Endocarditis 2015

1. ENDOCARDITIS
SAMIR EL ANSARY

2. Global Critical Care
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3. The important clinical
manifestations of
endocarditis

4. Several processes contribute to the
clinical signs and symptoms of infective
endocarditis, including valvular
involvement with intracardiac
complications, high-grade and
persistent bacteremia (which may lead
to metastatic foci), bland or septic
embolization to any organ, and immune
complex formation.

5. Fever occurs in 80% of patients, and
nonspecific symptoms, including
anorexia, weight loss, malaise, fatigue,
chills, weakness, nausea, vomiting, and
night sweats, are very common.
Although heart murmurs are common,
the so-called changing murmur is
relatively uncommon.
The incidence of peripheral
manifestations has decreased.

6. Osler nodes, although not specific for
endocarditis, may occur in 10% to 25% of all
cases and are generally seen in subacute
cases.
Janeway lesions (i.e., macular, painless
plaques on the palms and soles) are seen in
fewer than 10% of cases.
Clubbing may be seen if the disease is long-
standing and may occur 10% to 20% of the
time.
Splenomegaly occurs in 25% to 60% of
cases, generally those with subacute
disease.

7. Joint complaints may occur in
approximately 40% of patients and may be
relatively innocuous with low back pain or
myalgias and arthralgias.
Musculoskeletal symptoms may also be
quite severe,including frank septic arthritis
and severe low back pain.
Other less common musculoskeletal
manifestations include septic bursitis,
sacroiliitis, septic diskitis, and polymyalgia
rheumatica.

8. Long-standing subacute
endocarditis
may present as
Chronic wasting
syndrome mimicking
cancer or human
immunodeficiency virus
infection.

9. Signs and symptoms of
embolic episodes are
determined
By the location
of the embolism :

10. Patients with splenic emboli
may have left upper quadrant
pain, left-sided pleural
effusions, or a rub.
Renal infarction from a septic
embolus may present as flank
pain and hematuria.

11. Immune complex formation
may lead to renal insufficiency.
Cough and shortness of
breath
with chest pain often
accompany
Pulmonary emboli

12. Coronary emboli
Occur rarely and may present with
myocarditis, arrhythmias,
myocardial infarction, or a
combination of all
Extension into the pericardial
space may lead to purulent
pericarditis with severe chest pain
and hemodynamic compromise.

13. Unexplained heart failure in a
young patient without prior
cardiac disease should prompt
an investigation for
Infectious
endocarditis

14. Manifestations of
endocarditis
in elderly patients

15. There does appear to be an increased incidence
of endocarditis in elderly patients that may be
related to an increased life span in patients with
rheumatic and other cardiovascular diseases,
with a commensurate increase among patients
with calcific and degenerative heart disease.
In addition, the increase in prolonged catheter
use, implantable devices, and dialysis catheters
increases the incidence of nosocomial
endocarditis.

16. Endocarditis in elderly persons is more likely to
occur in men
with a ratio of approximately 2 to 8 :l
in patients older than 60 years of age.
Staphylococci and streptococci
account for approximately 80% of the cases in
elderly persons, and
Streptococcus bovis
may be noted more frequently in elderly patients
associated with underlying
colonic malignancy.

17. The clinical presentation of endocarditis
may be nonspecific, including lethargy,
fatigue, malaise, anorexia, failure to
thrive, and weight loss
(which may be attributed to aging or other
medical illnesses common in the elderly).
In addition, fever, which occurs in
roughly 80% of patients with
endocarditis, is more likely to be absent
in elderly patients.

18. Worsening heart failure and murmurs may be
attributed to underlying disease and therefore
erroneously neglected.
Consequently, a high index of
suspicion is necessary.

19. Duke criteria for the
diagnosis of
endocarditis
How have they been
modified?

20. The original Duke criteria for the diagnosis of
infective endocarditis stratified patients into
three categories
Definite: identified by using clinical or pathologic criteria
.
Possible: findings consistent with infective endocarditis
that fall short of definite, but the diagnosis cannot be
rejected
Rejected: firm alternative diagnosis for manifestations of
endocarditis or resolution of manifestations of
endocarditis, with antibiotic therapy for 4 days or less, or
no pathologic evidence of infective endocarditis at
surgery or autopsy, after antibiotic therapy for 4 days or
less .

