2. Introduction
•Infective endocarditis (IE) is a microbial infection of the
heart valves or the mural endocardium that leads to the
formation of vegetations
•The formed vegetations are usually composed of
thrombotic debris and organisms
•Formation of the vegetations is often associated with
destruction of the underlying cardiac tissues
3. Introduction
•The aorta, aneurysms, other blood vessels, and prosthetic
devices can also become infected
•Although fungi and other classes of microorganisms can
be responsible, most infections are bacterial (bacterial
endocarditis)
•Prompt diagnosis, identification of the offending agent,
and effective treatment of IE is important in limiting
morbidity and mortality
4. Risk factors of IE
• Risk factors for IE include the following:
• Healthcare interventions including pacer/defibrillators
• Aging with increased risk for degenerative valvular heart
disease (DVHDs)
• Pre-existing valve disease
• Increases the risk for bacterial infection
• The increased risk with regurgitant jets is due to direct
damage to the endocardium by the local haemodynamic
forces.
• Immunosuppression
• Bacteraemia
• Prosthetic valves
• Rheumatic fever
5. Risk factors of IE
• The major organisms involved in infective endocarditis include
• Streptococci spp and Staphylococci spp (representing ≥75%).
• Enterococcal infections account for many of the remaining cases
• However, small case series and case reports suggest that almost
all organisms that infect humans can be implicated at times
• However, a sizable number of ‘culture negative’ cases still occur
despite all the improvements in diagnostic methodology.
6. Risk factors of IE
• Streptococci of the types found in the mouth (viridans group)
• The organisms enter the blood from the mouth, classically after
dental work.
• Today, only about 15% of patients give a history of recent visits
to the dentist
• The majority of cases are, however, associated with poor oral
hygiene and gingivitis.
7. Risk factors of IE
• The range of β-haemolytic streptococci causing infective
endocarditis is far wider than that found 30 years ago.
• Streptococcus viridans is an extremely broad group of organisms
and common strains causing IE include:
• S. sanguis, S. mitis, S. milleri, S. mutans, and S. salivarius.
• The disease produced is subacute in its clinical type
• The male to female ratio is 2:1 and the peak age is 65 years.
8. Mechanisms of IE
• The normal endocardium is relatively resistant to infection, and the
constant flow of blood makes it particularly difficult for a microorganism
to adhere to and initiate a focal infection.
• Three general conditions appear to play critical roles in creation of an
endocarditic lesion:
• Endocardial abnormality-endocardial inflammation, endothelial injury
• Bacteremia-microorganism access to the bloodstream from oral, genitourinary, or
gastrointestinal sources; trauma; intravenous and subcutaneous injections)
• Microbial properties and associated components (microbial virulence properties
such as adhesion proteins and tissue-destructive factors, microbial quantity,
particulate and diluent materials, repetition of microbial entry into the
bloodstream).
9. Classification of IE
• Traditionally, IE has been classified on clinical grounds into
acute and subacute forms.
• This subdivision reflects the range of the disease severity and
tempo, which are determined in large part by the virulence of the
infecting microorganism and whether underlying cardiac disease
is present
• Acute infective endocarditis
• Is typically caused by infection of a previously normal heart valve by a
highly
• virulent organism (e.g., Staphylococcus aureus) that rapidly produces
necrotizing and destructive lesions.
• These infections may be difficult to cure with antibiotics alone, and
usually require surgery.
• Despite appropriate treatment, death can ensue within days to weeks
10. Classification of IE
•Subacute infective endocarditis
• This is characterized by organisms with lower virulence (e.g.,
viridans streptococci) that cause insidious infections of
deformed valves with overall less destruction.
• In such cases the disease may pursue a protracted course of
weeks to months, and cures can be achieved with antibiotics.
11. Staphylococcus aureus endocarditis
• Staphylococcus aureus is the archetypal organism capable of
settling on functionally normal valves and causes extensive
tissue damage and septic emboli
• Native valve staphylococcal IE is due to Staphylococcus aureus
while staphylococcal prosthetic valve IE is more frequently due
to coagulase negative staphylococci such as Staphylococcus
epidermidis
• Native valve endocarditis affects men nearly three times as
frequently as women
12. Enterococci IE
• Enterococci are now responsible for many cases of IE and are
more frequent than the viridans group in infections that follow
urogenital and gastrointestinal tract surgery, and in drug addicts.
• In general, the disease is subacute in type but it may on occasion
be more acute with septic emboli.
