Symptoms of liver cirrhosis: from initial to final stage

Cirrhosis of the liver is more common in men. Symptoms of cirrhosis of the liver are varied.

According to research data, 60% of patients have pronounced symptoms, in 20% of patients, liver cirrhosis is latent and is detected by chance during examination for some other disease, in 20% of patients, the diagnosis of liver cirrhosis is established only after death.

The main symptoms of liver cirrhosis are:

• pain in the right side and right hypochondrium and epigastric region, increasing after meals (especially after eating spicy, fatty foods), physical activity. The pain is caused by an enlarged liver and stretching of its capsule, concomitant chronic gastritis, chronic pancreatitis, cholecystitis, and biliary dyskinesia. With hyperkinetic dyskinesia of the biliary tract, pain in the right hypochondrium is colic-like, while with hypokinetic dyskinesia, it is usually not intense, nagging, and is often accompanied by a feeling of heaviness in the right hypochondrium;
• nausea, sometimes vomiting (bloody vomiting is possible with bleeding from varicose veins of the esophagus and stomach);
• a feeling of bitterness and dryness in the mouth;
• itching of the skin (with cholestasis and accumulation of a large amount of bile acids in the blood);
• fatigue, irritability;
• frequent loose stools (especially after eating fatty foods);
• bloating;
• weight loss;
• sexual weakness (in men), menstrual irregularities (in women).

Examination of patients reveals the following characteristic symptoms of liver cirrhosis:

• weight loss, in severe cases even exhaustion;
• pronounced muscle atrophy and a significant decrease in muscle tone and strength;
• delays in growth, physical and sexual development (if liver cirrhosis develops in childhood);
• dry, flaky, yellowish-pale skin. Severe jaundice is observed in the final stage of liver cirrhosis, with biliary cirrhosis, and also with the addition of acute hepatitis. Jaundice first appears on the sclera, the underside of the tongue, the palate, then on the face, palms, soles, and finally the entire skin is colored. Jaundice has different shades depending on the duration of its existence. At first, the skin is orange-yellow, then it acquires a greenish-yellow color, very long-term jaundice causes the skin to become brownish-bronze (for example, with primary biliary cirrhosis of the liver). Jaundice is caused by a violation of the ability of hepatocytes to metabolize bilirubin. In rare cases, with severe necrosis of the liver parenchyma, jaundice may be absent;
• xanthelasma (yellow lipid spots in the area of the upper eyelids) are more often detected in primary biliary cirrhosis of the liver;
• clubbed fingers with hyperemia of the skin at the nail beds;
• swelling of the joints and adjacent bones (mainly in biliary cirrhosis of the liver - "biliary rheumatism");
• dilation of the veins of the abdominal wall due to obstruction of blood flow in the liver due to the development of severe fibrosis in it. The dilated veins of the anterior abdominal wall are collaterals, bypass routes for blood outflow. In severe cases, this collateral venous network resembles the head of a jellyfish ("caput medusae"). Sometimes (with the development of collaterals through the umbilical veins) venous noise occurs on the anterior abdominal wall. Noise in the navel area is especially pronounced in cirrhosis of the liver in combination with non-closure of the umbilical vein (Cruveilhier-Baumgarten syndrome);

It is extremely important to detect minor signs of liver cirrhosis during examination:

• the appearance of "spider veins" on the skin of the upper half of the body - spider-like telangiectasias. It is characteristic that "spider veins" are never located below the navel, they are most pronounced during exacerbation of cirrhosis, and their reverse development is possible during the period of remission;
• angiomas at the edge of the nose, in the corner of the eyes (they can bleed);
• erythema of the palms - bright red lingonberry coloration of warm palms, diffused either in the thenar or hypothenar area, as well as in the area of the fingertips ("liver palms", "beer lovers' hands") (Weber); less often, such erythema occurs on the feet;
• varnished, swollen, uncoated tongue of cranberry-red color;
• carmine-red coloration of the mucous membrane of the oral cavity and lips;
• gynecomastia in men;
• atrophy of the genitals;
• reduction in the severity of secondary sexual characteristics (reduction in the severity of hair growth in the armpits and pubic area).

