al-anoud al-jifri consultant internal medicine,id nfective endocarditis infective endocarditis

AL-ANOUD AL-JIFRI

Consultant internal medicine ,ID

Infective nfective EndocarditisEndocarditis

Infective Endocarditis:Infective Endocarditis:DefinitionDefinition

A microbial infection of a cardiac valve or the endocardium caused by bacteria, fungi, or chlamydia.

Often categorized as acute or subacute based on the

rapidity of the clinical course Alternatively described by type of risk factor e.g.,

nosocomial, prosthetic valve, intravenous drug use - associated

Pathological findings include the presence of friable valvular vegetations containing bacteria, fibrin and inflammatory cells.

There is often valvular destruction with extension to adjacent structures. Embolic lesions may demonstrate similar findings.

Epidemiology of EndocarditisEpidemiology of Endocarditis

Incidence the same or slightly increased –1.7-6.2/100,000 depending on the population

The age of subjects with endocarditis has increased over the past 60 years (30-40 to 47-69).

Among injecting drug users the incidence is as high as 150 2000/100,000 person years.

There has been a major shift in nature of underlying valvular disorders.

There has also been a change in the microbiology of cases Increasing incidence of staphylococci.

There has been an increasing incidence of nosocomial endocarditis - both native and prosthetic valve.

There is an increased risk of IE among injecting drug users, patients on long-term hemodialysis, patients with intravenous catheters, diabetics and HIV-infected patients.

Risk Factors for Infective EndocarditisRisk Factors for Infective Endocarditis

Dental procedures, poor dental hygiene viridans streptococci, nutritionally variant

streptococci, HACEK Prosthetic valves

Early: coagulase negative staphylococci, S. aureus

Late: coagulase negative staphylococci, viridans streptococci

Gastrointestinal or genitourinary procedures enterococci or S. bovis (colon carcinoma)

Nosocomial S. aureus (including MRSA), Gram negatives ,

Candida speciesBrouqui and Raoult, Clin Microbiol Rev, 2001

Risk Factors for Infective EndocarditisRisk Factors for Infective Endocarditis

HIV S. aureus,MRSA.

Animal or farm exposure Coxiella , Chlamydia ,Brucella.

History of homelessness, alcoholism (body lice) Bartonella

Pathogenesis of IEPathogenesis of IE

The development of IE is the net result of the complex interaction between the bloodstream pathogen with matrix

molecules and platelets at sites of endocardial cell damage.

In addition, many of the clinical manifestations of IE origenate

from the host’s immune response to the infecting microorganism.

The following sequence of events is thought to result in IE: 1. formation of nonbacterial thrombotic endocarditis (NBTE) on

the surface of a cardiac valve or elsewhere that endothelial damage occurs

2. bacteremia 3. adherence of the bacteria in the bloodstream to NBTE4. proliferation of bacteria within a vegetation.

Dissemination of infection to other tissue sites and elicitation of systemic findings.

Pathogenesis of IEPathogenesis of IE Valvular endothelium

Congenital abnormalities,

turbulent blood flow

Trauma - damage at

tissue surface

Nonbacterial thrombus,

Native valves Transient bacteremia

Mucous membranes - otherperipheral tissue

Adherence and colonizationPlatelet adherence, fibrindeposition - vegetation

formationElaboration of bacterial

enzymes, proteases

HISTORYHISTORY

history of prior cardiac lesions/or rheumatic heart disease.

historical clues pointing toward a recent source of bacteremia: indwelling intravascular catheters intravenous drug use.

Epidemiological FeatureCommon Microorganism(s)

Injection drug useS aureus, including community-acquiredoxacillin-resistant strainsCoagulase-negative staphylococci-Hemolytic streptococciFungiAerobic Gram-negative bacilli, includingPseudomonas aeruginosaPolymicrobial

Indwelling cardiovascular medical devices

S aureusCoagulase-negative staphylococciFungiAerobic Gram-negative bacilliCorynebacterium sp

Genitourinary disorders, infection, manipulation, including pregnancy,delivery, and abortion

Enterococcus spGroup B streptococci (S agalactiae)Listeria monocytogenesAerobic Gram-negative bacilliNeisseria gonorrhoeae

Epidemiological Clues in Etiological Diagnosis ofCulture-Negative Endocarditis


Burn patientsS aureusAerobic Gram-negative bacilli, including PaeruginosaFungi

Chronic skin disorders, includingrecurrent infections

S aureus-Hemolytic streptococci

Poor dental health, dental procedure

Viridans group streptococci“Nutritionally variant streptococci”Abiotrophia defectivaGranulicatella spGemella spHACEK organisms

