Stroke medicine Flashcards
1
Q
Define stroke + its pathophysiology
A
Syndrome of rapid onset focal neurological deficit lasting >24h or leading to death
Hypoperfusion (O2+glucose) to endothelial lumen - depletes ATP - impaired membrane transport - AP not generated - stroke symptoms
2
Q
What is a stroke syndrome?
A
Neurological disturbance that evolves suddenly (AP cessation), is focal (only affects neurovascular units in the concerned territory) of predominantly negative symptoms that fit into a vascular territory
3
Q
What are the typical features of a stroke syndrome?
A
- Sudden onset i.e. <2s wish
- Focal
- Predominantly negative sx i.e. loss of a function
- Hypoperfusion to a vascular territory can explain the symptoms
- Symptoms don’t migrate
- Episodes do not usually stereotype (a repeat stroke would usually be in a different part of the vessel)
4
Q
What is stereotyping and does it occur in strokes?
A
Episodic recurrence of neuro disturbance with complete resolution between, e.g. migrainous aura or focal seizure. Not typical of strokes as a repeat stroke would affect a different area
however
capsular warning syndromes + intracranial stenosis causing global hypo perfusion (e.g. postural hypotension) are both examples of when it may be part of a stroke syndrome
5
Q
Define TIA
A
Rapid onset of symptoms that usually recovers within seconds-minutes, recovery is complete, and no infarction occurs
Usually due to microemboli from a carotid thrombus or atheromatous plaque
Is a retrospective diagnosis but a notice of an impending stroke/MI
6
Q
How may a TIA present based on where the ischaemia occurs?
A
- Anterior circulation-carotids: motor weakness/heaviness, hemisensory deficit (numb, aphasia, monocular blindness, amaurosis fugax, hemianopia)
- Posterior circ-vertebrobasilar: vertigo, diplopia, ataxia, amnesia, hemisensory loss, hemianopic/bilateral vision loss, paresis, LoC (rare), transient global amnesia
- Limb-shaking TIA -severe carotid stenosis
- Source of emboli: carotid artery bruit, valvular heart disease, AF, recent MI
7
Q
What are the risk factors for stroke events?
A
- Modifiable: smoking, HTN, DM, obesity, inactivity, dyslipidaemia, carotid artery stenosis, post-TIA, AF (responsible for 25% of strokes)
- Non-modifiable: black+Asian populations, age, genetics (e.g. SCD), being male, family history
8
Q
Outline stroke primary prevention (preventing a first episode)
A
- Risk assessment tools like QRISK2, ETHRISK
- Lifestyle - less fat, more fish, exercise moderate intensity 30m 5xweek (or whatever they safely can do), WL if fat, limit alcohol max 14U and avoid binges, STOP SMOKING
- Hypertension-NICE therapy guidance if raised
- Anti-thrombotic therapy if have had MI/other RF
- Aspirin low dose if benefits>risk (but no net effect on stroke, shouldn’t be used for stroke prevention cos bleeding but obv used for other things)
- Statin: if 20% 10y risk of stroke
- Manage AF with anticoagulant if needed
9
Q
How do you manage the risk of stroke in pt with atrial fibrillation?
A
CHADVASc - 1y risk of thrombotic event in a non-anticoagulated pt with AF. If score 0 (men) or 1 (female-only RF is female) don’t need anticoagulation
HAS-BLED - risk of major bleeding (ie needing hosp or Hb drop of 20) for a pt on anticoagulation. Point score translates to % risk
If score raised need warfarin or a DOAC (aspirin is less effective than anticoagulants and risk of bleeding means shouldn’t really be used for stroke prevention; used for MI prevention)
10
Q
What investigations are done in a stroke/TIA clinic and why?
A
- Bloods - FBC (plts), clotting, thrombophilia screen, U+E (general, renal function for drugs), LFT (general, needed for statins), CRP, lipid profile, HbA1c, ANCA (vasculitis)
- 24h ECG - see AF
- Echocardiogram - vegetations, valve incompetence, ASD/VSD
- Imaging with CT/MRI brain - evidence of infarcts, SOL. MRI better but limited by cost so only certain pt have
- Carotid artery doppler
11
Q
What are your differentials for a suspected TIA?
