Valproic acid toxicity: Difference between revisions
(Mechanism of hyperammonemia) |
(MOA of hyperammonemia) |
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**Elevated transaminases | **Elevated transaminases | ||
*Hyperammonemia | *Hyperammonemia | ||
**Secondary to L-Carnitine depletion | **Secondary to L-Carnitine and Acetyl-CoA depletion which inhibits urea cycle | ||
==Treatment== | ==Treatment== | ||
Revision as of 16:05, 7 November 2013
Background
- Peak concentration occurs within 4hr (12-18hr for controlled release forms)
Clinical Features
- CNS depression
- Hypotension
- Respiratory depression
Diagnosis
- Level
- Does not correlate well w/ toxicity
- Adverse effects increase w/ level >150
- Chemistry
- Hypocalcemia, hypernatremia, hypophosphatemia, AG metabolic acidosis
- LFT
- Elevated transaminases
- Hyperammonemia
- Secondary to L-Carnitine and Acetyl-CoA depletion which inhibits urea cycle
Treatment
- GI detox
- Activated charcoal PO x1 or multidose (for delayed-release preparations)
- l-carnitine
- Increases valproate metabolism
- Recommended for pts with:
- Lethargy, coma, hyperammonemia, hepatic dysfunction
- Give 50mg/kg/day IV in 3divided doses
- Naloxone
- May be effective in reversing CNS depression
- Dialysis
- Effective
Disposition
- Consider d/c for pt with declining levels and pt is asymptomatic
Source
Tintinalli