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STROKE

The acronym "F-A-S-T" can be used as a


memory aid for strokes: face, arm, speech,
time.

Abate W.
Clinical pharmacist
Debere Berhan University
Pharmacy Dept
6/2/2024 1
FAST
•F= face drooping
–Ask the person to smile or “show me your teeth."
Does one side of the face droop?
•A= arm weakness
–Ask the person to raise both arms. Does one arm
drift downward?
•S= speech difficulty
–Ask the person to say a simple sentence such as
“The sky is blue“. Is the sentence repeated
correctly?
•T= time to call Help
–Call to ambulance if a person has symptoms of
stroke, even if the symptoms go away.
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Introduction
 CEREBROVASCULAR DISEASE(CVD)- is any brain
abnormality caused by BV pathology.
 Includes : ischemic stroke, hemorrhagic stroke,
and Cerebrovascular anomalies such as
intracranial aneurysms and arteriovenous
malformations (AVMs)

 STROKE- is the most frequent clinical manifestation of


CVD although it may present, particularly in the elderly,
as a dementia .
 It is the abrupt onset of focal neurologic dysfunction that
lasts at least 24 hours and is caused by cerebral, spinal,
or retinal infarction.
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Stroke: What is it?
 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!

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Definition
 Clinically stroke is a sudden onset non convulsive
neurologic deficit characterised 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:
 So diagnosed clinically

 In stroke the evidence of brain dysfunction ( neurologic


deficit) lasts for at least 24h or more

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Def..
TRANSIENT ISCHEMIC ATTACK/TIA/
 A neurologic deficit that lasted less than
24hrs/usually few min./
 This abrupt onset of a neurologic deficit in
stroke/TIA is attributable to a focal vascular
cause.
 Generalized reduction in cerebral blood flow
causes syncope and if prolonged
watershed/ borderzone infarctions
Global hypoxia-ischemia
Hypoxic–ischemic encephalopathy
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Epidemiology
 Stroke is the fifth leading cause of death in the United
States, behind cardiovascular disease, cancer,
unintentional injuries, and chronic lower respiratory
diseases.
 Is the most common cause of severe physical disability
 The incidence rises steeply with age
 The incidence is rising in many developing countries
 African Americans have stroke rates that are 1.5 times
those of whites, and the difference is up to four times at
younger ages.

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 Ethiopia
A hospital based retrospective study was conducted at
St. Paul’s Teaching Referral Hospital in April 2016.
• The study has focused on review of medical records of all
stroke admissions to the hospital from September 1st, 2015
to August 30th, 2016.
•Results: A total of 163 stroke patients with
––M:F ratios of 1.3:1
–Hemorrhagic stroke was the most common type of stroke
accounting for 61.3% of cases.
–The most commonly identified risk factors were;
•Hypertension (60.7%),
•structural heart disease (18.4%),
•atrial fibrillation (14.7%) and
•diabetes mellitus (11%).
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Etiology
 Stroke is subdivided into either ischemic or hemorrhagic
types.
 Hemorrhagic stroke includes subarachnoid hemorrhage
(SAH) and intracerebral hemorrhage (ICH).
─ SAH occurs due to trauma, rupture of an intracerebral
aneurysm, or rupture of an arteriovenous malformation (AVM).
─ ICH occurs with the formation of a hematoma within the
brain. Uncontrolled HTN major cause.
 Hemorrhagic stroke, less frequent in occurrence, but
significantly higher mortality than ischemic stroke.
 Ischemic stroke is caused by occlusion within a cerebral
artery or emboli from a more proximal source resulting in
occlusion of a cerebral artery.

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Risk Factors

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ISCHEMIC STROKE
PATHOPHYSIOLOGY

 Occurs when a cerebral artery is blocked by a clot or other foreign


matter Causing ischemia (inadequate blood supply to tissue)

 Cerebral ischemia is caused by a reduction in blood flow that lasts


longer than several seconds
 If the cessation of flow lasts for more than a few minutes ischemia
Progresses to infarction (death of tissues).

 When blood flow is quickly restored, brain tissue can recover fully
and the patient's neurologic signs and symptoms resolve within 24
h: this is called a transient ischemic attack (TIA).
 If the neurologic signs and symptoms last for >24 h stroke has
occurred

 Classified as: Embolic Stroke or Thrombotic Stroke

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Pathophysiology of ischemic
stroke

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Clinical Presentation
General
• The patient may not be able to reliably report the history
due to cognitive or language deficits. A reliable history may
have to come from a family member or witness.
 Symptoms
 The patient may complain of weakness on one side of
the body, inability to speak, loss of vision, vertigo, and/or
falling.
 Ischemic stroke is not usually painful, but some patients
may complain of headache.
 Pain and headache, often severe, are more common
with hemorrhagic stroke.

