Case Report: Massive sustained-release valproate overdose with prolonged gastric tablet retention and partial...

Valproate poisoning is a potentially life-threatening condition that may result in central nervous system depression, hyperammonemia, metabolic disturbances, and multiorgan dysfunction. Management of massive sustained-release valproate overdose remains challenging because delayed gastrointestinal absorption may lead to prolonged toxicity despite conventional decontamination measures.

A 23-year-old woman with a history of previous suicide attempts was admitted approximately 6 hours after ingesting ninety 500-mg sustained-release valproate tablets (total dose 45 g) with alcohol. Upon arrival, she exhibited severe agitation and delirium. Endotracheal intubation was performed for airway protection because she was unable to cooperate with treatment and was at risk of aspiration. Gastric lavage and cathartic therapy were subsequently administered. The initial serum valproate concentration was 1,093.66 μg/mL. Because incomplete decontamination was suspected, bedside upper gastrointestinal endoscopy was performed approximately 11.5 h after ingestion. Fourteen intact and markedly swollen tablets were removed; some were separate, whereas others were adherent and partially aggregated, supporting partial pharmacobezoar formation and prolonged gastric drug retention. During intensive care unit management, the patient developed severe hyperammonemia (peak ammonia 205 μmol/L), hyperlactatemia with mixed metabolic acidosis and respiratory alkalosis, acute kidney injury, marked creatine kinase elevation, hypernatremia, and suspected transient central diabetes insipidus. Meropenem was administered empirically from May 31 to June 3 because impaired airway defenses after intubation raised concern for aspiration-related infection, although no definite infectious focus or causative pathogen was identified. Because of substantial financial hardship, extracorporeal treatment was initially deferred. It was initiated at 20:00 on June 1, approximately 62 h after ingestion and 56 h after hospital admission. Two consecutive 2-h sessions of hemoperfusion combined with CVVH were followed by CVVH alone until 08:30 on June 2. The serum valproate concentration decreased from 397.05 μg/mL before extracorporeal treatment to 12.72 μg/mL during ongoing CVVH and was 8.61 μg/mL approximately 70 h after treatment cessation. The patient was discharged on June 15 without evident neurological, cognitive, or motor impairment.

Massive sustained-release valproate overdose may cause prolonged gastric retention of intact and partially aggregated tablets, thereby sustaining systemic toxicity. In selected patients, endoscopic tablet removal may provide toxicological source control, while extracorporeal treatment may remain beneficial even when its initiation is delayed. The respective contributions of endoscopy, meropenem exposure, spontaneous elimination, and extracorporeal treatment cannot be separated in this single case.