As early as the 19th century diabetic coma without ketoacidosis (d.c.w.k.) was considered by some authors to be a disease differing from the common diabetic coma. During recent years more than 60 cases have been published in the literature, still carrying a mortality of 50%.
We have collected another five cases. None of the patients was in deep coma and only one died. Four of the patients had previously been treated with thiazides which, in some of the cases, might have induced the diabetes.
The mechanism of the development and the treatment of d.c.w.k. is discussed. Administration of insulin and large quantities of fluid parenterally is necessary if the high mortality is to be reduced. For rehydration purposes we prefer hypotonic saline containing 100 mEq NaCl per litre.
The effect of a respiratory stimulant must be investigated primarily by spirometric experiments. However, increased ventilation need not be tantamount to a beneficial effect. Most respiratory stimulants are central analeptics exerting a more or less marked systemic effect, which means that they induce convulsions when given in large doses. It is reasonable to assume, therefore, that ordinary therapeutic dcsa may not only stimulate respiration, but also increase the muscular tonus and thereby the metabolic rate. Such an effect leads to increased consumption of oxygen and increased production of carbon dioxide, so the applicability of such a drug depends upon whether its overall effect gives a sufficient reduction in alveolar and arterial carbon dioxide tension. If metabolic alterations in the acid-base balance can be ruled out, the arterial pC0, represents the total effect of the drug upon respiration and metabolism.The preceding paper by COLDING et al. (1963)' reports the results of spirometric investigations during administration of Dimefline*).
MATE R I A LA total of nine therapeutic experiments with Dimefline were performed on nine patients with respiratory insufficiency due to chronic bronchitis and pulmonary emphysema. Without oxygen therapy, all these patients had reduced oxygen saturation (45-82%), and eight had moderate hypercapnia (pCO,, 45-70 mm Hg).
ANALYTIC M E T H O D SArterial oxygen saturation was measured by the method of ZIJLSTRA ( 1953)6, and pC0, by the ASTRUP apparatus (1956)'. The capillary oxygen saturation
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