Cardiac cirrhosis

Any disease that causes obstruction of blood return from the inferior vena cava to the heart can lead to liver congestion, such as rheumatic heart valve disease, chronic constrictive pericarditis, hypertensive heart disease, ischemic heart disease, pulmonary heart disease, congenital heart disease, etc.

Rheumatic heart valve disease is the leading cause of heart源性 liver cirrhosis, with approximately 4% to 12% of rheumatic heart valve disease complicated by heart源性 liver cirrhosis. 53.2% of heart源性 liver cirrhosis is caused by rheumatic heart valve disease. When rheumatic heart valve disease causes congestive heart failure, the pressure in the right atrium and right ventricle increases, affecting the return of liver vein blood and causing liver congestion and cirrhosis.

During chronic constrictive pericarditis, the thickened pericardium compresses the heart, greatly limiting the filling of the diastolic period of the heart, causing the end-diastolic pressure of the right ventricle and the pressure of the right atrium to increase, leading to liver vein blood flow obstruction, continuous increase in liver vein pressure, central sinus dilation, congestion, and hemorrhage in the liver, leading to hypoxia and necrosis of liver cells, proliferation of reticular fiber tissue in the central area, and leading to heart源性 liver cirrhosis.

Patients with hypertension, coronary atherosclerosis, pulmonary origin, congenital heart disease, etc., with right heart failure, can also lead to liver vein blood flow obstruction, liver congestion, and liver cirrhosis.

Maceration of the liver can be seen macroscopically, presenting purple color and blunt edges. After death or at autopsy, the liver often becomes smaller, and the cut surface can show a 'nutmeg' shape, with alternating red and white colors. The red area is the hemorrhagic area, located around the portal vein. The severity of clinical congestive heart failure is not absolutely correlated with the degree of lobular necrosis.

Congestive liver injury initially involves the central zone of the lobule. The central vein of the lobule becomes congested and dilated, and the degree of dilation of the sinusoids varies with the distance from the central vein of the lobule. The central hepatocytes of the lobule are compressed, deformed, and atrophic. The cytoplasm shows granular change, with pyknosis, nuclear division, and cell necrosis, accompanied by brown pigment deposition. The brown pigment is located in the central area of the lobule and may be due to cholestasis. The most severe necrosis of the liver parenchyma adjacent to the central vein occurs, and with the worsening of congestion, necrotic tissue extends towards the portal area. In severe cases of congestion, only a small amount of normal liver tissue is present in the portal area. Over time, the reticular fibers around the central vein can collapse, and it can be seen that reticular fiber tissue and fine fiber bundles extend from the central vein to another central vein. This fibrous bridge-like connection between adjacent central veins of the lobules is a characteristic of heart源性 liver cirrhosis. Since most patients die of cardiovascular diseases, liver itself developing into a large area of extensive regeneration nodules is rare.

Prone to electrolyte imbalance, upper gastrointestinal bleeding, ascites, hepatic encephalopathy, and other complications.  

