Myke D Federman1, Robert Kelly, Rick E Harrison. 1. Division 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
Abstract
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.
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.
Authors: David G Vossler; Jacquelyn L Bainbridge; Jane G Boggs; Edward J Novotny; Tobias Loddenkemper; Edward Faught; Marta Amengual-Gual; Sarah N Fischer; David S Gloss; Donald M Olson; Alan R Towne; Dean Naritoku; Timothy E Welty Journal: Epilepsy Curr Date: 2020-08-21 Impact factor: 7.500
Authors: Nicolas Gaspard; Brandon Foreman; Lilith M Judd; James N Brenton; Barnett R Nathan; Blathnaid M McCoy; Ali Al-Otaibi; Ronan Kilbride; Ivan Sánchez Fernández; Lucy Mendoza; Sophie Samuel; Asma Zakaria; Giridhar P Kalamangalam; Benjamin Legros; Jerzy P Szaflarski; Tobias Loddenkemper; Cecil D Hahn; Howard P Goodkin; Jan Claassen; Lawrence J Hirsch; Suzette M Laroche Journal: Epilepsia Date: 2013-06-12 Impact factor: 5.864