A change in the sinusoid‐trabecular structure of the liver with hepatic venous outflow block

Hepatic Venous Outflow Obstruction: Suggestion of a New Classification

“…Blood cells dissecting and compressing the columns of liver cell plates result in atrophy and necrosis of hepatocytes (16). Similar changes were also reported in the experimental HV ligation (17) and in patients with heart failure (18).…”

Histologic changes mimicking biliary disease in liver biopsies with venous outflow impairment

“…Many studies have described the histopathologic findings in hepatic venous outflow impairment. 2,3,[6][7][8][9][10][11] Most patients show evidence of chronic passive congestion, which manifests as sinusoidal dilatation and varying degree of hepatic atrophy and necrosis. The congestion and necrosis are most marked in zone 3 of the acinus, but can involve zones 1 and 2 in more severe cases.…”

“…Extravasation of red blood cells in the space of Disse has also been described. 9 In chronic cases, these changes are accompanied by zone 3 sinusoidal fibrosis, which can progress to bridging fibrosis and cirrhosis. In all these reports, the description of liver pathology emphasizes the changes in liver sinusoids and hepatic parenchyma, and the patterns of fibrosis that are seen with chronic congestion.…”

“…These changes are well described in several articles and details of the changes in sinusoidal blood flow and mechanism of central-central and central-portal fibrosis have been studied. 2,3,[6][7][8][9][10][11] However, histologic features in portal tracts in liver biopsies with venous outflow impairment have not been detailed in any of these publications [1][2][3][4][5][6][7][8][9][10][11] or standard liver textbooks. 12,13 In our experience, abnormal portal tracts are often seen in venous outflow impairment and can mimic the findings of chronic biliary disease.…”

You've gotta have heart!

“…[39][40][41][42] Centrizonal necrosis was the predominant histological lesion of hepatic ischemia in most series of cases in which liver histology was available, [31][32][33][34][35][36][37][38]43 occasionally midzonal necrosis occurs too, 33,44 whereas sinusoidal changes likely reflect concomitant passive congestion. 33,45 The diagnosis maybe inferred when there is an abrupt and significant elevation of aminotransferases, 31,[35][36][37][38][46][47][48][49][50][51] usually without much in the way of alkaline phosphatase induction, and usually followed by normalization within 7-10 days. 52,53 In the context of the theme of the Yin-Yang of the liver-heart relationship, it is ironic to reflect that the serum enzyme activity assay that, as a medical student, Arthur Karmen devised for the diagnosis of acute myocardial infarction, the serum glutamic oxaloacetic transaminase 54,55 (SGOT, now known as serum aspartate aminotransferase, AST), should have been quickly applied to testing the liver 56 and adopted by hepatologists 57 and then abandoned by the cardiologists.…”