21. Pathologic Criteria
Pathologic criteria include
microorganisms demonstrated by
culture or histology in a vegetation or
in a vegetation that has embolized or
in an intracardiac abscess or
pathologic lesions, including
vegetation or intracardiac abscess,
confirmed by histologic analysis
showing active endocarditis.

22. Clinical Criteria
Clinical criteria include either
two major criteria or one major
and three minor criteria or five
minor criteria from the
following list:

23. Major criteria
Positive blood culture results with a typical
microorganism for infective endocarditis
from two separate blood cultures
(viridans streptococci, including
nutritionally variant strains; S. bovis,
HACEK group, or community-acquired S.
aureus or enterococci in absence of a
primary focus)

24. Major criteria
Persistently positive blood culture result,
defined as recovery of a microorganism
consistent with infective endocarditis from
blood cultures drawn more than 12 hours
apart or all of three or a majority of four or
more separated blood cultures with first
and last drawn at least 1 hour apart

25. Echocardiogram result positive for
infective endocarditis, including one of the
following:
Oscillating intracardiac mass on valve or
supporting structures, in the path of
regurgitant jets, or on implanted material
New partial dehiscence of prosthetic valve
New valvular regurgitation (increase or
change in preexisting murmur )

26. Minor criteria
Predisposition: predisposing heart condition or
IV drug use
Fever: body temperature >38" C (100.4" F)
Vascular phenomena: major arterial emboli,
septic pulmonary infarcts, mycotic aneurysm,
intracranial hemorrhage, conjunctival
hemorrhages, Janeway lesions
Immunologic phenomena: glomerulonephritis,
Osler nodes, Roth spots, rheumatoid factor

27. Minor criteria
Microbiologic evidence: positive blood culture
result but not meeting major criterion as noted
previously or serologic evidence of active
infection with organism consistent with infective
endocarditis.
Echocardiogram: consistent with infective
endocarditis but not meeting major criterion as
noted previously .

28. Since the original Duke
criteria were published in
1994, several refinements
have been made based on
studies evaluating the
sensitivity and specificity of
the criteria:

29. •Bacteremia with Staphylococcus aureus
was included as a major criterion only if it was
community acquired.
Subsequent research has shown that a
significant proportion of patients
with nosocomially acquired staphylococcal
bacteremia will have documented infective
endocarditis.
Consequently, S. aureus bacteremia is
now included as a major criterion
regardless of whether the infection is
nosocomial or community acquired.

30. •An additional major criterion was added as
follows:
•Single blood culture result
positive for Coxiella burnetii or anti-phase 1
immunoglobulin G antibody titer >1:800.
•An additional statement was added to the
major criteria regarding
endocardial involvement and an
echocardiogram positive for infective
endocarditis.

31. The statement now includes
the following:
Transesophageal echocardiography (TEE) is
recommended for patients with prosthetic
valves, diagnoses rated at least
"possible infective endocarditis"
by clinical criteria,or complicated infective
endocarditis (paravalvular abscess)
Transthoracic echocardiography (TTE) should
be the first test in other patients.

32. •The echocardiogram minor criterion was
eliminated.
•The category of "possible endocarditis"
was adjusted to include the following
criteria: one major and one minor criterion
or three minor criteria.
•This so-called floor was designated to
reduce the proportion of patients assigned
to the "possible" category.

33. The organisms that
most often cause
endocarditis

34. •The etiologic agents of infective
endocarditis include the following
•Streptococci: 60%-80% .
•Viridans streptococci: 30%-40% .
•Enterococci: 5%-18% .
•Gram-negative aerobic bacilli: 1% -13%
•Other streptococci: 15%-25%.
•Coagulase-positive organisms: 10%-27%
•Coagulase-negative organisms: 1 %-3%
•Fungi: 2%-4% Staphylococci: 20%-35%

35. Pseudomonas aeruginosa
Is also more commonly seen in patients using
IVdrugs.
•In patients with prosthetic valves, the
microbiology is somewhat dependent on
whether they have early (<2 months after valve
replacement) versus late (>I2 months)
endocarditis.
S. aureus tends to be the most
common etiologic agent of infective
endocarditis in intravenous (IV) drug
users.

