stroke Flashcards

1
Q

what is a stroke

A

Strokes result from ischaemic infarction or bleeding into part of the brain, manifest
by rapid onset (eg seconds–minutes) of focal CNS signs and symptoms. It is the major
neuro log ical disease of our time. Mortality after 1st stroke: 12% by day 56 (UK data;
was 21% in 1999). Incidence is falling too (now 1/1000/yr, perhaps due to a more
vigorous approach to risk factors in primary care, ie statin use and control of BP).

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2
Q

stroke modifyable risk factors

A

BP increase, smoking, DM, heart disease (valvular, ischaemic, AF),
peripheral vascular disease, past TIA, increased PCV, carotid bruit, the Pill, high lipids, high alcohol use,
high clotting (eg high plasma fi brinogen, low antithrombin III, p368), high homocysteine, syphilis

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3
Q

stroke signs

A

Sudden onset, maybe with further progression over hours (rarely days). In
theory, focal signs relate to distribution of the aff ected artery (p452), but collaterals
cloud the issue. Pointers to bleeding (unreliable!): Meningism, severe headache,
and coma within hours. Pointers to ischaemia: Carotid bruit, AF, past TIA, IHD.

• Cerebral infarcts: (50%) Depending on site there may be contralateral sensory loss
or hemiplegia—initially fl accid (fl oppy limb, falls like a dead weight when lifted),
becoming spastic (UMN); dysphasia; homonymous hemianopia; visuo-spatial defi cit.

• Brainstem infarcts: (25%) Wide range of eff ects, which include quadriplegia, disturbances
of gaze and vision, locked-in syndrome (aware, but unable to respond).

• Lacunar infarcts: (25%) In basal ganglia,3 internal capsule, thalamus, and pons. 5
syndromes: ataxic hemiparesis, pure motor, pure sensory, sensorimotor, and dysarthria/
clumsy hand. Cognition/consciousness are intact except thalamic stroke.

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4
Q

stroke - action to take in first hour

A

Action (1st hr; see p476–7 for later) Protect the airway to avoid hypoxia/aspiration.

 Pulse, BP and ECG: Is it an embolus from AF? NB: treating even very high BPs may
harm (unless there is encephalopathy, or aortic dissection): even a 20% fall may
compromise cerebral perfusion, as autoregulation is impaired. If on HRT, stop it.

 Blood glucose: If low, see p844. Aim for 4–11 mmol/L. Sliding scale (p591) if DM.

 Urgent CT/MRI if: Thrombolysis considered, cerebellar stroke (cerebellar haematomas
may need urgent referral for evacuation),92 unusual presentation (alternative
diagnosis likely?—BOX), or high risk of haemorrhage (GCS, signs of ICP, severe
headache, meningism, progressive symptoms, known bleeding tendency or anticoagulated).
Otherwise imaging can wait (aim <24h). Diff usion-weighted MRI is
most sensitive for an acute infarct, but CT helps rule out primary haemorrhage.

 Thrombolysis: Consider if onset of symptoms 4.5h ago; BOX.

 ‘Nil by mouth’: Only if swallowing attempts might lead to choking. Keep hydrated
(eg IVI), but don’t overhydrate (risk of cerebral oedema).

 Antiplatelet agents: Once haemorrhagic stroke is excluded, give aspirin 300mg.

Com municate fully with your patient, the relatives, and carers over diffi cult decisions,
eg deciding on the kindest/best level of intervention taking into account
quality of life, coexisting conditions, and prognosis. Is there a living will? See p478.

Take to a stroke unit with special nursing/physio to save life,93 and to motivate.

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5
Q

Thrombolysis in acute non-haemorrhagic stroke

A

seen within ~4.5h2, 3 of the onset of symptoms, and no contraindication exists (see
below), refer with utmost urgency for consideration of reperfusion with IV recombinant
tissue plasminogen activator (tPA: alteplase—eg 0.9mg/kg over 1h). This
reduces death and dependency (odds ratio 0.64) despite a small increase in intracranial
haemorrhage (these are usually small and asymptomatic). 99 Recent use of
antiplatelet agents does not appear to  this risk. 99 Always do CT 24h post-lysis to
identify bleeds (if +ve, register at SITS, www.acutestroke.org).

CI • Major infarct or haemorrhage on CT • Mild/non-disabling defi cit • Recent birth,
surgery, trauma, or artery or vein puncture at uncompressible site •Past CNS bleed
• AVM or aneurysm • Severe liver disease, varices or portal hypertension • Seizures
at presentation • Anticoagulants or INR >1 . 7 • Platelets 220/130.
The future: Those with CI may be eligible for a fl ow-restoration device, eg the Solitaire,
in large-vessel intracranial occlusive stroke (SWIFT and TREVO2 trials).100

2 Alteplase is licensed within 3h of onset of stroke, but ECASS3 and SITS studies show benefi t up to
4.5h,101, 102 IST3 + meta-analyses suggest at up to 6h (also if >80yrs old).103 Best results are at <90min;
don’t dawdle!104

Public health ‘Brain Attack’ awareness campaigns address this point: we should all know what the FAST acronym stands for: Facial weakness, Arm/leg weakness, or Speech difficulty = Time to act.

