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Hypoxia, Free Radicals, and Reperfusion Injury Following Cold Storage and Reperfusion of Livers for Transplantation
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Ronald G. Thurman, Wenshi Gao, Henry D. Connor, Sigrid Bachmann, Robert T. Currin, Ronald P. Mason, John J. Lemasters
Hepatic hypoxic injury commonly occurs with heart failure, where increased central venous pressure results in centrilobular venous stasis and necrosis.1 Causes of hypoxic injury to the liver that are more rare yet potentially more severe include hepatic artery thrombosis, thrombosis of the hepatic vein, and hepatic venoocclusive disease affecting the smaller hepatic vein tributaries and central veins. In contrast to heart or brain, hepatic regenerative capacity is great, and within two to three weeks complete recovery from hypoxic necrosis can occur. In hypoxic liver injury, the underlying circulatory problem is often the focus of attention rather than the liver itself. However, “ischemic hepatitis” is increasingly recognized clinically, and severe ischemic hepatitis has been associated with poor survival rates.2
Pregnancy and Sex-Related Deaths
Published in John M. Wayne, Cynthia A. Schandl, S. Erin Presnell, Forensic Pathology Review, 2017
John M. Wayne, Cynthia A. Schandl, S. Erin Presnell
Answer E is correct. Since the oxygenation to zone 3 of the liver is suboptimal, shock (systemic hypotension) can be seen in the liver as centrilobular congestion and necrosis or “shock liver.” One hallmark of diffuse intravascular coagulopathy that may be identified at autopsy is shock liver (also referred to as ischemic hepatitis).
Complications of Anesthesia
Published in Stephen M. Cohn, Matthew O. Dolich, Complications in Surgery and Trauma, 2014
Monique Espinosa, Albert J. Varon
Postoperative hepatic dysfunction can also occur due to ischemic hepatitis. This type of hepatic injury results from hepatic hypoperfusion, hypoxemia, or sepsis. Prevention strategies are nonspecific and include maintaining adequate systemic perfusion and oxygenation [21].
Prevalence, clinical characteristics and outcomes of hypoxic hepatitis in critically ill patients
Published in Scandinavian Journal of Gastroenterology, 2022
Sigrún Jonsdottir, Margrét B. Arnardottir, Jóhannes A. Andresson, Helgi K. Bjornsson, Sigrun H. Lund, Einar S. Bjornsson
Cut-off of aminotransferases has varied between studies from 400 to 3000 in AST with approximately half below 800 IU/L [11]. The cut-off levels for AST seem to be arbitrary and few studies have compared different cut-off levels. In 1984, Gibson and Dudley published a study on ischemic hepatitis and suggested a clinical and biochemical criteria based on an appropriate clinical setting, liver tests and time course of aminotransferase elevation. They did not specify a specific cut-off level of aminotransferases. In their study, they diagnosed 19 episodes of ischemic hepatitis by liver tests and characteristic liver pathology and AST ranged from between 255 and >3,000. They emphasized the importance of differentiating between ischemic hepatitis and acute viral or drug-induced hepatitis which was usually thought to be dependent on the demonstration of characteristic histological features in the absence of serological evidence of acute viral hepatitis. However, they mentioned that patients with ischemic hepatitis are seriously ill and a diagnostic liver biopsy must be considered undesirable in the clinical setting. Therefore, they suggested that a confident diagnosis of ischemic hepatitis might be made based on clinical and biochemical criteria alone [20]. Half of the cases recorded in Gibson’s and Dudley’s study had AST levels below 20 times the ULN. Thus, it is evident that with Henrion’s criteria a large part of patients with HH are missed since it is not always feasible to perform a liver biopsy.
Dili is rare amongst patients without liver metastases receiving cancer treatment in Iceland: a population-based cohort study
Published in Scandinavian Journal of Gastroenterology, 2022
H. K. Björnsson, A. Sverrisdottir, E. S. Björnsson
All patients with liver metastases at the onset of liver injury were excluded. Patients with bone metastases or kidney cancer and isolated ALP elevations on onset of liver injury were also excluded. When other non-DILI causes such as choledocholithiasis, ischemic hepatitis or viral hepatitis were identified they were categorized as ‘other specific causes’.