CURRENT TRENDS IN

THE MANGEMENT OF
CEREBROVASCULAR
ACCIDENT 1
Lecture Notes
 PRESENTATION OUTLINE
 INTRODUCTION
 EPIDEMIOLOGY
 PATHOPHYSIOLOGY
 RISK FACTORS
 CLINICAL MANIFESTATIONS

 INVESTIGATIONS
 MANAGEMENT
 ROLE OF PHARMACIST
 ACKNOWLEDGEMENT
 CASE STUDY
 REFERENCES
2
INTRODUCTION
 Cerebrovascular accident currently called brain attack is a rapidly
developing acute neurological events, presumed to be vascular in origin
lasting 24 hours or longer or leading to death.
 It is also known as stroke.
 Stroke happens when blood flow to the brain is interrupted depriving brain
cells of oxygen causing them to die within minutes
  It is always considered a medical emergency requiring prompt treatment
to prevent brain damage and complications

 Strokes can be prevented and managed.

3
TYPES OF STROKE
 Ischemic stroke
 Hemorrhagic stroke;

Intracerebral hemorrhage
Subarachnoid hemorrhage

 TIA: defined as a neurological deficit caused by interruption in blood supply

to the brain, in which all symptoms resolve within 24 hours

 Cryptogenic stroke A stroke in which no generally accepted cause is

identified after investigation.
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CLASSIFICATION OF STROKE

5
EPIDEMIOLOGY
 In 2005, estimates suggested that 58 million people died and chronic
diseases accounted for 35 million death, (60%). Cardiovascular disease
caused 17.5 million (WHO, Preventing chronic diseases: a vital investment.
Geneva: WHO 2005)

Stroke after heart disease is the second leading single cause of death.
(http://neurology .thelancet.com vol 6; 2007.)

 It is the most common cause of serious, long-term disability in

adults(zweifler rm. Management of acute stroke). South med
J. 2003;96:380–5

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 EPIDEMIOLOGY, CONT.
 In the united states, blacks have an age-adjusted risk of death from stroke that is 1.49
times that of whites.  Hispanics have a lower overall incidence of stroke than whites
and blacks but more frequent lacunar strokes and stroke at an earlier age.

 Men are at higher risk for stroke than women

 One third of strokes occur in persons younger than 65 years.

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EPIDEMIOLOGY, CONT.
 A literature search on stroke indicated that stroke is currently one of the
top five causes of deaths in Ghana and is also a frequent cause of
admission to hospitals. (University of Ghana, balme library, stroke burden
in Ghana 2012).

 In KBTH an unpublished research gave results leading to a conclusive fact

that stroke was associated with high mortality.

 They thereby made recommendations that awareness of stroke prevention

be made and a well equipped stroke unit be established to improve
prognosis of survival of stroke patients.

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TOP 10 CAUSES OF DEATH IN SME
(2011)
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300 295

250

200

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150

105
100 86
75 70 65
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PATHOPHYSIOLOGY
 Ischemic stroke

 Thrombotic stroke

 Embolic stroke

In the core area of a stroke, blood flow is so drastically reduced that cells
usually cannot recover and subsequently undergo cellular death.

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THE ISCHEMIC CASCADE

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 HAEMORRHAGIC STROKE
 Intracerebral hemorrhage.  A blood vessel in the brain bursts and spills into the
surrounding brain tissue.
 Subarachnoid hemorrhage an artery on or near the surface of your brain bursts
and spills into the space between the surface of your brain and your skull.
 Sudden and violent headache is characteristic of subarachnoid hemorrhage.
 Rupture of an aneurysm or atrio ventricular malformations(AVM), chronic
hypertension, trauma

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 RISK FACTORS-MODIFIABLE

 High blood pressure

 Cigarette smoking or exposure to secondhand smoke.
 High cholesterol
 Diabetes
 Obesity
 Sedentary lifestyle

 Heavy drinking
 Cardiovascular diseases, including heart failure, atrial fibrillaton, or coronary
artery disease

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 RISK FACTORS-NON MODIFIABLE

 Personal or family history of stroke, heart attack or TIA.

