(1569) Methylprednisolone-Induced Hyperlactatemia: A Case Report

Introduction: Lactic acidosis is commonly seen in the intensive care unit (ICU) and is often related to poor oxygen delivery and resultant anaerobic metabolism (type-A lactic acidosis).1 Importantly, however, hyperlactatemia can be due to other, non-perfusion related causes such as drugs or toxins (type-B lactic acidosis). While type-A lactic acidosis may be a harbinger of a life-threatening process, type-B lactic acidosis – particularly when medication-induced – is often benign. We present the first reported case of methylprednisolone-induced lactic acidosis in a healthy patient with acute spinal cord injury (SCI).

Description: A healthy 19-year-old female presented after a 12-foot fall with a chance fracture of T7 and T8 with spinal canal compromise. Initial laboratory and other imaging assessments were benign, and surgical fixation of the fracture was performed without complication. Protocolized care for acute SCI included maintenance of mean-arterial blood pressure >85 mmHg via a phenylephrine infusion, and fluid resuscitation. In addition, a bolus of 30 mg/kg methylprednisolone was given, followed by an infusion of 5.4 mg/kg over the following 23 hours. After methylprednisolone initiation, lactate rose to 6.4 mmol/L, peaking at 8.2 mmol/L.

Discussion: Steroid-induced elevations in lactate have been reported after perioperative use of high-dose dexamethasone in patients undergoing cardiopulmonary bypass, and in a single patient with COPD receiving a steroid burst.2,3 The mechanism is likely via steroid-induced hepatic gluconeogenesis, insulin resistance, and aerobic glycolysis.
When the etiology of lactic acidosis is unclear, a lactate-to-pyruvate ratio (LPR) can help to differentiate type-A and type-B lactic acidosis. In our patient, serial imaging and laboratory work were obtained to rule out type A lactic acidosis. Under normal, aerobic physiologic conditions, pyruvate is produced and then used by mitochondria to produce energy. This reaction occurs at a 1:10 ratio (LPR of ~10). When oxygen is not available, pyruvate accumulates, cellular acidosis develops, and the ratio of NADH-to-NAD increases, subsequently increasing the LPR (LPR>>10).1
Clinicians should be aware of this unusual complication and consider early assessment of the LPR to prevent unnecessary fluid resuscitation and imaging.