Liver Сirrhosis: Etiology, Clinical Manifestations, Diagnosis and Treatment

Liver cirrhosis is a generalized liver lesion characterized by the presence of parenchyma necrosis, diffuse fibrosis, the appearance of abnormal zones of liver tissue regeneration, resulting in disruption of the external and internal structure of the liver, as well as impairment of its function.

Classification of cirrhosis

By classification, cirrhosis of the liver can be divided according to the presence of structural changes, as well as stages of compensation.

By the presence of structural changes:

• Small nodal (diameter of nodes from 3 mm to 1 cm);
• Large nodal (node diameter greater than 1 cm);
• Mixed;
• Biliary.

3D Models of forms of liver cirrhosis according to the presence of structural changes:

Small-nodal cirrhosis of the liver.

Large-nodal cirrhosis.

Mixed cirrhosis

Biliary cirrhosis of the liver

By stages of compensation:

• Compensated;
• Subcompensated;
• Decompensated;
• Terminal.

There are clinical classifications that take into account clinical and laboratory manifestations (Child-Pugh).

Child-Pugh classification of liver cirrhosis

Results:

5-6 points – compensated cirrhosis (class A);

7-9 points – subcompensated (class B);

10-12 points – decompensated / terminal cirrhosis (class C).

Etiology of liver cirrhosis

According to the report of the European Association for the Study of the Liver, approximately 40% of liver transplants in Europe are performed for liver cirrhosis of viral etiology (viral hepatitis B, C, D), 33% – alcoholic, and 5% – due to a combination of these etiological factors.

Also the presence of autoimmune diseases or toxic effect of some drugs and systemic poisons affecting hepatic tissue contributes to the development of biliary cirrhosis associated with impaired outflow of bile through the intrahepatic and extrahepatic duct system.

Pathogenesis

The development of liver cirrhosis is based on direct damage to the hepatic lobule (structural and functional unit) by one of the etiologic factors.

The process of damage is long and can take a period of time from several months to several years. As a result of the lesion, areas of necrosis of hepatic parenchyma are formed. Around the areas of necrosis there are zones (nodules) of regeneration and chronic inflammation with the outcome in fibrosis.

In turn, regeneration nodules compress biliary tracts, which leads to congestion in the venous system of the liver with the formation of portal hypertension.

Clinical manifestations of liver cirrhosis

In the early stages of the disease, the disease may be asymptomatic.

With the progression of the disease, the following syndromes are distinguished:

1. A general syndrome characterized by weakness, headache, nausea, increased body temperature, arthralgia, a feeling of bitterness in the mouth, asthenia, and occasional abdominal pain;
2. Jaundice syndrome resulting from intrahepatic cholestasis (impaired bile outflow, increased blood concentration of direct bilirubin, increased concentration of bile acids). Increased concentration of bile acids in the blood is accompanied by pruritus;
3. Hepatomegaly and splenomegaly;
4. Portal hypertension syndrome occurs at the stage of decompensation. It is characterized by increased pressure in the portal vein system. Clinical manifestations of portal hypertension syndrome are: ascites, varicose veins of the esophagus, rectal veins, veins of the anterior abdominal wall. Often against the background of varicose veins bleeding occurs.

5. Pain syndrome arising against the background of biliary dyskinesia;
6. Liver encephalopathy, which occurs due to prolonged high concentrations of direct bilirubin. The latter, penetrating the blood-brain barrier, damages brain cells;
7. Violation of the synthetic and protective function of the liver.

It should be understood that the disease has stages and clinical manifestations will change with the progression of the disease. Thus, at the decompensation and terminal stages, not only the hepatobiliary system, but also other body systems (urinary, digestive, nervous, cardiovascular, etc.) are involved in the pathological process.

Diagnosis of liver cirrhosis

Diagnosis of the disease is based on the presence of clinical manifestations, etiologic factor, as well as instrumental and laboratory methods of investigation.

Instrumental methods of research

1. Ultrasound (fibroelastometry), Doppler ultrasound to assess blood flow in the portal vein system;
2. Computed tomography (CT) and magnetic resonance imaging (MRI);
3. Liver biopsy;
4. FGDS (fibrogastroduodenoscopy);
5. A review radiograph of the abdominal cavity.

Laboratory methods of research

1. Determination of antibodies to hepatitis B,C,D,E viruses;
2. Determination of alpha-fetoprotein in serum;
3. BAC (liver profile);
4. OAC;
5. Coagulogram;
6. OAM;
7. Determination of electrolyte composition.

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Treatment of liver cirrhosis

Treatment of cirrhosis of the liver should be comprehensive and include the following measures:

1. Withdrawal from alcoholic beverages;
2. Diet (liver table), correction of electrolyte composition (sodium, potassium, chlorine), correction of protein imbalance;
3. Limiting medications that have hepatotoxicity.

Medical treatment

1. Infusion therapy (in the presence of symptoms of intoxication);
2. The use of ursodeoxycholic acid preparations;
3. S-adenosyl-L-methionine preparations;
4. Glucocorticosteroids;
5. Prevention of hemorrhagic complications;
6. Taking diuretics;
7. Treatment aimed at eliminating viruses tropic to hepatic tissue;
8. Treatment of associated pathology.

Surgical treatments include laparocentesis and liver transplantation.

Indications for liver transplantation are:

• Presence of an irreversible pathologic process with a life prognosis of less than 12 months;
• Lack of effect from conservative therapy;
• Progressive cirrhosis with a life expectancy shorter than that of transplantation.