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Stroke > Cerebrovascular Disease Basics > Flashcards

Cerebrovascular Disease Basics Flashcards

1
Q

What is stroke?

A

Focal disturbance of blood flow into or out of brain
- Ischaemic (87%)
- Haemorrhagic (13%)

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2
Q

What is transient ischaemic attack (TIA)
- Definition
- Timing and resolution (standard vs contemporary)
- Pathophysiology

A

Abrupt onset neurological deficit due to interruption of blood flow to portion of the brain, with subsequent resolution of symptoms within 24 hours
- Contemporary definition defines as lasting under 1 hour
- Mostly resolves within 5 to 15 minutes

Normal imaging following TIA DOES NOT rule out TIA

If infarct identified on brain imaging -> classified as stroke regardless of druation of symptoms

Pathophysiology
Cause: same as stroke, commonly emboli, in-situ thrombosis
Occluded blood vessel reopens and function restored

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3
Q

Why is prompt recognition of TIA important?
(Epidemiology of TIA)

A

TIA - possibility of completed stroke
- Appropriate intervention prevent stroke and permanent disability (loading and treatment with DAPT)
- 90-day stroke rates >10-15% (highest within 48 hours to 7 days)
- Longer symptoms duration and large cerebral artery stenosis associated with higher risk of stroke

In the United States:
- > 795,000 cases of stroke per year
- > 250,000 cases of TIA per year

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4
Q

Risk factors for stroke

A

Non-modifiable
- Age (2nd biggest predictor)
- Sex, race

Modifiable
- Prior stroke (biggest predictor)
- Diabetes
- Hypertension
- Hyperlipidaemia
- Smoking
- Cardiac disease - AF, valvular disease
- Homocysteinaemia

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5
Q

Etiologies of Ischaemic Stroke
(TOAST -> CISS)

A
  1. Large vessel disease - intracranial (ICAD) , extracranial (ECAD)
    - Plaque rupture resulting in large in-situ thrombosis or artery-to-artery thromboembolism
  2. Small vessel disease - arteriolosclerosis, lipohyalinosis
    - Strong association with diabetes, hypertension
  3. Cardioembolic
  4. Embolic stroke of undetermine source (ESUS)
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6
Q

What are the classical clinical feature of large vessel disease?
(uncorrelated to real life)

A

Large vessel disease
- Occurs early in the morning hours or on waking up
- History of prior TIAs in same vascular distribution
- Symptoms fluctuate

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7
Q

What are the classical clinical feature of small vessel disease?
(uncorrelated to real life)

A

Small vessel disease
- History of diabetes, hypertension
- Diameter < 1.5cm (subcortical / lacunar)
- Occurs in subcortical regions - basal ganglia, thalamus, brainstem
- Lacking in cortical findings (aphasia, neglect)
- Symptoms fluctuate dramatically
- May have TIA with similar symptoms

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8
Q

What are the classical clinical feature of cardioembolic disease?
(uncorrelated to real life)

A

Cardioembolic disease (20%)
- History or features of heart disease
- Stoke symptoms maximal at onset (clot preformed already)
- TIA differing symptoms and embolism to different distributions
(fragment and lysed quickly)
- Associated with Valsalva
- Strokes of different ages in different vascular territories
- With reperfusion following prolonged ischaemia, development of petechial haemorrhages in ischaemic territory

Sites of lodge: intracranial ICA, MCA, PCA or their branches, rarely ACA

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9
Q

What cardiac conditions are considered source of cardioembolic stroke?

A
  1. Atrial fibrillation or flutter
  2. Mechanical valves
  3. Septic emboli
  4. Marantic endocarditis (sterile vegetations)
  5. PFO with left-to-right shunt and venous clot
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10
Q

What are rarer/other causes (ESUS) of stroke?

