Expansive liver pulsation
Clinical manifestations of cardiogenic cirrhosis. Patients with congestive heart failure and passive liver congestion are mostly symptoms and signs caused by severe heart failure, while liver involvement is secondary. There may be mild right upper abdominal discomfort, 10% to 20% have jaundice. Physical examination may have congestive heart failure, including jugular vein engorgement and positive jugular venous return. Most patients have hepatomegaly, a few can be highly swollen, 50% of patients have more than 5cm under the costal margin, and there are secondary three. The cusp regurgitation can reach the expansive liver pulsation. With the formation of liver fibrosis, the liver can be retracted to normal, 15% of patients have ascites, and 25% have splenomegaly.
Any disease that causes the blood in the inferior vena cava to be blocked can cause hepatic congestion, such as rheumatic valvular heart disease, chronic constrictive pericarditis, hypertensive heart disease, ischemic heart disease, pulmonary heart disease, congenital heart disease. Wait.
Rheumatic heart valve disease is the first in cardiogenic cirrhosis, rheumatoid heart valve disease is about 4% to 12% with cardiogenic cirrhosis, cardiogenic cirrhosis is 53.2% caused by rheumatic heart valve disease, rheumatic heart valve When the disease causes congestive heart failure, the right atrium and right ventricle pressure increase, affecting hepatic venous blood return and causing hepatic congestion and cirrhosis.
In chronic constrictive pericarditis, the hypertrophic pericardium compresses the heart, which greatly limits the diastolic filling of the heart, resulting in increased right ventricular end-diastolic pressure and right atrial pressure, resulting in obstruction of hepatic venous blood flow, continuous increase in hepatic venous pressure, liver Central hepatic sinus dilatation, congestion, hemorrhage, resulting in hypoxia and necrosis of hepatocytes, central reticular fibrous tissue hyperplasia, leading to cardiogenic cirrhosis.
Hypertensive, coronary atherosclerosis, pulmonary origin, congenital heart disease and other right heart failure, can also cause obstruction of hepatic venous blood flow, liver congestion and liver cirrhosis.
The liver is swollen, purple, and blunt. The liver tends to become smaller after the patient's death or at the time of autopsy. The cut surface may be in the form of "musk nutmeg", which is red and white, and the red area is the hemorrhage area, which is located around the portal vein. There is no absolute correlation between the severity of clinically congestive heart failure and the degree of hepatic lobular necrosis.
Congestive liver injury initially involves the central region of the lobules. The lobular central venous congestion, dilatation, and degree of hepatic sinus expansion are different from the distance of the hepatic sinus from the central vein of the lobule. Central hepatocytes of the lobules are compressed, deformed, and atrophied. There is a granular change in the cytoplasm, with nucleus pyknosis, nuclear fission, cell necrosis, accompanied by brown pigmentation. The brown pigment is located in the center of the leaflet and may be caused by cholestatic. The hepatic parenchymal degeneration and necrosis adjacent to the central vein is the most serious. With the aggravation of the congestion, the necrotic tissue extends to the portal area. Patients with severe congestion have only normal liver tissue in the portal area. Over time, the reticular fibers around the central vein can collapse, and the reticular fibrous tissue and fine fiber bundles extend from the central vein to the other central vein. The fiber bridge-like connection between the central veins of adjacent small leaves is cardiogenic. Characteristics of cirrhosis. Because the patient died of cardiovascular disease, it is rare for the liver to develop into a large area of extensive regenerative nodules.
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There was no absolute correlation between the degree of hepatic congestion and abnormal liver function, 80% had sulfonium bromide retention, and 25% to 75% had elevated serum bilirubin. Most of the serum alkaline phosphatase is normal or only slightly elevated, while most other liver diseases are accompanied by an increase in serum alkaline phosphatase, which can also be used to distinguish congestive liver disease from other liver diseases. In acute congested liver, serum transaminases (AST, ALT) were significantly increased, while chronic congested livers were only slightly elevated. Both acute and chronic hepatic congestion, accompanied by albumin reduction and elevated globulin, prolonged prothrombin time, the latter can not be corrected with vitamin K, and gradually returned to normal with the improvement of congestive heart failure. In addition, with congestive heart failure improved, other liver function indicators, especially serum transaminase, will soon return to normal, while sulfonate retention test can be restored after 1 to 2 weeks, low prothrombinemia for several weeks After recovery.
Biochemical indicators are difficult to distinguish between cirrhosis and non-cirrhosis. Cardiac cirrhosis has few abnormal biochemical indicators. It may have died of cardiovascular disease before the patient progressed to cardiogenic cirrhosis. Situation should consider the formation of cardiogenic cirrhosis:
1 severe rheumatic heart disease, especially mitral stenosis.
2 chronic constrictive pericarditis.
3 severe congestive heart failure recurrent or long-term existence.
4 severe liver congestion, but the liver is not large, ascites and splenomegaly.
5 The tricuspid regurgitation was incomplete, but the liver failed to reach the corresponding dilatational pulsation.
2. Liver biopsy is a diagnostic indicator, but hepatic venous pressure increases during congestive heart failure, so liver wear is easy to cause bleeding, need to correct heart failure, liver function can be corrected after liver biopsy. However, if a puncture is urgently needed to confirm the diagnosis, a liver biopsy may be feasible when the prothrombin time and platelets are allowed.
1 severe congestive heart failure patients with passive liver congestion, large liver, tenderness.
2 serum cholic acid and transaminase increased slightly, prothrombin time prolonged, serum alkaline phosphatase did not change significantly.
3 With the improvement of congestive heart failure, liver function tests improved rapidly.
4 liver biopsy tissue examination can help to confirm the diagnosis.
Liver enlargement: Under normal circumstances, the liver is in the upper right side of the abdominal cavity, surrounded by ribs, and under the diaphragmatic iliac crest, generally not accessible under the right rib. For example, when breathing calmly, 1.5 cm or more than 1.5 cm below the right rib can touch the liver, suggesting that the right lobe of the liver is swollen. In the middle of the upper abdomen, the liver should be within the upper third of the line between the xiphoid and the umbilical cord. If the indication is exceeded, the left lobe of the liver is swollen. This is a preliminary judgment of hepatomegaly. There are many causes of hepatomegaly, which can be caused by hepatitis, cirrhosis, portal hypertension or other organ generators.
Lifting a sample beat: refers to a slow, powerful beat of the heart, which can lift the tip of the finger and continue until the second heart sound begins. At the same time, the range of the apex beat increases, which is the body disease of left ventricular hypertrophy. The systolic pulsation of the lower left sternal border is a reliable indication of right ventricular hypertrophy.
Reverse pulsation: When the heart contracts, the anterior wall of the left ventricle hits the chest wall of the anterior region in the early stage of contraction, causing the ribs of the corresponding part to pulsate outward, called the apical beat. After left ventricular myocardial infarction, the ventricular wall is completely necrotic. About 10 to 38% of cases of necrotic myocardium are gradually replaced by fibrous scar tissue to form ventricular aneurysms. The ventricular wall of the thin layer of the lesion bulges outward, and the heart loses its mobility or exhibits abnormal movement when it contracts. The evolution of coronary artery obstruction, myocardial infarction, myocardial fibrosis, and left ventricular ventricular aneurysm was fully recognized as early as 1881.