This document is about infective endocarditis,a disease that affects mostly the heart valves

1. INFECTIVE
ENDOCARDITIS

2. Cont.
 Endocarditis is an inflammatory condition of
the mural endocardium characterized by large
crumbling vegetations toxaemia and
bacteraemia.
 There is the growth of microorganisms on an
endothelium usually a valve that occurs in a
pre-existing cardiac lesion.
 The organism is present in masses of
thrombus (vegetation). Multiple embolic
episodes occur.

3. Cont.
TYPES OF ENDOCARDITIS
1. Non-infective (non-microbial)
endocarditis
 Verrucous (acute rheumatic fever)
 Atypical verrucous (Libman-Sacks in
S.L.E)
 Non-bacterial thrombotic endocarditis
(NBTE)

4. Cont.
2. Infective (microbial)
 Mainly bacterial or fungal
 Rarely viral and rickettsial
 Destroys valve tissue in contrast with
non-infective
 Forms thrombosis with
microorganisms deep within it
(vegetations)
 Associated with thrombus formation

5. Cont.
CLASSIFICATION
 Acute bacterial Infective endocarditis
 Sub-acute bacterial Infective endocarditis
AETIOLOGY
 Alpha –haemolytic streptococci low virulence
organisms e.g. S. vividans (mouth and
pharynx commensals), S. sanguis and S.
Feacalis ,Staph aureas ,Strep boris (GIT) ,

6. Cont.
Staph epidermidis (skin) – from indwelling
venous catheters and artificial pace maker
wires ,Strep pneumoniae ,Haemophilus ssp.
,Diptheroids - skin/GIT ,Colliform bacilli -
“,Bacteroides ,Coxiella burnetti ,Neiserria
,Gram negative bacilli- pseudomonas
aeruginosa
 Fungal – drug addicts/Immunosuppresed e.g.
Candida, Aspergilla’s and Histoplama
 Rickettsia

7. Cont.
PREDISPOSING FACTORS
 Conditions causing:
 Bacteraemia
 Septicaemia
 Pyaemia
 E.g. Dental carries/extraction
,Boils/Carbuncles ,U.T.I ,Pneumonia
,Tonsillectomy/Adenoidectomy ,Surgery
(G.I.T, G.U.T, billiary and open Heart ,Drug
addicts

8. Cont.
 Cardiac lesions:
 Valve abnormalities
 Abrasions
 Mechanical & biological prosthetic valves
 Endocardial sutures & patches
 Degenerative heart disease
 Immunosuppression
 Decreased specific immunity
 Complement deficiency
 Inadequate function of lymphocytes

9. Cont.
 Haemodynamic factors
 Valvular abnormalities produce turbulent flow,
which damages the endocardium causing
deposition of platelets and fibrin forming
vegetations. The vegetations fall downstream
from an area of relatively higher pressure.
 Portals of entry of the organisms – blood.

10. Cont.
PATHOGENESIS
 The pathogenesis of infective endocarditis
is a result of three interactive processes
namely: -
 Host factors that predispose the
endothelium to infection
 Circumstances enhancing bacteraemia
 Tissue tropism and virulence of circulating
microorganisms

11. Cont.
PATHOLOGY
 Various changes occur in the heart and
heart valves
Macroscopy (Gross Appearances)
The Heart
 Heart reveals features of chronic
rheumatism or features of congenital
valvular heart disease .

12. Cont.
Microscopy
 The vegetations are composed of
platelets, fibrin, and colonies of
microorganism, scanty polymorphs and
calcification. Below the vegetation there is
heavy inflammation and vascularization.
 The Cusps are hyperaemic, vascularized,
thickened, fibrosed and oedematous with
necrotic tissues.

13. Cont.
 Their is cellular infiltration with polymorphs,
macrophages and giant cells
 The Kidneys are described as “flea-bitter”
because of the pinpoint red spots on
subcapsular (small haemorrhages at site of tuff
capillaries) due to immune – complex
deposition.
 They allow blood into glomeruli and renal
tubules causing haematuria.

14. Cont.
CLINICAL FEATURES
 The clinical features relate to: -
 Cardiac failure
 Systemic emboli
 Immunological manifestations.
 Cardiac Failure
 Cardiac failure results from volume overload
on left ventricle and myocardial damage due
to embolic and immune mechanisms.

15. Cont.
 Systemic emboli
 Spleen
 Mesenteric arteries
 Kidney (58% cases)
 Cerebral lesions
 Account for 20% cases and increases the
mortality and morbidity leading to
neurological problems – hemiplegia,
blindness, and dementia.