• Other bacterial causes include enterococci and the so-called
HACEK group (Haemophilus, Actinobacillus, Cardiobacterium,
Eikenella, and Kingella)
13. Gram-negative bacteria
• Gram-negative bacteria account for up to 10% of cases of IE in
some series and are relatively more common in drug addicts and
on prosthetic valves.
• A vast range of other organisms, many reported as single cases
or small series, can cause infective endocarditis.
• Previously, pneumococci and gonococci accounted for 10% of
cases of infective endocarditis but their frequency has now been
reduced to sporadic single cases
14. Other causes/forms of IE
• Rickettsia spp and Chlamydia spp -These cause a very chronic and
slowly progressive IE with an insidious onset as does brucella
endocarditis.
• Infection usually occurs on previously abnormal valves, and
diagnosis is made in life by serology rather than isolation of the
organism.
• A history of working with agricultural animals is present in more
than 50% of cases of brucella and Q-fever endocarditis.
15. Other causes/forms of IE
• There has been an increasing frequency of deep mycotic
infections complicating immunosuppression usually linked to
haematological malignancy.
• Candida sp. dominates, followed by Aspergillus sp.
• Histoplasma sp. predominates in cases with large vegetations.
• The probable source of infection is often bronchopneumonia or
an infected central venous catheter.
16. Clinical features of IE
• Acute endocarditis has a stormy onset with rapidly developing
fever, chills, weakness, and lassitude.
• Although fever is the most consistent sign of IE, it can be slight
or absent, particularly in older adults, and the only
manifestations may be nonspecific fatigue, loss of weight, and a
flulike syndrome.
• Murmurs are present in 90% of patients with left-sided IE, either
from a new valvular defect or from a preexisting abnormality
17. Clinical features of IE
• The so-called modified Duke criteria facilitate evaluation of
individuals with suspected IE that takes into account
predisposing factors, physical findings, blood culture results,
echocardiographic findings, and laboratory information.
18. Clinical manifestations of long-standing IE
• Microthromboemboli (manifest as splinter or subungual
hemorrhages)
• Erythematous or hemorrhagic nontender lesions on the palms or
soles (Janeway lesions)
• Subcutaneous nodules in the pulp of the digits (Osler nodes),
and retinal hemorrhages in the eyes (Roth spots)
19.
20. •Janeway lesions are small
erythematous or
hemorrhagic, macular,
nontender lesions on the
palms and soles and are the
consequence of septic
embolic events.
21.
22.
23. • Janeway lesions are small erythematous or hemorrhagic,
macular, nontender lesions on the palms and soles and are the
consequence of septic embolic events.
• Osler nodes are small, tender subcutaneous nodules that
develop in the pulp of the digits or occasionally more
proximally in the fingers and persist for hours to several days.
• Roth spots are oval retinal hemorrhages with pale centers.
24.
25. Diagnosis of IE
• Diagnosis by these criteria, requires either pathologic or clinical
criteria; if clinical criteria are used; 2 major + 3 minor, or 5 minor
criteria are required for diagnosis.
26. Complications of IE
• Obstruction to flow by vegetations is far more common in
prosthetic valves compared with native valves where the
predominant haemodynamic abnormality is regurgitation.
• Annular abscesses are a very common feature of prosthetic valve
endocarditis.
• Infection spreads in the tissue plane surrounding the sewing ring
of the valve and rapidly forms an abscess, which extends around
the whole annulus.
• Such vegetations may become large enough to cause obstruction
or to hinder the mechanical movement of the valve resulting in
regurgitation
27. Complications of IE
• The mortality of bacterial endocarditis remains high largely
because of a number of serious complications including the
following:
• Severe heart failure
• Neurological manifestations
• Septic shock
• Perivalvular extension
• Acute renal failure
• As vegetations grow and disintegrate, they embolize into the
brain, myocardium, spleen, and kidneys
• Glomerular antigen-antibody complex deposition causing
glomerulonephritis
28. Treatment of IE
• The cornerstone to the successful clinical treatment of IE is
isolation of the organism from blood cultures, with antibiotic
therapy being specifically matched to the sensitivity of the
organism.
• Surgery continues to play an important role, with large
vegetations, ruptured leaflets, and large abscesses criteria for
urgent surgery.
29. Nursing care.
• Consider removing existing venous access lines because they may
be contaminated.
• Continually check the patient's SpO 2.
• Monitor him for a worsened or returning fever and assess for
signs and symptoms of heart failure, such as dyspnea, orthopnea,
and crackles.
