Keywords
infective endocarditis, native valve endocarditis, prosthetic valve endocarditis
Step 1
Pathogenesis, Pathology, and Microbiology of Left-Sided Infective Endocarditis
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Infective endocarditis (IE) is the most severe and devastating complication of heart valve disease, whether it is native valve endocarditis (NVE), prosthetic valve endocarditis (PVE), or infection on another cardiac device. Despite advances in surgical technique, operations for IE remain associated with the highest mortality of any valve disease.
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IE patients require a multispecialty team approach, which includes an infectious disease specialist, cardiologist, and cardiac surgeon, with input from other specialties, such as neurology and nephrology, when needed. This is because the clinical scenarios presented by patients with IE are often very complex and require prompt diagnosis for the early institution of antibiotic treatment and decision making related to complications, including the risk of embolism and need for and timing of high-risk surgery.
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The microbiology of IE depends on whether the valve is native or prosthetic and whether the infection is community or hospital acquired. Staphylococci, streptococci, and enterococci are responsible for about 85% of all cases of IE.
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The infecting organisms produce and release virulence factors, including toxins, and enzymes. The enzymes produced are organism-specific regarding tissue specificity and efficiency. The severity of invasion and destruction, involvement of the valve annulus and beyond, occurs in stages—cellulitis, abscess, abscess cavity, and finally pseudoaneurysm—and are a function of virulence and time, with Staphylococcus aureus being the most aggressive and destructive.
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The capacity of biofilm production, which protects bacteria from host immune defenses and impedes antimicrobial efficacy, thus significantly reducing the ability of medical therapy alone to eradicate the infection, is a hallmark of microorganisms commonly causing IE.
Step 2
Diagnosis of Infective Endocarditis
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A high index of suspicion and low threshold to perform the examination and studies necessary to exclude IE are essential to diagnosis and early treatment. The diagnosis of IE is based on clinical symptoms, physical findings, microbiology results, echocardiograms, and other results. Echocardiography and blood cultures are the cornerstones of diagnosing IE. Whenever possible, blood cultures should be obtained before starting antibiotics.
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Transthoracic echocardiography (TTE) must be supplemented with transesophageal echocardiography (TEE) in most cases of suspected PVE. TEE is more sensitive than TTE and remains the present gold standard diagnostic modality for documenting IE. The role and added value of cardiac computed tomography (CT), magnetic resonance imaging (MRI), and other complementary imaging technologies are still unclear.
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Duke criteria or modified Duke criteria are used to confirm the certainty of the diagnosis. However, clinical judgment is very important on an individual basis, such as PVE and negative blood cultures, and so on ( Table 15.1 ).
Table 15.1
MAJOR CRITERIA
Blood culture positive for infective endocarditis
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Typical microorganisms consistent with infective endocarditis from two separate blood cultures: Streptococcus viridans, S. bovis HACEK group, S. aureus, or community-acquired enterococci, in the absence of a primary focus, or
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Microorganisms consistent with infective endocarditis from a persistently positive blood culture, defined as follows:
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At least two positive cultures of blood drawn >12 hours apart, or
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All of three or a majority of >four separate cultures of blood (with the first and last samples drawn at least 1 hour apart)
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Single positive blood culture for Coxiella burnetii or phase I IgG antibody titer to C. burnetii > 1:800
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Evidence of endocardial involvement:
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Echocardiogram positive for infective endocarditis: TEE recommended in patients with prosthetic valves, rated at least as “possible endocarditis” by clinical criteria, or complicated endocarditis, such as endocarditis with paravalvular abscess; TTE as the first test in other patients as follows:
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Oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation;
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Abscess:
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New partial dehiscence of prosthetic valve
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New valvular regurgitation (worsening or changing of preexisting murmur not sufficient)
MINOR CRITERIA
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Predisposition, predisposing heart condition, or injection drug use
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Fever
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Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
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Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor
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Microbiologic evidence: positive blood culture but does not meet a major criterion as noted above, or serologic evidence of active infection with an organism consistent with infective endocarditis
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Echocardiographic minor criteria eliminated
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Step 3
Special Considerations Related to Surgery for Infective Endocarditis
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Surgical treatment should be considered for patients with signs of heart failure, severe valve dysfunction, PVE, invasion with paravalvular abscess or cardiac fistulas, recurrent systemic embolization, large mobile vegetations, and persistent sepsis despite adequate antibiotic therapy for more than 5 to 7 days. Most patients with PVE will require surgery. See the next section for indications for surgery.
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Early surgery is recommended. Once a surgical indication is present, surgery should not be delayed. Early surgery is defined as being carried out “during initial hospitalization independently of completion of a full therapeutic course of antibiotics.”
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All patients with IE who require surgery but have neurologic symptoms should have a neurologic evaluation and brain imaging by CT or MRI before the planned operation. Imaging may need to be repeated in case of new or worsening symptoms.
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In general, surgery should be delayed for 1 to 2 weeks for patients with nonhemorrhagic strokes and 3 to 4 weeks for patients with hemorrhagic strokes. For those with nonhemorrhagic embolic strokes, earlier intervention may be justified. The risk of the worsening of stroke symptoms must be weighed against the indications for surgery and risk of additional emboli during the waiting period, in consultation with a neurologist.
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The need for preoperative coronary angiography should be guided by normal criteria. CT angiography is an alternative to assess coronary anatomy in patients with large aortic valve vegetations.
