Approach to hypokalemia: Clinical sciences

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Introduction0:00–0:45

Hypokalemia is defined as a low serum potassium level, usually below 3.5 milliequivalents per liter. Mild hypokalemia can be asymptomatic, but more severe hypokalemia can cause life-threatening symptoms like paralysis and cardiac arrhythmias.
Some common causes of hypokalemia include hypomagnesemia, low potassium intake, conditions associated with transcellular shift of potassium, as well as extrarenal potassium wasting, and increased mineralocorticoid activity.
Finally, keep in mind that hypokalemia can also occur due to acid base disorders.Now, if you suspect hypokalemia, you should first perform an ABCDE assessment to determine if your patient is unstable or stable.

Unstable patient0:45–1:23

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 drops in serum potassium can lead to dangerous cardiac arrhythmias, such as Torsades de Pointes and 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 patient1:23–3:41

If your patient is stable, first obtain a focused history and physical examination. Also obtain labs, including a comprehensive metabolic panel, and check a 12 lead ECG.
History typically reveals weakness, muscle cramps, or in extreme cases, even ascending paralysis. Also, there might be a history of diuretic or laxative use, while others may report severe diarrhea.
On the other hand, physical examination typically reveals an irregular pulse and decreased deep tendon reflexes; while lab results show a serum potassium level below 3.5 milliequivalents per liter.
Here’s a clinical pearl to keep in mind! Pseudohypokalemia refers to the falsely low potassium level, often caused by a blood sample being left in a warm environment several hours before processing.
This causes the potassium in the sample to shift from the extracellular space into the intracellular space, which gives a false impression of decreased potassium levels.
Additionally, leukemia can cause pseudohypokalemia due to excessive potassium uptake by cancerous cells. In addition to lab tests, check the ECG, which may reveal broad flat T waves, ST segment depression, and U waves.
Other findings include a prolonged PR interval or a prolonged QT interval. At this point, you can diagnose hypokalemia!Now, here’s a high-yield fact!
If severe hypokalemia results in ECG changes or cardiac arrhythmia, immediately administer an IV infusion of potassium to normalize the potassium level and stabilize the heart rhythm.
However, if Torsades de Pointes is present, give IV magnesium first, as this rhythm has a high likelihood of developing into ventricular fibrillation.Ok, once you confirm that your patient has hypokalemia, your next step is to order labs to check serum magnesium levels.

Hypomagnesemia3:41–4:19

If it’s below reference range, diagnose hypokalemia due to hypomagnesemia. Here’s another clinical pearl!
Hypomagnesemia can exacerbate hypokalemia by accelerating renal potassium wasting and impairing its reuptake. So, to restore potassium levels effectively, start with magnesium replenishment.
On the other hand, if the serum magnesium is not below the reference range, consider decreased potassium intake as the cause of hypokalemia.

Decreased potassium intake4:19–5:04

Low dietary intake of potassium can occur with profound malnutrition, alcohol overuse, or pica, which is the ingestion of inorganic material such as clay.
If the history reveals low potassium intake, you can diagnose hypokalemia due to low potassium intake. In the general population, hypokalemia from low dietary intake of potassium is uncommon, but in hospitalized patients who can't eat, it’s fairly common and can develop quickly, so watch out for this!Now, let’s say your patient’s history reveals a normal potassium intake, then consider conditions associated with transcellular shift of potassium, which actually refers to the movement of potassium from the extracellular fluid into intracellular space!

Transcellular shift of potassium5:04–6:58

Certain medications are known to cause a transcellular shift of potassium, such as beta agonists, theophylline, and insulin.
So if your patient is taking any of these drugs, you can diagnose medication-induced hypokalemia. On the flip side, another cause of transcellular potassium shift is hyperthyroidism.
Thyroid hormones increase sodium-potassium pump activity, causing an increase in cellular potassium uptake and subsequent hypokalemia.
So, if your patient has a known history or symptoms suggestive of hyperthyroidism, such as weight loss, heat intolerance, or palpitations, diagnose hypokalemia due to hyperthyroidism.
Now here’s a high-yield fact! Hypokalemia due to potassium transcellular shift can occur in several other conditions, such as familial hypokalemic periodic paralysis or FHPP.
This is a rare genetic disorder affecting skeletal muscle ion channels. A mutation in FHPP leads to rapid transcellular potassium shifts in the setting of exercise, high-carbohydrate meals, and stress, resulting in temporary muscle weakness or paralysis.
Another condition in which this can occur is thyrotoxic periodic paralysis, where severe thyrotoxicosis causes significant drops in serum potassium levels, and life-threatening paralysis.Ok, now if you rule out conditions associated with transcellular potassium shift, order labs to check urine potassium and creatinine, so you can calculate the urine potassium-to-creatinine ratio.

