3. INTRODUCTION
• Infective endocarditis (IE) is defined as an
infection of the endocardial surface of the
heart, which may include one or more heart
valves, the mural endocardium or a septal
defect.
• Its intracardiac effects include severe valvular
insufficiency, which may lead to intractable
congestive heart failure, and myocardial
abscesses.
4. BACKGROUND
• Lazaire Riviere first described gross autopsy
findings of the disease in 1723.
• In 1885, William Osler presented the first
comprehensive description of endocarditis in
English.
• Lerner and Weinstein presented a thorough
discussion of this disease in modern times.
• Endocarditis has evolved into several variations,
keeping it near the top of the list of diseases that
must not be misdiagnosed or overlooked.
5. • Currently, infection of intravascular lines has been
determined to be the primary risk factor for
Staphylococcus aureus bloodstream infections
(BSIs).
• Since the 1960s, the clinical characteristics of IE
have changed due to increase in recreational drug
use and of invasive vascular procedures.
• Varieties of IE that were uncommon in the early
antibiotic era have become prominent(NIE, IVDA
IE, PVE)
6. EPIDEMIOLOGY
• In the United States, the 2009 incidence of IE was
approximately 12.7 cases per 100,000 persons per
year.
• This incidence has significantly risen from that of the
previous 50 years which was 2-4 cases per 100,000
persons per year.
• The incidence in other countries is similar to that in
the United States from 1998-2009
• It is 3 times as common in males as in females
• No racial predilection
• It may occur in a person of any age.
7. • Between 1998 and 2009, the mean age of patients
has risen from 58 to 60 years. (Mendiratta et al.)
• In children it accounts for 4.6% of AHD in Nigeria.
• The proportion of people with intracardiac devices
increased from 13.3% to 18.9% while the proportion of
cases with a background of HIV drug abuse fell.
• Rheumatic heart disease currently accounts for less
than 20% of cases, and 6% of patients with rheumatic
heart disease eventually develop IE.
8. • A retrospective study (Jan 1982 to Dec 1989)
of infective endocarditis in 32 cases from
ABUTH, Zaria, Nigeria, found
– underlying heart disease in 30 patients (90%),
where
– 21 cases (66%) had RHD and
– nine cases (28%) had underlying congenital heart
diseases.
– Overall mortality was 47% due mostly to heart
failure and neurological complications.
9. CLASSIFICATION
• Acute (short incubation) vs. subacute (long
incubation)
• Culture-positive vs. culture-negative
• Right sided vs. left sided
• Nosocomial vs. community-acquired
• Native-valve endocarditis vs. prosthetic-valve
10. CLASSIFICATION
• Native valve endocarditis (NVE),
– acute and
– subacute
• Prosthetic valve endocarditis (PVE),
– early and
– late
• Intravenous drug abuse (IVDA) IE
• Nosocomial IE (NIE)
• Pacemaker IE
• Culture positive and culture negative IE
11. Native valve endocarditis
• Rheumatic valvular disease (30% of NVE) - Primarily
involves the mitral valve followed by the aortic valve
• Congenital heart disease (15% of NVE) - Underlying
etiologies include
– patent ductus arteriosus,
– ventricular septal defect,
– tetralogy of Fallot,
– native or surgical high-flow lesion.
• Mitral valve prolapse with an associated murmur (20%
of NVE)
• Degenerative heart disease - Including calcific aortic
stenosis due to a bicuspid valve or syphilitic disease
12. Native valve endocarditis
• Acute bacterial endocarditis (ABE)
• fulminant illness over days to weeks
• more likely due to Staphylococcus aureus and
group B Streptococci which has much greater
virulence, or disease-producing capacity
• frequently causes metastatic infection by
hematogenous seeding
• Destructive
• frequently of a previously normal heart valve
• leads to death within weeks if left untreated
13. • Subacute bacterial endocarditis (SBE)
– often due to alpha hemolytic streptococci and
enterococci of low virulence
– mild to moderate insidious illness which
progresses slowly over weeks and months
– low propensity to hematogenously seed to
extracardiac sites
– previously abnormal heart, particularly on
deformed valves
– recover after appropriate antibiotic treatment
14. Prosthetic valve endocarditis
• PVE accounts for 10-20% of cases of IE.
