Infective Endocarditis

1. ILESANMI ADEYINKA MARY #700 Infective Endocarditis

2. Definition: • Infection of the endocardialsurface of heart characterized by • - Colonization or invasion of the heart valves (native or prosthetic) or the mural endocardium by a microbe, • - leading to formation of bulky, friable vegetation composed of thrombotic debris and organisms • - often associated with destruction of underlying cardiac tissue.

3. Sitesinvolved: • Heart valves(commonly) • Mural endocardium • Intracardiac devices • Ventricular septum defects

4. RISK FACTORS FOR SPECIFIC PATHOGENS THAT CAUSE IE • Dental procedures, poor dental hygiene - viridans streptococci, nutritionally variant streptococci, HACEK • Prosthetic valves – Early: coagulase negative staphylococci, S. aureus – Late: coagulase negative staphylococci, viridans streptococci • Gastrointestinal or genitourinary procedures - enterococci or S. bovis (colon carcinoma) • Nosocomial - S. aureus (including MRSA), Gram negatives, Candida species

5. CLASSIFICATION : Infective endocarditis may have an indolent, subacute course or a more acute, fulminant course with greater potential for rapid decompensation. • Acute bacterial endocarditis (ABE): • usually develops abruptly and progresses rapidly (i.e, 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 Bhemolytic streptococci, pneumococci, or gonococci.

6. Subacute bacterial endocarditis (SBE): • usually develops insidiously • progresses slowly (i.e, over weeks to months). • Often, no source of infection or portal of entry is evident. • SBE often develops on abnormal valves after asymptomatic bacteremia due to periodontitis, GI, or GU infections. • 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, and fastidious Haemophilus sp.

7. CLINICAL MANIFESTION

8. Post oprativeendocarditis or PVE • develops in 2 to 3% of patients within 1 year 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, Aspergillussp). • Late-onset infections 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.

9. Microbiology: • Staphylococcus aureus(35%) : Either healthy or deformed valves, IV drug abusers (polymicrobial), devices • Streptococcus viridans(32%) : Native but previously damaged/abnormal valves • Enterococci (8 %) • Coagulase negative staphylococcus - S. epidermidis (4%): Prosthetic valve endocarditis, devices • Gram –ve bacilli of HACEK group (4%) • Yeast and Fungi(1%)

10. Pathogenesis: • Portal of entry: • Dental / Surgical Procedures • Contamination by IV drug use • Obvious infections (RS/Skin) • Occult source from gut, oral cavity • Trivial injuries. • Intravascular catheter infection • Nosocomial wounds • Chronic invasive procedures

12. Morphology: • Friable, bulky and potentially destructive vegetation containing fibrin, inflammatory cells, and microbes. • The vegetations form either systemic or septic emboli • Aortic and mitral valves involved most commonly. • Tricuspid valve involvement in iv drug users.

13. Symptoms: Acute High grade fever and chills SOB Arthralgias/ myalgias Abdominal pain Pleuritic chest pain Back pain Subacute Low grade fever Anorexia Weight loss Fatigue Arthralgias/ myalgias Abdominal pain

14. Signs: • Fever • Heart murmur • More specific signs - Osler’s Nodes, Janeway lesions, and Roth Spots • Nonspecific signs – petechiae, “splinter” hemorrhages, clubbing, splenomegaly, neurologic changes

16. Petechiae • Nonspecific • Often located on palpebral conjunctiva, buccal and palatal mucosa and the extremities

17. Splinter Hemorrhages • Non-specific • Non-blanching • Linear reddish-brown lesions found under the nail bed • Usually do NOT extend the entire length of the nail • Vessel damage from swelling of the blood vessels (vasculitis) or tiny clots that damage the small capillaries (microemboli).

18. Osler’s Nodes- immune • More specific • Painful, erythematous and subcutaneous nodules • Located on pulp of fingers and toes • More common in subacute IE

19. Janeway Lesions • More specific • Erythematous, blanching macules • Nonpainful • Located on palms and soles • Microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis.

