Rheumatic heart disease and infective endoarditis

1. Rheumatic Heart disease
and infective
endocarditis.
-M6 unit
-Prof Dr Samuel dinesh MD

2. Rheumatic fever (RF)
• Rheumatic fever (RF) is an acute, immune-
mediated, multisystem inflammatory disease that
occurs few weeks after an episode of A
streptococcal infection.
• Mainly follows pharyngitis, rarely streptococcal
infection at other sites, such as the skin.
• Rheumatic heart disease is the most serious
complication of rheumatic fever.
• It is the permanent heart valve damage resulting
from one or more attacks of acute rheumatic
fever.

4. PATHOGENESIS:
1. Organism Factors:
• Caused by an upper respiratory tract infection with
Group A Streptococcus especially the serotypes 1, 3,
,6, 14, 18, 19,24, 27, 29. Can also occur following a
streptococcal skin infections.
2. Host Factors:
• Genetic predisposition with HLA-DR4 AND HLA-DR7.
3. The immune response:
• Molecular mimicry by M protein and N-
acetylglucosamine of streptococcal carbohydrate.

5. CLINICAL FEATURES:
The average latent period for symptoms to develop is
around 3 weeks except for Chorea, which may take upto
6 months to manifest.
Heart involvement:
•Seen in around 75% of patients. Causes pancarditis.
•Valvular damage is characteristic. Mitral valve is almost
always involved followed by aortic valve.
• Initially causes mitral regurgitation which later evolves
into a stenotic lesion due to valve thickening.
•Secondary involvement of pulmonary and tricuspid
valve may occur due to pulmonary hypertension.

6. Joint involvement:
• Most common symptom is polarthritis- a migratory pattern
is seen.
• Polyarthralgia may also occur which also follows a
migratory pattern.
•The symptoms respond very well to NSAIDs/ salicylates, in
case it doesnt, then it is unlikely to be rheumatic fever.
Skin manifestations:
•Erythema marginatum- pink macules with central clearing
and peripherally enlarging. Most common in trunk and
limbs. Never occurs on face.
•Subcutaneous nodules: Small, painless, mobile lumps seen
over the the elbow, occiput, feet and hands.

7. Chorea:
• Has a long latent period, occurs in absence of other
clinical features.
•Characteristically involves the head and trunk with
darting movemet of tongue.

8. DIAGNOSIS:

10. Polyarthritis
Pancarditis

11. Subcutaneous nodules

12. Erythema marginatum

13. Consisting of central zone of fibrinoid degeneration/
fibrinoid necrosis surrounded by lymphocytes &
activated macrophages called “Anitschkow cells”
21
Distinctive lesion
Aschoff bodies: Similar to granuloma
Morphology of Acute RHD

14. Aschoff bodies
Aschoff bodies
Composed of aggregates of Anitschkow cells with
central degenerative/necrotic material
Cardiac muscles
Cardiac muscles

15. Anitschkow
cells
Anitschkow cells (pathognomonic for RF). These activated
macrophages having abundant cytoplasm and central
round to ovoid nuclei in which the chromatin is central,
elongated & wavy. They may become multinucleated.

16. Fish mouth appearance of
the stenosed mitral va3
l0
ve
The cardinal anatomic changes of the mitral valve in
chronic RHD are fibrosis, thickening and fusion → Fish
mouth appearance .
Aschoff bodies are rarely seen in patients with chronic
RHD, because of replacement of the lesions by fibrosis &
calcification.

17. TREATMENT:
There is only symptomatic therapy once the patient has
been confirmed to have ARF.
Antibiotics:
•In order to target the precipitating group A streptococcus.
•Penicillin and amoxycillin are used.
Aspirin and NSAID’s: Used for te treatment of arthritis,
fever and associated symptoms.
Management of Heart failure: As per existing heart failure
guidelines.

18. Mx of Chorea-
•Sodium valproate and carbamazepine are preferred
over haloperidol.
•Glucocorticoids at 0.5mg/kg have shown to have
some benefit in early recovery.
•IVIG- in cases of severe and refractory chorea.
PREVENTION:
Primary Prophylaxis:
•Elimination of risk factors of streptococcal infection
like overcrwding.
•Treatment of high risk patients with sore throat in
endemic areas with penicillin/ amoxycillin.

19. Secondary Prevention:

20. Infective Endocarditis

21. Definition
Infective Endocarditis (IE): An infection of the
heart’s endocardial surface. It is a febrile illness
that characterized by persistent bacteremia.The
prototypic lesion of infective endocarditis (IE),
the vegetation is a mass of platelets, fibrin,
microorganisms, and scant inflammatory cells.

22. Classification
1. Based on temporal evolution of disease-
Acute vs Sub acute endocarditis
2. Based on cause
3. Based on site of infection.
4. Based on predisposing risk factor- Prosthetic
valve endocarditis vs Native valve
endocarditis.

