Congestion in the liver symptoms. congestive cirrhosis

In heart failure, not only the patient's heart suffers, but also other organs, since they are closely related to each other in the process of functioning of the body. With an increase in pressure in the systemic circulation, an overload of the right sections of the heart muscle occurs. As a result, the liver is affected: there are pain, there is an increase in size. congested liver with heart failure a rare event, but when such symptoms appear, the patient needs treatment.

congested liver - pathological condition, characterized by stretching of the body due to stagnation of blood under the influence of high pressure in the veins.

One of secondary causes congestive conditions of the liver is a cardiac symptom. It means that primary factor the development of pathology was not a disease of the organ itself, but a dysfunction in the work of the heart. late stages chronic heart failure is observed in cardiac cirrhosis of the liver.

Insufficiency means the inability of the heart to disperse blood through the vessels with required speed. This leads to its accumulation in the organs, pressure rises, liver edema occurs. Stagnant blood reduces tissue oxygen saturation, and oxygen starvation. This inevitably leads to necrosis of the liver cells, provoking ischemia. Dead hepatocytes are replaced by fibrous tissue cells, cirrhosis gradually develops.

Factors that cause congestion in the liver include:

Lung heart.
Compressive pericarditis.
Mitral valve stenosis.
Tricuspid valve insufficiency.
Cardiomyopathy.
Consequences of the Fontan operation.
Severe pulmonary hypertension.

The primary manifestations of a decompensated state of the heart are shortness of breath and arrhythmia during physical exertion. Gradually, shortness of breath occurs at rest, tachycardia accompanies the patient everywhere. With insufficiency of the left ventricle, there is an accumulation of blood in the pulmonary circle.

The following manifestations are characteristic:

wheezing in the lungs;
sputum interspersed with blood;
blue tint of lips, fingers.

Cirrhosis of the liver is a manifestation of the disease of the right side of the heart. If the decrease in the efficiency of the right ventricle is not the primary phenomenon, blood stasis accompanies the pathology of the left side of the heart muscle for the second time.

At autopsy internal organ is heavy and dense in composition. The color depends on the duration of the stagnation, it varies from red to purple or bluish-brown. Sometimes yellowish spots are observed at the edges of the lobules due to fatty degeneration of the liver cells. In the center of the lobule, the cavity of the vein has a bluish-red color. Such a liver is called "nutmeg". With a long stagnant process, the pattern of the hepatic lobules is erased. fibrous tissue, formed at the site of dead hepatocytes, forms a "false lobularity". With a sudden onset of stagnation, a lot of hemorrhages are recorded.

Anatomical changes and impaired functioning of the liver appear when exposed to increased venous pressure and lack of oxygen at the same time.

Often, in people with heart failure, the manifestation of symptoms of congestive liver is predetermined. This disease inevitably occurs when diagnosing dysfunctions of the heart muscle in the later stages.

Signs of congestion weak heart one for all types of cirrhosis:

Increase in size (At the first stages, the organ grows in front and behind, is not palpable. With the progression of the pathology of the heart, an increase in the liver is seen, it is determined at the bottom of the right rib. Soreness is due to stretching of the liver capsule).
Intense pain under the right rib with a manifestation of heaviness and pressure.
Swelling of the limbs.
An increase in body temperature.
Nausea, vomiting, loss of appetite.
Lethargy, weight loss, fatigue.
Aggressiveness, Bad mood, sleep problems.
An increase in the size of the abdomen.
Symptoms of jaundice.

These manifestations are a reflection of an abnormal process occurring in the liver itself. The patient in parallel may experience pain associated with impaired functioning of the heart.

The cardiac cause of stagnation is indicated by symptoms that occur with right ventricular failure of the heart: swelling of the arms and legs, shortness of breath at rest or during exertion.

Cardiac cirrhosis usually results in ascites that does not respond to drug treatment.

A stagnant internal organ is always an unfavorable phenomenon. Cirrhosis causes activation of the pathological circuit and leads to further complications.

When a patient first visits a doctor, general inspection and clarifies the complaints of a sick person. Disease for a long time may be asymptomatic due to high compensation of liver cells.

Doctors distinguish cardiac cirrhosis from other types of liver damage by the following symptoms:

At the beginning, the enlarged liver has a soft density. Then it hardens and decreases in volume.
Treatment of the heart, which is the main cause of congestive processes, leads to an improvement in the patient's condition.
When you press the liver, the veins in the neck swell.

