3. Introduction
• Stroke is defined as a syndrome of rapid onset neurological deficit of
vascular origin caused by focal cerebral, spinal or retinal infarction or
hemorrhage
• TIA is defined as a transient episode of neurological dysfunction
caused by focal brain, spinal cord or retinal ischemia without
evidence of acute ischemia (AHA/ASA 2009)
4. • Stroke is the second leading cause of death worldwide, with
6.2million dying from stroke in 2015
• Stroke is a significant economic, social and medical problem
worldwide
• Stroke has grown in incidence worldwide , however it is declining
among the affluent and rising among those with less access to
medical care
5. Epidemiology
• 5th commonest cause of death, if considered separately from CVD
• Leading cause of disability worldwide
• In the US, annual incidence 795,000
• Prevalence increases with age
• Lifetime risk higher in women
• In Nigeria, prevalence is 1.14/1000, 30 day case fatality rate 40%
(Kolawole W. H)
6. • Stroke registry in Ibadan gave the annual incidence of stroke in
Nigerians as 26 per 100,000 populations
• At LASUTH stroke was the commonest cause of neurological
admissions
• In Nigeria cerebral ischemia accounted for 64%, ICH for 19% and SAH
for 6% of all strokes
• A cross sectional study between Jan 2010 and July 2013 in NHA
showed 62.5% had ischemic stroke while ICH 30.5% and SAH was
2.9%.[Nura H.A et-al]
7. • Stroke is classified into two major types
• Brain ischemia due to thrombosis, embolism, or systemic
hypoperfusion.
• Brain hemorrhage due to intracerebral hemorrhage (ICH) or
subarachnoid hemorrhage (SAH).
8. • Ischemic stroke represents a variety of conditions in which blood flow
to part or all of the brain is reduced resulting in tissue damage
• Ischemic stroke can be classified clinically using the TOAST
classification and Bamford classification
9.
10.
11. Watershed infarcts
• Defined as a brain ischemia localized to the vulnerable border zones
between the tissues supplied by ACA, MCA & PCA.
• The actual blockage site can be located far away from the infarcts.
• Comprise approximately 10% of all ischemic stroke cases
• particularly susceptible to infarction from global ischemia due to
hypoperfusion
• Memory loss, intellectual impairment, motor deficits
• Hypoxic ischemic encephalopathy due to prolonged hypoperfusion
13. Anatomy
• -Brain represents 2% body
mass
• -Requires 15-20% total cardiac
output to function
• - Blood supply through the
internal carotid artery &
vertebrobasilar artery
22. Cerebral autoregulation & cerebral perfusion
pressure
• The brain is able to autoregulate its blood flow within a mean arterial
pressure of 60-150mmhg (cerebral autoregulation)
• Beyond this pressure the brain is unable to compensate for changes
in perfusion pressure
• Cerebral auto regulation is impaired during ischemic stroke.
• In hypertensive individuals, autoregulation is adapted to occur in high
arterial pressure. Sudden reduction of BP to normal could exacerbate
Autoregulation derangement leading to further CBF reduction.
23. pathophysiology
• Acute occlusion of an intracranial vessel leads to a decrease in blood
flow to the brain region it supplies
• Reduction in cerebral blood flow to zero causes brain tissue death
within 4-10mins
• Blood flow <16-18ml/100g tissue/min leads to infarction within an
hour
• <20ml/100mg tissue/min ischemia without infarction unless
prolonged (hours-days)
24. • A TIA results when blood flow is restored to ischemic tissue before
significant infarction develops.
• Ischemic core is an affected area where blood flow is
<10ml/100g/min
• Ischemic penumbra, blood flow <25ml/100g/min
-area surrounding the ischemic core
-neurons are non functional
-structurally normal
-target of revascularization
27. • With decreasing cerebral blood flow the following occurs:
• Protein synthesis is initially inhibited and completely ceases
• Transient increase in glucose utilization then it drops dramatically
with conversion to anaerobic glycolysis
• There's accumulation of lactic acid with tissue acidosis
• Neuronal electrical failure and failure of membrane ion hemostasis
28. Brain ischemia initiates a cascade of events that eventually lead to cell
death, including:
• Depletion of adenosine triphosphate (ATP)
• Changes in ionic concentrations of sodium, potassium, and calcium
Increased lactate, acidosis
• Accumulation of oxygen free radicals
• Activation of proteolytic processes.
