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Infective Endocarditis

By Guy P. Armstrong, MD, Cardiologist;Cardiologist, North Shore Hospital, Auckland;Waitemata Cardiology, Auckland Valvular Disorders

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Infective endocarditis is infection of the endocardium, usually with bacteria (commonly, streptococci or staphylococci) or fungi. It may cause fever, heart murmurs, petechiae, anemia, embolic phenomena, and endocardial vegetations. Vegetations may result in valvular incompetence or obstruction, myocardial abscess, or mycotic aneurysm. Diagnosis requires demonstration of microorganisms in blood and usually echocardiography. Treatment consists of prolonged antimicrobial treatment and sometimes surgery.

Endocarditis usually refers to infection of the endocardium (ie, infective endocarditis). The term can also include noninfective endocarditis, in which sterile platelet and fibrin thrombi form on cardiac valves and adjacent endocardium. Noninfective endocarditis sometimes leads to infective endocarditis. Both can result in embolization and impaired cardiac function.

The diagnosis of infective endocarditis is usually based on a constellation of clinical findings rather than a single definitive test result.

Infective endocarditis can occur at any age. Men are affected about twice as often as women. IV drug abusers, immunocompromised patients, and patients with prosthetic heart valves and other intracardiac devices are at highest risk.

Etiology

The normal heart is relatively resistant to infection. Bacteria and fungi do not easily adhere to the endocardial surface, and constant blood flow helps prevent them from settling on endocardial structures. Thus, 2 factors are typically required for endocarditis:

  • A predisposing abnormality of the endocardium

  • Microorganisms in the bloodstream (bacteremia)

Rarely, massive bacteremia or particularly virulent microorganisms cause endocarditis on normal valves.

Endocardial factors

Endocarditis usually involves the heart valves. Major predisposing factors are congenital heart defects, rheumatic valvular disease, bicuspid or calcific aortic valves, mitral valve prolapse, hypertrophic cardiomyopathy, and prior endocarditis. Prosthetic valves and other intracardiac devices are a particular risk. Occasionally, mural thrombi, ventricular septal defects, and patent ductus arteriosus sites become infected. The actual nidus for infection is usually a sterile fibrin-platelet vegetation formed when damaged endothelial cells release tissue factor.

Infective endocarditis occurs most often on the left side (eg, mitral or aortic valve). About 10 to 20% of cases are right-sided (tricuspid or pulmonic valve). IV drug abusers have a much higher incidence of right-sided endocarditis (about 30 to 70%).

Microorganisms

Microorganisms that infect the endocardium may originate from distant infected sites (eg, cutaneous abscess, inflamed or infected gums, UTI) or have obvious portals of entry such as a central venous catheter or a drug injection site. Almost any implanted foreign material (eg, ventricular or peritoneal shunt, prosthetic device) is at risk of bacterial colonization, thus becoming a source of bacteremia and hence endocarditis. Endocarditis also may result from asymptomatic bacteremia, such as typically occurs during invasive dental, medical, or surgical procedures. Even toothbrushing and chewing can cause bacteremia (usually due to viridans streptococci) in patients with gingivitis.

Causative microorganisms vary by site of infection, source of bacteremia, and host risk factors (eg, IV drug abuse), but overall, streptococci and Staphylococcus aureus cause 80 to 90% of cases. Enterococci, gram-negative bacilli, HACEK organisms (Haemophilus sp, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae), and fungi cause most of the rest.

The disease develops in 3 stages:

  • Bacteremia: Microorganisms are present in the blood

  • Adhesion: The microorganism adheres to abnormal or damaged endothelium via surface adhesins

  • Colonization: Proliferation of the organism together with inflammation, leading to a mature vegetation

Many of the causative microorganisms produce polysaccharide biofilms that shield them from host immune defences and impede antibiotic penetration

Pathophysiology

Endocarditis has local and systemic consequences.

Local consequences

Local consequences of infective endocarditis include .

  • Myocardial abscesses with tissue destruction and sometimes conduction system abnormalities (usually with low septal abscesses).

  • Sudden, severe valvular regurgitation, causing heart failure and death (usually due to mitral or aortic valve lesions).

  • Aortitis due to contiguous spread of infection.