36. Staphylococci
account for 40% to 60% of the cases of
early onset prosthetic valve endocarditis.
Coagulase-negative
staphylococci
Account for approximately 30% to
35% of cases,
S. aureus
accounts for approximately 20% to
25%.

37. Patients who have fungal
endocarditis are often IV drug
users, have recently undergone
cardiovascular surgery, or have
received prolonged IV antibiotic
therapy.

38. HACEK organisms
How often do they cause
endocarditis?
HACEK is an acronym for a group of
fastidious, slow-growing, gram-negative
bacteria

39. •H: Haemophilus parainfluenzae,
Haemophilus aphrophilus,
Haemophilus paraphrophilus, .
Haemophilus influenzae .
•A : Actinobacillus
actinomycetemcomitans .
•C : Cardiobacterium hominis .
•E : Eikenella corrodens
•K: Kingella kingae, Kingella
denitrificans

40. These HACEK organisms account for
approximately 5% to 10% of cases of
community-acquired endocarditis.
Because an increasing number of these
organisms produce p-lactamase, they
should be considered resistant to
ampicillin.
The treatment of choice is
ceftriaxone or other third or fourth-
generation cephalosporins

41. associated
Endocarditis
Health care-associated native valve
endocarditis was present in 34% of non-IV
drug-using patients. Of these 54% had
nosocomial and 46% had nonnosocomial
infections (infections developing outside the
hospital but with extensive health care
contact [i.e., dialysis centers, outpatient
antibiotic programs, nursing homes]).
Patients with health care-associated native
valve endocarditis and without a history of
injection drug use were more likely to have S.
aureus (including methicillin-resistant S. aureus

42. prevalence of health care
associated
Endocarditis
Health care-associated native valve
endocarditis was present in 34% of non-IV
drug-using patients.
Of these 54% had nosocomial and 46% had
nonnosocomial infections (infections
developing outside the hospital but with
extensive health care contact [i.e., dialysis
centers, outpatient antibiotic programs,
nursing homes]).

43. Patients with health care-associated
native valve endocarditis and without
a history of injection drug use were
more likely to have S. aureus
(including methicillin-resistant S.
aureus [MRSA])
And had a higher mortality rate than
those with community-acquired
infections.

44. Role of echocardiography in the
diagnosis and
management of endocarditis
Echocardiography is an essential tool
in the diagnostic work-up of a patient
with suspected endocarditis.
The primary objective is to identify,
localize, and characterize valvular
vegetations.

45. However, echocardiography is also potentially
important in the management of endocarditis.
Identification of an abscess may indicate the
need for surgical intervention.
Patients may also benefit from repeating the
echocardiography once a definitive diagnosis
has been established to assess
complications, including congestive heart
failure and atrioventricular block, which
suggest worsening valvular and myocardial
function.

46. It is important to emphasize that
echocardiographic findings should
always be interpreted in
coordination with clinical
information.

47. The TEE is more sensitive than a TTE for the
diagnosis of endocarditis.
Sensitivities of the different modalities have
ranged from 48% to 100% for TEE and from
18% to 63% for TTE .
This is in part related to the fact that the
transesophageal approach allows closer proximity to
the heart and therefore can be performed at higher
frequencies, providing greater spatial resolution.
It can identify structures
as small as 1 mm.
TEE is the preferred modality in patients with
prosthetic valves.

48. The spatial resolution of the TTE may be limited
by overlying fat in obese patients or
hyperinflated lungs from chronic obstructive
pulmonary disease or mechanical ventilation.
The TTE may only be able to identify structures
as small as 5 mm.
TEE is the preferred modality in patients with a
higher pretest probability of disease or in
patients in whom the TTE would be less
sensitive, that is, with obesity, lung
hyperinflation, or prosthetic valves.