• Eventually, 5% of prosthetic valves become infected.
• Mechanical valves are more likely to be infected within the
first 3 months of implantation
• Bioprosthetic valves are more likely to be infected after one
year
• The valves in the mitral valve position are more susceptible
than those in the aortic areas
• Recent data suggest that S aureus may now be the most
common infecting organism in both early and late PVE
15. • Early PVE occurs within 60 days of valve implantation
– usually due to intraoperative contamination or a
postoperative bacterial contamination which is usually
nosocomial in nature.
– coagulase-negative staphylococci, gram-negative
bacilli, and Candida species most common.
• Late PVE occurs 60 days or more after valve implantation
– Late prosthetic valve endocarditis is usually due to
community acquired microorganisms
– Staphylococci, alpha-hemolytic streptococci, and
enterococci are the common causative organisms.
16. Intravenous drug abuse endocarditis
• No underlying valvular abnormalities are
noted in 75% of cases
• 50% of these infections involve the tricuspid
valve
• S. aureus is the most common causative
organism
17. Nosocomial infective endocarditis
• NIE is defined as an infection that manifests 48
hours after the patient is hospitalized or that is
associated with a hospital, based on a procedure
performed within 4 weeks of clinical disease
onset.
• The term healthcare-associated infective
endocarditis (HCIE) is preferable to NIE, since it is
inclusive of all sites that deliver patient care, such
as hemodialysis centers.
• An appropriate alternative term would be
iatrogenic IE.
18. – The right-sided variety affects a valve that has been
injured by placement of an intravascular line
– The left sided variety develops in a previously
damaged valve.
• S aureus has been the predominant pathogen of
NIE/HCIE since the recent prevalence of
intravascular devices.
• Enterococci are second most commonly isolated
pathogens usually from a genitourinary source.
19. Pacemaker infective endocarditis
• Infections of implantable pacemakers and cardioverter
defibrillators.
• They are infected within a few months of implantation
– Generator pocket (most common)
– Proximal leads
– Portion of leads in direct contact with endocardium, this
represents true pacemaker IE, is the least common (0.5%
of implanted pacemakers), and is the most challenging to
treat.
• Of pacemaker infections, 75% are produced by
staphylococci
20. • Risk factors for the development of pacemaker IE
– Surgical intervention to any part of the pacemaker
system, especially elective battery replacements.
Approximately 5 times the risk of initial implantation
(6.5% vs 1.4%)
– Diabetes mellitus
– Age
– Use of anticoagulants and corticosteroids
– Postoperative hematoma
– Inexperience of the surgeon
– Preceding temporary transvenous pacing
21. Culture positive and culture negative
endocarditis
• Culture-negative endocarditis can be due to
– micro-organisms that require a longer period of
time to be identified in the laboratory
– Fastidious organisms Aspergillus species, Brucella
species, Coxiella burnetii, Chlamydia species, and
HACEK bacteria.
– Fungal endocarditis
– Surface sterilization in S.aureus IE
– Prior antibiotic treatment.
22. PREDISPOSING/RISK FACTORS
• The most significant risk factor for IE is residual
valvular damage caused by a previous attack of
endocarditis.
• IVDA
• Prosthetic heart valves
• Structural heart disease: mitral valve prolapse with
mitral regurgitation and aortic stenosis.
• Congenital heart defects: Tetralogy of Fallot, bicuspid
aortic valves, Coarctation of the aorta, VSDs, and
patent ductus arteriosus.
23. PREDISPOSING/RISK FACTORS
• A predisposing abnormality of the endocardium
• RHD(8.5% in Nigeria)
• Myxomatous mitral valve
• Hypertrophic cardiomyopathy
• Degenerative calcific valvular stenosis
• Valvular damage from surgery, autoimmune conditions or old age.
