CT scanning is the preferred initial imaging study for diagnosing subarachnoid hemorrhage (SAH). CT scans can detect blood in the subarachnoid spaces around the brain and have a sensitivity of 93-100% within 24 hours. The amount of blood seen on CT scans correlates with risk of developing vasospasm and can help prognosticate. While CT is very accurate for diagnosing acute SAH, its sensitivity decreases after 5-7 days. If CT is negative but clinical suspicion remains, lumbar puncture should be performed.

1. Role of imaging in
subarachnoid hemorrhage

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CONTENTS :
1_ Introduction to subarachnoid hemorrhage
2_ Symptoms of SAH and its presentation
3_ Causes and risks of occurrence
4_Complications
5_ Pathology of SAH
6_ Diagnosis and role of imaging
- CT scan and its sensitivity/specificity
And the modified Fischer scale
- Role of MRI and Angiography and lumbar puncture following CT scan
- Use of ultrasonography and radiography and nuclear image as vasospasm, fracture assessment
7_ Treatment and prognosis
8_ Refrences

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INTRODUCTION / DEFINITION
Subarachnoid hemorrhage -SAH- is a life-threatening type of stroke caused by bleeding into
the space surrounding the brain. SAH can be caused by a ruptured aneurysm, AVM, or head
injury. One-third of patients will survive with good recovery; one-third will survive with a
disability; and one-third will die
Subarachnoid hemorrhage is uncommon type of intracranial hemorrhage which are group of
serious medical emergencies that the buildup of blood within the skull can lead to increases in
intracranial pressure furthermore to brain herniation
Approximately 10-30% of patients with subarachnoid hemorrhage die before reaching medical
attention. For those reaching a hospital alive, mortality rates for nontraumatic subarachnoid
hemorrhage have been reported in the 30-60% range.
Different types of Bleeding in various anatomical positiona of brain
/radiology: Figure 1
Figure 1

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SAH is bleeding into the subarachnoid space—the area between the arachnoid membrane and
the pia mater surrounding the brain
SYMPOTOMS/HOW IT IS PRESENTED!
When SAH develops, it has several symptoms. The main symptom is a sudden, severe
headache, which is more intense at the base of the skull. It is often described as the worst
headache people have ever experienced. Some people may even feel a popping sensation in
their head before the hemorrhage begins.
may also have:
2-neck pain 3-numbness throughout your body 4-shoulder pain 5-seizures 6-confusion 7-
irritability 8-sensitivity to light 9-decreased vision 10-double vision 11-nausea 12-vomiting
13-rapid loss of alertness
CAUSES AND RISKS TO SUBARACHNOID HEMORRHAGE:
1-Trauma 2-spontaneous 3-ruptured berry aneurysm: 85% 4-perimesencephalic hemorrhage:
10% 5-arteriovenous malformation 6-cerebral amyloid angiopathy 7-ruptured mycotic
aneurysm 8-reversible cerebral vasoconstriction syndrome 9-dural arteriovenous fistula 10-
spinal arteriovenous malformation 11-venous infarction 12-intradural arterial dissection 13-
pituitary apoplexy 14-cocaine use 15-cerebral vasculitis 16-anticoagulation therapy
In summary : often seen in the older people who have fallen and hit their head. Among the
young, the most common injury leading to SAH is motor vehicle accidents. Five to 10% of
strokes are caused by SAH
So aneurysmal hemorrhage may occur at any age, but it’s most common between age 40 and
65. Brain aneurysms are more common in women, in smokers, and in those with high blood
pressure

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COMPLICATIONS:
vasospasm, hydrocephalus, seizures, and rebleeding
and less commonly: hypothalamic dysfunction, hyponatremia, left ventricular dysfunction and
myocardial ischemia
PATHOLOGY OF {SAH} IN BRAIN
Three distinct patterns of subarachnoid hemorrhage have been described each with their own
etiology and treatment/prognostic implications:
Suprasellar cistern with diffuse peripheral extension; Figure 2
figure 2

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Perimesencephalic and basal cisterns;
Figure 3; the red arrow showing hyperdensity on an axial view of CT scan
figure 3
Isolated cerebral convexity;
Figure 4, hyperdenstity in axial view of CT scan the arrow; A, hyperinenstiy in
MRI; B and C
figure 4