49. Recently, echocardiography is
highly recommended
in patients with
at least one of the following
clinical prediction criteria:

50. Prolonged bacteremia
(> 4 days elapsed between the first
blood culture to yield S. aureus and
first negative follow-up blood culture,
or if the blood
cultures were not performed),
Presence of a permanent intracardiac
device, hemodialysis dependency, spinal
infection, and nonvertebral osteomyelitis.

51. Although echocardiography has
become an essential diagnostic tool
in patients with suspected
endocarditis
No definitive echocardiographic
features can reliably distinguish
infection from those lesions that
are noninfective.

52. Cardiac computed tomography (CT) and
magnetic resonance imaging have been used
in diagnosing complications of infective
endocarditis, and in at least one study cardiac
multislice CT was shown to be as effective as
TEE.
However, at this time they are not part of the
current standard of care in diagnosing
infective endocarditis.

53. A perivalvular abscess in patients
with endocarditis
The presence of a perivalvular abscess
should be considered in patients with
pericarditis, congestive heart failure
(CHF) , IV drug use, S. aureus infection,
prosthetic valve endocarditis, aortic valve
disease, or persistent fever or bact-
eremia while taking appropriate
antibiotics.

54. A perivalvular abscess in patients
with endocarditis
Formal evaluation has suggested that
previously undetected atrioventricular or bundle
branch block may be a significant correlate of a
perivalvular abscess.
Aortic valve involvement and IV drug use have
also been found to be signific-ant factors in
predicting the presence of a perivalvular
abscess.

55. The optimal timing,
volume, and number of
blood cultures for a
patient in whom
infective endocarditis
is suspected

56. Multiple blood cultures are necessary.
Two blood cultures performed with adequate
volumes of blood will identify approximately
99% of patients with culture-positive
bacteremia.
However, this does not apply to patients who
have received empirical antibiotics, patients
with fungal endocarditis, or organisms that are
difficult to culture.

57. Multiple blood cultures increase the yield,
help distinguish between contamination
and true bacteremia
And prove continuous bacteremia
Characteristic of infective endocarditis.
If the first set of blood culture results is
negative, it is important to realize that
repeating blood cultures may be important
if the pretest probability of endoc-arditis
remains high.

58. Although it makes sense that the
optimal time to obtain blood
culture specimens is
During the hour before the
onset of chills or fever spikes,
in reality this is not practical.

59. Because of the continuous bacteremia
associated with endocarditis, timing is less
important, and waiting to initiate therapy in a
patient with acute disease with a particularly
virulent organism such as S. aureus is not
warranted.
Two to three blood cultures should
be obtained within 5 minutes of
each other before initiation of
antimicrobial therapy.

60. However, if the patient has a
clinical course suggestive of
subacute endocarditis,
obtaining blood cultures over
several hours to document
continuous bacteremia would
be prudent.

61. In general, 20 mL of blood
should be obtained for each two-
bottle blood culture set.
It should also be stressed that
each blood culture set requires a
separate venipuncture site.

62. S. aureus bacteremia with endocarditis
could be identified on the basis of three
characteristics:
Community-acquired infection,
absence of a primary focus of
infection, and presence of metastatic
foci of infection.

63. However, in prospectively identified patients
with S. aureus bacteremia who undergo early
echocardiography, approximately 25% will
have evidence of endocarditis by TEE.
Clinical findings and predisposing heart
disease did not distinguish those with or
without endocarditis.
In addition, a substantial portion of these
patients had hospital-acquired S. aureus
bacteremia.

64. Nonbacterial thrombotic
endocarditis (NBTE)
NBTE refers to small, sterile vegetations on
cardiac valves from platelet-fibrin deposits.
The cardiac lesions most commonly resulting in
NBTE include mitral regurgitation, aortic
stenosis, aortic regurgitation, ventricular septal
defect, and complex congenital heart disease.

