Infective Endocarditis

On examination, the patient was acutely ill with distended neck veins. His pulse was 50 beats/min and blood pressure 110/50mm Hg. Systolic and diastolic murmurs were present. Blood cultures were drawn, and antibiotics started.

An electrocardiogram showed heart block. A temporary pacemaker was placed. A TEE revealed a huge atrial septal abscess with a fistula from the right atrium to the aorta. The patient was taken emergently to surgery, where the prosthesis was found to have nearly completely dehisced. The fistula was resected and the aortic valve replaced with a homograft. Postoperatively the patient remained in cardiogenic shock and died. Admission blood and valve cultures subsequently grew P. acnes.

Comment and Conclusions

Continued fevers despite appropriate antibiotic and medical management are cause for alarm. Ring abscesses may develop. This is a clear indication for surgical intervention. Fevers may also be caused by embolic events (arterial or venous), drug reactions, and intravascular catheter-related infections. Close monitoring is necessary to avoid major events. Vigilance should be maintained for widening pulse pressures and rhythm disturbances as these are ominous signs of progressive infection.

Indications for urgent surgery include progressive valvular dysfunction; aortic root, ring or septal abscesses; large vegetations (greater than l cm in diameter); and organisms such as VRE, MRSA, Pseudomonas species, and fungi refractive to antimicrobial therapy. It is important to note that, even with appropriate therapy and a bacteriologic “cure,” about one half of patients will have enough valve damage to require surgery later in life.

Despite our best efforts, the death rate from infective endocarditis remains in the range of 10–20%. Death is more likely with prosthetic valve endocarditis and when the organism is S. aureus. Patients still succumb from congestive heart failure, embolic phenomenon, and ruptured mycotic aneurysms, just as they did during Osler’s time.

It is clear there is room for improvement in the diagnosis and management of endocarditis. First, we must continue to refine microbiologic techniques, to allow diagnosis more quickly and accurately. Second, we must develop more effective antimicrobial therapy, especially for pathogens resistant to conventional antimicrobials. Third, we must learn how to combat biofilms. Perhaps in the future we can avoid removal of foreign materials. Finally, we must follow our patients closely and pursue timely surgical intervention when indicated. In recent years this has become more difficult, because patients, once stabilized, are often discharged home or to a skilled nursing facility to complete antibiotic therapy.

While we have learned more about infective endocarditis over the past quarter century, the challenges we face today are greater than ever before.

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