Dr. Hashemi MD
HEMORRHAGIC STROKE
Hemorrhagic stroke
Intracerebral Hemorrhage
(ICH)
What Is ICH?
 A hemorrhagic stroke is bleeding
(hemorrhage) that suddenly
interferes with the brain's
function. This bleeding can occur
either within the brain or
between the brain and the skull.
ICH background
 10-18% of strokes.
 Mortality rate : 25% and 60%.
 Mortality is strongly dependent on hematoma size and, to
a lesser extent, location.
 The main cause of ICH is hypertension~ 60-70%
 In both hypertensive and nonhypertensive patients, the
circadian rhythm of ICH onset, with peaks at 8 AM and 8 PM,
coincides with the physiological daily peaks of blood pressure,
pointing to the importance of blood pressure rises in the
pathogenesis of ICH.
Subarachnoid hemorrhage
 Bleeding from a damaged blood vessel causes blood
to accumulate at the surface of the brain.
 As blood flows into the cerebral spinal fluid, it
increases pressure on the brain, which causes an
immediate headache.
 In the days immediately following the bleeding,
chemical irritation from clotted blood can cause brain
arteries near to the clot to go into spasm. Artery
spasm can damage brain tissue.
 Most often, a subarachnoid hemorrhage happens
because of a saccular aneurysm, but it also can occur
because of leakage from an AVM.
Ischemic
versus
hemorrhagic
stroke
VASCULAR
ANATOMY
anatomy

Knowledge of cerebrovascular arterial anatomy and the brain regions
supplied by the arteries is useful in determining which vessels are involved in
acute stroke. Atypical patterns that do not conform to a vascular
distribution may indicate another diagnosis, such as venous infarction.

The cerebral hemispheres are supplied by 3 paired major arteries: the
anterior, middle, and posterior cerebral arteries. The anterior and middle
cerebral arteries are responsible for the anterior circulation and arise from
the supraclinoid internal carotid arteries. The posterior cerebral arteries
arise from the basilar artery and form the posterior circulation, which also
supplies the thalami, brainstem, and cerebellum. The angiograms in the
images below demonstrate some portions of the circulation involved in
hemorrhagic strokes.
Anterior circulation
Posterior circulation
Territories of the principle
cerebral arteries
Posterior circulation
Artery
Territory
Anterior circulation
Internal carotid
Anterior
choroidal Hippocampus, globus pallidus,
lower internal capsule
Anterior
Medial frontal and parietal
cerebral
cortex and subjacent white
matter, anterior corpus
callosum
Middle
cerebral
Lateral frontal, parietal,
occipital, and temporal cortex
and subjacent white matter
Lenticulostri
ate
branches
Caudate nucleus, putamen,
upper internal capsule
Vertebral
PICA
Medulla, lower cerebellum
Basilar
AICA
SCA
Posterior
cerebral
Lower and midpons,
mid cerebellum
Upper pons, lower
midbrain, upper
cerebellum
Medial occipital and
temporal cortex and
subjacent white matter,
posterior corpus
callosum, upper
midbrain
Thalamoperforat
e branches
Thalamus
Thalamogenicul
ate branches
Thalamus
Distribution of major
supratentorial
arterial territories

Frontal view of a cerebral
angiogram with selective injection
of the left internal carotid artery
illustrates the anterior circulation.
The anterior cerebral artery consists
of the A1 segment proximal to the
anterior communicating artery with
the A2 segment distal to it. The
middle cerebral artery can be
divided into 4 segments: the M1
(horizontal segment) extends to the
limen insulae and gives off lateral
lenticulostriate branches, the M2
(insular segment), M3 (opercular
branches), and M4 (distal cortical
branches on the lateral hemispheric
convexities)

