LBODP034 Metformin Associated Lactic Acidosis, Rare But Real

Abstract

Abstract Background Metformin has been widely used as a first-line agent to treat type 2 diabetes mellitus. Although metformin has become a drug of choice for the treatment of type 2 diabetes mellitus, some patients may not receive it owing to the risk of lactic acidosis. Metformin increases plasma lactate levels in a plasma concentration-dependent manner by inhibiting mitochondrial respiration predominantly in the liver. Elevated plasma metformin concentrations (as occur in individuals with renal impairment) and a secondary event or condition that further disrupts lactate production or clearance (e. g., cirrhosis, sepsis, or hypoperfusion), are typically necessary to cause metformin-associated lactic acidosis (MALA). Case description We present a case of a severe metformin-induced lactic acidosis in a patient with type 2 DM admitted to the emergency department with a history of dehydration due to diarrhea and complicated by acute renal failure Our patient is a 57-year-old female with a medical history of DM on metformin 1000 mg twice daily, hypertension, hyperlipidemia, and hypothyroidism who presented to the hospital with a concern of altered mental status. Upon presentation, the patient could not provide much history, but her daughter confirmed that she was in her normal state of health until 2 weeks ago when she started complaining of knee pain and stated that she was taking ibuprofen 600 mg every 8 hours for pain with good response. Later, 2 days prior to her presentation she started having severe nausea, vomiting, weakness and was noted to be confused so she was brought to the emergency department. Upon arrival the patient's blood pressure was noted to be 104/50, GCS 15, rest of the vitals were within normal. Potassium was 5.5(3.4 - 5.3 mmol/L), bicarbonate 5(22 - 33 mmol/L), creatinine 10.2(0.4 - 1.1 mg/dL) compared to normal creatinine 6 months ago, GFR<5(>59 ml/min/1.73 sq meters, anion gap 41(4-16), PH 6.7(7.33 - 7.43), After resuscitation, her severe acidemia persisted despite aggressive intervention with volume resuscitation and vasopressors, leading to the initiation of renal replacement therapy. After multiple dialysis treatments, her severe acidemia resolved and creatinine improved back to baseline after which she was discharged home in stable condition. Conclusion The reported incidence of lactic acidosis in clinical practice has proved to be very low (<10 cases per 100,000 patient-years). This literature-based review provides an update on the impact of renal function and other conditions (cirrhosis, sepsis, or hypoperfusion) on metformin plasma levels and the risk of MALA in patients with type 2 diabetes. As these secondary events may be unpredictable and the mortality rate for MALA approaches 50%, metformin has been contraindicated in moderate and severe renal impairment to minimize the potential for toxic metformin levels and MALA. Presentation: No date and time listed