Infective Endocarditis

INFECTIVE ENDOCARDITIS

DR ALIREZA AHMADIAssistant

Professor of Medical

University of Isfahan

DEFINITION 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.

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.

EPIDEMIOLOGYINCIDENCE

The incidence of endocarditis is approximately 1 case per 1000 pediatric hospital admissions.

In a review of several published studies between 1986 and 1995, the estimated incidence in children was 0.3 per 100,000 children per year with a mortality of 11.6%

The distribution of etiologies has shifted. Rheumatic heart disease, which was once common, is now a rare cause of endocarditis.

In contrast, the advent of sophisticated cardiac procedures and

Early intervention has led to an increase in the incidence of endocarditis in children with congenital heart disease.

Preexisting cardiac abnormalities are found in approximately 75-90% of children with bacterial endocarditis.

Endocarditis is rare in infancy; in this age group,it usually follows open heart surgery or is associated

with a central venous line.

The overall mortality rate for endocarditis in pediatric patients is approximately 16-25%.

Improved general health care, improved dental care, early treatment, and antibiotic prophylaxis have decreased the

mortality rate. Mortality is mostly due to secondary

congestive heart failure (CHF).

Infective endocarditis can also occur in children without any abnormal valves or cardiac malformations.

Patients with congenital heart lesions where there is turbulent blood flow due to a hole or stenotic orifice, especially if there is a high pressure gradient across the defect, are most susceptible to endocarditis.

This turbulent flow traumatizes the vascular endothelium, creating a substrate for

deposition of fibrin and platelets, leading to the formation of a nonbacterial thrombotic embolus (NBTE) that is thought to be the initiating lesion for infective endocarditis.

The development of transient bacteremia then colonizes this NBTE or biofilm, leading to proliferation of bacteria within the lesion.

Given the heavy colonization of mucosal surfaces (the oropharynx, or gastrointestinal, vaginal, or urinary tracts) by potentially

pathogenic bacteria, these surfaces are thought to be the origin of this transient bacteremia.

Transient bacteremia has been reported

to occur in 20-68% of patients after tooth brushing.

Maintenance of good oral hygiene may be a more important factor in decreasing the frequency and magnitude of bacteremia.

HIGHEST RISK OF ADVERSE OUTCOME AFTER INFECTIVE ENDOCARDITIS

prosthetic cardiac valves or other prosthetic material used for cardiac valve

repair, unrepaired cyanotic CHD (including those

palliated with shunts and conduits), completely repaired defects with prosthetic material or device during the 1st 6 mo after

repair,* repaired CHD with residual defects at or

adjacent to the site of a prosthetic patch

previous infective endocarditis. Patients with high velocity blood flow

lesions such as ventricular septal defects and aortic stenosis are also at high risk.

In older patients, congenital bicuspid aortic valves and mitral valve prolapse with regurgitation pose additional risks for

endocarditis.

Surgical correction of CHD may reduce but does not eliminate the risk of endocarditis, with the exception of repair of a simple atrial septal defect or patent ductus arteriosus without prosthetic material.

RELATIVE RISK OF ENDOCARDITIS FOR VARIOUS CARDIOVASCULAR AND UNDERLYING CONDITIONS

High risk  1. Prosthetic valves  2. Previous episode of endocarditis  3. Complex cyanotic CHD(e.g., single ventricle ,TGA,TOF)   4. Surgically constructed systemic artery“to“pulmonary artery shunts  5. Injection drug use  6. Indwelling central venous catheters

Moderate risk   Uncorrected PDA   Uncorrected VSD   Uncorrected ASD (other than secundum)   Bicuspid aortic valve   MVP with regurgitation   Rheumatic mitral or aortic valve disease   Other acquired valvar diseases   Hypertrophic cardiomyopathy

In ",30% of patients with infective endocarditis, a predisposing factor is presumably recognized.

Although a preceding dental procedure may be identified in 10-20% of patients, the time of the procedure may range from 1 to 6 mo prior to the

onset of symptoms. Primary bacteremia with Staphylococcus

aureus is thought to be another risk for endocarditis.

ETIOLOGY Viridans-type streptococci (a-

hemolytic streptococci) and Staphylococcus aureus remain the

leading causative agents for endocarditis in pediatric patients.

Other organisms cause endocarditis less frequently and,

in =6% of cases, blood cultures are negative for any organisms .

No relationship exists between the infecting organism and the type of congenital defect,

the duration of illness, or the age of the child. Staphylococcal endocarditis is more

common in patients with no underlying heart disease;

viridans group streptococcal infection is more common after dental procedures;

group D enterococci are seen more often after lower bowel or genitourinary manipulation;

Pseudomonas aeruginosa or Serratia marcescens is seen more

frequently in intravenous drug users;

fungal organisms are encountered after open

heart surgery. Coagulase-negative staphylococci

are common in the presence of an indwelling central venous catheter.

