Infrctive Endocarditis

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Infective Endocarditis

DR HAMISI SEMBE
DR NURU LETARA
OUTLINE
• Introduction
• Epidemiology
• Etiology
• Risk factors
• Pathogenesis
• Clinical features
• Management
• Complications
• Prognosis
Introduction
• Infection of the endocardial lining of the heart

• May involve
The endocardium of the valves
The mural endocardium
Endothelium of blood vessels

• The commonest site of infection is a diseased valve from where


the infection can spread along the endothelium.
Epidemiology
• Estimated annual incidence of approximately 0.5 per 100,
000 per year

• Significant cause of morbidity and mortality in children and


adolescents despite
advances in management and

Prophylaxis of the disease with antimicrobial agents.


Etiology

• Bacterial causes

• Non bacterial causes


Viruses
Fungi
Other microbial agents
Etiology
• Streptococcus viridans (alpha hemolytic) and Staphylococcus
aureus are the leading causative agent in pediatric patients.
• Viridans group streptococcal infection is more common after
dental procedures
• Group D enterococci are seen more often after lower bowel
or genital urinary manipulation
• Pseudomonas aeruginosa is seen more frequently in
intravenous drug users
Etiology
• Fungal endocarditis

Candida commonest

others : Aspergillus, Histoplasma etc.


Risk factor
• Survivors of cardiac surgery
Especially those with mechanical prosthesis
• RHD
• Unrepaired CHD
• Intravenous drug users
• Patients taking immunosuppressant medications
• Patients require chronic intravascular catheters
Pathogenesis
Pathogenesis
• Congenital or acquired heart lesion
• Turbulent blood flow because of hole or stenotic orifice
• Turbulent flow traumatizes the vascular endothelium, creating a
substrate for deposition of fibrin and platelets leading to the
formation of a nonbacterial thrombotic embolus (NBTE)
• Biofilms form on the surface of implanted mechanical devices such as
valves, catheters, or pacemaker wires that also serve as the adhesive
substrate for infection
• The development of transient bacteremia then colonizes this (NBTE)
or biofilm leading to proliferation of bacteria within the lesion.
Pathogenesis
• Bacteria surface proteins act as adhesion factors to the (NBTE ) or
biofilm after which bacteria can rapidly proliferate within the
vegetation
• Given the heavy colonization of mucosal surface ( the oropharynx, or
gastrointestinal, vaginal or urinary tracts) by potentially pathogenic
bacteria, these surfaces are thought to be the origin of this transient
bacteremia.
Clinical features
• Grouped into 3
Indicating presence of an infection
Indicating involvement of the cardiovascular system
Indicating the presence of an immunological reaction
to infection
Features indicating the presence of infection
• Fever
• Chills
• Rigors
• Night sweats
• General malaise and weakness
• Loss of appetite
• Weight loss
Features indicative of the involvement of the
CVS
• Appearance of left or right failure
• Development of a new murmur or change in a preexisting
murmur
• Presence of embolic episodes
Stroke from CNS embolism
Hematuria from renal infarct
Left flank pain from splenic infarct
Gastrointestinal hemorrhage from mesenteric embolism
Features of immunological response
presenting as vasculitis
• Arthralgia
• Mayalgia
• Clubbing
• Splenomegaly and microscopic hematuria
• Splinter hemorrhage
• Petechiae over skin
• Roth spots
• Osler nodes
• Janeway lesions
• Erythematous patches
Modified Duke criteria
• Major criteria
Positive blood culture for IE ( 1 of the following)
• Typical microorganism consistent with IE from 2 separate blood cultures
• Persistently positive blood culture
• Single positive blood culture for Coxiella burnetii

Evidence of endocardial involvement


• Echocardiography positive for IE
• New valvular regurgitation
Modified Duke criteria
• Minor criteria
Predisposition
• Iv drug users
• Presence of a predisposing heart condition
Fever-Temperature more or equal 38.0C
Vascular phenomena
Immunological phenomena
Microbiological evidence- positive blood cultures that do not meet
major criteria
Modified Duke criteria
• Definitive IE is established in the presence of the following
Pathological criteria
• Pathological lesions –vegetation or intracardiac abscess
• Microorganism- demonstrated by culture or histology of vegetation or
intrathoracic abscess
Clinical criteria
• 2 major clinical criteria
• 1 major and 3 minor criteria
• 5 minor clinical criteria
Modified Duke criteria
• Possible IE
Presence of 1 major and 1 minor clinical criteria or

Presence of 3 minor clinical criteria

• Rejected IE
A firm alternative diagnosis is made
Resolution of clinical manifestations occurs after less than 4 days of antibiotic
therapy
No pathological evidence of IE
Clinical criteria for possible or definitive IE not met.
Management
Investigations
• Blood culture- confirmatory
• Supportive
FBP
ESR
CRP
Urinalysis

• Echocardiogram
• CXR
Treatment
• Antibiotic therapy

• Surgical
IE associated valve dysfunction with CCF
Patients with persistent fevers and bacteremia despite appropriate antibiotic
therapy

• Empiric treatment
IE without acute symptoms (wait for B/C results 1 to 3 Days)
IE with symptoms; empiric treatment (Patients with hemodynamic instability,
clinical presentation suggestive of IE, fever, new murmur etc.)
Treatment
• Antibiotic for 6 weeks

• Penicillin and aminoglycosides

• MRRSA vancomycin for 6 weeks

• Antifungal for fungal infection


Complications
• Cardiac complications
 HF, perivalvular abscess, pericarditis.
• Forms of metastic infection
Septic embolization, metastatic abscess
• Neurologic complications
Stroke, brain abscess, meningitis
• Renal complications
Renal infarction or abscess following septic embolization, glomerulonephritis.
• Musculoskeletal complications
Vertebral osteomyelitis and septic athritis
Prognosis
• Six month mortality rate among patients with IE ranges up to 27%.

• Factors associated with increased risk of mortality


Microbiology
Heart failure
Embolization
Candidate for cardiac surgery
Prevention
• Oral hygiene for prevention of oral disease
• Antimicrobial prophylaxis for high risk patients when undergoing
invasive procedures
• Thank you for listening

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