65. NBTE may also result from
A hypercoagulable state, and sterile
vegetations
can be seen in systemic lupus erythematosus
(i.e., Libman-Sacks endocarditis),
Antiphospholipid antibody syndrome, and
collagen vascular diseases.
Noninfectious vegetations can also be seen
in patients with malignancy (e.g., renal cell
carcinoma or melanoma), burns, or even acute
septicemia.

66. Other lesions that may be somewhat
misleading include myxomatous valves,
benign cardiac tumors, and degenerative
thickening of the valves.
Lambl excrescences, which are multiple small
tags on heart valves seen in a large number of
adults at autopsy, can also be confused with
infectious vegetations; however, these tend to
be much more filamentous in appearance.

67. Causes of culture-negative
endocarditis
Approximately 2% to 30% of patients with
infective endocarditis will have sterile blood
culture specimens; however, it is more likely to
be 5% with use of strict diagnosis criteria.
Potential causes of culture-negative
endocarditis include the following:
•Prior antibiotic usage

68. Potential causes of culture-negative
endocarditis include the following:
•Prior antibiotic usage
•NBTE or an incorrect diagnosis
•Slow growth of fastidious organisms, including
anaerobes, HACEK organisms, nutritionally
variant streptococci, or Brucella species
•Obligate intracellular organisms, including
rickettsia, chlamydiae, Tropheryma whippelii, or
viruses

69. Potential causes of culture-negative
endocarditis include the following:
•Other organisms, including C. burnetii (the
etiologic agent of Q fever) and Legionella,
Bartonella, or Mycoplasma species .
•Subacute right-sided endocarditis .
•Fungal endocarditis
•Mural endocarditis, as in patients with
ventricular septal defects, post-myocardial
infarction thrombi, or infection related to
pacemaker wires
•Culture specimens taken at the end of a long
course, usually > 3 months

70. Conduction abnormalities can be
associated with endocarditis
Right and left bundle branch blocks, second-
degree atrioventricular block, and complete
heart block.
Heart block generally is the result of extension
of infection to the atrioventricular node or the
bundle of His.
Most patients with heart block have
involvement of the aortic valve.

71. Conduction abnormalities occurred in
approximately 10% of patients with native valve
endocarditis.
Mitral valve endocarditis
may cause first- or second-degree heart block,
but third-degree heart block would be unusual.
Aortic valve endocarditis
can cause first- or second-degree heart block
as well as bundle branch blocks, hemiblocks,
and complete heart blocks.

72. It should be remembered that the
electrocardiogram (ECG) is specific but
not sensitive for involvement of the
conduction system.
Consequently, one could have a valve
ring abscess but not have conduction
abnormalities on the ECG.
Complete heart block may be preceded
by prolongation of the PR interval or a left
bundle branch block.

73. Conduction abnormalities
in the setting of endocarditis may
occur for other
reasons as well, including
Myocardial infarction (rarely),
myocarditis, or pericarditis.

74. ECG findings may also have
prognostic implications because
patients with persistent
conduction abnormalities
have an
increased 1-year mortality
compared with patients who
have normal ECG findings.

75. The valves most
commonly affected in
patients with
endocarditis

76. This depends on the etiology of the
endocarditis.
In patients with native valve endocarditis, the
mitral valve alone is involved in 28% to 45%
of cases, 5% to 36% for the aortic valve
alone, and 0% to 35% for both valves
combined.
The tricuspid valve is involved alone 0% to
6% of the time, and the
pulmonic valve is involved in < 1% of the
cases of endocarditis.

77. Endocarditis occurs in approximately 5% to
15% of injection drug users admitted to the
hospital for acute infection.
In these patients, the frequency of
valvular involvement is as follows:
tricuspid valve alone or in combination,
50%; aortic valve alone, 19%; mitral valve
alone, 11%; and aortic plus mitral, 12%.

78. In patients with prosthetic valve
endocarditis, a difference does not seem to
exist in the incidence of endocarditis at the
aortic compared with the mitral location.
The overall risk of endocarditis is similar with
a mechanical valve compared with a
bioprosthetic valve; however, slight
differences exist in the risk on the basis of the
length of time after surgery.

