Infective endocarditis is an infection of the heart valves or endocardium. It has variable presentations ranging from acute and rapidly progressive to subacute and indolent. Key diagnostic criteria include identifying the infecting pathogen through blood cultures or other tests and detecting valvular vegetations or complications through echocardiography. Complications can involve the heart, brain, kidneys and other organs due to septic emboli. Treatment involves antibiotics and may require cardiac surgery.

1. By DR. RASHI SRIVASTAVA

2.  The prototypic lesion of infective
endocarditis, the vegetation is a mass of
platelets, fibrin, microorganisms, and scant
inflammatory cells.

4.  Acute endocarditis is a hectically febrile illness that rapidly
damages cardiac structures, 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 a
ruptured mycotic aneurysm

5.  EARLY PVE -PVE arising within 2 months of valve
 LATE PVE— The portals of entry and organisms causing cases
beginning >12 months after surgery.
 Delayed-onset nosocomial infection PVE due to
CoNS that presents 2–12 months after surgery often represents.

6. Involves the device or the endothelium at points
of device contact.
Occasionally, there is concurrent aortic or mitral
valve infection.
One-third of cases of CIED endocarditis present
within 3 months after device implantation or
manipulation,
one-third present at 4–12 months, and one-third
present at >1 year. S. aureus and CoNS, both of
which are often resistant to methicillin, cause the
majority of cases

7.  Community-associated IE develops in the absence
of recent contact with a health care setting, with diagnosis
established within 48 hours of hospital admission.
 Health care-associated IE develops in the context
of recent contact with a health care setting, with onset of
symptoms ≥48 hours after hospitalization

8.  Between 2000 and 2011, the incidence of IE
in the United States increased from 11 per
100,000 population to 15 per 100,000
population

9. Patient factors
 Age >60 years
 Male sex — Men predominate in most case series of IE;
male-to-female ratios range from 3:2 to 9:1.
 Injection drug use
 Poor dentition or dental infection

10. Comorbid conditions
 Structural heart disease — Approximately three-fourths of
patients with IE have a pre-existing structural cardiac abnormality at the time
that endocarditis develops

 Congenital heart disease
 History of infective endocarditis
 Indwelling intravascular device
 Nosocomial endocarditis - a diagnosis of IE made more than 72
hours after admission in patients with no evidence of IE on admission or
IE that develops within 60 days of a previous hospital admission during
which there was risk for bacteremia or IE

11.  Cardiac implantable electronic device
 Chronic hemodialysis
 HIV infection
 Cardiac bypass surgery

12.  Tricuspid or Pulmonic valve.
 Isolated right-sided IE - 10 percent .
 Concomitant left-sided and right-sided IE-- 13
percent of all IE cases .
 Risk factors for right-sided IE include
1. injection drug use,
2. presence of a cardiac implantable electronic device
(CIED) or other intravascular device, and
3. presence of an underlying right-sided cardiac anomaly.

13.  The undamaged endothelium is resistant to infection by most bacteria and to
thrombus formation.
 Endothelial injury (e.g., at the site of impact of high-velocity blood jets or on the
low-pressure side of a cardiac structural lesion) allows either direct infection by
virulent organisms or the development of a platelet–fibrin thrombus—a condition
called nonbacterial thrombotic endocarditis (NBTE).
 This thrombus serves as a site of bacterial attachment during transient bacteremia.
 The cardiac conditions most commonly resulting in NBTE are MR, AS, AR, VSD, and
complex CHD.
 NBTE also arises as a result of a hypercoagulable state; this phenomenon gives rise
to marantic endocarditis (uninfected vegetations seen in patients with malignancy
and chronic diseases) and to bland vegetations complicating systemic lupus
erythematosus and antiphospholipid antibody syndrome.

14.  Organisms that cause endocarditis enter the
bloodstream from mucosal surfaces, the skin,
or sites of focal infection.
 Except for more virulent bacteria (e.g., S.
aureus) that can adhere directly to intact
endothelium or exposed subendothelial
tissue, microorganisms in the blood adhere
at sites of NBTE.

16.  The clinical manifestations of infective
endocarditis (IE) are variable.
 IE may present as an acute, rapidly
progressive infection or as a subacute or
chronic disease with low-grade fever and
nonspecific symptoms

17.  Fever  most common symptom of IE (up to 90
percent of patients); it is often associated with
chills, anorexia, and weight loss.
 Patients with IE typically have continuous
bacteremia, regardless of whether fever is
present.
 Other common symptoms of IE include malaise,
headache, myalgias, arthralgias, night sweats,
abdominal pain, and dyspnea .
 Patients with IE associated with dental infection
may report tooth pain or related symptoms.

18.  Cardiac murmurs are observed in
approximately 85 percent of patients.
 Supportive signs include splenomegaly and
cutaneous manifestations such as petechiae
or splinter hemorrhages.