To detect blood clots, comprehensive examination, which includes the following methods:

Biochemistry of blood ( total protein, enzymes, bilirubin, alkaline phosphatase).
Analysis of the structure and volume of the liver using ultrasound.
Hemostasiogram (blood clotting test).
x-ray chest(examination of the lungs, determination of the size of the heart).
Electrocardiography, echocardiography (analysis of the work of the heart).
Laparocentesis (fluid withdrawal from the abdominal cavity).
Study coronary vessels heart by using angiography.
Puncture biopsy of the liver (with transplantation of the heart muscle).

For a correct diagnosis, the presence of hepatitis, inflammation, the presence of toxic elements in the blood (from alcohol, harmful production) and other types of pathology should be excluded.

Running conditions with stagnation in the liver are almost always asymptomatic. They are found only when clinical research in laboratory conditions.

The only method of preventing congestive cirrhosis is a timely appeal to a cardiologist. success therapeutic methods depends entirely on the correct recognition of the main disease - disorders of the heart. Doctors are not able to completely cure a sick person, but they are able to achieve an extension of life and alleviate the condition.

The life expectancy of patients suffering from cardiac cirrhosis is 3-7 years. Usually leads to death internal bleeding either offensive hepatic coma.

shown moderate rhythm life, reduction of motor loads and individually selected course physical activity. Limited use table salt and liquids. It is useful to follow a diet, balanced diet. Foods that load the liver are strictly prohibited: spices, smoked meats, alcohol, fried and fatty foods.

With low efficiency common events prescribe medications:

Cardiac glycosides (digoxin) for treatment and normal functioning heart muscle.
Beta-blockers (metoprolol) to normalize blood pressure and heart rhythms.

Heart failure (HF) in most cases is associated with dysfunction of the heart muscle. With HF, the level of providing the body with metabolic needs decreases.

Heart failure can be divided into:

systolic;
diastolic.

Systolic heart failure is characterized by contractility hearts. And diastolic is characterized by a failure of the relaxation ability of the heart muscle and an imbalance in the filling of the ventricles.

organic disorders;
Functional disorders;
birth defects;
Acquired diseases, etc.

HF symptoms

Physically, HF manifests itself in a decrease in working capacity and tolerance physical activity. This is demonstrated by the appearance of shortness of breath in heart failure and rapid fatigue. All these symptoms are associated with a quantitative decrease in cardiac output or fluid retention in the body.

As a rule, right ventricular HF is characterized by a whole list of liver disorders. Severe liver congestion is almost always asymptomatic and is detected only in laboratory and clinical studies. The main pathologies for the development of hepatic dysfunction include:

Passive venous congestion(due to pressure increase due to filling);
Impaired blood circulation and decreased cardiac output.

Complications of heart failure

With an increase in CVP (central venous pressure), as a result, the level of liver enzymes and direct and indirect serum bilirubin may increase.

The deterioration in perfusion received sharp decline cardiac output, can result in hepatocellular necrosis with elevated serum aminotransferase index. Liver shock, or cardiogenic ischemic hepatitis, is the result of severe hypotension in patients with HF.

Cardiac cirrhosis or fibrosis can be the result of long-term hemodynamic dysfunction, which is fraught with a functional disorder of the liver, accompanied by coagulation problems, as well as a deterioration in the digestibility of some cardiovascular drugs and make them undesirably toxic, reducing albumin production.

Unfortunately, it is difficult to determine the exact dosage of these preparations.

If we consider this problem From the perspective of pathophysiology and histology, we will see that liver problems associated with venous congestion are characteristic of patients with right-sided type of HF, adjacent to increased pressure in the right ventricle. and it doesn't matter what caused the right-sided heart failure. Any case can be the starting point of hepatic stagnation.

Factors causing stagnation in the liver

Such reasons include:

Constrictive pericarditis;
Severe pulmonary hypertension;
mitral valve stenosis;
Tricuspid valve insufficiency;
Pulmonary heart;
cardiomyopathy;
Consequences of the Fontan operation, with pulmonary atresia and hypoplastic syndrome of the left cardiac sections;
Tricuspid regurgitation (in 100% of cases). It occurs due to right ventricular pressure on the veins and sinusoids of the liver.

With an approximate study of the structure of a congestive liver, its overall increase. The color of such a liver acquires a purple or reddish hue. At the same time, it is supplied with full-blooded hepatic veins. The section clearly shows areas of necrosis and hemorrhage in the 3rd zone and intact or occasionally steatotic areas in the 1st and 2nd zones.

Microscopic examination of the venous hepatic hypertension shows us full-blooded central veins with sinus congestion and hemorrhages. Indifference and inaction in this matter leads to cardiac fibrosis and cirrhosis of the liver of the cardiac type.

