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YEAR 4 OLDER PEOPLE INTEGRATED CARE > Stroke presentations, assessment, management > Flashcards

Stroke presentations, assessment, management Flashcards

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1
Q

What is a stroke?

A

Sudden onset focal neurological deficit of vascular aetiology with symptoms lasting >24 hours (or with evidence of infarction on imaging)

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2
Q

Ischaemic vs haemorrhagic stroke?

A

85% strokes are ischaemic- when blood supply in cerebral vascular territory if reduced secondary to stenosis or complete occlusion of cerebral artery

15% stroke haemorrhagic- weakening of cerebral vessels leading to cerebral vessel rupture and haematoma formation- 3/4 of haemorrhagic strokes being intracerebral and the rest being subarachnoid

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3
Q

Stroke epidemiology?

A

110,000 first strokes/year
30,000 recurrent strokes/year
25% of strokes occur in under 65s

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4
Q

Prognosis after stroke?

A

20-30% die within a month
Accounting for 12% of all deaths
Leading cause of acquired disability

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5
Q

Types of Ischaemic stroke?

A

Thrombotic- thrombosis from larger vessel
Embolic- AF imp cause of this
Hypoxic

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6
Q

Types of haemorrhagic stroke?

A

Intracerebral
Subarachnoid

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7
Q

Ischaemic stroke RF?

A

Age
Hypertension
Smoking
Hyperlipidaemia
Male
DM
AF
Oestrogen containing therapies
Obesity

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8
Q

Rarer causes of Ischaemic stroke?

A

Primary vascular causes- vasculitis or aortic dissection
Haemotalogical causes- prothrombotic state e.g. pregnancy, factor V leiden

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9
Q

Ischaemia vs infarction?

A

Ischaemia- condition where insufficient blood flow (to the brain) to meet metabolic demands –> poor oxygen supply or cerebral hypoxia–> can lead to INFARCTION (death of the brain tissue)

Ischaemia- reversible
Infarction- irreversible

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10
Q

How does ischaemia turn to infarction?

A

1) tissue hypo perfusion- dysfunction
2) Early and reversible failure of the Na+ K+ pump- cerebral oedema
3) Irreversible tipping point reached–> sudden influx of Na+ ions–> cytotoxic oedema
4) BBB opens for macromolecules- vasogenic oedema
5) BBB opens for RBC’s–> haemorrhage into infarct

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11
Q

What is TIA

A

Transient ischaemic attack

Brief episode of neurological dysfunction causes by focal brain and/or retinal ischaemia with clinical symptoms <24 hours but typically lasting < 1hours and without evidence of acute infarction

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12
Q

What is a hyper acute infarct

A

the first 6 hours post symptoms

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13
Q

What classification is used for stroke?

A

Bamford/Oxford

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14
Q

What is a TACI (total anterior circulation infarct)?

A

Involves middle and ant cerebral arteries

Contralateral hemiparesis and/or hemisensroy loss of the face, arm, leg
AND
Contralateral homonymous hemianopia
AND
Higher cerebral dysfunction e.g. dysphasia/neglect

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15
Q

What is a PACS (partial anterior circulation stroke)

A

Involves smaller arteries of ant circulation e.g. upper or lower divisons of middle cerebral artery
2 of:

Contralateral hemiplegia or hemiparesis
Contralateral homonymous hemianopia
Higher cerebral dysfunction e.g. dysphasia

OR

higher cerebral dysfunction alone

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16
Q

What is a LACI?(lacunar infarct)

A

Pure motor or
Pure sensory or
Sensorimotor stroke or
Ataxic hemiparesis

NO Visual field defect, NO higher cerebral dysfunction and NO brainstem dysfunction

( occlusion of small penetrating arteries in the deep cerebral white matter (non cortical) that provide blood to the brain’s deep structures )

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17
Q

Where does a LACI affect?

