Farxiga
Started by gator2886
Also:
although from what I've read it's only case reports, but it resulted in an FDA warning, the physiology of it is a little suspect to me though
although from what I've read it's only case reports, but it resulted in an FDA warning, the physiology of it is a little suspect to me though
Have definitely seen multiple cases of euglycemic DKA post-operatively from it. That said, I can't say that any of them have clinically behaved like DKA, it's usually just an unexplained metabolic acidosis +/- lactemia. And I wonder whether all these patients would do fine eventually when they stop being NPO.
What was the clinical presentation? It must’ve been pretty bad for multiple case reports to get an fda warning, like they must’ve been re-intubated to get an abg and have it worked up. I’ll have to look into the case reports
Thanks for the info. Anyone else? Still not sure to hold or maintain for CHF.
All my patients were in the ICU for separate reasons related to their surgery and not the SGLT-i
Yeah don't agree with everything by AHA, but SGLT2 continued can absolutely lead to issues. Not in the OR, but mostly afterwards.
The acidosis can be a PITA in the OR but can certainly prolong intubation, ICU LOS, etc. Not sure if there is an increased mortality signal found in a study thus far, but wouldn't be the slightest surprised.
What's the benefit of continuing vs holding for 3 days? Some hyperglycemia and fluid retention?
For scheduled cases I’m not sure why we can’t give the patients the pre-surgical carb drink or even just a small amount of insulin. It seems the starvation state and lack of insulin seems to play a large role in the development of DKA.
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It isn’t DKA when SGLT2 are the cause. Different mechanism, different treatment.
I'm fully aware. The underlying mechanism of EDKA is secondary to a carbohydrate deficit resulting in generalized decreased serum insulin and excess glucagon and cortisol. Initial treatment is typically some sort of continuous insulin infusion following fluid replacement. In contrast to DKA management, since serum glucose in EDKA 'normal' you have to add dextrose to the mix somewhere.
Therefore, pre-emptively giving the patient carbs and insulin should therefore minimize and decrease the EDKA. Even if you don't consider it pre-emptive treatemnt, you can just call it treatment of presumed EDKA.
Or… just keep it simple and hold the med.
More to the point; https://www.jcvaonline.com/article/S1053-0770(23)00840-6/abstract seems to suggest that SGLT2 for heart failure appears to have a low to nearly non-existent risk of EDKA, if they don't have any history diabetes.
We used to see it all the time in our cvicu last 2 years. Insulin drip unit or 2 an hour overnight. Thats it. It's become routine @ this stage we don't even see it now really cause the nurses spot it and fix it themselves.
Doesn't delay discharge anymore or cause any harm that anyone's ever mentioned
Doesn't delay discharge anymore or cause any harm that anyone's ever mentioned
How did you diagnose EDKA? I’m curious, did you test for acetoacetate/B-hydroxybutarate? I know this is academic but I’m genuinely interested, were these cardiac cases? Im trying to unravel the physiology, like does this pose a risk for someone having a lap chole? What about someone who is npo and skips breakfast, are they going into profound acidemia if they skip lunch too? And I also had a topical cataract case get cancelled for this despite my and the surgeons protest which irritated me , because you know the nurse boss referred to ‘policy/protocol’ which has replaced clinical thinking for patients who’ve made life plans for surgery
And edit: I’ve been trying to use chatgpt and it actually said elective cataract surgery doesn’t need to be cancelled and the surgeon and anesthesiologist should be consulted, maybe AI will replace some administrators
In the OR I’ve seen low pH, pCO2 normal range, relatively normal glucose levels, lactic acid normal range. Never checked ketones because the result wouldn’t change my management. (Turned out my patient was taking spouses pills but didn’t tell anyone.) My colleagues have seen it in the cardiac rooms.
Just like any other acidotic situation there is a spectrum of clinical sequela.
Unexplained acidosis w/+ B-hydroxybutarate and hx of SGLT2i, these were after major surgeries. My guess is the length of surgery and magnitude of stress response play a role. Also one could always just run some dextrose/insulin intra-operatively as prophylaxis. I definitely would not cancel surgery for it.
For me, the decision to cancel for a SGLT2i depends on what case we’re doing, patient comorbidities, and possibly morning labs. We’ve had a couple euDKAs at our place related to patients in these meds so I’ve become a bit more strict especially if cases are truly elective. But if a patient wishes to proceed just make sure they understand the risk.
In the spirit of this thread had a patient the other day that didnt stop their SGLTi. Ran a dextrose gtt during the case, just 5% at 75cc/hr. Sugars stayed stable, but it logically should also help with risk of EDKA. Also encouraged eating immediately afterwards.
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