Approach to hyperkalemia: Clinical sciences

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Introduction0:00–1:01

Hyperkalemia refers to an elevated serum potassium level, usually above 5.5 milliequivalents per liter. Mild hyperkalemia can be asymptomatic, while severe hyperkalemia can cause life-threatening symptoms like paralysis and cardiac arrhythmias.
Some common causes of hyperkalemia include increased potassium intake and conditions associated with transcellular potassium shifts, like medication-induced hyperkalemia, metabolic acidosis, tumor lysis, rhabdomyolysis, or due to decreased effective arterial blood volume.
Another very important cause is reduced renal function, or renal failure. Lastly, other causes include tubular resistance to aldosterone, hyporeninemic hypoaldosteronism, and adrenal insufficiency.Now, if you suspect hyperkalemia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.

Unstable Patient1:01–1:38

If the patient is unstable, stabilize the airway, breathing, and circulation. Next, obtain IV access and put your patient on cardiac telemetry.
This is important because extreme elevations in serum potassium can lead to myocardial instability and dangerous cardiac arrhythmias, such as ventricular fibrillation.
You should also monitor vital signs and provide supplemental oxygen, if needed. Now that we're done with unstable patients, let’s go back to the ABCDE assessment and discuss the stable ones.

Stable Patient1:38–4:07

If your patient is stable, first obtain a focused history and physical examination. Next, obtain labs, including a comprehensive metabolic panel or CMP, and an arterial or venous blood gas, as well as a 12-lead ECG.
History typically reveals palpitations, paresthesias, muscle weakness, or even ascending paralysis in extreme cases. Additionally, there might be a known history of acute or chronic kidney disease.
On the flip side, physical examination usually reveals generalized weakness or a strength deficit, but you could also see fasciculations, or involuntary muscle twitching, as well as flaccid paralysis.
Lab findings will reveal a potassium above 5.5 milliequivalents per liter, and the ECG might demonstrate characteristic changes as the degree of hyperkalemia progresses.
The earliest manifestation is tall-peaked T waves, followed by p wave flattening, and prolongation of the PR interval. In severe cases, you might even see disappearance of P waves, widening of the QRS complex and the eventual development of a sine-wave appearance.
At this point, you can diagnose hyperkalemia! Now, here’s a clinical pearl to keep in mind!
Laboratory processing of blood specimens can affect your interpretation of potassium levels. If hemolysis or blood clotting occurs during blood collection and storage, intracellular potassium might be released into the extracellular fluid, causing a falsely elevated potassium level, or pseudohyperkalemia.
Alternatively, transfusing packed red blood cells can cause a true hyperkalemia. During storage, potassium can diffuse from the cellular layer to the plasma layer of donor blood.
So after transfusion, the potassium in the donor plasma causes a true, but generally brief, elevation in the recipient's serum potassium level.
If you suspect any of these scenarios, be sure to repeat the blood draw.Okay, now that you’ve diagnosed hyperkalemia, the first thing you should do is treat it.

Treatment4:07–5:49

The treatment options can be remembered with the mnemonic C BIG K Drop. This stands for Calcium gluconate, Beta-agonists or Bicarbonate, Insulin, Glucose, K-binders, and Diuretics or Dialysis.
Calcium gluconate helps stabilize the cardiac cell membrane, so it should be immediately given to patients with ECG changes or cardiac arrhythmia in the setting of severe hyperkalemia above 6.5 milliequivalents per liter.
Beta-agonists like albuterol, Bicarbonate, or Insulin help rapidly shift potassium into cells, decreasing its serum levels.
Keep in mind that the effect of medications that shift potassium into cells is only temporary, so they’re usually used while waiting for another treatment option to take effect.
Additionally, Glucose is given with insulin to prevent hypoglycemia, since insulin will also shift glucose into cells. Next, K-binders, like Sodium sulfonate, can be used prevent gastrointestinal absorption of potassium, increasing its fecal excretion; while Diuretics like furosemide in addition to IV saline infusion are given to help increase urinary excretion of potassium.
Lastly, Dialysis can be used to remove potassium from the body, but it’s typically reserved for refractory cases who don’t respond to any other treatment options, and for patients with renal failure.Ok, now that you’ve treated your patient’s hyperkalemia, let’s look for the cause.

