acute ischemic stroke, classification, risk factors,investigations,management according to latest aha/asa guidelines 2018

1. MANAGEMENT OF
ACUTE ISCHEMIC
STROKE INCLUDING TIA
BY: DR.DEEPANSHU KHANNA

2. DEFINITION
Stroke(CVA) is defined by the World Health Organization as a clinical
syndrome consisting of ‘rapidly developing clinical signs of focal (at
times global) disturbance of cerebral function, lasting more than 24 h
or leading to death with no apparent cause other than that of vascular
origin’.

3. TRANSIENT ISCHEMIC ATTACK(TIA)
• Transient ischemic attack is temporary focal neurological deficit of
sudden onset caused by ischemia of the brain, retina lasting less
than 24 hours followed by complete recovery.
• New definition: No objective evidence of acute infarction in the
affected region of brain or retina; < I hour
• Therefore, CT/MRI necessary to increase diagnostic
accuracy.

5. RISK FACTORS FOR ISCHEMIC STROKE
Non-modifiable
• Age>55
• Gender-Male
• Race
-African American
-Asian
-Hispanic
• Family history of stroke
• Low birth weight
• Genetics
Modifiable
• Hypertension-Most important risk factor
for ischemia stroke
• Atrial fibrillation-Most important and
treatable cardiac cause of stroke
• Other cardiac diseases-eg aortic arch
atheromatosis.
• Diabetes
• Dyslipidemia
• Sickle cell disease
• Asymptomatic carotid stenosis
• Postmenopausal hormone therapy, Oral
contraceptives
• Increased fibrinogen, elevated
homocysteine, elevated anticardiolipin
antibodies, low serum folate.
Lifestyle factors─ associated Cigarette
smoking, Alcohol, Obesity, Physical
inactivity, Diet

6. ISCHEMIC STROKE PATHOPHYSIOLOGY
The First Few Hours
“TIME ISBRAIN:
SAVETHE PENUMBRA”
Penumbra is zone of
reversible ischemia
around core of
irreversible infarction—
salvageable in first few
hours after ischemic
stroke onset
Penumbra damaged by:
• Hypoperfusion
• Hyperglycemia
• Fever
• Seizure

7. EMERGENCY EVALUATION AND
MANAGEMENT OF ACUTE ISCHEMIC STROKE
Assessment Goal:
• In first 10 minutes Assess ABCs, vital signs
• Provide oxygen by nasal cannula
• Obtain IV access; obtain blood samples (CBC, electrolytes, coagulation
studies)
• Obtain 12-lead ECG, check rhythm, place on monitor, Check blood sugar;
treat if indicated.
• Alert Stroke Team: neurologist, radiologist, CT technician
• Perform general neurologic screening assessment

8. EVALUATION OF STROKE
1. Determine if symptoms are due to stroke
2. Localize site of brain lesion
3. Establish the type of stroke
4. Ascertain the likely cause
• The clinical assessment (history, general examination, and neurological
examination) remains the cornerstone of the evaluation.
• The use of a stroke rating scale, preferably the NIHSS, is recommended (Class I;
Level of Evidence B).
• It has been recommended that patients with acute stroke <7 days or
progressive stroke should be admitted.

9. INVESTIGATIONS
• full blood count, serum electrolytes, renal
function
• tests, cardiac enzymes, and coagulation
studies
• Blood sugar is mandatory to exclude
hypoglycemia or diagnose diabetes
mellitus
• Full blood count to detect Polycythaemia,
ESR for endocarditis, clotting studies for
Hypercoagulable States.
• An electrocardiogram (ECG) : arrhythmias
and myocardial infarction. Baseline ECG is
recommended in all patients with
stroke(AHA/ASA Guidelines)
• Echocardiography : valve disease and
intra-cardiac clot

10. NIH STROKE SCALE

11. NIHSS INTERPRETATION
• NIHSS below 12-14 will
have an 80% good or
excellent outcome
• NIHSS above 20-26 will
have less than a 20%
good or excellent
outcome
• Lacunar infarct patients
had the best outcomes