Step 4
Indications for Surgery in Left-Sided Infective Endocarditis
1
Heart Failure
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Aortic or mitral IE or PVE with severe acute regurgitation or valve obstruction causing refractory pulmonary edema or cardiogenic shock.
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Aortic or mitral IE with severe acute regurgitation or valve obstruction and persisting heart failure or echocardiographic signs of poor hemodynamic tolerance (early mitral closure of pulmonary hypertension).
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Aortic or mitral IE or severe prosthetic dehiscence with severe regurgitation and no heart failure.
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Uncontrolled Infection
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Locally uncontrolled infection (e.g., abscess, pseudoaneurysm, fistula, enlarging vegetation).
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Persisting fever and positive blood cultures more than 7 to 10 days not related to an extracardiac cause.
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Infection caused by fungi or multiresistant organisms.
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PVE caused by staphylococci or gram-negative bacteria (most cases of early PVE).
3
Prevention of Embolism
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Aortic or mitral IE or PVE with large vegetations (> 10 mm) following one or more embolic episodes despite appropriate antibiotic therapy.
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Aortic or mitral IE or PVE with large vegetations (> 10 mm) and other predictors of complicated course (e.g., heart failure, persistent infection, abscess).
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Aortic or mitral or PVE with isolated very large vegetations (> 15 mm).
Step 5
Principles of Surgery for Infective Endocarditis
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Objectives of IE surgery are to prevent additional embolic events, débride and remove all infected and necrotic tissue and foreign material, and restore functional valve and cardiac integrity.
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Adequate surgical débridement requires good surgical exposure. A median sternotomy is required for most IE operations. Ministernotomy and right thoracotomy approaches are likely to provide insufficient exposure if unexpected or more advanced and invasive disease is encountered; these procedures are not recommended for IE surgery.
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Chest CT is recommended to assess the risk of sternal reentry in patients with previous cardiac surgery. When an arterial structure such as an ascending aorta, pseudoaneurysm, or important graft is in direct contact with the sternum, consideration should be given to peripheral cannulation and the institution of cardiopulmonary bypass before sternotomy. Intraoperative TEE is mandatory.
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Perfect myocardial protection is critical because the procedure is often long and complex. This is achieved with initial induction with antegrade and retrograde blood cardioplegia and repeat retrograde cardioplegia every 15 to 20 minutes. Open insertion of the retrograde coronary sinus cannula secures perfect cardioplegia delivery.
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For those infections limited to the native valve cusps or leaflets (so-called simple IE), valve repair or replacement with a biologic or mechanical valve prosthesis according to similar principles as for patients with noninfected valves should be done. For very sick patients and those with neurologic complications, a biologic valve is recommended to avoid added anticoagulation-related complexity in postoperative management.
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For infection beyond the cusp or leaflets (advanced pathologies), radical débridement and reconstruction may be required. Radical débridement means complete removal of foreign material, necrotic tissue, and vegetations; it does not mean excision with wide margins, which may cause additional damage, jeopardize valve repair, and make reconstruction more difficult.
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All infected areas must be opened, unroofed, and cleaned out. In patients with PVE, débridement should include removal of the old prosthesis and suture material.
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Dirty noncardiotomy suction should be used for the initial débridement and irrigation. The use of cardiotomy suction is avoided when the field is grossly contaminated to minimize blood contamination. Débridement is followed by generous irrigation. Surgical instruments and gloves should be exchanged after the completion of débridement and irrigation.
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The excised valve specimens should be handled properly and divided between pathology and microbiology. Molecular testing of the excised cardiac valves with a polymerase chain reaction (PCR) assay should be considered when there is uncertainty regarding the causative microorganism.
Step 6
Surgical Procedures
1
Native Aortic Valve Endocarditis a
a References .
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For limited localized infection and preserved cusp contour, repair may occasionally be possible. The resulting cusp defect after the removal of vegetation is repaired with an autologous pericardial patch. In most cases, cusp preservation is not possible, and valve replacement is required. The choice is based on the usual criteria, as mentioned earlier.
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For infection limited to the native aortic valve cusps, complete removal of the native valve cusps and replacement with a valve prosthesis should suffice. Extraaortic invasion of native valve endocarditis is usually localized, and subcommisural invasion is most common. Often, the site of annulus penetration is small, which hides a widely spread extraaortic infection that requires unroofing of the entire infected area for adequate débridement.
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For invasive pathology—infection beyond the valve cusps involving the annulus—radical resection of all infected tissue and foreign material is necessary. Adequate débridement is followed by reconstruction ( Fig. 15.1 ).
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We recommend caution so as not to lose track of anatomy, cause injury to coronary arteries, or sacrifice live left ventricular outflow tract (LVOT) muscle and surrounding structures to make reconstruction more difficult and risky.
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When additional material is required for reconstruction, autologous pericardium is our preference, but bovine pericardium or other materials can be used. Even in patients with invasive disease, the tissue destruction usually leaves the LVOT intact, and no additional material is required for the reconstruction in most cases.
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For invasive disease requiring aortic root reconstruction, an aortic allograft is our preferred choice. The more extensive and destructive the infection, the stronger is the argument in favor of an allograft over alternative conduits with prosthetic valves.
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Bioroots (bioprosthetic valve inside a graft), mechanical valve conduits, porcine aortic roots, and bovine pericardial root reconstruction may also work if the allografts are unavailable. This is also true for aortic PVE. The use of an allograft is no substitute for the radical débridement of all infected tissue!