 Being age 55 or older.
 Race — African-Americans have higher risk of stroke than people of other
races.
 Gender — Men have a higher risk of stroke than women. Women are
usually older when they have strokes, and they are more likely to die of
strokes than men.

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SIGNS AND SYMPTOMS

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SIGNS AND SYMPTOMS
Symptoms and signs develop rapidly, and are usually focal (although they
can be global)

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SIGNS AND SYMPTOMS CONT.
 Cerebral cortex is involved when the following symptons are seen;

 Aphasia-broca's or wernicke's area typically involved

 Dysarthria

 Apraxia (altered voluntary movements)

 Visual field defect

 Memory deficits (involvement of temporal lobe)

 Hemineglect (involvement of parietal lobe)

 Disorganized thinking, confusion, hypersexual gestures (with involvement

of frontal lobe)

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SIGNS AND SYMPTOMS CONT.

 Brain stem involvement brings about;

 Altered smell, taste, hearing, or vision (total or partial)

 Ptosis and weakness of ocular muscles

 Decreased reflexes: gag, swallow, pupil reactivity to light

 Decreased sensation and muscle weakness of the face

 Balance problems and nystagmus

 Altered breathing and heart rate

 Weakness in tongue movement

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SIGNS AND SYMPTOMS CONT

 Cerebellum involvement causes;

 Altered walking gait
 Altered movement coordination
 Vertigo and or disequilibrium

 Loss of consciousness, headache, and vomiting usually occurs more often

in hemorrhagic stroke than in thrombosis

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DIAGNOSIS
Use FAST for rapid diagnosis

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 DIAGNOSIS CONT.
 CT SCAN
 Magnetic resonance imaging (MRI) may also be done to find out the
amount of damage to the brain and help predict recovery.
 Ultrasound
 Echocardiogram
 Blood tests
 BUE Cr
 Serum lipids

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CT SCAN

23
MRI

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DIFFERENTIAL DIAGNOSIS
 Hypoglyceamia

 Migraine

 Neurological abnormalities

 Seizures

 Hyponatremia and hepatic encephalopathy

 Physical trauma including concussion

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PREVENTION
 Control high blood pressure  
 Quit tobacco use
 Control diabetes 
 Maintain a healthy weight (BMI 18.5-24.9 kg/m2)
 Maintain a healthy diet
 Exercise regularly. 
 Drink alcohol in moderation
 Avoid illicit drugs. 

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MANAGEMENT

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MANAGEMENT
 Goals of therapy:

 To limit the progression area of brain damage

 To prevent complications arising from unconsciousness and immobility

 To treat the underlying cause if possible

 To reduce mortality and recurrent stroke

 To improve the quality of life

 To institute measures to improve functional recovery

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SUPPORTIVE TREATMENT
 Monitor patient`s vital signs and neurological signs frequently

 Establish adequate airway in unconscious patients

 Prevent pressure sores by regular turning of patient every 2 hours in bed

 Insert nasogastric tube as early as possible for feeding and medications

 Early physiotherapy as soon as practicable

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SUPPORTIVE TREATMENT
 Blood sugar control (keep RBS 4-10)

 Elevate the head of the bed to 30°. This improves jugular venous outflow and
lowers intracranial pressure.

 Manage hyperpyrexia.

 Supplemental oxygen therapy if saturation falls below 95%

 Prevent or treat aspiration pneumonia

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MANAGEMENT OF TIA
 Immediate treatment
 Aspirin 300 mg daily should be started immediately
 Do not delay initiating aspirin treatment in people with uncontrolled blood
pressure.
 Consider gastroprotection
 Consider clopidogrel (75 mg daily — off-label use) only if the person is
allergic or cannot tolerate aspirin.
 Both aspirin and clopidogrel are contraindicated in people with active
gastrointestinal bleeding or ulceration.

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REFERRAL FOR TIA PATIENT
Consider admission if:
 The person has atrial fibrillation 

Refer immediately
 The person's ABCD 2 score is 4 or more .
 The person has had two or more TIAs within 1 week
 The person is on anticoagulation treatment — brain imaging is required to
exclude intracranial bleeding.

