Continuous Renal Replacement Therapy: Cause and Treatment of Electrolyte Complications

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Abstract
Continuous renal replacement therapy (CRRT) has become the modality of choice for critically ill patients. Although often hemodynamically better tolerated than intermittent dialysis, the continuous nature of this therapy may cause significant electrolyte complications. These complications commonly result from removal of electrolytes from the body without adequate replacement or because of the use of trisodium citrate as the anticoagulant. Both hypophosphatemia and hypokalemia frequently complicate prolonged treatment. These complications can be avoided by adding these electrolytes to the dialysate or replacement fluid. The use of citrate, especially if this anticoagulant is not used routinely following established protocols, can also result in several electrolyte abnormalities. Because citrate works by chelating calcium, hypo‐ and hypercalcemia occur because of under‐ or overreplacement of calcium. Because citrate is a base equivalent, if the bicarbonate concentration of the dialysate or replacement fluid is not decreased, a metabolic alkalosis may develop. Less commonly, in patients with severe liver dysfunction who cannot metabolize citrate back to bicarbonate, a metabolic acidosis may develop. Although CRRT may cause electrolyte complication it also can be the treatment of choice for the correction of certain electrolyte complications. In patients with acute or chronic renal failure who present with significant dysnatremias, intermittent hemodialysis may cause overly rapid correction of the serum sodium with serious neurologic sequelae. The ability to manipulate the sodium concentration of the dialysate or replacement fluid and the more sustained nature of the treatment allows for a slower correction thus avoiding complications.