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.
3/
You might say so what, I eat 4 bananas in one sitting, and I don’t get hyperkalemic.
Fair enough. Although do you?? And if you’re on an ACEi, don’t you??
But more importantly, there’s a difference between bananas and pure K+.
4/
40 mEq of K is actually a lot.
The total amount of potassium in our serum is only about 12 mEq (3L serum x 4 mEq per liter)!
By contrast, intracellular stores are MUCH higher: 50L cells x 100 mEq/L = 5000 mEq potassium.
5/
When we eat, the potassium in our food gets absorbed into the blood. Luckily, that potassium usually comes with carbohydrates (eg banana, potato, orange juice), which triggers insulin release, which puts the potassium into cells and keeps us from getting hyperkalemic.
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Does blood have enough carbohydrates in it to confer this protective effect? Maybe... maybe not. But even if we assume yes, there could still be an effect, especially since one can bleed more than a liter.
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If you bleed 2L/40% of your blood volume in a day, which isn’t unheard of - that’s 80mEq of potassium - and for someone with CKD, a subclinical RTA, on lisinopril... or an acutely depressed GFR from a brisk bleed... that might prove to be enough to raise serum levels.
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Many medicine procedures involve (1) pushing a needle into a fluid-filled space, (2) advancing a plastic catheter over the needle into the space, (3) pulling the needle out, and (4) leaving the catheter in either for drainage or infusion.
Things often go wrong at (2).
1/5
When you first get a “flash” (enter the fluid filled space with your needle), only the very tip/distal part of the needle/bevel is in the target space.
Let’s use paracentesis as an example.
In these photos, the paper is the peritoneum, with views from both sides of it.
2/
If you try to advance the catheter now, it will hit up against the peritoneum and you will feel resistance. The extra force you exert might even make the needle come out of the peritoneum completely, and you might end up advancing the catheter into subcutaneous tissue.
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I was taught, and continue to hear it taught, that the history of present illness (HPI) should be crafted to "convince the listener/reader of your suspected diagnosis."
I think this framing is problematic...
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The HPI should outline the patient's experience of illness chronologically, and include with some neutrality details relevant to the *differential* diagnosis.
As well as those symptoms particularly emphasized by the patient (in case you aren't thinking of all differentials).
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Teaching that the HPI should "sell" or "build a case for" a diagnosis essentially encourages us to ignore and hide inconvenient truths that don't fit with our top suspicion, or overemphasize those that do - which is the definition of confirmation bias.
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As you turned the corner on the second flight of stairs, you felt your breath pull a little deeper, the next one come a little earlier. Your heart said 👋🏼, bounding softly in your neck.
Ten seconds down the hall, all that faded. You were back to mulling some thought.
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But hold on. Let’s pause for a minute and retrace the steps.
A lot happened before the extra breath and the tug in your neck caught your attention.
And it’s all so damn cool.
2/
At the foot of the stairs, anticipation of exertion 🔔 and the stretch of muscle fibers 🦵🏽sent a signal to the sympathetic nervous system: start the car.
3/