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YEAR 4 OLDER PEOPLE INTEGRATED CARE > Stroke Brain imaging + ischaemic and haemorrhagic > Flashcards

Stroke Brain imaging + ischaemic and haemorrhagic Flashcards

https://www.youtube.com/watch?v=DdPRfPm9SI4&t=3043s https://www.youtube.com/watch?v=MgCjRfmPLQ4 https://www.youtube.com/watch?v=H4xErylBd1g&t=418s

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1
Q

What are different types of CT to visualise brain in stroke?

A

Unenhanced CT scan
CT angiogram (CTA)
CT perfusion scan (CTP_
CT venogram (CTV)
Contrast enhanced brain scan (CECT) for blood brain barrier disruption

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2
Q

What landmark should you look for to work out where in brain you are, which lobes etc?

A

Look for central sulcus - makes curve like greek letter omega
- anterior to this is frontal
- posterior to this is parietal

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3
Q

CT cut through basal ganglia - identify brain structures

A
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4
Q

A CT axial cut through sylvan fissure, identify Sylvian fissure and what lives there (v relevant for stroke!)

A

MCA lives in Sylvian fissure - in this image it is isodense (similar to surrounding brain tissue) so hard to see

When it is hyperdense (bright white) we have problems like stroke!

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5
Q

This is CT cut of midbrain - identify:

midbrain
basal cistern
Uncus (can herniate)
Lateral horn of the lateral ventricle (hydrocephalus -dilated)

A
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6
Q

CT cut to pontine level
identify:

Pons
Cerebello- pointine angle
4th ventricle

A
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7
Q

CT axial cut at the medulla - identify
medulla
4th ventricle
cerebellum

A
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8
Q

What are the two types of stroke?

A
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9
Q

Ischaemia vs infarction in stroke:

A

Ischaemia: insufficient blood flow to meet metabolic demand. Poor 02, cerebral hypoxia.
REVERSIBLE
but it can lead to ——> infarction

Infarction: cell and brain tissue death
IRREVERSIBLE

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10
Q

Describe the pathophysiology of how Ischaemia leads to infarction

A
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11
Q

What is a TIA?

A

“Brief episode of neurological dysfunction caused by focal brain and/or retinal ischeaemia, with clinical symptoms lasting <1hr and without evidence of acute infarction”

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12
Q

What are the four ages of an infarct (timings and how classed)

A

Hyperacute: <6 hours

Acute: < 7 days

Subacute : < 4 months

Chronic : >4 months

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13
Q

How do you treat a hyperacute infarct?

A

IV thrombolysis w/ Alteplase
window of 4.5 hours

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14
Q

Why does a suspected stroke need to be imaged?

A
  1. Thrombolysis (for hyperacute infarct) can only be given if excluded haemorrhage - need imaging
  2. Patients with stroke mimic e..g tumour - should NOT get thrombolysis - need to image
  3. BUT stroke is a clinical diagnosis might not need hyperacute infarct on imaging to prescribe thrombolysis
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15
Q

What are the benefits of CT scanning in stroke

A
  1. available 24/7
  2. Quicker than MRI
  3. Fewer contraindications / intolerances and need for MRI compatible resuscitation equipment
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16
Q

What is primary technique for stroke imaging and how does it aid clinicians in their decision making?

A

Unenhanced CT

-done ASAP post stroke

  • highly sensitive in detecting acute haemorrhage
  • sensitive to detect stroke mimics e.g tumour, arterial venous malformation (AVM) and to determine further investigations
  • may show the target thrombosed vessel
  • identify infarctions that are too big, or old for thrombolysis (due to increased risk of haemorrhage)
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17
Q

What appears hyperdense on CT?

A

Hyperdense = WHITE BRIGHT
mineralised structures: e.g. Ca bone or calcified lesions
Blood

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18
Q

What appears as hypodense on CT?

A

Hypodense = dark
Fluid appears dark on CT

so usually due to:
chronic lesions
Fluids
cysts
oedema

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19
Q

Unenhanced CT pf a cerebral infarct
What signs do you see?

