Stroke Flashcards

1
Q

What are the causes of stroke?

A

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2
Q

What are the differentials for stroke?

A

Differential diagnosis

M8S:

Migraine

Sugar: hypoglycaemia.

Seizures, especially Todd’s palsy.

Sepsis, encephalitis.

Syncope

SDH

Space occupying lesion.

OldStrokes with intercurrent illness.

Somatisation

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3
Q

What are the risk factors for stroke

A

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4
Q

What Investigations are done in an Acute stroke

A

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5
Q

What is the acute management of Stroke?

A

Acute management of ischaemic stroke

Patients should be approached in the DR ABCDE manner.

Airway protection (in patients presenting with depressed consciousness) and aspiration precautions (in patients presenting with swallowing impairment) are very important.

Subsequent stroke management depends on whether the stroke is ischaemic or haemorrhagic. CT head should be performed on arrival to the emergency department to distinguish ischaemic from haemorrhagic stroke.

Alteplase (tissue plasminogen activator) is indicated in patients presenting within 4.5 hours of symptom onset and with no contraindications to thrombolysis (e.g. recent head trauma, GI or intracranial haemorrhage, recent surgery, acceptable BP, platelet count, and INR).
Mechanical Thrombectomy can be performed in patients with anterior circulation strokes within 6 hours of symptom onset, provided that they have a good baseline functional status and lack of significant early infarction on initial CT scan. Mechanical Thrombectomy can also be performed in posterior circulation strokes up to 12 hours after onset.
If hyper-acute treatments are not offered, patients should receive aspirin 300 mg orally once daily for two weeks. If hyper-acute treatments are offered, aspirin is usually started 24 hours after the treatment following a repeat CT Head that excludes any new haemorrhagic stroke.

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6
Q

What is the chronic management of stroke?

A

Stroke investigations (post-acute)

Investigations in the post-acute phase aim to further define the cause of the stroke and to quantify vascular risk factors.

Further investigations to determine the cause of the stroke include, for example:

In ischaemic stroke: carotid ultrasound (to identify critical carotid artery stenosis), CT/MR angiography (to identify intracranial and extracranial stenosis), and echocardiogram (if a cardio-embolic source is suspected). In young patients further investigation e.g. a vasculitis screen or thrombophilia screen may be necessary.

In haemorrhagic stroke: serum toxicology screen (sympathomimetic drugs e.g. cocaine are a strong risk factor for haemorrhagic stroke).

Further investigations to quantify vascular risk factors include: serum glucose (all patients with stroke should be screened for diabetes with a fasting plasma glucose or oral glucose tolerance test), serum lipids (to check for raised total cholesterol/LDL cholesterol).

Stroke management (chronic)

The key steps in secondary stroke prevention can be remembered by the mnemonic HALTSS:

Hypertension: studies show there is no benefit in lowering the blood pressure acutely (as this may impair cerebral perfusion) unless there is malignant hypertension (systolic blood pressure >180 mmHg). Anti-hypertensive therapy should, however, be initiated 2 weeks post-stroke.
Antiplatelet therapy: patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy. In patients with ischaemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.
Lipid-lowering therapy: patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).
Tobacco: offer smoking cessation support.
Sugar: patients should be screened for diabetes and managed appropriately.
Surgery: patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy.
Rehabilitation and supportive management will include an MDT approach with involvement of physiotherapy, occupational therapy, speech and language therapy, and neurorehabiliation.

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7
Q

What is the nihss SCORE?

A

The NIH Stroke Scale (NIHSS) is a scoring system out of 42, which has been designed as a predictive score of clinical outcome in stroke.
This scoring system is completed on initial assessment of a patient with suspected stroke. It is important for the consideration of thrombolysis and clinical outcome.

A score < 4 is associated with a good clinical outcome. A high score (> 22) indicates a significant proportion of the brain is affected by ischaemia, and as such, there is higher risk of cerebral haemorrhage with thrombolysis. A score ≥ 26 is often considered a contraindication to thrombolysis.

