CASE

PRESENTATION

BY DR RAKESH KUMAR
PGDMRD
• CASE- A 55 year hypertensive female patient with on and off
headache SINCE 2 YRS.
• Now presented with sudden onset of severe diffuse headache
followed by unconsciousness .
• No neurological deficit.

• ON EXAMINATION
• Pulse-72/min
• Bp –140/90
• Hb-11.3
• In view of Pt. history and imaging findings …..

• is -subarachnoid haemorrhage localized to

• A contrast filled saccular outpouching measuring with
a mm wide neck oriented inferiorly and laterally arising
from M1 segment of right MCA. No arterial branches are
arising from it.
• No parenchymal hematoma
• The final diagnosis is SAH secondary to ruptured aneurysm
as described above.
DISCUSSIO
N
 Subarachnoid Space Overview
• The subarachnoid spaces (SASs) are CSF-filled cavities that lie between the
arachnoid and the pia.

• The SASs are crossed by numerous pia-covered trabeculae that extend

between the brain and the inner surface of the arachnoid.

• Prominent focal enlargements of the SASs, the cisterns, are found around the
base of the brain, midbrain/pineal region, brainstem, and cerebellum.

• Most subarachnoid cisterns are named for their adjacent structures

(e.g.suprasellar cistern, quadrigeminal cistern, cerebellopontine angle
cistern). A few are named for their size (the great cistern or “cisterna
magna”), shape, or sublocation.
Nontraumatic Subarachnoid
Hemorrhage
• Nontraumatic “spontaneous” SAH causes 3-5% of all acute “strokes.”

• Approximately 80% of these are caused by a ruptured intracranial

saccular aneurysm.

• The remainder are caused by a variety of entities including

dissections,venous hemorrhage or thrombosis, vasculitis, amyloid
angiopathy, and reversible cerebral vasoconstriction syndrome.
CAUSES OF
SPONTANEOUS SAH
Aneurysms
• The word “aneurysm” comes from the combination of two Greek words
meaning “across” and “broad.”They are widenings or dilatations of
intracranial arteries.
• Intracranial aneurysms are classified by their gross appearance-

• Saccular or “berry” aneurysms are the most common type and typically arise
eccentrically at vessel branch points.

• Pseudoaneurysms often resemble “true” saccular aneurysms (SAs) in shape

but are contained by cavitated clot, not components of arterial walls.

• Blood blister-like aneurysms are thin-walled hemispheric bulges that—as the

name suggests—resemble cutaneous blood blisters in appearance.
• Fusiform aneurysms are focal dilatations that involve the entire
circumference of a vessel, extend for relatively limited distances, and do not
arise at branch points.

• Ectasias refer to generalized arterial enlargement without focal

(“aneurysmal”) dilatation. While ectasias can affect any intracranial vessel,
the most common site is the posterior circulation
Pathophysiology Of Aneurysms
• It was previously thought that congenital defects in the tunica media
at arterial bifurcations were the source of aneurysm formation. This
has since been refuted and current beliefs hold that the mechanism
for aneurysm formation is acquired, and that aneurysms develop
gradually over one’s lifetime due to interactions with modifiable and
genetic factors

• Polycystic kidney disease, familial predisposition, hypertension,

atherosclerosis, smoking, excessive alcohol consumption (> 150
g/wk), age > 85 years, oral contraceptive use, and connective tissue
disorders have all been associated with aSAH
 Aneurysmal Subarachnoid Hemorrhage
• Aneurysmal SAH (aSAH) is an extravasation of blood into the space between the
arachnoid and pia.

• Etiology
• Aneurysmal SAH is most often caused by rupture of a saccular (“berry”) or (rarely) a
blood blister-like aneurysm.
• Other less common causes include intracranial dissections and dissecting aneurysms.

• Pathology
• LOCATION. Because most saccular aneurysms arise from the circle of Willis (COW) or the
middle cerebral artery (MCA) bifurcation, the most common locations for aneurysmal
SAH are the suprasellar cistern and sylvian fissures
• Occasionally anterior communicating artery (ACoA) aneurysm points upward and bursts
into the frontal lobe into the brain parenchyma
Clinical Issues
• DEMOGRAPHICS-peaks between the ages of 40 and 60 years.
M:F ratio is 1:2.
Aneurysmal SAH is rare in children(10%)

• PRESENTATION. Patients with aSAH present with sudden onset of the

“worst headache of my life.” The most severe form is a “thunderclap”
headache, an extremely intense headache that comes on “like a boom of
thunder” and typically peaks within minutes or even seconds.
• Other complains include neck pain,vomiting.

