stroke + TIA Flashcards

1
Q

definition

A

sudden onset

focal neuro deficit

vascular lesion in origin

lasting >24hrs

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2
Q

epidemiology

A

1/1000 per yr [falling due to improvement in rx]

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3
Q

pathogenesis

A

85% due to ischemia causing INFARCTION

15% due to intracerebral HEMORRHAGE

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4
Q

types of stroke

A

There are two main types of strokes:

1. ischaemic: these can be further subdivided between into episodes which last:

  • greater than 24 hours (termed an ischaemic stroke)
  • episodes where symptoms and signs last less than 24 hours (transient ischaemic attacks, TIAs, sometimes termed ‘mini-strokes’ by patients)

2. haemorrhagic

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5
Q

s/s

A

Stroke is defined by the World Health Organization as a clinical syndrome consisting of ‘rapidly developing clinical signs of focal (at times global) disturbance of cerebral function, lasting more than 24 hours or leading to death with no apparent cause other than that of vascular origin’. In contrast, with a TIA the symptoms and signs resolve within 24 hours.

Features include:

  • motor weakness
  • speech problems (dysphasia)
  • swallowing problems
  • visual field defects (homonymous hemianopia)
  • balance problems

Cerebral hemisphere infarcts may have the following symptoms:

  • contralateral hemiplegia: initially flaccid then spastic
  • contralateral sensory loss
  • homonymous hemianopia
  • dysphasia

Brainstem infarction

  • may result in more severe symptoms including quadriplegia and lock-in-syndrome

Lacunar infarcts

  • small infarcts around the basal ganglia, internal capsule, thalamus and pons
  • this may result in pure motor, pure sensory, mixed motor and sensory signs or ataxia
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6
Q

how are strokes classified

A

One formal classification system that is sometimes used is the Oxford Stroke Classification (also known as the Bamford Classification), whichclassifies strokes based on the initial symptoms. A summary is as follows:

The following criteria should be assessed:

  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
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7
Q

can you tell from the symptoms if the stroke is hemorrhagic or ischemic?

A

Whilst symptoms alone cannot be used to differentiate haemorrhagic from ischaemic strokes, patients who’ve suffered haemorrhages are more likely to have:

  • decrease in the level of consciousness: seen in up to 50% of patients with a haemorrhagic stroke
  • headache is also much more common in haemorrhagic stroke
  • nausea and vomiting is also common
  • seizures occur in up to 25% of patients
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8
Q

what is the public health campaign related to stroke

A

Over recent years there has been a public health campaign to raise awareness of stroke symptoms. The FAST campaign uses the following mnemonic:

  • Face - ‘Has their face fallen on one side? Can they smile?’
  • Arms - ‘Can they raise both arms and keep them there?’
  • Speech - ‘Is their speech slurred?’
  • Ttime - ‘Time to call 999 if you see any single one of these signs.’
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9
Q

Investigations

A

Patients with suspected stroke need to have emergency neuroimaging.

The main cause for urgency is to see whether a patient may be suitable for thrombolytic therapy to treat early ischaemic strokes.

The two types of neuroimaging used in this setting [within 1 hour] are:

  1. CT
  2. MRI

brain imaging should be performed immediately (ideally the next slot and definitely within 1 hour, whichever is sooner) for people with acute stroke if any of the following apply:

indications for thrombolysis or early anticoagulation treatment

  • on anticoagulant treatment
  • a known bleeding tendency
  • a depressed level of consciousness (Glasgow Coma Score below 13)
  • unexplained progressive or fluctuating symptoms
  • papilloedema, neck stiffness or fever
  • severe headache at onset of stroke symptoms

