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Refractory metabolic acidosis as a complication of high-dose midazolam infusion for pediatric status epilepticus
Myke D Federman1, Robert Kelly, Rick E Harrison
1Division of Pediatric Critical Care, Department of Pediatrics, Mattel Children's Hospital UCLA, 10833 Le Conte Ave., Los Angeles, CA 90095, USA. mfederman@mednet.ucla.edu
Insights
Continuous intravenous midazolam infusion for pediatric status epilepticus can cause severe metabolic acidosis. Healthcare providers should carefully monitor children receiving high-dose midazolam infusions.
Area of Science:
- Pediatric critical care medicine
- Neuropharmacology
Background:
- Midazolam is generally safe and effective for pediatric status epilepticus.
- Continuous intravenous infusions of midazolam show encouraging efficacy in pediatric patients.
Observation:
- A 9-year-old girl with refractory status epilepticus received high-dose, continuous intravenous midazolam.
- The patient developed severe hyperchloremic metabolic acidosis and hemodynamic compromise.
Findings:
- The complication is suspected to be due to hydrochloric acid in the midazolam preparation.
- Metabolic acidosis resolved within 5 hours of stopping the midazolam infusion.
- Inotropic and vasopressor support was weaned after midazolam discontinuation.
Implications:
- Caution is advised when administering continuous intravenous midazolam infusions to pediatric patients.
- Close clinical and laboratory monitoring is essential for pediatric patients receiving high-dose midazolam.
- This complication highlights potential risks associated with parenteral midazolam preparation.
Background:
The use of midazolam for the treatment of status epilepticus in children has generally been shown to be well tolerated and safe. Furthermore, encouraging efficacy has been observed when pediatric patients with status epilepticus have received continuous intravenous infusions of midazolam.
Case Presentation:
A 9-year-old girl was treated with high-dose, continuous intravenous infusion of midazolam for the management of refractory status epilepticus. The patient developed a severe hyperchloremic, non-anion gap metabolic acidosis and resultant hemodynamic compromise, necessitating significant inotropic support and the initiation of a vasopressor infusion. We speculate that this complication was due to the preparation of parenteral midazolam with hydrochloric acid. The midazolam infusion was stopped, and, in less than 5 hours, the patient's metabolic acidosis resolved. The patient's inotropic and vasopressor infusions could only be weaned after discontinuing the use of high-dose midazolam.
Conclusions:
Although this complication was observed in only 1 pediatric patient with cortical dysplasia, caution and close clinical and laboratory surveillance should be exercised when administering continuous intravenous infusions of midazolam to pediatric patients.
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