Prosthetic valve infections are particularly likely to involve valve ring abscesses, obstructing vegetations, myocardial abscesses, and mycotic aneurysms manifested by valve obstruction, dehiscence, and conduction disturbances.

Systemic consequences

Systemic consequences are primarily due to

  • Embolization of infected material from the heart valve

  • Immune-mediated phenomena (primarily in chronic infection)

Right-sided lesions typically produce septic pulmonary emboli, which may result in pulmonary infarction, pneumonia, or empyema. Left-sided lesions may embolize to any tissue, particularly the kidneys, spleen, and central nervous system. Mycotic aneurysms can form in any major artery. Cutaneous and retinal emboli are common. Diffuse glomerulonephritis may result from immune complex deposition.

Classification

Infective endocarditis may have an indolent, subacute course or a more acute, fulminant course with greater potential for rapid decompensation.

Subacute bacterial endocarditis (SBE), although aggressive, usually develops insidiously and progresses slowly (ie, over weeks to months). Often, no source of infection or portal of entry is evident. SBE is caused most commonly by streptococci (especially viridans, microaerophilic, anaerobic, and nonenterococcal group D streptococci and enterococci) and less commonly by S. aureus, Staphylococcus epidermidis, Gemella morbillorum, Abiotrophia defectiva (formerly, Streptococcus defectivus), Granulicatella sp, and fastidious Haemophilus sp. SBE often develops on abnormal valves after asymptomatic bacteremia due to periodontal, GI, or GU infections.

Acute bacterial endocarditis (ABE) usually develops abruptly and progresses rapidly (ie, over days). A source of infection or portal of entry is often evident. When bacteria are virulent or bacterial exposure is massive, ABE can affect normal valves. It is usually caused by S. aureus, group A hemolytic streptococci, pneumococci, or gonococci.

Prosthetic valvular endocarditis (PVE) develops in 2 to 3% of patients within 1 yr after valve replacement and in 0.5%/yr thereafter. It is more common after aortic than after mitral valve replacement and affects mechanical and bioprosthetic valves equally. Early-onset infections (< 2 mo after surgery) are caused mainly by contamination during surgery with antimicrobial-resistant bacteria (eg, S. epidermidis, diphtheroids, coliform bacilli, Candida sp, Aspergillus sp). Late-onset infections are caused mainly by contamination with low-virulence organisms during surgery or by transient asymptomatic bacteremias, most often with streptococci; S. epidermidis; diphtheroids; and the fastidious gram-negative bacilli, Haemophilus sp, Actinobacillus actinomycetemcomitans, and Cardiobacterium hominis.

Symptoms and Signs

Symptoms and signs vary based on the classification but are nonspecific.

Subacute bacterial endocarditis

Initially, symptoms of subacute bacterial endocarditis are vague: low-grade fever (< 39° C), night sweats, fatigability, malaise, and weight loss. Chills and arthralgias may occur. Symptoms and signs of valvular insufficiency may be a first clue. Initially, 15% of patients have fever or a murmur, but eventually almost all develop both. Physical examination may be normal or include pallor, fever, change in a preexisting murmur or development of a new regurgitant murmur, and tachycardia.

Retinal emboli can cause round or oval hemorrhagic retinal lesions with small white centers (Roth spots). Cutaneous manifestations include petechiae (on the upper trunk, conjunctivae, mucous membranes, and distal extremities), painful erythematous subcutaneous nodules on the tips of digits (Osler nodes), nontender hemorrhagic macules on the palms or soles (Janeway lesions), and splinter hemorrhages under the nails. About 35% of patients have CNS effects, including transient ischemic attacks, stroke, toxic encephalopathy, and, if a mycotic CNS aneurysm ruptures, brain abscess and subarachnoid hemorrhage. Renal emboli may cause flank pain and, rarely, gross hematuria. Splenic emboli may cause left upper quadrant pain. Prolonged infection may cause splenomegaly or clubbing of fingers and toes.

Acute bacterial endocarditis and prosthetic valvular endocarditis

Symptoms and signs of ABE and PVE are similar to those of SBE, but the course is more rapid. Fever is almost always present initially, and patients appear toxic; sometimes septic shock develops. Heart murmur is present initially in about 50 to 80% and eventually in > 90%. Rarely, purulent meningitis occurs.

Right-sided endocarditis

Septic pulmonary emboli may cause cough, pleuritic chest pain, and sometimes hemoptysis. A murmur of tricuspid regurgitation is typical.

