INTRODUCTION: We present a rare case of acute encephalopathy due to Valproate induced hyperammonemia required Hemofiltration (HF). CASE DESCRIPTION/METHODS: 45-year-old male was brought in by caregiver to the hospital with acute altered mental status, somnolent but arousable. PMHx of CP, Epilepsy, Left sided hemiplegia, Mental retardation, Abscess of thigh and wrist. Medications were Valproate and Phenytion. PE showed stable vitals, confused, was spitting to staff required restraints. Pupils equal, reactive to light. Neurological exam- left sided hemiplegia. Lab showed Na 140, K 4.0, HC03 30, BUN 7, Cr 1.18, Glucose 101, Osmolarity 287, ALT 24, AST 24, T Bil 1.1, Albumin 3.5, Al phos 79, Mg 2.0, lactic 1.2. WBC 6.9, hemoglobin 15.2, platelet 291, INR 1.2, Ammonia 402. Blood & urine culture and toxicology were negative. Acute hepatitis panel was non- reactive, Ceruloplasmin 32, ferritin 33.7, AMA < 20.1, Smooth muscle antibody < 1:40. Valproic acid level 125 mcg/ml (therapeutic level-50-100 mcg/ml). ECG was normal. Head CT showed no acute abnormality. Ultrasound showed fatty infiltration & Cholelithiasis. Unremarkable EGD. Lactulose & xifaxan were given for hyperammonemia, recurrent seizures occurred. RESULTS: Valproate was discontinued. L-carnitine 100 mg/kg IV loading dose was given. Received HF for 3hrs , and supportive care. Ammonia at 2hours post HF was 80. Patient’s mental status improved back to baseline over 24 hours. DISCUSSION: Acute encephalopathy due to valproate induced hyperammonemia required Hemofiltration is very rare. The incidence of valproate-induced hyperammonemia in the general population of patients taking VPA (Valproate acid) is not well established. Most cases of Valproate acid- toxicity are rather benign and resolve with supportive therapy. It is generally accepted that serum level >180 mcg/ml represents a high risk of toxicity. Our case was a first patient without chronic liver disease and valproate level was below high risk for toxicity who presented with acute encephalopathy due to valproate induced hyperammonemia and required Hemofiltration. Care of patients depends upon recognition of those at increased risk, anticipation & prevention, and appropriate response when they occur. Discontinuation of Valproate may require. L-carnitine has a significant mortality benefit in patient severe Valproate toxicity. HF is reserved for severely ill patients who have not responded to less invasive treatment.
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