Infective Endocarditis

Definition:Infection of the endocardial surface of heart characterized by

- Colonization or invasion of the heart valves (native or prosthetic) or the mural endocardium by a microbe,

- leading to formation of bulky, friable vegetation composed of thrombotic debris and organisms

- often associated with destruction of underlying cardiac tissue.

Sites involved:•Heart valves

•Mural endocardium

• Intracardiac devices

•Ventricular septum defects

CLASSIFICATION :Infective endocarditis may have an indolent, subacute course or a moreacute, fulminant course with greater potential for rapid decompensation.

Acute bacterial endocarditis (ABE):

• usually develops abruptly and progresses rapidly (ie, over days).• A source of infection or portal of entry is often evident. • When bacteria are virulent or bacterial exposure is massive, ABE can affect

normal valves. •It is usually caused by S. aureus, group B hemolytic streptococci,

pneumococci, or gonococci.

Subacute bacterial endocarditis (SBE):

• usually develops insidiously • progresses slowly (i.e, over weeks to months). •Often, no source of infection or portal of entry is evident.• SBE often develops on abnormal valves after asymptomatic bacteremia

due to periodontal, GI, or GU infections.• SBE is caused most commonly by streptococci (especially viridans,

microaerophilic, anaerobic, and nonenterococcal group D streptococci and enterococci) and less commonly by S. aureus, Staphylococcus epidermidis, and fastidious Haemophilus sp.

Post oprative endocarditis or PVE• develops in 2 to 3% of patients within 1 yr after valve replacement and in 0.5%/yr

thereafter. • It is more common after aortic than after mitral valve replacement and affects

mechanical and bioprosthetic valves equally. I. Early-onset infections

(< 2 mo after surgery) are caused mainly by contamination during surgery with antimicrobial-resistant bacteria (eg, S. epidermidis, diphtheroids, coliform bacilli, Candida sp, Aspergillus sp).

II. Late-onset infections caused mainly by contamination with low-virulence organisms during surgery or by transient asymptomatic bacteremias, most often with streptococci; S. epidermidis; diphtheroids; and the fastidious gram-negative bacilli, Haemophilus sp, Actinobacillus actinomycetemcomitans, and Cardiobacterium hominis.

CARDIAC AND VASCULAR ABNORMALITIES:

• RHD

• Myxomatous mitral valve

• Degenerative calcific valvular stenosis

• Bicuspid aortic valves

• Prosthetic valves

HOST FACTORS:

• Neutropenia

• Immunodeficiency

• Malignancy

• Therapeutic immunosuppression

• Diabetes mellitus

• Alcohol

• IV drug abuse

Predisposing factors:

Microbiology:•Staphylococcus aureus (35%) : Either healthy or deformed valves, IV drug

abusers (polymicrobial), devices

•Streptococcus viridans (32%) : Native but previously damaged/abnormal valves

•Enterococci (8 %)

•Coagulase negative staphylococcus - S. epidermidis (4%): Prosthetic valve endocarditis, devices

•G –ve bacilli of HACEK group (4%)

•Yeast and Fungi(1%)

•Culture negative endocarditis (5 %)

Pathogenesis:Portal of entry:◦ Dental / Surgical Procedures◦ Contamination by IV drug use◦ Obvious infections (RS/Skin)◦ Occult source from gut, oral cavity◦ Trivial injuries.◦ Intravascular catheter infection◦ Nosocomial wounds◦ Chronic invasive procedures

Endothelial Injury

Uninfected Platelet-Fibrin thrombus (NBTE)

Transient bacteremia and attachment at NBTE

Proliferation and pro-coagulant state

Infected, friable, bulky vegetation

Morphology:•Friable, bulky vegetation containing fibrin, inflammatory cells, and microbes

•Aortic and mitral valves involved most commonly.

•Right side valve involvement in iv drug users.

Symptoms:

Acute

◦ High grade fever and chills◦ SOB◦ Arthralgias/ myalgias◦ Abdominal pain◦ Pleuritic chest pain◦ Back pain

Subacute

◦ Low grade fever◦ Anorexia◦ Weight loss◦ Fatigue◦ Arthralgias/ myalgias◦ Abdominal pain

Signs:• Fever

• Heart murmur

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

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

Petechiae1. Nonspecific2. Often located on palpebral conjunctiva, buccal and palatal mucosa and the

extremities

Splinter Hemorrhages

1. Non-specific2. Non-blanching3. Linear reddish-brown lesions found under the nail bed4. Usually do NOT extend the entire length of the nail 5. Vessel damage from swelling of the blood vessels (vasculitis) or tiny clots that damage the small

capillaries (microemboli).

Osler’s Nodes- immune1. More specific2. Painful, erythematous and subcutaneous 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 soles5. Microabscess of the dermis with marked necrosis and inflammatory infiltrate not

involving the epidermis.

Roth SpotsOval, retinal

hemorrhages with pale centers.

Modified Dukes Criteria for diagnosis of Infective Endocarditis

Major Criteria:Positive blood culture ◦Typical organism from two cultures ◦Persistent positive blood cultures taken > 12 hours apart ◦Three or more positive cultures taken over more than 1 hour.

Endocardial involvement ◦Positive echocardiographic findings of vegetations ◦New valvular regurgitation

Minor Criteria:•Predisposition: Predisposing valvular or cardiac abnormality • Intravenous drug misuse •Pyrexia ≥38°C (≥100.4°F)•Embolic phenomenon •Vasculitic/ immunologic phenomenon •Blood cultures suggestive: -organism grown but not achieving

major criteria •Suggestive echocardiographic findings

Definitive Endocarditis if,- Two major or,- One major and three minor or,- five minor

Possible Endocarditis if,- One major and one minor or, - Three minor

Complications of Endocarditis:Cardiac 33-50%

Neurologic 25-35%

Emboli 15-35%

Metastatic Abscesses <5%

Cardiac complicationsCongestive heart failure

Valvular damage leads to valvular regurgitation

Valvular stenosis

Coronary embolism

Prosthetic dehiscence

Abscess extending to myocardium causing conduction disturbances extending to pericardium causing purulent pericarditis.

