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Infective Endocarditis

Nagesh S. Anavekar, md, Marcus Averbach, MD, and Bernard E. Bulwer, MD, mSc

Contents

Case Presentation

Introduction

Case Presentations

Role of Echocardiography in IE

Echocardiographic Characteristics Complications Summary

Suggested Reading case presentation 1

Clinical History

A 43-yr-old female with a past history of obesity, hypertension, and smoking was admitted with acute inferior myocardial infarction and underwent cardiac catheterization and balloon angioplasty with intracoronary stenting for blockage to her right coronary artery.

over the following week she experienced pleuritic chest pains that went largely ignored until chills and fever ensued. She was admitted 10 d later with a working diagnosis of pericarditis. Blood cultures were positive for Staphyloccus aureus. Shortly after admission, she developed acute respiratory distress, severe metabolic acidosis, rapid atrial fibrillation followed by acute heart block, coagulopathy, and anuria.

Echocardiography

Emergency transthoracic echocardiogram revealed a circumferential pericardial effusion (but no tamponade) and new onset severe aortic insufficiency.

No valvular vegetations were seen (Fig. 1). Transesophageal echocardiography (TEE) was requested but she was immediately whisked to the operating room for emergency surgery. The working diagnosis was aortic valve endocarditis complicated by a paravalvular abscess with involvement of her cardiac conduction system.

Surgical Findings inspection of the aortic valve at surgery revealed partial destruction and prolapse of the right and non-coronary cusps along with a contained rupture of the aortic root owing to an abscess cavity. The abscess had eroded into the interventricular septum causing complete heart block and a ventricular septal defect. Aortic valve replacement with a homograft valve, aortic root replacement, and repair of the ventricular septal defect using a pericardial patch were carried out. The patient never fully recovered, and she expired 2 d later. Autopsy confirmed the surgeon's findings (Fig. 2). Fibrinous pericarditis, cardiomegaly, and a friable thrombus on the adventitial aspect of the homograft were also noted.

From: Contemporary Cardiology: Essential Echocardiography: A Practical Handbook With DVD Edited by: S. D. Solomon © Humana Press, Totowa, NJ

Fig. 1. A 43-yr-old woman admitted with fever, septicemia, and pleuritic chest pain. The peri-aortic soft tissues (fine arrows) appear thickened. The aortic leaflets were barely visible on parasternal long axis (PLAX) views, but wide-open aortic regurgitation (arrow) was noted on Color flow Doppler (A,B). PLAX views showed a circumferential pericardial effusion (asterisks).

Circumferential Pericardial Effusion

Fig. 1. A 43-yr-old woman admitted with fever, septicemia, and pleuritic chest pain. The peri-aortic soft tissues (fine arrows) appear thickened. The aortic leaflets were barely visible on parasternal long axis (PLAX) views, but wide-open aortic regurgitation (arrow) was noted on Color flow Doppler (A,B). PLAX views showed a circumferential pericardial effusion (asterisks).

Ecocardiografia Immagini
Fig. 2. Infective endocarditis: peri-aortic abscess. See Case 1 for description.

introduction

Infective endocarditis (IE) is a microbial infection of the endothelial lining of the heart, most commonly involving the valves. Infection may also occur at the site of a septal defect, chordae tendinae, or mural endocardium. The diagnosis of IE is made on the basis of a combination of clinical, echocardiographic and pathological features using the modified Duke criteria (Table 1). Echocardiography features prominently in the diagnosis and follow-up of IE.

Damage to the endothelial surface of the valves or mural endocardium facilitates spontaneous platelet-fibrin deposition, giving rise to nonbacterial thrombotic

Table 1A

Modified Duke Criteria for the Diagnosis of Infective Endocarditis

Major criteria

Blood cultures positive for infective endocarditis

Positive blood cultures for typical organisms IE isolated from two separate blood cultures: Viridans streptococci, Streptococcus bovis, Staphylococcus aureus HACEK group, Enterococci (in the absence of a primary focus) Persistently positive blood cultures: recovery of microorganisms consistent with IE isolated from: >2 positive blood cultures >12 h apart

>3 positive cultures of blood, the 1st and the last sample >1 h apart Single blood culture for Coxiella burnetii Antiphase I IgG antibody titer of >1:800

Evidence of endocardial involvement

Positive Echocardiogram for IE (transesphageal echocardiography recommended for prosthetic valve, possible infective endocarditis by clinical criteria, or complicated IE [i.e., a paravalvular abscess]) Oscillating intracardiac mass (vegetation) on the valve or supporting structures in the path of regurgitant jets or on implanted material in the absence of an alternative anatomic explanation Abscess

New partial dehiscence of a valvular prosthesis

New valvular regurgitation (worsening or changing pre-existing murmur not sufficient)

HACEK, Haemophilus species (H. aprophilus and H. paraaphrophilus), Actinobacillus actinoinycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae.