Diagnosis

  • Blood cultures

  • Echocardiography and sometimes other imaging modalities

  • Clinical criteria

Because symptoms and signs are nonspecific, vary greatly, and may develop insidiously, diagnosis requires a high index of suspicion. Endocarditis should be suspected in patients with fever and no obvious source of infection, particularly if a heart murmur is present. Suspicion of endocarditis should be very high if blood cultures are positive in patients who have a history of a heart valve disorder, who have had certain recent invasive procedures, or who abuse IV drugs. Patients with documented bacteremia should be examined thoroughly and repeatedly for new valvular murmurs and signs of emboli.

Other than positive blood cultures, there are no specific laboratory findings. Established infections often cause a normocytic-normochromic anemia, elevated WBC count, increased ESR, increased immunoglobulin levels, and the presence of circulating immune complexes and rheumatoid factor, but these findings are not diagnostically helpful. Urinalysis often shows microscopic hematuria and, occasionally, RBC casts, pyuria, or bacteriuria.

Identification of organisms

  • Identification of the organism and its antimicrobial susceptibility is vital to guide treatment.

If endocarditis is suspected, 3 blood cultures (20 mL each) should be obtained within 24 h (if presentation suggests ABE, 2 cultures within the first 1 to 2 h). Each set of cultures should be obtained from a separate, fresh venipuncture site (ie, not from preexisting vascular catheters). Blood cultures do not need to be done during chills or fever because most patients have continuous bacteremia. When endocarditis is present and no prior antibiotic therapy was given, all 3 blood cultures usually are positive because the bacteremia is continuous; at least one culture is positive in 99%. Premature use of empiric antibiotic therapy should be avoided in patients with acquired or congenital valvular or shunt lesions to avoid culture-negative endocarditis. If prior antimicrobial therapy was given, blood cultures should still be obtained, but results may be negative.

Blood cultures may require 3 to 4 wk incubation for certain organisms; however, some proprietary, automated culture monitoring systems can identify positive cultures within a week. Other organisms (eg, Aspergillus sp) may not produce positive cultures. Some organisms (eg, Coxiella burnetii, Bartonella sp, Chlamydia psittaci, Brucella sp) require serodiagnosis; others (eg, Legionella pneumophila) require special culture media or PCR (eg, Tropheryma whippelii). Negative blood culture results may indicate suppression due to prior antimicrobial therapy, infection with organisms that do not grow in standard culture media, or another diagnosis (eg, noninfective endocarditis, atrial myxoma with embolic phenomena, vasculitis).

Imaging studies

Echocardiography, typically transthoracic (TTE) rather than transesophageal (TEE), should be done initially. TEE is more sensitive (ie, capable of revealing vegetations too small to be seen on TTE).

Transesophageal echocardiography should be done when

  • Patients have a prosthetic valve

  • Transthoracic echocardiogram is nondiagnostic

  • Diagnosis of infective endocarditis has been established clinically (done to detect perforations, abscesses, and fistulas)

CT is used occasionally when TEE fails to fully define paravalvular abscesses and for detection of mycotic aneurysms. PET scanning is an emerging tool for the diagnosis of endocarditis originating in prosthetic and intracardiac devices. CT and PET abnormalities are now included as major criteria in the European guidelines.

Diagnostic criteria

Infective endocarditis is definitively diagnosed when microorganisms are seen histologically in (or cultured from) endocardial vegetations obtained during cardiac surgery, embolectomy, or autopsy. Because vegetations are not usually available for examination, there are various clinical criteria for establishing a diagnosis. They include the revised Duke Criteria (with a sensitivity and specificity > 90%—see Table: Diagnostic Requirements for Infective Endocarditis According to the Revised Duke Criteria and Revised Duke Clinical Diagnostic Criteria for Infective Endocarditis) and the European Society of Cardiology (ESC) 2015 modified criteria (1).

The ESC criteria are similar to the modified Duke criteria but include expanded imaging results as major criteria as follows:

  • Vegetation, abscess, pseudoaneurysm, intracardiac fistula, valvular perforation or aneurysm, or new partial dehiscence of prosthetic valve identified by echocardiography

  • Abnormal activity around a prosthetic valve (implanted > 3 mo earlier) detected by PET/CT or SPECT/CT with radiolabelled leukocytes

  • Paravalvular lesions identified by cardiac CT

The ESC also differs from the modified Duke minor criteria by specifying that detecting silent vascular phenomena by imaging only is sufficient.

