2. INTRODUCTION
Stroke is generally defined as any disease process that interrupts blood flow to the brain.
Injury is related to the loss of oxygen and glucose substrates necessary for high-energy
phosphate production and the presence of mediators of secondary cellular injury.
Subsequent factors, such as edema and mass effect, may exacerbate the initial insult.
Ischemic stroke accounts for 87% of all strokes in hospitalized patients
Whereby 80% is from thrombotic ischemic CVA and 20% from embolic events
Hypoperfusion accounts for most of gross ischemic strokes in patients with cardiac failure which
lead to systemic hypotension
Stroke syndromes are defined by the type of cerebral vessels involved on accident
Thus we have MCA, ACA, ICA, PCA and vertebrobasilar stroke syndromes
3. ANATOMY AND PHYSIOLOGY OF THE BRAIN
Frontal Lobe roles
Movement of the body, Personality,
Concentration, planning, problem solving,
Meaning of words, Emotional reactions, Speech,
Smell
Parietal Lobe; Touch and pressure, Taste,
Body awareness
Temporal Lobe; Hearing, Recognizing faces,
Emotion, Long-term memory
Cerebellum; Latin for little brain
Fine motor (muscle) control,
Balance and coordination (avoid objects and
keep from falling)
5. BLOOD SUPPLY CONT………..
Blood is supplied to the brain by the anterior and posterior circulations.
The anterior circulation originates from the carotid system and perfuses 80% of the brain, including
the optic nerve, retina, and fronto-parietal and anterior-temporal lobes.
The first branch off the internal carotid artery is the ophthalmic artery, which supplies the optic
nerve and retina.
As a result, the sudden onset of painless monocular blindness (amaurosis fugax) identifies the stroke
as involving the anterior circulation (specifically the ipsilateral carotid artery) at or below the level
of the ophthalmic artery.
The internal carotid arteries terminate by branching into the anterior and middle cerebral arteries at
the circle of Willis.
6. BLOOD SUPPLY CONT………..
Although the posterior circulation is smaller and usually supplies only 20% of the brain,
It supplies the brainstem (which is critical for normal consciousness, movement, and sensation),
cerebellum, thalamus, auditory and vestibular centers of the ear, medial temporal lobe, and visual
occipital cortex.
The posterior circulation is derived from the two vertebral arteries that ascend through the transverse
processes of the cervical vertebrae.
The vertebral arteries enter the cranium through the foramen magnum and supply the cerebellum by
the posterior inferior cerebellar arteries.
They join to form the basilar artery, which branches to form the posterior cerebral arteries.
7. EPIDEMIOLOGY OF STROKE
Stroke claims about 5.8million of life every year worldwide
34.1% of all death from cardiovascular diseases
With incidence of 94.6 to 141.3/100,000 cases per year in high income countries
Published data with reliable methodology designs in low and middle income countries are limited.
However the range estimated to be 350 to 2120/100,000 cases per year
In sub-Saharan Africa incidence ranges between 15 and 1460/100,000 cases per year
In Tanzania recent data are limited, however estimated to be 109-316 cases per 100,000, from study
done in 2010
8. RISK FACTORS FOR ISCHEMIC STROKE
A; In situ thrombosis in ⅓ of these strokes
-Large vessels
• Occur at cerebral vessel branch points - e.g. internal carotid artery and caused by ulcerated
atherosclerotic plaque → platelet plugs, vasculitis in HIV, Polycythemia(hypercoagulable state)
- Small vessels
• Lacunar or small vessel strokes at the small terminal vessel end points [diabetes, hypertension]
B; Embolic obstruction in ¼ of all strokes
-Cardiac - atrial fibrillation; septic emboli from infective endocarditis.
Valvular vegetations, mural thrombi, fat emboli,
-Noncardiac- Extracranial proximal carotid plaque (amaurosis fugax)
C; AGE RELATED; More common in elderly however young age has not been spared
9. LOCATION OF STROKE AND SYMPTOMS
A; ANTERIOR CIRCULATION
1. Internal carotid artery stroke syndrome;
Presents with; tonic gaze deviation towards lesion, global aphasia, dysgraphia, dyslexia, dyscalculia
and disorientatation as the dominant lesion, spatial or visual neglect as non dominant lesion
2. Anterior cerebral artery stroke syndrome
Presents with; contralateral sensory and motor symptoms in extremities sparing face and hands,
urinary and bowel incontinence
-Primitive grasp and suck reflexes
-Left side occlusion; akinetic mutism, aphasia
- Right side occlusion with confusion
10. LOCATION OF STROKE AND
SYMPTOMS……….