79. Within the first 6 postoperative months,
mechanical valves have a slightly increased
risk of infection
However, no significant increased risk was
seen within the first 5 years after surgery with
mechanical valves compared with
bioprosthetic valves.
After 5 years, the risk for endocarditis for
bioprosthetic valves is slightly greater than
that for mechanical valves.

80. In patients with
fungal endocarditis
the aortic valve was involved 44% of
the time either alone or in combination
with other valves
The mitral valve, 26% alone or in
combination
And the tricuspid valve, 7%
Other locations were documented in
18% of patients.

81. The clinical differences
between right-sided and
left-sided
endocarditis

82. In patients with right-sided
endocarditis
(either the tricuspid or pulmonic
valve)
Particularly injection drug users
with tricuspid valve endocarditis
Only 35% will have an audible
murmur.

83. In general, symptoms and
complications arise from
involvement of the pulmonary
vasculature
And are characterized by multiple
pulmonary septic emboli that may
cause pulmonary infarction,
abscesses, pneumothoraces,
pleural effusions, or empyema.

84. In addition, multiple pulmonary
emboli may result in right-sided
heart failure with chamber dilatation
and worsening tricuspid
regurgitation.
Clinical symptoms associated with
these complications may include
chest pain, dyspnea, cough, and
hemoptysis.

85. Peripheral embolic phenomena and
neurologic involvement are
generally absent in patients with
right-sided endocarditis
And, when they do occur in the
setting of right-sided endocarditis,
involvement of the left side or
paradoxical embolization should be
considered.

86. Patients with left-sided endocarditis
(aortic or mitral)
Generally have greater
hemodynamic consequences
And are more likely to have
congestive heart failure.
Systemic embolization
(brain, kidney, spleen)
is more common with left-sided
lesions.

87. The appropriate empirical
therapy
(cultures pending)
for patients with
presumptive infective
endocarditis

88. Acute
Nafcillin or oxacillin, 2 g IV every 4
hours, plus gentamicin or tobramycin, 1
mg/kg IV every 8 hours, or vancomycin,
15 mg/kg every 12 hours IV (dosing
interval based on creatinine clearance)
plus gentamicin, 1 mg/kg every 8 hours.

89. Acute:
Some experts would add ampicillin,
2 g IV every 4 hours, to the
previously described nafcillin
regimen to cover the possibility of
enterococci.

90. Subacute
Ampicillin and sulbactam, 3 g IV
every 4 to 6 hours, plus gentamicin
or tobramycin, 1 mg/kg every 8
hours IV, or vancomycin, 15
mg/kg every 12 hours IV (dosing
interval based on creatinine
clearance), plus ceftriaxone, 2 g
every 12 hours IV.

91. Subacute
Prosthetic valve
Vancomycin, 15 mg/kg every 12
hours (dosing interval based on
creatinine clearance), plus
gentamicin, 1 mg/kg every 8 hours
IV, plus rifampin, 600 mg/day orally.

92. Surgical therapy

93. Clinical situations that warrant
surgical intervention include
moderate and severe (i.e., New York
Heart Association class Ill or IV) or
progressive and refractory CHF,
valve dehiscence, rupture, or
fistula.

94. Clinical situations that warrant
surgical
Although CHF has a worse prognosis with
medical therapy alone, an increased surgical
risk also exists.
Delay in surgery may also lead to worsening
cardiac decompensation or
perivalvular extension, which will increase
operative mortality as well as secondary
complications.

95. Several studies have shown
benefits in mortality statistics
with surgical intervention.
Progressive heart failure in the
presence of aortic or mitral valve
regurgitation requires surgery.

96. Right-sided endocarditis with
tricuspid regurgitation is
reasonably well tolerated if the
pulmonary vascular resistance is
not increased, and surgery is
often not required.

