Urgent considerations
See Differentials for more details
Other than pseudohyperkalaemia, any of the conditions that cause hyperkalaemia can increase serum potassium values sufficiently to result in life-threatening arrhythmias. The end-organ effects of potassium are more significant if hyperkalaemia has developed quickly.
Life-threatening hyperkalaemia occurs most commonly when there is acute-on-chronic renal failure and/or in the more advanced stages of chronic renal failure. The impact of renal failure on potassium excretion is most significant when concurrent potassium intake is high and/or drugs that reduce urinary potassium excretion, such as aldosterone receptor antagonists, are in use.[4]
Urgent treatment of hyperkalaemia
If potassium is ≥6.5 mmol/L (≥6.5 mEq/L) and cardiotoxicity is evident on ECG, protect the heart with intravenous calcium.[28][30] Calcium should also be given in lower level hyperkalaemia if ECG changes are present.[31][32] The protective effect of calcium begins within minutes but is short-lived. This therapy does not lower serum potassium. US guidelines recommend giving calcium via the intravenous or intraosseous route.[29]
If serum potassium is ≥6.5 mmol/L (≥6.5 mEq/L) with or without cardiotoxic changes on ECG, shift potassium into cells by giving an infusion of insulin/glucose and nebulised salbutamol.[28][29][31]
Each of these therapies can reduce the serum potassium by 0.5 to 1 mmol/L (0.5 to 1 mEq/L); their effect is generally evident within 15 minutes and can last up to 2 hours.
European and US guidelines recommend sodium bicarbonate by intravenous injection for cardiac arrest in patients with hyperkalaemia.[28][29][30]
Consider dialysis or extracorporeal cardiopulmonary resuscitation.[28][29][30][31]
Treat the underlying cause and prevent recurrence of hyperkalaemia.[28][31]
Cation-exchange resins/polymers, such as patiromer and sodium zirconium cyclosilicate, are oral agents that bind potassium in the gastrointestinal tract, leading to an increase in fecal potassium excretion and a fall in serum potassium. They are indicated for the treatment of chronic hyperkalaemia and may have a role in managing acute hyperkalaemia.[28][31]
In the UK, the National Institute for Health and Care Excellence advises that sodium zirconium cyclosilicate or patiromer may be used:[33][34]
in emergency care for acute life-threatening hyperkalaemia alongside standard care, or
for people with persistent hyperkalaemia and chronic kidney disease stage 3b to 5 or heart failure if they:
have a confirmed serum potassium level of at least 6.0 mmol/L, and
are not taking an optimised dosage of a renin angiotensin-aldosterone system (RAAS) inhibitor because of hyperkalaemia, and
are not on dialysis.
If RAAS inhibitors are no longer suitable, sodium zirconium cyclosilicate or patiromer should be stopped.[33][34]
Special considerations are required with specific causes of hyperkalaemia:
digitalis intoxication - digoxin-specific antibody fragments (digoxin-Fab) are recommended for digoxin poisoning. The pathophysiology of hyperkalaemia arising from digoxin poisoning differs from that of other causes of hyperkalaemia and, while the risk of harm from calcium administration has not been quantified, there is no evidence of benefit.[35]
rhabdomyolysis - pre-emptive treatment should be considered when creatinine kinase levels are rapidly rising and renal failure is present.
Evidence for the acute pharmacological management of hyperkalaemia is limited, with no clinical studies demonstrating a reduction in adverse patient outcomes.[36] Of the studied agents, salbutamol via any route and intravenous insulin/glucose appear to be most effective at reducing serum potassium. There is limited evidence to support the use of other interventions, such as intravenous sodium bicarbonate.[31][36]
Cardiac arrhythmias
Life-threatening arrhythmias occur most commonly when factors impairing cellular uptake of potassium coexist. Presence of hyponatraemia and/or hypocalcaemia can intensify the cardiotoxicity of hyperkalaemia. ECG findings are usually progressive and include first degree heart block (prolonged PR interval >0.2 s), flattened or absent P waves, tall, peaked (tented) T waves (i.e. T wave larger than R wave in more than 1 lead), ST-segment depression, widened QRS (>0.12 s), ventricular tachycardia, bradycardia and eventually cardiac arrest (pulseless electrical activity, ventricular fibrillation/paroxysmal ventricular tachycardia, asystole).[28] The presence of cardiotoxic ECG changes from hyperkalaemia require continuous monitoring until serum potassium values have been brought into a safe range and the ECG changes have been corrected.[Figure caption and citation for the preceding image starts]: ECG changes in patients with hyperkalaemiaBMJ 2009; 339:b4114. Copyright ©2009 by the BMJ Publishing Group [Citation ends].
Severe muscle weakness or paralysis
Severe muscle weakness is a complication of significant hyperkalaemia, commonly presenting as ascending paralysis. This process occurs as a function of depolarisation blockade.[37] Muscle weakness secondary to hyperkalaemia can be of sufficient severity to suppress respiratory effort. The effect of non-depolarising muscle relaxants can be accentuated by concurrent hyperkalaemia. Cardiac arrhythmias often, but not always, accompany muscle paralysis. Urgent reduction in serum potassium values is required.
Hyperkalaemic periodic paralysis
Hyperkalaemic periodic paralysis can episodically cause muscle weakness/stiffness. These episodes are brief, lasting for only minutes, and often occur during rest after exercise. In most patients, the level of potassium does not rise above normal when an attack occurs.[27] The term 'hyperkalaemic' is applied to this disturbance as the attacks may be prompted by administration of potassium or the ingestion of foods high in potassium content. Although it is difficult to capture the 'hyperkalaemic' component of this illness, repetitive sampling during attack-free intervals will often pick up high normal serum potassium values. The level of treatment is determined by the frequency of episodes. Patients with infrequent episodes can be managed by dietary means. Those with more frequent episodes require diuretic therapy (particularly acetazolamide), inhaled beta-agonists, and oral calcium gluconate.
Situations needing particular caution
In patients with significant hyperglycaemia there is movement of potassium from the intracellular to the extracellular compartment. The ensuing rise in serum potassium values is often of a sufficient magnitude that any underlying state of potassium depletion is poorly recognised. Treatment of the hyperglycaemia is required before the level of total body potassium depletion can be accurately gauged.
Hyperkalaemia which occurs with use of the aldosterone antagonist spironolactone can be prolonged owing to the very long half-life of its active metabolites. Measures implemented to reduce serum potassium values in such patients should be continued for 2 to 3 days after being started.
When diuretic therapy is used to increase urine flow rate and thereby potassium excretion, care should be taken not to allow the patient to become volume-depleted. Dehydration will slow urine flow rate and reduce sodium delivery to the distal tubular exchange site. As a result, potassium values may no longer drop with therapy and may even rise.
When calcium is being used as a physiological antagonist to the membrane effects of hyperkalaemia, care should be taken to use the correct dose of elemental calcium. Doses of calcium salts are not equivalent in terms of elemental calcium dose. Be alert to the risk of inadvertent underdosing if calcium gluconate is used instead of calcium chloride.[38]
There is a time lag for a potassium-lowering effect with cation-exchange resins/polymers that may be as long as several hours.[31]
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