Antiepileptic drugs
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Hyperammonaemia and drug-induced liver injury: case report A 6-year-old girl developed hyperammonaemia and drug-induced liver injury during treatment with gabapentin for paroxysmal sympathetic hyperactivity (PSH) and valproic acid, phenobarbital, phenytoin, potassium bromide, clonazepam, lamotrigine, lacosamide and perampanel for refractory epilepsy and thiopental sodium and midazolam for suspected exacerbation of epileptic seizures [not all routes stated; duration of treatments to reaction onsets not stated]. The girl had a generalised cerebellar disease (semilobar type) with refractory epilepsy and congenital hydrocephalus. Anamnesis revealed laryngeal tracheal separation, gastrostomy followed by tube feeding, insertion of vagal nerve stimulation device and ventral shunt. She had been receiving oral valproic acid 16 mg/kg/day, phenobarbital 10 mg/kg/day, phenytoin 3 mg/kg/day, potassium bromide 35 mg/kg/day, clonazepam 0.1 mg/kg/day, lamotrigine 3.6 mg/kg/day, lacosamide 8 mg/kg/day and perampanel 0.15 mg/kg/day for refractory epilepsy. Her water infusion was increased due to increase in viscosity of sputum two weeks prior. She required re-attachment of respiratory device due to poor oxygenation. She experienced spontaneous eye opening. She was examined at the outpatient department of the hospital. On examination, marked hyponatraemia was noted. She required immediate hospitalisation for further management and close monitoring. Based on physical and laboratory findings, a diagnosis of syndrome of inappropriate antidiuretic hormone secretion (SIADH) was made. She received sodium replacement with fluid therapy and water restriction. Hyponatraemia was corrected. On day 11 of illness, she experienced pupil dilation, vomiting, limb tonicity and increased body temperature and HR, and intermittent seizure with facial flushing. Initially, it was considered to be exacerbation of epileptic seizures, and she received additional antiepileptic drugs including phenytoin, phenobarbital and IV thiopental sodium [thiopental], but were ineffective. Afterwards, midazolam was administered, which was initially effective, but gradually showed poor response. PSH was suspected. EEG was performed and PSH was confirmed. She started receiving gabapentin and tizanidine on day 21 of illness. Tizanidine was effective initially, but the effect was poor and seizure did not completely resolved. On day 28 of illness, the dose of gabapentin was increased to 40 mg/kg/day, and the PSH attack disappeared. She was discharged on day 51 of illness. On day 58, blood sampling on an outpatient basis revealed increase in γ-glutamyl transpeptidase (GTP) and AST/ALT along with an increase in blood ammonia level to 198 g/dL. A diagnosis of drug-induced liver injury secondary to antiepileptic drugs was initially proposed due to hepatic disorder after drug adjustment. All the drugs were within an effective blood concentration, except phenobarbital which was increased. On day 60 of illness, blood tests revealed no improvement in hyperammonaemia. The girl’s v
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