Heart inflammation

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Infektive endocarditis

__ Infekční endokarditida (pediatrie)

Infective endocarditis (IE) is a disease caused by an infectious agent that affects the endocardium, heart valves and related structures. Inflammation can be caused by bacteria, fungi, chlamydia, rickettsiae or viruses.

Risk factors

Risk factors - children:

• congenital heart defects;
• rheumatic heart defects (rare);
• iatrogenic - long-established central venous catheters;
• intravenous drug use;
• bicuspid aortic valve;
• mitral valve prolapse with regurgitation;
• stp. cardiac surgery using conduits and vascular prostheses, with artificial valves[1].

In congenital heart disease, IE occurs most commonly in:

• Tetralogy of Fallot,
• ventricular septal defect,
• aortic stenosis, and
• patent ductus arteriosus

The risk is significantly lower in pulmonic stenosis and IE is virtually absent in atrial septal defect.

• The bicuspid aortic valve is a frequent site of IE, regardless of whether it causes stenosis or regurgitation.
• In mitral valve prolapse, patients are at risk of IE if the valve regurgitates.

IE is rare in neonates, infants, and young toddlers except for iatrogenic IE in critically ill children with catheter infection. The risk of IE increases with increasing age in individuals with heart disease.

Etiology

In children,  the most common cause of IE are:

• Streptococcus viridans,
• staphylococci,
• more rarely enterococci.
• Coagulase-negative staphylococci (Staphylococcus epidermidis) are typical triggers of IE after cardiac surgery.

• Gram-negative microorganisms and fungi rarely cause IE. They usually affect immunosuppressed individuals, patients with artificial valves and drug addicts. Mycotic IE is also a serious complication of long-term central venous catheters usually after repeated administration of broad-spectrum antibiotics

Pathogenesis

An important factor in the development of IE is the presence of turbulent blood flow that disrupts the endothelium. However, vegetations can also form as a result of the Venturi effect at the site of slow blood flow. A cluster of platelets and fibrin forms in the damaged endothelium, which is subsequently colonized by infectious agents. Bacteremia occurs in association with various diagnostic or therapeutic procedures. Transient bacteraemia may also occur during tooth brushing or biting of solid food. This mechanism explains the occurrence of IE in patients where a clear causative bacteraemia cannot be identified.

The main macroscopic findings are vegetations on the endocardium. They contain microbes and are covered by a layer composed of fibrin and leukocytes. Less virulent bacteria nestle in the thrombi, where fibrin protects them from phagocytosis and antibiotics.

The adjacent affected tissue is edematous, with cellular infiltration and poorly vascularized, which impairs antibiotic penetration. Fragility of vegetations causes recurrent bacteremia and embolization to the lungs or systemic circulation, depending on the site of cardiac involvement and the presence of intracardiac shunts. Embolization into the lung mimics pneumonia; an unrecognized lung abscess may perforate into the vascular system with subsequent fatal hemorrhage. In embolization into the systemic circulation, the skin, kidneys, spleen and brain are most commonly affected. In prolonged disease, the heart valves are destroyed. Virulent bacteria (Staphylococcus aureus) cause rapid destruction of the valve or invasion of the myocardium leading to abscess formation. Septic embolization into the coronary arteries is also a frequent finding. IE significantly activates the humoral and cellular immune system. For example, circulating immune complexes are responsible for the development of glomerulonephritis[1].

Classification

• IE native valves,
• IE of toxics (predisposes to tricuspid valve involvement with risk of pulmonary embolisation),
• IE of valve prostheses (early/late onset - threshold 2 months after surgery).

The division of IE into acute and subacute forms is obsolete and not used anymore. The division according to the causing agent is recommended. Microorganisms with low virulence (e.g. α-haemolytic streptococcus) usually induce the "subacute" form, whereas Staphylococcus aureus and other pyogenic bacteria induce the "acute" form.

Risks of infective endocarditis

High risk;

• Valve prostheses (lifelong),
• stp. cardiac surgery (up to 6 months after surgery),
• aortic defects,
• tetralogy of Fallot,
• mitral insufficiency,
• PDA,
• VSD,
• CoA,
• Marfan syndrome,
• history of IE.

Intermediate risk;

• Mitral stenosis,
• tricuspid defects,
• mitral prolapse,
• hypertrophic cardiomyopathy

Clinical picture

IE is always suspected in at-risk patients (see above) with a febrile state. Always bear in mind the mitigated forms of IE when p.o. antibiotic treatment has been given out of embarrassment, the febrile state may then even resolve. Endocarditis is most commonly manifested by fever and non-specific complaints such as myalgia, arthralgia, headache, fatigue. With a prolonged duration of the disease, splenomegaly is found, the skin is coloured with a hint of white coffee (caffé au lait). Other late symptoms are embolizing manifestations in the periphery: splinter-like subungual hemorrhages, petechiae on the skin or subconjunctivally, red spots on the palms (Janeway's spots), painful inductions on the bellies of the fingers (Osler's nodes). Embolization may reveal examination of the ocular background (hemorrhagic lesions on the retina = Roth spots) or hematuria. In up to 30% of patients, the first clinical sign of IE may be an acute embolic cause. Most commonly, the a. carotis interna basin is affected. Clinical signs are hemiplegia, aphasia, mental disorders, and rarely blindness when retinal arteries are affected. In general, IE of the left heart causes embolization to the periphery with subsequent ischemia, infarction in sterile emboli, abscesses in infective emboli, or mycotic aneurysms. Embolization from the right heart to the lungs is often asymptomatic because of good filtration properties of the lungs or presents with symptoms of pulmonary embolism followed by cough, auscultatory and radiographic findings on the lungs.

Sometimes there may be up to a picture of Löhlein's nephritis with hematuria, proteinuria and a decrease in glomerular filtration rate. It is a manifestation of microembolization to the kidney or a consequence of focal or diffuse glomerulonephritis, which causes deposits of immunocomplexes in the glomeruli. Up to 20% of children have neurological symptoms: meningitis, brain abscesses, toxic encephalopathy.

Significant findings are new-onset or altered heart murmurs due to valve involvement; more rarely, the inflammatory process may affect the cardiac conduction system and cause AV block. Heart failure is the most common cause of death.

CAVE!!! Always keep in mind the mitigated forms of IE when p.o. antibiotic treatment is given out of embarrassment, febrile episodes may then even subside!

Myocarditis

__ Myokarditida (pediatrie)

Pericarditis

__ Perikarditida (pediatrie)

Odkazy

Zdroj

• HAVRÁNEK, Jiří: Srdeční záněty. (upraveno)

Související články

• Infekční endokarditida
• Myokarditida
• Perikarditida

Kategorie:Pediatrie Kategorie:Vnitřní lékařství Kategorie:Kardiologie