The appearance of “minor signs” of cirrhosis is explained by most authors by hyperestrogenemia (the cirrhotically altered liver poorly participates in the metabolism of estrogens); in addition, the increase in the peripheral conversion of androgens into estrogens is important;

• In severe cases of liver cirrhosis, the appearance of ascites is characteristic.

All of the above symptoms determine the extremely characteristic appearance of patients with liver cirrhosis:

• emaciated face, unhealthy subicteric skin color, bright lips, prominent cheekbones, erythema of the cheekbone area, dilation of the capillaries of the facial skin; muscle atrophy (thin limbs);
• enlarged abdomen (due to ascites);
• dilation of the veins of the abdominal and chest walls, swelling of the lower extremities;
• Many patients exhibit hemorrhagic diathesis caused by liver damage with impaired production of blood clotting factors.

Hemorrhagic rashes of various types can be seen on the skin; nosebleeds are common, as well as bleeding in other locations (this is also facilitated by the development of portal hypertension).

When examining the internal organs, pronounced functional and dystrophic changes are detected. Myocardial dystrophy is manifested by palpitations, expansion of the heart border to the left, muffled tones, shortness of breath, on the ECG - a decrease in the ST interval, a change in the T wave (decrease, biphasic, in severe cases - inversion). Hyperkinetic type of hemodynamics is often detected (increase in minute blood volume, pulse pressure, rapid, full pulse ).

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Hepatorenal syndrome

The kidneys may undergo major changes (hepatorenal syndrome). A specific renal dysfunction develops: preservation of the renal epithelium functions and a disorder of the glomerular filtration function without pronounced anatomical changes. Many explain this by a disorder of the blood supply to the kidneys, an increase in blood flow through the renal medulla and shunting of blood around the glomerular capillaries; there is also an idea of a general increase in vascular resistance in the kidneys.

In severe cases of renal dysfunction, renal failure may develop. Its occurrence may be accelerated by such factors as bleeding from dilated veins of the esophagus, stomach, repeated punctures in ascites, use of diuretics, intercurrent infections.

Symptoms of hepatorenal syndrome have a number of features: the specific gravity of urine and its fluctuations differ little from the norm, protein is not always detected and in small quantities, pathological sediment (erythrocytes, cylinders) is not always expressed. Partial kidney functions change more often, in particular, glomerular filtration decreases. In very severe cases, especially with severe liver failure, arterial pressure may increase, oliguria develops, azotemia, and clinical signs of renal failure appear. The development of azotemia in liver cirrhosis is considered a sign of severe liver damage and imminent death.

Hypersplenism syndrome

Many patients with liver cirrhosis have an enlarged spleen and hypersplenism, which manifests itself as pancytopenia syndrome (anemia, leukopenia, thrombocytopenia).

Symptoms of enlarged spleen are explained by venous congestion in it, pulp fibrosis, the appearance of a large number of arteriovenous shunts, proliferation of reticulohistiocytic cells. Hypersplenism syndrome is caused by inhibition of bone marrow hematopoiesis, formation of antibodies to formed elements of blood, increased destruction of erythrocytes in the spleen.

Hypersplenism syndrome is manifested not only by pancytopenia in the peripheral blood, but also by a decrease in the number of myeloid cells in the bone marrow.

Digestive system disorders in liver cirrhosis

Reflux esophagitis is often determined with liver cirrhosis. Its main symptoms are belching of air, gastric contents, heartburn, and a burning sensation behind the breastbone. Reflux esophagitis is caused by increased intra-abdominal pressure due to ascites and the reflux of contents from the stomach into the esophagus. Chronic esophagitis may be accompanied by erosions and ulcerations of the mucous membrane of the lower third of the esophagus and the cardiac part of the stomach.

Very often, with liver cirrhosis, symptoms of chronic gastritis (usually superficial and hypertrophic) develop. It manifests itself as dull pain in the epigastrium, appearing after eating, nausea, a feeling of fullness and heaviness in the epigastric region, belching, and loss of appetite.

