1. INFECTIVE ENDOCARDITIS
Dr.Muayad AL-Qaisy
Tikrit University.

2. Infective Endocarditis
Colonisation or invasion of heart valves or mural endocardium by microbes
Formation of vegetations composed of thrombotic debris & organisms
Often associated with destruction of underlying cardiac tissue
Aorta, aneurysmal sacs, other blood vessels & prosthetic devices can be involved
Most cases bacterial

3. Acute IE
Infection of previously normal heart valve by a highly virulent organism that produces necrotising, ulcerative, destructive lesions
Difficult to cure with Abx & usually require Sx
Death can occur within days to weeks despite Rx

4. Subcute IE Organisms are usually of lower virulence
Cause insidious infections of deformed (native) valves that are less destructive
Can take prolonged course: weeks to months
More amenable to treatment with antibiotics

5. Aetiology & Pathogenesis
Incidence cases per
Female to male 1:2
Median age has increased from to yrs
Rheumatic HD is no longer the major risk factor in Western countries

6. Aetiology & Pathogenesis
More common causes now:
Mitral valve prolapse
Degenerative calcific valvular stenosis
Bicuspid aortic valve
Prosthetic valves
Congenital defects

7. Aetiology & Pathogenesis
Majority of cases of IE are caused by gram +ve bacteria
Staphylococcus aureus is now more common (31-54%) than oral Streptococci
MSSA is more frequent in community-acquired IE, infects mainly native valves & is associated with bacteraemia of unknown origin
MRSA is more related to nosocomial infection, wound infection, permanent IV catheters or surgery in previous 6/12

8. Aetiology & Pathogenesis
Strep viridans is now less common (12-26%) but difficult to isolate & confers partial resistance to ABx
Coag -ve Staph were main cause of prosthetic valve endocarditits in the past, esp within first 6-12/12 after valve surgery, MRSA is now more common

9. Aetiology & Pathogenesis
Enterococci
HACEK group:
Haemophilus group
Actinobacillus group
Cardiobacterium hominis
Eikenella corrodens
Kingella kingae
All commensals in the oral cavity

10. Other Causes
Candida & Aspergillus species cause the majority of fungal IE (1-3% of IE)
Patients with IVDU, prosthetic valve & long-term CVC are more likely to have fungal IE: needs to be considered in presence of bulky vegetations, metastatic infection, perivalvular invasion, or embolisation to large blood vessels despite -ve BLOOD CULTURES.
In 10-15% of all cases of endocarditis no organism can be isolated from BC (“culture-negative” endocarditis)

11. Other Causes
Whenever BC -ve IE is suspected other organisms such as Coxiella burnetti,, Brucella spp, &, Chlamydiae spp, must be considered

12. Aetiology & Pathogenesis
The most common factors predisposing to IE are those that cause bacteraemia:
Dental/surgical procedures
Needle sharing amongst IVDU
Breaks in skin
The risk in those with predisposing factors (eg valve abnormalities) can be lowered by using prophylactic Abx however the use of prophylactic Abx is no longer recommended

13. Morphology
Presence of friable, bulky, potentially destructive vegetations containing fibrin, inflammatory cells & infective organism (ie bacteria, fungi) on heart valves
Aortic & mitral most common sites
Right heart more common in IVDU
Vegetations can be single or multiple & may involve more than one valve
Vegetations can erode into underlying myocardium producing abscesses (ring abscess)

14. Morphology
Emboli can break off vegetations causing abscesses at distant sites where they lodge leading to sequelae such as septic infarcts or mycotic aneurysms
Vegetations of subacute endocarditis are associated with less valvular destruction than acute endocarditis
Gram +ve bacteria are particularly resistant to pts innate antibacterial activity (eg complement) which facilitates the adhesion & formation of vegetations

15. Morphology
When the left heart is involved vegetations most often develop on the ventricular aspect of the aortic valve & atrial surface of mitral valve, usually along the valve leaflets
Septic embolism has usually occurred before diagnosis
Up to 30% of patients have renal or splenic infarcts at the time of diagnosis
Septic emboli can also occur in the heart, brain, intestine & other large organs

18. Diagnosis
The modified Duke criteria based on clinical, microbiological & echo findings providing high sensitivity & specificity (~80%) for diagnosis of IE when applied to patients with native valve IE with +ve BC.

19. Modified Duke Criteria
Major Criteria:
• Posititive blood cultures
Positive echocardiogram for IE defined as:
1.Oscillating intracardiac mass
2.Intracardiac abscess
3.New partial dehiscence of prosthetic valve
Minor Criteria:
• Predisposition such as a heart condition or IV drug use
• Fever
• Vascular phenomena or immunological phenomena such as major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, & Janeway lesions
• Other microbial evidence such as PCR, serological tests, or a positive blood cuture but does not meet a major criterion.