A
- Mass lesions
- Focal epilepsy - usually recognised by LoC
- Cerebral amyloid angiopathy - seen on imaging, anti-plt contraindicated
- Migraine with aura - esp when no headache, differentiate as positive visual aura not seen in TIA, slower onset + evolution, limb weakness is uncommon
12
Q
What is the prognosis like for TIAs?
A
- 30% have a stroke in 5y post-TIA
- 15% have an MI 5y post-TIA
- Anterior circulation TIAs have a worse prognosis
ABCD2 score - used to use to rial-stratify but now not used
13
Q
Outline the pathophysiology of ischaemic stroke
A
Hypoperfusion –> ischaemia + neuronal injury
Osmotic activity –> oedema –> can cause subfalcine/tentorial herniation
14
Q
What causes ischaemic stroke?
A
- Thrombosis e.g. atherosclerotic plaque rupture, usually secondary to HTN
- Embolism in a cerebral vessel - cardiac source (from AF thrombosis in LA, mural thrombosis post-MI, infective vegetations), athero-emboli from the ICA/CCA/aortic arch (bruits), paradoxical embolism (when a DVT enters the left heart instead of lungs via an ASD [quite common to have asymptomatic] or PFO)
- Small vessel disease - HTN or DM - LACS/gradual diffuse changes
- Rarer causes - systemic hypo perfusion (e.g. post cardiac arrest), vasculitis like GCA or APS, carotid/vertebral artery dissections (higher risk in Marfan syndrome; CF include neck/face pain + Horner syndrome + lower CN palsies; blood goes between wall layers causing emboli), venous sinus thrombosis (higher risk in pregnancy + thrombotic disorders)
15
Q
What are the features of a MCA ischaemic stroke?
A
- c/l hemiplegia (UL>LL)
- hemisensory loss
- neglect syndromes (esp if non-dominant side-usually right)
- aphasia (esp dominant side-usually left)
- eye deviation to affected side, hemianopia
- coning
Branch occlusions less severe than full occlusions
16
Q
What are the features of an ACA ischaemic stroke?
A
- C/L hemiparesis LL>UL
- Minimal sensory loss, LL>UL
- May have frontal lobe deficits - apathy, apraxia, aphasia, urinary incontinence, dysarthria
17
Q
What are the features of a PCA ischaemic stroke?
A
- Homonymous hemianopia + macular sparing (u/l)
- Cortical blindness (b/l)
- C/L hemisensory loss in the DCML modalities
- Memory deficits
- Vertigo, nausea
- Prosopagnosia (right-‘face blindness’)
- Visual agnosia (left-not recognising)
18
Q
What are the features of brainstem infarction?
A
It depends on the location irt CN nuclei, tracts + brainstem connections
- Hemi/tetraparesis - affecting CSTs
- Sensory loss - affecting sensory tracts, CN V nucleus etc
- Facial weakness - CN VII nuclei
- Dysphagia/dysarthria - CN IX + X nuclei
- Nystagmus/vertigo - vestibular connections
- Horner syndrome - sympathetic fibres
- Altered consciousness - reticular formation
- Dysarthria, ataxia, hiccups, vomiting - cerebellar connections
- Locked in syndrome - basilar artery, paralysis of all voluntary muscles except eyelid+eye movement
- Lateral medullary syndrome - PICA/vertebral artery occlusion - ipsilateral Horner’s, CN X palsy, facial sensory loss, ataxia, c/l STT sensory loss, vertigo, dysphasia
- Medial medullary syndrome - ipsilateral loss of CN XII + c/l hemiparesis
- Vertebrobasilar artery - ipsilateral CN deficits, vertigo, tinnitus, hiccups, dysarthria, dysphasia, visual problems, ataxia, crossed paraesthesias, crossed hemiplegia
19
Q
What are the features of a cerebellar infarction?