       Upper gastrointestinal bleeding in liver cirrhosis is mostly due to esophageal and gastric fundus varices rupture, but it should be considered whether there is concurrent peptic ulcer, acute hemorrhagic erosive gastritis, esophageal variceal rupture syndrome, and other gastric mucosal lesions. Hemorrhage from variceal rupture is often caused by rough, hard, or angular foods that cause trauma, erosion of the esophagus by gastric acid reflux, severe vomiting, and other factors, leading to hematemesis and black stools. If the amount of bleeding is not much, only black stools may occur. If there is a large amount of bleeding, it can cause shock. Under the condition of ischemia and hypoxia of the liver, liver function often deteriorates, and bleeding causes the loss of plasma proteins, which can lead to the formation of ascites. After the blood in the intestines is decomposed by bacteria to produce ammonia and absorbed by the intestinal mucosa, it can induce hepatic encephalopathy and even lead to death. After bleeding, the previously enlarged spleen can shrink or even not be palpable. Infection, due to the decrease in immune function of the body, splenic hyperfunction, and the establishment of collateral circulation between the portal and systemic veins, the opportunity for pathogenic microorganisms to enter the systemic circulation is increased, so it is prone to various infections, such as bronchitis, pneumonia, tuberculous peritonitis, primary peritonitis, biliary tract infection, and Gram-negative bacillary sepsis, etc. Primary peritonitis refers to the acute peritoneal inflammation in the abdominal cavity of liver cirrhosis patients without organ perforation, with an incidence rate of 3% to 10%, which often occurs in patients with a large amount of ascites, and is mostly caused by Escherichia coli. The reason is that the phagocytic action of phagocytes is weakened during liver cirrhosis, bacteria in the intestines proliferate abnormally, enter the peritoneal cavity through the intestinal wall, and due to the change of vascular structures inside and outside the liver, bacteria can also cause sepsis or carry bacteria lymph fluid from under the liver capsule or from the lymphatic丛 around the hilum of the liver into the peritoneal cavity, causing infection. The clinical manifestations include fever, abdominal pain, abdominal distension, abdominal wall tenderness and rebound pain, increased ascites, increased blood leukocytes, cloudy ascites, which is between exudative and transudative fluid, ascites culture may have bacterial growth. A few patients have no abdominal pain and fever, but are manifested as hypotension or shock, refractory ascites, and progressive liver function failure. Hepatorenal syndrome: When liver cirrhosis is complicated with refractory ascites and not treated appropriately or with poor efficacy, it is easy to appear hepatorenal syndrome.

Changes in secondary sexual characteristics, liver palms, nausea, fatigue, ascites, abdominal distension, liver fibrosis, liver stellate cell proliferation, liver lobe atrophy, liver enlargement

Patients with congestive heart failure accompanied by passive liver congestion are mostly symptoms and signs caused by severe heart failure, while the liver involvement is of secondary importance, and there may be mild right upper abdominal discomfort, 10% to 20% have jaundice, physical examination may show signs of congestive heart failure, including jugular vein distension, positive hepatic jugular vein reflux sign, most patients have liver enlargement, a few can be highly enlarged, 50% of patients have liver size exceeding 5cm below the costal margin, patients with secondary tricuspid regurgitation may feel a distensible liver pulsation, as liver fibrosis forms, the liver can shrink back to normal, 15% of patients have ascites, and 25% have splenomegaly.

The main prevention is myocarditis, prevention and treatment of hypertension and other cardiovascular diseases. The prevention of liver cirrhosis requires the treatment of some etiologies that can cause liver cirrhosis. These disease factors include viral hepatitis, alcoholic liver cirrhosis, genetic and metabolic diseases. All of these are included in the prevention and treatment of liver cirrhosis. The occurrence of liver cirrhosis is closely related to some acute or subacute hepatitis, such as massive necrosis and fibrosis of liver cells, which can develop into liver cirrhosis. Therefore, the treatment of viral hepatitis can be considered as a part of the prevention of liver cirrhosis. In Western and European countries, alcoholic liver cirrhosis accounts for about 50%-90% of all liver cirrhosis. Liver cirrhosis caused by genetic and metabolic diseases, which gradually develop from liver diseases of genetic and metabolic diseases, needs to be prevented by timely treatment of these diseases. Secondly, the prevention of liver cirrhosis is to avoid contact with chemical toxins and drugs. Because long-term use of certain drugs such as diacetylmorphine, methyldopa, tetracycline, or long-term repeated contact with certain chemical toxins such as phosphorus, arsenic, and carbon tetrachloride, can cause toxic hepatitis, and eventually lead to liver cirrhosis. Therefore, in the prevention of liver cirrhosis, it is necessary to minimize contact with these easily accessible chemical toxins or take preventive measures when contacting them. At the same time, attention should be paid to nutritional balance in the prevention of liver cirrhosis to avoid malnutrition. This is mainly because liver cirrhosis caused by malnutrition also occurs occasionally.

