Endocarditis 101—diagnosis and treatment

In this video, from our Infectious Disease Essentials course, Dr John Fisher explains how to diagnose and treat infective endocarditis. He discusses important diagnostic clues and offers some priceless clinical pearls of wisdom.

[00:00:00] The pathogenesis of infective endocarditis begins with damaged heart valves from congenital heart disease, rheumatic fever, IV drug abuse, and the placement of intracardiac devices such as implantable defibrillators and pacemakers. Valve damage leads to sterile deposits of platelets, red blood cells, white blood cells, and fibrin called

[00:00:30] nonbacterial thrombotic endocarditis or NBTE. If a sufficiently virulent organism is present in the bloodstream in sufficient amounts, it may colonize the damaged valve and its associated NBTE and now the mass of bacteria and the NBTE becomes infective endocarditis. 80% of infective endocarditis is caused by Gram-positive cocci of which

[00:01:00] Staphylococcus aureus is the most common. The HACEK group of organisms consist of fastidious Gram-negative bacteria that are an unusual cause of infective endocarditis. They are together with fungal infections notoriously associated with large thrival vegetations which can easily break off and cause emboli to vital organs. Enterococcus causes about 10% of infective endocarditis.

[00:01:30] Enterococcus is a notorious problem if it causes endocarditis because agents that interfere with the organism's cell wall can inhibit these organisms but cannot kill them. However, bactericidal therapy is essential to prevent recurrence of endocarditis of any cause. Thus, for enterococcal endocarditis potentially toxic aminoglycosides must be added to cell wall agents for the entire period

[00:02:00] of treatment to eradicate the infection. Diagnosis is confirmed by multiple positive blood cultures and visible vegetation is noted on echocardiography. Definitive management of patients with infective endocarditis is best accomplished by an infectious disease specialist and the nuances of antimicrobial therapy are beyond the scope of this lesson. However, while awaiting cultural results, empirical therapy of native valve

[00:02:30] infective endocarditis with vancomycin plus ceftriaxone is recommended. For prosthetic valve endocarditis, the combination of vancomycin plus gentamicin plus oral rifampin is recommended because of the possibility of methicillin-resistant Staphylococcus aureus or MRSA. This combination is also recommended for methicillin-resistant Staphylococcus epidermidis, MRSE. Adjustment of antibiotics

[00:03:00] can be made by an infectious disease specialist when available. In some cases of endocarditis, valve replacement early in the course of endocarditis should be considered because it is associated with a lower mortality than elective valve replacement after prolonged antimicrobial treatment. This includes patients who exhibit congestive heart failure which is the most common cause of death from infected endocarditis. Patients with infection caused by organisms that are

[00:03:30] difficult to treat such as enterococcus especially on a prosthetic heart valve as well as Staph aureus, aerobic Gram-negative bacilli and fungi are also candidates for urgent valve replacement. Previous cerebral embolism or the presence of large vegetation which may embolize or compromised the heart's electrical conduction system leading to heart block or also indications for urgent replacement. The bottom line is this,

[00:04:00] if surgery is inevitable, early surgery has a better prognosis than delaying surgery. An endocarditis team consisting of a cardiologist, a cardiac surgeon, and infectious disease physician, a microbiologist and an intensivist who discussed patients in the hospital with infective endocarditis weekly and make decisions about surgery has been shown to reduce mortality substantially. To complete the picture

[00:04:30] as an outpatient, follow up by a cardiology and infectious disease specialist at 1, 3, 6, and 12 months after surgery is optimal.