• Host factors
• Neutropenia
• Immunodeficiency
• Malignancy
• Therapeutic immunosuppression
• Diabetes mellitus
• Alcohol
• IV drug abuse
24. PATHOPHYSIOLOGY
• Turbulent blood flow within the heart - most often (but not
always) – patient has risk factors for this
• Turbulent blood flow disrupts valve surface (endocardium)
to produce suitable (sticky) site for bacterial attachment
• Platelet deposition + fibrin may lead to non-bacterial
thrombus or vegetation(NBTE) providing a nidus for
bacterial adhesion.
• Bacteraemia – delivers organisms to the damaged (sticky)
endocardial surface resulting in adherence & colonisation.
• Eventual invasion of valve leaflets results in infected
vegetation (sheath of fibrin & platelets, ideal conditions for
further bacterial multiplications, protection from
polymorphs)
25. Bacteremia
• Most commonly from gingival disease.
• Pneumonias or pyelonephritis
• Most cases of subacute disease are secondary to the
bacteremias that develop from the activities of daily
living (e.g.brushing teeth).
• S aureus infection due to production of alpha toxin
which allows the organism to penetrate the
keratinocyte layer in the absence of any gross damage
to the epithelial layer.
• Endotheliosis by S aureus can increase the expression
of adhesion molecules and of procoagulant activity on
the cellular surface.
26. Invasive procedures
• Dental extractions - Rate of 40-100%; S viridans
• Transurethral resection of the prostate - Rate of 20-40%;
coliforms, enterococci, S aureus
• Endoscopy - Rate of 0-20%; coagulase-negative
staphylococci (CoNS), streptococci, diphtheroids
• Colonoscopy – Rate of 0-20%; Escherichia coli, Bacteroides
species
• Barium enema - Rate of 0-20%; enterococci, aerobic and
anaerobic gram-negative rods
• Transesophageal echocardiography - Rate of 0-20%; S
viridans, anaerobic organisms, streptococci
27. Adhesion of bacteria
• Damaged vascular endothelium will also promote
platelet and fibrin deposition, upon which
bacteria can take hold.
• Nonbacterial thrombotic endocarditis also may
result from stress, renal failure, malnutrition,
systemic lupus erythematosus or neoplasia.
• In acute IE, the thrombus may be produced by
the invading organism (i.e. S aureus) or by
valvular trauma from intravenous catheters or
pacing wires (i.e. NIE/HCIE).
28. Invasion of valvular leaflets
• Colonization of heart valves by microorganisms is a
complex process.
• Once microorganisms do establish themselves on the
surface of the vegetation, the process of platelet
aggregation and fibrin deposition accelerate at the site.
• As the bacteria multiply, they are covered by ever-
thickening layers of platelets and thrombin, which protect
them from neutrophils and other host defenses.
• Organisms deep in the vegetation hibernate because of the
paucity of available nutrients and are therefore less
susceptible to bactericidal antimicrobials that interfere with
bacterial cell wall synthesis.
29. • The cellular reaction in SBE is primarily that of
mononuclear cells and lymphocytes, with few
polymorphonuclear cells.
• The surface of the valve beneath the vegetation shows few
organisms.
• Proliferation of capillaries and fibroblasts is marked.
• Areas of healing are scattered among areas of destruction.
Over time, the healing process falls behind, and valvular
insufficiency develops secondary to perforation of the
cusps and damage to the chordae tendineae.
• Extension of the infectious process occurs beyond the
valvular leaflets.
30. Acute S. aureus IE with perforation of the
aortic valve and aortic valve vegetation.
Acute S. aureus IE with mitral valve ring
abscess extending into myocardium.
08-01-2016 Dr.T.V.Rao MD 30
32. MICROBIOLOGY
• Staphylococcus aureus
– most common cause of IE, including PVE, acute IE, and
IVDA IE.
– Approximately 35-60.5% of staphylococcal bacteremias are
complicated by IE.
– More than half the cases are not associated with
underlying valvular disease.
– The mortality rate of S aureus IE is 40-50%.
• Streptococcus viridans
– This organism accounts for approximately 50-60% of cases
of subacute disease.
– Most clinical signs and symptoms are mediated
immunologically.
33. • Streptococcus intermedius group
– These infections may be acute or subacute.
– S intermedius infection accounts for 15% of streptococcal
IE cases.
– S intermedius is unique among the streptococci; it can
actively invade tissue and can cause abscesses.
• Abiotrophia species (formerly known as nutritionally variant
streptococci)
– Approximately 5% of subacute cases of IE.
– This type of IE is associated with large vegetations that
lead to embolization and a high rate of posttreatment
relapse.
34. • Group D streptococci
– Most cases are subacute.
– The source is the gastrointestinal or genitourinary
tract.
– It is the third most common cause of IE.
– They pose major resistance problems for antibiotics.
• Nonenterococcal group D organisms
– The clinical course is subacute.
– Infection often reflects underlying abnormalities of
the large bowel (e.g. ulcerative colitis, polyps, cancer).
– The organisms are sensitive to penicillin.
35. • Group B streptococci
– Acute disease develops in pregnant patients and older patients
with underlying diseases (eg, cancer, diabetes, alcoholism).
– The mortality rate is 40%.
– Complications include metastatic infection, arterial thrombi, and
congestive heart failure.
– It often requires valve replacement for cure.
• Group A, C, and G streptococci
– Acute disease resembles that of S aureus IE (30-70% mortality
rate), with suppurative complications.
– Group A organisms respond to penicillin alone.
– Group C and G organisms require a combination of synergistic
antibiotics (as with enterococci).
36. • Coagulase-negative S aureus
– This causes subacute disease.
– It behaves similarly to S viridans infection.
– It accounts for approximately 30% of PVE cases and
less than 5% of NVE cases.
• Pseudomonas aeruginosa
– This is usually acute, except when it involves the right
side of the heart in IVDA IE.
– Surgery is commonly required for cure.
37. • HACEK organisms (Haemophilus aphrophilus,
Aggregatibacter actinomycetemcomitans,
Cardiobacterium hominis, Eikenella corrodens,
Kingella kingae)
– These organisms usually cause subacute disease.
– They account for approximately 5% of IE cases.
– They are the most common gram-negative organisms
isolated from patients with IE.
– Complications may include massive arterial emboli
and congestive heart failure.
– Cure requires ampicillin, gentamicin, and surgery.
38. SYMPTOMS
• Symptoms commonly are vague, emphasizing constitutional complaints
– Fever and chills are the most common symptoms
– anorexia,
– weight loss,
– malaise,
– headache,
– myalgias,
– night sweats,
– shortness of breath,
– cough,
– joint pains
– Dyspnea, cough, and chest pain are common complaints of
intravenous drug users.
39. • Primary cardiac disease may present with
signs of congestive heart failure due to
valvular insufficiency.
• Secondary phenomena could include focal
neurologic complaints due to an embolic
stroke or back pain associated with vertebral
osteomyelitis.
• As many as 20% of cases present with focal
neurologic complaints and stroke syndromes.
40. Subacute
Symptoms are subtle and nonspecific.
• Low-grade Fever (Absent In 3-15% Of Patients),
• Anorexia,
• Weight Loss,
• Influenza-like Syndromes,
• Polymyalgia-like Syndromes,
• Pleuritic Pain,
• Syndromes Similar To Rheumatic Fever (Fever, Dulled Sensorium As
In Typhoid, Headaches),
• Abdominal Symptoms (Right Upper Quadrant Pain, Vomiting,
Postprandial Distress, Appendicitis-like Symptoms).
• Palpitations
• Lumbosacral Pain
41. Acute
• Acute onset of high-grade fevers and chills
• Rapid onset of congestive heart failure with
marked dyspnoea and fatigue.
42. SIGNS
• The AHA (endorsed by the Infectious Diseases Society of
America [IDSA]) 2010 guideline update on cardiovascular
implantable electronic device (CIED) infections and their
management recommends that patients with CIED who
develop unexplained fever or bloodstream infection should
seek evaluation for CIED infection by cardiologists or
infectious disease specialists.
• Fever, possibly low-grade and intermittent, is present in
90% of patients.
• Heart murmurs are heard in approximately 85% of patients.
Change in the characteristics of a previously noted murmur
occurs in 10% of these patients and increases the likelihood
of secondary congestive heart failure.
43. • One or more classic signs of IE are found in as
many as 50% of patients. They include the
following:
– Petechiae - Common but nonspecific finding on
palpebral conjunctivae, the dorsa of the hands and
feet, the anterior chest and abdominal walls, the oral
mucosa, and the soft palate.
– Subungual (splinter) hemorrhages - Dark red linear
lesions in the nailbeds that do not extend for entire
length of nails
– Roth spots - Retinal hemorrhages with small, clear
centers; rare and observed in only 5% of patients
44. – Janeway lesions - irregular erythematosus and
painless macules (1-4 mm in diameter). They most
often are located on the thenar and hypothenar
eminences of the hands and feet.
– Osler nodes – Tender subcutaneous nodules in
pulp spaces of the terminal phalanges of the
fingers and toes, soles of the feet, and the thenar
and hypothenar eminences of the hands. Their
appearance is often preceded by neuropathic
pain. They last from hours to several days. They
remain tender for a maximum of 2 days.
45. Janeway Lesions
1. More specific
2. Erythematous, blanching macules
3. Nonpainful
4. Located on palms and soles
46. Splinter Hemorrhages
1. Nonspecific
2. Nonblanching
3. Linear reddish-brown lesions found under the nail bed
4. Usually do NOT extend the entire length of the nail
50. Osler’s Nodes
1. More specific
2. Painful and erythematous nodules
3. Located on pulp of fingers and toes
4. More common in subacute IE
51.
52. • Signs of neurologic disease occur in as many
as 40% of patients due to embolic stroke with
focal neurologic deficits, intracerebral
hemorrhage and multiple microabscesses.
• Signs of pulmonary and systemic septic emboli
• Signs of congestive heart failure, such as
distended neck veins
• Splenomegaly may be present.
53. • Other signs include the following:
– Stiff Neck
– Delirium
– Paralysis
– Hemiparesis
– Aphasia
– Conjunctival Hemorrhage
– Cardiac Arrhythmia
54. DIAGNOSIS
• Blood cultures
• Echocardiograhy
• ECG
– Rarely diagnostic
– Look for evidence of ischemia, conduction delay,
and arrhythmias
• Clinical criteria
55. • Because symptoms and signs are nonspecific, vary greatly,
and may develop insidiously, diagnosis requires a high index
of suspicion.
• Endocarditis should be suspected in patients with fever and
no obvious source of infection, particularly if a heart
murmur is present.
• Suspicion of endocarditis should be very high if blood
cultures are positive in patients who have a history of a
heart valve disorder, who have had certain recent invasive
procedures, or who abuse IV drugs.
• Patients with documented bacteremia should be examined
thoroughly and repeatedly for new valvular murmurs and
signs of emboli.
56. Blood Culture
• If endocarditis is suspected, 3 blood cultures (20 mL each)
should be obtained within 24 h (if presentation suggests
ABE, 2 cultures within the first 1 to 2 h).
• When endocarditis is present and no prior antibiotic
therapy was given, all 3 blood cultures usually are positive
because the bacteremia is continuous; at least 1 culture is
positive in 99%.
• Premature use of empiric antibiotic therapy should be
avoided in patients with acquired or congenital valvular or
shunt lesions to avoid culture-negative endocarditis.
• If prior antimicrobial therapy was given, blood cultures
should still be obtained, but they may be negative.
57. • Established infections often cause a
normocytic-normochromic anemia, elevated
WBC count, increased ESR, increased Igs,
circulating immune complexes, and
rheumatoid factor, but these findings are not
diagnostically helpful.
• Urinalysis often shows microscopic hematuria
and, occasionally, RBC casts, pyuria, or
bacteriuria.
58. Echocardiography
• Transthoracic echocardiography (TTE)
– First line if suspected IE
– Native valves
• Trans esophageal echocardiography (TEE)
– Prosthetic valves
– Intracardiac complications
– Inadequate TTE
– Fungal or S. aureus or bacteremia
59. Diagnosis
• Definitive diagnosis of infective endocarditis (IE)
is generally made by using the Duke criteria.
• Durack and colleagues developed diagnostic
criteria in 1994 that combine the
– clinical,
– microbiological,
– Pathological,
– echocardiographic characteristics of a specific case.
