RESUMEN

Valproate-induced hyperammonemic encephalopathy (VHE) is a rare and severe side effect that can occur with valproic acid (VPA) therapy, despite therapeutic doses and normal serum levels of valproate. The typical signs of this condition include a sudden onset of impaired consciousness, focal neurologic symptoms, and an increase in seizure frequency. The exact cause of VHE is unknown, but it is believed to be related to the accumulation of toxic VPA metabolites and increased levels of ammonia that can cause swelling of the astrocytes and cerebral edema. We present a case of a 19-year-old male patient with a history of bipolar disorder on valproic acid 250 mg daily, admitted to the hospital after a new-onset seizure. He was found to have elevated levels of ammonia in his blood, despite having therapeutic levels of valproate and no liver dysfunction. His symptoms improved with discontinuation of the medication and his ammonia levels decreased. We discuss possible mechanisms and risk factors leading to encephalopathy while on valproate therapy. VHE should be considered a possibility when patients treated with valproate show signs of impaired consciousness.

RESUMEN

Valproic acid poisoning can have mild to fatal consequences depending on its body concentration. There are rare case reports and barely any known controlled studies on the use of hemodialysis as a last treatment resort. We report a rare valproic acid poisoning case at One Brooklyn Health/Interfaith campus, New York City, warranting intubation and hemodialysis. The patient is a 47-year-old male with a past medical history of seizure disorder, polysubstance use disorder, schizophrenia, and gastroesophageal reflux disease (GERD) who was brought to the medical emergency department (ED) for intentional valproic acid overdose with 60 tablets of his prescribed home Depakote DR 500 mg (~30 g). The patient's other outpatient medications included valproic acid, trazodone, acetaminophen, famotidine, fluoxetine, folic acid, hydrocortisone-aloe, multivitamin, nicotine polacrilex, and thiamine. The patient's initial blood tests showed high valproic acid, ammonia, ethanol, and lactate. About six hours after ED admission, the patient became somnolent, desaturated to 74% on a non-rebreather oxygen mask, warranting intubation and hemodialysis after noticing persistently high serum concentrations of valproic acid. The relatively low molecular weight (144 Daltons) and low volume of distribution of valproic acid suggest a potential benefit from hemodialysis, especially at a serum concentration of >850 mg/L or in the event of a shock. In this patient, mentation and stability status were improved after hemodialysis. Hemodialysis appears to be the last treatment resort for severe valproic acid poisoning.

RESUMEN

Valproic acid (VPA), a common anti-epileptic with prevalent use, has many side effects such as alopecia, abdominal discomfort, thrombocytopenia, etc. Other than those documented, publications cite the drug's rare side effects, such as hepatotoxicity, coagulation disorders, hyperammonemic encephalopathy, rhabdomyolysis, etc. We present the case of a 24-year-old man who was started on valproic acid after a seizure episode and developed mild transaminitis and rhabdomyolysis within 24 hours of drug initiation. Cessation of the drug led to the resolution of raised creatinine kinase and transaminase levels.

RESUMEN

Valproic acid, a branching short chain fatty acid, is a popular drug to treat epilepsy and acts as a mood-stabilizing drug. The obstruction of ion channels and Gamma Amino Butyrate transamino butyrate GABA has been linked to antiepileptic effects. Valproic acid has been characterized as a Histone deacetylase inhibitor, functioning directly transcription of gene levels by blocking the deacetylation of histones and increasing the accessibility of transcription sites. Study has been extensively focused on pharmaceutical activity of valproic acid through various pharmacodynamics activity from absorption, distribution and excretion particularly in patients who are resistant to or intolerant of lithium or carbamazepine, as well as those with mixed mania or rapid cycling.

RESUMEN

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.

RESUMEN

Valproic acid is a commonly prescribed drug used in various conditions including seizures, bipolar disorder, mood disorder, and migraine headaches. Confusion and lethargy among patients on valproic acid need urgent attention as it can cause increased levels of ammonia, which can lead to the development of cerebral edema and even cerebral herniation in severe cases. Here, we describe a case of hyperammonemic coma induced by valproic acid toxicity. The condition was rapidly resolved using dual therapy involving extracorporeal removal and levocarnitine.

RESUMEN

WHAT IS KNOWN AND OBJECTIVE: The interaction between valproic acid (VPA) and carbapenem antibiotics is well described with previous reports suggesting a reduction in VPA half-life between 47% and 90%. As described in this case, this interaction might be beneficial in the setting of toxic VPA ingestion. CASE DESCRIPTION: An intubated, unresponsive patient arrived via emergency medical services after toxic VPA ingestion. Meropenem was prescribed for a suspected pneumonia and to take advantage of the VPA interaction. We observed a 56% decline in half-life with short-term meropenem dosing and an improvement in mental status shortly after administration. WHAT IS NEW AND CONCLUSION: Our findings suggest a potential role for short-term carbapenem therapy for VPA overdose.

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RESUMEN

BACKGROUND: Thrombotic microangiopathy (TMA) is a serious, sometimes life-threatening disorder marked by the presence of endothelial injury and microvascular thrombi. Drug-induced thrombotic microangiopathy (DI-TMA) is one specific TMA syndrome that occurs following drug exposure via drug-dependent antibodies or direct tissue toxicity. Common examples include calcineurin inhibitors Tacrolimus and Cyclosporine and antineoplastics Gemcitabine and Mitomycin. Valproic acid has not been implicated in DI-TMA. We present the first case of a patient meeting clinical criteria for DI-TMA following admission for valproic acid toxicity. CASE PRESENTATION: An adolescent male with difficult to control epilepsy was admitted for impaired hepatic function while on valproic acid therapy. On the third hospital day, he developed severe metabolic lactic acidosis and multiorgan failure, prompting transfer to the pediatric intensive care unit. Progressive anemia and thrombocytopenia instigated an evaluation for thrombotic microangiopathy, where confirmed by concomitant hemolysis, elevated lactate dehydrogenase (LDH), low haptoglobin, and concurrent oliguric acute kidney injury. Thrombotic thrombocytopenic purpura was less likely with adequate ADAMTS13. Discontinuing valproic acid reversed the anemia, thrombocytopenia, and normalized the LDH and haptoglobin, supporting a drug-induced cause for the TMA. CONCLUSION: To the best of our knowledge, this is the first report of drug-induced TMA from valproic acid toxicity.

Asunto(s)

RESUMEN

Valproic acid (VPA) is a commonly used broad-spectrum antiepileptic drug especially in children, with various side-effects reported with its usage. Hematologic toxicity is dose related and intracranial bleeding complications have been reported. We are reporting a rare case of massive scalp hematoma requiring surgical intervention, following a trivial fall associated with high-VPA levels.