A

Small, deep perforating arteries typically supplying internal capsule or thalamus

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18
Q

What is POCI? (posterior circulation infarct)

A

Involves vertebrobasilar arteries

Cerebelle dysfunction OR
Conjugate eye movement OR
Bilateral motor/sensory deficit OR
Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit OR
cortical blindness/isolated heminanopia

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19
Q

What does the ophthalmic artery supply?

A

Structures in the orbit as well as some structures in the nose, face and meninges

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20
Q

What does the posterior communicating artery supply?

A

Anteriorly connect ICA prior to terminal bifurcation of the ICA into the anterior cerebral artery and middle cerebral artery

Posteriorly communicates with the posterior cerebral artery

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21
Q

What does the anterior cerebral artery supply?

A

Supplies oxygenated blood to most midline portions of frontal lobes and superior medial parietal lobes

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22
Q

What is lateral medullary syndrome?

A

Posterior inferior cerebellar artery aka Wallenbergs syndrome

Ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horners
Contralateral: limb sensory loss

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23
Q

What is Weber’s syndrome?

A

Ipsilateral III palsy
Contralateral weakness

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24
Q

How does basilar artery occlusion present?

A

Locked in syndrome, Loss of consciouness, or sudden death

25
Q

Pt presents with:
contralateral hemiparesis and sensory loss
Lower extremities affected more than the upper

Wheres the lesion?

A

Anterior cerebral artery

26
Q

Pt presents with:
Contralateral hemiparesis and sensory loss
Upper extremities affected more than lower
Contralateral homonymous hemianopia
Aphasia

Where’s the lesion?

A

Middle cerebral artery

27
Q

Pt presents with:

Contralateral homonymous hemianopia WITH macular sparing
Visual agnosia

Where’s the lesion?

A

Posterior cerebral artery

28
Q

Pt presents with:

Amaurosis fugax

Where’s the lesion?

A

Retinal/opthalmic artery

29
Q

Immediate management of pt in ED with ?stroke

A

A-E assessment
Exclude hypoglycaemia
ROSIER score: >0 stroke is likely
Non-contrast CT

30
Q

What is the ROSIER score?

A

Loss of consciousness or syncope: - 1 point
Seizure activity: - 1 point
New, acute onset of:
* asymmetric facial weakness: + 1 point
* asymmetric arm weakness: + 1 point
* asymmetric leg weakness: + 1 point
* speech disturbance: + 1 point
* visual field defect: + 1 point

Stroke likely if >0

31
Q

What are we looking for in Non-contrast CT?

A

Is it ischaemic or haemorrhagic (or more rarely a tumour)

In an acute ischameic stroke:
* areas of low density in the grey and white matter of the territory (may take some time to develop)
* ‘Hyperdense artery’ sign- corresponding with the responsible arterial clot- tends to be visible immediately

Acute Haemorrhagic stroke
* typically shows hyperdense material (blood) surrounded by low density oedema

32
Q

When do you give thrombolysis with alteplase?

A

Administered within 4.5 hours of onset of stroke symptoms
Haemorrhage has definitely been excluded

33
Q

In an A-E assessment of stroke, what parameters do you need to aim for?

A

Blood glucose, hydration, o2 sats and temp- all should be maintained within normal limits
BP should NOT be lowered in the acute phase unless there are complications e.g. hypertensive encephalopathy

34
Q

ABSOLUTE contraindications to thrombolysis?

A

-Previous intracranial haemorrhage
- Seizure at onset of stroke
- Intracranial neoplasm
- Suspected subarachnoid haemorrhage
- Stroke or traumatic brain injury in preceding 3 months
- Lumbar puncture in preceding 7 days
- Gastrointestinal haemorrhage in preceding 3 weeks
- Active bleeding
- Pregnancy
- Oesophageal varices
- Uncontrolled hypertension >200/120mmHg

35
Q

RELATIVE contraindications to thrombolysis?

A
  • Concurrent anticoagulation (INR >1.7)
  • Haemorrhagic diathesis
  • Active diabetic haemorrhagic retinopathy
  • Suspected intracardiac thrombus
  • Major surgery / trauma in the preceding 2 weeks
36
Q

When should you offer a mechanical thrombectomy?

