Infective edocarditis
Post on 11-Jan-2016
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Infective edocarditis
Definition
an infection of the endocardium or vascular endothelium it may occur as fulminating or acute infection more commonly runs as subacute bacterial endocarditis (SBE)
SBE occurs on rheumatic or congenitally abnormal valves in mitral valve prolapse in calcified aortic valve
Congenital lesions: ventricular septal defect (VSD) Persistent ductus arteriosus (PDA)
Prosthetic valves
The lesion of infective endocarditis is a mass of
fibrin, platelets and infecting organisms known as a
vegetation.
Aetiology
Streptococcus viridans (50%) Enterococcus faecalis Staphylococcus aureus (50% of acute cases) Staphylococcus epidermidis Coxiella burnetti Gram-negative
Subacute endocarditis Fever Night sweats Weight loss Weakness Cardiac failure Embolism Heart murmur Onset of the disease is unknown
Acute endocarditis
Intravenous drug abusers Following an acute suppurative illness Persistence of fever Development of heart murmur Vasculitis Metastatic abscesses The onset of the illness: chordal rupture or acute
valvular destruction
Prosthetic endocarditis
develops soon after surgery Occurs late and follows a bacteraemia In both cases the valve ring in infected
Clinical features
Endocarditis must be suspected in a patients with a heart murmur and a fever
Cardiac findings
development of a new murmur
or
a change in the charakter of an existing murmur
Vascular lesions Vasculitis (small petechial or mucosal
haemorrhages, they are small, red, usually with a pale center, when seen on the retin – Roth spots, seen on the thenar or hypothenar eminences - Janeway lesions
Embolic lesions (hard, painful, tender, subcutaneous swellings occurs in the fingers, toes, palms and soles (Osler’ nodes)
Clinical Features
Clubbing of the fingers Splenomegaly Renal lesions (haematuria, proteinuria) Arthritis Infarcts
Investigaion
Blood (anaemia, leucocytosis, CRP) Liver biochemistry in often but mildly
disturbed Immunoglobulins are increased Total complement and C3 are decreased Urine:protein and blood (microscopic
haematuria)
Echocardiography
Is used to visualize vegetations
To document valvular dysfunction
To identify patients in need of urgent surgery
Drug therapy
Antibiotics are chosen on the basis of the results of the blood culture
The treatment should continue 4-6 weeks
Surgical treatment
Extensive damage to a valve Early infection of prosthetic material Worsening renal failure Persistent infection Large vegetations Progressive cardiac failure
Congenital heart disease
Aetiology
Maternal rubella infection Maternal alcohol abuse Maternal drug treatment and radiation Genetic abnormalities Chromosomal abnormalities (Turner’s and
Down’s syndrome)
Symptoms
Central cyanosis Pulmonary hypertension Clubbing of the fingers Paradoxical embolism Reduced growth syncope
Treatment
A significant ASD (pulmonary flow that in more than 50 % is increased when compare with systemic flow)
Ventrical septal defect Left ventricular pressure (LVP) is higher than
RVP blood moves from LV to RV and pulmonary blood flow obliterative pulmonary vascular changes may cause the pulmonary arterial pressure to equal the systemic pressure (Eisenmenger’s syndrome) the shunt is reduced or reversed and central cyanosis may develop
Clinical features
Small VSD systolic murmur Asymptomatic patients Usually close spontaneously
Moderate VSD Laud systolic murmur Some fatigue and dyspnoea Cardiac enlargement and prominent apex beat
Treatment
Surgery (moderate and large VSD)
Prophylaxis of endocarditis
Atrial Septal defect (ASD)
Type I ostium secundumsystolic murmur
Type II ostium primum
Common form of ASD is type I
Clinical features
Children
Most children are asymptomatic Pulmonary infection Dyspnoe and weakness
Clinical features
Age > 30: AF RVH RVF Second sound is wide and fixed Loud ejection systolic pulmonary flow murmur
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