Hypokalemia

Severity

• Mild: 3.0 to 3.4 mmol/L
• Moderate: 2.5 to 2.9 mmol/L
• Severe: <2.5 mmol/L

Causes

1. Reduced intake
   • Poor nutrition or starvation
   • Usually contributes rather than causes marked hypokalemia by itself, unless combined with other losses
2. Potassium loss
   • Gastrointestinal: diarrhea, vomiting or nasogastric suction, laxative use, intestinal fistulas
   • Renal: loop or thiazide diuretics, mineralocorticoid excess, renal tubular disorders, magnesium deficiency, some drugs such as amphotericin B
   • Vomiting causes renal potassium wasting indirectly through volume depletion, metabolic alkalosis, and increased aldosterone.
3. Shift into cells, without necessarily losing total-body potassium
   • Insulin administration
   • Beta-2 agonists, for example salbutamol/albuterol
   • Alkalosis
   • Thyrotoxic or familial periodic paralysis
   • Catecholamine excess

Symptoms and signs

• Fatigue, muscle cramps, myalgia
• Muscle weakness, which can progress to flaccid paralysis
• Constipation, ileus, or urinary retention
• Polyuria and polydipsia due to impaired renal concentrating ability
• Rhabdomyolysis in severe cases
• Respiratory muscle weakness or respiratory failure in extreme cases
• Palpitations, syncope, or arrhythmia

ECG findings

• Flattened or inverted T waves
• ST-segment depression
• Prominent U waves
• Apparent QT prolongation, often actually QU prolongation
• Ventricular ectopy and tachyarrhythmias when severe

Evaluation

1. Confirm the result
   • Repeat serum potassium if unexpected, to exclude laboratory error or pseudohypokalemia.
2. Assess urgency
   • Symptoms, ECG, cardiac history, digoxin use, kidney function, and ongoing losses.
   • Obtain an ECG in clinically significant hypokalemia.
3. Check associated tests
   • Magnesium, bicarbonate or blood gas, glucose, creatinine, and often phosphate.
   • Correct magnesium deficiency, because low magnesium promotes renal potassium wasting and can make hypokalemia refractory to treatment.
4. Determine whether losses are renal
   • If the cause is unclear, assess urinary potassium.
   • Low urinary potassium in hypokalemia suggests an appropriate renal response, favoring gastrointestinal loss, poor intake, or a cellular shift.
   • Inappropriately high urinary potassium suggests renal wasting, such as diuretics, mineralocorticoid excess, or tubulopathies.
   • Acid-base status and blood pressure then help narrow the cause.

Management principles

• Stop or adjust a causative medication when appropriate.
• Treat diarrhea, vomiting, endocrine disease, or renal losses.
• For recurrent diuretic-related hypokalemia, clinicians may adjust diuretic therapy, consider a potassium-sparing strategy when appropriate, and monitor potassium.

• Oral potassium chloride is preferred for stable patients with a functioning gastrointestinal tract and potassium generally >2.5 mmol/L.
• IV potassium is used for severe hypokalemia, significant symptoms, ECG abnormalities, inability to take oral replacement, or ongoing severe losses.
• IV replacement requires careful rate limits, repeat measurements, and cardiac monitoring when aggressive replacement is used. Glucose-containing IV solutions are generally avoided during acute correction because insulin release can shift potassium into cells.

• Potassium can rebound, particularly when the apparent low value is due to a transcellular shift rather than true depletion.
• Be particularly cautious in chronic kidney disease or reduced urine output because replacement can lead to hyperkalemia.

When it is an emergency

• Potassium ≤2.5 mmol/L
• Palpitations, fainting, chest discomfort, or an abnormal ECG
• Severe weakness, paralysis, or breathing difficulty
• Significant heart disease, digoxin therapy, or rapidly falling potassium
• Persistent vomiting/diarrhea or inability to take oral fluids

Key takeaway