An Extreme Case of Metformin-Associated Lactic Acidosis With a Remarkable Outcome

An Extreme Case of Metformin-Associated Lactic Acidosis With a Remarkable Outcome

Critical Care SESSION TITLE: Student/Resident Case Report Poster - Critical Care IV SESSION TYPE: Student/Resident Case Report Poster PRESENTED ON: Tu...

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Critical Care SESSION TITLE: Student/Resident Case Report Poster - Critical Care IV SESSION TYPE: Student/Resident Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM

An Extreme Case of Metformin-Associated Lactic Acidosis With a Remarkable Outcome John Watson MD*; and Adam Mora MD Baylor University Medical Center, Dallas, TX INTRODUCTION: Metformin-associated lactic acidosis (MALA) is a rare but well-documented phenomenon with an estimated incidence of 6 cases per 100,000 person-years (1). While often fatal, MALA carries a better prognosis than other etiologies of severe acidosis (2). CASE PRESENTATION: An 82 year-old man with non-insulin dependent diabetes mellitus (NIDDM) presented as a transfer for severe acidosis, respiratory failure requiring mechanical ventilation, profound shock requiring multiple pressor support, and renal failure. The patient presented to an outside hospital complaining of nausea and vomiting, was found to be hypotensive, and rapidly declined into shock with severe lactic acidosis. pH was 6.5 with a lactate of 28 mmol/L prior to transfer. Upon transfer, continuous renal replacement therapy (CRRT) was initiated, with hyperventilatory compensation for metabolic acidosis. The patient had a leukocytosis to 18.6 K/uL with a bandemia of 39%. His initial lactate was 28.6 mmol/L, and initial glucose was 16m g/dL with bicarbonate of 7mEq/L. A workup for infectious causes failed to yield positive results. Imaging studies did not support ischemic bowel contributing to his lactic acidosis. A metformin blood level was sent. The patient’s pH corrected from an initial value of 6.98 to 7.43 over 24 hours. The patient’s lactate began to decline, normalizing on hospital day #5. The patient was weaned from sedation on hospital day #3 and ultimately began following commands on hospital day #8. The patient was extubated on hospital day #9. The patient remained on CRRT, and urine output increased to 280cc per day by hospital day #10. On hospital day #11, metformin level returned at 11mcg/mL, suggesting his initial presentation was secondary to metformin toxicity. The patient’s overall status continued to improve with CRRT discontinued on hospital day #14. The patient was ultimately discharged to a skilled nursing facility. DISCUSSION: No randomized controlled trials exist to determine best treatment of MALA. Expert consensus and case reports suggest the use of CRRT can improve outcomes via both renal support and clearance of excess circulating metformin (2). Given the appropriate and adequate supportive measures, this case demonstrates that a pH of 6.5, when caused at least in part by metformin toxicity, can be survivable with aggressive medical management.

Reference #1: Salpeter SR, et al. Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Cochrane Database Syst Rev. 2010. p. CD002967. Reference #2: Allyn J, et al. Prognosis of patients presenting extreme acidosis (pH b7) on admission to intensive care unit. J Crit Care. 2016. 31(1): 243-248. Reference #3: Blough B, et al. Metformin-induced lactic acidosis with emphasis on the anion gap. Proc (Bayl Univ Med Cent). 2015. (1):31-3. DISCLOSURE: The following authors have nothing to disclose: John Watson, Adam Mora No Product/Research Disclosure Information DOI:

http://dx.doi.org/10.1016/j.chest.2016.08.454

Copyright ª 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

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CONCLUSIONS: This case highlights the importance of early recognition of the possibility of MALA in patients with severe lactic acidosis and a pH seemingly outside the realm of survivability.