ISCHEMIC STROKES  Alert Patient with any of following:

a. Mild pure motor weakness of one side of the body

STROKE IMPACT
 Stroke is BRAIN ATTACK
 Sudden onset of focal neurological deficit lasting
more than 24 hours due to an underlying vascular
pathology
 No. 2 killer worldwide
 No. 1 killer in Asia-Western Pacific, China, and
Japan
 20 million people every year with 5 million deaths
 Locally: 500 strokes per 100, 000 population
b. Pure sensory deficit
c. Slurred speech but intelligible
d. Vertigo with incoordination
Moderate Stroke
 Awake patient with significant motor and/or sensory
and/ or language and/or visual deficit
OR
 Disoriented, drowsy or stuporous patient but with
purposeful response to painful stimuli.

EPIDEMIOLOGY Severe Stroke

 Cerebrovascular disease is estimated to account for
7.8 million deaths yearly throughout the world and
represents about 13 percent of all causes of death
 Strokes cause significant physical, emotional, an
cognitive disabilities among survivors, accounting for
3.6 percent of total disability-adjustive life years
(DALYs) and thus placing stroke within the 10
leading causes of disability irrespective of the
development status of countries
THE NATURE OF STROKE
 There are all gradations of severity, but in all forms
of stroke the essential feature is abruptness with
which the neurologic deficit develops- usually a
matter of seconds that stamps the disorder as
vascular.
 In its most severe form, the patient with a stroke
becomes hemiplegic or even comatose.
 In its mildest form, a stroke may consist of a trivial
and transient neurologic disorder insufficient for the
patient even to seek medical attention.
 Comatose patient with non-purposeful response,
decorticate
OR
 Decerebrate posturing to painful stimuli or comatose
patient with no response to painful stimuli
DIAGNOSIS
 With the advent of numerous diagnostic modalities,
appropriate sequential diagnostic examinations are
most important to confirm the clinical diagnosis of
stoke
 First-line (emergent) diagnostic exam
 Second-line diagnostic investigations
Role of Diagnostic Exam
 Confirm and establish the clinic diagnosis
 Rule out stroke “mimickers”
 Determine pathologic type: Infarct, ICH, SAH
 Determine etiology and stroke mechanism
 Screen for medical and neurologic complications of
stroke

Anyone should consider stroke if they experience: Common Stroke “Mimickers”

 Sudden numbness or weakness in the face, arm, or
 Seizure  Transient global
leg specially on one side of the face or body
 Systemic infection amnesia
 Sudden confusion, trouble speaking or
 Brain tumor  Dementia
understanding
 Toxic-metabolic  Demyelinating
 Sudden trouble seeing in one or both eyes
encephalopathy disease
 Sudden trouble walking, dizziness, loss of balance
 Positional vertigo  Myasthenia gravis
or coordination
 Syncope  Parkinson’s disease
 Sudden severe headache with no known cause
 Trauma  Hypertensive
 Subdural hematoma encephalopathy
CLINICAL STROKE CLASSIFICATION
 Herpes encephalopathy  Bell’s palsy
 TIA and mild stroke
 Moderate stroke
 Severe stroke Differential Diagnosis of Stroke

