Spontaneous and Induced Water Intoxication in Two Cases of Hypopituitarism
Authors: V. Wynn, O. Garrod
Journal: BMJ (1955)

It has been known for many years that patients with adrenocortical failure, whether this be primary or secondary to anterior hypopituitarism, are unable to excrete ingested water at the normal rate (Rowntree and Snell, 1931; Robinson et al., 1941; Levy et al., 1946).Less recognized is the possibility that patients with hypopituitarism may retain water in excess of electro- lytes while on ordinary diets and without apparent forcing of their fluid intake.Such water retention* would lead to dilution of body fluids (hypotonicity) and, finally, to symptoms of water intoxication.Whittaker and Whitehead (1954) have described the case of a patient with hypopituitarism whose death they attributed to spontaneous water intoxication.The present report describes two such cases in which a similar, though reversible, abnormality was observed.Apart from its spontaneous occurrence, water intoxication is occasionally precipitated by water-diuresis tests in patients with hypopituitarism.Pickford and Watt (1950) have reported this complication, which also occurred in both of our patients, In primary water retention the plasma sodium con- centration falls, although the total body sodium may not be reduced.The plasma sodium concentration may also be low in severe sodium depletion, a finding which, by itself, is often regarded as evidence of depletion of this ion.It is important, therefore, to distinguish be- tween these two hyponatraemic states, since they differ in cause, metabolic effects, and treatment (Wynn and Rob, 1954).Briefly, sodium depletion leads to loss of body water and haemoconcentration.The patient loses weight, looks haggard, and shows loss of tissue turgor.The circulation is impaired, the blood urea rises, the plasma potassium may be raised, and there is usually a metabolic acidosis.If the kidneys behave normally there is little fall in plasma sodium concentration until loss of this ion is more than 300-500 mEq (McCance, 1936), because water is at first excreted to maintain a normal osmotic pressure of the body fluids.With primary water retention there is no dehydration but the reverse.The body weight exceeds normal, and the circulation does not fail unless hypotonicity is extreme.The plasma sodium concentration is always *Unfortunately the term " water retention" is used in two seaise in clinical medicine.Most commonly it is used to imply potonic retention of both water and sodium, a condition which Ially results in pitting oedema.The second sense, used in this report, means that water is retained alone or in excess of electro- btes.Since about two-thirds of this water is located in the celi (Wynn and Rob, 1954) the result is not pitting textracel1ular) oedema but intracellular overhydration and dilution of body A1ids.low; acidosis and urea retention may be absent, and the plasma potassium concentration may be normal or low.The symptoms of water intoxication are not unlike those of sodium depletion, but with certain differences (Wynn and Rob, 1954).Gross hypotonicity causes weakness or great prostration, lethargy, anorexia, vomiting, mental disturbances, and, finally, convulsions and coma, which may prove fatal.The following two cases of hypopituitarism illustrate the occurrence of water intoxication, both spontaneously and after a water-excretion test.