ACUTE BACTERIAL ENDOCARDITIS DR BASHIR

INFECTIVE ENDOCARDITIS : 

INFECTIVE ENDOCARDITIS By Dr Bashir Ahmed DarChinkipora Sopore KashmirAssociate Professor MedicineEmail drbashir123@gmail.com

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From Right to Left Dr.Smitha associate prof gynae Dr Bashir associate professor Medicine Dr Udaman neurologist Dr Patnaik HOD ortho Dr Tin swe aye paeds

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From RT to Lt Professor Dr Datuk rajagopal N Dr Bashir associate professor medicine Dr Urala HOD gynae Dr Nagi reddy tamma HOD-opthomology Dr Setharamarao Prof ortho

INFECTIVE ENDOCARDITIS : 

INFECTIVE ENDOCARDITIS A microbial infection of the endothelial lining of the heart; most commonly occurring as a vegetation on the valve leaflets

INFECTIVE ENDOCARDITIS : 

INFECTIVE ENDOCARDITIS Annual incidence: 15,000 to 20,000 Forth leading cause of life-threatening infectious disease Male:female ratio is 1.7:1 (median age 50)

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

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 factorsAlready damaged valves by RHD : 

Predisposing factorsAlready 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 : 

PREDISPOSING FACTORS Low risk isolated secundum atrial septal defect ASD, VSD, or PDA >6 months past repair “innocent” heart murmur “

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%

MICROBIAL AGENTS RESPONSIBLE FOR IE : 

MICROBIAL AGENTS RESPONSIBLE FOR IE Staphylococcus aureus: healthy or deformed valves, esp. in intravenous drug abusers and prosthetic valves. Prosthetic valve endocarditis during the perioperative period or 60 after operation also by s.epidermitides. Prosthetic valve endocarditis also occurs by Candida and aspergillosis but form large vegetations.

MICROBIAL AGENTS RESPONSIBLE FOR IE : 

MICROBIAL AGENTS RESPONSIBLE FOR IE HACEK group consists of Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, & Kingella (as I said are commensals of oral cavity)

MICROBIAL AGENTS RESPONSIBLE FOR IE : 

MICROBIAL AGENTS RESPONSIBLE FOR IE Enterococcus Normal inhabitants of the GI tract, occasionally anterior urethra Mostly subacute and affect men (mean age 59) after genitourinary manipulations or women (mean age 37) after obstetrics procedures. E. faecalis 85% of enterococcal IE

MICROBIAL AGENTS RESPONSIBLE FOR IE : 

MICROBIAL AGENTS RESPONSIBLE FOR IE Others are Fungi (Candida,aspergillosis). Rickettsiae Chlamydia These infections occur in a particular situation.

MICROBIAL AGENTS RESPONSIBLE FOR IE : 

MICROBIAL AGENTS RESPONSIBLE FOR IE Still other organisms are Pseudomonas Brucella Diphtheroids Listeria Bartonella Coxsiella Chlamydia

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

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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 The adherence of the organism to NBTE is a crucial step. 1. FimA is a surface adhesin of S.viridans that serves as an important colonization factor. Homologues of fimA genes were found in many S.viridans strains and enterococci. 2. Fibronectin is implicated as the host receptor within NBTE.

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 Petechiae, may result from local vasculitis or emboli Petechiae are red because they contain red blood that has leaked from the capillaries

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.

Summary of Infective Endocarditis : 

Summary of Infective Endocarditis Endothelial damage Platelet-fibrin thrombi Microorganism adherence

Summary of Pathogenesis BE : 

Summary of Pathogenesis BE Turbulent blood flow (from congenital or acquired heart dz)Endothelial trauma Platelets and fibrin deposit on damaged endothelium  Nonbacterial Thrombotic Endocarditis (NBTE) Bacteremia Colonization of NBTE  Bacterial Vegetation

THINGS TO REMEMBER IN INFECTIVE ENDOCARDITIS : 

THINGS TO REMEMBER IN INFECTIVE ENDOCARDITIS Infective endocarditis affects Left-sided valves 75% Right-sided valves 15% Both 5% Other 5%

THINGS TO REMEMBER IN INFECTIVE ENDOCARDITIS : 

THINGS TO REMEMBER IN INFECTIVE ENDOCARDITIS Mitral valve alone 35% Aortic valve alone 20% Mitral plus aortic 20% Tricuspid 14% Pulmonic 1% With changing murmurs in character pitch duration etc.fungal vegetations are large vegetations.

