Serum levels of potassium higher than the upper limit of normal is known as hyperkalaemia. The biggest concern with hyperkalaemia is the development of a dangerous cardiac arrhythmia, as potassium increases the excitability of cardiac cells.
Causes
Reduced Excretion
- AKI/CKD: Reduced glomerular filtration rate resulting in reduced excretion of potassium
- Drugs:
- Spironolactone: Antagonist to aldosterone. Aldosterone is a hormone released by the adrenals which is responsible for the retention of sodium, and excretion of potassium.
- Amiloride: Inhibits sodium reabsorption in the nephron which in turn reduces potassium excretion.
- ACEi/ARBs/NSAIDs: These all interfere with the autoregulatory mechanisms of renal blood supply which can result in hyperkalaemia.
- Addison’s disease: Due to deficient aldosterone production. Aldosterone is responsible for retention of sodium, and excretion of potassium.
Increased Intake
High intake of potassium rich foods although this is not a common cause in patients with normal renal function. Foods with high potassium include avocados, bananas, kiwis and dried fruit.
Intracellular to Extracellular Shifts
- Leaking from cells:
- Rhabdomyolysis e.g. following a crush injury or excessive exercise: Cells contain high amounts of potassium – therefore, injury to cells can result in the release of potassium into the extracellular space.
- Burns
- Tumour lysis syndrome
- Metabolic Acidosis e.g. diabetic ketoacidosis (DKA). This occurs due to increased exchange of hydrogen ions for potassium ions.
Pseudohyperkalaemia
This occurs when haemolysis occurs within the blood sample, releasing the intracellular potassium and causing a pseudohyperkalaemia. This can happen if:
- Tourniquet is left on for too long
- Excessive fist clenching during the withdrawal of the blood
- There is a delay in analysing the blood sample
- Haemolysis within the sample tube e.g. excessive shaking of the tube
Clinical Features
Clinical features are not always present and patients can be asymptomatic. When they are, they can include palpitations, muscle weakness, hyporeflexia, and ECG changes.
Investigations
Bedside
- 12-lead ECG +/- cardiac monitor: An ECG is an incredibly important investigative tool as ECG changes in the context of hyperkalaemia warrant urgent treatment. Patients will usually require cardiac monitors due to the risk of arrhythmias as well.
- Tall, tented T waves
- Wide QRS complexes
- Prolonged PR intervals
- Flattened P waves
- Sine wave: The wide QRS continues to widen until it ultimately merges with the following T wave to form a sine wave.
- Arrhythmias: Ventricular fibrillation and asystole are the risks with hyperkalaemia.
- Urine dipstick: If concerned about diabetes as an underlying cause. May be positive for glucose and ketones.
Bloods
- Venous blood gas: Can be used to confirm a hyperkalaemia in the acute setting as it provides an instant result. Can also be used to look for a metabolic acidosis in the case of DKA.
- Urea and electrolytes
- Diagnoses hyperkalaemia
- Also consider the renal function – is there an acute or chronic deterioration in kidney function, and is this the cause of the hyperkalaemia?
- HbA1c: Does the patient have diabetes (and therefore at risk of diabetic nephropathy/DKA)
- Creatine kinase (CK): If suspecting rhabdomyolysis
- FBC, LFT, CRP as a baseline
Classification of Hyperkalaemia
- Mild: 5.5-5.9 mmol/L
- Moderate: 6.0-6.5 mmol/L
- Severe: >=6.5mmol/L or ECG changes/symptoms present alongside any level of hyperkalaemia
Urgent intervention is warranted in case of ECG changes, if the patient is symptomatic, or a potassium level greater than 6 mmol/L.
Management
Different hospitals can have different guidelines for how to manage hyperkalaemia so doses of drugs or the time over which they should be administered can vary. Generally speaking, the following management plan is employed:
Stabilise the Cardiac Membrane
- Cardiac Monitoring: There is a risk of fatal arrythmias due to increased cardiac cell excitability so important to monitor the cardiac rhythm.
- IV Calcium gluconate 10% 10ml over 10 minutes:
- This is given prior to the administration of insulin + glucose and works to reduce the excitability of cardiac cells. It does NOT reduce the hyperkalaemia.
- ECG changes should improve in a 1-3 minutes following administration. If there is no improvement, further 10 mls can be administered.
- Patients on digoxin should receive this more slowly.
Shift Potassium Into the Cells
- IV 10 units of Actrapid insulin + dextrose (usually 50% 50ml or 20% 200ml – local guidelines should be consulted), usually over 30 minutes:
- Insulin will help to drive potassium into the cells, but patients should simultaneously be given glucose to avoid hypoglycaemia.
- Glucose should also be monitored before and after administration, up till at least 6 hours following administration of insulin.
- Monitor serum potassium for at least 24 hours (UK guidelines suggest 1, 2, 4, 6 and 24 hours).
- Nebulised salbutamol can also help to drive potassium into the cells. However, it can also cause a tachycardia so this should be used with caution, and it should not be used as a single agent for treating hyperkalaemia.
Remove Potassium From the Body
- If potassium fails to go down, patient may require referral for haemodialysis.
- Stop potassium sparing, or potassium containing drugs
- Calcium resonium helps to remove potassium from the gastrointestinal tract. This is not used in an emergency situation as it takes a long time to act but can be useful for milder cases/chronic problems.
References
https://www.ncbi.nlm.nih.gov/books/NBK470284/
https://www.nuh.nhs.uk/download.cfm?doc=docm93jijm4n690
https://rqia.org.uk/RQIA/files/6f/6f51b366-f8bf-44de-a630-6967d5353a87.pdf
https://renal.org/wp-content/uploads/2017/06/hyperkalaemia-guideline-1.pdf
