Sub Acute Bacterial Endocarditis By Dr Bashir Ahmed Dar Associate Professor Medicine Sopore Kashmir

INFECTIVE ENDOCARDITIS By Dr Bashir Ahmed Dar Chinkipora Sopore Kashmir Associate Professor Medicine Email [email protected]

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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 HODopthomology Dr Setharamarao Prof ortho

INFECTIVE ENDOCARDITIS A

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

INFECTIVE ENDOCARDITIS  Annual

incidence: 15,000 to 20,000  Forth leading cause of life-threatening infectious disease

Age Distribution 60% 50% 40% 30% 20% 10% 0% <30

 Male:female

ratio is

1.7:1 (median age 50)

31-60 Age

>60

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

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 damaged heart by CHD – Congenital heart disease (6-24%)

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 IV drug abusers

PREDISPOSING FACTORS Alcohol abuse & sepsis

PREDISPOSING FACTORS

Neutropenia & Immunosupression

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  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  Low

risk

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

PREDISPOSING FACTORS INVASIVE PROCEDURES – G.I.  

Barium enema Colonoscopy

– Genitourinary 

Prostatectomy

PREDISPOSING FACTORS INVASIVE PROCEDURES  Tooth

extraction  Periodontal surgery  Teeth cleaning  Tooth brushing, flossing  Using wooden toothpicks  Chewing food

PREDISPOSING FACTORS INVASIVE PROCEDURES  Biopsies,

suture removal, placing orthodontic bands 

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Tonsillectomy,Adenoid ectomy,Bronchoscopy. Resp tract procedure to drain abscess or empyema

PREDISPOSING FACTORS INVASIVE PROCEDURES  Central

venous catheterization  Bladder catheterization, Endoscopies, shaving,  Skin or musculoskeletal infections

PREDISPOSING FACTORS

– – – –

AIDS patients Cancer patients Leukemia Lymphomas

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 

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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.

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Prosthetic valve endocarditis also occurs by Candida and aspergillosis but form large vegetations.

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  Enterococcus  

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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  Others

are  Fungi (Candida,aspergillosis).  Rickettsiae  Chlamydia  These infections occur in a particular situation.

MICROBIAL AGENTS RESPONSIBLE FOR IE  Still

other organisms are  Pseudomonas  Brucella  Diphtheroids  Listeria  Bartonella  Coxsiella  Chlamydia

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  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)  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)  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)  Importance  Local

effect on valve unimportant  May produce emboli with resultant infarcts  May eventually heal with fibrosis.

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

Vegetation

Stick in Perforation

Mitral Valve

Infective endocarditis with perforation of mitral valve leaflet

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

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  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 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  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 Microscopic Pathology Fibrin, platelets, masses of organisms, +/- necrosis, +/- neutrophils Later: +/-lymphocytes, +/- macrophages, +/- fibroblasts, +/- fibrosis

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  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  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  Vegetations

may become detached and produce embolic effects.  Embolic phenomena are common (1535%). septic infarcts involving: renal, splenic, coronary, or cerebral circulation.  Risk for emboli is increased when vegetation >1cm.

IMMUNOLOGICAL EFFECTS OF IE  

IE cause both humural and cellular response Rheumatoid factor: – titers correlate with the level of hypergammaglobulinemia and decrease with

therapy

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Antinuclear antibodies: – may contribute to the musculoskeletal manifestations, low-grade fever, or

pleuritic pain

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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  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 Mycotic aneurysm is a localized, irreversible arterial dilatation due to destruction of the vessel wall by infection  More common with S.viridans 1.

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  Tend

to occur at bifurcation areas; middle cerebral artery is most common,Clinically silent until rupture

EFFECTS ON CNS,SPLEEN,LUNG 

CNS – cerebral emboli (>30% of IE) – Mycotic aneurysms

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Spleen – infarctions (44% of autopsy cases) – enlargement associated with hyperplasia of lymphoid follicles,

increase in secondary follicles, focal necrosis,abscess

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Lung – associated with right-sided IE – pulmonary embolism, acute pneumonia, pleural effusion, or

empyema

EFFECTS ON CNS,SPLEEN,LUNG 

CNS – cerebral emboli (>30% of

IE) – Mycotic aneurysms

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 

Lung – associated with right-sided

IE – pulmonary embolism, acute pneumonia, pleural effusion, or empyema

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  Osler

nodes, painful nodes on finger or toe pads  Due to immune complexes in dermal vessels

EFFECTS ON SKIN&EYE  1. 

