HEMORRHAGIC STROKE

OBJECTIVES

At the end of the presentation, the learners shall be able to :

Define Hemorrhagic Stroke

Correlate Anatomy and Physiologic Principles with the course of the
Hemorrhagic Stroke
Identify the Risk Factors, Etiology, Pathophysiology of Hemorrhagic
Stroke
Enumerate signs and symptoms of the disease
Discuss Treatment Options and Prognosis
Differentiate between Hemorrhagic and Ischemic Stroke
Differentiate ICH & SAH
Anatomy & physiology

• Layers from Scalp to Brain

Circle of willis
• Remember CIRCLE of WILLIS?
Anatomy & physiology

• Remember CIRCLE of WILLIS?

Circle of willis

• Angry -------------Anterior Cerebral Artery

• Alien-------------- Anterior Communicating Artery
• In ------------------ Internal CarotidArtery
• Our ---------------- Ophthalmic Artery
• Miserable --------- Middle Cerbral Artery
• Planet ------------- Posterior Communicating Artery
• Please--------------Pontine Arteries
• Save ---------------- Superior Cerebellar Artery
• Boring-------------- Basilar Artery
• And----------------- AICA
• Vain----------------- Vertebral Artery
• People--------------- PICA
• Amen-----------------Anterior Spinal
definition

• HEMORRHAGIC STROKE

• Hemorrhagic stroke results from weakened vessel that ruptures and bleeds
into the surrounding brain parenchyma

• 20% of strokes are hemorrhagic

• It usually affects a larger brain area

Ischemic VS hemorrhagic
EPIDEMIOLOGY

• Stroke is the Philippines' second leading cause of death

• Stroke remains among the five leading causes of death across

every income group in most countries in the last comprehensive
review by the World Health Organization in 2004

• The incidence of stroke varies with age, sex, ethnicity, and

socioeconomic status.

• According to the World Health Organization (WHO), 15 million

people suffer stroke worldwide each year. Of these, 5 million die
and another 5 million are left permanently disabled
Risk factors

• NON-MODIFIABLE RISK FACTORS

• Old age
• Male sex
• Asian ethnicity
• Cerebral amyloid angiopathy
• Cerebral microbleeds
• Chronic kidney disease
Risk factors

• MODIFIABLE RISK FACTORS

• Hypertension
• Current smoking
• Excessive alcohol consumption
• Decreased low density lipoprotein cholesterol,
low triglycerides
• Anticoagulation
• Use of antiplatelet agent
• Sympathomimetic drugs
TYPES OF HEMORRHAGIC STROKE

• Intracranial Hemorrhage
• the hemorrhage is into the substance or parenchyma of the brain

• Subarachnoid Hemorrhage
• bleeding originates in the subarachnoid spaces surrounding the brain and the
ventricular system
HEMORRHAGIC STROKE
STAGES

•As hematoma ages, hemoglobin

changes through several forms of
oxyhemoglobin, deoxyhemoglobin, and
methemoglobin before RBCs are broken
down into ferritin and hemosiderin
stages
PHASE TIME HEMOGLOBIN LOCATION

HYPERACUTE <24HRS OXYHEMOGLOBIN,

INTRACELLULAR

ACUTE 1-3DAYS DEOXYHEMOGLOBIN,

INTRACELLULAR

EARLY SUBACUTE >3DAYS METHEMOGLOBIN,

INTRACELULAR

LATE SUBACUTE >7DAYS METHEMOGLOBIN,

EXTRACELLULAR

CHRONIC >14DAYS FERRITIN & HEMOSIDEREIN,

EXTRACELLULAR
PRIMARY INTRACEREBRAL HEMORRHAGE

• third most frequent cause of stroke

• This is the often devastating "spontaneous" brain hemorrhage. It is

predominantly a result of chronic hypertension and degenerative
changes in cerebral arteries.

• is characterized by bleeding into the substance of the brain, usually from

a small penetrating artery

• Hypertension has been implicated as the cause of a weakening in the

walls of arterioles and the formation of microaneurysms (Charcot-
Brouchard)

• Maybe caused by trauma especially due to falls

PRIMARY INTRACEREBRAL HEMORRHAGE

• COMMON SITES
• (1) the putamen and adjacent internal capsule (Putaminal Hemorrhage)

• (2) the central white matter of the temporal, parietal, or frontal lobes (Lobar
Hemorrhage - not strictly associated with hypertension)

• (3) the thalamus ( Thalamic Hemorrhage)

• (4) one or the other cerebellar hemisphere (Cerebellar Hemorrhage)

• (5) the pons (Pontinal Hemorrhage)