A
  1. Dissection of cervical vessels -> neck/face pain, history of trauma
  2. Carotid injury -> Horner’s syndrome
  3. Illicit drug (cocaine, stimulant-induced spasms)
  4. Hypercoagulable state - cancer, genetic clotting disorder, autoimmune (lupus/ALPS)
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11
Q

What is haemorrhagic transformation?
(Haemorrhagic conversion)

A
  • Occurs in large or severe degree of ischaemia
  • Most likely in first days to a week post-stroke
  • Look out for clinical worsening -> immediate re-evalation with CT brain
  1. Tissues downstream becomes ischaemic - brain and vasculature
  2. Blood flow returns via weakened, damaged vessels
  3. Vessel leak -> petechial haemorrhage, or burst into haematoma
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12
Q

Stroke activation

A
  1. Onset and duration, time-to-needle
  2. Symptoms and signs
  3. Blood glucose - hypo or hyperglycaemia
  4. ECG, troponin
  5. Coagulation profile, FBC, RP
  6. NIHSS - at least 4 to 24
  7. CT brain - ASPECT (>5 for EVT, >7 for rtPA), ruled out intracranial bleeding and tumour
  8. Assess indications and contraindications for thrombolysis
  9. Blood pressure control if SBP > 185 for thrombolysis
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13
Q

What are the contraindications to rTPA?

A

Absolute Contraindications
1. > 4.5 hours from time patient last seen normal
2. Initial CT brain suggests time of onset inaccurate
3. Intracranial haemorrhage - SAH, ICH
4. Intracranial neoplasm or AVM
5. Active internal bleeding
6. Uncontrolled hypertension > 185/110mmHg despite antihypertensive
7. Current bacterial endocarditis
8. Head trauma, recent intracranial/intraspinal surgery within 3 months
9. Recent AMI within 3 months
10. Known coagulopathy - INR > 1.7, Plt < 100, elevated PTT
- DOAC within 24 hours (48 hours in CKD)
- Warfarin if reversible with vitamin K or PCC
- IV heparin within 48 hours with APTT > normal range

Relative Contraindications
1. Minor or rapidly resolving deficits
2. Seizure
3. Major surgery in previous 2 weeks
4. GI or urinary haemorrhage within 3 weeks
5. Puncture at non-compressible sites within 1 week (biospy, LP)

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14
Q

Pathophysiology of Ischaemic Stroke

A
  1. Acute occlusion of intracranial vessel and degree of cerebral occlusion resulting in brain tissue death
    - Complete occlusion: tissue death within 4-10 mins
    - <16-18mL/100g: within 1 hour
    - > 20mL/100g: ischaemia without infarct unless prolonged for several hours to days
  2. Infarction via 2 pathways:
    A. Necrotic pathway - cellular cytoskeletal breakdown
    B. Apoptotic pathway - programmed cell death
  3. Rise in intracellular calcium
    - Energy failure (starvation of glucose, oxygen resulting in failure of ATP production)
    > Membrane ion pump dysfunction (lack of ATP) causes neurons depolarisation, increases intracellular calcium
    - Glutamate release from synaptic terminals, excessive glutamate ->neurotoxic
    > activation of postynaptic glutamate receptors further increases calcium influx
  4. Free radials generation
    - Degradation of membrane lipids and mitochondrial dysfunction
    - Damages vital functions of cells, axons ,dentrites, glia
  5. Additional insults
    - Fever, hyperglycaemia
  6. Formation of ischaemic penumbra
    - Ischaemic but reversible dysfunctional tissue surroinding core area of infarct
    > Progresses to infarct if no restoration of flow
    (Goal of revascularisation therapy to reverse penumbra)
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15
Q

What are the complications of acute ischaemic stroke?

A
  1. Haemorrhagic transformation
  2. Alteplase-related orolingual oedema
  3. Cerebral oedema -> obtundation and herniation
  4. Cerebellar oedema -> hydrocephalus, brainstem compression
  5. Post-stroke depression
  6. Fatigue
  7. Aspiration pneumonia
  8. Bedridden complications - DVT, PE
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16
Q

Cerebral oedema occurs in 5-10% of stroke and may cause ___ and ___
- Dependent on ___ of infarct - __ and __

Oedema peaks on __-__ day, mass effect up to __ days

Herniation upward or downward through __ or __

Clinical features of herniation: (3)

Treatment with ___, __and ___ to raise serum osmolarity
Avoid ___ as it may worsen hypotension and infarct

Definitive treatment: __

A

Cerebral oedema occurs in 5-10% of stroke and may cause obtundation and cerebral herniation
- Dependent on size of infarct - large hemispheric infarct and cerebellar infarct

