Recently, I performed an incision and drainage on a patient with gas gangrene. I consulted an infectious disease specialist who said the patient had developed infective endocarditis. Prior to this, I knew very little about the condition. Here is what I have learned from the physician and my research.

The patient was a 56-year-old male with diabetes who presented to the hospital with gas gangrene of his right foot. I took him to the OR for an aggressive incision and drainage. His cultures revealed methicillin resistant Staphylococcus aureus (MRSA) in both his foot wound and blood cultures. Bacteremia was a direct result of the foot infection.

According to infectious disease specialist Andrew Catanzaro, MD, “If you have a patient who has repeat blood cultures that are positive for bacteremia and it is slow to clear from the blood stream for greater than 48 hours, then you should be suspicious of infective endocarditis.”1

The patient also had a prior history of receiving a peripherally inserted central catheter (PICC) line due to a previous foot infection. He was immunocompromised, which also increased the level of suspicion. Additionally, the patient had increased white blood cells, positive blood cultures and an elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP). Therefore, the next step was to order an echocardiogram to help with confirming infective endocarditis.

The patient had initial incision and drainage. Eventually, he had a transmetatarsal amputation after serial debridements. I monitored weekly ESR, CRP and vancomycin levels for this patient. He received six to eight weeks of IV antibiotics and will complete a repeat echocardiogram after his course of IV antibiotics. There was close follow-up with his primary care physician, podiatrist and infectious disease doctor.

A Quick Primer On Infective Endocarditis

Infective endocarditis is a type of endocarditis of the inner tissue of the heart caused by infectious agents. The incidence is two to 10 episodes per 100,000 people.2 It accounts for one in 1,000 hospital admissions. With this condition, the valves of the heart do not receive any dedicated blood supply. As a result, defensive immune mechanisms cannot directly reach the valves via the bloodstream. If an organism attaches to a valve surface and forms a vegetation, this blunts the host immune response. Many microorganisms can cause infective endocarditis.

The damaged part of a heart valve creates a local blood clot. The platelet and fibrin deposits that form as part of the blood clotting process allow bacteria to take hold and develop vegetations. The body has no direct methods of combating valvular vegetations because the valves do not have a dedicated blood supply. This combination of damaged valves, bacterial growth and lack of a strong immune response results in infective endocarditis.

Infective endocarditis has the following risk factors:
• Immunocompromised status
• Artificial heart valves
• Intracardiac devices such as implantable cardioverter defibrillators
• Unrepaired cyanotic congenital heart defects
• History of infective endocarditis
• Chronic rheumatic heart disease
• History of PICC line and/or recent bacteremia
• Age-related degenerative valvular lesions
• Hemodialysis
• History of diabetes, alcohol abuse, HIV/AIDS and intravenous drug use

There are several diagnostic modalities that can be helpful in detecting infective endocarditis.

Blood cultures. Physicians would look for Viridans streptococci, Staphylococcus aureus (MRSA or MSSA), HACEK organisms (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella), Streptococcus bovis or community-acquired Enterococcus in the absence of an alternative primary site of infection.

Echocardiogram (echo). This uses high-frequency sound waves to produce a graphic outline of the heart’s movement. The echo will show evidence of oscillating intracardiac mass without alternative explanation, abscess, new partial dehiscence of a prosthetic valve or new valvular regurgitation.

Transesophageal echo (TEE). This is a type of echo test in which the ultrasound transducer, positioned on an endoscope, goes down the patient’s throat into the esophagus. It can assess the overall function of the heart’s valves and chambers; determine the presence of many types of heart disease, such as valve disease, myocardial disease, pericardial disease, infective endocarditis, cardiac masses and congenital heart disease; evaluate the effectiveness of valve surgery and evaluate abnormalities of the left atrium.

A Guide To Treatment

For short-term treatment, the treating physician can administer high dose antibiotics intravenously for six to eight weeks to maximize the diffusion of the antibiotic.

For long-term treatment, patients typically continue on antibiotics for six to eight weeks, according to Dr. Catanzaro.1 He notes there is a 30 percent failure rate.

If infective endocarditis is left untreated, heart failure will occur and result in endocarditis, which can damage the heart valves and permanently destroy the heart’s inner lining. This can cause the heart to work harder to pump blood, eventually causing heart failure. If the infection progresses untreated, it is usually fatal.3

I now realize how important it is to look beyond the foot infection and always consult infectious disease with these complex patients.

1. Personal communication with Andrew Catanzaro, MD, board certified infectious disease specialist, Adventist Medical Group and Washington Adventist Hospital, Takoma Park, MD.
2. McDonald JR. Acute infective endocarditis. Infect Dis Clin North Am. 2009; 23(3):643-64.
3. Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America. Circulation. 2005; 111(23):e394-434.

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Original Posted on Podiatry Today.