Neurotoxicity and Status Epilepticus After Inadvertent Intrathecal Tranexamic Acid: A Case Report

Inadvertent intrathecal administration of tranexamic acid (TXA) is a rare but potentially fatal medication error that causes acute neurotoxicity, thought to be mediated by antagonism of gamma-aminobutyric acid type A (GABA-A) and glycine receptors.No treatment guidelines specific to intrathecal TXA toxicity exist.A man in his early 30s received an estimated 280 mg of TXA intrathecally instead of bupivacaine during spinal anaesthesia for ankle fracture fixation because of ampoule misidentification.No block developed; he reported severe back and gluteal pain and then developed myoclonus and generalised tonic-clonic convulsions that did not respond to midazolam.General anaesthesia was induced, phenytoin and levetiracetam were loaded, and fracture fixation was completed.Recurrent convulsions at the end of surgery, consistent with convulsive status epilepticus, were treated with diazepam, propofol and magnesium sulphate, after which no further convulsive activity was observed; because neuromuscular blockade had been given and electroencephalography (EEG) was unavailable, nonconvulsive seizures could not be excluded.Cerebrospinal fluid (CSF) lavage was then performed.Brain computed tomography on day one showed no acute abnormality.Consciousness remained impaired for several days: he was comatose on day three, still ventilated on day four, extubated and oriented by the morning of day five, and discharged home on day eight.A routine EEG at 11 weeks and brain magnetic resonance imaging at about three and a half months were normal, and at three months he had a normal neurological examination with no further clinically recognised seizures while taking levetiracetam.The contribution of individual interventions cannot be determined from a single case.The principal lesson is preventive: TXA must be stored and handled separately from neuraxial drugs, with independent pre-administration checks.