Infective endocarditis in children

INTRODUCTION — Infective endocarditis (IE) is an infection of the endocardium and/or heart valves that involves thrombus formation (vegetation), which may damage the endocardial tissue and/or valves. The process can involve native endocardium/endothelium or prosthetic material. Although uncommon in children, it is important to identify and treat IE because of its significant morbidity and mortality. Prompt diagnosis, rapid treatment, and recognition of complications are imperative for optimal patient outcomes.

IE is also referred to as bacterial endocarditis because bacteria are the predominant microbial pathogens. IE is used in this review to include both bacterial and fungal endocarditis.

Many aspects of IE are similar in children and adults, but there are some manifestations that are unique to children. An overview of IE in children is presented here. A number of other topics address particular issues in detail, some of which will be addressed here for children:

●Antibiotic prophylaxis of IE (see "Prevention of endocarditis: Antibiotic prophylaxis and other measures")

●Antimicrobial therapy for IE (see "Antimicrobial therapy of left-sided native valve endocarditis" and "Antimicrobial therapy of prosthetic valve endocarditis")

●Complications and outcome of IE (see "Complications and outcome of infective endocarditis")

●Diagnostic criteria and approach for IE (see "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis")

●Epidemiology, risk factors and microbiology of IE (see "Native valve endocarditis: Epidemiology, risk factors, and microbiology")

●Role of echocardiography in the diagnosis of IE (see "Role of echocardiography in infective endocarditis")

●Surgery for IE (see "Surgery for left-sided native valve infective endocarditis" and "Surgery for prosthetic valve endocarditis")

EPIDEMIOLOGY

Incidence — Reported incidence rates of pediatric IE in the United States range from 0.3 to 3.3 per 100,000 individuals per year [1,2]. Rates are higher among infants <1 year old compared with older children and adolescents. The highest rates are seen in children with congenital heart disease (CHD). In one study, the estimated cumulative risk of IE by age 18 years among children with CHD was 0.6 percent [3].

Rates of pediatric IE increased during the latter half of the twentieth century, likely due to dramatic improvements in survival of children with CHD and increased use of central venous catheters (CVC) [4,5]. Since the early 2000s, rates of IE appear to have plateaued or slightly decreased [1,2,6]. Studies evaluating pediatric hospital admission rates for IE in the United States before and after publication of the 2007 revised antibiotic prophylaxis guidelines did not detect a difference between the two eras [6,7].

Risk factors — Most children with IE have an identifiable risk factor for the disease.

Congenital heart disease — Children with CHD, especially those with cyanotic heart disease, are at increased risk of developing IE. Underlying CHD is present in approximately 35 to 60 percent of children with IE [2,4,6,8-10]. The risk of IE is highest in patients with complex cyanotic heart disease, especially in those who have had surgical intervention [3,8,11-16].

Reported incidence rates of IE in children with CHD range from 40 to 60 per 100,000 person-years, which is several orders of magnitude higher than in the general pediatric population [3,17]. In these reports, the CHD lesions at highest risk for IE included cyanotic lesions, endocardial cushion defect, left-sided lesions, and ventricular septal defects (VSD). Other risk factors included cardiac surgery within six months and age <3 years.

There appears to be an increased risk for IE in patients who undergo transcatheter pulmonary valve replacement (eg, following repair of tetralogy of Fallot); the risk is particularly high with bovine jugular vein prostheses [18]. This issue is discussed in greater detail separately. (See "Tetralogy of Fallot (TOF): Long-term complications and follow-up after repair", section on 'Pulmonary valve replacement (PVR)' and "Tetralogy of Fallot (TOF): Management and outcome".)

In a study of 3840 pediatric hospital admissions for IE from the Nationwide Inpatient Sample database (2000 to 2010), 54 percent had underlying cardiac conditions, of whom 81 percent had CHD [2]. The most common congenital heart defect was VSD (32 percent). Cyanotic lesions accounted for 25 percent of the CHD cases. A prosthetic valve was present in 7 percent, and other cardiac devices were present in 4 percent.

