9) Infective Endocarditis (IE)

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Q9.

Infective endocarditis (IE)

Definition: Infective endocarditis is an infection of the endocardial surface of the heart, which may
include one or more heart valves, the mural endocardium or a septal defect. Infective endocarditis
develops on damaged valves or congenital malformations. It can result in intracardiac effects such as:

 severe valvular insufficiency leading to congestive heart failure


 abscesses
 Systemic signs and symptoms through several mechanisms, including both sterile and infected
emboli and various immunological phenomena.

Types of infective endocarditis

Infective endocarditis is divided into native valve endocarditis and prosthetic valve endocarditis.

1. Native valve endocarditis:


- acute : involves normal valves and usually has an aggressive course e.g s.aureus and
group B streptococci.
- Subacute: typically effects only abnormal valves e.g. α-hemolytic streptococci or
enterococci.

2. Prosthetic valve endocarditis (10-20% cases) can be:


- early: within <60 days after valve implantation e.g. coagulase negative staphylococci,
gram negative basilli and candida species.
- late: 60 days or more after valve implantation e.g staphylococci, α-hemolytic
streptococci and enterococci.
3. Intravenous drug abuse endocarditis (50% of cases involves tricuspid valve caused by S.aureus)
4. Pacemaker infective endocarditis
5. Nosocomial infective endocardits ( hospital acquired)

Etiology

 streptococcus (causes subacute IE) - 70%


 Staphylococcus (causes acute IE) - 20%
 Gram (- ) bacteria: Klebsiella, E.coli , Proteus, Pseudomonas, Salmonella, Rickettsia
 Fungi: Candida , Histoplasma

Predisposing factors for the development of infective endocarditis:

 Pre-existing rheumatic fever and valvular damage


 Congenital malformations e.g. congenital heart disease, coarction of aorta, bicuspid aortic valve,
ventricular septal defect.
 ventricular septal defect
 Degenerative heart disease e.g mitral valve prolapse
 Asymmetric septal hypertrophy
 prosthetic valves and pacemakers
 Intravenous drug users
 alcohol abuse and sepsis
 invasive procedure e.g barium enema/ colonoscopy/prostatectomy/ tooth extraction / biopsies/
suture removal/ bronchoscopy/ tonsillectomy.

Pathophysiology (lecture +book):

 An infection penetrating the organism through a portal of entry, a suitable terrain (e.g. damaged
endothelium, valvular heart disease, congenital abnormality ) and the interaction between the
host and the pathogens are the main factors for the development of IE.
 Firstly, bacteraemia (nosocomial or spontaneous) delivers the organism to the surface of the
valve. Then there is adherence of the organism leading to eventual invasion of the valvular
leaflets.
 Sterile fibrin-platelet vegetations form on valves.
 Bacteraemia (spontaneous or due to an invasive procedure) infects the sterile fibrin-platelet
vegetation.
 The vegetations consists of fibrin, platelets, leukocytes, RBC and microorganisms. As valvular
destruction continues, valvular regurgitation occurs resulting in heart failure.
 Moreover, the vegetations can become emboli and can deposit in different organs such as kidney
, spleen, brain, skin.
 Infective endocarditis can enter the' immunologic phase' in which the organs are damaged by
autoimmune mechanisms.

Symptoms and signs

 Fever, chills, sweats (90% )


 heart murmurs (85% )
 splenomegaly
 anorexia , weight loss, malaise
 arthralgias, myalgias, low back pain
 systemic emboli
 congestive heart failure
 renal insufficiency
 sinus tachcardia
 skin may appear pale due to anemia
 Peripheral stigmata of IE:
- Janeway lesion = pink macuale
- roth's spots = retinal hemorrhages with pale centres
- splinter or subungual hermorrages = dark red linear streaks in the nail bed of fingers/toes
- Osler's nodes = small, tender subcutaneous nodules within the skin of finger/toe pads and
thenar/hypothenar eminences.
 Osler's (Austrian triad) = The classical triad consists of endocarditis ,pneumonia, meningitis, all
caused by Streptococcus pneumoniae. It is associated with alcoholism, elderly, diabetes (in
lecture).

complications

 embolisms
 valve destruction (most often aortic of mitral regurgitation)
 various immunological mechanisms
Laboratory finding

 ECG should be done in all patients with suspected IE (look for new LBBB/RBBB, prolonged PR
interval, complete heart block).
 Chest x-ray (look for pulmonary embolism , CHF)

Diagnosis
Dukes criteria for diagnosis of infective endocarditis requires:
 2 major criteria
 1 major and 3 minor criteria
 5 minor criteria
Major criteria:
 positvie blood culture at least two identical in 12 hours
 endocardial lesion - new regurgitation, vegetations, dehiscence of prosthesis, abscess formation.
 ECG - transthoracic echocardiogram or transesophageal echocardiography is an excellent
method to prove the diagnosis.

Small criteria

 Predisposition - anatomic or drug abuse


 Body temperature >38C
 Vascular phenomena
 immunologic phenomena

Differential diagnosis

 TB , sepsis, rheumatic fever, tumours

Treatment

 Main purpose of the treatment is the eradication of the microorganisms from the vegetation.
 PARENTERAL bactericidal antibiotics
 Always use a combination of at least 2 antibiotics for at least 4 weeks.
 High serum antibiotic required to penetrate the vegetation
 3 negative cultures are required to stop the antibiotic.
 Surgery is indicated in severe valvular destructions, septal or valvular abscess formation, most
cases of prosthetic endocarditis, massive vegetation with valvular obstruction and hypotension/
shock, repetitive embolic episodes.

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