liver failure (as in acute liver disease) and HCC. Clinical and laboratory findings are the main criteria used to gauge prognosis and disease progression. It some centers, portal venous wedge pressures are measured to assess the degree of vascular obstruction. Liver biopsy findings correlate with the presence and severity of portal hypertension. For example, specimens with thin fibrous septa and large islands of regenerated parenchyma are unlikely to be associated with portal hypertension, whereas broad bands of fibrosis and loss of parenchyma portend the development of portal hypertension and end-stage liver disease.
Some individuals after years of stable, well-compensated, chronic disease suddenly develop signs of acute liver failure. In such patients, there is often established cirrhosis with extensive vascular shunting, or large volumes of functioning liver parenchyma with a borderline vascular supply, both of which leave the liver vulnerable to  superimposed, potentially lethal insults. The short-term mortality of patients with this form of liver failure is around 50%.
Hepatic insults that cause sudden decompensation of patients with chronic liver disease include: hepatitis D superinfection in those with chronic hepatitis B; emergence of resistance to medical therapy in those with viral hepatitis; development of ascending bacterial cholangitis in patients with primary sclerosing cholangitis; or replacement of liver parenchyma by primary or metastatic carcinoma. In other instances the cause may be a systemic disorder, such as sepsis, acute cardiac failure or a superimposed toxic injury that tips a well-compensated cirrhotic patient into liver failure.
Liver failure may follow acute injury or chronic injury, or itmay occur as an acute insult superimposed on otherwise well-compensated chronic liver disease.
The mnemonic for causes of acute liver failure are as follows:
A: acetaminophen, hepatitis A, autoimmune hepatitis
B: hepatitis B
F: fatty change of the microvesicular type (fatty liver ofpregnancy, valproate, tetracycline, Reye syndrome)
Potentially fatal sequelae of liver failure include coagulopathy, encephalopathy, portal hypertension and ascites, hepatorenalsyndrome, and portopulmonary hypertension.
D: drugs/toxins, hepatitis D
E: hepatitis E, esoteric causes (Wilson disease, Budd-Chiarisyndrome)
The terminology for acute and chronic viral hepatitis can be confusing, because the same word, hepatitis, can be used to describe several different entities; careful attention to context can clarify its meaning in any situation. Firstly, hepatitis is the name applied to viruses (hepatitis A, B, C, D, and E virus) that are hepatotropic, that is, have a specific affinity for the liver. Secondly, hepatitis is applied to patterns of acute and chronic hepatic injuries that are produced not only by hepatotropic viruses, but also by damage produced by other viruses such as EBV, CMV , and yellow fever as well as autoimmune reactions, drugs, and toxins. In this section, we will focus on the main features of hepatotropic viruses, which are summarized in
Table 16.2 , and we will then discuss the clinicopathologic characteristics of acute and chronic viral hepatitis.