Infective endocarditis is an infection of the endocardium and the valves that separate the four chambers. It is a bacterial infection with symptoms such as fever, muscle, joint pain, shortness of breath, sweats, chills, and murmur.
In most patients, Janeway lesions, Osler nodes, and petechiae are also observed. A series of intracardiac and extracardiac problems might arise without prompt diagnosis and treatment.
Epidemiology
Infective endocarditis is an uncommon disease affecting 3 to 10 individuals per 100,000 people yearly. Traditionally, the disease process has shown a preference for men, with a male-to-female ratio of roughly 2:1. The typical age of patients with infected endocarditis is beyond 65.
This predominance for the elderly is most likely due to the greater incidence of risk factors, such as indwelling cardiac devices, prosthetic valves, acquired valvular disease, diabetes mellitus, and hemodialysis, in this population.
Despite being a prominent risk factor in the past, rheumatic heart disease now accounts for less than 5% of all occurrences in the current antibiotic age.
Anatomy
Pathophysiology
In most cases, the healthy endocardium is resistant to bacteria seeding. Overall, prodromal endocardial damage is required to develop infectious endocarditis, followed by a period of bacteremia. The initial endocardial rupture may occur because of turbulent flow around sick valves or direct mechanical damage produced by electrode or catheter placement.
In the context of intravenous drug usage, the requisite harm is caused by repeated valvular damage by co-injected particulates. Hemodynamics plays an essential role in pathogenesis, as indicated by the tendency for vegetation to grow on the ventricular surface of the aortic valve and the atrial surface of the mitral valve.
Since the vegetations are located directly downstream of the regurgitant flow, hypoperfusion of the intima increases the susceptibility of certain regions to endocardial damage. Moreover, infective endocarditis is more likely in lesions with significant turbulence, such as a minor ventricular septal defect with a stenotic valve or jet lesion; the high-pressure flow, presumably, causes more damage than defects with low flow or vast surface areas.
The bacteremia results from a long-standing infection source or emerges transiently because of intermittent hematogenous seeding of oral flora through gingival or dental manipulation. Although the minimal bacterial burden is unclear, slow 1 mL infusions of 106 colony-forming units of bacteria have been shown to cause instances of infected endocarditis.
Pathogenesis needs an organism capable of attaching to and promoting platelet-fibrin deposits, even in endocardial damage and bacteremia. Three S. aureus proteins, such as serine-aspartate repeat protein and clumping factors A and B, have been discovered to induce platelet aggregation independently.
Etiology
Gram-positive staphylococci, enterococci, and streptococci infections constitute most infective endocarditis cases. These three bacterial groups account for 80-90% of all cases, with S. aureus accounting for around 30% of infections in developed countries. Other prevalent oropharynx invaders, such as the HACEK organisms, are responsible in addition to other streptococci species.
Several bacteria have already been found, although they account for only around 6% of all cases. Finally, whereas fungal endocarditis occurs in less than 1% of cases, it is a potentially fatal consequence of systemic Candida and Aspergillus infection in immunocompromised patients.
Although the definition of nosocomial infections is debatable, in general, healthcare cases arise in the context of early prosthetic valve endocarditis occurring within the initial 60 days after the procedure or following recent hemodialysis, vascular catheterization, or extra-cardiac operative procedures. S. aureus is the most common pathogen in these settings, accounting for around half of all nosocomial infections.
Less virulent coagulase-negative staphylococci, such as S. epidermidis, are commonly associated with indwelling vascular devices or freshly implanted prosthetic valves. Enterococcal infection occurs similarly in both non-nosocomial and nosocomial infections, accounting for around 18% and 15% of cases, respectively.
Genetics
Prognostic Factors
The prognosis might differ significantly depending on the pathogen’s aggressiveness, the development of secondary infections, comorbidities, and the existence of a native vs. prosthetic valve.
The in-hospital mortality rate is roughly 18%, and one-year mortality might exceed 40%. Although surgical intervention is currently used in over half of all instances of infected endocarditis, it does not appear to increase the risk of in-hospital death.