20. Roth Spots Oval, retinal hemorrhages with pale centers.

21. Modified Dukes Criteria for diagnosis of Infective Endocarditis • Definitive Endocarditis if, • - Two major or, • - One major and three minor or, • - five minor • Possible Endocarditis if, • - One major and one minor or, • - Three minor

22. Major Criteria: • Positive blood culture • Typical organism from two cultures • Persistent positive blood cultures taken > 12 hours apart • Three or more positive cultures taken over more than 1 hour. • Endocardial involvement • Positive echocardiographic findings of vegetations • Myocardial abscess • Development of partial dehiscence of a prosthetic valve • New-onset valvular regurgitation

23. Minor Criteria: • Predisposition: Predisposing valvular or cardiac abnormality • Intravenous drug misuse • Fever≥38°C (≥100.4°F) • Vascular phenomenon; major arterial emboli, septic pulmonary infarcts, etc • Immunologic phenomenon; glomerulonephritis, osler nodes, etc • Blood cultures suggestive: -organism grown but not achieving major criteria • Suggestive echocardiographic findings

24. Complications The following are potential complications of IE: • Myocardial infarction, pericarditis, cardiac arrhythmia • Cardiac valvula insufficiency • Congestive heart failure • Aortic root or myocardial abscesses • Arterial emboli, infarcts, mycotic aneurysms • Arthritis, myositis • Glomerulonephritis, acute renal failure • Mesenteric or splenic abscess or infarct

25. Investigations • Blood cultures: • Key diagnostic investigation in infective endocarditis. • Isolation of microorganism from culture is important for diagnosis and also for treatment. • At least 3 sets of samples should be taken from different venepuncture sites over 24 hours. • Serology: • Can be sent when the diagnosis is suspected and the cultures are negative. • They aid in cases where the organisms will not grow in blood cultures(Coxiella,Legionella,Bartonella)

26. Chest x-ray • Look for multiple focal infiltrates and calcification of heart valves • EKG • Rarely diagnostic • Look for evidence of ischemia, conduction delay, and arrhythmias • Echocardiography • It can identify the presence and size of vegetations,detectintracardiac complications and assess cardiac function. • Transthoracic echocardiography is noninvasive and has high specificity for visualising vegetations. • Transoesophageal echocardiography is more sensitive than TTE.It can detect small vegetations,prostheticendocarditis and intra cardiac complications.

27. Complete blood counts may show anemia and increased WBC counts. • Urea and Creatinine: may be elevated due to glomerulonephritis • Inflammatory markers CRP,ESR are increased in infection .CRP also helps in monotoring response to therapy. • Urine proteinuria and hematuria occur frequently.

28. TREATMENT: Antibotic regimen for infective endocarditis: • Viridians Streptococci and Strep.bovis Penicillin G(12-18g million U IV q24h) continously Gentamicin(3mg/kg 8-12 hourly) 2 weeks Alternative Cefriaxone (2g once daily, iv) 4 weeks Vancomycin (15mg/kg 12 hourly) duration 6weeks

29. Enterococci • Ampicillin sensitive Ampicillin(12 g IV q24h in 6 divided doses) 4-6 weeks, and Gentamicin(3mg/kg IV or IM q24h in 1 dose for 4-6wk) • Ampicillin resistant Vancomycin+ Gentamicin

30. . • Staphylococcus aureus • Methicillin-susceptible Nafcillin (12g iv q24h in 4-6 divided doses for 6wk • Both penicillin and methicillin resistant Vancomycin(30mg/kg iv q24h in 2 divided doses for 6wks • Patients with unstable renal function: consider linezoid 600 mg IV q12h

31. . Surgery: Indications: • Failure of antibiotic therapy • patients with direct extension of infection to myocardial structures. • Prosthetic valve dysfunction. • Congestive heart failure. • Severely damaged valves. • IE caused by fungi or gram-ve or resistant organisms. • Large vegetations on echocardiography • Recurrent embolic attacks. • Abscess formation.

