Scholarlink

Background <p>Intentional or accidental intoxication is a common inciting cause of acute liver failure, which manifests as a severe clinical consequence of abrupt hepatocyte injury in the patient without any known underlying liver diseases (within 26&#xa0;weeks of illness duration). In addition, it often progresses to a lethal outcome. Thinner intoxication is a rare but non-negligible etiology of acute liver failure. Considering the potential neurotoxicity, myotoxicity, hepatotoxicity, nephrotoxicity, and cardiopulmonary toxicity of thinner, as well as the lack of effective specific reversal agents or antidotes, early and continuous supportive care by an artificial liver support system (Liu <i>et&#xa0;al.</i> in <i>Artif Organs</i> 49:762–777, 2025)—defined here as the integrated use of double plasma molecular adsorption system, plasma exchange, and continuous veno-venous hemofiltration—is conducive to remove thinner and ammonia from the blood, improve hepatic encephalopathy, replace lost liver function, alleviate thinner intoxication-induced multiorgan damage, restore hemodynamics and internal environment stability, modulate immune response, and maintain cytokine homeostasis. In this study, we presented the first reported case of acute liver failure induced by acute severe thinner intoxication in a Han Chinese adult, who was successfully rescued through the use of a double plasma molecular adsorption system, plasma exchange, and continuous veno-venous hemofiltration.</p> Case summary <p>A 46-year-old Asian man was admitted to the Department of Critical Care Medicine owing to nausea and vomiting for 4 days, abdominal pain and melena for 2 days, and disturbance of consciousness for 1 day after accidentally ingesting a mouthful of thinner (exact volume unknown) at a construction site. In the intensive care unit, the patient underwent orotracheal intubation, invasive mechanical ventilation, appropriate analgesia and sedation, infusion of blood products and hemostatic drugs, phlegm-removing, and correction of internal environment disorder. Subsequently, the patient received four double plasma molecular adsorption system treatments, two plasma exchanges (a total of 6000&#xa0;mL of fresh frozen plasma), and 79&#xa0;hours of continuous veno-venous hemofiltration during hospitalization. On the 8th day after admission, invasive mechanical ventilation was withdrawn, but the patient’s consciousness remained unclear. On the 36th day after admission, the patient was in remission and discharged. However, his liver function and coagulation parameters did not revert to normal.</p> Conclusion <p>Thinner intoxication is a rare but non-negligible etiology of acute liver failure. To the best of our knowledge, our case is the first attempt to combine double plasma molecular adsorption system treatment, plasma exchange, and continuous veno-venous hemofiltration for acute liver failure as a clinical manifestation of thinner intoxication. The combination of different therapeutic modalities of an artificial liver support system can compensate for the individual shortcomings and maximize their respective advantages, which requires a multidisciplinary team to determine their clinical application in suitable patients.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Combined application of double plasma molecular adsorption system treatment, plasma exchange, and continuous veno-venous hemofiltration to rescue an adult patient with acute liver failure induced by accidental acute severe thinner intoxication: a case report

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月21日

查看全文
  • Dong-Sheng Fei,
  • Xiao-Fei Bi,
  • Jian-Nan Zhang,
  • Yu-Jia Tang,
  • Di Wu,
  • Hui-Ying Liu,
  • Huan Meng,
  • Xiao-Hui Jiang,
  • Jia Xu,
  • Kuo Wang,
  • Ying-Fei Zhi,
  • Yang Gao,
  • Kai Kang

摘要

Background

Intentional or accidental intoxication is a common inciting cause of acute liver failure, which manifests as a severe clinical consequence of abrupt hepatocyte injury in the patient without any known underlying liver diseases (within 26 weeks of illness duration). In addition, it often progresses to a lethal outcome. Thinner intoxication is a rare but non-negligible etiology of acute liver failure. Considering the potential neurotoxicity, myotoxicity, hepatotoxicity, nephrotoxicity, and cardiopulmonary toxicity of thinner, as well as the lack of effective specific reversal agents or antidotes, early and continuous supportive care by an artificial liver support system (Liu et al. in Artif Organs 49:762–777, 2025)—defined here as the integrated use of double plasma molecular adsorption system, plasma exchange, and continuous veno-venous hemofiltration—is conducive to remove thinner and ammonia from the blood, improve hepatic encephalopathy, replace lost liver function, alleviate thinner intoxication-induced multiorgan damage, restore hemodynamics and internal environment stability, modulate immune response, and maintain cytokine homeostasis. In this study, we presented the first reported case of acute liver failure induced by acute severe thinner intoxication in a Han Chinese adult, who was successfully rescued through the use of a double plasma molecular adsorption system, plasma exchange, and continuous veno-venous hemofiltration.

Case summary

A 46-year-old Asian man was admitted to the Department of Critical Care Medicine owing to nausea and vomiting for 4 days, abdominal pain and melena for 2 days, and disturbance of consciousness for 1 day after accidentally ingesting a mouthful of thinner (exact volume unknown) at a construction site. In the intensive care unit, the patient underwent orotracheal intubation, invasive mechanical ventilation, appropriate analgesia and sedation, infusion of blood products and hemostatic drugs, phlegm-removing, and correction of internal environment disorder. Subsequently, the patient received four double plasma molecular adsorption system treatments, two plasma exchanges (a total of 6000 mL of fresh frozen plasma), and 79 hours of continuous veno-venous hemofiltration during hospitalization. On the 8th day after admission, invasive mechanical ventilation was withdrawn, but the patient’s consciousness remained unclear. On the 36th day after admission, the patient was in remission and discharged. However, his liver function and coagulation parameters did not revert to normal.

Conclusion

Thinner intoxication is a rare but non-negligible etiology of acute liver failure. To the best of our knowledge, our case is the first attempt to combine double plasma molecular adsorption system treatment, plasma exchange, and continuous veno-venous hemofiltration for acute liver failure as a clinical manifestation of thinner intoxication. The combination of different therapeutic modalities of an artificial liver support system can compensate for the individual shortcomings and maximize their respective advantages, which requires a multidisciplinary team to determine their clinical application in suitable patients.