• J Bauza, J Ortiz, M Dahan, M Justiniano, R Saenz, and M Vélez.
• Ponce University Hospital, Puerto Rico.
• Bol Asoc Med P R. 1998 Jul 1;90(7-12):108-12.

ObjectiveTo determine the prevalence of hypomagnesemia in diabetic children during diabetic ketoacidosis and following restitution of acid-base balance.MethodsEight consecutive diabetic children, ranging in age from 8 to 16 years, hospitalized in the pediatric intensive care unit with diabetic ketoacidosis from October 1st. through December 31st, 1995. A control group of 33 metabolically stable diabetic children, and a control group of 30 healthy children. Both control groups were similar in composition regarding age and sex to the study group. None of the patients in the study group and none of the controls had Magnesium supplementation given to them during the study period.MeasurementsTotal serum Magnesium concentrations were measured from peripheral venous blood in all 71 patients. For the study group serum Magnesium was determined in a serial fashion: 1. upon admission in diabetic ketoacidosis 2. 24 hours after admission 3. 72 hours after admissionResultsThe prevalence of hypomagnesemia was 62.4% in patients with diabetic ketoacidosis, (Group 1), 25% in patients after partial correction of ketoacidosis, (Group 2), and none in patients after resolution of ketoacidosis, (Group 3). The prevalence of hypomagnesemia was 6% for the chronic, metabolically stable diabetic control group, (Group 4), but 0% for the non-diabetic control group, (Group 5). Average serum Magnesium levels were significantly lower (p less than 0.05), in patients admitted in diabetic ketoacidosis compared to those of both the diabetic and the non-diabetic control groups. Also average serum Magnesium levels were significantly lower (p less than 0.05), in patients with corrected diabetic ketoacidosis than those of the healthy control group. But there were no significant differences (p = 0.59263) in average serum Magnesium levels between the diabetic control group and the diabetic patients after resolution of ketoacidosis.ConclusionsIn this study the prevalence of hypomagnesemia was documented to be higher than the average described elsewhere for pediatric, adult, and coronary intensive care units. As hypomagnesemia is an indication of Magnesium depletion, we speculate that the transient hypomagnesemia detected in our study group is an expression of a state of Magnesium depletion that is masked by correction of acidosis and the Magnesium shifts associated with it. Consequently serum Magnesium values ought to be considered most reliable during and not after correction of diabetic ketoacidosis. Since Magnesium was not supplemented to any of our patients, the normalization of their serum values must be the result of: a. decreased glycosuria-related urinary losses b. cessation of acidosis-related urinary losses c. Magnesium shifts from intra to extracellular space The high prevalence of hypomagnesemia and the significant lower average serum Magnesium levels in children with diabetic ketoacidosis reveals the magnitude of the problem and the potential for Magnesium depletion that occurs in diabetic children.

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