THINGS TO REMEMBER IN INFECTIVE ENDOCARDITIS : 

THINGS TO REMEMBER IN INFECTIVE ENDOCARDITIS Infective endocarditis may be culture negative either due to prior antibiotic treatment or due to atypical microbial organisms or due to fungus etc.then called as non bacterial endocarditis.

CLASSIFICATION OF BACTERIAL ENDOCARDITIS : 

CLASSIFICATION OF BACTERIAL ENDOCARDITIS 1. Acute Bacterial Endocarditis (“ABE”) usually fulminant, due to highly virulent organisms (e.g. Staphylococcus aureus) versus Subacute Bacterial Endocarditis (“SBE”) with insidious onset over weeks, due to less virulent organisms (e.g. viridans streptococci)

CLASSIFICATION OF BACTERIAL ENDOCARDITIS : 

CLASSIFICATION OF BACTERIAL ENDOCARDITIS Acute: Rapid progression of symptoms Less than 6 weeks duration Significant systemic signs/symptoms Fever Elevated systemic WBC/ left shift Subacute: Slower, more chronic progression of symptoms Low grade fevers Vague clinical signs/symptoms weakness, anorexia, malaise,etc.

CLASSIFICATION OF BACTERIAL ENDOCARDITIS : 

CLASSIFICATION OF BACTERIAL ENDOCARDITIS Acute Toxic presentation Progressive valve destruction & metastatic infection developing in days to weeks Most commonly caused by S. aureus Subacute Mild toxicity Presentation over weeks to months Rarely leads to metastatic infection Most commonly S. viridans or enterococcus

CLINICAL FEATURES OF ENDOCARDITIS : 

CLINICAL FEATURES OF ENDOCARDITIS Common Symptoms Fever 80% Chills 40% Weakness 40% Dyspnea 40%

CLINICAL FEATURES OF ENDOCARDITIS : 

CLINICAL FEATURES OF ENDOCARDITIS Uncommon Symptoms Cough 25% Sweats 25% Anorexia 25% Weight loss 25% Malaise 25% Skin lesions 20% Nausea/vomiting 20% Stroke 20%

CLINICAL FEATURES OF ENDOCARDITIS : 

CLINICAL FEATURES OF ENDOCARDITIS More Uncommon Symptoms Headache 15% Myalgia/arthralgia 15% Edema 15% Chest pain 15% Abdominal pain 15% Delirium/coma 15% Back pain 10% Hemoptysis 10%

CLINICAL FEATURES OF ENDOCARDITIS : 

CLINICAL FEATURES OF ENDOCARDITIS Common Physical Signs Fever 90% Heart murmur 85% Splenomegaly 30% Petechiae 30%

CLINICAL FEATURES OF ENDOCARDITIS : 

CLINICAL FEATURES OF ENDOCARDITIS Uncommon Physical Signs Osler nodes 15% (pea-sized tender finger/toe nodules) Subungual splinter hemorrhages 15% Changing heart murmur 10%

CLINICAL FEATURES OF ENDOCARDITIS : 

CLINICAL FEATURES OF ENDOCARDITIS More Uncommon Physical Signs Janeway lesions 5% (small palm/sole hemorrhages) New heart murmur 5% Roth spots (on retina) 2% (white dots with surrounding hemorrhage)

LABORATORY FINDINGS : 

LABORATORY FINDINGS Laboratory Findings Elevated ESR (mean 57 mm/hr) 95% (erythrocyte sedimentation rate) Circulating immune complexes 90% Anemia 80% Proteinuria 60%

LABORATORY FINDINGS : 

LABORATORY FINDINGS Laboratory Findings Rheumatoid factor 50% (anti-IgG antibodies) Hematuria 40% Leukocytosis 25% Hypergammaglobulinemia 25% Elevated creatinine 10% Leukopenia 10% Thrombocytopenia 10%

LABORATORY FINDINGS : 

LABORATORY FINDINGS ECG should be done in all pts with suspected IE Nonspecific usually Conduction abnormalities ( new LBBB, Prolonged PR interval, new RBBB, complete heart block) Junctional tachycardia Chest Xray Pulmonic emboli or CHF

LABORATORY FINDINGS : 

LABORATORY FINDINGS Blood cultures critical for specific diagnosis 3 sites 30-60 minutes apart before starting antibiotics. 86 – 96% of 1st cultures positive 98 – 100% of 1st 2 cultures positive Blood cultures may be negative if the patient has already received antibiotics; a few cases of infective endocarditis are “culture-negative”