Osler’s Nodes: red, raised lesions Tender, subcutaneous nodules.4 P’s:    

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Pink Painful Pea-sized Pulp of the fingers/toes.

Immunological origin?

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 

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

EFFECTS ON SKIN&EYE  Splinter

hemorrhage (linear lines beneath fingernails)

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 

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  Infective

endocarditis also can give rise to conjunctival haemorrhages

EFFECTS ON SKIN&EYE  Clubbing

is also known to occur in infective endocarditis.

Summary of Infective Endocarditis Endothelial damage

Platelet-fibrin thrombi

Microorganism adherence

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  Infective

endocarditis affects

Left-sided valves Right-sided valves Both Other

75% 15% 5% 5%

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  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 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  Acute:

Rapid progression of symptoms

– Less than 6 weeks duration – Significant systemic signs/symptoms  

Fever Elevated systemic WBC/ left shift

 Subacute:

symptoms

Slower, more chronic progression of

– Low grade fevers – Vague clinical signs/symptoms 

weakness, anorexia, malaise,etc.

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 Common Symptoms Fever Chills Weakness Dyspnea

80% 40% 40% 40%

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

25% 25% 25% 25% 25% 20% 20% 20%

CLINICAL FEATURES OF ENDOCARDITIS More Uncommon Symptoms Headache 15% Myalgia/arthralgia 15% Edema 15% Chest pain 15% Abdominal pain15% Delirium/coma 15% Back pain 10% Hemoptysis 10%

CLINICAL FEATURES OF ENDOCARDITIS Common Physical Signs Fever Heart murmur Splenomegaly Petechiae

90% 85% 30% 30%

CLINICAL FEATURES OF ENDOCARDITIS Uncommon Physical Signs Osler nodes (pea-sized tender finger/toe nodules)

15%

Subungual splinter hemorrhages

15%

Changing heart murmur

10%

CLINICAL FEATURES OF ENDOCARDITIS More Uncommon Physical Signs Janeway lesions (small palm/sole hemorrhages)

5%

New heart murmur

5%

Roth spots (on retina) 2% (white dots with surrounding hemorrhage)

LABORATORY FINDINGS Laboratory Findings Elevated ESR (mean 57 mm/hr) (erythrocyte sedimentation rate)

95%

Circulating immune complexes

90%

Anemia

80%

Proteinuria

60%

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  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  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  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  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 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 Criteria – Simplified  Requires

2 major,  or 1 major + 3 minor  or 5 minor 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  2.

Positive Echocardiogram showing  Vegetation  Abscess,  Detached prosthesis  Regurgitation

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  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 Heart failure

67%

Septic emboli to kidneys to heart to spleen to brain

55% 55% 50% 44% 33%

COMPLICATIONS OF INFECTIVE ENDOCARDITIS Uncommon Complications

Myocardial abscess20% Glomerulonephritis15% (immune complexes) “Mycotic aneurysm” Pericarditis (S.aureus)

10% rare

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  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  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  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       

Vaginal delivery Hysterectomy Local anesthetic injections Placement of oral rubber dams Post-op suture removal Placement of removable appliances Fluoride treatment

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Radiographs Orthodontic adjustments Shedding of primary teeth IUDs Circumcision MVP without regurgitation Pacemakers but see if not already infected Physiologic murmurs

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  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   

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Resection of mycotic aneurysms antibiotic-resistant pathogens) Local suppurative complications including perivalvular or myocardial abscesses Persistent vegetations after a major systemic embolic episode

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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  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  

  

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  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  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  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  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  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

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  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  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  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  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 





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 



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.

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



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  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  “If

anticoagulation is indicated for  Another reason it should be continued.  Anticoagulation does not prevent

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  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  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  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  Or

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

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