A

ASAP within 6hrs of symptoms onset, with IV thrombolysis (if within 4.5 hrs), to people who have:
* Acute ischaemic stroke AND
* Confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA

ASAP to people who were last known to be well between 6hrs- 24hrs previously (incl wake up strokes)
* Confirmed occlusion of proximal anterior circulation demonstrated by CTA or MRA and
* If there is potential to salvage brain tissue, as shown by CT perfusion or diffusion weighted MRI sequences showing limited infarct core volume

37
Q

When should you consider a thrombectomy with IV thrombolysis (if within 4.5hrs)?

A

People last known to be well up to 24 hours previously
* Who have ischaemic stroke and confirmed occlusion of proximal posterior circulation (that is basilar or posterior cerebral artery) demonstrated by CTA or MRA AND
* potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion weighted MRI sequences showing limited infarct core volume

38
Q

What is the role of aspirin in stroke management?

A

Aspirin 300mg orally or rectally should be given as soon as possible if a haemorrhagic stroke has been excluded

39
Q

Pt presents to ED within 2 hours of symptom onset, CT head is done which confirms ischaemic stroke, what are the next steps?

A

300mg oral or rectal aspirin
IV thrombolysis with alteplase
CTA/MRA- determine whether this is a candiate for mechanical thrombectomy

40
Q

Secondary prevention of stroke?

A
  • Clopidogrel 75mg once daily for long-term therapy- aspirin + modified release dipyridamole should only be used if clopidogrel is contraindicated/not tolerated
  • If pt has AF- DOACs should not be started until 14 days after inset of ischaemic stroke
  • If cholesterol is >3.5mmol/l pts should be commenced on a statin- usually 48hours after
  • Offer smoking cessation support
  • Pts screened for diabetes + managed
  • Carotid artery endarterectomy- if pt suffered stroke or TIA in the carotid territory and not severely disabled–> only considered if carotid stenosis > 70% according European Carotid Surgery Trialists or > 50% North American Symptomatic Carotid Endarterectomy Trial
41
Q

What post-acute investigations would you do in a pt with ischaemic stroke

To work out the cause

A
  • carotid USS- identify critical carotid artery stenosis
  • CTA/MRA- identify affected vessel and any possible stenosis
  • ECG- if cardioembolic source suspected
  • Young pts- vasculitis or thrombophilia screen may be necessary
42
Q

Post acute investigations for haemorrhagic stroke?

A

serum tox screen- sympathomimetic drugs e.g. cocaine are a strong RF for haemorrhagic stroke

43
Q

Importance of fluid management in stroke managment?

A

Hypovolaemia:
can worsen the ischaemic penumbra
Increase risk of infection, DVT, constipation and delirium

Over hydration:
cerebral oedema
cardiac failure
hyponatraemia

44
Q

Fluid managment recommendations for stroke pts?

A

Oral hydration in pts with a safe swallow
If not IV hydration may be necessary- isotonic saline without dextrose
Ensure you take electrolyte disturbances and CVS status when prescribing fluids

45
Q

What is the importance of monitoring BM post stroke?

A

Post stroke, pts with hyperglycaemia have increased mortality independent from age and severity
* likely due to increased tissue acidosis from anaerobic metabolism, free radical generation, and increased BBB permeability

46
Q

How to manage diabetic pts blood sugar post stroke?

A

Optimise insulin treatment using IV insulin and glucose infusions
Hypoglycaemia needs to be managed appropriately as well as can mimic neuronal injury

47
Q

When should anti- hypertensives be used for BP control in pts post- ischaemic stroke?

A

Hypertensive emergency:
* hypertensive encephalopathy
* hypertensive nephropathy
* hypertensive cardiac failure/MI
* aortic dissection
* pre-eclampsia/eclampsia

If treatment is needed, lower BP by approximately 15% in first 24 hours after stroke onset
Can use IV labetalol, nicardipine and clevidipine as first line agents, due to possibility for rapid and safe titration and to control BP

48
Q

What is the required BP for thrombolytic treatment?

