How to diagnose and treat hypokalemia (low potassium levels)?

How to Check Potassium Deficit

The most critical first step is checking serum magnesium levels concurrently with potassium, as hypomagnesemia is the most common reason for refractory hypokalemia and must be corrected before potassium levels will normalize. 1

Initial Laboratory Assessment

Essential Tests to Order

• Serum potassium level to establish severity: mild (3.0-3.5 mEq/L), moderate (2.5-2.9 mEq/L), or severe (<2.5 mEq/L) 2
• Serum magnesium level (target >0.6 mmol/L) - this is non-negotiable as magnesium depletion causes dysfunction of potassium transport systems and increases renal potassium excretion 1
• Renal function (creatinine, eGFR) to assess kidney's role in potassium wasting 1
• Urinary potassium excretion: A level ≥20 mEq/day in the presence of serum potassium <3.5 mEq/L indicates inappropriate renal potassium wasting 3
• Arterial blood gas or serum bicarbonate to identify metabolic alkalosis, which drives renal potassium losses 2

Verify the Result

Repeat the potassium sample to rule out fictitious hypokalemia from hemolysis during phlebotomy before initiating aggressive treatment 1

Electrocardiogram Assessment

Obtain a 12-lead ECG immediately to identify cardiac manifestations that indicate urgent treatment need, regardless of the absolute potassium value 1, 2

ECG Changes Indicating Urgent Treatment

• T-wave flattening or inversion 1, 2
• ST-segment depression 1, 2
• Prominent U waves 1, 2
• First or second-degree atrioventricular block 2
• Atrial fibrillation 2
• Ventricular arrhythmias (PVCs, ventricular tachycardia, torsades de pointes) 2

Estimating Total Body Potassium Deficit

Understand that serum potassium is an inaccurate marker of total-body potassium deficit - only 2% of body potassium is extracellular, so small serum decreases represent massive total body deficits 4, 5

Clinical Context Matters

• Diabetic ketoacidosis patients typically have total body potassium deficits of 3-5 mEq/kg body weight despite initially normal or even elevated serum levels 1
• Rapid potassium losses (acute vomiting, new diuretic therapy) may cause symptoms at higher serum levels than chronic, gradual depletion 2
• Clinical problems typically begin when potassium drops below 2.7 mEq/L, but this threshold varies based on rate of loss and comorbidities 2

Identifying the Underlying Cause

Medication Review (Most Common Cause)

• Loop diuretics (furosemide, bumetanide) - inhibit sodium/chloride reabsorption in ascending limb of loop of Henle 2
• Thiazide diuretics (hydrochlorothiazide) - inhibit sodium/chloride reabsorption in distal tubule 2
• Both cause significant hypokalemia and metabolic alkalosis 2
• Check for concealed diuretic use or herbal supplements containing licorice (mineralocorticoid effects) 2

Gastrointestinal Losses

• Vomiting causes hypokalemia primarily through renal losses, not direct gastric fluid loss - metabolic alkalosis from acid loss drives renal potassium excretion via enhanced ENaC activity 2
• High-output stomas or fistulas cause both direct losses and secondary hyperaldosteronism from volume depletion 2
• Diarrhea causes direct potassium losses 2

Renal Causes

• Primary hyperaldosteronism 2
• Secondary hyperaldosteronism (from volume depletion) 2
• Bartter syndrome or Gitelman syndrome 2
• Renal tubular acidosis 3

Transcellular Shifts

• Insulin excess 1
• Beta-agonist therapy 1
• Thyrotoxicosis 1

High-Risk Populations Requiring Aggressive Evaluation

Patients with cardiac disease, heart failure, or on digoxin require more aggressive investigation and correction even with mild hypokalemia due to increased risk of digitalis toxicity and life-threatening arrhythmias 1, 2

Common Pitfalls to Avoid

• Never supplement potassium without checking and correcting magnesium first - this is the most common reason for treatment failure 1
• Failing to address underlying volume depletion first in patients with GI losses - hypoaldosteronism from sodium depletion paradoxically increases renal potassium losses 1
• Overlooking secondary hyperaldosteronism in volume-depleted patients 2
• Not recognizing that transcellular shifts can cause potassium to rapidly shift back into extracellular space once the underlying cause is addressed 1