LABORATORY FINDINGS : 

LABORATORY FINDINGS All patients with suspected bacteremia should have blood cultures drawn in the ED prior to abx Blood cultures should be drawn in 3 different sites Minimum of 10 ml blood in each bottle Minimum of one hour between first and last bottle

LABORATORY FINDINGS : 

LABORATORY FINDINGS Negative culture can occur in 5% of patients. 1/3 to ½ are negative due to prior antibiotic use In patients with culture negative IE, advise lab to allow specialized testing to recover the causative organism which is needed to adequately treat

LABORATORY FINDINGS : 

LABORATORY FINDINGS Transthoracic (TTE)echocardiography 60% sensitivity for vegetations Transesophageal(TEE) echocardiography >90% sensitivity for vegetations The absence of vegetations on echocardiogram does not exclude the diagnosis of endocarditis

Duke’s Criteria For Diagnosis of Infective Endocarditis : 

Duke’s Criteria For Diagnosis of Infective Endocarditis Duke Criteria – Simplified Requires 2 major, or 1 major + 3 minor or 5 minor criteria

Duke’s Major Criteria : 

Duke’s Major Criteria Major Criteria 1. Positive blood culture typical microorganism (strep viridans, strep bovis, HACEK group, staph aureus or enterococci in the absence of a primary locus) for endocarditis from two separate blood cultures persistently positive blood culture from: blood cultures drawn more than 12 hr apart, or all of 3 or a majority of 4 or more separate blood cultures, with first and last drqwn at least 1 hr apart

Duke’s Major Criteria : 

Duke’s Major Criteria 2. Positive Echocardiogram showing Vegetation Abscess, Detached prosthesis Regurgitation

Duke’s Minor Criteria : 

Duke’s Minor Criteria Minor Criteria Predisposition (predisposing heart condition or iv drug use) Fever of 100.40F or higher Vascular phenomena (major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctive hemorrhages, Janeway lesions).

Duke’s Minor Criteria : 

Duke’s Minor Criteria Immunologic phenomena (glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor) Microbiologic evidence (positive blood culture not meeting major criteria or serologic evidence of active infection with organism consistent with IE) Echocardiogram (consistent with IE but not meeting major criteria)

COMPLICATIONS OF INFECTIVE ENDOCARDITIS : 

COMPLICATIONS OF INFECTIVE ENDOCARDITIS Heart failure 67% Septic emboli 55% to kidneys 55% to heart 50% to spleen 44% to brain 33%

COMPLICATIONS OF INFECTIVE ENDOCARDITIS : 

COMPLICATIONS OF INFECTIVE ENDOCARDITIS Uncommon Complications Myocardial abscess 20% Glomerulonephritis 15% (immune complexes) “Mycotic aneurysm” 10% Pericarditis (S.aureus) rare

INDICATIONS FOR PROPHYLAXIS : 

INDICATIONS FOR PROPHYLAXIS Prophylaxis is indicated for Prosthetic heart valves Congenital heart disease with manifestations Acquired heart disease with manifestations Hypertrophic cardiomyopathy Mitral valve prolapse with regurgitation Previous history of endocarditis Dental procedures known to produce bleeding Surgery involving GI, respiratory mucosa

INDICATIONS FOR PROPHYLAXIS : 

INDICATIONS FOR PROPHYLAXIS Tonsillectomy Esophageal dilation ERCP for obstruction Gallbladder surgery Cystoscopy, urethral dilation Urethral catheter if infection present Urinary tract surgery Tonsillectomy Rigid bronchoscopy.

INDICATIONS FOR PROPHYLAXIS : 

INDICATIONS FOR PROPHYLAXIS Esophageal sclerotherapy or stricture dilation Respiratory: Consider if pt will be cut or biopsied Periodontal procedures (surgery, scaling, and root planing, probing, and recall maintenance) Implant placement and reimplantation of avulsed teeth Endodontic instrumentation beyond the apex Subgingival placement of antibiotic fibers or strips Placement of orthodontic bands but not brackets.

