Exudative and proliferative inflammatory alterations of the endocardium caused by bacteria, fungi, or other infectious agents, characterized by the presence of vegetations on the surface of the endocardium or in the endocardium itself, and most commonly involving a heart valve, but sometimes affecting the inner lining of the cardiac chambers or the endocardium elsewhere.
- Frequency: the incidence in the United States is approximately 2-4 cases per 100,000 persons per year. This rate has not changed in the past 50 years. The incidence in other countries is similar to that in the United States.
Patients who inject narcotics intravenously may introduce infection which will travel to the right side of the heart. In other patients without a history of intravenous exposure, endocarditis is more frequently left-sided.
- Mortality: if left untreated, it generally is fatal. Anecdotal reports describe the resolution of right-sided valvular infection caused by S aureus in individuals who abuse intravenous drugs after just a few days of oral antibiotics.
- Sex: it occurs in males 3 times more often than in females.
- Age: it may occur in a person of any age. Frequency is increasing in elderly individuals, with 25-50% of cases occurring in those older than 60 years.
IE may be classified according to four different criterions:
- Acute: is a fulminant illness over days to weeks and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity
Subacute: is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months
- Short incubation: less than about six weeks
Long incubation: greater than about six weeks
Culture-negative: is due to micro-organisms that require a longer period of time to be identified in the laboratory. Such organisms are said to be ‘fastidious’ because they have demanding growth requirements. Some pathogens responsible for culture-negative endocarditis include Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species, and HACEK bacteria.
- Native-valve endocarditis
- Excessive sweating
- Night sweats (may be severe)
- Weight loss
- Muscle aches and pains
- Heart murmur
- Shortness of breath with activity
- Swelling of feet, legs, abdomen
- Joint pain
- Blood in the urine
- Abnormal urine color
- Red, painless skin spots on the palms and soles (Janeway lesions)
- Nail abnormalities (splinter hemorrhages under the nails)
- Red, painful nodes (Osler's nodes) in the pads of the fingers and toes
- Retinal hemorrhages with a central area of clearing (Roth's spots)
Note: symptoms of endocarditis may develop slowly (subacute) or suddenly (acute).
Fever is a hallmark of both. In the slower form, it may be present on a daily basis for months before other symptoms appear.
- Objective tests
- A history of congenital heart disease, rheumatic fever, recent dental work, or intravenous drug use raises the level of suspicion
- Physical examination may show an enlarged spleen
- The examiner may detect a new heart murmur, or a change in a previous heart murmur
- Examination of the nails may show splinter haemorrhages
- Eye examination may show retinal haemorrhages with a central area of clearing (Roth's spots), and petechiae (small, pinpoint haemorrhages) may be detected in the conjunctiva.
- Laboratory tests
- Repeated blood culture and sensitivity (best test for detection)
- ESR (erythrocyte sedimentation rate)
- CBC (complete blood count) may show low grade, microcytic (small red blood cells) anemia
- Instrument tests
- ECG (echocardiogram)
- Transesophageal echocardiogram
- Chest x-ray
- CT scan of the chest
ETIOLOGY AND RISK FACTORS
Endocarditis is usually a result of bacteremia (bacteria in the blood)
Organism clinical features
Preexisting conditions that increase the likelihood of developing endocarditis include:
Since Streptococcus viridans is often found in the mouth, dental procedures are the most common cause of bacterial endocarditis. This can put children with congenital heart conditions at risk. As a result, it is common practice for children with some forms of congenital heart disease, and adults with certain heart-valve conditions to start on antibiotics prior to any dental work but there is no evidence whether this prophylaxis is really effective.
Bacteremia can result from various invasive procedures, ranging from oral surgery to sclerotherapy of esophageal varices to genitourinary surgeries to various abdominal operations. The potential for invasive procedures to produce a bacteremia varies greatly. Procedures, rates, and organisms are as follows:
- Barium enema
- Dental extractions
- Transurethral resection of the prostate
- Transesophageal echocardiography
All cases of IE develop from a commonly shared process:
- bacteremia (nosocomial or spontaneous) that delivers the organisms to the valve's surface
- adherence of the organisms
- eventual invasion of the valvular leaflets
The common denominator for adherence and invasion is nonbacterial thrombotic endocarditis, a sterile fibrin-platelet vegetation. The development of subacute IE depends on a sufficient inoculum of bacteria to allow invasion of the preexistent thrombus. This critical mass is the result of bacterial clumping produced by agglutinating antibodies.
In acute IE, the thrombus may be produced by the invading organism or by valvular trauma from intravenous catheters or pacing wires. S aureus can invade the endothelial cells and increase the expression of adhesion molecules and of procoagulant activity on the cellular surface.
IE develops most commonly on the mitral valve, closely followed in descending order of frequency by the aortic valve, the combined mitral and aortic valve, the tricuspid valve, and, rarely, the pulmonic valve. Mechanical prosthetic and bioprosthetic valves exhibit equal rates of infection.
The microorganisms that most commonly produce endocarditis resist the bactericidal action of complement and possess fibronectin binding protein for the surface of the fibrin-platelet thrombus.
Among the many other characteristics of IE-producing bacteria demonstrated in vitro and in vivo, some features include the following:
Either a spontaneous bacteremia or one that is the result of an invasive procedure infects the sterile fibrin-platelet vegetation. BSIs develop from various extracardiac types of infection, such as pneumonias or pyelonephritis, but most commonly from gingival disease. Of those with high-grade gingivitis, 10% have recurrent transient bacteremias (usually streptococcal species). Most cases of subacute disease are secondary to the bacteremias that develop from the activities of daily living (eg, brushing teeth, bowel movements).
Colonization of heart valves by microorganisms is a complex process. Most transient bacteremias are short-lived, are without consequence, and often are not preventable. Bacteria rarely adhere to an endocardial nidus before the microorganisms are removed from the circulation by various host defenses. Once microorganisms establish themselves on the surface of the vegetation, acceleration of platelet aggregation and fibrin deposition occurs at the site. As the bacteria multiply, they are covered by ever-thickening layers of platelets and thrombin, which protect them from neutrophils and other host defenses. Organisms deep in the vegetation hibernate because of the paucity of available nutrients and, therefore, are less susceptible to bactericidal antimicrobials that interfere with bacterial cell wall synthesis.
Complications result from:
- slowly progressive valvular destruction
- various immunological mechanisms
- peripheral manifestations (eg, Osler nodes, Roth spots, subungual hemorrhages)
- various musculoskeletal abnormalities
- Janeway lesions (usually arised from infected microemboli)
The microscopic appearance of acute bacterial endocarditis differs markedly from that of subacute disease. Vegetations that contain no fibroblasts develop rapidly, with no evidence of repair. Large amounts of both polymorphonuclear leukocytes and organisms are present in an ever-expanding area of necrosis. This process rapidly produces spontaneous rupture of the leaflets, of the papillary muscles, and of the chordae tendineae.
The complications result from:
- intracardiac disease
- metastatic infection produced by suppurative emboli
Because of their shortened course, immunological phenomena are not a part of acute IE.
In addition to valvular insufficiency, other intracardiac complications include:
- aortocardiac and other fistulas
- aneurysms of the sinus of Valsalva
- intraventricular abscesses
- ring abscesses
- myocardial abscesses
- mycotic aneurysms
- septic coronary arterial emboli