Patient professional reference
Hyperkalaemia is defined as plasma potassium in excess of 5.5 mmol/L. The European Resuscitation Guidelines further classify hyperkalaemia as:
- Mild - 5.5-5.9 mmol/L.
- Moderate - 6.0-6.4 mmol/L.
- Severe - >6.5 mmol/L.
Potassium is the most abundant intracellular cation - 98% of it being located intracellularly. Hyperkalaemia has four broad causes:
- Renal causes - eg, due to decreased excretion or drugs.
- Increased circulation of potassium - can be exogenous or endogenous.
- A shift from the intracellular to the extracellular space.
The time of greatest risk is at the extremes of life. Reported incidence in hospitals is 1-10%, with reduced renal function causing a five-fold increase in risk in patients on potassium-influencing drugs. Men are more likely than women to develop hyperkalaemia, whilst women are more likely to experience hypokalaemia.
- Acute kidney injury (AKI).
- Chronic kidney disease (CKD):
- Normally all potassium that is ingested is absorbed and excretion is 90% renal and 10% alimentary.
- Most excretion by the gut is via the colon and in CKD this can maintain a fairly normal blood level of potassium.
- It seems likely that the elevated potassium levels in CKD trigger the excretion of potassium via the colon.
- Patients with CKD must be careful of foods rich in potassium.
- Hyperkalaemic renal tubular acidosis.
- Mineralocorticoid deficiency.
- Medicines that interfere with potassium excretion - eg, amiloride, spironolactone.
- Medicines that interfere with the renin-angiotensin axis - eg, angiotensin-converting enzyme (ACE) inhibitors, angiotensin-II receptor antagonists (AIIRAs), non-steroidal anti-inflammatory drugs (NSAIDs), heparin.
- Other drugs that can cause hyperkalaemia include - ciclosporin, tacrolimus, pentamidine, co-trimoxazole, ketoconazole, metyrapone.
- Also, remember to ask about herbal remedies.
Drugs that inhibit the renal excretion of potassium can cause hyperkalaemia but they are most dangerous if used in combination or if renal function declines.
Increased circulation of potassium
- Exogenous - eg, potassium supplementation.
- Endogenous - eg, tumour lysis syndrome, rhabdomyolysis, trauma, burns:
- Massive tissue damage leads to loss of potassium into the circulation.
- In crush syndrome this may be accompanied by renal impairment.
- Fresh water drowning is more swiftly fatal than salt water drowning because the fresh water enters the circulation from the lungs and osmotic pressure causes erythrocytes to swell and burst. The sudden release of potassium can stop the heart.
A shift from the intracellular to the extracellular space
- Acidosis - eg, diabetic ketoacidosis (DKA).
- Medications - eg, digoxin toxicity, suxamethonium, beta-blockade, theophylline.
- Hyperkalaemic periodic paralysis.
Hyperkalaemia is uncommon but serious. The diagnosis is based on a laboratory report and, especially if the result is unexpected, before initiating treatment, it is necessary to consider the possibility that the result may be spurious. There are a number of possible explanations for unexpectedly high results:
- Prolonged tourniquet time.
- There may have been difficulty collecting the sample.
- The fist may have been clenched.
- Test tube haemolysis - eg, blood may have been squirted through a needle into the bottle, or the tube may have been shaken.
- Use of the wrong anticoagulant, especially potassium EDTA.
- Excessive cooling of a specimen (in cold winter months, potassium in specimens from GP surgeries tends to be higher than in the summer).
- Length of storage of the specimen.
- Marked leukocytosis and thrombocytosis.
- Sample from limb receiving intravenous (IV) fluids containing potassium.
If there is doubt about the validity of the result, repeat it.
- Dehydration in a patient taking drugs that may cause hyperkalaemia can reduce renal output and lead to a dangerous increase in potassium levels.
- Even in sickle cell trait, strenuous exertion, especially in the unfit and dehydrated, can precipitate sickling, haemolysis and sudden death from hyperkalaemia.
- Patients with diabetes pose particular problems, as they may have impaired renal function, be on ACE inhibitors, and require a healthy diet for diabetes, which tends to be low in sodium and high in potassium. Managing patients with diabetes and congestive heart failure is a difficult balance but the heart failure must be treated aggressively with ACE inhibitors and a vasodilatory beta-blocker such as carvedilol.
