STROKE

Kassahun B.

1
Famous Victims

Vladimir Ilyitch Lenin

L. Pasteur
developed right
sustained stroke
hemiplegia with
at2 the age of 46
 Introduction

 Cerebrovascular Disease(CVD)- is
any brain abnormality caused by blood
vessel pathology
 Includes:ischemic stroke, hemorrhagic
stroke, and cerebrovascular anomalies
such as intracranial aneurysms and
arteriovenous malformations (AVMs)

3
 Introduction

 Stroke: Injury or death of brain tissue

due to oxygen deprivation; usually due
to an interruption of blood flow

 Also
referred to as “Brain Attack” or
“Cerebrovascular Accident” (CVA)

A true emergency!

4
Definition
 Clinically stroke is a sudden onset non
convulsive neurologic deficit characterized by
the rapid appearance (usually over minutes)
of a focal deficit of brain function, most
commonly a hemiplegia with or without
signs of focal higher cerebral dysfunction
(such as aphasia), hemisensory loss, visual
field defect or brain-stem deficit
 In stroke the evidence of brain dysfunction
(neurologic deficit) lasts for at least 24h or
more
5
 Definition…

Transient Ischemic Attack(TIA)

A neurologic deficit that lasted less than
24hrs (usually less than 30 minutes)
 This abrupt onset of a neurologic deficit
in stroke/TIA is attributable to a focal
vascular cause.

6
 Epidemiology
 Stroke is the second most common cause of death
worldwide and is the fifth leading cause of death in
the United States
 is the most common cause of severe physical
disability
 Stroke is a common medical emergency with an
annual incidence of between 180 and 300 per 100
000.
 The incidence rises steeply with age (esp after age
55)
 The incidence is rising in many developing countries
7
 Epidemiology…
 About one-fifth of patients with an acute
stroke will die within a month of the event,
and at least half of those who survive will
be left with physical disability (15% to 30%
of survivors are permanently disabled)
Ethiopia: hospital studies
 There is an increasing trend 35/yr 1970,
75/yr in 1980, 128/yr in 2000-1
 6.5% of admissions were due to stroke
8
Etiology
 Stroke can be either ischemic or hemorrhagic
(80% and 20%, respectively, of all strokes).
 Hemorrhagic strokes include
 Subarachnoid hemorrhage (SAH),
 intracerebral hemorrhage (ICH), and
 subdural hematomas.
 SAH: occurs when blood enters the
subarachnoid space (where cerebrospinal fluid is
housed) owing to
 Trauma or
 rupture of an intracranial aneurysm, or rupture of
an arteriovenous malformation (AVM).

9
Etiology…
 ICH: occurs when a blood vessel ruptures within
the brain parenchyma itself, resulting in the
formation of a hematoma.
 These types of hemorrhages very often are
associated with uncontrolled high BP and
sometimes antithrombotic or thrombolytic
therapy.
 Subdural hematomas: refer to collections of
blood below the dura (covering of the brain), and
they are caused most often by trauma
 Hemorrhagic stroke, although less common, is
significantly more lethal than ischemic stroke, with
30-day case-fatality rates that are two to six times
higher
10
Etiology…
 Ischemic strokes: are caused either by local
thrombus formation or by embolic phenomena,
resulting in occlusion of a cerebral artery.
 Atherosclerosis, particularly of the cerebral
vasculature, is a causative factor in most cases
of ischemic stroke, although 30% are
cryptogenic.
 Emboli can arise from either
 intracranial or extracranial arteries (including the
aortic arch) or,
 as is the case in 20% of all ischemic strokes, the
heart
11
Etiology…
 Cardiogenic embolism is presumed to
have occurred if the patient has
concomitant atrial fibrillation, valvular
heart disease, or any other condition of the
heart that can lead to clot formation.

12
Risk factors
Non-modifiable Modifiable
 Age (>55)  Hypertension (most Important
risk factor)
 Sex (males >  Atrial fibrillation(most
females at older important and treatable cardiac
ages) cause of stroke)
 Cigarette smoking
 Low birth weight  DM
 Race  High TC, LDL, low HDL
 Family history of  Sickle cell disease
stroke/TIA  High sodium diet, obesty,
inactivity,
 other cardiac disease (CAD,HF)
Transient ischemic attacks or prior
13 stroke (major independentrisk
factor)
Pathophysiology-Ischemic Stroke
 Ischemic stroke results from an occlusion of a
cerebral artery, leading to a reduction in cerebral
blood flow.
 Normal cerebral blood flow averages 50 mL/100 g
per minute, and this is maintained over a wide
range of BPs(MAP of 50 to 150 mm Hg) by a
process called cerebral autoregulation.
 Cerebral blood vessels dilate and constrict in
response to changes in BP, but this process can
be impaired by atherosclerosis, chronic
hypertension, and acute injury, such as stroke.
 Arterial occlusion leads to severe reductions in cerebral
blood flow leading to infarction.
14
 There are three major mechanisms
underlying ischemic stroke including
I. Occlusion of an intracranial vessel by an
embolus that arises from a distant site
(e.g., cardiogenic embolus),
II. In situ thrombosis of an intracranial
vessel, typically affecting the small
arteries, &
III. Hypoperfusion caused by flow-limiting
stenosis of a major extracranial artery