A
- DANISH
- No hemiparesis, unless part of a brainstem syndrome
- Swelling - brainstem compression/coma/obstructive hydrocephalus
20
Q
What are the features of a thalamic infarction?
A
- C/l hemiparesis + hemisensory loss
- Miotic unresponsive pupils
- Eyes deviate away from lesion
Thalamus involved in sensory system, consciousness + sleep. Supply by branches of PCA
21
Q
How may strokes of the extra cranial arteries present?
A
- ICA: neck/face pain, ipsilateral Horner’s, lower CN palsies, ipsilateral amaurosis fugax, signs of MCA stroke but collaterals often reduce infarct sign
- CCA: Horner’s, CN XII paralysis, signs of MCA infarct
- Vertebral artery: Wallenberg (lateral medullary) syndrome, neck pain, signs of PCA infarct
22
Q
What are watershed infarcts?
A
When there is infarct in the border zones between areas supplied by the ACA, MCA + PCA, due to severe cerebral hypo perfusion e.g. post-cardiac arrest
CF: complex visual loss patterns, memory loss, intellectual impairment, motor deficits, bilateral, signs of systemic hypo perfusion e.g. low BP
Comps: PVS, MCS
23
Q
Where do lacunar strokes arise?
A
Deep penetrating arteries in the white matter - affect basal ganglia, capsule, thalamus + pons
E.g. lenticulostriate artery occlusion
RF - HTN
24
Q
What are the CF of lacunar strokes?
A
- Lack of cortical signs like aphasia, agnosia
- Pure motor most common –> C/L hemiparesis
- Pure sensory –> C/L numbness/paraesthesia, usually thalamic
- Sensori-motor –> C/L hemiparesis + sensory sx
- Ataxic hemiparesis (2nd most common) –> C/L impaired coordination + weakness, LL>UL (mix of cerebellar + pyramidal)
- Dysarthria clumsy hand syndrome –> dysarthria, dysphagia, C/L face+hand weakness
- Hemiballismus –> infarct in sub thalamic nucleus causing c/l involuntary large flinging movements of arm/leg
25
What is multi-infarct dementia?
Multiple lacunar infarcts --> generalised intellectual loss with dementia, pseudo bulbar palsy + shuffling gait
26
What imaging is done in suspected stroke?
* MRI more sensitive for underlying causes
| * CT rapid, do non-contrast CT urgently to rule out haemorrhage, but ischaemic changes often not seen for 24-48h
27
What abnormalities may be seen on a non-contrast CT in stroke?
* Haemorrhage-bright white
* Early infarction: hyper dense artery (clot), early parenchymal changes (hypodense grey matter, loss of GM/WM differentiation cos of oedema from fluid/electrolyte shifts, effacement of sulci), increased attenuation
* 12-24h - hypodense
* After days - hyperdense
Can also be used to see a cause --> cardiac emboli, small indicates lacunar, watershed ischaemia (indicates carotid disease or intracranial stenosis), deep bleeds in BG/cerebellum (often HTN)
28
What are the rare causes of stroke?
Polycythaemia, hyper viscosity syndromes, antiphospholipid syndrome, low dose oestrogen-containing contraceptives, migraine, vasculitis (SLE, GCA), amyloidosis (cerebral haemorrhage), hyperhomocysteinaemia (thrombotic), neurosyphilis, mitochondrial diseases, sympathomimetic drugs e.g. cocaine
29
What is amaurosis fugax?
Sudden transient LoV in one eye, may be able to see the embolus if in retinal arteries
May occur in TIA - indicates ICA and is a warning of an impending ICA stroke
30
What is the ischaemic penumbra?
An area surrounding the infarct that is swollen + ischaemic so non-functioning but still structurally intact, so can regain function with revascularisation
31
Use Virchow's triad to explain why strokes occur
* Stasis - AF
* Altered blood components - dehydration, pregnancy, cancer, syndromes like APS
* Damaged vessel wall - atherosclerosis, GCA, dissection
32
What are the types of dysphasia?