In a similar study of 1588 pediatric hospital admissions for IE from the Kid's Inpatient Database (2000 to 2003), the most common CHD diagnoses were tetralogy of Fallot (20 percent), ventricular septal defect (18 percent), hypoplastic left heart syndrome (10 percent), congenital aortic regurgitation (8 percent), D-transposition of the great arteries (6 percent), and patent ductus arteriosus (5 percent) [8].

Central venous catheters — An indwelling CVC is another major risk factor for pediatric IE [19]. At-risk pediatric populations for IE include critically ill and premature infants and children with cancer or connective tissue disorders. The increased use of CVCs in these pediatric groups appears to be a major factor for IE [8,11,12,19,20]. The risk is similarly increased with use of other intracardiac devices (eg, ventriculoatrial shunts, pacemakers, implantable cardioverter-defibrillators, and prosthetic and bioprosthetic valves). In a study of 3840 pediatric hospital admissions for IE (2000 to 2010), 7 percent of patients with underlying cardiac conditions had a prosthetic valve and 4 percent had another cardiac device [2]. As use of these devices becomes more common, the relative proportion of device-related IE increases. (See "Intravascular catheter-related infection: Epidemiology, pathogenesis, and microbiology" and "Hydrocephalus in children: Management and prognosis", section on 'CSF shunt'.)

Rheumatic heart disease — In developed countries, the incidence of rheumatic heart disease has declined dramatically since the 1960s, and in the modern era, rheumatic heart disease is an uncommon predisposing condition for IE in children [4,8]. In a study of 3840 pediatric hospital admissions for IE (2000 to 2010), 15 percent of patients with underlying cardiac conditions had rheumatic heart disease [2]. In resource-limited settings, rheumatic heart disease remains an important risk factor. (See "Acute rheumatic fever: Epidemiology and pathogenesis", section on 'Epidemiology' and "Clinical manifestations and diagnosis of rheumatic heart disease".)

Other risk factors — Intravenous drug abuse (associated with right-sided IE) and degenerative heart disease, which are important predisposing factors in the adult population, are less commonly seen in children [4,21].

PATHOGENESIS — IE is the result of a series of complex interactions among blood-borne pathogens, damaged endothelium, fibrin, and platelets [22].

●The endocardial surface is initially injured by shear forces associated with turbulent blood flow in children with congenital heart disease (CHD), or indwelling central venous catheters in children without CHD.

●At the site of endothelial damage, fibrin, platelets, and occasionally red blood cells are deposited and initially form a noninfected thrombus.

●Transient bacteremia (which occurs in normal children) or fungemia results in adherence of microbial pathogens to the injured endocardium and thrombus. Subsequent fibrin and platelet deposition over the infected vegetation result in a protective sheath that isolates the organisms from host defenses and permits rapid proliferation of the infectious agent.

Involvement of other organs is secondary to embolization or immune-mediated processes (eg, glomerulonephritis). (See 'Clinical manifestations' below and 'Complications' below.)

MICROBIOLOGY — Although a variety of microorganisms can cause IE, staphylococci and streptococci species are the most common pathogens associated with IE in children [2,8,23]. In a large retrospective study that included culture results on >2500 children hospitalized for IE, the relative frequency of different pathogens varied according to whether the child had underlying heart disease [2]:

●Among children with underlying heart disease:

•Staphylococcus aureus – 28 percent

•Other Staphylococcus species – 7 percent

•Viridans streptococci – 33 percent

•Other streptococci – 17 percent

•Gram-negative bacilli – 5 percent

•Polymicrobial – 11 percent

●Among children without underlying heart disease:

•S. aureus – 47 percent

•Other Staphylococcus species – 6 percent

•Viridans streptococci – 18 percent

•Other streptococci – 10 percent

•Gram-negative bacilli – 8 percent

•Polymicrobial – 12 percent

These results demonstrate the relatively high incidence of endocarditis due to S. aureus, particularly among children without heart disease. IE caused by S. aureus is typically an acute fulminant process with a high mortality rate, as compared with IE due to most other pathogens. (See 'Clinical manifestations' below and 'Outcome' below.)