Diagnostic Requirements for Infective Endocarditis According to the Revised Duke Criteria

Clinical Diagnosis Status

Criteria

Definite endocarditis

One of the following:

  • 2 major criteria

  • 1 major and 3 minor

  • 5 minor

Possible endocarditis

One of the following:

  • 1 major and 1 minor

  • 3 minor

Endocarditis rejected

One of the following:

  • Firm alternative diagnosis explaining the findings of infective endocarditis

  • Resolution of symptoms and signs after ≤ 4 d of antimicrobial therapy

  • No pathologic evidence of infective endocarditis found during surgery or autopsy

  • Failure to meet the clinical criteria for possible endocarditis

Adapted from Durack DT, Lukes AS, Bright DK: New criteria for diagnosis of infective endocarditis: Utilization of specific echocardiographic findings; Duke Endocarditis Service. American Journal of Medicine 96 (3):200–209, 1994.

Revised Duke Clinical Diagnostic Criteria for Infective Endocarditis

Major criteria

Two positive blood cultures for organisms typical of endocarditis drawn >12 h apart

All of 3 or a majority of 4 or more positive blood cultures (with at least 1 h between first and last culture) for organisms consistent with endocarditis

Serologic evidence of Coxiella burnetii (IgG titer > 1:800) or one positive blood culture for Coxiella burnetii

Echocardiographic evidence of endocardial involvement:

  • Oscillating intracardiac mass on a heart valve, on supporting structures, in the path of regurgitant jets, or on implanted material without another anatomic explanation

  • Cardiac abscess

  • New dehiscence of prosthetic valve

  • New valvular regurgitation

Minor criteria

Predisposing heart disorder

IV drug abuse

Fever 38.0° C

Vascular phenomena:

  • Arterial embolism

  • Septic pulmonary embolism

  • Mycotic aneurysm

  • Intracranial hemorrhage

  • Conjunctival petechiae

  • Janeway lesions

Immunologic phenomena:

  • Glomerulonephritis

  • Osler nodes

  • Roth spots

  • Rheumatoid factor

Microbiologic evidence of infection consistent with but not meeting major criteria

Serologic evidence of infection with organisms consistent with endocarditis

Data from Durack DT, Lukes AS, Bright DK: New criteria for diagnosis of infective endocarditis: Utilization of specific echocardiographic findings; Duke Endocarditis Service. American Journal of Medicine 96 (3):200–209, 1994; Li JS, Sexton DJ, Mick N, et al: Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clinical Infectious Diseases 30:633–638, 2000

Diagnosis reference

1. Habib G, Lancellotti P, Antunes MJ, et al: 2015 ESC Guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). Eur Heart J 36:3075–3123, 2015.

Prognosis

Untreated, infective endocarditis is always fatal. Even with treatment, death is more likely and the prognosis is generally poorer for older people and people who have

  • Infection with resistant organisms

  • An underlying disorder

  • A long delay in treatment

  • Aortic valve or multiple valve involvement

  • Large vegetations

  • Polymicrobial bacteremia

  • Prosthetic valve infections

  • Mycotic aneurysms

  • Valve ring abscess

  • Major embolic events

Septic shock is more likely in patients with diabetes, acute renal insufficiency, S. aureus infection, vegetation size > 15 mm, and signs of persistent infection. The mortality rate for viridans streptococcal endocarditis without major complications is < 10% but is virtually 100% for Aspergillus endocarditis after prosthetic valve surgery.

The prognosis is better with right-sided than left-sided endocarditis because tricuspid valve dysfunction is tolerated better, systemic emboli are absent, and right-sided S. aureus endocarditis responds better to antimicrobial therapy.

Treatment

  • IV antibiotics (based on the organism and its susceptibility)

  • Sometimes valve debridement, repair, or replacement

  • Dental evaluation and treatment (to minimize oral sources of bacteremia)

  • Removal of potential source of bacteremia (eg, internal catheters, devices)

Treatment consists of a prolonged course of antimicrobial therapy (1). Surgery may be needed for mechanical complications or resistant organisms. Typically, antimicrobials are given IV. Because they must be given for 2 to 8 wk, home IV therapy is often used.