Alcoholism, cirrhosisBartonella spAeromonas spListeria spS pneumoniae-Hemolytic streptococci


Diabetes mellitusS aureus-Hemolytic streptococciS pneumoniae

Early (1 y) prosthetic valve placement

Coagulase-negative staphylococciS aureusAerobic Gram-negative bacilliFungiCorynebacterium spLegionella sp

Late (1 y) prosthetic valve placement

Coagulase-negative staphylococciS aureusViridans group streptococciEnterococcus speciesFungiCorynebacterium sp


AIDSSalmonella spS pneumoniaeS aureus

Dog–cat exposureBartonella spPasteurella spCapnocytophaga sp

Contact with contaminated milk orinfected farm animals

Brucella spCoxiella burnetiiErysipelothrix sp

Homeless, body liceBartonella sp

Pneumonia, meningitisS pneumoniae

Solid organ transplantS aureusAspergillus fumigatusEnterococcus spCandida sp

Gastrointestinal lesionsS bovisEnterococcus spClostridium septicum

PHYSICAL EXAMINATIONPHYSICAL EXAMINATION

cardiac examination for signs of new regurgitant murmurs or

heart failure. stigmata of endocarditis evidence of small and large

emboli with special attention to the fundi, conjunctivae, skin, and digits.

Associated peripheral cutaneous or mucocutaneous lesions of IE petechiae, splinter hemorrhages, Janeway lesions, Osler's nodes, and Roth spots.

involvement of other organs due to embolic events (eg, focal neurologic deficits, renal and

splenic infarcts) or a neurologic evaluation evidence of focal neurologic

impairment. a systemic immune reaction (eg, glomerulonephritis, arthritis). In right-sided endocarditis, septic pulmonary infarcts may be

seen.

Chest radiograph of a patient with tricuspid valve endocarditis due to S. aureus

Splinter hemorrhages in infective endocarditis

Roth spots

Osler's nodes

painful, violaceous nodules found in the pulp of fingers and toes and are seen more often in subacute than

acute cases of IE

Janeway lesions

macular, blanching, nonpainful, erythematous lesions on the palms

and soles

Modified Duke criteria for diagnosis of infective Modified Duke criteria for diagnosis of infective endocarditisendocarditis

Definite IEDefinite IEPathologic criteria Microorganism: demonstrated by culture or histology

in a vegetation, or in a vegetation that has embolized, or in an intracardiac abscess OR

Pathologic lesions: vegetation or intracardiac abscess, confirmed by histology showing active endocarditis.

Clinical criteria 2 major criteria OR 1 major and 3 minor criteria OR 5 minor criteria

Modified Duke criteria for diagnosis of infective Modified Duke criteria for diagnosis of infective

endocarditisendocarditis

Possible IE Possible IE 1 major criterion and 1 minor criterion OR 3 minor criteria Rejected IE Rejected IE Firm alternate diagnosis for manifestations of

endocarditis OR Resolution of manifestations of endocarditis, with

antibiotic therapy for four days or less OR No pathologic evidence of infective endocarditis at

surgery or autopsy after antibiotic therapy for four days or less

Does not meet criteria for possible infective endocarditis, as above


Major criteria

Positive blood cultures for IE Typical microorganism for infective endocarditis from two

separate blood cultures Viridans streptococci Streptococcus bovis, including nutritional variant strains HACEK group - Haemophilus spp,. Actinobacillus actinomycete

comitants, Cardiobacterium hominis, Eikenella spp, and Kingella kingae.

Staphylococcus aureus Community-acquired enterococci, in the absence of a primary

focus; OR Persistently positive blood culture, defined as recovery of a

microorganism consistent with IE from: Blood cultures drawn more than 12 hours apart OR All of three or a majority of four or more separate blood

cultures, with first and last drawn at least one hour apart Single positive blood culture for Coxiella burnetii or

antiphase I IgG antibody titer >1:800*

Modified Duke criteria for diagnosis of infective Modified Duke criteria for diagnosis of infective

endocarditisendocarditis

Evidence of endocardial involvement Evidence of endocardial involvement Positive echocardiogram for IE TEE recommended in patients with prosthetic valves,

rated at least "possible IE" by clinical criteria, or complicated IE [paravalvular abscess]; TTE as first test in other patients.

