Case Presentation: A 69-year-old woman, previously diagnosed with type 2 diabetes and managed with Metformin, along with a history of heart failure with preserved ejection fraction, was admitted to the hospital due to abdominal pain, nausea, vomiting, and diarrhea that had been ongoing for the three days leading up to her presentation. On arrival at the emergency department, she was afebrile with a blood pressure of 130/70 mmHg, heart rate of 75/minute, respiratory rate of 21/minute, and 99% saturation on room air. The patient was in moderate distress due to abdominal pain. Her physical examination was unremarkable. Laboratory findings were remarkable for a white blood cell count of 11.00, sodium level of 132 mmol/L, and bicarbonate level of 18 mmol. Her anion gap was 27 mmol/L, creatinine was 6.32 mg/dL, Her baseline was 0.9 mg/dL, and lactate was 11.0 mmol/L. CT scan of the abdomen showed no acute pathology, EKG indicated normal sinus rhythm, and blood and urine cultures were sent for evaluation.The patient was admitted to the intensive care unit for monitoring, where she underwent aggressive intravenous fluid resuscitation and was commenced on empiric antibiotics. There was a heightened concern for Metformin-associated Lactic Acidosis (MALA) due to acute kidney failure resulting from gastrointestinal losses and elevated lactate levels. Metformin levels were promptly assessed. Within two hours of admission, the patient developed hypotension and hypothermia. A chest X-ray revealed no significant findings. Subsequently, a norepinephrine and bicarbonate drip was started, while emergent hemodialysis was initiated to correct acid/base abnormalities and facilitate the clearance of Metformin.Following the second dialysis session, lactate levels normalized to 1.5 mmol/L, and creatinine decreased to 1.6 mg/dL, accompanied by improvements in anion gap, pH, and bicarbonate levels. Blood cultures and an echocardiogram yielded normal results. In the subsequent days, there was a noticeable improvement in blood pressure and oxygen requirements. Due to low suspicion of infection, antibiotics were discontinued within two days. Subsequently, the admission metformin levels were disclosed as 25 mcg/mL (the therapeutic concentration being 1-2 mcg/mL). The patient was discharged five days after admission, and Metformin was discontinued upon discharge, with an allergy notation added to her medical chart.

Discussion: Metformin-associated Lactic Acidosis (MALA) is a rare condition; in cases of suspected lactic acidosis from metformin toxicity, it is essential to consider five criteria: history of metformin use; significantly elevated lactate level (> 15 mmol/L) with elevated anion gap (> 20); severe acidemia (pH 7.1); notably low serum bicarbonate level (< 10 mmol/L); and history of renal insufficiency. A metformin level can be obtained if there is concern for MALA, and the levels do not always correlate with the severity of MALA. Supportive care is the primary treatment for MALA, but severe cases might require mechanical ventilation, vasopressors, and renal replacement therapies (RRT). In our patient, Continuous hemodialysis was performed, which resulted in improvement of acidosis and renal recovery.

Conclusions: Metformin-associated Lactic Acidosis (MALA) is a rare condition, Patients with MALA may exhibit nonspecific symptoms. Diagnosis relies on clinical criteria, including metformin history, elevated lactate, acidemia, low bicarbonate, and renal insufficiency. Supportive care is the key treatment for MALA.