Massive Transfusion-Associated Hyperkalaemia

Massive transfusion associated hyperkalaemia is a rise in plasma potassium (over 5.5 mmol/L, severe at over 6.5 mmol/L) caused by the potassium load in stored red cells, especially with rapid infusion, in neonates and in patients with renal impairment. A rebound fall in potassium commonly follows.

Epidemiology. It occurs in a minority of massive transfusions, but is more common in infants, in patients with kidney disease and with rapid central infusion. It has caused cardiac arrest in children undergoing surgery.

Causes and associations.

• Potassium leak from stored red cells: supernatant potassium reaches 5 to 10 mmol/L in the first days, and 30 to 50 mmol/L or more in older units (over 14 days), with irradiated units (up to 4 times more leak than non-irradiated within hours).
• Rapid transfusion (over 100 mL/kg/h in infants) directly into the central circulation.
• Acidosis, hypothermia, tissue injury, haemolysis and renal failure add to the risk.

Pathophysiology. Red cell membrane sodium potassium ATPase fails at 4 °C, so potassium leaks out during storage. After transfusion the cells resume uptake and potassium normalises over hours, hence a late fall (rebound hypokalaemia).

Presentation is peaked T waves, widened QRS, bradycardia, atrioventricular block, ventricular fibrillation, asystole, muscle weakness and cardiac arrest. Cardiac arrest may occur without warning in neonates and children.

Red flags.

• Potassium over 6.0 mmol/L or ECG changes during transfusion.
• Infant or child receiving a large volume rapidly, or patient with renal failure.
• Use of old or irradiated units.

Measure potassium by blood gas analyser every 30 to 60 minutes during massive transfusion (haemolysed samples give false results, and a point-of-care sample is preferred). Continuous ECG. Also measure ionised calcium, pH, magnesium, creatinine, glucose and lactate.

Differential diagnosis. Pseudohyperkalaemia from haemolysis, renal failure, rhabdomyolysis, tumour lysis, acidosis, suxamethonium, reperfusion and adrenal insufficiency.

Membrane protection. Calcium chloride 10% 10 mL IV (central line) or calcium gluconate 10% 30 mL IV over 5 to 10 minutes for ECG changes or arrest, repeated if ECG changes persist.

Shift potassium into cells.

• Soluble insulin 10 units IV (5 units in renal failure or older adults) with glucose 25 g IV, and glucose monitoring hourly for 6 hours.
• Salbutamol 10 to 20 mg nebulised (or 0.5 mg IV slowly in ventilated patients).
• Sodium bicarbonate 50 mmol IV (50 mL of 8.4%) when there is metabolic acidosis.

Remove potassium. Furosemide 40 to 80 mg IV if urine output is present, and dialysis (haemodialysis or continuous renal replacement) for refractory hyperkalaemia, oliguria or arrest.

Prevention.

• Use fresh red cells (under 7 days) or washed red cells for neonates, infants, patients with renal failure and those at highest risk.
• Irradiate units as close to the time of use as possible (within 24 hours), or wash after irradiation.
• Limit infusion rate in infants, give via a peripheral line when possible, and avoid direct right atrial infusion of large cold volumes.
• Use potassium adsorption filters where available.

Monitoring. Continuous ECG, potassium every 30 to 60 minutes during massive transfusion and for 6 hours afterwards, glucose, ionised calcium and urine output. Anticipate rebound hypokalaemia in 6 to 24 hours.

Referral and escalation. Anaesthesia, intensive care, nephrology and transfusion medicine.

Special groups. In children, calcium chloride 10% 10 to 20 mg/kg (0.1 to 0.2 mL/kg) IV and insulin 0.1 units/kg with glucose 0.5 g/kg. In renal failure, early dialysis.