Infective endocarditis is an infection of the endocardium and the valves that separate the four chambers. It is a bacterial infection with symptoms such as fever, muscle, joint pain, shortness of breath, sweats, chills, and murmur.
In most patients, Janeway lesions, Osler nodes, and petechiae are also observed. A series of intracardiac and extracardiac problems might arise without prompt diagnosis and treatment.
Infective endocarditis is an uncommon disease affecting 3 to 10 individuals per 100,000 people yearly. Traditionally, the disease process has shown a preference for men, with a male-to-female ratio of roughly 2:1. The typical age of patients with infected endocarditis is beyond 65.
This predominance for the elderly is most likely due to the greater incidence of risk factors, such as indwelling cardiac devices, prosthetic valves, acquired valvular disease, diabetes mellitus, and hemodialysis, in this population.
Despite being a prominent risk factor in the past, rheumatic heart disease now accounts for less than 5% of all occurrences in the current antibiotic age.
In most cases, the healthy endocardium is resistant to bacteria seeding. Overall, prodromal endocardial damage is required to develop infectious endocarditis, followed by a period of bacteremia. The initial endocardial rupture may occur because of turbulent flow around sick valves or direct mechanical damage produced by electrode or catheter placement.
In the context of intravenous drug usage, the requisite harm is caused by repeated valvular damage by co-injected particulates. Hemodynamics plays an essential role in pathogenesis, as indicated by the tendency for vegetation to grow on the ventricular surface of the aortic valve and the atrial surface of the mitral valve.
Since the vegetations are located directly downstream of the regurgitant flow, hypoperfusion of the intima increases the susceptibility of certain regions to endocardial damage. Moreover, infective endocarditis is more likely in lesions with significant turbulence, such as a minor ventricular septal defect with a stenotic valve or jet lesion; the high-pressure flow, presumably, causes more damage than defects with low flow or vast surface areas.
The bacteremia results from a long-standing infection source or emerges transiently because of intermittent hematogenous seeding of oral flora through gingival or dental manipulation. Although the minimal bacterial burden is unclear, slow 1 mL infusions of 106 colony-forming units of bacteria have been shown to cause instances of infected endocarditis.
Pathogenesis needs an organism capable of attaching to and promoting platelet-fibrin deposits, even in endocardial damage and bacteremia. Three S. aureus proteins, such as serine-aspartate repeat protein and clumping factors A and B, have been discovered to induce platelet aggregation independently.
Gram-positive staphylococci, enterococci, and streptococci infections constitute most infective endocarditis cases. These three bacterial groups account for 80-90% of all cases, with S. aureus accounting for around 30% of infections in developed countries. Other prevalent oropharynx invaders, such as the HACEK organisms, are responsible in addition to other streptococci species.
Several bacteria have already been found, although they account for only around 6% of all cases. Finally, whereas fungal endocarditis occurs in less than 1% of cases, it is a potentially fatal consequence of systemic Candida and Aspergillus infection in immunocompromised patients.
Although the definition of nosocomial infections is debatable, in general, healthcare cases arise in the context of early prosthetic valve endocarditis occurring within the initial 60 days after the procedure or following recent hemodialysis, vascular catheterization, or extra-cardiac operative procedures. S. aureus is the most common pathogen in these settings, accounting for around half of all nosocomial infections.
Less virulent coagulase-negative staphylococci, such as S. epidermidis, are commonly associated with indwelling vascular devices or freshly implanted prosthetic valves. Enterococcal infection occurs similarly in both non-nosocomial and nosocomial infections, accounting for around 18% and 15% of cases, respectively.
The prognosis might differ significantly depending on the pathogen’s aggressiveness, the development of secondary infections, comorbidities, and the existence of a native vs. prosthetic valve.
The in-hospital mortality rate is roughly 18%, and one-year mortality might exceed 40%. Although surgical intervention is currently used in over half of all instances of infected endocarditis, it does not appear to increase the risk of in-hospital death.
