INFECTIVE ENDOCARDITIS

INFECTIVE ENDOCARDITIS

INTRODUCTION

• Endocarditis is defined as an infection, usually bacterial, of the endocardial surface of the heart.

• Infective endocarditis primarily affects the cardiac valves, although the septa between the chambers or the mural endocardium may be involved in some cases.

• infective endocarditis has been categorized as acute or subacute, depending on the length of symptoms before presentation; . A classification that considers the causative organism and the valve involved is more clinically relevant

ACUTE IE

• Acute IE is most commonly caused by Staphylococcus aureus. It presents with marked toxicity and progresses over days to several weeks to valvular destruction and metastatic infection

SUB ACUTE IE

• Subacute IE, usually caused by viridans streptococci, enterococci, coagulase-negative staphylococci, or gram-negative coccobacilli, evolves over weeks to months with only modest toxicity and rarely causes metastatic infection.

Incidence Of Infective Endocarditis

• The incidence of infective endocarditis is approximately 1.7-6.2 cases per 100 000 patient /year,although rates are higher in at risk cohorts such as intravenous drug users.

• Men are more often affected than women (in a ratio of 2:1), and the incidence progressively increases with age. Underlying degenerative aortic and mitral valve disease now predominate over rheumatic disease, although in one recent French study 47% of patients with infective endocarditis presented without previous knowledge of an underlying cardiac disorder

 PREDISPOSING CONDITIONS ASSOCIATED WITH INCREASED RISK OF ENDOCARDITIS

• More Common• Mitral valve prolapse with murmur • Degenerative valvular disease• Intravenous drug use• Prosthetic valve.

• Congenital abnormalities (valvular or septal defect)

Less Common

• Rheumatic heart disease • Hypertrophic obstructive

cardiomyopathy• Pulmonary-systemic shunts.

• Coarctation of the aorta • Complex cyanotic congenital heart

disease

Infective endocarditis: patient groups

• Children with IE: congenital heart disease Staphylococcus (neonate), Streptococcus group B (children), S. pneumonia (rare)

• Adults with IE: Rheumatic heart disease: MV (F>M), AV (M>F)

Congenital heart disease: PDA, VSD, bicuspid AV

Infective endocarditis: patient groups

• IV drug abusers with IE: TV (46—78%) MV (24—32%) AV (8—19%) S. aureus, GNB (Pseudomonas), polymicrobial HIV: 73%; increased mortality (CD4 < 200)• Prosthetic valves with IE: early (< 60 days): surgical complication, late (> 60 days): community or nosocomial ring abscess, annular invasion, paravalvular regurgitation

Infective endocarditis: nosocomial

• Infected intracardiac device and catheter• GI or GU tract surgery or instrumentation• High mortality (40—56%)

• GPC ( S. aureus, CONS, Enterococcus)• S. aureus catheter related bacteremia .

Infective endocarditis: microorganism

• Streptococcus viridans: 35 — 65% NVE normal flora of the oropharynx• Streptococcus pneumoniae: alcoholism aortic valve concurrent pneumonia or meningitis • Enterococcus: normal GI tract flora and cause GU infection 5—15% NVE and PVE

Infective endocarditis: microorganism

• Staphylococcus: Coagulase-positive: S. aureus highly toxic febrile 30—50% CNS involvement

Coagulase-negative: S epidermidis Major cause of PVE

Infective endocarditis: microorganism

• Gram negative bacteria: upper respiratory tract and oropharyngeal flora P. aeruginosa: most common in GNB IE HACEK: haemophilus spp., Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae

• Fungus: drug abuser and prosthetic valve common: C. albicans (PVE); C. parapsilosis

(NVE)

Pathogenesis of Endocarditis

• Inoculation of bacteria colonizing a mucosal (e.g., oral mucosa) or peripheral tissue site into the bloodstream• Transient bacteremia of a serum-resistant pathogen

capable of adhering to a cardiac valvular surface.• Turbulent blood flow across the valve• • Bacterial adherence to cardiac valvular surface• Pathogen - host tissue interaction resulting in vegetation

formation and local tissue damage• – Bacterial persistence• Dissemination of infection to other tissue sites and

elicitation of systemic findings

Factors Contributing to the Pathogenesisof Endocarditis

• Hemodynamics - blood flow patterns

• Bacterial properties• Host factors

• Local destruction of intracardiac infection: valve, chordae tendineae, fistula, paravalvular abscess, conduction

• Distant embolization with infarct or infection:

• Hematogenous seeding with bacteremia: metasttic infection,

• Immune-complex or antibody reaction: IgM, IgA, IgG, Osler’s node, Rheumatoid factor, Roth’s spot

Differential Diagnosis: ABE

• Sepsis• Pneumonia• Meningitis• Brain abscess• Stroke• Malaria• Acute pericarditis

• Vasculitis• DIC

Differential Diagnosis: SBE

• As FUO• Rheumatic fever• Osteomyelitis• Tuberculosis• Meningitis• Abdominal infection• Glomerulonephritis