20. Diagnosis
The dx is confirmed in presence of 2 major criteria, 1 major + 2 minor or 5 minor criteria
IE considered in presence of 1 major + 1 minor or 3 minor

21. Clinical Features & Diagnosis
The modified Duke criteria have low sensitivity when BC -ve, infection affecting prosthetic valve/pacing system & when IE effects right heart
It’s not always useful for rapid diagnosis: one of its major criteria includes +ve blood cultures

22. Clinical Features
Fever, chills, weakness, lethargy, weight loss, flu-like illness (not always present)
Longstanding IE (rarely seen now with earlier diagnosis): splinter haemorrhages, Janeway lesions, Osler nodes, Roth spots
Murmurs are present in 90% of patients with left sided IE

23. Splinter Haemorrhages

24. Janeway Lesions

25. Osler Nodes

26. Roth Spots

27. Clinical Features
In IVDU right sided IE usually affect the tricuspid valve & occasionally the pulmonary valve, instead of systemic issues pulmonary embolism is the most important complication which can evolve into:
Pulmonary infarction
Pulmonary abscess
Bilateral pneumothoraces
Pleural effusion
Empyema

28. Clinical Features
The severity of valvular destruction depends on virulence of infecting organism & infection duration
Heart failure can be the initial presentation

29. Micro
+ve BC still the best method for identifying the causative agent: considered a major diagnostic criteria
BC are +ve in ~80% of cases
BC -ve in cases of intracellular or fastidious pathogens or after prior Abx treatment
BC are important in suspected IE (eg T > 38, new regurgative murmur, hx of valvular disease, and IVDU

30. Micro It is recommended to draw 3 sets of cultures
Culture -ve IE delays diagnosis + initiation of treatment/correct treatment
Using PCR has been proposed in these cases
PCR of excised valve tissue or embolic material should be performed in culture -ve IE (in cases of valve surgery or embolectomy)

31. Echo Important non-invasive technique for diagnosis & management
Sensitivity of TTE ranges from 45-60%
TOE offers better quality & sensitivity ranges from %, it is necessary whenever perivalvular complications or mitral valve involvement is suspected

32. Echo
Findings:
Vegetation (hallmark lesion of IE): mobile echodense mass attached to valvular leaflets or mural endocardium. Sensitivity TTE 75% TOE 90%
Periannular abscess
New dehiscence of valvular prosthesis

33. Echo Findings
~10% of IE involves right side of heart: most commonly the triscupid valve alone (98%).
Isolated right sided involvement is well detected by TTE & in those cases a TOE isn’t necessary
However ~15% IVDU associated IE affects left-sided valves & a TOE should be considered

34. Echo Findings
An abscess usually affects the aortic root & presents as a perivalvular zone of reduced echo density without blood flow. TTE (45-50%) TOE (>90%)
Important because the diagnosis of an abscess is an indication for early surgery
Aortic/mitral regurg is secondary to valvular necrosis, perforation or prolapse
~50-60% of pts with IE develop HF secondary to valvular destruction & require early surgery (mortality without surgery ~80%)

35. Echo Findings Vegetation size & mobility is important
Stroke complicates 20-40% of left-sided IE & is the second most common cause of death
*Vegetation > 10mm &/or high vegetation mobility are associated with increased embolic risk, & early surgery (within 1/52 of dx) is associated with improved long-term outcomes through reduction in systemic embolic events*
If vegetations are small or have already embolised, echo can provide false -ve results in ~15%. When suspicion is high a TOE can be repeated in 7-10 days

36. Prophylaxis
2008 National Institute of Clinical Excellence (NICE) produced guidelines re: antimicrobial prophylaxis for IE in pts undergoing interventional procedures
The guidelines suggest there is weak evidence to support routine preop Abx for pts at risk of IE
They state risk of allergic reaction, cost & resistance implications from Abx overuse
Therefore the routine use of Abx prophylaxis is no longer recommended

37. Antibiotics
Empirical treatment; flucloxacillin & gentamicin are the usual first line
Adjusted according to MCS
Vancomycin is used in pts with intracardiac prosthetic material or suspected MRSA
Benzylpenicillin is the first choice for Streptococcus or Enterococcus penicillin-susceptible strains
For vanc-resistant MRSA: teicoplanin, lipopeptide daptomycin or oxazilidones (linezolid) is recommended

38. Fungal IE Usually requires surgery
Amphotericin B doesn’t penetrate well into vegetations however is used successfully against Candida endocarditis
Caspofungin is usually fungicidal for Candida spp but its penetration into vegetations is unknown

39. Treatment Course
IV Abx is normally continued for 4-6 weeks, with the aim of sterilising the vegetations.

40. Surgery
Antimicrobial therapy can only offer curative treatment in ~50%
The other 50% require surgery
The surgical goal is valve repair but most require valve replacement
Pts with IE + large vegetations, intracardiac abscess (9-14%) or persisting infection (9-11%) almost always require surgery

41. Surgery
Anaesthetic can be complicated secondary to haemodynamic instability
Mitral or aortic regurg particularly challenging
Induction often complicated by hypotension despite hyerdynamic left ventricle & hypoxaemia secondary to severe pulmonary oedema
Some pts may develop acute RV dysfunction & severe tricuspid regurg
These pts require arterial pressure & CVP monitoring & may require inotropes/vasopressors

42. Surgery
Pts with peri-annular abscess have higher risk of para-valvular regurgitation & valve dehiscence after OT
Current IE perioperative mortality is 5-15%
If sepsis is under control the mortality is similar to non-infected valve replacement

43. Surgery Most common complications: Persistent septic shock
Coagulopathy
Acute renal failure
Stroke
Refractory heart failure
Conduction abnormalities

44. Summary Challenging diagnosis therefore diagnosis often delayed
Need to have a high index of suspicion: esp high risk pts
Clinical examination is still very important
Cultures are extremely important for diagnosis/treatment
The use of TTE/TOE is vital for Dx & Tx planning
Treatment needs to be started early to reduce morbidity/mortality
Many pts require surgical intervention
Pts can be haemodynamically unstable peri-operatively