ISCHEMIC STROKE
Dr. Syed Muhammad Ali Shah
RMO/PGR
Dept. of Medicine ABSTH/NSMC
HISTORY OF STROKE
• Hippocrates first recognized stroke over 2,400 years ago.
• At this time stroke was called apoplexy, which means
"struck down by violence" in Greek.
• In mid-1600s that Jacob Wepfer - bleeding in the brain or
blockage in one of the brain's blood vessels
• In 1928, apoplexy was divided into categories based on the
cause of the blood vessel problem.
• This led to the terms stroke or "cerebral vascular accident
(CVA)."
http://www.hopkinsmedicine.org/healthlibrary/conditions/nervous_system_disorders/history_of_stroke_85,P00223/
DEFINITION
• Stroke is defined as a syndrome of rapid onset
of cerebral deficit (usually focal) lasting >24 h
or leading to death, with no cause apparent
other than a vascular one.
Kumar & Clark’s Clinical Medicine 8th Ed.
Epidemiology of Stroke
• Stroke remains the third leading cause of
death worldwide.
• No large scale epidemiological studies are
available to determine the true incidence of
stroke in Pakistan.
• Estimated annual incidence is 250/100,000,
translating to 350,000 new cases every year.
http://www.jpma.org.pk/full_article_text.php?article_id=1444
RISK FACTORS
*Davidson’s Principles and Practice of Medicine 22nd Ed.
Classification of Stroke
CAUSES OF STROKE
Cardiac source
•Arrhythmias
•Valve disease
•Dilated cardiomyopathy
•Recent myocardial infarction
•Paradoxical emboli
•Aorta
Large-vessel disorders
•Atherosclerosis or dissection in the carotid or
vertebrobasilar system
Small-vessel occlusive disease
•Hypertension-induced disease
•Isolated central nervous system angiitis
•Systemic lupus erythematosus
Hematologic disorders
•Polycythemia
•Thrombocytosis
•Severe leukocytosis (acute leukemia)
•Antithrombin III defi ciency
•Protein C defi ciency,
•Protein S deficiency
•Factor V Leiden mutation
•Hypercoagulable state
Pathology
• Ischemia of brain occurs due to thromboembolic
event
• Reduction of blood flow reduces supply of oxygen
and hence ATP.
• H+ is produced by anaerobic metabolism of
available glucose.
• Energy-dependent membrane ionic pumps fail,
leading to cytotoxic oedema and membrane
depolarisation, allowing calcium entry and
releasing glutamate.
*Davidson’s Principles and Practice of Medicine 22nd Ed
Pathology
• Calcium enters cells via glutamate-gated channels
and activates destructive intracellular enzymes,
destroying intracellular organelles and cell
membrane, with release of free radicals.
• Free fatty acid release activates pro-coagulant
pathways that exacerbate local ischemia.
• Glial cells take up H+, can no longer take up
extracellular glutamate and also suffer cell death,
leading to liquefactive necrosis of whole arterial
territory.