13. NEUROIMAGING
• Brain CT scan: CT is sensitive to the intracranial blood and is
readily available.
• CT Scan changes in ischemic stroke may take several days
to develop.
• Urgent brain imaging is required in suspected stroke
• All should be imaged ≤ 20min of ED arrival
– The benefit of IV alteplase and thrombectomy are time dependent
– Reducing time from arrival to imaging can improve door to needle
time
• Non-contrast CT is adequate in most cases
– Primary goal is to exclude ICH
– Routine MRI is not cost-effective
• MRI will only change management in minority of cases Inadequate data to
establish who requires MRI

14. Acute (4 hours)
Infarction
Subtle blurring of gray-white junction & sulcal
effacement
Subacute (4 days) Infarction
Obvious dark changes & “mass effect”
(e.g., ventricle compression)
RR L L

17. MRI BRAIN IN HYPERACUTE ISCHEMIC STROKE
DWI ADC FLAIR
DWI & ADC: Early infarction visible
FLAIR: No signal changes; possible sulcal
effacement in area of infarction
R L R L

18. MULTIMODAL IMAGING
MULTIMODAL CT
• Typically includes non-contrast
CT, perfusion CT, and CTA
• Two types of perfusion CT
– Whole brain perfusion CT
– Dynamic perfusion CT
MULTIMODAL MRI
• Standard MRI sequences ( T1
weighted, T2 weighted, and
proton density) are relatively
insensitive to changes in
cerebral ischemia
• Multimodal adds diffuse-
weighted imaging (DWI) and PWI
(perfusion- weighted imaging)

21. Advanced imaging can select patients for thrombectomy
16-24 hours from last normal.
• Two recent RCTs
– CT Perfusion, or MRI/MR perfusion to select patients with salvageable brain tissue,
despite prolonged time from last normal
– Randomized to thrombectomy vs no-thrombectomy
– Both trials showed large benefit for thrombectomy
DAWN Trial: Good outcome (mRS 0-2) in 49% vs. 13% DEFUSE 3 Trial: Good
outcome (mRS 0-2) in 45% vs. 17%
Brain Imaging
Emergency Evaluation
.

22. MEDICAL MANAGEMENT
1.supportive management- airway, temperature, blood
pressure, blood glucose, cardiac assessement
2. thrombolysis – intravenous / intra arterial
3.antiplatelet drugs
4. anticoagulant drugs
5. hemodilution, vasodilators and induced
hypertension
6. Neuroprotective agents

23. SURGICAL MANAGEMENT
A) endovascular interventions
1) angioplasty and stenting
2) mechanical clot disruption
3) clot extraction
B)carotid endartectomy

24. AIRWAY AND VENTILATION
Patients with decreased consiousness AND or
patients with brainstem stroke are at the greatest
risk for airway compromise instroke
Seriously ill patients or those at riskfor
aspiration
Elective intubation may help in the
management of who have severely
increases ICT

25. SUPPLEMENTALOXYGEN – adequate tissue
oxygenation is important to prevent furtherbrain
injury(SPO2<94%)
Most common causes of hypoxia are partialairway
obstruction, hypoventilation. ,aspiration pneumonia,atelectasis..
Some patients develop cheynes stokes respiration which is readily
reversed by oxygen
Hyperbaric oxygen – studies done have been inconclusive or have
shown that it does not improve outcome

26. BLOOD PRESSURE MANAGEMENT
Reducing
formation of brain
edema
lessening
hemorrhagic
transformation
preventing early
recurrent stroke

27. HOWEVER ,,, aggressive treatment of blood
pressure may reduce the perfusion pressure to
the ischemic areas of the brain
In majority of patients decline in blood
pressure occurs within the first few hours
of stroke even without any treatment

28. WHENTOLOWERBLOODPRESSURE
the hypertension is extreme (systolic blood pressure >220 mmHg or diastolic
blood pressure >120 mmHg)
ischemic coronary disease, heart failure,
Aortic dissection
Hypertensive encephalopathy
Acute renal failure orpre-eclampsia/
Eclampsia