• Myocardial infarction• Stroke• Connective tissue

diseases• Occult malignancy• Chronic heart failure• Pericarditis

INFECTIVE ENDOCARDITIS:Symptoms

– High grade fever and chills

– SOB

– Arthralgias/ myalgias

– Abdominal pain

– Pleuritic chest pain

– Back pain

Signs• Fever • Changing Heart murmur

• Nonspecific signs – • petechiae, “splinter” hemorrhages, • clubbing, • splenomegaly, • neurologic changes

• More specific signs –• Osler’s Nodes, • Janeway lesions, • Roth Spots

Petechiae1.Nonspecific2.Often located on extremities

or mucous membranes

Splinter Hemorrhages

1. Nonspecific2. Nonblanching3. Linear reddish-brown lesions found under the nail bed4. Usually do NOT extend the entire length of the nail

Osler’s Nodes

1. More specific2. Painful and erythematous nodules3. Located on pulp of fingers and toes4. More common in subacute IE

Janeway Lesions

1. More specific2. Erythematous, blanching macules 3. Nonpainful4. Located on palms and soles

Duke Criteria For The Diagnosis Of Infective Endocarditis

• Major Criteria• Positive blood culture .• A). Typical micro-organism consistent with

infective endocarditis from two separate blood cultures :

• i) Streptococci viridans ,Streptococcus bovis HACEK group OR  (ii) community-acquired Staphylococcus aureus

enterococci, in the absence of a primary focus or

• B. Micro-organisms consistent with infective endocarditis from persistently positive blood cultures defined as:

i) at least two positive cultures of blood samples drawn > 12h apart or

ii) all three of these or a majority of four or more separate cultures of blood (with first and last sample drawn at least 1h apart).

• 2. Evidence of endocardial involvement

• A. Positive echocardiogram for infective endocarditis as defined as:

• (i) oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomical explanation or

  (ii) abscess or, (iii) new partial dehiscence of prosthetic valve.

B. New valvular regurgitation (worsening or changing of pre-existing murmur not sufficient)

Minor Criteria

• 1. Predisposition: predisposing heart condition or intravenous drug use2. Fever: temperature > 38 °C3. Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhages, and Janeway's lesions

• 4. Immunological phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor

• 5. Microbiological evidence: positive blood culture but does not meet a major criteria or serological evidence of active infection with organism consistent with infective endocarditis

• 6. Echocardiographic findings: consistent with infective endocarditis but do not meet a major criteria.

Lab: CBC

• Anemia– Mild to moderate– Normocytic normochromic

• Leukocytosis: not reliable

Routine Tests

• Elevated ESR: 90%• Elevated CRP: 96%• Urinalysis

– Microscopic hematuria or proteinuria: >50%– RBC casts & heavy proteinuria: glomerulonephritis– Gross hematuria: renal infarction

Blood Culture

• B/C should be done in all patients with undiagnosed fever and a heart murmur

• B/C send on the first day• Aerobic + anaerobic• Additional B/C on day 3 if necessary

(when diagnosis is likely but B/C yielded negative results)

ECG

• Repeated or even continuous ECG monitoring

• Frequent APC or PVC• Prolonged PR interval• Myocardial infarction

Echocardiography

• The diagnosis of infective endocarditis is frequently suggested on the basis of echocardiography, which is the diagnostic procedure of choice for detecting valvular vegetations.

• The echocardiographic features typical for infective endocarditis are

• (a) an oscillating intracardiac mass on a valve or supporting structure or in the path of a regurgitation jet or on a device,

• (b) abscesses, • (c) new partial dehiscence of a prosthetic valve,

or• (d) new valvular regurgitation. The initial

attachment site of a vegetation is usually on the ventricular surface of the semilunar valves and on the atrial surface of the atrioventricular valves

Image Study: CXR

• Provide evidence of early CHF• Valvular calcification• Multiple small, patchy infiltrates in the

lungs of an Iv drug user with fever: septic emboli from right-sided IE

Image Study: CT/MRI

• For defining the cause of focal neurologic lesions

• Cerebral emboli

Image Study: Cardiac Cath

• Indication:– In patients >40 y/o (for possible concurrent CAD)– When surgical intervention is considered

Diagnostic Criteria• DEFINITE INFECTIVE ENDOCARDITIS• Pathologically proven infective endocarditis or Clinical

criteria meeting either   Two major criteria or   one major and three minor criteria or   five minor criteria

• POSSIBLE INFECTIVE ENDOCARDITIS • One major or one minor or three minor criteria• REJECTED INFECTIVE ENDOCARDITIS• Firm alternative diagnosis or Resolution of infective

endocarditis syndrome with antibiotic therapy of ≤4 days or No pathologic evidence of infective endocarditis at surgery or autopsy with antibiotic therapy of ≤4 days

Culture-Negative Infective Endocarditis• Blood cultures fail to isolate an etiologic agent in 3% to 23% of cases .

