Endocarditis by siva

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Endocarditis :

Endocarditis Prepared & Presented by Dr. Siva Reddy Challa , Professor & HOD, Dept. of Pharmacology KVSR Siddhartha College of Pharmaceutical Sciences, Siddhartha Nagar, Vijayawada-520010 Andhra Pradesh, INDIA Email: sivareddypharma@gmail.com

PowerPoint Presentation:

INFECTIVE ENDOCARDITIS 100% fatal if undiagnosed and untreated 20% fatal even if diagnosed and treated appropriately. 70% streptococcal 20% staphylococcal

Roths spots in eye:

Roths spots in eye

Oslers nodes :

Oslers nodes

Petechial rash:

Petechial rash

Splinter hemorrhages :

Splinter hemorrhages

Risk factors :

Intravenous drug abuse Artificial heart valves and pacemakers Acquired heart defects Calcific aortic stenosis Mitral valve prolapse with regurgitation Congenital heart defects Intravascular catheters Risk factors

Predisposing factors:

Predisposing factors Any type of structural heart disease Rheumatic heart disease (37-76%) like MS,AS,AI,MI,etc Congenital heart disease (6-24%) Like ASD,VSD,PDA,etc Degenerative cardiac lesions (30-40%) Other (including prosthetic valves)

Predisposing factors Already damaged valves by RHD:

Predisposing factors Already damaged valves by RHD

Predisposing factors Already damaged damaged heart by CHD:

Predisposing factors Already damaged damaged heart by CHD Congenital heart disease (6-24%)

Predisposing factors Prosthetic valves & pacemakers:

Predisposing factors Prosthetic valves & pacemakers High risk prosthetic cardiac valve prior episodes of endocarditis surgically constructed systemic-pulmonary shunts or conduits Pacemakers & pacemaker leads

Predisposing factors Prosthetic valves & pacemakers:

Predisposing factors Prosthetic valves & pacemakers

PREDISPOSING FACTORS IV drug abusers:

PREDISPOSING FACTORS IV drug abusers

PREDISPOSING FACTORS Alcohol abuse & sepsis:

PREDISPOSING FACTORS Alcohol abuse & sepsis

PREDISPOSING FACTORS:

PREDISPOSING FACTORS Neutropenia & Immunosupression

PREDISPOSING FACTORS:

PREDISPOSING FACTORS Staph aureus accounts for the majority of cases of endocarditis in case of IV drug abusers and is recurrent polymicrobial tricuspid valve, either alone or in combination, is most often infected

PREDISPOSING FACTORS:

PREDISPOSING FACTORS Moderate risk patent ductus arteriosus VSD, primum ASD coarctation of the aorta bicuspid aortic valve hypertrophic cardiomyopathy acquired valvular dysfunction MVP with mitral regurgitation

PREDISPOSING FACTORS INVASIVE PROCEDURES:

PREDISPOSING FACTORS INVASIVE PROCEDURES G.I. Barium enema Colonoscopy Genitourinary Prostatectomy

PREDISPOSING FACTORS INVASIVE PROCEDURES:

PREDISPOSING FACTORS INVASIVE PROCEDURES Tooth extraction Periodontal surgery Teeth cleaning Tooth brushing, flossing Using wooden toothpicks Chewing food

PREDISPOSING FACTORS INVASIVE PROCEDURES:

PREDISPOSING FACTORS INVASIVE PROCEDURES Biopsies, suture removal, placing orthodontic bands Tonsillectomy,Adenoidectomy,Bronchoscopy. Resp tract procedure to drain abscess or empyema

PREDISPOSING FACTORS INVASIVE PROCEDURES:

PREDISPOSING FACTORS INVASIVE PROCEDURES Central venous catheterization Bladder catheterization, Endoscopies, shaving, Skin or musculoskeletal infections

PREDISPOSING FACTORS:

PREDISPOSING FACTORS AIDS patients Cancer patients Leukemia Lymphomas

MICROBIAL AGENTS RESPONSIBLE FOR IE:

MICROBIAL AGENTS RESPONSIBLE FOR IE The commonest cause is streptococci (alpha hemolytic) and constitutes about 70%.among which Streptococci viridans is 35% that reside in oral cavity along with HACK associated with dental procedures. Then is streptococcus bovis that resides in oral & colon.colonic cancers 15% Then is enterococci 10% And other streptococci 10%

ORIGINAL CLASSIFICATION (Prior to Antibiotic era):

ORIGINAL CLASSIFICATION (Prior to Antibiotic era)

Current Criteria for Classification:

Current Criteria for Classification Underlying Anatomy: › Native Valve Endocarditis › Prosthetic Valve Endocarditis Infecting Organism › Serves as basis for therapy and prognosis

Native Valve Endocarditis Underlying Predisposing Conditions:

Native Valve Endocarditis Underlying Predisposing Conditions ›› 60 - 80% of non IV Drug abusers have a predisposing condition › Mitral Valve Prolapse 30 - 50% › Rheumatic Heart Disease 20 - 40% › Degenerative Aortic and 20 - 30% Mitral valve disease › Congenital Heart Disease 10 - 20%

Native Valve Endocarditis Microbiology:

Native Valve Endocarditis Microbiology ›› Streptococci 50 - 70% Viridans Streptococci (50% of all Strep) ›› Staphylococci ~ 25% Mostly Coagulase +ve Staph. Aureus Staph. Epidermidis ›› Enterococci ~ 10%

Native Valve Endocarditis Microbiology:

Native Valve Endocarditis Microbiology Viridans Streptococci Infect primarily abnormal valves Indolent clinical course Highly sensitive to Penicillins Staph. aureus Infect normal and abnormal valves Fulminant course with rapid destruction of valves and multiple metastatic abscesses Mostly resistant to Penicillins and sensitive to penicillinase resistant ß-lactams Common with soft tissue infections, and infected IV catheters

Native Valve Endocarditis Microbiology:

Native Valve Endocarditis Microbiology Staph. Epidermidis Indolent Course Affects abnormal valves Enterococci Normally affects damaged valves Recent history of genitourinary or gastrointestinal manipulation, disease or trauma Usually sensitive to Penicllin+Gentamicin Resistant strains prevalent

Prosthetic valve endocarditis:

Prosthetic valve endocarditis 5 - 15% of all Infective Endocarditis Overall incidence 1 - 4% Risk of PVE peaks at 15 days postop. , then rapidly declines by 150 days

Prosthetic Valve Endocarditis Classification:

Prosthetic Valve Endocarditis Classification Early ( < 60 days ) Reflects perioperative contamination Incidence around 1% Microbiology Staph (45 - 50%) Staph. Epiderm (~ 30%) Staph. Aureus (~ 20%) Gram -ve aerobes (~20%) Fungi (~ 10%) Strep and Entero (5-10%) Late ( > 60 days) After endothelialization Incidence 0.2 -0.5 % / pt. year Transient bacteraemia from dental, GI or GU Microbiology resembles native valve endocarditis

IE in IV Drug Abusers:

IE in IV Drug Abusers Right sided predilection Tricuspid Valve ~ 55% Aortic Valve ~ 25% Mitral Valve ~ 20% Pulmonary Valve 1 - 1.5% Mixed Rt. And Lt. Side 5 - 6%

Causative organisms:

Causative organisms

PowerPoint Presentation:

Causative organisms

Pathophysiology:

Pathophysiology

PATHOGENESIS OF INFECTIVE ENDOCARDITIS:

PATHOGENESIS OF INFECTIVE ENDOCARDITIS Previously damaged endocardial surface of valve for example by rheumatic heart disease forms rough surface over the damaged valve. Due to this rough surface palatelets stick and adhere to this area forming small small thrombi over the cusp of valves.fibrin also deposits on this area, the lesions now called as Nonbacterial Thrombotic Endocarditis (NBTE).

