Valproate-induced hyperammonemic encephalopathy: A reminder of rare complication of valproate

Gurjar, Mohan; Singhal, Sanjay; Baronia, AK; Azim, Afzal; Poddar, Banani

doi:10.4103/0974-2700.82240

Cited by 5 publications

(5 citation statements)

References 6 publications

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“…However, adverse factors including hyperammonemia and thrombocytopenia were present in patients prescribed with prophylactic anticonvulsants. Upon review of previous studies, complications including hyperammonemia and thrombocytopenia could be caused by valproate or levetiracetam 13 , 27) . One study demonstrated an association between phenytoin prophylaxis and more fever, worse clinical examination, and a worse functional outcome at follow-up 21) .…”

Section: Discussionmentioning

confidence: 99%

Seizures after Spontaneous Intracerebral Hemorrhage

Woo

Yang

Cho

2012

J Korean Neurosurg Soc

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ObjectiveIn patients with spontaneous intracerebral hemorrhage (ICH), the risk factors for seizure and the effect of prophylactic anticonvulsants are not well known. This study aimed to determine the risk factor for seizures and the role for prophylactic anticonvulsants after spontaneous ICH.MethodsBetween 2005 and 2010, 263 consecutive patients with spontaneous ICH were retrospectively assessed with a mean follow-up of 19.5 months using medical records, updated clinical information and, when necessary, direct patient contact. The seizures were classified as early (within 1 week of ICH) or late (more than 1 week after ICH). The outcomes were measured with the Glasgow Outcome Scale at discharge and the modified Rankin Scale (mRS) at both 2 weeks and discharge.ResultsTwenty-two patients (8.4%; 9 patients with early seizures and 13 patients with late seizures) developed seizures after spontaneous ICH. Out of 263 patients, prophylactic anticonvulsants were administered in 216 patients. The prophylactic anticonvulsants were not associated with a reduced risk of early (p=0.094) or late seizures (p=0.326). Instead, the factors associated with early seizure were cortical involvement (p<0.001) and younger age (60 years or less) (p=0.046). The risk of late seizure was increased by cortical involvement (p<0.001) and communicating hydrocephalus (p=0.004). The prophylactic anticonvulsants were associated with a worse mRS at 2 weeks (p=0.024) and at last follow-up (p=0.034).ConclusionCortical involvement may be a factor for provoked seizures. Although the incidence of early seizures tended to decrease in patients prescribed prophylactic anticonvulsants, no statistical difference was found.

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Section: Discussionmentioning

confidence: 99%

Seizures after Spontaneous Intracerebral Hemorrhage

Woo

Yang

Cho

2012

J Korean Neurosurg Soc

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“…[ 5 ] For a diagnosis of VHE to be made, the serum ammonia level should be raised, and the clinical picture should improve with VPA withdrawal or dose adjustment. [ 6 ] In all the cases discussed above serum ammonia levels were raised, and there was improvement on stopping VPA. Naranjo et al .…”

Section: Discussionmentioning

confidence: 98%

The Menacing Side of Valproate: A Case Series of Valproate-induced Hyperammonemia

Elwadhi¹,

Prakash

Gupta

2017

Indian Journal of Psychological Medicine

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Valproate (VPA) is a well-tolerated and commonly used drug to treat variety of psychiatric and neurological disorders. VPA-induced hyperammonemic encephalopathy is a rare adverse effect which can commonly occur in the background of normal liver function and therapeutic serum levels. Any delay in treatment of VPA-induced hyperammonemic encephalopathy can lead to life-threatening coma thus a strong clinical suspicion, fair understanding of the pathophysiology, and management of this drug-related complication can prevent fatal outcome. We hereby report a series of cases admitted to a tertiary care center that developed hyperammonemia and all patients recovered on stopping VPA. This case series cautions the clinicians about hyperammonemia as an uncommon but highly plausible life-threatening side effect, emphasizing astute observation, and high degree of clinical suspicion to prevent mortality and limit morbidity. Early recognition of subtle gastrointestinal, cognitive, and behavioral signs can lead to immediate intervention with satisfying results.

