Paracetamol overdose
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Paracetamol overdose Acute liver failure and acute kidney injury following an overdose of paracetamol: case report
A 27-year-old woman developed acute liver failure and acute kidney injury following an overdose of paracetamol [time to reactions onsets not stated]. The woman with a remote history of focal segmental glomerular sclerosis, presented at an emergency department due to nausea, vomiting and abdominal pain radiating to the chest for 2 weeks. To manage the pain, she had ingested >50 tablets of paracetamol [acetaminophen; dosage not stated] over 3–4 days prior to the presentation. In the emergency department, she was haemodynamically stable except for mild tachycardia. Her BP was 135/85mm Hg and HR was 104 beats/minute. Her body temperature was found to be normal. She did not have tachypnoea. Her oxygen saturation was 100% on room air. She had generalised abdominal tenderness. Her cardiac and pulmonary examination were found to normal. Her mental status and neurological exam were intact upon presentation. Investigations revealed leukocytosis and elevated aminotransferases (elevated levels of AST and ALT). Her total bilirubin was 2.9 mg/dL, ALP was 97 U/L and INR was 1.7. She had a mild acute kidney injury with a creatinine of 1.04 mg/dL (baseline of 0.8 mg/dL). Lactate was 12.9 mEq/L and D-dimer was 21830 ng/mL. Paracetamol level was found to be elevated. Her chest x-ray was found to be normal. An abdominal and pelvic CT scan demonstrated diffuse colonic wall thickening most pronounced in the cecum, ascending and sigmoid colon. There was no evidence of hepatic steatosis on imaging. A COVID-19 nasopharyngeal swab was obtained in view of diarrhoea and abdominal pain and was found to be positive. Despite positive test, she did not have respiratory symptoms at the time of presentation. She received treatment with N-acetylcysteine. She was shifted to the ICU for further management and close monitoring of acute liver injury secondary to paracetamol overdose and COVID-19. Testing of acute viral hepatitis was found to be negative. Additionally, serological testing for autoimmune and genetic etiologies of liver disease were found to be negative. Two days after the admission, her hepatic synthetic function significantly worsened. Her total bilirubin increased to 4.3 mg/dL and INR increased to 6.3. Additionally, her aminotransferases (AST and ALT levels) were found to be elevated further. Her kidney function worsened, and she became oliguric. Later that day, frequent neurological examinations showed progressive changes in her mental status and she met criteria for acute liver failure which was attributed to paracetamol overdose. Hepatic encephalopathy eventually progressed to grade 3 of West Haven Grading system. An urgent CT brain showed diffusely small cerebral sulci and basal cisterns concerning for brain swelling. Arterial ammonia was 196 µmol/L and she was started on replacement therapy and eventually required intubation for airway protection. Neurology and neurosurgery were consulted, and it was decided to
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