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Acute phosphate intoxication in seven infants under parenteral nutrition
D Biarent1, C Brumagne, M Steppe
1Free University of Brussels, Intensive Care Unit for Children, Hôpital Universitaire des Enfants, Reine Fabiola, Belgium.
Insights
Infants receiving intravenous phosphate instead of calcium developed hyperphosphatemia and hypocalcemia but remained asymptomatic. Normalization occurred with glucose-in-water infusion, highlighting the importance of correct parenteral nutrition formulation.
Area of Science:
- Pediatric Nephrology
- Clinical Nutrition
- Intensive Care Medicine
Background:
- Parenteral nutrition is crucial for infants post-major surgery.
- Accurate electrolyte management is vital in neonatal intensive care.
- Phosphate and calcium balance are critical for infant homeostasis.
Purpose of the Study:
- To report a case series of infants mistakenly administered monosodium phosphate.
- To describe the resulting biochemical abnormalities and clinical outcomes.
- To compare findings with existing literature on acute phosphate intoxication.
Main Methods:
- Retrospective analysis of seven infants (4-29 weeks) receiving incorrect parenteral phosphate infusion.
- Biochemical monitoring of serum phosphate and calcium levels.
- Literature review of symptomatic acute phosphate intoxication cases in pediatrics.
Main Results:
- Infants developed significant hyperphosphatemia (8.0–14.4 mg/100 mL) and hypocalcemia (4 infants).
- All infants remained asymptomatic despite severe electrolyte disturbances.
- Biochemical parameters normalized within 24 hours after switching to glucose-in-water infusion.
Conclusions:
- Accidental monosodium phosphate administration can cause severe hyperphosphatemia and hypocalcemia in infants.
- Continuous infusion may lead to asymptomatic electrolyte derangements, unlike high-dose bolus phosphate intoxication.
- Prompt correction with hydration is effective in normalizing calcium and phosphate levels.
Abstract:
After major surgery, seven infants aged 4 to 29 weeks, under parenteral nutrition, received monosodium phosphate (4.2 to 14.3 mEq/kg body weight) instead of prescribed calcium gluconate. The wrong solution was perfused during 16 hours. At the 15th hour, blood samples showed hyperphosphatemia in all (8.0 to 14.4 mg/100 mL) and hypocalcemia in four infants (6.1 to 8.0 mg/100 mL), but all were asymptomatic. Under a perfusion of glucose in water, calcemia and phosphatemia returned to normal within 24 hours. In a review of the pediatric literature, we found 11 subjects with symptomatic acute phosphate intoxication, who also presented with hypocalcemia and hyperphosphatemia. The differences were that they received high bolus doses of phosphate orally or rectally and showed symptomatic features. Normalization of the calcemia occurred only when hyperphosphatemia was corrected throughout intravenous hydration.