Hyperkalaemia

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What is hyperkalaemia?

Hyperkalaemia is defined as plasma potassium in excess of ≥ 5.5 mmol/L.1,2

Hyperkalaemia is further classified by the European Resuscitation Guidelines as follows:

  • Mild – 5.5-5.9 mmol/L
  • Moderate – 6.0-6.4 mmol/L
  • Severe – >6.5 mmol/L

The incidence of complications rises with increasing severity of hyperkalaemia.

The rate at which serum potassium rises also an important factor which influences the likelihood of complications occurring.

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Aetiology

Renal causes of hyperkalaemia

In healthy individuals, the kidneys are responsible for 90% of potassium excretion, with the remainder excreted via the gastrointestinal tract. As a result, renal impairment is one of the commonest causes of hyperkalaemia.

  • Acute kidney injury (AKI)
  • Chronic kidney disease (CKD)
  • Hyperkalaemic renal tubular acidosis

Iatrogenic causes of hyperkalaemia

Many medications can cause or contribute to hyperkalemia directly or indirectly:

  • ACE inhibitors
  • Angiotensin receptor blockers
  • Potassium-sparing diuretics
  • NSAIDs/COX 2 inhibitors
  • Digoxin (in toxicity)
  • Trimethoprim
  • Beta-blockers – selective and non-selective can cause it
  • Nicorandil
  • Heparin – unfractionated and LMWH
  • Ciclosporin
  • Tacrolimus
  • Renin-inhibitors (e.g. aliskiren)
  • Potassium supplements

Intravenous fluids containing potassium also have the potential to cause hyperkalaemia when prescribed inappropriately.

Blood transfusion is another potential cause of hyperkalaemia.

Trauma and burns

Tissue damage sustained secondary to trauma or burns results in the release of significant volumes of potassium from damaged cells.

Diabetic ketoacidosis

In diabetic ketoacidosis (DKA) potassium shifts from the intracellular to the extracellular space due to a lack of insulin, resulting in hyperkalaemia.

Addison’s disease

Aldosterone promotes excretion of potassium by the kidneys.

In Addison’s disease, the adrenal glands are unable to produce adequate levels of aldosterone which results in reduced renal excretion of potassium.

Pseudohyperkalaemia

Pseudohyperkalaemia can occur for a wide variety of reasons including:

  • Haemolysis (e.g. prolonged tourniquet time, prolonged sample transport time, use of incorrect blood bottles)
  • Blood sample being taken from a limb receiving IV fluids containing potassium
  • Leukocytosis and thrombocytosis

If there are concerns about pseudohyperkalaemia, a sample should be urgently repeated to check the validity of the result.


Clinical features

History

Symptoms of hyperkalaemia are typically vague and including general weakness and fatigue.

In some cases, patients may experience palpitations, chest pain or shortness of breath.

Clinical examination

In most cases, there are no obvious clinical signs of hyperkalaemia.

Potential clinical signs include:

  • Bradycardia secondary to hyperkalaemia-induced atrioventricular block
  • Depressed or absent tendon reflexes

Investigations

Laboratory tests

U&Es should be performed to:

  • confirm the presence of hyperkalaemia and assess other electrolytes (a repeat sample should be sent if hyperkalaemia is noted)
  • assess renal function (the kidneys are responsible for 90% of potassium excretion)

FBC should be performed to:

  • rule out haemolysis (e.g. normocytic normochromic anaemia)
  • rule out leukocytosis or thrombocytosis

Capillary blood glucose should be performed to rule out hyperglycaemia (e.g. DKA).

An arterial blood gas should be performed to rule out metabolic acidosis (e.g. hyperkalaemic renal tubular acidosis or DKA).

Serum cortisol should be performed to rule out Addison’s disease (low serum cortisol is found in Addison’s).

A digoxin level should be performed to rule out toxicity (if relevant).

