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:
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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)
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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:
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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
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Before tweeting the original post, I texted two trusted cardiologists, who trained and practice at different institutions. Caveat, only one is an interventionalist.
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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
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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:
Op report: “gangrenous cholecystitis with extremely friable tissue. Purulent drainage with manipulation of gallbladder.”
I've seen this many times.
Thread
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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.
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.
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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?
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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.
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...
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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.
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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.
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