23. CAUSES:

24. Risk Factors
1. Intravenous drug abuse (IVDA)
2. Artificial heart valves and pacemakers
3. Structural heart disease:
• Congenital heart defects
• Acquired heart defects
4. Intravascular catheterization
5. Aging, infective endocarditis is more common in
elderly

25. Infective Endocarditis
Pathogenesis & sequels
Endothelial damage
Platelet-fibrin thrombi
+
Microorganism adherence
Infected Vegetations
These infected
vegetations may dislodge
from the heart &
transported through
blood to any region of the
body→ the serious
metastatic septic emboli.

26. Organisms
Fibrin
Fibrin
Organisms
Organisms
Microscopically, vegetations are composed of
fibrin & platelets with abundant organisms &
few inflammatory cells
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2019 Professor Intisar Salim Pity

27. Differential diagnosis of vegetative endocarditis:
1. The rheumatic heart disease (RHD) is marked by small vegetations
along the lines of closure of the valve leaflets.
2. Infective endocarditis (IE) is characterized by large, irregular &
destructive masses on the valve cusps that can extend onto the
chordae
3. Nonbacterial thrombotic endocarditis (NBTE): One or many, typically
bland vegetations (larger than those of RHD) at the line of closure.
4. Libman-Sacks endocarditis (LSE) (a sequel of SLE): Variably sized
vegetations on both sides of the valve leaflets.
2019
27
Professor Intisar Salim Pity

29. A. Initially begins with history of non-cardiac infection
(e.g. tooth infection)→ bacteremia → infective
endocarditis.
B. There is interval between bacteremia & onset of
symptoms usually <2 weeks.
1. Fever is the most common sign
2. Murmur already present in 80 – 85%
3. → Changing murmur
4. Embolization – usually septic
5. Bleeding tendency
6. Hematogenous seeding of infection →metastatic
abscesses.
7. Immune complications- Osler nodes,focal “embolic”
glomerulonephritis, arteritis
Clinical manifestations

30. Signs of infective
endocarditis:
Bleeding tendency
like petechia & splinter
hemorrhages
50

31. Splinter Hemorrhages

32. Splinter Hemorrhages in the brain
32
2019 Professor Intisar Salim Pity

33. Could be
subconjunctival
Splinter Hemorrhages

34. Osler’s Nodes
1. More specific than splinter hemorrhage
2. Painful and erythematous nodules
3. Located on pulp of palm, fingers and toes

35. Embolic Complications
• Systemic emboli form the most serious
complication of IE.
• Common: occurring in up to 40% of patients.
• Incidence decreases significantly after initiation
of effective antibiotics.

36. DIAGNOSIS:

37. Blood cultures in Infective endocarditis:
Three two-bottle blood culture sets containing the
appropriate
volume of blood (10 mL per bottle) should be obtained from
different
venipuncture sites over 1–2 hours.
Serological tests:
These are used for identification of organisms that cannot
be grown in blood cultures like Brucella, Bartonella, T.
whipplei, and C. burnetii. PCR is used in these cases.

38. Cardiac imaging in IE:
 Trans Thoracic Echocardiograpy (TTE)
– rapid, non-invasive – excellent specificity (98%) but
poor sensitivity
– obesity, chronic obstructive pulmonary disease and chest
wall deformities
 Transesophageal Echo (TOE)
– more invasive, sensitivity up to 95%, useful for
prosthetic valves and to evaluate myocardial
invasion
– Negative predictive valve of 92%

39. TREATMENT:
Complete sterilization of the valvular vegetations with
prolonged, high dose, bactericidal intravenous
antibiotics is the preferred treatment of choice.
Organism specific therapy:
1. Streptococci/Enterococci
– Determine MIC of Penicillin
– Penicillin +/- aminoglycoside
– Ceftriaxone alone
– Vancomycin +/- aminoglycoside

40.  Staphylococci
– Native valve
» Flucloxacillin +/- aminoglycoside
» Vancomycin +/- aminoglycoside/ rifampicin
– Prosthetic valve
» Flucloxacillin + aminoglycoside + rifampicin
» Vancomycin + aminoglycoside + rifampicin
 HACEK group of organisms:
– Cefotaxime/ceftriaxone

41. Surgical Therapy:
 Indications:
– Congestive cardiac failure
– perivalvular invasive disease
– uncontrolled infection despite maximal antimicrobial
therapy
– Presence of prosthetic valve endocarditis unless late
infection
– Large vegetation
– Major embolus
– Heart block

43. Prophylaxis:
 The pathogenesis of infective endocarditis (IE) is presumed
to involve the
following sequence of events
●Formation of a small thrombus on an abnormal
endothelial surface
●Secondary infection of this nidus with bacteria that are
transiently circulating in the bloodstream
●Proliferation of bacteria resulting in the formation
of vegetations on the endothelial surface
 Since the occurrence of bacteremia is crucial to the
initiation of an episode of IE, in theory it is reasonable to
conclude that preventing or promptly treating transient
bacteremia can prevent the above events.