Endocarditis

Martin E. Goldman

Infective endocarditis (IE) is an infection of the endothelium of the heart or blood vessels. Heart valves are particularly susceptible, but IE can occur on any endothelial lined surface, including the papillary muscles, walls of the atria or ventricles, pulmonary artery, or endothelialized surfaces of prosthetic valves or implanted devices such as catheters, pacemakers, and automatic implantable cardioverter-defibrillators (AICDs).1,2 Structural heart disease is the most common predisposing risk factor for IE, which includes acquired valvular disease, congenital abnormalities, prosthetic heart valves, and indwelling devices.

Echocardiography is the imaging technology of choice for the diagnosis of IE and recognition of its potential complications.3–5 Once IE is confirmed by blood cultures and echocardiography, appropriate treatment with bactericidal antibiotics and surgery (if indicated) can reduce the morbidity and mortality of IE. Unrecognized and untreated, IE is invariably fatal. ⁶ Perioperative echocardiography must be performed in IE to help the surgeon in the assessment and management of these patients. ⁷

The American Heart Association (AHA) estimates the incidence of IE in the United States to be 10,000 to 15,000 new cases annually. ⁸ The pathophysiologic mechanism of IE is blood flowing from a zone of relatively high pressure to one of lower pressure. If the Reynolds number is surpassed, turbulent flow will be generated and cause endothelial damage, forming a susceptible nidus for implantation and subsequent infection with an adhering organism during bacteremia or fungemia. As part of the native immune response, adherence factors such as fibrin, platelets, and inflammatory cells are drawn to the infective surface, creating a heterogeneous irregular meshwork called vegetation. Vegetations are typically located on the low-pressure side of high-velocity turbulence, on the atrial side of mitral or tricuspid regurgitation, on the ventricular side of aortic or pulmonic regurgitation, on the ventricular side of mitral stenosis, or on the aortic side of aortic stenosis ( Figs. 20-1 and 20-2; Videos 20-1 and 20-2). Similarly, if there is a ventricular septal defect (VSD) with left-to-right shunting, the vegetation will be on the low-pressure side, or in this specific scenario, the right ventricular side of the defect. An atrial septal defect (ASD) usually has low pressure on either side of the defect and subsequently does not create a turbulent jet, resulting in a much lower likelihood of developing endocarditis.

Figure 20-1 Four-chamber view showing vegetations on both anterior and posterior leaflets.

Figure 20-2 Three-dimensional en face view of same valve seen Figure 20-1 and Video 20-1 . Vegetations seen in both commissures and at A2.

The definitive diagnosis of endocarditis by echocardiography is detection of a vegetation diagnosed with either transthoracic or transesophageal echocardiography (TTE, TEE). This is identified as an irregularly shaped echogenicity mass that may be sessile or pedunculated, mobile or immobile, fibrinous or multilobar and usually has a distinct separation and echogenicity (tissue density) from the underlying valve or endocardial tissue. Infection may involve the valve leaflet or its support apparatus. Any endocardial surface that is attached or adherent to an indwelling cardiac device can also become the site for formation of a vegetation ( Video 20-3 ).

The echocardiogram can also diagnose complications of IE including abscess formation, ruptured chordae or papillary muscle, leaflet or sinus of Valsalva perforation, prosthetic valve dehiscence, development of fistulous tracts, and suppurative pericarditis ( Fig. 20-3 and Video 20-4 ). The differential diagnosis of a vegetation includes Libman-Sacks lesions, which are nonbacterial thrombotic lesions found in inflammatory disorders such as systemic lupus erythematosus in up to 18% of patients.^9,10 These broad-based lesions may appear on the basilar portion of the valve leaflets (not necessarily associated with jet lesions) and are usually sessile. Marantic endocarditis can also occur in patients with advanced neoplasms such as melanoma and may be difficult to differentiate from endocarditis in a patient with malignancy and fever. Lambl excrescences are small, fibrinous, filiform lesions usually seen on aortic valve leaflet coaptation points as a result of mechanical trauma. They can also appear on the mitral valve (MV).

Figure 20-3 Commissure view showing aneurysm and perforation of anterior leaflet.

Duke Criteria

The Duke criteria for diagnosis of IE, originally published in 1994 and modified in 2000, includes endocardial involvement as documented by positive TTE or TEE as one of the two major criteria in the diagnosis of endocarditis, the other being positive blood cultures ( Box 20-1).^3,11,12 Minor criteria include a broader range of clinical findings: predisposing cardiac conditions, elevated temperature/fever, vascular phenomena, immunologic phenomena, and certain microbiological findings. The criteria also define three diagnostic categories: (1) “definite” by pathologic or clinical criteria, (2) “possible,” and (3) “rejected.” ³ The category “possible IE” is defined as having at least one major criterion and one minor criterion or three minor criteria. ¹¹

BOX 20-1 MAJOR AND MINOR DUKE CRITERIA FOR DIAGNOSIS OF INFECTIVE ENDOCARDITIS

Major Criteria

• Positive blood cultures for infective endocarditis. Typical microorganism for infective endocarditis from two separate blood cultures in the absence of a primary focus:

• Viridans streptococci

• Streptococcus bovis, including nutritional variant strains

• HACEK group—Haemophilus spp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella spp., and Kingella kingae

• Community-acquired Staphylococcus aureus or enterococci

• Persistently positive blood culture, defined as recovery of a microorganism consistent with infective endocarditis from:

• Blood cultures drawn more than 12 hours apart OR

• All of three or a majority of four or more separate blood cultures, with first and last drawn at least 1 hour apart

• Evidence of endocardial involvement

• Positive echocardiogram for infective endocarditis

• Oscillating intracardiac mass on valve or supporting structures, or in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation OR

• Abscess OR

• New partial dehiscence of prosthetic valve OR

• New valvular regurgitation (increase or change in preexisting murmur not sufficient)

Minor Criteria

• Predisposition—predisposing heart condition or intravenous drug use

• Fever—38.0°C (100.4°F)

• Vascular phenomena—major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions

• Immunologic phenomena—glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor

• Microbiologic evidence—positive blood culture but not meeting major criterion as noted previously (excluding single positive cultures for coagulase-negative staphylococci and organisms that do not cause endocarditis) OR serologic evidence of active infection with organism consistent with infective endocarditis

• Echocardiogram—consistent with infective endocarditis but not meeting major criterion as noted previously

From Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med. 1994;96:200-209.

The Duke criteria have also been validated in the intravenous drug user (IVDU) population, in whom right-sided endocarditis, especially involving the tricuspid valve, occurs much more frequently than in the non-IVDU population (Video 20-5 ). ¹³ IVDUs with definite diagnosis of IE more commonly have vascular phenomena (arterial embolism, septic pulmonary infarction, mycotic aneurysm, intracranial hemorrhage, or Janeway lesions) and multiple opacities on chest radiography than those with possible endocarditis.