In 10-18% of patients with liver cirrhosis, symptoms of gastric and duodenal ulcers are detected. A characteristic feature of these ulcers is the absence or weak expression of pain syndrome. Often, these ulcers first manifest themselves with bleeding symptoms. One of the reasons for the development of ulcers is the high content of histamine in the blood. Histamine bypasses the liver during the development of portocaval anastomoses and, therefore, is not neutralized in it. It stimulates excessive secretion of hydrochloric acid by the glands of the stomach, which contributes to the formation of ulcers. Hypergastrinemia, often observed in liver cirrhosis, is also important.

Damage to the pancreas manifests itself as symptoms of chronic pancreatitis with exocrine insufficiency, damage to the intestines - as symptoms of chronic enteritis with impaired absorption capacity ( malabsorption syndrome ).

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Endocrine system disorders in liver cirrhosis

The endocrine system undergoes major changes in liver cirrhosis:

• 50% of patients show symptoms of carbohydrate metabolism disorder in the form of decreased carbohydrate tolerance, accompanied by increased insulin levels in the blood. These changes indicate relative insulin deficiency, which is caused by hyperproduction of counter-insular hormones ( glucagon, somatotropin ) and decreased sensitivity of peripheral tissues to insulin. In 10-12% of patients, approximately 5-7 years after the onset of obvious symptoms of liver cirrhosis, clinically expressed diabetes mellitus develops. It is possible that liver cirrhosis converts genetic predisposition to diabetes mellitus into a clinically manifest form of the disease;
• In decompensated liver cirrhosis, the functional state of the sex glands in men is disrupted, which is manifested in a decrease in the blood testosterone content, an increase in estrogens, prolaetin, and sex hormone-binding globulin. Hyperestrogenemia is due to reduced degradation of estrogens in the liver, as well as increased peripheral conversion of androgens to estrogens. Clinically, these changes are manifested in hypogonadism (atrophy of the testicles, penis, decreased severity of secondary sexual characteristics, sexual weakness), gynecomastia, feminization. In women, pathology of the reproductive system is expressed in menstrual irregularities; atrophy of the mammary glands, decreased sexual desire;
• Disruption of the functional state of the adrenal glands is expressed in symptoms of hyperaldosteronism, which contributes to the development of ascites in patients with liver cirrhosis.

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Central nervous system damage

Damage to the central nervous system manifests itself with symptoms of toxic encephalopathy. It is characterized by asthenia, sleep disturbances (sleepiness during the day, insomnia at night), memory loss, headaches, paresthesia in the arms and legs, trembling fingers, apathy, and indifference to others. The extreme manifestation of hepatic encephalopathy is hepatic coma.

The liver is defined as enlarged, dense, often lumpy, with a sharp edge. The functional capacity of the liver is significantly impaired, especially in the late, final phases of the disease.

Hepatocellular failure

The general condition of patients and the prognosis for liver cirrhosis are determined by the syndromes of hepatocellular insufficiency and portal hypertension.

Hepatocellular hypertension is always based on damage to hepatocytes (dystrophy and necrosis) and the development of cytolytic, cholestatic, and excretory-biliary syndromes.

Symptoms of hepatocellular hypertension:

• "poor nutrition" syndrome (loss of appetite, nausea, intolerance to alcohol, tobacco, belching, flatulence, abdominal pain, bowel disorders, weight loss, dry flaky skin, manifestations of hypovitaminosis);
• fever due to autolysis processes in the liver and the entry of toxic products and a pyrogenic steroid, etiocholanolone, into the blood (its inactivation in the liver is impaired);
• jaundice;
• skin changes (minor signs of cirrhosis);
• symptoms of endocrine changes.
• liver odor from the mouth (appears in severe liver failure and resembles the sweet smell of raw liver);
• hemorrhagic diathesis (due to impaired synthesis of blood clotting factors in the liver and thrombocytopenia).

The following stages of hepatocellular insufficiency are distinguished:

The compensated (initial) stage is characterized by the following symptoms:

• general condition is satisfactory;
• moderate pain in the liver and epigastric region, bitterness in the mouth, bloating;
• no weight loss or jaundice;
• the liver is enlarged, dense, its surface is uneven, the edge is sharp;
• the spleen may be enlarged;
• liver function tests have changed slightly;
• There are no clinically expressed manifestations of liver failure.

