The mechanisms involved in the production, maintenance and progression of the state of nonketotic, hyperosmolar coma of mild diabetic patients are discussed; and a method is outlined for both initial therapy (before insulin activity is sufficiently increased) and subsequent therapy. Factors involved in the development of the syndrome include: (1) Persistence of enough insulin production to prevent ketoacidosis but very severe suppression of insulin release in relation to the level of blood glucose. (2) Insidious development of extreme hyperglycemia, increasingly great osmotic diuresis, severe depletion of body water and large volumes of urine. (3) Lack of appropriate response of the thirst center as the sensorium becomes inadequate.

Because the mortality of this condition now approaches 50 per cent, careful attention to details of therapy is imperative. Delay in recognition and, therefore, of therapy leads to fatalities.

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