83seizures persisted. MRI brain revealed left temporal and occipital gliosis. Electroencephalography show epileptiform discharges from the left temporal region.Child was subsequently started on VPA (17 mg/kg/day), LTG (6 mg/kg/day) by neurologist and phenytoin was gradually stopped. Seizures frequency decreased and Carbamazepine was also added after 10 days (11.8 mg/kg/day). Thereafter, child remained seizure free for next 4 months.At present, child had fever and cough, treated with paracetamol, amoxycilin and clavulanic acid. Within 24 h she developed rash and was hospitalized. LTG, carbamazepine and amoxicillin were stopped. VPA was continued and rash continued to increase. Subsequently VPA was stopped and phenobarbitone was added. Child was referred to us in view of worsening of rash and hepatic involvement.At admission, child was hemodynamically stable. Extensive vesicobullous lesions with nikolsky sign positivity were present. 30% of body surface area had cutaneous detachment. Mucosal surfaces, bilateral conjunctiva were also involved. Cornea was spared.
ABSTRACTEpilepsy is common childhood problem and advent of newer anticonvulsant drugs has led to injudicious uses. Anticonvulsant hypersensitivity syndrome (AHS) has been previously described developing secondary to aromatic anticonvulsants such as phenytoin and carbamazepine. AHS developing secondary to non-aromatic anticonvulsant agents such as lamotrigine (LTG) and valproic acid (VPA) is rare. We present a case of an 11-year-old girl with known epilepsy on VPA, LTG and carbamazepine therapy that developed fever with the clinical pattern of Steven-Johnson syndrome/toxic epidermal necrolysis requiring pediatric intensive care. Judicious use of anticonvulsant should be done in appropriate dose especially in pediatric population and when used in combination to prevent AHS like life-threatening event.