Centrilobular Hepatic Necrosis in Cardiac Failure

Gadeholt, Hermod; Haugen, J

doi:10.1111/j.0954-6820.1964.tb00957.x

Cited by 12 publications

(3 citation statements)

References 2 publications

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“…). Severe cholestasis with jaundice mimicking biliary obstruction is a rare course of HH . Prolonged hemodynamic failure, sepsis and renal failure are risk factors.…”

Section: Atypical Course Of Hypoxic Hepatitis and Particular Circumstmentioning

confidence: 99%

Hypoxic hepatitis

Henrion

2011

Liver International

173

143

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Hypoxic hepatitis (HH), an acute liver injury also known as 'ischaemic hepatitis' or 'shock liver', is frequently observed in intensive care units. HH is heralded by a massive but transient rise in serum aminotransferase activities caused by anoxic necrosis of centrilobular liver cells. Cardiac failure, respiratory failure and toxic-septic shock are the main underlying conditions accounting for more than 90% of cases, but HH may also occur in other circumstances. Until recently, liver ischaemia, i.e. a drop in hepatic blood flow, was considered the leading, and even the sole, hemodynamic mechanism responsible for HH, and it was generally held that a shock state was required. In reality, other hemodynamic mechanisms of hypoxia, such as passive congestion of the liver, arterial hypoxaemia and dysoxia, play an important role while a shock state is observed in only 50% of cases. Accordingly, 'ischaemic hepatitis' and 'shock liver' are misnomers. Therapy of HH depends primarily on the nature of the underlying condition. The prognosis is poor, with more than half of patients dying during the hospital stay.

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“…). Severe cholestasis with jaundice mimicking biliary obstruction is a rare course of HH . Prolonged hemodynamic failure, sepsis and renal failure are risk factors.…”

Section: Atypical Course Of Hypoxic Hepatitis and Particular Circumstmentioning

confidence: 99%

Hypoxic hepatitis

Henrion

2011

Liver International

173

143

View full text Add to dashboard Cite

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“…We reviewed the medical records of 293 [2] (e.g., hypotension), decreased oxygen availability [3] (e.g., sepsis) and increased oxygen consumption [4] (e.g., hyperthermia).…”

Section: Study Patientsmentioning

confidence: 99%

“…Though clinically significant, impairment of hepatic function is unusual in shock, a transient (5-25 days), and often marked (10-300 times the upper limit of normal) change in serum enzyme levels in association with centrilobular hepatic necrosis has been described (1)(2)(3)(4)(5)(6)(7)(8)(9). Historically referred to as "shock liver", clinical and experimental reports over the last five decades have confirmed that the liver is a target organ during certain hypotensive states (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Hypoxic Hepatopathy: Pathophysiology and Prognosis

Birrer

Takuda

Takara³

2007

Intern. Med.

196

184

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Severe hyperbilirubinemia and coma in chronic congestive heart failure

et al. 1982

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A 64-year-old man developed severe hyperbilirubinemia of predominantly conjugated fraction in 1978, eight years after a myocardial infarction and development of congestive heart failure. In 1975, he was admitted elsewhere for symptoms suggestive of chronic hepatitis, but liver biopsy revealed replacement of hepatocytes by red blood cells which was interpreted as a result of left-sided cardiac failure. In 1978, liver biopsy showed congestive liver disease with cardiac sclerosis. Despite initial improvement, his condition deteriorated, he became encephalopathic, and died in a coma. This case is reported to illustrate that chronic congestive heart failure can present with severe jaundice and terminate in hepatic coma.

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Centrilobular Hepatic Necrosis in Cardiac Failure

Cited by 12 publications

References 2 publications

Hypoxic hepatitis

Hypoxic hepatitis

Hypoxic Hepatopathy: Pathophysiology and Prognosis

Severe hyperbilirubinemia and coma in chronic congestive heart failure

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