BACTERIAL AGENTS IN PEDIATRICINFECTIVE ENDOCARDITIS

COMMON: NATIVE VALVE OR OTHER CARDIAC LESIONS

Viridans group streptococci (Streptococcus mutans, Streptococcus sanguinis,

Streptococcus mitis) Staphylococcus aureus Group D streptococcus (enterococcus)

(Streptococcus bovis, Streptococcus Faecalis)

UNCOMMON: NATIVE VALVE OR OTHER CARDIAC LESIONS

Streptococcus pneumoniae Haemophilus influenzae Coagulase-negative staphylococci Coxiella burnetii (Q fever)' Neisseria gonorrhoeae Brucella * Chlamydia psittaci* Chlamydia trachomatis* Chlamydia pneumoniae* Legionella* Bartonella *

HACEK GROUP

Streptobacillus moniliformis* Pasteurella multocida* Campylobacter fetus HACEKgroup includes Haemophilus species

(H. paraphrophilus, H. parainfluenzae, H. aphrophilus), Actinobacillus

actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella speciesCulture negative (6% of cases)

PROSTHETIC VALVE

Staphylococcus epidermidis Staphylococcus aureus Viridans group streptococcus Pseudomonas aeruginosa Serratia marcescens Diphtheroids Legionella species" HACEK qroup' Fungi

HISTORY

Prior congenital or rheumatic heart disease

Preceding dental, urinary tract, or intestinal procedure

Intravenous drug use Central venous catheter Prosthetic heart valve

SYMPTOMS Fever Chills Chest and abdominal pain Arthralgia, myalgia Dyspnea Malaise, weakness Night sweats Weight loss CNS manifestations (stroke, seizures, headache)

SIGNS Elevated temperature Tachycardia Embolic phenomena (Roth spots,

petechiae, splinter nail bed hemorrhages, Osler

nodes, CNS or ocular lesions) Janeway lesions New or changing murmur

SIGNS Splenomegaly Arthritis Heart failure Arrhythmias Metastatic infection (arthritis, meningitis,

mycotic arterial aneurysm, pericarditis, abscesses, septic pulmonary emboli) Clubbing

CLINICAL MANIFESTATIONS

Early manifestations are usually mild, especially when viridans group streptococci are the infecting organisms.

Prolonged fever without other manifestations (except, occasionally, weight loss) that persists for as long as several months may be the only

symptom.

Alternatively, the onset may be acute and severe, with

high, intermittent fever and prostration. The symptoms are often nonspecific and

consist of low-grade fever with afternoon elevations, fatigue, myalgia,

arthralgia, headache, and, chills, nausea, and vomiting.

CLINICAL FINDINGS IN INFECTIVE ENDOCARDITIS PATIENTS

Symptoms NVE (%) (n = 60) PVE (%) (n = 30)

Fever 75 87 Weight loss 52 20 Skin lesions 51 47 New murmur 33 33 Splenomegaly 20 20

New or changing heart murmurs are common, particularly with associated heart failure.

Splenomegaly and petechiae are relatively common. Serious neurologic : embolic strokes, cerebral abscesses, mycotic aneurysms, and hemorrhage are most often associated with staphylococcal disease and may be late

manifestations.

Meningismus, increased intracranial pressure, altered sensorium, and focal neurologic signs are

manifestations of these complications.

Myocardial abscesses may occur with staphylococcal disease and may damage the cardiac conducting system, causing

heart block, or may rupture into the pericardium and

produce purulent pericarditis. * Pulmonary and other systemic emboli are infrequent, except with fungal disease

Many of the classic skin findings develop late in the course of the disease; they are seldom seen in appropriately treated patients.

include Osler nodes (tender, pea-sized intradermal nodules in the pads of the fingers and toes),

Janeway lesions (painless small erythematous or hemorrhagic lesions on the palms and soles),

and splinter hemorrhages (linear lesions beneath the nails).

These lesions may represent vasculitis produced by circulating antigen-antibody complexes.

Identification of infective endocarditis is most often based on

a high index of suspicion during evaluation of an infection in a

child with an underlying risk factor.

LABORATORY Positive blood culture Elevated erythrocyte sedimentation

rate; may be low with heart or renal failure

Elevated C-reactive protein Anemia Leukocytosis

Immune complexes Hypergammaglobulinemia Hypocomplementemia Cryoglobulinemia Rheumatoid factor Hematuria Renal failure: azotemia, high creatinine

(glomerulonephritis

DIAGNOSIS

The critical information for appropriate treatment of infective endocarditis is obtained from blood cultures.

