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Stroke Flashcards

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1
Q

Risk factor for haemorrhagic transformation

A

Large infarcts + high NIHSS score
Established infarcts
Poor collaterals
Thrombocytopenia

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2
Q

Absolute CI to haemolysis

A 
Extensive hypoattenuation on CT
Suspicious of SAH (thunderclap headache followed by weakness)
Current/previous ICH
Intracranial neoplasm
Severe head trauma last 3/12
Intracranial or intraspinal surgery
Plat <100
INR >1.7
APTT >40
Clexane last 24 hours
Suspicious for current endocardtisi
Active GI or internal bleed
Aortic arch dissection
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3
Q

What kind of clots does thrombolysis do well in?

A

Smaller clots

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4
Q

Broad indications for clot retrieval

A

ICA, basilar, M1, M2 (needs to be appropriate) occlusion
CTP: large penumbra, small core
CTB: no extensive infarct
Good premorbid function

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5
Q

Do you give tPA for clot retrieval?

A

Yes unless you’re not eligible

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6
Q

BP target post thrombolysis

A

<185/110

Use IV labetalol or hydralazine

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7
Q

BP target if no TPA

A

<220/120
Need the cerebral perfusion to perfuse through collaterals

Wait 48-72 hours then can start lowering BP = aim 120-130/80-90

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8
Q

Hemicraniectomy for swelling and herniation post stroke has what outcomes?

A

Reduce deaths

But not necessarily reduce disability

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9
Q

Target lipids for stroke

A

LDL <1.8

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10
Q

Ticagrelor or clopidogrel in stroke?

A

Clopidogrel has lower bleeding rates

Similar efficacy

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11
Q

What’s symptomatic carotid stenosis?

A

When you have a stroke on the same side

We don’t treat asymptomatic carotid stenosis

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12
Q

Rx symptomatic carotid stenosis

A

CEA
70-99% stenosis of ipsilateral carotid artery
50-69% select patients (especially men)
Best benefits within 2 weeks, <3 months at least (any longer the plaque has stabilised so no point)
Intensive vascular secondary prevention therapy

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13
Q

Stent or CEA?

A

Stent for

  • Unfavourable anatomy ie tortuous
  • Symptomatic re-stenosis after CEA
  • Previous stenting
  • Aged <70 years
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14
Q

Dissection often occurs where?

A

Carotid and vertebral arteries

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15
Q

How does dissection occur?

A

Trauma (can be minimal) with hyperextension of neck
Genetic predisposition
Fibromuscular dysplasia
CT disorders

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16
Q

Presentation of dissection

A

Neck pain
Headache - migraines, raeder’s syndrome (trigeminal neuralgia), thunderclap headache
Stroke - dependent on migratory
Partial Horner’s syndrome (do an angiogram to look for dissection)
- Sympathetic ganglion lie at carotid birfurcation
- Sympathetic pathway runs with internal carotid
- No anhidrosis as fibres for sweat travel with the external carotid
CN 6 or lower cranial nerve palsy
SAH if rupture

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17
Q

Rx dissection

A

Aspirin

Generally good prognosis

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18
Q

What happens in dissection?

A

Tear in the vessel wall, intima –> leads to thrombus formation in the wall artery which can expand towards intima or adventita –> creates stenosis, tapering or pseudoaneurysm –> thrombus can embolise or occlude the artery

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19
Q

When to close a PFO in stroke?

A

If <60 years with no other cause found apart from PFO who have associated atrial septal aneurysm or moderate to large R to L shunt

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20
Q

Preferred NOAC for AF in stroke?

A

Apixaban and dabigatran preferred

Rivaroxaban linked to breakthrough stroke (often wake up in the morning just before 8am daily dose)

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21
Q

How long do TIAs usually last?

A

Usually less than 1 hour (usually <10 minutes)

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22
Q

How to treat ischaemic stroke with no AF?

A

Load 300mg for both DAPT

3 weeks DAPT–> monotherapy

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23
Q

BP target for ICH

A

SBP <140

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24
Q

Rx ICH

A

BP management
Reverse INR if on warfarin
Reverse dabigatran
Safe to recommence antiplatelets 4-6/52 after ICH
Don’t operate unless there is cerebellar haemorrhage (tight space/decompress)
EVD in intraventricular haemorrhage to prevent hydrocephalus

