International Journal of Clinical Case Reports and Reviews Copy rights@ Parackrama Karunathilake et.al. Auctores Publishing LLC – Volume 9(1)-170 www.auctoresonline.org ISSN: 2690-4861 Page 1 of 3 Acetaminophen Intoxication with Fulminant Hepatic Failure Salvaged by Plasmapheresis Rumesh Ranasinghe 1 , Shifa Azher 1 , Parackrama Karunathilake 2 *, Udaya Ralapanawa 2 1 National Hospital Kandy, Kandy, Sri Lanka. 2 Department of Medicine, Faculty of Medicine, University of Peradeniya, Peradeniya, Sri Lanka. *Corresponding Author: Parackrama Karunathilake, Department of Medicine, Faculty of Medicine, University of Peradeniya, Sri Lanka. Received Date: 23 August 2021 | Accepted Date: 22 November 2021 | Published Date: 30 November 2021 Citation: R Ranasinghe, S Azher, P Karunathilake, U Ralapanawa. (2021). Acetaminophen Intoxication with Fulminant Hepatic Failure Salvaged by Plasmapheresis. International Journal of Clinical Case Reports and Reviews. 9(1); DOI:10.31579/2690-4861/170 Copyright: © 2021 Parackrama Karunathilake, This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Abstract Introduction: Acetaminophen-induced liver injury is the most common cause of acute liver failure, where multiple ingestions or a delay in the presentation may lead to a poor prognosis. N-acetylcysteine (NAC) is the conventional antidote used to treat acute acetaminophen toxicity, and plasmapheresis can be used as an adjunct, though there are no systematic studies to prove its effectivity. Case Presentation: An 18-year-old girl was admitted with reduced responsiveness for one day with a few episodes of diarrhea. On admission, she was febrile and had a GCS of 10/15, otherwise normal neurology. She had marked right hypochodrial tenderness, deep icterus, and a pulse of 120 beats per minute, with a blood pressure of 80/50 mmHg; fluid resuscitation with inotropic support was done. Initial investigations revealed severe metabolic acidosis, hemoglobin of 9.5 g/dL, white blood cell count 13,500/mm3, and platelet 119,000 per μL. The prothrombin time (PT) international normalized ratio (INR) was 4.7, and the activated partial thromboplastin time (APTT) was 38.6. The alanine aminotransferase (ALT) level was 8118 U/L, and aspartate aminotransferase (AST) was 3883 U/L with a total bilirubin of 107 μmol/L. The diagnosis of acute liver failure following acetaminophen intoxication was made and managed with intravenous NAC, pantoprazole cover, intravenous ceftriaxone, metronidazole, thiamine, and vitamin K. Fresh frozen plasma and platelets were given for severe coagulopathy. She was started with plasmapheresis at the intensive care unit (ICU), where she had a significant improvement, though she developed hospital-acquired pneumonia, which was successfully managed. Subsequently, her liver functions returned to the baseline, and she was discharged after a psychiatric assessment. Conclusion: A high degree of suspicion needs to be adopted to diagnose acetaminophen-induced acute liver failure when a patient presents with hepatic encephalopathy, and plasmapheresis can be considered a life-saving measure adjunct to the NAC. Keywords: acetaminophen; fulminant hepatic failure; acute liver failure; plasmapheresis; n-acetyl cysteine Abbreviations NAC: N-acetylcysteine; GCS: Glasgow Coma Scale; NCCT: Non- contract Computed Tomography; PT: Prothrombin Time; INR: International Normalized Ratio; APTT: Activated Partial Thromboplastin Time; ALT: Alanine aminotransferase; AST: Aspartate aminotransferase; ICU: Intensive Care Unit; NAPQI: N-acetyl parabenzoquinone imine Introduction Acetaminophen is the most widely used analgesic – antipyretic agent since its clinical introduction in 1965. In therapeutic doses, it is considered safe, but its overdose could cause fatal and nonfatal hepatic necrosis. Nevertheless, in susceptible individuals like alcoholics, therapeutic or slightly excess doses can be hepatotoxic [1]. The other reported risk factors for hepatotoxicity of acetaminophen include chronic malnutrition, advanced age, genetic factors, and use of cytochrome P450 inducers [2]. In the United States, 20% of liver transplantations are due to acetaminophen-induced acute liver failure [1]. In managing acetaminophen toxicity, serum acetaminophen concentration is measured after four hours of single ingestion, and the values plotted in a Rumack-Matthew nomogram are used for therapeutic decision-making. N-acetylcysteine (NAC) is the antidote that will be started based on this nomogram [2]. In cases of multiple ingestions or when there is a delay in presentation, the prognosis is poor. Those patients may require intensive care management and anticipate the possibility of liver transplantation [3]. Though the mainstay of treatment in acetaminophen intoxication is Open Access Case Report International Journal of Clinical Case Reports and Reviews Parackrama Karunathilake * AUCTORES Globalize your Research