Oedema peaks on 2nd-3rd day, mass effect up to 10 days

Herniation upward or downward through tentorium or under falx cerebri

Clinical features of herniation: somnolence, pupils dilatation (CN3 compression), increased ICP (nausea, vomiting)

Treatment with fluid restriction, hyperventilation and IV mannitol to raise serum osmolarity
Avoid hypovolaemia as it may worsen hypotension and infarct

Definitive treatment: surgical decompression

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17
Q
  1. Dosing and administration of IV rtPA
  2. Management of hypertension during rtPA
  3. Management of hypotension during rtPA
A

IV rtPA alteplase 0.9mg/kg up to 90mg maximum
- 10% given as bolus over 30-60 seconds
- 90% infusion over 60 minutes

Keep BP below 185/110 prior to rtPA and at least 24 hours after rtPA initiation
- Every Q15 mins for 2 hours after therapy
- Every Q30 mins for next 6 hours
- Every Q1 H until 24 hours post-rtPA

If BP >180/105 or higher
- Increase vitals monitoring to Q5 mins
- Continue IV rtPA
- Choice of antihypertensives:
A. IV Labetalol 10mg over 1-2 minutes, repeatable or doubled every 10-20 minutes, up to total 150mg
(10-20-40-80)
B. IV GTN 2.5 up to 400 mcg/min

If BP >230/140
- Stop rtPA infusion, give IV antihypertensives
- Consider other agents if poor response
- Resume rtPA only if BP within acceptable limits

If SBP < 100
- Give fluid challenge IV NS 100-500mL fast bolus
- If no response, start IV dopamine at 5 mcg/kg/min, titrate upwards until BP > 120, do not start below 5
- Monitor for signs of major haemorrhage
- KIV 4-6 units FFP

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18
Q

What happens if NIHSS worsens by 4 or more points from baseline during rtPA

A
  1. Stop rtPA immediately if still infusing
  2. Send FBC, coagulation panel, fibrinogen, GXM, antibody screen
  3. Urgent CT brain
  4. In the event of ICB, consider 4-6 units FFP/platelet/cryo/EACA
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19
Q

National Institute of Neurological Disorders and Stroke (NINDS) Stroke Study

A

Regime: IV rTPA 0.9mg/kg max 90mg
Timing: within 3 hours of onset

Haemorrhage: 5.8% increased incidence
6.4% rtPA vs 0.6% placebo

Resolution: 12% absolute increase
44% rtPA vs 32% placebo

Mortality: 4% non-significance reduction
17% rtPA vs 21% placebo

–> Benefits and improved clinical outcomes outweighs risks if given within 3 hours of stroke onset

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20
Q

European Cooperative Acute Stroke Study III (ECASS III)

A

Timing: 0 - 4.5 hours
Exclusion: > 80 years old, diabetic patients with previous stroke

Haemorrhage: 2.2% increased incidence
2.4% rtPA vs 0.2% placebo

Resolution: 7.2% absolute increase (lower than NINDS)
52.4% rtPA vs 45.2% placebo

–> rtPA approved for 3-4.5H window in Europe and Canada, however only 0-3H in USA

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21
Q

Japan Trial on IV rtPA

A

Dosing: 0.6mg/kg
Rationality: Asian descent higher propensity to bleed

Observation of > 600 patients
- Similar outcomes to historical controls
- Lower rate of ICB

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22
Q

Tenecteplase trial

A

Dosing: IV tenecteplase 0.25mg/kg bolus over 5 seconds

Not directly tested against IV rtPA

Benefits: Given bolus. No need for 1 hour infusion
- Improved effifiency of transfer to stroke centre
- Trials found tenecteplase prior to EVT to be safe

23
Q

Alteplase induced anaphylaxis or peri-oral/orolingual angioedema

A

Features:
- Swelling of tongue/lips
- Airway tightening - wheeze/stridor/bronchospasm
- Dyspnoea
- Rash/urticaria

Management:
1. Stop rtPA immediately
2. ABC
3. Early activation of airway team
4. IV hydrocortisone 100-200mg STAT
5. IV diphenhydramine 10-50mg STAT
6. SC adrenaline 0.5-1mL (1:1000 dilution)
7. Salbutamol inhalers

