ENDOCARDITIS

SAMIR EL ANSARY

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The important clinical

manifestations of

endocarditis

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.

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.

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.

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.

Long-standing subacute

endocarditis

may present as

Chronic wasting

syndrome mimicking

cancer or human

immunodeficiency virus

infection.

Signs and symptoms of

embolic episodes are

determined

By the location

of the embolism :

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.

Immune complex formation

may lead to renal insufficiency.

Cough and shortness of

breath

with chest pain often

accompany

Pulmonary emboli

Coronary emboliOccur 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.

Unexplained heart failure in a

young patient without prior

cardiac disease should prompt

an investigation for

Infectious

endocarditis

Manifestations of

endocarditis

in elderly patients

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.

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 streptococciaccount for approximately 80% of the cases in

elderly persons, and

Streptococcus bovismay be noted more frequently in elderly patients

associated with underlying

colonic malignancy.

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.

Worsening heart failure and murmurs may be

attributed to underlying disease and therefore

erroneously neglected.

Consequently, a high index of

suspicion is necessary.

Duke criteria for the

diagnosis of

endocarditis

How have they been

modified?

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 .

Pathologic CriteriaPathologic 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.

Clinical CriteriaClinical criteria include either

two major criteria or one major

and three minor criteria or five

minor criteria from the

following list:

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)

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

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 )

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

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 .

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:

•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.

•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.

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.

•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.

The organisms that

most often cause

endocarditis

•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%

Pseudomonas aeruginosaIs 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.

Staphylococciaccount 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. aureusaccounts for approximately 20% to

25%.

Patients who have fungal

endocarditis are often IV drug

users, have recently undergone

cardiovascular surgery, or have

received prolonged IV antibiotic

therapy.

HACEK organisms

How often do they cause

endocarditis?

HACEK is an acronym for a group of

fastidious, slow-growing, gram-negative

bacteria

•H: Haemophilus parainfluenzae,

Haemophilus aphrophilus,

Haemophilus paraphrophilus, .

Haemophilus influenzae .

•A : Actinobacillus

actinomycetemcomitans .

•C : Cardiobacterium hominis .

•E : Eikenella corrodens

•K: Kingella kingae, Kingella

denitrificans

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

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]).

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

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]).

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.

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.

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.

It is important to emphasize that

echocardiographic findings should

always be interpreted in

coordination with clinical

information.

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.

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.

Recently, echocardiography is

highly recommended

in patients with

at least one of the following

clinical prediction criteria:

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.

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.

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.

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.

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.

The optimal timing,

volume, and number of

blood cultures for a

patient in whom

infective endocarditis

is suspected

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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

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

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

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.

Conduction abnormalities occurred in

approximately 10% of patients with native valve

endocarditis.

Mitral valve endocarditismay cause first- or second-degree heart block,

but third-degree heart block would be unusual.

Aortic valve endocarditiscan cause first- or second-degree heart block

as well as bundle branch blocks, hemiblocks,

and complete heart blocks.

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.

Conduction abnormalities

in the setting of endocarditis may

occur for other

reasons as well, including

Myocardial infarction (rarely),

myocarditis, or pericarditis.

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.

The valves most

commonly affected in

patients with

endocarditis

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.

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%.

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.

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.

In patients with

fungal endocarditisthe 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.

The clinical differences

between right-sided and

left-sided

endocarditis

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.

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.

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.

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.

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.

The appropriate empirical

therapy

(cultures pending)

for patients with

presumptive infective

endocarditis

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.

Acute:

Some experts would add ampicillin,

2 g IV every 4 hours, to the

previously described nafcillin

regimen to cover the possibility of

enterococci.

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.

Subacute

Prosthetic valveVancomycin, 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.

Surgical therapy

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.

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.

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.

Right-sided endocarditis with

tricuspid regurgitation is

reasonably well tolerated if the

pulmonary vascular resistance is

not increased, and surgery is

often not required.

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.

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.

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%.

The neurologic

manifestations of

endocarditis

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.

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.

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).

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.

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.

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.

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.

•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.

•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.

•If hemorrhage has been

confirmed and surgery is

considered, conventional

angiography is still the most

appropriate diagnostic procedure

to pinpoint location and anatomic

relationships.

Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/145161011512

9555/ Wellcome in our new group ..... Dr.SAMIR EL ANSARY

GOOD LUCK

SAMIR EL ANSARY

ICU PROFESSOR

AIN SHAMS

CAIRO

elansarysamir@yahoo.com