Venous congestion in the liver treatment. Cardiac cirrhosis: causes and consequences

When there is stagnation in the systemic circulation, the liver is usually short time able to take in a significant amount of blood. Its role in infancy and childhood is of paramount importance. A congestive liver is always a sign of failure of the right half of the heart, even if the depletion of the right half of the heart is not primary, but secondary to the failure of the left half of the heart. Pathological changes and functional disorders occur under the influence of the combined effect of increased venous pressure and hypoxia.

Upon autopsy, the liver appears larger, heavier, and denser than normal. With fresh stagnation its color is red, with older stagnation it is bluish-brownish-red. With prolonged stagnation, the liver capsule thickens. Due to secondary fatty degeneration, the liver may have yellowish spots. With short-term stagnation, the pattern on the section is pronounced, in the center of the lobules the central veins gape red and at the edges of the hepatic beams - capillaries. The color of the hepatic ligaments is very pale compared to the red spots of the gaping vessels. After long-term stagnation, the liver cells at the edges of the lobules undergo fatty degeneration and therefore acquire yellowish color, and in the center of the lobule there is a central vein filled with bluish-red blood (“nutmeg liver”). With long-term stagnation, the pattern of the hepatic lobules is erased, and the connective tissue that takes the place of the dead hepatic substance leads to the appearance of “false lobulation.” In the center of these false lobules there is yellow liver tissue that has undergone fatty degeneration; seemingly gaping vessels are distributed along the edges. With sudden congestion in the liver substance and under the capsule, many hemorrhages are visible. The microscopic picture is characterized by dilated central veins and capillaries, compressed between them by liver cells with fat droplets and pigment grains. In the center of the lobules, liver cells often die. Microscopic hemorrhages are common.

With sudden congestion in the liver, the patient usually feels sharp pain in the liver area, which may resemble pain caused by a gallstone. Often confused with pleurisy. The pain is caused by sudden tension of the liver capsule. Muscular protection may exist over the liver area. A congested liver also affects the function digestive tract: it is accompanied by vomiting, nausea, flatulence, diarrhea and lack of appetite.

IN infancy in acute infectious diseases, it is sometimes difficult to decide whether a sudden enlargement of the liver is a consequence of heart failure or toxic damage. In such cases, you can navigate based on other symptoms (increased venous pressure, tachycardia, ECG, etc.). It should be noted here that although the basis of liver congestion is venous congestion, severe liver congestion can still occur without an increase in venous pressure. Veins because of their great ability expand sometimes over time able to balance high blood pressure, and by the time the increase in venous pressure becomes measurable, liver congestion has long since occurred.

In childhood, recognition and clarification of congestive liver is already easier. The lower edge of the liver extends beyond the costal arch; percussion can also establish that the liver is enlarged upward. She lifts right side diaphragm and can compress the lower parts of the lungs. In such cases, the percussion sound above the diaphragm is shortened, and bronchial breathing is heard. Palpation usually reveals a uniformly compacted liver with a smooth surface and a hard, sharp or rounded edge. It rarely pulsates. In childhood, even with insufficiency of the tricuspid valves, it is very difficult to recognize the pulsation of the liver, because the liver tissue is very elastic and the greater ability to accept blood equalizes the intense action of the blood flowing back. In chronic decompensation, the proliferation of connective tissue makes the liver so hard that its pulsation can no longer be taken into account. In cardiac pseudocirrhosis, the size of the liver, despite stagnation, may be less than normal.

The functional disorder of the liver with a slight stagnation is insignificant, however, with a larger or long-term stagnation it is still significant. We have to take into account a functional disorder even if it is not detected by functional liver tests, because based on the literature data and our own experience, we believe that functional tests in some cases do not reflect changes in the liver. The content of urobilinogen in urine increases. Some authors attach a relationship between the severity of hepatic congestion and the content of urobilinogen in the urine diagnostic value. According to other authors positive result The Ehrlich reaction is caused not by urobilinogen, but by stercobilinogen. A significant increase in the concentration of lactic acid in the blood is explained by the disorder liver function. Serum bilirubin increases significantly only after severe or prolonged stagnation. In such cases, the patient develops mild jaundice. The reason for this phenomenon is not entirely clear. It is assumed that liver damage resulting from hypoxia and hemolysis play a role in the occurrence of this jaundice. The latter is supported by the observation of Magyar and Toth: an increase in the content of bilirubin in the urine. Jaundice develops slowly and also disappears slowly. In feces, the amount of coloring substances formed from bile pigment increases.

Disorder of liver function is, with its long-term existence, one and perhaps the most important cause of hypoproteinemia accompanying failure of the right half of the heart. The decrease in the content of serum proteins in heart patients is partly explained by insufficient nutrition, poor absorption conditions, and loss of protein with edematous fluid, but undoubtedly the leading role is played by a decrease in the ability of the liver to form proteins. Due to hypoproteinemia, drug removal of edema is often unsuccessful after restoration of heart strength for a long time.

With scarring of the pericardium or with prolonged decompensation, so-called cardiac cirrhosis often occurs. With abundant growth of connective tissue, it is characterized by the death of the liver substance and, in places, islands of regenerating liver cells. The growth of connective tissue occurs not only around the lobules, but also in their central part. If the growth of connective tissue merges, then the pattern of the hepatic substance becomes unidentifiable. With prolonged stagnation, the capsule thickens due to perihepatitis. The occurrence of liver cirrhosis is characterized by the fact that the liver becomes hard, small, with sharp edges, its size is fixed. At the same time, due to portal hypertension, the spleen begins to swell. It becomes larger and harder. In this state, under the influence of treatment acting on the heart and blood circulation, neither the magnitude nor functional disorder livers do not change. Cardiac cirrhosis is usually accompanied by ascites that is not amenable to drug treatment.

Liver for heart disease.

Professor Ambalov Yuri Mikhailovich - Doctor medical sciences, Head of the Department of Infectious Diseases of Rostov State Medical University, Member of the RAE, Chairman of the Association of Infectious Diseases Rostov region, Head of the Rostov branch of the RAE, Chief consultant of the Hepatological Center of Rostov-on-Don, Hepatologist of the highest qualification category

Khomenko Irina Yurievna — Candidate of Medical Sciences, Head of Infectious Diseases Department No. 4, Moscow Healthcare Institution “ City Hospital No. 1 named after N.A. Semashko, Rostov-on-Don", Chief freelance hepatologist of the Ministry of Health of the Rostov region, Member Russian Society for the study of the liver (ROPIP), infectious disease specialist, hepatologist of the highest qualification category

Book: “Liver Diseases” (S.D. Podymova; 1981)

Liver for heart disease.

In heart disease, the liver is affected due to an acute or chronic increase in central venous pressure, as well as a decrease in cardiac output. Usually there are phenomena of stagnation, necrosis, fibrosis, and less often cirrhosis, which can exist separately, but are often combined depending on the clinical situation. The term “cardiogenic liver” has been proposed to refer to these disorders.