3. Middle cerebral artery stroke syndrome
Presents with; hemiparesis, facial plegia, sensory loss contralateral
Motor deficits; more on upper extremities than lower extremities
Dominant hemisphere; aphasia
Wernicke(receptive aphasia) and Broca’s (expressive aphasia)
Dominant hemisphere; dysarthria, hemianopsia, gaze preference towards
affected side and agnosia
11. LOCATION OF STROKE AND
SYMPTOMS………
B; POSTERIOR CIRCULATION
-Posterior cerebral artery and vertebrobasilar stroke syndrome:
affect the brainstem, cranial nerves, cerebellum, and reticular activating system (RAS)
-Ipsilateral CN deficit without contralateral motor weakness
-Multiple complaints of LOC, N/V, alexia and visual agnosia
-5Ds;Dizziness, Dysarthria, Dystaxia, Diploplia and Dysphagia
16. INHOSPITAL DIAGNOSIS
LAB TEST;
Blood glucose test PTT, INR, CBC
RADIOLOGICAL
ECG; To exclude atrial fibrillation or acute MI
Cranial imaging (CT or CT/CTA)
NB;
Most acute ischemic strokes are not visualized by a non contrast brain CT
in the early hours of a stroke.
Therefore, the utility of the first brain CT is primarily to exclude intracranial
bleeding, abscess, tumor, and other stroke mimics, as well as to detect
current contraindications to thrombolytic
17. MANAGEMENT APPROACH AT ED
All patients
Assessment of airway, breathing, circulation Immediate life threats must be addressed before
other interventions are undertaken.
Actively manage airway if necessary.
Establish IV access; for possible thrombolytic therapy.
(Do not delay brain imaging for prolonged IV access attempts.)
Pulse oximetry; To detect hypoxia.
Oxygen administration (only if hypoxia is present)
Cardiac monitoring; Dysrhythmias, especially atrial fibrillation, are not infrequent in acute
stroke and may predict 3-month mortality.
Prophylactic administration of antidysrhythmic agents is not indicated.
18. MANAGEMENT APPROACH AT ED……..
Bedside glucose determination
-To rapidly rule out hypoglycemia mimicking stroke.
-Treat hypoglycemia (<60 milligrams/dL) with IV dextrose.
Noncontrasted brain CT or MRI
To exclude intracerebral hemorrhage, other contraindications to IV thrombolytics, or stroke mimics.
-ECG; ACS, dysrhythmias (especially atrial fibrillation), ECG changes and abnormal cardiac
biomarkers are frequently associated with acute stroke
- ECG abnormalities and abnormal troponin T levels may also predict short-term and 3-mo mortality.
19. MANAGEMENT APPROACH AT ED……..
CBC including platelet count; To detect polycythemia, thrombocytosis, or
thrombocytopenia.
Coagulation studies
To detect preexisting coagulopathy when thrombolytics are being indicated
Electrolyte levels; To detect electrolyte-imbalance stroke mimics (Na+ and
Ca2+).
Cardiac biomarker levels; may be useful in detecting cardiac etiologies of
ischemic stroke.
Nothing by mouth (NPO) order; To protect against aspiration.
20. MANAGEMENT APPROACH AT ED……..
-Strict bed rest in the ED
To protect against falls and seizures (in the period immediately after stroke).
-In patients who can maintain oxygenation,
supine position has been suggested to possibly improve patient outcomes by
enhancing cerebral blood flow
21. Selected patients
Chest radiograph; Routine chest radiography in asymptomatic patients is not recommended and
should be reserved only for situations where a cardiopulmonary contraindication to thrombolytics is
suspected or if immediate management would be significantly impacted by chest radiograph
findings.
Urinalysis; To detect infectious stroke mimics or stroke-associated infections.
Pregnancy test (if female of childbearing age) Pregnancy influences diagnosis and management
considerations.
Toxicology screen and/or blood alcohol level (if ingestion suspected) To detect stroke mimics as well
as potential causes of stroke such as ingestion of a sympathomimetic (e.g., cocaine,
methamphetamine, phencyclidine).
Lumbar puncture (if infection or subarachnoid hemorrhage suspected)
To detect stroke mimics.
