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proceed with close monitoring given the risk of rebound hyperkalemia.
When potassium loss is accompanied by acid–base disturbance, a
redistribution effect should be factored when losses are estimated.
Magnesium supplementation is indicated in hypokalemia associated with
hypomagnesemia. In all cases of significant hypokalemia, monitoring for
ECG changes and muscle strength is imperative, and if abnormalities are
present, immediate replacement is warranted.
The choice of oral or IV replacement will depend on the severity of the
disorder and the ability to tolerate enteral salts. If the child is clinically well,
oral therapy is preferable and can be provided two to four times per day as
potassium chloride. Dosing may start at 2 to 5 mEq/kg/day and be adjusted
on the basis of serial laboratory assessment. If there is concurrent metabolic
acidosis, potassium citrate or bicarbonate can be provided. If the child is
unable to take oral medications or is symptomatic, IV potassium should be
provided. If the child is not symptomatic, potassium can be added to the
maintenance fluids. If intermittent infusion is indicated, this can begin with
an IV dose of 0.5 to 1 mEq/kg (typical maximum 30 to 40 mEq/dose).
Potassium chloride is typically used, but potassium phosphate may be used
in the treatment of DKA or documented severe hypophosphatemia.
Potassium acetate or its equivalent may be used if there is metabolic
acidosis. The infusion rate for clinically stable patients should provide 0.25
mEq/kg/hr, though emergent conditions may warrant the maximal rate of
0.5 to 1 mEq/kg/hr (maximum 15 to 40 mEq/hr depending on local policy)
with continuous ECG monitoring.
Hyperkalemia
Hyperkalemia is typically defined as serum potassium concentration
exceeding 6 mEq/L in neonates or 5.5 mEq/L in children or adults. Serum
potassium concentration is determined by the interplay of potassium intake,
distribution between the intracellular and extracellular space, and renal
excretion. Hyperkalemia can therefore result from excessive load,