15
Pathophysiology-Hemorrhagic
Stroke
 The presence of blood in the brain
parenchyma causes damage to the
surrounding tissue through
I. the mechanical effect it produces (mass
effect) and
II. the neurotoxicity of the blood
components and their degradation
products
 Approximately 30% of ICHs continue to
enlarge
over the first 24 hours, most within 4
hours.
16
 Hemorrhage volumes >60 mL are
associated with 71% to 93% mortality at
30 days.
 Much of the early mortality of hemorrhagic
stroke (up to 50% at 30 days) is caused by
the abrupt increase in intracranial
pressure that can lead to herniation and
death.
 There is also evidence to support that both
early and late edema contributes to
worsened outcome after ICH
17
 Clinical Presentation and Diagnosis
 General
 The patient may not be able to reliably report the
history owing to cognitive or language deficits.
 A reliable history may have to come from a
family member or another witness.
 Symptoms
 The patient may complain of weakness on one
side of the body, facial droop, inability to speak,
loss of vision, vertigo, or falling.
 Stroke patients may complain of headache;
however, with hemorrhagic stroke, the headache
can be very severe.
18
 Clinical Presentation and Diagnosis

 Signs (Ischemic)
 Hemiparesis or monoparesis occur
commonly, as does hemisensory deficit.
 Patients with double vision are likely to
have posterior circulation involvement.
 Aphasia is seen commonly in patients
with anterior circulation strokes.
 Patients may also suffer from dysarthria,
visual field defects, and altered levels of
consciousness.
19
 Signs and Symptoms (Hemorrhagic Stroke)
 A sudden severe headache, nausea, vomiting,
and photophobia may be the first signs and
symptoms. Patients may complain the headache
is “the worst headache of my life.”
 Neck pain and nuchal rigidity (stiffness) may
also be experienced.
 It is important to note that diagnosis of type of
stroke cannot be made solely on signs and
symptoms because overlap occurs between
types of stroke.

20
 Clinical Presentation and Diagnosis

 Laboratory Tests
 A computed tomography (CT) scan of the head:
identifying that a hemorrhage has occurred.
 The CT scan may take 24 hours (rarely
longer) to reveal the area of infarction.
 Magnetic resonance imaging (MRI): reveal
areas of ischemia earlier and with better
resolution than a CT scan.
 Carotid Doppler studies-to identify stenosis
 ECG-to identify AF
 ECHO-to identify the source of emboli
21
 TREATMENT OF ISCHEMIC STROKE

DESIRED TREATMENT OUTCOMES

 Short-term goals
 Reducing secondary brain damage by re-
establishing and maintaining adequate
perfusion to marginally ischemic areas of
the brain and to protect these areas from the
effects of ischemia (i.e., neuroprotection).
 Long-term goals
 Prevention of a recurrent stroke through
reduction and modification of risk factors and
by use of appropriate treatments.
22
 GENERAL APPROACH TO TREATMENT

 Allpatients should have a brain CT scan

or MRI scan to differentiate an ischemic
stroke from a hemorrhagic stroke,
 as the treatment will differ accordingly
and thrombolytic (fibrinolytic) therapy
must be avoided until a hemorrhagic
stroke is ruled out (in other words,
until it is determined that it is not a
hemorrhagic stroke).
23
General Approach…
 Identification
of the time and manner of
ischemic stroke onset is an important factor
for reperfusion therapy.
 The
time the patient was last without
symptoms is used as the time of stroke onset.
 Elevated BP should remain untreated in the
acute period (first 24 hrs) after ischemic
stroke to avoid decreasing cerebral blood
flow and worsening symptoms.