TIA and Mild Stroke
 Transient Ischemic Attack – deficits resolved within
24 hours including transient blindness in one eye
OR
 If any of the following conditions is presents, stroke
is probably unlikely
o Pure hemifacial weakness (e.g. Bell’s palsy)
o Fever prior to onset of symptoms
1
 o Trauma o Cardiomyopathy
o Recurrent seizures
o Weakness with atrophy 3. Miscellaneous
o Recurrent headaches o Fat emboli
o Air emboli
Emergent Diagnostic Exam o Tumor emboli
1. Plain cranial CT scan C. Diseases of Blood e.g Coagulopathies or
2. CBC, PT/PTT, Blood sugar Hemoglobinopathies
3. Electrocardiogram D. Cerebral Venous Thrombosis
 Thrombosis of cerebral veins may occur with
Second Line Diagnostic Studies infection, dehydration or in association with
estrogen excess, either post-partum or
 Neurovascular studies
combined oral contraceptive use.
o Carotid duplex
E. Decreased Cerebral Perfusion
o Transcranial doppler studies (TCD)  Hypotension, from cardiac arrhythmia or GI
o Catheter angiography bleed, can lead to infarction in the watershed
o CT angiography between arterial territories.
o Magnetic Resonance Angiography (MRA)
 Cardiac Investigations PATHOLOGY
o Echocardiography
o 24 hour Holter
 Hematologic studies
o Hypercoagulable state- Protein C, S,
Fibrinogen Antithrombin III
o APAS-ANA, Anticardiolipin Ab, Lupus
anticoagulant, Homocysteine
 Drug levels- e.g. Metamphetamine
 Biopsy- e.g. Vasculitis, temporal arteritis
 Genetic- Familial homocystinuria, CADASIL
 Within brain and spinal cord tissue the adventitia is
CAUSES usually very thin and the elastic lamina between
media and adventitia less apparent.
A. OCCLUSION (50%)  The intima is an important barrier to leakage of blood
 Atheromatous/thrombotic and constituents into the vessel wall.
1. Large vessel occlusion or stenosis (e.g. carotid  In the development of the atherosclerotic plaque
artery) damage to the endothelium of the intima is the
 Non-atheromatous diseases of the vessel wall primary event.
1. Collagen disease e.g. rheumatoid arthritis, SLE
2. Vasculitis e.g. polyarteritis nodosa, temporal The Atherosclerotic Plaque
arteritis
3. Granulomatous vasculitis e.g. Wegener’s  Following intimal damage:
granulomatosis
4. Miscellaneous e.g. trauma fibromuscular
dysplasia syphilitic vasculitis

B. Embolization (25%) from:

1. Atheromatous plaque in the intracranial or
extracranial arteries OR from aortic arch
2. The heart
o VHD
 Hemorrhage may occur within the plaque or the
o Arrhythmias plaque may ulcerate into the lumen of the vessel
o Ischemic heart disease forming an intraluminal mural thrombus. Either way,
o Bacterial and non0bacterial endocarditis the lumen of the involved vessel is narrowed
o Atrial myxoma (stenosed) or blocked (occluded).
o Prosthetic valves  The plaque itself may give rise to emboli.
o Paradoxical emboli via patent foramen ovale Cholesterol is present partly in crystal form and
2
 fragments following plaque rupture may be
sufficiently large to occlude the lumen of distal
vessels. The cholesterol esters, lipids and
phospholipids each play a role in the aggregation of
such emboli.
 The carotid bifurcation in the neck is a frequent site
at which the atheromatous plaque causes stenosis
or occlusion.
o The development of infarction is a
consequence of the degree of reduced flow and
the duration of such a reduction.
o If flow is restored to an area of brain within the
critical period, ischaemic symptoms will reverse
themselves.
o TIAs may be due to:

 Platelet emboli arise from thrombus developed over

the damaged endothelium.
 This thrombus is produced partly by platelets coming
into contact with exposed collagen fibers.
 Endothelial cells synthesize PROSTACYCLIN which
is a potent vasodilator and inhibitor of platelet
aggregation.
 THROMBOXANE A2, synthesized by platelets, has
opposite effects.
 In thrombus formation these two Both mechanisms occur. Emboli are accepted as the
PROSTAGLANDINS actively compete with each cause of the majority of TIAs.
other

CEREBROVASCULAR DISEASE –
PATHOPHYSIOLOGY

 Normal cerebral blood flow at rest in the normal

adult brain is approximately 50-55mL/100g/min
 When blood flow decreases to 18ml/100g/min, the
brain reaches a threshold for electrical failure.
 When blood decreases to 8mL/100g/min, cell death
can result A small number of transient ischaemic attacks are
 These thresholds mark the upper and lower blood- difficult to fit convincingly into either anterior or posterior
flow limits of the ischemic penumbra. circulation, e.g. dysarthria with hemiparesis.
 The natural history of TIAs
ISCHEMIC STROKES o Following a TIA, 5% of patients will develop
 Transient Ischemic Attacks (TIAs) infarction within 1 week and 12% within 3
 Large Vessel Occlusion months.
 Embolization o The risk of infarction is greatest in older
patients with more risk factors (hypertension
A. TRANSIENT ISCHAEMIC ATTACKS (TIAs) and diabetes) who have had longer
 Are episodes of focal neurological symptoms due to hemispheric TIAs.
inadequate blood supply to the brain. o About 10% of patients who have a stroke have
 Attacks are sudden in onset, resolve within 24 hours had a warning TIA.
or less and leave no residual deficit.
 These attacks are important as warning episodes or
precursors of cerebral infarction. B. LARGE VESSEL OCCLUSION
 The pathogenesis of transient ischaemic attacks  Internal Carotid Artery
o A reduction of cerebral blood flow below 20–30  Anterior cerebral artery
ml/100 g/min produces neurological symptoms.  Middle cerebral artery
 Vertebral artery
 Basilar artery
3
 Posterior cerebral artery

