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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
04/12/2023 49
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