Infective endocarditis represents an acquired disease caused by various pathogenic agents, affecting the valvular or mural endocardium or the surface of septal defects, leading to abscess formation, valvular regurgitation or even rupture. The disease causes heart failure and is often lethal if left unaddressed.
Presentation depends on whether the disease is acute or subacute. An acute infective endocarditis patient usually presents with high fever, chills and rapid onset of heart failure symptoms or peripheral embolic phenomena. Associated complaints include fatigability, myalgia, night sweats, headache, anorexia, weight loss, dulled sensorium, back pain, pleuritic pain, cough or dyspnea. Other findings like right upper quadrant pain or abdominal postprandial distress are not uncommon. The physician must inquire about the existence of known congenital heart defects, about recent dental, surgical or other invasive procedures or intravenous drug use. The history of the disease helps differentiate between an acute and a subacute endocarditis episode: a subacute patient will usually be diagnosed about 6 weeks after the pathological process has started, whereas an individual suffering from acute endocarditis will be obligated to present sooner by dramatic symptoms.
Peripheral embolism may manifest as stroke , hemiplegia, hematuria, unilateral blindness, myocardial or pulmonary infarction. If the disease goes undiagnosed for a longer period of time, the physician will notice Janeway lesions, petechiae, splinter hemorrhages, Roth spots and Osler nodes, caused by immune-mediated vasculitis. Right-sided endocarditis sometimes presents in a similar manner to pulmonary empyema. Mycotic aneurysms suggest Pseudomonas aeruginosa etiology.
Internal cardiac defibrillators associated endocarditis patients have a two-fold higher mortality rate than single-chamber pacemaker endocarditis individuals . Their disease is usually caused by coagulase-negative staphylococci . Also, these cases may report accompanying pericarditis and mediastinitis signs, almost always along with fever. Signs of congestive heart failure, such as distended jugular veins or changes in previously known murmurs result from mitral valve involvement, which occurs in in eighty percent of methicillin-resistant Staphylococcus aureus endocarditis cases associated with dialysis catheters . Additional findings may include splenomegaly, gallop or arrhythmia, pericardial or pleural rubs, rales, pallor, acute septic monoarticular arthritis or delirium.
Echocardiography is usually the first imaging method applied. Transthoracic and transesophageal can help in diagnosis. They are able to characterize the dimensions of the vegetations and their effect on the underlying structures, such as valvular regurgitation or rupture. Anterior myocardial abscesses are better observed with transthoracic echocardiography, while abscesses in other locations are visualized by transesophageal studies . Embolization can be predicted to some extent, based on vegetation dimensions and echogenicity. Color Doppler echo can diagnose cusp perforation and valvular regurgitation apart and showcase intracardiac fistulas, especially when used in transesophageal views. Advanced harmonic imaging techniques add accuracy to these methods .
A thoracic radiograph showing pulmonary pyogenic abscesses suggest tricuspid endocarditis. Atrioventricular blocks and new interventricular conduction delays may be seen on the electrocardiogram and suggest a poor prognosis. Computer tomography is used to ascertain cerebral abscesses , but also to characterize vegetations and valvular anatomy .