Treatment: Hypokalemia

The goals of therapy in hypokalemia are to prevent life-threatening and/or serious chronic consequences, to replace the associated K⁺ deficit, and to correct the underlying cause and/or mitigate future hypokalemia. The urgency of therapy depends on the severity of hypokalemia, associated clinical factors (cardiac disease, digoxin therapy, etc.), and the rate of decline in serum K⁺. Pts with a prolonged QT interval and/or other risk factors for arrhythmia should be monitored by continuous cardiac telemetry during repletion. Urgent but cautious K⁺ replacement should be considered in pts with severe redistributive hypokalemia (plasma K⁺ concentration <2.5 mM) and/or when serious complications ensue; however, this approach has a risk of rebound hyperkalemia following acute resolution of the underlying cause. When excessive activity of the sympathetic nervous system is thought to play a dominant role in redistributive hypokalemia, as in thyrotoxic periodic paralysis, theophylline overdose, and acute head injury, high-dose propranolol (3 mg/kg) should be considered; this nonspecific β-adrenergic blocker will correct hypokalemia without the risk of rebound hyperkalemia. It should be noted that hypokalemia is refractory to correction in the presence of Mg⁺⁺ deficiency, which also should be corrected when present; renal wasting of both cations may be particularly prominent after renal tubular injury, e.g., from cisplatin nephrotoxicity.

Oral replacement with K⁺-Cl^- is the mainstay of therapy in hypokalemia. Potassium phosphate, oral or IV, may be appropriate in pts with combined hypokalemia and hypophosphatemia. Potassium bicarbonate or potassium citrate should be considered in pts with concomitant metabolic acidosis. The deficit of K⁺ and the rate of correction should be estimated as accurately as possible; renal function, medications, and comorbid conditions such as diabetes should also be considered so as to gauge the risk of overcorrection. In the absence of abnormal K⁺ redistribution, the total deficit correlates with serum K⁺ such that serum K⁺ drops by approximately 0.27 mM for every 100-mmol reduction in total-body stores. Notably, given the delay in redistributing potassium into intracellular compartments, this deficit must be replaced gradually over 24-48 h, with frequent monitoring of plasma K⁺ concentration to avoid transient over-repletion and transient hyperkalemia if otherwise appropriate. If hypokalemia is severe (<2.5 mmol/L) and/or if oral supplementation is not feasible or tolerated, IV KCl can be administered through a central vein with cardiac monitoring in an intensive care setting, at rates that should not exceed 20 mmol/h. KCl should always be administered in saline solutions, rather than dextrose; the dextrose-induced increase in insulin can acutely exacerbate hypokalemia.

Strategies to minimize K⁺ losses should also be considered. These measures may include minimizing the dose of non-K⁺-sparing diuretics, restricting Na⁺ intake, and using clinically appropriate combinations of non-K⁺-sparing and K⁺-sparing medications (e.g., loop diuretics with angiotensin-converting enzyme inhibitors).