Could There Be an Alternative Explanation for Cardiomyopathy in an Infant Following Fosphenytoin Overdose?

We read the recent report by Grageda et al with great interest. ¹ While we agree with the authors that profoundly elevated phenytoin concentrations might be responsible for the patient’s myocardial depression, we would like the authors to provide some missing information to help solidify their diagnosis.

Fosphenytoin is a prodrug form of phenytoin that is metabolized by blood and tissue phosphatases into phenytoin and phosphate. ² Metabolism of fosphenytoin has been shown to yield high serum phosphate concentrations following administration. ³ Resulting hyperphosphatemia has been shown to produce significant hypocalcemia with electrocardiogram changes. ⁴ Hypocalcemia itself has also been shown to cause reversible cardiomyopathy in infants, presenting as cardiogenic shock. ⁵

We would like to request that the authors provide the electrocardiogram and serum calcium and phosphate concentrations. While the temporal relationship to the medication error is evident, the omitted data points may help clarify the exact etiology of the cardiovascular compromise.