Speaking about the importance of hemodynamic disorders in the pathogenesis of liver damage in heart disease, it should be emphasized that the liver’s need for oxygen is comparable to the need of the brain and heart, and hypoxia significantly impairs its functions.

IN clinical picture nevertheless, one factor of liver damage often predominates: either the phenomena of stagnation due to right ventricular failure, or the insufficiency of arterial perfusion of the liver due to left ventricular failure, or signs of liver cirrhosis against the background of prolonged stagnation. This division allows us to better understand the mechanism of formation of individual symptoms.

Congestive liver. Any heart disease that causes increased pressure in the right atrium leads to stagnation of blood in the liver. The most common causes are mitral valve disease, tricuspid valve insufficiency, cor pulmonale for chronic respiratory failure or recurrent thrombosis of small branches pulmonary artery, constrictive pericarditis, right ventricular myocardial infarction, right atrial myxoma.

Dependence of liver blood supply on functional state of the right heart is determined by the topographic relationship between the right atrium and the hepatic veins, the liver is called a reservoir for stagnant blood, the pressure gauge of the right atrium.

The increased central venous pressure is transmitted to the hepatic veins and interferes with the flow of blood to the central part of the lobule. Slowing blood circulation increases the overflow of blood into the central veins, the central part of the lobules. Developing central portal hypertension has predominantly mechanical origin, hypoxia joins it.

Localized central hypoxia causes atrophy and even necrosis of hepatocytes. Cell loss leads to collapse and condensation of the reticulum, active necrosis stimulates the formation of collagen, causing sclerosis of the veins. Further, the development of connective tissue leads to the movement of the central veins to the place of the portal veins. Connective tissue cords connect the central veins of neighboring lobules, and the liver architecture is disrupted.

Macroscopically, the liver in heart failure is enlarged, dark red, congested, it is rarely nodular. Dilated, stretched veins protrude on the cut surface; the liver looks like nutmeg(centrilobular red areas of stagnation and yellow remaining part of the lobules).

Microscopically, expansion of the central veins and sinusoids containing red blood cells is observed; in some cases, the centers of the hepatic lobules look like “lakes of blood.” The trabecular structure is erased in the central areas, hepatocyte atrophy and balloon degeneration develop here, and as the process progresses, centrilobular focal necrosis is revealed. The pigment lipofuscin in the form of delicate or coarse clusters of golden yellow or brown color is contained in the center of hepatocytes.

Clinical picture. The first symptom of liver congestion is its enlargement. When pressing on the liver area, a hepatojugular reflex (Plesch's symptom) occurs - swelling of the neck veins. In the initial stage of circulatory failure, the liver protrudes slightly from under the costal arch, its edge is rounded, smooth, and the surface is soft.

In the future, the organ can reach enormous sizes, descending below the scallop ilium. The edge of the liver becomes sharper, the surface becomes dense. A. L. Myasnikov (1949) rightly emphasizes the variety of clinical manifestations of congestive liver: severe heart failure with large edema and ascites and a slight enlargement of the liver is possible, and, on the contrary, the liver can become significantly enlarged with other mild symptoms of stagnation. The different reaction of the liver to stagnation in it depends on its previous lesions - alcoholism, medicinal effects, as well as on the duration of stagnation.

Noteworthy is the sensitivity and, in some cases, pain of the congestive liver upon palpation. With acutely developing circulatory failure, intense spontaneous pain in the right half of the abdomen may be observed, associated with stretching of the liver capsule. A characteristic feeling of heaviness and fullness that occurs during eating, sometimes nausea. Distinctive feature congestive liver is the variability of its size, associated with the state of central hemodynamics and treatment, in particular with cardiac glycosides and diuretics.

Jaundice is usually mild. The combination of jaundice and cyanosis creates a peculiar color of the skin. An increase in bilirubin, mainly due to the bound fraction, is detected in 20-50% of patients [Bondar 3. A., 1970; Bluger A.F., 1975]. Usually it is moderately elevated - up to 34.2-51.3 µmol/l (2-3 mg%), rarely up to 68.4-85.5 µmol/l (4-5 mg%). The mechanism of hyperbilirubinemia consists of impaired excretion, regurgitation and uptake of bilirubin by the liver.

Sometimes, against the background of chronic stagnation in the liver, jaundice quickly and significantly increases, which requires differential diagnosis with a number of diseases.

A. A. Krylov, O. G. Sprinson (1982) observed 25 patients in whom increasing jaundice did not have additional etiological factors and arose as a result of congestive liver. Bilirubinemic crises in these patients with a rise in bilirubin from 71.1 to 167.6 µmol/l (4.16-9.8 mg%) due to the predominance of the direct fraction were accompanied by circulatory failure of the right ventricular type.

An increase in venous pressure, a positive venous pulse, and enlargement and hardening of the liver were noted. Most often, increasing jaundice was preceded or accompanied by pain in the right hypochondrium.

The causes of bilirubinemic crises in congestive liver are not entirely clear. The main significance in their origin, apparently, is the further, sometimes paroxysmal, deterioration of intrahepatic circulation, increasing liver hypoxia, the appearance of hepatocyte necrosis, impaired excretion of bile through the intrahepatic bile ducts due to increasing intravascular pressure in the sinusoids of the liver.

Hemolytic jaundice is rare. The sudden appearance of jaundice with indirect bilirubin is characteristic of pulmonary infarctions, spleen or kidneys, which without heart failure do not cause jaundice. This is due to the fact that an additional hemoglobin depot is created at the site of the infarction, and bilirubin is formed from it. Excess pigment cannot bind to altered liver cells. Pulmonary congestion also leads to increased hemolysis and an increase in the indirect bilirubin fraction.

When studying the functional state of the liver, the most pronounced changes are detected with a bromsulfalein test, as well as a study of blood flow and the absorptive-excretory fraction of the liver with 1311. In some cases, moderate hypoalbuminemia, a decrease in the prothrombin index, and a mild increase in the activity of serum aminotransferases are noted.

Insufficient liver perfusion. Both functional and morphological liver disorders can occur with a decrease in arterial blood supply. The cause of such disorders may be acute left ventricular failure or prolonged collapse.

They are sometimes referred to as ischemic hepatitis. It should be highlighted acute heart attack myocardium, complicated by cardiogenic shock, arrhythmogenic collapses, post-resuscitation conditions, pulmonary embolism.

With a decrease in perfusion heat pressure in the liver, sufficient oxygen saturation of the blood is observed only in the periportal zones and quickly drops when approaching the central part of the lobule, which is most sensitive to metabolic damage. Severe hypoxia of centrilobular liver cells leads to the development of necrosis and, in some cases, infarction.