60. • Definitive Endocarditis
–Two major or,
–One major and three minor or,
–five minor
• Possible Endocarditis
–One major and one minor or,
–Three minor
• Rejection criteria
Modified Dukes Criteria for diagnosis
of Infective Endocarditis
61. • Major blood culture criteria include the following:
– Two blood cultures positive for organisms typically
found in patients with IE (S viridans, Streptococcus
bovis, a HACEK group organism, community-acquired
S aureus, or enterococci in the absence of a primary
focus)
– Blood cultures persistently positive for one of the
above organisms from cultures drawn more than 12
hours apart
– Three or more separate blood cultures drawn at least
1 hour apart, positive for organisms consistent with IE
62. • Major echocardiographic criteria include the
following:
– Echocardiogram positive for IE, documented by an
oscillating intracardiac mass on a valve or on
supporting structures in the path of regurgitant jets,
or on implanted material in the absence of an
alternative anatomical explanation
– Myocardial abscess
– Development of partial dehiscence of a prosthetic
valve
– New-onset valvular regurgitation
63. • Minor criteria include the following:
– Predisposing heart condition or intravenous drug use
– Fever of 38°C (100.4°F) or higher
– Vascular phenomenon, including major arterial emboli, septic
pulmonary infarcts, intracranial hemorrhage, conjunctival
hemorrhage, or Janeway lesions
– Immunological phenomenon such as glomerulonephritis, Osler
nodes, Roth spots, and rheumatoid factor
– Positive blood culture results not meeting major criteria or
serologic evidence of active infection with an organism consistent
with IE (Brucella, C burnetii [Q fever], Legionella)
– Rheumatoid factor
– Echocardiogram results consistent with IE but not meeting major
echocardiographic criteria
64. • Rejection criteria for the diagnosis of IE are as
follows:
– The presence of a firm alternative diagnosis of the
manifestations of endocarditis
– Resolution of manifestations of endocarditis after
4 or fewer days of antimicrobial therapy
– No pathologic evidence of IE at surgery or autopsy
after 4 or fewer days of antimicrobial therapy
66. TREATMENT
• The major goals of therapy for infective
endocarditis (IE) are to
– eradicate the infectious agent from the thrombus
– address the complications of valvular infection.
• General measures include the following:
– Treatment of congestive heart failure
– Oxygen
– Hemodialysis (may be required in patients with
renal failure)
67. • Antibiotics remain the mainstay of treatment for
IE.
• In acute IE, institute antibiotic therapy as soon as
possible to minimize valvular damage.
• In subacute IE, treatment may be safely delayed
until culture and sensitivity results are available.
• Initial antibiotic choice is empiric in nature,
determined by clinical history and physical
examination findings.
68. • High dose antibiotics are administered by the
intravenous route to maximize diffusion of
antibiotic molecules into vegetation(s) from
the blood filling the chambers of the heart.
• This is necessary because neither the heart
valves nor the vegetations adherent to them
are supplied by blood vessels.
• Antibiotics are continued for a long time,
typically two to eight weeks.
69. • Bactericidal antibiotics are considered
necessary for cure of valvular infection.
• Orally administered antibiotics have been
used as suppressive therapy for incurable
valvular infections (inoperable PVE).
• Treat all patients in a hospital or skilled
nursing facility to allow adequate monitoring
of the development of complications and the
response to antibiotic therapy.
70. • The American Heart Association (AHA) has developed guidelines for
treating IE caused by the most frequently encountered microorganisms.
• Adult NVE caused by penicillin-susceptible S viridans, S bovis, and other
streptococci
– Penicillin G at 12-18 million U/d IV by continuous pump or in 6 equally
divided doses for 4 weeks
– Ceftriaxone at 2 g/d IV for 4 weeks or IM for short periods .ceftriaxone
allows once-a-day outpatient IV therapy for clinically stable patients.
