Clinical presentation: infectious endocarditis refers to a rare bacterium or virus of a fungus of the heart valves. The endothelium virus extracardíacas is called "
endarteritis" and can cause disease that is clinically similar to endocarditis.
One of the most typical aspects that predispose to infective endocarditis is the structurally abnormal presence of heart valves. Patients with a history of rheumatic or
congenital heart disease, mitral valve with an audible hum, a heart valve prosthesis or a history of prior endocarditis prolapse are therefore more likely to infective endocarditis.
Infection involves the left side of the heart (mitral and aortic valves), almost exclusively, except in patients injecting drug users or, less commonly, in patients with pulmonary artery (Swan-Ganz) valve catheter, in which the virus of the right side of the tricuspid (lung) heart valve could occur.Etiology: Typical infectious agents that cause native valve endocarditis is a Gram-positive, including Streptococcus bacteria viridans, S aureus and enterococci. In particular, often causing bacterial endocarditis is be anticipated on the basis of host items.Injecting drug users in general, enter S aureus blood when the non-sterile needle is used or the skin is not sufficiently cleaned before inserting the needle. Those affected with dental work recent are transient bacteremia with oral microbiota, notably viridans S, with subsequent endocarditis possibility.With enterococci Genitourinary tract infections can lead to damaged bacteremia and subsequent planting heart valves. Patients with prosthetic heart valves are also at increased risk of resulting infective endocarditis of flora of the skin such as epidermidis S or S aureus.Before the availability of antibiotics, the infective endocarditis is a progressive disease fatal. Even with antibiotics, case fatality of endocarditis approaches 25%, and the definitive cure often require prolonged administration of antibiotics and emergency surgery to replace infected heart valves.Pathogenesis: A number of hemodynamic factors predispose patients to endocarditis: (1) a high speed jet stream producing turbulent blood flow, (2) are derived from a high pressure to a relatively narrow camera low pressure, and (3) a hole that separates the two cameras that creates a pressure gradient.The lesions of infective endocarditis tend to form on the surface of the valve heart Chamber with the lowest (for example, near the surface pressure ventricular an abnormal aortic valve and the auricular surface an abnormal mitral valve).Endothelium damaged by turbulent blood flow results in exposure of extracellular matrix, the promotion of the deposition of fibrin and platelets, which form sterile vegetations (thrombotic not bacterial endocarditis) or endocarditis marantic proteins. Infectious endocarditis occurs when microorganisms deposited in these sterile vegetations during the course of the bacteremia.Not all bacteria also adhere to these web sites. For example, e. coli, a common trigger of bacteremia, rarely involved as a trigger of endocarditis. On the contrary, the virulent agencies, for example, the S aureus can invade intact, causing endocarditis in the absence of pre-existing alterations valvular endothelium.Once infected, these vegetations continue to grow in additional platelet and fibrin deposition, providing the bacteria in a sanctuary of mechanisms for leukocytes polymorphonuclear example and complement. Accordingly, as soon as the virus takes hold, infected vegetation continues to grow in a way largely unimpeded.Long (4-6 weeks) bactericidal antibiotic that is needed to penetrate the vegetation and cure this disease management. Bacteriostatic antimicrobial agents that inhibit but do not kill bacteria, are insufficient.Surgical removal of the infected sometimes valve is required for healing, especially to infection by fungi, and Gram-negative bacilli and if there is mechanical valve resulting congestive heart failure, or valve prosthesis infections dysfunction. A distinctive feature of infective endocarditis is a persistent bacteremia, which stimulates the immune system humoral and cellular.A variety of immunoglobulins are expressed, giving rise to the formation of immune complex increased nonspecific serum levels of rheumatoid aspect, and hipergammaglobulinemia. deposition of complex immune from the kidney glomerular basement membrane can result in the development of acute Glomerulonephritis, and kidney failure.Clinical manifestations: infectious endocarditis is a multiple system disease protein demonstrations. For these reasons, signs may be nonspecific and diagnosis can not be included first in the differential diagnosis. Cutaneous findings suggestive of endocarditis consist of nodules of Osler, painful papules on the fingertips of hands and feet believed to be secondary to the deposit of immune; complex and injuries of Janeway, painless bleeding lesions on the palms and soles caused by septic microembolias. The signs and symptoms of endocarditis can be acute, subacute or chronic. Clinical manifestations mainly reflect (1) the valve damage haemodynamic changes, (2) target organs symptoms and septic emboli (emboli side right into the lungs, the left side to the brain emboli, spleen, kidney, and limb) indicators, (3) target organs symptoms and signs of the deposition of the immune complex, and (4) persistent bacteremia with planting metastatic abscesses (septic joints) virus. Death is usually caused by the hemodynamic collapse or septic emboli to the central nervous system, giving rise to brain abscesses or aneurysms fungi and intracerebral hemorrhage.Elements of chance a fatal outcome of the virus are valve on the left side, bacterial etiology different viridans S, medical co-morbidities, complications of endocarditis (congestive heart failure, the ring of the valve or disease Embolic abscess), and a study, the medical treatment without valvular surgery.