Broca (expressive) - lesion to inferior frontal gyrus (superior MCA)
Wernicke (receptive) - lesion to superior temporal gyrus (inferior MCA)
Conduction aphasia - lesion to arcuate fasciculus, fluent speech but abnormal comprehension + poor repetition (whereas Broca + Wernicke's repetition is good)
Transcortical sensory aphasia-lesion to temporo-occipital region
33
Left MCA stroke
Right hemiplegia with face+arms>legs, dysphasia
34
Right MCA stroke
Left hemiplegia with face+arms > legs, visual/sensory neglect, denial of disability
35
Vascular basis + clinical features of TACS
Hemiparesis/hemisensory deficit of face arm + leg
AND
homonymous hemianopia
AND
higher cerebral dysfunction (dysphasia, visuospatial disorder)
Proximal MCA or ICA occlusion, large stroke affecting areas supplied by both the MCA+ACA
36
Vascular basis + clinical features of PACS (partial anterior circ stroke)
Two of hemiparesis, higher cortical dysfunction or hemianopia; or isolated higher cortical dysfunction
Branch of MCA occluded-only part of anterior circulation compromised
37
Vascular basis + clinical features of POCS (posterior circ stroke)
* CN palsy AND c/l motor/sensory deficit
* B/l motor/sensory deficit
* Conjugate eye movement disorder e.g. horizontal gaze palsy
* Cerebellar dysfunction
* Isolated homonymous hemianopia (PCA)
Vertebral, basilar, cerebellar or posterior cerebral vessels
38
Vascular basis + clinical features of LACS (lacunar syndrome)
Pure motor/pure sensory/sensorimotor/ataxic hemiparesis
* unilateral
* motor weakness may affect face/arm/leg or all of them
Due to lenticulostriate branches of the MCA, supply to the brainstem or deep WM supply
39
What is the TOAST classification for stroke?
Another way to classify ischaemic stroke, based on the cause e.g. large artery atherosclerosis, cardio-embolic, small vessel disease or undetermined/multiple causes
40
Outline the pathophysiology of haemorrhagic stroke
Blood breaks parenchyma - WM fibres split - neurones don't function - blood expands causing more damage/trans-tentorial coning
Cerebellar haematomas can cause obstructive hydrocephalus or coma from brainstem compression
41
What causes haemorrhage strokes?
* Intracerebral haemorrhage
1. Chronic HTN causing ruptured micro aneurysms (Charcot-Bouchard aneurysms) + degeneration small deep arteries, usually causes a massive haemorrhage
2. Cerebral amyloid angiopathy (elderly): lobar ICH, esp posterior, a/w particular ApoE subtypes
3. Secondary causes: AV malformations (commonest cause in children), aneurysms, dural venous thrombosis, CNS infection, stimulant drugs, anticoagulant drugs, thrombolysis, haemorrhagic transformation of a large ischaemic infarct
* Subarachnoid haemorrhage (5%, can also be caused by trauma but this wouldn't be a stroke)
1. Ruptured berry aneurysm at branching points in CoW, round saccular aneurysms
2. Ruptured AVM
3. Other: cortical thrombosis, neoplasm, infection
42
How would you differentiate ischaemic from haemorrhagic strokes if you didn't have a CT scanner?
* No reliable CF to distinguish
* ICH more often causes severe headache, coma or meningism
* On anticoagulants - ICH until proven otherwise
* SAH: sudden thunderclap headache, occipital, vomiting, neck stiffness, papilloedema, subhyaloid haemorrhage (on fundoscopy)
* Berry aneurysms: may have h/o sentinel headaches from small bleeds, may LoC, may have h/o ADPKD/NF1/Marfans etc
43
What findings are seen on imaging after haemorrhagic stroke?
CT: seen immediately, intraparenchymal/intraventricular/subarachnoid bleed.