Davidson’s Principles and Practice of Medicine 22nd Ed
Arterial Cerebral Circulation
• The arterial cerebral circulation is normally
divided into
– Anterior cerebral circulation
– Posterior cerebral circulation
http://emedicine.medscape.com/article/1916852-clinical
Symptoms & Signs
• Hemiparesis
• Monoparesis
• Hemisensory deficits
• Monocular or binocular
visual loss
• Visual field deficits
• Diplopia
• Dysarthria
• Facial drop
• Ataxia
• Vertigo (rarely in
isolation)
• Aphasia
• Sudden decrease in the
level of consciousness
http://emedicine.medscape.com/article/1916852-clinical
Stroke, April 2003, Adams et al, Management of Patients With Ischemic Stroke
Stroke, April 2003, Adams et al, Management of Patients With Ischemic Stroke
Rapid Assessment of Suspected
Stroke
ROSIER scale
– Unilateral facial weakness +1
– Unilateral grip weakness +1
– Unilateral arm weakness +1
– Unilateral leg weakness +1
– Speech loss +1
– Visual field defect +1
– Loss of consciousness −1
– Seizure −1
Total (−2 to +6); score of > 0 indicates stroke is possible cause
Exclude hypoglycaemia
• Bedside blood glucose testing
Davidson’s Principles and Practice of Medicine 22nd Ed
Investigations
Management
General Management1
• Airway
– Perform bedside swallow screen and keep patient nil by mouth if
swallowing unsafe or aspiration occurs
• Breathing
– Check respiratory rate and oxygen saturation and give oxygen if
saturation < 95%
• Circulation
– Check peripheral perfusion, pulse and blood pressure and treat
abnormalities with fluid replacement, anti-arrhythmics and inotropic
drugs as appropriate
• Hydration
– If signs of dehydration, give fluids parenterally or by nasogastric tube
www.pakneurology.net
Davidson’s Principles and Practice of Medicine 22nd Ed
http://jama.jamanetwork.com/article.aspx?articleid=195305
• Nutrition
– Assess nutritional status and provide nutritional supplements if necessary
– If dysphagia persists for > 48 hrs, start feeding via a nasogastric tube
• Medication
– If patient is dysphagic, consider alternative routes for essential medications
• Blood pressure
– Unless there is heart or renal failure, evidence of hypertensive
encephalopathy or aortic dissection, do not lower blood pressure in first week
as it may reduce cerebral perfusion.
– Target blood pressure in patients who are not candidates for rt-PA should have
a systolic blood pressure of less than 220 mm Hg and a diastolic blood
pressure of less than 120 mm Hg.
– A blood pressure less than these values does NOT warrant anti-hypertensive
medicines.
– Blood pressure often returns towards patient’s normal level within first few
days
http://jama.jamanetwork.com/article.aspx?articleid=195305
• Blood glucose
– Hyperglycemia has detrimental outcomes after stroke.
It increases the chances of hemorrhagic conversion.
– Persistent hyperglycemia at the rate of > 200 mg / dl
independently predicts stroke expansion
– Monitor closely to avoid hypoglycaemia
• Temperature
– Increased body temperature in the setting of acute
stroke is associated with poor neurologic outcomes
as raised brain temperature may increase infarct
volume
– If pyrexic, investigate and treat underlying cause &
control with antipyretics
– Common reasons are aspiration pneumonia, IV line
phlebitis and urinary tract infection.
• Pressure areas
– Reduce risk of skin breakdown
– Treat infection
– Maintain nutrition
– Provide pressure-relieving mattress
– Turn immobile patients regularly
• Incontinence
– Check for constipation and urinary retention; treat
appropriately
– Avoid urinary catheterisation unless patient is in acute
urinary retention or incontinence is threatening
pressure areas
• Mobilisation
– Avoid bed rest
Thrombolysis
• IV thrombolytic therapy with recombinant tissue
plasminogen activator (rtPA; 0.9 mg/kg to a
maximum of 90 mg, with 10% given as a bolus
over 1 minute and the remainder over 1 hour) is
effective in reducing the neurologic deficit in
selected patients
• Patients should receive tPA within 1 hour after
arriving to the hospital but not more than 4.5
hours after the onset of ischemic symptoms.
CMDT 2015
www.pakneurology.net
http://jama.jamanetwork.com/article.aspx?articleid=195305
• In patients not eligible for thrombolytic
therapy, the immediate administration of
aspirin 325 mg orally daily is indicated.
• Anticoagulant drugs ONLY be started in the
setting of atrial fibrillation with warfarin
(target INR 2.0–3.0) or dabigatran (150 mg
twice daily)
Davidson’s Principles and Practice of Medicine 22nd Ed
CMDT 2015
http://jama.jamanetwork.com/article.aspx?articleid=195305
• Elevated intracranial pressure is managed by
head elevation and osmotic agents such as
mannitol.
• Decompressive hemicraniectomy for
malignant middle cerebral artery infarctions
may reduce mortality and improve functional
outcome in some instances.
Davidson’s Principles and Practice of Medicine 22nd Ed
CMDT 2015
http://jama.jamanetwork.com/article.aspx?articleid=195305
Physical Therapy
• Passive movements at an early stage will help prevent
contractures.