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25
Cerebral amyloid angiopathy syndrome | Presentation
Lobar haemorrhage (peripheral) Cortical microhaemorrhages Cortical superficial siderosis/convexity SAH White matter disease and cortical infarcts Dementia CAA-related inflammation
26
Rx Cerebral amyloid angiopathy syndrome
BP Control | Avoid anticoagulation, antiplatelet, Tpa
27
Risk factor for cerebral venous sinus thrombosis
``` Woman Pregnancy Obesity Thrombophilia including OCP Local infections Chronic inflammatory diseases Malignancy ```
28
When to start anticoagulation post acute stroke?
``` 0, 3, 6, 12 rule Day 0 for TIA Day 3 for minor stroke Day 6 for moderate stroke Day 12 for significant stroke ```
29
Should you anticoagulate stroke of unknown source? Ie you think its coming from the heart but you can't prove it
No | Treat with antiplatelet therapy
30
Surgical occlusion of the left atrial appendage in those post stroke with AF undergoing cardiac surgery for another indication has shown ...
Benefit in preventing further stroke + Usual anticoagulation Need AF and CHADSVASC2 2+
31
How does amaurosis fugax present?
Curtain coming down one eye Transient monocular vision loss lasting seconds-minutes May be recurrent
32
Pathophysiology of amaurosis fugax
``` Retinal ischaemia (retinal artery occlusion) Associated with ipsilateral severe carotid artery stenosis (ICA --> opthalmic artery) ```
33
What might you see on fundoscopy in amaurosis fugax?
Retinal emboli or hypoperpfusion
34
What's the difference between primary and secondary ICH?
``` Primary ICH > Deep perforation vasculopathy - BG or brainstem - White matter lesions, lacuna strokes - Vascular risk factors - HTN, binge drinking, smoking > Cerebral amyloid angiopathy - Lobar intracerebral haemorrhage ``` ``` Secondary ICH > Metastasis - Grey-white junction - Significant oedema >AVM, aneurysms, cavernomas, cerebral venous sinus thrombosis, IE ```
35
Pathophysiology of cerebral amyloid angiopathy
Amyloid protein deposition in leptomeningeal and cortical vessels of cerebrallar and cerebral lobes --> necrosis of vessel wall --> rupture/small vessel occlusion Increasing number of microbleeds = increasing risk of ischaemic stroke and ICH
36
Pathophysiology of cerebral venous sinus thrombosis
Thrombosis --> increased capillary and venular pressure --> decreased perfusion --> ischaemia and oedema Venous and capillary rupture --> haemorrhage Poor CSF obstruction -> raised intracranial pressure
37
Presentation of cerebral venous sinus thrombosis
> Isolated intracranial hypertension (90%) - Symptoms of raised pressure - Subacute headache, generalised or local - Visual changes, papilloedema > Focal neurological abnormalities (44%) > Seizures (33%) > Encephalopathy usually elderly
38
Rx cerebral venous sinus thrombosis
1) Anticoagulation to prevent clot propagation Heparin infusion (fast offset) vs therapeutic clexane (fast onset). Transition to oral anticoagulant. 3-6/12 in provoked and 6-12/12 in unprovoked Indefinite if severe thrombophilia or systemic thrombosis Can do follow up imaging to see if recanalised 2) Direct fibrinolysis only in severe cases, no evidence 3) Hemicraniectomy 4) Raised intracranial pressure - Acetazolamide - not suggested by european guidelines - May need surgical intervention if severe
39
Prognosis of cerebral venous sinus thrombosis
Overall mortality 5% (herniation) 10% have permanent neurological deficit Otherwise excellent recovery Women who have it during pregnancy or postpartum may need prophylactic anticoagulation during next pregnancy
40
COVID19 Vaccine-induced immune thrombotic thrombocytopenia 1) Presentation 2) How many days post vaccine? 3) Risk factors
1) Similar to heparin-induced thrombocytopenia (HIT) Thrombocytopenia, thrombosis and ab to platelet factor 4 Systemic thrombosis with higher rates of cerebral venous sinus thrombosis 2) Develops 8-10 days post vaccine 3) Female sex, age <60
41
Rx COVID19 Vaccine-induced immune thrombotic thrombocytopenia
Anticoagulation with non-heparin IVIG Steroids Severe cases consider PLEX, rituximab, eculizumab
42
Stroke patients need to go to a stroke care unit within ... hours
24-48 hours
43
For large vessel occlusive stroke, ECR or lysis?
Do both! Use alteplase with ECR/mechanical thrombectomy when indicated 10% of clot is gone before you do ECR
44
How does tenecteplase compare to altephase?
Tenecteplase is better than alteplase Reperfusion before ECR 22% vs alteplase 10% Much better at recanulisation but not standard practice yet
45
GA or conscious sedation for ECR?
Doesn't matter | As long as you keep the BP up so collaterals keep working
46
When do you close a PFO in embolic stroke?
47
Hematoma evacuation - any evidence?
NO
48
What is Idarucizumab?
Fragmented ab binds dabigatran TGA approved and in general use Stops dabigatran activity within 5 minutes of infusion
49
How long to use DAPT for after ischaemic stroke?
DAPT for 3 weeks then switch to monotherapy (aspirin or clopidogrel long-term)
50
Carotid or vertebral artery dissection Risk of embolisation is very high in the first 1-2 weeks Which blood thinner to use?