Neurologic Complications

•Acute encephalopathy

•Meningitis

•Embolic stroke

•Cerebral hemorrhage

•Brain abscess

Embolic Phenomena

•Stroke

•Ischemic extremities

•Pulmonary emboli

•Paralysis due to embolic infarction of either the brain or spinal cord

•Hypoxia from pulmonary emboli

•Abdominal pain (splenic or renal infarction

Metastatic Spread of InfectionMetastatic abscess ◦ Kidneys, spleen, brain, soft tissues

Meningitis and/or encephalitis

Vertebral osteomyelitis

Septic arthritis

INVESTIGATIONS

.

Microbiology: Blood cultures:Key diagnostic investigation in infective endocarditis. Isolation of microorganism from culture is important for diagnosis and also

for treatment.At least 3 sets of samples should be taken from different venepuncture sites

over 24 hours.

Serology: Can be sent when the diagnosis is suspected and the cultures are negative.They aid in cases where the organisms will not grow in blood

cultures(Coxiella,Legionella,Bartonella

Imaging:Chest x-ray

◦ Look for multiple focal infiltrates and calcification of heart valvesEKG

◦ Rarely diagnostic◦ Look for evidence of ischemia, conduction delay, and arrhythmias

Echocardiography

Septic Pulmonary Emboli:

.

Echocardiography It can identify the presence and size of vegetations,detect intracardiac

complications and assess cardiac function.Transthoracic echocardiography is noninvasive and has high specificity for

visualising vegetations.Transoesophageal echocardiography is more sensitive than TTE.It can detect

small vegetations,prosthetic endocarditis and intra cardiac complications.

Complete blood counts may show anemia and increased WBC counts.

Urea and Creatinine: may be elevated due to glomerulonephritis

Liver biochemistry: Serum alkaline phosphatase may be increased

Inflammatory markers CRP,ESR are increased in infection .CRP also helps in monotoring response

to therapy.

Urine proteinuria and hematuria occur frequently.

TREATMENT:Antimicrobial Therapy

•Therapy requires identification of specific pathogen and its susceptibility to antimicrobials.

•Empirical therapy should be started as soon as possible targeting most likely pathogens.

•Bactericidal drugs should be used.

• Resolution of fever occurs in 5 to 7 days.if fever persists patient should be evaluated for complications like paravalvular abscess and extracardiac abscess.

• Serologic abnormalities resolve slowly and do not reflect response to treatment.

Antibotic regimen for infective endocarditis: Viridians Streptococci and Strep.bovis Benzyl penicillin (1.2g 4 hourly) 4-6 weeks

Gentamicin (1mg/kg 8-12 hourly) 2 weeks

Alternative

Cefriaxone (2g once daily, iv)

Vancomycin (15mg/kg 12 hourly)

duration 4 weeks

Enterococcio Ampicillin sensitive Ampicillin (2 g 4 hourly) 4-6 weeks, and Gentamicin (1mg/kg 8-12 hourly) o Ampicillin resistant Vancomycin(1g 12hourly) 4-6 weeks, and Gentamicin (1mg/kg 8-12 hourly) Alternative Cefriaxone (2g once daily, iv) Vancomycin (15mg/kg 12 hourly) duration 4 weeks

StaphycoccioPenicillin sensitive

Benzyl penicillin I.V(1.2 g 4 hourly)oPenicillin resistant but methicillin sensitive

Flucloxacillin I.V (2g 4 hourly )oBoth penicillin and methicillin resistant

Vancomycin I.V (1g 12 hourly) and

Gentamicin (1mg/kg 8 hourly)

duration 4-6 weeks

.

Surgery:Indications:Failure of antibiotic therapy patients with direct extension of infection to myocardial structuires.Prosthetic valve dysfunction.Congestive heart failure.Badly damaged valves.IE caused by fungi or gram-ve or resistant organisms.Large vegetations on echocardiographyRecurrent embolic attacks.Abscess formation.

.

Prophylaxis: High risk category: Prosthetic cardiac valvesPrevious bacterial endocarditis,even in absense of heart disease.Complex cyanotic congenital heart disease (TOF) Surgically constructed systemic pulmonary shunts.

Moderate risk category:

Rheumatic and other valvular dysfunctionCongenital cardiac malformationsHypertrophic cardiomyopathyMitral valve prolapse with valvular regurgitation

Regimen for IE prophylaxis: Standard oral regime

Amoxicillin 2 g 1hr before procedure

Inability to take oral medication Ampicillin 2g IV or IM 1hr before procedure

Penicillin allergy

Clindamycin 600 mg

Clarithromycin 500 mg

Cephalexin 2 g.

Poor Prognostic Factors:• Female

• S. aureus

• Vegetation size

• Aortic valve

• Prosthetic valve

• Older age

• Diabetes mellitus

• Low serum albumen

• Apache II score

• Heart failure

• Paravalvular abscess

• Embolic events

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Prevention – the procedure• Dental procedures known to produce

bleeding

• Tonsillectomy

• Surgery involving GI, respiratory mucosa

• Esophageal dilation

• ERCP for obstruction

• Gallbladder surgery

• Cystoscopy, urethral dilation

• Urethral catheter if infection present

• Urinary tract surgery, including prostate

• I&D of infected tissue