The subcompensated stage has the following symptoms:

• pronounced subjective manifestations of the disease (weakness, pain in the right hypochondrium, flatulence, nausea, vomiting, bitterness in the mouth, diarrhea, loss of appetite, nosebleeds, bleeding gums, itchy skin, headaches, insomnia);
• weight loss;
• jaundice;
• "minor symptoms" of liver cirrhosis;
• hepatomegaly, splenomegaly;
• initial manifestations of hypersplenism: moderate anemia, leukopenia, thrombocytopenia;
• changes in liver function indicators: bilirubin levels in the blood are increased by 2.5 times, alanine aminotransferase levels are increased by 1.5–2 times compared to the norm, the thymol test is increased to 10 units, the albumin content in the blood is reduced to 40%, and the sublimate test is reduced to 1.4 ml.

The stage of severe decompensation (the last stage) is characterized by the following symptoms and laboratory manifestations:

• pronounced weakness;
• significant loss of body weight;
• jaundice;
• skin itching;
• hemorrhagic syndrome;
• edema, ascites;
• liver odor from the mouth;
• symptoms of hepatic encephalopathy;
• changes in liver function indicators: bilirubin levels in the blood are increased by 3 or more times, alanine aminotransferase levels are more than 2-3 times higher than normal; prothrombin levels are less than 60%, total protein levels are less than 65 g/l, albumin levels are below 40-30%, and cholesterol levels are less than 2.9 μmol/l.

Portal hypertension syndrome

Portal hypertension syndrome is an important symptom of cirrhosis and consists of increased pressure in the portal vein basin.

Portal hypertension in liver cirrhosis occurs due to a reduction in blood flow through the sinusoids. This is due to the following factors:

• compression of small hepatic veins by nodes of regenerating hepatocytes;
• reduction of the terminal and larger branches of the portal vein and hepatic artery as a result of the inflammatory process in the liver;
• narrowing of the sinusoid lumen by proliferating endothelial cells and inflammatory infiltrates. Due to the reduction in blood flow, portal pressure begins to increase and anastomoses develop between the portal vein and the vena cava.

The most important are the following portocaval anastomoses:

• in the cardiac part of the stomach and the abdominal part of the esophagus, connecting the vessels of the portal and superior vena cava through the azygos vein system;
• superior hemorrhoidal veins with the middle and inferior hemorrhoidal veins, connecting the portal and inferior vena cava basins;
• between the branches of the portal vein and the veins of the anterior abdominal wall and diaphragm;
• between the veins of the gastrointestinal tract, the retroperitoneal and mediastinal veins, these anastomoses connect the portal and inferior vena cava.

Of greatest clinical significance are anastomoses in the cardiac region of the stomach and esophagus, since at very high pressure severe bleeding may occur in them, which can cause death.

The appearance of ascites is also associated with an increase in venous pressure in the portal vein.

The main symptoms of portal hypertension:

• persistent dyspeptic symptoms, especially after eating;
• bloating and a feeling of fullness in the stomach after eating any food (“wind before the rain”);
• a feeling of a constantly full intestine;
• progressive weight loss and signs of polyhypovitaminosis with a fairly complete diet;
• periodic diarrhea without pain and fever, after which the patient feels better;
• splenomegaly;
• ascites;
• oliguria;
• caput medusa;
• varicose veins of the esophagus and stomach, detected by X-ray examination of the stomach and FGDS;
• gastric and hemorrhoidal bleeding;
• increased pressure in the splenic vein (detected using splenoportometry). Typically, after bleeding, the pressure in the splenic vein decreases, and the spleen may contract.

The following stages of portal hypertension are distinguished:

The compensated stage is characterized by the following main symptoms:

• pronounced flatulence;
• frequent loose stools, after which flatulence does not decrease;
• dilation of the veins of the anterior abdominal wall;
• increased pressure in the portal and hepatic veins (determined by catheterization of these veins; catheterization of the hepatic veins also allows one to judge the sinusoidal pressure);
• an increase in the diameter of the portal vein and its insufficient expansion during inhalation (determined using ultrasound examination).

Initial decompensation of portal hypertension has the following symptoms:

• varicose veins of the lower third of the esophagus (determined by X-ray examination of the stomach and FEGDS);
• often pronounced hypersplenism;
• The remaining symptoms are the same as in the first stage.