24
General Approach…
 BP should be lowered if it exceeds
220/120mm Hg or there is evidence of
 aortic dissection, acute myocardial infarction
(MI), pulmonary edema, or hypertensive
encephalopathy.
 If BP is treated in the acute phase, short-
acting parenteral agents (eg, labetalol,
nicardipine, nitroprusside) are preferred.
 When treatment is indicated, cautious
lowering of BP by approximately 15% during
the first 24 hours after stroke onset is
suggested
25
General Approach…
 Antihypertensive medications should be
restarted at approximately 24 hours after
stroke onset in patients with preexisting
hypertension who are neurologically
stable.
 However, patients with extracranial or
intracranial large artery stenosis may require
a slower reduction in BP(eg, over 7 to 10
days after ischemic stroke), as some degree
of BP elevation may be necessary to
maintain cerebral blood flow to ischemic
brain regions.
26
General Approach…
 InICH, patients may require external
ventricular drainage (EVD) if there is
intraventricular blood and evolving
hydrocephalus (enlargement of the
ventricles)

27
General Approach…

Supportive Measures
• Oxygen
• Volume status and electrolytes should be corrected
• Blood glucose should be corrected, as both
hyperglycemia and hypoglycemia may worsen brain
ischemia.
Hypoglycemia (<60 mg/dl)  bolus with 50%
dextrose
Hyperglycemia (>126 mg/dl)  subcutaneous
insulin (<300 mg/dL)
• Febrile: acetaminophen
•28DVT prophylaxis: Heparin 5000 units subcutaneously
Pharmacologic Therapy-
Ischemic Stroke
 For acute treatment, the only two
pharmacologic agents with class I
recommendations are
I. IV tissue plasminogen activator (tPA)
within 4.5 hours of onset and
 Early reperfusion (<4.5 hours from onset) with
IV tPA has been shown to reduce the ultimate
disability caused by ischemic stroke
II. Aspirin within 48 hours of onset.
 But it should never be given within 24 hours
of the administration of tPA because it can
increase the risk of bleeding
29
Thrombolytic Therapy
Alteplase
• In carefully selected patients, alteplase is
effective in limiting the infarct size and
protecting brain tissue from ischemia and
cell death by restoring blood flow.
• Treatment must be given within 4.5 hours of
the onset of symptoms and offers no benefit
if given beyond this time period
• Dose: 0.9 mg/kg (max 90 mg) is
recommended; the first 10% is given as an
IV bolus over 1 minute and the remainder is
infused over 1 hour
30
Criteria for Alteplase Use

Inclusion Criteria
• 18 years of age or older
• Clinical diagnosis of ischemic stroke
causing a measurable deficit
• Time of symptom onset well
established to be less than 4.5 hrs
before treatment would begin

31
Alteplase Use…
Exclusion Criteria
• Evidence of intracranial hemorrhage on CT scan
• Only minor or rapidly improving stroke symptoms
• Active internal bleeding (GI bleeding with in 21
days)
• Known bleeding diathesis, including but not limited
to
(1) Platelet count less than 100 × 10 3/mm3 (100 ×
109/L);
(2) Heparin within 48 hours with an elevated aPTT; or
(3) Current oral anticoagulant use (e.g., warfarin) or
recent use with an elevated PT (greater than 15
32
seconds) or INR (greater than 1.7)
Alteplase Use…

Exclusion Criteria….

 Intracranialsurgery, serious head trauma,

or previous stroke within 3 months
 Major surgery or serious trauma within 14
days
 Lumbar puncture within 7 days
 Recent acute myocardial infarction
 SBP greater than 185 mm Hg or DBP
greater than 110 mm Hg at the time of
33
treatment
Alteplase Use…

 Antiplatelet agents,
anticoagulants, and invasive
procedures such as the insertion of a
central line or the placement of a naso-
gastric tube should be avoided for 24
hours after the infusion of alteplase to
prevent bleeding complications.
 Bladder catheterization should also
be avoided for 30 minutes post-
infusion.
34
Alteplase Use…

 The major adverse effects of thrombolytic

therapy are bleeding, including
intracerebral hemorrhage and serious
systemic bleeding.
 Mentalstatus changes and a severe
headache may indicate an intracerebral
hemorrhage.
 Signs of bleeding include easy bruising;
hematemesis; guaiac-positive stools; black,
tarry stools; hematoma formation;
hematuria; bleeding gums; and nosebleeds
35
Aspirin
 Early aspirin therapy is recommended in most
patients with acute ischemic stroke within the
first 24 to 48 hours after stroke onset and
should be continued for at least 2 weeks.
 Antiplatelet therapy is the cornerstone of
antithrombotic therapy for the secondary prevention
of ischemic stroke and should be used in non-
cardioembolic strokes.
 ASA or clopidogrel are considered first-line
antiplatelet agents

