Hi all, Jessica here, and welcome to CritIC.
In this video we’ll go through not only the workup, but we’ll focus a bit more on
the treatment of hyperkalemia.
Let’s go, shall we?
There are a couple of statements I made in previous videos on potassium that are helpful
in remembering the workup to hyperkalemia:
first, potassium resides prominently inside of our cells.
Second, our kidneys are great at retaining sodium and excreting potassium
so it’s pretty rare to have hyperkalemia with normal renal function, but it does happen.
And third, potassium shifts over the cellular membrane.
Let’s go through these quickly.
The extracellular potassium (the one you measure in serum) is around 4.5 mmol/l, while the
intracellular concentration is 30-fold!
Being around 150 mmol/l.
So cracking open a cell like an egg will spill potassium and result in hyperkalemia.
This is the case in hemolysis, rhabdomyolysis, excessive burns, tumor lysis syndrome and
crush trauma.
If our kidneys are great at excreting potassium, it goes without saying that renal failure
can result in hyperkalemia.
If GFR falls, less potassium will be presented in urine.
Potassium excretion is furthermore governed by the mineralocorticoid action of aldosterone,
and by tubular secretion.
So a defect in either of these systems will cause hyperkalemia.
Examples of aldosterone deficiency are drug related (like ACE-inhibitors, ARBs and potassium
sparing diuretics like spironolactone) or an adrenal crisis (Addison’s).
Examples of impaired tubular secretion are some forms of renal tubular acidosis.
If you’ve seen my video on hypokalemia, you know that potassium is prone to transcellular shifts.
Flip the causes, and you’ll get the ones that result in hyperkalemia: acidosis, hyperthermia
(note that I’ve never seen it in fever) and beta-blockers.
Now let’s briefly touch upon pseudohyperkalemia.
Just like in pseudohyponatremia, this is an erroneous measurement.
So you’re not to be worried about possible complications from hyperkalemia.
The most common cause is prolonged tourniquet use while getting a venous sample.
The tourniquet crushes the red blood cells that get into your sample.
So the measurement is correct (high potassium) but it’s only in your sample
and not in the entire body.
If you’re unsure if this is the cause, get a new sample.
Still unsure, get an arterial sample.
Pseudohyperkalemia is also seen in severe thrombocytosis and leukocytosis as they cause
in vitro release of potassium from inside of the cells.
If your patient has hyperkalemia above 6.0, your immediate action is to monitor your patient
and get an ECG stat, as hyperkalemia can cause heart blocks and ventricular fibrillation.
Symptoms of hyperkalemia are not really specific, but include tingling sensations, muscle weakness
and paralysis.
Symptoms or ECG abnormalities call for immediate cardiac monitoring (so admit to a cardiac
or medium care) and immediate treatment, the first of which is the administration of calcium.
The following steps of treatment should be on your mind:
First:
Calcium.
Calcium doesn’t lower serum potassium levels, but it stabilizes cellular membrane of the
heart, decreasing excitability and thus decreasing the chance of cardiac arrest.
It should be given to symptomatic patients, especially patients with ECG abnormalities
like QRS widening or when the ST-segment resembles a sine pattern.
It should not be given to patients that use digoxin, because it can lead to digitalis
intoxication, or in combination with bicarbonate, as it may form depositions.
So what should you do?
When in doubt and to prevent delay, just administer calcium, as there is very little harm.
Give 10cc’s of calciumgluconate 10%.
This buys you about 30 minutes.
If your patient is unstable, use calciumchloride, as this is more potent and can be administered
faster, but can cause severe thrombophlebitis
Second:
Insulin-glucose solution.
Remember that insulin causes a transcellular shift of potassium towards intracellular.
So it is only a temporary solution!
The glucose is added to prevent hypoglycemia.
Typical dose is 10 units of insulin (the rapid kind, like actarapid or novorapid) combined
with 50cc’s of 50% glucose.
The onset of effect is around 20-30 minutes, and it will lower potassium with about 1 mmol/l.
Reduce the dose of insulin in patients with renal failure (try 6).
This step will buy you around 4-6 hours.
So what do you do?
Give it to all patients that are symptomatic or have ECG changes.
If your patient is asymptomatic and without ECG abnormalities, give it if hyperkalemia
is above 6.0 and you can’t remove the cause within a few hours.
Just like with calcium, there’s not much you can do wrong in this case.
Third:
Potassium binders, like sodium polystyrene sulfonate (resonium) or calcium polystyrene
sulfonate (sorbisterit).
These are insoluble molecules that bind potassium in the large intestine, preventing them from
being absorbed.
The effect starts after 2 to 4 hours and lasts for several hours.
So it won’t help you in the acute setting, but still is considered very important, and
it may be repeated.
So what do you do?
Always give a potassium binder, just realize it’s not the first step in treatment.
I prefer a calcium preparation over the sodium one.
This is because as mentioned before, a lot of patients with hyperkalemia have impaired
renal function, and administration of sodium could cause renal fluid overload.
With the calcium preparation, just be careful with digoxin and with sodium bicarbonate.
Fourth:
Salbutamol.
Nebulizing with salbutamol causes a transcellular shift.
Again, it is a temporary fix and should only be used if above measures aren’t sufficient.
Don’t nebulize instable patients with cardiac arrhythmias, as salbutamol causes beta stimulation
and thus tachycardia.
The effect on potassium is immediate and lasts for about 2 to 4 hours.
Consider the following treatments for specific conditions:
Dialysis in renal failure
Diuretics in fluid overload in in patients that still have urinary production
Sodiumbicarb for acidosis.
Give 100cc’s of 8.4% solution, and repeat if necessary.
Give hydrocortisone for adrenal insufficiency.
100mg intravenously.
All steps should be considered for every patient with hyperkalemia, but for asymptomatic patients
without ECG changes, we usually start with the insulin glucose solution, followed by
a dietary restriction combined with potassium binders.
And we treat the underlying cause.
To sum this up: remember that in hyperkalemia, your first actions should be to check for
symptoms and get an ECG stat.
If they’re good, you’ve bought yourself some time to think about the cause.
Remember that in people with normal renal function, the most common cause is
pseudohyperkalemia, which doesn’t require treatment.
Repeat the analysis, preferably in a blood gas sample, because that will also help you
with the workup.
Measure serum kreatinine levels for the estimated GFR.
For treatment, when in doubt, or when delayed (sometimes, ECG’s can take forever)
remember that there is little harm in administering calcium
(though it is contraindindicated in patients with digoxin)
there is little harm in administering insulin-glucose-solution
(though be careful in patients with renal failure)
and there is little harm giving a potassium binder.
That’s all!
Drop me a line in the comments with your thoughts!
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