Hyperkalaemia

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Hyperkalaemia\: plasma potassium ≥ 5.5 mmol/L, classi
life-threatening arrhythmias increases with severity.
Renal causes\: acute kidney injury, chronic kidney disease (stages 4/5, dialysis), hyperkalaemic renal tubular acidosis.
Iatrogenic causes\: ACE inhibitors, ARBs, potassium-sparing diuretics, NSAIDs, digoxin toxicity, beta-blockers, heparin,
potassium supplements, inappropriate IV
Other causes\: trauma, burns, diabetic ketoacidosis (DKA), Addison’s disease (low aldosterone), pseudohyperkalaemia
(haemolysis, incorrect sampling).
Clinical features\: often asymptomatic; may present with bradycardia or absent tendon re
waves, prolonged PR,
Investigations\: U&Es, venous blood gas for rapid potassium check, ECG to detect cardiotoxicity, FBC, serum cortisol,
digoxin levels.
Management\:
Stop potassium sources
Administer IV calcium (10ml 10% calcium chloride or 30ml 10% calcium gluconate) if ECG changes to stabilise myocardium.
Insulin-glucose infusion (10 units insulin, 25g glucose), salbutamol; potassium binders (sodium zirconium, patiromer),
haemodialysis if resistant hyperkalaemia.
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A comprehensive topic overview

Introduction

Hyperkalaemia is de≥ 5.5 mmol/L.
1,2
Hyperkalaemia is further classi
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 hyperkalemia. The rate at which serum potassium rises is
also an important factor in
Severe hyperkalaemia is a medical emergency due to the risk of life-threatening arrhythmias. Hyperkalaemia is one of the
reversible causes of cardiac arrest. Prompt treatment is vital, especially in patients who have ECG changes. This article will
cover the causes, investigation and emergency management of hyperkalaemia.

Aetiology

Renal causes of hyperkalaemiaThe kidneys are responsible for 90% of potassium excretion in healthy individuals, with the remainder excreted via the
gastrointestinal tract.
As a result, renal impairment is one of the most common causes of hyperkalaemia.
Acute kidney injury (AKI)
Chronic kidney disease (CKD)\: especially patients on dialysis, or CKD stages 4 and 5
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
Blood transfusion is another potential cause of hyperkalaemia.
Trauma and burns
Tissue damage sustained secondary to trauma or burns results in the release of signi
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 the excretion of potassium by the kidneys.
In Addison's disease, the adrenal glands cannot produce adequate aldosterone levels, 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
Leukocytosis and thrombocytosis
If there are concerns about pseudohyperkalaemia, a sample should be urgently repeated to check the validity of the
result.

Clinical features

HistoryHyperkalaemia is usually asymptomatic, although patients may have symptoms related to an acute illness causing the
hyperkalaemia. If present, symptoms of hyperkalaemia are typically vague and non-speci
The history may identify risk factors for hyperkalemia such as renal impairment or a medication known to cause
hyperkalaemia.
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 re

Investigations

Serum potassium is reported as part of urea & electrolytes (U&Es).
The
should be sent. A venous blood gas can be used to rapidly con
Bedside investigations
Relevant bedside investigations include\:
12-lead ECG\: to identify ECG changes which suggest cardiotoxicity
Blood gas (venous or arterial)\: to exclude metabolic acidosis (e.g. hyperkalaemic renal tubular acidosis or DKA) and
rapidly check serum potassium
Capillary blood glucose\: to exclude hyperglycaemia (e.g. DKA)
ECG changes in hyperkalaemia
An ECG is an essential investigation in the context of hyperkalaemia. Abnormalities can include\:
Tall tented T waves (early sign)
Prolonged PR interval
Flattened P waves
Wide QRS complexes
Sine wave pattern (late sign)
Arrhythmias
Progression of ECG changes in hyperkalaemia
Laboratory investigations
Relevant laboratory investigations include\:
U&E\: a repeat U&E sample should be sent
Full blood count\: to exclude haemolysis (e.g. normocytic normochromic anaemia) and leukocytosis or thrombocytosisSerum cortisol\: to exclude Addison's disease (low serum cortisol is found in Addison's)
Digoxin level\: to exclude toxicity (if relevant)