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DIAGNOSIS AND THE ROLE OF IMAGING
Computed tomography (CT) scanning without intravenous contrast enhancement is the
preferred initial diagnostic study, with cerebral angiography the next procedure of choice
Computed Tomography
On CT scans, subarachnoid hemorrhage {SAH} looks like a high-attenuating, amorphous
substance that fills the normally dark, CSF which filled subarachnoid spaces around the brain.
The normally black subarachnoid cisterns and sulci may show white in acute hemorrhage.
These findings are most evident in the largest subarachnoid spaces, such as the suprasellar
cistern and Sylvian fissures.
Subarachnoid hemorrhage (SAH). A nonenhanced computed tomography scan of the brain that
demonstrates an extensive SAH filling the basilar cisterns in a patient with a ruptured
intracranial aneurysm; Figure 5
Figure 5

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A computed tomography scan obtained after angiography of a rupturing bilobed aneurysm of
the posteroanterior cerebellar artery. This image shows a subarachnoid hemorrhage and contrast
medium filling the right sylvian fissure, the interhemispheric fissure, and the lateral and third
ventricles; Figure 6
Figure 6
Over the cerebral hemispheres, SAH is exhibited by the filling in of normally low-attenuating
(black) sulci with high-attenuating (white) subarachnoid blood. SAH is most conspicuous
within 2-3 days of the onset of acute bleeding. Acute SAH is typically 50-60 Hounsfield units
(HU). The protein content of the hemoglobin molecule is predominantly responsible for the
attenuating effect of blood; therefore, the absolute measurement in HU varies somewhat with
the hematocrit value.
When CT scanning is performed several days or weeks after the initial bleed, the findings are
more subtle. The initial high-attenuation of blood and clot tend to decrease, and these appear as
intermediate gray. These findings can be isointense relative to normal brain parenchyma. If the
patient presents during this subacute period, evidence of SAH includes decreased visualization
of the normally hypoattenuating fluid within the sulci and basal cisterns and enlargement of the
ventricles caused by communicating hydrocephalus.

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In addition to detecting SAH, CT scanning is useful for localizing the source of bleeding. This
is particularly important in cases of multiple intracranial aneurysms, which occur in 20% of
patients. Localization of SAH on CT scans correlates with the location of the ruptured
aneurysm. The presence of blood in the anterior interhemispheric fissure or the adjacent frontal
lobe suggests rupture of an anterior communicating artery aneurysm. Sylvian fissure clot
correlates with an ipsilateral middle cerebral artery aneurysm. Blood predominantly localized
in the posterior fossa suggests bleeding from a posterior circulation aneurysm.
The ability to discern the location of an aneurysm rupture is limited by the fact that many
patients with SAH have a diffuse distribution of blood in the subarachnoid spaces and basal
cisterns on CTscans. The effect of gravity has been suggested as a possible cause for misleading
patterns of blood distribution. Published studies report a wide variation in the accuracy of CT
scanning in localizing the bleeding source.
In addition to the diagnosis of SAH and the localization of the bleeding site, CT scanning also
allows for some degree of prognostication, particularly in the probability of the development of
vasospasm. In 1980, Fisher originally demonstrated that the amount of blood and the presence
of localized clots in the subarachnoid space are correlated with a higher incidence of delayed
symptomatic arterial spasm; this correlation has since been well validated.
A specialized CT scanning technique involving the inhalation of xenon gas allows for the
quantitative determination of regional cerebral blood flow, which can be of value in monitoring
the severity and effect of cerebral vasospasm.
Degree of confidence
Nonenhanced CTscanning of the brain is the study of choice for the initial evaluation of patients
with potential SAH. The sensitivity is 93-100% in patients presenting with SAH within 24 hours
of symptom onset. Conversely, the detection of SAH on CTscanning has a 0-7% false-negative
rate during this period. As the time from the onset of the bleeding episode increases, the
sensitivity of CT scanning decreases. At 5 days, the sensitivity is approximately 85%; at 1 week,
it is approximately 50%.
If a high clinical concern for SAH exists and the CT brain scan is negative, a lumbar puncture
(LP) is indicated. Although LP is considered to have a higher sensitivity than that of CT
scanning, its specificity is lower. Additionally, LP is an invasive procedure.