INDICATIONS FOR PROPHYLAXIS : 

INDICATIONS FOR PROPHYLAXIS ERCP Billiary surgery Prostate surgery Cystoscopy Cardiac transplants Extractions of teeth Intraligamentary injections Prophylactic cleaning of teeth or implants where bleeding is anticipated

No Prophylaxis : 

No Prophylaxis Vaginal delivery Hysterectomy Local anesthetic injections Placement of oral rubber dams Post-op suture removal Placement of removable appliances Fluoride treatment Radiographs Orthodontic adjustments Shedding of primary teeth IUDs Circumcision MVP without regurgitation Pacemakers but see if not already infected Physiologic murmurs

Indications for Surgery : 

Indications for Surgery (When removal of an infected valve is necessary). Refractory CHF Severe valvular dysfunction Uncontrolled infection Valve perforation Dehiscence Fistula Abscess

Indications for Surgery : 

Indications for Surgery Embolic event with persistent large vegetation or >1 episode of embolization Prosthetic valve infection Fungal IE New heart block Refractory CHF Uncontrolled infection Ineffective antimicrobial therapy

Indications for Surgery : 

Indications for Surgery Resection of mycotic aneurysms antibiotic-resistant pathogens) Local suppurative complications including perivalvular or myocardial abscesses Persistent vegetations after a major systemic embolic episode Large (>1cm diameter) anterior mitral valve vegetation Acute mitral insufficiency Valve perforation or rupture Increase in vegetation size 4 weeks after antibiotic therapy

Indications for Surgery : 

Indications for Surgery Periannular extension of infection Infected prosthetic material: less than 1 year out from original heart surgery Refractory congestive heart failure (Leading cause of death) Unresponsive infection/ continued infection despite appropriate antibiotics

Indications for Surgery : 

Indications for Surgery Pt. experiences more than 1 major emboli Severe valvular dysfunction: Acute CHF or impaired hemodynamic status Relapsing prosthetic valve endocarditis Fungal endocarditis New conduction defects or arrhythmias Persistent bacteremia Acute AR or MR with heart failure. Acute AR with tachycardia and early closure of the MV. Annular or aortic abscess. Sinus or aortic aneurysm. Persistent bacteremia and valve dysfunction

Indications for Surgery : 

Indications for Surgery Recurrent emboli after appropriate Abx. Mobile vegetations >10 mm. Persistent pyrexia and leucocytosis with negative blood cultures. Increase in vegetation size after antimicrobial therapy Valvular dysfunction Fungal endocarditis

TREATMENT OF INFECTIVE ENDOCARDITIS : 

TREATMENT OF INFECTIVE ENDOCARDITIS Purpose of Prophylaxis To give antibiotics and kill blood-borne bacteria or interfere with their metabolism, hindering their ability to adhere to a damaged heart valve. However antibiotic resistance is increasing. Only administered prior to “high risk” surgeries Include dental procedures, surgery on the gastrointestinal or urinary tract, surgery on infected tissues

TREATMENT OF INFECTIVE ENDOCARDITIS : 

TREATMENT OF INFECTIVE ENDOCARDITIS 50% of some valvular infections do not respond to antimicrobial therapy or surgery Today’s highly virulent causative agents have led to an increase in dangerous complications Don’t need to memorize individual procedures

PROPHYLACTIC TREATMENT : 

PROPHYLACTIC TREATMENT Standard Prophylactic Regimen Single dose, 30-60 min prior to any procedure Amoxycillin 2.0 grams orally or iv Ampicillin 2gm IV/IM or Ceftriaxone 1g IV/IM IV, PCN-allergic Ceftriaxone 1g IV/IM

PROPHYLACTIC TREATMENT : 

PROPHYLACTIC TREATMENT Prophylaxis for Patients Already Taking Amoxycillin or have allergy to pencillin or microbial may have developed resistance to Amoxycillin options then are Ceftriaxone 1g IV/IM before and after procedure Clindamycin 600mg PO or Clarithromycin 500 mg or Azithromycin 500mg PO Quinolones or IV Vancomycin not recommended for prophylaxis due to concern of creating new drug resistance

SUMMARY PROPHYLACTIC TREATMENT : 

SUMMARY PROPHYLACTIC TREATMENT Summary of Standard Regimen Ampicillin 1g IM/IV Gentamicin 1 to 1.5 mg/kg IV/IM (MAX 120 mg) Ceftriaxone 1gm IV Vancomycin 1g IV over 1-2h

TREATMENT OF IE GENERAL COMMENTS : 

TREATMENT OF IE GENERAL COMMENTS IE treatment should be considered in All febrile IDUs Pts with a cardiac prosthesis and fever Pts with new murmur or change in murmur with evidence of vasculitis or embolization Any cardiac risk factor with unexplained fever Any patient with a prolonged fever (>2 weeks)

