A reply

Abstract

We thank you for the opportunity to respond to Dr Horsey's comments on our case report and to clarify any ambiguity. The blood preparation given was indeed red cells in an SAGM preparation but Dr Horsey's calculations are somewhat misleading. Each SAGM unit contains around 220 ml red cells and 150 ml supernatant (100 ml SAGM anticoagulant plus 50 ml plasma). During storage, potassium leaks from the red cells (intracellular potassium concentration is approximately 100 mmol.l−1) down a concentration gradient into all components of the supernatant (plasma and SAGM solution not just the plasma component). Supernatant levels of around 30 mmol.l−1 can be expected after 3 weeks storage. We transfused 2 units (748 ml) of SAGM blood preparation; this amounts to a total potassium load of 9 mmol. In a 42-kg cachectic woman with a calculated blood volume of 2520 ml (plasma volume of around 1500 ml) this potassium load has the potential to raise the potassium level by 6 mmol.l−1. But this would assume that complete intravascular retention takes place, whereas it is known that potassium usually equilibrates rapidly between the plasma and the extracellular fluid. The laboratory potassium level of 9.5 mmol.l−1 and the ECG changes confirm that there was indeed significant intravascular retention. We appreciate that modest transfusions of this nature are usually safe and in our article tried to explore other avenues for such a marked effect. Some suggestions given in our paper were: endogenous potassium release (tumour manipulation), reduced circulating volume and cardiac output, rapid pressure bag infusion, etc. However, the timing of the cardiac arrest and clinical presentation would suggest the transfusion must be implicated. Anaesthetists should not be lulled into a false sense of security simply because modest volumes of blood preparations are being transfused.