• As cooperation increases and some recovery begins,
active movements will improve strength and
coordination.
• In all cases, early mobilization and active rehabilitation
are important.
• Occupational therapy may improve morale and motor
skills
• Speech therapy may help expressive dysphasia or
dysarthria.
CMDT 2015
www.pakneurology.net
Steroids
• Treatment with corticosteroids did not appear to
show any improvement in functional outcomes of
stroke survivors.
• Usage of steroids in these cases may elicit unwanted
adverse effects such as hyperglycemia and infections.
Neuroprotection and Neurotonics
• No single trial has shown convincing benefit of stroke
neuroprotection and efficacy of intervention is
doubtful.
Qizilbash N, Lewington SL, Lopez-Arrieta JM. Corticosteroids for acute ischaemic stroke. Cochrane Database Syst Rev. 2002:CD000064
Lutsep HL, Clark WM. Neuroprotection in acute ischemic stroke. Current status and future potential. Drugs R D. 1999; 1:3-8
Wahlgren NG, Ahmed N. Neuroprotection in cerebral ischemia: Facts and fancies—the need for new approaches. Cerebrovasc Dis. 2004; 17 Suppl 1:153-
166
Secondary Prevention
• Antithrombotic therapy
– Aspirin in a dose ranging from 75 to 300 mg is efficacious
in stroke prevention.
– Clopidogrel is marginally better at increased cost and is
therefore suggested in those with concomitant peripheral
vascular disease and / or intolerance to aspirin.
• Dose adjusted warfarin is suggested in an INR 2-3 for
those who have intermittent or continous atrial
fibrillation.
Davidson’s Principles and Practice of Medicine 22nd Ed
CMDT 2015
www.pakneurology.net
http://jama.jamanetwork.com/article.aspx?articleid=195305
• Lipid Control1
– Atorvastatin 80 mg/day significantly reduced the risk of
stroke in patients who previously had a stroke or (TIA) and
who had no known cardiovascular disease.
– Target goal for cholesterol lowering LDL-C of <100 mg/dL
and LDL-C of <70 mg/dL for very-high-risk persons with
multiple risk factors
• Blood Pressure Control2’3
– Mean blood pressure fall of 5 mm Hg leads to a one third
reduction of stroke
– If BP > 130/70 mmHg 1–2 weeks after onset use thiazide
diuretic and/or ACE inhibitor
1. Stroke Prevention by Aggressive Reduction of Cholesterol Levels (SPARCL) study
2. PROGRESS trial
3. Davidson’s Principles and Practice of Medicine 22nd Ed
www.pakneurology.net
http://jama.jamanetwork.com/article.aspx?articleid=195305
• Smoking
• Obesity
• Exercise- regular physical activity
• Dietry salt restriction
www.pakneurology.net
http://jama.jamanetwork.com/article.aspx?articleid=195305
Surgical Interventions
Carotid Endarterectomy
When arteriography reveals a surgically
accessible highgrade stenosis (70–99% in
luminal diameter) on the side appropriate to
carotid ischemic attacks - operative treatment
(carotid endarterectomy) or endovascular
intervention reduces the risk of ipsilateral
carotid stroke
CMDT 2015
http://jama.jamanetwork.com/article.aspx?articleid=195305
Stroke in Future
Folate Supplements for Stroke Prevention1
Among adults with hypertension in China without
a history of stroke or MI, the combined use of
enalapril and folic acid, compared with enalapril
alone, significantly reduced the risk of first stroke.
These findings are consistent with benefits from
folate use among adults with hypertension and
low baseline folate levels.
1.http://jama.jamanetwork.com/article.aspx?articleid=2205876
Stroke in Future
Endovascular Therapy for Ischemic Stroke with
Perfusion-Imaging Selection
In patients with ischemic stroke with a proximal
cerebral arterial occlusion and salvageable tissue
on CT perfusion imaging, early thrombectomy
with the Solitaire FR stent retriever, as compared
with alteplase alone, improved reperfusion, early
neurologic recovery, and functional outcome.
http://www.nejm.org/doi/full/10.1056/NEJMoa1414792#t=abstract
Ischemic stroke

Ischemic stroke

  • 1.