Direct liver damage from acute disorders blood circulation in patients with myocardial infarction was described by B. I. Vorobyov, L. I. Kotelnitskaya (1976). Ch. Stambolis et al. (1979), V. Aroidi et al. (1980), W. Beckert (1980) observed massive centrilobular necrosis of the liver in patients who died from circulatory failure.

In the clinical picture, the most important are jaundice, sometimes intense, and high levels of aminotransferases (usually a 5-fold increase above normal), which is often interpreted as acute viral hepatitis.

O. Nouel et al. (1980) described the development of acute liver failure in 6 patients with transient episodes of acute heart failure against the background of chronic congestion in the liver. Jaundice and hepatic encephalopathy developed 1–3 days after the episodes acute failure blood circulation, when hemodynamic parameters have already returned to normal. All patients had massive centrilobular necrosis without inflammatory cell infiltration.

Cardiac cirrhosis of the liver. According to various authors, the incidence of cirrhosis in patients with congestive liver ranges from 0.7 to 6.9% [Bondar Z. A., 1970; Valkovich E.I., 1973; Filippova L. A., Tikhonova G. N., 1975; Sherlock S., 1968]. Most often it is detected against the background of prolonged congestion in the liver with tricuspid valve insufficiency or constrictive pericarditis.

However, liver cirrhosis cannot be considered a common consequence of heart failure. A number of authors propose the term “liver cirrhosis in heart diseases occurring with circulatory failure,” emphasizing the multifactorial genesis of the disease. In addition to chronic stagnation, insufficient perfusion with the formation of necrosis in the liver, prolonged drug therapy, protein and vitamin deficiency.

Morphological examination, in addition to changes characteristic of stagnation, reveals periportal fibrosis, regenerated nodes, and restructuring of lobular architectonics.

The clinical picture of cardiac cirrhosis does not have characteristic features. In the foreground is increasing heart failure, congestive liver, which is becoming increasingly dense, often with acute and uneven edge; sometimes the spleen enlarges. Ascites develops after long period edema and is usually refractory to digitalis-diuretic therapy. Other signs of portal hypertension are observed on late stage diseases.

Cardiac cirrhosis of the liver occurs at the dystrophic stage of heart failure, when emaciation (to the point of cachexia), asthenia, anorexia, darkening of the skin, hair loss, and brittle nails are severe.

A functional study of the liver reveals slight hyperbilirubinemia, hypoalbuminemia, hypoprothrombinemia, a moderate increase in gamma globulins, a decrease in cholinesterase activity, an increase in aminotransferases and gamma-glutamyl transpeptidase. Cardiac cirrhosis occurs latently, without significant exacerbations.

Among 603 patients with cirrhosis, A.I. Khazanov discovered muscat cirrhosis with a pronounced restructuring of the liver structure in 22 cases; Histological examination revealed layers of fibrous tissue and regenerated nodes. The majority of patients were found to have severe disturbances functional tests liver; in the terminal period, 5 people developed a deep coma.

Liver is a gland involved in the metabolism of proteins, fats, and vitamins. The liver produces bile, the lack of which in the body leads to disturbances in the digestive process. The liver filters the blood circulating throughout the body to prevent toxic substances and microorganisms from entering the body through the gastrointestinal tract. The most common liver diseases are hepatitis A and B, fatty liver due to alcoholism, gallstones formed due to stagnation of bile, infection, and disruption of cholesterol metabolism.

Traditional healers offer many ways liver cleansing. There is a cleaning method according to G. Malakhov, according to E. Shchadrin, according to A. Zaraev, according to O. Eliseeva, according to K. Nishi, according to N. Walker. In general, a lot and using various ingredients. The procedures are responsible, and the attending physician should recommend them, since he knows the condition of your liver and the general state of health. Before using the author’s methods of cleansing the liver and gallbladder, you should undergo an examination. Large stones are not removed; they can only be removed surgically. Moreover, if you proceed to expel gallstones without examining them, you may provoke an emergency surgical intervention. Be extremely responsible in relation to your health.

But the fact that the liver will need to be constantly helped to cope with its functions is something everyone who has abnormalities in liver health needs to know. Doctors often prescribe choleretic herbs and drugs in such cases.

Traditional methods of treating congestion in the liver They suggest cleansing the liver with choleretic herbs and herbs.

Liver indicates problems with bitterness in the mouth, heaviness and pain in the right hypochondrium, stool instability, as well as problems with the health of the pancreas.
Of course, in such cases there should be a consultation with the attending physician.
But there are also folk remedies, herbs that have choleretic, diuretic and analgesic effects.

10 gr. Place (1.5 tbsp) St. John's wort herb in an enamel bowl, pour a glass of boiling water (200 ml), close the lid and simmer in a water bath for 30 minutes. Cool, strain, top up boiled water up to 200 ml. Drink 1/3 glass 3 times a day 30 minutes before meals. The decoction can be stored in a cool place for no more than 2 days.

Wash 3 fresh beets. cut into small cubes, put in a three-liter jar, add 2 tablespoons of white flour, 500 grams of sugar. Close the jar with a plastic lid and place in a dark place at room temperature for two days. Stir twice a day. Then add 700 grams of seedless and stemless raisins, 4 cups of sugar, ½ cup of water and leave to ferment for 7 days. Strain, you get 1 liter of beet kvass. The cleansing course requires 3 liters of beet kvass. Take 1 tablespoon before meals 30 minutes. After a 3-month break, repeat the course.

Take 1 tablespoon of a mixture of wild strawberry berries and leaves, brew and leave for 20 minutes. Then strain the infusion and take ½ - 1 glass of infusion 3 times a day for up to 3 weeks. After 2 weeks, treatment can be repeated. Not only the liver is treated, but also the vascular system from salt deposits. Traditional medicine recommends it for diseases of the gastrointestinal tract, gastritis, kidney stones, and vitamin deficiencies. Both fresh fruits and leaves, their aqueous infusion, are used for general loss of strength, anemia, liver disease and biliary tract, with uterine bleeding, jaundice, rickets, hemorrhoids. Very useful for children, especially those weakened after illness fresh berries with milk and sugar - as a nutritious and tonic. The outstanding Swedish botanist Carl Linnaeus, who suffered from gout for many years, got rid of this disease using only one medicine - fresh strawberries.

With the help of smoke weed you can remove bitterness in your mouth, and with the help of chicory you can increase the secretion of bile and eliminate congestion in the liver.
Infusion: 2.tsp. Infuse dry fume grass for 2 hours in 2 cups of boiling water, strain. Drink 0.5 cups 3 times a day before meals for diseases of the liver and biliary tract, cholelithiasis.

Decoction: 1 teaspoon of chopped chicory roots pour 2 tbsp. boiling water, boil for 10-15 minutes. Drink 0.5 tbsp. 3 times a day half an hour before meals.

Infusion: 1 tbsp. crushed chicory roots, pour 1 cup of boiling water, leave for 2 hours, strain. Drink ¼ glass 3-4 times a day before meals.

