Carbamazepine/zuclopenthixol Toxic epidermal necrolysis: case reportA 27-year-old man developed toxic epidermal necrolysis (TEN) during treatment with carbamazepine for aggressive behavior and zuclopenthixol [not all indications and durations of treatments to reaction onset stated; routes and dosages not stated].The man presented with worsening of aggression and violent behavior. He had been receiving various concomitant medications for autism spectrum disorder. Subsequently, he started receiving carbamazepine for aggressive behavior. However, eleven days post carbamazepine initiation, he developed a fever. His fever persisted for 3 days despite empirical therapy with unspecified antibiotics. Due to the mild derangements in his liver function tests, an infective aetiology was suspected and extensive investigations were done. However, no sources of sepsis or occult infection was noted. Following 4 days of the fever onset, he started developing erythematous macules on his trunk, upper thighs and arms. Hence, a dermatology consultation was done, and he was diagnosed with TEN.The man's therapy with carbamazepine was stopped due to possible implication as a causative agent. His skin biopsy demonstrated vacuolar interface changes associated with numerous apoptotic bodies at the dermal-epidermal junction. At that time, his rash progressed rapidly with the formation of flaccid blisters and erosions, along with conjunctival and oral mucosal involvement. Nikolsky's sign was positive with a body surface area of 50%, and a diagnosis of TEN was confirmed. Due to tachycardia, and the affected body surface area of >10%, the score of TEN (SCORTEN) was 2 at the time of diagnosis. He was then initiated on supportive treatment, along with ciclosporin. During detailed investigations regarding his exposure to new drugs in the recent 3 months prior to the onset of TEN, few potential culprits were identified, namely carbamazepine and zuclopenthixol. His TEN was attributed to carbamazepine and zuclopenthixol. In the subsequent days, he persistently remained febrile and tachycardic, with the progression of his involved BSA to 80 to 90%. He was managed with meticulous supportive care with unspecified fluids, regularly scheduled dressing changes using non-adherent dressings, and ciclosporin. He remained clinically stable, although initial improvement in his cutaneous and mucosal involvement was marginal. However, after 6 days, he was shifted to the burns unit. He developed type I respiratory failure and fluid overload. Therefore, for fluid overload, he was started on furosemide, to which he responded initially. However, he rapidly deteriorated overnight, and eventually died due to cardiac arrest.
