Mechanisms of Hepatocyte Injury, Multiorgan Failure, and Prognostic Criteria in Acute Liver Failure

2003 ◽  
Vol 23 (3) ◽  
pp. 203-216 ◽  
2020 ◽  
Vol 2020 ◽  
pp. 1-4
Author(s):  
Bertram K. Woitok ◽  
Shawki Bahmad ◽  
Gregor Lindner

Background.Exertional heat stroke is a life-threatening condition often complicated by multiorgan failure. We hereby present a case of a 25-year-old male presenting with syncope after a 10  km run in 28°C outside temperature who developed acute liver failure. Case Presentation. Initial temperature was found to be 41.1°C, and cooling measures were rapidly applied. He suffered from acute renal failure and rhabdomyolysis and proceeded to acute liver failure (ASAT 6100 U/l and ALAT 6561 U/l) due to hypoxic hepatitis on day 3. He did not meet criteria for emergency liver transplantation and recovered on supportive care. Conclusions. Acute liver failure due to heat stroke is a life-threatening condition with often delayed onset, which nevertheless resolves on supportive care in the majority of cases; thus, a delayed referral to transplant seems to be reasonable.


Author(s):  
Cynthia Wang ◽  
Michelle Y. Braunfeld

Acute liver failure produces widespread physiologic derangements including encephalopathy, coagulopathy, peripheral vasodilation, a systemic inflammatory response, and multiorgan failure. Morbidity is significant, and mortality is 50%. The classification of liver failure and the various etiologies, including viral hepatitis, drug-induced, toxins, and autoimmunity are reviewed here. The multisystem effects of acute liver failure influence all aspects of perioperative care and adequate supportive care during this time is crucial to providing the best possible outcome for the patient. Specific treatment objectives and recommendations are discussed, and the anesthetic management with regard to drug choices, hemodynamic goals, and intraoperative monitoring is reviewed.


2018 ◽  
Vol 39 (05) ◽  
pp. 513-522 ◽  
Author(s):  
Priyanka Rajaram ◽  
Ram Subramanian

AbstractAcute liver failure (ALF) is a condition that can rapidly progress to multiorgan failure. This article focuses on the diagnosis and management of ALF. We provide a detailed review of the common etiologies of ALF, including acetaminophen overdose, viral hepatitis, drug-induced liver injury, Wilson's disease, and autoimmune hepatitis. The article then addresses how to recognize ALF and reviews the role of common laboratory and imaging tests in establishing this diagnosis. The remainder of the article details the management of hepatic and extrahepatic organ dysfunctions in ALF. The article concludes with a discussion regarding the prognostication of patients with ALF and the criteria for considering liver transplantation.


2012 ◽  
Vol 12 (8) ◽  
pp. 635-642 ◽  
Author(s):  
Judith van Paassen ◽  
Martijn P Bauer ◽  
M Sesmu Arbous ◽  
Leo G Visser ◽  
Jonas Schmidt-Chanasit ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Janja Tarčuković ◽  
Lara Valenčić ◽  
Željka Polonijo ◽  
Ana Fućak ◽  
Boban Dangubić ◽  
...  

Tumour lysis syndrome (TLS) is a group of pathophysiological processes caused by rapid degradation of tumour cells with subsequent release of intracellular contents into the extracellular space. It is characterized by the development of systemic metabolic disturbances with or without clinical manifestations. The process usually occurs in highly proliferative, large tumours after induction of cytotoxic therapy. Rarely, however, spontaneous TLS can develop, as well as signs of multiorgan failure triggered by an excessive metabolic load and sterile inflammation. The combination of the aforementioned is thus quite unique. Here, we present a 63-year-old male in which spontaneous TLS was accompanied with acute liver failure and delineated underlying nonHodgkin lymphoma. Initial laboratory findings included hyperkalaemia, hyperphosphataemia, hypocalcaemia, uraemia, and increased creatinine levels indicating the onset of TLS with acute kidney injury. Moreover, the patient showed signs of jaundice, coagulopathy, and hepatic encephalopathy. Development of TLS with multiorgan failure prompted rapid initiation of critical care management, including vigorous intravenous fluid therapy, allopurinol treatment, high flow continuous venovenous haemodiafiltration, and commencement of chemotherapy. The case highlights the possibility of TLS as a differential diagnosis in patients presenting with multiorgan failure and the importance of early detection of this potentially challenging and fatal diagnosis.


2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Guo-Zhen Liu ◽  
Xu-Wen Xu ◽  
Shu-Hui Tao ◽  
Ming-Jian Gao ◽  
Zhou-Hua Hou

Abstract Background Acute liver failure (ALF) is a syndrome of severe hepatocyte injury with high rate of mortality. Hepatitis B virus (HBV) infection is the major cause of ALF worldwide, however, the underlying mechanism by which HBV infection leads to ALF has not been fully disclosed. Methods D-GalN-induced hepatocyte injury model and LPS/D-GalN-induced ALF mice model were used to investigate the effects of HBV X protein (HBx) in vitro and in vivo, respectively. Cell viability and the levels of Glutathione (GSH), malondialdehyde (MDA) and iron were measured using commercial kits. The expression of ferroptosis-related molecules were detected by qRT-PCR and western blotting. Epigenetic modification and protein interaction were detected by chromatin immunoprecipitation (ChIP) assay and co-immunoprecipitation (co-IP), respectively. Mouse liver function was assessed by measuring aspartate aminotransferase (AST) and alanine aminotransferase (ALT). The histological changes in liver tissues were monitored by hematoxylin and eosin (H&E) staining, and SLC7A11 immunoreactivity was assessed by immunohistochemistry (IHC) analysis. Results D-GalN triggered ferroptosis in primary hepatocytes. HBx potentiated D-GalN-induced hepatotoxicity and ferroptosis in vitro, and it suppressed SLC7A11 expression through H3K27me3 modification by EZH2. In addition, EZH2 inhibition or SLC7A11 overexpression attenuated the effects of HBx on D-GalN-induced ferroptosis in primary hepatocytes. The ferroptosis inhibitor ferrostatin-1 (Fer-1) protected against ALF and ferroptosis in vivo. By contrast, HBx exacerbates LPS/D-GalN-induced ALF and ferroptosis in HBx transgenic (HBx-Tg) mice. Conclusion HBx facilitates ferroptosis in ALF via EZH2/H3K27me3-mediated SLC7A11 suppression.


2000 ◽  
Vol 6 (2) ◽  
pp. 163-169 ◽  
Author(s):  
A. Obaid Shakil ◽  
David Kramer ◽  
George V. Mazariegos ◽  
John J. Fung ◽  
Jorge Rakela

2000 ◽  
Vol 6 (2) ◽  
pp. 163-169 ◽  
Author(s):  
A SHAKIL ◽  
D KRAMER ◽  
G MAZARIEGOS ◽  
J FUNG ◽  
J RAKELA

Sign in / Sign up

Export Citation Format

Share Document