Paracetamol
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Mortier P, et al. Hepatic encephalopathy resulting in mania, a possible role of bilirubin and glutamate?. Bipolar Disorders 21: 565-567, No. 6, Sep 2019. Available from: URL: http://doi.org/10.1111/bdi.12818 - Spain 803436189
Various toxicities following drug overdose: case report A 50‐year‐old woman developed hepatotoxicity, hepatic encephalopathy and mania secondary to drug intoxication following an intentional overdose of paracetamol with an unclear suicidal intent [not all times to reactions onset stated]. The woman was admitted due to severe depressive episode with psychotic features and treated with electroconvulsive therapy (ECT). After receiving 19 sessions of ECT, on day 106 of admission, she took an intentional overdose of paracetamol [acetaminophen] 16g with unclear suicidal intent. Additionally, she was receiving treatment with various medications concomitantly. Subsequently, she received activated charcoal and was shifted to the emergency department. During admission, laboratory investigation showed normal Glasgow Coma Scale score and had normal liver function tests with an unconjugated bilirubin (UCB) of 0.18 mg/dL and a total bilirubin of 0.45 mg/dL. Four hours after the ingestion of paracetamol, the serum level of paracetamol had increased to 56 mg/L, which did not require the administration of acetylcysteine [N‐acetylcysteine]. Following a short observation, she was shifted back to the psychiatric ward. On day 108 of admission, as scheduled, she received the next ECT session. Approximately 72 hours after the ingestion of paracetamol (on day 109 of admission), laboratory investigation showed substantial increased in ALT, AST, total bilirubin and gamma‐glutamyl transferase, which were consistent with hepatotoxicity associated with paracetamol. Subsequently, she was shifted to a high‐care emergency unit, where she developed jaundice, mild flapping tremor and motor lag. Thereafter, she was treated with acetylcysteine along with pantoprazole for prevention of stress ulcers. On day 110 of admission, her ammonia level increased to 118 µmol/L. She developed symptoms of hepatic encephalopathy, including decreased sense of orientation and somnolence, which was treated with lactulose. Initial IV infusion of glucose caused mild hypokalaemia, which was treated with potassium replacement therapy. Her ECT and psychopharmacological treatments were stopped. During the following days, she was monitored at the medium care unit, and her clinical course was favourable; but, with an expected full recuperation of liver function over the subsequent weeks. On day 110 of admission, she was shifted back to the psychiatric ward, where she had irritability and increased talkativeness. Her young mania rating scale (YMRS) score was 8 points. There were no signs of persistent encephalopathy, disorientation or cognitive impairment, and her consciousness was clear at all times. Eleven days after the intoxication (day 117 of admission), the total bilirubin had increased further. She had an incre
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