eMedicine Specialties > Emergency Medicine > Toxicology

Toxicity, Valproate: Treatment & Medication

Author: Timothy Wiegand, MD, Clinical Assistant Professor of Medicine, University of Vermont College of Medicine and Maine Medical Center; Associate Medical Director, Northern New England Poison Center
Coauthor(s): Kent R Olson, MD, FACEP, Clinical Professor of Medicine and Pharmacy, University of California San Francisco; Medical Director, San Francisco Division, California Poison Control System; Herbert E Hern Jr, MD, Assistant Clinical Professor, Department of Emergency Medicine, University of California, San Francisco; Residency Director, Department of Emergency Medicine, Highland General Hospital
Contributor Information and Disclosures

Updated: Jan 26, 2009

Treatment

Prehospital Care

Stabilize all acute life-threatening conditions.

  • Ensure a patent airway. Intubate if necessary, such as to manage profound respiratory depression.
  • Establish intravenous (IV) lines.
  • Obtain information about the overdose, including the following:
    • Amount of pills
    • Dosage
    • Last date the prescription was filled. (The bottles should be brought to the hospital if possible.)
  • Check blood sugar levels with a bedside test, or administer a bolus of dextrose if bedside testing is not available.
  • Naloxone may be indicated if the patient has stupor or coma, depressed respiration, and small pupils.
  • Rare reports describe a positive response to naloxone in patients without findings of opiates on toxicology screen; the mechanism is unexplained.

Emergency Department Care

Treatment of patients with valproic acid poisoning is mainly supportive such as management of airway, breathing, and circulation (ABCs); oxygenation; administration of intravenous fluids; and monitoring. However, respiratory depression and cardiopulmonary arrest have been documented. Proceed with resuscitative maneuvers (eg, intubation, defibrillation) if appropriate. Ventilate the patient and provide circulatory assistance as needed.