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In patients with a negative noncontrast CT and xanthochromia detected on lumbar puncture, a
CT angiography (CTA) can be performed to evaluate for a saccular aneurysm. Although some
institutions will perform catheter angiography after a negative CTA on clinical grounds,
multiple studies have reported that CTA is adequate to exclude aneurysms in cases with no
visible blood on CT.
False positives/negatives
Various normally attenuating extra---axial structures perhaps are misinterpreted as SAH, and
these can lead to false-positive results. The falx cerebri, tentorium cerebelli, and intracranial
blood can be confused for small amounts of SAH. Streak artifacts from bone at the skull base
and partial volume-averaging artifacts may also lead to a false diagnosis of SAH. False-negative
studies may occur from errors in interpretation or from failure of the technology itself.
Perceptual errors aside, several conditions may lead to the inability of CT scanning to detect a
SAH.
An interval of days to weeks between the bleeding episode and the CT scan allows for the
breakdown and resorption of some or all of the hemoglobin from the subarachnoid space,
decreasing the contrast between the SAH and CSF. Similarly, small amounts of SAH may be
masked by dilution by the CSF and/or CT volume averaging with CSF. Motion artifacts
occurring in the scans of agitated or confused patients can lead to either false-positive or false-
negative SAH diagnoses.
"Pseudosubarachnoid hemorrhage" can occur when high-density areas are seen in the cisterns
and cortical sulci in the setting of severe brain edema. Although the mechanism is not clear, it
may be related to a combination of decreased attenuation of the brain parenchyma and
distention of the superficial vessels secondary to elevated intracranial pressure. {Yuzawa et al}
suggested that "pseudosubarachnoid hemorrhage" can be differentiated from true subarachnoid
hemorrhage by a lower attenuation (pseudosubarachnoid hemorrhage is < 43 HU) and an
absence of intraventricular high attenuation (patients with subarachnoid hemorrhage, however,
may not have intraventricular blood).
In a study of patients with aneurysmal SAH, CT evidence of SAH was present but went
unrecognized in 4% (18 of 452 cases), according to the final radiology report in cases of
presumed CT-negative aSAH

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The modified Fisher scale
is a method for grading subarachnoid hemorrhage (SAH) secondary to intracranial aneurysm
rupture, seen on non-contrast CT. It was developed from the original Fisher scale which was
modified to account for patients with thick cisternal blood and concomitant intraventricular
(IVH) or intraparenchymal hemorrhage.
Moreover, the risk of developing vasospasm progressively increases with each grade of the
modified Fisher scale. Whereas the risk was highest for grade 3 and then decreased for grade 4
while using the original Fisher scale.
Classification
grade 0
no subarachnoid hemorrhage (SAH)
no intraventricular hemorrhage (IVH)
incidence of symptomatic vasospasm: 0% 3
grade 1
focal or diffuse, thin SAH
no IVH
the incidence of symptomatic vasospasm: 24%
grade 2
thin focal or diffuse SAH
IVH present
the incidence of symptomatic vasospasm: 33%
grade 3
thick focal or diffuse SAH
no IVH
the incidence of symptomatic vasospasm: 33%

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grade 4
thick focal or diffuse SAH
IVH present
the incidence of symptomatic vasospasm: 40%
Magnetic Resonance Imaging
Fluid attenuated inversion recoveryy {(flair) is the most sensitive MRI pulse sequence for the
detection of subarachnoid hemorrhage (SAH). On flair images, SAH looks like a high signal-
intensity…white… in normally low signal-intensity (black) CSF spaces. In cases of SAH, flair
and CT scanning have similar findings. T2 and T2 weighted images could potentially
demonstrate SAH as low signal/intensity in normally high signal.intensity subarachnoid spaces.
On T1 weighted images, acute SAH often appear as intermediate-intensity or high-intensity
sigal in the subarachnoid space
MRA could be useful for estimating aneurysms and other vascular lesions that cause SAH. The
low sensitivity for aneurysms smaller than 5 mm, the inability to evaluate small aneurysm
contour irregularities, and difficulty in obtaining high-quality images in patients who are
agitated or confused limits the utility of MRI in the diagnosis of acute SAH.
Onee of studies that performed on 49 patients with aneurysmal SAH found that T2 was highly
predictive of the location of the initial hemorrhage (positive predictive value, 95%), especially
in the Sylvian cisterns (positive predictive value, 100%) and the anterior interhemispheric
fissure (positive predictive value, 90%).
Axial FLAIR cerebral MRI ; Figure 7
Figure 7

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Subarachnoid sulcal hemorrhages (A, orange box) are investigated by comparison
with subarachnoid hemorrhages affecting the basal cisternae (A, white box); Figure 8
Figure 8
Degree of confidence
In many types of studies suggest that Flair MRI is as sensitive as or more sensitive than CT
scannings in the evaluatiion of acute SAH; however, compared with lumbar puncture, Flair
MRI cannot exclude SAH. Relative to CTscanning, MRI is often more valuable in the subacute
phase of SAH, in which the density of hemorrhage on CT scans decreases. In patients with
equivocal findings on CT scanning or angiography or in those patients who cannot undergo CT