97. Other indications for surgery include
perivalvular extension of infection, persistent
bacteremia without evidence of an
extracardiac source of bacteremia, mechanical
valve obstruction, fungal endocarditis,
prosthetic endocarditis, and difficult-to-treat
organisms, including Pseudomonas species,
G. burnetii, Brucella species.
Surgery may also be indicated to avoid
embolizations.

98. Conventional wisdom has been that indications
for surgery to avoid embolization have been
two or more major embolic events during
therapy.
The risk of embolization also decreases
significantly during the first 1 to 2 weeks of
antibiotic therapy.

99. Relationship between duration of antibiotic
therapy before surgery and operative
mortality
Although it is important to have adequate
antibiotic coverage during surgery, the duration
of antibiotic therapy does not generally
influence operative mortality.
The incidence of reinfection of newly
implanted valves is approximately
3% and may be as high as 10%.

100. The neurologic
manifestations of
endocarditis

101. Overall, the incidence of central nervous
system involvement during the course of
infective endocarditis ranges between
20% and 40%.
Neurologic symptoms are the presenting
manifestations in endocarditis
approximately 16% to 23% of the time;
however, there are generally other clues
to the diagnosis.

102. The most common neurologic
manifestation is stroke, and this
accounts for approximately 50% to
60% of all neurologic complications.
Stroke generally occurs from
cerebral emboli with infarction, but
hemorrhage or abscess may occur
as well.

103. Other neurologic manifestations with their
associated main clinical presentations include
encephalopathy (decreased level of
consciousness), seizures, severe or localized
headache, psychiatric syndromes from minor
personality changes to more severe psychiatric
syndromes (generally in elderly patients),
various dyskinesias, visual disturbances,
spinal cord involvement (paraplegia or
tetraplegia), peripheral nerve involvement
(mononeuropathy), and meningitis, which is
more common with S. aureus and
Streptococcus pneumoniae (with or without
focal signs).

104. Ocular complications include acute
embolic occlusion of the central retinal
artery, which may result in sudden vision
loss.
Other complications that have been well
documented include involvement of
cranial nerves Ill, IV, and VI,
{ Occulomotor ,Trochlear and Abducent
nerves }
which can lead to diplopia, deviation of
the eyes, nystagmus or unequal pupils,
retinal hemorrhages, and
endophthalmitis.

105. Intracranial mycotic aneurysms
(ICMAs) occur
ICMAs are uncommon, and although
they constitute only 2% to 6% of all
intracranial aneurysms
80% of these are identified in the
setting of infective endocarditis.

106. Intracranial mycotic aneurysms
(ICMAs) occur
•Among patients with endocarditis, only 1
% to 5% will have a recognized ICMA.
•The mortality rate is approximately 60%,
and many patients are seen initially with a
sudden subarachnoid or intracerebral
hemorrhage.
•Rupture of an ICMA may occur while the
patient is being treated for endocarditis or
after completion of therapy.

107. The warning signs of ICMA? How
is it diagnosed
•Serious warning signs that should
prompt further investigation for the
possibility of an ICMA include
severe localized headache and
other focal neurologic signs, such as
seizures, ischemic deficits, and
cranial nerve abnormalities.

108. •Although sudden rupture is not an
uncommon presentation of an ICMA
Some aneurysms may leak slowly
before rupture and produce
meningeal irritation manifested by
cerebrospinal fluid that is sterile but
shows a moderate number of red
cells and a neutrophilic reaction.

109. •When hemorrhage is suspected, either
a CT angiogram or magnetic resonance
angiography (MRA) should be obtained.
•Recent studies have shown that
CT angiography and MRA
Have similar results in the detection of
noninfectious intracranial aneurysms,
and it is likely that the same would be
true for infectious intracranial aneurysms.

110. •If hemorrhage has been
confirmed and surgery is
considered, conventional
angiography is still the most
appropriate diagnostic procedure
to pinpoint location and anatomic
relationships.

111. Global Critical Care
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Wellcome in our new group ..... Dr.SAMIR EL ANSARY

112. GOOD LUCK
SAMIR EL ANSARY
ICU PROFESSOR
AIN SHAMS
CAIRO
elansarysamir@yahoo.com