Abstract: SA-PO505
Linezolid-Induced Lactic Acidosis
Session Information
- Acid-Base, Calcium, Potassium, and Magnesium Disorders: Clinical
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Seethapathy, Ritu, Landmark Medical Center, Woonsocket, Rhode Island, United States
- Klufas, Andrew, Roger Williams Medical Center, Providence, Rhode Island, United States
- Monsour, Michael J., Landmark Medical Center, Woonsocket, Rhode Island, United States
Introduction
Linezolid inhibits bacterial protein synthesis by preventing formation of 70S initiation complex needed for bacterial reproduction. This site of action is unique to linezolid, distinguishing it from other protein synthesis inhibitors.
Case Description
A 93-year-old woman presented to the hospital after nursing home labs showed elevated creatinine, nitrite positive urinalysis, and normal lactic acid. Urine culture grew VRE susceptible to linezolid and she was discharged on a course of linezolid.
Two weeks post-discharge, the patient was readmitted with dyspnea, with labs showing AKI and significant lactic acidosis (LA). CT C/A/P revealed bilateral opacities consistent with pneumonia. She was started on a bicarbonate drip per Nephrology recommendations. Her FeUrea was consistent with prerenal AKI and urine output was ~400 cc/dy.
Unfortunately, the patient then became hypotensive requiring pressor support, thought to be secondary to her significant LA causing her hemodynamic instability, rather than the inverse. Linezolid toxicity was the leading diagnosis and she was switched to meropenem and started on IV thiamine. Although the patient’s pH normalized, her LA worsened. Hemodialysis was declined per the family’s wishes and patient was made CMO after extensive goals of care discussion.
Discussion
Linezolid Induced Lactic Acidosis (LILA) is due to an interaction between the drug and mitochondrial ribosomes; inhibition of mitochondrial protein synthesis causes impaired oxidative phosphorylation, thus limiting aerobic energy production.
LILA is a diagnosis of exclusion after ruling out common causes of LA and has been found to cause hemodynamic instability in patients. Previous studies have shown that mortality from LILA does not have a strong correlation with age, gender or duration of treatment, however, mortality is as high as 50% in patients with shock.
LILA can often be associated with hypoglycemia however our patient was normoglycemic throughout hospitalization. Management of LILA consists of withdrawal of the drug and supportive care. Previous case reports suggest that critically ill patients further benefit from concurrent renal replacement therapy, like treatment of metformin induced lactic acidosis.
LILA is a poorly understood side effect of patients treated with even a short course of linezolid. Given high rate of mortality, further investigation is warranted to study etiology of LILA to prevent its occurrence.