• Between 10-25% of patients experience symptoms days or even weeks

before the onset of overt SAH. These “sentinel” or “warning” leaks may
presage aneurysm rupture and should not be ignored
Subarachnoid Hemorrhage Clinical Severity Scales

• There are multiple clinical scales to assess the severity of aSAH.

• The 2 most widely used are the Hunt and Hess scale and the World
Federation of Neurological Surgeons (WFNS) scale,with the latter
primarily used in the research community.
•
The Hunt and Hess and WFNS scales correlate with mortality; the
higher the score, the higher the inpatient mortality.

• A third scale, the Fisher Grade, uses quantity of blood on CT

appearance to predict the risk of symptomatic cerebral vasospasm,
which is currently a relatively common complication of aSAH
• Without treatment, ruptured saccular aneurysms have a rebleed rate of 20% within
the first two weeks following the initial hemorrhage.

• Unfavorable outcome is associated with several factors

• including increasing age,
• worsening neurological grade,
• aneurysm size,
• large amounts of SAH on initial NECT scan,
• parenchymal hematoma,
• intraventricular hemorrhage,
• and vascular risk factors such as hypertension and myocardial infarction.
TREATMENT OPTIONS

• The goals of aSAH treatment in patients who survive their initial bleed
are to

• (1) obliterate the aneurysm (preventing potentially catastrophic

rebleeding) and

• (2) prevent or treat vasospasm

• GENERAL FEATURES.The first three days after ictus, a negative NECT scan is usually sufficient to
exclude SAH.Lumbar puncture is generally unnecessary if the NECT is negative.

• CT FINDINGS- The basal cisterns—especially the suprasellar cistern—are generally filled with
blood
• SITE OF SAH AND HEMATOMA GIVES A CLUE TO THE VESSEL OF ORIGIN FROM WHICH
ANEURYSM ARISES.
• ACoA aneurysms tend to rupture superiorly into the anterior interhemispheric fissure.
• MCA bifurcation aneurysms usually rupture into the sylvian fissure.
• Internal carotid-posterior communicating artery (IC-PCoA) aneurysms generally rupture into
the suprasellar cistern.
• Vertebrobasilar aneurysms often fill the fourth ventricle, prepontine cistern, and foramen
magnum with blood.
• Intraventricular hemorrhage (IVH) is present in nearly half of all patients with aSAH and is
associated with a higher likelihood of complications and poorer three-month post-SAH
• MR FINDINGS.
• Acute aSAH is isointense with brain on T1WI .

• The CSF cisterns may appear smudged or “dirty.” Because aSAH is hyperintense to
brain on T2WI, it may be difficult to identify.

• FLAIR is the best sequence to depict aSAH . Hyperintense CSF in the sulci and
cisterns is present.

• Other causes of “bright” CSF on FLAIR include

hyperoxygenation, meningitis, neoplasm, and artifact.

• MR may also be a helpful additional examination when no structural cause for

nontraumatic SAH is identified on screening NECT or CTA.
• ANGIOGRAPHY. CTA is positive in 95% of aSAH cases if the “culprit” aneurysm
is two millimeters or larger.

• DSA is still considered the gold standard for detecting and delineating
aneurysm angioarchitecture.

• Standard DSA occasionally fails to demonstrate a “culprit” aneurysm. So-

called angiogram-negative SAH.

• With the addition of three-dimensional rotational angiography and 3D shaded

surface displays (SSDs), the rate of “angiogramnegative” SAH decreases.

• CTA is recommended in patients with diffuse-type SAH if the initial DSA is

negative.
IMAGING-BASED GRADING OF
SAH

• A simple scale based on NECT findings, the modified Fisher scale, has
been proposed to grade aSAH
• Stepwise increases in modified Fisher grade have a moderately linear
relationship with the risk of vasospasm, delayed infarction, and poor
clinical outcome
Differential Diagnosis
1.TRAUMATIC SAH

• The major differential diagnosis of aSAH is traumatic SAH.

• Aneurysmal SAH is generally much more widespread, often filling the

basal cisterns.

• tSAH typically occurs adjacent to cortical contusions or lacerations

and is therefore most common in the superficial sulci.
• 2) Perimesencephalic nonaneurysmal SAH (pnSAH)

-(pnSAH) is much more limited than aSAH and is localized to the

interpeduncular, ambient, and prepontine cisterns.
Occasionally, pnSAH spreads into the posterior aspect of the suprasellar
cistern.
It rarely extends into the sylvian fissures
THE IMPORTANCE : ITS VENOUS BLEED ,LOW PRESSURE BLEED THEREFORE
HAS BETTER PROGNOSIS. HAS NO CHANCE OF REBLEED.
• 3) Convexal SAH is, as the name implies, localized to
superficial sulci over the cerebral convexities.
• Often only a single sulcus is affected.

