Cirrhosis is a quite common condition worldwide. It is related to severe damage of liver tissue and usually also to the impairment of liver functions. Cirrhosis itself is a mark of liver regeneration processes that unfortunately result in formation of chaotically organized tissue. Cirrhotic liver is not fully capable of processing nutrients, removing waste products and detoxification of external pollutants. Blood flow through cirrhotic liver is more difficult.
Cirrhosis is usually an outcome of liver inflammation processes. These include chronic infectious hepatitis B and hepatitis C, non-alcoholic steatohepatitis (NASH) and chronic liver effects of alcohol in alcoholics. Cirrhosis usually occurs in daily drinkers and it is quite difficult to estimate the dose needed for its development, but it is generally assumed that women are more sensitive to alcohol than men.
Cirrhosis also accompanies some metabolic disorders that cause abnormal deposition of certain substances in the liver tissue. The se include Wilson's disease (copper) and hemochromatosis (iron). Autoimmune diseases of liver and biliary tract usually lead to chronic liver damage followed by cirrhosis. We can mention for example autoimmune hepatitis, primary biliary cirrhosis and primary sclerosing cholangitis. More frequent liver cirrhosis was observed in people with congenital deficiency of alpha-1-antitrypsin.
Rarely, the cirrhosis may be related to long-term changes after acute liver injury by certain toxins such as mushroom toxins (“death cap” poisoning) or toxic substances used in industry.
There are many symptoms of cirrhosis and its decompensation. Cirrhosis significantly shortens life and its signs are mostly derived from impaired liver functions, liver failure and impaired blood flow through cirrhotic liver.
The yellowish discoloration of skin and mucous membranes is caused by elevated concentration of substance known as bilirubin. It is a product of decomposed hemoglobin that is further metabolized in liver and excreted into bile. Cirrhotic liver is sometimes unable to properly eliminate the bilirubin causing jaundice.
This is a classic complication of advanced cirrhosis that can be defined as increased pressure in the portal vein. Portal vein takes venous blood from stomach and intestines and leads it towards the liver tissue. This is an effective way to immediately process nutrients from digested food and detoxify ingested harmful substances. Within the liver tissue, the portal vein branches into smaller vessels that later converge into hepatic veins leaving the liver and leading to inferior vena cava. There are also other connections between portal vein and inferior vena cava than the above mentioned liver vessels such as veins running in esophageal wall but these are not important in a healthy person. In cirrhotic patients the blood may have problems to flow through the liver tissue and accumulates in the portal vein causing portal hypertension.
This condition is a dangerous complication of portal hypertension. Blood from portal vein attempts to bypass the cirrhotic liver tissue, flows to venous connections in the esophagus and through them towards the vena cava. Esophageal veins are not built for a large blood flow, they expand and there is a risk of their sudden perforation. In such case, the affected person begins to vomit blood and can quickly exsanguinate. Small varices are monitored; their therapy consists of cirrhosis management and administration of beta-blockers. Larger varices or acutely bleeding varices are treated by ligation performed during upper GI endoscopy. Other therapeutic option of endoscopically unsolvable varices is the so-called TIPS. The TIPS is an abbreviation for transjugular intrahepatic portosystemic shunt and it means the creation of an artificial connection between liver veins and portal vein leading through liver tissue. This leads to sharp decrease of portal blood pressure but on the other hand the blood flowing through the TIPS is not purified by the liver tissue and toxic substances can easily damage the brain, thus accelerating the liver encephalopathy.
Ascites means the accumulation of fluid in the abdominal cavity. In cirrhotic patients it occurs because of portal hypertension followed by fluid leakage into the abdominal cavity. Large forms of ascites can be quite unpleasant for the patient as the fluid can oppress the chest and lungs in horizontal position and cause shortness of breath. Ascitic fluid may also get infected by bacteria. The best therapeutic options are diuretic drugs. Ascites may be also let out by a puncture of abdominal cavity by a thick needle that drains the fluid. Ascites resisting this therapy may be solved by TIPS insertion.
Brain damage (liver encephalopathy)
This is a common complication of cirrhosis resulting from inadequate detoxification of metabolic waste products. These get to brain and damage its function. The symptoms may be various such as change the circadian rhythm (waking at night, sleeping during the day), confusion, aggression, behavioral changes and eventually loss of consciousness. The therapy of liver encephalopathy consists mainly of reducing the amount of pollutants absorbed in the intestine, especially ammonia produced by intestinal microflora. We use drugs to encourage bowel activity to prevent constipation, reduce the protein intake and administrate antibiotics to suppress the intestinal microflora.
Renal failure is a severe complication of cirrhosis. It is caused by impaired blood flow through the kidneys. The condition is referred to as the hepatorenal syndrome. It is related to the effort of the organism to keep the blood flow through the portal vein by restricting blood supply to the kidneys.
This dangerous malignant tumor often arises in cirrhotic tissue. Patients with known cirrhosis should be regularly checked by ultrasound and any tumor should be surgically solved. If that is not possible, the prognosis is very serious.
Cirrhotic liver may inadequately produce clotting factors dependent on vitamin K disrupting blood coagulation and increasing the risk of bleeding. Vitamin K can be supplemented in oral or injection form.
Decompensated cirrhosis is often accompanied by impaired production and excretion of bile. Lack of bile pigments in the intestine causes discoloration of stool from brown to pale color.
Cirrhosis has many dangerous complications. As you have surely noticed, their treatment does not solve the cirrhosis itself. Cirrhosis is incurable by any medication or conventional therapy. The only ultimate solution is the liver transplantation. This option, however, means a quite risky surgical intervention with many possible complications.