Cerebrovascular Disease Flashcards

1
Q

What is ischaemic stroke?

A

-Acute focal neurological dysfunction due to focal infarction at single or multiple sites of the brain or retina. Blockage in blood vessel, 85%
=Symptoms lasting >24hrs
=Imaging findings in the clinically relevant area of the brain
=Thrombotic (thrombosis from carotid)/ embolic (blood clot/ fat/ air/ bacteria/ AF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk factors for ischaemic stroke

A

General risk factors for cardiovascular disease
age
hypertension
smoking
hyperlipidaemia
diabetes mellitus

Risk factors for cardioembolism
atrial fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is an intracerebral haemorrhage?

A

Acute neurological dysfunction from haemorrhage in brain parenchyma or ventricular system
=Blood vessel bursts, 15%
=Intracerebral haemorrhage vs subarachnoid haemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Risk factors haemorrhagic stroke

A

age
hypertension
arteriovenous malformation
anticoagulation therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is a TIA?

A

-Transient focal neurological symptoms due to cerebral ischaemia without evidence of infarction
=a subtype of ischaemic stroke is a transient ischaemic attack (TIA). This describes the sudden onset of a focal neurologic symptom and/or sign lasting typically less than an hour, brought on by a transient decrease in blood flow. This is sometimes referred to by patients as a ‘mini-stroke’
=The original definition of a TIA was time-based: a sudden onset of a focal neurologic symptom and/or sign lasting less than 24 hours, brought on by a transient decrease in blood flow. However, this has now changed as it is recognised that even short periods of ischaemia can result in pathological changes to the brain. Therefore, a new ‘tissue-based’ definition is now used: a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is infarction

A

Positive imaging or symptoms at 24hr follow up

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are focal symptoms?

A

-Motor weakness, clumsiness, sensory alteration in limb(s) on the same side
-Speech or language disturbance (dysphasia)
-Swallowing problems
-Loss of vision in eye/part of eye/ homonymous hemianopsia
-Sensory alteration, ataxia, imbalance, unsteadiness not associated with vertigo
-2 or more diplopia, dysphagia, dysarthria, or vertigo

Cerebral hemisphere infarcts:
=contralateral hemiplegia: initially flaccid then spastic
contralateral sensory loss
homonymous hemianopia
dysphasia

Brainstem infraction
=Quadriplegia
=Locked in syndrome

Lacunar
=Pure motor/ pure sensory/ mixed motor and sensory signs or ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Symptoms less likely to be TIA

A

-Disturbances of vision with flashes, objects, distorted-view tunnel vision or image moving
-Tiredness/ heavy sensation in limb(s)
-Sensory symptoms or gradual spread of sensory symptoms
-Isolated disorder of swallowing or articulation, double vision, dizziness, or uncoordinated movements
-Unconsciousness, limb jerking, tingling of limbs/lips, disorientation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Stroke classification system

A

-Oxford/ Bamford

  1. Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ROSIER scoring

A

Exclude hypoglycaemia first, then assess the following:
-Loss of consciousness or syncope (-1)
-Seizure activity (-1)

-New acute onset of:
=Asymmetric facial weakness (+1)
=Asymmetric arm weakness (+1)
=Asymmetric leg weakness (+1)
=Speech disturbance (+1)
=Visual field defect (+1)

A stroke is likely if > 0.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of carotid stenosis

A

Endarterectomy
=Atheroma removal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Primary and secondary prevention of stroke

A

-DOAC= more convenient than warfarin (monitoring, slow onset of action, bridging, and multiple drug interactions)
=Reduce risk of stroke or systemic embolic events compared with warfarin and reduce bleeding
=Warfarin has role in renal failure and mechanical heart valves
-Antiplatelet (clopidogrel)/ aspirin 300mg
-Blood pressure lowering
-LDL-cholesterol lowering
-Look for AF
-Look for carotid stenosis
-Stopping smoking advice
-Diet advice
-Look for PFO (patent foramen Ovale)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of SAH

A

-intracranial aneurysm (saccular ‘berry’ aneurysms)
=accounts for around 85% of cases
=conditions associated with berry aneurysms include hypertension,adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta
-arteriovenous malformation
-pituitary apoplexy
-mycotic (infective) aneurysms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Presentation of subarachnoid haemorrhage

A

-Sudden-onset thunderclap headache, severe, occipital, peaking in intensity 1-5 minutes
=Maybe history of less-severe ‘sentinel’ headache in weeks prior
-Nausea and vomiting
-Meningism (photophobia, neck stiffness)
-Coma
-Seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diagnosis of subarachnoid haemorrhage

A

-Non-contrast CT head= hyperdense/ bright on CT. If done within 6 hours and normal, not LP, alternative diagnosis
-If CT done more than 6 hours after symptom onset and is normal= LP (at least 12 hours following onset of symptoms to allow xanthochromia), normal or raised opening pressure
-CT angiography to identify cause
-ECG changes including ST elevation may be seen
=this may be secondary to either autonomic neural stimulation from the hypothalamus or elevated levels of circulating catecholamines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Management of subarachnoid haemorrhage

A

-Pain relief, bed rest, VTE prophylaxis, discontinue antithrombotic
-Enteral nimodipine for ruptured aneurysm
-Endovascular coiling, or neurosurgical clipping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Complications of SAH

A

-re-bleeding
=happens in around 10% of cases and most common in the first 12 hours
=if rebleeding is suspected (e.g. sudden worsening of neurological symptoms) then a repeat CT should be arranged
=associated with a high mortality (up to 70%)
-hydrocephalus
=hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculoperitoneal shunt
-vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset
=ensure euvolaemia (normal blood volume)
=consider treatment with a vasopressor if symptoms persist
-hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH))
-seizures

Important predictive factors in SAH:
conscious level on admission
age
amount of blood visible on CT head

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Presentation of subdural haemorrhage

A

The typical presentation of a subdural haematoma (SDH) often involves a history of head trauma, which may range from minor to severe. Patients frequently exhibit a lucid interval followed by a gradual decline in consciousness. This pattern is particularly common in chronic SDH. Other hallmark features include headache, confusion, and lethargy.

-Acute/ subacute/ chronic.
-Headache, often unilateral, worsening
-Nausea and vomiting (ICP)
-Cushing’s triad: bradycardia, hypertension, respiratory irregularities (ICP)
-Diminished GCS/ fluctuations in consciousness
-Confusion, memory loss (chronic), irritability, apathy, depression, cognitive impairment
-Loss of bowel and bladder continence
-Localised weakness, aphasia, visual field defect
-Seizure.
-Papilloedema (raised ICP)
-Pupil changes: unilateral dilated pupil, ipsilateral, compression of third cranial nerve
-Gait abnormalities: ataxia or weakness in one leg
-Hemiparesis or hemiplegia: mass effect/ midline shift

-ACUTE= high impact trauma, incidental finding vs severe coma and coning due to herniation. 48 hours, rapid neurological deterioration

-SUBACUTE= days to weeks post-injury, more gradual progression

-CHRONIC= weeks to months, rupture of small bridging veins causing slow bleeding, elderly and alcoholic (brain atrophy), progressive history of confusion, reduced consciousness, neurological deficit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Investigation of subdural haemorrhage

A

-Non-contrast CT imaging (crescentic collection not limited by suture lines, large= mass effect= midline shift or herniation).
-ACUTE= hyperdense
-CHRONIC= hypodense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Management of subdural haemorrhage

A

-Prophylactic antiepileptic
-Correction of coagulopathy
-ICP lowering.
-ACUTE= conservative/ surgical decompressive craniectomy, monitoring of ICP.
-Surgical decompression with burr holes= chronic, confusion, neurological deficit.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Presentation of extradural haemorrhage/ haematoma

A

-Trauma (low impact)
-Often in temporal-parietal region (middle meningeal artery).
-Initially loses, briefly regains, then loses again consciousness (lucid interval).
-Lost when expands and herniation= fixed and dilated pupil due to compression of third cranial nerve.
-Fracture of temporal bone, headache.