Blood specimens for culture should be obtained as promptly as possible, even if the child feels well and has no other physical findings.

Three to five separate blood collections should be

obtained after careful preparation of the phlebotomy site.

The timing of collections is not important because bacteremia can be expected to be relatively constant.

In 90% of cases of endocarditis, the causative agent is recovered from the 1st 2 blood cultures.

The laboratory should be notified that endocarditis is suspected so that, if necessary, the blood can

be cultured on enriched media for longer than usual (>7 days) to detect nutritionally deficient and fastidious bacteria or fungi.

Antimicrobial pretreatment of the patient reduces the yield of blood cultures to 50-60%.

Other specimens that may be cultured include scrapings from

cutaneous lesions, urine, synovial fluid, abscesses, and, in the presence of manifestations of

meningitis, cerebrospinal fluid.

Serologic diagnosis or PCR of resected valve tissues is

necessary in patients with unusual or fastidious

microorganisms.

Chest radiograph: bilateral infiltrates, nodules, pleural effusions Echocardiographic : valve vegetations, prosthetic valve dysfunction or leak, myocardial abscess, new-onset valve insufficiency

The combination of transthoracic and transesophageal echo cardiography enhances the ability to diagnose endocarditis.

Two-dimensional echocardiography can identify the size, shape, location, and mobility of the

lesion; when combined with Doppler studies, the presence of valve dysfunction (regurgitation,

obstruction) can be determined and its effect on left ventricular performance.

Echo is helpful in predicting embolic complications, given that lesions >1 cm and fungating masses are at greatest risk for embolization.

* The absence of vegetations does not exclude endocarditis, and vegetations are often not visualized in the early phases of the disease or in patients with complex congenital heart lesions.

THE DUKE CRITERIA The Duke criteria help in the diagnosis of endocarditis. Major criteria include: (1) positive blood cultures (2 separate cultures for a usual pathogen, 2 or more

for less typical pathogens), and (2) evidence of endocarditis on echocardiography

(intracardiac mass on a valve or other site, regurgitant flow near a prosthesis, abscess, partial dehiscence of prosthetic valves, or new valve regurgitant flow).

MINOR CRITERIA include predisposing conditions, fever, embolic-vascular signs, immune complex phenomena (glomerulonephritis, arthritis, rheumatoid factor,

Osler nodes, Roth spots), a single positive blood culture or serologic evidence

of infection, and echo cardiographic signs not meeting the major

criteria.

Two major criteria, or one major + three minor, or five minor criteria suggest definite endocarditis.

The following minor criteria are added to those above list:

the presence of newly diagnosed clubbing, splenomegaly, splinter hemorrhages, and petechiae; a high ESR; a high CRP; and the presence of central nonfeeding lines,

peripheral lines, and microscopic hematuria.

TREATMENT Antibiotic therapy should be instituted

immediately once a definitive diagnosis is made.

When virulent organisms are responsible,

small delays may result in progressive endocardial damage and are associated with a greater likelihood of severe complications.

Empirical therapy before the identifiable agent is recovered may

be initiated with vancomycin plus gentamicin in patients without a prosthetic valve and when there is a high risk of S. aureus

enterococcus or viridans streptococci (the 3 most common organisms).

A total of 4-6 wk of treatment is usually recommended.

Depending on the clinical and laboratory responses, antibiotic therapy may require modification

and, in some instances, more prolonged treatment is required.

With highly sensitive viridans group streptococcal infections,shortened regimens that include oral penicillin for some portion have been recommended.

In nonstaphylococcal disease, bacteremia usually resolves in 24-48 hr, whereas fever

resolves in 5-6 days with appropriate antibiotic therapy.

Resolution with staphylococcal disease takes longer.

Surgical intervention for infective endocarditis

is indicated for severe aortic or mitral valve involvement with intractable heart failure.

2007 STATEMENT OF THE AMERICAN HEART ASSOCIATION (AHA): PROPHYLACTIC ANTIBIOTIC REGIMENS FOR A DENTAL PROCEDURE Oral Amoxicillin 2g,(50 mg/kg)

Age Frequency Percent

< 2 years 7 30%

2-6 years 7 30%

7 -12 years 5 20%

13-18 years 5 20%Total 24 100%

Sex

MaleFemale

Frequency PercentStaph negative coagulase

4 40%

Staph aureus 2 20%Hemophilus 1 10%Ecoli 1 10%Pesudomonas 1 10%Fungal 1 10%Total 10 100%

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