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neuro > Stroke > Flashcards

Stroke Flashcards

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
Q

Cerebral amyloid angiopathy syndrome

Presentation

A

Lobar haemorrhage (peripheral)
Cortical microhaemorrhages
Cortical superficial siderosis/convexity SAH
White matter disease and cortical infarcts
Dementia
CAA-related inflammation

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26
Q

Rx Cerebral amyloid angiopathy syndrome

A

BP Control

Avoid anticoagulation, antiplatelet, Tpa

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27
Q

Risk factor for cerebral venous sinus thrombosis

A 
Woman
Pregnancy
Obesity
Thrombophilia including OCP
Local infections
Chronic inflammatory diseases
Malignancy
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28
Q

When to start anticoagulation post acute stroke?

A 
0, 3, 6, 12 rule
Day 0 for TIA
Day 3 for minor stroke
Day 6 for moderate stroke
Day 12 for significant stroke
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29
Q

Should you anticoagulate stroke of unknown source? Ie you think its coming from the heart but you can’t prove it

A

No

Treat with antiplatelet therapy

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30
Q

Surgical occlusion of the left atrial appendage in those post stroke with AF undergoing cardiac surgery for another indication has shown …

A

Benefit in preventing further stroke
+ Usual anticoagulation

Need AF and CHADSVASC2 2+

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31
Q

How does amaurosis fugax present?

A

Curtain coming down one eye
Transient monocular vision loss lasting seconds-minutes
May be recurrent

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32
Q

Pathophysiology of amaurosis fugax

A 
Retinal ischaemia (retinal artery occlusion)
Associated with ipsilateral severe carotid artery stenosis (ICA --> opthalmic artery)
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33
Q

What might you see on fundoscopy in amaurosis fugax?

A

Retinal emboli or hypoperpfusion

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34
Q

What’s the difference between primary and secondary ICH?

A 
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
Q

Pathophysiology of cerebral amyloid angiopathy

A

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
Q

Pathophysiology of cerebral venous sinus thrombosis

A

Thrombosis –> increased capillary and venular pressure –> decreased perfusion –> ischaemia and oedema

Venous and capillary rupture –> haemorrhage

Poor CSF obstruction -> raised intracranial pressure

37
Q

Presentation of cerebral venous sinus thrombosis

A

> 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
Q

Rx cerebral venous sinus thrombosis

A

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
Q

Prognosis of cerebral venous sinus thrombosis

A

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
Q

COVID19 Vaccine-induced immune thrombotic thrombocytopenia

1) Presentation
2) How many days post vaccine?
3) Risk factors

A

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
Q

Rx COVID19 Vaccine-induced immune thrombotic thrombocytopenia

A

Anticoagulation with non-heparin
IVIG
Steroids

Severe cases consider PLEX, rituximab, eculizumab

42
Q

Stroke patients need to go to a stroke care unit within … hours

A

24-48 hours

43
Q

For large vessel occlusive stroke, ECR or lysis?

A

Do both!

Use alteplase with ECR/mechanical thrombectomy when indicated

10% of clot is gone before you do ECR

44
Q

How does tenecteplase compare to altephase?

A

Tenecteplase is better than alteplase

Reperfusion before ECR 22% vs alteplase 10%
Much better at recanulisation but not standard practice yet

45
Q

GA or conscious sedation for ECR?

A

Doesn’t matter

As long as you keep the BP up so collaterals keep working

46
Q

When do you close a PFO in embolic stroke?

A
47
Q

Hematoma evacuation - any evidence?

A

NO

48
Q

What is Idarucizumab?

A

Fragmented ab binds dabigatran
TGA approved and in general use
Stops dabigatran activity within 5 minutes of infusion

49
Q

How long to use DAPT for after ischaemic stroke?

A

DAPT for 3 weeks then switch to monotherapy (aspirin or clopidogrel long-term)

50
Q

Carotid or vertebral artery dissection
Risk of embolisation is very high in the first 1-2 weeks
Which blood thinner to use?

A

No clear winner between antiplatelet vs anticoagulation, hence, probably neither.

Answer: admit to stroke unit

51
Q

LDL target following atherosclerotic stroke

A

LDL <1.8

52
Q

Clopidogrel or ticagrelor in secondary stroke prevention?

A

Ticagrelor and aspirin prevent more stroke BUT much more bleeding
So in practice, we use clopidogrel + aspirin

53
Q

Do we treat asymptomatic carotid stenosis?

A

No

54
Q

Risk factors for recurrent stroke

A 
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
Q

Antihypertensive in ischaemic stroke

A

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
Q

BSL target post stroke

A

BSL <11
Reduces disability and death in the acute window
Don’t use insulin infusion = just causes lots of hypoglycaemia!

57
Q

Should you mobilise them straight after stroke?

A

No

Mobilise after 24 hours

58
Q

Tenecteplase vs alteplase within 4.5h in small artery strokes

A

Similar

Default is alteplase at the moment (standard of care)

59
Q

Evolocumab in stroke prevention?

A

Evolocumab reduces CV death, MI and stroke by 20% in patients with CV disease

Due to effective LDL reduction

60
Q

Pioglitazone in stroke prevention?

A

Reduces risk of stroke, MI and development of diabetes (in insulin resistance)

AE: weight gain, oedema, bone #

Benefits > risks

61
Q

Minor stroke is NIHSS of …

A

<4

The other definition is based on volume of infarct on scan

62
Q

Extracranial vs intradural arterial dissection

What’s the difference?

A

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
Q

What’s the time window for the following? What management occurs in each window?

Hyperacute window post stroke

Acute stroke

Subacute

A

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
Q

What’s the 1, 3, 6, 12 rule re restarting NOAC post stroke?

A

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
Q

Amyloid angiopathy

A

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
Q

Hypertensive haemorrhages

A

White matter
Perforating arteries
Basal ganglia

67
Q

AVM, SAH bleeding pattern

A

basal cisterns secondary to berry aneurysms

68
Q

Acute ICH management

A

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
Q

SAH investigation

A

CT sensitivity >95% first 12-24h

Do LP at least 12h later to look for xanthochromia

70
Q

When do you start lowering BP after ischaemic stroke?

A

After 3 day window (no evidence)

Keep it as low as possible until you get side effects

71
Q

NOACs vs warfarin in ischaemic stroke related to AF

A

NOACs
Less intracerebral haemorrhage
Slightly more GI bleed

72
Q

Watershed infarct between 2 major circulations

Likely cause

A

Embolic or Haemodynamic

73
Q

Lacunar infarct

Likely cause

A

Small vessel ischaemia

74
Q

Juxtacortical infarct

Likely cause

A

Embolic

75
Q

Straitocapsular infarct

Likely cause

A

Embolic

76
Q

Wedge MCA branch infarct

Likely cause

A

Embolic

77
Q

What’s DWI-FLAIR mismatch on MRI?

A

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
Q

Time window for thrombolysis

A

Within 4.5h of symptom onset

Within 9h if favourable perfusion

79
Q

Prophylactic clexane after ischaemic stroke?

A

24h after

80
Q

Time window for ECR

A

6 hours if no perfusion

24 hours if favourable perfusion

81
Q

Benefits of the acute stroke unit

A

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
Q

Extensive stroke <60 years

Should Hemicraniectomy be done?

A

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
Q

Cerebral venous sinus thrombosis

Treatment

A

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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