Scrutiny of trials involving glargine and detemir has increased our understanding of how best to dose basal insulins. An individualized approach is still necessary however, and several questions remain that require further research.
An overall hospital mortality rate of 3.9% was found in 929 episodes of diabetic ketoacidosis treated in single centre over a 21-year period. The mortality rate in the first half of the survey (4.4%) was not significantly different from that in the second half of the survey (3.4%). Six deaths in patients under 50 years of age occurred in the first half, but only one death under 50 years occurred in the second half of the survey. The number of deaths from a metabolic cause where no other illness was identified also fell from nine (43% of deaths) in the first half to five (33% of deaths) in the second half of the study (not significant). The remaining deaths were due to concurrent illness, mainly myocardial infarction and serious infections. Many of the residual deaths occurred in elderly patients with such medical illness in addition to the ketoacidosis. It may, therefore, prove difficult to reduce mortality further in diabetic ketoacidosis.
The original criteria described for euglycaemic ketoacidosis (initial blood glucose less than 16.7 mmol/l and plasma bicarbonate equal to or less than 10 mmol/l) were identified in 23 of 722 consecutive episodes (3.2%) of diabetic ketoacidosis. True euglycaemic ketoacidosis (initial blood glucose 10 mmol/l or less) was rare, occurring in 0.8-1.1% of all episodes depending on the defining plasma bicarbonate concentration. Management of euglycaemic ketoacidosis with low-dose continuous intravenous infusion of insulin together with adequate fluid replacement was effective. The clinical and biochemical data did not support the concept of euglycaemic ketoacidosis as a separate entity. The importance of ketone testing rather than glucose testing in the diagnosis of ketoacidosis is, however, emphasized. The importance of adequate insulin and fluid therapy in those few episodes where blood glucose is normal or near normal at presentation is also highlighted.
The mortality rate from myocardial infarction is disproportionately high in diabetic patients. One explanation for this may be that diabetic patients incur more extensive myocardial necrosis. This possibility was examined in a three part study. Firstly, peak serum aspartate aminotransferase concentrations of all diabetic and non-diabetic patients admitted with myocardial infarction over a 16 year period were compared retrospectively. Secondly, peak aspartate aminotransferase concentrations in a series of diabetic patients and controls matched by age and sex were examined retrospectively. Thirdly, creatine kinase MB release and electrocardiographic measures of infarct size were investigated prospectively in a case/control study. Although cardiac failure and death were more common in the diabetic groups, there were no significant differences in estimates of infarct size between diabetic and non-diabetic patients in any of the studies. Therefore, the high case fatality rate amongst diabetic patients is not caused by increased myocardial damage. Presumably survival is prejudiced by factors operating before the infarction.
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