitivity as low as 50% in some studies.

tinyurl.com/4d2dcyw6

2/ Image
The specificity is decent. If a clinical syndrome generates moderate or high pre-test probability, and US shows typical signs like

distended GB
thickened walls
fluid around it
sonographic Murphy’s

...you have a diagnosis.

But you can have none of those, and still have chole
Read 14 tweets
Sep 1, 2022
Making a thread of some POCUS gifs from @thepocusatlas

Will be referring to these during a basic POCUS workshop where learners practice scans on normal volunteers.

Non-scanning learners can pull up and show some abnormal examples in parallel with live demo of normal findings
00 - Normal parasternal long-axis (PLAX) view
01 - LV dysfunction in PLAX
Read 19 tweets
Mar 4, 2022
Let's play a little fremitus game, just for fun:

Press the hypothenar edge of your hand firmly against your own ribcage. You're gonna keep it there the whole time while you say some stuff and feel the amount of vibrations transmitted.

Let's go.

1/5
Experiment # 1:

Compare the amount of fremitus/vibration when you say:

ninety-nine
noy-noy-noy
one-two-three

Feel free to repeat a couple times.

Did any of them cause more vibration than others?

2/5
Experiment #2

Pick any one of the three chants above.

Compare the amount of vibrations when you say the phrase in the lowest (deepest) voice you can muster... vs. a high-pitched (e.g. falsetto-y) voice.

Did one cause more vibration than the other?

3/5
Read 5 tweets
Nov 1, 2021
If you eat yourself, will you get hyperkalemic?

Sorry, let me rephrase:

Can upper GI bleeding cause hyperkalemia in predisposed people?

I feel like I’ve gotten that vibe from a couple patients. I can’t find any reports from others.. but I can think of a mechanism...

1/
Blood contains a lot of protein.

When a significant amount of it is introduced into the proximal GI lumen (and some of it absorbed), it can elevate your BUN, or trigger hepatic encephalopathy.

2/
The concentration of potassium in RBCs is ~100 mMol, meaning 100 mEq/L. If you start at a hematocrit of 40 and bleed 20% of your blood volume into your stomach...

That’s ~1 liter blood = 400 cc of red cells = 40 mEq of potassium.

3/
Read 9 tweets

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