Topic Resources
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.
Overview of Infective and Noninfective Endocarditis
VIDEO
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:
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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, urinary tract infection) 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 species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae), and fungi cause most of the rest.
The disease develops in 3 stages:
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Bacteremia: Microorganisms are present in the blood
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Adhesion: The microorganism adheres to abnormal or damaged endothelium via surface adhesions
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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
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Myocardial abscesses with tissue destruction and sometimes conduction system abnormalities (usually with low septal abscesses)
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Sudden, severe valvular regurgitation, causing heart failure and death (usually due to mitral or aortic valve lesions)
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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 of endocarditis 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 species, and fastidious Haemophilus
species. SBE often develops on abnormal valves after asymptomatic
bacteremia due to periodontal, gastrointestinal, or genitourinary
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 year after valve replacement and in 0.5%/year
thereafter. It is more common after aortic than after mitral valve
replacement and affects mechanical and bioprosthetic valves equally.
Early-onset infections (< 2 months after surgery) are caused mainly by contamination during surgery with antimicrobial-resistant bacteria (eg, S. epidermidis, diphtheroids, coliform bacilli, Candida species, Aspergillus
species). 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 species, 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 central nervous system (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 acute bacterial endocarditis and prosthetic
valvular endocarditis are similar to those of subacute bacterial
endocarditis, 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
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Blood cultures
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Echocardiography and sometimes other imaging modalities
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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 white blood cell count,
increased erythrocyte sedimentation rate, 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, red blood cell
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 samples for culture (20-mL
each) should be obtained within 24 hours (if presentation suggests acute
bacterial endocarditis, 2 cultures within the first 1 to 2 hours). 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 weeks of incubation for certain
organisms; however, some proprietary, automated culture monitoring
systems can identify positive cultures within a week. Other organisms
(eg, Aspergillus) may not produce positive cultures. Some organisms (eg, Coxiella burnetii, Bartonella species, Chlamydia psittaci, Brucella species) require serodiagnosis; others (eg, Legionella pneumophila) require special culture media or polymerase chain reaction (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
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Patients have a prosthetic valve
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Transthoracic echocardiogram is nondiagnostic
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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. Positron
emission tomography (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 tables Diagnostic Requirements for Infective Endocarditis 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:
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Vegetation, abscess, pseudoaneurysm, intracardiac fistula, valvular perforation or aneurysm, or new partial dehiscence of prosthetic valve identified by echocardiography
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Abnormal activity around a prosthetic valve (implanted > 3 months earlier) detected by PET/CT or single-photon emission computed tomography (SPECT)/CT with radiolabeled leukocytes
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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.
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
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Infection with resistant organisms
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An underlying disorder
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A long delay in treatment
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Aortic valve or multiple valve involvement
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Large vegetations
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Polymicrobial bacteremia
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Prosthetic valve infections
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Mycotic aneurysms
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Valve ring abscess
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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
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IV antibiotics (based on the organism and its susceptibility)
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Sometimes valve debridement, repair, or replacement
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Dental evaluation and treatment (to minimize oral sources of bacteremia)
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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 weeks, 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).
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 hour) 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
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Native valves: Vancomycin 15 to 20 mg/kg IV every 8 to 12 hours (not to exceed 2 g per dose)
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Prosthetic valve: Vancomycin 15 to 20 mg/kg IV every 8 to 12 hours (not to exceed 2 g per dose) plus gentamicin 1 mg/kg every 8 hours plus either cefepime 2 g IV every 8 hours or imipenem 1 g IV every 6 to 8 hours (maximum dose 4 g per day)
As soon as possible, the empiric drug regimen should be adjusted based on culture results.
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 every 4 hours plus gentamicin 1 mg/kg IV every 8 hours for 2 weeks is effective, as is a 4-week oral regimen of ciprofloxacin 750 mg twice a day plus rifampin 300 mg twice a day. Left-sided endocarditis does not respond to 2-week courses.
For left-sided endocarditis, current guidelines recommend 6 weeks
of parenteral antibiotic therapy . However, a recent multi-center,
randomized, non-blinded study of uncomplicated left-sided endocarditis
found that switching to oral antibiotics (after a minimum of 10 days of
parenteral therapy) to be non-inferior to continued parenteral therapy.
In addition, length of hospital stay was shortened in the patients
switched to oral therapy. This approach has the potential to reduce the
psychologic stress and some of the risks inherent to prolonged inpatient
parenteral therapy (2).
Cardiac valve surgery
Surgery (debridement, valve repair, or valve replacement) is sometimes required for treatment of infectious endocarditis (3). Surgery is typically indicated in
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Patients with heart failure (particularly those with prosthetic, aortic or mitral native valve endocarditis, and those with pulmonary edema or cardiogenic shock)
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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)
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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 hours of antimicrobial therapy.
In patients with prosthetic valves, surgery may be required when
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Transesophageal echocardiography shows valve dehiscence on a paravalvular abscess
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Valve dysfunction precipitates heart failure
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Recurrent emboli are detected
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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 weeks. Antibiotic retreatment may
be effective, but surgery may also be required. In patients without
prosthetic valves, recrudescence of endocarditis after 6 weeks 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 year 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.
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2. Iversen K, Ihlemann N, Gill SU, et al: Partial oral versus intravenous antibiotic treatment of endocarditis. N Engl J Med 380:415–424, 2019. DOI: 10.1056/NEJMoa1808312
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3. 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
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Prosthetic heart valves, including transcatheter implanted prostheses
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Prosthetic material used for heart valve repair (eg, annuloplasty rings, chords)
-
Previous infective endocarditis
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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
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 gastrointestinal, genitourinary, or
musculoskeletal procedures that involve an area with an established
infection (see table Procedures Requiring Antimicrobial Endocarditis Prophylaxis). Guidelines for endocarditis prophylaxis vary geographically.
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] orally) 6 hours later.
For gastrointestinal, genitourinary, 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 gastrointestinal and genitourinary 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
-
1. Cahill TJ, Baddour LM, Habib G, et al: Challenges in infective endocarditis. J Am Coll Cardiol 69(3):325–344, 2017.
Key Points
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Because the normal heart is relatively resistant to infection, endocarditis occurs mainly when there is a predisposing abnormality of the endocardium.
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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.
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Local cardiac consequences include myocardial abscess, conduction system abnormalities, and sudden, severe valvular regurgitation.
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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, central nervous system, skin, and retina (with left-sided endocarditis).
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Do blood cultures and diagnose using Duke or European Society of Cardiology clinical criteria.
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Treat with a prolonged course of antimicrobial therapy; surgery may be needed for mechanical complications or resistant organisms.
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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.
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