  • Decontamination
    • Activated charcoal should be administered to patients presenting within 1 hour unless contraindications are present. The optimum activated charcoal–to-toxin ratio is 10:1.
    • If the patient presents more than 1 hour after the ingestion, activated charcoal may still be indicated because of the potentially delayed absorption with enteric-coated or extended-release preparations (eg, Depakote, Depakote ER).
    • Whole-bowel irrigation (WBI) may be useful when large amounts of sustained-release products (eg, Depakote, Depakote ER) are ingested.
  • Enhancement of elimination: As levels rise, the percentage of valproic acid bound to protein decreases; procedures to enhance elimination may be considered.
    • Hemodialysis and hemoperfusion: These therapies can decrease the elimination half-life, as described in many case series, reviews, and reports. Dialysis removes valproic acid metabolites and ammonia. One of the most dramatic reports describes hemoperfusion and hemodialysis in series, which reduced the half-life of valproic acid from 13 hours before treatment to 1.7 hours during hemodialysis.5 Four hours after treatment and within 20 hours of ingestion, the patient was alert, responsive, and following commands. However, indications for dialysis are not well established; some advocate hemodialysis in cases of refractory hemodynamic instability and metabolic acidosis not responsive to fluid resuscitation. Hemodialysis is ideally started before the onset of hemodynamic compromise. Consider dialyses when levels are greater than 850-1000 mg/L because these levels are associated with increased morbidity and mortality.
    • High-flux hemodialysis without hemoperfusion has been shown to significantly decrease the elimination half-life, as described in case reports of valproic acid overdoses. 
      • In one case, high-flux hemodialysis was used in a 25-year-old patient who developed hypotension and lactic acidosis as valproic acid level concentrations increased to greater than 1200 mcg/mL. High-flux hemodialysis was performed for 4 hours.6  The half-life during dialysis was 2.74 hours compared to 23.41 hours posthemodialysis. The patient recovered as her serum levels of valproic acid declined. 
      • Multiple other reports describe successful use of hemodialysis without hemoperfusion for severe valproic acid overdose. In fact, in review of the literature regarding high-flux dialysis and/or hemoperfusion for valproic acid overdose, toxic concentrations of valproic acid can be effectively removed via high-flux dialysis without concomitant hemoperfusion. Use of this single method of elimination eliminates the associated risks that hemoperfusion may bring.
    • Use of multidose activated charcoal (MDAC): Despite case reports in which MDAC decreased the serum half-life of valproic acid, this treatment did not affect the elimination half-life in volunteer studies. MDAC may be considered in conjunction with WBI in cases of massive ingestion or ingestion of extended-release products (see Decontamination above).
    • Continuous venovenous hemodialysis (CVVHD): In cases of hemodynamic compromise, continuous renal-replacement therapy such as CVVHD may improve the elimination half-life compared with the patient's baseline function. Whether it may decrease the potential hemodynamic instability compared with standard dialysis, in particular, low-flux dialysis, is up for debate. One case report discusses a potentially fatal valproic acid overdose that did not respond to CVVHD but was successfully treated with low-flux hemodialysis.7
  • Isolated case reports have described reversal of sedation with naloxone.
    • Naloxone has been postulated to act as a GABA antagonist or inhibit postsynaptic GABA transport due to valproic acid in addition to its opioid receptor antagonism.
    • However, the administration of naloxone (including aggressive administration of 30 mg total) with no response has been reported. The literature is varied in regard to the efficacy of naloxone in reversing VPA-induced coma. In one case report, naloxone administration in 2 separate doses reversed coma with VPA level of 487.8 mg/L.8 On the other hand, in cases of severe valproate intoxication with plasma concentrations exceeding 850 mg/L, administration of naloxone has been unsuccessful. 
    • Many medical toxicologists and pharmacologists believe that reversal of coma in cases of VPA-associated coma may actually be due to reversal of opiate/opioid effects where an opioid/opiate was unsuspected or not confirmed via urine toxicology screen (eg, a negative opiate screen on a drugs of abuse assay). Many opioids will not be positive on such assays including fentanyl, oxycodone, and meperidine.
  • L-carnitine
    • L-carnitine is the active form of carnitine and is an essential cofactor in the beta-oxidation of fatty acids in the liver. Long-term use of valproic acid is associated with depletion of serum carnitine levels. This is due to 2 distinct mechanisms. First, valproic acid combines with carnitine to form valproylcarnitine, which is freely excreted in the urine. Additionally, during treatment with valproic acid, renal reabsorption of both free carnitine and acylcarnitine is decreased.
    • Ultimately, carnitine deficiency effects mitochondrial metabolism of valproic acid as well as energy synthesis. Hyperammonemia may also develop with carnitine deficiency as the production of urea is disrupted within the mitochondria. Thus, carnitine deficiency plays a large role in the development of hyperammonemia and VPA-induced hyperammonemic encephalopathy. This is associated with chronic or high-dose VPA use as well as overdose. Carnitine also plays a direct role in the metabolism and elimination of VPA.         
    • L-carnitine supplementation, then, is thought to provide benefit, particularly in patients with concomitant hyperammonemia, encephalopathy, and/or hepatotoxicity.
    • One case report documented the administration of L-carnitine oral supplementation to a patient with acute valproic acid overdose.9 Levels of beta-oxidation metabolites (from mitochondrial metabolism, normal pathway) of valproic acid were low, levels of omega and omega-1 metabolites (non-mitochondrial–mediated metabolic byproduct) were elevated before treatment. After treatment, the former levels increased, and the latter decreased. Toxic metabolites (eg, 4-en-valproate, products of omega oxidation) initially detected in the urine were no longer present after carnitine supplementation. Carnitine supplementation makes sense, physiologically, in cases where hepatotoxicity occurs or is potential.
    • The optimum route and dose of L-carnitine has not been determined. In a retrospective review of patients with hepatotoxicity secondary to valproic acid, improved outcomes were noted in patients who received intravenous L-carnitine compared with those receiving oral L-carnitine or control subjects who received only supportive care. Some dosing guidelines included patients with acute overdose of valproic acid and without hepatic enzyme abnormalities or hyperammonemia can receive prophylactic carnitine of 100 mg/kg/day, divided every 6 hours, to a maximum dose of 3 g/d. For patients with symptomatic hyperammonemia or hepatotoxicity, dosing is more aggressive. A loading dose of 100 mg/kg intravenously is administered (up to a maximum of 6 g) over 30 minutes followed by 15 mg/kg every 4 hours over 10–30 minutes until clinical improvement occurs.
    • The toxicity profile of L-carnitine has been found to be relatively benign. In a systematic review of 674 acute valproic acid overdoses, 55 doses of L-carnitine were given to 19 patients with isolated valproic acid ingestion and 196 doses were given to patients with mixed overdoses that included valproic acid.10 No patient developed hypotension or had an allergic reaction or other adverse effect.
    • One group recommends intravenous administration of L-carnitine, stating, "in any patient with coma, despite falling VPA concentrations, and climbing ammonia levels and (pending further study), in all patients with VPA concentrations greater than 450 mcg/mL (mg/L)."11 However, no dose for intravenous therapy was given.
    • L-carnitine is best administered in consultation with a regional poison control center certified by the American Association of Poison Control Centers or a medical toxicologist certified by the American Board of Emergency Medicine or the American College of Medical Toxicology.
    • Despite physiologic sense and case reports documenting favorable outcomes, further study, in particular randomized controlled studies, is needed before the use of carnitine for valproate toxicity becomes a true standard of care.

