High anion gap metabolic acidosis (HAGMA) in diabetes is commonly attributed to diabetic ketoacidosis (DKA); however, concurrent causes should be considered when severity is disproportionate or fails to respond to standard therapy.

A 90-year-old woman who was independent with no significant comorbidities, type 2 diabetes mellitus, hypertension and dyslipidaemia presented with confusion, recurrent falls and reduced oral intake following a recent upper respiratory tract infection. Prior outpatient pathology demonstrated reasonable glycaemic control (HbA1c 8.1%) and preserved renal function (creatinine 78 µmol/L, eGFR 65 mL/min) on metformin 1 g daily and linagliptin.

On admission she was haemodynamically stable but had severe HAGMA (pH 7.15, bicarbonate <4 mmol/L), hyperglycaemia (35 mmol/L), mild ketosis (3.4 mmol/L), marked lactataemia (7.7 mmol/L) and acute kidney injury (creatinine 656 µmol/L, eGFR 4 mL/min). She was treated initially as DKA with intravenous fluids and insulin infusion.

Despite insulin infusion, acidosis worsened with rising lactate and worsening hypotension requiring vasopressor support. Inflammatory markers were only mildly elevated (WCC 12 ×10⁹/L, CRP 12 mg/L) and she remained afebrile, making sepsis less likely. There were no clinical features of bowel ischaemia or perforation, and imaging options were limited by renal failure. ECG demonstrated borderline QRS widening, inferior T-wave inversions and non-specific ST-T changes in the setting of severe lactic acidosis.

Given preserved baseline renal function, ongoing metformin exposure, profound dehydration and acute renal failure, impaired metformin clearance was considered the main contributor to the progressive lactic acidosis and clinical deterioration, likely contributing to cardiovascular collapse. ^1,2 The patient progressed to multi-organ failure, and, after multidisciplinary discussion, care was transitioned to palliation. She died the following day.

Persistent or worsening HAGMA and lactataemia despite standard DKA therapy should prompt reassessment for alternative pathology, including metformin-associated lactic acidosis, particularly in patients with acute kidney injury and ongoing metformin exposure.