29. When treatment is indicated, cautious lowering of
blood pressure by approximately 15percent during
the first 24 hours after stroke onset is suggested
Systolic blood pressure > 185 and diastolic > 110 is
a contraindication for thrombolysis

30. • Ideal blood pressure in AIS remains unknown
– Observational studies variable
• No clear data on fluid choice, volume, or duration
• BP with IV alteplase:
– BP <185/110 prior to administration
– BP <180/105 for 24 hours after administration
• BP with Intra-arterial Therapy
– Optimal BP unknown
– RCTs largely excluded BP >185/110
– Reasonable to use <185/110 as guideline
General Supportive Care and Emergency Treatment
BLOOD PRESSURE

31. BP treatment options in AIS patients eligible for reperfusion:
• Labetalol: 10-20mg IV over 1-2 min, may repeat x1
– If continues to be elevated, 10mg IV x1 followed by infusion 2-8mg/min
• Nicardipine: 5mg/h IV, titrate 2.5mg/h every 5-15 min (max 15
mg/h)
• Clevidipine: 1-2mg/h IV, double dose every 2-5 minutes to
titrate (max 21 mg/h)
• Other agents may be considered (hydralazine, enalaprilat)
Monitoring BP after reperfusion:
• Every 15 min x 2 hours
• Every 30 min x 6 hours
• Every 60 min x 16 hours
y
General Supportive Care and Emergency Treatment
BLOOD PRESSURE

32. BLOOD GLUCOSE LEVELS
Hyperglycemia may augment brain injury by several
mechanisms including
increased tissue acidosis from anaerobic metabolism
free radical generation
increased blood brain barrier permeability.
The American Heart Association/American Stroke Association
guidelines(2018) recommend to achieve blood glucose in the
range of >140 to 185mg/dL (>7.8to 10.3 mmol/L)

33. HYPOGLYCEMIA- Hypoglycemia can cause
focal neurologic deficits mimicking stroke, and
severe hypoglycemia alone can cause neuronal
injury
Check the blood sugar and rapidly correct low
serum glucose(<60mg/dl) in AIS.
Normoglycemia is the desired goal while
avoiding marked elevation of serum glucose.

34. • Peak temperature in first 24 hours <37°C and
>39°C associated with increased risk of in hospital
death compared to normothermia
– Retrospective cohort study of 9366 pts w/ AIS
• Hypothermia is a promising strategy but benefit
not proven and studies suggest increased risk of
infection
y
General Supportive Care and Emergency Treatment
TEMPRATURE

35. INTRAVENOUS THROMBOLYSIS
-Results from the NINDS trial showed that intravenous alteplase (recombinant
tissue-type plasminogen activator or tPA) improves functional outcome at three
months, if given within 3 hours of symptom onset.
-The ECASS 3 clinical trial found that intravenous alteplase is beneficial when
given up to 4.5 hours after stroke onset

36. Despite recommendations, less than 1% of
potentially eligible patients are currently being
treated in India
Principle behind the time dependency of
thrombolysis is that of penumbra – the salvageable
tissue which decreases every minute afterstroke

37. Alteplase Dosing: 0.9mg/kg, maximum 90mg, over 60
minutes with initial 10% given as a bolus over 1 minute.
y
General Supportive Care and Emergency Treatment
Intravenous Alteplase: Indications
Indications (Class I): Within 3 hours
Age ≥18 years of age; equally recommended for <80 and >80 years of age
under 3 hours.
Severity Recommended for severe strokes and for mild but disabling strokes.
Indications (Class I): 3-4.5 hours
Age, Severity
and Other
Considerations
<80 and without history of both diabetes and prior stroke, NIHSS <25,
not on Oral anticoagulants, and without imaging evidence of ischemia
of >1/3 of the MCAterritory.