19.  Petechiae are observed in 20 to 40 percent of
patients; they may be present on the skin
(usually on the extremities) or on mucous
membranes such as the palate or
conjunctivae (picture 1).

20.  Splinter hemorrhages consist of nonblanching
linear reddish-brown lesions under the nail
bed .

21. ●Janeway lesions – Nontender erythematous
macules on the palms and soles

22.  ●Osler nodes – Tender subcutaneous
violaceous nodules mostly on the pads of the
fingers and toes, which may also occur on
the thenar and hypothenar eminences

23.  Janeway lesions  more common in acute than subacute IE.
 Histologically, they reflect microabscesses with neutrophil
infiltration of capillaries.
 Osler nodes and Roth spots occur most frequently in the setting
of a protracted time course of endocarditis.
 They probably represent the sequelae of vascular occlusion by
microthrombi leading to localized immune-mediated vasculitis.
 Roth spots (also described as Litten spots) occur in 2 percent of
patients with IE .
 Osler nodes were commonly observed among patients with IE in
the preantibiotic era, but are now uncommon since IE is
frequently diagnosed and treated before their development.

24.  IE is associated with a broad array of systemic
complications due to septic embolization, which may
be associated with localized thrombosis, bleeding,
infection, and/or development of immune reactions.
 Cardiac complications (up to 50 percent of patients) –
Valvular insufficiency, heart failure, and others.
 Neurologic complications (up to 40 percent of
patients) – Embolic stroke, intracerebral hemorrhage,
brain abscess, and others.

25.  Septic emboli (up to 25 percent of patients) – Infarction of
kidneys, spleen, and other organs. In patients with concomitant
right-sided endocarditis, septic pulmonary emboli may be seen

26.  Metastatic infection (such as vertebral
osteomyelitis, septic arthritis, splenic or
psoas abscess).
 Systemic immune reaction (eg,
glomerulonephritis)

28.  Signs of new regurgitant murmurs or heart
failure,
 Chest examination
1. Crackles,
2. Consolidation, or
3. Diminished breath sounds), and
4. Evaluation for evidence of septic emboli
with special attention to the fundi,
conjunctivae, skin, and digits.

29. Evaluation for bone or joint abnormalities
focal back discomfort, suggesting vertebral
osteomyelitis, discitis, and/or epidural
abscess),
Abdominal pain
(particularly left upper quadrant pain, which
may reflect splenic infarction), and
costovertebral angle tenderness (which may
reflect renal infarction or psoas abscess).
 Neurologic examination

30.  Routine laboratory findings relatively
nonspecific;
 Elevated ESR, CRP, NCNC ANEMIA and positive
RA.
 Hyperglobulinemia, cryoglobulinemia, circulating
immune complexes, hypocomplementemia, and
false-positive serologic tests for syphilis occur in
some patients.
 Urinalysis  microscopic hematuria, proteinuria,
and/or pyuria.
 The presence of red blood cell casts on urinalysis
is generally indicative of glomerulonephritis,
which is a minor diagnostic criterion for IE

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32. 1. Identification of the infecting pathogen by
blood culture, serologic testing, or
molecular testing
(1) Cardiac imaging to identify a valvular
vegetation, paravalvular abscess, or other
structural complication of infection.
 The accepted criteria for diagnosis of IE are
the modified Duke criteria,

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35.  Blood cultures and Echocardiography:
 At least 3 sets of blood cultures  separate
venipuncture sites (ideally spaced over 30 to
60 minutes) prior to initiation of antibiotic
therapy.
 The decision to start or withhold antibiotic
therapy prior to a microbiologic diagnosis
must be individualized.

36.  Serologic tests can be used to implicate
organisms that are difficult to recover by
blood culture: Brucella, Bartonella,
Legionella, Chlamydia psittaci, and C.
burnetii.

37.  Echocardiography  standard imaging modality for
evaluation of cardiac valves.
 FDG PET/CT an adjunctive imaging modality.
 Transesophageal echocardiography (TEE) has
higher sensitivity than TTE and is better for detection of
cardiac complications such as abscess, leaflet perforation,
and pseudoaneurysm.
 FDG PET/CT diagnostic tool for IE, which can identify
infection of native valves and paravalvular areas, as well
as extracardiac sites of infection.

40. 2 clinical categories:
 Presence of bacteremia in the absence of
valvular vegetation
 Presence of valvular vegetation(s) in the
absence of bacteremia.
 Patients with bacteremia in the absence of
evidence for valvular vegetation should be
evaluated for alternative causes of
bacteremia (which may coexist with IE),
including:

41.  Intravascular catheter infection
 Cardiac device infection
 Prosthetic joint infection –
 Hematogenous osteomyelitis
 Septic thrombophlebitis
 Infected arterial aneurysm

42.  Pneumonia
 Pulmonary embolism/infarction
 Hypersensitivity pneumonitis