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 more
acute, 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.

Predisposing factors:
CARDIAC AND VASCULAR ABNORMALITIES:

• RHD
• Myxomatous mitral valve

• Degenerative calcific valvular
stenosis

HOST FACTORS:

• Neutropenia
• Immunodeficiency
• Malignancy
• Therapeutic
immunosuppression

• Bicuspid aortic valves

• Diabetes mellitus

• Prosthetic valves

• Alcohol
• IV drug abuse

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

Subacute

◦ High grade fever and chills

◦ Low grade fever

◦ SOB
◦ Arthralgias/ myalgias
◦ Abdominal pain
◦ Pleuritic chest pain
◦ Back pain

◦
◦
◦
◦
◦

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

Petechiae
1. Nonspecific
2. Often located on palpebral conjunctiva, buccal and palatal mucosa and the
extremities

Splinter Hemorrhages

1.
2.
3.
4.
5.

Non-specific
Non-blanching
Linear reddish-brown lesions found under the nail bed
Usually do NOT extend the entire length of the nail
Vessel damage from swelling of the blood vessels (vasculitis) or tiny clots that damage the small
capillaries (microemboli).

Osler’s Nodesimmune
1.
2.
3.
4.

More specific
Painful, erythematous and subcutaneous nodules
Located on pulp of fingers and toes
More common in subacute IE

Janeway Lesions

1.
2.
3.
4.
5.

More specific
Erythematous, blanching macules
Nonpainful
Located on palms and soles
Microabscess of the dermis with marked necrosis and inflammatory infiltrate not
involving the epidermis.

Roth Spots
Oval, 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

Neurologic
Emboli

Metastatic Abscesses

33-50%

25-35%
15-35%

<5%

Cardiac complications
Congestive 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 Infection
Metastatic abscess
◦ Kidneys, spleen, brain, soft tissues

Meningitis and/or encephalitis

Vertebral osteomyelitis
Septic arthritis

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 valves

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

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

Enterococci
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
o

 Staphycocci
oPenicillin 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 echocardiography
Recurrent embolic attacks.
Abscess formation.

.
Prophylaxis:
High risk category:

 Prosthetic cardiac valves
Previous 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 dysfunction
Congenital cardiac malformations
Hypertrophic cardiomyopathy
Mitral 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

• Diabetes mellitus

• S. aureus

• Low serum albumen

• Vegetation size

• Apache II score

• Aortic valve

• Heart failure

• Prosthetic valve

• Paravalvular abscess

• Older age

• Embolic events

Prevention – the procedure
• Dental procedures known to produce
bleeding
• Tonsillectomy
• Surgery involving GI, respiratory mucosa

• Esophageal dilation
• ERCP for obstruction

2/23/2014

• Gallbladder surgery
• Cystoscopy, urethral dilation
• Urethral catheter if infection present
• Urinary tract surgery, including prostate
• I&D of infected tissue

49

Infective endocarditis

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