36
 Inpatients with atrial fibrillation
and a presumed cardiac source of
embolism, oral anticoagulation is
recommended for secondary stroke
prevention.
 The choice of other oral
anticoagulants (e.g., dabigatran)
over vitamin K antagonism
(warfarin) may be recommended in
some patients
37
 Treatment of elevated BP after ischemic
stroke reduces risk of stroke recurrence.
 Treatment guidelines recommend BP reduction in
patients with ischemic stroke or TIA after the
acute period (first 7 days).
 Early blood pressure lowering can worsen symptoms
 Statins reduce risk of stroke by
approximately 30% in patients with coronary
artery disease and elevated plasma lipids.
 Treat ischemic stroke patients, regardless of
baseline cholesterol, with high-intensity statin
therapy to achieve a reduction of at least 50% in
LDL for secondary stroke prevention.
38
 Low-molecular-weight heparin (enoxaparin 40
mg daily) or low-dose subcutaneous
unfractionated heparin (5000 units three times
daily) is recommended for prevention of DVT in
hospitalized patients with decreased mobility due
to stroke and should be used in all but the most
minor strokes.
 within 48 hours of acute ischemic stroke onset
 For patients who are treated with intravenous
thrombolysis for acute ischemic stroke, IPC
should be started on admission, while
anticoagulation should be delayed until 24
hours after intravenous thrombolysis.
39
PREVENTION OF ACUTE ISCHEMIC
STROKE

Primary Prevention
 Aspirin is beneficial in the primary prevention of
MI, but not for primary stroke prevention.
 Statin: use may reduce the incidence of a first
stroke in high-risk patients (e.g., hypertension,
coronary heart disease, or diabetes) including
patients with normal lipid levels.
 Blood Pressure Management: Lowering blood
pressure in patients who are hypertensive has
been shown to reduce the relative risk of stroke,
both ischemic and hemorrhagic
40
Secondary Prevention
 ASPIRIN: Aspirin is typically considered to be
the first-line secondary prevention agent for
ischemic stroke and decreases the risk of
subsequent stroke by approximately 25%
with previous transient ischemic attacks or
stroke.
 WARFARIN: In patients with atrial fibrillation,
long-term anticoagulation with warfarin is
recommended and is effective in both
primary and secondary prevention of stroke
41
 Blood Pressure Management
 Inpatients with a previous history of
stroke or TIA, a diuretic and an ACE-
I are recommended

43
Hemorrhagic Stroke- Treatment
 There are currently no standard
pharmacologic strategies for treating ICH
 When ICH occurs in a patient on oral
anticoagulants, reversal of anticoagulation
to prevent expansion
and allow surgical intervention is
recommended.
 Other managements include
 Control of BP
 Management of increased intracranial pressure
 Management of other complications
44
BP control guidelines (AHA) for acute ICH
I. For patients with SBP b/n 150 and 220mmHg,
consider lowering of SBP to a target of 140 mmHg,
ideally within the first one hour of presentation,
provided the patient remains clinically stable
II. For patients who present with SBP >220 mmHg,
we suggest rapid lowering of SBP to <220 mmHg.
Thereafter, the blood pressure is gradually reduced
(over a period of hours) to a target range of 140 to
160 mmHg, provided the patient remains clinically
stable
 Patients who deteriorate clinically during this period
may require reduction of acute antihypertensive
therapy. The optimal blood pressure goal is uncertain,
but an SBP of 140 to 160 mmHg is a reasonable
target for patients who remain clinically stable
45
Drug Selection
 For most patients with an initial SBP ≥160
mmHg, we prefer nicardipine for initial
treatment because it is fast-acting and can be
quickly titrated
 For most patients with an initial SBP <160
mmHg, we start with labetalol for its ease of
administration and long duration of effect.

