Methylprednisolone-Induced Hyperlactatemia: A Case Report

Lactic acidosis is commonly encountered in critical care and can be a harbinger of life-threatening conditions and end-organ ischemia. Importantly, however, other etiologies of lactic acidosis exist. We review the first case of methylprednisolone-induced lactic acidosis in a previously healthy patient who suffered from traumatic spinal cord injury (SCI). A 19-year-old female presented to a level 1 trauma center after a fall resulted in lower extremity paralysis. After imaging revealed a chance fracture dislocation of T7-8 along with spinal cord compromise and swelling, the patient underwent emergent T5-T11 instrumented fusion. Postoperatively, she was given high-dose methylprednisolone in hopes of improving neurologic outcome; soon after administration, she developed lactic acidosis. After workup ruled out hypoperfusion and type A lactic acidosis, we determined that methylprednisolone likely induced non-ischemic, type B, lactic acidosis. The lactate quickly returned to baseline after steroid discontinuation. It is important for clinicians to consider type B lactic acidosis in the ICU in patients with persistent lactic acidosis after tissue hypoperfusion has been ruled out.