Lateral view of a cerebral angiogram
illustrates the branches of the anterior
cerebral artery (ACA) and sylvian
triangle. The pericallosal artery has been
described as arising distal to the anterior
communicating artery or distal to the
origin of the callosomarginal branch of
the ACA. The segmental anatomy of the
ACA has been described as follows: (1)
the A1 segment extends from the
internal carotid artery (ICA) bifurcation
to the anterior communicating artery, (2)
A2 extends to the junction of the
rostrum and genu of the corpus
callosum, (3) A3 extends into the bend of
the genu of the corpus callosum, and (4)
A4 and A5 extend posteriorly above the
callosal body and superior portion of the
splenium. The sylvian triangle overlies
the opercular branches of the middle
cerebral artery, with the apex

Frontal projection from a right
vertebral artery angiogram
illustrates the posterior circulation.
The vertebral arteries join to form
the basilar artery. The posterior
inferior cerebellar arteries (PICA)
arise from the distal vertebral
arteries. The anterior inferior
cerebellar arteries (AICA) arise from
the proximal basilar artery. The
superior cerebellar arteries (SCA)
arise distally from the basilar artery
before its bifurcation into the
posterior cerebral arteries.
Diagnosis
 Brain imaging is a crucial step in the evaluation
of suspected hemorrhagic stroke and must be
obtained on an emergent basis.
 Brain imaging aids in excluding ischemic
stroke, and it may identify complications of
hemorrhagic stroke such as intraventricular
hemorrhage, brain edema, and
hydrocephalus.
 Either noncontrast computed tomography
(NCCT) scanning or magnetic resonance
imaging (MRI) is the modality of choice.
Risk factors
 The risk of hemorrhagic stroke is increased
with the following factors:
• Advanced age
• Hypertension (up to 60% of cases)
• Previous history of stroke
• Alcohol abuse
• Use of illicit drugs (cocaine, other
sympathomimetic drugs)
Hypertension
Hypertensive small-vessel
disease results from tiny
lipohyalinotic aneurysms
that subsequently rupture
and result in
intraparenchymal
hemorrhage.
Typical locations include the
basal ganglia, thalami,
cerebellum, and pons.
Nonhypertensive Causes of
Intracerebral Hemorrhage
 Vascular malformations (saccular or mycotic aneurysms,

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arteriovenous malformations, cavernous angiomas)
Intracranial tumors
Bleeding disorders, anticoagulant and fibrinolytic
treatment
Cerebral amyloid angiopathy
Granulomatous angiitis of the central nervous system and
other vasculitides, such as polyarteritis nodosa
Sympathomimetic agents (including amphetamine and
cocaine)
Hemorrhagic infarction
Trauma
Arteriovenous malformations

Numerous genetic causes may
predispose to AVMs in the brain,
although AVMs are generally
sporadic. Hereditary hemorrhagic
telangiectasia (HHT), previously
known as Osler-Weber-Rendu
syndrome, is an autosomal
dominant disorder that causes
dysplasia of the vasculature.