Any apparent source of bacteremia must be managed: necrotic tissue debrided, abscesses drained, and foreign material and infected devices removed. People with infective endocarditis should be evaluated by a dentist and treated for oral diseases that could cause bacteremia and subsequent endocarditis. Existing IV catheters (particularly central venous ones) should be changed. If endocarditis persists in a patient with a newly inserted central venous catheter, that catheter should also be removed. Organisms within biofilms adherent to catheters and other devices may not respond to antimicrobial therapy, leading to treatment failure or relapse. If continuous infusions are used instead of intermittent boluses, infusions should not be interrupted for long periods.

Antibiotic regimens

Drugs and dosages depend on the microorganism and its antimicrobial susceptibility. (for typical regimens, see Table: Some Antibiotic Regimens for Endocarditis in the United States).

Although most patients are stable enough to wait for culture results, empiric antibiotic therapy before organism identification may be necessary in seriously ill patients. Antibiotics should not be given until adequate blood cultures (2 or 3 samples from different sites over 1 h) have been obtained. Antibiotics should be broad spectrum to cover all likely organisms, typically including sensitive and resistant staphylococci, streptococci and enterococci. Empiric antibiotic regimens should reflect local patterns of infection and antibiotic resistance; however, typical examples of broad-spectrum antibiotic coverage may include

  • Native valves: Vancomycin 15 to 20 mg/kg IV q 8 to 12 h (not to exceed 2 g per dose)

  • Prosthetic valve: Vancomycin 15 to 20 mg/kg IV q 8 to 12 h (not to exceed 2 g per dose) plus gentamicin 1 mg/kg q 8 h plus either cefepime 2 g IV q 8 h or imipenem 1 g IV q 6 to 8 h (maximum dose 4 g/day)

As soon as possible, the empiric drug regimen should be adjusted based on culture results.

Some Antibiotic Regimens for Endocarditis in the United States

Type

Drug And Dosage for Adults

Drug and Dosage for Adults Allergic to Penicillin

Streptococci susceptible to penicillin (penicillin G MIC 0.1 µg/mL)

For NVE: Penicillin G 12–18 million units/day IV continuously or 2–3 million units q 4 h for 4 wk or, if gentamicin 3 mg/kg* IV or IM once/day is given concurrently, for 2 wk

For PVE: Penicillin G 24 million units/day IV continuously or 4 million units q 4 h for 6 wk or, if gentamicin 3 mg/kg* IV or IM (up to 80 mg) is given concurrently, for 2 wk

Ceftriaxone 2 g once/day IV or IM for 4 wk for NVE (6 wk for PVE) or, if gentamicin 3 mg/kg* IV or IM once/day is given concurrently, for 2 wk If there is no history of penicillin anaphylaxis

or

Vancomycin 15 mg/kg IV q 12 h for 4 wk for NVE (6 wk for PVE)

Streptococci resistant to penicillin (penicillin G MIC >0.1 µg/mL)

For NVE: Gentamicin 3 mg/kg* IV or IM once/day for 2 wk plus penicillin G 24 million units/day IV continuously or 4 million units q 4 h for 4 wk

For PVE: Gentamicin 3 mg/kg* IV or IM once/day for 2 wk plus penicillin G 24 million units/day IV continuously or 4 million units q 4 h or ceftriaxone 2 g once/day IV or IM for 6 wk

Vancomycin 15 mg/kg IV q 12 h for 4 wk for NVE (6 wk for PVE)

Enterococci

For NVE and PVE: Ampicillin 2 g IV q 4 h plus ceftriaxone 2 g IV q 12 h for 6 wk

For NVE and PVE: Vancomycin 15 mg/kg q 12 h IV plus gentamicin 3 mg/kg IV or IM once/day or gentamicin 1 mg/kg IV or IM q 8 h for 6 wk

or

For NVE and PVE: Linezolid 600 mg po or IV q 12 h for 6–8 wk

or

For NVE and PVE: Daptomycin 10–12 mg/kg once/day IV for 6–8 wk

Staphylococci susceptible to oxacillin

For NVE: Oxacillin or nafcillin 2 g IV q 4 h for 6 wk

For PVE: Oxacillin or nafcillin 2 g IV q 4 h for 6–8 wk plus gentamicin 1 mg/kg* IV q 8 h for 2 wk plus rifampin 300 mg IV or po q 8 h for 6–8 wk