for all people with acute stroke without indications for immediate brain imaging, scanning should be performed as soon as possible (within a maximum of 24 hours after onset of symptoms)

~~~~~~~

The objectives of identifying stroke risk factors are:

  1. to identify specific pathophysiological subtypes of cerebral infarction with different management and prognosis
  2. to ascertain specific risk factors and their possible prevention

Investigations that might contribute to these goals include:

  • chest X-ray - cardiac enlargement in hypertension or valvular disease
  • retinal examination - retinopathy in hypertension, embolic disease
  • ECG - ventricular enlargement and/or arrhythmias in hypertensive/embolic disease; recent MI in embolic disease; conduction defect - embolic / output failure
  • blood glucose - for hyperglycaemia in diabetes mellitus
  • serum cholesterol and lipids - hyperlipidaemia in patients under 65 years
  • ESR, auto-antibodies - for vasculitis, collagen vascular disease
  • full blood count - for polycythaemia, thrombocytopenia
  • urine analysis - polyarteritis, thrombocytopenia
  • other haematological tests as indicated - e.g. neurosyphilis
  • cervical spine X ray - for atlanto-axial subluxation
  • note drug history - oral contraceptives, amphetamines, opiates

Further investigations as indicated:

  • blood culture - if suspected infective endocarditis
  • sickle cell screen, plasma electrophoresis, viscosity studies
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10
Q

Selected points relating to the management of acute stroke include:

A
  • blood glucose, hydration, oxygen saturation and temperature should be maintained within normal limits
  • blood pressure should not be lowered in the acute phase unless there are complications e.g. Hypertensive encephalopathy*
  • aspirin 300mg orally or rectally should be given as soon as possible if a haemorrhagic stroke has been excluded
  • with regards to atrial fibrillation, the RCP state: ‘anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke’
  • if the cholesterol is > 3.5 mmol/l patients should be commenced on a statin. Many physicians will delay treatment until after at least 48 hours due to the risk of haemorrhagic transformation

Thrombolysis

  • Thrombolysis should only be given if:
  • it is administered within 4.5 hours of onset of stroke symptoms (unless as part of a clinical trial)
  • haemorrhage has been definitively excluded (i.e. Imaging has been performed)
  • Alteplase is currently recommended by NICE.
  • Contraindications to thrombolysis attached as picture
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11
Q

Acute management: ABC

A

1. Airways/Breathing: protect – prevent hypoxia and aspiration

2. Circulation:
o Pulse (AF)
o BP: Rx severe HTN can → ↓ cerebral perfusion

  1. Disability/don’t forget glucose:

o Blood glucose: hypoglycaemia  N.B. aim: 4-11mmol/L – Rx sliding scale

  1. Imaging:
    o Urgent CT/MRI: thrombolysis
     Diffusion-weighted MRI is most sensitive for acute infarct
     CT will exclude primary haemorrhage
  2. Thrombolysis: onset <4.5h (onset of symptoms)
    o Alteplase (rh-tPA) IV 0.9mg/kg
    o → ↓ death and dependency (OR 0.64)
    o CT 24h post-thrombolysis to look for haemorrhage
  3. Nil by mouth: choking risk – IVI hydration
  4. Antiplatelet agents: Aspirin 300mg (+PPI) – once haemorrhagic stroke ruled out.
    o Clopidogrel if aspirin CI
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12
Q

2ry prevention

A

Recommendations from NICE include:

  • clopidogrel is now recommended by NICE ahead of combination use of aspirin plus modified release (MR) dipyridamole in people who have had an ischaemic stroke
  • aspirin plus MR dipyridamole is now recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated, but treatment is no longer limited to 2 years’ duration
  • MR dipyridamole alone is recommended after an ischaemic stroke only if aspirin or clopidogrel are contraindicated or not tolerated, again with no limit on duration of treatment

With regards to carotid artery endarterectomy:

  • recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled
  • should only be considered if carotid stenosis > 70% according ECST** criteria or > 50% according to NASCET*** criteria

~~~~~~~~~~~~~~~~~~~~~~~~~

Primary Prevention (pre-stoke)

 Control RFs: HTN, ↑ lipids (statin ↓ risk 17%), DM, smoking, cardiac disease

 Exercise: ↑ HDL, ↑glucose tolerance

 Folate supplements: ↓ plasma homocysteine

 Smoking cessation

 life-long anticoagulation: consider in AF (use CHADS2)

Secondary Prevention (prevent stroke)
 Risk factor control as above
o Start anti-hypertensives and statin

 Antiplatelet therapy: Aspirin / clopi 300mg for 2wks after stroke then either
o Clopidogrel 75mg OD (preferred option)
o Aspirin 75mg OD + dipyridamole MR 200mg BD

 Anticoagulation: Warfarin instead of aspirin/clopidogrel if
o Cardioembolic stroke or chronic AF
o Start from 2wks post-stroke (INR 2.5-3.5)
o Don’t use aspirin and warfarin together.

 Carotid endarterectomy if good recovery + ipsilat stenosis ≥70%

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13
Q

Management

Ischaemic strokes

A

Urgent neuroimaging classifies the stroke as either ischaemic or haemorrhagic.

If the stroke is ischaemic, and certain criteria are met, the patient should be offered thrombolysis.

Example criteria include:

  • patients present with 4.5 hours of onset of stroke symptoms
  • the patient has not had a previous intracranial haemorrhage, uncontrolled hypertension, pregnant etc

Once haemorrhagic stroke has been excluded patients should be given aspirin 300mg as soon as possible and antiplatelet therapy should be continued.

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14
Q

Transient ischaemic attacks

A

Remember with TIAs the, by definition, symptoms last less than 24 hours although in the vast majority of cases the duration is much shorter, typically 1 hour or so. For this reason most patients symptoms will have resolved before they see a doctor.

The ABCD2 prognostic score has previously been used to risk stratify patients who present with a suspected TIA. However, data from studies have suggested it performs poorly and it is therefore no longer recommended by NICE Clinical Knowledge Summaries. Instead, NICE recommend:

Immediate antithrombotic therapy:

give aspirin 300 mg immediately, unless contraindicated e.g. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)

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
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15
Q

management: Haemorrhagic strokes

A

If imaging confirms a haemorrhagic stroke neurosurgical consultation should be considered for advice on further management.

The vast majority of patients however are not suitable for surgical intervention.

Management is therefore supportive as per haemorrhagic stroke.

  • Anticoagulants (e.g. warfarin) and antithrombotic medications (e.g. clopidogrel) should be stopped to minimise further bleeding.
  • If a patient is anticoagulated this should be reversed as quickly as possible.
  • Trials have shown improved outcomes in patients who have their blood pressure lowered acutely and this is now part of many protocols for haemorrhagic strokes.
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16
Q

stroke by anatomy: Anterior cerebral artery

A

Contralateral hemiparesis and sensory loss, lower extremity > upper

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17
Q

stroke by anatomy: Middle cerebral artery

A

Contralateral hemiparesis and sensory loss, upper extremity > lower

Contralateral homonymous hemianopia
Aphasia

18
Q

stroke by anatomy: Posterior cerebral artery

A

Contralateral homonymous hemianopia with macular sparing

Visual agnosia

19
Q

stroke by anatomy: Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain)

A

Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity

20
Q

stroke by anatomy: Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)

A

Ipsilateral: facial pain and temperature loss

Contralateral: limb/torso pain and temperature loss

Ataxia, nystagmus

21
Q

stroke by anatomy: Anterior inferior cerebellar artery (lateral pontine syndrome)

A

Symptoms are similar to Wallenberg’s (see above),

but:
Ipsilateral: facial paralysis and deafness

22
Q

stroke by anatomy: Retinal/ophthalmic artery

A

Amaurosis fugax

23
Q

stroke by anatomy: Basilar artery

A

‘Locked-in’ syndrome

[pt is cognively intact but completely paralysed except for eye muscles]

24
Q

stroke by anatomy: Lacunar strokes

A

present with either isolated hemiparesis, hemisensory loss or hemiparesis with limb ataxia

strong association with hypertension

common sites include the basal ganglia, thalamus and internal capsule

25
Q

stroke: assessment [ROSIER SCORE]

A

The FAST screening tool (Face/Arms/Speech/Time) is widely known by the general public following a publicity campaign. It has a positive predictive value of 78%.

A variant of FAST called the ROSIER score is useful for medical professionals. It is validated tool recommended by the Royal College of Physicians.

ROSIER score

Exclude hypoglycaemia first, then assess the following:

26
Q

complications

A
  • Aspiration pneumonia
    • Pressure sores
    • Contractures
    • Urinary or Faecal incontinence
    • Constipation
    • Depression
27
Q

Rehabilitation: MENDS

A

🍰 MDT: physio, SALT, dietician, OT, specialist nurses, neurologist, family

🍰 Eating
o Screen swallowing: refer to specialist
 Avoid NG/PEG: only w/ severe dysphagia
o Screen for malnutrition (MUST tool)
 Supplements if necessary

🍰 Neurorehab: physio and speech therapy
o Botulinum can help spasticity

🍰 DVT Prophylaxis

🍰 Sores: must be avoided @ all costs

🍫 Depression: TCA or SSRI

Occupational Therapy
 Impairment: e.g. paralysed arm
 Disability: e.g. inability to write
 Handicap: e.g. can’t work as accountant
 OT aims to minimise disability and abolish handicap

