Abstract
The treatment of type 1 (ketosis-prone) or insulin-depend ent diabetes has not changed radically since the introduc tion of insulin into clinical practice in the 1920s. Modifications and improvements in the purity , supply , for mulations and regimens of insulin have provided signifi cant progress in diabetic management, but the presently available range of insulins and methods of delivery are still far removed from simulating the normal physiology of insulin secretion and action. The loss of the normal homeostatic mechanisms which maintain blood glucose within a narrow physiological range, render the diabetic individual susceptible to wide excursions in blood glucose and the intermittent hazard of metabolic extremes. This occurs with chronic hyperglycaemia and diabetic ketoaci dosis, which is fortunately now relatively infrequent, and acute hypoglycaemia which is an exceedingly common therapeutic side effect of insulin. Hypoglycaemia will be addressed in more detail here because of its potential effects on the diabetic eye.
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