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Hypokalaemia: Difference between revisions
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(Created page with "'''Hypokalaemia''' is a disorder of potassium homeostasis characterised by low levels of potassium (<3.5 mmol/L). It's a relatively common electrolyte abnormality. == Grading of severity == {| class="wikitable" |+ !Potassium level !Severity |- |3.5 - 3.0 |Mild |- |2.9 - 2.5 |Moderate |- |< 2.5 |Severe |} == Etiology == Hypokalaemia can occur due to increased potassium loss, redistribution of potassium into cells, or (rarely) insufficient potassium intake. Because the k...") |
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Hypokalaemia can occur due to increased potassium loss, redistribution of potassium into cells, or (rarely) insufficient potassium intake. Because the kidneys can reduce potassium excretion to a minimum, and the daily potassium requirement is really low, insufficient intake of potassium rarely causes hypokalaemia by itself, but it may contribute to hypokalaemia due to other causes | Hypokalaemia can occur due to increased potassium loss, redistribution of potassium into cells, or (rarely) insufficient potassium intake. Because the kidneys can reduce potassium excretion to a minimum, and the daily potassium requirement is really low, insufficient intake of potassium rarely causes hypokalaemia by itself, but it may contribute to hypokalaemia due to other causes | ||
{| class="wikitable" | {| class="wikitable" | ||
|+ | |+Most common causes of hypokalaemia | ||
!Increased potassium loss | !Increased potassium loss | ||
!Redistribution of potassium into cells | !Redistribution of potassium into cells | ||
| Line 27: | Line 27: | ||
|Excessive insulin (treatment of [[diabetic ketoacidosis]] or [[hyperglycaemic hypoerosmolar syndrom]], [[refeeding syndrome]]) | |Excessive insulin (treatment of [[diabetic ketoacidosis]] or [[hyperglycaemic hypoerosmolar syndrom]], [[refeeding syndrome]]) | ||
|- | |- | ||
|Vomiting or other gastrointestinal loss | |[[Vomiting]] or other gastrointestinal loss | ||
|Excessive beta-adrenergic activity (severe stress (like [[myocardial infarction]], [[traumatic head injury]], [[alcohol withdrawal]]), administration of [[Beta-adrenergic agonist|beta-adrenergic agonists]]) | |Excessive beta-adrenergic activity (severe stress (like [[myocardial infarction]], [[traumatic head injury]], [[alcohol withdrawal]]), administration of [[Beta-adrenergic agonist|beta-adrenergic agonists]]) | ||
|- | |- | ||
|Hyperaldosteronism, e.g. due to | |Hyperaldosteronism, e.g. due to hormone-producing [[adrenal adenoma]] | ||
|Alkalosis | |[[Alkalosis]] | ||
|} | |} | ||
Upper gastrointestinal fluids don't contain much potassium, so loss of the fluid itself does not cause severe hypokalaemia. However, the resulting hypovolaemia can cause hyperaldosteronism, which can cause hypokalaemia. | Upper gastrointestinal fluids don't contain much potassium, so loss of the fluid itself does not cause severe hypokalaemia. However, the resulting hypovolaemia can cause hyperaldosteronism, which can cause hypokalaemia. Lower gastrointestinal fluids, however, contain much potassium, and so loss of these fluids (usually due to diarrhoea) can cause hypokalaemia. | ||
== Pathomechanism == | |||
Hypokalaemia causes the resting membrane potential of muscle cells to be lower than normal (that is, more negative, also called ''hyperpolarised''). This makes the membranes harder to excite, which causes weakness. | |||
Hypokalaemia has many effects on the heart: | |||
* Hypokalaemia decreases Na-K-ATPase activity, leading to increased intracellular sodium, which inhibits Na-Ca exchanger activity, leading to increased intracellular calcium, which stimulates Ca<sup>2+</sup>/calmodulin-dependent protein kinase II, which eventually leads to ventricular arrhythmia | |||
* In the conducting system of the heart, hypokalaemia paradoxically causes depolarisation by triggering sodium influx into cells. This increases membrane excitability in the conducting system, predisposing to arrhythmia. | |||
* In ventricular cells, hypokalaemia delays ventricular repolarisation | |||
== Clinical features == | |||
Symptoms are more severe if the drop in serum potassium is rapid than if it is chronic. Mild hypokalaemia is usually asymptomatic. Moderate hypokalaemia can cause muscle weakness, constipation, ileus, and restless legs. Severe hypokalaemia can cause arrhythmia, rhabdomyolysis, and paresis. Hyporeflexia is a possible sign. | |||
Severe hypokalaemia can cause ECG changes: | |||
* Low or inverted T-waves | |||
* Presence of U-waves | |||
* ST depression | |||
* Supraventricular or ventricular tachyarrhythmia | |||
* Prolonged QT interval | |||
== 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 hypokalaemia is usually evident from the list of medications, the anamnesis, or from clinical features of the underlying cause. | |||
A urine potassium of > 20 mmol/L in the setting of hypokalaemia is indicative of renal loss of potassium. | |||
== Management == | |||
Mild hypokalaemia does not usually require hospitalisation, but moderate, severe, or symptomatic hypokalaemia requires hospitalisation. Severe hypokalaemia requires [[intensive care]]. Severe cases should be continously monitored with ECG. The underlying cause should be adressed if possible. Any concomitant hypomagnesaemia must also be treated, as hypomagnesaemia maintains hypokalaemia. | |||
Potassium can be supplemented p.o. or i.v. P.o is the first choice, while i.v. is used in severe hypokalaemia, if there is a high risk of arrhythmia, or if p.o. supplementation is insufficient. | |||
== Complications == | |||
Arrhythmia in case of hypokalaemia can be fatal and is the most dangerous complication. Elderly, as well as people with heart disease, previous ventricular arrhythmia, or digitalis treatment are at extra high risk for arrhythmia. | |||