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8
Q

Contraindications for thrombolysis

A

Contraindications to thrombolysis:

Absolute

  • 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

relative

  • Concurrent anticoagulation (INR >1.7)
  • Haemorrhagic diathesis
  • Active diabetic haemorrhagic retinopathy
  • Suspected intracardiac thrombus
  • Major surgery / trauma in the preceding 2 weeks
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9
Q

When is a thrombectomy done?

A

Mechanical thrombectomy is an exciting new treatment option for patients with an acute ischaemic stroke. NICE incorporated recommendations into their 2019 guidelines. It is important to remember the significant resources and senior personnel to provide such a service 24 hours a day. NICE recommend that all decisions about thrombectomy take into account a patient’s overall clinical status:
NICE recommend a pre-stroke functional status of less than 3 on the modified Rankin scale and a score of more than 5 on the National Institutes of Health Stroke Scale (NIHSS)

Offer thrombectomy as soon as possible and within 6 hours of symptom onset, together with intravenous thrombolysis (if within 4.5 hours), to people who have:
acute ischaemic stroke and
confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA)

Offer thrombectomy as soon as possible to people who were last known to be well between 6 hours and 24 hours previously (including wake-up strokes):
confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA and
if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume

Consider thrombectomy together with intravenous thrombolysis (if within 4.5 hours) as soon as possible for people last known to be well up to 24 hours previously (including wake-up strokes):
who have acute ischaemic stroke and confirmed occlusion of the proximal posterior circulation (that is, basilar or posterior cerebral artery) demonstrated by CTA or MRA and
if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume

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10
Q

What advice would you give them regarding driving?

A

stroke or TIA: 1 month off driving, may not need to inform DVLA if no residual neurological deficit
multiple TIAs over short period of times: 3 months off driving and inform DVLA

chronic neurological disorders e.g. multiple sclerosis, motor neuron disease: DVLA should be informed, complete PK1 form (application for driving licence holders state of health)

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11
Q

When is carotid endartectomy done?

A

patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy.

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12
Q

How many recover after stroke?

A

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13
Q

Scoring systems used in stroke?

A

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14
Q

Cardiac causes of stroke

A

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15
Q

Mechanism of anti platelet agents?

A

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16
Q

Whats the CHADSVASC score?

A

NICE categorise CHA2DS2-VASc scores as:

Low risk - 0 (if a woman has no other risk factors gender is no longer significant).
Intermediate risk - 1
High risk ≥ 2 - anticoagulation.
NICE CG 180 recommend anticoagulation in all patients with a score of 2 or more. It should be considered in men with a score of 1. In women with a score of 1 due to gender, NICE do no consider this an indication for treatment.

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17
Q

What is the HASBLED score

A

The HAS-BLED score helps the identification of those at risk of significant bleeding on anticoagulation therapy.
A point is given for each of the following factors shown. HAS-BLED can be used to remember the factors though this does combine drugs and alcohol, as well as abnormal liver function and abnormal renal function to make it fit. The prescence of each of these factors scores an individual point.

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18
Q

What are the different types of AF

A
Atrial fibrillation (AF) refers to irregular atrial contraction, caused by chaotic impulses.
AF is increasingly common, NHS studies indicate a prevalence of 1-2% in the UK. It is a major cause of morbidity, in particular stroke, which is largely preventable with appropriate anticoagulation.

AF can be classified as paroxysmal, persistent or permanent:

Paroxysmal
Recurrent (more than 1 episode ≥30 seconds in duration).
Terminates spontaneously within 7 days (usually within 48 hours of presentation).
Persistent
Lasts longer than 7 days or requires termination by pharmacological / electrical cardioversion.
Permanent
Refractory to cardioversion.
Sinus rhythm cannot be restored or maintained.
AF is accepted as a final rhythm.

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19
Q

What can cause AF?