24
Q

Endovascular therapy (EVT) in large vesel occlusion

A

Large vessel: basilar artery, intracranial ICA, MCA
- Often large clot volume and fails to open with IV rtPA

Overall meta-analysis: odds ratio 2.49, CI 95%

Timing studies:
- Good outcomes under 6H from stroke with/without pre-treatment with IV rtPA
- OR > 3 within 2 hours; OR 2 if 8 hours elapse
- >80% EVT within 1 hour of arrival to ED had good outcome, 1/3 if 6 hours elapsed

Outcome studies:
- EVT discharge 2 months earlier than medical
- Recovery to mRS 0-2: 46% EVT vs 26.5% medical
- Mortality benefits

25
Q

EVT beyond 6 hours - clinical trials

A

Imaging: CT or MR perfusion studies
- must demonstrate good vascular collaterals
- can be treated up to 24 hours

A. Clinical Mismatch in Triage of Wake Up and Late Presenting Strokes Undergoing Neurointervention with Trevo (DAWN) trial
- 47% EVT vs 13% medical

B. Endovascular Therapy Following Imaging Evaluation for Ischaemia Stroke 3 (DEFUSE-3) Trial
- 45% EVT vs 17% medical up to 16 hours from onset

C. Non-randomised data for bvasilar occlusion
- Safe up to 24 hours
- Lower mRS score in 3 months

26
Q

Aspirin in acute stroke trials

A

Aspirin is the only antiplatelet that has shown effectivness in acute treatment of stroke
(while other agents are for secondary prevention)

A. International Stroke Trial (IST), Chinese Acute Stroke Trial (CAST)
- Aspirin within 48 hours reduced recurrence and mortality minimally
- Mortality: 9% aspirin vs 9.4% placebo
- Recurrence: 2.8% aspirin vs 3.9% placebo
- Haemorrhage: 0.9% aspirin vs 0.8% placebo
- Dependency: 30.5% aspirin vs 31.6% placebo

NNT for every 1000 cases
~prevents 9 deaths or non-fatal stroke recurrence
~ prevents 13 deaths or dependent at 6 months

27
Q

ABCD2 score for TIA

A

A: age > 60 years
B: BP > 140/90
C: clinical symptoms - weakness (2), speech (1)
D: duration - >60m (2), 10-59m (1)
D: DM

Score of 4 or more indicates high risk TIA -> DAPT for 3 weeks and lifelong SAPT

High risk for 3-month rate of stroke (>8%)

28
Q

Treatment for TIA

A
  1. DAPT - aspirin and clopidogrel for 3 weeks, then lifelong aspirin (POINT study)
    - Asians may have CYP2C19 polymorphism causing poor metabolism of clopidogrel to active form (less efficacy)
  2. ## Control CVRFRecent trials on DAPT with aspirin ticagrelor showed benefit in preventing stroke
    - No genetic heterogenicity in platelet inhibition
29
Q

What are the causes of cardioembolic strokes?

A

Atrial fibrillation (non-valvular)
Mural thrombus
Myocardial infarct (transmural or anteroapical ventricular wall)
Dilated cardiomyopathy
Valvular lesions
Mitral stenosis (rheumatic heart disease)
Mechanical valve
Bacterial endocarditis
Paradoxical embolus - ASD, PFO

30
Q

PFO occurs in ___ of general population

What is the clinical significance of PFO?
How to diagnose patent foramen ovale?
What are the current guidelines for PFO?

A

PFO occurs in 15-25% of general population
Mostly confers little if any stroke risk
————–
Paradoxical embolisation
- Venous thrombi migrate to arterial circulation via PFO or ASD
- Others: fat/tumour emboli, bacterial endocarditis, IV air, amniotic fluid embolism
————–
Bubble-contrast study (TTE or TCD)
- IV injection of agitated saline demonstrating (right-to-left cardiac shunt) or (bubble signature in MCA)
————–
Percutaneous occlusion device closure
(1% per year absolute reduction, hazard ratio 0.41)

Previously CLOSURE 1 trial did not demonstrate any benefit in 2-year follow up

31
Q

What is the appearance of bacterial endocarditis infarcts?

A
  • Multifocal symptoms and signs
  • Infarcts microscopic size
  • May develop into brain abscess or cause haemorrhage
  • Mycotic aneurysms -> SAH, ICH
32
Q

What is artery-to-artery embolism?
What are the causes of artery-to-artery embolic stroke?

A
  • Thrombus formation of atherosclerotic plaques embolise to intracranial arteries
  • Can occur in any diseased vessel

Causes of artery-to-artery embolic stroke
1. Thromboembolism at atherosclerotic plaque
- Extracranial arteries
- Intracranial arteries
2. Diseased vessel acutely thrombose and embolise
3. Dissection of arteries - ICA, vertebral arteries, COW
> EDS type 4, Marfan, cystic medial necrosis, fibromuscular dysplasia, trauma, spinal manipulative therapy

33
Q

When is hemicraniectomy recommended?

A

Malignant MCA occlusion, cerebellar infarct- high risk of cerebral oedema and herniation

NNT: 2 hemicraniectomies save 1 life

Prognosis:
- MCA: < 10% achieve functional decompression, but fewer people die.
- Cerebellar: good recovery

34
Q

What are the goals of hospitalisation for ischaemic stroke?

A
  1. Determine stroke mechanism and secondary stroke prevention strategy
  2. Prevent complications
  3. Plan for functional recovery - rehabilitation
35
Q

How to prevent systemic complications of stroke?

A
  1. DVT prophylaxis - mechanical
    - Calf pumps, TED stockings
    - Early mobilisation
  2. Swallowing deficits
    - Bedside swallowing test (BSST)
    - NBM until safety established
    - Speech therapy review and diet modification
  3. Immobility
    - Regular bed turning
    - PT OT support
    - Early removal of urinary catheter
    - Fall precaution
36
Q

Young stroke

A

Neurofibromatosis
Fabry disease
Connective tissue disease
Endocarditis
Cardiac abnormalities
Hypercoagulability

Standard Investigations
History - personal and family history of clotting, autoimmune, trauma and cardiac disease
Cardiac evaluation - TTE, Telemetry
MRI brain, vessel imaging

Additional Investigations
Hypercoagulable state workup
CRP, ANA, ANCA, RF, SLE
Infective - syphilis, HIV
Lumbar puncture

37
Q

Hypercoagulable state and workup

A
  • Family history - clotting, miscarriage, vascular risk factors
  • Hormone use - OCP, testosterone replacement, hormon replacement
  • Malignancy

Workup:
- AT III
- Protein C and protein S
- Activated protein C resistance
- Factor V leiden mutation
- Prothrombin mutation
- Lupus anticoagulant, anticardiolipin, anti-beta 2 glycoprotein antibodies (ALPS)
- CT TAP for malignancy

38
Q

North American Symptomatic Carotid Endarterectomy Trial (NASCET) and European Carotid Surgery Trial (ECST)
(Management of carotid stenosis with endarterectomy)

A

Symptomatic: retinal or hemispheric symptoms

  • Symptomatic + 70% carotid stenosis: reduces recurrent stroke risk in 2 years by half (absolute benefit of 14%)
  • Symptomatic + 50-69% carotid stenosis: only reduces 3 year recurrent stroke risk by 6%, with similar surgical risk
  • Asymptomatic patient: little to no recurrent stroke risk reduction, with similar surgical risk
    (Natural history of ~2% stroke rate per year)
  • Most beneficial when endarterectomy performed within 2 weeks of symptoms onset, men > women
39
Q

Stenting and Aggressive Medical Management for Preventing Recurrent Stroke in Intracranial Stenosis (SAMMPRIS) trial
(Management of intracranial atherosclerosis stenosis)

A

Intracranial atherosclerosis managed medically
- DAPT aspirin, clopidogrel for 3 months, then lifelong aspirin
- Aggressive CVRF control

Stenting causes increase in recurrent stroke!

SAMMPRIS trial: compares 70-99% stenosis to stenting + medical vs medical only
- 14.7% stenting arm had stroke within 30 days (most within 1 day!) vs 5.8% in medical arm
- 1 year stroke risk: 20% stent arm 12.2% medical arm
–> Terminated early due to adverse stenting outcomes

40
Q

Common locations of carotid artery atherosclerosis
Incidence in ischaemic stroke

A
  1. Common carotid bifurcation
  2. Proximal internal carotid artery
  3. Carotid siphon (portion within cavernous sinus)

Incidence ~10% of ischaemic stroke

41
Q

What is symptomatic carotid disease?

