DefinitionInfection of the endocardial surface of heart characterized by - Colonization or invasion of the heart valves (native orprosthetic) or the mural endocardium by a microbe, - leading to formation of bulky, friable vegetation composedof thrombotic debris and organisms - often associated with destruction of underlying cardiactissue.
Classification ACUTE ENDOCARDITIS SUBACUTE ENDOCARDITIS• Destructive and tumultuous • Organisms of low virulence infection, frequently of a causing infection in a previously normal heart previously abnormal valve, with a highly virulent heart, particularly on organism deformed valves.• Hematogenoulsy seeds • Disease appear insidiously and pursue a protracted course of• If untreated, leads to death weeks to month within weeks • Recover after appropriate antibiotic treatment
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 %)• CoNS - S. epidermidis (4%): Prosthetic valve endocarditis, devices• G –ve bacilli of HACEK group (4%)• Yeast and Fungi(1%)• Culture negative endocarditis (5 %)
PathogenesisPortal 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.
Clinical features Symptoms Constitutional symptoms - Damage to intracardiac --- Cytokine release ?structures - Embolization of vegetationfragments - Hematogenous infection - Immune complex
Sub-acute Endocarditis• Persistent fever• Constitutional symptoms• New signs of valve dysfunction• Heart failure• Embolic Stroke• Peripheral arterial embolism• Other features
Modified Dukes Criteria for diagnosisof Infective Endocarditis 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
Major CriteriaPositive 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
.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)ECG To detect complications like MI,conductionabnormalities.CHEST X RAY
.EchocardiographyIt 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 anamia and increased WBC counts.Urea and Creatinine: may be elevated due to glomerulonephritisLiver biochemistry: Serum alkaline phosphatase may be increasedInflammatory markers CRP,ESR are increased in infection .CRP also helps in monotoring response to therapy.Urine proteinuria and hematuria occur frequently.
TREATMENTAntimicrobial 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 feverpersists patient should be evaluated for complicationslike paravalvular abscess and extracardiac abscess. Serologic abnormalities resolve slowly and do notreflect response to treatment.
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
.Surgery Indications 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.
Prophylaxis High risk category prosthetic cardiac valvesPrevious bacterial endocarditis,even in absense of heart disease.Complex cyanotic congenital heart disease(TGA,TOF) Surgically constructed systemic pulmonary shunts.
Moderate risk categoryRheumatic 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 procedurePenicillin allergy Clindamycin 600 mg Clarithromycin 500 mg Cephalexin 2 g.