Cefazolin 2 g IV q 8 h if there is no history of penicillin anaphylaxis for 6 wk for NVE (6–8 wk for PVE)

or

Vancomycin 15 mg/kg IV q 12 h for 4 wk for NVE (6–8 wk for PVE)

or

For right-sided NVE: Daptomycin 6 mg/kg once/day IV for 6 wk

Staphylococci resistant to oxacillin

Vancomycin 15 mg/kg IV q 12 h alone for 6 wk for NVE (6–8 wk for PVE), plus gentamicin 1 mg/kg IV* q 8 h for 2 wk plus rifampin 300 mg po q 8 h for 6–8 wk for PVE

or

For right-sided NVE: Daptomycin 6 mg/kg once/day IV for 6 wk

HACEK microorganisms

Ceftriaxone 2 g once/day IV or IM for 4 wk for NVE (6 wk for PVE)

or

Ampicillin 2 g IV q 4 h for 4 wk for NVE (6 wk for PVE)

or

Ciprofloxacin 1000 mg once/day po or 400 mg q 12 h IV for 4 wk for NVE (6 wk for PVE)

Ceftriaxone 2 g once/day IV for 4 wk for NVE (6 wk for PVE) if there is no history of penicillin anaphylaxis

Noncoliform bacilli

Sensitivity-proven beta-lactam antimicrobial (eg, ceftriaxone 2 g IV q 12–24 h or ceftazidime 2 g IV q 8 h) plus an aminoglycoside (eg, gentamicin 2 mg/kg* IV q 8 h) for 6 wk

*Based on ideal rather than actual weight in obese patients.

With vancomycin, serum levels must be monitored if doses > 2 g/24 h are administered.

XX

HACEK microorganisms: Haemophilus parainfluenzae, H. aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae.

NVE = native valve endocarditis; PVE = prosthetic valve endocarditis.

Adapted from Baddour LM, Wilson WR, Bayer AS, et al: Infective endocarditis in adults: Diagnosis, antimicrobial therapy, and management of complications; A scientific statement for healthcare professionals from the American Heart Association. Circulation 132 (15):1435–1486, 2015. doi: 10.1161/CIR.0000000000000296.

IV drug abusers frequently do not adhere to treatment, abuse IV access lines, and tend to leave the hospital too soon. For such patients, short-course IV or (less preferably) oral therapy may be used. For right-sided endocarditis caused by methicillin-sensitive S. aureus, nafcillin 2 g IV q 4 h plus gentamicin 1 mg/kg IV q 8 h for 2 wk is effective, as is a 4-wk oral regimen of ciprofloxacin 750 mg po bid plus rifampin 300 mg po bid. Left-sided endocarditis does not respond to 2-wk courses.

Cardiac valve surgery

Surgery (debridement, valve repair, or valve replacement) is sometimes required for treatment of infectious endocarditis (2). Surgery is typically indicated in

  • Patients with heart failure (particularly those with prosthetic, aortic or mitral native valve endocarditis, and those with pulmonary edema or cardiogenic shock)

  • Patients with uncontrolled infection (those with persistent infection, infection with fungal or resistant organisms, recurrent prosthetic valve endocarditis, or endocarditis complicated by heart block, abscess, aneurysm, fistula, or enlarging vegetation)

  • Patients at risk for embolism (particularly those with prosthetic, aortic or mitral native valve endocarditis, and large vegetations [defined in the United States as > 10 mm] or those with recurrent emboli)

Timing of surgery requires experienced clinical judgment. If heart failure caused by a correctable lesion is worsening (particularly when the organism is S. aureus, a gram-negative bacillus, or a fungus), surgery may be required after only 24 to 72 h of antimicrobial therapy. In patients with prosthetic valves, surgery may be required when TEE shows valve dehiscence on a paravalvular abscess, when valve dysfunction precipitates heart failure, when recurrent emboli are detected, or when the infection is caused by an antimicrobial-resistant organism.

Right-sided endocarditis is usually managed medically. If surgery is necessary (due to heart failure or lack of therapeutic response), then valve repair is preferred over replacement to avoid future prosthetic valve infection due to any continued IV drug use.