A

Aetiology
A large number of conditions may predispose too AF.
Cardiac

Hypertension
IHD
Valvular disease (RHD)
Cardiomyopathy
Non-cardiac
Respiratory
COPD
Pneumonia
Pulmonary embolism
Pleural effusion
Lung cancer
Endocrine
Thyrotoxicosis 
Diabetes mellitus
Infection
Electrolyte disturbances
Drugs
Bronchodilators
Thyroxine
Lifestyle

Alcohol
Caffeine (contribution is debated, there is no evidence that at normal levels of consumption caffeine causes AF)

athophysiology
Despite the range of risk factors and causative conditions, common changes to the electrophysiology of the heart may occur.
Atrial myocardium

Atrial myocardium has a number of interesting electrophysiological properties. It possesses a short action potential with a refractory period that reduces with an increasing rate.

These properties permit rapid contraction.

Generation of arrhythmia

As mentioned, AF is caused by disruption of the electrophysiology in the atrial myocardium. Many mechanisms have been proposed with varying degrees of evidence to support their existence. Most likely, they occur simultaneously.

Two of the most commonly discussed mechanisms are:

Multiple wavelets - proposes that wavefronts (spontaneous waves of excitation) become fragmented resulting in multiple daughter wavelets.
Autonomic foci - these foci, located primarily in the pulmonary veins, act to initiate AF.
Ultimately, the physiological sinoatrial node rhythm is superseded by these rapid and chaotic impulses.

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20
Q

What investigations and treatment options are available for AF?

A

anagement of AF may be achieved with rate or rhythm control.
Underlying causes should be identified and treated. Patients may be anticoagulated to reduce the risk of thrombo-embolic events.

Rate control

Most common type of management. Aimed at controlling rapid heart rate.

First line therapies:

Beta blockers (e.g. metoprolol)
Rate-limiting calcium channel blockers (e.g. verapamil).
Other therapies:

Digoxin monotherapy - may be used in sedentary patients (in active patients sympathetic action may easily overcome the effects of digoxin).
Sotalol - should only be prescribed by a cardiologist due to life-threatening side effects.
Rhythm control

Cardioversion is aimed at reverting the heart back to a normal (sinus) rhythm.

Decision made by specialists, may be indicated when:

New onset
Identifiable reversible cause.
Heart failure (caused by or exacerbated by AF).
There are two forms of cardioversion:

Electrical - typically indicated in AF that has been present > 48hrs.
Pharmacological - amiodarone, sotalol.
In new-onset AF establishing time of onset is important. Firstly, ventricular rate should be appropriately controlled. If onset < 48hrs, immediate cardioversion can take place. If > 48hrs or timing is uncertain, anticoagulation (for at least three weeks) is required before cardioversion. This is due to potential thrombus generation in the atrial appendage.

Anticoagulation

Anticoagulation may take two main forms:

Vitamin K antagonists (e.g. warfarin): has been the mainstay for many years. Regular INR measurements required.
Direct-acting oral anticoagulants (DOACs): newer agents such as Rivaroxaban (direct Xa inhibitor) and Dabigatran (direct thrombin inhibitor).
If the above are contraindicated dual anti-platelet therapy (aspirin and clopidogrel) may be used. Aspirin or clopidogrel monotherapy is no longer advised.

Ablation therapy

Catheter and surgical ablation therapy offers an additional treatment option. NICE recommends its use when drug treatment has failed. The potential risks and benefits should be discussed with the patient. It is a complex procedure requiring mapping of circuits and can fail.

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21
Q

What are the complications of AF

A

notable complications include
cardiac tamponade
stroke
pulmonary valve stenosis
success rate
around 50% of patients experience an early recurrence (within 3 months) of AF that often resolves spontaneously
longer term, after 3 years, around 55% of patients who’ve had a single procedure remain in sinus rhythm. Of patient who’ve undergone multiple procedures around 80% are in sinus rhythm

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22
Q

How can stroke’s be classified?

A

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23
Q

What are the cerebellar stroke syndromes and how do they present?

A

-

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24
Q

What the comment artery affected in stroke?

A

-

25
Q

Visual field defects

A

-

26
Q

Indications for stroke within an hour?

A

-

27
Q

Visual rehab services?

A

-

28
Q

Stroke MDT

A

-

29
Q

How would swallow be assessed post stroke?

