Discussion 95 



McCance: It is a question of definition. Do you mean by dehydration 

 a rise in the tonicity of the extracellular fluid due to an increase in the 

 quantity of sodium there, or do you mean by dehydration a decrease in 

 the total amount of water in the body? 



Adolph : I think one type of dehydration would exist if we are satisfied 

 that there is no change in the concentration, but a decrease in the volume. 



Fourman : In the patients with hypernatraemia who have an increased 

 volume of the extracellular fluid, is this increase appropriate or inappro- 

 priate to the requirements of the cells? Is the hypotonicity something 

 determined by the cells or something imposed upon them? Water in- 

 toxication with its characteristic symptoms (Weir, J. F., Larsen, E. E., 

 and Rowntree, L. G. (1922). Arch, inter?!. Med., 29, 306) exemplifies an 

 inappropriate imposition; here the hypotonicity of the extracellular 

 fluid is accompanied by a swelling of the cells. An "appropriate" fall in 

 tonicity and increase in volume of the extracellular fluid is not associated 

 with these symptoms. The patients I mentioned earlier do not have 

 evidence of water intoxication. 



After every stress, these patients with hyponatraemia returned to 

 their original low concentration of extracellular fluid. One feels that the 

 concentration is determined by the cells — a new steady state. We do 

 believe that this low concentration of the extracellular fluid must be the 

 result of a low osmotic pressure of the cells. There are obviously different 

 kinds of hypotonicity of the extracellular fluid, with and without symp- 

 toms of water intoxication. When there are symptoms, the cells are 

 swollen. Miss Leeson and I have been wondering whether a lack of 

 symptoms means the cells are not swollen, but merely hypotonic. 



Swyer: I was referring to the opposite problem, namely that in labour 

 dehydration is accompanied by lack of potassium. Presumably this 

 increase in specific gravity of the plasma and the apparent loss of plasma 

 potassium would not be consistent with normal functioning of the cells. 

 It might therefore complicate still further the prolongation of labour. 



Fourman: I do need convincing that any case of high serum sodium, 

 which these patients have, is not a case of dehydration. 



You made another very fascinating statement which I would be very 

 glad to have amplified. Not being a paediatrician I do not see very much 

 of these adrenogenital syndromes. In Addison's disease, on the other 

 hand, I think it would be exceptional to find that the patient with a high 

 plasma potassium as a leading feature would die of a cardiac arrest as a 

 result. The general experience is to find that there is depletion of sodium 

 and, incidentally, but not clinically important, a raised serum potassium. 

 I wonder whether there is a different abnormality in a simple lack of 

 sodium-retaining hormone, which would account for the — to me rather 

 surprising — predominance of changes in the serum potassium. We have 

 one patient who is being maintained after adrenalectomy with cortisone 

 but because she has heart failure we are not giving her any sodium- 

 retaining hormone. To my astonishment our problems in her are those 

 of transient paralysis with very high plasma potassium (9 m-equiv./l.). 



Swyer: High plasma potassium is one of the outstanding features, as I 

 think Dr. Talbot wfll also agree, in adrenal hyperplasia. In the salt-losing 



