Recognizing infective endocarditis

  I. What is infective endocarditis?  Infective endocarditis refers to inflammation of the heart valves or endocardial wall due to direct infection by bacteria, fungi and other microorganisms (such as viruses, rickettsia, chlamydia, spirochetes, etc.), as distinct from non-infective endocarditis due to rheumatic fever, rheumatoid fever, systemic lupus erythematosus, etc. The cause of infective endocarditis?  1. Patients receiving prolonged intravenous treatment, addiction to intravenous narcotics, immune suppression caused by drugs or diseases.  Endocarditis in the left side of the heart mainly involves the aortic and mitral valves, especially in those with mild to moderate closure insufficiency. Endocarditis in the right side of the heart is less common and mainly involves the tricuspid valve. Of the various congenital heart diseases, patent ductus arteriosus, ventricular septal defect, and tetralogy of Fallot are the most frequent. Among the individual valve lesions, bileaflet aortic stenosis is the most likely to occur, and valve prolapse (aortic valve, mitral valve) is also susceptible to this disease. It is also more likely to develop after valve replacement.  What are the manifestations of infected endocardium?  The most common are fever, heart murmur, anemia, embolism (which can occur in any organ and cause symptoms in the corresponding organ), skin lesions, splenomegaly, and positive blood cultures.  Fourth, the common pathogenic bacteria? Staphylococcus aureus, Streptococcus streptococcus V. Ultrasound Ultrasound ultrasound can be used to detect redundancies on valves, especially in infective endocarditis with positive blood cultures, and can detect the location, size, number and shape of redundancies. Transesophageal 2D echocardiography is significantly better than trans-thoracic wall 2D echocardiography. 90% of the cases can detect the redundant organisms and can detect smaller redundant organisms of 1-1.5 mm in diameter.  Six, early treatment can improve the cure rate, but in the application of antibiotic treatment should be taken before sufficient blood culture, according to the severity of the disease delayed antibiotic treatment for a few hours or even 1 to 2 days, does not affect the cure rate and prognosis of the disease. And clarifying the pathogen and using the most effective antibiotics are the most fundamental factors in curing this disease: it is generally believed that larger doses of bactericidal agents such as penicillins, streptomycins, and cephalosporins should be chosen, which can penetrate the superfluous matrix of platelet-fibrin and kill bacteria to achieve eradication of infection of the valves and reduce the risk of recurrence. The mortality rate of fungal endocarditis is as high as 80% to 100%, and drug cure is extremely rare. The affected valve tissue should be surgically removed early during antifungal therapy, especially in fungal prosthetic endocarditis, and postoperative antifungal therapy should be continued to provide a chance of cure.  Surgery In recent years, the development of surgical treatment has reduced the mortality rate of infective endocarditis, especially in those with significant heart failure.  The main surgical treatments for natural valve endocarditis are refractory heart failure; other infections with uncontrollable drugs, especially fungal and antibiotic-resistant gram-negative bacillary endocarditis; multiple emboli; and septic complications such as septic pericarditis, sinusoidal aneurysm (or rupture) of the Varicella, perforation of the interventricular diaphragm, and myocardial abscess. When complete or high atrioventricular block is present, temporary artificial pacing may be given, and permanent pacing therapy may be given when necessary.  The death rate for prosthetic valve endocarditis is higher than that for natural valve endocarditis. The mortality rate of prosthetic valve infective endocarditis treated with antibiotics alone is 60%, and the mortality rate can be reduced to about 40% with the use of antibiotics and prosthetic valve reoperation. Therefore, once prosthetic valve infective endocarditis is suspected, it is advisable to treat it with at least two antibiotics after at least three blood cultures are taken within a few hours. Early stage prosthetic valve infective endocarditis is mostly aggressive and early surgery is generally advocated. Most late stage prosthetic valve infective endocarditis is caused by streptococci, and medical therapy is preferred. The fungal prosthetic valve infective endocarditis is treated with medical drugs only as an adjunct to emergency surgical revalvularization, and early revalvularization should be performed. Early surgical treatment of drug-resistant Gram-negative bacilli prosthetic valve infective endocarditis is also advisable. Others, such as moderate or severe heart failure due to valve dysfunction, severe perivalvular leakage or tearing of the bioprosthetic valve and valve stenosis, and the appearance of new conduction block. Recalcitrant infections, recurrent peripheral embolism, should all be considered for replacement of the infected prosthetic valve.  Pharmacologic treatment of the vast majority of right-sided cardiac endocarditis is effective, while surgical treatment is generally not considered because the right ventricle is well tolerated to tricuspid and pulmonary valve insufficiency. Surgery is often required to remove or replace the tricuspid valve in cases of progressive heart failure and Pseudomonas aeruginosa and fungal infections where medical therapy is ineffective.  To reduce the rate of residual infection after surgery during active infection, vitamins should be used continuously for 4 to 6 weeks after surgery.