Valproate overdose: a comparative cohort study of self poisonings (original) (raw)
Related papers
Massive valproic acid overdose, a misleading case
American Journal of Emergency Medicine, 2008
Seizures are often attributed to a low plasma concentration of antiepileptic drugs, although sometimes it can be due to a high plasma concentration of the antiepileptic drug. This case report describes a very severe valproic acid intoxication including paradoxical seizures, which was initially held for a subtherapeutic valproic acid treatment. Applied treatment strategy based on available evidence is discussed. A more careful clinical evaluation at admission might have guided the treating physicians to the right diagnoses from the start. The important lesson is that several antiepileptic medicines, as valproic acid, can cause seizures in overdose.
Favorable results after conservative management of 316 valproate intoxicated patients
Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences, 2015
Valproic acid (VPA) is an effective antiepileptic drug widely used worldwide. Despite several studies indicating the usefulness of intravenous L-carnitine in the treatment of VPA poisoning, this drug is not readily available in Iran. The aim of this study was to determine whether supportive care without antidote would result in acceptable outcomes in VPA poisoned patients. In an observational, retrospective, single-center case series, all patients >12-year-old with VPA overdose who had referred to a tertiary center between 2009 and 2013 were consecutively enrolled. Patients' demographic and presenting features, physical examinations, clinical management, laboratory data, and outcomes were recorded. A total of 316 patients were enrolled with pure VPA toxicity. The most common presenting signs/symptoms were drowsiness, nausea and vomiting, vertigo, and headache. In the course of the disease, 14 patients (4.4%) were intubated and three (0.9%) required hemodialysis with mean dial...
Cureus
Patients presenting with hyperammonemic encephalopathy are likely to have hepatic encephalopathy. However, valproate (an anticonvulsant and mood stabilizer) can also cause hyperammonemic encephalopathy and belongs on the differential for patients taking it, especially if there are recent contributory medication changes. We present a case report of a 61-year-old woman with valproate-induced hyperammonemic encephalopathy but with an initial valproate level within the therapeutic range (50-100 mcg/dL). After withholding valproate and before additional treatment could be initiated, she became fully alert and oriented. We present a literature review exploring valproate toxicity and treatment. Our case shows that clinical suspicion for valproate-induced hyperammonemic encephalopathy is warranted even if the valproate level is within the therapeutic range.
Valproic acid poisoning: An evidence-based consensus guideline for out-of-hospital management*
Clinical Toxicology, 2008
A review of US poison center data for 2004 showed over 9000 ingestions of valproic acid. A guideline that determines the conditions for emergency department referral and prehospital care could potentially optimize patient outcome, avoid unnecessary emergency department visits, reduce health care costs, and reduce life disruption for patients and caregivers. An evidence-based expert consensus process was used to create the guideline. Relevant articles were abstracted by a trained physician researcher. The first draft of the guideline was created by the lead author. The entire panel discussed and refined the guideline before distribution to secondary reviewers for comment. The panel then made changes based on the secondary review comments. The objective of this guideline is to assist poison center personnel in the appropriate out-of-hospital triage and initial out-of-hospital management of patients with a suspected ingestion of valproic acid by 1) describing the process by which an ingestion of valproic acid might be managed, 2) identifying the key decision elements in managing cases of valproic acid ingestion, 3) providing clear and practical recommendations that reflect the current state of knowledge, and 4) identifying needs for research. This guideline applies to the acute ingestion and acute-on-chronic ingestion of immediate-release and extended-release dosage forms of valproic acid, divalproex, and valproate sodium alone. Co-ingestion of additional substances could require different referral and management recommendations depending on the combined toxicities of the substances. This review focuses on the ingestion of more than a single therapeutic dose and the effects of an overdose. Although therapeutic doses of valproic acid can cause adverse effects in adults and children, some idiosyncratic and some dose-dependent, these cases are not considered. This guideline is based on an assessment of current scientific and clinical information. The expert consensus panel recognizes that specific patient care decisions might be at variance with this guideline and are the prerogative of the patient and the health professionals providing care, considering all of the circumstances involved. This guideline does not substitute for clinical judgment. Recommendations are in chronological order of likely clinical use. The grade of recommendation is in parentheses. 1) All patients with suicidal intent, intentional abuse, or in whom a malicious intent is suspected (e.g., child abuse or neglect) should be referred to an emergency department (Grade D). 2) Patients who are symptomatic (more than somnolence or exhibiting coma or seizures) after a valproic acid ingestion should be referred to an emergency department (Grade C). 3) Asymptomatic patients with an unintentional acute ingestion of 50 mg/kg or more or asymptomatic patients who are taking the drug therapeutically and who take an additional single acute ingestion of 50 mg/kg or more of any valproic acid formulation should be referred to an emergency department for evaluation (Grade C). 4) Patients with unintentional ingestions of immediate-release valproic acid formulations, who are asymptomatic, and more than 6 hours has elapsed since the time of ingestion, can be observed at home (Grade C). 5) Patients with unintentional ingestions of delayed-release or extended-release formulations of valproic acid who are asymptomatic, and more than 12 hours has elapsed since the time of ingestion, can be observed at home (Grade C). 6) Pregnant women who ingest below the dose for emergency department referral and do not have other referral conditions should be directed to their primary care obstetrical provider for evaluation of potential maternal and fetal risk. Routine referral to an emergency department for immediate care is not required (Grade D). 7) Do not induce emesis (Grade C). 8) Activated charcoal can be administered to asymptomatic patients who have ingested valproic acid within the preceding hour (Grade C). Prehospital activated charcoal administration, if available, should only be carried out by health professionals and only if no contraindications are present. Poison centers should follow local protocols and experience with its use. Do not delay transportation in order to administer activated charcoal (Grades D). 9) In patients who have ingested valproic acid and who are comatose, naloxone can be considered for prehospital administration in the doses used for treatment of opioid overdose, particularly if the patient has respiratory depression (Grade C). 10)