1. Occlusion of The Internal Carotid Artery

o may present in a ‘stuttering’ manner due to
progressive narrowing of the lumen or recurrent
emboli.
o The degree of deficit varies – occlusion may be
asymptomatic and identified only at autopsy, or
a catastrophic infarction may result.

Clinical Features

o The anterior cerebral artery may be occluded by

embolus or thrombus. The clinical picture
depends on the site of occlusion (especially in
relation to the anterior communicating artery)
and anatomical variation, e.g. both anterior
cerebral arteries may arise from one side by
enlargement of the anterior communicating
o The outcome of carotid occlusion depends on artery.
the collateral blood supply primarily from the
circle of Willis, but, in addition, the external
carotid may provide flow to the anterior and
middle cerebral arteries through meningeal
branches and retrogradely through the
ophthalmic artery to the internal carotid artery.

3. Occlusion of the MIDDLE CEREBRAL ARTERY

2. Occlusion of the ANTERIOR CEREBRAL
ARTERY
o The anterior cerebral artery is a branch of the
internal carotid and runs above the optic nerve
to follow the curve of the corpus callosum. Soon
after its origin the vessel is joined by the anterior
communicating artery. Deep branches pass to
the anterior part of the internal capsule and
basal nuclei.
o Cortical branches supply the medial surface of
the hemisphere:
a. Orbital
b. Frontal
o The middle cerebral artery is the largest branch
c. Parietal
of the internal carotid artery. It gives off
(1) deep branches (perforating vessels –
lenticulostriate) which supply the anterior limb of
the internal capsule and part of the basal nuclei.
It then passes out to the lateral surface of the
cerebral hemisphere at the insula of the lateral
sulcus. Here it gives off cortical branches (2)
temporal,
(3) frontal,
4
 (4) parietal
Clinical Features
o The middle cerebral artery may be occluded by
embolus or thrombus. The clinical picture
depends upon the site of occlusion and whether
dominant or non-dominant hemisphere is
affected.
Clinical Features
o When cortical branches are affected individually,
the clinical picture is less severe, e.g.
involvement of parietal branches alone may
produce Wernicke’s dysphasia with no limb
weakness or sensory loss.
o The deep branches (perforating vessels) of the
middle cerebral artery may be a source of
haemorrhage or small infarcts
4. VERTEBRAL ARTERY OCCLUSION
5. BASILAR ARTERY OCCLUSION
o The vertebral artery arises from the subclavian
artery on each side.
o Underdevelopment of one vessel occurs in 10%.
o The vertebral artery runs from its origin through
the foramen of the transverse processes of the
mid-cervical vertebrae. It then passes laterally
through the transverse process of the axis, then
upwards to the atlas accompanied by a venous
plexus and across the suboccipital triangle to the
vertebral canal. After piercing the dura and
arachnoid matter, it enters the cranial cavity
through the foramen magnum. At the lower
border of the pons, it unites with its fellow to
form the basilar artery.
o The vertebral artery and its branches supply the
medulla and the inferior surface of the
cerebellum before forming the basilar artery.
o Occlusion of the vertebral artery, when low in
the neck, is compensated by anastomotic
channels.
o When one vertebral artery is hypoplastic,
occlusion of the other is equivalent to basilar
artery occlusion.
o Only the posterior inferior cerebellar artery
(PICA) depends solely on flow through the
vertebral artery. Vertebral artery occlusion may
therefore present as a PICA syndrome.
o The close relationship of the vertebral artery to
the cervical spine is important. Rarely, damage
at intervertebral foramina or the atlanto-axial
joints following subluxation may result in intimal
damage, thrombus formation and embolization.
o Vertebral artery compression during neck
extension may cause symptoms of intermittent
vertebrobasilar insufficiency.
o The basilar artery supplies the brain stem from
medulla upwards and divides eventually into
posterior cerebral arteries as well as posterior
5
 communicating arteries which run forward to join
the anterior circulation (circle of Willis).