There are many choleretic herbs, such as immortelle, St. John's wort, milk thistle, calendula, corn silk, strawberry leaves, rose hips, etc. When selecting herbs, it is important to select anti-inflammatory properties, choleretic properties, blood purifying properties, antispasmodic properties.

Pay attention to milk thistle, which not only has choleretic properties, but also restores liver cells during inflammation and restores intestinal motility. Milk thistle is the king herb for liver restoration. You can use it for a long time, up to a year or more, up to full recovery liver cells. Kholmovaya Solyanka has the same property. Milk thistle oil has the same properties. But, I emphasize, it is best to use ground milk thistle powder. The main component of milk thistle is a rare biologically active substance - silymarin. It is silymarin that has a hepatoprotective effect, restoring the affected areas of the liver. It stimulates the formation of new liver cells, protects the liver and kidneys from destruction by alcohol, and has an anti-inflammatory and wound-healing effect in diseases of the gastrointestinal tract. Also used for cirrhosis, hepatitis, jaundice, and weakened immunity. Directions for use: during meals you can take 1 teaspoon of dry powder, or pour a little boiled water and eat with food.

You can consume up to 3 times a day, depending on your health condition. Doctors often recommend to us karsil, a medicine for liver disease, medicinal beginning There is also silymarin there. The course of treatment with Karsil is up to 3 months. But, I think it’s easier and safer to cook it yourself. considering that our pharmacology is now far from reliable.

Make sure that the herbs you consume do not thicken your blood, as this complicates the functioning of the liver.

Grind 1 cup of rose hips in a porcelain or wooden mortar (vitamin C is oxidized in an iron mortar), pour in 1 liter of boiling water, wrap well and leave to infuse for a day. 3 cups oats, rinsed warm water, pour into a 5-liter enamel pan and fill with 4 liters cold water, then close the lid and leave for 24 hours, then add 2 tablespoons of birch buds, 3 tablespoons of lingonberry leaves, bring the mixture to a boil and simmer over low heat for 5 minutes. Then add 2 tablespoons of corn silk and 3 tablespoons of knotweed and simmer over low heat for 15 minutes. Leave the mixture for 45 minutes, strain. Add the prepared rosehip infusion, pour the mixture into dark glass bottles and refrigerate. Take 150 ml 4 times a day half an hour before meals. The last appointment must be no later than 19:00. The course of treatment is 10 days, i.e. you need to prepare 2 such servings of the medicinal composition.

Take a few beets, peel, wash and cook. Next, cook this mixture until it becomes like syrup. Drink ¾ glass several times a day. Experts say that gallstones will dissolve fairly quickly.

And yet, to cleanse the liver of toxins, stagnant bile, cholesterol, and mucus, you sometimes have to do liver tubage. This procedure is simple and can be done with different ingredients. True, the stones are not expelled or dissolved during this procedure. But this procedure will undoubtedly help relieve and help the liver, although you should not abuse this procedure; it is better to do it no more than once a week.

With honey: dilute 1 tablespoon of honey in 1 glass of warm mineral water, drink in sips, put warm heating pad Lie on the liver area for 30 minutes. Then another 1 glass of warm mineral water and leave for 45 minutes. Then have a light breakfast.

With cholenzyme: pour 5-6 dragees into 1 tbsp. warm mineral water and then according to the same principle as described above.

With xylitol: dilute 2-3 teaspoons in 0.5 liters of warm water, divide into 2 doses. And take it the same way as in the first two methods.

For biliary dyskinesia, pay attention to nervous system, eliminate stress in your life.

Liver enlargement- hepatomegaly - noted in cases where the size of this the most important body exceeds natural, anatomically determined parameters. As doctors emphasize, this pathology cannot be considered a separate liver disease, since it is a symptom characteristic of many diseases, including those affecting other human organs and systems.

The danger of liver enlargement lies in complications of liver failure and other pathological conditions that disrupt normal functioning of this body and create many serious problems with health.

Therefore, it is worth talking about such a common pathology as liver enlargement in more detail.

Causes of liver enlargement

Perhaps the list below, including the causes of liver enlargement, is incomplete, but it should make one realize the true scale of its pathogenesis and get an answer to the question - is liver enlargement dangerous?

So, an enlarged liver in an adult can be a consequence of:

As a rule, there is an increase in the lobe of the liver, and an increase in the right lobe of the liver (which has a higher functional load in the functioning of the organ) is diagnosed more often than an enlargement of the left lobe of the liver. However, there is nothing good in this either, since left lobe is so close to the pancreas that it may be this gland that is causing the problem.

Simultaneous enlargement of the liver and pancreas is possible due to inflammation of the pancreas (pancreatitis). Inflammation is accompanied by intoxication, and it removes toxins from the blood liver. If the course of pancreatitis takes particularly severe forms, the liver may not cope with its task and increases in size.

Diffuse enlargement of the liver is a clearly non-localized change in the size of its lobules, consisting of hepatocytes (liver cells). For one of the above reasons, hepatocytes begin to die, and glandular tissue gives way to fibrous. The latter continues to grow, thereby enlarging (and deforming) individual areas of the organ, squeezing the hepatic veins and creating the preconditions for inflammation and swelling of the parenchyma.

Symptoms of liver enlargement

A person may not feel a slightly pronounced pathology - an enlargement of the liver by 1 cm or an enlargement of the liver by 2 cm. But the process of changing the natural size of the liver sooner or later begins to manifest itself with more obvious clinical symptoms.

The most typical symptoms of liver enlargement are: weakness and fatigue, which patients feel even in the absence of intense exercise; discomfort(heaviness and discomfort) in the abdominal cavity; attacks of nausea; weight loss. Further heartburn, halitosis (permanent bad smell from the mouth) itchy skin and dyspepsia.

Liver enlargement due to hepatitis is accompanied not only by general malaise, but also by yellowness of the skin and sclera, increased temperature, aches in all joints, nagging pain in the area of the right hypochondrium.

Liver enlargement in cirrhosis occurs against the background of the same set of symptoms, which are accompanied by the following signs of this disease: abdominal pain and an increase in its size, a quickly onset feeling of satiety when eating, increased drowsiness during the day and insomnia at night, nosebleeds and bleeding gums, weight loss, hair loss, decreased ability to remember information. In addition to the enlargement of the liver with cirrhosis (first of both lobes, and then more of the left), the size of the spleen in half of the patients also increases, and doctors determine that they have hepatosplenomegaly - an enlargement of the liver and spleen.

In the clinical manifestation of damage to the body by the human immunodeficiency virus, liver enlargement in HIV is diagnosed at stage 2B - in acute HIV infection without secondary diseases. In addition to the enlargement of the liver and spleen, at this stage there are febrile state, skin swelling and rashes on the mucous membranes of the mouth and pharynx, enlarged lymph nodes, as well as dyspepsia.