    ISCHEMIC STROKE Dr. SyedMuhammad Ali Shah RMO/PGR Dept. of Medicine ABSTH/NSMC
  • 2.
    HISTORY OF STROKE •Hippocrates first recognized stroke over 2,400 years ago. • At this time stroke was called apoplexy, which means "struck down by violence" in Greek. • In mid-1600s that Jacob Wepfer - bleeding in the brain or blockage in one of the brain's blood vessels • In 1928, apoplexy was divided into categories based on the cause of the blood vessel problem. • This led to the terms stroke or "cerebral vascular accident (CVA)." http://www.hopkinsmedicine.org/healthlibrary/conditions/nervous_system_disorders/history_of_stroke_85,P00223/
  • 3.
    DEFINITION • Stroke isdefined as a syndrome of rapid onset of cerebral deficit (usually focal) lasting >24 h or leading to death, with no cause apparent other than a vascular one. Kumar & Clark’s Clinical Medicine 8th Ed.
  • 4.
    Epidemiology of Stroke •Stroke remains the third leading cause of death worldwide. • No large scale epidemiological studies are available to determine the true incidence of stroke in Pakistan. • Estimated annual incidence is 250/100,000, translating to 350,000 new cases every year. http://www.jpma.org.pk/full_article_text.php?article_id=1444
  • 5.
    RISK FACTORS *Davidson’s Principlesand Practice of Medicine 22nd Ed.
  • 6.
  • 7.
    CAUSES OF STROKE Cardiacsource •Arrhythmias •Valve disease •Dilated cardiomyopathy •Recent myocardial infarction •Paradoxical emboli •Aorta Large-vessel disorders •Atherosclerosis or dissection in the carotid or vertebrobasilar system Small-vessel occlusive disease •Hypertension-induced disease •Isolated central nervous system angiitis •Systemic lupus erythematosus Hematologic disorders •Polycythemia •Thrombocytosis •Severe leukocytosis (acute leukemia) •Antithrombin III defi ciency •Protein C defi ciency, •Protein S deficiency •Factor V Leiden mutation •Hypercoagulable state
  • 8.
    Pathology • Ischemia ofbrain occurs due to thromboembolic event • Reduction of blood flow reduces supply of oxygen and hence ATP. • H+ is produced by anaerobic metabolism of available glucose. • Energy-dependent membrane ionic pumps fail, leading to cytotoxic oedema and membrane depolarisation, allowing calcium entry and releasing glutamate. *Davidson’s Principles and Practice of Medicine 22nd Ed
  • 9.
    Pathology • Calcium enterscells via glutamate-gated channels and activates destructive intracellular enzymes, destroying intracellular organelles and cell membrane, with release of free radicals. • Free fatty acid release activates pro-coagulant pathways that exacerbate local ischemia. • Glial cells take up H+, can no longer take up extracellular glutamate and also suffer cell death, leading to liquefactive necrosis of whole arterial territory. Davidson’s Principles and Practice of Medicine 22nd Ed
  • 10.
    Arterial Cerebral Circulation •The arterial cerebral circulation is normally divided into – Anterior cerebral circulation – Posterior cerebral circulation http://emedicine.medscape.com/article/1916852-clinical
  • 12.
    Symptoms & Signs •Hemiparesis • Monoparesis • Hemisensory deficits • Monocular or binocular visual loss • Visual field deficits • Diplopia • Dysarthria • Facial drop • Ataxia • Vertigo (rarely in isolation) • Aphasia • Sudden decrease in the level of consciousness http://emedicine.medscape.com/article/1916852-clinical
  • 13.
    Stroke, April 2003,Adams et al, Management of Patients With Ischemic Stroke
  • 14.
    Stroke, April 2003,Adams et al, Management of Patients With Ischemic Stroke
  • 15.
