A74-year-old woman with insulin-dependent diabetes was admitted to the medical high dependency unit with a 2-day history of increasing nausea and confusion. On examination she was afebrile, dehydrated and confused. Systemic examination was unremarkable. Capillary blood glucose by self-monitoring strip was 10.6 mmol/litre and urinalysis demonstrated 3+ ketones and 3+ glucose. Biochemical examination revealed plasma glucose 11.9 mmol/litre, sodium 127 mmol/litre, potassium 5.1 mmol/litre, urea 13.9 mmol/litre and creatinine 87 mmol/litre. Arterial blood gas analysis showed pH 7.30, partial pressure of carbon dioxide = 4.4 kPa, partial pressure of oxygen = 9.0 kPa, bicarbonate = 15.3 mmol/litre, base excess -9.2 mmol/litre and oxygen saturation 97%. She was treated with intravenous dextrose-saline and low dose insulin infusion. She made a good recovery and was well within 48 hours of presentation.

We present two cases of diabetic ketoacidosis in type 1 diabetic patients who presented with normal glucose levels. The clinical picture and biochemical profile were typical of diabetic ketoacidosis, although if only the blood glucose level at presentation had been taken into account the unwary would have missed the diagnosis. The two cases highlight that ketoacidosis in diabetes can occur with near‐normal blood glucose and that levels of blood glucose and development of ketoacidosis do not necessarily correlate. ‘Euglycemic ketoacidosis’ was originally described whereby the initial blood glucose was less than 16.7 mmol/L and plasma bicarbonate equal to or less than 10 mmol/L. The cause of preserved ‘euglycemia’ could be greater urinary loss of glucose triggered by counter‐regulatory hormones or decreased rate of hepatic glucose production observed during a fast as in a state of diabetic ketoacidosis. Better education and home blood glucose monitoring with appropriate increase in insulin doses during intercurrent illness may be another factor responsible for the rising incidence of euglycemia. One must use urinary ketones and arterial blood gas measurement in all known diabetic patients who are unwell on presentation to diagnose ‘euglycaemic diabetic ketoacidosis’ and treat them with cautious use of low‐dose insulin infusion and intravenous fluids, otherwise a potentially treatable condition may be missed. We discuss euglycaemic diabetic ketoacidosis, an entity we believe is possibly on the rise and discuss the available, albeit controversial and scarce, literature. Copyright © 2001 John Wiley & Sons, Ltd.

Acute onset quadriparesis can be a manifestation of a variety of neurological and metabolic conditions. We report the case of a 47‐year‐old alcoholic gentleman who presented with acute onset weakness of all four limbs associated with hypokalemia and very high blood glucose (hyperosmolar nonketotic diabetes—HNKD) detected for the first time. He was confirmed as having type 2 diabetes (detectable insulin and C‐peptide levels) and his quadriparesis completely resolved on potassium replacement and treatment with insulin. HNKD is discussed along with the possible mechanisms of hypokalemia in this patient presenting with reversible limb weakness as an initial manifestation of type 2 diabetes. Copyright © 2002 John Wiley & Sons, Ltd.

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