Journal of Clinical Toxicology, 2015
Introduction: Intoxication with Sodium valproate (SVP) is a growing concern owing to its increased use and availability. SVP intoxication may result in cerebral, cardiovascular, respiratory, gastrointestinal, and hematological complications. However, SVP use does not seem to be associated with significant cardiovascular effects and electrocardiographic (ECG) abnormalities. Thus, we aimed to describe SVP intoxication in a series of patients by focusing on ECG findings. Method: Between February 2011 and February 2012, we enrolled all consecutive patients who referred to Loghman-Hakim Poison Hospital complaining of poisoning and subsequently diagnosed with SVP intoxication. For each patient, we recorded age, sex, and history of SVP use, including indication for use, number of pills ingested, time of ingestion, and total daily dose. We also inquired whether the patient took SVP chronically with or without prescription and whether the ingestion was intentional (suicide attempt). Result: A total of 194 patients with SVP poisoning at a mean ± SD age of 28.91 ± 11.24 years and a male-tofemale ratio of 1:2.8 were admitted. Regarding cardiac presentations, all the subjects were in sinus rhythm, and 1.5% experienced PR prolongation, 16.8% QTc widening, and 0.5% QRS widening. There were no significant correlations between ECG abnormalities and the ingested dose, plasma level of SVP, admission duration, time to reach the hospital, and PH. Conclusion: The possibility of QT prolongation due to an overdose of the SVP anticonvulsant drug requires particular consideration.
PHENYTOIN AND SODIUM VALPROATE INTOXICATION AND MANAGEMENT, A CASE REPORT
Phenytoin Toxicity Is Challenging Due To Its Pharmacokinetic Properties And Narrow Therapeutic Index. Serum Values In Valproate Toxicity Do Not Correlate With Its Side Effects. In This Case Report, Patient Consumed 100 Tablets Of Phenytoin And 15 Tablets Of Sodium Valproate Causing Her Serum Levels Of Phenytoin And Valproate Rise To 100mcg/Ml And 1.4mcg/Ml Respectively. Her Conditioned Worsened And Suffered Cardiac Arrest On 9th Day Of Admission During Supportive Therapy. Plasma Pheresis Was Done As Rescue Measure Which Decreased Phenytoin Levels. Her Neurological Condition Improved And Was Discharged After 40 Days Of Hospital Stay.
Open Access Emergency Medicine, 2018
A 51-year-old woman, who intentionally ingested a massive dose of ~60 g of valproic acid which she was using as a mood stabilizer for bipolar affective disorder, presented within 30 minutes of ingestion to the emergency department. The patient was asymptomatic and was immediately started on decontamination therapy with activated charcoal (AC). Drug serum levels, liver functions, and ammonia levels were tested and followed up during treatment. Due to the massive ingestion and continuous rise in serum drug levels, the patient received regular multiple doses of AC, as well as l-carnitine for liver protection. The patient was started on extracorporeal therapy in the form of renal replacement therapy in the intensive care unit (ICU), followed by intermittent hemodialysis. Drug serum levels dropped significantly. Ammonia levels showed improvement with treatment. The patient was discharged from the ICU after 14 days of treatment. She was stable and in good condition with no residual hepatic or central nervous system (CNS) manifestations.
Delayed toxicity following acute ingestion of valpromide
Human & Experimental Toxicology, 2004
As valpromide is a prodrug of valproic acid (valproate), the clinical presentation of overdoses with either valpromide or valproate sodium is generally considered similar. Whereas plasma peak levels and signs of central nervous system depression occur within a few hours after the acute ingestion of regular-release forms of valproate sodium, delayed toxicity and time to peak levels following valpromide ingestion can be seen as shown by the three reported cases. They were initially considered as mild because patients presented with no or only moderate symptoms and serum valproate levels were below or at therapeutic levels on admission more than 3 hours post-ingestion in two of the three patients. Serum valproate levels were not monitored until marked deterioration more than 10 hours after ingestion. At the time of deterioration, serum valproate was at toxic level in the three reported cases. Therefore, large intake of valpromide should be closely monitored because no or moderate symptoms together with low plasma levels in the first few hours after ingestion do not exclude a subsequent severe intoxication. Despite the usual favourable outcome and the poor correlation between plasma levels and toxic symptoms, patients should not be discharged until plasma levels are documented to remain at low levels for at least 10 hours after the ingestion of valpromide and the patient asymptomatic. Human & Experimental Toxicology (2004) 23, 145 ]/148 series of valproic acid ingestion: serum concentrations and toxicity. J Toxicol Clin Toxicol 2000; 38: 755 ]/60.
Life-threatening Valproate Overdose Successfully Treated with Haemodialysis
Archives of Industrial Hygiene and Toxicology, 2000
Valproate (VPA) poisoning is an increasing clinical problem. The most common finding in VPA overdose is the depression of the central nervous system, which may progress to coma and death. This type of poisoning is difficult to treat, as no antidote exists. This report describes a case with a 16-year-old girl who poisoned herself with valproate. Initial treatment included naloxone, but she did not respond. She became comatose, with serum VPA concentration of 1320 µg mL -1 . Three sessions of haemodialysis were performed, effectively eliminating VPA and decreasing the serum concentration. The patient regained consciousness and fully recovered. To our knowledge, this is the highest serum VPA concentration reported by now in children aged 16 or less. Haemodialysis has proved to be the treatment of choice for life-threatening acute VPA overdose in children.