You’re the paediatric registrar on call. You get a phone call from ED who have kindly performed some blood tests on a 4-year-old who ‘looks a bit dry’. The caller sounds panicked. The potassium is 6.9mmol. They have started a salbutamol neb but want some help. You ask for cardiac monitoring, check the dose of calcium gluconate and start thinking about insulin. But what is the best fluid to prescribe?
The management of hyperkalaemia is something that gets drilled into us from medical school. Despite lots of erroneous samples in neonates and children, treating true hyperkalaemia happens rarely, leaving some feeling flustered and under-confident. Rubens and Kanaris, in a recent Archives article, take a delve into the depths of hyperkalaemia management, including some enlightening and perhaps what may feel initially controversial IV fluid choices.
Rubens M, Kanaris C. Fifteen-minute consultation: Emergency management of children presenting with hyperkalaemia. Arch Dis Child Educ Pract Ed. 2021 Aug 3:edpract-2021-322080. doi: 10.1136/archdischild-2021-322080. Epub ahead of print. PMID: 34344762.
What do we mean by hyperkalaemia and why does it happen?
Commonly defined as serum potassium >5.5mmol/L, hyperkalaemia is a cause for concern. It can lead to life-threatening cardiac arrythmias and death. It can be difficult to predict how common it really is since it can be a manifestation of disease.
Essentially it is caused by:
Take it back to physiology
98% of potassium should be kept in cells (stored in the intracellular compartment mostly in liver and skeletal muscle). As the most common intracellular cation, even small extracellular shifts can cause serum potassium levels to creep up. Most of our dietary potassium (this is where the bananas come in) is excreted via the kidneys, with a small amount excreted via the gastrointestinal tract. So, when someone has hyperkalaemia, the body moves some of the excess potassium intracellularly while the kidneys catch up and try to excrete more. This can take a few hours.
An acidotic environment is bad news for potassium. It encourages K+ to move out of cells into the extracellular compartment. When the extracellular compartment is hyperosmotic, relative to the intracellular compartment, water will follow (moving out of the cells) concentrating the intracellular potassium and causing movement through potassium-permeable channels into the extracellular compartment.
So what can we do?
Simply put, the aims of hyperkalaemia treatment are to:
Stabilising the myocardium (The PRIMARY GOAL of treatment)
The big worry with hyperkalaemia is that it can cause lethal cardiac arrythmias. This is due to the reduction in resting membrane potential of the myocardium, resulting in a very excited myocardial membrane.
ECG changes (which may be the first signs of this myocardium becoming excitable) are as follows:
Luckily, we have calcium gluconate in our back pocket. This reduces this membrane excitability by increasing the resting potential of the myocardium.
0.5mls/kg of calcium gluconate 10% (0.11mmol/kg) over five to ten minutes given centrally.
This will do the job. If there is no central access, calcium gluconate may require dilution – see local guidance.
Phew! Our myocardium has chilled out, but this is a temporary measure. It WON’T reduce the overall serum potassium level.
Get that potassium moving…
Everyone’s friend. This drug is commonly used and easy to access and of course we all remember that it binds to beta-adrenergic receptors and facilitates the conversion of ATP (adenosine triphosphate) to CAMP (cyclic AMP) which works on the Na+/K+ pump to increase the uptake of intracellular potassium. Great – no brainer – we all love salbutamol. But BEWARE – tachycardia is a common side effect. In children with that unstable myocardium, be cautious.
Salbutamol 2.5- 5mg via nebuliser (can be repeated).
Metabolic acidosis (as mentioned above) is not your friend in hyperkalaemia. We can cause the opposite effect (moving potassium back into cells) by making the environment more alkalotic. Cue sodium bicarbonate. BUT this will only work in an acidotic environment AND there is evidence to suggest that ISOTONIC bicarbonate preparations (8.4% is HYPERTONIC) are more effective (remember we mentioned the effect of a hyperosmolar extracellular environment).
Sodium Bicarbonate 1mmol/ kg or ‘half correction’ (0.15x weight x base deficit).
But check the ionised calcium level, as correction of acidosis can exacerbate hypocalcaemia.
Insulin also works by activating the Na+/K+ ATPase pump. The effect can start within the first 15 minutes and last hours. BEWARE watch out for hypoglycaemia and dextrose must be administered simultaneously to avoid this.
Insulin infusion: 0.1- 0.6units/ kg/ hour (neonates), 0.05- 0.2units/kg/hour (>1month).
Kick that potassium out…
All the treatments so far are great, but they are the removal team of the hyperkalaemia world, just moving things around. We need the bouncers to get the potassium kicked out.
We can do this by encouraging potassium diuresis with loop diuretics (e.g., furosemide). Gastrointestinal losses of potassium can be increased by using cation exchange resins, such as calcium resonium. These cause potassium to be bound in the gut to increase excretion in stool.
Furosemide 1mg/ kg/ dose (higher doses may be required- discuss with nephrology consultant).
Calcium resonium 0.5- 1g/ kg PO or PR (contraindicated in neonates with reduced gut motility and obstructive bowel disease)
Haemodialysis, or CVVH, may be used to kick out potassium.
A note on IV Fluids… (may be slightly different to what you’re used to)
As one of the causes of hyperkalaemia may be due to prescribing IV fluids containing potassium, the logical thing would be to not prescribe IV fluid with any potassium in.
(AB)normal saline (0.9% saline) contains no potassium but lots of chloride (154mmol in 1L). This influx of chloride ions causes a hyperchloremic acidosis. The acidosis causes an extracellular movement of potassium and acidaemia as we have learnt reduces the excretion of potassium.
So, what should we use?
Balanced solutions (Plasma-lyte or Hartmanns) even though they do contain some potassium (both 5mmol per 1L) are solutions that have similar ion concentrations to the extracellular space. They don’t cause hyperchloremic alkalosis and the effects described above. They have a net alkalinising effect due to the ‘buffers’ contained within these solutions, namely lactate in Hartmann’s and acetate in Plasma-lyte. By increasing the pH, we get an intracellular movement of potassium – causing a drop in serum potassium. A viral twitter thread explaining the concept well can be found here:
Hang on, I thought lactate caused more acidosis?
Lactate and acetate are metabolised to citrate – which enters the citric acid cycle – and results in a production of water and carbon dioxide. These are converted to bicarbonate, which has an alkalinising effect on serum. And as we learned, a higher pH encourages potassium movement into cells and an overall drop in serum potassium.
With the move to balanced fluids as primary resus fluids (see DFTB’s summary on Resus Council updates in paediatrics) this may be another reason to ask what your local department has in stock. The fluid management in in hyperkalaemia should be managed as per local guidance
So, hyperkalaemia management is easy right?
Just remember to
- MOVE IT
- LOSE IT
For more DFTB resources on hyperkalemia, check out the third PEM adventure.
Lehnhardt A, Kemper MJ, Pathogenesis KMJ. Pathogenesis, diagnosis and management of hyperkalemia. Pediatr Nephrol 2011;26:377–84.
Rubens M,Kanaris C. 15 minute consultation: Emergency Management of Children presenting with Hyperkalaemia Arch Dis Child Educ Pract Ed Epub ahead of print. doi:10.1136/ archdischild-2021-322080
Semler MW, Kellum JA. Balanced crystalloid solutions. Am J Respir Crit Care Med 2019;199:952–60.
Team PEM Adventures. PEM adventures chapter 3, Don’t Forget the Bubbles, 2021. Available at: