INFECTIVE ENDOCARDITIS DR ANJUM M CHUGHTAI - PowerPoint Presentation

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INFECTIVE ENDOCARDITIS

DR ANJUM M CHUGHTAI

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OUTLINE

DEFINITION

EPIDEMIOLOGY : CURRENT INDIAN SCENARIO

RISK FACTORS

MICROBIOLOGICAL PROFILE

DIAGNOSIS

CLINICAL FEATURES

TREATMENT

PROPHYLAXIS

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DEFINITION

Infective endocarditis

is a form of

endocarditis

, or inflammation of the inner tissue of the heart (such as its valves) caused by infectious agents.

The prototypic lesion of infective endocarditis, the

vegetation

, is a mass of platelets, fibrin,

microcolonies

of microorganisms, and scant inflammatory cells.

Infection most commonly involves heart valves (either

native disorganized valves, at times normal valve

or prosthetic) but may also occur on the low-pressure side of a ventricular

septal

defect, on the mural endocardium where it is damaged by aberrant jets of blood or foreign bodies, or on

intracardiac

devices themselves.

The analogous process involving

arteriovenous

shunts,

arterioarterial

shunts (patent

ductus

arteriosus

), or a

coarctation

of the aorta is called

infective endarteritis

.

Acute endocarditis

is a hectically febrile illness that rapidly damages cardiac structures,

hematogenously

seeds

extracardiac

sites, and, if untreated, progresses to death within weeks.

Subacute

endocarditis

follows an indolent course; causes structural cardiac damage only slowly, if at all; rarely metastasizes; and is gradually progressive unless complicated by a major embolic event or ruptured

mycotic

aneurysm.

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VEGETATIONS

SCHEMATIC

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EPIDEMIOLOGY : CURRENT INDIAN SCENARIO

The

incidence IS

(11.6/100,000

).It

increases in certain areas where

IVDAs

are common

A study by

Garg

N et al. in Indian patients during the last decade indicates that 76% of the patients with IE were younger than 40 years (median age 27.6 ± 12 years)

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RISK FACTORS

Most commonly due to

DENTAL PROCEDURES

• Increased longevity has added the burden of degenerative heart disease to IE

• Medical instrumentation of gastrointestinal, genitourinary (GU) tracts, etc.

• Invasive therapeutic procedures:

Intracardiac

pacemaker, implantable

cardioverter

defibrillator (ICD), AV fistula

• Immunosuppressive therapy • Immune compromised states: Human immunodeficiency virus (HIV), uncontrolled diabetes, etc. • Intravenous drug abuse. Hence in India, we are facing the traditional IE due to rheumatic heart disease (RHD) and modern IE on normal heart valves

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MICROBIOLOGICAL PROFILE

STAPH

AUREUS

40-50

25

30-40

25-30

STREPTOCOCCI VIRIDANS

15-20

40-50

33-65

30-45

COAGULASE

NEGATIVE STAPH

10

5

3-10

5-10GRAM NEGATIVE BACTERIA1054-85 ENTEROCOCCI45-815FUNGI1011RAREOTHER STREPTOCOCCI12POLYMICROBIAL41RARECULTURE NEGATIVE40-153-105

REFERENCE: BRAUNWALD’S CHAPTER 67 TABLE 1

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SPECIFIC MICROBIOLOGY

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VIRIDANS STREPTOCOCCI

cause 18% to 30% of NVE cases unrelated to drug abuse and health care.

Normal inhabitants of oropharynx.

Alpha-

hemolytic

Nontypable

by

lancefield

classification

Streptococcus

mitior, 31% of cases; Streptococcus sanguis, 24%; Streptococcus

bovis

,

27%;

Streptococcus

mutans

,

7%; Streptococcus milleri 4%; Streptococcus faecalis (now Enterococcus faecalis), 7%; and Streptococcus salivarius and other species, 2%highly susceptible to penicillin and synergistic action of penicillin+gentamicin

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STREPTOCOCCUS BOVIS

Streptococcus

gallolyticus

(formerly

S.

bovis

), part of the gastrointestinal tract normal flora, causes 20% to 40% of the episodes of streptococcal NVE.