o Branches can be classified into:
a. Posterior cerebral arteries
b. Long circumflex branches
c. Paramedian branches.
Clinical features
o Prodromal symptoms are common and may take
the form of diplopia, visual field loss, intermittent
memory disturbance and a whole constellation
of other brain stem symptoms:
o vertigo
o ataxia
o paresis
o paraesthesia
o The complete basilar syndrome following
occlusion consists of:
o impairment of consciousness → coma
o bilateral motor and sensory dysfunction
o cerebellar signs
o cranial nerve signs indicative of the level
of occlusion.
o The clinical picture is variable. Occasionally
basilar thrombosis is an incidental finding at
autopsy.
o ‘Top of basilar’ occlusion: This results in lateral
midbrain, thalamic, occipital and medial
temporal lobe infarction. Abnormal movements
(hemiballismus) are associated with visual loss,
pupillary abnormalities, gaze palsies, impaired
conscious level and disturbances of behaviour.
o Paramedian perforating vessel occlusion gives
rise to the ‘LOCKED-IN’ SYNDROME and
LACUNAR infarction
6. Occlusion of the POSTERIOR CEREBRAL
ARTERY
o The posterior cerebral arteries are the terminal
branches of the basilar artery. Small perforating
branches supply midbrain structures, choroid
plexus and posterior thalamus. Cortical
branches supply the undersurface of the
o temporal lobe – temporal branch
o occipital and visual cortex – occipital
and calcarine branches.
Clinical Features
o Proximal occlusion by thrombus or embolism will
involve perforating branches and structures
supplied:
o Midbrain syndrome – III nerve palsy with
contralateral hemiplegia – WEBER’s
SYNDROME
o Thalamic syndromes – chorea or
hemiballismus with hemisensory
disturbance.
o Occlusion of cortical vessels will produce a
different picture with visual field loss
(homonymous hemianopia) and sparing of
macular vision (the posterior tip of the occipital
lobe, i.e. the macular area, is also supplied by
the middle cerebral artery).
o Posterior cortical infarction in the dominant
hemisphere may produce problems in naming
colors and objects.
7. BASILAR ARTERY – LONG CIRCUMFLEX
BRANCH OCCLUSION
o It can be seen that a vascular lesion in the
territory of these vessels will produce, not only
cerebellar, but also brain stem symptoms and
signs localizing to:
(a) superior pontine,
(b) inferior pontine
(c) medullary levels.
Clinical Features
6

Posterior inferior cerebellar artery syndrome (lateral
medullary syndrome) results in:
o At the midbrain level damage to the nucleus or
the fasciculus of the oculomotor nerve (III) will
result in a complete or partial III nerve palsy;
damage to the red nucleus (outflow from
opposite cerebellar hemisphere) will also
produce contralateral tremor – referred to as
BENEDIKT’S SYNDROME.
o At the pontine level an abducens nerve (VI)
palsy will occur with ipsilateral facial (VII)
weakness and contralateral sensory loss – light
touch, proprioception (medial lemniscus
damage) when the lesion is more basal.
Abducens and facial palsy may be accompanied
by contralateral hemiplegia – MILLARD-
GUBLER SYNDROME.
o At the medullary level, bilateral damage usually
occurs and results in the ‘LOCKED-IN’
SYNDROME. The patient is paralyzed and
unable to talk, although some facial and eye
movements are preserved. Spinothalamic
sensation is retained, but involvement of the
medial lemniscus produces loss of
‘discriminatory’ sensation in the limbs. The
syndrome usually follows basilar artery
occlusion and carries a grave prognosis.
LACUNAR STROKE
 Occlusion of deep penetrating arteries produces
subcortical infarction characterized by preservation
of cortical function – language, other cognitive and
visual functions.
 Clinical syndromes are distinctive and normally
result from longstanding hypertension.
 In 80%, infarcts occur in periventricular white matter
and basal ganglia, the rest in cerebellum and brain
stem.
 Areas of infarction are 0.5 –1.5cm in diameter and
occluded vessels demonstrate lipohyalinosis,
microaneurysm and microatheromatous changes.
7
 Lacunar or subcortical infarction accounts for 17% of
all thromboembolic strokes and knowledge of
commoner syndromes is essential.