Serum alkaline phosphatase, vitamin K, chest X-ray, Doppler echocardiography, liver disease ultrasound diagnosis, electrocardiogram, abdominal X-ray, liver upper and lower margin percussion

Laboratory examination

There is no absolute correlation between the degree of liver congestion and liver function abnormalities. 80% have bromosulfophthalein retention, 25% to 75% have increased serum bilirubin, serum alkaline phosphatase is mostly normal or only slightly increased, while most other liver diseases are accompanied by increased serum alkaline phosphatase, so it can also be used to differentiate congestive liver disease from other liver diseases. In acute congestive liver disease, serum transaminases (AST, ALT) are significantly increased, while chronic congestive liver disease only has slight increase. Whether acute or chronic liver congestion, it is accompanied by decreased albumin and increased globulin, prolonged prothrombin time, which cannot be corrected by vitamin K, and gradually recover to normal with the improvement of congestive heart failure. In addition, with the improvement of congestive heart failure, other liver function indicators, especially serum transaminases, will recover quickly to normal, while the bromosulfophthalein retention test can recover after 1-2 weeks, and hypoprothrombinemia can recover after several weeks.

It is difficult to differentiate liver cirrhosis from non-cirrhosis based on biochemical indicators, and there are few abnormal biochemical indicators in cardiogenic liver cirrhosis, which may be due to the fact that patients die of cardiovascular lesions before they progress to cardiogenic liver cirrhosis. When the following situations occur, consider the formation of cardiogenic liver cirrhosis:

① Severe rheumatic heart disease, especially mitral stenosis;

② Chronic constrictive pericarditis;

③ Recurrent or long-standing severe congestive heart failure;

④ Severe liver congestion, but the liver is not large, with ascites and splenomegaly; ⑤ Tricuspid regurgitation, but the liver has not been palpated with corresponding dilatation pulsation.

Liver biopsy

It is a diagnostic indicator, but when there is congestive heart failure, the pressure in the hepatic veins increases, so liver puncture is prone to bleeding. Heart failure needs to be corrected and liver function needs to be restored before liver biopsy can be performed. However, if urgent liver biopsy is needed to clarify the diagnosis, liver biopsy can also be performed if the prothrombin time and platelet levels are permitted.

1. It is not advisable to eat too much or too varied to avoid excessive growth of intestinal bacteria, leading to bacterial translocation and causing primary peritonitis.

2. Abstain from alcohol, and it is best not to drink at all to avoid exacerbating liver damage.

3. Liver cirrhosis with esophageal varices should absolutely avoid various刺激性 spicy, hot, and hard foods, and vegetables with a high content of dietary fiber should also be eaten cautiously.

4. If there is edema or ascites, a low-salt diet should be followed.

5. Early liver cirrhosis patients can take high-protein diets appropriately to promote liver cell regeneration and enhance the body's immunity. However, if the liver function is poor and there is a tendency towards hepatic coma, a low-protein light diet should be adopted, mainly composed of carbohydrates, and fresh fruits and vegetables should be eaten regularly.

The main treatment for heart failure is to correct or alleviate it, which can be achieved by using diuretics, cardiotonics, and drugs to reduce the afterload of the heart. However, some symptoms of these patients are caused by the liver, such as refractory hypoglycemia and disturbance of consciousness, the latter is also related to reduced cardiac output.

Primary liver cirrhosis itself does not cause severe portal hypertension and esophageal variceal rupture and bleeding, but can lead to splenomegaly and ascites. Liver palms, spider nevi, and 'sea snake heads' are rare. Clinically, the improvement of cardiac function, such as artificial valve replacement, the relief of constrictive pericarditis, and the correction of congenital heart disease, can gradually and even quickly improve liver cell function.