S.

gallolyticus

is highly penicillin susceptible.

S. gallolyticus type I endocarditis is frequently associated with coexistent polyps or malignant disease in the colon; accordingly, colonoscopy is warranted in these patients.

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STREPTOCOCCUS PNEUMONIA

accounts for only 1% to 3% of NVE cases.

Pneumococcal IE frequently involves a normal aortic valve and progresses rapidly with valve destruction, myocardial abscess formation, and acute CHF.

The clinical presentation, complications, and outcome of endocarditis caused by penicillin-susceptible and penicillin-resistant

S.

pneumoniae

are similar. Many require surgery.

Mortality (35%) is related to left-sided heart failure.

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ENTEROCOCCI

E.

faecalis

and

Enterococcus

faecium

cause 85% and 10% of cases of

enterococcal

IE, respectively.

part of the normal gastrointestinal flora.

Enterococci infect abnormal valves and prosthetic valves. IE may be acute or subacute. Bactericidal antienterococcal activity can be achieved by combining an inhibitory cell wall–active agent and streptomycin or gentamicin.

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STAPHYLOCOCCI AUREUS

S.

aureus

is the most common cause of IE noted in large international series from tertiary care

centers

.

In general, 25% to 30% of isolates are methicillin resistant; however, among nosocomial and health care–associated cases, rates of methicillin resistance are 57% and 40%, respectively.

S.

aureus

IE is characterized by a highly toxic febrile illness, frequent focal metastatic infection, 30% to 50% rate of CHF, and central nervous system complications.

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COAGULASE- NEGATIVE STAPHYLOCOCCI

S.

epidermidis

,

are a major cause of PVE, an important cause of nosocomial IE, and the cause of 8% to 10% of NVE, usually in the setting of prior valve abnormalities .

Non-

epidermidis

species cause NVE that is not associated with health care. Coagulase-negative staphylococcal NVE is often complicated and fatal.

Staphylococcus

lugdunensis

, a community-acquired, antibiotic-susceptible coagulase-negative species, causes valve damage and frequently requires surgical intervention.

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GRAM NEGATIVE BACTERIA

The HACEK organisms

Haemophilus

parainfluenzae

,

Aggregatibacter

[previously

Haemophilus

]

aphrophilus, Aggregatibacter [previously Actinobacillus] Actinomycetemcomitans

Cardiobacterium

hominis

Eikenella

corrodens, and Kingella kingae,Part of the upper respiratory tract and oropharyngeal flora, infect abnormal cardiac valves, causing subacute NVE and PVE that occurs a year or more after valve surgery. Although fastidious and slow growing, HACEK organisms are usually detected in blood cultures within 5 days of incubation; more prolonged incubation is occasionally required. HACEK NVE has been associated with large vegetations and a high incidence of systemic emboli.

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OTHERS

Corynebacterium

species, called

diphtheroids

, although often contaminants in blood cultures, cannot be ignored when they are isolated from multiple blood cultures. They are an important cause of PVE and cause endocarditis involving abnormal valves.

Listeria

monocytogenes

occasionally infects abnormal left-sided heart valves and prosthetic devices.

Tropheryma

whipplei, the cause of Whipple disease, causes a cryptic afebrile form of IE with associated arthralgias but without diarrhea

as well as

valvular

disease as part of typical Whipple disease. The diagnosis has been established by identification of the organism on excised valves by periodic acid–Schiff stain or by polymerase chain reaction (PCR). IE caused by

T.

whipplei

often does not

fulfill the Duke criteria for diagnosis ,thus detection requires a high index of suspicion.Bordetella and brucella cause chronic slow growing vegetation.

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DIAGNOSIS

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DUKE CRITERIA

Definite endocarditis is defined by documentation of two major criteria, of one major criterion and three minor criteria, or of five minor criteria

MAJOR CRITERIA

POSITIVE BLOOD CULTURE

Typical microorganism for infective endocarditis from two separate blood cultures

Viridans

streptococci,

Streptococcus

gallolyticus

, HACEK group,

Staphylococcus

aureus

Community-acquired enterococci in the absence of a primary focus

 Persistently positive blood culture, defined as recovery of a microorganism consistent with infective endocarditis

EVIDENCE OF ENDOCARDIAL INVOLVEMENT

 Positive echocardiogram

Oscillating intracardiac mass on valve or supporting structures or in the path of regurgitant jets or in implanted materialAbscesses New partial dehiscence of prosthetic valve New valvular regurgitationMINOR CRITERIAPredisposition: predisposing heart condition or injection drug useFever 38.0°C (100.4°F)Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions.Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth's spots, rheumatoid factor.Microbiologic evidence: positive blood culture but not meeting major criterion as noted previously or serologic evidence of active infection with organism consistent with infective endocarditis

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BLOOD CULTURES

Isolation of the causative microorganism from blood cultures is critical for diagnosis, determination of antimicrobial susceptibility, and planning of treatment.

In the absence of prior antibiotic therapy, three 2-bottle blood culture sets, separated from one another by at least 1 h, should be obtained from different

venipuncture

sites over 24 h.

If the cultures remain negative after 48–72 h, two or three additional blood culture sets should be obtained, and the laboratory should be consulted for advice regarding optimal culture techniques.

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NON BLOOD CULTURE TESTS

Serologic tests can be used to implicate causally some organisms that are difficult to recover by blood culture:

Brucella

,

Bartonella

,

Legionella

,

Chlamydophila

psittaci, and C. burnetii. Pathogens can also be identified in vegetations by culture, microscopicexamination

with special stains (i.e., the periodic acid–Schiff stain for

T.

whipplei

), or direct fluorescence antibody techniques and by the use of polymerase chain reaction (PCR) to recover unique microbial DNA or 16S

rRNA

that, when sequenced, allows identification of organisms.

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ECHOCARDIOGRAPHY

A

llows anatomic confirmation of infective endocarditis, sizing of

vegetations

, detection of

intracardiac

complications, and assessment of cardiac function

.Transthoracic echocardiography (TTE) is

noninvasive

and exceptionally specific; however, it cannot image

vegetations <2 mm in diameter, TTE detects vegetations in only 65% of patients . TTE is not adequate for evaluating prosthetic valves or detecting intracardiac

complications.

TEE is safe and detects

vegetations

in >90% of patients with definite endocarditis; nevertheless, initial studies may be false-negative in 6–18% of endocarditis patients.

When endocarditis is likely, a negative TEE result does not exclude the diagnosis but rather warrants repetition of the study in 7–10 days.

TEE is the optimal method for the diagnosis of PVE or the detection of myocardial abscess, valve perforation, or

intracardiac fistulae.

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CLINICAL FEATURES

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CLINICAL FEATURES

SYMPTOMS(PERCENTAGE)

FEVER (80-85)

CHILLS(42-75)

SWEATS(25)

ANOREXIA(25-55)

WEIGHT LOSS(25-55)

MALAISE(25-40)

DYSPNEA(20-40)

COUGH(25)

STROKE(13-20)HEADACHE(15-30)NONSPECIFIC(35-45)SIGNS(PERCENTAGE)

FEVER(80-96)

MURMUR(80-85)

CHANGING OR NEW MURMUR(10-40)

NEUROLOGICAL ABNORMALTIES(30-40)

EMBOLIC EVENT(20-40)

SPLENOMEGALY(15-50)

CLUBBING(10-20)PERIPHERAL MANIFESTATIONOSLER NODES(7-10)SPLINTER HEMORRHAGES(5-15)PETECHIAE(10-40)JANEWAY LESION(6-10)ROTH SPOTS(4-10)

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FEVER

Fever is almost universal.