22
Q

Investigations of extradural haemorrhage

A

-Non-contrast CT= biconvex/ lentiform, hyperdense collection limited by the suture lines of the skull.

23
Q

Management of extradural haemorrhage

A

-Clinical and radiological observation in patients with no neurological deficit
-Craniotomy and evacuation of haematoma.

24
Q

Presentation and investigation of cerebral arterial dissection

A

-Presentation: haematoma in wall of cervical or intracranial artery. Leads to brain infarction, stroke, and subarachnoid haemorrhage. Head and neck pain

-Investigation: Angiography (catheter cerebral), CT, MRI

25
Q

Presentation and investigation of cerebral venous thrombosis

A

-Presentation
=Raised ICP
=Seizures
=Focal neurological symptoms.
=CORTICAL= aphasia, hemiparesis, epilepsy.
=CAVERNOUS= eye symptoms, headache, reduced sensation in trigeminal first division.
=SUPERIOR SAGITTAL SINUS= headache, papilledema, seizures, resemble idiopathic intracranial hypertension.
=TRANSVERSE= hemiparesis, seizures, papilledema.
=Causes= dehydration, pregnancy, idiopathic, infection of cranial sinuses, thrombophilia.

-Diagnosis: MR venography= filling defect in affected vessel.

26
Q

Presentation of TIA

A

-Brief period of sudden onset neurological deficit typically lasting less than an hour/ completely resolved within 24hrs- ischaemia without acute infarction.
-Unilateral weakness or sensory loss, aphasia or dysarthria, ataxia, vertigo, loss of balance, visual problems (amaurosis fugax, diplopia, homonymous hemianopia)

unilateral weakness or sensory loss.
aphasia or dysarthria
ataxia, vertigo, or loss of balance
visual problems
sudden transient loss of vision in one eye (amaurosis fugax)
diplopia
homonymous hemianopia

27
Q

Investigation of TIA

A

-Assessed within 24hours by stroke specialist clinician/ If a patient presents more than 7 days ago they should be seen by a stroke specialist clinician as soon as possible within 7 days
-Exclude hypoglycaemia, intracranial haemorrhage (all pts on anticoagulants or with similar risk factors should be admitted for urgent imaging)

-MRI to determine territory of ischaemia or detect haemorrhage. Preferred to CT to determine territory if ischaemia, same day preferable
-Carotid doppler= atherosclerosis can be source of emboli, carotid endarterectomy of carotid stenosis >70%.
-CT if bleeding disorder or taking anticoagulation: exclude haemorrhage. NICE recommend that CT brains should not be done ‘unless there is clinical suspicion of an alternative diagnosis that CT could detect’ (e.g. anticoagulant and haemorrhage concern)

Carotid imaging
atherosclerosis in the carotid artery may be a source of emboli in some patients
patients who are considered candidates for carotid intervention should have carotid imaging performed within 24 hours of assessment
carotid duplex ultrasound or either CT angiography or MR angiography
carotid endarterectomy is recommend if the patient has suffered a stroke or TIA in the carotid territory and is not severely disabled NICE
should only be considered if the stenosis > 50% according to North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria
+ it should be noted that previous guidelines have used other reporting methods, that have resulted in different cut-offs, e.g. European Carotid Surgery Trial (ECST) with a cut-off of 70%
it should be performed as soon as possible within 7 days

28
Q

Management of TIA

A

-Immediate antithrombotic therapy (aspirin 300mg unless anticoagulated, already taking low-dose aspirin, contraindicated)
-It should be noted that DAPT is not currently recommended for ‘major’ ischaemic stroke as the risk of haemorrhagic transformation is too high.

