INFECTIVE ENDOCARDITIS

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Presentation transcript:

INFECTIVE ENDOCARDITIS

INFECTIVE ENDOCARDITIS: DEFINITION Microbial infection of the endothelial surface of the heart Characteristic lesion: VEGETATION

IE: DEFINITION: VEGETATIONS Mass of platelets and fibrin, rich in bacteria, scanty inflammatory cells Sites: heart valves, septal defect, chordae tendineae or mural endocardium

INFECTIVE ENDOCARDITIS: DEFINITION Infection of arteriovenous shunts or PDA or coarctation of the aorta is called infective endarteritis, but clinically resembles IE

INFECTIVE ENDOCARDITIS: DEFINITION Causative organism: bacteria, fungi, and rickettsiae Most frequent organisms: streptococci, staphylococci, enterococci, and fastidious gram-negative coccobacilli

INFECTIVE ENDOCARDITIS: PATHOGENESIS vegetations Bacterial proliferation Colonization with bacteria during bacteremia Deposition of platelets & fibrin Endocardial damage High pressure jet

Vegatations on the mitral valve

Vegetations on top of mitral stenosis

Vegetations on a biologic valve

IE: UNDERLYING HEART DISEASE High pressure gradient or narrowed tracts: Mitral regurgitation Aortic regurgitation VSD Aortic stenosis Mitral stenosis Tetralogy of Fallot Coarctation of the aorta, PDA

IE: UNDERLYING HEART DISEASE Cardiac lesions with low or no pressure gradients are unlikely to be complicated by IE e.g. ASD

IE: MICRO-ORGANISMS S. viridans Enterococcus fecalis Staphylococcus aureus Coagulase negative Staphylococci Gram-negative bacilli Brucella Rickettsia Fungi

CLINICAL MANIFESTATIONS The local destructive effects of intracardiac infection Embolization of bland or septic fragments of vegetations to distant sites: infarction or infection Hemato seeding of remote sites during continuous bacteremia Antibody response to MO: immune complex deposition or Ab-complement interaction

IE: CLINICAL MANIFESTATIONS Fever Heart murmur Splenomegaly Peripheral manifestations

IE: PERIPHERAL MANIFESTATIONS Splinter hemorrhage Osler’s nodes: subcutaneous nodules, tender

Osler’s nodes

Dermal infarcts

IE: EYE MANIFESTATIONS Janeway’s lesions: macular non-tender lesions Roth’s spots: on fundoscopy

IE: EYE MANIFESTATIONS Subconjunctival hemorrhage

IE: PERIPHERAL MANIFESTATIONS: THE EYE Petechiae: conjunctiva, buccal mucosa, limbs

CLINICAL MANIFESTATIONS The local destructive effects of intracardiac infection Embolization of bland or septic fragments of vegetations to distant sites: infarction or infection Hemato seeding of remote sites during continuous bacteremia Antibody response to MO: immune complex deposition or Ab-complement interaction

LOCAL DESTRUCTIVE EFFECTS Destruction of valve leaflets, ruptured chordae Abscess formation Perforations or fistulas Disruption of conductive system Large vegetations lead to valve obstruction

IE: SYSTEMIC EMBOLI CNS embolization: focal neurologic deficits Spleen: pain, splenomegaly Limbs: ischemia and gangrene Mesenteric: abdominal pain, hematochezia

IE: NEUROLOGICAL MANIFESTATIONS Headache Confusion Convulsions Long tract signs & focal neurological deficit Meningeal irritation

IE: RENAL MANIFESTATIONS Renal failure: immune-complex deposition Congestive heart failure drug-induced Glomerulonephritis Focal renal infarcts: hematuria

IE: CLINICAL SETUP depending on the clinical presentation: Acute IE: Subacute IE (SBE) Postoperative IE: following cardiac surgery

ACUTE IE Caused by virulent organisms on top of normal heart: Usually staphylococcus aureus E.g. cannula infection, staphylococcal septicemia, drug abusers

ACUTE IE 5:Vegetations on top of normal endocardial tissue 1:Bacteremia or septicemia 2:Direct damage of endocardium 3:Colonization: virulent organisms 4:Deposition of platelets & fibrin 5:Vegetations on top of normal endocardial tissue

ACUTE IE: CLINICAL MANIFESTATIONS Severe febrile illness Petechiae Embolic events common Rapid progression of cardiac and renal failure

SUBACUTE IE Caused by infection with low-virulence organisms on top of pre-existing cardiac disease Persistent fever, tiredness, weight loss, night sweats

PROSTHETIC VALVE ENDOCARDITIS IE following cardiac surgery Early postoperative IE: infection is acquired at the time of surgery High mortality: repeat surgery often required Late postoperative IE: Community-acquired infection Complication rates lower than early form

IE: INVESTIGATIONS Blood cultures Echocardiography: transthoracic (TTE) and transesophageal (TEE) Vegetations Serial follow up Valve damage Abscess fromation

Vegatations on the aortic valve

VEGETATIONS

IE: INVESTIGATIONS High ESR Anemia of chronic disease Neutrophil leucocytosis CRP Hematuria Proteinuria Low serum complement Rheumatoid factor

IE: INVESTIGATIONS ECG: Heart block Bundle branch block arrhythmia

IE: TREATMENT Combination antibiotic therapy according to culture & sensitivity Empirical regimes pending the results of blood culture

IE: TREATMENT Large doses Given intravenously Protracted duration of therapy: usually 4 weeks 6 weeks in PVE

Combination AB therapy Benzyl penicillin or ampicillin i.v Plus gentamycin For penicillin resistant or allergic: vancomycin infusion plus gentamycin Oral rifampicin when staphylococcal infection suspected or confirmed

CARIAC SURGERY: INDICATIONS Failure to respond to medical treatment Heart failure due to valve insufficiency Large vegetations Abscess formation

PREVENTION OF IE Susceptible patients: those with valvular or congenital heart disease Good dental hygiene

PREVENTION OF IE Avoidance of bacteremia Antibiotic prophylaxis: Dental manipulation Genito-urinary tract catheterization or surgery

PROPHYLAXIS For dental procedures: Oral amoxicillin given 30 min before and 6 hours after the procedure