Antiepileptics
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Antiepileptics Non-convulsive status epilepticus (NCSE) and hyperammonaemic encephalopathy: case report
A 57-year-old woman developed non-convulsive status epilepticus (NCSE) and hyperammonaemic encephalopathy following treatment with lacosamide, levetiracetam, midazolam, perampanel and valproate for generalised tonic-clonic seizures [not all routes, dosages and outcomes stated; durations of treatments to reactions onsets not stated]. The woman had a history of chronic kidney disease secondary to interstitial nephropathy, kidney transplant, chronic graft rejection, and on haemodialysis. She had been on prednisone. Around six months prior to the admission, she experienced the first episode of generalised tonic-clonic seizures after a dialysis session. Based on lab examinations, a potential metabolic imbalance due to dialysis was suspected. Following one month, the second episode of generalised tonic-clonic seizure had observed. Therefore, she had started receiving valproate 500mg every 12 hours. However, she experienced recurrent episodes of generalised tonic-clonic seizures. Therefore, levetiracetam 500mg every 12 hours was added to her treatment. Around one month prior to the current admission, she developed agitation, hetero-aggression and autolytic ideation, requiring hospitalisation. During the previous hospitalisation, olanzapine and lorazepam had been added to her treatment, and dose of levetiracetam reduced. One week following the current admission, a fluctuation in the level of alertness and repeated generalised tonic-clonic seizures were observed. Due to incomplete recovery of the level of consciousness, she was admitted to the ICU. Examination showed Glasgow 3 index, medium isocoric pupils with normal reaction, multi-focal movements of the limbs and fluctuating episodes of irregular clonic. Therefore, she underwent orotracheal intubation and IV valproate and IV levetiracetam were initiated. Her psychiatric treatment was interrupted. EEG showed NCSE compatible tracing. Therefore, lacosamide was added to her treatment. General laboratory and brain CT neuroimaging studies were performed without significant alterations, maintaining normal kidney function with no changes. Control EEGs showed no significant changes. Therefore, perampanel, midazolam and propofol were gradually increased. The control EEG showed progression to a flattening trace with flares in which sustained acute graphoelements continued to be observed. Her valproate levels were consistently below therapeutic range. However, serum ammonia levels were found to be elevated (NCSE secondary to hyperammonaemic encephalopathy). Therefore, the woman’s treatment with valproate was discontinued, 8 days after admission to the ICU. Consequently, an EEG controls showed improvement in her with less acute, non-sustained activity. Therefore, sedation was gradually decreased. Eventually, the ammonia level and level of consciousness normalised. Viloria Alebesque A, et al. Non-convulsive status epilepticus secondary to valproate-induced hyperammonaemic ence
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