Definition of positive echocardiogram Oscillating intracardiac mass, on valve or supporting

structures, or in the path of regurgitant jets, or on implanted material, in the absence of an alternative anatomic explanation OR

Abscess OR New partial dehiscence of prosthetic valve

New valvular regurgitation Increase in or change in preexisting murmur


Minor criteria Predisposition - predisposing heart condition or

intravenous drug use Fever - 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 spots, rheumatoid factor.

Microbiologic evidence - positive blood culture but not meeting major criterion as noted previously (excluding single positive cultures for coagulase-negative straphylococci and organisms that do not cause endocarditis) OR serologic evidence of active infection with organism consistent with IE.

Complications of IEComplications of IE

can be broadly categorized as:can be broadly categorized as: Cardiac Septic Embolic Neurologic Musculoskeletal Renal Associated with medical treatment

complications in terms of their pathogenesis, which leads complications in terms of their pathogenesis, which leads to different groupingsto different groupings: Embolic (eg, cerebral infarct) Local spread of infection (eg, heart valve destruction) Metastatic infection (eg, vertebral osteomyelitis) Immune-mediated damage (eg, glomerulonephritis)


CARDIAC COMPLICATIONS Heart failure Perivalvular abscesses extravalvular complications

Pericarditis, which may be suppurative or nonsuppurative, can rarely cause pain or even cardiac tamponade

Fistulous intracardiac connections (eg, aorta-atrial or aorta-ventricular) due to extension of infection from the valve to adjacent myocardium may rarely result in large aneurysms, a pseudoaneurysm if the aortic wall is involved , or even myocardial perforation.


EMBOLIZATION Emboli consisting of vegetation fragments can occlude or

damage virtually any blood vessel, large or small, in the systemic or pulmonary arterial circulation.

As a result, emboli can produce: Stroke Blindness Painful ischemic or frankly gangrenous extremities Unusual pain syndromes (eg, due to splenic or renal

infarction). Hypoxia (due to pulmonary emboli in right-sided

endocarditis). Paralysis (due to embolic infarction of either the brain or

spinal cord).


NEUROLOGIC COMPLICATIONS Embolic stroke Acute encephalopathy Meningoencephalitis Purulent or aseptic meningitis Cerebral hemorrhage (due to stroke or a

ruptured mycotic aneurysm) Brain abscess or cerebritis Seizures (secondary to abscess or embolic

infarction)


RENAL DISEASE Renal infarction (due to emboli). Drug-induced acute interstitial nephritis. Glomerulonephritis (due to deposition of

immunoglobulins and complement in the glomerular membrane).

Rarely , renal abscess can occur in patients with IE.


METASTATIC ABSCESSES Rarely, metastatic abscesses develop in the

kidneys, spleen, brain or soft tissues (eg, the psoas muscle) in the setting of IE.

MUSCULOSKELETAL COMPLICATIONS Vertebral osteomyelitis is a well known but

relatively rare complication of IE. Osteomyelitis more frequently complicates S.

aureus endocarditis than IE due to other microorganis


Acute septic arthritis, involving one or more joints, may be the first clue to the presence of IE in a small percentage of patients.

IE should be strongly considered in selected cases of septic arthritis:

When infections spontaneously arise in joints of the axial skeleton (eg, sacroiliac, pubic, or manubriosternal joints).

When organisms with a known propensity to cause IE (eg, S. aureus, viridans streptococci or non-group A beta-hemolytic streptococci) grow from a joint aspirate, particularly in patients without a history of recent surgery, joint infection, or trauma.

When multiple joints are infected.

COMPLICATIONS OF MEDICAL OR SURGICAL COMPLICATIONS OF MEDICAL OR SURGICAL

THERAPYTHERAPY Associated with prolonged parenteral antimicrobial therapy

or surgery Aminoglycoside-induced ototoxicity or nephrotoxicity Secondary bacteremia due to central vascular lines Mediastinitis or early postoperative prosthetic valve

endocarditis Intravenous catheter-associated phlebitis Drug fever Allergic or idiosyncratic reactions to various antimicrobial

agents Bleeding due to disturbances in coagulation caused by

anticoagulants (in prosthetic valve endocarditis)

Principles of TherapyPrinciples of Therapy

Bactericidal antibiotics must be used. Prolonged therapy is necessary (6 weeks). Treatment is best started after multiple

sets of blood cultures have been taken. Urgency in the initiation of therapy is

required for acute but not subacute endocarditis.

Synergistic combinations of antibiotics are used when available.

