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Background <p>Linezolid-induced hyperlactatemia may be masked by metabolic alkalosis, creating diagnostic challenges. This case demonstrates how acid–base disturbances can delay toxicity recognition in geriatric patients.</p> Case presentation <p>An 82-year-old Han Chinese woman with carbapenem-resistant&#xa0;<i>Acinetobacter baumannii</i>&#xa0;pneumonia developed severe hyperlactatemia (peak 17&#xa0;mmol/L) during linezolid therapy (600&#xa0;mg every 12&#xa0;hours for 14&#xa0;days). Despite progressive lactate elevation (1.6 → 17&#xa0;mmol/L), alkalotic pH (7.45–7.51) and normal anion gap (8–12&#xa0;mmol/L) obscured the diagnosis.</p> Interventions <p>Serial monitoring included arterial blood gas analysis and serum lactate levels. Linezolid was discontinued upon recognition of hyperlactatemia. Continuous renal replacement therapy was initiated post-discontinuation.</p> Outcomes <p>A lactate/HCO<sub>3</sub><sup>−</sup> ratio &gt; 0.17 (day 20) preceded metabolic decompensation by 5&#xa0;days. Renal replacement failed to correct lactate accumulation, suggesting irreversible mitochondrial damage.</p> Conclusion <p>pH-based monitoring inadequately detects linezolid toxicity in alkalotic patients. Lactate/HCO<sub>3</sub><sup>−</sup> ratios (&gt; 0.17) should be incorporated into geriatric antimicrobial protocols for early intervention.</p>

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Linezolid-associated severe hyperlactatemia masked by metabolic alkalosis in a geriatric patient: a case report

  • 期刊论文

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  • 发表日期：

    2025年11月18日

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  • Zhiyong Fei,
  • Chunye Dong,
  • Hua Xu,
  • Hong Dong

摘要

Background

Linezolid-induced hyperlactatemia may be masked by metabolic alkalosis, creating diagnostic challenges. This case demonstrates how acid–base disturbances can delay toxicity recognition in geriatric patients.

Case presentation

An 82-year-old Han Chinese woman with carbapenem-resistant Acinetobacter baumannii pneumonia developed severe hyperlactatemia (peak 17 mmol/L) during linezolid therapy (600 mg every 12 hours for 14 days). Despite progressive lactate elevation (1.6 → 17 mmol/L), alkalotic pH (7.45–7.51) and normal anion gap (8–12 mmol/L) obscured the diagnosis.

Interventions

Serial monitoring included arterial blood gas analysis and serum lactate levels. Linezolid was discontinued upon recognition of hyperlactatemia. Continuous renal replacement therapy was initiated post-discontinuation.

Outcomes

A lactate/HCO3− ratio > 0.17 (day 20) preceded metabolic decompensation by 5 days. Renal replacement failed to correct lactate accumulation, suggesting irreversible mitochondrial damage.

Conclusion

pH-based monitoring inadequately detects linezolid toxicity in alkalotic patients. Lactate/HCO3− ratios (> 0.17) should be incorporated into geriatric antimicrobial protocols for early intervention.