Causes of convexal SAH are numerous and include

 TRAUMA
 cortical vein occlusion,
 Amyloid angiopathy,
 vasculitis, and
 reversible cerebral vasoconstriction syndrome.
 MOYA MOYA DISEASE.
4)Pseudo-SAH is caused by severe
cerebral edema. The hypodensity of the
brain makes blood in the cerebral
arteries and veins appear dense,
mimicking the appearance of SAH.

• Pseudoaneurysms are usually caused

by a specific inciting event—e.g.,
trauma, infection, drug abuse,
neoplasm, or surgery—that initially
weakens and then disrupts the normal
arterial wall
• they lack normal vessel wall
components, & are especially prone to
repeated hemorrhage
• 5) Sulcal-cisternal FLAIR hyperintensity on MR is a
nonspecific imaging finding and does not always denote subarachnoid
hemorrhage.

• Incomplete CSF nulling artefact,Pyogenic meningitis, meningeal carcinomatosis,

and high inspired oxygen concentration may also cause CSF hyperintensity on
FLAIR.

• Prior administration of gadolinium chelates (with or without decreased renal

clearance) can result in diffuse delayed CSF enhancement.

• Other etiologies of sulcal-cisternal FLAIR hyperintensity include hyperintense

vessels with slow flow (e.g., acute arterial strokes, pial collaterals developing
after cerebral ischemia-infarction, Sturge-Weber syndrome, moyamoya, and
reversible cerebral vasoconstriction syndrome).)
Special Circumstances
• Pregnant And Postpartum Women
• Acute headache in pregnant or postpartum women requires
additional understanding and expansion of the differential diagnosis.
• As pregnancy and the acute postpartum period represent
hypercoagulable states, emergency clinicians should strongly consider
ischemic stroke and cerebral venous thrombosis.
• Other etiologies more common in the peripartum period that may
present with headache are reversible cerebral vasoconstriction
syndrome, pre-eclampsia, and posterior reversible encephalopathy
syndrome
 Delayed cerebral ischaemia DCI and vasospasm

• DCI occurs in more than 60% of patients, with the greatest risk between days
4 and 10 after the SAH, and is associated with worse outcome. DCI and
vasospasm are often assumed to be synonymous

• Patients with poor grade SAH, large subarachnoid blood load, intraventricular
haemorrhage, and smokers are particularly at risk for the development of
vasospasm
• Pathological changes occur within intracranial arteries causing
thickening of the vessel walls and narrowing of the lumen, impaired
vascular relaxation, and associated impairment of vascular reactivity
and autoregulation.Together these result in reduced cerebral blood
flow (CBF) and ischaemia in affected areas.
• Clinical symptoms include reduced level of consciousness,changes to
speech, or the development of focal motor deficits and onset may be
sudden or insidious.

• Diagnosis is often difficult, particularly in patients who already have a

neurological deficit or in those who are sedated.

• Of note, both vasospasm and DCI may be asymptomatic

• “Triple H” therapy (hypervolemia, hypertension, and hemodilution)
has been used in combination with calcium antagonists in an attempt
to increase cerebral perfusion and improve outcome following aSAH
 Techniques used to aid diagnosis

• 1)Transcranial Doppler ultrasonography is a non-invasive bed-side technique

that measures blood flow velocity in basal cerebral arteries.A diagnosis of
vasospasm is made if flow velocities are >120 cm s, velocities increase (>50 cm
s /day from baseline) or the Lindegaard ratio (ratio of flow velocity in ipsilateral
middle cerebral and internal carotid arteries)is >3. This technique is operator-
dependent and, because it measures flow velocity, is able only to assess
relative changes in CBF.

• 2)CT angiography (CTA) is highly specific (85–95%) for the diagnosis of

angiographic vasospasm but has a tendency to overestimate the degree of
stenosis. It is often used as a screening tool for vasospasm reducing the need
for DSA.
• 3)DSA is the gold standard for detecting vasospasm but is unable to
assess the adequacy of brain tissue perfusion. DSA is often combined
with endovascular treatment, usually transluminal balloon
angioplasty and intraarterial nimodipine

• 4)CT perfusion imaging provides information on regional brain tissue

perfusion. A delayed mean transit time (>6.4 s) with arterial
narrowing on CTA can be used to predict the need for DSA and
intervention for vasospasm. It is best when used for anterior
circulation vasospasm.
• The most relevant guidelines for emergency clinicians are the 2008
American College of Emergency Physicians (ACEP) Clinical Policy on
acute headache ,the 2012 American Heart Association (AHA)
Guidelines for the Management of Aneurysmal Subarachnoid
Hemorrhage, and the 2011 Neurocritical Care Society (NCS)
Guidelines on the critical care management of patients with aSAH
THANK
YOU