Euglycaemic Diabetic Ketoacidosis

Abstract

liferative glomerulonephritis, two had total kidney infarction, and one had severe interstitial nephritis with, on biopsy, what appeared to be severe tubular compression. The remaining patient had a combination of extensive tubular blockage due to myeloma protein and glomerulonephritis.The possible mechanisms underlying the development of these various nephrographic patterns have been recently reviewed (Fry and Cattell, 1972). Space precludes any further discussion of these at this time. It must, however, be reemphasized that the diagnostic value of the nephrographic pattern relates to the changes in density observed with time. Precise measurement of absolute density is difficult, depending as it does on many independent variable factors. In general, doubtful changes in density should be ignored and only unequivocal changes recorded. On no account should a diagnosis be attempted when the urographic technique has resulted in unsatisfactory radiographs.Though based on relatively small numbers of cases these observations confirm that distinctive nephrographic patterns are observed in patients with acute renal failure. They also indicate that more extensive observations are required both to assess more fully the diagnostic value of the nephrographic pattern and to define more clearly the mechanisms underlying the development of the different patterns.We would like to record our appreciation of the work of the radiographers responsible for these examinations, especially Miss Jill Baldock, Miss Anne Casey, and Miss Jane Cooper who were the superintendent radiographers. We would also like to thank Mrs. Sylvia Welsh for her invaluable help throughout the study.

Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis

“…The development of blood ketone meters allows us to focus on the underlying metabolic abnormality (ketonaemia). This simplifies treatment of patients who present with only modest elevation of blood glucose, but with acidosis secondary to ketonaemia-'euglycaemic diabetic ketoacidosis' [1,13,14]. This clinical presentation is encountered more frequently as improved patient education with increased blood glucose and ketone monitoring has led to partial treatment of diabetic ketoacidosis prior to admission and lower blood glucose levels at presentation.…”

90 years of insulin therapy – analysis of its success and failure

“…A "very simple" solution has been found: decreased concentration of plasmatic insulin is the cause of HHNS, its absolute deficiency is the cause of DKA. But successively appeared reports which casted doubt on the role of insulin in the development of DKA: the existence of euglycemic DKA [6] and even DKA in hypoglycaemia [7] is difficult to explain as consequence of insulin deficiency.…”

An unexpected hazard of insulin injection

“…Their discussion centres on historical descriptions, particularly by Munro et al, where euglycaemia was originally described when the blood glucose was less than 16.7 mmol/L, and the ensuing debate regarding whether a lower glucose should be used 2,3 .…”