• Intracellular accumulation of water leading to cytotoxic edema
29. • Ischemia also directly results in dysfunction of the cerebral
vasculature with breakdown of the blood-brain barrier
• Influx of proteins and water into the extracellular space leading to
vasogenic edema.
• Extravasation of peripheral blood from disrupted blood brain barrier
can also occur hemorrhagic transformation
30. Clinical presentation
• Common signs and symptoms :
• Hemiparesis, monoparesis or quadriparesis
• Hemisensory deficits
• Monocular or binocular visual loss, visual field deficits, diplopia
• Dysarthria, aphasia, facial droop
• Ataxia, Vertigo
• Sudden decrease in level of consciousness
31. Management
• Focused hx and examination to establish the lesion, localize region of
brain dysfunction and identify risk factors.
• Airway, breathing and circulation
• Vital signs
• Head and neck exam
• Major organ system examination: CVS, neurologic
• National Institute of Health Stroke Score: NIHSS
32. Investigations
• Emergent Non contrast brain CT
• CT perfusion, CT angiography
• Brain MRI: structural details and show early cerebral edema
• MRI angiography
• Carotid Doppler
• ECG, ECHO
36. • Acute phase
-mass effect
• Chronic phase
-gliosis
-hypodensity with negative mass effect
-cortical mineralization (hyperdense)
37.
38. Treatment
• AIMS:
-redeem the ischemic penumbra
-achieve timely recanalization of occluded artery & reperfusion of
ischemic tissue
-optimize collateral flow
-apply principles of acute stroke care
-avoid secondary brain injury
39. • ABC: airway, breathing, circulation
• Stabilize the patient as necessary
• Complete initial evaluation and assessment all within 60 mins of
patient arrival
• Address comorbidities: antipyretics, oxygen supplementation, IVF ,
vasopressor therapy
• Blood glucose control. : maintain blood glucose level between 140-
180mg/dl (7.7-10mmol/L)
40. Blood pressure control
• For patients who are not candidates for fibrinolytic therapy, current
guidelines recommend permitting moderate hypertension in most
patients with acute ischemic stroke.
• The exceptions would be patients who have active comorbidities (eg,
aortic dissection, acute myocardial infarction [MI],
• Acute antihypertensive therapy is typically indicated when blood
pressure is >220/120 mm Hg,(ASA 2013)
• For those who have received IV thrombectomy blood pressure should
be maintained
41. Fibrinolytic therapy
• IV thrombolysis with rtPA is proven to be effective in improving functional
outcomes after an ischemic stroke up to 4.5 hours after symptom onset
• Fibrinolytic therapy with alteplase (rt-PA).
• Indications for administration of rtPA for AIS
– Clinical diagnosis of stroke
– Onset of symptoms to time of drug administration ≤ 4.5 h
– CT scan showing no hemorrhage or edema of >1/3 of the MCA territory
– Age ≥ 18 years
-persisting neurological deficit
42.
43. • Endovascular therapy with mechanical thrombectomy :
• for patients in whom fibrinolysis is ineffective or contraindicated.
Within 6-16hrs post event
• 4 devices have been approved :
1. Merci retriever
2. Penumbra system
3. Solitaire FR Revascularization Device
4. Trevo
44.
45. Antithrombotic therapy
• AHA/ASA recommend giving aspirin 325mg PO within 24-48hrs of
ischemic stroke onset
• Aspirin therapy reduces the risk of stroke recurrence within 14 days (
International Stroke Trial )
• Aspirin treatment started within 48 hrs of onset of AIS and continued
for up to 4 weeks reduced mortality to 3.3% (CAST)
46. • DAPT -is recommended in the short term and only for specific
patients: those with early arriving minor stroke and high-risk TIA or
severe symptomatic stenosis
• Treatment with DAT (aspirin + clopidogrel) started within 24hrs of
onset and continued up to 21 days is effective in reducing ASI
recurrence within 90 days.
47. Anticoagulation
• Atrial Fibrillation- 2 weeks after AF
• Arterial dissection- immediately due to high risk of re stroke
• Venous sinus/ cortical vein thrombosis
- Warfarin
- DOAC: thrombin inhibitors- dabigatran
factor Xa inhibitor- rivaroxaban/apixaban
48. Supportive care
• Nutritional support: enteral feeding NG Tube feeding if there’s
dysphagia
• Screen for dysphagia, to prevent aspiration
• Intermittent pneumatic compression for immobile patients
• Use of prophylactic-dose subcutaneous heparin has not been
established as beneficial
49. • • Use of hemodilution, IV albumin, to increase CBF has no any
benefit.
