In this segment, we review some of the key treatments of severe acidosis in the DKA patient.
po Mag, right? Just what is the order you use for po Mag? Love the series.
Thanks for the feedback! In answer to your question about magnesium repletion, I actually much prefer IV Mg++ rather than PO Mg++ in this situation.
In sick DKA, often the rate limiting step for correcting the acidosis ends up being the serum potassium, ie: you can't rapidly give the patient enough insulin to correct their acidosis because you keep dropping the K+ too far. As such, repleting the potassium aggressively from the very beginning is a major priority in a sick DKA patient. If the patient is hypomagnesemic, then it is going to be very difficult to adequately replete their K+. If you are interested in the detailed mechanism of why that is, this paper gives a good description: https://jasn.asnjournals.org/content/18/10/2649. (In brief, one of the major mechanisms has to do with the fact that Mg++ is an important determinant of K+ secretion vs reabsorption in the distal nephron because intracellular Mg++ blocks channels responsible for K+ secretion; low Mg++ unblocks the channels and allows for increased K excretion).
There are two main reasons that I give IV Mg++ when I am trying to rapidly increase Mg++ serum concentrations in DKA to support my K+ repletion:
1) The IV route of Mg++ administration seems to result in a larger and more rapid increase in the serum Mg++ concentration (Am J Health Syst Pharm. 2012 Jul 15;69(14):1212-7). You can give IV Mg++ pretty quickly (for example, in asthma exacerbations, most protocols give 2gm over 20 minutes), meaning you are not tying up one of your IV lines for hours while the Mg++ is infusing.
2) These patients are often nauseous and vomiting. In a patient with a good mental status, I will still try to give them lots of ondansetron and see if I can get them to participate in some PO electrolyte repletion, HOWEVER if they are already nauseous I want to minimize the number of pills I am asking them to swallow. And I am prioritizing PO intake of K+ over Mg++ because K+ takes FOREVER to replete IV (most hospitals set upper limits at 10mEq per hour via a peripheral IV and 20mEq/hr via a central line), and so if your patient can tolerate it, it can be much faster to replete the K+ PO. In practice, I usually start PO and IV K+ at the same time in case the patient does start throwing up after I give them the PO K+ (also most people can only take 40-60mEq of K+ at a time before they start feeling pretty nauseous).
Hope that helps!
Hi, just had time to watch your (excellent) acid-base in DKA discussion. One comment on your comment about "loading the patient up with zofran" when they arrive in the ED knowing that you are going to give them PO potassium: ondansetron (Zofran) prolongs the QT, hypokalemia prolongs the QT and low magnesium (often along with low potassium) prolongs the QT. I have given zofran to a patient with a low K and caused Torsades (not a spectacular day - didn't check the ECG first). Learn from my experience - check the QTc early on before you pick your antiemetic.
She's really good.Great speaker!
Thank you so much for this!
How often are you redosing the oral potassium? And after how much K replacement or time are you rechecking it?
Is it safe to give 60 meq of potassium via peripheral line
What you do matters.