Profound Hyperbilirubinemia During Severe Carbon Monoxide Poisoning and Subsequent Multiorgan Failure: A Case Report.
- 1Internal Medicine Department University of Toledo Toledo Ohio USA.
- 2Department of Medicine, Faculty of Medicine and Health Sciences An-Najah National University Nablus Palestine.
- 3Gastroenterology Department University of Toledo Toledo Ohio USA.
Abstract
Carbon monoxide poisoning is classically associated with neurologic and cardiovascular toxicity, while severe exposure may also cause systemic toxic-hypoxic injury. Profound direct-predominant hyperbilirubinemia without mechanical biliary obstruction is rarely described. We report a 55-year-old woman with alcohol use disorder, chronic tobacco use, COPD, and hepatic steatosis who presented with altered mental status and jaundice after suspected household carbon monoxide exposure. Her carboxyhemoglobin level was > 30%, and she required intubation, intensive care, vasopressor support, and three hyperbaric oxygen treatments. Initial testing showed total bilirubin of 23.1 mg/dL and direct bilirubin of 13.1 mg/dL, despite only mild AST elevation and near-normal ALT and alkaline phosphatase. Imaging showed hepatic steatosis and cholelithiasis without convincing biliary obstruction, and the documented workup for viral, autoimmune, metabolic, hemolytic, and vascular causes was unrevealing. Her liver dysfunction was considered multifactorial, with possible carbon monoxide-related toxic-hypoxic injury superimposed on underlying steatotic or alcohol-related liver vulnerability. After transient improvement, she developed coagulopathy, acute kidney injury, recurrent shock with clinical and imaging concern for acute cholecystitis, worsening hyperbilirubinemia peaking near 49-50 mg/dL, encephalopathy, respiratory failure, and multiorgan failure. Cholecystostomy yielded dark green bile without documented purulence, and aspirate cultures showed no growth; biliary sepsis was therefore not microbiologically confirmed. She died in the hospital after goals-of-care discussions. The initial bilirubin-predominant pattern was atypical for classic hypoxic hepatitis and may have reflected overlapping hepatic insults. This case emphasizes broad evaluation and cautious causal interpretation; it does not establish that carbon monoxide exposure alone caused the initial hyperbilirubinemia.
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BibTeX
@article{joma2026profound,
title = {{Profound Hyperbilirubinemia During Severe Carbon Monoxide Poisoning and Subsequent Multiorgan Failure: A Case Report.}},
author = {Marwan Joma and Anwar Zahran and Abdulrahman Karam and Bisher Sawaf and Wasef Sayeh and Thomas Sodeman and Yaseen Alastal},
journal = {Clinical case reports},
year = {2026},
month = nov,
doi = {10.1002/ccr3.73833},
url = {https://europepmc.org/article/MED/42997175},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Profound Hyperbilirubinemia During Severe Carbon Monoxide Poisoning and Subsequent Multiorgan Failure: A Case Report.
AU - Marwan Joma
AU - Anwar Zahran
AU - Abdulrahman Karam
AU - Bisher Sawaf
AU - Wasef Sayeh
AU - Thomas Sodeman
AU - Yaseen Alastal
PY - 2026
DA - 2026/11/06
JO - Clinical case reports
DO - 10.1002/ccr3.73833
UR - https://europepmc.org/article/MED/42997175
AB - Carbon monoxide poisoning is classically associated with neurologic and cardiovascular toxicity, while severe exposure may also cause systemic toxic-hypoxic injury. Profound direct-predominant hyperbilirubinemia without mechanical biliary obstruction is rarely described. We report a 55-year-old woman with alcohol use disorder, chronic tobacco use, COPD, and hepatic steatosis who presented with altered mental status and jaundice after suspected household carbon monoxide exposure. Her carboxyhemoglobin level was > 30%, and she required intubation, intensive care, vasopressor support, and three hyperbaric oxygen treatments. Initial testing showed total bilirubin of 23.1 mg/dL and direct bilirubin of 13.1 mg/dL, despite only mild AST elevation and near-normal ALT and alkaline phosphatase. Imaging showed hepatic steatosis and cholelithiasis without convincing biliary obstruction, and the documented workup for viral, autoimmune, metabolic, hemolytic, and vascular causes was unrevealing. Her liver dysfunction was considered multifactorial, with possible carbon monoxide-related toxic-hypoxic injury superimposed on underlying steatotic or alcohol-related liver vulnerability. After transient improvement, she developed coagulopathy, acute kidney injury, recurrent shock with clinical and imaging concern for acute cholecystitis, worsening hyperbilirubinemia peaking near 49-50 mg/dL, encephalopathy, respiratory failure, and multiorgan failure. Cholecystostomy yielded dark green bile without documented purulence, and aspirate cultures showed no growth; biliary sepsis was therefore not microbiologically confirmed. She died in the hospital after goals-of-care discussions. The initial bilirubin-predominant pattern was atypical for classic hypoxic hepatitis and may have reflected overlapping hepatic insults. This case emphasizes broad evaluation and cautious causal interpretation; it does not establish that carbon monoxide exposure alone caused the initial hyperbilirubinemia.
SN - 2050-0904
ER -