16. Cont.
 Immunological Complications
 The release of bacterial antigens into
circulation leads to immune complex
formation.
 The high levels of circulating immune –
complexes are associated with the
arthritis, splinter haemorrhages, purpura
and glomerulonephitis.
 The Osler’s nodes (small red tender
nodes) are embolic in origin.

17. Cont.
CRITERIA FOR DIAGNOSIS (DUKE
UNIVERSITY ENDOCARDITIS SERVICE)
 Definitive diagnosis
 Pathology/microbiology of vegetations obtained at
surgery or autopsy
 Two major criteria
 One major/three minor criteria
 Possible diagnosis – findings consistent with
but fall short of definitive diagnosis of
endocarditis
 No endocarditis – no pathology at surgery or
autopsy or clinical resolution with 3 days of
antimicrobial therapy,

18. Cont.
 Major criteria
 Blood culture
 2 separate cultures positive for S. viridans and S. auras
 Positive blood cultures > 12 hours apart
 Positive blood culture 3 out 3, one hour apart.
 Echocardiography

19. Cont.
 Minor criteria
 Predisposing/risk factors
 Fever
 Systemic or pulmonary emboli
 Immunologic phenomenon
 Echocardiography

20. Cont.
INVESTIGATIONS
 Full heamogram and ESR - shows reduced
haemoglobin (Hb), increased white blood cells
(wbc’s), reduced platelets and increased C –
reactive proteins
 Blood cultures At least six samples
 Liver biochemistry (LFTS) - reduced Serum
alkaline Phosphotase
 Immunoglobins and complement - raised Serum
Ig, reduced total complement and C3 complement
due to immune-complex formation, circulating
immune complexes and rheumatoid factor

21. Cont.
 Serological tests
 Urea/Electrolytes
 Urinalysis
 ECG – evidence of myocardial infarction
 Echocardiography
 Chest X-Ray - evidence of Heart failure and
emboli in right-sided endocarditis.

22. Cont.
COMPLICATIONS
Intracardiac
 Severe valve deformities and obstruction of
valves or outlet tract
 Abscess
 Fistula
 Embolism into coronary artery (ischaemic
heart disease)
 Cardiac failure

23. Cont.
Extra-cardiac
 Systemic emboli to major organs
 Kidney (renal failure)
 Liver (hepatic failure)
 Retina (retinopathy)
 Brain (cerebro-vascular accident – CVA)

24. Cont.
 Mycotic aneurysm formation
 Pyemia
 Septicaemia
 Glomerulonephritis (secondary to immune
complexes)
 Anaemia
 Other toxic or allergic inflammation of vessel
walls leading to petechiae and/or splinter
haemorrhages in the skin, mucosa, conjunctiva
and retina.

25. Cont.
INDICATIONS FOR SURGERY
 Extensive damage to a valve
 Early infection of prosthetic material
 Worsening renal failure
 Persistent infection but failure to culture
 Embolism
 Large vegetations
 Progressive cardiac failure

26. 7. RHEUMATIC HEART
DISEASE
 At the end of the lesson the student should be
competent to: -
 Define rheumatic heart disease and rheumatic
fever
 Outline causes of RHD and RF
 Describe the pathogenesis and
pathophysiology of ARF and RHD

27. Cont.
 Evaluate the basis of signs and symptoms of
ARF and RHD
 Outline features of ARF and RHD
 Make a diagnosis of ARF and RHD
 Describe investigations in ARF and RHD
 Describe the complications of ARF and RHD

28. Cont.
ACUTE RHEUMATIC FEVER (ARF)
 Rheumatic fever is an immunologically
mediated inflammatory disease, that occurs as
a delayed sequel to group A streptococcal
throat infection, in genetically susceptible
individuals.
 The disease involves the heart, joints, skin,
and brain.
INCIDENCE
 The first attack occurs between 5 – 15 yrs of
age (peak age 8 years).

29. Cont.
CLINICAL FEATURES
 Clinical features depend on organs
involved
General Features
 Fever
 Joint pains
 General malaise
 Loss of appetite

30. Cont.
Cardiac Features
 Cardiomegally
 Congestive cardiac failure (CCF)
 Pericardial effusion
 ECG change(Raised ST segment in pericarditis and
inverted or flat T-wave in myocarditis)
 AV block
 Cardiac Arrthymias
 Changing murmurs (Diastolic mitral - Carey
Coomb’s murmur)

31. Cont.
Extra-Cardiac Features
Respiratory System
 Epistaxis
 Tachypnoea
Musculo-skeletal system
 Polyarthritis (knees, elbows, ankles,
wrists)
 Swollen, red and tender joints

32. Cont.
The Skin
 Erythema marginatum (trunk and
limbs)
 Subcutaneous nodules (tendons and
joints bony prominences)
The Central Nervous System
 The is chorea

