Hyperkalaemia

Hyperkalaemia is an electrolyte disorder characterized by a serum potassium concentration of ≥5.5 mmol/L. It is a potentially life-threatening medical emergency because elevated potassium levels impair cardiac electrical conduction and may result in fatal cardiac arrhythmias. Hyperkalaemia commonly occurs in patients with chronic kidney disease (CKD), acute kidney injury (AKI), diabetes mellitus, and in those receiving medications that impair potassium excretion.

Severity is classified as:

• Mild: 5.5–6.0 mmol/L

• Moderate: 6.1–6.5 mmol/L

• Severe: >6.5 mmol/L

The presence of electrocardiographic (ECG) changes indicates severe hyperkalaemia regardless of the serum potassium level and requires immediate treatment.

Epidemiology

Hyperkalaemia is frequently encountered in patients with impaired kidney function, particularly those with CKD Stages 4–5 and acute kidney injury. The risk increases with the use of renin-angiotensin-aldosterone system (RAAS) inhibitors, potassium-sparing diuretics, and other medications that reduce renal potassium excretion. Hyperkalaemia is associated with increased hospitalization, cardiovascular events, and mortality if not promptly recognized and treated.

Risk factors

Common risk factors include:

• Chronic kidney disease

• Acute kidney injury

• Diabetes mellitus

• Heart failure

• Hypoaldosteronism

• Metabolic acidosis

• Excessive dietary potassium intake

• Renin-angiotensin-aldosterone system inhibitors (ACE inhibitors, ARBs)

• Potassium-sparing diuretics

• Non-steroidal anti-inflammatory drugs (NSAIDs)

• Potassium supplements

• Tissue breakdown (rhabdomyolysis, tumour lysis syndrome, severe trauma)

• Massive blood transfusion

Pathophysiology

Potassium is predominantly an intracellular ion. Hyperkalaemia develops when potassium excretion is impaired, excessive potassium is released from cells, or potassium shifts from the intracellular to the extracellular compartment.

Elevated extracellular potassium reduces myocardial resting membrane potential, resulting in impaired cardiac conduction, progressive ECG abnormalities, and potentially fatal ventricular arrhythmias or cardiac arrest. In CKD, impaired renal potassium excretion is the principal mechanism, while metabolic acidosis further promotes extracellular potassium accumulation.

Clinical presentation

Symptoms depend on the severity and rate of potassium elevation.

Patients may present with:

• Ascending muscle weakness

• Muscle fasciculations

• Flaccid paralysis

• Fatigue

• Palpitations

• Shortness of breath

• Chest discomfort

• Syncope

Clinical signs may include:

• Bradycardia

• Cardiac conduction abnormalities

• Cardiac arrhythmias

• Muscle weakness

• Reduced or absent deep tendon reflexes

• Cardiac arrest in severe cases

Diagnostic criteria

Hyperkalaemia is diagnosed when:

• Serum potassium concentration is ≥5.5 mmol/L.

Severity is classified as:

Hyperkalaemia with ECG abnormalities should be treated as a medical emergency regardless of the potassium level.

Investigations

Recommended investigations include:

Laboratory investigations

• Serum potassium (repeat at 0, 1, and 3 hours or as clinically indicated)

• Serum creatinine

• Blood urea nitrogen (BUN)

• Serum bicarbonate

• Serum electrolytes

• Full blood count

• Random blood glucose

• Lipid profile (total cholesterol and LDL cholesterol)

• Serum uric acid

Cardiac assessment

• Electrocardiogram (ECG)

Common ECG findings include:

• Tall, peaked T waves

• Flattening or disappearance of P waves

• PR interval prolongation

• Widening of the QRS complex

• Sine-wave pattern in severe hyperkalaemia

• Ventricular arrhythmias

• Cardiac conduction abnormalities

Additional investigations should identify the underlying cause of hyperkalaemia.

Management

Management aims to:

• Stabilize the myocardium.

• Shift potassium into the intracellular compartment.

• Remove excess potassium from the body.

• Treat the underlying cause.

• Prevent recurrence.

Non-pharmacological treatment

General measures include:

• Discontinue potassium-containing supplements.

