Portal field

In the portal tract (= Glisson s triangle, portal field) (E Glisson, 1659), the perivascular connective tissue with its enclosed (and protected) radicles of the portal veins, the hepatic arterioles, bile ducts, lymph vessels and nerve fibres terminates in the connective tissue covering of the... 

Fig. 2.15 Diagram of the liver lobule and the acinus arranged like a clover leaf around the portal field according to the acinar structure (modified from D. Sasse, t986) central hepatic vein (CV) or terminal hepatic vein, periportal field (P). Circulatory and meta-bolically different zones zone t (periportal), zone 2 (intermediate), zone 3 (perivenous)...

It must, however, be considered that a biopsy punch of 1.5-3.0 cm in length is proportionate to approx. 1/ 50000 of the normal liver volume (J. Volmer et al., 1981). For histological assessment, the punch should be > 1.5 cm long and include at least 4 portal fields the weight of such a bioptate generally amounts to 20-30 mg. The smaller the sample, the more difficult is the histological... 

Eosinophilic infiltrations in the portal fields generally point to intrahepatic cholestasis. By contrast, ductular changes with bile cylinders, ballooning, acidophilia of the liver cells at the lobular centres, bile infarcts, increase in the copper content, etc. are usually signs of extrahepatic cholestasis, (s. fig. 13.5) (s. tab. 13.10)... 

Granulomas are generally distributed focally throughout the liver, mostly within the liver lobules and less frequently in the portal fields. As a rule, the normal lobular architecture is not affected. Granulomas located on the surface can be visualized laparoscopically as small, greyish-white foci, which can be conveniently collected by forceps biopsy for histological examination. 

The classical inflammation criteria such as exudation, cellulation and proliferation can only be applied to the liver with some reservations, since the emphasis in this instance is on the sinusoids, which already display maximum permeability under normal conditions. The increase in capillary permeability, required by the definition of infiammation, is really only applicable to the area of the vascularized portal fields, e.g. in purulent cholangitis. The definition of inflammation can only be applied to classic acute viral hepatitis, (s. p. 415)... 

Fibrosis is usually the consequence or concomitant symptom of a chronic hepatobiliary disease, the course of which can itself in turn be unfavourably influenced by the fibrosis. The matrix substances, which are being produced in greater quantities, are increasingly deposited in Disse s space in the portal field and periportal area as well as around the terminal liver vein. 

A fibrotic widening of the portal fields (with differing intensity and often variable regional distribution) is a frequent finding in chronic hepatitis, and it plays an important role in staging, (s. p. 694) However, it may also be a remnant of previous hepatitis. In many cases, strands of connective tissue extend into the periportal parenchyma. Mostly, there is portal/periportal fibrosis with an irregular star-shaped pattern, (s. fig. 21.14)... 

The transformation of the lobular architecture is initiated and maintained by at least two histomorphological processes (i.) piecemeal necrosis and (2.) bridging necrosis, which provides string-like links between the central veins and the portal fields. Portocentral shunts, which are of significance for the fate of cirrhosis, make use of these bridges as routes for their development. During the course of time, these channels, which acquire solid basal membranes like capillaries, carry the portal blood directly to the venous flow-off. As a result, blood is withdrawn from the respective acini these areas become more susceptible to disruption and damage and are forced to restructure anew, (see chapter 35)... 

The classical criteria of inflammation (7.) exudation, (2.) cellulation and (3.) proliferation can only partly be applied to the liver, since this organ is predominantly characterized by sinusoids rather than capillaries. An essential problem thus arises in the morphological context of the term hepatitis . Due to this specific vascular feature, the otherwise valid association between the terms inflammation and infection is only marginally true in the case of the liver. In fact, this association is only given with infectious changes within the vascularized fibrous tissue of the portal fields. The problem concerning the definition of hepatitis has already been outlined in detail in the last chapter, (s. p. 404)... 

The respective lesions in the area of the lobules and portal fields and at the hepatocytes, the mesenchyma and connective tissue differ in intensity from case to case (also depending on the respective stage of the disease) - yet the picture of acute hepatitis predominates. In each case of liver disease which remains unresolved in terms of differential diagnosis, thought must be given to the possibility of acute hepatitis with its wide range of aetiological causes, (s. fig. 22.6)... 

In severe hepatic necrosis with large losses of parenchyma, the regenerating epithelium is not always able to restore the affected area completely. There is a development of fibrous bundles, which are in some places connected with pronounced and partly fringed fibrotic tissue in the portal field. Moreover, extensive cicatricial areas are formed, occasionally embedded in small parenchymal islets, (s. fig. 22.14)... 

In the portal fields, plasmacellular and lymphocytic infiltrates prevail. However, they are also present in the liver parenchyma, arranged linearly inside the sinusoids, which is why this finding can indeed be mistaken for hepatitis mononucleosa. There are no granulocytic components. 

Fig. 25.4 Granuloma close to a portal field. Clinical diagnosis Toxoplasmosis...

From a morphological perspective, any kind of alcohol-induced fatty liver or alcoholic hepatitis has the potential to develop into cirrhosis. The fibrous ramifications of the various portal fields make contact with one another as well as with other centrilobular fibre formations. This ultimately causes pronounced fibrosis of the liver, which leads to a cirrhotic transformation if alcohol consumption continues, (s. fig. 28.7)... 

Occasionally, ductopenia (= vanishing bile duct syndrome) is observed. This condition is given when more than half of the portal fields in a large biopsy specimen fail to feature a bile duct. The irregular distribution of the lesions can make it very difficult to form a diagnosis based on just one biopsy specimen. The safest way is to carry out several biopsies (e. g. with the help of laparoscopy) and to make an assessment based on more than 20 portal areas. (8, 31, 93, 118, 128) (s. tabs. 29.3 29.10)... 

In this context, cell infiltrates consisting of leucocytes and lymphocytes can be found within the acinus and/or in the portal field in contrast, in immunological-allergic impairment mechanisms, it is primarily lymphocytic and eosinophilic-leucocytic infiltrations that become manifest. This cellular reaction is also reversible. 

Fig. 31.13 Cholesterol ester storage disease. Fine-droplet fatty changes in the hepatocytes. Widely extensive small and larger lipid vacuoles in the liver cells and foam cells of the portal field (Sudan black) (s. fig. 21.5). Same patient as in fig. 31.14...

The inflammatory mesenchymal reactions in the portal field and lobular periphery induce extremely low-cell perilobular and tylotic fibrosis. (425, 442) Slowly, starshaped portal fibrosis, so-called holly-leaf fibrosis, develops. This morphological picture, similar to that of chronic hepatitis, was termed chronic siderophile hepatitis by H. Kalk (1962). The hepatic lobules are gradually... 

Acute cholangitis Thickened bile-duct walls with inflammatory infiltration as well as focal ulcerations are found histologically. The portal fields are expanded by oedema and reveal pericholangiolar and intracholangiolar infiltrations from leucocytes. Ductal tortuosity reflects increased pressure in the biliary ducts. Periductular abscesses can develop during the course of cholangitis, (s. fig. 32.2)... 

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