Hypoxic hepatitis: underlying conditions and risk factors for mortality in critically ill patients

Fuhrmann, Valentin; Kneidinger, Nikolaus; Herkner, Harald; Gisslinger, Heinz; Nikfardjam, Mariam; Bojic, Anja; Schellongowski, Peter; Angermayr, Bernhard; Kitzberger, Reinhard; Warszawska, Joanna; Holzinger, Ulrike; Schenk, Peter; Madl, Christian

doi:10.1007/s00134-009-1508-2

Cited by 173 publications

(228 citation statements)

References 35 publications

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“…The reported incidence of this event ranges between 0.03% in the internal normal ward to 1.5% in the intensive care unit (ICU) [1,2]. Recently, we reported that high international normalized ratio (INR), presence of septic shock, and high sequential organ failure assessment (SOFA) score were independent predictors of mortality in patients with HH [3]. Although it is reported that hyperbilirubinemia and other abnormal ''liver function tests'' on ICU admission may have a prognostic impact [4,5], there are a lack of studies evaluating the influence of specific disease entities of acute hepatic injury-like HH-on outcome in critically ill patients.…”

Section: Introductionmentioning

confidence: 99%

Impact of hypoxic hepatitis on mortality in the intensive care unit

et al. 2011

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Section: Introductionmentioning

confidence: 99%

Impact of hypoxic hepatitis on mortality in the intensive care unit

et al. 2011

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“…Transaminases and LDH levels reach their peak 1-3 days after the acute event and return to normal limits within 7-10 days if the patient's hemodynamics recover (19,56,57). In ACLI, an early and rapid increase of LDH levels in parallel with transaminase levels, a ratio of ALT to LDH <1.5, and a decrease in ALT levels by more than 50% within 72 h are characteristic findings that can be useful in the differential diagnosis of acute viral, alcoholic, or drug-induced hepatitis (29,58,59). Other laboratory findings are mild elevations of serum bilirubin and AP levels and prolongation of prothrombin time (11,19,29).…”

Section: Clinical Findings and Implications Of The Laboratory Changesmentioning

confidence: 99%

How to interpret liver function tests in heart failure patients?

Cagli

Başar²,

Tok³

et al. 2020

Turk J Gastroenterol

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Cardiac hepatopathy has generally been used to describe any liver damage caused by cardiac disorders in the absence of other possible causes of liver damage. Although there is no consensus on the terminology used, cardiac hepatopathy can be examined as congestive hepatopathy (CH) and acute cardiogenic liver injury (ACLI). CH is caused by passive venous congestion of the liver that generally occurs in the setting of chronic cardiac conditions such as chronic HF, constrictive pericarditis, tricuspid regurgitation, or right-sided heart failure (HF) of any cause, and ACLI is most commonly associated with acute cardiocirculatory failure resulting from acute myocardial infarction, acute decompensated HF, or myocarditis. Histologically, CH is characterized by sinusoidal dilation, replacement of hepatocytes with red blood cells extravasating from the sinusoids, and necrosis/apoptosis of zone 3 of the Rappaport acinus, and it could progress to cirrhosis in advanced cases. In ACLI, however, massive necrosis of zone 3 is the main histological finding. Primary laboratory findings of CH are elevated serum cholestasis markers including bilirubin, alkaline phosphatase, and γ-glutamyl-transpeptidase levels, whereas those of ACLI are a striking elevation in transaminase and lactate dehydrogenase levels. Both CH and ACLI have a prognostic value for identifying cardiovascular events and mortality and have some special implications in the management of patients undergoing ventricular assist device implantation or cardiac transplantation. There is no specific treatment for CH or ACLI other than treatment of the underlying cardiac disorder.

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“…Die zentrilobuläre Leberzellnekrose bei HH tritt infolge einer Sauerstoffunterversorgung der Leber zumeist nach kardiogenem, septischem oder seltener auch respiratorischem Schockgeschehen auf [28,29]. Die HH ist die häufigste Ursache eines akuten Transaminasenanstiegs auf der Intensivstation und wird mit einer Inzidenzrate von 10 % beschrieben [30,31].…”

Section: Hypoxische Hepatitisunclassified

Hepatokardiale Wechselwirkungen

Horvatits

Drolz

Rutter

et al. 2015

Med Klin Intensivmed Notfmed

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Interactions between the hepatic portal and cardiovascular systems are frequently found in patients with liver disease. Cirrhotic cardiomyopathy (CCMP) is defined as reduced cardiac function in patients with liver cirrhosis in the absence of other known causes of cardiac disease. The typical hyperdynamic circulatory state by means of increased cardiac output and reduced systemic vascular resistance may mask left ventricular failure. Portopulmonary hypertension (POPH) is defined as increased pulmonary arterial pressure and the presence of portal hypertension, and is associated with increased mortality. Targeted medical therapies include vasodilators such as prostanoids, endothelin receptor antagonists and phosphodiesterase-5 inhibitors. Hypoxic or ischaemic hepatitis (HH) is defined by a sharp increase of serum aminotransferase levels due to liver cell necrosis as result of cardiac, circulatory or respiratory failure. An overview of these diseases is provided in this article.

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Hypoxic hepatitis: underlying conditions and risk factors for mortality in critically ill patients

Abstract: Hypoxic hepatitis is the consequence of multiorgan injury. Outcome is influenced by the severity of liver impairment and the etiology and severity of the basic disease.

Cited by 173 publications

References 35 publications

Impact of hypoxic hepatitis on mortality in the intensive care unit

Impact of hypoxic hepatitis on mortality in the intensive care unit

How to interpret liver function tests in heart failure patients?

Hepatokardiale Wechselwirkungen

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