Fatty hepatosis with liver enlargement

Fatty hepatosis (or steatosis), according to the latest WHO data, affects 25% of European adults and up to 10% of children and adolescents. In Europe, “fatty liver” develops in 90% of alcohol abusers and 94% of obese people. Regardless of the underlying cause of the pathology, fatty hepatosis with liver enlargement progresses to cirrhosis within eight years in 10-12% of patients. And when accompanying inflammations liver tissue - into hepatocellular carcinoma.

In addition to alcohol intoxication of the liver and obesity, this disease is associated with impaired glucose tolerance in type II diabetes mellitus and pathology of the metabolism of cholesterol and other fats (dyslipidemia). From the point of view of pathophysiology, fatty hepatosis with or without liver enlargement develops due to metabolic damage fatty acids, which can be caused by an imbalance between energy consumption and energy expenditure. As a result, an abnormal accumulation of lipids, in particular triglycerides, occurs in the liver tissue.

Under the pressure of accumulated fat and the resulting fatty infiltrates, parenchyma cells lose viability, the size of the liver grows, and the normal functioning of the organ is disrupted.

On early stages fatty hepatosis may not have obvious symptoms, but over time, patients begin to complain of nausea and increased gas formation in the intestines, as well as heaviness or pain in the hypochondrium on the right.

Liver enlargement in heart failure

The functional interaction of all body systems is so close that liver enlargement in heart failure is an indicator of a decrease in blood output from the right ventricle of the heart and a consequence of circulatory disorders.

At the same time, blood circulation in the liver vessels slows down, venous stagnation forms (hemodynamic dysfunction), and the liver swells, increasing in size. Since heart failure is most often chronic, prolonged oxygen deficiency inevitably leads to the death of some liver cells. In their place, connective tissue cells grow, forming entire areas that disrupt the functioning of the liver. These zones enlarge and thicken, and at the same time the liver (most often its left lobe) enlarges.

In clinical hepatology, this is called hepatocellular necrosis and is diagnosed as cardiac cirrhosis or cardiac fibrosis. And cardiologists in such cases make a diagnosis of cardiogenic ischemic hepatitis, which, in essence, is an enlargement of the liver in heart failure.

Enlarged liver in a child

There are many reasons for an enlarged liver in a child. So, it could be syphilis or tuberculosis, generalized cytomegaly or toxoplasmosis, congenital hepatitis or bile duct abnormalities.

With this pathogenesis, not only a moderate enlargement of the liver, but also strong increase liver with significant compaction of the parenchyma can be established by the end of the first year of the child’s life.

Enlargement of the liver and spleen in infants - the so-called hepatolienal syndrome or hepatosplenomegaly - is the result of a congenital elevated level of immunoglobulins in the blood (hypergammaglobulinemia). This pathology, in addition to the enlargement of these organs, manifests itself in a delay general development child, poor appetite and very pale skin. Enlargement of the liver and spleen (with icteric symptoms) occurs in newborns with congenital aplastic anemia, which occurs due to the destruction of red blood cells, as well as due to extramedullary hematopoiesis - when red blood cells are formed not in the bone marrow, but directly in the liver and spleen.

Fatty hepatosis with liver enlargement in children develops in almost half of cases due to a significant excess age standards body weight. Although this pathology can occur with some chronic diseases Gastrointestinal tract, after long-term use of non-steroidal anti-inflammatory drugs, antibacterial or hormonal therapy.

Diagnosis of liver enlargement

Diagnosis of liver enlargement begins with a physical examination of the patient and palpation of the internal organs of the abdominal cavity to the right of the midline of the abdomen - in the epigastric region.

During a medical examination, the doctor may detect severe enlargement of the liver. What does it mean? This means that the liver protrudes from under the edge of the costal arch much more than expected by the anatomical norm (in an adult of average height this is no more than 1.5 cm), and can be felt significantly below the edge of the ribs. Then it is stated that the liver is enlarged by 3 cm, the liver is enlarged by 5 cm, or the liver is enlarged by 6 cm. But the final “verdict” is made only after a comprehensive examination of the patient, primarily using ultrasound.

An enlarged liver on ultrasound confirms that there is, for example, “an enlarged liver of a homogeneous hyperechoic structure with a displacement towards the stomach, the contours are unclear” or that “diffuse hyperechogenicity of the liver and unclear vascular pattern and borders of the liver have been identified.” By the way, in an adult, a healthy liver has the following parameters (on ultrasound): the anteroposterior size of the right lobe is up to 12.5 cm, the left lobe is up to 7 cm.

In addition to ultrasound examination, the following is used in the diagnosis of liver enlargement:

biochemical analysis

laboratory tests

radioisotope scanning

Enlarged liver lymph nodes during ultrasound examination are noted by hepatologists in all types of liver cirrhosis, viral hepatitis, tuberculosis of the lymph nodes, lymphogranulomatosis, sarcoidosis, Gaucher disease, drug-induced lymphadenopathy, HIV infection, pancreatic cancer.

Treatment of liver enlargement

Treatment of liver enlargement is treatment of the symptom, but, by and large, complex therapy of the specific disease that led to pathological change of this body.

Drug therapy for a hypertrophied liver must be supported by proper nutrition, diet and vitamin intake. According to experts, in some diseases accompanied by liver enlargement, damaged parenchyma and normal sizes the organ can be restored.

For the regeneration of liver cells, they normal functioning and protection from negative impact Hepatoprotective drugs are used - special medications for liver enlargement.

The drug Gepabene is a hepatoprotector of plant origin (synonyms - Karsil, Levasil, Legalon, Silegon, Silebor, Simepar, Geparsil, Hepatofalk-Planta). The active substances of the drug are obtained from extracts of fumaria officinalis (protipin) and milk thistle fruits (silymarin and silibinin). They stimulate the synthesis of proteins and phospholipids in damaged liver cells, inhibit the formation of fibrous tissue and accelerate the process of parenchyma restoration.

This drug is prescribed for toxic hepatitis, chronic inflammatory diseases of the liver, disorders of its metabolism and functions with liver enlargement of various etiologies. It is recommended to take one capsule three times a day (with meals). The minimum course of treatment is three months. Among the contraindications of this drug are acute forms of inflammation of the liver and bile ducts, age under 18 years. For hemorrhoids and varicose veins, Gepabene is used with caution. During pregnancy and lactation, the drug is used only as prescribed by a doctor and under his supervision. Possible side effects manifested by laxative and diuretic effects, as well as the appearance skin rash. Taking Gepabene is incompatible with drinking alcohol.

The therapeutic effect of the drug Essentiale (Essentiale Forte) is based on the action of phospholipids (complex fat-containing compounds), which are similar in structure to the natural phospholipids that make up human tissue cells, ensuring their division and restoration in case of damage. Phospholipids block the growth of fibrous tissue cells, due to which this drug the risk of developing liver cirrhosis is reduced. Essentiale is prescribed for liver steatosis, hepatitis, cirrhosis of the liver and its toxic lesions. Standard dose is 1-2 capsules three times a day (with meals). Side effects (in the form of diarrhea) are rare.

