Preventing and Managing Catastrophic Drug Errors in Neuraxial Anaesthesia: The Tranexamic Acid Experience

Background: Accidental intrathecal administration of tranexamic acid (TXA) is a rare but potentially fatal medication error during neuraxial anaesthesia. TXA, an antifibrinolytic agent, inhibits plasminogen activation to reduce bleeding but causes severe neurotoxic and cardiotoxic effects when administered intrathecally (1,2). Neurotoxicity results from competitive antagonism of GABA_A and glycine receptors in the spinal cord and brain, producing neuronal hyper-excitability, seizures, and myoclonus (3,4,5). Ventricular arrhythmias may result from sympathetic overactivity (6,7). We report an ASA grade II patient undergoi Case Presentation: ng haemorrhoidectomy who inadvertently received 300 mg intrathecal TXA instead of 15 mg hyperbaric 0.5% bupivacaine. Lack of anaesthetic effect led to a repeat subarachnoid block within 20 minutes, masking early signs of TXA toxicity. Postoperatively, the patient developed abdominal myoclonic jerks, refractory seizure and ventricular arrhythmias. Lower limb myoclonus was initially unnoticed. Isoflurane anaesthesia was instituted to induce coma and reduce cerebral metabolic demand. A cerebrospinal fluid (CSF) tap was considered but deferred, as the drug had already widely distributed within the CNS. Intensive supportive management and close monitoring enabled full recovery by day 7. This case emphasises the catastrophic consequences of intrathecal TXA and the importance of strin Discussion: gent verification protocols, segregation of look-alike vials, and careful evaluation of block failure before repeating neuraxial anaesthesia (4,8,9). Symptomatic management includes anticonvulsants, haemodynamic support, sedation, and, in selected cases, CSF lavage to reduce TXA concentration (6,10,11,12). Despite such measures, mortality remains significant in reported cases. Prevention through rigorous anaesthetic safety practices and improved pharmaceutical packaging differentiation is critical. Further research is required to clarify TXA's neurotoxic and cardiotoxic mechanisms and optimise treatment strategies.