38. INTRAVENOUS ALTEPLASE: INDICATIONS
: Indications
Indications (Class I): Overall
Urgency Treatment should be initiated as quickly as possible. Time to treatment
strongly associated with outcomes.
BP Recommended in those whose BP can be safely lowered to <185/110 prior to
starting IV alteplase.
Glucose Recommended in otherwise eligible patients with glucose >50 mg/dL.
CT Recommended in setting of mild to moderate early ischemic changes on NCCT.
Prior
Antiplatelets
Recommended in those taking single antiplatelet drug; benefit outweighs
possible small increased risk of sICH.
End-stage
renal disease
Recommended in those with normal aPTT; those with elevated aPTT
might be at higher risk of hemorrhage.

39. INTRAVENOUS ALTEPLASE: CONTRAINDICATIONS
y
3.5 Intravenous Alteplase: Contraindications
Contraindications (Class III Overall)
Time of onset Not recommended if unclear time of onset or >3 or 4.5hours
Not recommended in wake-up strokes last normal >3 or 4.5hours.
CT Not recommended if CT shows acute intracranial hemorrhage
Insufficient evidence to identify clear threshold for hypoattenuation severity
or extent that affects treatment response, but treating with IV alteplase not
recommended with extensive hypoattenuation.
AIS within 3 months May be harmful in patients with AIS within 3months
Potential for increased risk of hemorrhage and associated morbidityand
mortality exists but not well established.
Severe head trauma Contraindicated within 3 months given risk of bleeding.
Intracranial/
Intraspinal surgery
Potentially harmful within 3 months of procedure.
History of Intracranial
Hemorrhage
Potentially harmful in patients with a history of ICH.
Subarachnoid Hemorrhage Contraindicated in patients presenting with signs/symptoms most
consistent with SAH.
GI malignancy or GI bleed GI malignancy or GI bleed within 21 days is high risk.
Coagulopathy IV alteplase should not be administered if platelets <100,000/mm3,INR
>1.7, aPTT >40, or PT >15 as safety and efficacy unknown.

40. INTRAVENOUS ALTEPLASE: CONTRAINDICATIONS
y
3.5 Intravenous Alteplase: Contraindications
Contraindications (Class III): Continued
Low-molecular-weight
Heparin
Should not be administered if treatment dose LMWH given within 24
hours.
Thrombin or Xa inhibitors Use not fully established, but may be harmful. IV alteplase should not
be administered in those taking these agents unless no dose given in
prior 48 hours or laboratory tests (aPTT, INR, platelets, ecarin clotting
time, thrombin time, or appropriate direct factor Xa activity assays)
are normal.
Glycoprotein IIb/IIIa
inhibitors
Should not be administered concurrently with IV alteplase outside of
clinical trials.
Infective Endocarditis IV alteplase should not be administered due to increased risk of
hemorrhage.
Aortic arch dissection Potentially harmful and should not be administered.
Intra-axial intracranial
neoplasm
IV alteplase potentially harmful.

41. 3.5 Intravenous Alteplase: Additional Recommendations
Additional Recommendations (Class II): Cardiac Disease
Cortical Microbleeds Treatment is reasonable in otherwise eligible patients withsmall
number (1-10) of CMBs.
Treatment may be associated with increased risk of sICH in patients
with high burden of CMBs (>10), may be reasonable if there is
potential for substantial benefit.
Extra-axial intracranial neoplasms Probably recommended.
Acute MI For concurrentAIS and MI, treat at cerebral ischemia dose, then
coronary angioplasty and stenting ifindicated.
Recent MI (within 3 months) Reasonable if non-STEMI.
Also reasonable if STEMI involving right or inferior myocardium.
May be reasonable if STEMI involving left anterior myocardium.

42. • Stop alteplase infusion
• CBC, PT (INR), aPTT, fibrinogen level, and type and cross-match
• STAT non-enhanced head CT
• Cryoprecipitate (includes factor VIII)
– 10 units over 10-30 minutes
– If fibrinogen <200 mg/dL, administer additional dose
• Tranexamic acid (TXA) 1,000 mg IV infused over 10 minutes or ɛ-
aminocaproic acid (EACA) 4-5 g over 1 hour, followed by 1 g IV until
bleeding controlled
• Hematology and Neurosurgery consults
• Supportive therapy: BP management, ICP, CPP, MAP, temperature, and
glucose control
General Supportive Care and Emergency Treatment
Management of sICH after IV Alteplase