A

Hypoattenuating
Cortical-sub cortical
within a vascular territory

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20
Q

Images demonstrate the territories of ACA, Middle cerebral artery MCA and posterior cerebral artery on CT and drawing - try and visualise

A
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21
Q

Describe the early signs of infarction pictured here

A
  • Hypoattenuation Right side
    -Sulcal effacement in right MCA territory
    -RIGHT Middle cerebral artery infarct
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22
Q

Describe early signs of infarction pictured here

A
  • Loss of gray matter - white matter differentiation of the left basal ganglia
  • sulcal effacement in the left MCA territory
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23
Q

Describe early signs of infarction pictured here

A

-Hyperattenuating left MCA
-Intra -arterial thrombus (30% of cases)
- False positives: Calcifications, dolichoectasia, polyscythaemia, increased haematocrit

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24
Q

What are the causes of acute infarction due to cerebral ischaemia?

A

Embolism (most common)
e..g cardiac/ carotid / paradoxical / aorta

Thrombosis e.g. arteriosclerotic disease

Arterial dissection

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25
Q

The role of MRI in stroke imaging

A

MRI is more sensitive in detection and diagnosis of acute infarction
- diffusion weighted imaging
- positive from 2 hours - 3 weeks

Good to use if:
Previous CVD makes CT difficult
Difficult location for CT - e.g. posterior fossa
Equivocal case - ? tumour
sensitivity - TIA clinic

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26
Q

Hyperacute findings of acute infarction on CT
when might you be able to visualise a clot?

A

see hyperdense artery (clot w/in lumen of artery)
clot = hyperdense compared to flowing blood

gets more hyperdense with time - often see immediately on CT as the thrombo- embolism has often travelled from somewhere else in body

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27
Q

Hyperacute findings of acute infarction on CT
when might you be able to visualise early parenchymal signs ?

A

hypoattenuation

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28
Q

Where is the thromboembolsim in these 2 unenhanced CTs?

How would you confirm visualisation of the clot?

A

LEFT image: Right MCA = hyperdense
RIGHT image: Hyperdense seen in top of basilar artery

Confirm with: CT angiography
Result: the hyperdense area seen on non-contrast CT imaging will become a filling defect on CT angiography

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29
Q

What does this unhenanced CT show?

A

Chronic Right MCA stroke

hypo-dense = chronic lesions
well defined, wedge shaped, same density as CSF and conforms to vascular territory

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30
Q

What does this unenhanced CT scan show?

A

Acute right MCA infarction
see hypodensity in MCA territory

From scan 8 hours post symptom onset
(acutely ischaemic neurons swell, but oedema takes 6-8 hours to show on CT. this scan taken later - we can see. Early CT scans of ischaemic stroke can often look falsely normal!)

31
Q

What does this show?

A

This is (left to right)

Unenhanced CT
MRI
CT angiography

of ACUTE RIGHT MCA infarction

32
Q

What is Alteplase licensed for?

A
  • licensed to first 4.5 hours post stroke

-This leads to current preferred model of ‘clinical prescribing’ of Alteplase: limits use of CT to eliminate haemorrhage and stroke mimics

33
Q

How does a perfusion CT of brain work?

A
  • use iodinated CT contrast
  • repeated images of the same few levels of brain tissue are taken during the first pass of the contrast through the brain
  • the transient hyperattenuation is proportional to the amount of contrast in the vessels of that region
34
Q

What are the parameters used in CT Perfusion

A

MTT : Mean transit time
CBV : cerebral blood volume

from this can work out CBF : cerebral blood flow
CBF= CBV/MTT

These parameters are displayed as visual maps to be analysed

35
Q
A

RIGHT = ischaemic penumbra

The ischaemic penumbra surrounds the infarct core
- increased MTT/Tmax
- moderately reduced CBF
- near-normal or increased CBV(due to autoregulatory vasodilatation)

https://radiopaedia.org/articles/ct-perfusion-in-ischaemic-stroke

36
Q
A

The infarct core is the part of the ischaemic brain which has already infarcted or is destined to infarct regardless of therapy.

  • increased MTT
  • markedly decreased CBF
  • markedly decreased CBV

Can overestimate infarct core if use Note, that if one uses CBF alone to visually assess core size, it is easy to overestimate infarct core, as the penumbra often has reduced CBF also. So, even though some automated processes used CBF to define the core, CBV is a safer parameter if ‘eye-balling’ the scan.

https://radiopaedia.org/articles/ct-perfusion-in-ischaemic-stroke

37
Q

What is the relevance of identifying

  1. the infarct core
  2. the ischaemic penumbra

in acute ischaemic stroke on CT perfusion studies?

