Author: Martin Crook
Disorders of plasma potassium concentration (Box 86.1) may be an acute effect of drugs, or result from disordered renal plasma potassium handling, release of potassium from damaged cells or excessive gut loss of potassium.
Hyperkalaemia must be excluded in any patient with acute kidney injury (AKI) or advanced chronic kidney disease (CKD). Severe hyperkalaemia may be asymptomatic until it results in cardiac arrest.
If the plasma potassium is discordant with the clinical picture, consider pseudohyperkalaemia, for example haemolysis, potassium-EDTA contaminated sample, old sample, sample kept in fridge or severe thrombocytosis/leukocytosis.
Treat the underlying disorder: causes of hyperkalaemia are given in Table 86.1.
Check renal function and address any reversible causes of renal impairment.
Review acid-base status, as hyperkalaemia can be associated with metabolic acidosis.
If the patient is taking digoxin, check plasma digoxin drug level.
Stop drugs which may be contributing to hyperkalaemia, and reduce the dietary intake of potassium.
To increase excretion of potassium, the options are to improve renal function, start renal replacement therapy, or use an ion-exchange resin such as calcium resonium to bind potassium in the gut.
Severe hyperkalaemia with ECG abnormalities
If the plasma potassium is >7 mmol/L or the ECG has abnormalities associated with hyperkalaemia (widening of the QRS complex, loss of the P wave, peaking of the T wave or a sine wave pattern) then:
- Give 10 mL of calcium chloride 10% IV over 5–10 min to stabilize cardiac muscle. This can be repeated every 5 min up to a total dose of 50 mL. Calcium chloride is more toxic to veins than calcium gluconate, but provides more calcium per ampoule (272 mg of calcium in 10 mL of calcium chloride 10%; 94 mg of calcium in 10 mL of calcium gluconate 10%). The ECG may change within a couple of minutes.
- Consider 10–20 mg nebulized salbutamol (contraindicated if unstable angina or acute MI); this may reduce potassium by about 0.5–1.0 mmol/L in 15–30 min and lasts for a couple of hours.
- Give insulin and glucose IV: add 10 units of Actrapid® to 50 mL of glucose 50% and infuse over 30 min. Avoid hypoglycaemia by monitoring blood glucose. The plasma potassium should decrease by about 0.6–1.0 mmol/L in 15 min and the reduction lasts for about an hour. Recheck plasma potassium 30 min afterwards and monitor plasma electrolytes and renal function 1–2h later.
- The use of intravenous sodium bicarbonate in severe hyperkalaemia in the face of severe acidosis is controversial and expert opinion should be consulted.
- Stop potassium supplements or any drugs (e.g. ACE inhibitors, angiotensin receptor blockers, potassium-retaining diuretics, spironolactone), which may be contributing to hyperkalaemia. Start calcium resonium (15g 8-hourly PO or 30g by retention enema).
- Recheck plasma potassium after 2h. If hyperkalaemia is due to AKI or CKD, renal replacement therapy may need to be started to prevent a recurrence: discuss this with a nephrologist.
Mild or moderate hyperkalaemia
Stop potassium supplements or any drugs which may be contributing to hyperkalaemia, and reduce the dietary intake of potassium.
Start calcium resonium (15g 8-hourly PO or 30g daily by retention enema) in patients with hyperkalaemia complicating renal failure.
Hypokalaemia may result in muscle weakness and arrhythmias. When plasma potassium falls below 2.5 mmol/L, muscle necrosis may occur; below 2 mmol/L, there may be ascending paralysis. Cardiac arrhythmias may occur when plasma potassium is <3 mmol/L, especially in patients with underlying cardiac disorders or taking anti-arrhythmic drugs. The ECG may show flattened T waves, ST depression and prominent U waves. In patients with cardiac arrhythmias, target plasma potassium is 4–4.5 mmol/L.
Treat the underlying disorder: causes of hypokalaemia are given in Table 86.2.
A spot urine potassium concentration may help distinguish between predominately non-renal versus renal causes: a urine potassium >20 mmol/L in a patient with hypokalaemia suggests renal potassium loss. Each 0.3 mmol/L reduction in plasma potassium concentration reflects 100 mmol/L deficit in body potassium stores.
Hypokalaemia is most often due to diuretic therapy or gut loss of potassium, and replacement of sodium and water may also be needed. Magnesium depletion commonly coexists with potassium depletion: check plasma magnesium (normal range 0.70–1.20 mmol/L) in patients with hypokalaemia, and correct hypomagnesaemia (Chapter 88) with IV or oral supplements.
Review acid-base status as hypokalaemia can be associated with metabolic alkalosis.
Severe Hypokalaemia or Hypokalaemia Associated with Cardiac Arrhythmias
Attach an ECG monitor.
Give potassium by IV infusion, initally 40 mmol over 4h, and then recheck potassium. Give further potassium as needed, up to 200 mmol over 24h. The maximum rate of infusion should not exceed 20 mmol/h. Potassium given via a peripheral vein may cause pain at the infusion site and tissue necrosis if there is extravasation: administration via a central vein is preferable.
Mild or moderate hypokalaemia without cardiac arrhythmias
Give oral potassium, for example Sando-K 2 tablets (12 mmol per tablet) 8-hourly PO for 3–7 days, and increase the dietary intake of potassium; beware of gastric irritation particularly with Slow-K preparations.
If hypokalaemia is due to the use of a loop diuretic, consider adding a potassium-retaining diuretic (e.g. amiloride or spironolactone), but avoid in patients with renal impairment.