Write a short note on hyperkalaemia.

Definition

Hyperkalaemia is a serum potassium above the upper limit of normal (conventionally > 5.5 mEq/L), graded as mild, moderate and severe. It is a medical emergency because of the risk of fatal cardiac arrhythmia, and is the commonest life-threatening electrolyte disorder.

Causes

Pseudohyperkalaemia (exclude first): haemolysis of the sample, prolonged tourniquet application with fist clenching, delayed sample processing, marked leucocytosis or thrombocytosis. A raised potassium in a well patient with a normal ECG should always prompt a repeat sample.

Reduced renal excretion — the commonest true cause:

• Acute kidney injury and chronic kidney disease (especially eGFR < 20).
• Drugs: ACE inhibitors, ARBs, potassium-sparing diuretics (spironolactone, amiloride), NSAIDs, trimethoprim, heparin, tacrolimus, beta-blockers, and potassium supplements.
• Hypoaldosteronism — Addison's disease, type 4 renal tubular acidosis (common in diabetic nephropathy).

Transcellular shift out of cells:

• Metabolic acidosis (inorganic acids), insulin deficiency and hyperglycaemia as in diabetic ketoacidosis, rhabdomyolysis, tumour lysis syndrome, massive haemolysis, extensive burns and crush injury, suxamethonium, digoxin toxicity, and beta-blockade.

Increased intake: rarely a cause alone unless renal function is impaired — potassium supplements, salt substitutes (widely used and easily overlooked), stored blood transfusion.

Clinical Features

Often asymptomatic until cardiac arrest — the danger of this disorder. When present: muscle weakness, flaccid paralysis (ascending, sparing respiratory muscles until late), paraesthesiae, and palpitations.

ECG Changes — Progressive and Critical

The ECG matters more than the absolute number, and changes broadly follow this sequence:

1. Tall, peaked, narrow-based T waves — the earliest change.

2. Flattening and loss of the P wave; PR prolongation.

3. Widening of the QRS complex.

4. Sine wave pattern — merging of QRS and T.

5. Ventricular fibrillation or asystole.

Management — Three Steps in Order

1. Stabilise the myocardium (works in minutes, does not lower potassium):

• Intravenous calcium gluconate or calcium chloride — antagonises the membrane effect of potassium. Onset within 1–3 minutes, duration 30–60 minutes; repeat if ECG changes persist. Use with great caution in digoxin toxicity.

2. Shift potassium into cells (works in 15–30 minutes, temporary):

• Insulin with dextrose — the most reliable shifting measure; monitor blood glucose for several hours afterwards, as delayed hypoglycaemia is a common iatrogenic complication.
• Nebulised salbutamol — additive to insulin; may cause tachycardia.
• Sodium bicarbonate — only if there is significant metabolic acidosis; of limited value otherwise.

3. Remove potassium from the body (definitive):

• Loop diuretics with adequate hydration if renal function permits.
• Potassium binders — sodium or calcium polystyrene sulphonate; newer agents (patiromer, sodium zirconium cyclosilicate) act faster and are better tolerated.
• Haemodialysis — the definitive treatment in renal failure, refractory or severe hyperkalaemia, or where potassium continues to rise.

Also: stop all contributing drugs and potassium-containing fluids; restrict dietary potassium (bananas, citrus, coconut water, tender coconut, dates, potatoes and salt substitutes); treat the underlying cause; and recheck potassium and the ECG frequently, since shifting agents wear off and rebound is common.