patients with TIA or minor ischaemic stroke should be given antiplatelet therapy provided there is neither a contraindication nor a high risk of bleeding
-for patients within 24 hours of onset of TIA or minor ischaemic stroke and with a low risk of bleeding, the following DAPT regimes should be considered:
=clopidogrel (initial dose 300 mg followed by 75 mg od) + aspirin (initial dose 300 mg followed by 75 mg od for 21 days) followed by monotherapy with clopidogrel 75 mg od
=ticagrelor + clopidogrel is an alternative
-if not appropriate for DAPT:
clopidogrel 300 mg loading dose followed by =75 mg od should be given
-proton pump inhibitor therapy should be considered for DAPT

-Resolved TIA symptoms, awaiting specialist review within 24 hours: aspirin
-Reviewed by specialist, initial 21 days when at high risk of further events: aspirin + clopidogrel
-Long-term prevention after 21 days: clopidogrel

-high-intensity statin (such as atorvastatin 20-80 mg daily) - the aim of statin therapy is to reduce non-HDL cholesterol by more than 40%

29
Q

Presentation of anterior cerebral stroke

A

-Contralateral hemiparesis and sensory loss, lower extremity > upper

-Total anterior circulation infarct (15%)
=Involves middle and anterior cerebral arteries
=All 3 Oxford criteria

-Partial anterior circulation infarcts (PACI, 25%)
=Involves smaller arteries of anterior circulation (e.g. upper or lower division of middle CA)
=2 of Oxford criteria

30
Q

Presentation of middle cerebral stroke

A

-Sudden onset contralateral hemiparesis and sensory loss
-Contralateral Homonymous hemianopia with eye deviation
-Altered speech (aphasia)
-Difficulty answering questions or naming objects.
-Upper > lower.

31
Q

Presentation of posterior cerebral stroke

A

-POCI, 25%
-Acute vestibular syndrome (acute, persistent, continuous vertigo or dizziness with nystagmus, nausea, vomiting, head motion intolerance, new gait unsteadiness).
-Contralateral homonymous hemianopia with macular sparing. Visual agnosia

involves vertebrobasilar arteries
presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia

32
Q

Presentation of lacunar stroke (LACI)

A

-Isolated hemiparesis
-Hemisensory loss or hemiparesis with limb ataxia
-Hypertension.
-25%

involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

33
Q

Presentation of basilar artery stroke

A

Locked in syndrome

34
Q

Lateral medullary syndrome and anterior inferior cerebellar artery

A

(posterior inferior cerebellar artery)
aka Wallenberg’s syndrome
ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
contralateral: limb sensory loss

Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

-Anterior inferior cerebellar artery/ lateral pontine syndrome:
symptoms similar to Wallenberg’s but ipsilateral facial paralysis and deafness

35
Q

Retinal/ ophthalmic artery

A

Amaurosis fugax

36
Q

Weber’s syndrome

A

ipsilateral III palsy
contralateral weakness of upper and lower extremity

Branches of posterior cerebral artery that supply midbrain

37
Q

Haemorrhagic stroke symptoms

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

38
Q

Diagnosis of stroke

A

-ECG to exclude arrhythmia
-Non-contrast CT head (hypoattenuation of brain parenchyma, sulcal effacement, loss of grey matter-white matter differentiation, hyperattenuating indicates clot in artery)
=may show areas of low density in the grey and white matter of the territory. These changes may take time to develop
=other signs include the ‘hyperdense artery’ sign corresponding with the responsible arterial clot - this tends to visible immediately
=Acute haemorrhagic: hyperdense material (blood) surrounded by low density (oedema)

-Routine bloods
-CT angiography or MRI in patients with suspected large vessel occlusion candidates for thrombectomy.
-MRI if diagnosis uncertain.
-Carotid ultrasound, echo.

