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Do you have a systematic approach for the causes of hypokalemia? It’s important to step back and ask WHY is that potassium low? Remember, don’t just replete, treat!


So, let’s start with the big idea, which is that when a patient is hypokalemic, that means there’s either too little potassium going in, too much going out, or potassium hiding inside of cells.


This gives us our framework for understanding the causes of hypokalemia, which consists of four main buckets:

Number 1, poor oral intake

2, GI losses

3, urinary losses

And 4, intracellular shifts. 


First, let’s talk about hypokalemia from poor intake. 

Poor oral intake of potassium as a sole driver of hypokalemia is pretty uncommon. Patients would generally have to consume less than 1g/day to become hypokalemic. Usually, these patients have poor nutrition overall, as we may see with those hospitalized with alcohol use disorder or eating disorders.


Next up, we have GI losses of potassium. Potassium can be lost in both directions, either by vomiting or by losses from stool… Anything that increases stool losses can result in hypokalemia. So ask yourself- has your patient been having diarrhea, repeated enemas, or laxatives? This might be where their potassium is being lost… But what about loss of potassium due to vomiting?


Vomiting does cause hypokalemia, but maybe not for the reason you would expect. Acid losses in emesis in the form of hydrochloric acid result in an excess of bicarbonate. Our kidneys are great at compensating for this by excreting the excess bicarb… but what goes out with all that excess bicarb? Potassium follows bicarb into the urine, which causes hypokalemia.


And speaking of urinary causes, that’s our third bucket! There are a lot of things that cause urinary losses of potassium, so it’s helpful to divide them into four groups. (1) medications, (2) uncontrolled diabetes,  (3) renal tubular acidosis or RTA, and (4) hypomagnesemia. 


First, let’s look at the med list for possible culprits. Diuretics, particularly loop diuretics and thiazides result in potassium wasting in the urine. Certain antibiotics, such as penicillins, fluoroquinolones,and aminoglycosides are also common offenders. And steroids, particularly mineralocorticoids or glucocorticoids in high doses, trigger potassium excretion by mimicking aldosterone. A helpful way to remember these meds is using the Pesky P’s: Pee, for diuretics, Penicillin, for antibiotics, and Prednisone, for steroids. And remember, in the GI bucket, we talked about laxatives, so you tack on a P for poop to help you remember those meds, too!


Next up in our causes of urinary losses is uncontrolled diabetes. If they have uncontrolled hyperglycemia, then they may be losing potassium through osmotic diuresis. Or is your patient in DKA, and losing potassium along with beta-hydroxybutyrate in the urine? 


Now onto our third cause of urinary losses, renal tubular acidosis. Types 1 and 2 can cause hypokalemia. In Type 1 or Distal RTAs, potassium is lost due to a defect in secretion of hydrogen ions. The excess hydrogen ions in the urine create an acidic environment that predisposes patients to stones! So the presence of hypokalemia and kidney stones may clue you in to a type 1 RTA.


 Next, we have Type 2 or Proximal RTA, which occurs due to a defect in bicarb reabsorption, and potassium is lost along with bicarb in the urine.


Our fourth and last group of urinary causes is hypomagnesemia. If your patient has a low mag, this can contribute to potassium wasting in the urine. And what medication can cause Mg wasting and contribute to hypokalemia? PPIs, which are another one of those Pesky P medications! 


Now, for the last big bucket in our framework for hypokalemia, we have intracellular shifts. One reason that potassium shifts into cells is because of excess catecholamines. Think about patients who are having uncontrolled alcohol withdrawal, an active MI, or panic attacks. All these scenarios cause a rise in beta-adrenergic activity that promotes potassium movement into cells by activating the sodium-potassium pumps. 

Similarly, any meds that are beta-agonists also shift potassium into cells. Two common ones are albuterol, when it’s given in high doses, and insulin. 

Shifts also occur when hematopoietic cells are rapidly dividing, like during therapy with GM-CSF, B12, or folate. So whereas cell destruction leads to potassium leakage and hyperkalemia (think – TLS), the opposite happens during proliferative states, where potassium shifts into cells. 

Lastly, alkalotic states promote intracellular movement of potassium. A trick for remembering this is that in alka-low-sis, potassium is usually low. 


While it’s helpful to think about the causes of hypokalemia separately using this framework, it is important to remember that many patients are going to have more than one reason for being hypokalemic. It’s up to you as their clinician to think critically about what is driving that low number so you can treat the cause and not just the number. 

That’s all for now! Check out our website for a handy infographic and show notes that may be good to pull up next time on rounds! 

Original Episode (Infographic and Show Notes)

Hypokalemia & Potassium Repletion: 5 Pearls Segment

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