28
Q

prognosis

A

10% recurrence

  • - PACS

 20% mortality
 1/3 of survivors independent
 2/3 of survivors dependent

  • - TACS is much worse

 60% mortality
 5% independence

29
Q

ddx of stroke

A
  • Head injury ± haemorrhage
    • ↑↓ glucose
    • SOL
    • Hemiplegic migraine
    • Todd’s palsy
      • = a post-ictal - post-seizure - focal neurologic deficit which following a series of seizures, is characterised by persistent weakness - for several hours or longer - at the affected site.
      • t may occur in association with hemiplegia in which seizures often accompany the outset.
      • It is often confused with a cerebrovascular event.
    • Infections: encephalitis, abscesses, Toxo, HIV, HTLV
    • Drugs: e.g. opiate overdose
30
Q

TIA: define

A
  • Sudden onset focal neurological deficit lasting <24h due to temporary occlusion of part of the cerebral circulation
  • ~15% of 1st strokes are preceded by TIAs
31
Q

TIA: epidemiology

A
  • Incidence: 0.4/1000/yr
  • 15% of 1 st strokes were preceded by TIA
32
Q

TIA: aetiology

A
  • Atherothromboembolism: from carotids is main cause
  • Cardioembolism: post-MI, AF, valve disease
  • Hyperviscosity: polycythaemia, SCD, myeloma
  • vasculitis: SLE, PAN, syphilis
33
Q

TIA: s/s

A

Signs of a TIA
 Symptoms usually brief
 Global events (e.g. syncope, dizziness) are not typical
 Signs mimic those of CVA in the same arterial territory
 Amaurosis fugax: emboli pass to the retinal artery – loss of
vision in one eye ‘like a curtain descending’
 limb shaking TIA

34
Q

TIA: signs of causes

A

Signs of Causes
 Carotid bruits – N.B. stenosis may = no bruit
 ↑BP
 Heart murmur – valve disease
 AF
 funduscopy: emboli in retinal artery

35
Q

TIA: assessment + referral

A

The ABCD2 prognostic score has previously been used to risk stratify patients who present with a suspected TIA. However, data from studies have suggested it performs poorly and it is therefore no longer recommended by NICE Clinical Knowledge Summaries. Instead, NICE recommend:

Immediate antithrombotic therapy:

give aspirin 300 mg immediately, unless

  1. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage)
  2. the patient is already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist
  3. Aspirin is contraindicated: discuss management urgently with the specialist team

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.

36
Q

TIA: ix

A

Aim to find cause and define vascular risk

  • Bloods: FBC, U&E, ESR glucose, lipids
  • Imaging:
  •  CXR
  •  ECG
  •  Echo
  •  Carotid doppler ± angiography
  •  Consider brain imaging

o Diffusion weighted MRI is best

37
Q

TIA: mx

[ACAS]

A

ACAS

 Time to intervention is crucial (Reduction of risk of stroke)
o Intervention w/i 72hrs (2% strokes @ 90d)
o Intervention w/i 3wks (10% strokes @ 90d)

 Avoid driving for 1mo – must inform DVLA if multiple attacks in short period

  1. Antiplatelet Therapy / Anti-coagulate
     clopidogrel 75mg/d
    o MOA: inhibits platelet aggregation
     Aspirin 300mg/d for 2wks  75mg/d
     Add dipyridamole MR to aspirin
    o MOA: ↑cAMP and ↓ thromboxane A2
     Warfarin if cardiac emboli: AF, MI, MS
  2. Control Cardiac Risk Factor
     BP (aim: <140/85mmHg), lipids, DM, smoking
     Exercise
     Diet: ↓ salt
  3. Assess risk of subsequent stroke
     ABCD2 score
  4. Specialist referral to TIA clinic
     ABCD2 ≥4: w/i 24hrs
     ABCD2 <4: w/i 1wk

Carotid Endarterectomy
 Beneficial if ≥70% symptomatic stenosis (internal carotid arteries)
 50-70% stenosis may benefit if operative risk is <3%
 Surgery should be performed w/i 2wks of 1 st presentation
 Endovascular carotid artery stenting is an alternative, but safety and long-term benefits (in-stent restenosis is common) are still
under Ix.
 Major complications are stroke and death.

38
Q

ABCD2 Score

A

 Predicts stroke risk following TIA

39
Q

TIA: prog

A

Combined risk of stroke and MI is ~9%/yr
- 3x ↑ in mortality cf TIA-free populations

40
Q

TIA: ddx

A

Vascular: CVA, migraine aura, retinal bleed

  • Focal Epilepsy
  • Hyperventilation
  • Hypoglycaemia
  • Malignant HTN
  • pheochromocytoma
  • MS
  • peripheral neuropathy
  • intracranial tumour
  • somatization