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Hyperkalaemia: Difference between revisions
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{{Infobox medical condition | <section begin="clinical biochemistry" />{{Infobox medical condition | ||
| name = Hyperkalaemia | | name = Hyperkalaemia | ||
| definition = Serum potassium > 5.0 | | definition = Serum potassium > 5.0 | ||
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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. | 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. | [[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.<section end="clinical biochemistry" /> | ||
== Pathomechanism == | == Pathomechanism == | ||
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Hyperkalaemia also interferes with the cardiac action potential, for reasons I don't understand. | Hyperkalaemia also interferes with the cardiac action potential, for reasons I don't understand. | ||
<section begin="clinical biochemistry" /> | |||
== Clinical features == | == 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. | 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. | ||
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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. | 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. | ||
<section end="clinical biochemistry" /> | |||
== Treatment == | == 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. | 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. | ||