Potassium deficits and shifts by far pose the most immediate electrolyte-based risk. On average, potassium losses range from 3 to 5 meq/kg, though deficits as high as 10 meq/kg body weight have been reported. Despite these total body deficits, initial serum laboratory measurements may be normal. Serum potassium may even be high in the presence of acidemia. Patients whose initial serum potassium measurements are low are at highest risk for cardiac dysrhythmia and respiratory arrest and should be treated with urgency. Insulin therapy will likely correct acidemia while increasing renal potassium losses as GFR is restored. Also, insulin therapy may cause precipitous shift of potassium into the cell. Usually well within the first 12 h of therapy, most patients will be hypokalemic if replacement therapy has not begun.

With adequate urinary output, potassium replacement should begin at serum K + of 4.5 to 5.0 meq/L. In general, potassium should be replaced at a rate of 10 to 20 meq/h, though life-threatening hypokalemia may warrant utilizing infusion rates of up to 60 meq/h. Some authors feel that potassium infusion through a central venous catheter poses risk for conduction defects and should be avoided. If properly diluted, peripheral infusions of potassium through two peripheral intravenous lines are well tolerated. Monitoring of serum potassium should occur every hour until a steady state has been achieved.

Sodium deficits are replenished fairly rapidly, considering the amount of normal saline and half-normal saline given during fluid replacement. Phosphate and magnesium levels should be measured. In cases of severe hypophosphatemia or hypomagnesemia, replacement therapy is indicated.

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