22. THERAPEUTIC MANAGEMENT AT ED
The big picture of current therapies are:
Prevention of secondary neurologic injury by:
Avoiding dehydration
Maintaining saturation above 92%
Preventing fever
Maintaining glucose between 140 and 180mg/dl
Bed elevation above 30 degrees
23. THERAPEUTIC MANAGEMENT AT ED…..
○ Blood Pressure management
-tPA candidate; Lower SBP<185, DBP to<110, goal MAP <110
Drug options labetalol, nitroglycerin or nicardipine
-Non tPA candidate; Allow permissive hypertension unless SBP>220 Or DBP>120
where you lower by 25% over 24hrs MAP goal of <150
○ Anticoagulation
Aspirin 325mg within 24-48hrs
Clopidogrel 600mg loading dose then 75mg daily for 30-90days
However is not recommended in acute stroke or A. fibrilation
24. THERAPEUTIC MANAGEMENT AT ED….
○ Thrombolytic therapy
-Recommended to patients who present at ED within 3hrs to 4.5hrs from when
the attack has occurred
-inclusion criteria
1. Age >18yrs,
2. Diagnosis of ischemic stroke causing measurable neurologic deficit.
3. Clear onset last witnessed well, less than 3 to 4.5hrs
25. THROMBOLYTICS USE IN ISCHEMIC
STROKE
Exclusion criteria for thrombolytics
Prior stroke or head injury in the past 3months
Hx of intracebral hemorrhage
Abnormal coagulation profile
Uncontrolled HTN above 185/110mmhg
Using direct thrombin inhibitors dabigatran or factor Xa inhibitors rivaroxaban
Myocardial infarction in the past 3months
GIT or any system presented with bleeding in the past 27days
26. Endovascular Therapy
Mechanical clot removal for large vessel occlusions (e.g. M1 occlusion, basilar artery occlusion)
Early trials MR RESCUE, SYNTHESIS, and IMSIII showed no benefit and potential harm
MR CLEAN Trial show promising outcomes[14]
Participants had proximal intracranial artery occlusions
Intervention was conducted within 6 hrs
Functional independence of 32.6% with endovascular treatment and 19.1% with typical therapy
27. Eligibility for the procedure
AHA guidelines say the following patients are eligible for mechanical thrombectomy:
0-6 hours: pre-stroke modified ranking score (mRS)
major vessel occlusion,
age > 18,
NIHSS > 5,
Goal SBP <160 after endovascular therapy
28. SPECIAL CONSIDERATIONS
TRANSIENT ISCHEMIC STROKE (T.I.A)
A brief episode of neurologic dysfunction caused by focal brain, spinal cord or retinal ischemia,
with clinical symptoms typically lasting less than one hour, and without evidence of acute
infarction.
Clinical Features
Focal weakness (Paralysis or paresis of the face, arm, or leg and typically unilateral)
Dysarthria or dysphasia or aphasia
Vision changes (Field deficits, blindness, or diplopia)
Changes in balance or coordination
A Patient with TIA should be admitted and investigated full
Risk of developing stroke within two days is too high and extends up to 90 days
Therefore 90days follow up is mandatory
29. WORK UPS
Stroke Work-Up
Labs
POC glucose
CBC
Chemistry pannel
Coagulation profile
Troponin
Radiology; ecg, ct head and CTA, MRI done to differentiate TIA vs CVA
30. T.I.A SCORES
ABCD2 Scoring system
Age >60yr (1 pt)
BP (SBP >140 OR diastolic >90) (1
pt)
Clinical Features
Isolated speech disturbance (1 pt)
Unilateral weakness (2 pts)
Duration of symptoms
10-59 min (1 pt)
>60 min (2 pts)
Diabetes mellitus (1 pt)
Interpretation
Points Stroke Risk 2 Days 7 Days 90 Days
0-3 Low 1.0% 1.2% 3.1%
4-5 Moderate 4.1% 5.9% 9.8%
6-7 High 8.1% 11.7% 17.8%
31. Canadian TIA Score
Item Scoring
Clinical Findings:
1. First TIA (in lifetime) (2 pt)
2. Symptoms ≥10 minutes (2 pt)
3. Past history of carotid stenosis (2 pt)
4. Already on antiplatelet therapy (3 pt)
5. History of gait disturbance (1 pt)
6. History of unilateral weakness (1 pt)
7. History of vertigo (-3 pts)
8. Initial triage diastolic blood pressure ≥110
mm Hg (3 pt)
9. Dysarthria or aphasia (history or
examination) (3 pt)
Investigations in the emergency department:
1.Atrial fibrillation on electrocardiogram (2 pt)
2.Infarction (new or old) on computed tomography (1 pt)
3.Platelet count≥400×109/L (2 pt)
4.Glucose ≥15 mmol/L (3pt)
interpretation
-3-3 Low
4-8 Medium Risk
≥9 High
32. ACUTE ISCHEMIC STROKE AND ACS
Troponin elevation in acute ischemic stroke is common,
Is associated with multiple disease processes
Like acute coronary syndrome, congestive heart failure, renal failure,
myopericarditis, chronic obstructive pulmonary disease,
pulmonary embolism, sepsis atrial fibrillation
For patients presenting with concurrent AIS [acute ischemic stroke] and acute MI [myocardial infarction],
treatment with IV alteplase at the dose appropriate for cerebral ischemia, followed by percutaneous
coronary angioplasty and stenting if indicated is reasonable.