– Penicillin G and gentamicin at 1 mg/kg every 8 hours for 2 weeks;
short-course therapy with ceftriaxone and gentamicin for 2 weeks in
uncomplicated NVE caused by sensitive S viridans and of less than 3
months’ duration
– Vancomycin at 30 mg/kg/d IV in 2 equally divided doses for 4 weeks;
the vancomycin dose should not exceed 2 g/d
71. • NVE caused by relatively penicillin resistant
streptococci
– Penicillin G at 18 million U/d IV, either by continuous
pump or in 6 equally divided doses, for 4 weeks
– Cefazolin at 6 g/d IV in 3 equally divided doses for 4
weeks
– Both of the above regimens are combined with
gentamicin at 1 mg/kg IM or IV every 8 hours for the
first 2 weeks of therapy
– Vancomycin at 30 mg/kg/d IV in 2 equally divided
doses for 4 weeks
72. • IE caused by nonresistant enterococci, resistant S
viridans or nutritionally variant S viridans
• PVE caused by penicillin-G–susceptible S viridans or S
bovis should be treated as follows:
– Penicillin G at 18-30 million U/d IV, either by continuous
pump or in 6 equally divided doses daily, combined with
gentamicin at 1 mg/kg IM or IV every 8 hours for 4-6 weeks
– Ampicillin at 12 g/d by continuous infusion or in 6 equally
divided doses daily, combined with gentamicin at 1 mg/kg
IM or IV every 8 hours for 4-6 weeks
– Vancomycin at 30 mg/kg/d in 2 equally divided doses. This
may be combined with gentamicin for 4-6 weeks.
73. • NVE caused by methicillin-sensitive S aureus
(MSSA) should be treated as follows:
– nafcillin or oxacillin at 2 g IV every 4 hours for 4-6
weeks
– cefazolin at 2 g IV every 8 hours for 4-6 weeks
– vancomycin at 30 mg/kg for 4-6 weeks
74. • P aeruginosa
– Cefepime, or imipenem, combined with high-dose tobramycin at 8
mg/kg/d in 3 divided doses for 6 weeks
• Enteric gram-negative rods (E coli, Proteus mirabilis)
– Ampicillin, ceftriaxone, or cefepime combined with gentamicin for 4-6
weeks
• Streptococcus pneumoniae
– Ceftriaxone at 2 g/d IV or vancomycin for 4 weeks
• Diphtheroids
– Penicillin G at 18-24 million U/d in 6 divided doses or vancomycin
combined with gentamicin for 4 weeks
• Q fever (C burnetii infection)
– Doxycycline combined with rifampin, for 3-4 years
75. • Anticoagulation is controversial.
• Evidence indicates patients who are
anticoagulated have worse outcomes than those
who are not anticoagulated.
• Patients who are treated with anticoagulation
appear to have a higher rate of intracerebral
bleeding.
• If an established reason for anticoagulation (deep
venous thrombosis) exists, a standard regimen of
anticoagulation should be followed.
76. Indications for surgery
• Congestive heart failure refractory to standard
medical therapy
• Fungal IE (except that caused by Histoplasma
capsulatum)
• Persistent sepsis after 72 hours of appropriate
antibiotic treatment
• Recurrent septic emboli, especially after 2 weeks of
antibiotic treatment
• Rupture of an aneurysm of the sinus of Valsalva
• Conduction disturbances caused by a septal abscess
77. • A second relapse, during or after completion of
treatment, requires replacement of the valve.
• Paravalvular abscess and intracardiac fistula
• Patients with culture-negative NVE who remain
febrile for more than 10 days.
• Persistent hypermobile vegetations
• Patients with multi-resistant organisms
(enterococci)
• Metastatic infections (macroabscesses of the
brain and spleen)
78. Monitoring
• Blood cultures taken after 3-4 days of treatment to
document eradication of the bacteremia.
• Blood cultures during treatment are essential if
persistent fever or other signs develop that suggest
failing treatment.
• Failure to sterilize the bloodstream should prompt a
search for metastatic infection (abscesses, especially
splenic, or mycotic aneurysm).
• Fever lasting longer than 10 days into therapy should
prompt a search for suppurative complications.
79. • Approximately 30% of patients have a return of
fever after the initial response. This is usually
caused by an intracardiac abscess or metastatic
infection.
• Causes of unresponsive fever include myocardial
or septal abscesses, large vegetations that resist
sterilization, and metastatic infection.
• Patients with staphylococcal endocarditis tend to
respond more slowly.
