From the Research
Liposomal amphotericin B causes cardiac ectopy on telemetry primarily through electrolyte disturbances, especially hypokalemia and hypomagnesemia, as a result of renal tubular dysfunction that impairs potassium and magnesium reabsorption, as seen in a case report of a neonate with persistent dyselectrolytemia induced by liposomal amphotericin B 1. When administered intravenously, amphotericin B can lead to significant electrolyte wasting, which alters cardiac cell membrane potentials and disrupts normal cardiac conduction, manifesting as premature atrial or ventricular contractions on telemetry. The development of hypokalemia is a well-known adverse effect of liposomal amphotericin B, with a study analyzing 56 episodes in 40 children and adolescents showing that hypokalemia occurred in 55.4% of episodes, with a median onset of 10 days after starting treatment 2. To prevent these complications, clinicians should monitor serum electrolytes (particularly potassium and magnesium) before, during, and after amphotericin B administration, with aggressive replacement as needed. Some key points to consider include:
- Premedication with normal saline (500-1000mL) can help reduce nephrotoxicity
- Slower infusion rates (over 2-4 hours) may help reduce the risk of arrhythmias compared to rapid administration
- Liposomal amphotericin B is as effective as conventional amphotericin B for empirical antifungal therapy in patients with fever and neutropenia, and it is associated with fewer breakthrough fungal infections, less infusion-related toxicity, and less nephrotoxicity 3
- The mechanism of nephrotoxicity involves direct cell membrane actions to increase permeability, as well as indirect effects secondary to activation of intrarenal mechanisms and/or release of mediators 4
- Solubilizing the standard amphotericin B preparation with 10% lipid emulsion may attenuate nephrotoxicity 5