WEEK 3: Infective endocarditis Flashcards
What is infective endocarditis?
Endocarditis is an inflammation of the endocardium.
State the possible causes of infective endocarditis.
Caused by bacterial or fungal infections.
OR
Non-bacterial thrombotic endocarditis: in absence of infection
IE is a characterized by a vegetation. What does that mean?
Without treatment, what is the mortality %?
Even with treatment, 6-month mortality rate ≈ how many %?
a mass of platelets, fibrin, microcolonies of microorganisms and scant inflammatory cells.
Even with treatment, 6-month mortality rate ≈ 25%
Outline parts which may be involved in infective endocarditis.
- Valves (most common)
- Septal defects
- Arteriovenous shunts
- Arterioarterial shunts (e.g., PDA)
Discuss the epidemiology of infective endocarditis.
Male: Female 2:1
Aortic valve and Mitral valve most common
Tricuspid rare (iv drug abusers)
Pulmonary valve exceedingly rare
Discuss Infective endocarditis,– aetiology and sources of infection
View diagram on slides.
- MOUTH
Discuss the Pathophysiology of IE.
The endothelium and valves are normally resistant to infection with bacteria and fungi.
State the 2 major predisposing causes of IE.
Development of IE requires two major predisposing causes:
-Presence of organisms in the bloodstream.
-Abnormal cardiac endothelium facilitating their adherence and growth.
Outline different way in which bacteria enters the body.
Poor dental hygiene,
Intravenous drug use,
Soft tissue infections)
Diagnostic or therapeutic procedures (dental treatment, intravascular cannulae, cardiac surgery or permanent pacemakers).
Outline Predisposing Factors to IE.
- Age
-Degenerative valvular dz.
-Increased exposure to nosocomial bacteremia
-Prosthetic valves - Medical conditions :
-Long term HD
-DM
-Poor dental hygiene
-HIV (independent) - Congenital defects
-MVP: Mitral Valve Prolapse (MVP):
Description: MVP is a condition where the flaps (cusps) of the mitral valve do not close properly, causing them to bulge (prolapse) into the left atrium during ventricular contraction. This can lead to leakage of blood back into the left atrium, known as mitral regurgitation.
-Atrial Septal Defect (ASD)
-Ventricular Septal Defect (VSD)
- Injection-drug use (TV)
- Long-term indwelling intravenous catheters
- Rheumatic heart dz.
- Gender
Discuss the Pathogenesis: Events of IE.
- Endothelial damage
Produced by various local and systemic stresses, including blood turbulence and high-velocity flows
induces thrombogenesis, leading to nonbacterial thrombotic endocarditis (NBTE). - Deposition of platelets and fibrin
-Form sterile vegetation the lesions of nonbacterial thrombotic endocarditis (NBTE)
-Suitable site for bacterial attachment and colonization.
- Bacteria colonization of NBTE
-organisms to adhere and grow, leading to an infected vegetation - Bacterial multiplication and vegetation growth
-Surface covered with a protective sheath of platelets and fibrin.
-Mature vegetation consist of fibrin, platelets, leukocytes, red blood cell debris, and dense clusters of bacteria.
Define bacteremia.
Bacteremia is a medical condition characterized by the presence of bacteria in the bloodstream.
Normally, the bloodstream is sterile, meaning it does not contain any bacteria.
However, bacteremia occurs when bacteria from an infection site elsewhere in the body, such as the skin, lungs, urinary tract, or gastrointestinal tract, enter the bloodstream and circulate throughout the body.
Describe Clinical Manifestations and Complications of IE.
Most patients develop symptoms within 2 wks. of the inciting bacteremia.
Symptoms and signs are protean (capable of assuming many different forms or roles).
Any organ system may be involved.
*Malaise
*Clubbing
*CARDIAC: Murmurs. Cardiac failure
*Arthralgia
*Pyrexia
*SKIN LESIONS: Jane way, Osler’s, splinter hemorrhages, petechiae
*EYES:
-Conjuctival splinter hemorrhages.
-Roth spots: oval retinal hemorrhages with pale centers
*Splenomegaly
*Hematuria
*NEUROLOGICAL: Cerebral emboli, mycotic aneurysm
Discuss the diagnosis of IE.
*Frequently difficult
-Highly variable and often non-specific presentation.
*Look for predisposing anatomy or behavior
*Blood cultures
*Echocardiography
-Trans Thoracic Echocardiography (TTE) – 60% sensitive
During a TTE procedure, a transducer (a device that emits and receives ultrasound waves) is placed on the chest wall, and sound waves are directed toward the heart. These sound waves bounce off the heart structures, creating detailed images of the heart chambers, valves, and surrounding structures.
-Trans Esophageal Echocardiography (TEE) – 80 – 95% sensitive
During a TEE procedure, a specialized transducer is attached to the end of a flexible tube (probe) that is passed through the mouth and into the esophagus, which lies directly behind the heart.
By positioning the transducer close to the heart, TEE provides clearer and more detailed images compared to TTE, as the ultrasound waves do not have to pass through the chest wall and lungs.
Discuss Diagnosis-Duke Criteria: Major criteria
Major criteria:
1. Persistently positive blood cultures
*Typical organisms for IE
*Persistent bacteremia
2. Evidence of endocardial involvement
*Positive ECHO
*New valvular regurgitation
*Immunologic phenomena
-Glomerulonephritis, Osler nodes, Roth spots, or rheumatoid factor
*Microbiologic evidence
-Positive blood cultures that do not meet major criteria, OR serologic evidence of active infection with organism consistent with IE
Discuss Diagnosis-Duke Criteria: Minor criteria
Minor criteria:
- Predisposition
Intravenous drug use or presence of a predisposing heart condition (prosthetic heart valve or a valve lesion associated with significant regurgitation or turbulence of blood flow) - Fever – Temperature ≥38.0°C (100.4°F)
*Vascular phenomena
-Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, or Janeway lesions
