SUB ACUTE BACTERIAL ENDOCARDITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIR

INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS

By Dr Bashir Ahmed DarChinkipora Sopore KashmirAssociate Professor MedicineEmail [email protected]

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

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


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


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)

0%

10%

20%

30%

40%

50%

60%

Age

Age Distribution

<30 31-60 >60

INFECTIVE ENDOCARDITIS

100% fatal if undiagnosed and untreated

• 20% fatal even if diagnosed and treated appropriately.

•70% streptococcal• 20% staphylococcal

Predisposing factorsPredisposing 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 factorsPredisposing factorsAlready damaged valves by Already damaged valves by

RHDRHD

Predisposing factorsPredisposing factors Already damaged damaged Already damaged damaged

heart by CHDheart by CHD– Congenital heart

disease (6-24%)

Predisposing factors Predisposing factors Prosthetic valves & Prosthetic valves &

pacemakerspacemakers High risk

– prosthetic cardiac valve

– prior episodes of endocarditis

– surgically constructed systemic-pulmonary shunts or conduits

– Pacemakers & pacemaker leads

Predisposing factors Predisposing factors Prosthetic valves & Prosthetic valves &

pacemakerspacemakers

PREDISPOSING FACTORS PREDISPOSING FACTORS IV drug abusersIV drug abusers

PREDISPOSING FACTORS PREDISPOSING FACTORS Alcohol abuse & sepsisAlcohol abuse & sepsis

PREDISPOSING FACTORSPREDISPOSING FACTORS

Neutropenia

&

Immunosupression


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


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


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

PREDISPOSING FACTORS PREDISPOSING FACTORS INVASIVE PROCEDURESINVASIVE PROCEDURES

– G.I. Barium enema Colonoscopy

– Genitourinary Prostatectomy


Tooth extraction Periodontal surgery Teeth cleaning Tooth brushing,

flossing Using wooden

toothpicks Chewing food


Biopsies, suture removal, placing orthodontic bands

Tonsillectomy,Adenoidectomy,Bronchoscopy.

Resp tract procedure to drain abscess or empyema


Central venous catheterization

Bladder catheterization, Endoscopies, shaving,

Skin or musculoskeletal infections


– AIDS patients– Cancer patients– Leukemia– Lymphomas

MICROBIAL AGENTS MICROBIAL AGENTS RESPONSIBLE FOR IERESPONSIBLE 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%


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.


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


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


Others areFungi (Candida,aspergillosis).RickettsiaeChlamydiaThese infections occur in a particular

situation.


Still other organisms are Pseudomonas Brucella Diphtheroids Listeria Bartonella Coxsiella Chlamydia

PATHOGENESIS OF PATHOGENESIS OF INFECTIVE ENDOCARDITISINFECTIVE 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).


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

NONBACTERIAL NONBACTERIAL THROMBOTIC THROMBOTIC

ENDOCARDITIS (NBTE)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



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



Importance Local effect on valve unimportantMay produce emboli with resultant infarctsMay eventually heal with fibrosis.


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 EndocarditisInfectious Endocarditis

Infective endocarditis with perforation of mitral valve leaflet

Vegetation

Mitral Valve

Stick in Perforation


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 EffectVenturi Effect


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


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.


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


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.


Microscopic Pathology

Fibrin, platelets, masses of organisms,

+/- necrosis, +/- neutrophils

Later: +/-lymphocytes, +/- macrophages,

+/- fibroblasts, +/- fibrosis

LOCAL EFFECTS OF LOCAL EFFECTS OF INFECTIVE ENDOCARDITISINFECTIVE 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.


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 abscessFistulaeProsthetic dehiscence


Valvular distortion/destruction chordal rupture.

Conduction abnormalitiesPurulent pericarditisFunctional valve obstructionWith treatment, healing occurs by fibrosis

and occasionally calcification.

DISTANT EFFECTS OF DISTANT EFFECTS OF INFECTIVE ENDOCARDITISINFECTIVE 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 IEIMMUNOLOGICAL 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 KIDENYEFFECTS 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 lesion2. GN can occur with right-sided IE3. GN is rare in acute IE even though large vegetation result in

metastatic abscess formation4. IF staining reveals IC-typical distribution5. Antibacterial antibodies eluted from lesions

OTHER EFFECTS OF IEOTHER EFFECTS OF IE

1. Mycotic aneurysm is a localized, irreversible arterial dilatation due to destruction of the vessel wall by infection

More common with S.viridans


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


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

EFFECTS ON EFFECTS ON CNS,SPLEEN,LUNGCNS,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


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 SKIN&EYEEFFECTS 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


Osler nodes, painful nodes on finger or toe pads

Due to immune complexes in dermal vessels


Osler’s Nodes:

1. red, raised lesions Tender, subcutaneous

nodules.4 P’s: Pink Painful Pea-sized Pulp of the fingers/toes.

– Immunological origin?


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.


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 LesionsJaneway Lesions


Splinter hemorrhage (linear lines beneath fingernails)


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


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.


Infective endocarditis also can give rise to conjunctival haemorrhages


Clubbing is also known to occur in infective endocarditis.

