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.


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.

 

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.

 

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.

Symptoms and Clinical Signs

Symptoms

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 Signs

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

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

FBC

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

Capillary blood glucose

  • To rule out hyperglycaemia (i.e. DKA)

Arterial blood gas

  • To rule out metabolic acidosis (e.g. hyperkalaemic renal tubular acidosis or DKA)

Serum cortisol

  • To rule out Addison’s

Digoxin level

  • To rule out toxicity (if relevant)

ECG

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 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.

Acute management⁴

Prevent further accumulation of potassium

  • Stop any IV fluids containing potassium
  • Suspend any medications that have the potential to increase serum potassium
  • Suspend 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 into the cells

Insulin-glucose infusion

  • Administer an insulin-glucose intravenous infusion (typically 10 units of soluble insulin are added to 25g of glucose).
  • Insulin helps to shift potassium from the extracellular to the intracellular compartment, whilst the glucose helps to maintain capillary blood glucose levels.
  • Capillary blood glucose needs to be monitored closely, to avoid hypoglycaemia.
  • Potassium should be re-checked 30 minutes after the infusion and U&Es should be checked 1-2 hours later.
  • The reduction in potassium from this intervention would be expected to last for approximately 60 minutes.

Salbutamol

  • Salbutamol is often used as adjuvant therapy for hyperkalaemia.
  • It promotes the movement of potassium into cells and therefore out of the serum.
  • The onset of action is approximately 15 – 30 minutes
  • The duration of effect is approximately 2 hours

 

Remove potassium from the body

Removing potassium from the body is not usually possible in the acute setting (other than urgent haemodialysis) and therefore this forms part of the longer-term management strategy.

Calcium Resonium

  • Calcium polystyrene sulfonate resin (Calcium Resonium) can be used to remove potassium via the gastrointestinal tract.
  • Calcium Resonium is recommended in the treatment of mild and moderate hyperkalaemia (in the non-acute setting, due to a delayed onset of action of 2 hours).
  • The typical oral dose for an adult is 15 grams 3-4 times a day.

Correction of the underlying cause

  • To fully address hyperkalaemia in the long-term, the underlying cause needs to be identified and treated (e.g. IV fluids for acute kidney injury, suspension of the causative drug).
  • If the underlying cause is treated, the kidneys should be able to resume their normal function of excreting adequate volumes of potassium via the urine.

Haemodialysis

  • Haemodialysis is an invasive treatment reserved as a last resort for resistant hyperkalaemia that has failed to respond to all other therapies.

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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