Infective Endocarditis

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Transcript Infective Endocarditis

Infective Endocarditis
Dr. Hussein Amrat
Cardiologist PHH-MOH
Microbiology: Organisms
Responsible

Bacteria are the predominant cause
 Fungi
 Rickettsia
 Chlamydia
 Microorganisms vary dependent on risk
factors predisposing patient to IE
 Staph Aureus= single most common cause
Native Valve Endocarditis

Streptococcus responsible for more than
50% of cases
 Staphylococci
 Enterococci
 Infection occurs most frequently in those
with preexisting valvular abnormality
Staphylococci

Causes endocarditis in those with normal
and abnormal valves
 Most are coagulase positive S.Aureus
 Causes destruction of valves, multiple distal
abscesses, myocardial abscesses,
conduction defects, and pericarditis
Enterococci

Patients generally have underlying valvular
disease
 May occur following manipulation of
genitourinary or lower gastrointestinal tract
 Remainder of cases caused by Haemphilus
Actinobacillus, Cardiobacterium, Eikenella,
Kingella, Bartonella, or Coxiella Burnetti
Diagnosis

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
IDU associated IE

Skin flora and contaminated injection devices are
the most frequent sources involved in IDUassociated IE
 S. Aureus – Most common (50% of cases)
 Streptococcal species
 Gram negative Bacilli
– Pseudomonas
– Serratia species

Fungi
– Candida
Prosthetic Valve Endocarditis

Most commonly occur during the perioperative
period
 S. epidermidis
– Most frequently isolated organism

Early PVE (w/i 60 days of surgery)
– Assoc. with valve dysfunction and fulminant clinical
course

Late PVE (beyond 60 days postop)
– Disease course is less fulminant

Mycotic PVE (Aspergillus and Candida)
– Larger vegetations
Clinical Features

Acute IE – Rapid onset of high fevers and rigors
with hemodynamic deterioration and death within
days to weeks if not treated
– Assoc. with highly virulent organisms such as Staph
Aureus

Subacute IE – Indolent course with progressive
constitutional signs and symptoms and gradual
deterioration
– Assoc. with avirulent organisms such as viridans
streptococci
Clinical Features

Bacteremia can produce signs and symptoms that
are often nonspecific usually within 2 weeks of
infection
– Most common course of disease (fevers, chills, nausea,
vomiting, fatigue and malaise)
– Fever is the most common symptom
– Fever can be absent in pts with antibiotic use,
antipyretic use, severe CHF, or renal failure

Prosthetic valve patient with a fever requires IE
work up
Cardiac Clinical Features

Heart murmurs are present in up to 85% of cases
of IE.
– Most commonly regurgitant lesions secondary to
valvular destruction

Acute or progressive CHF is the leading cause of
death in patients with IE (70% of patients)
– Distortion or perforation of valvular leaflets
– Rupture of the chordae tendinae or papillary muscles
– Perforation of the cardiac chambers (rare)

Valvular abscesses and Pericarditis
 Heart blocks and Arrhythmias
Embolic Clinical Features

Extracardiac manifestations are the result of arterial
embolization of fragments of the friable vegetation
– CNS complications occur in 20-40% of cases (embolic
stroke with MCA affected most frequently)
– Retinal artery emboli may cause monocular blindness
– Mycotic aneurysm may cause a SAH
– IVDU can cause right sided lesions (tricuspid valve) –
Pulmonary complications
– Pulmonary complications ( pulmonary infarction,
pneumonia, empyema, or pleural effusion)
– Coronary artery emboli (Acute MI or myocarditis with
arrhythmias)
– Splenic infarction (LUQ abdominal pain)
– Renal emboli (flank pain or hematuria)
Clinical Features

Persistent bacteremia can stimulate the humoral and
cellular immune systems resulting in circulating immune
complexes
 Petechiae – Red, nonblanching lesions that become brown
after several days (20-40%)
– Conjunctivae, buccal mucosa, and extremities
 Splinter hemorrhages – Linear dark streaks under the
fingernails (15%)
 Osler’s nodes – Small tender subcutaneous nodules that
develop on the pads of the fingers or toes (25%)
 Janeway lesions – Small hemorrhagic painless plaques
located on the palms or soles
 Roth spots – Oval retinal hemorrhages with pale centers
Diagnosis

Diagnosis of IE requires hospitalization
– Cultures
– Echocardiogram
– Clinical observation

Duke Criteria – 90% sensitive
– Major Criteria
– Minor Criteria
Major Criteria

Positive blood culture for:
– Strep bovis, Strep viridans, or HACEK group
– Staph aureus or Enterococci
– Microorganisms c/w IE from persistent positive
blood cultures