46
INTRACRANIAL PRESSURE
MANAGEMENT
 Patients with space-occupying lesions such as
acute ICH are at risk for progressive neurologic
impairment from brain compression due to
increased intracranial pressure (ICP).
 Acute ICH may lead to elevated ICP due to several
mechanisms. These include:
 Mass effect of the initial hematoma
 Expansion or re-bleeding of the ICH
 Cerebral edema surrounding the hemorrhage
 Hydrocephalus from ventricular outflow obstruction
 Treatment interventions include cerebrospinal fluid
drainage and osmotic therapy. Selected patients
with ICH may benefit from surgical interventions
47
 Surgical candidates
 Acute ICH >3cm in diameter or acute
neurological deteroration
 Hemispheric ICH and life threatening mass
effect
 Obstructive hydrocephallus
 Preventive Measures
 Head of bed > 30 degree
 Sedation for confort
 Antipytretics for temp > 38oC
 Serum Na>135 meq/L
 Avoidance of hypotonic fluids
48
Monitoring of ICP
 Clinical exam findings include new or
worsening:
 Pupillary changes, including impaired
reactivity to light
 Cranial nerve VI palsy; alert patients may
report horizontal diplopia
 Progressive drowsiness
 Cushing triad consisting of bradycardia,
respiratory depression, and hypertension
 Focal symptoms related to herniation
syndromes
49
 Osmotic therapy: Acute ICP elevation or life-
threatening mass effect can be treated with
hypertonic saline or mannitol
 For initial therapy and for patients with
evidence of life-threatening or progressive
deterioration, we use
 Mannitol 1 g/kg as a bolus via a central
intravenous line.
 For other patients, we use mannitol at a dose of
0.25 to 0.5 g/kg every six hours

50
SEIZURE MANAGEMENT
 Patients with acute ICH are at risk for early
seizures (within one to two weeks of ICH) and
late (post-stroke) seizures.
 Early seizures may be self-limited, attributed
to transient neurochemical changes
associated with the acute ICH.
 By contrast, late seizures are felt to be due to
structural changes and are likelier to become
recurrent
 For patients with acute ICH who have a
seizure, immediate intravenous antiseizure
medication treatment should be initiated to
reduce the risk of a recurrent seizure
51
 The optimal duration of antiseizure medication
therapy for patients with ICH and a seizure is
uncertain.
 For patients who have an early seizure (<14 days from
ICH onset), we typically continue treatment for several
days and then wean when patients are clinically stable if
seizures do not recur.
 For patients who have a late seizure (>14 days from ICH
onset), we typically continue long-term seizure therapy.
 For patients with acute ICH who do not have a
seizure, we do not start antiseizure medication
prophylaxis (AHA guidelines)
 Early seizures are more common than poststroke
epilepsy
52
Prevention of venous
thromboembolism
 Intermittent pneumatic compression should
be started on the first day of hospital
admission for patients with ICH and impaired
mobility
 Use anti-coagulants for most patients one to
four days after ICH stability is documented

53
TREATMENT OF ACUTE HEMORRHAGIC
STROKE

• Surgical
• Medical
 Protecting airway
 Managing BP before and after
aneurysm Rx
 Preventing rebleeding
Vasospasm- nimodipine

54
Initial assessment and management of
acute stroke
 Supplemental oxygen to maintain oxygen
saturation >94%
 Diagnosing an ICH or SAH as soon as possible
can be lifesaving. The history may be helpful
in this regard. The presence of acute onset
headache and vomiting favor the diagnosis of
ICH or SAH compared with a thrombo-embolic
stroke
 While the abrupt onset of impaired cerebral
function without focal symptoms favors the
diagnosis of SAH.
 Another important element of the history is
whether the patient takes anticoagulant
55
 The physical examination should include
careful evaluation of the neck and retroorbital
regions for vascular bruits, and palpation of
pulses in the neck, arms, and legs to assess
for their absence, asymmetry, or irregular
rate. The heart should be auscultated for
murmurs
 The three most predictive examination
findings for the diagnosis of acute stroke are
facial paresis, arm drift/weakness, and
abnormal speech
 Urgent lab tests include non-contract CT/MRI,
blood glucose, and oxygen saturation
56
Acute stroke mgt issues
 Fluids: Intravascular volume depletion is frequent in
the setting of acute stroke and may worsen cerebral
blood flow.
 Isotonic saline without dextrose is the agent of choice
 Mgt of hypoglycemia or hyperglycemia is important
 Swallowing assessment: Dysphagia is common
after stroke and is a major risk factor for developing
aspiration pneumonia. It is important to assess
swallowing function prior to administering oral
medications or food
 Head and body position
 Fever: may contribute to brain injury in patients with
an acute stroke.
57
 Summary

 Rapid evaluation is essential for use of

time-sensitive treatments such as
thrombolysis.
 However, patients with acute stroke often
do not seek medical assistance on their
own, both because they are rarely in pain,
as well as because they may lose the
appreciation that something is wrong
(anosagnosia); it is often a family member
or a bystander who calls for help.
58
 Summary

 Therefore, patients and their family

members should be counseled to call
emergency medical services immediately
if they experience or witness the sudden
onset of any of the following: loss of
sensory and/or motor function on one side
of the body (nearly 85% of ischemic stroke
patients have hemiparesis); change in
vision, gait, or ability to speak or
understand; or if they experience a
sudden,
59 severe headache