Profound systemic hypotension in myocardial infarction, exacerbation of HF, and pulmonary embolism often become good reasons for the development of acute ischemic hepatitis. Conditions such as: obstructive sleep apnea syndrome, respiratory failure, increased metabolic demand is a signal of ischemic hepatitis.

Hepatitis and HF

The use of the term "hepatitis" in this case is not entirely correct, since the inflammatory conditions that infectious hepatitis we don't watch.

development chronic hypoxia in the liver is accompanied by specific protective processes. This process is characterized by an increase in the production of oxygen by liver cells from past (through the liver) flowing blood. But there are conditions under which defense mechanism It does not work. These are persistent inadequate target organ perfusion, tissue hypoxia, and acute hypoxia. In case of damage to hepatocytes, sharp rise: ALT, AST, LDH, serum prothrombin time. It is also possible the onset of functional renal failure.

Temporal development of cardiogenic ischemic hepatitis varies from 1 to 3 days. Normalization of the disease occurs from the fifth to the tenth day from the moment of the first episode of the disease.

Clinical manifestations in patients with left-sided HF are:

shortness of breath;
Orthopnea;
Paroxysmal nocturnal dyspnea;
cough;
Rapid onset of fatigue.

Right-sided CH is characterized by:

peripheral edema;
Ascites;
Hepatomegaly;
Dull stretching pains in the upper right quadrant of the abdomen (rare).

Hepatomegaly is inherent in right-sided chronic heart failure. But it happens that hepatomegaly develops in acute heart failure.

For ascites, only 25% of the total number sick. As for jaundice, it is mostly absent. There is a presystolic pulsation of the liver

Ischemic hepatitis proceeds, in the majority of cases, benignly.

Diagnostics

It is diagnosed inadvertently when an enzymatic increase is detected after systemic hypotension. But systemic hypotension does not only lead to an increase in liver enzymes. Also, after such episodes, createnin increases, nausea, vomiting, impaired eating behavior, pain symptoms in the right upper abdominal quadrant, oliguria, jaundice, tremor, hepatic encephalopathy.

Last year I found out that I have bile stasis. I am within for long years she suffered from pain under her right ribs, suffered from heaviness in her stomach and did not even know what was the matter. When they appeared, I thought that the reason was the fatty and fried foods that were often present in my diet. I got rid of all this quite simply. I took and ate Activated carbon- this eliminated pain in the liver. And the reason, as it turned out later, was in poor bile secretion. But this leads to the fact that the whole process of digestion is disturbed. The liver and intestines suffer. The doctors advised me to stimulate the production of bile. After that, I began to study what can contribute to this process. In the literature, I came across the following advice: in the morning on an empty stomach you need to drink a glass of hot water. Of course, you do not need to drink boiling water, but still the water should be hot enough and boiled. Drinking a glass of water before breakfast will digestive system which will make breakfast easier to digest. Water ensures the awakening of the digestive and biliary systems after a night's sleep.
After that, I began to study products that are useful for stagnation of bile. I have limited sweets. They provoke a weakening of bile secretion. I started cooking vegetable dishes for myself. vegetable oil, especially the vinaigrette, which has beneficial effect for digestion.
Among all the products that are useful for me, I found my favorite. This is a zucchini that I first tried when I was a child. It turned out that it helps to unload the liver. Yes, it also helps good digestion. It contains within itself a large number of substances. A large number of antioxidants that have a rejuvenating effect on the body contained in this vegetable pleased me the most. But for the active manifestation of all this benefit that this vegetable I used it raw. I made salads out of it. Sometimes it was extinguished, but not for long. Pretty simple in terms of cooking is mine favorite dish, which I often cook from zucchini.
To prepare it, you need to take a raw zucchini, wash it, and then cut it into strips. Then add the same amount of cucumber to the resulting mass. After that, the salad is dressed with sour cream. You can decorate it with an egg and slices of tomatoes, which you need to take half as much as cucumbers. You can add a variety of greens.
I think this dish is not only very useful, but also delicious. This healing salad is eaten with great pleasure by many grandchildren. When I have heaviness in the liver area, I exclude the egg from this salad. And then my bile secretion comes in order, thanks to raw zucchini. In the summer months in the country, I consider this salad indispensable, because everyone has zucchini, cucumbers, tomatoes and herbs in the country.
At the personal premiere, I was convinced that the body starts to work better when you tweak your diet a little. It's much better than swallowing pills.