Table 1B

Modified Duke Criteria for the Diagnosis of Infective Endocarditis

Minor criteria

• Predisposing heart disease or injection drug use

• Vascular phenomenon:

Major arterial emboli Septic pulmonary infarcts Mycotic aneurysm

Intracranial or conjunctival hemorrhage Janeway's lesions

• Immunological phenomenon:

Glomerulonephritis Osler's nodes Roth's spots Rheumatoid factor

• Microbiological evidence: a positive blood culture that does not meet a major criterion (as previously noted) or serological evidence of active infection with an organism consistent with IE

Definite endocarditis: two major criteria or one major and three minor criteria or five minor criteria. Possible endocarditis: one major plus one minor, or three minor criteria.

Table 2

Infective Endocarditis: Predisposing Cardiac Lesions

Higher risk

Intermediate risk

Low or no increased risk

Prosthetic valves

Previous endocarditis Aortic valve disease

Mitral regurgitation

Combined mitral regurgitation and stenosis Congenital heart disease, especially cyanotic congenital heart disease, patent ductus arteriosus, ventricular septal defect, coarctation of the aorta

Mitral valve prolapse with regurgitation Mitral stenosis Tricuspid valve disease

Pulmonary valve disease

Assymetrical septal hypertrophy

Intracardiac lines (in right atrium) Intracardiac implants (nonvalvular) Degenerative valvular disease in the elderly

Cardiac pacemakers

MVP with no regurgitation Cardiac lesions—post surgical correction Tricuspid regurgitation with normal valves Atrial septal defect, secundum variety

Adapted from Fuster V, Alexander RW, O'Rourke RA. Hurst's: The Heart, 11th ed. New York: McGraw Hill, 2004.

endocarditis. These sites are susceptible to microbial seeding during episodes of bacteremia culminating in the characteristic "vegetation" that consists of an amorphous mass of platelets, fibrin, inflammatory cells, and microorganisms. Factors contributing to endocardial injury and the genesis of nonbacterial thrombotic endocarditis include: a high-velocity jet impacting the endothelium, flow from a high- to low-pressure chamber, and high-velocity flow across a narrow orifice. This explains the increased risk of endocarditis in certain patients (e.g., those with pre-existing valvular lesions or intracardiac prosthetic devices) as well as the common sites of vegetations (i.e., atrial surface of mitral valve, ventricular surface of aortic valve). However, in approx 30% of reported cases, no predisposing cause can be found. The incidence of this disease is relatively uncommon, approx 4.2 per 100,000 patient-years. With the advent and increased use of various intracardiac devices, the number of reported cases of infectious endocarditis is expected to rise. Cardiac lesions predisposing to IE are listed in Table 2.

If IE is not detected and managed in a timely manner, it can lead to devastating outcomes. Prompt recognition of IE requires a high index of clinical suspicion. The diagnosis must be considered and aggressively investigated when individuals with fever also present with bacteremia, predisposing cardiac lesions, prosthetic valves, other intracardiac devices, evidence of an active endo-cardial process, or embolic phenomena. The following cases exhibit diverse presentations and differential diagnoses of IE.

case presentation 2

An 86-yr-old female was admitted with ascending cholangitis, but developed streptococcal meningitis shortly thereafter. Subsequent transthoracic echocar-diography (TTE) findings were suggestive of endocarditis. Patient developed acute renal failure, sepsis, and later demised. Her images appear in Figs. 3-5 (please see companion DVD for corresponding video for Fig. 3). Compare these to the findings shown in Figs. 6 and 7.

case presentation 3

A 72-yr-old man with end-stage renal disease and an atrioventricular fistula for hemodialysis presented to hospital with an infected graft and Methicillin-resistant Staphylococcus aureus bacteremia. He complained of increasing shortness of breath and orthopnea. Images from his transesophageal echocardiogram are shown in Fig. 8 (please see companion DVD for corresponding video).

