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Infective endocarditis is infection of the endocardium, usually with bacteria (commonly, streptococci and staphylococci) or fungi. It causes 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 can occur at any age. Men are affected about twice as often. IV drug abusers and immunocompromised patients 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 generally required for endocarditis: a predisposing abnormality of the endocardium and 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, and hypertrophic cardiomyopathy. Prosthetic valves 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—see Gram-Negative Bacilli: HACEK Infections), and fungi cause most of the rest. Why streptococci and staphylococci frequently adhere to vegetations and why gram-negative aerobic bacilli seldom adhere are unclear. However, the ability of S. aureus to adhere to fibronectin may play a role, as may dextran production by viridans streptococci.
After colonizing vegetations, microorganisms are covered by a layer of fibrin and platelets, which prevents access by neutrophils, Ig, and complement and thus blocks host defenses.
Pathophysiology
Endocarditis has local and systemic consequences.
Local consequences
Local consequences include formation of myocardial abscesses with tissue destruction and sometimes conduction system abnormalities (usually with low septal abscesses). Severe valvular regurgitation may develop suddenly, causing heart failure and death (usually due to mitral or aortic valve lesions). Aortitis may result from 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 and, primarily in chronic infection, immune-mediated phenomena. 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 CNS. 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, 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.
SBE
Initially, symptoms 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's 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's 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.
ABE and PVE
Symptoms and signs 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
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.
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). 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 they may be negative.
Echocardiography, typically transthoracic (TTE) rather than transesophageal (TEE), should be done. Although TEE is somewhat more accurate (ie, capable of revealing vegetations too small to be seen on TTE), it is invasive and more costly. TEE should be done when endocarditis is suspected in patients with prosthetic valves, when TTE is nondiagnostic, and when diagnosis of infective endocarditis has been established clinically.
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 Igs, 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 the organism and its antimicrobial susceptibility is vital to guide treatment. 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).
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, clinical criteria for establishing a diagnosis (with a sensitivity and specificity > 90%) have been developed (see Table 1: Endocarditis: Revised Duke Clinical Diagnostic Criteria for Infective Endocarditis ).
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Table 1
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| Revised Duke Clinical Diagnostic Criteria for Infective Endocarditis |
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Major criteria
Two positive blood cultures for organisms typical of endocarditis
Three positive blood cultures for organisms consistent with endocarditis
Serologic evidence of Coxiella burnetii
Echocardiographic evidence of endocardial involvement:
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Oscillating intracardiac mass on a heart valve, on supporting structures, in the path of regurgitant jets, or on implanted material without another anatomic explanation
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Cardiac abscess
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New dehiscence of prosthetic valve
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New valvular regurgitation
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Mnior criteria
Predisposing heart disorder
IV drug abuse
Fever ≥ 38° C
Vascular phenomena:
Immunologic phenomena:
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Glomerulonephritis
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Osler's nodes
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Roth's spots
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Rheumatoid factor
Microbiologic evidence of infection consistent with but not meeting major criteria
Serologic evidence of infection with organisms consistent with endocarditis
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For definite clinical diagnosis: 2 major criteria or 1 major and 3 minor criteria, or 5 minor criteria.
For possible clinical diagnosis: 1 major criterion and 1 minor criterion or 3 minor criteria.
For rejection of diagnosis: Firm alternative diagnosis explaining the findings of infective endocarditis, resolution of symptoms and signs after antimicrobial therapy for ≤ 4 days, no pathologic evidence of infective endocarditis found during surgery or autopsy, or failure to meet the clinical criteria for possible endocarditis.
Adapted from 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.
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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, or a long delay in treatment. The prognosis is also poorer for people with aortic or multiple valve involvement, large vegetations, polymicrobial bacteremia, prosthetic valve infections, mycotic aneurysms, valve ring abscess, and major embolic events. 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
Treatment consists of a prolonged course of antimicrobial therapy. 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. 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 2: Endocarditis: Antibiotic Regimens for Endocarditis ). Initial therapy before organism identification (but after adequate blood cultures have been obtained) should be broad spectrum to cover all likely organisms. Typically, patients with native valves and no IV drug abuse receive ampicillin 500 mg/h continuous IV infusion plus nafcillin 2 g IV q 4 h plus gentamicin 1 mg/kg IV q 8 h. Patients with a prosthetic valve receive vancomycin 15 mg/kg IV q 12 h plus gentamicin 1 mg/kg q 8 h plus rifampin 300 po q 8 h. IV drug abusers receive nafcillin 2 g IV q 4 h. In all regimens, penicillin-allergic patients require substitution of vancomycin 15 mg/kg IV q 12 h.