Surgery is usually delayed for a month after intracranial hemorrhage or major ischemic stroke.

Response to treatment

After starting therapy, patients with penicillin-susceptible streptococcal endocarditis usually feel better, and fever is reduced within 3 to 7 days. Fever may continue for reasons other than persistent infection (eg, drug allergy, phlebitis, infarction due to emboli). Patients with staphylococcal endocarditis tend to respond more slowly. Diminution of vegetation size can be followed by serial echocardiography. Echocardiography should be done at the completion of therapy to establish a new baseline for valvular appearance (including sterile vegetations) and insufficiency.

Relapse usually occurs within 4 wk. Antibiotic retreatment may be effective, but surgery may also be required. In patients without prosthetic valves, recrudescence of endocarditis after 6 wk usually results from a new infection rather than a relapse. Even after successful antimicrobial therapy, sterile emboli and valve rupture may occur up to 1 yr later. Risk of recurrence is significant, so ongoing life-long dental and cutaneous hygiene is advised. Patients who require antibiotic therapy for any reason should have at least 3 sets of blood cultures drawn before antibiotics are started.

Treatment references

1. Baddour LM, Wilson WR, Bayer AS, et al: Infective endocarditis in adults: Diagnosis, antimicrobial therapy, and management of complications: A scientific statement for healthcare professionals from the American Heart Association. Circulation 132:1435–1486, 2015.

2. Cahill TJ, Baddour LM, Habib G, et al: Challenges in infective endocarditis. J Am Coll Cardiol 69(3):325–344, 2017.

Prevention

Preventive dental examination and therapy before surgery to repair heart valves or congenital heart lesions is recommended.

Measures to reduce health care–acquired bacteremia aim to curb the rising incidence of iatrogenic bacteremia and subsequent endocarditis.

Dental and cutaneous hygiene is recommended for the general population but particularly for patients at intermediate risk (those with native valve disease) and high-risk.

High-risk patients

The American Heart Association (AHA) recommends antimicrobial prophylaxis for patients at high risk of an adverse outcome from infective endocarditis (see AHA Guidelines). Such patients include those with

  • Prosthetic heart valves, including transcatheter implanted prostheses

  • Prosthetic material used for heart valve repair (eg, annuloplasty rings, chords)

  • Previous infective endocarditis

  • Certain congenital heart diseases (CHD): Unrepaired cyanotic CHD (including palliative shunts and conduits), completely repaired CHD during the first 6 mo after surgery if prosthetic material or device was used, repaired CHD that has residual defects at or adjacent to the site of repair

  • Heart transplant recipients with valvulopathy

ESC prophylaxis regimens are described in reference 1.

Procedures requiring antibiotic prophylaxis

Most procedures for which prophylaxis is required for high-risk patients are oral-dental procedures that manipulate the gingiva or the periapical region of teeth or perforate the oral mucosa. Other procedures include those respiratory tract procedures in which mucosa is incised, vaginal delivery in some high-risk patients (patients with prosthetic cardiac valve or prosthetic material used for cardiac valve repair and for patients with unrepaired and palliated cyanotic congenital heart disease), and GI, GU, or musculoskeletal procedures that involve an area with an established infection (see Table: Procedures Requiring Antimicrobial Endocarditis Prophylaxis in High-Risk Patients in the US). Guidelines for endocarditis prophylaxis vary geographically.

Procedures Requiring Antimicrobial Endocarditis Prophylaxis in High-Risk Patients in the US

Type

Examples

Oral-dental*

Dental extraction

Dental implant placement or reimplantation of avulsed teeth

Periodontal procedures, including surgery, scaling, root planing, and probing

Prophylactic cleaning of teeth or implants when bleeding is anticipated

Root canal instrumentation or surgery beyond the apex

Respiratory tract

Bronchoscopy if mucosa is to be incised

Procedures done during an established infection

Tonsillectomy, adenoidectomy, or both

Vaginal delivery

n/a

GI tract

None, unless procedure is done during an established infection

GU tract

None, unless procedure is done during an established infection (eg, cystoscopy during known enterococcal UTI)

Musculoskeletal

None, unless procedure involves infected tissue

Skin

None, unless procedure involves infected tissue

*Examples of oral-dental procedures that do not require prophylaxis are anesthetic injection through uninfected mucosa and placement of orthodontic brackets.