Extrarenal potassium wasting6:58–7:27

If the ratio is equal to or less than 1.5 milliequivalents per millimole, diagnose extrarenal potassium wasting, which occurs in conditions like severe diarrhea, laxative overuse, or excessive sweating.
On the other hand, if the urine potassium-to-creatinine ratio is greater than 1.5 milliequivalents per millimole, consider renal potassium wasting.

Renal potassium wasting7:27–10:44

Next, evaluate for hypertension or signs of hypervolemia. If they are present, diagnose hypokalemia due to increased mineralocorticoid activity, because mineralocorticoids induce potassium wasting.
But, at the same time, mineralocorticoids retain sodium and subsequently water, and that’s why these patients typically present with hypertension or fluid overload.
Hypokalemia due to increased mineralocorticoid activity is commonly seen in conditions like primary and secondary aldosteronism, congenital adrenal hyperplasia, and Cushing syndrome.
Here’s a high-yield fact! Glycyrrhizin, the main ingredient in black licorice, is known to impair the renal metabolism of mineralocorticoids.
When ingested in excess, black licorice can lead to an increase in mineralocorticoid activity, which in turn can cause hypokalemia and hypertension.Okay, now, let’s assess renal potassium wasting when your patient has no hypertension or signs of hypervolemia.
First, evaluate their acid-base status by obtaining an ABG or VBG. If labs reveal a pH below 7.35 and low serum bicarbonate, your patient has hypokalemia due to metabolic acidosis.
This can be seen in several conditions, including renal tubular acidosis types 1 and 2, acetazolamide use, and diabetic ketoacidosis.
Now, here’s a clinical pearl to keep in mind! In diabetic ketoacidosis, the kidneys also attempt to eliminate the excess glucose by increasing urine production, a process known as osmotic diuresis.
But, with glucose, potassium is lost in the urine due to an osmotic gradient, which eventually leads to a decrease in serum potassium levels.
On the flip side, if your patient has a normal pH and a normal serum bicarbonate level, check to see if your patient is taking medications like hippurate or penicillin.
These medications are excreted by the kidneys as non-resorbable anions, which increases renal potassium excretion, eventually leading to hypokalemia.
If this is the case, your patient’s hypokalemia is due to non-resorbable anions. Finally, if your patient’s pH is above 7.45 with an elevated serum bicarbonate level, there’s a high chance that their hypokalemia is due to metabolic alkalosis.
This can be caused by vomiting, use of diuretics, or genetic conditions like Bartter or Gitelman syndrome.Alright, as a quick recap...
If you diagnose hypokalemia, check the serum magnesium levels. If it’s below the reference range, diagnose hypokalemia due to hypomagnesemia; if it’s within range, check your patient’s potassium intake.

Review10:44–12:11

If it’s decreased, diagnose hypokalemia due to low potassium intake; but if it’s normal, think of potassium transcellular shift, such as medication-induced hypokalemia or hyperthyroidism.
If there’s no shift, calculate the urine potassium-to-creatinine ratio. If it’s equal to or less than 1.5, diagnose extrarenal potassium wasting; but if it’s greater, consider renal potassium wasting and evaluate for hypertension or hypervolemia.
If present, diagnose increased mineralocorticoid activity. If absent, evaluate your patient’s acid-base status.
If the pH is less than 7.35 and serum bicarbonate is low, diagnose metabolic acidosis. If pH and bicarbonate are normal, consider hypokalemia due to non-resorbable anions.
Finally, if pH is above 7.45 and there’s elevated bicarbonate,