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 KBTH POLYCLINIC OTHER
OTHERHOSP.
HOSP.
OPD
OPD KBTH
KBTH

KBTH SME Team on duty sees

Review by stroke team
Suspicion of stroke Admission criteria
+/- CT scan • Rosier score>0
• ABCD 2 score>6
• Head CT confirmed
INITIATE MGT & CONSULT STROKE TEAM
• First and second stroke

ADMIT
ADMIT TO
TO STROKE
STROKE UNIT
UNIT
•• MEDICAL
MEDICAL TEAM
TEAM
•• PHARMACIST
PHARMACIST
Previous stroke with other medical conditions •• NURSES
NURSES
•• PHYSIOTHERAPIST
PHYSIOTHERAPIST
•• SPEECH
SPEECH & & LANGUAGE
LANGUAGE
THERAPIST
THERAPIST
•• DIETICIAN
DIETICIAN
ADMIT •• PSYCHOLOGIST
ADMIT TO
TO GENENRAL
GENENRAL WARD
WARD TO
TO BE
BE CO-
CO- PSYCHOLOGIST
MANAGED •• NEUROSURGEON
NEUROSURGEON
MANAGED WITH
WITH STROKE
STROKE TEAM
TEAM •• SOCIAL
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SOCIAL WORKER
WORKER
 ISCHAEMIC

REDUCING
ANTIHYPERTEN ANTICONVULSAN
THROMBOLYSIS STATINS SURGERY INTRACRANIA
SIVES TS
L PRESSURE

ANTICOAGULANT CAROTID ANGIOPLAST

S FIBRINOLYTICS ANTIPLATELETS IV
ENDARTERECTO Y AND IV
MANNITO
MY STENTS DEXAMETHASONE
L

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 HAEMORRAGIC
STROKE

REDUCING
ANTIHYPERTENSIVE ANTICONVULSANTS SURGERY INTRACRANIAL
STATINS
S PRESSURE

SURGICAL IV MANNITOL IV
AVM REMOVAL
CLIPPING DEXAMETHASONE

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MANAGEMENT
FIBRINOLYTICS
 Tissue plasminogen activator- Alteplase

tPA works by dissolving the clot and improving blood flow

 Should be administered within 3 hours and up to 4.5 hours on onset
 by intravenous administration over 60 minutes, 900micrograms/kg (max.
90mg);
 initial 10% of dose by intravenous injection, remainder by intravenous
infusion;
 ELDERLY over 80 years not recommended
 Anticoagulants and antiplatelet drugs are not used within 24 h of treatment
with tPA.

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Exclusion Criteria for Use of Tissue Plasminogen Activator in Stroke
> 4.5 h after symptom onset
Intracranial hemorrhage on CT scan
Multilobar infarct (hypodensity in more than one third of the territory supplied by the middle cerebral artery)
on CT scan
Rapidly decreasing symptoms
Presentation suggesting subarachnoid hemorrhage even if CT is negative

History of intracranial hemorrhage

Intracranial aneurysm, arteriovenous malformation, or tumor

History of stroke or head trauma within the past 3 months

Systolic BP >185 mm Hg or diastolic BP > 110 mm Hg after antihypertensive treatment

Arterial puncture at noncompressible site or lumbar puncture in the past 7 days

Major surgery or serious trauma in the past 14 days

Active internal bleeding

GI or urinary tract hemorrhage in the past 21 days

Suspected bleeding disorder

Platelet count < 100,000/μL
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WARFARIN
 Prophylaxis and treatment of systemic embolic complications including
stroke associated with atrial fibrillation (AF)
 Initial dose: 2-5 mg qDay × 2 days
 Check INR and adjust dose according to results
 Typical maintenance dose ranges between 2-10 mg/day
 Interferes with hepatic synthesis of vitamin K-dependent clotting factors II,
VII, IX, and X
 The administration of anticoagulants is contraindicated during the first 24
hours after IV thrombolytic therapy
 Given with enoxaparin1.5 mg/kg (150 units/kg) every 24 hours
 until adequate oral anticoagulation established
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CURRENT ANTICOAGULANTS
 Efficacious alternatives to warfarin for patients with nonvalvular atrial
fibrillation
 Rivaroxaban (xarelto)
 A direct factor xa inhibitor
 20 mg once/day for patients without severe renal failure (creatinine
clearance < 15 ml/min)
 Dabigatran (Pradaxa)

