Treating hypokalaemia

Introduction

Before starting urgent treatment for apparent hypokalaemia, the diagnosis should be confirmed on a further serum sample. Assessing kidney function and acid–base and volume status is essential for optimal choice of therapy.

Management of confirmed hypokalaemia may require any of the treatments listed below, depending on the clinical context and degree of urgency. Intravenous potassium replacement is best carried out in a hospital setting, where infusion rates, clinical condition and potassium concentration can be closely monitored.

Therapy may not be successful until the mechanism of ongoing potassium loss has been identified and corrected. If hypokalaemia does not respond to treatment, continuing loss should be suspected (eg due to diuretic drug abuse, acid–base disturbance, associated magnesium deficiency).

Oral treatment

Oral potassium supplements are adequate for most patients but can be difficult to swallow. Use:

For patients unable to swallow tablets, an effervescent formulation may be appropriate. Use:

Intravenous treatment

Intravenous potassium is required:

• when oral intake is not possible
• for severe hypokalaemia (lower than 3 mmol/L) with associated muscle paralysis
• for cardiac rhythm disturbance with electrocardiogram (ECG) evidence of hypokalaemia.

Regardless of the severity of the overall deficit, rapid intravenous infusion of potassium may cause fatal hyperkalaemia. Unless special circumstances apply (eg emergency management of diabetic ketoacidosis), the:

• rate of potassium infusion should not exceed 10 mmol/hour
• potassium concentration through a peripheral vein should not exceed 40 mmol/L.

Use:

Potassium chloride should be given in premixed infusion bags. Extemporaneously adding ampoules of potassium chloride to intravenous fluids is not safe. Inadequate mixing may result in potassium being delivered at a lethal concentration. Premixed preparations are available in varying concentrations and volumes, most commonly in 1000 mL of compatible fluids. Premixed potassium chloride is also available in a smaller volume at a high concentration (10 mmol/100 mL). Choice of preparation depends on the amount of potassium required, whether intravenous access is central or peripheral, and how much fluid the patient can tolerate.

During potassium replacement, the ECG should be monitored and the serum potassium concentration measured every 2 hours. If resources are not available to monitor the venous potassium concentration every 2 hours, it should be measured as often as possible.

Additional considerations

Potassium replacement needs special care in cachectic patients. Their low muscle mass increases the chance of overcorrecting the deficit, leading to hyperkalaemia. Rebound hyperkalaemia is also a danger when hypokalaemia is due to acute potassium shift into cells (eg caused by periodic paralysis or insulin excess).

In hypokalaemia due to proven or suspected diuretic drug abuse, suddenly stopping a high-dose loop diuretic can cause marked fluid retention. Diuretic dosage should be reduced gradually, while restricting sodium and water intake.

When hypokalaemia results from fixed mineralocorticoid excess (eg in primary hyperaldosteronism), restricting sodium intake is also key in achieving potassium repletion.

When potassium depletion is associated with severe metabolic alkalosis (eg from vomiting acid stomach contents), potassium repletion may not be possible until the chloride deficit is corrected.

Potassium sparing drugs

Potassium-sparing drugs have no place in managing acute hypokalaemia but can be useful for maintenance. Use:

The response to continuing treatment with potassium-sparing drugs should be reviewed every 1 to 2 weeks until the serum potassium concentration is stable. This is to avoid overcorrection of the deficit and the development of potentially dangerous hyperkalaemia. The lowest effective dose should be used. Spironolactone has adverse effects in women and men.