Infective Endocarditis

Supervisor: Dr: Mohammed Al marwala

Presented by: Dr :Areej Aljabali

Items of Presentation

• General definitions• Pathology • Pathogenesis• Pathophysiology• Clinical features• Diagnosis • Treatment• Prevention

Definition :Infective endocarditis is characterized

by colonization or invasion of the heart valves or the mural endocardium by a microbe, leading to the formation of bulky friable vegetations

composed of thromb and organisms, often associated with destruction of the underlying cardiac tissues.

 

Acute ◦Toxic presentation◦Progressive valve destruction &

metastatic infection developing in days to weeks

◦Most commonly caused by S. aureusSub acute

◦Mild toxicity◦Presentation over weeks to months◦Rarely leads to metastatic infection◦Most commonly S. viridans or

enterococcus

55-75% of patients with native valve endocarditis (NVE) have underlying valve abnormalities

MVP Rheumatic Congenital I.v. drug abuse

◦7-25% of cases involve prosthetic valves

◦25-45% of cases predisposing condition can not be identified

Pathology :

◦NVE infection is largely confined to leaflets

◦PVE infection commonly extends beyond valve ring into annulus/peri annular tissue Ring abscesses Septal abscesses Fistulae Prosthetic dehiscence

◦Invasive infection more common in aortic position and if onset is early

Pathogenesis :

Endothelial damage

Platelet-fibrin thrombi

Microorganism

adherence

Nonbacterial Thrombotic EndocarditisEndothelial injuryHypercoagulable state

◦Lesions seen at coaptation points of valves Atrial surface mitral/tricuspid Ventricular surface aortic/pulmonic

Modes of endothelial injury High velocity jet Flow from high pressure to low

pressure chamber Flow across narrow orifice of high

velocity◦Bacteria deposited on edges of low

pressure or site of jet impaction

: PathophysiologyClinical manifestations

◦Direct Constitutional symptoms of infection

(cytokine)◦ Indirect Local destructive effects of infection Embolization – septic or bland Hematogenous seeding of infection may

present as local infection or persistent fever, metastatic abscesses may be small

Immune response Immune complex or complement-mediated

Local destructive effects Valvular distortion/destruction Chordal rupture Perforation/fistula formation Paravalvular abscess Conduction abnormalities Purulent pericarditis Functional valve obstruction

Embolization

Clinically evident 11 – 43% of patients

Pathologically present 45 – 65% High risk for embolization

Large > 10 mm vegetationHypermobile vegetationMitral vegetations (esp. anterior leaflet)

Pulmonary (septic) – 65 – 75% of i.v. drug abusers with tricuspid IE

: Clinical Features

• Fever, chills, weakness, lethargy, weight loss, flu-like illness (not always present)

• Longstanding IE (rarely seen now with earlier diagnosis): splinter haemorrhages, Janeway lesions, Osler nodes, Roth spots

• Murmurs are present in 80 - 85% of patients with left sided IE

Feature Frequency, %Fever 80–90Chills and sweats 40–75Anorexia, weight loss, malaise 25–50Myalgias, arthralgias 15–30Back pain 7–15Heart murmur 80–85New/worsened regurgitant murmur 10–40Arterial emboli 20–50Splenomegaly 15–50Clubbing 10–20Neurologic manifestations 20–40Peripheral manifestations (Osler's nodes, subungual hemorrhages, Janeway lesions, Roth's spots)

2–15

Petechiae 10–40Laboratory manifestations Anemia 70–90Leukocytosis 20–30Microscopic hematuria 30–50Elevated erythrocyte sedimentation rate >90Elevated C-reactive protein level >90Rheumatoid factor 50Circulating immune complexes 65–100Decreased serum complement 5–40

Splinter Haemorrhages

Janeway Lesions

Osler Nodes

Roth Spots

• In IVDU right sided IE usually affect the tricuspid valve & occasionally the pulmonary valve, instead of systemic issues pulmonary embolism is the most important complication which can evolve into:

• Pulmonary infarction• Pulmonary abscess• Bilateral pneumothoraces• Pleural effusion• Empyema

• The severity of valvular destruction depends on virulence of infecting organism & infection duration

• Heart failure can be the initial presentation

: Diagnosis

Modified Duke criteria It is based on clinical, microbiological & echo

findings providing high sensitivity & specificity (~80%) for diagnosis of IE when applied to patients with native valve IE with +ve BC

Modified Duke CriteriaMajor Criteria:

Positive blood cultures Typical microorganism for IE from 2 separate blood

culures Viridans sreptococci Sreptococcus bovis HACEK group Saph . Auresus Community acquired enerococci , in the absence

of primary focus

Persistently positive blood culture , defined as recovery of a microorganism consistent with IE from:

Blood culture drawn more than 12 h apart OR

All of 3or majority of 4 or more separate blood cultures , with first last drawn at least one h apart

Single positive blood culture for Coxiella burnetii or antiphase I IgG AB titer more than 1: 800

Evidence of endocardial involvementPositive echocardiogram for IE TEE recommended in patients with

PV ,rated at least possible IE by clinical crieria ,or complicated IE ( paravalvular abscess ) TTE as first test in other patients

Definition of positive ECHO - Oscillating intracardiac mass, on valve or

supporting structures , or in the path or regurgitant jets , or on implanted material , in he absence of an alternative anatomic explanation

- Intracardiac abscess - New partial dehiscence of prosthetic valveNew valvular regurgitation Increase in or change in preexisting murmur not

sufficent

Minor Criteria Predisposition such as a heart condition or IV

drug use Fever Vascular phenomena - major arterial emboli,

septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhage, & Janeway lesions

immunological phenomena – glomerulonephritis , Osler s nodes , Roth spots , rheumatoid factor

Other microbial evidence - serological tests, or a positive blood culture but does not meet a major criteria ( excluding single positive cultures for coagulase negative staph and organisms that do not cause endocarditis )

Definite IE 2 major criteria OR 1 major + 3 minor OR 5 minor criteria

Possible IE 1 major + 1 minor OR 3 minor

Rejected : Firm alternate diagnosis for

manifestation of endocarditis OR Resolution of manifestation of

endocarditis , with antibiotic therapy for 4 days or less OR

No pathologic evidence of IE at surgery or autopsy after antibiotic therapy for 4 days or less

Does not meet criteria for possible IE , as above

TREATMENT:

Goals of Therapy

Eradicate infectionDefinitively treat sequelae of

destructive intra-cardiac and extra-cardiac lesions

: Antibiotics

• Benzylpenicillin is the first choice for Streptococcus or Enterococcus penicillin-susceptible strains

• Empirical treatment; flucloxacillin & gentamicin are the usual first line

• Vancomycin is used in pts with intracardiac prosthetic material or suspected MRSA

• For vanc-resistant MRSA: teicoplanin, lipopeptide daptomycin or oxazilidones (linezolid) is recommended

• IV Abx is normally continued for 4-6 weeks, with the aim of sterilising the vegetations

Indications for Cardiac Surgical Intervention in Patients with EndocarditisSurgery required for optimal

outcome Moderate to severe congestive heart

failure due to valve dysfunctionPartially dehisced unstable prosthetic

valvePersistent bacteremia despite optimal

antimicrobial therapyLack of effective microbicidal therapy

(e.g., fungal or Brucella endocarditis)S. aureus prosthetic valve endocarditis

with an intracardiac complication Relapse of prosthetic valve

endocarditis after optimal antimicrobial therapy

Surgery to be strongly considered for improved outcomea

Perivalvular extension of infectionPoorly responsive S. aureus

endocarditis involving the aortic or mitral valve

Large (>10-mm diameter) hypermobile vegetations with increased risk of embolism

Persistent unexplained fever (10 days) in culture-negative native valve endocarditis

Poorly responsive or relapsed endocarditis due to highly antibiotic-resistant enterococci or gram-negative bacilli

Complications1. Congestive heart failure• Most common complication• Main indication to surgical treatment• ~60% of IE patients

2. Uncontrolled infection• Persisting infection • Perivalvular extension in infective endocarditis

3. Systemic embolism• Brain, spleen and lungs• 30% of IE patients• May be the first symptom

5. Neurologic events6. Acute renal failure7. Rheumatic problems8. Myocarditis

High-Risk Cardiac Lesions for Which Endocarditis Prophylaxis Is Advised before Dental ProceduresProsthetic heart valves Prior endocarditis Unrepaired cyanotic congenital heart

disease, including palliative shunts Completely repaired congenital heart

defects during the 6 months after repair Incompletely repaired congenital heart

disease with residual defects adjacent to prosthetic material

Valvulopathy developing after cardiac transplantation

Antibiotic Regimens for Prophylaxis of Endocarditis in Adults with High-Risk Cardiac Lesionsa,b

A. Standard oral regimen1. Amoxicillin 2.0 g PO 1 h before

procedure

B. Inability to take oral medication

1. Ampicillin 2.0 g IV or IM within 1 h before procedure

C. Penicillin allergy1. Clarithromycin or azithromycin 500

mg PO 1 h before procedure2. Cephalexinc 2.0 g PO 1 h before

procedure3. Clindamycin 600 mg PO 1 h before

procedureD. Penicillin allergy, inability to

take oral medication1. Cefazolinc or ceftriaxonec 1.0 g IV or

IM 30 min before procedure2. Clindamycin 600 mg IV or IM 1 h

before procedure

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