The decompensated (complicated) stage of portal hypertension is characterized by significant hypersplenism; hemorrhagic syndrome; pronounced dilation of the veins of the lower third of the esophagus and stomach and bleeding from them, edema and ascites; portocaval encephalopathy.

Spontaneous bacterial peritonitis

In case of decompensated liver cirrhosis in the presence of ascites, spontaneous bacterial peritonitis may develop (in 2-4% of patients). Its most common pathogen is E. coli.

The main symptoms of spontaneous bacterial peritonitis are:

• acute onset with fever, chills, abdominal pain;
• tension of the muscles of the anterior abdominal wall;
• weakening of intestinal peristaltic sounds;
• lowering blood pressure;
• worsening of symptoms of hepatic encephalopathy, in severe cases - development of hepatic coma;
• leukocytosis in peripheral blood with a shift to the left;
• intra-abdominal fluid is turbid, rich in cellular elements (more than 300 cells per 1 mm2, with neutrophilic leukocytes predominating among the cells); poor in protein (less than 20 g/l); in most cases, an infectious agent is isolated from the fluid;
• The mortality rate is 80-90%.

Mesenchymal inflammatory syndrome (immune inflammation syndrome)

Mesenchymal inflammatory syndrome (MIS) is an expression of the processes of sensitization of cells of the immune competent system and activation of the RES. MIS determines the activity of the pathological process.

The main symptoms of MIS:

• increase in body temperature;
• enlarged spleen;
• leukocytosis;
• acceleration of ESR;
• eosinophilia;
• increase in thymol test;
• reduction of the sublimate test
• hyper alpha2- and y-globulinemia;
• oxyprolinuria;
• increase in serotonin content in platelets;
• the appearance of C-reactive protein;
• immunological manifestations are possible: the appearance of antibodies to liver tissue, LE cells, etc.

The course of liver cirrhosis

The course of liver cirrhosis is chronic, progressive, with exacerbations and remissions and is determined by the activity of the pathological process in the liver, the severity of the syndromes of hepatocellular insufficiency and portal hypertension. During the period of the active process, the symptoms of liver cirrhosis and the severity of liver failure and portal hypertension are aggravated.

An important indicator of liver cirrhosis activity is the high intensity of the mesenchymal-inflammatory process, it indicates the ongoing progression of the pathological process. The active phase of liver cirrhosis is characterized by an increase in body temperature, hypergammaglobulinemia, hypoalbuminemia, an increase in ESR, Ig content of all classes, a high level of alanine and aspartic aminotransferases in the blood, sensitization of T-lymphocytes to a specific liver lipoprotein, confirming the participation of autoimmune mechanisms in the progression of the process.

Depending on the severity of laboratory indicators, moderate and severe activity of liver cirrhosis are distinguished.

Degrees of activity of liver cirrhosis

Blood serum parameters	Moderate activity of liver cirrhosis	Severe activity of liver cirrhosis
A2-Globulins	Up to 13%	Tmore than 13%
Gamma globulins	Up to 27-30%	More than 27-30%
Thymol test	Up to 8-9%	More than 8-9 OD
AlAT	1.5-2 times	3-4 times or more
Sublimate test	From 1.8 to 1.2 ml	Less than 1.2 ml

The active pathological process is also characterized by clinical symptoms: deterioration of health, pain in the liver, weight loss, jaundice, increased body temperature, the appearance of new stellate telangiectasias. Histologically, the active phase is manifested by the proliferation of Kupffer cells, inflammatory cell infiltration inside the liver lobules, the appearance of a large number of step necroses of hepatocytes, and increased fibrogenesis.

The manifestations of the active phase of viral liver cirrhosis and chronic replicative hepatitis B are very similar and can be combined. In this regard, many hepatologists suggest distinguishing "liver cirrhosis with active hepatitis" or "chronic active hepatitis in the phase of liver cirrhosis." (HBV-CAH-cirrhosis). Some scientists believe that liver cirrhosis develops mainly in chronic hepatitis B induced by mutant strains lacking the ability to synthesize HBeAg.

In long-term liver cirrhosis, there may be no signs of active inflammatory process (the active process has already ended, in the figurative expression of S. N. Sorinson, cirrhosis has “burned out”), and decompensation and signs of portal hypertension are pronounced.