HHT is most frequently diagnosed
when patients present with
telangiectasias on the skin and
mucosa or with chronic epistaxis
from AVMs in the nasal mucosa.
Additionally, HHT can result in AVMs
in any organ system or vascular bed.
Arteriovenous malformations
Intracranial tumors
Noncontrast CTscan of acute left putaminal intracerebral hemorrhage (CT done
3 hours after symptom onset) with a large amount of surrounding hypodensity edema
and mass effect. Biopsy of tissue adjacent to the hemorrhage at the time of surgical
drainage revealed typical features of gliobastoma multiform.
Amyloidosis
Cerebral amyloidosis affects
people who are elderly and may
cause up to 10% of intracerebral
hemorrhages. Rarely, cerebral
amyloid angiopathy can be caused
by mutations in the amyloid
precursor protein and is inherited
in an autosomal dominant
fashion.
80-year-old woman with numerous punctate foci of hypointensity (black dots)
on MRI gradient-echo (GRE) sequence (left), suggesting multiple lobar
microbleeds caused by cerebral amyloid angiopathy.
Coagulopathies
Coagulopathies may be
acquired or inherited. Liver
disease can result in a
bleeding diathesis. Inherited
disorders of coagulation
such as factor VII, VIII, IX, X,
and XIII deficiency can
predispose to excessive
bleeding, and intracranial
hemorrhage has been seen
in all of these disorders.
Hemorrhagic transformation of
ischemic stroke
 Hemorrhagic transformation represents the
conversion of a bland infarction into an area of
hemorrhage (20-40% of patients with ischemic
infarction).
 Mechanisms:
 Reperfusion of ischemically injured tissue, either
from recanalization of an occluded vessel or from
collateral blood supply to the ischemic territory
 Disruption of the blood-brain barrier
Hemorrhagic transformation of
ischemic stroke
 Hemorrhagic transformation of an ischemic
infarct occurs within 2-14 days postictus, usually
within the first week. It is more commonly seen
following cardioembolic strokes and is more
likely with larger infarct size.
 Hemorrhagic transformation is also more likely
following administration of tissue plasminogen
activator (tPA) in patients whose noncontrast
computed tomography (CT) scans demonstrate
areas of hypodensity.
Noncontrast computed tomography scan (left) obtained in a 75-year-old man who
was admitted for stroke demonstrates a large right middle cerebral artery
distribution infarction with linear areas of developing hemorrhage. These become
more confluent on day 2 of hospitalization (middle image), with increased mass
effect and midline shift. There is massive hemorrhagic transformation by day 6
(right), with increased leftward midline shift and subfalcine herniation. Obstructive
hydrocephalus is also noted, with dilatation of the lateral ventricles, likely due to
compression of the foramen of Monroe. Intraventricular hemorrhage is also noted
layering in the left occipital horn.
CLINICAL FEATURES
 The clinical presentation of ICH has two main elements: symptoms
that reflect the effects of intracranial hypertension and those that
are specific for the location of the hematoma.
 The general clinical manifestations of ICH related to increased
intracranial pressure (lCP) (headache, vomiting, and depressed
level of consciousness) vary in their frequency at onset of ICH.
 A characteristic of ICH at presentation is the frequent progression
of the focal neurological deficits over periods of hours . This early
course reflects the progressive enlargement of the hematoma.
 Seizures at the time of presentation of ICH are rare, except for
lobar ICH, in which they occur in as many as 28% of patients.
Symptoms of a hemorrhagic stroke

ICH —Symptoms worsen over a
period of 30 to 90 minutes.
Symptoms can include:

SAH — When caused by a ruptured
aneurysm, symptoms can include:
 A very severe headache that
 Sudden weakness
 Paralysis or numbness in