A

a patient with a small core and a large penumbra is most likely to benefit from reperfusion therapies.

38
Q

How do CT perfusion maps help work out what is salvageable brain tissue?

A
39
Q

What does this show?

A

Brain stem infarction in a 43yr old woman admitted unconscious

  • Large potine infarct
  • Hyperattenuating basilar artery

Brainstem infarcts:
-Slower to appear
-Slower to evolve
- Longer theraputic window

40
Q

Spontaneous Intracranial haemorrhage (ICH):
1. % of strokes
2. Clinical clues an ICH

A
  1. 15% of strokes
  2. Clincial clues:
    - possible underlying causes
    - reduced level of consciousness at admission
    - Hx of headache
    - seizures
41
Q

Intracranial haemorrhage can be

  1. Primary (small vessel) haemorrhage
  2. Secondary haemorrhage

What are some causes of 1…?

A
  • Hypertension
  • Cerebral amyloid angiopathy (CAA)
42
Q

Intracranial haemorrhage can be

  1. Primary (small vessel) haemorrhage
  2. Secondary haemorrhage

What are some causes of 2./.?

A
  • Haemorrhagic transformation infarct - venous sinus thrombosis infarct and venous infarct
  • Tumour - GBM, anaplastic astrocytoma, mets
  • Vascular - aneurysm, AV<. vasculitis

-Coagulopathy - warfarin, aspirin

  • Cocaine / alcohol
43
Q

Outline what can happen in the brain during an intracranial haemorrhage?

A
44
Q

What are some factors of intracranial haemorrhage that predict outcomes? e.g. early mortality, poor outcomes, clinical

A
45
Q

Intracranial haemorrhages can be located where in the brain?

A
46
Q

What imaging can you use to diagnose Intracranial haemorrhage?

A

CT first then MRI

47
Q

Outline how CT is used in the diagnosis of intracranial haemorrhage?

A

-Acute bleed and immediate complications of acute bleed
- time course
- uderlying cause - CTA, CTV, CEET

48
Q

How is MRI used in the diagnosis of intracranial haemorrhage ?

A
49
Q

How is Intracranial haemorrhage managed ?

A

Neurosurgery:
- clot reduction, decompression craniotomy
(mandated in cerebellar haemorrhage with
GCS <14 and haematoma >40mls)
-Intraventricular shunting
(mandated in hydorcephalus)

Medical:
-Suportive
- Blood pressure
- Mass effect
- seizures
- secondary prevention

50
Q

How does an acute haemorrhage look on CT?

A
  • Large globulin molecule of blood stops attenuating X-rays - so high density - hyperattenuating
  • Lesion density depends on age of haematoma. As globulin is broken down density will fall until dark protein fluid (like CSF) is left

small bleeds - disappear in a week
large - take months

51
Q

How do you class the stages on CT of an acute haematoma?

A
52
Q

What does this show

A

Typical hypertensive bleed

in Basal ganglia
- 2/3rd putamen
- 1/4 thalamas

53
Q

What does this show?

A

Bleed due to Cerebral Amyloid Angiopathy

(a condition in which proteins called amyloid [amyloid-beta (Aβ)] build up on the walls of the arteries in the brain. CAA causes bleeding into the brain (hemorrhagic stroke) and dementia.

54
Q

Intratumoral Haemorrhage……what are some clues / action / Primary malignancy it could be?

A

Clues:
-History - stutering onset
- Oedema
- Irregular nature of the clot

Action:
ASAP CE-MRI (contrast enhanced)

Primary malignancy:
Glioblastoma multiforme / anaplastic astrocytoma
Mets: Lung, renal, melanoma, choriocarcinoma, thyroid

55
Q

Arteiovenous malformation haemorrhage .what are some…clues….action ?

A

Clues:
- age
-abnormal vessels

Action:
- CTA / CTV or MRA / MRV
- urgent neurosurgical referral as may be further bleeding
- DSA and endovascular treatment

56
Q

What is this? What could it be caused by?

A
57
Q

What are some complications of Intracranial Haemorrhage ?

A

MASS EFFECT :
- effacement of ventricles
- Displacement of ventricles
- Midline shift
- Twisted ventricle
- Hydrocephalus
- Cerebral herniation (subfalcine, uncal, tenting, coning)
- Raised ICP

58
Q

Mass effect and midline shift in intracerebral haemorrhage ( lots of detail but think seeing images helpful to get an idea of what looks like)

A
59
Q

What complication of intracerebral haemorrhage does this depict?