- Potassium is often raised in DKA (prior to treatment). Insulin pushes both glucose and potassium into cells, and potassium levels must be monitored during treatment. Glucagon impairs the intracellular shift of potassium.
Symptoms are nonspecific and include weakness and fatigue. Occasionally, a patient presents with muscular paralysis or shortness of breath. They may also complain of palpitations or chest pain.
- There is little abnormality except occasional bradycardia due to heart block or tachypnoea from respiratory muscle weakness.
- Muscle weakness and flaccid paralysis.
- Depressed or absent tendon reflexes.
- Physical examination is unlikely to suggest the diagnosis, except if severe bradycardia is present or if muscles are tender as well as weak, suggesting rhabdomyolysis.
- Any unexpected result should be repeated. If blood has been left standing for a long time or shaken vigorously, damage to erythrocytes will result in potassium loss from cells, giving a spurious result. Check urea, other electrolytes and creatinine too.
- Check 24-hour urine volume and electrolytes.
- FBC - looking for normocytic, normochromic anaemia (which may suggest acute haemolysis), thrombocytosis and/or leukocytosis.
- Capillary blood glucose and plasma glucose.
- If the patient takes digoxin, check blood levels.
- Arterial blood gas - looking for a metabolic acidosis (will also give a potassium level which can be compared to the laboratory result).
Serum potassium will monitor the extracellular concentration but the best way to assess the intracellular situation is an ECG and, in severe cases, continuous monitoring is required. In hyperkalaemia the ECG may show:
- Peaked T waves - can be difficult to determine.
- Prolongation of the PR interval.
- Widening of the QRS.
- Reduced, or loss of, P wave.
- AV dissociation.
- Sine wave pattern.
- In patients with heart disease and abnormal baseline ECG, bradycardia may be the only new ECG abnormality.
Cardiac conduction disturbances are more likely when there is a rapid rise in potassium - eg, AKI and/or if hypoxia of any cause is present.
The aggression of treatment will depend upon the level of potassium, the rate of rise and ECG abnormalities. All patients should be assessed using ABCDE (Airway, Breathing, Circulation, Disability and Everything else) and have an Early Warning Score documented and an escalation plan put in place.
Treatment of hyperkalaemia involves the following steps:
- Establishing whether it is true hyperkalaemia: any doubt warrants an urgent repeat (getting an ABG can provide an almost instant result).
- Determine severity of hyperkalaemia: mild, moderate, severe.
- Get a 12-lead ECG and look for changes as above. However, remember the following:
- ECG may be normal even in severe hyperkalaemia.
- The absence of ECG changes does not mean no need for treatment.
- Presence of ECG changes means a need for urgent treatment.
- Severity of ECG changes does not always relate to the severity of hyperkalaemia.
- Try to determine why hyperkalaemia has occurred (once the patient has been stabilised):
- Take a full history and full medication history.
- Establish whether there is a past medical history of CKD.
- Check medication and fluid prescription chart.
- Examine as above and also look for the presence of bladder distension.
- Reduce potassium:
Stop further potassium accumulation:
- Stop any potassium supplements or drugs that conserve potassium.
- Consider stopping digoxin and beta-blockers, as these may prevent buffering of intracellular potassium and reduce effectiveness of insulin-glucose.
- Decrease high intake of potassium in the diet.
- Give 10 ml 10% calcium gluconate (calcium chloride is an alternative ideally given via central access) which will improve ECG changes within 1-3 minutes; however, this effect only has a transient effect of 30-60 minutes.
- If there is no improvement then give 10 ml every 10 minutes until ECG normalises (may need up to 50 ml).
- In patients who are taking digoxin, give calcium gluconate in an infusion (add to 100 ml glucose 5%) and run over 20 minutes (otherwise, can precipitate myocardial digoxin toxicity).
- The use of calcium gluconate in the absence of ECG changes is controversial and is best avoided, as the risks of extravasation outweigh the benefits.
- Insulin-glucose infusion - usually 10 units of soluble insulin are added to 25 g of glucose and administered by IV infusion.
- Capillary blood glucose needs to be checked before, during and after.