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Signs
• Hemiparesis or monoparesis occurs commonly, as does a
hemisensory deficit.
• Aphasia
• dysarthria, visual field deficits, and altered levels of
consciousness.
 Laboratory Tests
 Blood glucose, platelet count, coagulation parameters,
tests for hypercoagulable states (protein C/S deficiency,
antiphospholipid antibody)
 Other Diagnostic Tests
 MRI,
 CT scan; determine whether the injury is ischemic or
hemorrhagic…..major role.
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CHA2DS2-VASc score: Stroke Risk
 CHF = 1 point; Hypertension = 1 point; Age 75 or older =
2 points; Diabetes = 1 point; prior Stroke, TIA, or
thromboembolism = 2 points; Vascular disease (aortic
plaque, peripheral artery disease, or history of MI) = 1
point; Age 65 to 74 years = 1 point; Sex category female
= 1 point.
 Scores correlate with approximate annual stroke risk
(based on a 2001 hospitalized cohort):
 0 = 0% risk
 1 = 1.3% risk
 2 = 2.2% risk
 3 = 3.2% risk
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Management
 The goals of treatment of acute stroke are
to;
(a) reduce the ongoing neurologic injury in
the acute setting to reduce mortality and
long-term disability,
(b) prevent complications secondary to
immobility and neurologic dysfunction, and
(c) prevent stroke recurrence.

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A) ACUTE ISCHEMIC STROKE
 1)Medical support
-Giving acute care
-ABCs of life
-BP management
-MAP increases following ischemic stroke
- Lowering BP is associated with clinical
deterioration
- Recommendation is to withhold the
antihypertensive till 10 to 14 days unless the pt
has the following conditions.
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 BP >/= 220/130
 Acute coronary heart disease event
 Heart failure
 Aortic dissection
 Thrombolysis is anticipated
-Fever and hyperglycemia management
- Prevention of complications/ DVT,infection etc

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2) Thrombolysis
 Tissue plasminogen activator, at 0.9mg/kg in the first three
hours of the onset of stroke
 Alteplase is the only FDA-approved treatment for acute
ischemic stroke.
 IV lteplase is first-line therapy, provided that treatment is
initiated within 4.5 hours of clearly defined symptom onset.
 Indication- Ischemic stroke after CT imaging
- </= 3hr
- No hemorrhage or edema
- Age >18, Consent
 C/I – Hypertension
- bleeding Hx or tendency
- coma/ stupor….
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3) Anticoagulation
- In cardioembolic stroke - Anticoagulants

4) Neuroprotection
5) Rehabilitation-
By giving appropriate rehabilitation recovery can be hastened
PREVENTIVE STRATEGIES

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B) Risk modification
 Individualized intervention to decrease the recurrence of
stroke
 MODIFIABLE

 Arterial hypertension- Dyslipidemia


 TIA Smoking
 Prior stroke Excessive alco
 carotid stenosis High fibrinogen
 Carotid disease High homocystein
 DM Low folate
 Obesity Anticardiolipin Ab

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RISK MODIFICATION
 HPN
• A patient's BP must be controlled if alteplaseis to be given.
–SBP > 185 mmHg or DBP > 110 mmHg are contraindications to
using antithrombotic therapy.
• If BP is high, IV labetalol or nicardipineare reasonable choices
for lowering blood pressure prior to administration of alteplase.
• In addition, blood pressure should be maintained below 180/105
mmHg for at least the first 24 hours after treatment with alteplase.
• For patients who don't receive thrombolytic therapy, high blood
pressure should not be treated acutely unless the systolic blood
pressure is > 220 mmHg, the diastolic blood pressure is > 120
mmHg, or the patient is at increased risk due to underlying
conditions (i.e. heart failure, hypertensive encephalopathy, acute
renal failure, etc.)
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 DM - 2-4X increase risk
- +HPN---4X inc risk
- Role of tight glycemic control in decreasing the risk
is not well substantiated/proved.

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 DYSLIPEDEMIA
 Higher total and LDL is associated with atherosclerosis
 Statins decrease CVD risk and benefit stroke survivors
 Statins slow progress of plaque formation and may also cause
regression/failure of plaque

 ATRIAL FIB
- 5-6X increased risk, 2X higher mortality
- warfarin with INR 2-3
 SMOKING
- 2-3 X increase risk
- Cessation decrease risk after 5 yrs
 ALCOHOL
- safe up to 2 drinks per day distributed equally over the week
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Ischemic Stroke; Nonpharmacologic Therapy

 Endovascular intervention and thrombectomy…. to


reperfuse ischemic brain tissue.

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Secondary prevention of
Ischemic Stroke
 Antiplatelet
 Anticoagulant
 Statin
 Antithrombotic agents
 Life style modification
 Control modifiable risk factors

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Antiplatelets
 After treatment with intravenous alteplas, antiplatelets
such as aspirin, and other anti-platelet agents (e.g.,
clopidogrel, tirofiban, eptifibatide) are contraindicated
during the first 24 hours.
 Oral aspirin, at an initial dose of 325 mg per day, should
be started within 24 to 48 hours after ischemic stroke
onset in most patients.
 Aspirin improves mortality and outcomes with its primary
effects on reduction of early recurrent stroke.
 Aspirin should not be started sooner than 24 hours after
IV administration of alteplase.

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Intracranial Hemorrhage

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 Intracranial hemorrhage is caused by
bleeding directly into or around the brain;

 it produces neurologic symptoms by


producing a mass effect on neural
structures, from the toxic effects of blood
itself, or by increasing intracranial pressure.