C. EMBOLISATION
 Emboli consist of friable atheromatous material,
platelet-fibrin clumps or well-formed thrombus.
 The diagnosis of embolic infarction depends on:
o The identification of an embolic source, e.g.
cardiac disease.
o The clinical picture of sudden onset.
o Infarction in the territory of a major vessel or
large branch.
CT Findings in Hyper Acute Infarction (0-6 hours)
 Almost 60% of CT scans done in the first few hours
of ischemic stroke: NORMAL
 However, the following signs may be seen:
o Hyperdense artery (“dense MCA sign)
o Obscuration of lentiform nuclei
o Loss of grey-white interphase along
lateral insula (“insular ribbon sign”)
o Effacement of sulci
 Early signs of infarction on Cranial CT

Cranial CT in Acute Ischemic Stroke

 Infarction: focal hypodense area in cortical,

subcortical, or deep gray or white matter, following a
STENOTIC/OCCLUSIVE DISEASE –
vascular territory or watershed distribution.
INVESTIGATIONS

1. Computerized tomography (CT scan)

 Infarction is evident as a low-density lesion
which conforms to a vascular territory, i.e.
usually wedge shaped.
 Subtle changes occur within 3 hours in some
patients; most scans become abnormal within
48 hours.
 CT scan also identifies: CT Findings in Subacute/Chronic Infarction
o the site and size of the infarct, providing
a prognostic guide
o the presence of haemorrhagic infarction
where bleeding occurs into the infarcted
area
o intracerebral haemorrhage or tumor.

8
 Limitations of Cranial MRI

 More expensive and less widely available

 Longer acquisition time compared to CT (difficult in
uncooperative patients)
 Contraindicated in patients with metallic implants
(e.g. Pacemaker)
 Not sensitive in detecting acute hemorrhage

NEUROVASCULAR EVALUATION

2. Magnetic resonance imaging (MRI)  Ultrasound technique

 Catheter angiography
Advantages of Cranial MRI  CT angiography
 More sensitive in detecting  MR angiography
o Small lesion/lacunar infarcts Rationale for Neurovascular Evaluation
o Early infarction
o Brainstem/posterior fossa lesions  Identifying occlusive artery disease
 Can detect lesions as early as 6 hours from onset of o Is there blockage?
stroke (as early as 90 mins for Diffusion MRI)  Localizing the occlusion
o Where? Carotid? Intracranial?
Early Signs of Infarction on MRI  Quantifying the pathology
o Athero? Dissection? Others?
 Identifying other vascular lesions

Recommendations for Neurovascular Imaging in

Patients with Stroke

 A non-invasive screening technique is indicated as

an initial diagnostic test
 A conventional radiographic angiography may be
indicated based on findings of non-invasive
screening procedures (i.e. severe stenosis,
occlusion)
 Cerebral arteriography may also be required when a
diagnosis of vasculitis, dissection, vascular
malformation needs confirmation or exclusion.

1. Vascular Ultrasound “Neurosonology”

2. Carotid Duplex
 Established technique to identify extracranial
MRI in Brainstem Infarction carotid/vertebral artery disease
 Advantages: non-invasive, bedside, availability, low-
cost
 Disadvantages: operator dependent, unable to
differentiate occlusion from near occlusion

9
3. Transcranial Doppler  Treatment aims
 Established technique to evaluate basal intracranial o Recanalized blocked vessels
arteries o Prevent progression of present event
 Stablished utility in stroke (e.g. stenosis, vasospasm, o Prevent immediate complication
increased ICP, vasomotor reactivity) o Prevent the development of subsequent
 Advantages: non-invasive, bedside availability, low- events
cost, allows serial monitoring, detects micro emboli. o Rehabilitate the patient
 Disadvantages: operator dependent, poor temporal
window, circle of Willis variation. Guidelines for TIA and MILD STROKE
 TCD Applications in Strokes
o Stenosis/occlusion  Management priorities
o Emboli detection o Ascertain clinical diagnosis of stroke or TIA
o Collateralization o Exclude common stroke mimickers
o Vasospasm o Monitor and manage blood pressure
o Increased ICP/ brain death  SBP: 220 or DBP: 120
o Cerebral auto regulation  MAP: 130
 Avoid precipitous drop in BP >20%
4. Other Non-invasive Neurovascular Imaging of baseline MAP
Procedure  No rapid acting sublingual agents
 MR Angiography  Use oral or easily titratable IV
 CT Angiography antihypertensive
o Ensure appropriate hydration
5. Catheter Angiograpy  No hypotonic IV fluid
 “Gold Standard”  Emergent Diagnosis
o Severe carotid stenosis o CBC
o Vertebral artery stenosis o Blood sugar (CBG, HGT, or RBS)
o MCA stenosis o ECG atrial fibrillation or possible cardio
embolic source
CARDIAC EVALUATION o PT/PTT
o Plain cranial CT scan as soon as possible
 Holter monitor
 2D echocardiography  Early Specific Treatment for Thrombotic or Lacunar
Recommendations for Echocardiography in Patients Stroke (CT scan Confirmed)
with Stroke o Aspirin 160-325 mg start as early as
possible for 14 days
 Clinical evidence of heart disease o Neuroprotection
 Less than or equal 45 years of age o Early rehabilitation within 72 hours
 Older patients, without evidence of extra or o Anticoagulation with IV heparin or
intracranial occlusive disease or other obvious cause subcutaneous LMWH
 Abrupt occlusion of major peripheral or visceral o Or Aspirin 160-235 mg/day (If
artery
anticoagulation not available)
 Suspect embolic disease (non-lacunar syndrome,
o If infective endocarditis is suspected, give
multiple arterial territory involvement)
antibiotics and do not anticoagulated.
 Clinical therapeutic decision will depend on results of
echocardiography
Ischemic-noncardiogenic (Thrombotic/Lacunar)
o If within 3 hours of stroke onset, consider
Proper Use of Diagnostic Examinations in Strokes
rTPA treatment and refer to specialist
Requires an Understanding of:
o Aspirin 160-325mg/day start as early as
 Underlying disease process possible
 Principles of test involved o Neuroprotection
 Advantages and limitations of each procedure o Early supportive rehabilitation
 How each investigation influences patient
management Pharmacologic Treatment

Cerebral Infarction Management 1. Tissue Plasminogen Activator (TPA)

 Total dose 90 mg
10
  Administration: 10% of the total dose as an
initial IV bolus over 1 minute and the
remainder infused over 60 minutes
Eligibility Criteria for the Treatment of Acute Ischemic
Stroke with Intravenous Alteplase (Recombinant Tissue
Plasminogen Activator or TPA)
 Inclusion Criteria
o Age ≥18 years
o Onset of symptoms <4.5 hours before
beginning treatment; if the exact time of
stroke onset is not known, it is defined as
the last tie the patient was known to be
normal or at neurologic baseline
o Clinical diagnosis of ischemic stroke causing
measurable neurologic deficit.
 Exclusion Criteria (Patient history)
o Ischemic stroke or severe trauma in the
previous three months
o Previous intracranial hemorrhage
o Intra-axial intracranial neoplasm
o Gastrointestinal malignancy
o Gastrointestinal hemorrhage in the previous
21 days
o Intracranial or intraspinal surgery within the
prior three months
 Exclusion criteria (Clinical)
o Symptoms suggestive of subarachnoid
hemorrhage
o Persistent blood pressure elevation (systolic
≥185mmHg or diastolic ≥110 mmHg
o Active internal bleeding
o Presentation consistent with infective
endocarditis
o Stroke known or suspected to be associated
with aortic arch dissection
o Acute bleeding diathesis, including but not
limited to conditions defined under
“Hematologic”
INR, ECT, TT, or appropriate factor Xa
activity assays.
 Exclusion Criteria (Head CT)
o Evidence of hemorrhage
o Extensive regions of obvious hypodensity
consistent with irreversible injury
 Warning
o Only minor and isolated neurologic signs or
rapidly improving symptoms
o Serum glucose <50 mg/dL (<2.8 mmol/L)
o Serious trauma in the previous 14 days
o Major surgery in the previous 14 days
o History of GI or GU bleeding
o Seizure at the onset of stroke with postictal
neurologic impairments
o Pregnancy
o Arterial puncture at a noncompressible site
in the previous seven days
o Large (≥10 mm), untreated, unruptured
intracranial aneurysm
o Untreated intracranial vascular malformation
 Additional warnings for treatment from 3 to 4.5
hours from symptom onset
o Age >80 years
o Oral anticoagulant use regardless of INR
o Severe stroke (NHSS score >25)
o Combination of both previous ischemic
stroke and diabetes mellitus
Other Pharmacologic Treatment