39
Q

Management of ischaemic stroke

A

-Within 4.5 hours and thrombolysis not contraindicated (no previous intracranial haemorrhage, uncontrolled hypertension, pregnancy): Alteplase/ mechanical thrombectomy (proximal anterior circulation).
-Otherwise, aspirin 300mg orally one haemorrhagic stroke excluded, antiplatelet therapy, VTE prophylaxis, high-intensity statin.
-Blood pressure not lowered in acute phase unless complications (hypertensive encephalopathy)
-blood glucose, hydration, oxygen saturation and temperature should be maintained within normal limits
-blood pressure should not be lowered in the acute phase of ischaemic stroke unless there are complications e.g. Hypertensive encephalopathy or they are being considered for thrombolysis (see below)
-blood pressure control should be considered for patients who present with an acute ischaemic stroke, if they present within 6 hours and have a systolic blood pressure > 150 mmHg
-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

40
Q

Criteria for thrombolysis

A

-Patients with an acute ischaemic stroke, regardless of age or stroke severity, who were last known to be well more than 4.5 hours earlier, should be considered for thrombolysis with alteplase if:
=treatment can be started between 4.5 and 9 hours of known onset, or within 9 hours of the midpoint of sleep when they have woken with symptoms, AND
=they have evidence from CT/MR perfusion (core-perfusion mismatch) or MRI (DWI-FLAIR mismatch) of the potential to salvage brain tissue
-This should be irrespective of whether they have a large artery occlusion and require mechanical thrombectomy.
-There are specific criteria in the guidelines that determine the imagine criteria that determine whether thrombolysis should be performed

Blood pressure should be lowered to 185/110 mmHg before thrombolysis.

41
Q

Contraindications to thrombolysis

A

-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
- Oesophageal varices
- Uncontrolled hypertension >200/120mmHg

-Relative
=Pregnancy
- Concurrent anticoagulation (INR >1.7)
- Haemorrhagic diathesis
- Active diabetic haemorrhagic retinopathy
- Suspected intracardiac thrombus
- Major surgery / trauma in the preceding 2 weeks

42
Q

Thrombectomy for acute ischaemic stroke

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

43
Q

Secondary prevention for ischaemic strokes

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 is recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated

Carotid endarterectomy is recommend if the patient has suffered a stroke or TIA in the carotid territory and is not severely disabled
should only be considered if the stenosis > 50% according to North American Symptomatic Carotid Endarterectomy Trial (NASCET) criteria
- it should be noted that previous guidelines have used other reporting methods, that have resulted in different cut-offs, e.g. European Carotid Surgery Trial (ECST) with a cut-off of 70%
it should be performed as soon as possible within 7 days

44
Q

Management of TIA

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. 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

45
Q

Management of 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.

46
Q

Fluid management for stroke

A

As in all patients in hospital, regular assessment for fluid status must be undertaken to ensure patients remain normovolaemic
The NICE guidelines recommend assessing the hydration of all patients with acute stroke on admission, with regular review during their stay
Greater than 80% of patients who cannot swallow post stroke will recover within 2-4 weeks
However, it is important to manage fluids in this immediate post-event period as hypovolaemia can worsen the ischaemic penumbra, as well as increase risk of other complications such as infection, deep vein thrombosis, constipation and delirium
Conversely, over-hydration can also complicate matters by leading to cerebral oedema, cardiac failure and hyponatraemia, therefore it is important to regularly review fluid status in these patients
Recommendations for management:
Oral hydration is preferable in all patients who are able to safely swallow
Intravenous hydration may be necessary otherwise, and although studies have remained contentious regarding choice of intravenous fluid, UptoDate currently recommend isotonic saline without dextrose as the agent of choice in most patients
Other factors to take into consideration when choosing fluid agent include electrolyte disturbances and/or cardiovascular status

47
Q

Glycaemic management in stroke

A

It is important to closely monitor and control blood sugar, particularly if they are nil by mouth due to concerns regarding swallowing safety post stroke, and/or in diabetics
Post stroke, patients with hyperglycaemia have increased mortality independent from their age and the severity of stroke
This is likely due to increased tissue acidosis from anaerobic metabolism, free radical generation, and increased blood brain barrier permeability post injury
The NICE guidelines recommend maintaining a blood sugar level between 4 and 11 mmol/L in people with acute stroke
Diabetic patients
It is important to provide intensive management for diabetics post acute stroke
The NICE guidelines suggest optimising insulin treatment using intravenous insulin and glucose infusions
Hypoglycaemia also needs to be managed appropriately, as alone it can cause neuronal injury as well as mimic stroke-related neurological deficits