Consultations

  • Consult a regional poison control center certified by the American Association of Poison Control Centers or a medical toxicologist certified by the American Board of Emergency Medicine or the American College of Medical Toxicology.
  • Consultation with a nephrologist may be necessary for emergency hemodialysis and hemoperfusion.
  • Consider consultation with a neurosurgeon if the head CT scan reveals severe cerebral edema.
    • One case report discusses management of cerebral edema and increased intracranial pressure (ICP) with ventriculostomy, hyperventilation to maintain a perfusion pressure at 60-70 mm Hg, and 1 dose of mannitol 25 g and dopamine 1-8 mcg/kg/min.12
    • If the patient's illness requires ventriculostomy, high-flux hemodialysis or hemoperfusion to enhance elimination is appropriate.

Medication

Despite favorable reviews and outcomes in case reports, it remains to be seen, prospectively, whether the use of L-carnitine in valproic acid (VPA) overdose impacts clinical outcome. Despite this lack of evidence, however, some groups advocate use when the VPA levels exceed 450 mg/L, VPA-associated hepatotoxicity and/or encephalopathy occurs and in any case of primary carnitine deficiency (particularly relevant in the pediatric population). Specific recommendations regarding the optimal dose, frequency, or route of administration are limited (some recommendations are given above). L-carnitine should be administered in consultation with a medical toxicologist or a poison control center certified by the American Association of Poison Control Centers.

Antidotes

These agents are used in the emergency treatment of poisoning caused by drugs and chemicals.


Naloxone (Narcan)

Pure competitive opioid antagonist used for reversal of respiratory depression after opioid exposure.
Reversal in VPA exposure may be due to nonspecific action of naloxone or due to reversal of the effect of undetected opioid (coingestant).

Adult

0.4-2 mg IV can reverse respiratory depression in majority of opioid exposure
Some clinicians recommend lower doses at 0.05-0.1 mg IV as initial dose in order to avoid complications of precipitous opioid withdrawal (eg, vomiting, aspiration)
(In VPA exposure, administration of large cumulative dose of naloxone, up to 10 mg, may be required in order to reverse respiratory depression and/or change of mental status)

Pediatric

Patients weighing <20 kg or <5 years: 0.1 mg/kg
Patients weighing >20 kg or >5 years: 0.1-0.2 mg/kg
If cumulative dose of 10 mg of naloxone does not produce improvement of symptoms, it is very unlikely that naloxone will have any effect

Decreases analgesic effects of narcotics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients who have opioids in their system may experience precipitous withdrawal and consequent vomiting and aspiration
Pregnant patients who are opioid dependent can experience precipitous withdrawal and consequent labor complications after naloxone administration
Infants of pregnant mothers who are opioid dependent can experience severe/life-threatening withdrawal after administration of naloxone


Activated charcoal (Liqui-Char, Actidose-Aqua, Insta-Char)

Has network of pores present that absorbs 100-1000 mg drug per gram charcoal. Does not dissolve in water. For maximum effect, administer within 0.5-1 h of poison ingestion.