Although patients with indwelling catheters are at risk for bacteremia with gram-negative organisms, gram-negative bacterial endocarditis is rare. This is probably due to the poor ability of gram-negative bacteria to adhere to the endocardium.

In neonates with IE, likely etiologic agents include S. aureus, coagulase-negative staphylococci, Klebsiella pneumonia, and Enterobacter species, among others [24].

Similar to adults, blood cultures remain negative in 5 to 7 percent of children with IE [4,21,22,25]. Potential mechanisms include previous administration of antimicrobial agents, inadequate microbiologic techniques, or infection with highly fastidious bacteria or nonbacterial pathogen. Consultation with an infectious disease expert is recommended in all cases of culture-negative endocarditis.

Fungal endocarditis is rare and is typically caused by Candida species [4]. Indwelling catheters and high glucose concentrations in parenteral nutrition have contributed to the occurrence of fungal endocarditis, especially in premature infants [12]. Fungal endocarditis is frequently associated with large, friable vegetations that can embolize, producing important complications. (See 'Complications' below and "Clinical manifestations and diagnosis of Candida infection in neonates", section on 'Endocarditis'.)

CLINICAL MANIFESTATIONS

Presentation — The clinical presentation of pediatric IE is variable and depends upon the extent of the local cardiac disease, degree of involvement of other organs (eg, embolization), and the causative agent.

IE is generally classified as a subacute or acute process.

●Subacute — The subacute presentation is characterized by a prolonged course of low-grade fever and nonspecific complaints including fatigue, arthralgias, myalgias, chills, weight loss, exercise intolerance, and diaphoresis. The presence of a cluster of these symptoms in a patient at risk for IE (ie, those with preexisting heart disease or indwelling central venous catheter) should raise the possibility of IE as a potential diagnosis. In addition, there is a risk of immunologic sequelae, such as immune-mediated glomerulonephritis. The less virulent pathogens, such as viridans group streptococci and coagulase-negative staphylococci, are usually the causative agents for subacute IE.

●Acute — Acute IE is a rapidly progressive and fulminant disease. These patients typically have high spiking fevers, and appear severely ill. An acute presentation is commonly seen in patients with IE due to S. aureus, which can cause rapid destruction of heart valve tissue, abscess formation, embolic phenomena, and a rapidly progressive deterioration in hemodynamic status.

Clinical findings — The clinical findings of IE correspond to the underlying pathologic phenomena of bacteremia/fungemia, valvulitis, immunologic response, and embolization [22].

●Symptoms associated with bacteremia or fungemia include fever, and vasodilation and tachycardia due to decreased systemic vascular resistance. (See "Pathophysiology of sepsis", section on 'Circulation'.)

●Valvulitis may result in a new or changing murmur. In some patients, tachypnea and hypotension are signs of heart failure, which occurs because of perforation of a valve, chordal rupture, or poor ventricular function.

●In children with cyanotic congenital heart disease (CHD) with either a systemic-pulmonary shunt or conduit procedure, the murmur may not change, but a decline in systemic oxygen saturation may occur due to obstruction of blood flow.

●Glomerulonephritis may develop in children who present with subacute IE as a consequence of immune-mediated disease. Other immunologic sequelae (ie, Roth's spots, Janeway lesions, and Osler nodes) are less common in children than they are in adults. These are described in greater detail elsewhere. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis", section on 'Clinical manifestations'.)

●In children with IE, septic emboli are common, resulting in extracardiac infection (eg, osteomyelitis or pneumonia) or infarction to major vessels and organs. Emboli to the brain may result in neurologic symptoms (eg, seizures, headache, strokes, or altered mental status). Other major organs that may be at risk for embolic episodes include the kidney, gastrointestinal tract, limbs, and lungs. Ophthalmic evaluation might reveal retinal hemorrhagic lesions (Roth spots).

