sterile vegetation
Introduction
Introduction A cockroach is a general term for various protrusions formed in the pathological process inside and outside the body or organ. According to its nature, it can be divided into non-neoplastic and neoplastic. In the former, such as bacterial endocarditis, the neoplasms on the endocardium, which are mostly caused by tumors protruding into the heart valve, are affected by blood flow and can be embolized by organs such as brain, kidney and spleen. . Aseptic neoplasms are most common in turbulent areas, scars (such as after infective endocarditis) and areas of intimal damage caused by factors inside and outside the heart. Bacterial infection of aseptic neoplasms depends on: 1 the frequency of bacteremia and the number of bacteria in the circulation, the latter related to the severity of the wound, the infection and the number of bacteria in the mucous membrane of the skin; 2 The ability of bacteria to adhere to platelet microthrombus and fibrin. Streptococcus mutans has a high chance of entering the bloodstream from the oral cavity and has strong adhesion, so it is the primary cause of subacute infective endocarditis. Escherichia coli has poor adhesion, although it is a common bacteremia, but it is rarely heart-felt. Endometritis.
Cause
Cause
The cause has not yet been elucidated. Gross et al believe that rheumatic valvular disease is an important cause of non-bacterial thrombotic endocarditis. Allen and Sirota believe that allergies and vitamin C deficiency are prone to the disease. Williams believes that allergic reactions and circulating immune complexes are the immunological basis of valvular lesions.
1. Mechanisms Williams believes that allergic reactions and circulating immune complexes are the immunological basis of valvular lesions. Mcray and Warlor believe that malignant tumors (especially gastric cancer, pancreatic cancer and lung cancer) and DIC hypercoagulable state, high blood clotting fluid in the valve The turbulence formed by the closure line is an important factor in the formation of a thrombus. Tumor mucin and thrombocytosis, increased levels of fibrinogen or coagulation factors V, VII, XI, and IX, increased fibrinolytic products, accelerated fibrin decomposition, and procoagulant substances produced by tumor cells, all of which cause thrombosis of the valve. important reason. Therefore, any disease that can produce primary or secondary hypercoagulable state is the etiology and pathological basis of non-bacterial thrombotic endocarditis.
Non-bacterial thrombotic endocarditis can involve any heart valve, primarily affecting the mitral and aortic valves. Second, the tricuspid sputum is located in the atrial aortic valve, the pulmonary valve is more than the collateral non-bacterial thrombotic endocarditis, the main pathological change is the formation of aseptic neoplasms on the valve, early changes For the valvular collagen under the influence of allergies, vitamin deficiency, hemodynamic damage and aging, degenerative changes and matrix edema occur, followed by partial exfoliation of the intima of the valve, which exposes collagen and matrix to the bloodstream. When the antibody is in a hypercoagulable state, platelets and the like are liable to adhere to the surface to form non-bacterial thrombotic neoplasms. The lesions are often less inflammatory than the superficial regions, and once the sputum is shed, the signs of arterial embolism may occur.
2. Pathological changes: Allen and Sirota divide the pathological manifestations of non-bacterial thrombotic endocarditis into five types:
Type I: a single small sickle lesion with a diameter <3mm light brown to dark brown, more adherent to the valve.
Type II: Single large scorpion, >3 mm in diameter, yellow-brown, granular, adhering to the valve.
Type III: multiple small sickle lesions, 1 to 3 mm in diameter, fragile, often arranged in a beaded shape along the valve closure line.
Type VI: multiple large sputum lesions, all > 3mm soft and brittle, the same size and color.
Type V: old type (healing type), the surface is covered with epithelial cells, and the color and density are similar to the attached valve tissue. The early pathological changes of the disease are caused by factors such as valvular allergic reaction, vitamin C deficiency, hemodynamic damage and aging. Degenerative changes and stromal edema are followed by local exfoliation of the intima of the valve, exposing collagen and matrix to In the blood flow, especially when the body is in a hypercoagulable state, it is easy to cause platelets and the like to adhere to the collagen tissue, and the non-bacterial thrombotic neoplasms often have no inflammatory reaction locally, and the lesions are more superficial. Once the neoplasm is shed, it can cause signs of arterial embolism.
Examine
an examination
Related inspection
Lung imaging
Mcray proposed a triad for clinical diagnosis of non-bacterial thrombotic endocarditis:
1. A disease in which non-bacterial thrombotic endocarditis can occur.
2. The heart has a murmur or a new murmur or the original murmur changes.
3. The body has multiple embolisms.
In addition, DIC laboratory diagnosis of venous thrombosis and multiple negative blood cultures contribute to the diagnosis of non-bacterial thrombotic endocarditis. If combined with UCG, it is more conducive to diagnosis.
Diagnosis
Differential diagnosis
Infectious neoplasms: The basic pathological change of infective endocarditis is the attachment of neoplasms composed of platelets, fibrin, red blood cells, white blood cells, and infectious pathogens on the surface of the heart valve. Infective endocarditis refers to the inflammation of the heart valve or the lining of the ventricular wall caused by direct infection of bacteria, fungi and other microorganisms (such as viruses, rickettsia, chlamydia, spirochetes, etc.), which is different from Non-infectious endocarditis caused by rheumatic fever, rheumatoid, systemic lupus erythematosus, and the like. In the past, this disease was called bacterial endocarditis, which is not used because it is not comprehensive enough. Typical clinical manifestations of infective endocarditis include fever, murmur, anemia, embolism, skin lesions, splenomegaly, and blood culture positive.
The bright red papillary sputum is protruding into the urethra cavity: the symptoms of paraurethral adenocarcinoma, the lesion may be bright red papillary sputum to the urethral cavity and the urethra. Middle and lower urethral cancer may be discovered by visual inspection or palpation examination.
Thrombotic neoplasm: The neoplasm is a general term for various protrusions formed in the pathological process inside and outside the body or organ. Thrombotic neoplasms are more common in non-bacterial thrombotic endocarditis. Non-bacterial thrombotic endocarditis can involve any heart valve, primarily affecting the mitral and aortic valves. Second, the mitral mites are mostly located in the atrial surface, and the aortic and pulmonary valves are mostly located on the ventricular surface. The main pathological change of non-bacterial thrombotic endocarditis is the formation of aseptic neoplasms on the valve. The early changes are the degeneration of valvular collagen under the influence of allergies, vitamin deficiency, hemodynamic damage and aging. The matrix edema, followed by partial exfoliation of the intima of the valve, exposes the collagen and the matrix to the bloodstream. When the antibody is in a hypercoagulable state, platelets and the like easily adhere to the surface to form non-bacterial thrombotic neoplasms. The lesions are more superficial, and there is often no inflammatory reaction in the local area. Once the neoplasms fall off, the signs of arterial embolism can be generated.
Mcray proposed a triad for clinical diagnosis of non-bacterial thrombotic endocarditis:
1. A disease in which non-bacterial thrombotic endocarditis can occur.
2. The heart has a murmur or a new murmur or the original murmur changes.
3. The body has multiple embolisms.
In addition, DIC laboratory diagnosis of venous thrombosis and multiple negative blood cultures contribute to the diagnosis of non-bacterial thrombotic endocarditis. If combined with UCG, it is more conducive to diagnosis.
