Dysregulation of calcium homeostasis after severe burn injury in children: Possible role of magnesium depletion

Objective: To determine the cause and extent of hypocalcemia observed in children after severe burns. Design: We studied 10 children with burns covering 57% ± 17% (SD) body surface area, ages 9.6 ± 4.7 years, who were admitted consecutively during a 6-month period. Diet supplied a minimum of 2.7 gm/m² of calcium, 0.3 gm/m² of magnesium, and 2.2 gm/m² phosphate. Blood specimens were obtained daily for 10 ± 5 days for the following tests: (1) simultaneous analysis for ionized calcium, magnesium, and intact parathyroid hormone (group A); (2) two of these children, randomly selected, had serial 2-hour determinations on a single day (group B); (3) a modified Ellsworth-Howard test, consisting of a 10-minute infusion of synthetic parathyroid hormone 18 ± 10 days postburn and associated changes in urinary cyclic adenosine monophosphate excretion and renal threshold phosphate concentration (group C). Three of these children, when normomagnesemic, also received a standard magnesium infusion to determine magnesium retention (group D). Data were analyzed with chi-square, regression analysis, and nonparametric testing as appropriate. Results: All patients showed sustained hypocalcemia and hypomagnesemia; intact parathyroid hormone response was inappropriately low and response to synthetic parathyroid hormone infusion was blunted. Lowest ionized calcium levels were associated with hypomagnesemia. Conclusion: Hypoparathyroidism and blunted renal response to parathyroid hormone suggest that magnesium depletion may contribute to their pathogenesis. Magnesium repletion and monitoring are recommended.