Introduction

Mild-moderate hyperkalaemia (K+ 7-8 mmol/l) is not uncommon in the neonatal period, especially in the most immature infants. When potassium levels in this range are encountered, it is essential to consider the likely underlying cause and these infants should also be discussed with the consultant.  Because newborn infants seldom show signs of toxicity until the plasma potassium concentration is greater than 8 mmol/l, it may be that treatment will not be started unless the level is approaching or exceeding 8 mmol/l, depending on the trend and on the cause. Severe hyperkalaemia (K+ > 8mmol/l) may be life-threatening and will require treatment.

Clinical features

There are unlikely to be any clinical signs specifically related to hyperkalaemia other than those attributable to cardiotoxicity. This may be evident from the presence of widened QRS complexes or tall, tented T-waves on ECG. Serious arrhythmias such as ventricular tachycardia or fibrillation may develop.

Causes

• Sample error due to haemolysis during or following sampling. Always send an urgent repeat specimen to verify the level, aiming to obtain a good free-flowing specimen
• Oliguria. In health, any excess potassium is readily excreted by the kidneys. Ensure that the blood pressure is adequate and that the baby is not dehydrated. Discontinue indometacin if it is in use
• Congenital adrenal hyperplasia
• Genuine haemolysis
• Medication/ fluid prescription error
• Immaturity. Extremely preterm infants may have immature potassium excreting capacity in the distal tubule
• Acidosis. Potassium leaks out of the cells into the extracellular fluid when there is acidosis

Treatments

Aim to improve the underlying cause to whatever extent possible as all of the following treatments are only temporary measures. The measures outlined below should then be considered in order.

• Remove all sources of potassium intake and review fluid balance and blood pressure
• In all infants who require more aggressive treatment, administer calcium resonium 4-6 hourly rectally. This is the only treatment which removes potassium from the body. It takes 1-2 hours to act and lasts around 6 hours.
• Normalise acid base balance. If there is metabolic acidosis, give bicarbonate i.v. If there is respiratory acidosis, attempt to increase CO2 elimination. This will drive some of the potassium into the cells within 5-10 minutes and the effect should last around 2 hours
• If there is evidence of myocardial excitability, give calcium gluconate i.v. This will not lower the potassium levels but will help to prevent arrhythmias. It takes 5-10 minutes to act and the protection may be effective for 30-60 minutes. Aim to normalise the plasma calcium with maintenance treatment.
• Salbutamol infusion promotes intracellular uptake of potassium by inducing Na+/K+-ATPase. It will lower potassium levels over about 40 minutes. Maintain a continuous infusion as long as potassium remains dangerously high. Start with 200 nanograms per kg per minute. Discuss dose alterations with the consultant.
• Glucose and insulin drive potassium into the cells. Increase the rate of glucose infusion to around 10mg/kg/min. This is approximately equivalent to 150mls/kg/day of 10% glucose, so if this was already your background intake you may need to go higher. Remember that you can increase the glucose concentration as well as the infusion rate. Titrate insulin to maintain normal blood glucose.
• Bicarbonate, salbutamol and glucose and insulin work through different mechanisms and may be used in combination with one another.
• Exchange transfusion will lower potassium levels for 12 hours or more.