The drug Essliver differs from Essentiale in the presence in its composition - along with phospholipids - of vitamins B1, B2, B5, B6 and B12. And the combined hepatoprotective medicine Phosphogliv (in capsules), in addition to phospholipids, contains glycyrrhizic acid, which has anti-inflammatory and antioxidant properties. It helps reduce damage to hepatocyte membranes during inflammation and liver enlargement, as well as normalize metabolic processes. The method of administration and dosage of the last two drugs are similar to Essentiale.

Medicines for liver enlargement include a drug based on the artichoke sativum plant - Artichol (synonyms - Hofitol, Cynarix, Artichoke extract). This medicine helps improve the condition of liver cells and normalize their functioning. Doctors recommend taking this drug 1-2 tablets three times a day (before meals). The course of treatment lasts from two weeks to a month, depending on the severity of the disease. Side effects may include heartburn, diarrhea, and stomach pain. And contraindications to its use are obstruction urinary tract and bile ducts, gallstones, as well as severe forms of renal and liver failure.

Besides the fact that medicinal plants are the basis of many hepatoprotective drugs; herbs for liver enlargement are widely used in the form of infusions and decoctions prepared at home. For this pathology, herbalists advise using dandelion, corn silk, calendula, sandy immortelle, yarrow, peppermint. Standard recipe water infusion: for 200-250 ml of boiling water, take a tablespoon of dry herbs or flowers, brew with boiling water, infuse until cool, strain and take 50 ml 3-4 times a day (25-30 minutes before meals).

Diet for liver enlargement

A strictly followed diet for liver enlargement is the key successful treatment. With a hypertrophied liver, you need to completely avoid eating fatty, fried, smoked and spicy foods, since such foods overload the liver and the entire digestive system.

In addition, the diet for liver enlargement is incompatible with such food products, like legumes, radishes, radishes, spinach and sorrel; sausage and spicy cheeses; margarine and spreads; white bread and pastries; vinegar, mustard and pepper; cream confectionery, chocolate and ice cream; carbonated drinks and alcohol.

Everything else (especially vegetables and fruits) can be eaten, at least five times a day, but little by little. It is not recommended to eat after 19:00 even if the liver is healthy, and if the liver is enlarged, it is strictly forbidden. But a glass of water with a spoonful of natural honey is possible and necessary.

IN daily diet there should be 100 g of animal proteins, about the same amount of vegetable proteins and 50 g vegetable fats. The volume of carbohydrate food is 450-500 g, while sugar consumption should be reduced to 50-60 g per day, and salt to 10-12 g. The daily volume of liquid (excluding liquid food) is at least 1.5 liters.

Prevention of liver enlargement

The best prevention of liver enlargement caused by excess weight or addiction to strong drinks, you know what it is. Nothing will work out here without following the principles of a healthy lifestyle...

Unfortunately, it is impossible to predict how the liver will behave and how much it may enlarge, for example, with hepatitis, mononucleosis, Wilson's disease, hemochromatosis or cholangitis. But even in such cases rational nutrition, consumption of vitamins, physical activity, hardening and giving up bad habits will help the liver cope with cleansing the blood of toxins, producing bile and enzymes, regulating protein, carbohydrate and fat metabolism in the body. Also, to help the liver when there is a threat of hepatomegaly, B vitamins, vitamin E, zinc (to restore liver tissue) and selenium (to increase overall immunity and reduce the risk of inflammatory liver diseases) are especially needed.

Forecast for liver enlargement

The prognosis for liver enlargement is quite alarming. Since pronounced signs This pathology does not appear immediately; treatment in a third of cases begins when the process reaches the “point of no return.” And most likely consequences liver enlargement – partial or complete loss of its functionality.

Liver in congestive heart failure

Morphological changes

In those who die from heart failure, the process of autolysis in the liver occurs especially quickly. Thus, the material obtained during autopsy does not make it possible to reliably assess intravital changes in the liver in heart failure.

Macroscopic picture. The liver, as a rule, is enlarged, with a rounded edge, its color is purple, the lobular structure is preserved. Sometimes nodular accumulations of hepatocytes (nodular regenerative hyperplasia) can be detected. The section reveals dilatation of the hepatic veins, their walls may be thickened. The liver is full of blood. Zone 3 of the hepatic lobule is clearly defined with alternating yellow (fatty changes) and red (hemorrhage) areas.

Microscopic picture. As a rule, the venules are dilated, the sinusoids flowing into them are full-blooded in areas of varying length - from the center to the periphery. In severe cases, severe hemorrhages and focal necrosis of hepatocytes are determined. They contain various degenerative changes. In the area of the portal tracts, hepatocytes are relatively preserved. The number of unchanged hepatocytes is inversely related to the degree of atrophy of zone 3. During biopsy, pronounced fatty infiltration is detected in a third of cases, which does not correspond to the usual picture at autopsy. Cellular infiltration is insignificant.

The brown pigment lipofuscin is often found in the cytoplasm of degenerative zone 3 cells. When hepatocytes are destroyed, it can be located outside the cells. In patients with severe jaundice, bile thrombi are detected in zone 1. In zone 3, hyaline bodies resistant to diastase are detected using the PHIK reaction.

The reticular fibers in zone 3 are compacted. The amount of collagen is increased, sclerosis is determined central vein. Eccentric thickening of the venous wall or occlusion of zone 3 veins and perivenular sclerosis extend deep into the hepatic lobule. In long-term or recurrent heart failure, the formation of “bridges” between the central veins leads to the formation of a ring of fibrosis around the unchanged area of the portal tract (“reverse lobular structure”). Subsequently, as the pathological process spreads to the portal zone, mixed cirrhosis develops. True cardiac cirrhosis of the liver is extremely rare.

Pathogenesis

Hypoxia causes degeneration of zone 3 hepatocytes, dilation of sinusoids and slower bile secretion. Endotoxins entering the system portal vein through intestinal wall, may exacerbate these changes. The absorption of oxygen from the blood of the sinusoids increases compensatoryly. A slight impairment of oxygen diffusion may result from sclerosis of the space of Disse.

A decrease in blood pressure with low cardiac output leads to necrosis of hepatocytes. The increase in pressure in the hepatic veins and the associated stagnation in zone 3 are determined by the level of central venous pressure.

Thrombosis arising in the sinusoids can spread to the hepatic veins with the development of secondary local portal vein thrombosis and ischemia, loss of parenchymal tissue and fibrosis.