Viral cirrhosis of the liver

Viral cirrhosis of the liver has the following clinical and laboratory features that must be taken into account when diagnosing it.

1. Most often, viral cirrhosis of the liver is observed in young and middle age, and more often in men.
2. A clear connection can be established between the development of liver cirrhosis and acute viral hepatitis. There are two types of viral liver cirrhosis: early, developing during the first year after acute hepatitis B, and late, developing during a long latent period. Hepatitis D and C viruses have pronounced cirrhotic properties. Chronic hepatitis caused by these viruses often transforms into liver cirrhosis. Chronic hepatitis C can proceed clinically quite benignly for a long time and still naturally leads to the development of liver cirrhosis.
3. Viral cirrhosis of the liver is most often macronodular.
4. Symptoms of liver cirrhosis resemble the acute phase of viral hepatitis and also manifest as pronounced asthenovegetative, dyspeptic syndromes, jaundice, and fever.
5. Functional liver failure in the viral form of cirrhosis appears quite early (usually during periods of exacerbation of the disease).
6. In the stage of established liver cirrhosis, varicose veins of the esophagus and stomach, hemorrhagic syndrome with viral etiology of cirrhosis are observed more often than with alcoholic cirrhosis.
7. Ascites in viral cirrhosis of the liver appears much later and is observed less frequently than in alcoholic cirrhosis.
8. Thymol test values in viral cirrhosis reach the highest values compared to alcoholic liver cirrhosis.
9. Viral liver cirrhosis is characterized by the detection of serological markers of viral infection.

Alcoholic cirrhosis of the liver

Alcoholic liver cirrhosis develops in 1/3 of people suffering from alcoholism, within 5 to 20 years. The following clinical and laboratory features are characteristic of alcoholic liver cirrhosis:

1. Anamnestic indications of long-term alcohol abuse (however, most patients tend to hide this).
2. Characteristic "alcoholic appearance": puffy face with reddened skin, small telangiectasias, purple nose; tremor of hands, eyelids, lips, tongue; edematous cyanotic eyelids; slightly bulging eyes with injected sclera; euphoric behavior; swelling in the parotid glands.
3. Other manifestations of chronic alcoholism (peripheral polyneuropathy, encephalopathy, myocardial dystrophy, pancreatitis, gastritis).
4. Severe dyspeptic syndrome (loss of appetite, nausea, vomiting, diarrhea) in the advanced stage of alcoholic liver cirrhosis, caused by concomitant alcoholic gastritis and pancreatitis.
5. Telangiectasias and Dupuytren's contracture (in the area of the tendons of the palm), as well as testicular atrophy and hair loss are more characteristic of alcoholic cirrhosis of the liver than of other etiologic forms of cirrhosis.
6. Portal hypertension (including one of its most important manifestations - ascites) develops much earlier than with viral cirrhosis of the liver.
7. The spleen enlarges significantly later than in viral cirrhosis of the liver; in a significant number of patients, splenomegaly is absent even in the advanced stage of the disease.
8. Leukocytosis (up to 10-12x10 ⁷ l) with a shift to band cells, sometimes up to the appearance of myelocytes and promyelocytes (leukemoid reaction of the myeloid type), anemia, increased ESR. Causes of anemia are blood loss due to erosive gastritis, the toxic effect of alcohol on the bone marrow; impaired absorption and alimentary deficiency of folic acid (this can cause the megaloblastic type of hematopoiesis); impaired pyruvadoxine metabolism and insufficient heme synthesis (this causes the development of sidero-achrestic anemia); sometimes hemolysis of erythrocytes.
9. Characterized by high levels of IgA in the blood, as well as an increase in the activity of y-glutamyl transpeptidase in the blood - by 1.5-2 times (the normal value for men is 15-106 U/l, for women - 10-66 U/l).

