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A lecture on common problem infective endocarditis prepared by IslamGhanem Ahmed Ghanem assistant lecturer of cardiology Zagazig university 2013
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Infective Endocarditis (IE): an infection of the heart’s endocardial surface
The valves involved› Mitral 28-45%› Aortic 5-36%› Both 0-35%
› Tricuspid 0-6%› Pulmonary <1%
Incidence - varies according to location Males > females May occur at any age and increasingly
common in elderly Mortality 20-30% Decline in incidence of rheumatic fever The commonest cause in adults is mitral
valve prolapse with regurgitation More prosthetic valves More nosocomial cases, injected drug
use More staphylococcal infection
Native IE: Streptococcus
viridnas Streptococcus bovis Staphylococcus
aureus Staphylococcus
epidermidis HACEK organisms
Prosthetic IE: Early (>1year) Staphylococcus
epidermidis Staphylococcus
aureus Streptococcus
viridnas Enerococci Late(<1year) As native IE
Haemophilus aphrophilus, H. paraphrophilus, parainfluenzae
Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingella kingae
High risk› MVP with regurgitaion› Prosthetic cardiac valve› Prior episodes of endocarditis› Degenerative valvular diseases› Complex congenital cardiac defect› Surgical systemic-pulmonary shunts
– Intravenous drug abuse – Intravascular catheters
Moderate risk› PDA, VSD, primum ASD› Co-Aorta› Bicuspid aortic valve› Hypertrophic cardiomyopathy
Low risk› Isolated secundum atrial septal defect› ASD, VSD, or PDA > 6 months past repair
Infective Endocarditis: a changing disease
new high-risk subgroups
IVDA elderly intracardiac devices nosocomial diseases
more difficult to prevent more difficult to treat
1. Endocardium is resistant to infection
2. Turbulent blood flow disrupts the endocardium making it “sticky”
3. Bacteremia delivers the organisms to the endocardial surface
4. Adherence of the organisms to the endocardial surface
5. Eventual invasion of the valvular leaflets
Alteration of the valvular endothelial surface leading to deposition of platelets and fibrin
Bacteremia with seeding of non-bacterial thrombotic vegetation (NBTE)
Adherence and growth, further platelet and fibrin deposition
Extension to adjacent structures› Papillary muscle, aortic valve ring
abscess, conduction system
Low pressure side of structural lesion› Atrial side of mitral valve (MR)› Ventricular side of aortic valve (AR, AS with R)› But, Non infective endocarditis vegetations occur
at atrial side of mitral valve, aortic side of aortic valve
› Congenital abnormality (MV prolapse, bicuspid AV)
› Scarring from rheumatic heart disease or sclerosis as a consequence of aging
› Prosthetic valves Other turbulence, high-velocity jets
› Ventricular septal defect› Stenotic valve
Direct mechanical damage from catheters, pacemaker leads
The clinical manifestation IE result from:
1. The local destructive effects of intracardial infection;
2. The embolization of septic fragments of vegetations to distant sites, resulting in infarction or infection;
3. The hematogenous seeding of remote sites during continuous bacteremia and
4. An antibody response to the infecting organism with subsequent tissue injury due to deposition of preformed immune complexes.
Vegetations on valve closure lines Destruction and perforation of valve
leaflet Rupture of chordae tendinae,
intraventricular septum, papillary muscles
Valve ring abscess Myocardial abscess Conduction abnormalities
Heart murmurs› It has been found that 15% don’t have
murmurs at initial diagnosis, however most develop a murmur during the course of the disease
› Changing murmurs – factors other than valvular integrity like change in cardiac output, temperature, hematocrit may play a role. However new onset regurgitant murmur in a setting of acute sepsis is virtually diagnostic.
MORPHOLOGY The hallmark of IE is presence of friable, bulky, potentially
destructive vegetations containing fibrin, inflammatory cells and bacteria or other organisms.
Aortic and mitral valve most common sites, valves of right heart may be involved particularly in intravenous drug abusers.
Vegetations sometimes erode into the underlying myocardium and produce an abscess (ring abscess).
Emboli may shed from the vegetation leading to abscesses formation at the site where emboli lodged, this may lead to sequelae such as septic infracts or mycotic aneurysms.
The vegetations of subacute endocarditis are associated with less valvular destruction than acute endocarditis.
Microscopically vegetations of typical subacute IE often have granulation tissue indicating healing at the bases.
With time fibrosis, calcification and a chronic inflammatory infiltrate can develop.
The aortic valve with a large, irregular, reddish tan vegetation
Here, infective endocarditis on the mitral valve has spread into the septum all the way to the tricuspid valve, producing a fistula.
Microscopically, the valve in infective endocarditis demonstrates friable vegetations of fibrin and platelets (pink) mixed with inflammatory cells and bacterial colonies (blue). The friability explains how portions of the vegetation can break off and embolize.
Here is a valve with infective endocarditis. The blue bacterial colonies on the lower left are extending into the pink connective tissue of the valve. Valves are relatively avascular, so high dose antibiotic therapy is needed to eradicate the infection.
Acute bacterial endocarditis caused by Staphylococcus aureus with perforation of the aortic valve and aortic valve vegetations.
Acute bacterial endocarditis caused by Staphylococcus aureus with aortic valve ring abscess extending into myocardium.
Bartonella henselae bacilli in cardiac valve of a patient with blood culture-negative endocarditis The bacilli appear as black granulations.
S. Aureus mitral valve vegetation, anterior leaflet
Systemic embolism is reported to occur in over 50% cases in autopsy studies.
Most common sites are brain, kidneys, skin, spleen, eye and CNS (coronary embolization is rare).
There is increasing evidence to show that embolic phenomena actually represent “immune complex” deposition in small systemic arteries.
Cutaneous manifestations› Petichiae (20-40%)› Subcunjunctival and subungual splinter hemorrhages
due to lipid microembolism.› Osler nodes
Tender, purplish erythematous papules in pulp of distal fingers
Due to hypersensitive angitis – cultures are negative› Janeway lesions
Erythematous, non-tender nodules on palms or soles.› Clubbing found only in 10-20%.
Ocular manifestations› Roth spot- flame shaped hemorrhage occasionally takes
the form of cotton wool spot(rounded red with pale center).
Janeway lesions
Splinter hemorrhages
Osler node
Petechial rash. He was diagnosed with right-sided staphylococcal endocarditis. Osler nodes
Osler's nodes on a finger and foot.
Janeway lesions are Flat, painless, erythematous lesions seen on the palm of this patient's hand. Frequently associated with bacterial endocarditis.
Seen here in the finger at the right are small splinter hemorrhages in a patient with infective endocarditis. These hemorrhages are subungual, linear, dark red streaks. Similar hemorrhages can also appear with trauma.
Roth spots: it has pale center and red periphery
Renal› Immune complex mediated
glomerulonephritis (improve with effective antibiotics)
› Focal glomerulonephritis and embolic renal infarct manifest with hematuria but rarely leading to renal failure
› Renal failure is mostly due to impaired hemodynamics, antibiotics toxicity
Splenic enlargement, infarction
Septic or bland pulmonary embolism
Neurological (mostly Staph.aureus)› Embolic stroke is the commonest (Antibiotic is the
anticoagulant in this case, Thrombolytics and anticoagulants are relatively contraindicated)
› Intracranial hemorrhage (rupture of mycotic aneurysm, septic arteritis, hemorrhage into an infarct)
Mycotic aneurysm: Focal dilatations of arteries occuring at points in the arterial wall that have been weakened by infection in the vasa vasorum or where septic emboli have lodged.
› Encephalopathy,cerebritis, brain abcesses, meninigitis
Acute› Affects normal
heart valves› Rapidly
destructive› Metastatic foci› Commonly Staph.› If not treated,
usually fatal within 6 weeks
Subacute› Often affects
damaged heart valves
› Indolent nature› If not treated,
usually fatal by one year
The terms acute and subacute are used to define duration of infection, however are older terms and should not be used
Symptoms› Fever, sweats, chills› Anorexia, malaise, weight loss
Signs› Anemia (normochromic, normocytic)› Splenomegaly› Microscopic hematuria, proteinuria› New or changing heart murmur, CHF› Embolic or immunologic dermatologic signs› Hypergammaglobulinemia, elevated ESR,
CRP, RF
SYMPTOM AND SIGNS
SBE: Initially, symptoms are vague: low-grade fever (< 39° C), night sweats, fatigability, malaise, and weight loss. Chills and arthralgias may occur. Symptoms and signs of valvular insufficiency may be a first clue. Initially, ≤ 15% of patients have fever or a murmur, but eventually almost all develop both. Physical examination may be normal or include pallor, fever, change in a preexisting murmur or development of a new regurgitant murmur, and tachycardia.
Retinal emboli can cause round or oval hemorrhagic retinal lesions with small white centers (Roth's spots).
Cutaneous manifestations include petechiae (on the upper trunk, conjunctivae, mucous membranes, and distal extremities), painful erythematous subcutaneous nodules on the tips of digits (Osler's nodes), nontender hemorrhagic macules on the palms or soles (Janeway lesions), and splinter hemorrhages under the nails.
About 35% of patients have CNS effects, including transient ischemic attacks, stroke, toxic encephalopathy, and, if a mycotic CNS aneurysm ruptures, brain abscess and subarachnoid hemorrhage.
Renal emboli may cause flank pain and, rarely, gross hematuria.
Splenic emboli may cause left upper quadrant pain. Prolonged infection may cause splenomegaly or clubbing of fingers and toes.
ABE and PVE: Symptoms and signs are similar to those of SBE, but the course is more rapid. Fever is almost always present initially, and patients appear toxic; sometimes septic shock develops. Heart murmur is present initially in about 50 to 80% and eventually in > 90%. Rarely, purulent meningitis occurs.
Right-sided endocarditis: Septic pulmonary emboli may cause cough, pleuritic chest pain, and sometimes hemoptysis. A murmur of tricuspid regurgitation is typical.
Congestive heart failure Extravalvular cardiac manifestations( myocarditis, conduction disturbances) Systemic and pulmonary embolism Mycotic aneurysm Neurologic – stroke, neuropsychiatric
syndromes Renal – glomerulonephritis, renal infarcts Hematological – anemia, TTP
Most patients with infective endocarditis should respond within 48 hours of initiation of appropriate antibiotic therapy.
If persistent fever consider: perivalvular extension of infection and possible
abscess formation. Extracardiac embolic complications Pulmonary embolism (secondary right-sided
endocarditis or prolonged hospitalization). Drug reaction (the fever should promptly resolve
after drug withdrawal) Nosocomial infection (i.e. venous access site,
urinary tract infection)
Echocardiography: esp transesophageal echocardiography.
Blood culture. Serology(Immunoglobulins and
compliment). ECG: Conduction abnormalities. CBC: Normocytic normochromic
anemia, leukocytosis. ESR. Urine exam: proteinurea and
microscopic hemeturia is common
Transthoracic› Relatively low sensitivity› Good specificity
Transesophageal› Detection of valve ring abscess (87% vs. 28%
sensitivity for TTE)› Detection of prosthetic valve IE especially in
mitral position› Detection of small vegetations (less than 2mm)› Echocardiography cannot distinguish• between infective and non infective
vegetations• Between vegetation, thrombus and pannus• Between active and healed endocarditis
Limited thoracic windows = TTE low sensitivity
Prosthetic valves Prior valvular abnormality S. aureus bacteremia and suspected
IE Bacteremia with organisms likely to
cause IE= high prior probability of IE
mitral valve vegetation
MULTIPLE BLOOD CULTURES BEFORE EMPIRIC THERAPY
If not critically ill› 3 blood cultures over 12-24 hour period› ? Delay therapy until diagnosis confirmed
If critically ill› 3 blood cultures over one hour
20 cm each sample from 3 different puncture sites
Not mandatory during the fever
Less common with improved blood culture methods
Causes: Prior antibiotic therapy(40%) Fastidious(slowly growing organisms):HACEK, Brucella, Bartonella, TropherymaWhipplei Non bacterial organisms: Marantic, fungal
endocarditis Special media required
› Brucella, Mycoplasma, Chlamydia, Histoplasma, Legionella, Bartonella
Longer incubation may be required› HACEK
Coxiella burnetii (Q Fever), Trophyrema whipplei will not grow in cell-free media(Serology)
Electrocardiogram› Conduction delays› Ischemia or infarction (coronary embolism)
Chest X-ray› Septic emboli in right-sided IE› Valve calcification (degenerative heart
disease)› CHF
PCR› Coxiella burnetii› Tropheryma whipplei› Bartonella henselae
Serology› Coxiella burnetii› Bartonella› Brucella› Legionella› Chlamydophila psittaci
1977 Pelletier and Petersdorf criteria 1981 von Reyn criteria 1994 Duke criteria 2000 Modified Duke criteria: It is of
limited value in PVE, CDRIE, BCNIE and should not replace the clinical judgment
Major criteria: A. Positive blood culture for Infective Endocarditis1- Typical microorganism consistent with IE from 2 separate blood
