Hemorrhagic Stroke
Dr. Grant Stotts, Director Ottawa Stroke Program
09 FEB 2016
Faculté de médecine | Faculty of Medicine
uOttawa.ca
2
Hemorrhagic Stroke
• 2 major types
– Subarachnoid
Hemorrhage (SAH)
– Intracerebral
Hemorrhage (ICH)
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Hemorrhagic Stroke Objectives
①
②
③
④
⑤
⑥
⑦
4830 Discuss the epidemiology and etiology of cerebral
aneurysms.
4831 List the common anatomic sites of aneurysmal
formation.
4832 Describe the common clinical manifestations of a) a
sentinel bleed and b) an aneurysmal rupture and c)
compression from giant unruptured
aneurysms.
4833 Describe the investigation and management principles
of patients with suspected subarachnoid hemorrhage (SAH).
4834 Discuss potential complications of SAH, including
vasospasm and
hydrocephalus.
4835 Discuss how hemorrhagic stroke differs from ischemic
stroke in its clinical and radiologic presentation.
4836 List the most common causes and manifestations of
subarachnoid and intracerebral hemorrhage.
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Objective 4835
DISCUSS HOW HEMORRHAGIC STROKE DIFFERS
FROM ISCHEMIC STROKE IN ITS CLINICAL AND
RADIOLOGICAL PRESENTATION
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Intracerebral Hemorrhage (ICH)
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Presentation of ICH
 Acute onset neurological deficit
 Deficit depends on location of bleed – same as ischemic stroke
 Contralateral hemiparesis/sensory loss and visual field deficits are
common with hemispheric ICH
 Ataxia can develop with cerebellar hemorrhage
 Brainstem deficits can occur with ICH in the brainstem or if it creates
pressure on the brainstem
 Often:
 Headache
 Vomiting
 Progressive deterioration in level of consciousness and/or worsening
deficits
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Clinical Differentiation of Ischemic
and Hemorrhagic Stroke
 Clinically, a stroke is more likely hemorrhagic if:



Rapid deterioration in level of consciousness
Headache +/- Vomiting
History of trauma
 However:

Imaging is necessary to verify

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Usually CT scan
Radiological Differentiation of
Ischemic and Hemorrhagic Stroke
•
Computed tomography (CT) is the most
widely used imaging modality to determine
acute stroke type
•
Hemorrhagic Stroke
–
Blood (acutely) is more dense than brain
tissue
• Will appear bright on CT
immediately
•
Ischemic stroke
–
–
–
–
Initially CT Head may be normal
With tissue death there is (cytotoxic) edema
involving cellular swelling
This leads to a decrease in tissue density
May take hours to develop
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Management of ICH
Initial CT
• Limit progression of hematoma
–
–
Reverse anticoagulation if taking warfarin or
newer anticoagulant agents
Control blood pressure
• Investigate for underlying cause of
hemorrhage
–
Vascular malformations
•
–
CT or MR Angiogram often done initially
Other causes can be investigated if this testing is
negative
3 Hours Later
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Courtesy: Dr. D. Dowlatshahi
CT Angiogram Demonstrates
Vasculature
CT Head
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CT Angiogram
Arteriovenous Malformation
Abnormal network of vessels between arteries and veins without intervening
capillaries.
CT Angiogram
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Catheter Angiogram
Objective 4836
LIST THE MOST COMMON CAUSES AND
MANIFESTATIONS OF SUBARACHNOID AND
INTRACEREBRAL HEMORRHAGE
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Causes of Intracerebral Hemorrhage:
Location is Associated with Etiology
1.
Subcortical
• Hypertension most common cause
2.
Lobar
• Involving major lobes of the brain
• Hemorrhage extends out to the cortex
• Examples:
• Amyloid angiopathy
• Anticoagulant-associated hemorrhage
• Coagulopathy-associated hemorrhage
Subcortical
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Lobar
Subcortical Hemorrhage Etiology
• Hypertension leads to formation of microaneurysms in
small, penetrating arteries
– Lenticulostriate vessels, branches usually from
middle cerebral artery, degenerate with prolonged
hypertension
– Note these same vessels are responsible for lacunar
ischemic infarcts as the vessels can also develop
hypertrophy with prolonged hypertension
– These vessels are too small to be seen on any
available imaging.