2 positive blood cultures drawn >12 hrs apart
All of 3 or a majority of 4 or more positive blood
cultures
Major Criteria

Echocardiographic involvement:
– Mass on valve
– Abscess
– Dehiscence of prosthetic valve
– New valvular regurgitation
Minor Criteria

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Predisposition: Heart condition or injection drug
use
Fever > 38 degrees C
Vascular: Emboli, conjunctival hemorrhages,
janeway lesions
Immunological: Glomerulonephritis, osler’s
nodes, roth spots, and rheumatoid fever
Positive blood cultures
Echocardiographic findings c/w IE
Duke Criteria

Definite infective endocarditis
– Microorganisms demonstrated by culture or histologic
examination of vegetation or emboli
– Abscess with active endocarditis
– Two major criteria
– One major and three minor criteria
– Five minor criteria
 Possible endocarditis
– Findings c/w IE that fall short of definite, but not rejected
 Rejected
– Firm alternate diagnosis
– Resolution of manifestations of IE with abx for < 4 days
– No pathologic evidence of IE at surgery or autopsy after 4 days
of abx
DDx and Consideration of IE

IE should be considered in:
– All febrile IDUs
– Pts with a cardiac prosthesis and fever (or
malaise, vasculitis or new murmur)
– 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)
Evaluation of Bacteremia

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
Diagnostic Tests

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

Nonspecific lab tests
– Anemia (70-90% of cases)
– Elevated ESR (>90% of cases)
– Hematuria
Echocardiography



Mandatory in all pts with possible IE
Transthoracic Echo(TTE) should be done first.
– Specificity for vegetations is 98%
– Sensitivity varies but it is the highest with IDUs
because they more often have larger vegetations, right
sided valvular lesions and favorable precordial
windows.
Transesophageal Echo(TEE) has a higher sensitivity and
specificity than TTE
– Recommended for the following:

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Prosthetic valves
Pts with obesity, chest wall deformities, COPD
Intermediate or high probability of IE
Treatment

Initial Stabilization
– Rapid airway stabilization secondary to possible
respiratory or hemodynamic compromise( acidosis,
altered mental status, sepsis)
– Cardiac decompensation may occur secondary to left
sided valvular rupture
 Intraaortic balloon counterpulsation may be
indicated
– Neurologic complications such as stroke

Standard stroke protocol
Empiric Treatment

Therapy of suspected Bacterial Endocarditis
– Uncomplicated history

Ceftriaxone or nafcillin plus gentamycin
– IVDU, Congenital heart disease, MRSA, current abx
use

Nafcillin plus gentamycin plus vancomycin
– Prosthetic heart valve


Vancomycin plus gentamycin plus rifampin
Most patients will require 4 to 6 weeks of
antibiotic therapy
Surgical Treatment

Indications for surgical management:
– Severe valvular dysfunction: Acute CHF or
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–
–
–
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impaired hemodynamic status
Relapsing prosthetic valve endocarditis
Major embolic complications
Fungal endocarditis
New conduction defects or arrhythmias
Persistent bacteremia
Anticoagulation

Anticoagulation for native valve
endocarditis has not been shown to be
beneficial
– Increase the 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
IE Prophylaxis


Prophylaxis is indicated for:
– Prosthetic heart valves
– Congenital cardiac manifestations
– Acquired valvular dysfunction
– Hypertrophic cardiomyopathy
– Mitral valve prolapse with documented regurgitation
– History of endocarditis
Not indicated for the following:
– MVP without regurgitation
– Pacemakers
– Physiologic murmurs
– Prior CABG, angioplasty, ASD repair, VSD, or PDA
IE Prophylaxis

Dental, oral, respiratory or esophageal
procedures
– Amoxicillin or Ampicillin or Clindamycin

Genitourinary, gastrointestinal procedures
– Ampicillin plus Gentamycin plus Ampicillin
(post) or Amoxicillin
– Alternate regimen: Vancomycin plus
Gentamycin
Question 1:

T/F Streptococcus is responsible for more
than 50% of Native Valve Endocarditis.
Question 2:

Embolic clinical features of infective
endocarditis include:
A) CNS complications
B) Pulmonary complications
C) Coronary Artery Emboli
D) All of the above
Question 3:

Small hemorrhagic painless plaques located
on palms or soles are called?
A) Janeway lesions
B) Osler’s nodes
C) Roth Spots
D) Splinter hemorrhages
Answers

1) T
 2) D
 3) A