Clinical manifestations

Patients are usually slightly icteric. Severe jaundice is rare and is found in patients with chronic congestive insufficiency due to ischemic heart disease or mitral stenosis. In hospitalized patients, the most common cause An increase in the concentration of bilirubin in the serum is caused by diseases of the heart and lungs. Long-term or recurrent heart failure leads to increased jaundice. In edematous areas, jaundice is not observed, since bilirubin is bound to proteins and does not enter the edematous fluid with low content squirrel.

Jaundice is partly hepatic in origin, and the greater the extent of zone 3 necrosis, the greater the severity of the jaundice.

Hyperbilirubinemia due to pulmonary infarction or stagnation of blood in the lungs creates an increased functional load on the liver under hypoxic conditions. In a patient with heart failure, the appearance of jaundice in combination with minimal signs of liver damage is characteristic of a pulmonary infarction. An increase in the level of unconjugated bilirubin is detected in the blood.

The patient may complain of pain in the right abdomen, most likely caused by stretching of the capsule of the enlarged liver. The edge of the liver is dense, smooth, painful, and can be detected at the level of the navel.

Increased pressure in the right atrium is transmitted to the hepatic veins, especially with tricuspid valve insufficiency. When using invasive methods, the curves of pressure changes in the hepatic veins in such patients resemble the pressure curves in the right atrium. Palpable expansion of the liver during systole can also be explained by pressure transmission. In patients with tricuspid stenosis, presystolic pulsation of the liver is detected. Liver swelling is detected by bimanual palpation. In this case, one hand is placed in the projection of the liver in front, and the second - on the area of the posterior segments of the right lower ribs. Increasing the size will make it possible to distinguish liver pulsation from pulsation in epigastric region, transmitted from the aorta or hypertrophied right ventricle. It is important to establish the connection between pulsation and the phase of the cardiac cycle.

In patients with heart failure, pressure on the liver area leads to increased venous return. The impaired functionality of the right ventricle does not allow it to cope with the increased preload, which causes an increase in pressure in the jugular veins. Hepatojugular reflux is used to detect the pulse in the jugular veins, as well as to determine the patency of the venous vessels connecting the hepatic and jugular veins. In patients with occlusion or block of the hepatic, jugular or main veins of the mediastinum, reflux is absent. It is used in the diagnosis of tricuspid regurgitation.

Pressure in the right atrium is transmitted to the vessels up to the portal system. Pulsed duplex Doppler can detect increased portal vein pulsation; in this case, the amplitude of the pulsation is determined by the severity of heart failure. However, phasic fluctuations in blood flow are not found in all patients with high pressure in the right atrium.

Ascites has been associated with significantly increased venous pressure, low cardiac output, and severe necrosis of zone 3 hepatocytes. This combination is found in patients with mitral stenosis, tricuspid valve insufficiency, or constrictive pericarditis. In this case, the severity of ascites may not correspond to the severity of edema and clinical manifestations congestive heart failure. The high protein content in ascitic fluid (up to 2.5 g%) corresponds to that in Budd-Chiari syndrome.

Brain hypoxia leads to drowsiness and stupor. Sometimes there is a detailed picture hepatic coma. Splenomegaly is common. Other signs of portal hypertension are usually absent, except in patients with severe cardiac cirrhosis in combination with constrictive pericarditis. At the same time, in 6.7% of 74 patients with congestive heart failure, autopsy revealed esophageal varices, of which only one patient had an episode of bleeding.

On CT immediately after intravenous administration of a contrast agent, retrograde filling of the hepatic veins is noted, and in the vascular phase there is a diffuse uneven distribution of the contrast agent.

In patients with constrictive pericarditis or long-term decompensated mitral disease heart with the formation of tricuspid insufficiency, one should assume the development cardiac cirrhosis liver. With implementation surgical methods treatment of these diseases, the incidence of cardiac cirrhosis has decreased significantly.

Changes in biochemical parameters

Biochemical changes are usually moderate and are determined by the severity of heart failure.

The serum bilirubin concentration in patients with congestive heart failure usually exceeds 17.1 µmol/L (1 mg%), and in a third of cases it is more than 34.2 µmol/L (2 mg%). Jaundice may be severe, with bilirubin levels greater than 5 mg% (up to 26.9 mg%). Bilirubin concentration depends on the severity of heart failure. In patients with advanced mitral heart disease normal level serum bilirubin during its normal uptake by the liver is explained by the organ’s reduced ability to excrete conjugated bilirubin due to a decrease in hepatic blood flow. The latter is one of the factors in the development of jaundice after surgery.

Alkaline phosphatase activity may be slightly elevated or normal. Maybe slight decrease Serum albumin concentrations, which are facilitated by intestinal protein loss.

Forecast

The prognosis is determined by the underlying heart disease. Jaundice, especially severe, is always an unfavorable sign in heart disease.

Cardiac cirrhosis in itself is not a bad prognostic sign. With effective treatment of heart failure, compensation for cirrhosis can be achieved.

Liver dysfunction and cardiovascular abnormalities in childhood

In children with heart failure and “blue” heart defects, liver dysfunction is detected. Hypoxemia, venous congestion, and decreased cardiac output lead to increased prothrombin time, increased bilirubin levels, and increased serum transaminase activity. The most pronounced changes are found with reduced cardiac output. Liver function is closely related to the condition of the cardiovascular system.

Liver with constrictive pericarditis

In patients with constrictive pericarditis, clinical and morphological signs of Budd-Chiari syndrome are detected.

Due to significant compaction, the liver capsule resembles icing sugar (“ glazed liver » — « Zuckergussleber"). Microscopic examination reveals a picture of cardiac cirrhosis.

There is no jaundice. The liver is enlarged, compacted, and sometimes its pulsation is detected. There is pronounced ascites.

It is necessary to exclude liver cirrhosis and hepatic vein obstruction as a cause of ascites. Diagnosis is facilitated by the presence of paradoxical pulsus, venous pulsation, pericardial calcifications in the patient, characteristic changes with echocardiography, electrocardiography and cardiac catheterization.

Treatment is aimed at eliminating cardiac pathology. Patients who have undergone pericardiectomy have a favorable prognosis, but recovery of liver function is slow. Within 6 months after successful operation There is a gradual improvement in functional indicators and a decrease in liver size. You can't expect complete reverse development cardiac cirrhosis, but fibrous septa in the liver become thinner and become avascular.

Cardiac cirrhosis of the liver

Cardiac, or cardiac cirrhosis of the liver develops as a consequence of chronic heart failure.

This type of cirrhosis is classified as secondary, because It is not caused by liver pathology, but by a disease of another organ.

What is chronic heart failure?

Chronic heart failure is a chronic pathological condition, which is due to a decrease contractility myocardium.

This condition can be caused by many factors, including high blood pressure, heart defects, alcohol abuse, diabetes mellitus, inflammatory heart diseases, ischemic disease hearts, etc.

There are left and right ventricular heart failure. It is chronic failure of the right ventricle in the final stages that leads to cardiac cirrhosis of the liver.