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any part of the body
Inability to speak
Inability to control eye
movements correctly
Vomiting
Difficulty walking
Irregular breathing
Stupor
Coma
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starts suddenly
(thunderclap)
Loss of consciousness
Nausea and vomiting
Inability to look at bright
light
Stiff neck
Dizziness
Confusion
Seizure
Patients with hemorrhagic stroke present with
focal neurologic deficits similar to those of
ischemic stroke but tend to be more ill than are
patients with ischemic stroke. However, though
patients with intracerebral bleeds are more likely
to have headache, altered mental status,
seizures, nausea and vomiting, and/or marked
hypertension, none of these findings reliably
distinguishes between hemorrhagic and ischemic
stroke.
Differences between ICH and
hemorrhagic stroke
ICH
Hemorrhagic infarct
Clinical
Onset
Raised ICP
Embolic source
Sudden, with progression
Prominent
No
Maximal from onset
Absent
Yes
CT scan
High attenuation
Mass effect
Location
Distribution
Enhancement
Ventricular blood
Dense, homogeneous
Prominent
Subcortical, deep
Beyond arterial territory
Ring- type
Yes
Spotted, mottled
Absent or mild
Cortex > subcortical WM
Along branch distribution
Gyral- type
No
MRI
Hypo intense blood Homogeneous
Hyper intense
Thin peripheral halo
edema
Patchy, mottled
Extensive, territorial
Angiography
Branch occlusion
Mass effect, avascular
Putaminal Hemorrhage
 A wide spectrum of clinical severity relates to
hematoma size, from minimally symptomatic cases
presenting with pure motor hemiparesis, or slight
hemiparesis and dysarthria, to the extreme of coma
with decerebrate rigidity in instances of massive
hematomas with rupture into the ventricles.
 Modern CT series of putaminal hemorrhage
document a mortality rate of 37%.
 Ventricular extension carries an invariably poor
prognosis in putaminal hemorrhage.
Putaminal Hemorrhage
 The most common variety of ICH,
putaminal hemorrhage, represents
approximately 35% of the cases.
Lobar hemorrhage
 Nonhypertensive mechanisms, including AVMs,
sympathomimetic agents (in young patients), and
CAA (in elderly patients) are frequent causes.
 The clinical features reflect location : hemiparesis
of upper limb predominance in frontal hematomas,
sensorimotor deficit and hemianopia in parietal
hemorrhages, fluent aphasia with relatively
preserved repetition in dominant temporal
hematomas, and homonymous hemianopia in
occipital lobe hemorrhages.
Lobar Hemorrhage
 Lobar hemorrhage is
second to putaminal
hemorrhage in
frequency, accounting
for approximately 25%
of the cases.
Thalamic Hemorrhage
 10% to 15% of the cases of ICH
 Its onset tends to be more abrupt than that of putaminal
hemorrhage, and slow progression of deficits is less
common.
 Early communication of the medially located hematoma
with the third ventricle
 The prognosis in thalamic hemorrhage relates to
hematoma size and level of consciousness at
presentation, presence of hydrocephalus, a complication
that occasionally occurs abruptly, as a result of
aqueductal obstruction by an intraventricular clot.
 ventriculostomy may result in a reversal of symptoms.
Right thalamic hemorrhage with
ventricular extention
Cerebellar Hemorrhage
 5% to 10% of the cases
 Its clinical presentation is characteristic, with
abrupt onset of vertigo, headache, vomiting,
and inability to stand and walk, with absence
of hemiparesis or hemiplegia.
 Triad of appendicular ataxia, horizontal gaze
palsy, and peripheral facial palsy, all ipsilateral
to the hemorrhage.
 There is a notorious tendency for abrupt
deterioration to coma and death after a period
of clinical stability under hospital observation.
Large midline and left sided
hemispheric cerebellar hemorrhage
GENERAL MANAGEMENT OF STROKE
 Control of HTN
 Surgical treatment
 Nutritional status and fluid requirements
 Prevention of hyperthermia
 Prevention of pulmonary complications
 DVT prophylaxis
 Pressure sores
 Rehabilitation
 Treatment of depression
Prognosis
 About 30% to 60% of people with an intracerebral
hemorrhage die. In those who survive long enough to
reach an emergency room, bleeding usually has
stopped by the time they are seen by a doctor. Many
people with ruptured aneurysms or subarachnoid
hemorrhages also do not survive long enough to reach
a hospital. Of those who do, about 50% die within the
first month of treatment. However, in people with
subarachnoid hemorrhages resulting from
arteriovenous malformations, the risk of death is only
about 15%.
Prognosis
Among the 25% of people who survive an intracerebral hemorrhage,
many experience a major improvement in their symptoms as their
bodies naturally and gradually reabsorb the clotted blood within the
brain.
Among those who survive a bleeding aneurysm, about 50% suffer
long-term neurological problems. People who bleed from an
aneurysm or AVM and do not have this problem treated are at risk
for having a repeat bleeding event. If the blood vessel is not repaired
or removed, one out of 5 survivors of subarachnoid hemorrhage have
bleeding again within 14 days if the abnormal blood vessel was not
repaired or removed. 50% who do not have surgical treatment have
a repeat bleed within 6 months. When surgery is used to clip a
bleeding aneurysm, there is a good chance of success, but there is
also a 5% risk of death or long-term disability after surgery.
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