• Diminution of vegetation size can be followed by
serial echocardiography
80. COMPLICATIONS
• Valvular dysfunction, usually insufficiency of the
mitral or aortic valves
• Myocardial or septal abscesses
• Congestive heart failure
• Metastatic infection
• Embolic phenomenon
• Organ dysfunction resulting from immunological
processes
• Relapse
81. Recurrence
• Relapse of IE usually occurs within 2 months of finishing clinically
effective therapy.
– Infection with S aureus, enterococci, and gram-negative organisms
(especially P aeruginosa) is associated with a high rate of relapse.
– Enterococcal infection of the mitral valve has the greatest potential for
relapse.
– Recurrent IE occurs most often in individuals who abuse IV drugs.
– Valvular infections in these patients recur at a rate of 40%.
– Those with pretreatment symptoms of IE of more than 3 months’
duration are at greater risk for relapse.
• Other significant risk factors for recurrence include a previous
episode of IE, the presence of a prosthetic valve, and congenital
heart disease.
82. PREVENTION
• Preventive dental examination and therapy
before surgery to repair heart valves or
congenital heart lesions is recommended.
• The American Heart Association (AHA)
recommends antimicrobial prophylaxis for
patients at high risk of an adverse outcome
from infective endocarditis.
83. Such patients include those with
• Prosthetic heart valves
• Previous infective endocarditis
• Congenital heart diseases (CHD):
– Unrepaired cyanotic CHD (including palliative shunts
and conduits),
– completely repaired CHD during the 1st 6 months
after surgery if prosthetic material or device was used
– repaired CHD that has residual defects at or adjacent
to the site of repair
• Heart transplant recipients with valvulopathy
84. • Any procedure involving manipulation of gingival
tissue or the periapical region of teeth, or
perforation of the oral mucosa
• Any procedure involving incision in the
respiratory mucosa
• Procedures on infected skin or musculoskeletal
tissue including incision and drainage of an
abscess
• Prophylaxis is no longer routinely recommended
for gastrointestinal or genitourinary procedures.
85. ROUTE DRUGS AND DOSAGE IN
ADULTS (AND CHILDREN)
DRUGS AND DOSAGE IN
ADULTS (AND CHILDREN)
ALLERGIC TO PENICILLIN
ORAL (GIVEN 1 HOUR BEFORE
PROCEDURE)
AMOXYCILLIN 2g (50mg/kg) PO CLINDAMYCIN 600mg
(20mg/kg) PO or
CEPHALEXIN 2g (50mg/kg) or
AZITHROMYCIN or
CLARITHROMYCIN 500mg
(15mg/kg) PO
PARENTERAL (GIVEN 30 MINS
BEFORE PROCEDURE)
AMPICILLIN 2g (50mg/kg) IM/IV CLINDAMYCIN 600mg
(20mg/kg) IV or
CEFAZOLIN 1g (25mg/kg) IM/I
86. PROGNOSIS
• In contemporary population-based studies of infective
endocarditis in industrialized countries, in-hospital
mortality ranges from 15 to 22% and 5-year mortality is
approximately 40%.
• In-hospital mortality is less than 10% among patients
with right-sided lesions or oral streptococcal, left-
sided, native-valve lesions, whereas it is 40% or more
among patients with prosthetic-valve infective
endocarditis due to Staphylococcus aureus.
• Independent predictors of mortality included higher
age, S. aureus infection, heart failure, cerebrovascular
and embolic events.
88. REFERENCES
• International journal of general medicine, march 2013.
• Bode-Thomas F, Ige O.O, Yilgwan C. Childhood acquired
heart diseases in Jos, north central Nigeria. Niger Med J
2013
• National center for biotechnology information journal,
2007
• New England Journal of Medicine. Bruno Hoen, M.D., Ph.D.,
and Xavier Duval, M.D., Ph.D. April, 2013
• Mitchell RS, Kumar V, Robbins SL, Abbas AK, Fausto N
(2007). Robbins Basic Pathology (8th ed.).
• Kasper DL, Brunwald E, Fauci AS, Hauser S, Longo DL,
Jameson JL (May 2005). Harrison's Principles of Internal
Medicine.