●In the neonate, the signs and symptoms of IE are variable and nonspecific [26,27]. They include feeding intolerance, tachycardia, respiratory distress, hypotension, and a new or changing murmur. Fever may not be present with either subacute or acute IE. Those with right-sided IE in association with central venous catheters characteristically have little clinical evidence of disease other than persistently positive blood cultures in the setting of appropriate antibiotic treatment [24]. Fungal IE is more common in the newborn infant and may present as an acute fulminant disease [12]. The IE presentation may be indistinguishable from septicemia or heart failure.

Laboratory findings — Nonspecific laboratory findings that support the diagnosis of IE include:

●Low hemoglobin/hematocrit demonstrating anemia (either hemolytic or anemia of chronic disease), which is a common feature of IE

●Elevated erythrocyte sedimentation rate and C-reactive protein indicative of inflammation

●Urinalysis showing hematuria, proteinuria, and red cell casts is suggestive of glomerulonephritis, a minor diagnostic criterion

ECG and chest radiograph findings

●Electrocardiography (ECG) – ECG is generally not helpful in the diagnosis of IE with the exception of IE with periannular extension, in which prolongation of the PR interval or frank heart block can occur.

●Chest radiography – The chest radiograph is often normal. Nonspecific findings may include cardiomegaly, pulmonary edema, and focal pulmonary infiltrates in patients with pulmonary septic emboli.

DIAGNOSIS — The diagnosis of IE is based upon history, physical examination, blood cultures, laboratory tests, and echocardiography.

Blood cultures — Blood cultures are performed in all patients since one of the two major diagnostic criterion is positive blood cultures for typical organisms associated with IE from at least two separate specimens. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)

A minimum of three blood cultures should be obtained over a time period of a few hours to two days depending upon the severity of the illness. In most patients, three blood cultures are obtained from separate venipunctures in the first 24 hours and an additional two blood cultures in the next 24 hours if there is no growth [28]. In critically ill children, three separate venipunctures for blood cultures should be performed as quickly as possible (with <1 hour) and empiric antibiotic therapy started promptly. In children who are not acutely ill, antibiotic therapy can be withheld for at least 48 hours while the blood cultures are collected [28].

Unless there has been prior antibiotic therapy, more than five blood cultures over two days is generally not warranted. Since bacteremia is generally continuous, the blood cultures do not have to be obtained at any particular time in the fever cycle.

It is important to obtain adequate volumes of blood for culture. However, in children, it is often not possible to obtain the large volumes of blood (10 to 20 mL) recommended for adults with suspected IE. In most pediatric settings, the obtained volume of blood for culture is approximately 1 to 3 mL in infants and young children and 5 to 7 mL in older children. If there is a limited volume of blood, preferential culturing of the aerobic culture bottle is suggested because almost all cases of bacterial IE are due to aerobic organisms, and culturing for anaerobes is rarely useful.

Cardiac imaging

Echocardiography — An echocardiogram should be performed on all patients in whom there is a reasonable suspicion of IE, as it may detect the presence of a vegetation, a major diagnostic Duke criterion. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis", section on '2023 Duke-ISCVID criteria'.)

Risk factors for IE including preexisting heart disease, indwelling central lines, presence of prosthetic material, persistent bacteremia, or infection with organisms most associated with IE should prompt early evaluation. Other echocardiographic findings of IE include intracardiac abscess, new or progressive valvular regurgitation, and, in patients with a prosthetic valve, evidence of partial dehiscence.

In patients with IE, echocardiography can identify the size and location of a vegetation, extent of valve damage and the degree of valvar stenosis or regurgitation, perivalvar extension of infection, conduit or shunt obstruction, ventricular function, and the presence of a pericardial effusion. It can be used to serially monitor hemodynamic and valvular function, and the resolution of vegetations in response to medical treatment. (See "Role of echocardiography in infective endocarditis".)

In most pediatric cases of suspected IE, transthoracic echocardiography (TTE) is adequate to detect the presence of a vegetation, especially in infants and younger children (<10 years and <60 kg), and to monitor hemodynamic and valvular function. TTE is a much more sensitive diagnostic tool in children compared with adults [22,29,30].

