C49-10 Fatal Metformin-Associated Lactic Acidosis Mimicking COPD Exacerbation

Abstract A 71-year-old female, with a history of chronic obstructive pulmonary disease (COPD) on home oxygen, type 2 diabetes mellitus complicated by neuropathy (on Janumet), chronic kidney disease (CKD) stage 3, hypertension, dyslipidemia, and multiple comorbidities, presented to the emergency department with acute shortness of breath of one day’s duration. Emergency Medical Services found her hypoxic with SpO2 at 80%, requiring oxygen supplementation. On arrival, she reported bilateral lower back and leg pain. Despite bronchodilators, steroids, antibiotics, and fluid resuscitation, her respiratory status deteriorated rapidly, necessitating intubation for acute hypoxic respiratory failure, initially presumed to be due to COPD exacerbation. In the ED, she developed severe hypotension unresponsive to fluids and required vasopressor support with norepinephrine and vasopressin. Initial laboratory findings revealed acute kidney injury on CKD, high anion gap metabolic acidosis, and markedly elevated lactate (6.4 → 12.68 mmol/L). Arterial blood gas showed profound acidosis (pH 7.05, pCO2 27.8, pO2 93). White blood cell count was elevated at 18,000, possibly steroid-induced, and proBNP was 648, suggesting cardiac strain. Imaging studies including chest X-ray and CT scans excluded pneumonia, pulmonary embolism, or other acute pathology. Blood and urine cultures remained negative. In the medical ICU, she remained intubated, sedated, and in shock with cold extremities. EKG revealed new junctional rhythm. Given the severe lactic acidosis, renal impairment, and use of metformin (Janumet 50/1000 mg BID), metformin-associated lactic acidosis (MALA) was suspected as the primary etiology. Differential diagnoses included sepsis, distributive shock, and cardiogenic shock. Broad-spectrum antibiotics were continued empirically, and continuous renal replacement therapy (CRRT) was initiated to address metabolic derangements. Despite transient improvement, lactate levels remained critically elevated, and the patient’s hemodynamics failed to stabilize with multiple vasopressors. Over the following days, the patient’s condition progressively worsened with refractory shock and multiorgan failure. In 3 days since admission, despite maximal supportive measures, she suffered cardiac arrest and was pronounced dead. This case underscores the diagnostic difficulty of metformin-associated lactic acidosis (MALA), especially in patients with comorbid COPD and CKD. The presentation resembled a COPD exacerbation with respiratory failure, delaying recognition of the metabolic cause. Although rare, MALA has a high mortality rate and should be suspected in patients with unexplained high anion gap acidosis and elevated lactate, particularly with renal dysfunction and metformin use. Early diagnosis and prompt dialysis are essential, but outcomes remain poor in severe cases. This abstract is funded by: None