Culture-negative IE is most often associated with antibiotic use within the previous 2 weeks. Less frequently, intracellular pathogens not detected using standard culture approaches may be the cause . If blood cultures are negative , consideration should be made to analyze serum for Bartonella, Coxiella, and Chlamydia species antibodies . If the patient requires valve surgery, RNA polymerase chain reaction amplification of valve tissue often yields an etiologic agent

• the search for a causative organism remains fruitless, consider noninfectious etiologies such as marantic or Libman-Sacks endocarditis and atrial myxoma.

Clinical Criteria

• 2 major• 1 major + 3 minor• 5 minor

 INDICATIONS FOR SURGERY IN ENDOCARDITIS

IndicationNATIVE VALVE ENDOCARDITIS

• Acute aortic insufficiency or mitral regurgitation with heart failure I • Acute aortic insufficiency with tachycardia and early closure of the

mitral valve on echocardiogram I • Fungal endocarditis I • Evidence of annular or aortic abscess; sinus or aortic true or false

aneurysm; valve dehiscence, rupture, perforation, or fistula I• Evidence of valve dysfunction and persistent infection after a

prolonged period (7–10 days) of appropriate therapy, provided there are no noncardiac causes for infection I

• Recurrent emboli after appropriate antibiotic therapy I • Infection with gram-negative organisms or organisms with a poor

response to antibiotics in patients with evidence of valve dysfunction I

• Anterior mitral leaflet vegetation (especially >10 mm) or persistent vegetation after systemic embolization IIa

• Increase in vegetation size despite appropriate antimicrobial therapy IIb

• Early infections of the mitral valve that can probably be repaired III

• Persistent fever and leukocytosis with negative blood cultures III

PROSTHETIC VALVE ENDOCARDITIS  • Early prosthetic valve endocarditis (<2 months

after surgery) I• Heart failure with prosthetic valve dysfunction I • Nonstreptococcal endocarditis I• Evidence of perivalvar leak, annular or aortic

abscess, sinus or aortic true or false aneurysm, fistula formation, or new-onset conduction disturbances I

• Persistent bacteremia after 7–10 days of appropriate antibiotic therapy without noncardiac causes for bacteremia IIa

• Recurrent peripheral embolus despite therapy Iia• Vegetation of any size seen on or near the

prosthesis IIb • Class III: Conditions for which there is evidence

and/or general agreement that the procedure/treatment is not useful and in some cases may be harmful

PROPHYLAXIS

AGAINST INFECTIVE ENDOCARDITIS

PROPHYLACTIC ANTIBIOTICREGIMENS

Dental , oral , respiratory & oesophageal procedures

Oral Amoxycillin 2 gm 1 hour before the procedure

• if allergic to penicillin : Clindamycin 600 mg or Azithromycin or clarithromycin 500

mg 1 hour before the procedure

Gastrointestinal & Genitourinary procedures

parenteral amoxicillin 2 gm + gentamycin 1.5 mg / kg 1 hour before and 6 hours after the

procedure• if allergic to penicillin : Vancomycin 1 gm over 1-2 hours + gentamycin 1.5 mg / kg IV or IM

Patients receiving antibiotics for other reasons

• the main danger is resistant organisms

• Clindamycin , Azithromycin or Clarithromycin are alternatives

Patients undergoing cardiac surgery or procedures

involving infected tissue :

• Clindamycin or Vancomycin +Aminoglycosides are effective

• Prognosis • Untreated, infective endocarditis is uniformly fatal. Aggressive medical

and surgical management, however, has dramatically improved the outcome. Mortality overall from both native and prosthetic valve endocarditis remains fairly high, ranging from 17 to 36%. Certain subgroups carry a lower risk of death (endocarditis related to viridans streptococci); endocarditis due to S. aureus, fungal endocarditis, and zoonotic endocarditis have higher mortalities. Heart failure and CNS events are the most frequent causes of death.

• Endocarditis recurs in 12 to 16% of patients and is more common in injection drug users, elderly people, and patients with prosthetic valves. The rate of relapse also varies according to the causative organism. Easily treated infections, such as those with α-hemolytic streptococci, have a low rate of relapse ( 5%), whereas infections with organisms that are ∼more difficult to eradicate may have significantly higher rates.

• Future Directions • As cardiac imaging technology continues to improve, the

duration of treatment of endocarditis may be dictated in part by the characteristics of visualized vegetations. In addition, now that large vegetations have been demonstrated to cause more embolic events, interventions to remove vegetations “prophylactically” (e.g., valve repair and vegectomy) or to introduce agents that prevent the formation or promote the dissolution of vegetations may be feasible. Finally, novel therapeutic approaches (for instance, antibacterial antibodies and cell wall–specific enzymes) that act as adjuncts to antibiotics in facilitating bacteriologic clearance are in development.

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