PATHOGENESIS OF INFECTIVE ENDOCARDITIS:

PATHOGENESIS OF INFECTIVE ENDOCARDITIS This deposition of sterile vegetations in the form of thrombi on the leaflets of cardiac valves, is also called MARANTIC ENDOCARDITIS

NONBACTERIAL THROMBOTIC ENDOCARDITIS (NBTE):

NONBACTERIAL THROMBOTIC ENDOCARDITIS (NBTE) These vegetations are sterile, nondestructive, noninflammatory & small (1-5mm),made of platelets,fibrin & other blood elements and may occur singly or multiply along the lines of closure of heart valves

NONBACTERIAL THROMBOTIC ENDOCARDITIS (NBTE):

NONBACTERIAL THROMBOTIC ENDOCARDITIS (NBTE) Probably occurs as a consequence of a hypercoagulable state Seem with concomitant venous thrombosis &/or pulmonary embolism May be seen with hyperestrogenic state, extensive burns, or endocardial trauma from indwelling catheters

NONBACTERIAL THROMBOTIC ENDOCARDITIS (NBTE):

NONBACTERIAL THROMBOTIC ENDOCARDITIS (NBTE) Importance Local effect on valve unimportant May produce emboli with resultant infarcts May eventually heal with fibrosis.

PATHOGENESIS OF INFECTIVE ENDOCARDITIS:

PATHOGENESIS OF INFECTIVE ENDOCARDITIS Bacteria reach this thrombotic vegetation site and produce colonization and deposit deep within this thrombi and remain hidden and protected and then multiply easily there. The surface may further covered by platelets and fibrin.

Infectious Endocarditis:

Infectious Endocarditis

PowerPoint Presentation:

Infective endocarditis with perforation of mitral valve leaflet Vegetation Mitral Valve Stick in Perforation

PATHOGENESIS OF INFECTIVE ENDOCARDITIS:

PATHOGENESIS OF INFECTIVE ENDOCARDITIS The reason why bacteria lodge there is because of Venturi effect as the blood carrying bacteria flows with high jet and force from high pressure to low pressure chamber below. Since the valve is deformed and stenosed so bubbles of blood are sprinkled that fall over the atrial surface of valve along free margins and deposit within thrombi.

Venturi Effect:

Venturi Effect

PATHOGENESIS OF INFECTIVE ENDOCARDITIS:

PATHOGENESIS OF INFECTIVE ENDOCARDITIS In systemic lupus erythematosus the vegetations may form on the undersurface of valve towards ventricular side called as libman sacks syndrome.

PATHOGENESIS OF INFECTIVE ENDOCARDITIS:

PATHOGENESIS OF INFECTIVE ENDOCARDITIS Adherence of some streptococci to blood clot is facilitated by dextran (a cell wall component) (especially of Streptococcus mutans, a viridans group. Further Some strains of bacteria are stimulators of platelet aggregation

PATHOGENESIS OF INFECTIVE ENDOCARDITIS:

PATHOGENESIS OF INFECTIVE ENDOCARDITIS Once these thrombotic vegetations are laden with microbial organisms they become large even upto 3cms,friable and easily detachable in contrast to vegetations of RHD that are not easily detachable. The colour of vegetations is tan grey red or brown and situated along the line of closure of valve.

PATHOGENESIS OF INFECTIVE ENDOCARDITIS:

PATHOGENESIS OF INFECTIVE ENDOCARDITIS Microscopic Pathology Fibrin, platelets, masses of organisms, +/- necrosis, +/- neutrophils Later: +/-lymphocytes, +/- macrophages, +/- fibroblasts, +/- fibrosis

LOCAL EFFECTS OF INFECTIVE ENDOCARDITIS:

LOCAL EFFECTS OF INFECTIVE ENDOCARDITIS First the leukocytes are unable to penetrate the vegetations as additional layers of fibrin are added. Treatment with antibiotics can also be problematic because the bacteria within the vegetation often become less metabolically active, and many antibiotics require active bacterial growth to be effective.

LOCAL EFFECTS OF INFECTIVE ENDOCARDITIS:

LOCAL EFFECTS OF INFECTIVE ENDOCARDITIS Infection may extends beyond valve cusp may erode & perforate valve, & may erode into underlying myocardium to produce an abscess (ring abscess) or Paravalvular abscess Septal abscesses & adjacent abscess Fistulae Prosthetic dehiscence

LOCAL EFFECTS OF INFECTIVE ENDOCARDITIS:

LOCAL EFFECTS OF INFECTIVE ENDOCARDITIS Valvular distortion/destruction chordal rupture. Conduction abnormalities Purulent pericarditis Functional valve obstruction With treatment, healing occurs by fibrosis and occasionally calcification.