43. Multiple randomized trials have shown thrombectomy benefit, up
to 24 hours after symptom onset.
• MR CLEAN, ESCAPE, REVASCAT, SWIFT PRIME, EXTEND-IA,
THRACE, DAWN, DEFUSE 3 Trials
• Benefit was consistent across age groups
• Patient selection criteria varies based on time
16-24 hours since last normal, advanced imaging with CT perfusion
or MRI/MR Perfusion is necessary to select patients
• Reperfusion to TICI 2b/3 should be achieved as early as possible
– Better outcomes with faster times to reperfusion
• Stent retrievers are preferred devices
• Eligible patients should receive IV alteplase even if
thrombectomy is being considered.
General Supportive Care and Emergency Treatment
Mechanical Thrombectomy

44. Mechanical thrombectomy
Patients should receive mechanical thrombectomy with a stent retriever if
they meet all the following criteria:
(1) prestroke mRS score of 0 to 1
(2) causative occlusion of the internal carotid artery or MCA segment 1
(M1).
(3) age ≥18 years
(4) NIHSS score of ≥6
(5) ASPECTS of ≥6
(6) treatment can be initiated if groin puncture within 6 hours of symptom
onset.
3.7 Mechanical Thrombectomy: within 6 hours

45. Mechanical thrombectomy over 6 hours
– DAWN AND DEFUSE 3 TRIALS
– CT Perfusion, or MRI/MR perfusion to select patients with salvageable brain tissue,
despite prolonged time from last normal
– Randomized to thrombectomy vs no-thrombectomy
– Both trials showed large benefit for thrombectomy
DAWN Trial: Good outcome (mRS 0-2) in 49% vs. 13%
DEFUSE 3 Trial: Good outcome (mRS 0-2) in 45% vs. 17%
In selected patients with AIS onset within 6-16 hours, anterior circulation large vessel occlusion, and who meet other DAWN or
DEFUSE 3 eligibility criteria, mechanical thrombectomy is recommended.
In selected patients with AIS within 16 to 24 hours of last known normal who have LVO in the anterior circulation and meet other
DAWN eligibility criteria, mechanical thrombectomy is reasonable.

46. MERCIDevice
Source: St. Petersburg Times, October 2003

47. ANTIPLATELET TREATMENT:ASPIRIN
• AIS- within 24 to 48 hours after onset.
• Treated with IV alteplase- delayed until 24 hours later.
• The efficacy of IV tirofiban and eptifibatide is not well established.
• Glycoprotein IIb/IIIa receptor antagonists, including abciximab is
potentially harmful and should not be performed.
• In patients with minor stroke, treatment for 21 days with dual antiplatelet
therapy (aspirin and clopidogrel) begun within 24 hours can be beneficial
for early secondary stroke prevention for a period of up to 90 days from
symptom onset.
• Ticagrelor is not recommended (over aspirin) in the acute treatment of
patients with minor stroke

48. ANTICOAGULANTS
• Urgent anticoagulation with the goal of preventing early recurrent
stroke, halting neurological worsening, or improving outcomes after
AIS is not recommended for treatment of patients with AIS.
• The usefulness of urgent anticoagulation in patients with severe
stenosis of an internal carotid artery ipsilateral to an ischemic stroke,
nonocclusive, extracranial intraluminal thrombus is not well
established.
• At present, the usefulness of argatroban, dabigatran, factor Xa
inhibitors or other thrombin inhibitors for the treatment of patients
with AIS is not well established. Further clinical trials are needed.

49. VOLUME EXPANSION/HEMODILUTION
• Hemodilution by volume expansion is not recommended for
treatment of patients with AIS.
• The administration of high-dose albumin is not recommended for the
treatment of patients with AIS.
• The administration of vasodilatory agents, such as pentoxifylline, is
not recommended for AIS.

50. NEUROPROTECTIVE AGENTS
At present, no pharmacological or non-pharmacological
treatments with putative neuroprotective actions have
demonstrated efficacy in improving outcomes after ischemic
stroke, and therefore, other neuroprotective agents are not
recommended.