case presentation 4

A 40-yr-old man with a history of daily heroin abuse presented with sudden onset of left lower extremity pain, intermittent blindness, delayed clotting to a small cut to his hand, and a fever recorded at 103.9°F. He recently tested positive for hepatitis C and HIV. At the time of examination, he was noted to have a grade 2/6 holosystolic crescendo-decrescendo

Fig. 3. An 86-yr-old woman with generalized sepsis. Transesophageal echocardiogram shows a well-circumscribed echodensity attached to atrial surface of the posterior mitral valve leaflet (white arrow; also seen in A,C-E). Color flow Doppler revealed new onset moderate-to-severe mitral regurgitation (B). Note the linear echodensity (pacer wire) in the right heart chambers (A,F). An undulating cuvilinear echodensity (arrow head; A,E) was seen in the right atrium and was thought to be clot or vegetation attached to the pacer wire (twin arrows; A,F), or even possibly Chiari's network. (Please see companion DVD for corresponding video.)

Fig. 3. An 86-yr-old woman with generalized sepsis. Transesophageal echocardiogram shows a well-circumscribed echodensity attached to atrial surface of the posterior mitral valve leaflet (white arrow; also seen in A,C-E). Color flow Doppler revealed new onset moderate-to-severe mitral regurgitation (B). Note the linear echodensity (pacer wire) in the right heart chambers (A,F). An undulating cuvilinear echodensity (arrow head; A,E) was seen in the right atrium and was thought to be clot or vegetation attached to the pacer wire (twin arrows; A,F), or even possibly Chiari's network. (Please see companion DVD for corresponding video.)

Right Atrium Chiari Network

Fig. 4. An 86-yr-old woman with generalized sepsis. Parasternal long-axis still frame (suboptimal quality) show an echodense lesion near the posterior mitral valve annulus, the most common site for mitral annular calcification. On transesophageal echocardiography, a circumferential opacity with a central echolucent region was seen (see Fig. 5).

Fig. 4. An 86-yr-old woman with generalized sepsis. Parasternal long-axis still frame (suboptimal quality) show an echodense lesion near the posterior mitral valve annulus, the most common site for mitral annular calcification. On transesophageal echocardiography, a circumferential opacity with a central echolucent region was seen (see Fig. 5).

murmur heard best at the right lower sternal border. rhythm, right bundle branch block, and left anterior

No peripheral stigmata of endocarditis was present. fascicular block. His echocardiography images

His initial electrocardiogram (ECG) showed sinus appear in Fig. 9.

Stigmata Endocarditis

Fig. 5. An 86-yr-old woman with generalized sepsis. A large vegetation attached to the atrial surface of the posterior mitral valve leaflet is shown (left panel). A flesh-colored mass was adherent to the pacerwire. On histology, it proved to be organized thrombi with superimposed infection. (Pathology specimens courtesy of Robert Padera, MD, Brigham and Women's Hospital.)

Fig. 5. An 86-yr-old woman with generalized sepsis. A large vegetation attached to the atrial surface of the posterior mitral valve leaflet is shown (left panel). A flesh-colored mass was adherent to the pacerwire. On histology, it proved to be organized thrombi with superimposed infection. (Pathology specimens courtesy of Robert Padera, MD, Brigham and Women's Hospital.)

Mitral Valve Regurgitation Mode

Fig. 6. Images from an 83-yr old woman with aortic and mitral regurgitation showed heavy calcification of the posterior mitral valve annulus with leaflet encroachment (white arrows). No fever or other symptoms that suggested infective endocarditis were present. Mitral annular calcification results from degenerative changes that become more prevalent with aging. M-mode through thickened mitral annulus shows echo-bright region that moves concordantly with cardiac chambers during the cardiac cycle (B).

Fig. 6. Images from an 83-yr old woman with aortic and mitral regurgitation showed heavy calcification of the posterior mitral valve annulus with leaflet encroachment (white arrows). No fever or other symptoms that suggested infective endocarditis were present. Mitral annular calcification results from degenerative changes that become more prevalent with aging. M-mode through thickened mitral annulus shows echo-bright region that moves concordantly with cardiac chambers during the cardiac cycle (B).

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