ONSD showed right pupil 6.8mm and left pupil 5.6mm in diameter. Relatives were counseled to identify a donar for emergency liver transplant.Īround 48 h post admission, right –sided pupil developed sluggish reaction to light which was managed with intravenous mannitol (0.5g/kg). N –acetyl cysteine (NAC) and 3% NS were started as per protocol. Arterial blood gases, blood sugar and electrolyte were monitored and managed. Core temperature was maintained at 35-36 0C. The patient was nursed in slight head up position with no physical stimulation. Haemodynamics were maintained on high dose nor adrenaline and low dose vasopressin infusions. Invasive haemodynamic monitoring helped guided fluid management. Trechea was electively intubated in view of encephalopathy with etomidate, fentanyl and rocuronium and mechanical ventilation instituted targrting an end tidal CO 2 of 30-35 mmhg. The patient was managed according to institute protocol for ALF. Other lab parameters were as follow haemoglobin 9 gm% TLC: 10,400 mm3 platelet count 1.24 lacs mm3 bilirubin 42.2 mg% AST: 453 IU/ml ALT:719 IU/ml INR:5.43 sodium: 134 meq/l potassium: 3.52 meq/L serum creatinine 0.9 mg%. A provisional diagnosis of ALF with unknown etiology was made. On examination patient was in hepatic encephalopathy grade 4 with bilateral equal mid dilated pupil sluggish reacting to light. In this situation patient was reffered to our institute. Patient was apparently normal 20 days back then she developed fever which is acute in onset not associated with chills and rigor but associated with nausea and vomiting and jaundice which was insidious in onset, gradually progressive in nature and not associated with pruritis or clay coloured stool for which she was admiited in local hospital there she developed altered sensorium which is acute in onset, started as confusion and progressed to agitation followed by non responsive to verbal stimuli. A 42 old years female patient with no other co morbidities.
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