DISTANT EFFECTS OF INFECTIVE ENDOCARDITIS:

DISTANT EFFECTS OF INFECTIVE ENDOCARDITIS Vegetations may become detached and produce embolic effects. Embolic phenomena are common (15-35%). septic infarcts involving: renal, splenic, coronary, or cerebral circulation. Risk for emboli is increased when vegetation >1cm.

IMMUNOLOGICAL EFFECTS OF IE:

IMMUNOLOGICAL EFFECTS OF IE IE cause both humural and cellular response Rheumatoid factor: titers correlate with the level of hypergammaglobulinemia and decrease with therapy Antinuclear antibodies: may contribute to the musculoskeletal manifestations, low-grade fever, or pleuritic pain Circulating immune complexes: Connected with long duration of illness, extravascular manifestations, hypocomplemenemia May cause diffuse glomerulonephritis, and some of the peripheral manifestations such as Osler nodes

EFFECTS OF IE ON KIDENY:

EFFECTS OF IE ON KIDENY Pathological processes: abscess, infarction, glomerulonephritis (focal, segmental), membranoproliferative GN May be normal is size or slightly swollen 10 to 15% of IE exhibit immune complex GN (as in SLE). Supporting IC rather than emboli: 1. Bacteria rarely seen in lesion 2. GN can occur with right-sided IE 3. GN is rare in acute IE even though large vegetation result in metastatic abscess formation 4. IF staining reveals IC-typical distribution 5. Antibacterial antibodies eluted from lesions

OTHER EFFECTS OF IE:

OTHER EFFECTS OF IE Mycotic aneurysm is a localized, irreversible arterial dilatation due to destruction of the vessel wall by infection More common with S.viridans

OTHER EFFECTS OF IE:

OTHER EFFECTS OF IE May arise by the following mechanisms: direct bacterial invasion of the arterial wall with subsequent abscess formation or rupture septic or bland emoblic occlusion of the vasa vasorum immune complex deposition with resultant injury to arterial wall

OTHER EFFECTS OF IE:

OTHER EFFECTS OF IE Tend to occur at bifurcation areas; middle cerebral artery is most common,Clinically silent until rupture

EFFECTS ON CNS,SPLEEN,LUNG:

EFFECTS ON CNS,SPLEEN,LUNG CNS cerebral emboli (>30% of IE) Mycotic aneurysms Spleen infarctions (44% of autopsy cases) enlargement associated with hyperplasia of lymphoid follicles, increase in secondary follicles, focal necrosis,abscess Lung associated with right-sided IE pulmonary embolism, acute pneumonia, pleural effusion, or empyema

EFFECTS ON CNS,SPLEEN,LUNG:

EFFECTS ON CNS,SPLEEN,LUNG CNS cerebral emboli (>30% of IE) Mycotic aneurysms

EFFECTS ON CNS,SPLEEN,LUNG:

EFFECTS ON CNS,SPLEEN,LUNG Spleen infarctions (44% of autopsy cases) enlargement associated with hyperplasia of lymphoid follicles, increase in secondary follicles, focal necrosis,abscess

EFFECTS ON CNS,SPLEEN,LUNG:

EFFECTS ON CNS,SPLEEN,LUNG Lung associated with right-sided IE pulmonary embolism, acute pneumonia, pleural effusion, or empyema

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Infective endocarditis also can give rise to conjunctival haemorrhages

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Clubbing is also known to occur in infective endocarditis.

Petechiae: Peripheral sign:

Petechiae: Peripheral sign

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Osler nodes, painful nodes on finger or toe pads Due to immune complexes in dermal vessels

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Osler’s Nodes: red, raised lesions Tender, subcutaneous nodules.4 P’s: Pink Painful Pea-sized Pulp of the fingers/toes. Immunological origin?

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Janeway lesions (due to septic emboli), painless plaques on palms or soles. non-tender, small erythematous or hemorrhagic macular or nodular lesions on the palms or soles only a few millimeters.