Adult

1 g/kg PO initially; may administer MDAC 10-20 g (0.25 g/kg/h) NG q2-4h; ideal dosing for overdose is 10:1 charcoal to ingested toxin

Pediatric

1-2 g/kg PO; 15-30 g total

May inactivate syrup of ipecac if used concomitantly; effectiveness of other medications decrease with coadministration; do not mix charcoal with sherbet, milk, or ice cream (decreases absorptive properties of activated charcoal)

Documented hypersensitivity; poisoning or overdose of acid or alkali mixtures; poisoning with substances that charcoal does not bind (eg, metals, alcohols); unprotected airway with absent gag reflex, obstruction or ileus, concomitant GI bleed (consult gastroenterologist before administering and carefully weigh risk and benefit)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Not effective in poisonings of ethanol, methanol, iron salts, lithium, or other metals; protect airway during administration; check for bowel sounds before each dose to minimize risk of charcoal ileus; avoid charcoal-sorbitol mixtures in children (risk of vomiting, hypernatremia, and dehydration)


L-Carnitine

Levocarnitine is endogenous carboxylic acid involved in fatty-acid metabolism. Carnitine deficiency can result from dietary deficiency, inborn errors of metabolism, therapy with many anticonvulsants, and VPA toxicity. VPA may interrupt fatty-acid metabolism, impairing mitochondrial function and ultimately urea metabolism, leading to hyperammonemia. Carnitine deficiency may allow for production of hepatotoxic VPA metabolites by increasing alternate routes of metabolism (gamma oxidation). Effectively treats hyperammonemia associated with chronic VPA toxicity. Carnitine also improves outcome in hepatotoxicity and coma associated with acute VPA ingestion.

No consensus on dose, frequency, and route in VPA overdose. Supplementation appears to be well tolerated; few adverse reactions reported.

Adult

Initial dose of 100 mg/kg IV (not to exceed 6 g) with additional doses of 15 mg/kg IV q4h over 30 min
Note that recommendations vary; some groups advocate limiting total dose to 3 g/d, although the basis for this recommendation is unclear

Pediatric

Overdose or hyperammonemia: 150-500 mg/kg/d IV; not to exceed 3 g/d or until clinical improvement observed
1996 Pediatric Neurology Advisory Committee consensus guidelines: 100 mg/kg/d PO; not to exceed 2 g/d in divided doses

Documented hypersensitivity to carnitine or L-carnitine

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Monitor vital signs in ICU setting during IV administration; monitor serum chemistries daily during therapy

More on Toxicity, Valproate

Overview: Toxicity, Valproate
Differential Diagnoses & Workup: Toxicity, Valproate
Treatment & Medication: Toxicity, Valproate
Follow-up: Toxicity, Valproate
References
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Further Reading

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Keywords

valproic acid, toxicity valproate, valproate overdose, valproate poisoning, VPA, valproic acid overdose, anticonvulsant, antiseizure, seizure treatment, valproate, divalproate, sodium valproate toxicity, dipropylacetic acid toxicity, divalproex sodium toxicity, valproate semisodium toxicity, 2-propylpentanoic acid toxicity, 2-propylvaleric acid toxicity, Depacon, Depakene, Depakote, Depakote ER, Epilim, Ergenyl, Leptilan, Valkote, Sprinkles

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Contributor Information and Disclosures

Author

Timothy Wiegand, MD, Clinical Assistant Professor of Medicine, University of Vermont College of Medicine and Maine Medical Center; Associate Medical Director, Northern New England Poison Center
Timothy Wiegand, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, American College of Physicians, and Maine Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Kent R Olson, MD, FACEP, Clinical Professor of Medicine and Pharmacy, University of California San Francisco; Medical Director, San Francisco Division, California Poison Control System
Kent R Olson, MD, FACEP is a member of the following medical societies: American Academy of Clinical Toxicology and American College of Medical Toxicology
Disclosure: Nothing to disclose.

Herbert E Hern Jr, MD, Assistant Clinical Professor, Department of Emergency Medicine, University of California, San Francisco; Residency Director, Department of Emergency Medicine, Highland General Hospital
Herbert E Hern Jr, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Lance W Kreplick, MD, MMM, FAAEM, FACEP, Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC
Lance W Kreplick, MD, MMM, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physician Executives
Disclosure: Nothing to disclose.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & St. Joseph's Hospitals
John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists
Disclosure: Nothing to disclose.

Managing Editor

Fred Harchelroad, MD, FACMT, FAAEM, FACEP, Chair, Department of Emergency Medicine, Director of Medical Toxicology - Allegheny General Hospital, Associate Professor, Department of Emergency Medicine, Drexel University College of Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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