• Stop medications that increase serum potassium, including:

  • ACE inhibitors.

  • Angiotensin receptor blockers.

  • Potassium-sparing diuretics.

  • Non-steroidal anti-inflammatory drugs (NSAIDs).

• Restrict dietary potassium intake.

• Avoid potassium-rich foods such as bananas, potatoes, and green leafy vegetables.

• Treat the underlying cause.

• Monitor cardiac rhythm continuously in patients with severe hyperkalaemia.

Pharmacological treatment

Cardiac membrane stabilization

Patients with serum potassium >6.5 mmol/L or ECG changes should receive immediate intravenous calcium.

Adults:

• Calcium gluconate 10% 10–30 mL intravenously immediately.

OR (reserved for Intensive Care Unit administration through a central venous line)

• Calcium chloride 10% 10 mL intravenously immediately.

If ECG abnormalities persist, the calcium dose may be repeated after 5–10 minutes.

Do not administer intravenous calcium simultaneously with sodium bicarbonate through the same intravenous line.

Shift potassium into the intracellular compartment

Adults:

• Short-acting insulin 5–10 units intravenously together with 50 mL of 50% glucose.

Glucose should be administered only if random blood glucose is below 11 mmol/L.

Monitor blood glucose closely to detect hypoglycaemia.

Repeat insulin therapy every 4–6 hours if necessary.

Children:

• Short-acting insulin 0.1 units/kg intravenously together with dextrose 0.5 g/kg administered over 30 minutes.

In addition:

• Salbutamol nebulization 2.5–10 mg every 4–6 hours.

Patients with metabolic acidosis who are not fluid overloaded may receive:

• Sodium bicarbonate 1 mEq/kg intravenously over 15 minutes.

Removal of potassium from the body

To enhance potassium elimination:

• Calcium (or sodium) polystyrene sulphonate 15–30 g orally every 8 hours for 3 days.

This may also be administered three times weekly for selected patients with chronic recurrent hyperkalaemia.

Caution: Polystyrene sulphonate is associated with a risk of bowel perforation.

In addition:

• Furosemide 40–80 mg orally or by slow intravenous injection every 12 hours, provided adequate urine output is present.

Patients with severe or refractory hyperkalaemia should undergo urgent haemodialysis, particularly those with advanced kidney failure.

If potassium-binding resins are unavailable:

• Lactulose 10–30 mL orally every hour until rapid bowel evacuation occurs, followed by 30 mL every 8 hours for 24 hours.

Referral

Urgently refer patients to a higher-level facility or nephrologist when:

• Serum potassium exceeds 6.5 mmol/L.

• ECG abnormalities are present.

• Hyperkalaemia persists despite emergency treatment.

• Advanced CKD or acute kidney injury is present.

• Emergency haemodialysis is required.

• Recurrent hyperkalaemia occurs despite appropriate management.

Patients with severe hyperkalaemia should be managed in a facility capable of continuous cardiac monitoring and emergency dialysis.

Complications

Potential complications include:

• Life-threatening cardiac arrhythmias.

• Complete heart block.

• Ventricular tachycardia.

• Ventricular fibrillation.

• Asystole.

• Cardiac arrest.

• Respiratory muscle paralysis.

• Sudden death.

Prognosis

The prognosis depends on the severity of hyperkalaemia, the underlying cause, the presence of ECG abnormalities, and the timeliness of treatment. Early recognition and prompt correction usually result in favorable outcomes, whereas delayed treatment may lead to fatal cardiac arrhythmias, cardiac arrest, and death. Patients with recurrent hyperkalaemia due to advanced CKD require ongoing monitoring and long-term management.

Prevention

Preventive measures include:

• Regular monitoring of serum potassium in patients with CKD and those receiving RAAS inhibitors.

• Appropriate dose adjustment of medications that impair potassium excretion.

• Avoidance of unnecessary potassium supplements.

• Dietary counselling to reduce potassium intake in high-risk patients.

• Early treatment of acute kidney injury and chronic kidney disease.

• Prompt correction of metabolic acidosis.

• Regular monitoring of kidney function and electrolytes.

• Early referral of patients with recurrent or severe hyperkalaemia to nephrology services.