A

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30
Q

What advice can we give regarding falls

A

-

31
Q

Effect of early cathertization?

A

-

32
Q

How can spasticity be managed?

A

-

33
Q

How can process post stroke be measured?

A

-

34
Q

How can mood be managed?

A

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35
Q

Activities than can engage the patient and make the process more enjoyable?

A

-

36
Q

Test for visual apraxia, agnosia, perceptional function and spatial ability?

A

-

37
Q

How to differentiate ischemic and haemorrgic stroke?

A

-

38
Q

How to manage a haemorrhage stroke?

A

-

39
Q

CNS bleeds

A

-

40
Q

CT findings

A

-

41
Q

Rosiers score?

A

-

42
Q

Early and late complications following stroke?

A

-

43
Q

What are the most common sites of crescendo attacks?

A

critical intracranial stenosis-superior division of MCA

44
Q

When clopidogrel is contraindicated?

A

aspirin 75mg od with dipyridamole

45
Q

How can TIA be managed?

A

Management
Any patient with a suspected TIA should be treated with 300 mg of aspirin unless contraindicated.
The management of TIA can be divided into acute treatment, secondary prevention and lifestyle measures.

Acute treatment

The principle management for TIA is 300 mg of aspirin that is usually continued for two weeks. This is followed by treatment with 75 mg of clopidogrel as long-term vascular prevention.

Patients with atrial fibrillation or significant carotid artery disease require a different treatment pathway.

Atrial fibrillation (AF): should be offered and counselled about starting an oral anticoagulant
Carotid artery disease (CAD): urgent referral for consideration of carotid endarterectomy if significant disease. Based on NASCET or ECST criteria for stenosis.
NASCET: 50-99% stenosis
ECST: 70-99% stenosis
Secondary prevention

Patients with a TIA should be offered secondary prevention treatments to optimise their cardiovascular risk

Anti-hypertensives: as per hypertension guidelines (tolerate higher if significant bilateral CAD)
Lipid modification: offer high-dose statin therapy unless contraindication.
Diabetic control: treat any new diagnosis of diabetes and optimise control of pre-existing disease
Obstructive sleep apnoea: referral to specialist sleep medicine/respiratory clinic if suspected
Pre-menopause: use of combined oral contraceptive pill contraindicated.
Lifestyle measures

Basic advice on physical activity, smoking cessation, diet optimisation and alcohol intake should be given to all patients

46
Q

When is urgent admission warranted?

A

Certain features warrant urgent admission to hospital because of the high risk of stroke, bleeding or deterioration.
≥1 suspected TIA (crescendo TIA): typically within the last 7 days
Suspected cardioembolic source or severe carotid stenosis
Vulnerable patient: lack of reliable observer at home to monitor for worsening symptoms
Bleeding disorder or taking an anticoagulant
Any patient with ongoing symptoms needs to be treated as an acute stroke and urgently referred to a stroke unit.

ABCD2 SCORE 4 HIGH RISK,greater than 6 very high risk

47
Q

What investigations are done for TIA?

A

Investigations
MRI is the key investigation in a patient with suspected TIA.
Bloods

Haematology: full blood count (FBC), HbA1c +/- haemoglobin electrophoresis
Routine biochemistry: Urea & electrolytes (U&Es), bone profile, liver function tests (LFTs), lipid profile
Coagulation: routine clotting
Special (as indicated): ‘young stroke screen’ (e.g. thrombophilia screen, Fabry’s)
Cardiac investigations

ECG: assessment for arrhythmias, especially atrial fibrillation
Echo: not routinely offered unless suspicion of heart disease or confirmed stroke
Imaging

MRI head with diffusion-weighted imaging (DWI): preferred to CT unless alternative diagnosis suspected that CT could detect. Enables detection of small infarcts.
Carotid dopplers: all patients who are candidates for carotid endarterectomy.

48
Q

When would you refer patient with TIA?

A

All patients with a suspected TIA should be referred to a specialist TIA clinic and be seen within 24 hours.
At the TIA clinic, patients should have a comprehensive medical assessment including blood tests, electrocardiogram (ECG) and imaging. If the episode occurred > 1 week ago, the assessment should be within 7 days.

