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[Anesthetic-induced heart arrest. A case report of 2 infants with previously unrecognized muscular dystrophy]
J Stelzner1, F J Kretz, A Rieger
1Klinik für Anaesthesiologie und operative Intensivmedizin, Freie Universität Berlin.
Insights
Two infants experienced cardiac arrest during anesthesia induction due to suspected anesthesia-induced acute rhabdomyolysis or malignant hyperthermia, highlighting risks in pediatric patients with undiagnosed muscular dystrophy.
Area of Science:
- Pediatric Anesthesiology
- Neuromuscular Disorders
- Critical Care Medicine
Background:
- Anesthesia induction carries risks, especially in infants with potential underlying myopathies.
- Congenital muscular dystrophies can present with severe complications during surgical procedures.
Observation:
- Two boys (4 months and 10 months) suffered cardiac arrest post-anesthesia induction.
- Both infants received halothane, N2O/O2, atropine, and succinylcholine.
- One infant experienced immediate cardiac arrest with rigidity; the other developed bradycardia progressing to asystole.
Findings:
- The younger infant showed extreme hyperkalemia and elevated creatine phosphokinase, with muscle biopsy revealing congenital muscular dystrophy.
- The older infant survived after resuscitation, exhibiting myoglobinuria and significantly elevated creatine phosphokinase, with biopsy confirming muscular dystrophy (Duchenne excluded).
- Potential causes discussed include anesthesia-induced acute rhabdomyolysis and malignant hyperthermia.
Implications:
- Highlights the critical need for careful anesthetic management in infants with suspected or undiagnosed neuromuscular conditions.
- Suggests that severe hyperkalemia and rhabdomyolysis can be triggered by specific anesthetic agents in susceptible pediatric patients.
- Emphasizes the importance of prompt recognition and management of cardiac arrest and related complications during pediatric anesthesia.
Abstract:
We report two boys aged 4 and 10 months who suffered cardiac arrests after induction of anaesthesia. Both infants had no personal or family history of myopathy. In both cases anaesthesia was induced by inhalation with halothane and N2O/O2 (70/30). To facilitate tracheal intubation both were given succinylcholine after the administration of atropine. The 4-month-old developed muscle rigidity and cardiac arrest occurred immediately after tracheal intubation. Resuscitation was unsuccessful. Laboratory findings during resuscitation showed elevated serum potassium levels of more than 10 mmol/l and serum creatine phosphokinase 17.700 IU/l. Histopathologic examination of the skeletal muscle revealed congenital muscular dystrophy. In the older boy no muscle contractures were noted after administration of succinylcholine. He developed bradycardia that progressed to asystole 15 min after induction of anaesthesia. After 1 h of resuscitation a sinus rhythm could be established. The boy developed myoglobinuria and his serum creatine phosphokinase reached a maximum level of 45,000 IU/l on the 2nd day. The child survived and made a complete recovery. Two months later a muscle biopsy taken from the quadriceps showed marked muscular dystrophy. Duchenne's muscular dystrophy could be excluded. The most likely underlying reasons for these complications are discussed: anaesthesia-induced acute rhabdomyolysis or malignant hyperthermia.