However, in some children, TTE provides inadequate imaging due to suboptimal echocardiographic windows, which may be circumvented by transesophageal echocardiography (TEE). Inadequate TTE imaging is most likely to occur in the following patients [22]:

●Overweight children.

●Muscular children.

●Children with significant respiratory disease.

●Children with surgically repaired complex congenital heart disease (CHD), as artifacts from prosthetic material (grafts and conduits) and valves may interfere with TTE imaging [31]. Suboptimal echocardiographic windows are frequently present in the postoperative patient.

●Children with chest wall disruption from prior surgery or trauma.

●Children with congenital anomalies involving the thoracic cage (eg, severe pectus excavatum).

In addition, in children with aortic valve IE, TEE is superior to TTE for the detection of aortic root abscess. Thus, TEE may be warranted if there are findings on TTE consistent with periannular extension (eg, changing aortic root dimensions) or if there are concerning findings on electrocardiogram (eg, prolonged PR interval or heart block) [28,32,33].

Both TTE and TEE may give false-negative results if the vegetations are small or if embolization of the vegetation has occurred. The absence of visible vegetations on echocardiogram does not exclude IE.

Other imaging modalities — Other imaging modalities such as cardiac magnetic resonance imaging, computed tomography, or cardiac positron emission tomography may be useful in select clinical situations, including when suspicion for endocarditis is high but TTE or TEE have been unrevealing. Additional benefits include the ability to identify distant emboli and early spread of infection prior to anatomic changes. These modalities are discussed in greater detail separately. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis".)

Diagnostic criteria — The diagnostic criteria used most commonly for the diagnosis of pediatric IE are the Duke-International Society for Cardiovascular Infectious Disease (ISCVID) criteria, which categorize patients as "definite IE," "possible IE," and "rejected IE" based on pathologic and clinical criteria [34]. These criteria are outlined separately. (See "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis", section on '2023 Duke-ISCVID criteria'.)

TREATMENT — In general, the principles of treatment of IE in children are the same as in adults. In patients with acute IE, blood cultures should be obtained as quickly as possible so appropriate antibiotic therapy can be started. Patients with IE-associated valve dysfunction causing symptomatic heart failure and patients with persistent fevers and bacteremia despite appropriate antibiotic therapy may be candidates for surgical intervention.

Antibiotic regimens — Antibiotic choice, dose, and duration of treatment are dependent upon the underlying causative microbial agent, and are discussed in greater detail separately. (See "Antimicrobial therapy of left-sided native valve endocarditis".)

Antibiotic regimens for common bacterial pathogens in pediatric IE are summarized in the tables:

●Viridans group streptococci and Streptococcus bovis (table 1A-D)

●Enterococci (consultation with an infectious disease specialist is recommended (table 2))

●Staphylococci (table 3A-B)

●Gram-negative organisms (including Haemophilus sp, Aggregatibacter sp, Cardiobacterium hominis, Eikenella corrodens, and Kingella sp [ie, the HACEK group]) (table 4)

Culture-negative endocarditis (CNE) occurs rarely in children and may be diagnosed when a patient has clinical or echocardiographic evidence of IE but persistently negative blood cultures [28]. Patients with suspected CNE should be managed in consultation with a pediatric infectious disease specialist. Important considerations in determining the treatment regimen include prior antibiotic exposure, route of acquisition of the infection, whether the infection is community acquired or nosocomial, whether the valve infected is native or prosthetic, and whether the infection is acute or subacute [28].

Surgical intervention — Determination of the need for surgical intervention should be individualized using a multispecialty approach, including involvement of experts in infectious disease, cardiology, and cardiothoracic surgery. Considerations in children are generally similar to those in adults with IE. The most common reasons for surgical intervention include congestive heart failure, progressive valve dysfunction, and embolic phenomena [28,35,36]. Limited pediatric data are available, and clinical practice is largely guided by adult guidelines.

Recommendations for surgical intervention in patients with IE are reviewed in detail elsewhere. (See "Surgery for left-sided native valve infective endocarditis".)