 A direct thrombin inhibitor, inhibits thrombin-induced platelet aggregation

 Apixaban (Eliquis)

 A direct factor Xa inhibitor

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ANTI PLATELETS
 Aspirin
 Blocks prostaglandin synthetase action prevents the formation of platelet-
aggregating thromboxane A2
 Clopidogrel(plavix)
 Inhibitor of adenosine diphosphate (ADP)-induced pathway for platelet
aggregation
 Dipyridamole
 Inhibition of Thromboxane A2 formation (vasoconstrictor and a stimulator
of platelet activation)

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ANTI PLATELETS
 High-dose aspirin is usually continued for about 2 weeks after the event,
and then low–dose long–term antiplatelet treatment is started.
 Clopidogrel (75 mg daily) is the preferred antiplatelet for secondary
prevention of ischaemic stroke.

 If clopidogrel is contraindicated or not tolerated, give a combination of

modified-release dipyridamole (200 mg twice daily) and aspirin 75 daily

 Consider a proton pump inhibitor to reduce G.I bleeding in people at high

risk of G.I. bleeding or to relieve aspirin-induced dyspepsia.

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ANTIHYPERTENSIVES
 For people with a TIA: consider starting antihypertensive treatment as soon
as possible.
 For people with an acute stroke treatment will usually be initiated in
secondary care about 2 weeks after the event
 For people with established cardiovascular disease the aim is to reduce
blood pressure preferably to 130/80 mmHg.

 For people with bilateral, severe (more than 70%) stenosis of the internal
carotid arteries: a slightly higher target blood pressure

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ANTIHYPERTENSIVES
 If systolic BP is over 200 mm Hg or mean arterial pressure (MAP) is over
150 mm Hg, then consider reduction of BP with continuous IV infusion;
check BP every 5 minutes to < 110 mm Hg (SBP < 160 mm Hg) for 24
hours is required

 In patients presenting raised intracranial pressure, lowering of MAP to <

130 mm Hg (SBP < 180 mm Hg) for 24 hours is required

 For patients with aneurysmal subarachnoid hemorrhage, the 2012 AHA/ASA

guidelines recommend lowering BP below 160 mmHg to reduce rebleeding.

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 Nicardipine
 Ca channel blocker
 5mg/hr by slow infusion
 2.5mg/hr every 15mins if desired outcome not achieved

 Labetalol
 Beta blocker with slight alpha 1 activity

I.V injection 50mg within a min. repeat after 5mins(max. 200mg)

I.V infusion 2mg/min (max. 50-200mg)

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ANTIHYPERTENSIVES
 Thiazide diuretics

 Calcium channel blockers (amlodipine)

 Angiotensin-converting enzyme inhibitors (ramipril, perindopril)

 Angiotensin receptor blockers (losartan)

 Beta blockers (carvedilol)

 (HOPE) study, the addition of the ACEI ramipril

 (PROGRESS), a regimen based on perindopril, an ACEI, was superior to placebo

  Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT)

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 The Losartan Intervention for Endpoint Reduction in Hypertension Study (LIFE)
STATINS
 Started as soon as possible for people with a transient ischaemic attack (TIA).

 48 hours after the event for people with an acute ischaemic stroke.