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Table 2
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| Antibiotic Regimens for Endocarditis |
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Type
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Drug And Dosage for Adults
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Drug and Dosage for Adults Allergic to Penicillin
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Penicillin-susceptible streptococci (penicillin G MIC ≤ 0.1 µg/mL), including most viridans streptococci
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Penicillin G 12–18 million units/day IV continuously or 2–3 million units q 4 h for 4 wk or, if gentamicin 1 mg/kg* IV (up to 80 mg) q 8 h is given concurrently, for 2 wk
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Ceftriaxone 2 g once/day IV for 4 wk or, if gentamicin 1 mg/kg* IV (up to 80 mg) q 8 h is given concurrently, for 2 wk through a central venous catheter (can be given on outpatient basis) if there is no history of penicillin anaphylaxis
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Vancomycin† 15 mg/kg IV q 12 h for 4 wk
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Streptococci relatively resistant to penicillin (penicillin G MIC > 0.1 µg/mL), including enterococci, some other streptococcal strains, and Abiotrophia defectiva (previously Streptococcus defectivus)
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Gentamicin 1 mg/kg* IV q 8 h plus penicillin G 18–30 million units/day IV or ampicillin 12 g/day IV continuously or 2 g q 4 h for 4–6 wk‡
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Desensitization to penicillin
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Vancomycin† 15 mg/kg IV (up to 1 g) q 12 h plus gentamicin 1mg/kg* IV q 8 h for 4–6 wk
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Pneumococci or group A streptococci
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Penicillin G 12–18 million units/day IV continuously for 4 wk if susceptible to penicillin
or
Vancomycin† 15 mg/kg IV q 12 h for 4 wk for pneumococci with penicillin G MIC ≥ 2 µg/mL
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Ceftriaxone 2 g once/day IV for 4 wk through a central venous catheter (can be given on outpatient basis) if there is no history of penicillin anaphylaxis
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Vancomycin† 15 mg/kg IV q 12 h for 4 wk
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Penicillin-resistant Staphylococcus aureus strains
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For patients with a left-sided native valve: Oxacillin or nafcillin 2 g IV q 4 h for 4–6 wk§
For patients with a right-sided native valve: Oxacillin or nafcillin 2 g IV q 4 h for 2–4 wk plus gentamicin 1 mg/kg* IV q 8 h for 2 wk
For patients with a prosthetic valve: 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 po q 8 h for 6–8 wk
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Cefazolin 2 g IV q 8 h for 4–6 wk if staphylococci are susceptible to oxacillin or nafcillin and if there is no history of penicillin anaphylaxis
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Cefazolin 2 g IV q 8 h for 2–4 wk plus gentamicin 1 mg/kg* IV q 8 h for 2 wk
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Cefazolin 2 g IV q 8 h for 4–6 wk plus gentamicin 1 mg/kg* IV q 8 h for 2 wk plus rifampin 300 mg po q 8 h for 6–8 wk
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Vancomycin† 15 mg/kg IV q 12 h alone if native valve, plus gentamicin 1 mg/kg* IV q 8 h for 2 wk plus rifampin 300 mg po q 8 h for 4–6 wk if prosthetic valve
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Oxacillin and nafcillin-resistant S. aureus strains
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Vancomycin† 15 mg/kg IV q 12 h alone if native valve, plus gentamicin 1 mg/kg IV* q 8 h for 2 wk plus rifampin 300 mg po q 8 h for 6–8 wk if prosthetic valve
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HACEK microorganisms
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Ceftriaxone 2 g once/day IV for 4 wk
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Ampicillin 12 g/day IV continuously or 2 g q 4 h plus gentamicin 1 mg/kg* IV q 8 h for 4 wk
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Ceftriaxone 2 g once/day IV for 4 wk or, if gentamicin 1 mg/kg* IV (up to 80 mg) q 8 h is given concurrently, for 2 wk if there is no history of penicillin anaphylaxis
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Coliform bacilli
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Sensitivity-proven β-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 4–6 wk
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Pseudomonas aeruginosa
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Ceftazidime 2 g IV q 8 h or cefepime 2 g IV q 8 h or imipenem 500 mg IV q 6 h plus tobramycin 2.5 mg/kg q 8 h for 6–8 wk; amikacin 5 mg/kg q 12 h substituted for tobramycin if bacteria are susceptible
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Ceftazidime 2 g IV q 8 h or cefepime 2 g IV q 8 h plus tobramycin 2.5 mg/kg q 8 h for 6–8 wk; amikacin 5 mg/kg q 12 h substituted for tobramycin if bacteria are susceptible only to amikacin
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*Based on ideal rather than actual weight in obese patients.