33. Cont.
DIAGNOSIS
Jones Criteria
Major Criteria
 Pancarditis (friction rub, murmur, cardiomegaly, CCF,
and ECG changes)
 Arthritis (migratory polyarthritis, swollen, tender, red)
 Chorea-abnormal involuntary movement disorder of
muscle
 Subcutaneous nodules
 Erythema marginatum
Pneumonic-PACSE

34. Cont.
 Carditis is the only manifestation of ARF that
is potentially life-threatening and capable of
causing chronic disease.
 Approximately half of patients with ARF are
affected.
 When pancarditis is present, endocarditis and
resultant valvulitis is the most important
contributor to acute congestive heart failure
(CHF).
 Myocarditis and pericarditis can contribute to
cardiac dysfunction.

35. Cont.
 The mitral valve is most commonly affected,
with the aortic valve a distant second.
 Valvular insufficiency is present acutely
(although stenosis develops years later in
some patients). The physical examination is
used to diagnose carditis.
 The apical, holosystolic murmur of mitral
insufficiency and the blowing, early diastolic
murmur of aortic incompetence are classic.
 Resting tachycardia (out of proportion to any
fever) suggests carditis.

36. Cont.
 Arthritis is the most common manifestation of
ARF, occurring in approximately 75% of
patients.
 Classically, an asymmetric migratory arthritis
of the large joints (knees, ankles, elbows, and
wrists) is present.
 Each joint tends to be affected for a few days
to a week. Arthritis rarely lasts beyond 4 weeks
in ARF and is usually responsive to salicylate
therapy.
 Arthritis of longer duration or with poor
responsiveness to aspirin suggests another

37. Cont.
 Sydenham chorea is seen in approximately
5% to 15% of ARF cases.
 It often starts with emotional lability and
progresses to involuntary purposeless
movements.
 After puberty, chorea is much more common in
female patients.
 It often appears 1 to 6 months after group A
streptococcal pharyngitis.

38. Cont.
 Erythema marginatum, an erythematous,
macular, nonpruritic rash with serpiginous
borders that spread outward with central
clearing, is seen in less than 5% of patients.
 It is seen on the trunk, buttocks, and proximal
limbs and does not involve the face.

39. Cont.
 Subcutaneous nodules are also seen in
fewer than 5% of patients and are associated
with active carditis.
 These small, freely mobile nodules are found
on extensor surfaces (especially the occiput,
over the vertebral spines, and on the elbows,
knees, and wrists).

40. Cont.
Minor Criteria
 Clinical
 Previous Rheumatic fever or RHD
 Arthralgia
 Fever
 Laboratory
 Acute phase proteins (ESR, positive C-
reactive proteins, leucocytosis)
 Prolonged P-R interval on ECG

41. Cont.
 Supporting evidence of Group A
streptococcal infection
Raised antibody titres of
Streptococcal antibodies
Positive throat culture for group A
streptococci

42. Cont.
RHEUMATIC HEART DISEASE (RHD)
 Rheumatic heart disease occurs as an
aftermath of destructive effects of rheumatic
fever on the endocardium and the heart
valves.
 The destruction results in healing by fibrosis of
the damaged surfaces resulting in valve
disorders and incompetence (stenosis and
regurgitation).
 RHD can be acute or chronic RHD.

43. Cont.
1. ACUTE RHD
 This presents as acute rheumatic fever (ARF)
which occurs mainly in children. It presents
with cardiac and extra-cardiac features. It
recurs in 50 – 70% of young children and
causes chronic rheumatic valvulitis.
 The cardiac features which are elaborate
include pancarditis (occurs in 40% of acute
RHD presenting as: -

44. Cont.
 Endocarditis (verrucous) – valve destruction
and murmurs of stenosis
 Myocarditis – cardiac enlargement, cardiac
failure, dilatation of ventricles and mitral ring
resulting in mitral regurgitation (insufficiency),
aschoff nodules
 Pericarditis – friction rub
 The other features of ARHD include rheumatic
polyarthritis, subcutaneous nodules, erythema
marginatum and Sydenham’ chorea.

45. Cont.
CHRONIC RHD
 Chronic RHD occurs mainly in adults as a
sequale of earlier ARF (ARHD) with
destruction of heart valves.
 It presents mainly as valvular heart disease
predominantly affecting left sided valves
(almost always the mitral valve).

46. Cont.
 It affects the valves in the following order of
decreasing frequency – mitral, aortic, tricuspid
and pulmonary.
 The mitral valve is affected alone in 48% of
cases and together with the aortic valve in
42% cases.
 The right sided valves are rarely affected but
tricuspid regurgitation (insufficiency) is usually
due to congestive cardiac failure.