hyperkalemia guideline

[paramatt_]

Hello all,

My employer recently came up with a new policy that enables us to suggest changes or new interventions to our guidelines. I’ve been looking at the use of (s)albuterol for hyperkalemia both in the context of crush injury as well as other etiologies. Now I’ve done the research…there’s lots out there on the topic, but was wondering if anyone uses beta-2 agonists for suspected hyperkalemia. And if so, what is the implementation of the protocol/guidline based upon (all crush injury pateints, EGC changes, etc). Anyways, I'm just curious to see what others out there are doing...any feedback appreciated

[Kiwiology]

Nebulised salbutamol for hyperkalaemia is possible in NZ

[Eydawn]

I would be leery of using Beta-agonists due to their cardiac effects... even just looking at crush injury/compartment syndrome type stuff, unless you know the full medical history you could possibly cause more harm than good in my opinion. Without knowing what the actual potassium value is, it seems more prudent to provide supportive care until those values can be known and then to use insulin/D-50 to treat a known hyperkalemia.

What criteria were you going to use for justifying intervention? What's the odds for potential harm from the hyperkalemia vs. beta agonist effects?

I guess the advantage would be reducing hyperkalemia if you had an extended transport time; however, I would want the receiving facility to be on board with it... especially in terms of crush injuries that will be going to OR expeditiously...

Kiwi- what do the protocols say, other than NZ "has capacity" for it? It's all well and good to say "oh yea, we do that here" but I want to know the details!!

Wendy

CO EMT-B

RN-ADN Student

[croaker260]

We use it here. 10 mg nebbed, or if intubated, all 10 mg squirted directly down the tube (i.e. in a code where Kyper-K is suspected) and bagged in.

[Kiwiology]

We just give 'em 5mg of salbutamol if they have clinically significant hyperkalaemic changes on ECG but such is only very rarely done

I think in this case it would be better to use calcium than insulin to treat the hyperkalaemia. Certainly you want to use insulin in somebody who is hyperkalaemic because of diabetic ketoacidosis although remember hyperkalaemia in DKA is only pseudo hyperkalaemia because the V H+/K+ ATPase swaps extracellular hydrogen (because of the acidosis) for intracellular potassium as one of the acid/base homeostasis mechanisms so this is only a "pseudo hyperkalemia" and that patients with DKA are often actually profoundly hypokalemic. Do not just give your DKA patients an insulin drip and leave them in the corner cos they will croak and die from hypokalaemic cardiac arrest rather quickly

[Eydawn]

I might disagree... I've seen insulin/D50 used in hyperkalemic patients who were not DKA. And it is true that DKA patients are often given D5.45 with 20meq of K+ as their maintenance fluid (at least in my limited exposure) to prevent this and treat the systemic hypokalemia, along with Q4-6 lab draws to closely monitor potassium level (as well as being on continuous telemetry monitoring).

In someone with a crush injury, how is introducing Ca+ going to be more beneficial than just getting the serum K+ level down?

Wendy

CO EMT-B

RN-ADN Student

[Kiwiology]

If you give insulin to somebody who is normoglycaemic wont they become hypoglycaemic?

I am getting fuddled and biochemistry is not my strong suit at 4am

Mmmm ... metabolic pathway valiumz

[Eydawn]

Did you miss that it's given with a BOLUS OF D50??

Sugar... to go into the cells and take K+ with it... leaving person normoglycemic (or slightly hypo which is then corrected)

Just sayin'...

Wendy

CO EMT-B

RN-ADN Student

[Just Plain Ruff]

If you give insulin to somebody who is normoglycaemic wont they become hypoglycaemic?

I am getting fuddled and biochemistry is not my strong suit at 4am

Mmmm ... metabolic pathway valiumz

Then go to bed Kiwi. Might some of your fuddlement be caused by your being awake at 4am? You might think more clearly if you got more sleep.

Edited July 27, 2012 by Captain ToHellWithItAll

[paramatt_]

Thanks for the replies.

Looking at the research, calcium glutonate seems to be the preferred treatment, though not possible as we don't carry it. Same goes for the insulin/glucose. Though beta-2 agonists can take 30mins+ to take effect, it’s all we really have to work with. Also our transport times that can be well over an hour, so I suppose it is possible to see a change in patient condition if implemented in the field.

What criteria were you going to use for justifying intervention?

That's what I was wondering...what criteria is being used, as obviously all we have to work with is a patient's history and ECG changes. I'll I'm doing is proposing the use of beta-2 agonists for hyper-K, including the research, patient's likely to be at risk (crush injury, renal failure, burns, etc), suggestive ECG changes, and potential doses.

It will be the higher-ups that will go through the proposal, see if it’s worth implementing, make a decision, tweak accordingly, and come out with a final guideline if they see it as appropriate. As there is lots of literature on the subject and we already carry both IV and nebulized beta-2 agonists I don't see any reason why a guideline wouldn't be formulated.

What's the odds for potential harm from the hyperkalemia vs. beta agonist effects?

In terms of risk vs benefit, some transient sympathetic stimulation will occur, and granted, some patients will have a greater predisposition to adverse reactions. At the end of the day the benefit is high. The ability to prevent/correct any of the 4 H's and T's prehospitally isn’t always possible, but when it is, I'd say that's a pretty strong step in the right direction.