It may be absent or minimal in those with CHF, severe debility, or chronic renal failure.

OCCURS IN 80-85% CASES

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MURMURS

Emblematic of the lesion predisposing to IE.

Murmurs are commonly not audible in patients with tricuspid valve IE.

The new or changing

regurgitant

murmurs indicative of valve damage are relatively infrequent in

subacute

NVE and are more prevalent in acute IE and PVE (e.g., that due to

S.

aureus

). They are frequently harbingers of CHF

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PETECHIAE

The classic peripheral manifestations of IE are encountered infrequently today and are virtually absent in IE restricted to the tricuspid valve.

Petechiae

, the most common of these manifestations, are found on the palpebral conjunctiva, the

buccal

and palatal mucosa, and the extremities.

  

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SPLINTER HEMORRHAGES

Splinter or

subungual

hemorrhages

are dark red, linear, or occasionally flame-shaped streaks in the proximal

nailbed

.

Distal lesions at the nail tip are probably caused by trauma.

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OSLER NODES

Osler nodes are small, tender subcutaneous nodules in the pulp of the digits, or occasionally more proximal, that persist for hours to several days.

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JANEWAY LESIONS

Janeway

lesions are small erythematous or

hemorrhagic

macular

nontender

lesions on the palms and soles and are the consequence of septic embolic events.

Embolic infarcts in the digits are common in left-sided

S.

aureus

IE.

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ROTH SPOTS

Roth spots, oval retinal

hemorrhages

with pale

centers

, are infrequent findings in IE.

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TREATMENT

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PRINCIPLES

Always go for parenteral antibiotics

Use bactericidal drugs

Combination therapy is must

Duration usually for 4-6 weeks

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STREPTOCOCCI

(PENICILLIN SUSCEPTIBLE)

REGIMENS

Penicillin G (2–3

mU

IV q4h for 4 weeks)

 Ceftriaxone (2 g/d IV as a single dose for 4 weeks)

 

Vancomycin

c

(15 mg/kg IV q12h for 4 weeks)Penicillin G (2–3 mU IV q4h) or ceftriaxone (2 g IV qd) for 2 weeks

plus

 

Gentamicin

d

(3 mg/kg

qd

IV or IM, as a single dosee or divided into equal doses q8h for 2 weeks)NOTESCan use ceftriaxone in patients with nonimmediate penicillin allergyUse vancomycin in patients with severe or immediate -lactam allergyAvoid 2-week regimen when risk of aminoglycoside toxicity is increased and in prosthetic valve or complicated endocarditis

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STREPTOCOCCI

(RELATIVELY PENICILLIN RESISTANT)

REGIMENS

Penicillin G (4

mU

IV q4h) or ceftriaxone (2 g IV

qd

) for 4 weeks

plus

 

Gentamicind (3 mg/kg qd IV or IM, as a single dosee or divided into equal doses q8h for 2 weeks)

 

Vancomycin

c

as noted above for 4 weeks

NOTES

Penicillin alone at this dose for 6 weeks or with gentamicin during initial 2 weeks preferred for prosthetic valve endocarditis caused by streptococci with penicillin MICs of 0.1 g/mL

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STREPTOCOCCI

(MODERATELY PENICILLIN RESISTANT)

REGIMENS

Penicillin G (4–5

mU

IV q4h) or ceftriaxone (2 g IV

qd

) for 6 weeks

plus

Gentamicin

d (3 mg/kg qd IV or IM as a single dosee or divided into equal doses q8h for 6 weeks)

 

Vancomycin

c

as noted above for 4 weeks

NOTES

Preferred for prosthetic valve endocarditis caused by streptococci with penicillin MICs of >0.1 g/mL