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The CIBA Collection of Medical
Illustrations volume I, Nervous System
Part II, Neurologic and Neuromuscular
Disorders. Frank H. Netter. Pg. 59
Lobar Hemorrhage Etiologies
• Major Etiologies:
–
–
–
–
–
Bleed into tumor
Bleed after ischemic infarct
Anticoagulant medications
Coagulopathy
Amyloid angiopathy
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Amyloid Angiopathy: Connection to Alzheimer’s Disease
(not on objective list)
•
•
Amyloid Precursor Protein is cleaved into 2
predominant fragments
– Soluble fragment (Aβ40) deposits in
muscular layers of cerebral arteries and
capillaries
• Vessels become fragile and
spontaneously rupture
• Major cause of bleeding in the
elderly
– Insoluble fragment (Aβ42) deposits lead
to amyloid plaque which is one of the
major pathological findings in
Alzheimer’s Disease
These conditions can overlap but may also
occur independently
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Stroke 2009;40;2601-2606
Objective 4830
DISCUSS THE
EPIDEMIOLOGY AND
ETIOLOGY OF CEREBRAL
ANEURYSMS
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Cerebral Aneurysms: Background
• Intracranial aneurysms occur in 1 to 5% of the population
– Autopsy studies
– 50 – 80% do not rupture
• More common in:
– Adults
– Women
• Associated factors:
– Hypertension
– Smoking
– Excessive EtOH use
• Familial forms are less common (10%)
• Strong association with polycystic kidney disease
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Two Major Factors of Cerebral
Aneursym Formation
Location at artery
bifurcation
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Defect in arterial wall:
tunica media
Factors Influencing Cerebral
Aneurysm Rupture Risk
• More likely to rupture
if
– Larger (> 7 mm)
– Growth with time
• Other factors
– HTN
– Smoking
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Causes of Subarachnoid Hemorrhage
• Majority due to trauma
• Spontaneous SAH
– Aneurysm 85%
• Clinically one of the most
important presentations to
recognize
• Mortality rate: 30-40%
• Most survivors are disabled
– Other: cocaine, vasculitis,
coagulopathy
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Objective 4831
LIST THE COMMON ANATOMIC SITES
OF ANEURYSMAL FORMATION
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Cerebral Aneurysm Locations
Cerebral aneurysms
tend to occur at
arterial bifurcations
NEJM 2006;355:928-39.
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Cerebral Aneurysms Occur at
Arterial Bifurcations
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Major Cerebral Arteries Travel in the
Subarachnoid Space
• Cerebral arteries follow
subarachnoid space
– The subarachnoid space
is continuous through
the brain and spine.
– Therefore, a lumbar
puncture can test for
blood products even if
the hemorrhage was
intracranial.
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Objective 4832
DESCRIBE THE COMMON CLINICAL
MANIFESTATIONS OF:
- ANEURYSMAL RUPTURE
- A SENTINEL BLEED
- COMPRESSION FROM GIANT
UNRUPTURED AN ANEURYSMS
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Compression from Giant Aneurysms
What is the deficit?
Which CN nerve raises the eyelid?
Which CN lowers the eyelid?
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Compression from Giant Aneurysms
• Cranial nerve deficits
– CN III palsy from
Posterior
Communicating Artery
aneurysm most common
• Headache
• Seizure
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Clinical Manifestations of SAH
• Thunderclap Headache
– Maximal at onset
• Predominant clinical
feature
– Severe in intensity
(10 out of 10)
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Aneurysmal Rupture
• Clinical Presentation
– Acute, thunderclap,
headache
– Acute loss of
consciousness
– Nausea, vomiting
– Seizure
– Clinical deficits may occur
if pressure is high enough
to injure surrounding
tissue
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Sentinel Bleed
• Sentinal = Minor bleed
– Likely represents minor hemorrhage
with rapid thrombus formation
within the aneurysm
• Occurs in ~ 20% of SAH cases
– 80% will not have clinical warning
• Rebleed rate: 50% in 1 week
• Clinical recognition allows for time
window to detect aneurysms
– Symptoms similar to SAH with
thunderclap headache
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Objective 4833
DESCRIBE THE INVESTIGATION AND
MANAGEMENT PRINCIPLES OF PATIENTS
WITH SUSPECTED SUBARACHNOID
HEMORRHAGE (SAH)
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Investigation of Thunderclap
Headache for Possible SAH
• CT Head
– 95% sensitivity for
detecting hemorrhage
– Most sensitive if done
< 12 hours
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Investigation of Thunderclap
Headache for Possible SAH
• If a CT Head is normal with
a person presenting with
thunderclap headache then
a lumbar puncture is
necessary.