TREATMENT OF IE GENERAL COMMENTS : 

TREATMENT OF IE GENERAL COMMENTS Most patients will require 4 to 6 weeks of antibiotic therapy. Antifungals alone are not enough to cure fungal IE, although Amphotericin B is often administered in conjunction with surgery. Culture-negative native-valve endocarditis should be individualized and generally includes ampicillin, Ceftriaxone, or Vancomycin, +/- Aminoglycoside

TREATMENT OF IE GENERAL COMMENTS : 

TREATMENT OF IE GENERAL COMMENTS Complete eradication takes weeks, relapses may occur. This is due to: 1. The infection exists in an area of impaired host defense and is tightly encased in a fibrin meshwork 2. The bacteria reach very high population densities, such that the organism may exist in a state of reduced metabolic activity and cell division

TREATMENT OF IE GENERAL COMMENTS : 

TREATMENT OF IE GENERAL COMMENTS Etiologic agent must be isolated in pure culture. MIC and MBC should be determined. All patients with suspected bacteremia should have blood cultures drawn in the ED prior to abx Blood cultures should be drawn in 3 different sites Minimum of 10 ml blood in each bottle Minimum of one hour between first and last bottle Aspirin may decrease the growth of vegetative lesions and prevent cerebral emboli

TREATMENT OF IE GENERAL COMMENTS : 

TREATMENT OF IE GENERAL COMMENTS Parenteral antibiotics are recommended over oral drugs Antibiotic combinations should produce a rapid effect Selection of antibiotics should be based on susceptibility tests, and treatment should be monitored with clinical improvement. Blood cultures should be obtained during the early phase of therapy to ensure eradication Use of anticoagulants during therapy for native valve IE is not recommended. With mechanical valves, anticoagulation should be maintained (if indicated) within therapeutic range

TREATMENT OF IE GENERAL COMMENTS : 

TREATMENT OF IE GENERAL COMMENTS Effective antimicrobial treatment should lead to defervescence within 7 – 10 days Persistent fever in IE may be due to staph, pseudomonas, culture negative IE or with microvascular complications/major emboli or due to drug reaction. OOPS! You didn’t premedicate patient and you encounter unexpected bleeding!Don’t Panic Stop procedure, administer antibiotics, and resume working Antibiotics administered up to 2 hours following a procedure may still protective

TREATMENT OF IE GENERAL COMMENTS : 

TREATMENT OF IE GENERAL COMMENTS Anticoagulation for native valve endocarditis has not been shown to be beneficial because of Increase of risk of intracranial hemorrhage Pts with prosthetic valves who are treated with anticoagulation can be maintained on their regimen with proper caution for CNS complications

TREATMENT OF IE GENERAL COMMENTS : 

TREATMENT OF IE GENERAL COMMENTS “If anticoagulation is indicated for Another reason it should be continued. Anticoagulation does not prevent

TREATMENT OF IE : 

TREATMENT OF IE Highly penicillin-susceptible Streptococcus viridans or bovis Once-daily ceftriaxone for 4 wks cure rate > 98% Or Once-daily ceftriaxone 2 g for 2wks followed by oral Amoxycillin qid for 2 wks

TREATMENT OF IE : 

TREATMENT OF IE If organisms are resistant to this then give Vancomycin, 15mg/kg IV 12 hourly daily, plus Gentamicin 1 to 1.5 mg/kg 8 hourly, both 4 to 6 weeks.

TREATMENT OF IE : 

TREATMENT OF IE Ampicillin 2gm 4 hourly plus Gentamicin 60-80mg 8 hourly HACEK organisms (IE) Ceftriaxone monotherapy (1 to 2gm IV/BD daily) or Ampicillin Plus Gentamicin x 4 to 6 weeks.

TREATMENT OF IE : 

TREATMENT OF IE Staph IE with Prosthetic Material Triple drug regimens Methicillin-sensitive staph spp. Nafcillin/Oxacillin Plus Rifampin (6 weeks) Methicillin-resistant staph spp Vancomycin Plus Rifampin 300mg PO 8hrly (6 to 8 weeks) Plus Ampicillin &Gentamicin (2 weeks).

TREATMENT OF IE : 

TREATMENT OF IE Or Ceftriaxone (2 g/d IV as a single dose for 4 weeks) plus Rifampicin (300 mg PO q8h for 6-8 weeks).

THANK YOUHELP THOSE IN SUFFERING : 

THANK YOUHELP THOSE IN SUFFERING