i nfective endocarditis
DESCRIPTION
I nfective Endocarditis. AL-ANOUD AL-JIFRI Consultant internal medicine ,ID. Infective Endocarditis : Definition. 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 - PowerPoint PPT PresentationTRANSCRIPT
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
Epidemiological FeatureCommon Microorganism(s)
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
Epidemiological FeatureCommon Microorganism(s)
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
Epidemiological FeatureCommon Microorganism(s)
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
Modified Duke criteria for diagnosis of infective Modified Duke criteria for diagnosis of infective endocarditisendocarditis
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
Modified Duke criteria for diagnosis of infective Modified Duke criteria for diagnosis of infective endocarditisendocarditis
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)
Complications of IEComplications of IE
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.
Complications of IEComplications of IE
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).
Complications of IEComplications of IE
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)
Complications of IEComplications of IE
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.
Complications of IEComplications of 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
Complications of IEComplications of IE
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