Hypernatraemia and Hyponatraemia 43 



not respond, as does the ordinary case of diabetes insipidus, 

 with thirst. (He recovered spontaneously from his diabetes 

 insipidus, and from his hypernatraemia, after three months.) 

 Although this type of hypernatraemia might be termed cere- 

 bral, it is in fact a water deficiency due to the breakdown of 

 one of the mechanisms that normally ensure water balance. 



Renal effects of water deficiency. Before leaving the 

 question of hypernatraemia due to w^ater deficiency it may 

 be noted that in many of the reported cases the disturbance 

 apparently produced a disorder of tubular function, mani- 

 fested by oliguria with isosthenuria or by the excretion of 

 urine with a high pH in the presence of a systemic acidosis 

 (Cooper and Crevier, 1952 (Case 4); Gordon and Goldner, 1957; 

 Allott, 1957). This suggests that severe water deficiency may 

 be accompanied by tubular damage; Allott (1939) noted a 

 tubular degeneration in two of his cases post mortem. 



A tubular damage would help to explain the acidosis in at 

 least one of the patients of Higgins and his co-workers (1951). 

 It is not possible to say with any certainty whether these 

 patients were water-deficient, but all of them had a high 

 blood urea and in relation to this the urine volumes were 

 certainly small. It is also possible that in some patients 

 (e.g. Allott, 1957) polyuria with hyposthenuria represented 

 the diuretic phase of a tubular necrosis, itself the result of 

 dehydration. 



To sum up the question of "cerebral" hypernatraemia, a 

 failure of the thirst mechanism, with or without a diabetes 

 insipidus, accounts for some of the cases that have been 

 described; and, as Gordon and Goldner (1957) have ably 

 illustrated, unrecognized renal or extrarenal losses of fluid 

 must account for many more. 



If, as we believe, cerebral hypernatraemia is the result of 

 water deficiency then water will correct it, but only if enough 

 is given. Unfortunately most authors have underestimated 

 the amount of water required to correct a severe deficit. 

 Higgins and co-workers (1954) gave up to four litres to the 

 patients they thought were water-deficient. We give nearly 