PRIMARY INTRACEREBRAL HEMORRHAGE
Microscopic changes
CAUSES
SPONTANEOUS SUBARACHNOID
HEMORRHAGE
• Fourth most frequent cerebrovascular disorder

• When the blood is localized to the surrounding membranes and cerebrospinal

fluid

• It is most frequently caused by leakage of blood from a cerebral aneurysm

• The combination of congenital and acquired factors leads to a degeneration of

the arterial wall and the release of blood under arterial pressures into the
subarachnoid space and cerebrospinal fluid

• Saccular aneurysms also have been called "berry" aneurysms

SPONTANEOUS SUBARACHNOID
HEMORRHAGE
• COMMON SITES
• (1) the proximal portions of the anterior communicating artery

• (2) at the origin of the posterior communicating artery from the stem of the
internal carotid

• (3) at the first major bifurcation of the middle cerebral artery

• (4) at the bifurcation of the internal carotid into middle and anterior cerebral
arteries
SPONTANEOUS SUBARACHNOID
HEMORRHAGE
PATHOPHYSIOLOGY

• The hypertensive vascular lesion that leads to

arterial rupture in most cases appears to arise from
an arterial wall altered by the effects of
hypertension, lipohyalinosis and false aneurysm
(microaneurysm)

• Developmental defects in media & elastica

• Focal destruction of internal elastic membrane

PATHOPHYSIOLOGY

•H.Stroke was once considered to be a simple,

monophasic, rapid bleeding event that
stopped quickly as a result of clotting and
tamponade. But it has been shown by seria
CT Scans to b a dynamic and complex process
involving several distinct phases
PATHOPHYSIOLOGY

• Expansion of Hematoma- Many hemorrhages continue to grow and

expand over several hours after onset of symptoms
• Acute HPN, a local coagulation deficit, or both, may be associated

• Secondary Brain Injury and edema develops for the 1st 24-96 hrs and
slowly resolves over several weeks
PATHOPHYSIOLOGY
Chronic Hypertension
+
Degenerative
Changes

Charcot-
Bouchard
Aneurysm
ICH
SIGNS AND SYMPTOMS
SIGNS & symptoms

• ICH
• Almost occur while px is awake
• Abrupt onset of focal neurological deficit
• Diminished LOC
• Signs of Increased ICP

• Putamen Hemorrhage--Contralateral Hemiparesis (sentinel sign especially

from Putamen site)
• Face sag, Slurred Speech

• Thalamic Hemorrhage—prominent sensory deficit,Aphasia, Anisocoric

Pupils, and several ocular disturbances
SIGNS & symptoms

• ICH
• Pontine Hemorrhage- deep coma with quadriplegia, pinpoint pupils,
decerebrate rigidity , hyperhydrosis, Severe Hypertension, impaired
horizontal eyemovements

• Cerebellar-may develop over several hours, occipital headache, vertigo,

vomiting, gait ataxia, dysarthia, dysphagia,
SAH
SIGNS & symptoms

• SAH
• Signs may depend on the site of bleed

• “Worst Headache” or Thunderclap Headache

• Subhyaloid Hemorrhage per Fundoscopic

Examination

• Meningeal Irritation Signs

• Third Nerve Palsy

DIAGNOSTICS

• ICH
• NeuroImaging
• CT scan----Method of choice to evaluate the
presence of ICH. Evaluates:
• size
• location of the hematoma
• extension into the ventricular system
• degree of surrounding edema
• anatomic disruption
• Hematoma volume (predictor of 30-day
mortality) calculation from CT scan images:
diagnostics
diagnostics

•Hematoma volume (predictor of 30-day

mortality) calculation from CT scan images:

•-ABC/2 (multiply the diameter of the

hematoma in 3 dimensions and divide by
two.
 diagnostics
• SAH
• CT angiography - reveal
secondary ICH due to
andaneurysm or
arteriovenous
malformation or active
contrast extravasation
into the clot (“spot
sign”)- implies increased
risk of early hematoma
growth
 diagnostics

• Others :
• CBC
• Glucose - higher serum glucose is associated with worse outcome
• PT (with INR) - warfarin-related hemorrhages are associated with an
increased hematoma volume, greater risk of expansion, and increased
morbidity and mortality
• Toxicoloy screen- to detect cocaine and other sympathomimetic drugs of
abuse which are asociated with ICH.
diagnostics
• Neurodiagnostic examination

• CT scan - hyperdense blood in the basal cisterns

is usually diagnostic, but parenchymal clot in the
temporal or basal frontal, and intraventricular
hemorrhage are also suggestive of ruptured
aneurysm.