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Pathologically, the Janeway lesion is described to be a microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis, which is due to the deposition of circulating immune complexes in small blood vessels.

Janeway Lesions:

Janeway Lesions

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Splinter hemorrhage (linear lines beneath fingernails)

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Eye Roth spots Roth's spots are retinal hemorrhages with white or pale centers composed of coagulated fibrin. They are typically observed via fundoscopy (using an ophthalmoscope to view inside the eye) or slit lamp exam

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Eye Roth spots They are usually caused by immune complex mediated vasculitis often resulting from bacterial endocarditis. Roth's spots may be observed in leukemia, diabetes, subacute bacterial endocarditis, pernicious anemia, ischemic events, and rarely in HIV retinopathy.

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Infective endocarditis also can give rise to conjunctival haemorrhages

EFFECTS ON SKIN&EYE:

EFFECTS ON SKIN&EYE Clubbing is also known to occur in infective endocarditis.

Duke Criteria for diagnosis :

Duke Criteria for diagnosis

Duke criteria: Minor criteria:

Duke criteria: Minor criteria Predisposition Predisposing heart condition or IV drug abuser Fever > 38.0º C Vascular phenomena arterial emboli, septic pulmonary infarct, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, Janeway’s lesion Immunologic phenomena glomerulonephritis , Osler’s nodes, Roth’s spots, rheumatoid factors Microbiologic evidence positive blood culture but does not meet major criteria as noted Echocardiographic evidence consistent with IE but does not meet major criteria as noted

Echocardiography:

Echocardiography

Echocardiography:

Echocardiography

TTE-Transt-horacic echocardiography TOE-Trans-oesophagal echocardiography:

TTE-Transt-horacic echocardiography TOE-Trans-oesophagal echocardiography

Endocarditis prophylaxis recommended:

Endocarditis prophylaxis recommended High-risk Prosthestic cardiac valves Previous bacterial endocarditis Complex cyanotic heart disease Surgically constructed systemic-pulmonary shunts or conduits Moderate-risk Most other congenital heart disease Acquired valvar dysfunction Hypertrophic cardiomyopathy Mitral valve prolapse WITH regurgitation and/or thickened leaflets

Endocarditis prophylaxis NOT recommended:

Endocarditis prophylaxis NOT recommended Isolated secundum ASD Surgically repaired VSD, ASD, or PDA after 6 months (no residua) s/p CABG MVP without MR Previous Kawasaki disease w/o valvar dysfunction Previous rheumatic fever w/o valvar dysfunction Pacemakers and AICDs Flow murmurs

Dental procedures and IE prophylaxis: Recommended:

Dental procedures and IE prophylaxis: Recommended Dental extractions Periodontal procedures Dental implants and reimplantation of avulsed teeth Endodontic proceures Subgingival placement of antibiotic fibers and strips Initial placement of orthodontic bands (not brackets) intraligamentary local anesthetic injections Prophylactic cleaning

Dental procedures and IE prophylaxis: Not recommended:

Dental procedures and IE prophylaxis: Not recommended Restorative dentistry Non-intraligamentary local anesthetic injections Taking oral impressions Fluoride treatments Oral radiographs Orthodontic appliance adjustment Shedding primary teeth

Other procedures and IE prophylaxis: Recommended:

Other procedures and IE prophylaxis: Recommended Respiratory T&A Surgical procedures involving respiratory mucosa Rigid bronchoscopy Gastrointestinal Sclerotherapy Esophageal stricture dilation ERCP with biliary obstruction Surgery involving biliary tract or intestinal mucosa Genitourinary tract Prostatic surgery, cystoscopy Urethral dilation

Other procedures and IE prophylaxis: Not recommended:

Other procedures and IE prophylaxis: Not recommended Respiratory Endotracheal intubation PE tubes Flexible bronchoscopy Gastrointestinal Transesophageal echocardiography Endoscopy (with or without biopsy) Circumcision Genitourinary tract Vaginal hysterectomy, and vaginal or Caesarean deliveries In uninfected tissues: urethral catheterization, uterine D&C, therapeutic abortions, sterilization procedures, insertion or removal of IUDs

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