51. EMERGENCY CAROTID INTERVENTION
• The usefulness of emergency or urgent CEA when clinical indicators
or brain imaging suggests a small infarct core with large territory at
risk (eg, penumbra), compromised by inadequate flow from a critical
carotid stenosis or occlusion, or in the case of acute neurological
deficit after CEA, in which acute thrombosis of the surgical site is
suspected, is not well established.
• In patients with unstable neurological status (eg, stroke-in-
evolution), the efficacy of emergency or urgent CEA is not well
established.

52. GENERAL ACUTE TREATMENT FOR
HOSPITALISED PATIENTS
• The use of comprehensive specialized stroke care (stroke units) that incorporates
rehabilitation is recommended.
• The use of standardized stroke care order sets is recommended to improve general
management.
• Dysphagia screening before the patient begins eating, drinking, or receiving
oral medications is reasonable to identify patients at increased risk for aspiration.
• Enteral diet should be started within 7 days of admission after an acute stroke.
• For patients with dysphagia, it is reasonable to initially use nasogastric tubes for feeding
in the early phase of stroke (starting within the first 7 days) and to place percutaneous
gastrostomy tubes in patients with longer anticipated persistent inability to swallow
safely (>2-3 weeks).
• Nutritional supplements are reasonable to consider for patients who are malnourished
or at risk of malnourishment.
• Implementing oral hygiene protocols to reduce the risk of pneumonia after stroke may
be reasonable, antibacterial rinse with chlorhexidine may reduce pneumonia.

53. DVT PROPHYLAXIS
• In immobile stroke patients without contraindications, intermittent
pneumatic compression in addition to routine care (aspirin and
hydration) is recommended over routine care to reduce the risk of
DVT.
• Prophylactic-dose subcutaneous heparin [unfractionated heparin
(UFH) or LMWH] in immobile patients with AIS is not well
established.
• In ischemic stroke, elastic compression stockings should not be used.

54. DEPRESSION SCREENING
– Post-stroke depression (PSD) is common (~25-30%)
– Structured screening is recommended
– Pts with PSD should be treated with antidepressants and the response monitored.

55. OTHER
• Routine use of prophylactic antibiotics-not beneficial.
• Routine placement of indwelling bladder catheters- should not be
performed(associated risk of catheter-associated urinary tract
infections).
• During hospitalization and inpatient rehabilitation, regular skin
assessments are recommended with objective scales of risk such as
the Braden scale.

56. REHABILITATION
• Rehabilitation
– Assessment
• Pts with stroke need formal multidomain assessments before discharge
• Pts with residual deficits should have an assessment by a clinician with expertise in rehab
– Timing and intensity
• High-dose and very early (within 24 hrs) should not be performed
• --AVERT trial (46% vs 50%) compared with usual care Reduced likelihood
of favorable outcome
• Intensity commensurate with benefit and tolerance
• Effectiveness of fluoxetine/other SSRIs is unclear

57. TREATMENT OF ACUTE COMPLICATIONS
1. CEREBELLAR AND CEREBRAL EDEMA
-CEREBELLAR EDEMA: Edema after large cerebellar infarction
can cause neurologic deterioration via:
– Acute obstructive hydrocephalus
– Direct brainstem compression
• When hydrocephalus is present, emergent ventriculostomy is a reasonable first
step
• When brainstem compression occurs despite medical therapy, decompressive
suboccipital craniectomy should be performed
– Outcome after suboccipital craniectomy can be good

58. Cerebral Edema After Large MCA Infarct
• High risk for neurologic deterioration
• Care options should be discussed early
• In those with neurologic deterioration within 48 hours, decompressive
hemicraniectomy

59. 2. SEIZURES
• Recurrent seizures after stroke should be treated in a manner similar
to when they occur with other acute neurological conditions, and
anti-seizure drugs should be selected based upon specific patient
characteristics.
• Prophylactic use of anti-seizure drugs is not recommended.