Management

The potassium level and the presence/absence of associated ECG changes determine the urgency by which
hyperkalemia needs to be treated.
A potassium level of ≥6.5 mmol/L and/or a hyperkalaemia-associated ECG changes requires urgent treatment (a
medical emergency).
All patients with hyperkalaemia will ultimately require further monitoring and management.
Prevent further accumulation of potassium
Further accumulation of potassium can be prevented by\:
Stopping any intravenous
Suspending any medications that have the potential to increase serum potassium
Suspending any supplements containing potassium
Stabilise the cardiac membrane (protect the heart)
If ECG changes are present, then administer intravenous calcium\:
10mls 10% calcium chloride
30mls 10% calcium gluconate
This stabilises the myocardium temporarily for 30-60 minutes and reduces the risk of fatal arrhythmia.
Further doses may be required if ECG changes persist. Usually, ECG changes begin to improve within 1-3 minutes of
administering calcium. The administration of calcium without hyperkalaemia-associated ECG changes is not
recommended.
The role of intravenous calcium
Intravenous calcium stabilises the myocardium and reduces the risk of life-threatening arrhythmias.
Calcium does not reduce serum potassium levels.
The role of intravenous calcium is to buy time until potassium-lowering treatments can be initiated.
Shift potassium intracellularly (reduce serum potassium)
Treatments which can shift potassium into cells and out of the serum include\:
Insulin-glucose infusion\: insulin shifts potassium from the extracellular to the intracellular compartment, while glucose
helps maintain capillary blood glucose levels
Salbutamol\: often used as adjuvant therapy for hyperkalaemia as it promotes the movement of potassium into cells and
out of the serum
Patients receiving an insulin-glucose infusion should undergo regular monitoring of blood glucose levels and serum
potassium levels.
Insulin-glucose infusion
Usually, 10 units of insulin is given in 25 grams of glucose over 15-30 minutes, however always follow local guidelines.
Patients with pre-treatment blood glucose \<7 mmol/L will require a glucose infusion to prevent hypoglycaemia.Remove potassium from the body
Methods to remove potassium from the body include\:
Potassium binders (sodium zirconium cyclosilicate and patiromer)\: these are both newer potassium binders which have
been approved for the treatment of hyperkalaemia
Correction of the underlying cause\: the kidneys should then 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.

Example ECG

A 62-year-old woman on haemodialysis presents feeling unwell. She has recently missed a dialysis session.
JETem. License\: [CC BY-SA 4.0]
What does the ECG show?
This ECG shows\:
1. Tall, tented T-waves
2. Flattened or absent P waves
3. Broad QRS complexes
These ECG changes are consistent with severe cardiotoxicity seen in hyperkalaemia.
This patient had a K+ level of 7.6mmol/L on her VBG. She was treated with calcium gluconate, insulin + dextrose and
admitted to critical care for urgent haemo

References

Soar J, Perkins GD, Abbas G et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Resuscitation
2010; 81\: 1400-1433.
Nyirenda MJ, Tang JI, Pad
Tonelli M and Clase CM. Emergency interventions for hyperkalaemia (Review). Cochrane Review, Cochrane Library Issue 2,
2008
Emerg Med Clin N Am 23 (2005) 723–747. Disorders of Potassium. Timothy J. Schaefer, MDa,b,
*
, Robert W. Wolford, MD,
MMMc,d
Clinical Practical Guidelines. Treatment of acute hyperkalaemia in adults. UK Renal Association. 2023. Available from\: [LINK]Related notes
Acute Kidney Injury (AKI)
Chronic Kidney Disease (CKD)
Glomerular Disease (Glomerulonephropathies)
Haemodialysis
Henoch-Schönlein Purpura (IgA Vasculitis)