* Hypodense lesion in hyper acute phase
* Hyperdense lesion + hypodense oedema in acute phase
* May show midline shift
Later - MRI + MRA to look for aneurysms or AVM
LP - for suspected SAH, do after 12h to see xanthochromia (rather than blood from trauma of LP)
44
Outline the management of haemorrhagic stroke
* Non-contrast CT to confirm haemorrhage
* Medical (stroke unit or ICU): reverse anticoagulation (e.g. warfarin -give IV vit K+prothrombin complex concentrate/FFP), control HTN, reduce ICP, in SAH you give IV CCB for 3w (nifedipine, reduces vasospasm as this can induce ischaemic stroke)
* Surgical: cerebellar needs urgent craniotomy + clot evacuation; for others depends on neurosurgery opinion. Hydrocephalus may have ventricular drain/serial LPs/VP shunt, SAH aneurysms may have clipping/endovascular coiling to prevent re-bleeding
45
What are stroke mimics and when would you suspect them?
Conditions that resemble an acute stroke
May suspect if can't fit symptoms into a presentation or the syndrome is gradual, non-focal, mostly positive and shows evolution of symptoms or stereotyping
Some are recognised on imaging easily e.g. MS/SDH, some diagnosed clinically e.g. TIA/vestibular disorders/syncope, others are more subtle and need specialist assessment e.g. complex migraine with aura/functional syndromes
46
Give examples of stroke mimics
```
*HEMI most common:
Hypoglycaemia
Epilepsy e.g. Todd's palsy (post-ictal paresis) or focal seizures that stereotype
Migraine (cortical spreading depression)
Intracranial infection/tumour
```
*Others: syncope, sepsis, peripheral vestibular disorder, EDH/SDH, drugs/alcohol, transient global amnesia, functional syndromes, apparent neurological deficit
47
What are stroke chameleons?
Conditions where presentation suggest another cause, but it is actually a stroke!
48
Give some examples of stroke chameleons
* Venous infarct - gradual onset, may have seizure
* Small cortical strokes - may present as peripheral nerve lesions
* Limb shaking TIA - may look like a movement disorder/seizure
* Occipital stroke - if predominant feature is confusion/delirium
* Stroke amnestic syndromes
* Stroke that mimics vestibular dysfunction
49
What investigations are done in suspected stroke?
* CT brain non-contrast
* Bloods-FBC for plt/polycythaemia, ESR (GCA), glucose, lipids, U+E + LFT
* ECG - rule out AF
* Carotid doppler studies in anterior circ strokes to identify stenosis needing surgery
* Others done if young.no cause: CT/MR angiography, prolonged cardiac monitoring, echo, carotid USS, vasculitis screen, APS antibodies, thrombophilia screen
* MRI brain - good for underlying causes, mimics like demyelination
* LP - definitive test in SAH if CT inconclusive. Xanthochromia, high opening pressure, high RBC, normal glucose
50
What is the cause of deep vs lobar bleeds?
Deep - HTN
| Lobar - secondary causes e.g. mass lesions
51
What is apparent neurological deficit?
Area of damaged brain - residual scar tissue (gliosis) forms new connections that can function normally if physiology is optimal, but if something offsets it e.g. infection/hypotension/hypoglycaemia a stroke picture can damage
52
What do you look for on the immediate CT head done in suspected stroke?
Pipes, parenchyma, perfusion + penumbra
ASPECTS score: different areas of MCA given a score based on if normal or not, out of 10 where 10/10=normal and 0/10=extensive ischaemia (1 point deducted for each abnormal area)
53
What immediate management is done once haemorrhagic stroke is confirmed?
* Do not give drugs that affect clotting
* Control BP, control clotting, may evacuate haematoma/insert drains - as they cause RICP
* Anticipate + prevent comps
* Neurosurgery discussion - balance between stability _ accessibility e.g. thalamus isn't accessible
54
What is the purpose of thrombolysis and how is it done?
Reduction of infarct size to reduce disability - activate plasminogen to form plasmin - degrades fibrin - breaks up thrombi
Indicated where there is an acute ischaemic stroke + persisting neuro deficit + well-established timing of onset
IV alteplase given within 4.5h (preferably 3h) of sx, bolus over 1min then over 1h
55
What are the contraindications to thrombolysis?
