Hypoglycemia and lactic acidosis outperform King's College criteria for predicting death or transplant in acetaminophen toxic patients Journal Article uri icon
Overview
abstract
  • IMPORTANCE: Acetaminophen toxicity is common and is characterized by hepatic failure. In cases that are not improving with standard medical therapy with N-acetylcysteine, some patients may require hepatic transplant. While there are various criteria to predict patients who might benefit from transplant, the King's College criteria remain one of the most widely used. However, the King's College criteria have several limitations and do not incorporate glucose, an important marker of hepatic function. OBJECTIVE: The primary objective of this study is to compare the presence of hypoglycemia, coagulopathy, and metabolic acidosis with the King's College criteria for predicting a composite endpoint of death or transplant. DESIGN: This study is a retrospective cohort study of adult patients admitted with a discharge diagnosis of acetaminophen-induced liver failure. SETTING: The patients were admitted at one of six university-affiliated teaching hospitals in the United States. RESULTS: A total of 334 subjects were identified who met inclusion criteria. Fifty-one subjects (15.3%) met the composite endpoint of death or transplant. Ninety-six (28.7%) subjects met the King's College criteria for transplant. The presence of hypoglycemia increased the odds of reaching the composite endpoint by 3.39-fold. This model performed better than the King's College criteria (pseudo R(2) for the area under the curve of 0.93 vs. 0.20 for the King's College criteria). CONCLUSIONS: The combination of hypoglycemia, coagulopathy, and lactic acidosis performed better than the King's College criteria for predicting death or transplant.

  • Link to Article
    publication date
  • 2018
  • Research
    keywords
  • Drugs and Drug Therapy
  • Emergency Medicine
  • Injuries
  • Liver
  • Mortality
  • Poisoning
  • Retrospective Studies
  • Transplantation
  • Additional Document Info
    volume
  • 56
  • issue
  • 7