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[Tetraparesis in an infant after prolonged administration of pancuronium]
F Bordet1, B Contamin, J C Berthier
1Service de Réanimation Pédiatrique, Hôpital Debrousse, Lyon.
Insights
Prolonged pancuronium infusion in a pediatric patient led to severe tetraparesis. This rare neuromuscular complication resolved over three months, suggesting axonal degeneration.
Area of Science:
- Neurology
- Pediatric Critical Care
- Pharmacology
Background:
- Long-term pancuronium use for ventilatory support in adults with ARDS can cause severe tetraparesis.
- This adverse effect is uncommon in pediatric intensive care units.
Observation:
- A 9-month-old girl with severe bronchopneumonia required prolonged mechanical ventilation.
- She received an 11-day infusion of pancuronium (approx. 120 mg) to manage chest wall rigidity.
- Following discontinuation, she developed severe tetraplegia with areflexia, but maintained normal head movements.
Findings:
- Electromyography confirmed normal neuromuscular transmission.
- Other causes of peripheral neuropathy were ruled out through comprehensive testing.
- The patient's recovery pattern indicated regeneration following axonal degeneration.
Implications:
- This case highlights the potential for severe neuromuscular complications, including tetraparesis, from prolonged high-dose pancuronium administration in pediatric patients.
- Concurrent use of corticosteroids and aminoglycosides may be associated with these neuromuscular adverse effects.
- Understanding these risks is crucial for optimizing neuromuscular blockade management in critically ill children.
Abstract:
Long-term administration of pancuronium for ventilatory support of adults with ARDS may result in severe tetraparesis, with areflexia and atrophy of distal muscles. This adverse effect occurs rarely in paediatric intensive care units. We describe a case of tetraparesis after prolonged pancuronium infusion in a 9-month-old girl who experienced a severe bronchopneumonia caused by para-influenza virus, requiring endotracheal intubation and mechanical ventilation. To decrease chest wall rigidity, pancuronium was administered over 11 days, with a total dose of approximately 120 mg of pancuronium bromide. The day after discontinuation of the muscle relaxant she had a severe tetraplegia with areflexia, but normal head movements. Electromyography showed a normal neuromuscular transmission. She recovered from tetraplegia three months later. Other causes of peripheral neuropathy were eliminated. Electroencephalograms and head CT-scans were normal. The recovery pattern observed in our patient corresponded to the process of regeneration seen after axonal degeneration. It is suggested that these neuromuscular complications were caused by prolonged high-dosage pancuronium treatment, associated with corticosteroid and aminoglycoside administration.