MONITORING — The following tests are helpful in monitoring the patient's clinical course during treatment and after completion of antibiotic therapy:

●Antimicrobial levels – Patients receiving treatment with gentamicin or vancomycin should have blood levels for these drugs checked at least once a week. The dose of gentamicin should be adjusted for a target peak level of 3 to 4 mcg/mL and a trough level of <1 mcg/mL, although higher levels may be required for some gram-negative infections [28]. For vancomycin, the target trough level is 10 to 15 mcg/mL, though higher levels (ie, 15 to 20 mcg/mL) may be required initially for methicillin-resistant staphylococci. Children with renal insufficiency require dose adjustments for these agents [28].

●Echocardiography – Repeat echocardiogram may be warranted during treatment of IE to assess for changes in vegetations and evaluate valve and myocardial function. This is particularly true of patients exhibiting clinical deterioration, new murmurs, persistent fevers, or bacteremia. Once treatment is completed, repeat evaluation may be necessary to establish a new baseline of valvar and myocardial function for the patient [37].

●Repeat blood cultures – Repeat blood cultures are always warranted if there is recurrence of symptoms. Cultures performed after completion of antibiotic therapy may be helpful to demonstrate adequacy of treatment in certain cases (eg, in a patient with S. aureus prosthetic valve infection associated with prolonged bacteremia); however, repeat blood cultures may also result in isolation of a contaminant [28].

PREVENTION — Strategies to prevent IE in children include oral hygiene for prevention of oral disease and antimicrobial prophylaxis for high-risk patients when undergoing invasive procedures [28]. We provide antibiotic prophylaxis in children who are at highest risk for IE based upon guidance from the American Heart Association [38]. Antibiotic IE prophylactic regimens for children are summarized in the table (table 5). Antibiotic prophylaxis for IE is discussed in detail separately, including discussion of patient selection and relevant procedures. (See "Prevention of endocarditis: Antibiotic prophylaxis and other measures".)

OUTCOME

Mortality — Reported mortality rates among children with IE range from 1 to 5 percent [2,6,8,10]. Mortality is highest among patients with underlying cyanotic congenital heart disease (CHD) and with infection caused by S. aureus [2,8]. In addition, the risk of mortality is increased in patients who develop complications from IE, particularly heart failure, perivalvular abscess, stroke, or septic emboli with distant abscesses.

Complications — Complications seen in children with IE are generally similar to those seen in adults; however, as a general rule, these complications occur less commonly in children compared with adults.

Factors that predispose to the development of complications in children with IE include [22].

●Prosthetic cardiac valves

●Left-sided involvement

●S. aureus or fungal IE

●Previous IE

●Prolonged symptoms (≥3 months)

●Cyanotic congenital heart disease

●Systemic-to-pulmonary shunts

●Poor clinical response to antimicrobial therapy

Complications of IE include cardiac sequelae and end-organ infection or infarction due to embolic events:

●Cardiac complications – Cardiac complications include the following (see "Complications and outcome of infective endocarditis", section on 'Cardiac complications'):

•Heart failure – Heart failure can be caused by perforation of the valve, rupture of an infected chordae, or perivalvar leaks or dehiscence in patients with prosthetic valve. Poor ventricular function often accompanies worsening valvar regurgitation. Heart failure is the most common indication for surgical intervention in patients with IE. (See "Surgery for left-sided native valve infective endocarditis".)

•Perivalvular abscess – Extension of infection beyond the endothelium may result in a fistula tract or perivalvular infection (eg, abscess), which may cause an arrhythmia or atrioventricular heart block. Transesophageal echocardiography (TEE) is more sensitive for detection of myocardial abscess than transthoracic echocardiography (TTE). (See "Role of echocardiography in infective endocarditis", section on 'Perivalvular abscess or fistula'.)

•Extension of infection into a prosthetic shunt or conduits may occlude the graft. These infections require surgical intervention because they rarely respond to medical management.

●Metastatic infection – Infection at other sites can occur from septic emboli resulting in osteomyelitis, pneumonia, or distal abscesses in the kidneys, spleen, brain, or soft tissues.

