Infective Endocarditis
| Overview |
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- Infective Endocarditis refers to infection of the endocardium. The prototypical physical manifestation of Infective Endocarditis is termed the "Vegetation", and represents a mass of thrombotic debris and bacteria adherent to the endocardial surface with few immune cells. Infective Endocarditis can be categorized along many axes, highlighting the location of infection, the responsible bacterial species, by a patient's predisposing risk factor, or by the speed of clinical progression.
| Pathogenesis |
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- Overview
- The smooth endocardium is normally resistant to infection; however, the set of pathogenic events described below are thought to be the sequence by which the endocardium is injured and rendered prone to infection, thus forming the physical substrate upon which infective vegetations can develop.
- Endocardial Injury
- Physical injury of the endocardium initiates the pathogenic sequence which ultimately leads to its infection. In most cases, injury is due to hemodynamic trauma associated with localized turbulent flow. Such turbulent flow can occur on the endocardium covering deformed heart valves or at the endocardial impact site of high-velocity jets of blood. Foreign bodies such as in-dwelling cardiac catheters or prosthetic heart valves can also incite endocardial injury.
- Thrombus Formation
- Endocardial Injury results in thrombosis and the formation of an adherent thrombus at the site of injury. The consequent localized mass of fibrin and platelets is termed a "Nonbacterial Thrombotic Endocarditis (NBTE)" and likely represents the sterile precursor lesion to a full infective vegetation. It should also be pointed out that the material of prosthetic heart valves is highly prone to spontaneous thrombus formation and thus development of surface NBTEs. NBTEs are thought to provide a physical substrate upon which bacteria present within the blood stream can attach and proliferate.
- Bacterial Entry
- Bacteria can gain access to the blood stream anytime a colonized epithelial surface is traumatized. Mild, transient episodes of bacteremia likely happen fairly regularly due to everyday activities such as teeth brushing or may occur more profoundly following dental procedures, surgical procedures, or IV drug abuse. Whatever the case, in most normal patients these episodes are self-limited and inconsequential. However, in individuals harboring NBTEs, hematogenous bacteria can colonize and proliferate within the adherent thrombi and in doing so damage the underlying endocardium as well as physically expand the vegetation.
| Etiology |
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- Overview
- Culprit organisms must be able to survive within the bloodstream long enough to travel from their site of inoculation to the heart itself. Most cases of infective endocarditis (~90%) are caused by the gram positive bacteria mentioned below, likely because gram negative bacteria and fungi are rapidly destroyed by plasma complement proteins.
- Organisms
- Staphylococci: Mostly Staphylococcus aureus with some cases caused by Staphylococcus epidermidis
- Streptococci: Mostly Viridans Streptococci and Enterococci
- Other Organisms: The remaining 10% of cases can be caused by a variety of gram negative bacteria and some fungi
| Epidemiology |
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- Overview
- The major risk factors for infective endocarditis are conditions which predispose an individual's endocardium to injurious hemodynamic trauma. In many cases, patients are categorized by their risk factors as certain bacterial etiologies are more or less common among these different demographic groups.
- Pre-existing Valvular Pathology
- Valvular deformities generate significant turbulent flow adjacent to the valvular endocardium. Thus, pre-existing Valvular Heart Diseases of any etiology and a history of conditions such as Rheumatic Fever which give rise to valvular deformities are major risk factors for the development of infective endocarditis. Empirically, patients with mitral regurgitation, aortic stenosis, and aortic regurgitation are those with the highest risk. Additionally, patients with hypertrophic cardiomyopathy are at an increased risk due to repeated trauma to the mitral valve as described on its respective page.
- Prosthetic Heart Valves
- Patient with valvular prostheses are at a significantly greater risk of developing endocarditis not only because endocardial injury is an inherent part of their implantation but also because prostheses are less able to resist inappropriate thrombosis. Furthermore, surgical placement of prostheses often results in a transiently increased burden of bloodstream bacteria and the risk of infective endocarditis development gradually declines following valvular replacement. In developed countries, nearly 30% of all cases of infective endocarditis are associated with valvular prostheses.
- Pre-existing High-velocity Jets
- Architectural defects of the heart that result in the development of high-velocity jets of blood can pre-dispose the endocardial impact sites of the jet to injury. Such jets can be created by Ventricular Septal Defects, Patent Ductus Arteriosus, or Tetralogy of Fallot.
- IV Drug Abuse
- IV Drug Abusers are at a higher risk of developing infective endocarditis likely because of repeated exposure to transient bacteremic episodes associated with non-sterile injection. Because bacteria first encounter the tricuspid valve and pulmonic valve, these valves are particularly at risk for infection in this particular demographic.
| Clinical Consequences |
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- Overview
- The clinical course of infective endocarditis represents a spectrum from rapid progression (Acute Endocarditis) to an indolent progression (Subacute Endocarditis). Acute Endocarditis is characterized by rapid development of high fevers and intense chills, indicative of a profound microbial infection. In contrast, Subacute Endocarditis is characterized by a low-grade fever and other constitutional symptoms] such as fatigue, malaise, myalgia, and anorexia. The primary, although not exclusive, factor which determines the course of disease is the causative organism
- In general, Acute Endocarditis is caused by Staphylococcus aureus whereas other microbial species usually give rise to a Subacute course. It is important to note that the signs and symptomology of endocarditis are relatively non-specific and a high degree of clinical suspicion must be employed with an eye toward the risk factors delineated above.
- Cardiac Consequences
- The presence of vegetations often results in physical damage to the underlying endocardium. When vegetations are present on heart valves this can give rise to or aggravate pre-existing Valvular Heart Disease. For example, large vegetations can lead to valvular stenosis but more commonly destruction of the heart valve leads to valvular regurgitation. Acute endocarditis can cause valvular damage rapidly, within days, whereas damage following a subacute course can progressively worsen over months. Often, infective endocarditis can be detected by the development of new or changing heart murmurs representing new or evolving valvular damage.
- Embolization
- The extra-cardiac clinical consequences of infective endocarditis are primarily due to embolization of vegetations which can seed nearly any organ
- Microemboli to skin: Present as small "Splinter Hemorrhages" under the nails, petechiae, or as small, painful nodules on the fingers and toes, termed "Osler's Nodes"
- Emboli to vaso vasorum of large arteries: Can lead to mycotic aneurysms
- Emboli to kidneys: Can lead to renal infarctions
- Emboli to cerebral arteries: Can lead to cerebral infarctions or meningitis
- Emboli to lungs: Occurs only in right-sided infective endocarditis observed in IV drug abusers and can lead to septic pulmonary emboli
- Immune-Complex Disease
- For poorly-understood reasons immune complexes are developed during the sustained immune response to prolonged cases of infective endocarditis. These immune complexes can deposit within the glomerulus and cause glomerulonephritis similar to Acute Proliferative Glomerulonephritis or Membranoproliferative Glomerulonephritis