• DOI:10.1136/bmj.1.5068.435
• Corpus ID: 38775487

Salt Retention and Uraemia in Brain Injury

@article{Metz1958SaltRA,
  title={Salt Retention and Uraemia in Brain Injury},
  author={Robert J. Metz and W. F. Cooper},
  journal={British Medical Journal},
  year={1958},
  volume={1},
  pages={435 - 438}
}

• R. J. Metz, W. Cooper
• Published 22 February 1958
• Medicine, Biology
• British Medical Journal

sium chloride (2-10%), given within a matter of minutes. A few were observed after a 1.14% solution of potassium chloride (155 mEq of potassium per litre) had been given at the rate of 3-5 ml. a minute. However, during the treatment of diabetic ketosis, once diuresis has started, solutions containing up to 30 mEq of potassium per litre are frequently given at a rate of 3 ml. a minute without causing pain. In our case pain was caused by an infusion containing practically the same concentration of potassium (25 mEq /1. as potassium citrate plus 5-7 mEq/l. in the plasma of the blood), given at the same rate, suggesting that a low threshold of excitability was present in the pain receptors in the vein wall. It is known that spontaneous activity may be induced experimentally in nerve fibres by exposing them to potassium, which lowers the threshold of excitability (Brown' and MacIntosh 1939). The same effect may be produced by sodium citrate, which removes ionized calcium and increases the ratio of potassium to calcium ions acting on the nerve fibre (Katz, 1936; Brink and Bronk, 1937; Lehmann, 1937). Presumably the non-medullated nerve fibrils which subserve pain respond in a similar manner. In our case the blood being transfused contained 2 g. (1%) of disodium citrate as an anticoagulant, as well as 1.5 g. (0.278%) of added potassium citrate. It is probable, therefore, that the lowering of the pain threshold was due to potentiation of the potassium effect by the citrate.