Cirrhosis

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Cirrhosis is among the top ten causes of death in the Western world. Although it is the result of alchol abuse, other major contributors include chronic hepatitis, biliary disease, and iron overload. This end stage of chronic liver disease is defined by three characteristics:

Bridging fibrous septa in the form of delicate bands or broad scars replacing multiple adjacent lobules

Parenchymal nodules created by regeneration of encircled hepatocytes, varying from small(<3 mm in diameter micronodules) to large (several centimeters in diameter, macronodules)

Disruption of the architecture of the entire liver

Several features should be underscored.

The parenchymal injury and consequent fibrosis are diffuse, extending throughout the liver; focal injury with scarring does not constitute cirrhosis.

Nodularity is requisite for the diagnosis and reflects the balance between regenerative activity and constrictive scarring.

The fibrosis, once developed is generally irreversible, although regression is observed in rare instances of sehistosomiasis and hemochromatosis,

Vascular architecture is recognized by the parenchymal damage and scarring. With the formation of abnormal interconnections between vascular inflow and hepatic vein outflow channels.

There is no satisfactory classification of cirrhosis save for specification of the presumed underlying cause.The terms micronodular and macronodular should not be used as a primary classification, although the size of the nodules may provide clues to etiology. Many forms of cirrhosis (particularly alcholic)are initially micronodular, but there is a tendency for nodules to increase in size with time, counterbalanced by the constraints imposed by fibrous scaring.

The etiology of cirrhosis varies both geographically and socially. The following is the spproximate frequency of etiologic categories in the Western world:

Alcholic liver disease 60-70%
Viral hepatitis 10%
Biliary disease 5-10%
Primary hemochromatosis 5%
Wilson disease – rare
Ü- Antitrypsin deficiency - rare
Cryptogenic cirrhosis 10-15%

Infrequent types of cirrhosis include (1) the cirrhosis developing infants and children with galactosemia and tyrosinosis (2) liver destruction by a diffusely infiltrative cancer; (3) drug-induced cirrhosis and (4) syphilis. Severe sclerosis can occur in the setting of cardiac disease. After all the categories of cirrhosis of known causation have been excluded, a substantial number of cases remain. The magnitude of this “wastebasket” category referred to as cryptogenic cirrhosis, speaks eloquently to the difficulties in discerning the many origins of cirrhosis. Once cirrhosis is established, it is usually difficult to clearly distinguish an etiologic diagnosis on morphologic grounds alone.

The central pathogenetic process in cirrhosis is progressive fibrosis. In the normal liver, interstitial collagens (types I and III) are concentrated in portal tracts and around central veins, with occasional bundles in the space of Disse. The collagen (reticulin) coursing alongside hepatocytes is composed of delicate strands of type IV collagen in the space of Disse. In cirrhosis types I and III collagen are deposited in the lobule, creating delicate or broad septal tracts. New vascular channels in the septa connect the vascular structures in the portal region (hepatic arteries and portal veins) and terminal hepatic veins, shunting blood around the parenchyma. Continued deposition of collagen in the space of Disse within preserved parenchyma is accompanied by the loss of fenestrations in the sinusoidal endothelial cells. In the process, the sinusoidal space comes to resemble a capillary rather than a channel for exchange of solutes between hepatocytes and plasma. In particular, hepatocellular secretion of proteins (e.g., albumin, clotting factors, lipoproteins) is greatly impaired.

The major source of excess collagen in cirrhosis appears to be perisinusoidal hepatic stellate cells (Ito cells), which lie in the space of Disse. Although normally functioning as vitamin A fat-storing cells, they become activated during the development of cirrhosis, lose their retinyl ester stores, and transform into myofibroblast like cells.

Clinical Features

All forms of cirrhosis may be clinically silent. When symptomatic, they lead to nonspecific clinical manifestations; anorexia, weight loss, weakness, osteoporosis, and in advanced disease, frank debilitation. In cipient or overt hapatic failure may develop usually precipitated by superimposition of a metabolic load on the liver as from systemic infection or a gastrointestinal hemorrage. Imbalances of pulmonary blood flow which are poorly understood, may lead to severly impaired oxygenation (hepatopulmonary syndrome) further stressing the patient.

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