Data from Wilson W, Taubert KS, Gewitz M, et al: Prevention of infective endocarditis. Circulation 116 (15):1736–1754, 2007 and Warnes CA, Williams RG, Bashore TM, et al: ACC/AHA 2008 Guidelines for the Management of Adults with Congenital Heart Disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2008;118(23):e714.

Prophylactic antibiotic regimens

For most patients and procedures, a single dose shortly before the procedure is effective. For oral-dental and respiratory procedures, a drug effective against viridans group streptococci is used (see Table: Recommended Endocarditis Prophylaxis During Oral-Dental or Respiratory Tract Procedures*). For vaginal delivery, give ampicillin 2 g IV or IM plus gentamicin 1.5 mg/kg (maximum 120 mg) IV administered within 30 minutes before delivery, followed by ampicillin 1 g IV or IM (or amoxicillin 1 g [as the trihydrate] po) 6 hours later.

Recommended Endocarditis Prophylaxis During Oral-Dental or Respiratory Tract Procedures*

Route

Drug and Dosage in Adults (and Children)

Drug and Dosage in Adults (and Children) Allergic to Penicillin

Oral (given 1 h before procedure)

Amoxicillin 2 g (50 mg/kg) po

Clindamycin 600 mg (20 mg/kg) po

or

Cephalexin or cefadroxil 2 g (50 mg/kg) po

or

Azithromycin or clarithromycin 500 mg (15 mg/kg) po

Parenteral (given 30 min before procedure)

Ampicillin 2 g (50 mg/kg) IM or IV

Clindamycin 600 mg (20 mg/kg) IV

or

Cefazolin 1 g (25 mg/kg) IM or IV

*For patients without active infection.

Adapted from Wilson W, Taubert KS, Gewitz M, et al: Prevention of infective endocarditis. Circulation 116(15):1736–1754, 2007.

For GI, GU, and musculoskeletal procedures on areas involving infected tissue, antibiotics should be selected based on the known organism and its sensitivities. If infection is present but the infecting organism has not been identified, antibiotics for GI and GU prophylaxis should be effective against enterococci (eg, amoxicillin or ampicillin, or vancomycin for patients who are allergic to penicillin). Antibiotics for skin and musculoskeletal prophylaxis should be effective against staphylococci and beta-hemolytic streptococci (eg, a cephalosporin or vancomycin or clindamycin if infection with methicillin-resistant staphylococci is possible).

Prevention reference

Key Points

  • Because the normal heart is relatively resistant to infection, endocarditis occurs mainly when there is a predisposing abnormality of the endocardium.

  • Predisposing cardiac abnormalities include congenital heart defects, rheumatic valvular disease, bicuspid or calcific aortic valves, mitral valve prolapse, hypertrophic cardiomyopathy, prior endocarditis, and intracardiac devices.

  • Local cardiac consequences include myocardial abscess, conduction system abnormalities, and sudden, severe valvular regurgitation.

  • Systemic consequences include immune phenomena (eg, glomerulonephritis) and septic emboli, which may affect any organ put particularly the lungs (with right sided endocarditis), kidneys, spleen, CNS, skin, and retina (with left-sided endocarditis).

  • Do blood cultures and diagnose using Duke or European Society of Cardiology clinical criteria.

  • Treat with a prolonged course of antimicrobial therapy; surgery may be needed for mechanical complications or resistant organisms.

  • Give antimicrobial prophylaxis for patients at high risk of an adverse outcome from infective endocarditis, including those with prosthetic heart valves or heart valve repair, previous infective endocarditis, certain congenital heart diseases, or who are heart transplant recipients with valvulopathy.

Resources In This Article

Drugs Mentioned In This Article

  • Drug Name
    Select Trade
  • CILOXAN, CIPRO
  • CLEOCIN
  • BIAXIN
  • No US brand name
  • NALLPEN IN PLASTIC CONTAINER
  • VANCOCIN
  • AMOXIL
  • ZITHROMAX
  • ZYVOX
  • CUBICIN
  • RIFADIN, RIMACTANE
  • FORTAZ, TAZICEF
  • KEFLEX
  • ANCEF, KEFZOL
  • MAXIPIME
  • ROCEPHIN
  • GENOPTIC
  • BACTOCILL IN PLASTIC CONTAINER