While mild hyperkalaemia is usually asymptomatic, high potassium levels may cause life-threatening cardiac arrhythmias, muscle weakness, or paralysis. The aetiology and treatment approach to hyperkalaemia is penned down in this article.

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Hyperkalaemia

Hyperkalaemia is defined as a serum potassium level greater than 5.5 mEq/L. Symptoms usually develop at higher levels, 6.5 mEq/L to 7 mEq/L, but the rate of change is more important than the numerical value.

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Aetiology

1. Pseudohyperkalaemia 

It is one of the common causes of hyperkalaemia due to haemolysis of the sample, causing intracellular potassium to be measured in the serum. Haemolysis is more common when a syringe is used than a vacuum device. Using tourniquets and excessive fist-pumping during the blood draw also increases the risk

2. Increased potassium intake

Increased potassium intake from food is a very uncommon cause of hyperkalaemia in adult patients with normal renal function but can be an important cause in those with kidney disease.

Many vegetables that are also high in potassium include spinach, potatoes, tomatoes, broccoli, beets, carrots, and squash. High-potassium-containing fruits include kiwis, mangoes, oranges, bananas, and cantaloupe. Red meats are also rich in potassium.

Intravenous intake through high potassium-containing fluids, particularly total parenteral nutrition, medications with high potassium content and massive blood transfusions can significantly elevate serum potassium levels.

3. Intracellular potassium shifts

1. Rhabdomyolysis from a crush injury, excessive exercise, or other haemolytic processes.
2. Metabolic acidosis may cause intracellular potassium to shift into the extracellular space without red cell injury. Metabolic acidosis is most frequently caused by decreased, effective circulating arterial blood volume. Sepsis or dehydration may lead to hypotension and decreased tissue perfusion leading to metabolic acidosis with subsequent potassium elevation.
3. Insulin deficiency and diabetic ketoacidosis may cause dramatic extracellular shifts causing measured serum potassium to be elevated in the setting of whole-body potassium depletion.
4. Medications, such as succinylcholine, may cause severe, acute potassium elevations in patients with up-regulation of receptors, particularly in subacute neuromuscular disease. Medications that may predispose to the development of hyperkalaemia include digoxin, potassium-sparing diuretics, non-steroidal anti-inflammatory drugs and ace-inhibitors.
5. Tumour lysis syndrome, particularly in patients receiving chemotherapy for hematogenous malignancy, may cause acute hyperkalaemia due to massive cancer cell death.
6. Hyperkalemic periodic paralysis is a rare, autosomal dominant condition that causes potassium to shift into the extracellular space due to impaired sodium channel function in skeletal muscle.

Impaired potassium excretion

Acute or chronic kidney disease is a common cause of hyperkalaemia. Hyperkalaemia is usually not seen until the glomerular filtration rate falls below 30 ml/min. Tubular dysfunction due to aldosterone deficiency or insensitivity can also cause hyperkalaemia.

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Approach to the patient

A. History and physical examination

Most patients are relatively asymptomatic with mild and even moderate hyperkalaemia. Elevated potassium is often discovered in screening labs done in patients with nonspecific complaints. Patients may complain of weakness, fatigue, palpitations, or syncope.

B. Laboratory tests

The first test that should be ordered in a patient with suspected hyperkalaemia is an ECG since the most lethal complication of hyperkalaemia is cardiac condition abnormalities which can lead to dysrhythmias and death

Elevated potassium causes ECG changes in a dose-dependent manner:

• K = 5.5 to 6.5 mEq/L ECG will show tall, peaked t-waves
• K = 6.5 to 7.5 mEq/L ECG will show loss of p-waves
• K = 7 to 8 ECG mEq/L will show a widening of the QRS complex
• K = 8 to 10 mEq/L will produce cardiac arrhythmias, sine wave pattern, and asystole

Additional laboratory testing should include;

1. Serum blood urea nitrogen and creatinine to assess renal function and urinalysis to screen for renal disease.
2. Urine potassium, sodium, and osmolality.
3. Serum calcium levels should also be checked because hypocalcemia may exacerbate the cardiac effects of hyperkalaemia.
4. Serum glucose and blood gas analysis should be ordered in diabetics and patients with suspected acidosis.
5. LDH should be ordered in patients with suspected haemolysis.
6. CPK and urine myoglobin should be ordered in patients with suspected rhabdomyolysis.
7. Uric acid and phosphorus should be ordered in patients with suspected tumour lysis syndrome.
8. Digoxin toxicity may cause hyperkalaemia, so serum levels should be checked in patients on digoxin.
9. If no other cause is found, consider cortisol and aldosterone levels to assess for mineralocorticoid deficiency.

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Management

Treatment is usually prescribed in the following manner;

1. Exogenous sources of potassium should be immediately discontinued.
2. Treatment of the reversible cause should begin along with the management of hyperkalaemia.
3. Calcium therapy will stabilise the cardiac response to hyperkalaemia and should be initiated first in the setting of cardiac toxicity. Calcium does not alter the serum concentration of potassium but is a first-line therapy in hyperkalaemia-related arrhythmias and ECG changes. Intravenous Calcium gluconate is the initial drug of choice in patients with evidence of cardiac toxicity. As a precaution, calcium should never be given in bicarbonate-containing fluids, as it can cause the precipitation of calcium carbonate.
4. Insulin and glucose, or insulin alone in hyperglycemic patients, will drive the potassium back into the cells, effectively lowering serum potassium. A common regimen is ten units of regular insulin given with 100 ml of a 25% dextrose solution.
5. Beta-2 adrenergic agents such as salbutamol will also shift potassium intracellularly. To be effective, beta-2 agonists are given in much higher doses than those commonly used for bronchodilation. Sodium bicarbonate infusion may be helpful in patients with metabolic acidosis. Bolus dosing of sodium bicarbonate is less effective.
6. Loop or thiazide diuretics may help enhance potassium excretion. They may be used in non-oliguric, volume-overloaded patients but should not be used as monotherapy in symptomatic patients. In hypervolemic patients with preserved kidney function (e.g., patients with congestive cardiac failure), 40 mg of intravenous furosemide is administered every 8 hours or may be given as a continuous infusion. In euvolemic or hypovolemic patients with preserved kidney function, an isotonic saline infusion is given before as needed to the patient before administering 40 mg of intravenous furosemide every 12 hours or a continuous furosemide infusion.
7. Gastrointestinal cation exchangers such as sodium polystyrene sulfonate, though commonly used, are falling out of favour due to lack of effectiveness and adverse effects, particularly bowel necrosis in elderly patients. If used due to a lack of alternatives, it should be given with lactulose.
8. Haemodialysis should be performed in patients with end-stage renal disease or severe renal impairment.

Disclaimer- The views and opinions expressed in this article are those of the author and do not necessarily reflect the official policy or position of M3 India.

About the author of this article: Dr Bhavin Mandowara is a practising nephrologist at Zydus Hospital, Ahmedabad.