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bridging necrosis
Tuesday 27 January 2004
Definition: Bridging necrosis is the term given to confluent necrosis linking terminal venules to portal tracts. The term "Bridging necrosis" has been used for necrosis linking any of the vascular structures, but it is now more often restricted to the linking of terminal hepatic venules (centrilobular veins) to portal tracts (central-portal bridging necrosis).
Bridging necrosis describes the location rather than the type of necrosis. It usually results from extensive necrosis of confluent necrosis type of hepatocytic necrosis. A possible explanation for this location is that it represents the entire zone 3 of an acinus, a view supported by the curved shape of many bridges.
Bridging necrosis is a manifestation of severe acute hepatitis but its distribution even within a single biopsy may be irregular.
Necrosis and inflammation linking adjacent portal tracts without involvement of terminal venules should not strictly be called bridging because it almost certainly has different pathogenetic significance; it results from widening of portal tracts, with or without periportal necrosis.
Bridges of confluent necrosis with subsequent collapse may be mistaken for the septa of chronic hepatitis and chronic liver disease.
In making the important distinction between them, the pathologist is often helped by stains for elastic tissue. Unlike stains for collagens, these normally give negative results in the parenchyma, but elastic tissue accumulates as septa age. Recent collapse is therefore negative, whereas old septa are positive.
Substantial amounts of elastic tissue take months or years to accumulate, but small amounts can be detected by sensitive methods such as Victoria blue as early as 1 or 2 months after onset of hepatitis.
Physiopathology
A possible explanation for this type of bridging is that it represents necrosis of acinar zones 3, which touch both the veins and the larger portal tracts.
Linking of portal tracts to each other (portal-portal bridging necrosis) is common in conditions in which portal tracts are widened, for example by chronic hepatitis or biliary tract disease; this is partly because the chance of obtaining a longitudinal section of a widened portal tract is greater than for one of normal width.
Linking of perivenular areas to each other (central-central bridging necrosis) by is found in some examples of parenchymal hypoperfusion and venous outflow obstruction.
Bridging of terminal hepatic venules to portal tracts (central-portal bridging necrosis) is a fairly common feature of acute hepatitis of viral type, when the bridges contain few or no elastic fibres. It is also seen in exacerbations of chronic hepatitis. Old bridges contain elastic fibres as well as collagen fibres.
Such bridging fibrosis is an important component both of the more severe examples of chronic viral hepatitis and of steatohepatitis.
Contraction of collagen-rich bridges may produce rapid and severe distortion of the normal hepatic microstructure, with correspondingly rapid progression to cirrhosis.
Types
central-central bridging necrosis
central-portal bridging necrosis
portal-portal bridging necrosis
See also
hepatic necrosis
hepatocytic necrosis
hepatic lesions