A

Stroke or TIA within vascular distribution of the diseased artery

42
Q

What is the relationship between arterial narrowing and risk of stroke?

A

Greater degrees of arterial narrowing associated with higher risk of stroke
(except near occlusions - lower risk -> possibly due to development of collaterals)

43
Q

Dissection of intracranial arteries is ___, precedes stroke by __.
Intracranial dissection causes __ and __, requiring urgent treatment and surgery to prevent re-rupture.

Dissection of extracranial arteries does not cause __ due to tough adventitia of vessels, and pseudoaneurysms of ECA __ require treatment

Most dissections heal spontaneously, stroke or TIA uncommon beyond __.

Trial: no difference if stroke prevention with aspirin compared with anticoagulation, low recurrence stroke rate __

A

Dissection of intracranial arteries is painful, precedes stroke by several hours to days.
Intracranial dissection causes SAH and pseudoaneurysm, requiring urgent treatment and surgery to prevent re-rupture.

Dissection of extracranial arteries does not cause haemorrhage due to tough adventitia of vessels, and pseudoaneurysms of ECA does not require treatment

Most dissections heal spontaneously, stroke or TIA uncommon beyond 2 weeks.

Trial: no difference if stroke prevention with aspirin compared with anticoagulation, low recurrence stroke rate 2%

44
Q

What is small vessel disease ischaemic stroke?
What is the incidence of small vessel disease stroke?

A

Occlusion of small penetrating artery due to atherothrombotic or lipohyalinotic process
Accounts for 20% of all strokes

45
Q

Pathophysiology of small vessel disease stroke

A
  1. Small penetrating artery branches
    - Major arteries give rise to 30-300 um branches that penetrate deep gray and white matter
  2. Atherothrombotic or lipohyalinotic t hickening occlusion
  3. Development of infacts size 3mm up to 2cm (usually < 1.5cm)
46
Q

What are the causes of stroke?

A
47
Q

What are the risk factors for development of venous sinus thrombosis? (7)

A
  • Contraceptives
  • Pregnancy
  • Postpartum
  • Inflammatory bowel diseases
  • Intracranial infections
  • Dehydration
  • Thrombophilia, antiphospholipid syndromes, protein deficiencies
  • Polycythaemia
  • Sickle cell anaemia
  • Homocysteinaemia
  • Prothrombin G20210 mutation
48
Q

What is the ultrasound characteristics of fibromuscular dysplasia?

A

Multiple rings of segmental narrowing alternating with dilatation

49
Q

How do drugs like amphetamine and cocaine cause stroke?

A
  1. Acute hypertension crisis
  2. Drug induced vasculopathy - vasospasm, atherosclerosis, vasculitis
50
Q

What is moyamoya disease?

A

Occlusive disease of large intracranial arteries
Involving distal ICA, stem of MCA and ACA

Lenticulostriate arteries develop rich collateral circulation around occlusive lesion (puff of smoke appearance)
Rupture of moyamoya collaterals cause ICH

Occurs in Asian children or young adult

51
Q

What is extracranial-to-intracranial (EC-IC) bypass surgery and current studies (2023)?

A

Current trial: recent stroke with associated carotid occlusion and evidence of inadequate brain perfusion of NM brain perfusion imaging

Proven ineffective for atherosclerotic stenoses that are inaccessible to conventional CEA.

No benefit of EC-IC bypass was found in a trial stopped for futility

52
Q

Risk of Paradoxical Embolism (RoPE) Score
- Evaluation of stroke-related PFO in patients with cryptogenic stroke

A
  1. No hypertension
  2. No diabetes
  3. No previous stroke or TIA
  4. Non-moker
  5. Cortical infarct on imaging
  6. Younger age higher risk

Score of 4 and above warrants PFO closure

53
Q

Bubble Study Grading of PFO

A
  1. Grade 1 (1-5 bubbles)
  2. Grade 2 (6-19 bubbles)
  3. Grade 3 (20 or more bubbles)
  4. Grade 4 (complete opacification)

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