Some Observations on the Water-Drinking Test in Glaucomatous and Non-Glaucomatous Subjects

THE imbibition of water is known to cause a rise in intra-ocular pressure in glaucomatous subjects, particularly in those in whom the intra-ocular pressure is raised initially (Leydhecker and Niesel, 1954).Although the test in its present form is of limited diagnostic value in cases of suspected glaucoma, it is of some academic interest in respect of the relationship of intra-ocular pressure to accompanying changes in the extracellular fluid of the body.This paper is a preliminary study of the nature of diuresis and of the alterations in diffusible and non-diffusible constituents of the blood in relation to intra-ocular pressure.The most noticeable effect of the imbibition of a large volume of water is a considerable diuresis, yet there is no gross dilution of the plasma (Haldane and Priestley, 1916).In glaucomatous subjects, Marx (1925), de Decker (1929), Wegner (1930 a, b), and Schmidt (1931) observed that the rise in intra-ocular pressure coincided with an initial dilution of the plasma, and that the latter was followed by phasic variations (as shewn by the haemo- globin content) which appeared to be due in sequence to (a) loss of water by diuresis and (b) migration of fluid from the plasma into and out of the tissues.These variations bore no relationship to the actual volume of water taken, nor to the diuresis (de Decker, 1929).There is no doubt that fluid interchanges in the body, as well as excretion, account for such con- flicting evidence as that of Marx (1926a), who found an initial fall of 12 per cent. in the plasma proteins with a return to normal level after 1 hours, and of Verney (1929), who later observed that there was no change in the plasma protein concentration even at the height of diuresis.The accumulated physiological evidence shews that in normal subjects (Best and Taylor, 1950) after water imbibition, the great bulk of ingested fluid leaves the vessels and is followed or accompanied by salt which serves to preserve the isotonicity of the tissue fluids:The load is subsequently discharged from the tissues in a slow but steady stream and transported to the kidneys (p.457).Further, the diuresis which follows is largely due to the inactivation of the antidiuretic factor (Verney, 1929) through a fall in the osmotic pressure *