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A 13-year-old adolescent presented for correction of an 85-degree idiopathic thoracic scoliosis. She was known to have Prader-Willi syndrome. Previous general anaesthesia for non-spinal surgery had been uneventful. On two occasions following uneventful induction and total intravenous anaesthesia (TIVA) maintenance, she developed severe recalcitrant bradycardia with hypotension that was resistant to anticholinergics, inotropes and vasopressors upon prone positioning. Immediate resolution occurred upon a return to the supine position. On each occasion, she emerged from anaesthesia with no untoward sequelae. Cardiac investigations, including echocardiography, electrocardiography (ECG), troponin and creatine kinase-MB fraction levels were all within the normal range, and ventricular function was good. It was necessary to urgently proceed with the surgery as the scoliosis was progressive, with risks of cardiovascular and respiratory compromise. Additionally, she was scheduled to recommence growth hormone therapy postoperatively to treat her growth retardation. Ultimately, she received propofol for induction of anaesthesia and TIVA with propofol and remifentanil infusions for the maintenance of anaesthesia. Post-induction, a transvenous pacing wire was placed under ECG guidance. A transoesphageal probe was inserted and cardiac function monitored throughout the procedure. Upon prone positioning, she again developed a bradycardia which responded to pacing and surgery was carried out uneventfully. Clinical examination and extensive investigations had failed to demonstrate any specific underlying cause for her repeated positional arrhythmia. Therefore, we deduced that the bradycardia was due to a hypervagal response provoked by prone positioning and because of the severity of the scoliosis. We are unaware of reports of such a complication in the literature.Keywords: anaesthesia, cardiovascular, scoliosis, bradycardia, pacing

We describe a case of a 2-year-old boy who ingested 35 mg.kg(-1) of amitriptyline. He developed central nervous system toxicity, as demonstrated by coma and seizures and cardiac toxicity (cardiac arrest) within 1 h of ingestion. The cardiac toxicity was refractory to standard therapy. His cardiac rhythm alternated between ventricular tachycardia and pulseless ventricular tachycardia/ventricular fibrillation for a period of 17 h. Following prolonged cardiopulmonary resuscitation and aggressive supportive management, the patient recovered both cardiovascularly and neurologically. An echocardiogram and MRI brain were subsequently performed and were normal. The patient was discharged 2 weeks later with normal cognitive, behavioral and motor function. We discuss the benefit of prolonged and effective cardiopulmonary resuscitation in the management of this potentially fatal poisoning.

Genetic analysis of 617 first-degree relatives of 97 patients with idiopathic cardiomyopathy suggests that this disease has both dominant and recessive modes of transmission.