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A well-recognized complication of the transfusion of red blood cells (RBCs) is hyperkalaemia. This occurs in paediatric or adult patients receiving massive transfusion and can lead to cardiac arrest. Hyperkalaemia may follow the transfusion of 'stored' RBCs and/or haemolysed units, and depends on the quantity and rate of transfusion. We report on an unusual case of hyperkalaemia-induced cardiac arrest during transfusion of a 'fresh' blood unit. A 62-day-old baby girl was scheduled for a construction of a Blalock-Taussig shunt, after the completion of anastomosis, and upon release of vascular control, there was bleeding at the anastomotic site that was controlled with a suture placement. To compensate for the blood loss, a stat order was given for a push of 120 mL of RBCs over 10 min through the inferior vena cava central line. The blood unit was 6 days old and had been gamma-irradiated 48 h earlier. Shortly after the transfusion, the patient's electrocardiogram showed changes typical of hyperkalaemia; she then went into cardiac asystole. The blood unit potassium concentration was 55.3 mmol L-1, which flushed the atrioventricular node during transfusion. This is the first report of a high potassium level found in a 'fresh', less than 7 days old, nonhaemolysed RBC blood unit. The high concentration of potassium in this unit seems to be due to accelerated alterations of the RBC sodium/potassium adenosine triphosphatase pump (Na+/K+ pump), resulting in the release of intracellular potassium. This early and severe alteration of the pump and the unusually high potassium level may be due to as yet unexplained causes, warranting awareness, future investigation and routine saline washing of 'fresh' RBCs for paediatric patients who are candidates for central line transfusion.

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The tumour suppressor p53 induces cell death by launching several pathways that are either dependent on or independent of gene transcription. Accumulation of the sphingolipid ceramide and reactive oxygen species are among these pathways. Crossregulation of these two pathways is possible owing to the demonstrated inhibition of neutral sphingomyelinase by glutathione, the predominant cellular antioxidant, and has been observed in some cytokine-dependent cell-death models. In a model of irradiation-induced cell death of Molt-4 leukaemia cells, it was found that ceramide accumulation and glutathione depletion were dependent on p53 up-regulation. The loss of p53 owing to expression of the papilloma virus E6 protein inhibited both pathways after irradiation. However, in this model, these two pathways appeared to be independently regulated on the basis of the following observations: (1) glutathione supplementation or depletion did not alter irradiation-induced ceramide accumulation, (2) exogenous ceramide treatment did not induce glutathione depletion, (3) glutathione depletion was dependent on new protein synthesis, whereas ceramide accumulation was independent of it and (4) caspase activation was required for ceramide accumulation but not for glutathione depletion. Furthermore, caspase 9 activation, which is dependent on the release of mitochondrial cytochrome c, was not required for ceramide accumulation. This suggested that a caspase, other than caspase 9, was necessary for ceramide accumulation. Interestingly, Bcl-2 expression inhibited these pathways, indicating a possible role for mitochondria in regulating both pathways. These findings indicate that these two pathways exhibit cross-regulation in cytokine-dependent, but not in p53-dependent, cell-death models.