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Abstract: FR-PO606

Treatment of Severe Metformin-Associated Lactic Acidosis (MALA) with Continuous High Flux Hemodialysis and Tris-Hydroxymethyl Aminomethane (THAM)

Session Information

  • Trainee Case Reports - III
    October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 102 AKI: Clinical, Outcomes, and Trials

Authors

  • Tiwary, Abhinav K., UMMS-Baystate , Springfield, Massachusetts, United States
  • Landry, Daniel L., Kidney Care and Transplant Services of New England, Springfield, Massachusetts, United States
  • Abdullin, Marat, Kidney Care and Transplant Services of New England, Springfield, Massachusetts, United States
  • Tiru, Bogdan, Baystate Medical Center, Springfield, Massachusetts, United States
  • Papamarkakis, Kostas, Baystate Medical Center, Springfield, Massachusetts, United States
  • Braden, Gregory Lee, Kidney Care and Transplant Services of New England, Springfield, Massachusetts, United States
Introduction

Hemodialysis is the preferred modality for severe lactic acidosis due to MALA. We report a case of ingestion of 480 grams of metformin. After 33 hours of high flux hemodialysis (HFHD) his severe MALA was reversed by THAM. This is the first case report of the use of THAM to treat severe MALA not responding to HFHD alone.

Case Description

A 43-year-old suicidal man with type 2 diabetes ingested the largest reported dose of metformin, 480000 mgs. Initial serum potassium was 4.9 mmol/L, bicarbonate (HCO3) 16 mmol/L, anion gap 22, serum lactate 6.2 mmol/L, & an ABG showed a ph 7.16, pCO2 36, PO2 247 & HCO3 12 mmol/L. He was intubated for airway support & activated charcoal & polyethylene glycol given by NG tube. Repeat labs showed a potassium of 7.4 mmol/L, lactate of 6.6 mmol/L, & pH of 7.06. Emergent high flux HFHD was initiated. After 12 hours of dialysis the metformin dialyzer clearance was 416 ml/min which is significantly better than earlier reports of 68-228 ml/min. Due to a persistent lactate of 22.6 - 31.4 mmol/L we continued HFHD for a total of 33 hours. The next day the serum ph was only 7.11 and the serum HCO3 10` mmol/L. A dose of THAM was calculated as follows: THAM (ml of 0.3 mol/L solution) = lean body weight (kg) x base deficit (mmol/L).We chose 3 times the usual base deficit to increase serum HCO3 by 15 mmol/L rather than the usual 5. We gave 1280 ml of THAM over 12 hours, enough to increase the serum HCO3 by 15 mmol/L. Levophed & vasopressin for hemodynamic support were rapidly weaned. The serum lactate corrected dramatically after THAM from 31.4 to 6.2 mmol/L. In fact, over the next 24-hours, the serum lactate normalized along with pH & HCO3 levels.

Discussion

Our study is the first successful use of THAM with continuous HFHD in a patient with severe MALA complicated by anuria. THAM rapidly equilibrates into the intracellular space of liver, muscle & intestine. We hypothesize that the rapid increase in tissue pH inhibits lactate dehydrogenase & increases the activity of pyruvate dehydrogenase & pyruvate carboxylase leading to rapid inhibition of lactate production & enhanced metabolism of lactate. Our case supports the use of THAM to augment continuous HFHD for the correction of severe acidemia associated with MALA.