Infective Endocarditis

1. Infective Endocarditis

2. Infective Endocarditis DR ALIREZA AHMADI Assistant Professor of Medical University of Isfahan

3. 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. Definition

5. 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. EpidemiologyIncidence

6. 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.

7. 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.

8. 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).

9. Infective endocarditiscan 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.

11. 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 bacteremiathen colonizes this NBTE or biofilm, leading to proliferation of bacteria within the lesion.

13. 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.

16. 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.

17. 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 highest risk of adverse outcome after infective endocarditis

18. 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.

19. Surgical correction of CHD may reduce but does not eliminate the risk of endocarditis, with the exception of repair of a simple atrialseptal defect or patent ductusarteriosus without prosthetic material.

20. 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 RELATIVE RISK OF ENDOCARDITIS FOR VARIOUS CARDIOVASCULAR AND UNDERLYING CONDITIONS

21. 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

22. 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 bacteremiawith Staphylococcus aureus is thought to be another risk for endocarditis.

23. Viridans-type streptococci (a-hemolytic streptococci) and Staphylococcus aureusremain the leading causative agents for endocarditisin pediatric patients. Other organisms cause endocarditisless frequently and, in =6% of cases, blood cultures are negative for any organisms . Etiology

24. No relationship exists between the infecting organism and the typeof congenital defect, the durationof illness, or the ageof the child. Staphylococcal endocarditis is more common in patients with no underlying heart disease;

25. viridans group streptococcal infection is more common after dental procedures; group D enterococciare seen more often after lower bowel or genitourinary manipulation; Pseudomonas aeruginosa or Serratiamarcescensis seen more frequently in intravenous drug users;

26. fungal organisms are encountered after open heart surgery. Coagulase-negative staphylococci are common in the presence of an indwelling central venous catheter.

27. 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) BACTERIAL AGENTS IN PEDIATRICINFECTIVE ENDOCARDITIS

28. Streptococcus pneumoniae Haemophilusinfluenzae Coagulase-negative staphylococci Coxiellaburnetii (Q fever)' Neisseriagonorrhoeae Brucella * Chlamydia psittaci* Chlamydia trachomatis* Chlamydia pneumoniae* Legionella* Bartonella * UNCOMMON: NATIVE VALVE OR OTHER CARDIAC LESIONS

29. Streptobacillusmoniliformis* Pasteurellamultocida* Campylobacter fetus HACEKgroupincludes Haemophilus species (H. paraphrophilus, H. parainfluenzae, H. aphrophilus), Actinobacillusactinomycetemcomitans, Cardiobacteriumhominis, Eikenellacorrodens, and KingellaspeciesCulturenegative (6% of cases) HACEK group

30. Staphylococcus epidermidis Staphylococcus aureus Viridans group streptococcus Pseudomonas aeruginosa Serratiamarcescens Diphtheroids Legionella species" HACEK qroup' Fungi PROSTHETIC VALVE

31. Prior congenital or rheumatic heart disease Preceding dental, urinary tract, or intestinal procedure Intravenous drug use Central venous catheter Prosthetic heart valve HISTORY

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

33. Elevated temperature Tachycardia Embolic phenomena (Roth spots, petechiae, splinter nail bed hemorrhages, Osler nodes, CNS or ocularlesions) Janeway lesions New or changing murmur SIGNS

34. Splenomegaly Arthritis Heart failure Arrhythmias Metastatic infection (arthritis, meningitis, mycotic arterial aneurysm, pericarditis, abscesses, septic pulmonary emboli) Clubbing SIGNS

37. 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. CLINICAL MANIFESTATIONS

38. 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.

39. 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 Clinical Findings in Infective Endocarditis Patients

40. New or changing heart murmurs are common, particularly with associated heart failure. Splenomegaly and petechiae are relatively common. Serious neurologic : embolic strokes, cerebral abscesses, mycoticaneurysms, and hemorrhage are most often associated with staphylococcal disease and may be late manifestations.

42. Meningismus, increased intracranial pressure, altered sensorium, and focal neurologic signs are manifestations of these complications.

43. 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. *Pulmonaryand other systemic emboli are infrequent, except with fungal disease

44. 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), Janewaylesions (painless small erythematousor 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.

48. 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.