50mg/kg intravenously/intramuscularly 30-60 minutes prior to the procedure. Do not exceed 1g
According to American Heart Association (AHA) recommendations: High-risk individuals only should get endocarditis prophylaxis
https://www.ncbi.nlm.nih.gov/books/NBK557641/
medtigo
Infective endocarditis
Updated :
October 10, 2022
Infective endocarditis is an infection of the endocardium and the valves that separate the four chambers. It is a bacterial infection with symptoms such as fever, muscle, joint pain, shortness of breath, sweats, chills, and murmur.
In most patients, Janeway lesions, Osler nodes, and petechiae are also observed. A series of intracardiac and extracardiac problems might arise without prompt diagnosis and treatment.
Infective endocarditis is an uncommon disease affecting 3 to 10 individuals per 100,000 people yearly. Traditionally, the disease process has shown a preference for men, with a male-to-female ratio of roughly 2:1. The typical age of patients with infected endocarditis is beyond 65.
This predominance for the elderly is most likely due to the greater incidence of risk factors, such as indwelling cardiac devices, prosthetic valves, acquired valvular disease, diabetes mellitus, and hemodialysis, in this population.
Despite being a prominent risk factor in the past, rheumatic heart disease now accounts for less than 5% of all occurrences in the current antibiotic age.
In most cases, the healthy endocardium is resistant to bacteria seeding. Overall, prodromal endocardial damage is required to develop infectious endocarditis, followed by a period of bacteremia. The initial endocardial rupture may occur because of turbulent flow around sick valves or direct mechanical damage produced by electrode or catheter placement.
In the context of intravenous drug usage, the requisite harm is caused by repeated valvular damage by co-injected particulates. Hemodynamics plays an essential role in pathogenesis, as indicated by the tendency for vegetation to grow on the ventricular surface of the aortic valve and the atrial surface of the mitral valve.
Since the vegetations are located directly downstream of the regurgitant flow, hypoperfusion of the intima increases the susceptibility of certain regions to endocardial damage. Moreover, infective endocarditis is more likely in lesions with significant turbulence, such as a minor ventricular septal defect with a stenotic valve or jet lesion; the high-pressure flow, presumably, causes more damage than defects with low flow or vast surface areas.
The bacteremia results from a long-standing infection source or emerges transiently because of intermittent hematogenous seeding of oral flora through gingival or dental manipulation. Although the minimal bacterial burden is unclear, slow 1 mL infusions of 106 colony-forming units of bacteria have been shown to cause instances of infected endocarditis.
Pathogenesis needs an organism capable of attaching to and promoting platelet-fibrin deposits, even in endocardial damage and bacteremia. Three S. aureus proteins, such as serine-aspartate repeat protein and clumping factors A and B, have been discovered to induce platelet aggregation independently.
Gram-positive staphylococci, enterococci, and streptococci infections constitute most infective endocarditis cases. These three bacterial groups account for 80-90% of all cases, with S. aureus accounting for around 30% of infections in developed countries. Other prevalent oropharynx invaders, such as the HACEK organisms, are responsible in addition to other streptococci species.
Several bacteria have already been found, although they account for only around 6% of all cases. Finally, whereas fungal endocarditis occurs in less than 1% of cases, it is a potentially fatal consequence of systemic Candida and Aspergillus infection in immunocompromised patients.
Although the definition of nosocomial infections is debatable, in general, healthcare cases arise in the context of early prosthetic valve endocarditis occurring within the initial 60 days after the procedure or following recent hemodialysis, vascular catheterization, or extra-cardiac operative procedures. S. aureus is the most common pathogen in these settings, accounting for around half of all nosocomial infections.
Less virulent coagulase-negative staphylococci, such as S. epidermidis, are commonly associated with indwelling vascular devices or freshly implanted prosthetic valves. Enterococcal infection occurs similarly in both non-nosocomial and nosocomial infections, accounting for around 18% and 15% of cases, respectively.
The prognosis might differ significantly depending on the pathogen’s aggressiveness, the development of secondary infections, comorbidities, and the existence of a native vs. prosthetic valve.
The in-hospital mortality rate is roughly 18%, and one-year mortality might exceed 40%. Although surgical intervention is currently used in over half of all instances of infected endocarditis, it does not appear to increase the risk of in-hospital death.
https://www.ncbi.nlm.nih.gov/books/NBK557641/
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