The ABCD2 is a prognostic score that was traditionally used to identify people at high risk of stroke after a TIA score. It was originally used to triage the urgency of TIA referrals and treatment with aspirin. NICE no longer recommend its use.

49
Q

What are the differentials for TIA

A

Numerous conditions can present similarly to TIA, which are collectively referred to as ‘stroke mimics’.
Toxic/metabolic: hypoglycaemia, drug and alcohol consumption
Neurological: seizure, migraine, Bell’s palsy
Space occupying lesion: tumour, haematoma
Infection: meningitis/encephalitis, systemic infection with ‘decompensation’ of old stroke
Syncope: extremely uncommon presentation of TIA, consider causes of syncope

50
Q

What are the differentials for amaurosis fugax

A

Amaurosis fugax

This is a classical syndrome of short-lived monocular blindness, which is often described as a black curtain coming across the vision. It is a term usually reserved for transient visual loss of ischaemic origin.

The principle cause of amaurosis fugax is transient obstruction of the ophthalmic artery, which is a branch of the internal carotid artery. However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion. An important differential of transient visual loss, particularly in young patients, is migraine.

51
Q

How does TIA present?

A

A TIA presents with sudden, focal neurological deficit that reflects the area of the brain devoid of blood flow.
A variety of neurological deficits can present in TIA, but the majority of symptoms will resolve within 1-2 hours.

Neurological deficit

Unilateral weakness or sensory loss
Dysphasia
Ataxia, vertigo, or incoordination
Amaurosis fugax: see below
Homonymous hemianopia: visual field loss on the same side of both eyes
Cranial nerve defects: particularly if associated with contralateral sensory/motor deficits

52
Q

What is the aetiology of TIA?

A

TIA is caused by temporary blockage to blood flow, which leads to ischaemia.
Ischaemia refers to the absence of blood flow to an organ, which deprives it of oxygen. Cerebral ischaemia may be due to in situ thrombosis, emboli, or rarely, dissection.

Thrombosis: local blockage of a vessel due to atherosclerosis. Precipitated by cardiovascular risk factors (e.g. hypertension, smoking) or small vessel disease (e.g. vasculitis, sickle cell). Listen for bruits

Emboli: propagation of a blood clot that leads to acute obstruction and ischaemia. Typically due to atrial fibrillation or carotid artery disease. valve disease prosthetic valves

Dissection: a rare cause of cerebral ischaemia from tearing of the intimal layer of an artery (typically carotid). This leads to an intramural haematoma that compromises cerebral blood flow. May be spontaneous or secondary to trauma.

Hyperviscosity-polycythemia,sickle cell,myeloma

Vasculitis-SLE,PAN,syphilis

During a TIA, there is a transient reduction in blood flow to an area of cerebral tissue that causes neurological symptoms. TIA commonly occurs secondary to embolisation from atrial fibrillation or carotid artery disease.

53
Q

What is the diagnostic criteria for TIA?

A

Traditionally, transient neurological dysfunction with resolution within 24 hours was diagnostic of TIA. However, up to a third of patients whose symptoms have resolved within 24 hours have evidence of infarction on imaging. Consequently, the definition is now ‘tissue-based’ rather than ‘time-based’ with the incoporation of the phrase ‘without evidence of acute infarction’. Thus, the end-point is biological tissue damage, not an arbitrary time cut-off.

54
Q

What is is risk of a patient developing stroke following a TIA?

A

within the first week following a TIA, the risk of stroke is up to 10%. The estimated incidence of TIA within the UK is 50 per 100,000 people per year.

55
Q

What is a TIA?

A

TIA is defined as transient neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without evidence of acute infarction. It is a medical emergency

56
Q

Who likely are patients to be independent post stroke?

A

less than 40 -depe

57
Q

What is

A

MCA provides a branch to central part causing macular sparing

58
Q

Pressure ulcers classification and scoring

A

Water low and broaden score

59
Q

Dvla criteria for driving

A

Ib