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Toxic epidermal necrolysis: case report An 8-year-old boy developed toxic epidermal necrolysis (TEN) during treatment with paracetamol and levetiracetam for acute epileptic seizure secondary to a febrile viral episode [not all routes stated; dosages not stated]. The boy, who had a history of post-traumatic cerebral palsy and epilepsy treated 3 years previously with levetiracetam for 1 year without any side effects, was hospitalised with an acute epileptic seizure secondary to a febrile viral episode. He started receiving levetiracetam, paracetamol [acetaminophen] and diazepam. Following 24 hours with unremarkable laboratory results and no further epileptic seizures, he started receiving oral levetiracetam and paracetamol, and he was discharged. However, after 72 hours, he presented with hypotension and erythematous patches on the trunk, arms and face with blisters and areas of detached skin, and he had a temperature of 38.5°C. The boy was admitted to the paediatric ICU (PICU) on day 0, and he started receiving unspecified broad-spectrum antibacterials along with supportive care. During the first 24 hours, he required volume expansion with crystalloid, packed erythrocytes [red blood cells] and inotropic support with dopamine and norepinephrine along with mechanical ventilation. Dermatological examination showed red patches with grayish blisters, which covered 30% body surface area (BSA) and affected the trunk, face, arms and genital area. He had positive Nikolsky’s sign. Also, he had haemorrhagic crusting of the lips with erosive stomatitis and bilateral conjunctivitis. A skin biopsy demonstrated histopathological findings, which were consistent with TEN, and he was diagnosed with TEN based on 30% of skin detachment, positive Nikolsky’s sign and mucosal involvement. Levetiracetam and paracetamol were suspected to have caused the TEN. Laboratory tests showed low haemoglobin, acute renal failure with an elevated creatinine and an elevated CRP. Therefore, the boy’s levetiracetam and paracetamol treatment was promptly stopped, and he was immediately treated with methylprednisolone and immune-globulin. However, after 48 hours (on day 2), he experienced a rapid progression of skin detachment, melaena and epistaxis. Haemoglobin was noted to have decreased to 50 g/dL, for which he required blood transfusion. Due to the progression of TEN and significant mucosal involvement, on day 3, he was treated with etanercept. Over the following 24 hours (on day 4), the blistering stopped, the erythema and mucosal involvement improved, and he showed negative Nikolsky’s sign. He received a second dose of etanercept after a week (on day 10), without any complications related to the drug. On day 19 after admission, he exhibited complete re-epithelisation. He was discharged from the PICU on day 25. After a total of 25 days, the rash resolved, and the crusts remained only on the lips. Eye involvement included moderate ocular surface inflammation, which was managed with ciclosporin [cyclosporine], tetracycline, autologous serum eye drop