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

At autopsy, the liver is found to be 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 hepatic capsule thickens. Due to secondary fatty degeneration, the liver may have yellowish spots. With a short-term stagnation, the pattern on the section is pronounced, in the center of the lobules the central veins gape redly and at the edges of the hepatic balustrades - capillaries. The color of the liver bumps is very pale compared to the red spots of the gaping vessels. After a long existing 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 a 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 a yellow hepatic tissue that has undergone fatty degeneration, and gaping-looking vessels are distributed along the edges. With a sudden onset of stagnation in the hepatic substance and under the capsule, many hemorrhages are seen. The microscopic picture is characterized by dilated central veins and capillaries, squeezed between them by hepatic cells with fatty drops and with pigment grains. In the center of the lobules, liver cells often die. Microscopic hemorrhages are common.

With a sudden onset of stagnation in the liver, the patient usually feels sharp pain in the area of the liver, which may feel like pain caused by gallstone. Often confused with pleurisy. The pain is caused by a sudden pull on the hepatic 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 with acute infectious diseases sometimes it is difficult to decide whether a sudden enlargement of the liver is a consequence of heart failure or toxic injury. In such cases, you can navigate on the basis of other symptoms (increased venous pressure, tachycardia, ECG, etc.). It should be noted here that, although the basis of congestive liver is venous congestion, there may still be a pronounced congestive liver without an increase in venous pressure. Veins because of great ability expand sometimes over time able to balance high blood pressure, and by the time the increase in venous pressure becomes measurable, congestive liver has long been established.

IN childhood recognition and elucidation of congestive liver is already easier. The lower edge of the liver goes beyond the costal arch, percussion can also establish an increase in the liver upwards. 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. On palpation, a liver is usually evenly compacted with a smooth surface, 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 great ability to receive blood equalizes the tense action of the blood flowing back. In chronic decompensation, growth connective tissue makes the liver so hard that it is no longer possible to reckon with its pulsation. With cardiac pseudocirrhosis, the size of the liver, despite stagnation, may be less than normal.

The functional disorder of the liver with a small stagnation is insignificant, however, with a larger or long-term stagnation, it is still significant. A functional disorder must also be considered 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 the urine increases. Some authors attribute the relationship between the severity of hepatic congestion and the content of urobilinogen in the urine diagnostic value. According to other authors positive result Ehrlich reaction is caused not by urobilinogen, but by stercobilinogen. A significant increase in the concentration of lactic acid in the blood is due to a disorder hepatic function. The content of bilirubin in serum increases significantly only after severe or prolonged stagnation. The patient in such cases has a slight jaundice. The reason for this phenomenon is not fully understood. It is assumed that in the cause of this icterus, liver damage, which occurs in connection with hypoxia, and hemolysis play a role. In favor of the latter is the observation of Magyar and Thoth: an increase in the content of bilirubin in the urine. Jaundice develops slowly and also slowly disappears. In feces, the amount of coloring substances formed from the bile pigment increases.

A disorder of the hepatic function is, with its long existence, one and, possibly, the main reason hypoproteinemia accompanying insufficiency of the right half of the heart. The decrease in the serum protein content of heart patients is partly due to malnutrition, poor conditions absorption, 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 pumping out of edema is often ineffective for a long time after the restoration of the strength of the heart.

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 islets of regenerating liver cells. The proliferation of connective tissue takes place not only around the lobules, but also in their central part. If the proliferation of connective tissue merges, then the pattern of the liver substance becomes unrecognizable. With prolonged stagnation, the capsule thickens due to perihepatitis. For the occurrence of cirrhosis of the liver, it is characteristic that the liver becomes hard, small, with sharp edges, its size is fixed. At the same time, due to portal hypertension, the spleen also begins to swell. It becomes bigger and more solid. In this condition, under the influence of treatment acting on the heart and circulation, neither the magnitude nor functional disorder the liver does not change. Cardiac cirrhosis is usually accompanied by ascites that is not amenable to medical treatment.

In those who died from heart failure, the process of autolysis in the liver proceeds especially rapidly. 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 determined. On the cut, an expansion of the hepatic veins is found, their walls can be thickened. The liver is full-blooded. Zone 3 of the hepatic lobule is clearly defined with alternating yellow ( fat 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 various lengths - from the center to the periphery. In severe cases, pronounced hemorrhages and focal necrosis of hepatocytes are determined. They find various degenerative changes. In the area of the portal tracts, hepatocytes are relatively intact. The number of unchanged hepatocytes is inversely related to the degree of zone 3 atrophy. fatty infiltration are detected in a third of cases, which does not correspond to the usual picture at autopsy. Cellular infiltration is insignificant.

In the cytoplasm of degeneratively altered cells of zone 3, the brown pigment lipofuscin is often found. With the destruction of hepatocytes, it can be located outside the cells. In patients with severe jaundice, biliary thrombi are determined in zone 1. In zone 3, diastasis-resistant hyaline bodies are detected using the PAS reaction.

