Hypoxic hepatitis : a contribution to the clinical syndrome and the hemodynamic patterns
(2000)
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- Authors
- Supervisors
- Heller, Francis
- Abstract
- In the mid-1950’s, when the determination of serum aminotransferase activities became current practice, it appeared rapidly obvious that the blood elevation of these enzymatic activities was not specific for myocardial infarction, but could be also observed in hepato-biliary diseases. Soon after, a strong association between massive elevation of serum aminotransferase activities and presence of a clinical condition of shock was noted. In this setting, a centrilobular liver cell necrosis was generally observed when histologic examination of the liver was performed. The terms “ischemic hepatitis” were first coined by Bynum et al. (Dig. DIs. Sci., 1979, 24 : 129 – 135) in 1979, because of the clinical (asthenia, anorexia, abdominal discomfort) and biochemical (serum aminotransferase activity elevation) analogy between this newly reported syndrome and viral hepatitis. During a ten-year period, we had the opportunity to collect 142 episodes of hypoxic hepatitis in the intensive care units of the Jolimont hospital. This prospective, observational series represents the basis of this monograph. Patients at risk of hypoxic hepatitis are patients with cardiac failure (100 episodes), particularly with decompensated congestive heart failure, patients with exacerbated chronic respiratory failure (19 episodes), and patients with circulatory shock mainly of septic origin (19 episodes). In contrast with a widely held opinion, a shock state is not a prerequisite for the occurrence of hypoxic hepatitis, and in the Jolimont series, was observed in only 55% of the cases. The clinical signs of liver injury are generally overshadowed by obvious signs of cardio-circulatory failure. The typical pattern of the alteration in liver biochemistry is characterized by a dramatic increase in the serum activities if liver cell cytosolic enzymes and a marked decline in the prothrombin activity that recover in a few days. The outcome of hypoxic hepatitis is poor and depends on the underlying condition. The in-hospital fatality rate average 50% (1-month mortality rate of 53% in the Jolimont series). <BR> The major contribution of the Jolimont series is to have assessed systemic and hepatic hemodynamics in hypoxic hepatitis. It remains widely agreed that, in hypoxic hepatitis, the sole hemodynamic mechanism responsible for hepatic hypoxia is ischemia, i.e. a fall in hepatic blood flow. It was our aim to demonstrate that passive congestion of the liver in heart failure, arterial hypoxemia in respiratory failure and inability to oxygen uptake in toxic/septic shock were also relevant mechanisms in the occurrence of hypoxic hepatitis. Actually, from a hemodynamic viewpoint, hypoxic hepatitis is multifactorial and encompasses different hemodynamic patterns accordingly to the underlying condition. It is the reason why we estimated that the commonly used terms of “ischemic hepatitis” or ‘”shock liver” are misnomers and should be replaced by “hypoxic hepatitis”
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Citations
Henrion, J. (2000). Hypoxic hepatitis : a contribution to the clinical syndrome and the hemodynamic patterns. https://hdl.handle.net/2078.5/111077