Increased Potassium Load and Transcellular Shift of Potassium5:49–8:11

First, consider increased potassium load. If your patient has a high dietary potassium intake, either through potassium rich foods or supplements, you can diagnose hyperkalemia due to increased potassium load.
On the other hand, if the history suggests a normal potassium load, you should consider conditions associated with transcellular shift of potassium, which actually refers to the movement of potassium from the intracellular to the extracellular space.If your patient has received medications such as beta blockers, digoxin, or succinylcholine, consider medication-induced hyperkalemia as the cause.
Alternatively, if your patient's labs reveal a pH below 7.35, a low serum bicarbonate, and a normal anion gap, diagnose hyperkalemia due to metabolic acidosis with a normal anion gap.
This occurs due to a compensatory mechanism involving the exchange of intracellular potassium ions for extracellular hydrogen ions.Next, if history reveals malignancy or recent chemotherapy, think hyperkalemia due to tumor lysis syndrome.
Extensive lysis of tumor cells releases intracellular contents, including potassium, into the circulation. Similarly, a history of recent muscular trauma or extreme muscular exertion can lead to myocyte injury.
This can release intracellular contents and potassium into the circulation. In this situation, rhabdomyolysis is the cause of hyperkalemia.Here’s a clinical pearl to keep in mind!
Hyperkalemic periodic paralysis is a rare genetic condition affecting a gene coding for skeletal muscle ion channels. The mutation causes rapid transcellular shifts of potassium after strenuous exercise, resulting in hyperkalemia, episodic muscle weakness or even temporary paralysis.
Ok, now let’s take a look when you rule out conditions associated with transcellular shift of potassium. Consider decreased renal potassium excretion, so order urine electrolytes and review the urine sodium level.
If it’s below 25 millimoles per liter, this is due to decreased effective arterial blood volume or EABV, which typically occurs in the setting of congestive heart failure and hypovolemia.

Decreased Renal Potassium Excretion8:11–10:48

On the other hand, if your patient’s urine sodium is greater than or equal to 25 millimoles per liter, then calculate the estimated glomerular filtration rate, or eGFR for short, to determine renal function.
AnThe eGFR less than or equal to 20 suggests that hyperkalemia is due to reduced renal function, which can be seen in acute kidney injury and chronic kidney disease.
If the eGFR is greater than 20, consider aldosterone deficiency or aldosterone resistance, so your next step is to check aldosterone level.
If the serum aldosterone level is normal or elevated, suspect tubular resistance to aldosterone. Some causes include the effects of medications like spironolactone and trimethoprim, as well as systemic disorders, such as pseudohypoaldosteronism and obstructive uropathy.
Now, if the serum aldosterone is low, check a renin level. If the renin is low, diagnose hyporeninemic hypoaldosteronism.
Some important causes include the effects of medications like NSAIDs and beta blockers, as well as systemic disorders like diabetic nephropathy or HIV infection.
Finally, if the renin is normal or high, diagnose adrenal insufficiency. Some important causes of adrenal insufficiency include systemic disorders, such as primary hypoaldosteronism or Addison disease.
One last high-yield fact! You may also find high renin levels in patients who take certain medications, such as ACE inhibitors and angiotensin receptor blockers.
That’s because these medications work by lowering aldosterone levels, which can in turn lead to potassium retention and hyperkalemia, and may lead to a compensatory increase in renin.
Alright, as a quick recap… If you diagnose hyperkalemia, first treat with the mnemonic C BIG K Drop for Calcium gluconate, Beta-agonists or Bicarbonate, Insulin, Glucose, K-binders, and Diuretics or Dialysis.
Then, check for history of increased potassium intake. If so, diagnose hyperkalemia due to increased potassium load.
However, if intake is normal, consider transcellular potassium shift, like medication-induced hyperkalemia, metabolic acidosis, tumor lysis, and rhabdomyolysis.

Review10:48–12:27

If there’s no transcellular shift, check urine electrolytes; if urine sodium is less than 25, suspect hyperkalemia due to decreased effective arterial blood volume; if it’s greater than or equal to 25, calculate the eGFR.
If eGFR is less than or equal to 20, diagnose hyperkalemia due to reduced renal function; if it’s above 20, check serum aldosterone levels.
If normal or high, diagnose tubular resistance to aldosterone; if low, check renin levels. If renin is low, diagnose hyporeninemic hypoaldosteronism; but if it’s normal or high, diagnose adrenal insufficiency.
due to decreased affective arterial blood volume if it s greater than or equal to 25 Calculate the EGFR if EGFR is less than or equal to 20 diagnose hyperkalemia due to reduced renal function If it's above 20 check serum aldosterone levels if normal or high diagnose tubular resistance to aldosterone if low check renin levels If Rennin is low diagnose hypo remic hyperaldosteronism But if it s normal or high diagnose