Summary of Infective Summary of Infective EndocarditisEndocarditis

Endothelial damage

Platelet-fibrin thrombi

Microorganism adherence

Summary of Summary of Pathogenesis BEPathogenesis 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 THINGS TO REMEMBER IN INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS

Infective endocarditis affects Left-sided valves 75%

Right-sided valves 15%Both 5%Other 5%


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.


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 CLASSIFICATION OF BACTERIAL ENDOCARDITISBACTERIAL 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 CLASSIFICATION OF BACTERIAL ENDOCARDITISBACTERIAL 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 CLASSIFICATION OF BACTERIAL ENDOCARDITISBACTERIAL 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 CLINICAL FEATURES OF ENDOCARDITISENDOCARDITIS

Common Symptoms Fever 80%Chills 40%Weakness 40%Dyspnea 40%


Uncommon Symptoms

Cough 25%Sweats 25%Anorexia 25%Weight loss 25%Malaise 25%Skin lesions 20%Nausea/vomiting 20%Stroke 20%


More Uncommon Symptoms

Headache 15% Myalgia/arthralgia 15% Edema 15% Chest pain 15% Abdominal pain 15% Delirium/coma 15% Back pain 10% Hemoptysis 10%


Common Physical Signs Fever 90%Heart murmur 85% Splenomegaly 30%Petechiae 30%


Uncommon Physical Signs

Osler nodes 15%(pea-sized tender finger/toe nodules)

Subungual splinter hemorrhages 15%

Changing heart murmur 10%


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 FINDINGSLABORATORY FINDINGS

Laboratory Findings

Elevated ESR (mean 57 mm/hr) 95%(erythrocyte sedimentation rate)

Circulating immune complexes 90%

Anemia 80%

Proteinuria 60%


Laboratory Findings

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


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


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”


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 bottleMinimum of one hour between first and last

bottle


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


Transthoracic (TTE)echocardiography 60% sensitivity for vegetations

Transesophageal(TEE) echocardiography >90% sensitivity for vegetations

The absence of vegetations on echocardiogramdoes not exclude the diagnosis of endocarditis

Duke’s Criteria For Diagnosis Duke’s Criteria For Diagnosis of Infective Endocarditisof Infective Endocarditis

Duke Criteria – Simplified

Requires 2 major, or 1 major + 3 minor or 5 minor criteria

Duke’s Major CriteriaDuke’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 CriteriaDuke’s Major Criteria

2. Positive Echocardiogram showingVegetationAbscess,Detached prosthesisRegurgitation

Duke’s Minor CriteriaDuke’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 CriteriaDuke’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 COMPLICATIONS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS

Heart failure 67%

Septic emboli 55% to kidneys 55%

to heart 50% to spleen 44% to brain 33%

COMPLICATIONS OF COMPLICATIONS OF INFECTIVE ENDOCARDITISINFECTIVE ENDOCARDITIS

Uncommon Complications

Myocardial abscess 20%

Glomerulonephritis 15%(immune complexes)

“Mycotic aneurysm” 10%

Pericarditis (S.aureus) rare

INDICATIONS FOR INDICATIONS FOR PROPHYLAXISPROPHYLAXIS

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


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


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.


ERCP Billiary surgery Prostate surgery Cystoscopy Cardiac transplants Extractions of teeth Intraligamentary injections Prophylactic cleaning of teeth or implants where

bleeding is anticipated

No ProphylaxisNo 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 SurgeryIndications for Surgery

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


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


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


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


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


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 TREATMENT OF INFECTIVE ENDOCARDITISENDOCARDITIS

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 TREATMENT OF INFECTIVE ENDOCARDITISENDOCARDITIS

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 PROPHYLACTIC TREATMENTTREATMENT

Standard Prophylactic RegimenSingle dose, 30-60 min prior to any

procedureAmoxycillin 2.0 grams orally or iv

Ampicillin 2gm IV/IM or Ceftriaxone 1g IV/IM

IV, PCN-allergic Ceftriaxone 1g IV/IM

PROPHYLACTIC PROPHYLACTIC TREATMENTTREATMENT

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 SUMMARY PROPHYLACTIC TREATMENTTREATMENT

Summary of Standard RegimenAmpicillin 1g IM/IV Gentamicin 1 to 1.5 mg/kg IV/IM (MAX

120 mg)Ceftriaxone 1gm IVVancomycin 1g IV over 1-2h

TREATMENT OF IE TREATMENT OF IE GENERAL COMMENTSGENERAL 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)


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


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


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


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


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


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


“If anticoagulation is indicated forAnother reason it should be continued. Anticoagulation does not prevent

TREATMENT OF IETREATMENT 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


If organisms are resistant to this then giveVancomycin, 15mg/kg IV 12 hourly daily,

plus Gentamicin 1 to 1.5 mg/kg 8 hourly, both 4 to 6 weeks.


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.


Staph IE with Prosthetic MaterialTriple drug regimensMethicillin-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).


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

THANK YOUTHANK YOUHELP THOSE IN HELP THOSE IN

SUFFERINGSUFFERING

SUB ACUTE BACTERIAL ENDOCARDITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIR

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Transcript of SUB ACUTE BACTERIAL ENDOCARDITIS BY DR BASHIR AHMED DAR ASSOCIATE PROFESSOR MEDICINE SOPORE KASHMIR