48
Q

Blood pressure management in stroke

A

Use of anti-hypertensive medications should only be used for blood pressure control in patients post ischaemic stroke if there is a hypertensive emergency with one or more of the following serious concomitant medical issues (according to the NICE guidelines):
Hypertensive encephalopathy
Hypertensive nephropathy
Hypertensive cardiac failure/myocardial infarction
Aortic dissection
Pre-eclampsia/eclampsia
This is because lowering blood pressure too much can potentially compromise collateral blood flow to the affected region, and possibly hasten the time to complete and irreversible tissue infarction
If if treatment is indicated, UptoDate recommend cautious lowering of blood pressure by approximately 15% in the first 24-hours after stroke onset
UptoDate suggest using intravenous labetalol, nicardipine and clevidipine as first-line agents, due to the possibility for rapid and safe titration to control blood pressure

However, in patients who are candidates for thrombolytic therapy for acute stroke, blood pressure should be reduced to 185/110mmHg or lower
Elevated BP can affect thrombolytic eligibility and delay treatment
Timely management of elevated BP is crucial when patients are otherwise eligible for intravenous thrombolysis
After thrombolytic therapy, UptoDate recommend ensuring that the blood pressure is stabilised and maintained at or below 180/105mmHg for at least 24 hours after treatment

49
Q

Feeding assessment and management in stroke

A

All patients presenting with acute stroke must be screened for safe swallowing function prior to further oral intake, as dysphagia is common after stroke
This is to reduce the risk of aspiration and subsequent complications
This includes prior to any oral intake of food, fluids, and/or medications
If there are any concerns regarding swallowing, the NICE guidelines recommend specialist assessment of swallowing
This should preferably within 24 hours of admission and not greater than 72 hours after
Prior to assessment is undertaken, a patient should remain nil by mouth to prevent complications
Recommendations for patients deemed unsafe for oral intake:
Patients should receive nasogastric tube feeding, ideally within 24 hours of admission, unless they have had thrombolytic therapy
If nasogastric tube feeding is not tolerated, patients should be considered for a nasal bridle tube/gastrostomy instead
Medications need to be assessed to determine if formulations are available for nasogastric feeding, or if conversion to subcutaneous or intravenous forms are required
Nutritional support may be required for patients at risk of malnutrition post stroke, whether a result from dysphagia, poor oral health or reduced ability to self-feed due to weakness or paralysis

50
Q

Disability scales in stroke

A

Stroke can result in a number of complications and subsequent disability, therefore disability scales are often used as a measure of functional decline post event and subsequent improvement after medical intervention
Disability, often measured in terms of functional status (notably, basic activities of daily living), is often the leading cause of morbidity after stroke
After a patient is medically stabilised after a stroke, they may require transfer to a rehabilitation team for ongoing treatment depending on their level of disability
Disability is most commonly measured using the Barthel index (BI), an outcome measure for stroke
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
This index should be used to assess the functional status of a patient post stroke, and to monitor their improvement with ongoing rehabilitation to regain independence after the event

51
Q

Atrial fibrillation post-stroke

A

following a stroke or TIA it is obviously important to exclude a haemorrhage before starting any anticoagulation or antiplatelet therapy
for longer-term stroke prevention, NICE recommend warfarin or a direct thrombin or factor Xa inhibitor
the timing of when to start depends on whether it is a TIA or stroke
following a TIA, anticoagulation for AF should start immediately once imaging has excluded haemorrhage
in acute stroke patients, in the absence of haemorrhage, anticoagulation therapy should be commenced after 2 weeks. Antiplatelet therapy should be given in the intervening period. If imaging shows a very large cerebral infarction then the initiation of anticoagulation should be delayed