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Related Experiment Videos

[Deep lactic acidosis after valproate self-poisoning].

D Blayac1, A Roch, P Michelet

  • 1Département d'anesthésie-réanimation, hôpital Sainte-Marguerite, 270, boulevard Sainte-Marguerite, 13009 Marseille, France.

Annales Francaises D'Anesthesie Et De Reanimation
|October 27, 2004
PubMed
Summary

Severe Depamide (Valpromide) overdose in a patient led to coma and hypotension. Treatment with sodium bicarbonate and continuous venovenous haemodiafiltration facilitated recovery.

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Area of Science:

  • Toxicology
  • Critical Care Medicine
  • Pharmacology

Background:

  • Depamide (Valpromide) is an anticonvulsant medication.
  • Valpromide overdose can lead to severe toxicity, including neurological and cardiovascular complications.

Observation:

  • A 60-year-old female ingested 430 mg/kg of Valpromide, resulting in coma (Glasgow Coma Score 3), bilateral mydriasis, hypotension, acidosis, and hyperlactatemia.
  • Peak serum valproic acid concentration reached 342 mg/l, significantly exceeding the therapeutic range of 35-85 mg/l.
  • The patient required tracheal intubation, mechanical ventilation, and epinephrine infusion for hemodynamic support.

Findings:

  • Continuous infusion of sodium bicarbonate and continuous venovenous haemodiafiltration were initiated.
  • The patient showed progressive hemodynamic improvement and neurological recovery.

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  • Extubation was possible at 36 hours post-ingestion.

    • Implications:

    • This case highlights the potential severity of Valpromide overdose and the critical role of intensive care management.
    • Combined therapy with sodium bicarbonate and haemodiafiltration may be effective in managing severe valproic acid toxicity.
    • Prompt and aggressive supportive care is crucial for patient survival and recovery from Valpromide poisoning.