No clear winner between antiplatelet vs anticoagulation, hence, probably neither. Answer: admit to stroke unit
51
LDL target following atherosclerotic stroke
LDL <1.8
52
Clopidogrel or ticagrelor in secondary stroke prevention?
Ticagrelor and aspirin prevent more stroke BUT much more bleeding So in practice, we use clopidogrel + aspirin
53
Do we treat asymptomatic carotid stenosis?
No
54
Risk factors for recurrent stroke
``` Strongest risk factors for recurrence #1 multiple infarctions on imaging #2 large artery artherosclerosis = 'hot' carotid #3 ABCD2 6-7 = very heavy vascular risk profile ```
55
Antihypertensive in ischaemic stroke
All are good EXCEPT beta blockers in the prevention of stroke (however if they need beta blocker for MI, just use it) CCB are better at preventing stroke
56
BSL target post stroke
BSL <11 Reduces disability and death in the acute window Don't use insulin infusion = just causes lots of hypoglycaemia!
57
Should you mobilise them straight after stroke?
No | Mobilise after 24 hours
58
Tenecteplase vs alteplase within 4.5h in small artery strokes
Similar | Default is alteplase at the moment (standard of care)
59
Evolocumab in stroke prevention?
Evolocumab reduces CV death, MI and stroke by 20% in patients with CV disease Due to effective LDL reduction
60
Pioglitazone in stroke prevention?
Reduces risk of stroke, MI and development of diabetes (in insulin resistance) AE: weight gain, oedema, bone # Benefits > risks
61
Minor stroke is NIHSS of ...
<4 The other definition is based on volume of infarct on scan
62
Extracranial vs intradural arterial dissection | What's the difference?
Extracranial - risk of ischaemic stroke. However we don't know how to prevent the stroke. Often need intravascular intervention. Intradural - risk of haemorrhage, bleeding into the dura
63
What's the time window for the following? What management occurs in each window? Hyperacute window post stroke Acute stroke Subacute
Hyperacute 6-24 hours - lysis, ECR Acute 1-3 days - acute stroke unit care, FAST, keep BSL down, keep temp under 37.5, consider decompressive hemicraniectomy Subacute 24h to 3 weeks - DAPT after TIA/ischaemic stroke, vascular risk factor mx
64
What's the 1, 3, 6, 12 rule re restarting NOAC post stroke?
After 1 day- restart day 1 if TIA or super small stroke 3 - restart after 3 days if small 6 - restart after 6 days if moderate 12 - restart after 12 days if large i.e. whole MCA territory Not evidence based!! Clinician dependent
65
Amyloid angiopathy
Amyloid angiopathy Old Dementia Haemorrhage in the lobar distribution MRI: multiple microhaemorrhages in the lobar distribution These patients are also at risk of ischaemic strokes or TIAs Hence very difficult to prevent further episodes as they can bleed and clot
66
Hypertensive haemorrhages
White matter Perforating arteries Basal ganglia
67
AVM, SAH bleeding pattern
basal cisterns secondary to berry aneurysms
68
Acute ICH management
Reduce BP <140/90 (intracerebral haemorrhage, not SAH, AVM, fistula) for the first 7 days reduces death or disability Embolise any bleeds Reverse antithrombotics Correct coagulopathy Decompress or assist CSF drainage if high ICH, hydrocephalus Stroke unit/ICU
69
SAH investigation
CT sensitivity >95% first 12-24h Do LP at least 12h later to look for xanthochromia
70
When do you start lowering BP after ischaemic stroke?
After 3 day window (no evidence) | Keep it as low as possible until you get side effects
71
NOACs vs warfarin in ischaemic stroke related to AF
NOACs Less intracerebral haemorrhage Slightly more GI bleed
72
Watershed infarct between 2 major circulations | Likely cause
Embolic or Haemodynamic
73
Lacunar infarct | Likely cause
Small vessel ischaemia
74
Juxtacortical infarct | Likely cause
Embolic
75
Straitocapsular infarct | Likely cause
Embolic
76
Wedge MCA branch infarct | Likely cause
Embolic
77
What's DWI-FLAIR mismatch on MRI?
FLAIR (T2) looks for oedema, water in the interstitium (between cells). Means cells have died. DWI - neuronal dysfunction If there is a DWI and FLAIR mismatch, it means there is a penumbra
78
Time window for thrombolysis
Within 4.5h of symptom onset Within 9h if favourable perfusion
79
Prophylactic clexane after ischaemic stroke?
24h after
80
Time window for ECR
6 hours if no perfusion 24 hours if favourable perfusion
81
Benefits of the acute stroke unit
Temp <37.5 NBM until swallow ax BSL <11 The above seems to largely contribute to improved outcome post stroke in the first 3 days (less death and disability)
82
Extensive stroke <60 years | Should Hemicraniectomy be done?
Do it early Let dead brain herniate so it doesn't squash good brain Reduces mortality but NOT disability Don't do it >60 years
83
Cerebral venous sinus thrombosis | Treatment
Clexane regardless of the presence of intracerebral haemorrhage They're bleeding not because they're gushing out of an artery, they're bleeding cause the brain is so oedemetaous and blood is leaking out (anticoagulate to ty break down the clot thats causing the congestion) For those that progress despite anticoagulation: endovascular thrombectomy or thrombolysis may improve outcomes

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