Abstract Metformin-associated lactic acidosis (MALA) is a rare but life-threatening complication of Type 2 Diabetes Mellitus therapy, characterized by profound metabolic acidosis and refractory vasoplegic shock. In severe acidosis, adrenergic receptor responsiveness is markedly reduced, limiting the effectiveness of conventional vasopressors. Angiotensin II, which restores vascular tone through the renin-angiotensin-aldosterone pathway, offers a non-adrenergic mechanism of hemodynamic support. We describe a case of severe MALA successfully treated with angiotensin II following failure of standard vasopressor therapy. A 77-year-old man with hypertension, Type 2 Diabetes Mellitus, coronary artery disease, and anoxic brain injury presented with three days of malaise, fatigue, and altered mental status. He lived in an assisted living facility where staff administered his medications, including metformin, and reported poor oral intake preceding symptom onset. On presentation, he was borderline hypotensive, afebrile, and breathing comfortably on room air. Laboratory results showed a BUN of 64 mg/dL, creatinine 6.17 mg/dL, lactate 9.4 mmol/L, and an anion gap of 28. Osmolar gap and urine toxicology were unremarkable, and viral testing was positive for a non-COVID-19 coronavirus. He was admitted to the ICU for worsening hypotension, renal failure, and metabolic acidosis. Imaging and liver function tests revealed no alternative cause for lactic acidosis. His lactate and anion gap peaked at 20.5 mmol/L and 44, respectively, by hospital day 3. He required intubation for airway protection and was started on norepinephrine, vasopressin, hydrocortisone, and renal replacement therapy (RRT). Despite these interventions, shock persisted. Metformin levels later returned elevated at 21 mcg/mL. Angiotensin II was initiated with rapid improvement in blood pressure and RRT tolerance. He was weaned off vasopressors and discharged from the ICU without further dialysis requirements. In severe MALA, acidosis impairs catecholamine receptor sensitivity and reduces endogenous angiotensin II synthesis, contributing to refractory vasoplegia. Angiotensin II offers a physiologic mechanism to restore vascular tone independent of adrenergic pathways. In this patient, its use led to prompt hemodynamic recovery when conventional therapy failed. Although reports remain limited, this case highlights the potential role of angiotensin II as adjunctive therapy in refractory acidotic vasoplegia, aligning with post-hoc findings from ATHOS-3 demonstrating benefit in vasodilatory shock with renal failure. This abstract is funded by: None
Lam et al. (Fri,) studied this question.