- What is Infective Endocarditis (IE)
- Statistics on Infective Endocarditis (IE)
- Risk Factors for Infective Endocarditis (IE)
- Progression of Infective Endocarditis (IE)
- Symptoms of Infective Endocarditis (IE)
- Clinical Examination of Infective Endocarditis (IE)
- How is Infective Endocarditis (IE) Diagnosed?
- Prognosis of Infective Endocarditis (IE)
- How is Infective Endocarditis (IE) Treated?
- Infective Endocarditis (IE) References
What is Infective Endocarditis (IE)
Infective endocarditis is an infection (usually bacterial, occasionally fungal) of the endocardium (the inner lining of the heart). It is a serious disease with significant morbidity and mortality. Prompt diagnosis and treatment are essential to minimize sequelae.
Statistics on Infective Endocarditis (IE)
The incidence of Infective Endocarditis is approximately 6-7 cases per 100,000 per year in developed countries but is significantly higher in developing countries.
Risk Factors for Infective Endocarditis (IE)
1) Rheumatic heart disease and existing valvular disorders.
2) Prosthetic heart valves.
3) Compromised immunity for any reason.
4) Intravenous drug abuse (commonly leads to endocarditis affecting the right heart valves).
5) Dental procedures and poor dentition.
6) Congenital cardiac lesions. Nonetheless, at least half of all endocarditis occurs on otherwise normal heart valves.
Progression of Infective Endocarditis (IE)
The disease process can follow one of several courses resulting in the frequently made clinical distinction between sub-acute bacterial endocarditis or SBE and acute bacterial endocarditis or ABE. SBE usually occurs on normal valves and follows a smouldering course of many weeks. Micro-organisms from a source of sepsis attach to the heart valves and proliferate there, inducing further thrombosis and the formation of vegetations. The presence of bacteraemia and generalised sepsis may also cause a peripheral syndrome of vasculitic changes. The significant outcomes of SBE include heart failure, embolisms of vegetation fragments and abscess formation. ABE occurs more commonly in intravenous drug abusers and on prosthetic valves and or after acute suppurative illness such as pneumonia and meningitis and follows a much more fulminant course with vasculitis and abscesses in other organs. The vasculitic syndromes (inflammation of blood vessels) can produce renal failure. IE can also produce almost any valvular heart disorder.
How is Infective Endocarditis (IE) Diagnosed?
1) Full blood count to assess anaemia and leukocytosis (marker of infection).
2) Urea and electrolytes: assess any renal failure.
3) ESR is almost always raised (>50mm/h).
4) ECG: may show myocardial infarction either as a differential diagnosis or as a silent complication following vegetation embolism to a coronary artery.
5) Chest X-ray: shows early manifestation of cardiac failure.
Prognosis of Infective Endocarditis (IE)
It is almost universally fatal if untreated. Untreated, the average time from onset of disease to death in SBE is about 6 months, 4 weeks in ABE. Heart Failure is by far the strongest negative prognostic indicator. Despite advances in antibacterial therapies, early and late mortality rates in patients with IE remain high, due to co-morbidities and late detection of the disease.
How is Infective Endocarditis (IE) Treated?
The mainstay of IE treatment is antibiotic therapy to eradicate the infection. This is facilitated by correct isolation of the causative agent through culture and establishment of sensitivities. Bactericidal rather than bacteristatic agents should be de rigueur. Due to the nature of the infection, intravenous treatment is required for at least 4 weeks requiring home administration or specialised central/PICC lines. Surgical replacement of seriously damaged valves should be considered to reverse cardiac failure. Complications such as heart failure, and renal failure should be treated with medications and dialysis respectively. Renal function often returns to normal after eradication of the infection.
Infective Endocarditis (IE) References
- Hurst’s The Heart 8th Edition, McGRAW-HILL 1994.
- Kumar and Clark Clinical Medicine 4th Edition, W.B SAUNDERS 1998.
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