A
60
Q

What complications of intracerebral haemorrhage does this depict?

A
61
Q

What complications of intracerebral haemorrhage does this depict?

A
62
Q

What does this depict?

A

Cerebellar haemorrhage on unenhanced CT

63
Q

Explain what makes up cerebral perfusion?

A
64
Q

What is an elevated ICP?

A

e.g with mass lesion / mass effect

Elevated = >20 mmHg

65
Q

For intracranial pressure monitoring what BP / ICP and CCP (cerebral perfusion pressure) is ideal / aim for?

A

Rule of thumb:

  • BP less than 130 mm Hg (to reduce bleeding) but above 90 to maintain CPP

-ICP less than 20 mm Hg

  • Ensure CPP is >70 mm Hg (if below brain will usffer iscahemic injury)
66
Q

Outline the membranes that surround the brain

A
67
Q

Diagnosis?
Presentation?
Pathophysiology?

A

Diagnosis:
- Extradural / epdiural haematoma
- Bi- convex (lemon shape) as blood spread is limited by sutures of brain, appears hyperdense

Presentation:
- Young men
- trauma - 90% have skull fracture - examine for closely
- LOC, consciousness, LOC (lucid intervals)

Pathophysiology:
- Blood collects between periosteum of blood inner table of bone and inner layer of dura
- often middle meningeal artery

68
Q

Diagnosis ?
Presentation ?
Pathophysiology?

A

Diagnosis:
- Actue (L) and chronic (R) subdural haemorrhage
- concave, cross suture lines, hyperdense

Presentation:
- elderly
- trauma

Pathophysiology:
- Blood collection between arachnoid and dura
- Torn bridging veins
- brain atrophy

69
Q

Diagnosis ?
Presentation?

A

Diagnosis:
Subarachnoid haemorrhage

Presentation:
- older pt
- HTN
- smoker
- thunderclap headache
- nausea and vomiting
- LOC

Pathophysiology:
- arteriovenous malformations
- berry aneurysm

70
Q

Is MRI helpful in Intracerebral haemorrhage?

A

Not practical in hyperacute / acute pt as the first way to diagnose a pt. Acute bleed - CT

MRI good for:
- Identifying underlying causes
- Great at ageing bleeds to see if subacute / chronic
- seeing haemorrhage transformation of an infarct (diffusion weighted imaging)

71
Q

How do Saccular aneurysms (berry aneurysms) develop?

A
  • Aneurysms develop due to pressures on the arterial wall (vessels in subarachnoid space)
  • Usually at bifurcation points
  • Large cerebral arteries in anterior circle of Willis most affected
  • Intracranial arteries lack external elastic lamina and have thin adventitia
  • Small aneurysms(<5mm) unlikely to rupture

Risk factors for developing aneurysms (not conclusive)
Same as cardiovascular- hypertension, smoking etc
Alcohol++, APDK

72
Q

investigations for suspected subarachnoid haemorrhage?

A

Imaging:
- 1st line- CT scan (catch 93% w/in 24 hrs of bleed)

Other:
- lumbar puncture (hx suggests but CT negative)
wait 6 hours (12+ is preferable)- for lysis of RBC (Xanthochromia)
CSF: high protein, WCC not raised, glucose normal

Once diagnosis confirmed:
- Angiography is performed to confirm location of aneurysm

73
Q

Management of subarachnoid haemorrhage?

A
  • A- E - airway support?
  • cardiovascular monitoring
  • CCB e.g. Nimodipine (to prevent vasospasm and secondary ischaemia)

Surgery:
- pts w/ good neurological status within 72 hours -to prevent re-bleeding
- Clipping (surgeons) clamp neck of aneurysm (with spring clip)
- Coiling (neuro-radiologists) insertion of wire into aneurysm sac which causes thrombosis of blood within aneurysm

74
Q

Appearance of blood on MRI in T1 vs T2 over time
Acute, subacute, chronic
(taken image from a youtube tutorial link included, quicker way than the PP which was very long and convoluted)

A

https://www.youtube.com/watch?v=DdPRfPm9SI4&t=3043s

YEAR 4 OLDER PEOPLE INTEGRATED CARE (21 decks)

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