• sensitivity depends on the timing of imaging in

relation to ictus from hemorrhage.
diagnostics

•Duration of SAH (subarachnoid hemorrhage)

•CT scan sensitivity
•24 hours--90-95 %
•3 days--80%
•1 week--50%
diagnostics
diagnostics
 diagnostics
• MRI - can also be
used to detect a
completely
thrombosed
aneurysm if the
initial angiogram is
negative.
• shows
hyperintensity on
subarachnoid space
on FLAIR.
diagnostics

• Lumbar puncture with CSF analysis in the absence of focal

neurological signs is strongly recommended if cranial CT scan
is negative.
• Important considerations in the examination of CSF:
• Timing of lumbar puncture in relation to SAH
• RBC and WBC - usual ratio of 1:700
• Presence of xanthocromia - may take up to 12 hours to
appear and disappear in about 2 weeks unless
hemorrhage recurs.
• multiple specimens should be collected to rule out
traumatic tap. Opening pressure should be measured.
diagnostics
 diagnostics
• Angiography - definite
diagnostic procedure in
determining intracranial
aneurysms and defining their
anatomy.

• Four vessel
angiogram is
mandatory when CT
and MRA is negative.
management
management

• ICH
• Stabilize vital signs -adequate ventilation
• Monitoring and control of intracranial pressure-
Mannitol
• Acute hypertension-beta blocking
agents(esmolol, labetalol)
• Diuretics
• Drain-acute hydrocephalus
• Surgical Evacuation of cerebral hematoma
• >4 cm or more in largest diameter, esp in the
vermis
management

• ICH
• Anticoagulation leads to more hematoma growth
and higher mortality
• Reverse warfarin promptly and aggressively
• FFP or prothrombin complex concentrates
(PCCs)

• IV vitamin K
• Faster than SQ/PO but a small risk of
anaphylactoid reaction
SURGICAL MANAGEMENT

• For patients presenting with lobar clots >30 cc and

within 1 cm of the surface, evacuation of
supratentorial ICH by standard craniotomy might be
considered
 management
• SAH
• Protecting the airway
• Managing the blood pressure--nicardipine, labetolol, esmolol
• Managing vasospasm- leading cause of morbidity following
aneurysmall SAH--Calcium channel antagonist(Nimodipine)
• Symptomatic --Increasing the cerbral perfusion pressure by
raising the mean arterial pressure
• 1) plasma volume expansion
• 2) IV vasopressor agent
• phenylephrine
• Norepinephrine
3.) Persistent
-Vasodilators
-verapamil and nicardipine
management

• Treating hydrocephalus
-Temporary ventricular drainage
• Treating hyponatremia
-supplemental oral salts coupled with normal
saline
-Intravenous hypertonic saline
• Limiting secondary brain insults
• Preventing pulmonary embolism
-pneumatic compression stockings
-Unfractionated heparin
prognosis
RISK FACTORS

•FOR RECURRENT ICH

•Lobar ICH
•Older age
•Anticoagulation
•Apo E e2 or e4 alleles
•Increased number of “microbleeds” on MRI
RISK FACTORS

•FOR RECURRENT SAH

•REBLEEDING
•Fever
•Cerebral Ischemia
•Non obliterated aneurysms
 prognosis
Neurons Brain Synapses Axons Accelerated
Lost Cells Lost Lost Lost Aging

Per 582 12.2 4.2 trillion 2470 18 years

Stroke million billion miles

Per Hour 58 million 1.2 billion 420 billion 247 miles 2 years

Per 1 million 20 million 6.9 billion 4 miles 1.5 weeks

Minute

Per 16,000 340,000 115 120 yards 4.4 hours

Second million
 GENERAL COMPLICATIONS
• Permanent loss of movement or sensation of a part of the
body

• Joint contractures

• Muscle spasticity

• Permanent loss of cognitive or other brain functions

• Disruption of communication, decreased social interaction

• Decreased ability to function or care for self

• Decreased life span

• Urinary and respiratory tract infections

SPECIAL CHALLENGES

• Early recognition of signs

• Within several days of admission, the mechanism of the

cerebral ischemia or hemorrhage should be identified in the
majority of patients; this allows institution of effective
management sooner rather than later.

• Patients who are neurologically unstable should be admitted

to an intensive care unit.

• Need for a Multidisciplinary approach toward the various

special needs of the patient with acute stroke
SOURCES

• American Heart Association website

• American Stroke Association
• Adam’s and Victor’s-Principle of Neurology 10thEd
• Harrison’s Principle of Internal Medicine 19th ed
• Medscape.com
• Merrit’s Neurology 12th Ed
• www.emedicine.medscape.com
• www.nlm.nih.gov