Anesthetic considerations in Stevens-Johnson syndrome with epilepsy for bilateral amniotic membrane grafting in eye.

Sir,

Stevens–Johnson syndrome (SJ syndrome) and toxic epidermal necrolysis (TEN) are life-threatening, delayed type hypersensitivity reactions. Epidermal separation is observed in less than 10% of the body surface in SJ syndrome, more than 30% in TEN, and 10–30% in SJ syndrome/TEN.[1]

We present the anesthetic management of a 12-year-old child, weight 28 kg, with SJ syndrome for bilateral amniotic membrane grafting in eye. The child had history of operation for transposition of great arteries at the age of 4 months and was on antiepileptic treatment. He developed SJ syndrome following initiation of treatment with Perampanel 2 mg. This precipitating drug was stopped. Levetiracetam and clonazepam were added to topiramate and clobazam for seizure control in perioperative period. On examination, there were severe mouth ulcers, lip swelling, and peeling of skin on touch. He had history of occurrence of sudden tachycardia and bradycardia. Two dimensional echocardiography and 24 h Holter monitoring were normal. All basic laboratory investigations and chest X-ray were normal. A triple-lumen catheter was inserted in the femoral vein. In premedication, pantoprazole 20 mg intravenous was given. The arm was wrapped with cotton bandage before putting blood pressure (BP) cuff to avoid peeling of skin by pressure during BP measurement. Heart rate was 68/min, BP 110/60 mmHg, and SpO2 99% on room air. General anaesthesia was induced with intravenous ketamine 1.5 mg/kg and midazolam 0.05 mg/kg, glycopyrrolate 0.01 mg/kg. Oxygen was supplemented through nasal prongs at a flow rate of 6 L/min. Ketamine 0.5 mg/kg was repeated twice over 15 min. Infusion of dexmedetomidine was started at 0.5 μ/kg/h after a bolus of 0.5 μ/kg and continued for 2 h. Spontaneous ventilation was maintained. Paracetamol 250 mg intravenous was given for postoperative pain relief. The child was hemodynamically stable intraoperatively and postoperatively.

Drugs causing SJ syndrome/TEN are anti-infective sulphonamides, antiepileptic drugs, non-steriod anti-inflammatory drugs (NSAIDs) of the oxicam type, allopurinol, and nevirapamine.[2] The incidence is 1–3 per million and the mortality rates are 1–5% for SJ syndrome and 25–30% for TEN.[34] Induction with ketamine or etomidate could provide better cardiovascular stability in hypotensive patients.[567] We used ketamine as an induction agent followed by dexmedetomidine later as maintenance sedative agent. Ketamine was used initially because the child had history of bradycardia, but after ketamine induction and use of glycopyrrolate heart rate remained between 100–120/min. We therefore used dexmedetomidine for sedation with close monitoring of heart rate. The intravenous cannula was inserterd over an area of normal skin. We did not intubate the trachea and maintained spontaneous respiration because of lesions involving the oral mucosal lesions. There are chances of desquamation of skin, so care should be taken during face mask ventilation. Pulmonary complications can present early or during the first 48 h after admission or afterwards.[8]

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