 Exclusion criteria (Hematologic)

o Platelet count <100,000/mm3
o Current anticoagulant use with an INR >1.7
or PT /.15 secs or aPTT />40secs
o Therapeutic doses of LMWH received within
24 hours (e.g. to treat VTE and ACS); tis
exclusion does not apply to prophylactic
doses (e.g. to prevent VTE)
o Current use of (i.e, last dose within 48 hours
in a patient with normal renal function) of a
direct thrombin inhibitor or direct factor Xa
inhibitor with evidence of anticoagulant
effect by laboratory tests such as aPTT,
11

GUIDELINES FOR SEVERE STROKE
 Management Priorities
o Basic emergent supportive care (ABC of
resuscitation)
o Neurovital: BP, CR, RR, Temperature,
pupils, GCS
o Recognize and treat early signs of increased
ICP
o Monitor and manage blood pressure. Treat if
SBP is 220 or DBP of 120 or MAP >130
 Precautions: Avoid precipitous drop
in BP >20%
 MAP. No sublingual agents.
o Ascertain clinical diagnosis, exclude stroke
mimickers
o Identify co-morbidities, (cardiac disease,
gastric ulcer, etc)
 Early Specific Treatment for Cadioembolic (CT scan
Confirmed)
 Noncardiogenic (Thrombotic/Lacunar)
o Aspirin 160-325 mg start as early as
possible
o Neuroprotection
o If cerebellar infarct, consult Neurosurgeon
ASAP
o Early supportive rehabilitation
 Place of treatment:
o Hospital
o ICU
o Acute Stroke Unit
Rationale for Acute Stroke Treatment
 In the complete absence of blood flow, neuronal
death occurs within 2-3 minutes from exhaustion of
energy stores.
 However, in most strokes, there is salvageable
penumbra (tissue at risk) that retains viability for a
period of time through suboptimal perfusion from
collaterals.
 Progression of local cerebral edema resulting from
the ischemic injury results in compromise of these
collaterals and progression of ischemic penumbra to
infarction if flow is not restored and maintained.
SUMMARY
 Determine by history if stroke or not
o Rule out stroke mimickers
 History and PE, NE should be done immediately on
patients with stroke
 Do emergent diagnostic tests to determine patient’s
eligibility for rTPA
 CT scan remains to be the most important brain
imaging test. Cranial MRI is not recommended for
routine evaluation of acute strokes.
 Differentiation of ischemic and hemorrhagic stroke is
important because of marked difference in the
management
 Second line diagnostic tests need not be done in the
ER setting and should not delay treatment
Primary Prevention Strategies Have Proven to
Reduce Stroke Incidence
 Management of hypertension
 Use of warfarin in patients with atrial fibrillation or
antiphospholipid antibody syndrome
 Lipid reduction with statins in patients with
preexisting ischemic heart disease
 Use of aspirin (ASA) in women 45 years or older but
not men.
Secondary Prevention Strategies Have Proven to
Reduce Stroke Incidence
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 Antiplatelet ASA, ASA+ dipyridamole, clopidogrel
(slightly better)
 Warfarin in atrial fibrillation. Risk of intracerebral
hemorrhage is 0.3% to 0.6% per year.
 Symptomatic carotid stenosis >70%: carotid
endarterectomy
 ACEi (possibly independent of BP)
 Statins reduce the risk of stroke and their effect
might be independent of the cholesterol levels.

END

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