* Historical: stroke/head trauma in past 3m, prev ICH, major surgery in past 14d, GI/GU bleeding in last 21d, arterial puncture at non-compressible site/LP in past 7d
* Clinical: rapidly improving sx, minor/isolated neuro signs, persistent HTN, pregnancy, active bleeding, active #
* Lab: plt <100, high/low glucose, INR>1.7, on warfarin, elevated PTT if on heparin
56
What outcomes are there after thrombolysis?
1/3 improve
1/10 make a complete recovery
1/20 get a symptomatic haemorrhage
57
What are the complications of thrombolysis?
* Extracerebral haemorrhage-thin thready pulse, low BP, melaena/haematemesis, distended abdomen
* Intracerebral haemorrhage-neuro decline, new headache, rising BP, N+V
* Anaphylaxis
58
What management is done for ischaemic strokes not eligible for thrombolysis?
* Aspirin 300mg per day for 2w then switch to clopidogrel
* Mechanical thrombectomy
* Decompressive hemicraniectomy
59
Mechanical thrombectomy
Emerging, plans to make this future of care similar to PCI for MI but currently only done in specialist centres --> used if large vessel occlusion within 6h of sx
60
What is the role of the NIHSS score?
Used to grade severity of stroke-related neurological deficit
Used in assessment + prediction of prognosis + charting recovery
61
Decompressive hemicraniectomy
Do within 48h to manage malignant oedema in younger/fitter patients in large MCA strokes to prevent coning
Can preserve life, but balance with significant dependency
62
What management is undertaken in the stroke unit?
* Plan discharge early on-shouldn't be kept longer than necessary, need proactive plan for rehab
* Antiplatelets
* Anticoagulants
* Treat BP e.g. enalapril if high or midodrine if low (permissive hypertension to ensure adequate perfusion) -- aim for <130/90
* Lipid control total cholesterol <4, LDL <2
* Glycaemic control HbA1c < 7
* Carotid endarterectomy
* MDT: asses swallow, VTE prophylaxis, treat medical complications or causes like AF, investigate RF, begin PT/OT input, secondary stroke prevention, early mobilisation, pt education + support, nutritional support if unsafe swallow with NG/PEG
63
Antiplatelets after ischaemic stroke
300mg aspirin
* Immediately in suspected TIA or on confirmation of ischaemic stroke
* 24h post-thrombolysis
* Aspirin for 2w, then switch to clopidogrel
64
Anti-Thrombotic + anticoagulant therapy after ischamic stroke
Aspirin initially then switch to clopidogrel after 2w for antiplatelets
Anticoagulant:
* Assess if needed using CHADVASC + HASBLEd
* Started immediately in TIA, after a few days for small strokes or after 2w for large strokes
* Wait 2w in large strokes as infarcted area at higher risk of bleeding
* If AC contraindicated but have AF can refer for left atrial appendage closure
65
Carotid endarterectomy after stroke
Do within 2w for symptomatic disease with >50% occlusion of lumen
Reduce recurrent stroke by BP control + statins + dual anti platelet therapy
Can also try to stabilise the plaque if surgery not suitable, as it is an embolic source
66
Outline the process of stroke rehabilitation
* Specialised unit e.g. community hospital, or in community
* In hospital sort out transfers, positioning, swallowing, orientation, pressure areas, continence, communication, nutrition, hydration
* Vision: functional task practice for neglect, orthoptics, eye movement therapy for hemianopia
* Memory: consistent environment + routines, aids like medication alarms
* Emotional: opportunity to talk, support + educate, manage depression/anxiety
* Swallowing: screen for dysphagia, mouth care to reduce aspiration, nutrition support
* Communication: SALT, minimise environmental barriers, appreciate their frustration
* Motor: strength + balance training, walking practice, use of walking aids, splints for high tone
* Self-care: OT assess ADLs, equipment, home adaptations
* Management of return to wider participation in society
* Monitor for comps - mood, bowel + urine, progress of stroke impairments, DVT, blood results
* Impact on pt + family: education + support to understand impact + extent of deficits, recognising these vary over time/setting, help train communication e.g. using props
67
Outline secondary stroke prevention
Begin within a week of the stroke
* Lifestyle
* Review RF
* Stroke register - annual FU
* Lifelong anti-thrombotic therapy with clopidogrel or if CI dipyridamole+/- aspirin (preferred if have also had MI)
* Anti-lipid unless CI usually simvastatin
* Carotid artery endarterectomy or stenting
* Anti-hypertensive: lower BP slowly
68
When can you drive after a stroke or TIA?
