Cirrhosis is always fatal
Cirrhosis of the liver
Cirrhosis of the liver(Shrink liver): Progressive destruction of the liver over the years, associated with nodular and scarred changes and shrinkage of the liver. Liver cirrhosis is feared as the end stage of almost all liver diseases. 50% of the cases are due to chronic alcohol abuse, a third to hepatitis infections and the rest to less common causes, e.g. B. primary biliary cholangitis. 70% of the sick are men, 30% women.
If the destruction cannot be stopped, the disease leads to death from liver failure within months to a few years. There is hope for a liver transplant for a minority of those affected. For most of the sick - especially alcohol addicts - this is not possible because of their concomitant diseases.
- Fatigue, weight loss, decreased performance
- Skin abnormalities such as vascular stars, reddened palms, lacquer tongue
- Dilated veins under the skin of the abdomen as a result of bypass circulation in portal hypertension
- Loss of libido, breast formation in men, menstrual irregularities in women as a result of hormonal disorders
- Pronounced jaundice with yellowing of the conjunctiva and skin, itching all over the body
- Dementia-like symptoms such as memory loss, disorientation, mood swings, and inappropriate behavior due to brain damage.
The signs of a severe liver disease such as cirrhosis of the liver are: yellow eyes, torn corners of the mouth (rhagades), scratches on the skin (due to itching), red palms (palmar erythema), growth of mammary gland tissue (gynecomastia), star-shaped new blood vessels (spider naevi), abdominal dropsy (Ascites), varicose veins around the navel (caput medusae), edema in the legs, reddened and smooth tongue (lacquer tongue), loss of pubic hair and shrinkage of the testicles.
Georg Thieme Verlag, Stuttgart
When to the doctor
In the next few days at
- You experience one or more of the above symptoms
Disease emergence and causes
Alcohol, hepatitis and some less common pre-existing conditions lead to the death of liver cells. If the liver is permanently exposed to harmful influences, it cannot replace the dying tissue with functional liver cells, so that it scars and instead thick connective tissue forms.
Hereditary metabolic diseases such as Wilson's disease and hemochromatosis are also among the pre-existing conditions that lead to cirrhosis of the liver. In Wilson's disease, the copper metabolism is disturbed, combined with increased copper storage in the liver; In hemochromatosis, the iron metabolism is disturbed, combined with increased iron deposition in the liver.
Another important cause of the development of liver cirrhosis are autoimmune liver diseases, in which inflammatory processes against the body's own tissue attack the liver and biliary tract. These include primary biliary cholangitis, primary sclerosing cholangitis and autoimmune hepatitis.
Once the liver tissue has been transformed into nodular connective tissue, this leads to a multitude of problems:
Healthy liver cells produce many vital proteins. If liver cells are lost in favor of simple connective tissue, these proteins are missing. These include, for example, coagulation factors, i.e. proteins that are responsible for blood clotting. If too few coagulation factors are formed, there is an increased tendency to bleeding and thus an increased risk of bleeding.
The transport proteins for the blood, especially the albumin, are also no longer sufficiently formed. As a result of this lack of albumin in the blood, the so-called colloid osmotic pressure drops. As a result, the water can no longer be held in the vessels, it escapes into the surrounding tissue. Depending on where it flows, edema, a pleural effusion or ascites develops.
The connective tissue remodeling of the liver tissue narrows and destroys the biliary tract in the liver. This leads to bile drainage disorders (intrahepatic jaundice) with jaundice, itching and fat digestion disorders.
If the blood vessels in the liver constrict as a result of the remodeling processes, the blood builds up on its way from the liver to the heart. This congestion leads to increased pressure in the portal vein, the central vessel of the liver. Doctors then speak of one Portal hypertension (portal hypertension). This backlog is also noticeable in other blood vessels, e.g. B.
- in the spleen by swelling of the spleen (splenomegaly), which is associated with an increased breakdown of blood cells
- in the esophagus through esophageal varicose veins, which can burst easily and lead to life-threatening bleeding
- in the area of the anus due to hemorrhoids.
Complications arise when the damaged liver no longer performs its detoxification function. Syndromes like thatHepatic encephalopathy or the hepatic coma can be explained by the fact that too much ammonia accumulates in the blood. The metabolic toxin ammonia directly affects the functioning of the brain, so that the patients show various neurological and psychological abnormalities. At the beginning there are mostly "only" concentration disorders and mood swings. People with hepatic encephalopathy also have less ability to react due to the reduced concentration and alertness. As a result, they make driving mistakes more often than healthy people. Many traffic accidents can be traced back to liver disease, but there are no exact numbers.
In the worst case, there is a risk of impaired consciousness or even loss of consciousness. Doctors call this a fatal hepatic coma.