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ENTEROCOCCI

REGIMENS

Penicillin G (4–5

mU

IV q4h)

plus

Gentamicin

d

(1 mg/kg IV q8h), both for 4–6 weeks

 Ampicillin (2 g IV q4h)

plus Gentamicind (1 mg/kg IV q8h), both for 4–6 weeks 

Vancomycin

c

(15 mg/kg IV q12h)

plus

Gentamicin

d

(1 mg/kg IV q8h), both for 4–6 weeksNOTESCan use streptomycin (7.5 mg/kg q12h) in lieu of gentamicin if there is not high-level resistance to streptomycinUse vancomycin plus gentamicin for penicillin-allergic patients, or desensitize to penicillin

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STAPHYLOCOCCI

(METHICILLIN SUSCEPTIBLE)

REGIMENS

 

Nafcillin

or

oxacillin

(2 g IV q4h for 4–6 weeks)

 

Cefazolin

(2 g IV q8h for 4–6 weeks) Vancomycinc (15 mg/kg IV q12h for 4–6 weeks)

NOTES

Can use penicillin (4

mU

q4h) if isolate is penicillin-susceptible (does not produce -lactamase)

Can use

cefazolin

regimen for patients with nonimmediate penicillin allergyUse vancomycin for patients with immediate (urticarial) or severe penicillin allergy

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STAPHYLOCOCCI

(METHICILLIN RESISTANT)

REGIMENS

 

Vancomycin

c

(15 mg/kg IV q8–12h for 4–6 weeks) - NATIVE VALVES

 

Vancomycin

c

(15 mg/kg IV q12h for 6–8 weeks) plus Gentamicind (1 mg/kg IM or IV q8h for 2 weeks) plus 

Rifampin

i

(300 mg PO q8h for 6–8 weeks)-PROSTHETIC VALVES

NOTES

No role for routine use of

rifampin

for native valve infection.

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HACEK ORGANISMS

REGIMENS

 Ceftriaxone (2 g/d IV as a single dose for 4 weeks)

 Ampicillin/

sulbactam

(3 g IV q6h for 4 weeks)

NOTES

Can use another third-generation cephalosporin at comparable dosage

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ROLE OF SURGERY

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SURGICAL INDICATIONS

OPTIMAL OUTCOME

  Moderate to severe congestive heart failure due to valve dysfunction

  Partially dehisced unstable prosthetic valve

  Persistent bacteremia despite optimal antimicrobial therapy

  Lack of effective

microbicidal

therapy (e.g., fungal or

Brucella

 endocarditis)

  S. aureus prosthetic valve endocarditis with an

intracardiac

complication

  Relapse of prosthetic valve endocarditis after optimal antimicrobial therapy

IMPROVED OUTCOME

  

Perivalvular

extension of infection  Poorly responsive S. aureus endocarditis involving the aortic or mitral valve  Large (>10-mm diameter) hypermobile vegetations with increased risk of embolism  Persistent unexplained fever (10 days) in culture-negative native valve endocarditis  Poorly responsive or relapsed endocarditis due to highly antibiotic-resistant enterococci or gram-negative bacilli

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ANTIBIOTIC PROPHYLAXIS

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Regimens for Prophylaxis of Endocarditis in Adults with High-Risk Cardiac Lesion

STANDARD ORAL REGIMEN

- Amoxicillin: 2 g PO 1 h before procedure.

INABILITY TO TAKE ORAL MEDICATION

- Ampicillin: 2 g IV or IM within 1 h before procedure.

PENICILLIN ALLERGY

-

Clarithromycin or azithromycin: 500 mg PO 1 h before procedure

Cephalexin

c

: 2 g PO 1 h before procedureClindamycin: 600 mg PO 1 h before procedurePENICILLIN ALLERGY, INABILITY TO TAKE ORAL MEDICATION

-

Cefazolin

c

or

ceftriaxone

c

: 1 g IV or IM 30 min before procedureClindamycin: 600 mg IV or IM 1 h before procedure3A- AMPICILLIN/AMOXYCILLIN/AZITHROMYCIN3C-CLARITHROMYCIN/CEPHALOSPORIN/CLINDAMYCIN

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THANK YOU

V