- Potassium will decrease (0.6-1.0 mmol/L) in 15 minutes and the reduction lasts for 60 minutes.
- Check potassium 30 minutes afterwards and if there is a good response, check U&E 1-2 hours later.
- Also give 10-20 mg nebulised salbutamol - this reduces potassium (0.5-1.0 mmol/L) in 15-30 minutes and lasts for two hours.
- Sodium bicarbonate is not recommended, as the risks outweigh the benefits.
- Calcium polystyrene sulfonate resin (Calcium Resonium®) with regular lactulose will remove potassium via the gastrointestinal tract. It may be useful for mild-to-moderate hyperkalaemia when given over several days but has no role in the acute situation, due to its slow onset of action. Sodium polystyrene sulfonate (SPS) is an alternative if hypercalcaemia is to be avoided; however, it is contra-indicated in congestive heart failure, oedema and hypertension.
- Each gram removes approximately 1 mmol of potassium but onset is slow, taking over two hours.
- The adult dose (of the generic form) is 15 g 3-4 times a day orally. It can also be given rectally, 30 g retained for nine hours followed by irrigation to remove the resin. See British National Formulary for dosage details.
- Haemodialysis will also remove potassium from the body (see note below).
- Newer potassium-binding agents which have greater efficacy - such as sodium zirconium cyclosilicate and patiromer - are being developed.
- It may be necessary to give further glucose and IV insulin and/or IV calcium.
- The use of IV diuretics (eg, furosemide) is more contentious. However, this would be a good choice if other comorbidities are present - eg, congestive cardiac failure.
- If, despite repeated glucose and IV insulin infusions, potassium remains too high then the case should be discussed with renal physicians.
- Sodium bicarbonate may be useful in the setting of resistant hyperkalaemia with acidosis. However, it can be dangerous and thus is best used after discussion with renal specialists. It is best avoided in DKA.
- Haemodialysis may be required but is invasive.
Hyperkalaemia is an independent risk factor for death and most fatal cases are complicated by AKI.
Much dangerous hyperkalaemia is iatrogenic. If patients take two drugs that reduce potassium excretion, check U&E if they develop diarrhoea or vomiting. Beware of NSAIDs with these drugs. In patients with renal impairment, the ACE inhibitors and AIIRAs are very effective and reduce blood pressure and possible albumin loss. However, they must be used with care to prevent hyperkalaemia.
Further reading and references
Martin-Perez M, Ruigomez A, Michel A, et al; Impact of hyperkalaemia definition on incidence assessment: implications for epidemiological research based on a large cohort study in newly diagnosed heart failure patients in primary care. BMC Fam Pract. 2016 May 417:51. doi: 10.1186/s12875-016-0448-5.
Clinical Practice Guidelines: Treatment of Acute Hyperkalaemia in Adults; UK Renal Association (2014)
Kuijvenhoven MA, Haak EA, Gombert-Handoko KB, et al; Evaluation of the concurrent use of potassium-influencing drugs as risk factors for the development of hyperkalemia. Int J Clin Pharm. 2013 Dec35(6):1099-104. doi: 10.1007/s11096-013-9830-8. Epub 2013 Aug 22.
Lehnhardt A, Kemper MJ; Pathogenesis, diagnosis and management of hyperkalemia. Pediatr Nephrol. 2011 Mar26(3):377-84. doi: 10.1007/s00467-010-1699-3. Epub 2010 Dec 22.
Isnard Bagnis C, Deray G, Baumelou A, et al; Herbs and the kidney. Am J Kidney Dis. 2004 Jul44(1):1-11.
Smellie WS; Spurious hyperkalaemia. BMJ. 2007 Mar 31334(7595):693-5.
Iyngkaran P, Toukhsati SR, Thomas MC, et al; A Review of the External Validity of Clinical Trials with Beta-Blockers in Heart Failure. Clin Med Insights Cardiol. 2016 Oct 1210:163-171. eCollection 2016.
British National Formulary; 72nd Edition (Sep 2016) British Medical Association and Royal Pharmaceutical Society of Great Britain, London
Chaitman M, Dixit D, Bridgeman MB; Potassium-Binding Agents for the Clinical Management of Hyperkalemia. P T. 2016 Jan41(1):43-50.
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