Chronic heart failure develops under the influence of pathological factors that lead to the following:

Organic or functional disorders of the heart muscle, heart valves (heart defects)
Excessive heart work (alcoholism, diabetes, blood pressure, etc.)
Combination of the first two factors

For these reasons, symptoms of chronic right ventricular heart failure develop:

Shortness of breath, first during exercise, then at rest
Decreased performance
Edema of the upper and lower extremities
Liver damage

Causes of development of cardiac cirrhosis of the liver

Right ventricular failure means that the heart does not fully perform its function as a blood pump. The speed of blood flow decreases big circle blood circulation, which includes the liver.

Blood stagnation begins, both in the liver and in other organs. Due to high blood pressure, the liquid part of the blood passes into the liver tissue, causing swelling.

Hypoxia of hepatocytes
Reduction and necrosis of hepatocytes
Development of portal hypertension
Collagen formation, fibrosis
With increased blood stagnation, the proliferation of connective tissue and the destruction of the liver structure intensify

Symptoms of cardiac cirrhosis of the liver

Liver cirrhosis associated with cardiac pathology is characterized by all the symptoms of other types of disease:

Fatigue, loss of appetite, weight loss
Gastrointestinal disorders (flatulence, vomiting, nausea)
Varicose veins
Abdominal enlargement, ascites
Edema of the lower extremities
Bleeding from the esophagus, stomach, etc.
Jaundice
Increased body temperature
Signs of hepatic encephalopathy (changes in the rhythm of sleep and wakefulness, difficulty performing usual activities, changes in behavior, etc., up to impairment of consciousness)
Pain in the right hypochondrium
Enlarged liver, spleen
Jellyfish head - dilation of veins on the skin of the abdomen

There are also signs that are typical for congestive liver:

Disappearance or reduction of symptoms of cardiac cirrhosis after treatment of heart failure, bringing positive results
On initial stages during the process, the liver is enlarged, soft to the touch, later the liver becomes of a typical dense consistency
With palpation and pressure on the liver area, the veins of the neck swell

However, when further development process, treatment of heart failure does not affect liver pathology. This means that cardiac cirrhosis of the liver has fully developed.

Also, cardiological cirrhosis of the liver is characterized by changes in blood tests (anemia, leukocytosis), urine (erythrocytes, protein), feces (acholia - decreased stercobilin), blood biochemistry (increased transaminases, alkaline phosphatase, gamma-GGT, fructose-1-phosphate aldolase, arginase, prothrombin time, bilirubin, globulin, decreased albumin, cholesterol, fibrinogen, prothrombin.

Ultrasound reveals an enlarged liver with uniformly increased echogenicity and an enlarged spleen. Liver biopsy gives a characteristic picture of cirrhosis if possible.

Cardiac cirrhosis of the liver: treatment

First of all, a diet is prescribed with a limit on fatty, fried, smoked foods, salt and spices are limited. A complete rejection of bad habits is necessary.

The following drugs are used to correct chronic heart failure:

Cardiac glycosides (digoxin, dobutamine) are used to strengthen and protect the myocardium
Beta-blockers (atenolol, bisoprolol, metoprolol, propronalol, bopindolol, timolol) are necessary to normalize blood pressure
Diuretics (hypothiazide, spironolactone, furosemide) reduce swelling, they also help in the treatment of ascites

For the treatment of cardiac cirrhosis of the liver, various groups of drugs are used, depending on the degree of activity and stage of compensation:

Vitamin therapy (vitamins of groups B, C are prescribed)
Hepatoprotectors – drugs that protect the liver from damage (Essentiale, Heptral)
If complications occur, they are treated

Cardiac cirrhosis of the liver: prognosis

The prognosis, as in the case of other types of cirrhosis, depends on the stage of compensation. Compensated cirrhosis allows you to live quite a long time, often more than 10 years.

Decompensated cardiac cirrhosis of the liver has a much worse prognosis: most often the life expectancy is no more than 3 years. If bleeding develops, the prognosis is poor: mortality is about 40%.

Ascites also affects life expectancy for the worse. The 3-year survival rate is only 25%.

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Congestive liver is observed in chronic heart failure, which is a common complication all organic heart diseases (defects, hypertension and coronary disease, constrictive pericarditis, myocarditis, infective endocarditis, fibroelastosis, myxoma, etc.), a number chronic diseases internal organs (lungs, liver, kidneys) and endocrine diseases(diabetes mellitus, thyrotoxicosis, myxedema, obesity).

The appearance of the first signs of heart failure depends on a number of reasons, including a combination of several diseases, the patient’s lifestyle, and the addition of intercurrent diseases. In some patients, from the moment organic disease In the heart, decades pass before the first signs of heart failure appear, and sometimes it develops quite quickly following organic damage to the heart.

Clinical picture

The first signs of chronic heart failure are palpitations and shortness of breath during exercise. Over time, tachycardia becomes constant, and shortness of breath occurs at rest, and cyanosis appears. IN lower parts Moist rales are heard from the lungs. The liver enlarges, swelling appears in the legs, then fluid accumulates in the subcutaneous tissue and on the body, in the serous cavities, anasarca develops.

In the first stages of heart failure, the liver enlarges in the anteroposterior direction and is not palpable. An enlarged liver can be detected using instrumental studies(rheohepatography, ultrasound). With the increase of heart failure, the liver noticeably enlarges, and it is palpated in the form of a painful edge protruding from the hypochondrium. Liver pain on palpation is associated with stretching of its capsule. The severity and pressing pain in the right hypochondrium, bloating. The liver is noticeably enlarged, sensitive or painful, its surface is smooth, its edge is sharp. Jaundice is often observed. Liver function tests are moderately altered. These changes are in most cases reversible.

Histological examination of liver biopsies reveals dilation of the central veins and sinusoids, thickening of their walls, atrophy of hepatocytes, and the development of centrilobular fibrosis (congestive liver fibrosis). Over time, fibrosis spreads to the entire lobule (septal congestive cirrhosis liver).

Diagnostics

Identify a disease that may be causing heart failure. Correct assessment of tachycardia and detection of signs of venous stagnation play an important role. Of no small importance is the favorable dynamics of symptoms during treatment with cardiac glycosides and diuretics.

Treatment

Treatment is successful if the underlying disease that led to heart failure is correctly recognized and appropriate causal therapy is carried out. Patients are limited in physical activity, fluid intake and table salt.

In case of insufficient efficiency general events cardiac glycosides are used orally, long-term or permanently (digoxin, digitoxin, isolanide, celanide, acetyldigitoxin, adonis infusion), thiazides (furosemide, brinaldix, hypothiazide, yurinex, burinex, uregit, etc.) and potassium-sparing diuretics (triamterene, triampur, amiloride, moduretic, veroshpiron). The choice of a diuretic drug and the method of its use are determined by the degree of edema syndrome, the stage of heart failure and tolerability.