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†With vancomycin, serum levels must be monitored if doses > 2 g/24 h are administered.
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‡If enterococcal endocarditis lasts > 3 mo and involves large vegetations or vegetations on prosthetic valves, treatment should last for 6 wk.
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§Some clinicians add gentamicin 1 mg/kg IV q 8 h for 3–5 days if patients have a native valve.
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HACEK microorganisms: Haemophilus parainfluenzae, H. aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae.
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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 replacement) is frequently required for abscess, persistent infection despite antimicrobial therapy (ie, persistent positive blood cultures or recurrent emboli), or severe valvular regurgitation.
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.
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.
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.
Prevention
Preventive dental examination and therapy before surgery to repair heart valves or congenital heart lesions is recommended.
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
Procedures
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, and GI, GU, or musculoskeletal procedures that involve an area with an established infection (see Table 3: Endocarditis: Procedures Requiring Antimicrobial Endocarditis Prophylaxis in High-Risk Patients).
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Table 3
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| Procedures Requiring Antimicrobial Endocarditis Prophylaxis in High-Risk Patients |
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Type
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Examples
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Oral-dental*
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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
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Respiratory tract
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Bronchoscopy if mucosa is to be incised
Procedures done during an established infection
Tonsillectomy, adenoidectomy, or both
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GI tract
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None, unless procedure is done during an established infection
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GU tract
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None, unless procedure is done during an established infection (eg, cystoscopy during known enterococcal UTI)
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Musculoskeletal
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None, unless procedure involves infected tissue
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Skin
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None, unless procedure involves infected tissue
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*Examples of oral-dental procedures that do not require prophylaxis are anesthetic injection through uninfected mucosa and placement of orthodontic brackets.
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Data from Wilson W, Taubert KS, Gewitz M, et al: Prevention of infective endocarditis. Circulation 116(15): 1736–1754, 2007.
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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 4: Endocarditis: Recommended Endocarditis Prophylaxis During Oral-Dental or Respiratory Tract Procedures*)
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Table 4
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| Recommended Endocarditis Prophylaxis During Oral-Dental or Respiratory Tract Procedures* |
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Route
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Drug and Dosage in Adults (and Children)
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Drug and Dosage in Adults (and Children) Allergic to Penicillin
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Oral (given 1 h before procedure)
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Amoxicillin 2 g (50 mg/kg) po
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Clindamycin 600 mg (20 mg/kg) po
or
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Cephalexin or cefadroxil 2 g (50 mg/kg) po
or
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Azithromycin or clarithromycin 500 mg (15 mg/kg) po
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Parenteral (given 30 min before procedure)
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Ampicillin 2 g (50 mg/kg) IM or IV
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Clindamycin 600 mg (20 mg/kg) IV
or
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Cefazolin 1 g (25 mg/kg) IM or IV
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*For patients without active infection.
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Adapted from Wilson W, Taubert KS, Gewitz M, et al: Prevention of infective endocarditis. Circulation 116(15):1736–1754, 2007.
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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, and vancomycin for patients who are allergic to penicillin). Antibiotics for skin and musculoskeletal prophylaxis should be effective against staphylococci and β-hemolytic streptococci (eg, a cephalosporin or vancomycin or clindamycin if infection with methicillin-resistant staphylococci is possible).
Last full review/revision November 2006 by Lawrence L. Pelletier, Jr., MD
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