Hepatorenal syndrome. The damage associated with cirrhosis of the liver also results in kidney failure in the end-stage. Signs of this are water retention (edema) and decreased urine output. A combined liver and kidney failure is usually no longer treatable.
Based on the clear symptoms and the findings of the physical examination, the doctor usually quickly suspects cirrhosis of the liver. Examination methods such as laboratory, ultrasound and, if necessary, a laparoscopy can confirm the diagnosis and assess the extent of liver damage and existing complications. Typical examinations and findings are
- Transaminases and GLDH increased due to liver cell damage
- Gamma-GT, alkaline phosphatase, bilirubin increased due to impaired bile drainage
- Albumin and total protein as well as cholinesterase decreased due to the disturbed protein synthesis
- Ammonia increases due to the impaired detoxification function
- Blood count: anemia due to a lack of vitamins or blood loss in the case of a coagulation disorder
- Blood values to search for the cause of cirrhosis: hepatitis viruses (hepatitis), autoantibodies (primary biliary cholangitis), iron (hemochromatosis), copper (Wilson's disease)
- Ultrasound: nodular remodeling of the liver tissue, changes in the vessels and biliary tract, signs of portal hypertension
- Possibly liver biopsy if the cause is unclear
- Reflection of the stomach and esophagus: look for varicose veins (varices).
Above: Healthy liver in laparoscopy (laparoscopy). The liver surface is smooth and well supplied with blood. Bottom: Cirrhotically altered liver in a patient with moderate cirrhosis of the liver. The nodular remodeling of the liver is easy to see; Deposits of connective tissue lead to a lightening of the liver surface.
Georg Thieme Verlag, Stuttgart
In addition to basic nutritional measures (compensating for vitamin or mineral deficiencies and adequate calorie intake), the therapy of cirrhosis of the liver focuses on averting further damage. This includes:
- The flushing out of the water in the abdominal cavity (ascites) by means of water tablets (diuretics)
- The obliteration of varicose veins in the esophagus and stomach in order to prevent any unstoppable bleeding
- Alcohol is strictly forbidden for the patient in order not to put even more strain on the liver.
Treatment can at least reduce the effects of portal hypertension. One option is to make a short-circuit connection between the portal vein and the vena cava, one portosystemic shunt. It guides the blood past the damaged liver so that pressure is relieved. However, this procedure is associated with an increased risk of hepatic encephalopathy, as the blood is no longer adequately detoxified in the liver. The procedure is not without risk; the risk of death is 5–10%, in emergency operations even 50%.
The hope for many patients is Liver transplant Unfortunately, many patients come because of exclusion criteria, e. B. Alcohol addiction, not on the waiting lists. Even if this hurdle has been overcome, the waiting times are relatively long. If a transplant occurs, the doctors either transfer an entire organ (corpse donation) or only part of the liver (split liver transplantation, corpse donation and living donation possible). The 5-year survival rate is then 80%.
In the treatment of hepatic encephalopathy, hepatic coma and hepatorenal syndrome, a cure or causal treatment is not possible. In this case, doctors concentrate on ensuring that the circulatory system is functioning properly.
The prognosis depends on the extent of the cirrhosis and whether there are complications. Doctors often classify cirrhosis of the liver into 3 classes based on 5 factors (albumin level, coagulation, bilirubin, encephalopathy and ascites; Child-Pugh score).
The 1-year survival rate for cirrhosis of the Child A type is almost 100%, for the Child B type 85% and for the Child C type 35%.
Child-Pugh classification   points 1 2 3 Serum albumin concentration in g / dL> 3.5 2.8–3.5 <2.8 Serum bilirubin concentration in mg / dL <2.0 2, 0–3.0> 3.0 Coagulation (Quick value in%)> 70 40–70 <40 Ascites (ascites, sonographic) not moderate Hepatic encephalopathy none Grade I – II> Grade II Child A: 5–6 points ; Child B: 7-9 points; Child C: 10–15 points Your pharmacist recommends
Extracts from milk thistle have a supportive effect in the therapy of liver cirrhosis and other liver damage. The active ingredient complex silymarin stabilizes the liver cell membrane, stimulates the build-up of protein in the liver cells and thereby promotes the regeneration of the liver cells. Silymarin is available as a capsule, tablet, or tincture. It is best to discuss with your doctor whether a therapy with milk thistle extracts is an option for you.
AuthorsDr. med. Arne Schäffler, Dr. Bernadette Andre-Wallis in: Health Today, edited by Dr. med. Arne Schäffler. Trias, Stuttgart, 3rd edition (2014). Revision and update: Dr. med. Sonja Kempinski | last changed on at 10:06
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