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scanning or conventional angiography, MRI and…or MRA may provide clinically useful
information.
False positives/negatives
Magnetic field inhomogeneity can lead to artifactual increase in signal intensity in sulci over
the cerebral convexities on FLAIR images, which can mimic SAH. CSF flow artifacts can
mimic the appearance of SAH on either T1- or T2-weighted images. Intracranial thrombus can
appear similar in signal to flowing blood on time-of-flight (TOF) gradient-echo (GRE) MRA.
In uncooperative patients, motion artifacts may produce images that can lead to either false-
positive or false-negative interpretations.
Hyperintensity in the subarachnoid space on Flair images can also be secondary to other
pathologies, such as meningitis or meningeal carcinomatosis. It is important to know whether
recent contrast-enhanced MRIs have been performed, as delayed leakage of gadolinium into
the subarachnoid space can result in hyperintense signal on Flair images. This has been reported
to result from contrast studies performed 24-48 hours before MRI scanning in patients with
intact renal function and an intact blood-brain barrier. However, this is typically associated with
abnormalities that can alter perfusion and disrupt the blood-brain barrier (eg, acute ischemic
stroke and after carotid artery and balloon stenting), as well as found in patients with renal
failure or who are receiving high doses of gadolinium Substantial increases in subarachnoid
FLAIR signal have also been reported in patients receiving 100% supplemental oxygen
Angiography
Cerebral angiography is considered the standard imaging technique for the detection of
intracranial aneurysms, arteriovenous malformations (AVMs), and fistulae. Aneurysms are
detected as focal areas of outpouching or dilatation of the arterial wall. These frequently occur
at arterial branching points in characteristic locations within or near the circle of Willis.
Cerebral angiography should include anteroposterior (AP), lateral, and one or more oblique
views of both carotid and vertebral artery contrast injection studies. A submentovertical view
is sometimes useful in demonstrating the neck of a middle cerebral artery bifurcation aneurysm
or anterior communicating artery aneurysm.

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An angiogram showing a bilobed aneurysm of a posteroinferior cerebellar artery immediately
before rupturing ; Figure 9
Figure 9
An angiogram showing the onset of an aneurysmal rupture, with extravasation of contrast
material into the subarachnoid space from the anterosuperior aspect of a bilobed aneurysm in a
posteroinferior cerebellar artery; Figure 10
Figure 10

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A later-phase angiogram of a rupturing bilobed aneurysm of a posteroinferior cerebellar artery
shows progressive opacification of the subarachnoid space in the posterior fossa; Figure 11
Figure 11
A late angiogram demonstrating contrast medium filling the posterior fossa subarachnoid
spaces, including the ambient, prepontine, and perimedullary cisterns; Figure 12
Figure 12

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Compression of the contralateral carotid artery should be performed during carotid cerebral
angiography to demonstrate the anterior communicating artery if it does not fill spontaneously
during one of the internal carotid artery injections. Carotid artery compression should be done
on a segment of the common carotid artery without atherosclerotic plaque, if possible. One
vertebral arteriogram is occasionally omitted by some angiographers if there is abundant reflux
proximal to the origin of the posterior inferior cerebellar artery of that vertebral artery when the
contralateral vertebral artery is injected with contrast medium. This technique does not,
however, depict all aneurysms. The most reliable method of aneurysm detection is the
invariable selective injection of contrast medium into both common or internal carotid arteries
and both vertebral arteries.
Cerebral angiography reliably demonstrates the presence or absence of an intracranial aneurysm
or an AVM, and it establishes the number and locations of aneurysms. Morphologic
information, such as aneurysm size and shape, helps to determine which aneurysm has bled in
a patient with multiple aneurysms. Specifically, the presence of a lobulation, tit, or a daughter
aneurysm is highly suggestive that the aneurysm is the one that has bled. In the absence of any
distinguishing aneurysm shape features or hemorrhage localization by a CT scan, the largest
aneurysm is the most likely to have bled. Features such as aneurysm location, shape, neck size,
and neck-to-maximal diameter ratio are crucial in determining whether the aneurysm is better
treated with open craniotomy or with an endovascular technique.
Degree of confidence
Cerebral angiography provides a high degree of accuracy. A small false-negative rate does
occur, probably in the range of 1-2%. A repeat cerebral arteriogram at 10-14 days is indicated
if the initial angiogram does not demonstrate the cause of a subarachnoid hemorrhage (SAH).
In a small number of patients, a follow-up angiogram will detect an aneurysm that was not
demonstrated on the initial study.
Bilateral selective external and internal carotid artery angiograms can be performed to exclude
a dural arteriovenous fistula, which is a rare cause of SAH. Bilateral vertebral arteriograms of
the neck (and, if necessary, selective thyrocervical trunk and/or careful injections of the right
superior intercostal artery) demonstrate the arterial and venous circulation of the cervical spinal
cord. In rare cases, they show a spinal vascular malformation or neoplasm, such as
hemangioblastoma, as the cause of SAH.

