Hyperkalaemia
| Hyperkalaemia | |
|---|---|
| Definition | Serum potassium > 5.0 |
| Symptoms | Muscle weakness |
| Complications | Fatal arrhythmia |
| Causes | Chronic kidney disease, RAAS inhibitors |
| Treatment | Calcium gluconate i.v., insulin + glucose |
Hyperkalaemia is a disorder of potassium homeostasis characterised by high levels of potassium (>4.5 mmol/L). It's a relatively common electrolyte abnormality, and more common than hypokalaemia. Hyperkalaemia almost always occurs in the context of reduced potassium excretion by the kidneys, either due to kidney disease or due to medications which reduce the excretion. The most common symptom is muscle weakness, and the most dangerous complication is fatal arrhythmia. Treatment involves stabilising the cardiac membrane by using calcium, moving potassium into cells by using insulin and glucose, and by increased potassium removal from the body by dialysis, potassium-losing diuretics, or a gastrointestinal cation exchanger.
Grading of severity
| Potassium level | Severity |
|---|---|
| 5.1 - 5.9 | Mild |
| 6.0 - 6.9 | Moderate |
| > 7.0 | Severe |
Etiology
| Increased potassium release from cells | Decreased renal potassium excretion |
|---|---|
| Metabolic acidosis | Chronic kidney disease, especially end-stage |
| Massive cell death (rhabdomyolysis, haemolysis, tumor lysis syndrome, burn injury) | Acute kidney injury |
| Non-selective beta blockers | Potassium-sparing diuretics (mineralocorticoid receptor antagonists, amiloride) |
| ACE inhibitors, angiotensin II blocker | |
| Addison disease | |
| Trimethoprim, NSAIDs |
The most common cause of hyperkalaemia is chronic kidney disease and acute kidney injury. In healthy people, the kidney can excrete usually excrete any potassium which is superfluous, but in case of kidney disease, this mechanism doesn't work, and so people with kidney disease are at risk for hyperkalaemia if ingesting potassium-rich foods.
Metabolic acidosis causes hyperkalaemia as the cells tries to buffer the acidosis by movement of H+ ions from the extracellular to the intracellular space. In exchange, cells move K+ ions out, to maintain electrical neutrality.
Non-selective beta blockers inhibit beta-2-adrenergic stimulation of potassium movement into cells. Selective beta blockers don't inhibit the beta-2 receptor and therefore don't cause this effect.
Trimethoprim blocks sodium channels in the collecting tubule, which indirectly impairing potassium secretion. NSAIDs somewhat impair renin secretion and aldosterone release, potentially causing mild hyperkalaemia, but only rarely causes more severe potassium elevation.
Haemolysis of the blood sample causes release of potassium from RBCs, which causes the laboratory to falsely report hyperkalaemia. This is known as pseudohyperkalaemia. Most labs should be able to detect when haemolysis occurs, so this shouldn't be a big problem. Clenching the hand of the arm the blood sample is taken from also causes falsely elevated potassium, as the "exercise" causes potassium release from skeletal muscle.
Pathomechanism
Hyperkalaemia causes the resting membrane potential of muscle cells to be higher than normal (less negative, closer to 0. This makes the membrane more easily excitable initially, but the cell compensates for this by inactivating sodium channels in the membrane, which ultimately decreases membrane excitability. This makes the membranes harder to excite, which causes weakness.
Hyperkalaemia also interferes with the cardiac action potential, for reasons I don't understand.
Clinical features
Symptoms are more severe if the increase in serum potassium is rapid than if it is chronic. Mild hyperkalaemia is asymptomatic. Moderate or severe hyperkalaemia can cause ascending muscle weakness.
Hyperkalaemia can cause ECG changes. These changes are not necessarily proportional to potassium level:
- Early changes
- Tall peaked T-waves
- Shortened QT interval
- Later changes
- Prolonged PQ interval
- Wide QRS, eventually
- Supraventricular or ventricular tachyarrhythmia
- Shrinkage, later absence of P wave
- Bundle branch block (left or right)
- AV block
Diagnosis and evaluation
The serum potassium level may be up to 0,5 units higher than the true level of potassium in the blood, due to release of potassium from thrombocytes. To get the most accurate potassium value, an arterial blood gas should be taken.
The cause of hyperkalaemia is usually trivial to determine from anamnesis, clinical features, or regular blood test. It's simple to determine whether there is kidney injury, based on creatinine and urea levels. If no cause is immediately obvious, aldosterone levels should be measured.
Treatment
Mild or moderate asymptomatic hyperkalaemia does not need urgent treatment, and can usually be managed less emergently. Severe or symptomatic hyperkalaemia, or in case of late ECG changes, need emergency treatment. If there is a known underlying cause, like administration of a RAAS inhibitor, it should be managed or the drug withheld.
Emergency treatment involves administration intravenous insulin administered together with glucose. This stimulates movement of potassium from the extracellular to the intracellular space, which decreases the serum potassium, but doesn't actually decrease the amount of potassium in the body. Glucose is added to prevent hypoglycaemia. Administration of a beta-2-adrenergic agonist may also be used to move potassium intracellularly.
In addition to measures to move insulin into cells, treatment to remove potassium from the body is indicated. This can be either dialysis (in the most severe cases), a potassium-losing diuretic like a loop diuretic or thiazide diuretic, or a gastrointestinal cation exchanger.
If there are ECG changes, administration of intravenous calcium gluconate or calcium chloride is indicated. Calcium gluconate stabilises the cardiac membrane, reducing the risk of arrhythmia. Calcium gluconate does not decrease the potassium level. Patients with ECG changes must have cardiac monitoring.
Less severe hyperkalaemia can be managed with potassium-losing diuretic or gastrointestinal cation exchanger alone.
Prevention in chronic kidney disease
People with chronic kidney disease are at risk for hyperkalaemia. Affected people must keep a low-potassium diet as well as avoid medications which decrease potassium excretion.
Complications
Arrhythmia
Hyperkalaemia can cause many different arrhythmias, the worst of which are lethal. Arrhythmias include LBBB and RBBB, AV block, sinus bradycardia, sinus arrest, ventricular tachycardia, ventricular fibrillation, or asystole.
Metabolic acidosis
Hyperkalaemia may cause metabolic acidosis by reducing renal excretion of ammonia.