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Magnesium-chloride/magnesium-oxide/tacrolimus High stool output, metabolic acidosis and exacerbation of hypomagnesaemia: case report

A 7-year-old boy experienced exacerbation of hypomagnesaemia during treatment with tacrolimus. Additionally, he also experienced high stool output and metabolic acidosis during treatment with magnesium chloride and magnesium oxide [not all routes and dosages stated; durations of treatments to reactions onsets not stated]. The boy, who had Gitelman syndrome (GS), was referred for acute onset right-sided hemiplegia and aphasia. Head CT showed an ischaemic stroke of the left middle cerebral artery. Echocardiogram identified severely depressed biventricular function with ejection fraction of 18%, dilated cardiomyopathy and no atrial shunt. Echocardiogram 2 years previously had showed normal biventricular function. He was stabilised by milrinone treatment, which was then changed to magnesium supplementation (magnesium chloride and magnesium oxide) and unspecified enteral heart failure medications, as well as unspecified anticoagulation prophylaxis for potential cardioembolic stroke. At discharge, he had right-sided weakness and mild expressive aphasia. Within 4 months, he developed decompensated heart failure, necessitating readmission for transplant evaluation and listing. He was bridged to transplant with dobutamine and milrinone, along with a high-dose magnesium infusion. He was listed status 1A by exemption. Owing to the history of stroke, he was not offered a ventricular assist device as the risk of systemic anticoagulation was assumed to outweigh the benefit of mechanical circulatory support. Following 7 months of waitlist time, he underwent heat transplantation. Other than the requirement of multiple potassium and magnesium replacements to maintain the serum levels, no additional operative or anaesthetic management issues related to his GS were observed. Normal graft function was observed on subsequent echocardiograms. Posttransplant, tacrolimus use in the setting of the underlying GS induced exacerbation of recalcitrant hypomagnesemia. His postoperative course was complicated by ventricular tachycardia with no evidence of rejection, coronary artery abnormality or reperfusion injury. The boy was started on lidocaine and subsequently switched to enteral amiodarone. Additionally, he developed remarkable tetany and cramping in the extremities limiting mobility, which ameliorated with higher serum magnesium levels. Both unique postoperative symptoms were treated with the use of magnesium infusion (up to 33 mg/kg/day magnesium chloride and 73 mg/kg/day magnesium oxide). Transition to enteral magnesium was found to be challenging with high stool output and resultant metabolic acidosis. Eventually, he was discharged home 79 days after the transplant (289 hospitalisation days including waitlist time) achieving goal magnesium levels of 1.2 mEq/L with 6–7 loose stools per day. Subsequently, his serum magnesium level had ameliorated to average 1.7 mEq/L, and the amount of magnesium suppl