1m - normal driving
1y - HGV
Inform DVLA if there are persisting deficits (don't need to inform if no residual neuro deficit)
69
What aspects of palliative care apply to stroke?
Pain control, mouth + skin care, agitation, airway secretions, communication w families
Usually feed orally + accept risk of aspiration as less invasive
70
What is the Modified Rankin Scale?
A measure of global disability to assess baseline function + evaluate outcomes.
0-no sx
1-some sx but can do everything
2-slight disability, can look after own ADLs but not all previous activities
3-moderate disability, needs some help but can walk unassisted
4-moderate to severe, can't attend to own bodily needs without assistance, needs help to walk
5-severe disability, constant nursing care, bedridden, incontinent
6-death
71
What is the Rosier scale?
A tool used to recognise stoke in the emergency department, for initial differentiation of acute stroke from stroke mimics
72
How is the stroke prognosis determined?
* Tools like NIHSS, OCSP class
* Pattern + number of complications
* Recovery trajectory: indicates neuroplasticity @ site of damage, continues until pt reaches their plateau.
Generally TIA/minor stroke early high functioning plateau, TACS - early low functioning plateau, or most moderate strokes medium functioning plateau reached after a delay
73
What is the ABCD2 prognostic score?
Used to be used for TIA, was in workbook but now NICE don't recommend it. If score is 4 high risk of a stroke so have aspirin 300mg daily + specialist assessment
* Age 60+ (1)
* BP >140/90 (1)
* Clinical features: 2 for u/l weakness, 1 if speech disturbance
* Duration: 2 for >1h, 1 for 10-59min
* Diabetes (1)
74
List the early complications of stroke
* Death - if affects brainstem or causes RICP
* RICP -haematoma expansion, malignant oedema, haemorrhagic transformation, hydrocephalus
* Recurrent stroke due to unaddressed RF, or suboptimal physiology causing loss of ischaemic penumbra
* Infections: aspiration pneumonia, UTI (poor hydration or incomplete emptying from constipation/supine)
* Immobility: VTE, constipation, pressure ulcers
* Visual impairment
* Bladder/bowel problems
* Swallow impairment-dehydration, malnutrition, aspiration
* Seizure
* Vasospasm 5-7d after haemorrhagic can lead to ischaemic
* SIADH
75
List the long-term complications of stroke
* Death
* cognitive dysfunction-concentration, memory, spatial awareness, apraxia, executive function e.g. planning
* mood changes - mood disorders, disturbed social interaction, disinhibition, aggression
* bladder, bowel or sexual dysfunction
* inability to complete ADLs
* vascular dementia
* MSK: spasticity, balance/tone/movement/sensation
* secondary epilepsy
* post stroke pain + fatigue: multifactorial like the spasticity, injury sustained from stroke, neuropathic pain, fatigue from pain/pain from fatigue, poor sleep, meds, brain cell damage
76
Outline the provision for stroke services in the NHS
* Rapid access TIA clinics
* Hyperacute stroke units with access to neurosurgical + interventional radiology services
* Acute stroke wards
* Inpatient rehab
* Outpatient rehab inc early supported discharge services
* Outpatient stroke clinics
77
How would you treat a clinically suspected TIA?
300mg aspirin immediately for clinically suspected TIA (+ gastroprotection if indicated) - unless bleeding disorder/on anticoagulant/already on low dose aspirin
Refer for specialist review within 24h if has happened within the last week, or if happened >1w ago then refer within 7d
Don't drive until have been seen
After specialist is usually clopidogrel daily (or aspirin + dipyridamole 2nd line), carotid endarterectomy if had TIA in carotid territory and stenosis >70%
