Hepatic encephalopathy
Hepatic encephalopathy is a potential complication of cirrhosis. It may lead to functional neurological impairment ranging from mild confusion to coma. Goal of treatment is reducing ammonia. This can can achieved by administering lactulose or lactitol to increase potassium. Hydration and nutritional support is also provided. Protein uptake is encouraged. The underlying cause may also need to be identified and treated. Causes include alcohol use, excess protein, gastrointestinal bleeding, infection, constipation, and vomiting/diarrhea. Drugs like benzodiazepines, diuretics, or narcotics can also precipitate hepatic encephalopathy. A low protein diet is recommended with gastrointestinal bleeding. Rifaximin is administered if mental state does not improve in 48 hours. Antibiotic treatment may need to be continued for at least 3 months. The grading or severity of hepatic encephalopathy is determined by mental status. Hepatorenal syndrome
Hepatorenal syndrome is a serious complication of end-stage cirrhosis when kidney damage is also involved. Spontaneous bacterial peritonitis
People with ascites due to cirrhosis are at risk of spontaneous bacterial peritonitis. Portal hypertensive gastropathy
Portal hypertensive gastropathy refers to changes in the mucosa of the stomach in people with portal hypertension, and is associated with cirrhosis severity. Infection
Cirrhosis can cause immune system dysfunction, leading to infection. Signs and symptoms of infection may be nonspecific and are more difficult to recognize (for example, worsening encephalopathy but no fever). Moreover, infections in cirrhosis are major triggers for other complications (ascites, variceal bleading, hepatic enecphalopathy, organ failures, death). Hepatocellular carcinoma
Hepatocellular carcinoma is the most common primary liver cancer, and the most common cause of death in people with cirrhosis.
Cirrhosis is defined by its features on microscopy: (1) the presence of regenerating nodules of hepatocytes and (2) the presence of fibrosis, or the deposition of connective tissue between these nodules. The pattern of fibrosis seen can depend on the underlying insult that led to cirrhosis. Fibrosis can also proliferate even if the underlying process that caused it has resolved or ceased. The fibrosis in cirrhosis can lead to destruction of other normal tissues in the liver: including the sinusoids, the space of Disse, and other vascular structures, which leads to altered resistance to blood flow in the liver, and portal hypertension. As cirrhosis can be caused by many different entities which injure the liver in different ways, cause-specific abnormalities may be seen. For example, in chronic hepatitis B, there is infiltration of the liver parenchyma with lymphocytes. In congestive hepatopathy there are erythrocytes and a greater amount of fibrosis in the tissue surrounding the hepatic veins. In primary biliary cholangitis, there is fibrosis around the bile duct, the presence of granulomas and pooling of bile. Lastly in alcoholic cirrhosis, there is infiltration of the liver with neutrophils.Macroscopically, the liver is initially enlarged, but with the progression of the disease, it becomes smaller. Its surface is irregular, the consistency is firm, and if associated with steatosis the color is yellow. Depending on the size of the nodules, there are three macroscopic types: micronodular, macronodular, and mixed cirrhosis. In the micronodular form (Laennecs cirrhosis or portal cirrhosis), regenerating nodules are under 3 mm.