Enormous Breadth Of Liver Pathology:
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Introduction:
There are very few actual specialists in the subject because of the vastness of liver pathology, which would require a lifetime of study and practise to even begin to master. As a result, the goal of this chapter is not to make the reader into one of those specialists, but rather to provide a useful overview of some of the most prevalent and significant entities found in the field of paediatric liver pathology. The two main categories of liver pathology are neoplastic liver and nonneoplastic, or medical, liver. The majority of samples examined under a pathologist's microscope are neoplastic, but it goes without saying that liver tumours and a timely identification of one can significantly alter a child's and their family's quality of life. Last but not least, the practise of liver pathology is one of the branches of pathology that significantly relies on the opinions of the multidisciplinary group, which includes hepatologists, radiologists, surgeons, and oncologists among many others.
The diagnostic issue is cirrhosis:
Usually, but not always, it is simple to make the histologic diagnosis of cirrhosis and hepatitis. Because the liver reacts to a large range of damage in only a limited number of ways, it can often be challenging to identify the aetiology of an inflammatory or fibrotic process in the liver. However, specific damage patterns and other microscopic characteristics, when used in the right clinical environment, can aid in differentiating distinct causes of such processes.
Difficult to diagnose Cirrhosis:
Lack of normal architecture, or loss of typical central-portal interactions, should be the initial criterion for cirrhosis diagnosis. In order to make this observation, the specimen needs to be large enough to have a number of undamaged portal and core portions. Particularly if regenerative cell plates (also known as "twin plates," which are two cells thick) are present or if the fragments have rounded edges, suggestive of nodularity, a specimen that is fragmented into small pieces of hepatic parenchyma with scant connective tissue, no normal portal tracts, and possibly an irregular pattern of central veins may suggest a cirrhotic process.
The connective tissue component that connects the cirrhotic nodules stays in situ even if the nodules themselves can be easily removed from the liver during a biopsy of a cirrhotic liver using a cutting core needle. There may still be some connective tissue around the borders of the excised spherical fragments; this connective tissue is easier to see on trichrome or reticulin stains. Reticulin improves areas of regeneration by more clearly showing the existence of multiple cell plates. The atypical enlargement of nuclei with little to no corresponding increase in the nuclear: cytoplasmic ratio, also known as "large cell change" (or previously as "large cell dysplasia"), is very common in cirrhotic livers. However, this cytologic aberration should only be used as an adjunct to the diagnostic clues of regeneration and architectural abnormalities for identifying cirrhosis.
Highly thin bands of collagen partially or completely partition hepatocytic nodules in the extremely unusual condition of incomplete septal cirrhosis. There are a few atypical cell plates or regions that resemble nodular regenerative hyperplasia foci (see section below on partial nodular transformation). The main problem with this type of macronodular cirrhosis is portal hypertension; otherwise, liver function is usually not compromised. Needle biopsies make it very difficult to distinguish connective tissue, thus if areas of regeneration or rounded fragments are not noticed by the pathologist, cirrhosis may go undetected.
Because the subcapsular connective tissue can be more pronounced and extend into the portal triads within 1 cm of the capsule, wedge biopsies can present unique diagnostic challenges. This is especially true for specimens taken from the acute anterior border of the liver. Additionally, rather than being scar tissue, a piece or zone of fibrous tissue may be a normal portal tract if it comprises a sizable artery and sizable duct. A final possibility in the differential diagnosis of cirrhosis is nodular regenerative hyperplasia if regeneration without fibrosis is evident in a clinical situation of portal hypertension (as discussed below with partial nodular transformation).
Conclusion:
However, for all biopsies, depending on the level of suspicion, a diagnosis of "probable cirrhosis," "possible cirrhosis," or "cannot exclude cirrhosis" should be made if the tissue is scant or if the degree of fibrosis is difficult to assess (i.e., if diffuse disease with portal-portal, central-portal, or central-central bridging fibrosis is not definitely present). The phrase "early cirrhosis" should generally only be used to describe focal bridging fibrosis when the duration of a cirrhotic condition or advancement of fibrosis has been clinically or histologically verified. The term end-stage cirrhosis is more appropriate than severe cirrhosis to characterise an extensive fibrosis with little residual parenchyma. (For a glossary of additional terms, see "Chronic Hepatitis and Cirrhosis").
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