33. SCD AND ISCHEMIC STROKE
Highest incidence in homozygous HbS group
Causes are cerebral aneurysm and abnormal arteries with hypercoagulable state
Due to raise platelets and increased arterial vascular pressure from abnormal RBCs which stack in the
intima
Initial approach is similar to other non sickler stroke patients
Iv thrombolytic can be safely administered
Exchange blood transfusion with PRBCS is a recommended
Goal is to achieve HbS<30% OR Hb of 10g/dl
However if not available simple PRBCS can safely be given
34. ISCHEMIC STROKE IN PREGNANCY
Pregnancy-associated ischemic stroke is rare
But can be devastating
Recanalization therapy should not be systematically withheld
Women who are at risk for stroke should be followed carefully,
Providers caring for pregnant women should be educated regarding stroke signs and symptoms.
Causes of ischemic stroke include atherosclerotic disease, pregnancy induced HTN,
embolisms, thrombi and hypotension
Evaluation is similar to other stroke patients with no pregnancy
Both intravenous tissue plasminogen activator (tPA) and endovascular thrombectomy have been used
successfully to treat pregnant women with acute ischemic stroke who meet criteria for tPA
36. REFFERENCES CONT……………………..
6. Terón I, Eng MS, Katz JM. Causes and Treatment of Acute Ischemic Stroke
During Pregnancy. Curr Treat Options Neurol. 2018 May 21;20(6):21. doi:
10.1007/s11940-018-0506-5. PMID: 29785465
7. Hertz J.T.a , Madut D.B.b, William G.c, Maro V.P.d, Crump J.A.e, Rubach M.P.
Perceptions of Stroke and Associated Health-Care-Seeking Behavior in Northern
Tanzania: A Community-Based Study; Neuroepidemiology 2019;53:41–
47https://doi.org/10.1159/000499069
-The boundary zones between the areas supplied by individual arteries (watershed zones) are the areas at most risk from ischemia during periods of systemic hypotension
-Ischaemic damage in these areas leads to watershed infarcts.
Amaurosis fugax; emboli from proximal carotid artery plaque embolizes to the ophthalmic artery and cause transient monocular blindness
Wernicke; Patient is not able to understand verbal communication and can not process sensory input
Brocas; understands verbally but cant communicate
Agnosia; cant recognize previous known subjects
CPSS; sensitivity = 66%, specificity = 87% for acute stroke.)
-Los Angeles Prehospital Stroke Screen (If answers to all items 1–6 are “Yes” or “Unknown,” sensitivity = 91% [95% confidence interval (CI) 76%–98%],
specificity = 97% [95% CI 93%–99%] for acute stroke.)
-Melbourne Ambulance Stroke Screen (If answers to all items 1–4 are “Yes” PLUS at least one of 5–8 is present, sensitivity = 90% [95% CI 81%–96%], specificity = 74% [95% CI 53%–88%] for acute stroke.)
-however, a cluster-randomized, crossover trial found no difference in stroke patient outcomes between lying flat for 24 hours and head of bed elevation to at least 30 degrees.
-However, significant methodologic concerns about this study have been raised, and optimal head positioning for stroke remains controversial.
-That said, it is probably reasonable to consider raising the head of the bed to 15 to 30 degrees in patients at risk for hypoxia, airway compromise, aspiration, or suspected increased intracranial pressure.
LABETALOL DOSE; 10MG IV Over 1 to 2 minutes, may be repeated after every 10 to 20minutes maximum 300mgor infusion 2-8mg/min
NICARDIPINE DOSE; 5MG/HR BY SLOW INFUSION 50MLS PER OUR initialy may be increased by 2.5mg/hr every 15minutes not to exceed 15mg/hr
Uncontrolled BP can be treated by nitroprusside 0.5-10mcg/kg/minute
Alteplase dosage 0.9mg/kg iv max 90mg total, 10% as bolus the rest in 60minutes
Monitor; neurological status every 15min for 2hrs, SBP<180, DBP <105
No anticoagulation or antiplatelet for 24hrs
MR CLEAN
`
. "Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute Ischemic Stroke in the Netherlands
mRS used to assess the pts prestroke baseline level of function
-Studies have failed to validate the ABCD2 score,
-and may cause physicians to incorrectly classify ~8% of patients as low risk,
-with sensitivity of the score for high risk patients only ~30%
-This clinical policy recommends that current risk stratification instruments such as ABCD2 should not be used to identify TIA patients who can be safely discharged home.
The score offers better performance than ABCD2 in predicting stroke risk after TIA, particularly low risk.