Background

Starvation ketoacidosis is an uncommon cause of high anion gap metabolic acidosis and is generally characterised by only mild to moderate ketosis and acidaemia. Severe biochemical derangement approaching that seen in diabetic ketoacidosis is rarely reported and may present a significant diagnostic challenge, particularly in patients with type 2 diabetes.

Case presentation

A 65-year-old woman with well-controlled type 2 diabetes mellitus (HbA1c 6.2%) presented with several days of markedly reduced oral intake, recurrent falls, hypothermia and documented hypoglycaemia (blood glucose 2.0 mmol/L prior to presentation). She was being treated with gliclazide and linagliptin and had never received a sodium-glucose cotransporter 2 (SGLT2)-inhibitor. Her medical history included ischaemic heart disease, chronic kidney disease and peripheral vascular disease.

Initial investigations demonstrated profound high anion gap metabolic acidosis (pH 7.05, bicarbonate 9 mmol/L, anion gap 27 mmol/L) with marked ketonaemia (7.0 mmol/L) and euglycaemia (blood glucose 7.8 mmol/L). The severity of the biochemical abnormalities closely resembled euglycaemic diabetic ketoacidosis. She was admitted to the intensive care unit and treated with intravenous insulin, dextrose and fluid resuscitation, resulting in rapid resolution of ketosis and acidosis. Her admission was complicated by Klebsiella oxytoca urinary tract infection, type 2 myocardial infarction and recurrent hypoglycaemia during insulin therapy. A C-peptide concentration of 0.5 nmol/L together with her low HbA1c, preceding prolonged fasting and absence of SGLT2-inhibitor exposure supported a diagnosis of severe starvation ketoacidosis precipitated by intercurrent infection rather than euglycaemic diabetic ketoacidosis.

Conclusion

Although typically regarded as a mild metabolic disturbance, starvation ketoacidosis can rarely present with life-threatening biochemical severity that closely mimics euglycaemic diabetic ketoacidosis. Recognition of prolonged fasting, recurrent hypoglycaemia and absence of SGLT2-inhibitor use are important clinical clues when evaluating euglycaemic high anion gap metabolic acidosis, as accurate diagnosis is essential to guide management and minimise complications such as treatment-related hypoglycaemia.