60. Secondary prevention of stroke
• Management of hypertension (goal <140/85 mm Hg)
• Diabetes control (goal<126 mg/dL)
• Lipid management: Statins (goal cholesterol<200 mg/dL,
LDL<100 mg/dL)
• Anticoagulants: Warfarin (target INR 2 to 3); esp.
recommended in patients with cardioembolic stroke
• Appropriate life style modification (cessation of smoking,
exercise, diet etc)
• Antiplatelet agents:Antiplatelet agents such as
aspirin(300mg) reduce the risk of recurence of all ischaemic
stroke & for patients with TIAs.
• Aspirin is not useful for preventing a first stroke in persons
at low risk (Class III; Level of Evidence A).

61. SECONDARY PREVENTION:
1.VASCULAR IMAGING
• Vascular Imaging
– Extracranial
• For patients with non-disabling (mRS 0-2) AIS in the carotid territory who are candidates
for carotid endarterectomy or stenting, non- invasive imaging of the cervical vessels
should be performed routinely within 24 hours of admission
• Revascularization via CEA or CAS feasible in a 2-7 day time window
– Intracranial
• Routine imaging is not recommended
• In some pts reasonable to perform intracranial imaging to help plan secondary
prevention strategies

62. 2.CARDIAC EVALUATION
– Cardiac monitoring
• Atrial fibrillation is a common cause of AIS and anticoagulation is
associated with reduced stroke incidence compared with ASA
• Monitoring should be performed at least 24 hrs
• Prolonged monitoring identifies more atrial fibrillation but thus far the
clinical benefit is uncertain
– Echocardiography
• Routine use is not recommended as evidence of cost-effectiveness is
insufficient
• In some pts ECHO data may help plan secondary preventive strategies
• -Intracardiac thrombus
• -PFO(patent foramen ovale) in selected pts

63. 3.Glucose
– Screening for DM is reasonable in AIS pts
• Fasting glucose
• HbA1c (may be more accurate in the acute setting)
• Oral glucose tolerance test

64. 4.CHOLESTROL
• Cholesterol
– The 2013 ACC/AHA Cholesterol Guidelines recommend statins for pts with
atherosclerotic cardiovascular disease (ASCVD), including stroke of atherosclerotic
origin
– No data for treatment or titration to a specific LDLlevel
– Measurement in stroke pts
• No benefit to measuring cholesterol routinely in atherosclerotic stroke pts not already taking a
high-intensity statin
• Maybe some benefit in measuring cholesterol levels in pts already on optimized statin as
they might benefit from PCSK9 inhibitor treatment
• Maybe some benefit in measuring cholesterol levels in pts with non-atherosclerotic origin
stroke as primary prevention guidelines are based on LDL-C levels

65. Other Tests for Secondary Prevention
– Recommended
• Troponin
– Not recommended
• Routine screening for hyperhomocysteinemia
• Routine antiphospholipid antibody testing unless APS findings or no alternative
explanation
• Routine OSA screening
• -OSA is highly prevalent but RCTs have not found treating these pts with CPAP prevents
cardiovascular events or death in pts with stroke
• Routine thrombophilia screening

66. Antithrombotic Treatment
– Antiplatelet therapy
• Recommended for non-cardioembolic AIS
• Increasing ASA or switching agents is not well established
• -SPS-3: no benefit to adding clopidogrel to ASA
• -WARSS: no difference in stroke recurrence after switching to warfarin
• -WASID: no difference after switching to warfarin
– Anticoagulation for AIS due to atrial fibrillation
• Reasonable to initiate 4-14 days after AIS for most pts
– Dissection: antiplatelet or anticoagulation is reasonable (CADISS).
If recurrence, the value of stenting is not well established

67. STATINS
• Statins
– Pts already on a statin: reasonable to continue
– Pts ≤75yo with ASCVD: reasonable to continue or start
– Pts ≥75yo with ASCVD: evaluate risk-reduction
– Clinical ASCVD
• Acute Coronary Syndrome
• History of MI
• Stable or unstable angina
• Coronary or other arterial revascularization Stroke/TIA
• Peripheral artery disease
– ‘High intensity’ statin: atorvastatin 80mg or rosuvastatin 20mg

