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ENDOCARDITISSAMIR EL ANSARY
Global Critical Carehttps://www.facebook.com/groups/1451610115129555/#!/groups/1451610115129555/
Wellcome in our new group ..... Dr.SAMIR EL ANSARY
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 asChronic wasting
syndrome mimicking cancer or human
immunodeficiency virus infection.
Signs and symptoms of embolic episodes are
determined
By the locationof 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 ofregurgitant jets, or on implanted material
New partial dehiscence of prosthetic valveNew 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 resultpositive 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 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.
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 organismsHow 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 isceftriaxone 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
those with community-acquired infections.
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 withat 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 bacteremiaAnd 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 isDuring 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 fromA hypercoagulable state, and sterile
vegetationscan 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 abnormalitiesin the setting of endocarditis may
occur for otherreasons as well, including
Myocardial infarction (rarely), myocarditis, or pericarditis.
ECG findings may also have prognostic implications because
patients with persistent conduction abnormalities
have anincreased 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 thepulmonic 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 infectionHowever, 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-sidedendocarditis
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 orperivalvular 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
mortalityAlthough 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/1451610115129555/
Wellcome in our new group ..... Dr.SAMIR EL ANSARY