Echocardiographic Features That Suggest Potential Need for Surgical Intervention

VegetationVegetation Persistent vegetation after systemic embolization. Anterior mitral leaflet vegetation, particularly with size 10 mm. 1 embolic events during first 2 wk of antimicrobial therapy. Increase in vegetation size despite appropriate antimicrobial

therapy.Valvular dysfunctionValvular dysfunction Acute aortic or mitral insufficiency with signs of ventricular failure. Heart failure unresponsive to medical therapy. Valve perforation or rupture.Perivalvular extensionPerivalvular extension Valvular dehiscence, rupture, or fistula. New heart block. Large abscess or extension of abscess despite appropriate

antimicrobial therapy.

Predictors of deathPredictors of death

Several studies have attempted to identify predictors of death in patients with IE.

Each patient may have one or more of the following: Infection with S. aureus , while mortality is lower with

streptococcal infection. Heart failure. Diabetes mellitus. Embolic events . Perivalvular abscess . Larger vegetation size. Female gender. Contraindication to surgery. Low serum albumin. Persistent bacteremia. Abnormal mental status. Poor surgical candidacy.

Mimics of Infective EndocarditisMimics of Infective Endocarditis

Atrial myxoma. Marantic endocarditis. Left atrial thrombus. Acute rheumatic fever with carditis. Collagen vascular disease (SLE). Neoplasms (carcinoid).

Antimicrobial Prophylaxis of EndocarditisAntimicrobial Prophylaxis of Endocarditis

Potential MechanismsPotential Mechanisms Bactericidal activity. Reduce bacterial adherence. Reduce bacterial density in the wound at

the time of surgery (for prosthetic valves).

Prevention of Infective EndocarditisPrevention of Infective Endocarditis

High risk– Prosthetic valve– Complex congenital heart disease– Previous endocarditis

Moderate risk– Acquired valvular dysfunction (e.g. rheumatic

valve)– Mitral valve prolapse with regurgitation

Negligible risk– Mitral valve prolapse without regurgitation– Rheumatic fever without valvular dysfunction

Cardiac Conditions Associated With the Highest Riskof Adverse Outcome From Endocarditis for Which ProphylaxisWith Dental Procedures Is Reasonable

Prosthetic cardiac valve or prosthetic material used for cardiac valve repair.

Previous IE. Congenital heart disease (CHD)

Unrepaired cyanotic CHD, including palliative shunts and conduits.

Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure.

Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization).

Cardiac transplantation recipients who develop cardiac valvulopathy.

Dental Procedures for Which EndocarditisDental Procedures for Which EndocarditisProphylaxis Is ReasonableProphylaxis Is Reasonable

All dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa.

The following procedures and events do not need prophylaxis:

routine anesthetic. injections through noninfected tissue. taking dental radiographs . placement of removable prosthodontic or orthodontic

appliances. adjustment of orthodontic appliances. Placement of orthodontic brackets . shedding of deciduous teeth. bleeding from trauma to the lips or oral mucosa.

ENDOCARDITIS PROPHYLAXIS FOR DENTAL ENDOCARDITIS PROPHYLAXIS FOR DENTAL PROCEDURESPROCEDURES

ORALAdult Dosage (30-60 minutesbefore procedure)

Pediatric Dosage(30-60 minutesbefore procedure)

Amoxicillin2 g P.O.50 mg/kg

Penicillin allergy:Cephalexin(Keflex, and others)

2 g P.O.50 mg/kg

OR Clindamycin600 mg P.O.20 mg/kg

OR Azithromycin (Zithromax, and others)or Clarithromycin(Biaxin, and others)

500 mg P.O.15 mg/kg

PARENTERAL (FOR PATIENTS UNABLE TO PARENTERAL (FOR PATIENTS UNABLE TO TAKE ORAL DRUGS)TAKE ORAL DRUGS)

Adult Dosage(30-60 minutes before procedure

Pediatric Dosage(30-60 minutesbefore procedure)

Ampicillin2 g IM or IV50 mg/kg IM or IV

OR Cefazolin or Ceftriaxone

1 g IM or IV 50 mg/kg IM orIV

Penicillin allergy:Cefazolin or Ceftriaxone

1 g IM or IV 50 mg/kg IM or IV

OR Clindamycin600 mg IM or IV 20 mg/kg IV

al-anoud al-jifri consultant internal medicine,id nfective endocarditis infective endocarditis

Documents

cardiac valve

risk factors

increased risk

bacteremia adherence

valvular destruction

nbteproliferation of

injecting drug users

similar findings