46 Paul Fourman and Patricia M. Leeson 



Water excess 



Water excess is a well recognized cause of hyponatraemia 

 when patients are given too much water while unable to 

 excrete it at the normal rate (Wynn, 1956). This may happen 

 in renal failure, in adrenal and pituitary insufficiency, and 

 postoperatively, particularly after mitral valvotomy (Bruce 

 et at., 1955). Hyponatraemia from this cause is usually obvious 

 from the circumstances. Such patients may have no symp- 

 toms; sometimes they have the syndrome of water intoxica- 

 tion, with fits and other profound neurological disturbances. 

 They may have hypertension; they certainly do not have 

 hypotension. The face looks bloated, not drawn. 



Both sodium deficiency and simple water excess respond to 

 the administration of hypertonic saline with a rise in the 

 plasma [Na] to normal which is subsequently maintained. 



There remains for consideration a large group of cases 

 where the hyponatraemia does not produce symptoms and its 

 mechanism is obscure. Elkinton (1956) and McCrory and 

 Macaulay (1957) have recently reviewed this problem. The 

 hyponatraemia appears to be associated with an expanded 

 volume of ECF; and the kidneys do not excrete water or 

 retain sodium to bring back the tonicity of the plasma to 

 normal (Leaf and Mamby, 1952). 



There are at least two possible explanations. The first is 

 that there is an abnormal stimulus to antidiuresis, say from 

 the "volume receptors", operating through the secretion of 

 ADH or in some other way (Kleeman et al., 1955; Ginsburg 

 and Brown, 1957). Pitressin given experimentally to normal 

 people leads to a retention of water, a fall in the plasma [Na] 

 and eventually an increased renal loss of sodium in spite of 

 the low plasma [Na] (Leaf et al., 1953; Weston et al., 1953; 

 Wrong, 1956). 



The second possibility is that an abnormal hypotonicity of 

 the cells determines the hypotonicity of the ECF (Sims et al., 

 1950; Rapoport, West and Brodsky, 1951). 



McCrory and Macaulay (1957) described an infant with 

 diffuse cerebral damage and hyponatraemia. Her ECF 