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 zone 3 vein occlusion and perivenular sclerosis extends 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 zone of the portal tract ("reverse lobular structure"). Later, as it spread pathological process develops into the portal zone mixed cirrhosis. True cardiac cirrhosis of the liver is extremely rare.

Pathogenesis

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

decline blood pressure at low cardiac output leads to hepatocyte necrosis. 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 hepatic veins with the development of secondary local thrombosis of the portal vein 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 against the background of coronary artery disease or mitral stenosis. In hospitalized patients, the most common cause elevated serum bilirubin levels are associated with heart and lung diseases. Long-term or recurrent heart failure leads to increased jaundice. Jaundice is not observed in the edematous areas, 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 prevalence of zone 3 necrosis, the greater the severity of jaundice.

Hyperbilirubinemia due to pulmonary infarction or pulmonary congestion creates increased functional load on the liver under hypoxic conditions. In a patient with heart failure, the appearance of jaundice, combined with minimal signs of liver damage, is characteristic of 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 determined at the level of the navel.

An increase in pressure in the right atrium is transmitted to the hepatic veins, especially with tricuspid valve insufficiency. Using invasive methods pressure curves in the hepatic veins in such patients resemble pressure curves in the right atrium. Palpable enlargement of the liver during systole may also be due to pressure transmission. Patients with tricuspid stenosis show presystolic pulsation of the liver. 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 region of the posterior segments of the right lower ribs. An increase in size will make it possible to distinguish the pulsation of the liver from the pulsation in epigastric region transmitted from the aorta or a hypertrophied right ventricle. It is important to establish a 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. Violated functionality the right ventricle is not allowed to cope with the increased preload, which leads to an increase in pressure in the jugular veins. Hepatojugular reflux is used to detect the pulse on 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.

The pressure in the right atrium is transmitted to the vessels up to the portal system. With pulse duplex Doppler study it is possible to determine the increase in the pulsation of the portal vein; while the amplitude of the pulsation is determined by the severity of heart failure. However, phase 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. High content protein in ascitic fluid (up to 2.5 g%) corresponds to that in Budd-Chiari syndrome.

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

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

In patients with constrictive pericarditis or long-term decompensated mitral defect heart with the formation of tricuspid insufficiency should be assumed to develop cardiac cirrhosis liver. With the introduction surgical methods treatment of these diseases, the incidence of cardiac cirrhosis of the liver has decreased significantly.

Changes in biochemical parameters

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

Serum bilirubin concentration in patients with congestive heart failure usually exceeds 17.1 µmol/l (1 mg%), and in a third of cases 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%). The concentration of bilirubin depends on the severity of heart failure. Patients with advanced mitral heart disease normal level serum bilirubin during its normal uptake by the liver is explained by the reduced ability of the organ to release conjugated bilirubin due to a decrease in hepatic blood flow. The latter is one of the factors in the development of jaundice after surgery.

ALP activity may be slightly elevated or normal. Maybe slight decrease serum albumin concentrations, aided by intestinal protein loss.

Forecast

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

By itself, cardiac cirrhosis is not a poor prognostic sign. At effective treatment heart failure can compensate for cirrhosis.

Impaired liver function and anomalies of the cardiovascular system in childhood

In children with heart failure and "blue" heart defects, abnormal liver function is detected. Hypoxemia, venous congestion and reduced cardiac output lead to an increase in prothrombin time, an increase in bilirubin levels and serum transaminase activity. The most pronounced changes are found with reduced cardiac output. The function of the liver is closely related to the condition of cardio-vascular system.

Liver in constrictive pericarditis

In patients with constrictive pericarditis, clinical and morphological features Budd-Chiari syndrome.

Due to the significant compaction, the liver capsule takes on a resemblance to icing sugar (" glazed liver» - « Zuckergussleber"). At microscopic examination reveal a picture of cardiac cirrhosis.

Jaundice is absent. The liver is enlarged, compacted, sometimes its pulsation is determined. There is marked ascites.

Cirrhosis of the liver and obstruction of the hepatic veins should be excluded as a cause of ascites. Diagnosis is facilitated by the presence in the patient of a paradoxical pulse, pulsation of the veins, calcification of the pericardium, characteristic changes with echocardiography, electrocardiography and cardiac catheterization.

Treatment is aimed at eliminating cardiac pathology. Patients who have undergone pericardectomy have a good prognosis, but recovery of liver function is slow. Within 6 months after successful operation there is a gradual improvement functional indicators and shrinkage of the liver. Can't expect full reverse development cardiac cirrhosis, however, fibrous septa in the liver become thinner and become avascular.