Hyperglycemic Crises: DKA and HHS - Part 2 of 2

[@StrongMed]

In HHS, practice is more variable, with some clinicians using the blood sugar of 250 as indication that the HHS has improved to the point that the insulin infusion is no longer necessary (and thus don't add dextrose). Other clinicians treat HHS in a similar fashion as DKA where the blood sugar level only dictates when dextrose should be added, and resolution (or near resolution) of the clinical syndrome (dehydration, AMS) dictates when the insulin infusion is switched to long-acting.

[@JJAngleton]

Dear Eric, thanks for sharing. All your videos are very nice to refresh :) However, if I just may add something about the K+ issue that I always found a little bit confusing for students: if patient with DKA come in, they might present with hyperkalemia because the cells try to correct the acidosis by taking up protons in exchange to K+. Later by insulin administration, the K+ drops due to the reasons you provided. That's actually one of the stumbling blocks why rapid insulin administration can get you into big trouble with exactly the opposite: hypokalemia.

[@StrongMed]

Medimarc Thanks for note. Totally agree.

[@bn9891]

Wonderful video as usual!! Loved the"corrected"sodium explanation in particular

[@StrongMed]

In my own experience, I've never seen a situation in which excessively rapid administration of K led to hyperkalemia due to poor renal function from dehydration. I think iatrogenic hyperkalemia is largely prevented by the combination of the rapid improvement in renal function with IVF & the insulin-induced intracellular shift of K. I'm sure we could think up a pt in whom it would be a concern (e.g. pt with ATN + on spironolactone), but it's not something I particularly worry about in DKA.

[@StrongMed]

In DKA, most clinicians transition off of the insulin infusion once the anion gap has returned to normal. Usually the glucose will drop below 250 first, prompting addition of dextrose, and 4-8 hrs later the anion gap will "close" (i.e. normalize), prompting switching of insulin infusion to long-acting insulin (with 30-120 min overlap).

[@sarahneslund712]

I'm an MS3 and this is sooo helpful for the surgery and IM clerkships!

[@khanhduong88]

According to ADA concensus 2009, we use corrected Sodium for choosing normal saline or half saline, not measured Sodium. You can find this reference at care.diabetesjournals.org/content/32/7/1335.full

[@StrongMed]

Y Khoa Thanks for the comment. I've been meaning to update and revise this video for a while, and will review the literature and physiology on this specific issue.

[@xXxTamara01xXx]

Absolutely great! best videos out there about hyperglycemic crises!! Thank you so incredibly much!

[@suleimanbaba1776]

What an excellent way of explanation!

[@behrouznavabakhsh8886]

Hello Dear Sir, I found some inconsistencies between the Uptodate's article on DKA and your great video and would love your input on that: 1. Uptodate recommends 1/2 Saline in normal sodium levels and that is corrected sodium levels rather than measured sodium levels (I guess they are more concerned with CPM than Cerebral edema???). Based on your video however, even if the measured sodium is normal (for which the corrected would probably be higher than normal) we should still administer N.S. 2. You suggest a maximum correction of 50-70 mg/dL in serum glucose concentrations during DKA treatment, while Uptodate sets that as the minimum correction value. It also states that you can't possibly cause higher drops in Glc concentrations with higher insulin doses since the receptors are already saturated on the lower dosages... Again thanks for your great work and all the videos.

[@StrongMed]

Thanks for the comment. This video is one of the oldest on the channel (that hasn't already been replaced) and is in bad need of an update - I just haven't gotten around to it yet.

[@hmrpharmacist9370]

great video , really informative .I really loved the simplicity of the video . Dr.Gill

[@drabhijeetchopade]

Brilliant educator

[@iloveafter]

Thanks Dr. Strong. Have a good holiday!

[@syednajmulhassanshah6186]

Great teaching!Keep it up Dr Eric.Badly Waiting for upcoming updated vedios.

[@amodghimire]

Thanks alot. Loads of informations. Loved watching it.

[@jakewong6943]

Thank you Dr. Strong for another helpful video. In your section about precipitating causes (10:06), are those triggers only for people who have diabetes (either type 1 or 2)? In other words, is it possible that a UTI, stroke, etc. can cause DKA or HHS even in a patient without diabetes?

[@sunving]

Thank you very much Doctor Strong

[@zbjordan23]

wow totally awesome -grateful intern

[@khanhduong88]

May i ask you one question. at 2:50, in case of mild volume depletion, normal corrected Na+, you use normal saline. But in the ADA concensus, in case of normal corrected Sodium, they use half normal saline. Can you explain this to me? I think you are right, because there is no use to use half normal saline if the Sodium concentration of the patient is normal. But they use half normal saline in that situation. You can make reference at: img.medscape.com/article/706/727/706727-fig2.jpg

[@ktykts]

Could you fix the volume? Im having some trouble hearing, is very low.

[@AwakenCompassion]

Great Lecture!! Thanks!

[@MikeBirkhead]

I recently watched your videos on Sodium regulation; In those videos and in this one, you mention that hyponatremia is due to: - Transcellular fluid shift - Salt loss from diuresis My question is: 1. Hyperosmolarity induces ADH release -- Does ADH release contribute to the hyponatremia? 2. Diuresis, alone, would lead to volume depletion and activation of RAAS--> leading to Sodium retention (and possibly mild hypernatremia)? I think you mentioned the possibility of Hyperglycemia causing both hypo- and hyper- natremia in your videos on the subject -- is this the proposed mechanism for possible hypernatremia or is there an alternative pathway? Thanks!

[@umeshwadile]

when sugar level

[@adlesal24]

thanks doctor strong for nice review of DKA/HHS mx. As you mentioned in hyponatremia lectures, correction of hypovolemic state will usually correct hyponatremia rapidly. so, i ask in case of DKA with hyponatremia, with initiation of normal saline to hydrate the pt and sodium started to rapidly corrected, shall i follow the same rule of hyponatremia correction and slow down the NS rate or shall i give the priority for correcting the dehydration status.

[@meanderingdave]

Hi there - At 8:38 you mispoke. Might want to throw a not in on your video addressing it. Should have said "hypokalemia" instead of "hypoglycemia". This is a great presentation. Thank you, sir! Dr Dave

[@FatimaNaeemMalik]

Hello Eric. You have always been very helpful with your videos and I, as a resident can not thank you enough. Each of your video has been of great help. I however have a question here. You have mentioned that for choosing IV fluids, one needs to look at measured serum sodium, but UpToDate suggests to use corrected sodium for choosing fluid. Kindly tell which one to follow. Thanks.

[@goerizal1]

commonly there maybe a pre-renal azotemia component from the negative fluid status and/ or renal azotemia exacerbation. how slow would you like the K replacement then? thanks.

[@russellmachin109]

Hi additionally to the osmotic effect of hyperglycaemia on sodium can't it also cause a degree of pseudohyponatraemia?

[@wendychng7864]

is 0.45% normal saline can be used in hhs with hypernatremia, will it lead to cerebral edema?

[@StrongMed]

Thanks for the correction Dr. Dave.

[@jinyousif5095]

greaaat video !

[@n.upadhyay7478]

excellent

[@nakiaally7136]

thanx

[@nsas955]

thanks a lot but the sound is too low ....we could barely hear!!!

[@StrongMed]

Sorry about the sound. There were both audio and video problems with some of my earlier videos. I'll hopefully be rerecording this particular one soon.

[@chintalavenkatarakesh9316]

please update the video sir