By Jeremy Hughes; Ashley Jefferson; John Iredale
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G. g. potassium-sparing diuretics, tubulointerstitial disease, obstructive nephropathy). It should be noted that diabetic patients with diabetic nephropathy may develop hyporeninaemic hypoaldosteronism and troublesome hyperkalaemia at an earlier stage than non-diabetic patients with chronic renal impairment, often necessitating the institution of renal replacement therapy at an earlier stage. 5 mmol/L then emergency treatment is merited. Check the ECG trace for signs of cardiac instability and proceed to emergency treatment if ECG changes are present.
Give intravenous calcium gluconate (10%, 10 mL administered over 5 min) to antagonise the effects of hyperkalaemia on the heart and stabilise the myocardium. This drug is short acting and may need to be repeated. 2. Shift potassium into cells by giving insulin and dextrose (6 units fast-acting insulin and 50 mL 50% dextrose) over 10 min. Commence an insulin and dextrose infusion (6 units fast-acting insulin, 50 mL 50% dextrose in 500 mL 5% dextrose) with monitoring of blood glucose levels. d. 1 Emergency therapy of hyperkalaemia 2 Hyperkalaemia over 1–2 h).
Consider pseudohyperkalaemia in situations where there is a marked leukocytosis (>11 Â 106/mL) or thrombocytosis (>400 Â 106/mL). In this case the serum K concentration will be raised but the plasma K level will be normal. High potassium intake Increased potassium intake per se is not a cause of hyperkalaemia as the kidneys can excrete a large potassium load. A high potassium intake, however, may be a significant contributing factor especially in patients with impaired renal function. High intake may be dietary (fruits, certain vegetables) or iatrogenic (secondary to excessive K replacement).
Clinical chemistry made easy by Jeremy Hughes; Ashley Jefferson; John Iredale