cultures, as noted below:viridans streptococci, Streptococcus bovis, or HACEK group, or
community-acquired Staphylococcus aureus or enterococci, in the absence of a primary focus
or2- Microorganisms consistent with IE from persistently positive
blood cultures defined as: 2 positive cultures of blood samples drawn >12 hours apart, or all of 3 or a majority of 4 separate cultures of blood (with first
and last sample drawn 1 hour apart)(Persistntly +ve blood cultures The best)
Single positive blood culture for Coxeilla burnetti or phase IgG antibody titer < 1 : 800
B. Evidence of endocardial involvement1- Positive echocardiogram for IE defined as : (vegetation) oscillating intracardiac mass on valve or
supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation, or
(abcess) , or new partial dehiscence of prosthetic valve2- New valvular regurgitation (New or changing of preexisting
murmur)
Minor criteria:
1- Predisposition: predisposing heart condition or intravenous drug use
2- Fever: temperature > 38.0° C (100.4° F)3- Vascular phenomena: major arterial emboli, septic
pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
4- Immunologic phenomena: glomerulonephritis, Osler's nodes, Roth spots, and rheumatoid factor
5- Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE
Diagnosis Definite: Pathological criteria: Microorganisms demonstrated by histological examination of a vegeation or
intracardiac abcess or peripheral embolus showing active endocarditis Clinical criteria : Definite:• Two major criteria, or• One major and three minor criteria, or• Five minor criteria Possible:• One major and one minor criteria, or• Three minor criteria Rejected:• Firm alternative diagnosis, or• Resolution of IE syndrome (fever) ≥ 4 days of antibiotics, or• No pathological evidence of IE at surgery or autopsy with antibiotic therapy
for ≥ 4 days
Noninfected (sterile) vegetation are caused by non bacterial thrombotic endocarditis
The endocarditis of SLE called Libman-sacks endocarditis.
NBTE is characterized by deposition of small sterile thrombi on the leaflet of cardiac valve
Grossly the lesions are 1mm-5mm in size occur singly on the line of closure of leaflets (at atrial side of mitral valve, aortic side of aortic valve).
Histologically :they composed of bland thrombi(Platelets+Fibrin, No bacteria or inflammatory cells) that are loosely attached.
They are source of systemic emboli that produce infarcts in brain,heart or elsewhere.
NBTE or marantic endocarditis also occur in debilitated patient.
NBTE occur in DVT, mucinous adenocarcinoma, is part of Trousseau syndrome of migratory thrombophelebitis.
Endocarditis of SLE ( Libman-Sacks Disease). Mitral and tricuspid valvulitis with small sterile vegetations.
Here is another marantic vegetation on the leftmost cusp. These vegetations are rarely over 0.5 cm in size. However, they are very prone to embolize.
The valve is seen on the left, and a bland vegetation is seen on the right. It appears pink because it is composed of fibrin and platelets. It displays about as much morphologic variation as a brown paper bag. Such bland vegetations are typical of the non-infective forms of endocarditis.
Libman-sacks endocarditis. Here are flat, pale tan, spreading vegetations over the mitral valve surface and even on the chordae tendineae.
Non infective Endocarditis (as in SLE, Antiphospholipid Syndrome)
Cardiac Neoplasms, Primary Vegetations from pannus, thrombus
Resolution of fever within 5-7 days Blood culture become sterile within 2 days
(Except in Staph. up to 9 days) Blood culture should be repeated daily
until sterile, rechecked if recrudescent fever , performed again 4-6 weeks after therapy to document cure
Blood tests to detect renal, hepatic, hematological toxicity should be done periodically (especially in 3rd w. of therapy)
Emergent: Within 24h. Urgent: Within few days. Elective: After 1-2w.of antibiotics. If there is indication for surgery& Cerebral hemorrhage: Postpone for 4w. Cerebral infarction: Postpone for 2w.
Use ampho B and flucytosine ( toxic to B. marrow and kidneys)
Almost always needs surgery . Long term oral prophylaxis is often
given to prevent relapse
513 patients with complicated IE , 230 (40%) surgical therapy513 patients with complicated IE , 230 (40%) surgical therapy 6 month mortality6 month mortality
Impact of surgery on mortalityImpact of surgery on mortality