68. Carotid Revascularization
– Indication
• Minor, nondisabling stroke (mRS 0-2) in distribution of the
artery
– Timing
• 2-7 days after index event is reasonable
• Stroke risk is highest in the first few days after the event
• No high quality data supporting emergent
revascularization

69. SMOKING CESSATION INTERVENTION
• Therapeutic options include:
– Counseling
– Nicotine products
– Varenicline
• In-hospital initiation of any of the above is reasonable

70. STROKE EDUCATION
Discussion before discharge regarding:
-What is a stroke
-Stroke risk factors
-Medications
-When to call emergency
-Any other stroke-related questions

71. TIA: MANAGEMENT
-ABCD2
SCORE: The ABCD2
score is a risk assessment tool designed to
improve the prediction of short-term stroke risk after a transient ischemic
attack (TIA). The score is optimized to predict the risk of stroke within 2 days
after a TIA, but also predicts stroke risk within 90 days. The ABCD2
score is
calculated by summing up points for five independent factors.

72. ABCD2 SCORE
• Higher ABCD2
scores are associated with greater risk of stroke
during the 2, 7, 30, and 90 days after a TIA (Figure). The
authors of the ABCD2
score made the following
recommendations for hospital observation:1
ABCD2
Score
2-day Stroke Risk
Comment
0-3 1.0%
Hospital observation may be unnecessary
without another indication (e.g., new atrial
fibrillation)
4-5 4.1% Hospital observation justified in most
Situations.
6-7 8.1% Hospital observation worthwhile

73. MANAGEMENT OF TIA
Initial Evaluation: Prompt initial evaluation (within 12h);
evaluation completed within 48 hours
Hospitalization: Should be considered to facilitate early therapy
and secondary prevention
Lab testing: Full blood count, serum electrolytes and creatinine;
fasting blood glucose and lipids
Electrocardiography: Recommended within 48 hours
Brain imaging study: CT or MRI within 48 hours
Vascular imaging: Carotid imaging, CT or MR angiography, or
transcranial Doppler within 48 hours

74. MEDICAL MANAGEMENT
 Antithrombotic Therapy
o Atherothrombotic TIA: Daily long-term antiplatelet therapy: combination extended-release
dipyridamole plus aspirin (reasonable as first choice), clopidogrel, or aspirin alone.
• Anticoagulation is not recommended
o Cardioembolic TIA: Long-term anticoagulation for atrial fibrillation (continuous or paroxysmal).
If patient intolerant to anticoagulation, aspirin 325 mg daily; clopidogrel 75 mg daily if intolerant to aspirin.
 Hypertension: Lower blood pressure to <140/90 mm Hg or <130/80 mm Hg for diabetics, with an
ACE inhibitor alone or in combination with a diuretic, or with an angiotensin-receptor blocker
 Lipids: Initiate a daily statin. Goal LDL-cholesterol level <2.59 mmol/l (<100mg/dl)
 Smoking: Initiate a cessation program
 Diabetes: Fasting blood glucose goal <126mg/dl
 Physical activity: Recommend ≥10 min of exercise such as walking, bicycling, running, or swimming ≥3 times/week

75. SURGICAL MANAGEMENT
Carotid endarterectomy: Preferably within 2 weeks of cerebral or
retinal TIA in those with TIA attributed to a high-grade internal carotid
artery stenosis:
o 70-99% internal carotid artery stenosis: Recommended
o 50-69% stenosis: Recommended for certain patients and only at
centers with perioperative complication rate <6%
o <50% stenosis: Not recommended
Bypass surgery: Not recommended

76. REFERENCES
• AHA/ASA GUIDELINES: 2018 Guidelines for the Early Management of
Patients with Acute Ischemic Stroke.
• HARISSON’S TEXTBOOK OF INTERNAL MEDICINE-19th edition
• BRADLEY’S NEUROLOGY IN CLINICAL PRACTICE-7th edition
• GOLDMAN CECIL MEDICINE- 24th edition.