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Cervical spinal MRI and/or MRA may indicate the necessity of an additional arteriographic
study. If thorough arteriographic studies do not demonstrate a specific cause for an SAH, a
presumptive diagnosis of idiopathic perimesencephalic hemorrhage is sometimes made.
False positives/negatives
The reason that some aneurysms are not initially diagnosed by angiography and are only
detected on subsequent follow-up angiograms is not always evident. Vasospasm is believed to
be the most common cause. Arteriography double densities simulating aneurysm or apparent
areas of vessel wall bulge or outpouching may be caused by arterial tortuosity and
atherosclerosis or overlap of adjacent arteries on standard angiogram views. This can usually
be determined by comparing all angiographic views and, if necessary, obtaining additional
oblique arteriography views
Ultrasonography
Echoencephalography is useful for diagnosing germinal matrix and intraventricular hemorrhage
in the newborn; however, ultrasonography has no direct role in the diagnosis of subarachnoid
hemorrhage (SAH) in the adult patient. Conversely, transcranial Doppler ultrasonography has
become increasingly used in the diagnosis and management of vasospasm in patients with SAH.
Flow is most easily measured in the middle cerebral arteries, which have been found to have
flow velocities normally in the 30-80 cm/s range. Elevation to 120 cm/s indicates moderate
vasospasm, and elevation to 200 cm/s indicates severe vasospasm
The sensitivity of transcranial Doppler ultrasonographic imaging for the detection of vasospasm
has been reported to be 85-90%. Because not all vasospasm is necessarily symptomatic, the
finding must be correlated with a clinical neurologic examination to determine the appropriate
therapy.

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Nuclear Imaging
Like ultrasonography, nuclear medicine studies are not useful in the initial diagnosis of
subarachnoid hemorrhage (SAH), but they can play a role in the diagnosis of related vasospasm.
Plain radiographs
plain radiographs of the skull and orbits may be used to exclude the presence of aneurysm clips
or intraorbital foreign bodies. Plain radiographs may also be useful for evaluating facial or
cervical spinal fractures
Some neuroradiologists use skull radiographs in their routine follow-up care of patients with
aneurysm treated with coil embolization. Interval follow-up skull radiographs can be compared
with baseline studies to check for coil compaction.
DIFFERENTIAL DIAGNOSIS OF SAH
It is important to realize that apparent hyperdensity in the subarachnoid space is not
pathognomonic of subarachnoid hemorrhage. Other diagnostic possibilities include:
pseudosubarachnoid hemorrhage
bacterial meningitis
tuberculous meningitis
granulomatous meningitis
neurosarcoidosis

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TREATMENT AND PROGNOSIS
Treatment will vary according to the underlying cause, however, regardless of the source of
subarachnoid blood, a number of treatment principles and potential complications are
encountered:
elevated intracranial pressure
often require ICP monitoring
serial non-invasive screening possible in equivocal cases using sonographic indices of elevated
ICP
hydrocephalus may require extraventricular drain placement
cerebral vasospasm causing delayed cerebral ischemia
triple H therapy (Haemodilution, Hypertension, Hypervolaemia)
calcium channel blockers (e.g. nimodipine)
endovascular intervention (e.g. intra-arterial delivery of vasodilating agents (such as NO)
and/or balloon angioplasty)
hyponatremia
coronary spasm
neurogenic pulmonary edema
pulseless electrical activity (PEA) 13
Prognosis varies greatly depending on:
cause of subarachnoid hemorrhage
grade of subarachnoid hemorrhage
presence of other injuries/pathologies/co-morbidities

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A small amount of traumatic subarachnoid hemorrhage or small perimesencephalic blood has
an excellent prognosis with little if any significant long-term sequelae. A grade V aneurysmal
subarachnoid, on the other hand, has a dismal prognosis, despite aggressive treatment.
REFERENCES:
1_ Linda R. Gray .Subarachnoid Hemorrhage: Epidemiology, Management and Long-Term
Health Effect Book.2015;1:59-98
2_ Abner Gershon, MD. Imaging in Subarachnoid Hemorrhage.2016;1
3_ M.Edjlali. Subarachnoid hemorrhage in ten questions.2015;96:655-666

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