32. . • Prophylaxis: High risk category: • Prosthetic cardiac valves • Previous bacterial endocarditis,even in absense of heart disease. • Complex cyanotic congenital heart disease (TOF) • Surgically constructed systemic pulmonary shunts. Moderate risk category: • Rheumatic and other valvular dysfunction • Congenital cardiac malformations • Hypertrophic cardiomyopathy • Mitral valve prolapse with valvular regurgitation

33. Regimen for IE prophylaxis: • Standard oral regime Amoxicillin 2gPO 1hr before procedure • Inability to take oral medication Ampicillin 2g IV or IM 1hr before procedure • Penicillin allergy Clindamycin 600 mg PO Clarithromycin 500 mg PO Cephalexin 2 g PO

34. CARDIAC MYXOMA

35. Cardiac Myxoma • WHO defines cardiac myxoma as a neoplasm composed of stellate to plump, cytologically bland mesenchymal cells set in a myxoidstroma • Most common type of primary cardiac tumor (1/3 to ½ of all cases) • Most commonly in 3rd – 6th decade; female > male • Usually solitary and develop in the atria, 75%originating in the left atrium and 15-20% in the right atrium • Arise from or near the interatrial septum at the border of the fossaovalis membrane

36. Other sites-posterior wall anterior wall appendage • RA myxoma-broader base larger area • Ventricular-free wall/IVS • Multiple- 5% (biatrialcommon).

37. Etiology • Sporadic vs familial • Majority are sporadic; 90-95% • some are familial which typically arise as part of the CARNEY COMPLEX – a heritable disorder that includes spotty pigmentation of skin and endocrinopathy. PRKAR1A mutation(70%) • LAMB SYNDROME – lentigines, atrialmyxoma and blue nevi • NAME SYNDROME – nevi, atrialmyxoma, myxoidneurofibromas and ephelides

38. Myxoma

39. Morphology • Range in size from 1-15 cm in diameter. • Polypoid with a smooth or gently lobulated surface, often pedunculated, and characteristically arise from a narrow stalk. • Polypoid myxomas rarely embolise • Villous or papillary myxomas have multiple fine fragile villous extensions -greatest risk of embolisation.

40. Histologically-sparsely distributed uniform spindle- and stellate-shaped cells within an extensive myxoidstroma. • Generally hypocellular • stroma and the tumor cells stain positive with PAS, whereas only the stroma shows positive staining with Alcian blue

42. Myxoma – Symptoms and Signs

43. Myxoma – Symptoms and Signs

44. Clinical presentation • Systemic or cardiovascular findings • Cardiovascular findings: • Atrial • s/sx resemble mitral valve disease  most common clinical presentation • Stenosis – tumorprolapse into the mitral orifice during diastole • Regurgitation – injury to the valve by tumor-induced trauma • Ventricular – outflow obstruction  syncope

45. Diagnosis • Two-dimensional transthoracic or trans-esophageal echocardiography • Determine site of tumor attachment and tumor size • Screening of 1st degree relatives for familial or syndrome myxoma • CT scan and MRI • Tumor size, shape, composition, and surface characteristics • Cardiac catheterization • Risk of tumor emboli; for suspected CAD

46. Myxoma TEE showing a large mass (M), in the left atrium with attachment to interatrial septum and prolapsing through the mitral valve into the left ventricular cavity in diastole. (M = myxoma).

47. Treatment • Surgical en bloc resection with a margin of normal tissue, if anatomically feasible, is considered curative and is the treatment of choice

48. Prognosis • Overall risk of recurrence after resection is 13%, but is much more common with familial myxomas (10-20%) than with sporadic tumours (1-3%). • Hazard of recurrence increases linearly for 4 years after resection, after which risk of recurrence is low. • Based on this observation, semi-annual surveillance echocardiographic follow-up has been recommended for 4 years following surgery

49. Immediate postoperative mortality in most series ranges from 0 to 7.5 percent. • Common postoperative complications include arrhythmias • Recurrence of myxoma in the brain- • Growth of the embolizedtumor fragments, • Difficult to manage, but chemotherapy is not recommended because embolic myxomas do not truly represent meta-static diseases. • Rare but potentially life-threatening complication is the development of cerebral aneurysm secondary to embolic tumor fragments.

50. Thank you