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