3 Intra-arterial r-tPA has a role seen between 3 and 6h post symptom onset.105

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6
Q

Public health ‘Brain Attack’ awareness campaigns

A

2 Alteplase is licensed within 3h of onset of stroke, but ECASS3 and SITS studies show benefi t up to
4.5h,101, 102 IST3 + meta-analyses suggest at up to 6h (also if >80yrs old).103 Best results are at <90min;
don’t dawdle!104

Public health ‘Brain Attack’ awareness campaigns address this point: we should all know what the FAST acronym stands for: Facial weakness, Arm/leg weakness, or Speech difficulty = Time to act.

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7
Q

primary prevention of stroke

A

Control risk factors (p474): Look
for and treat hypertension, DM, high lipids (p704; statins risk by ~17%),106 and cardiac
disease (see BOX). Exercise helps (increase HDL, increase glucose tolerance). Folate supplements1
may also help somewhat (serum homocysteine).107

Help quit smoking: p87. In
middle-aged men (esp. if BP), quitting risk of stroke, with benefi ts seen in ≤5yrs
(switching to pipes or cigars achieves little; former heavy smokers retain some excess
risk). Use lifelong anticoagulation if rheumatic or prosthetic heart valves on
left side, and consider in chronic non-rheumatic atrial fibrillation (AF), especially if
there are other vascular risk factors (see BOX). For prevention post-TIA see p480

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8
Q

secondary prevention of stroke

A

Secondary prevention (ie preventing further strokes) Control risk factors (as
Primary prevention above). Several large studies suggest considerable advantages
from lowering blood pressure and cholesterol (even if not particularly raised).
Antiplatelet agents after stroke: (assuming no primary haemorrhage on CT)
Clopidogrel monotherapy is the best way to prevent CNS and heart events and is
probably superior to aspirin plus slow-release dipyridamole. Anticoagulation after
stroke from AF: Start warfarin if indicated (BOX), 2wks after the stroke (if
clinically and radiologically small, from 7–10 days). Use antiplatelet therapy until
anticoagulated; if anticoagulated already, replace with antiplatelet for 1wk. Warfarin
CI: p344.

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9
Q

what is a TIA

A

The sudden onset of focal CNS phenomena due to temporary occlusion of part of the
cerebral circulation, usually by emboli, is termed a TIA if symptoms last <24h (often
much shorter). Incidence: 0.4/1000/yr. 15% of 1st strokes are preceded by TIAS; they
are also harbingers of MI, so…good management may avert disaster

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10
Q

signs of TIA

A

Attacks are single or many. Features of a TIA should always mimic those
of a stroke in the same arterial territory (p453), and may be the same or diff erent
for each TIA. Global events (eg syncope, dizziness) are not typical of TIAs. Multiple
highly stereotyped attacks suggest a critical intra cranial stenosis (commonly the
superior division of the MCA, p452). Emboli may also pass to the retinal artery, causing
amaurosis fugax (one eye’s vision is progressively lost “like a curtain descending
over my fi eld of view”). Limb-shaking TIAS may be mistaken for a focal motor seizure

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11
Q

tests in TIA

A

Aim to fi nd the cause and defi ne vascular risk: FBC, ESR, U&Es, glucose, lipids,
CXR, ECG, carotid Doppler ± angiography, CT or diff usion-weighted MRI (any existing
infarcts? If bilateral, it suggests cardioembolism), echo cardio gram (rarely shows
cardiac cause if no suggestive signs).

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12
Q

TIA treatment

A

Time to intervention is crucial. Risk of stroke within 90 days of TIA is
2% in those treated within 72h of TIA, compared to 10% in those treated by 3wks. 126

• Control cardiov ascular risk factors: BP (cautiously lower; aim for <3%.129 Intra-operative transcranial Doppler
can monitor middle cerebral artery fl ow. Using patches may reduce chance of
restenosis. Do not stop aspirin beforehand. Endovascular carotid artery stenting
is an alternative if not suitable for surgery, but safety and long-term benefi ts (instent
restenosis is common) remain under investigation.108
Driving Avoid for 1 month; patients in the UK should inform the DVLA only if multiple
attacks in short period or residual defi cit

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13
Q

When should TIA lead to prompt or emergency referral?

A

An ABCD2 score 131 of ≥6 (see TABLE) strongly predicts a stroke (8 . 1% within 2 days,
35.5% in the next week). Patients with a score ≥4 should be assessed by a specialist
within 24h, and all patients with a suspected TIA should be seen within 7 days. In assessing urgency, bear in mind Warlow’s 2005 data: in stroke patients who had
a preceding TIA, 17% occurred on the day of the stroke, 9% on the previous day, and
43% at some point during the 7 days before the stroke. 132 These sobering fi gures
should remind us to rehearse routes for referral for emergency endarterectomy—
at present this is typically performed >90 days post-TIA. 133

Age ≥60 yrs old 1 point
Blood pressure ≥140/90 1 point

Clinical features
Unilateral weakness 2 points
Speech disturbance without weakness 1 point

Duration of symptoms
Symptoms lasting ≥1h 2 points
Symptoms lasting 10–59min 1 point
Diabetes 1 point

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