    Rapid Assessment ofSuspected Stroke ROSIER scale – Unilateral facial weakness +1 – Unilateral grip weakness +1 – Unilateral arm weakness +1 – Unilateral leg weakness +1 – Speech loss +1 – Visual field defect +1 – Loss of consciousness −1 – Seizure −1 Total (−2 to +6); score of > 0 indicates stroke is possible cause Exclude hypoglycaemia • Bedside blood glucose testing Davidson’s Principles and Practice of Medicine 22nd Ed
  • 16.
  • 17.
    Management General Management1 • Airway –Perform bedside swallow screen and keep patient nil by mouth if swallowing unsafe or aspiration occurs • Breathing – Check respiratory rate and oxygen saturation and give oxygen if saturation < 95% • Circulation – Check peripheral perfusion, pulse and blood pressure and treat abnormalities with fluid replacement, anti-arrhythmics and inotropic drugs as appropriate • Hydration – If signs of dehydration, give fluids parenterally or by nasogastric tube www.pakneurology.net Davidson’s Principles and Practice of Medicine 22nd Ed http://jama.jamanetwork.com/article.aspx?articleid=195305
  • 18.
    • Nutrition – Assessnutritional status and provide nutritional supplements if necessary – If dysphagia persists for > 48 hrs, start feeding via a nasogastric tube • Medication – If patient is dysphagic, consider alternative routes for essential medications • Blood pressure – Unless there is heart or renal failure, evidence of hypertensive encephalopathy or aortic dissection, do not lower blood pressure in first week as it may reduce cerebral perfusion. – Target blood pressure in patients who are not candidates for rt-PA should have a systolic blood pressure of less than 220 mm Hg and a diastolic blood pressure of less than 120 mm Hg. – A blood pressure less than these values does NOT warrant anti-hypertensive medicines. – Blood pressure often returns towards patient’s normal level within first few days http://jama.jamanetwork.com/article.aspx?articleid=195305
  • 19.
    • Blood glucose –Hyperglycemia has detrimental outcomes after stroke. It increases the chances of hemorrhagic conversion. – Persistent hyperglycemia at the rate of > 200 mg / dl independently predicts stroke expansion – Monitor closely to avoid hypoglycaemia • Temperature – Increased body temperature in the setting of acute stroke is associated with poor neurologic outcomes as raised brain temperature may increase infarct volume – If pyrexic, investigate and treat underlying cause & control with antipyretics – Common reasons are aspiration pneumonia, IV line phlebitis and urinary tract infection.
  • 20.
    • Pressure areas –Reduce risk of skin breakdown – Treat infection – Maintain nutrition – Provide pressure-relieving mattress – Turn immobile patients regularly • Incontinence – Check for constipation and urinary retention; treat appropriately – Avoid urinary catheterisation unless patient is in acute urinary retention or incontinence is threatening pressure areas • Mobilisation – Avoid bed rest
  • 21.
    Thrombolysis • IV thrombolytictherapy with recombinant tissue plasminogen activator (rtPA; 0.9 mg/kg to a maximum of 90 mg, with 10% given as a bolus over 1 minute and the remainder over 1 hour) is effective in reducing the neurologic deficit in selected patients • Patients should receive tPA within 1 hour after arriving to the hospital but not more than 4.5 hours after the onset of ischemic symptoms. CMDT 2015 www.pakneurology.net http://jama.jamanetwork.com/article.aspx?articleid=195305
  • 22.
    • In patientsnot eligible for thrombolytic therapy, the immediate administration of aspirin 325 mg orally daily is indicated. • Anticoagulant drugs ONLY be started in the setting of atrial fibrillation with warfarin (target INR 2.0–3.0) or dabigatran (150 mg twice daily) Davidson’s Principles and Practice of Medicine 22nd Ed CMDT 2015 http://jama.jamanetwork.com/article.aspx?articleid=195305
  • 23.
    • Elevated intracranialpressure is managed by head elevation and osmotic agents such as mannitol. • Decompressive hemicraniectomy for malignant middle cerebral artery infarctions may reduce mortality and improve functional outcome in some instances. Davidson’s Principles and Practice of Medicine 22nd Ed CMDT 2015 http://jama.jamanetwork.com/article.aspx?articleid=195305
  • 24.