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Lumbar Puncture
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What would you expect to see in the
CSF if there was a SAH?
A.
B.
C.
D.
High
High
High
High
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protein
glucose
red blood cell count
platelet count
Traumatic Tap
• The spinal needle may
pierce a blood vessel
before reaching the
subarachnoid space.
• A test is needed to
determine if the blood is
from the CSF.
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Testing for a Traumatic Tap:
Compare First Tube with Later Tube
• RBC count is tested in the
first and last CSF tube
collected
– SAH, the RBC count
will be similar between
the 2 tubes
– Traumatic LP: cell
count will drop by the
last tube if it is diluted
by normal CSF
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SAH:
First Tube RBC =
Last Tube RBC
Traumatic Tap:
First Tube RBC >
Last Tube RBC
If CT Normal and CSF Negative for RBCs:
Test for Xanthochromia
•
You should wait approximately 2
hours after headache onset before the
LP is performed
– Xanthochromia is a yellowish
discoloration due to bilirubin from
hemoglobin breakdown
– Takes at least 2 hours to develop
– Helpful if RBC count is low in the case
of a sentinel bleed where there is no
active bleeding
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Xanthochromia
Imaging of Cerebral Aneuryms
•
When a SAH is detected by any of the
previous tests, the next step is to
determine if there is an underlying cerebral
aneurysm.
•
Non-invasive imaging: used first
– CT Angiogram
– MR Angiogram
•
Invasive imaging may be necessary
– Catheter cerebral angiogram
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Cerebral Aneurysm Management
Surgical Clipping
Historically the most common way
to treat cerebral aneurysms
Endovascular Coiling
Generally considered first-line
treatment for the majority of
aneurysms presently
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NEJM 2006;355:928-39.
Cerebral Aneurysm Coiling
• Catheter usually inserted into the
femoral artery
• Angiograms can be performed to see
position of catheter during the
procedure
• Detachable coils are inserted into the
aneurysm until it is filled
• Coils are thrombogenic
• Patients are followed by MR scanning
to evaluate possibility of regrowth
• Avoids craniotomy
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NEJM 2006;355:928-39.
Cerebral Aneurysm Coiling
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Courtesy: Dr. C. Lum, Interventional Neuroradiology, Ottawa Hospital
Objective 4834
DISCUSS POTENTIAL
COMPLICATIONS OF SAH,
INCLUDING VASOSPASM AND
HYDROCEPHALUS
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Complications of SAH
• Immediate
– Decreased Level of
Consciousness
– Airway Protection
– Cardiac Effects
• Arrhythmia
– Seizure
• Delayed
1. Rebleeding
2. Hydrocephalus
3. Vasospasm
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Immediate Management of SAH
• ABCs
• ECG to look for cardiac
arrhythmia
• Admit to hospital even if
small SAH and patient looks
currently stable in order to
monitor for the possibility of
delayed complications.
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Management of Delayed
Complications of SAH
1. Rebleeding
– Secure aneurysm by
endovascular coiling
or surgical clipping
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Management of Delayed
Complications of SAH
2. Hydrocephalus
– Blood obstructs CSF outflow pathways (arachnoid
villi)
– CSF accumulates and expands, increasing
intracranial pressure
– Surgically drain CSF if required
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Management of Delayed
Complications of SAH
3. Vasospasm
– Uncertain cause,
components of blood
breakdown suspected
– Severe vasospasm can
lead to ischemia
(stroke)
– Usually 3 - 7 days after
onset of SAH
– Treated with BP
elevation and
vasodilators
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Conclusions
SAH
• Diagnosis
– Thunderclap headache
– CT
– Lumbar Puncture when
necessary
• Management
– Stabilize and observe
– Secure aneurysm
– Watch for delayed
hydrocephalus or
vasospasm
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ICH
• Location correlates
with etiology
– Subcortical:
Hypertension
– Cortical: Amyloid
angiopathy
• Management:
– Control blood pressure
– Investigate for
underlying vascular
cause