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“…Rarely valproate induced hyperammonemia produces delirium like state of non hepatic origin and if not timely suspected may also lead to valproate induced encephalopathy or even death [2]. Hyperammonemia could be asymptomatic [3] or may progress to focal neurological deficit, seizure, marked sedation, coma, due to encephalopathy [4].…”

Section: Discussionmentioning

confidence: 99%

Valproate Induced Delirium due to Hyperammonemia in a Case of Acute Mania: A Diagnostic Dilemma

Dixit¹

2015

JCDR

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A 31-year-old male with no past history of any significant medical illness manifested with acute onset of behavioural problems of seven-eight days duration in form of increased psychomotor activity, elated mood, verbosity, distractibility, enhanced self esteem, hyper-religiosity, delusion of grandiosity, impaired biodrives (sleep, appetite and libido) in absence of any perceptual disturbance and with intact sensorium. There was no history of fever, altered sensorium, neurological deficit and significant weight loss prior to onset of behavioural abnormalities. There were no developmental issues. Physical examination revealed pulse 82/min, BP 130/82 mm of Hg, afebrile, respiratory rate was 16/min, no digital tremors or hyperhydrosis. Lab investigations including heamogram, LFT, urea, creatinine, blood sugar, lipid profile, serum electrolyte, X-ray chest, CT Scan Brain, T3, T4, and TSH was within normal limits and HIV status was negative. He was diagnosed as a case of mania with psychotic symptoms as per International Classification of Diseases 10 (ICD10) [1] and started on mood-stabilizer tab divalproex sodium 500 mg BD and olanzapine 5 mg BD. Patient started showing improvement. By 10 th day his symptoms remitted to about 40% however his hyper-religiosity, self esteem and grandiose manners though less severe persisted, however on 13 th day patient complained of headache right hemi-cranium lasting for half hour to one hour accompanied by nausea and vomiting. His pulse, BP and temp were normal. MRI brain and fundoscopy revealed no abnormality. A neurophysician referral resulted in prescription of tab topiamate 25 mg BD in view of vascular headache and the same evening (15 th day of admission) after receiving tab topiramate patient developed disorientation, confusion, unsteadiness of gait, irrelevant talks and agitation which continued for next three-five days. His topiramate was stopped immediately. His MMSE score was 13/30. Subsequently divalproex sodium was increased to 1500 mg along with 15 mg of olanzapine by 22 nd day. EEG revealed normal bilateral symmetrical 9-12 Hz posteriorly dominant alfa rhythms. Patient did not show any improvement and continued to remain puzzled, dazed, confused and disoriented during day time with irrelevant talk and exhibited more hyperactivity towards evening with altered sleep-Wake schedule. His physical examination revealed pulse 88/min, BP 136/88 mm of Hg, respiratory rate 18/ min. There were no menningeal, cerebellar or extra pyramidal signs. keywords: Bipolar disorder, Encephalopathy, Non hepatic hyperammonemia, Valproic acidHis neurological examination was non contributory. His repeat liver function, electrolyte, urea, creatinine and CPK levels were within normal range. A pre-anesthetic check up was done and after taking appropriate consent of patient and relatives, he was taken up for electroconvulsive therapy (ECT) on 29 th day suspecting it to be a case of Delirious mania. ECT was planned twice a week. Before starting ECT dose of divalproex sodium was reduced to 250 mg BD t...

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Valproate-induced hyperammonemic encephalopathy: A reminder of rare complication of valproate

Cited by 5 publications

References 6 publications

Seizures after Spontaneous Intracerebral Hemorrhage

Seizures after Spontaneous Intracerebral Hemorrhage

The Menacing Side of Valproate: A Case Series of Valproate-induced Hyperammonemia

Valproate Induced Delirium due to Hyperammonemia in a Case of Acute Mania: A Diagnostic Dilemma

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