An ECG is an essential investigation in the context of hyperkalaemia, abnormalities can include:

  • Tall tented T waves
  • Wide QRS complexes
  • Prolonged PR interval
  • Flattened P waves
  • AV block
  • Bradycardia
Hyperkalaemia associated ECG changes
Hyperkalaemia associated ECG changes5

Management

The urgency by which hyperkalemia needs to be treated is determined by the level of potassium and the presence/absence of associated ECG changes.

A potassium level of ≥7.0 mmol/L and/or a patient with hyperkalaemia associated ECG changes requires URGENT treatment.

All patients with hyperkalaemia will ultimately require some form of further monitoring and management.

Prevent further accumulation of potassium

Further accumulation of potassium can be prevented by:

  • Stopping any intravenous fluids containing potassium
  • Suspending any medications that have the potential to increase serum potassium
  • Suspending any supplements containing potassium

Stabilise the cardiac membrane

Administer intravenous calcium gluconate (10mls of 10% solution) if there are hyperkalaemia associated ECG changes present. This should help to stabilise the myocardium temporarily for 30-60 minutes and reduce the risk of fatal arrhythmia.

Further doses may be required if ECG changes persist (you would expect ECG changes to begin to improve within 1-3 minutes from the administration of calcium gluconate). The administration of calcium gluconate in the absence of hyperkalaemia associated ECG changes is not recommended.

Shift potassium intracellularly

Treatments which can shift potassium into cells and out of the serum include:

  • Insulin-glucose infusion: insulin helps to shift potassium from the extracellular to the intracellular compartment, whilst the glucose helps to maintain capillary blood glucose levels.
  • Salbutamol: often used as adjuvant therapy for hyperkalaemia as it promotes the movement of potassium into cells and therefore out of the serum.

Remove potassium from the body

Methods to remove potassium from the body include:

  • Calcium polystyrene sulfonate resin (Calcium resonium) can be used to remove potassium via the gastrointestinal tract.
  • Correction of the underlying cause: the kidneys should then be able to resume their normal function of excreting adequate volumes of potassium via the urine.
  • Haemodialysis is an invasive treatment reserved as a last resort for resistant hyperkalaemia that has failed to respond to all other therapies.

Key points

  • Hyperkalaemia is defined as plasma potassium in excess of ≥ 5.5 mmol/L.1,2
  • There is a wide range of causes of hyperkalaemia including renal, iatrogenic, trauma/burns, DKA and Addison’s disease.
  • Symptoms of hyperkalaemia are typically vague and including general weakness and fatigue.
  • In most cases, there are no obvious clinical signs of hyperkalaemia.
  • Key investigations in hyperkalaemia include U&Es, ECG, serum cortisol, FBC and capillary blood glucose.
  • Typical ECG findings in hyperkalaemia include tall tented T waves, broad QRS complexes, prolonged PR intervals and flattened P waves.
  • Management of hyperkalaemia involves preventing further accumulation of potassium, stabilising the cardiac membrane (if ECG changes present), shifting potassium intracellularly and removing potassium from the body.

References

  1. Soar J, Perkins GD, Abbas G et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Resuscitation 2010; 81: 1400-1433.
  2. Nyirenda MJ, Tang JI, Padfield PL, et al. Hyperkalaemia. BMJ 2009; 339: 1019-1024.  Mahoney BA, Smith WAD, Lo DS, Tsoi K, Tonelli M and Clase CM. Emergency interventions for hyperkalaemia (Review). Cochrane Review, Cochrane Library Issue 2, 2008
  3. Emerg Med Clin N Am 23 (2005) 723–747. Disorders of Potassium. Timothy J. Schaefer, MDa,b,*, Robert W. Wolford, MD, MMMc,d
  4. Clinical Practical Guidelines. Treatment of acute hyperkalaemia in adults. UK Renal Association. 2012
  5. Häggström, Mikael (2014). WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 2002-4436.

 

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