●Mycotic aneurysms – Can occur in any systemic artery and result from septic embolization or, occasionally, from contiguous spread of infection. This complication is usually an indication for surgery.

●Stroke – Stoke occurs in 5 to 15 percent of pediatric IE cases, chiefly in the setting of left-sided IE [2,10,39].

●Acute kidney injury (AKI) – AKI can be caused by renal infarction, glomerulonephritis (as a result of an immune-mediated secondary process), and drug-induced acute interstitial nephritis. AKI occurs in approximately 10 percent of pediatric patients with IE [2].

●Other embolic events, including:

•Pulmonary embolism (typically occurs in the setting of right-sided IE)

•Ischemia of the extremities

•Splenic infarction

•Visual impairment (due to embolism or due to endophthalmitis as a result of bacteremic seeding)

•Acute myocardial infarction

The complications of IE are discussed in greater detail separately. (See "Complications and outcome of infective endocarditis".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Treatment and prevention of infective endocarditis".)

SUMMARY AND RECOMMENDATIONS

●Incidence – Infective endocarditis (IE) is uncommon in children, with an estimated annual incidence of approximately 0.43 per 100,000 per year. Most children with IE have an identifiable risk factor of either preexisting heart disease and/or an indwelling central venous catheter (CVC) or other device. (See 'Incidence' above and 'Risk factors' above.)

●Microbiology – Streptococci and staphylococci species are the most common pathogens associated with IE in children, although a variety of microorganisms can cause IE. (See 'Microbiology' above.)

●Clinical presentation – The clinical presentation of pediatric IE is variable and is generally classified as either a subacute or acute process. (See 'Presentation' above.)

•Subacute presentation is characterized by a prolonged course of low-grade fevers and nonspecific complaints, including fatigue, chills, arthralgias, myalgias, weight loss, exercise intolerance, and diaphoresis.

•Acute IE is a rapidly progressive fulminant disease with high, spiking fevers and an increased likelihood of complications, including hemodynamic instability and heart failure. Staphylococcus aureus is the organism most commonly associated with acute IE and carries a higher mortality risk.

●Physical findings – Physical findings consistent with a diagnosis of IE include a new regurgitant heart murmur and evidence of embolic events. (See 'Clinical findings' above.)

●Diagnosis – The clinical diagnosis of IE is made by fulfilling the 2023 Duke-International Society for Cardiovascular Infectious Disease (ISCVID) criteria, which are based upon blood cultures, echocardiogram findings, and other clinical findings. (See 'Diagnosis' above and "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis", section on '2023 Duke-ISCVID criteria'.)

●Treatment – The principles of treatment of IE in children are the same as those for adults (see 'Treatment' above):

•Antibiotic therapy – The choice, dose, and duration of antibiotic therapy depend upon the underlying causative microbial agent (see 'Antibiotic regimens' above):

-Viridans group streptococci and Streptococcus bovis (table 1A-D)

-Enterococci (consultation with an infectious disease specialist is recommended (table 2))

-Staphylococci (table 3A-B)

-Gram-negative organisms (including Haemophilus sp, Aggregatibacter sp, Cardiobacterium hominis, Eikenella corrodens, and Kingella sp [ie, the HACEK group]) (table 4)

•Surgical intervention – Determination of the need for surgical intervention should be individualized using a multispecialty approach, including involvement of experts in infectious disease, cardiology, and cardiothoracic surgery. Considerations in children are generally similar to those in adults with IE. (See "Surgery for left-sided native valve infective endocarditis".)

●Prevention – Prophylactic antibiotic therapy for IE (table 5) is reserved for patients with the highest risk of IE, as discussed separately. (See "Prevention of endocarditis: Antibiotic prophylaxis and other measures".)

●Outcome – The mortality rate for pediatric IE is approximately 1 to 5 percent. Prematurity, cyanotic CHD, and IE due to S. aureus are important risk factors for mortality. (See 'Mortality' above.)

Complications of IE include cardiac sequelae (eg, heart failure, perivalvular abscess) and end-organ infection or infarction due to embolic events. (See 'Complications' above and "Complications and outcome of infective endocarditis".)