 Seek specialist advice before initiating a statin in people with a history of

hemorrhagic stroke, particularly those with inadequately controlled
hypertension

 Consider higher-intensity statin therapy if the total cholesterol level does not
decrease to below 4 mmol/L or the low-density lipoprotein cholesterol level
does not decrease to below 2 mmol/L. 46
 Atorvastatin, oral,
 10-40 mg daily

 80 mg once/day is recommended for patients with evidence of atherosclerotic stroke and LDL (low-
density lipoprotein) cholesterol ≥ 100 mg/dL.
 Rosuvastatin, oral,

 5-10 mg daily

 Or

 Simvastatin, oral
 20-40mg at night

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ANTICONVULSANTS
 Early seizure activity occurs in 4-28% of patients with intracerebral
hemorrhage; these seizures are often nonconvulsive
   (AHA/ASA) 2010 guidelines for the management of spontaneous
intracerebral hemorrhage for patients with clinical seizures accompanied
by a change in mental status should be treated with antiepileptic drugs
 Phenytoin
 20 mg/kg slowly at rate no greater than 50 mg/minute
 Diazepam
 10 mg slowly over 23 minutes (approximately 2.5 mg every 30 seconds)

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PIRACETAM
 A derivative of the neurotransmitter gamma-aminobutyric acid (GABA)

 Has neuroprotective and anticonvulsant properties

 At a vascular level, it appears to reduce erythrocyte adhesion to vascular

endothelium, hinder vasospasm, and facilitate microcirculation

 Increase in weight

 Feeling nervous or shaky

 Drowsiness

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NIMODIPINE
 Indicated for the improvement of neurological outcome by reducing the
incidence and severity of ischemic deficits with subarachnoid hemorrhage

 60 mg PO q6hr for 21 days; begin therapy within 96 hours of subarachnoid

hemorrhage

 Ca channel blocker with minimal effects on conduction in heart; primary

effect is upon cerebral arteries to prevent vasospasm
 Highly lipophilic, allowing it to cross the blood-brain barrier

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REDUCTION OF
INTRACRANIAL PRESSURE
 I.V manitol

 Reduction of intracranial pressure and treatment of cerebral edema

 1.5-2 g/kg IV infused over 30-60 minutes 8hrly

 I.V dexamethasone

 10 mg IV, then 4 mg IM q6hr until clinical improvement is observed; may

be reduced after 2-4 days and gradually discontinued

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RESIDUALS OF STROKES
 Paralysis or loss of muscle movement.

 
 Difficulty talking or swallowing. 

 Memory loss or thinking difficulties

 Emotional problems (depression)

 Changes in behavior and self-care.

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COMPLICATIONS OF STROKE
 Intracranial pressure and hydorocephalus

 Aspiration pneumonia

 Vasospasm

 Seizures

 Deep vein thrombosis leading to pulmonary embolism

 Another stroke

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 Coma.
ROLE OF THE PHARMACIST
 Advice team on evidence-based medicine guidelines

 Monitoring of newly prescribed and existing drug therapies

 Advice on correct management of stroke complications

 Strict adherence counselling

 Assessment of potential compliance

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 CASE
STUDY
55
 Name: Y.O
 Age : 56 years
 DOA : 15/02/14
 Sex : F
 PC-severe headache and sudden collapse
 Brief History

Patient is not a known hypertensive nor diabetic. Was apparently well until 3
days ago prior to presentation when she experienced with the above
symptoms. She presented with a BP of 240/140mmHg. A head Ct scan showed
intracerebral bleed and was referred for further management
 SHx– lives at Pokuase , married with 5 children, plantain trader, not alcoholic,
doesn’t smoke, and not on health insurance
DHx from referral source– Nifedepine 30mg bd
Losartan 100mg dly
Bendroflumethiazide 2.5mg dly
 O/E

BP 180/110 mmHg

 15/02/14

 FBC, BUE, Cr, LFT, Chest x-ray, ECG, Urine Re and Cs

 Lisinopril 10mg dly

 Tab Nimodipine 30mg 8hrly

 4hrly bp check

 4hrly RBS check

 16/02/14

 Increase Lisinopril to 20mg dly

 Add bendrofluazide 2.5mg dly

QUESTIONS
1. What could be the possible diagnosis

2. What are the possible risk factors of her condition

3. What are the pharmaceutical care issues

4. What are the counselling points.

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