High blood levels of y-glutamyl transpeptidase usually indicate long-term alcohol abuse, alcoholic liver disease, and are considered by many authors as a biochemical marker of alcoholism. The test can be used to screen alcoholics and control them during abstinence (the enzyme activity decreases by half only after 3 weeks of stopping alcohol intake). However, it should be taken into account that y-glutamyl transpeptidase activity can be increased in diabetes mellitus, myocardial infarction, uremia, pancreatic tumors, pancreatitis, and the use of cytostatics, antiepidemic drugs, barbiturates, and indirect anticoagulants. Chronic alcoholism is accompanied by increased blood levels of acetaldehyde (an alcohol metabolism product that is more toxic than alcohol itself), and increased urinary excretion of salsolin (an acetaldehyde and dopamine condensation product). Often, with alcoholic cirrhosis of the liver, the level of uric acid in the blood is increased.

10. The following symptoms are revealed in liver biopsies:

• Mallory bodies (accumulation of alcoholic hepatic acid in the liver lobule);
• accumulation of neutrophilic leukocytes around hepatocytes;
• fatty degeneration of hepatocytes; pericellular fibrosis;
• relative preservation of portal tracts.

11. Stopping alcohol consumption leads to remission or stabilization of the pathological process in the liver. With continued alcohol consumption, liver cirrhosis steadily progresses.

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"Congestive liver" and cardiac cirrhosis of the liver

Congestive liver is a liver disorder caused by blood stagnation in the liver due to high pressure in the right atrium. Congestive liver is one of the main symptoms of congestive heart failure.

The most common causes are mitral valve defects, tricuspid valve insufficiency, chronic pulmonary heart disease, constrictive pericarditis, right atrial myxoma, myocardial sclerosis of various origins. The main mechanisms of development of "congestive liver" are:

• overflow of blood into the central veins, the central part of the liver lobules (development of central portal hypertension);
• development of local central hypoxia in the liver lobules;
• dystrophic, atrophic changes and necrosis of hepatocytes;
• active synthesis of collagen, development of fibrosis.

As congestion in the liver progresses, connective tissue develops further, connective tissue strands connect the central veins of adjacent lobules, the architecture of the liver is disrupted, and cardiac cirrhosis of the liver develops.

Characteristic symptoms of liver cirrhosis with "congestive liver" are:

• hepatomegaly, the liver surface is smooth. In the initial stage of circulatory failure, the consistency of the liver is soft, its edge is rounded, later the liver becomes dense, and its edge is sharp;
• liver pain upon palpation;
• positive Plesh's sign or hepatojugular "reflex" - pressure on the area of the enlarged liver increases swelling of the jugular veins;
• variability of liver size depending on the state of central hemodynamics and the effectiveness of treatment (positive results of treatment of congestive heart failure are accompanied by a decrease in liver size);
• minor severity of jaundice and its reduction or even disappearance with successful therapy of congestive heart failure.

In severe congestive heart failure, edematous-ascitic syndrome develops, in which case there is a need for differential diagnosis with liver cirrhosis with ascites.

With the development of cardiac cirrhosis, the liver becomes dense, its edge is sharp, its size remains constant and does not depend on the effectiveness of the treatment of heart failure. When diagnosing cardiac cirrhosis of the liver, the underlying disease that caused heart failure, the absence of signs of chronic alcohol abuse and markers of viral infection are taken into account.

Assessing the severity of liver cirrhosis

Clinical assessment of the stage and severity of liver cirrhosis is based on the severity of portal hypertension and hepatocellular insufficiency. The severity of liver cirrhosis can also be assessed using the Child-Pugh diagnostic complex, which includes an assessment of the serum bilirubin, albumin, prothrombin levels, as well as the severity of liver encephalopathy and ascites.

The severity of liver cirrhosis according to Child-Pugh highly correlates with patient survival rates and liver transplantation results; the life expectancy of patients belonging to class A is on average 6-7 years, and for class C - 2 months.

The most important task of clinical and laboratory examination of the patient is the timely recognition of complications of liver cirrhosis.

The most important complications of liver cirrhosis are:

• encephalopathy with the development of hepatic coma;
• profuse bleeding from varicose veins of the esophagus and stomach;
• bleeding from varicose inferior hemorrhoidal veins;
• portal vein thrombosis;
• the addition of a secondary bacterial infection (pneumonia, sepsis, peritonitis);
• progressive hepatorenal failure);
• transformation of liver cirrhosis into cirrhosis-cancer.

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