A

185/110 or lower
after thrombolytic therapy, BP should be stabilised and maintained at or below 180/105mmHg for at least 24 hours after treatment

49
Q

Why does BP not need to be lowered unless it’s an emergency in stroke pts?

A

This is because lowering BP too much can potentially compromise collateral blood flow to the affected region and increase time to complete and irreversible tissue infarction

50
Q

How do we assess feeding after a stroke?

A
  • screen for safe swallow prior to ANY oral intake- reduces risk of aspiration and subsequent complications
  • any concerns about swallow: specialist assessment 24 hours of admission and not greater than 72 hours, prior to assessment pt should remain NBM
51
Q

How do you manage stroke pt with unsafe swallow?

A

NG tube within 24 hours of admission, unless they have had thrombolytc therapy
NG tube not tolerated- pts should be considered for a nasal bridle tube/gastrostomy
Assess meds if there is NG formulations or may need to prescribe IV or SC

52
Q

How is disability post stroke measured?

A

In terms of functional status- basic ADLS
Barthel Index

The Barthel Index (BI) measures the extent to which somebody can function independently and has mobility in their activities of daily living (ADL) i.e. feeding, bathing, grooming, dressing, bowel control, bladder control, toileting, chair transfer, ambulation and stair climbing.

53
Q

Outline the Barthel Index?

A

Describes 10 tasks, and is scored according to amount of time or assistance required by the patient for each given task

Tasks: feeding, moving from wheelchair to bed, personal toileting, getting on/off toilet, bathing, walking on level surface, ascending/descending stairs, dressing, controlling bowels and controlling bladder

The total score is from 0 to 100, with 0 being completely dependent, and 100 being completely independent

54
Q

Clinical features of TIA?

A

Similar to stroke
Sudden onset, focal neurological deficit, resolves typically within an hour

  • unilateral weakness or sensory loss
  • aphasia or dysarthria
  • ataxia, vertigo or loss of balance
  • visual problems- amaurosis fugax, diplopia, homonymous heminanopia
    *
55
Q

Managment for pts with TIA

A

give 300mg aspirin immediately unless
1) pt has bleeding disorder or on anticoagulant
2) pt already taking low dose aspirin regularly- continue the current dose until reviewed
3) apirisn is contraindicated

Clopidogorel long-term first line (aspirin and dipyridamole if not tolerated)
Carotid artery endarterectomy if stroke/TIA in the carotid territory adn are not severely disabled (only consider if carotid stenosis >70% or >50% depending on the source you read)

56
Q

When do you refer TIA patient to specialist?

A

if the patient has had more than 1 TIA (‘crescendo TIA’) or has a suspected cardioembolic source or severe carotid stenosis:
discuss the need for admission or observation urgently with a stroke specialist

If the patient has had a suspected TIA in the last 7 days:
arrange urgent assessment (within 24 hours) by a specialist stroke physician

if the patient has had a suspected TIA which occurred more than a week previously:
refer for specialist assessment as soon as possible within 7 days

Advise the person not to drive until they have been seen by a specialist.

57
Q

What imaging should you do in a TIA?

A

CT brain should NOT be done unless clinical suspicion of an alternative diagnosis that CT could detect

MRI (including diffusion-weighted and blood-sensitive sequences) is preferred to determine territory of ischaemia, or to detect haemorrhage or alt patholgies- same day as specialist assessment

Urgent carotid doppler to rule out atherosclerosis in carotid artery as source of emboli, UNLESS pt is not suitable for carotid endartectomy

58
Q

From BB

what clinical signs would you expect when examining a pt who has had a posterior circulation infarct?

A
  • motor and /or sensory deficit bilaterally or associated with cranial nerve defect on the opposite side
  • homonymous hemianopia or new diplopia
  • ataxia and other cerebellar signs
  • higher cerebral signs normal or reduced GCS

YEAR 4 OLDER PEOPLE INTEGRATED CARE (21 decks)

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