    Physical Therapy • Passivemovements at an early stage will help prevent contractures. • As cooperation increases and some recovery begins, active movements will improve strength and coordination. • In all cases, early mobilization and active rehabilitation are important. • Occupational therapy may improve morale and motor skills • Speech therapy may help expressive dysphasia or dysarthria. CMDT 2015 www.pakneurology.net
  • 25.
    Steroids • Treatment withcorticosteroids did not appear to show any improvement in functional outcomes of stroke survivors. • Usage of steroids in these cases may elicit unwanted adverse effects such as hyperglycemia and infections. Neuroprotection and Neurotonics • No single trial has shown convincing benefit of stroke neuroprotection and efficacy of intervention is doubtful. Qizilbash N, Lewington SL, Lopez-Arrieta JM. Corticosteroids for acute ischaemic stroke. Cochrane Database Syst Rev. 2002:CD000064 Lutsep HL, Clark WM. Neuroprotection in acute ischemic stroke. Current status and future potential. Drugs R D. 1999; 1:3-8 Wahlgren NG, Ahmed N. Neuroprotection in cerebral ischemia: Facts and fancies—the need for new approaches. Cerebrovasc Dis. 2004; 17 Suppl 1:153- 166
  • 26.
    Secondary Prevention • Antithrombotictherapy – Aspirin in a dose ranging from 75 to 300 mg is efficacious in stroke prevention. – Clopidogrel is marginally better at increased cost and is therefore suggested in those with concomitant peripheral vascular disease and / or intolerance to aspirin. • Dose adjusted warfarin is suggested in an INR 2-3 for those who have intermittent or continous atrial fibrillation. Davidson’s Principles and Practice of Medicine 22nd Ed CMDT 2015 www.pakneurology.net http://jama.jamanetwork.com/article.aspx?articleid=195305
  • 27.
    • Lipid Control1 –Atorvastatin 80 mg/day significantly reduced the risk of stroke in patients who previously had a stroke or (TIA) and who had no known cardiovascular disease. – Target goal for cholesterol lowering LDL-C of <100 mg/dL and LDL-C of <70 mg/dL for very-high-risk persons with multiple risk factors • Blood Pressure Control2’3 – Mean blood pressure fall of 5 mm Hg leads to a one third reduction of stroke – If BP > 130/70 mmHg 1–2 weeks after onset use thiazide diuretic and/or ACE inhibitor 1. Stroke Prevention by Aggressive Reduction of Cholesterol Levels (SPARCL) study 2. PROGRESS trial 3. Davidson’s Principles and Practice of Medicine 22nd Ed www.pakneurology.net http://jama.jamanetwork.com/article.aspx?articleid=195305
  • 28.
    • Smoking • Obesity •Exercise- regular physical activity • Dietry salt restriction www.pakneurology.net http://jama.jamanetwork.com/article.aspx?articleid=195305
  • 30.
    Surgical Interventions Carotid Endarterectomy Whenarteriography reveals a surgically accessible highgrade stenosis (70–99% in luminal diameter) on the side appropriate to carotid ischemic attacks - operative treatment (carotid endarterectomy) or endovascular intervention reduces the risk of ipsilateral carotid stroke CMDT 2015 http://jama.jamanetwork.com/article.aspx?articleid=195305
  • 31.
    Stroke in Future FolateSupplements for Stroke Prevention1 Among adults with hypertension in China without a history of stroke or MI, the combined use of enalapril and folic acid, compared with enalapril alone, significantly reduced the risk of first stroke. These findings are consistent with benefits from folate use among adults with hypertension and low baseline folate levels. 1.http://jama.jamanetwork.com/article.aspx?articleid=2205876
  • 32.
    Stroke in Future EndovascularTherapy for Ischemic Stroke with Perfusion-Imaging Selection In patients with ischemic stroke with a proximal cerebral arterial occlusion and salvageable tissue on CT perfusion imaging, early thrombectomy with the Solitaire FR stent retriever, as compared with alteplase alone, improved reperfusion, early neurologic recovery, and functional outcome. http://www.nejm.org/doi/full/10.1056/NEJMoa1414792#t=abstract