• Use of pharmacological and Non pharmacological neuroprotective
medications has no benefits.
• Regular skin assessment and skin hygiene.
• Use of prophylactic antibiotics and indwelling catheter should be
AVOIDED.
50. • Management of Cerebral edema:
• IV mannitol may be used to raise the serum osmolality.
• Hemicraniotomy reduces mortality by 50%
• Seizure control: antiepileptics for secondary prevention of
subsequent seizures.
51. Supportive care
• Rehabilitation : multidisciplinary approach
• Planning for discharge
• formal evaluation of the patients ADL
• ability to communicate and functional mobility
• Depression screening : use of antidepressants for diagnosed
depression
52. Prevention
• Primary prevention
• Healthy diet
• Smoking avoidance and cessation
• Blood pressure control: BP target <130/80mmHg
-SBP <120mmHg reduces risk of stroke & MI by 43% (SPRIN-Trial)
• Weight reduction, Increased physical activity
• Low dose statin
• Antiplatelet therapy: aspirin, clopidogrel
53. Secondary prevention (prevent further
strokes)
• Treatment of dyslipidemia:
- dietary, lifestyle modifications
- High intensity statin therapy : goal is to lower LDL-C by 50% or more in
patients <75yrs
- Screen for atrial fibrillation and initiate anticoagulant drug therapy to
reduce recurrent events
- Control of blood pressure in hypertensive patients
- Smoking cessation
- Screening and management of diabetes mellitus
- Surgery & stenting for carotid stenosis
57. Conclusion
• Acute ischemic stroke is a medical emergency in which every minute
counts.
• Achievement of reperfusion can reverse neurologic deficits, even if
severe, and allow patients to regain function
58. References
• Wahab KW. The burden of stroke in Nigeria. Int J Stroke. 2008 Nov;3(4):290-2. doi:
10.1111/j.1747-4949.2008.00217.x. PMID: 18811746.
• Arshad Majid, MB, ChB, FRCP, Mounzer Kassab, MD , Pathophysiology of ischemic stroke
https://www.uptodate.com/contents/pathophysiologyof-ischemic-stroke#H21816470
• Natalia S Rost, Alexis Simpkins Overview of secondary prevention of ishemic stroke
• Edward C Jaunch Ischemic Stroke https://emedicine.medscape.com/article/1916852-
overview
• Wade S. Smith, S. Claiborne Johnston, J. Claude Hemphill, Ischemic stroke :
• Harrison Principle of Internal Medicine 20th Edition. 6. CONTINUUM (MINNEAP
MINN)2020;26(2, CEREBROVASCULAR DISEASE):435–456.
• https://www.stroke-manual.com/toast-stroke-classification/#1631720401843-ec8ba1b8-
1bb6
Editor's Notes
Causes of cardiormbolic
Infective endocarditis
Mural thrombus
Paradoxical thrombosis if there’s patent foramen ovale.
Af
Atrial flutter
What arteries are affected in lacuna infarts.
The lentiostratical branches
Subthalamic nucleus the globus pallidus and putamen
embolismcardiac embolism
atrial fibrillation
ventricular aneurysm
endocarditis
paradoxical embolism: from a dvt through a shunt vsd,and or pfa
atherosclerotic embolism
fat embolism
air embolism
Drugs : through vasospams or haemorrhagic stroke more from damage to the blood vessels.
Renovasocular disease: fibromuscilar dysplasia
Myoamyoa
Related to handheld of water
T2 csf is white in T2.
T1. Csf is black
Carotid dappled to check for stenosis of ICA > 70% is significant and should be done in 2weeks of stroke to prevent repeat
Other contraindications- symptoms of subarachnoid hemoorhage, plt count <100,000, INR 1.7, rbs <2.8/>26.2
Complications of TPA: orolingual edema, symptomatic intracranial hemorrhage
MERCI- mechanical embolus removal in cerebral ischemia
Trevo- stent retriever
DAPT (dual antiplatelet therapy)
DOAC- wider therapeutic index
Less drug interactions
Lower risk of hemorrhage
Do not require drug monitoring
