INFECTIVE ENDOCARDITIS
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.
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)
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
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) ,
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
Cont.
PREDISPOSING FACTORS
Conditions causing:
Bacteraemia
Septicaemia
Pyaemia
E.g. Dental carries/extraction
,Boils/Carbuncles ,U.T.I ,Pneumonia ,Tonsillect
omy/Adenoidectomy ,Surgery (G.I.T, G.U.T,
billiary and open Heart ,Drug addicts
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
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.
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
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 .
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.
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.
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.
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.
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.
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,
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
Cont.
Minor criteria
Predisposing/risk factors
Fever
Systemic or pulmonary emboli
Immunologic phenomenon
Echocardiography
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
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.
Cont.
COMPLICATIONS
Intracardiac
Severe valve deformities and obstruction of valves
or outlet tract
Abscess
Fistula
Embolism into coronary artery (ischaemic heart
disease)
Cardiac failure
Cont.
Extra-cardiac
Systemic emboli to major organs
Kidney (renal failure)
Liver (hepatic failure)
Retina (retinopathy)
Brain (cerebro-vascular accident – CVA)
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.
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
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
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
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).
Cont.
CLINICAL FEATURES
Clinical features depend on organs involved
General Features
Fever
Joint pains
General malaise
Loss of appetite
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)
Cont.
Extra-Cardiac Features
Respiratory System
Epistaxis
Tachypnoea
Musculo-skeletal system
Polyarthritis (knees, elbows, ankles, wrists)
Swollen, red and tender joints
Cont.
The Skin
Erythema marginatum (trunk and limbs)
Subcutaneous nodules (tendons and
joints bony prominences)
The Central Nervous System
The is chorea
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
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.
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.
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 diagnosis.
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.
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.
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).
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
Cont.
Supporting evidence of Group A
streptococcal infection
Raised antibody titres of Streptococcal
antibodies
Positive throat culture for group A
streptococci
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.
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: -
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.
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).
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.