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ICH Epidemiology

 7000 operations annually in USA to remove


blood
 HEMORRHAGIC stroke in Ethiopia contribute to
57% stroke

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HEMORRHAGIC STROKE or/& Intracranial
bleeding can be
 Intraparenchymal hemorrhage (hypertensive or
related to other cause of hemorrhage)=ICH
 Subarachnoid hemorrhage
 Epidural
 Subdural
 Intraventricular
 Cerebellar

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Hypertensive Intraparenchymal
Hemorrhage/ICH/

 Spontaneous rupture of deep, small penetrating


artery
 Commonest Sites
 Putamen, Thalamus, Pons, Cerebellum
 Occur when pt is awake and sometimes stressed

 Abrupt onset of focal deficit , then raised ICP

 Focal deficit worsens over 30-90 minutes,

 Seizures are uncommon 33


6/2/2024
Pathophysiology:
- After rupture of a small penetrating artery
blood dissects the brain tissue and
compress adjacent tissue & may disect into
the ventricular space and cause
hydrocephalus.

- The hematoma is associated with increase


ICP through mass effect.

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Other Etiologies

 Trauma
 Vascular malformation-
 Aneurysm
 Tumor
 Coagulopathy
 Vasculitis

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Clinical presentation

 Depend on the site of bleeding !! ….

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ICH Rx Key Concepts
 Two key concepts:

1. Intracranial pressure
 Elevated when ICP >20 mm Hg

2. Cerebral perfusion pressure


 CPP=MAP-ICP
 Must maintain CPP > 70 mm Hg

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Increased ICP Treatment
 Intracranial Pressure (ICP):
-considered a major contributor to mortality when elevated
 Controlling ICP is essential
 BP Management
 Lower blood pressure to decrease risk of ongoing
bleeding from ruptured small arteries (SBP: 140-160)
 Overaggressive treatment of blood pressure may
decrease cerebral perfusion pressure and worsen brain
injury
 Especially with elevated ICP

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 Management of hypertension
- increase BP increases the bleeding
- decrease BP decreases CPP
* Monitor ICP and decrease BP to CPP of 60-
70 mmHg
* Drugs- labetelol,Nitroprusside,nicardipine
 Management of increase ICP
Osmotic agents, induced hyperventilation
Monitor ICP and consider ventriculostomy

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Surgery-

Hematoma evacuation in cerebellar
hemorrhage
 immediately if >3cm
 1-3 cm with change in consciousness and
respiratory failure
 Treat other causes of bleeding if …

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Initial Treatment Approach.. Hemorrhagic
Strokes
 Any underlying hemostatic abnormalities should be
corrected if possible.. because.
 Patients on oral anticoagulants account for 12% to 20%
of intracranial hemorrhages.
 Rapid correction of INR is recommended for any patient
on an oral anticoagulant.
 Most patients should wait four weeks prior to restarting
anticoagulation.
 Aspirin doesn't seem to increase bleeding
recurrence(can start within 48hr patient with DVT) and
can be restarted within a few days (at 10 days
rebleeding in unlikely).

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Initial Treatment Approach
 Systolic blood pressure should kept below 140 mmHg,
but clinicians must take care to not overshoot with
antihypertensive therapy and cause hypotension.
 IV nicardipineis titratable and may be a good option to
control blood pressure.
 Control of fevers, seizure prophylaxis, and the use of
fludrocortisone and hypertonic saline for correction of
hyponatremia should also be considered where
appropriate in hemorrhagic stroke.
 Deep vein thrombosis (DVT) prophylaxis with intermittent
pneumatic compression should be started on the day of
admission.
 Once bleeding is controlled, consider starting
pharmacological prophylaxis (e.g., enoxaparin, etc)
within the first few days
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Secondary Prevention
 Reduction in all modifiable risk factors;
 Recent modifications to the lipid-lowering
recommendations
a. High-intensity statin therapy should be initiated or
continued as first-line therapy if less than 75 years of age
who have had stroke or TIA
b. In individuals with stroke or TIA in whom high-intensity
statin therapy would otherwise be used, moderate-intensity
statin should be used as the second option if tolerated
Can we use thrombolytic, antiplatelets, and
anticoagulant for patients with hemorrhagic stroke
secondary prevention?

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Case 1
 B.S is a 65 years old male with HTN,
dyslipidemia, and seizure disorder
presents to the emergency department
after experiencing face drooping, arm
weakness, and speech difficulties.
 V/s; BP 150/90, HR 110, RR 14, T 36 oc.

 Investigations
 CT scan indicate Ischemic stroke, ICP >
20mm Hg.
 RFT,LFT, and CBC within normal range.
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Questions
1.What modifiable and non-modifiable risk
factor of acute ischemic stroke are present
in this patient?
2.What sign and symptoms indicate the
presence of acute ischemic stroke?
3. How do we estimate his stroke risk?
4. List all possible treatment options use in
acute phase and secondary prevention.
5. Which class of drug we use for secondary
45
prevention of his problem?
6/2/2024
THANK YOU!!

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